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Title: A System of Practical Medicine By American Authors, Vol. III
       Diseases of the Respiratory, Circulatory, and HÃ¦matopoietic Systems

Author: Various

Editor: William Pepper
        Louis Starr

Release Date: October 17, 2016 [EBook #53305]

Language: English

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*** START OF THIS PROJECT GUTENBERG EBOOK SYSTEM OF PRACTICAL MEDICINE, VOL 3 ***




Produced by Ron Swanson





A SYSTEM OF PRACTICAL MEDICINE.

BY AMERICAN AUTHORS.




EDITED BY WILLIAM PEPPER, M.D., LL.D.,

PROVOST AND PROFESSOR OF THE THEORY AND PRACTICE OF MEDICINE AND OF
CLINICAL MEDICINE IN THE UNIVERSITY OF PENNSYLVANIA.


ASSISTED BY LOUIS STARR, M.D.,

CLINICAL PROFESSOR OF DISEASES OF CHILDREN IN THE HOSPITAL OF THE
UNIVERSITY OF PENNSYLVANIA.




VOLUME III.

DISEASES OF THE RESPIRATORY, CIRCULATORY, AND HÆMATOPOIETIC SYSTEMS.




PHILADELPHIA:
LEA BROTHERS & CO.
1885.




Entered according to Act of Congress, in the year 1885, by

LEA BROTHERS & CO.,

in the Office of the Librarian of Congress at Washington. All rights
reserved.





WESTCOTT & THOMSON,
_Stereotypers and Electrotypers, Philada._

WILLIAM J. DORNAN,
_Printer, Philada._




CONTENTS OF VOLUME III.


DISEASES OF THE RESPIRATORY SYSTEM.
                                                                   PAGE
LARYNGOSCOPY AND RHINOSCOPY. By CARL SEILER, M.D. . . . . . . . .    19

DISEASES OF THE NASAL PASSAGES. By HARRISON ALLEN, M.D. . . . . .    41

NEUROSES OF THE LARYNX. By HOSMER A. JOHNSON, M.D., LL.D. . . . .    59

ACUTE CATARRHAL LARYNGITIS (FALSE OR SPASMODIC CROUP).
  By ABRAHAM JACOBI, M.D. . . . . . . . . . . . . . . . . . . . .    92

PSEUDO-MEMBRANOUS LARYNGITIS. By ABRAHAM JACOBI, M.D. . . . . . .   100

DISEASES OF THE LARYNX. By LOUIS ELSBERG, A.M., M.D.  . . . . . .   109

DISEASES OF THE TRACHEA. By LOUIS ELSBERG, A.M., M.D. . . . . . .   133

TRACHEOTOMY. By GEORGE M. LEFFERTS, A.M., M.D.  . . . . . . . . .   145

DISEASES OF THE BRONCHI. By N. S. DAVIS, M.D., LL.D.  . . . . . .   164

BRONCHIAL ASTHMA. By W. H. GEDDINGS, M.D. . . . . . . . . . . . .   184

HAY ASTHMA. By W. H. GEDDINGS, M.D. . . . . . . . . . . . . . . .   210

DILATATION OF THE BRONCHIAL TUBES, CIRCUMSCRIBED AND DIFFUSED.
  By SAMUEL C. CHEW, M.D. . . . . . . . . . . . . . . . . . . . .   227

EMPHYSEMA. By SAMUEL C. CHEW, M.D.  . . . . . . . . . . . . . . .   232

COLLAPSE OF THE LUNG (ATELECTASIS). By SAMUEL C. CHEW, M.D. . . .   250

CONGESTION AND OEDEMA OF THE LUNGS (HYPOSTATIC PNEUMONIA).
  By SAMUEL C. CHEW, M.D. . . . . . . . . . . . . . . . . . . . .   258

HÆMOPTYSIS. By WILLIAM CARSON, M.D. . . . . . . . . . . . . . . .   266

PULMONARY APOPLEXY. By WILLIAM CARSON, M.D. . . . . . . . . . . .   293

ABSCESS OF THE LUNG. By WILLIAM CARSON, M.D.  . . . . . . . . . .   296

GANGRENE OF THE LUNG. By WILLIAM CARSON, M.D. . . . . . . . . . .   301

CROUPOUS PNEUMONIA. By ALFRED L. LOOMIS, M.D., LL.D.  . . . . . .   307

CATARRHAL PNEUMONIA. By WILLIAM PEPPER, M.D., LL.D. . . . . . . .   353

PULMONARY EMBOLISM. By BEVERLEY ROBINSON, M.D.  . . . . . . . . .   373

PULMONARY PHTHISIS (FIBROID PHTHISIS OR CHRONIC INTERSTITIAL
  PNEUMONIA). By AUSTIN FLINT, M.D. . . . . . . . . . . . . . . .   391

SYPHILITIC DISEASE OF THE LUNG. By EDWARD T. BRUEN, M.D.  . . . .   447

PNEUMONOKONIOSIS. By EDWARD T. BRUEN, M.D.  . . . . . . . . . . .   454

CANCER OF THE LUNGS. By EDWARD T. BRUEN, M.D. . . . . . . . . . .   460

PULMONARY HYDATIDS. By EDWARD T. BRUEN, M.D.  . . . . . . . . . .   466

ACUTE MILIARY TUBERCULOSIS. By JOHN S. LYNCH, M.D.  . . . . . . .   472

DISEASES OF THE PLEURA. By FRANK DONALDSON, M.D.  . . . . . . . .   483


DISEASES OF THE CIRCULATORY SYSTEM.

DISEASES OF THE SUBSTANCE OF THE HEART. By WILLIAM OSLER, M.D.  .   601

ENDOCARDITIS AND CARDIAC VALVULAR DISEASES.
  By ALFRED L. LOOMIS, M.D., LL.D.  . . . . . . . . . . . . . . .   639

CYANOSIS AND CONGENITAL ANOMALIES OF THE HEART AND GREAT VESSELS.
  By MORRIS LONGSTRETH, M.D.  . . . . . . . . . . . . . . . . . .   687

CARDIAC THROMBOSIS. By BEVERLEY ROBINSON, M.D.  . . . . . . . . .   718

NEUROSES OF THE HEART. By AUSTIN FLINT, M.D.  . . . . . . . . . .   747

DISEASES OF THE PERICARDIUM. By J. M. DACOSTA, M.D., LL.D.  . . .   769

THE OPERATIVE TREATMENT OF PERICARDIAL EFFUSIONS.
  By JOHN B. ROBERTS, A.M., M.D.  . . . . . . . . . . . . . . . .   794

DISEASES OF THE AORTA. By G. M. GARLAND, M.D. . . . . . . . . . .   800

DISEASES OF THE CORONARY, PULMONARY, SUPERIOR MESENTERIC,
  INFERIOR MESENTERIC, AND HEPATIC ARTERIES, AND OF THE COELIAC
  AXIS. By ELBRIDGE G. CUTLER, M.D. . . . . . . . . . . . . . . .   828

DISEASES OF THE VEINS. By ANDREW HEERMANCE SMITH, M.D.  . . . . .   843

THE CAISSON DISEASE. By ANDREW HEERMANCE SMITH, M. D. . . . . . .   854

DISEASES OF THE MEDIASTINUM. By EDWARD T. BRUEN, M.D. . . . . . .   861


DISEASES OF THE BLOOD AND OF THE HÆMATOPOIETIC SYSTEM.

DISEASES OF THE BLOOD AND BLOOD-GLANDULAR SYSTEM.
  By WILLIAM OSLER, M.D.  . . . . . . . . . . . . . . . . . . . .   882

DISEASES OF THE SPLEEN. By I. EDMONDSON ATKINSON, M.D.  . . . . .   951

DISEASES OF THE THYROID GLAND. By D. HAYES AGNEW, M.D., LL.D. . .   974

SIMPLE LYMPHANGITIS. By SAMUEL C. BUSEY, M.D. . . . . . . . . . .   983


INDEX.  . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   993




CONTRIBUTORS TO VOLUME III.


AGNEW, D. HAYES, M.D., LL.D.,
  Professor of Principles and Practice of Surgery in the University of
  Pennsylvania, Philadelphia.

ALLEN, HARRISON, M.D.,
  Emeritus Professor of Physiology in the University of Pennsylvania,
  Philadelphia.

ATKINSON, I. EDMONDSON, M.D.,
  Professor of Pathology and Clinical Medicine and Clinical Professor
  of Dermatology in the University of Maryland, Baltimore.

BRUEN, EDWARD T., M.D.,
  Assistant Professor of Physical Diagnosis in the University of
  Pennsylvania; Physician to Philadelphia (Blockley) Hospital; Lecturer
  on Pathology in the Woman's Medical College, Philadelphia.

BUSEY, SAMUEL C., M.D.,
  Attending Physician and Chairman of the Board of Hospital
  Administration of the Children's Hospital, Washington, D.C.

CARSON, WILLIAM, M.D.,
  Physician to and Clinical Lecturer at the Cincinnati Hospital,
  Cincinnati.

CHEW, SAMUEL C., M.D.,
  Professor of Materia Medica, Therapeutics, and Clinical Medicine in
  the University of Maryland, Baltimore.

CUTLER, ELBRIDGE G., M.D.,
  Clinical Instructor in Auscultation in the Harvard Medical School;
  Physician to Out-Patients, Massachusetts General Hospital.

DACOSTA, J. M., M.D., LL.D.,
  Professor of Theory and Practice of Medicine in the Jefferson Medical
  College, Philadelphia.

DAVIS, N. S., M.D., LL.D.,
  Professor of Principles and Practice of Medicine in the Chicago
  Medical College, Chicago.

DONALDSON, FRANK, M.D.,
  Clinical Professor of Diseases of the Throat and Chest in the
  University of Maryland, Baltimore.

ELSBERG, LOUIS, A.M., M.D.,
  Late Professor of Laryngology and Rhinology in the New York
  Polyclinic and in Dartmouth Medical College; Physician to Charity
  Hospital, Blackwell's Island (Throat Wards), New York.

FLINT, AUSTIN, M.D.,
  Professor of the Principles and Practice of Medicine and Clinical
  Medicine in the Bellevue Hospital Medical College, New York.

GARLAND, G. M., M.D.,
  Formerly Professor of Thoracic Diseases in the University of Vermont,
  and Assistant in Clinical Medicine in Harvard Medical School.

GEDDINGS, W. H., M.D.,
  Aiken, South Carolina, and Bethlehem, N.H.

JACOBI, ABRAHAM, M.D.,
  Clinical Professor of Diseases of Children in the College of
  Physicians and Surgeons, New York, etc.

JOHNSON, HOSMER A., M.D., LL.D.,
  Emeritus Professor of Practical Medicine in the Chicago Medical
  College, Chicago.

LEFFERTS, GEORGE M., A.M., M.D.,
  Professor of Laryngoscopy and Diseases of the Throat in the College
  of Physicians and Surgeons, New York; Consulting Laryngoscopic
  Surgeon to St. Luke's Hospital, etc.

LONGSTRETH, MORRIS, M.D.,
  Physician to the Pennsylvania Hospital, Philadelphia.

LOOMIS, ALFRED L., M.D., LL.D.,
  Professor of Pathology and Practice of Medicine in the University of
  the City of New York.

LYNCH, JOHN S., M.D.,
  Professor of Principles and Practice of Medicine in the College of
  Physicians and Surgeons, Baltimore.

OSLER, WILLIAM, M.D.,
  Professor of Clinical Medicine in the University of Pennsylvania;
  formerly Professor of the Institutes of Medicine in McGill
  University, Montreal.

PEPPER, WILLIAM, M.D., LL.D.,
  Professor of the Theory and Practice of Medicine and of Clinical
  Medicine in the University of Pennsylvania, Philadelphia.

ROBERTS, JOHN B., A.M., M.D.,
  Professor of Applied Anatomy and Operative Surgery in the
  Philadelphia Polyclinic and College for Graduates in Medicine.

ROBINSON, BEVERLEY, M.D.,
  Clinical Professor of Medicine in the Bellevue Hospital Medical
  College, New York.

SEILER, CARL, M.D.,
  Instructor in Laryngoscopy in the University of Pennsylvania;
  Professor of Acoustics and Vocal Physiology at the National School of
  Oratory, Philadelphia.

SMITH, ANDREW HEERMANCE, M.D.,
  Professor of Therapeutics and Clinical Medicine in the New York
  Post-Graduate Medical School; Physician to the Presbyterian Hospital,
  New York.




ILLUSTRATIONS.

FIGURE                                                             PAGE
 1. LARYNGEAL MIRROR . . . . . . . . . . . . . . . . . . . . . . .   21

 2. HEAD REFLECTOR . . . . . . . . . . . . . . . . . . . . . . . .   23

 3. SEILER'S ELECTRIC ILLUMINATOR FOR THE LARYNGOSCOPE . . . . . .   24

 4. POSITION OF HAND IN HOLDING THE LARYNGEAL MIRROR . . . . . . .   27

 5. SECTION OF THE HEAD, SHOWING THE POSITION OF LARYNGEAL MIRROR
      IN THE PHARYNX . . . . . . . . . . . . . . . . . . . . . . .   27

 6. ELSBERG'S SPONGE-HOLDER AND EPIGLOTTIS FORCEPS . . . . . . . .   29

 7. LARYNGEAL IMAGE DURING RESPIRATION . . . . . . . . . . . . . .   31

 8. LARYNGEAL IMAGE DURING PHONATION . . . . . . . . . . . . . . .   31

 9. LARYNGOSCOPIC DIAGRAM, SHOWING VOCAL CORDS WIDELY DRAWN APART,
      AND THE POSITION OF THE VARIOUS PARTS DURING QUIET BREATHING   31

10. THE SAME, SHOWING APPROXIMATION OF VOCAL CORDS AND POSITION OF
      THE VARIOUS PARTS DURING VOCALIZATION  . . . . . . . . . . .   31

11. VERTICAL SECTION OF THE HEAD . . . . . . . . . . . . . . . . .   33

12. NASAL SPECULUM . . . . . . . . . . . . . . . . . . . . . . . .   36

13. BOSWORTH'S NASAL DILATOR . . . . . . . . . . . . . . . . . . .   36

14. SEPTOMETER FOR MEASURING THICKNESS OF NASAL SEPTUM . . . . . .   37

15. FOLDING TONGUE DEPRESSOR . . . . . . . . . . . . . . . . . . .   38

16. COHEN'S TONGUE DEPRESSOR . . . . . . . . . . . . . . . . . . .   38

17. JARVIS'S RHINOSCOPIC MIRROR AND TONGUE DEPRESSOR . . . . . . .   39

18. RHINOSCOPIC IMAGE  . . . . . . . . . . . . . . . . . . . . . .   39

19. SHOWING ANTERO-POSTERIOR SECTION OF BONES OF THE FACE IN
      POSITION . . . . . . . . . . . . . . . . . . . . . . . . . .   48

20. BELLOCQ'S CANULA . . . . . . . . . . . . . . . . . . . . . . .   52

21. ALLEN'S NASAL FORCEPS  . . . . . . . . . . . . . . . . . . . .   54

22. THE GALVANO-CAUTERY SNARE  . . . . . . . . . . . . . . . . . .   56

23. DOUBLE BATTERY AND FLEMING ELECTRODE FOR USE IN NASAL DISEASES   56

24. TWO ELECTRODES OF PECULIAR SHAPE, FOR USE IN NASAL DISEASES  .   58

25. ACUTE TRACHEITIS: ANTERIOR WALL  . . . . . . . . . . . . . . .  135

26. SAME CASE AS FIG. 25: POSTERIOR WALL . . . . . . . . . . . . .  135

27. TUBERCULOUS ULCERATION OF THE TRACHEA, AS SEEN DURING LIFE . .  137

28. SAME CASE AS FIG. 27: POST-MORTEM APPEARANCE . . . . . . . . .  137

29. SYPHILITIC ULCERATION OF TRACHEA, AS SEEN DURING LIFE  . . . .  137

30. SAME CASE AS FIG. 29: POST-MORTEM APPEARANCE . . . . . . . . .  138

31. PAPILLOMA OF TRACHEA . . . . . . . . . . . . . . . . . . . . .  141

32. INVOLUTION OF TRACHEA, DUE TO ANEURISM . . . . . . . . . . . .  142

33. A TYPICAL CASE OF LOBAR PNEUMONIA IN THE ADULT: RECOVERY . . .  324

34. LOBAR PNEUMONIA, WITH CRISIS MARKED BY EVENING EXACERBATIONS
      REACHING NEARLY THE HIGHEST PYREXIA OF THE SECOND STAGE  . .  325

35. A TYPICAL CASE OF LOBAR PNEUMONIA IN A CHILD: RECOVERY . . . .  326

36. A CASE OF LOBAR PNEUMONIA IN A BOY TEN YEARS OLD, IN WHICH
      TEMPERATURE WAS TAKEN EVERY FOUR HOURS . . . . . . . . . . .  327

37. A TYPICAL CASE OF SENILE LOBAR PNEUMONIA . . . . . . . . . . .  327

38. CROUPOUS PNEUMONIA IN THE ADULT, TERMINATION OF, IN PURULENT
      INFILTRATION . . . . . . . . . . . . . . . . . . . . . . . .  333

39. ACUTE LOBAR (CROUPOUS) PNEUMONIA IN A CHILD: RECOVERY  . . . .  341

40. ACUTE LOBULAR (CATARRHAL) PNEUMONIA IN A CHILD: RECOVERY . . .  341

41. SPHYGMOGRAPHIC TRACING OF AORTIC OBSTRUCTION (AFTER FOSTER)  .  656

42. SPHYGMOGRAPHIC TRACING OF AORTIC REGURGITATION . . . . . . . .  662

43. SPHYGMOGRAPHIC TRACING OF AORTIC OBSTRUCTION AND REGURGITATION  662

44. SPHYGMOGRAPHIC TRACING OF MITRAL OBSTRUCTION . . . . . . . . .  667

45. SPHYGMOGRAPHIC TRACING OF MITRAL AND AORTIC OBSTRUCTION AND
      REGURGITATION  . . . . . . . . . . . . . . . . . . . . . . .  669

46. SPHYGMOGRAPHIC TRACING OF MITRAL REGURGITATION . . . . . . . .  672

47. SPHYGMOGRAPHIC TRACING OF MITRAL AND AORTIC REGURGITATION  . .  672

48. SPHYGMOGRAPHIC TRACING OF TRICUSPID REGURGITATION  . . . . . .  679

49. ROBERTS'S PERICARDIAL ASPIRATING TROCAR  . . . . . . . . . . .  797

50. SPHYGMOGRAPHIC TRACING OF NORMAL PULSE . . . . . . . . . . . .  809

51. SPHYGMOGRAPHIC TRACING OF RIGHT AND LEFT RADIAL PULSE IN
      ANEURISM OF THE AORTA  . . . . . . . . . . . . . . . . . . .  810

52. ARCH OF AORTA DURING EARLY FOETAL LIFE . . . . . . . . . . . .  826

53. SARCOMATOUS TUMOR OF ANTERIOR MEDIASTINUM  . . . . . . . . . .  866

54. SECONDARY MYELOID SARCOMA OF MEDIASTINUM . . . . . . . . . . .  868

55. RESECTION OF STERNUM FOR REMOVAL OF ENCHONDROMA  . . . . . . .  880




DISEASES OF THE RESPIRATORY SYSTEM.


LARYNGOSCOPY AND RHINOSCOPY.     | CONGESTION AND OEDEMA OF THE LUNGS
                                 | (HYPOSTATIC PNEUMONIA).
DISEASES OF THE NASAL PASSAGES.  |
                                 | HÆMOPTYSIS.
NEUROSES OF THE LARYNX.          |
                                 | PULMONARY APOPLEXY.
ACUTE CATARRHAL LARYNGITIS       |
  (FALSE OR SPASMODIC CROUP).    | ABSCESS OF THE LUNG.
                                 |
PSEUDO-MEMBRANOUS LARYNGITIS.    | GANGRENE OF THE LUNG.
                                 |
DISEASES OF THE LARYNX.          | CROUPOUS PNEUMONIA.
                                 |
DISEASES OF THE TRACHEA.         | CATARRHAL PNEUMONIA.
                                 |
TRACHEOTOMY.                     | PULMONARY EMBOLISM.
                                 |
DISEASES OF THE BRONCHI.         | PULMONARY PHTHISIS (FIBROID PHTHISIS
                                 |   OR CHRONIC INTERSTITIAL
BRONCHIAL ASTHMA.                |    PNEUMONIA).
                                 |
HAY ASTHMA.                      | SYPHILITIC DISEASE OF THE LUNG.
                                 |
DILATATION OF THE BRONCHIAL      | PNEUMONOKONIOSIS.
  TUBES, CIRCUMSCRIBED AND       |
  DIFFUSED.                      | CANCER OF THE LUNGS.
                                 |
EMPHYSEMA.                       | PULMONARY HYDATIDS.
                                 |
COLLAPSE OF THE LUNG             | ACUTE MILIARY TUBERCULOSIS.
  (ATELECTASIS).                 |
                                 | DISEASES OF THE PLEURA.




{19}

LARYNGOSCOPY AND RHINOSCOPY.

BY CARL SEILER, M.D.


The laryngoscope is a combination of instruments designed for the
examination of the interior of the larynx and upper part of the
trachea, while the rhinoscope is a similar combination of instruments
designed to explore the posterior nasal cavity; and both are
comparatively recent inventions.

HISTORY OF THE LARYNGOSCOPE.--In medical literature before the middle
of the eighteenth century no mention is made of an instrument or
apparatus resembling the laryngoscope, but recent excavations at
Pompeii have brought to light small polished metal mirrors attached to
slender handles which are supposed to have been used to inspect the
cavities of the human body. The first authenticated attempt at
laryngoscopy and rhinoscopy was made by the distinguished French
accoucheur M. Levret in the year 1743, who invented, among other
surgical instruments, an apparatus by means of which polypoid growths
in the cavities of the nose, throat, ear, etc. could be seen, and a
ligature be passed around them for their removal.[1] This apparatus
consisted mainly of a polished metal mirror which "reflected the
luminous rays in the direction of the tumor," and on whose surface the
image of the growth was seen to be reflected. The great value of this
apparatus for the diagnosis and treatment of nasal and laryngeal
diseases was, however, not recognized, and it shared the fate of many
other valuable discoveries which were made before the world was ready
to receive them: it was forgotten.

[Footnote 1: _Mercure de France_, 1743, p. 2434.]

In 1807 a certain Dr. Bozzini, living in Frankfort-on-the-Main,
published a work describing an apparatus which he had invented for the
illumination and examination of the cavities of the human body.[2] This
apparatus consisted of a peculiarly-shaped lamp and of a number of
metal tubes, polished on their inner surface, of various shapes and
sizes adapted for the different cavities of the body. The one intended
for the examination of the larynx was bent near its end at a right
angle, and had a mirror placed at the bend, which served to throw the
light downward toward the opening of the larynx when the tube was
inserted into the mouth. When reflected light was to be used, the
interior of the tube or speculum was divided into two portions by a
longitudinal septum, and two mirrors were inserted at the bend--one for
the reflection of the light downward, and the other for receiving the
reflected image. This invention of Bozzini was treated, however, with
derision by the medical profession, probably on account of the
extravagant descriptions given of it in the papers, which were not
verified by its performances.

[Footnote 2: "Der Lichtleiter," Philipp Bozzini, _Med. und Chir. Dr._,
Weimar, 1807.]

In 1825, Cagniard de Latour, an investigator of the physiology of the
voice, made some unsuccessful attempts to examine the living larynx.[3]

[Footnote 3: _Physiologie de la Voix_, par Ed. Tournié, Paris, 1865.]

{20} Senn of Geneva in 1827 endeavored to examine the larynx of a
little girl suffering from an affection of the throat by means of a
small mirror which he had made and which he inserted into the pharynx,
but he failed to see the glottis, because, as he says, the mirror was
too small, and because he used neither direct nor reflected light to
illuminate the cavity below the mirror.[4]

[Footnote 4: _Journal de Progrès des Sciences, etc._, 1829.]

In the year 1829, Benjamin Guy Babington published[5] an account of
what he called the glottiscope, an apparatus which consisted mainly of
two mirrors. One of these was small and attached to a slender stem, and
was used to receive the image, while the other, an ordinary hand-glass,
was used to reflect the rays of the sun or ordinary daylight upon the
smaller mirror in the fauces. This combination was essentially the same
as is used at the present day in the laryngoscope, with the difference
that we now use artificial light in most instances, and a concave
mirror instead of a plane one for reflecting the light.

[Footnote 5: _Lond. Med. Gazette_, 1829, vol. iii.]

While Babington was still engaged in perfecting his instruments, a
mechanic named Selligue, who suffered from an affection of the throat,
in 1832 invented a speculum for his physician, Bennati of Paris, with
which the latter was able, as he asserted,[6] to see the vocal cords.
This instrument was similar to the one invented by Bozzini, and
consisted of a double speculum bent at right angles and carrying two
mirrors--one for illuminating the cavity, and the other for reflecting
the image. Selligue was rewarded for his efforts by a complete cure of
his affection.

[Footnote 6: _Recherches sur le Mécanisme de la Voix humane_.]

A number of others worked in the same direction, and endeavored to see
the interior of the larynx in the living subject by employing different
apparatus and methods of illumination. Thus, in 1838, Baumès of Lyons
described a mirror the size of a two-franc piece (1-1/8 inches in
diameter) as useful in examining the larynx and posterior nares.[7]
Then Liston in 1840 used a dentist's mirror,[8] and Warden of Edinburgh
employed a prism of flint glass attached to a long stem as a laryngeal
mirror.[9] In the latter part of the same year Avery of London employed
a speculum with a mirror in its end for examining the larynx, using as
an illuminator a concave reflector with a central opening, which was
supported by a frame to be worn on the head of the operator.[10]

[Footnote 7: _Compte Rendu des Travaux de la Société de Médecine de
Lyons_, 1836-38.]

[Footnote 8: _Practical Surgery_, 1840.]

[Footnote 9: _Lond. Med. Gazette_, vol. xxiv. p. 256.]

[Footnote 10: _Med. Circ._, June, 1862.]

Up to this time all efforts at laryngoscopy had been made with a view
to diagnose diseases of the larynx, with the exception of those made by
Latour. In the year 1854, however, Signor Manuel Garcia of London,
without any knowledge of previous efforts, conceived the idea of
studying the changes in the larynx during phonation in his own throat.
For this purpose he placed a small dentist's mirror against the uvula
and reflected the rays of the sun into his mouth and upon the small
mirror by means of a hand-glass held in the other hand. By arranging
his position in relation to the sun in such a manner that he could see
the reflected image of the small mirror in his throat in the
hand-glass, and in it the illuminated image of his larynx, after a few
ineffectual attempts his efforts at auto-laryngoscopy were crowned with
such success that he was enabled to study the movements of the vocal
cords during phonation, and accurately describe the registers of the
voice in a paper read before the Royal Society of London in 1855.[11]
Although Garcia was the first who practised laryngoscopy successfully,
his communication to the Royal Society attracted little attention, and
would have been forgotten if it had not been that, in 1857, Tuerk of
Vienna, having heard of Garcia's paper, began to use the laryngeal
mirror on the patients in the K. K. Algem. Krankenhaus for {21}
diagnostic purposes.[12] At first he was not very successful in his
attempts, and began to experiment with laryngeal mirrors of different
sizes and shapes. While thus engaged Czermak borrowed Tuerk's mirrors,
and modified them until he succeeded in the greater number of cases in
seeing the vocal cords,[13] using artificial light for illuminating the
larynx. Meanwhile, Tuerk continued his experiments, and also succeeded
in almost all cases of throat disease which came to his department of
the hospital in seeing the interior of the larynx and in treating the
lesions. Both Tuerk and Czermak improved their apparatus, and
especially the latter, who by substituting artificial light for
sunlight, and by inventing a number of different illuminating
apparatuses, has given us the laryngoscope in the form in which it is
used at the present day. It is but natural that Tuerk should have
claimed priority in the successful use of this instrument, and in
consequence of this claim a controversy was carried on for a number of
years in the medical press between him and Czermak, which at times
became quite spirited, but which left Czermak master of the field. In
the winter of 1858-59, Madam E. Seiler, having heard of Czermak's
experiments, had a laryngeal mirror constructed from his description,
practised laryngoscopy successfully on herself and others, among them
the writer, with a view to study the physiology of the voice. Her
efforts being crowned with success, she was able not only to verify
Garcia's observations in regard to the registers, but also discovered
the so-called head register of the female voice, as well as two small
cartilages in the vocal cords.[14]

[Footnote 11: _Proc. Royal Society of London_, vol. vii. No. 13, 1855.]

[Footnote 12: _Zeitschrift der Ges. der Aerzte zu Wien_, April, 1858.]

[Footnote 13: _Wien. Medicin. Wochenschrift_, March, 1858.]

[Footnote 14: _Altes und Neues_, Leipzig, 1861.]

HISTORY OF THE RHINOSCOPE.--Rhinoscopy, or the art of viewing the
naso-pharyngeal space by placing a small mirror behind the velum
palati, naturally suggested itself almost as soon as any attempts at
laryngoscopy were made, but in the literature we find that Bozzini was
the first to clearly express the idea.[15]

[Footnote 15: _Loc. cit._]

A number of years later Wilde endeavored to see the opening of the
Eustachian tubes by means of a small mirror: an account of these
experiments he published in his famous work on the diseases of the ear.

In 1836, Baumès used the rhinoscope, and claimed to have seen
ulcerations in the naso-pharyngeal cavity.[16] It remained, however,
for modern times to develop this field of research, and it is again
Czermak whom we have to thank for the perfection of this valuable means
of diagnosis.

[Footnote 16: _Loc. cit._]

THE LARYNGOSCOPE.--The laryngoscope as it is used at the present day,
both by the specialist and the general practitioner of medicine,
consists of a so-called laryngeal mirror and of an illuminating
apparatus more or less complicated. The laryngeal mirror is a small
circular glass mirror mounted in a metal frame varying in size from ¾
inch to 1½ inches in diameter, and attached to a wire stem at an angle
of 120°. This stem, about 4 inches in length and about 1/10 inch in
thickness, should be soldered to the back of the mirror in such a
manner that the rim of the frame forms the angle with the stem, and
should not be below it, as this would increase the diameter of the
instrument without increasing its reflecting surface. The stem is made
to slide into a hollow handle of wood, ivory, or ebonite, and is
clamped at any desired length by a set-screw. This arrangement is
preferable to having the stem permanently fixed in the handle, inasmuch
as the stem can be pushed entirely into it, thus economizing space and
rendering the instrument more portable, and also allowing an adjustment
of the length of the stem when in use. The handle should be 4 inches in
length, and of the thickness of an ordinary lead-pencil (Fig. 1).

[Illustration: FIG. 1. Laryngeal Mirror.]

Mirrors of various shapes have been used, but it has been found that
the circular form is the one most easily borne by the patient, and can
be used in {22} a greater number of cases than any other shape, at the
same time giving the largest reflecting surface for its size. However,
in cases where an hypertrophy of the tonsils is present an oval mirror
can be introduced between the protruding glands more easily than a
round one.

This laryngeal mirror, however, would be of little or no value as an
instrument of diagnosis if used by itself, for in order to see the
cavity of the larynx it must be illuminated, lying as it does far below
the level of the back of the tongue; and this cannot be done
satisfactorily by merely allowing ordinary daylight to fall into the
oral cavity. It becomes, therefore, necessary to use a stronger light
to illuminate the larynx, and for this purpose either direct or
reflected artificial or sunlight may be used.

Direct illumination, by allowing a strong artificial light or sunlight
to fall into the patient's mouth, although it is used by several of the
eminent laryngologists of Europe, is both inconvenient and
unsatisfactory, because the observer must either place his head in the
path of the light in order to be able to see the surface of the
laryngeal mirror, as in the case when sunlight is used, or he must
place the lamp, candle, or other source of light between himself and
the patient, which materially interferes with the freedom of his
motions. For these reasons reflected light is now almost universally
employed in laryngoscopy.

Reflected light may be obtained by throwing the light of a lamp,
candle, gas-jet, or light from any other source into the mouth of the
patient by means of a round concave reflector. This concave
mirror--which, when made of glass, should be silvered and not backed
with amalgam--is from 3 to 4 inches in diameter, and should have a
focus of from 12 to 14 inches. The metal frame in which it is mounted
is attached by means of a ball-and-socket joint to some contrivance by
which it can be supported on the observer's head or be attached to the
source of illumination if a stationary artificial light, such as a
gas-lamp, is used at the physician's office.

A variety of devices for fastening the reflector on the head of the
observer is in use, among which the head band, introduced by Cramer,
will be found the most serviceable. It consists of a broad strap of
some strong material which passes around the head and is fastened at
the back by a buckle. To the part of the band or strap resting on the
forehead is attached a padded plate, to which the reflector is fastened
with its ball-and-socket joint (Fig. 2). The reflector usually either
has a small hole in the centre or a small space in the centre is left
unsilvered. This opening is intended to be brought before the pupil of
one or the other eye of the observer in such a manner that the line of
vision and that of light have exactly the same direction. Using the
reflector in this way like the reflector of the ophthalmoscope, it is
easier to obtain the image of the larynx well illuminated, but with the
great disadvantage of {23} monocular vision, which makes all objects
appear on the same plane and prevents a correct interpretation of
distances--a very important point in laryngoscopy. It will therefore be
found more advantageous to place the reflector on the forehead, and
from thence reflect the light into the patient's larynx. Both eyes may
thus be employed in viewing the laryngeal image, and a correct idea of
the relations of parts in regard to distance may be formed.

[Illustration: FIG. 2. Head Reflector.]

The line of vision and the path of the beam of light in order to obtain
the best results should be in the same plane as though the light
emanated from the pupil of the observer; but practically the position
of the reflector upon the forehead is nearly as good as when the hole
in it is brought before the eye, because a line drawn from the pupil of
the eye to the laryngeal mirror, and a line from the reflector upon the
forehead to the mirror, do not form an angle sufficient to make any
very great difference in the reflection of the light downward, and very
little difficulty will be experienced in obtaining the desired image.

The head reflector should be concave when artificial light or ordinary
daylight is used, but be plane when direct sunlight is employed, for
the concentration of the sun's rays by a concave reflector produces so
much heat as to become painful to the patient.

THE SOURCE OF LIGHT.--As an artificial source of light a candle, coal
oil lamp, gas-flame, or incandescent electric lamp suffices for
ordinary purposes. But frequently it is desirable to have a much
stronger light than can be obtained without concentration, and several
forms of apparatus for concentrating artificial light have been
constructed and are in use. Among these, Tobold's lamp and Mackenzie's
light concentrator are the most convenient and most universally used.

Tobold's lamp consists of a brass tube containing several lenses, which
are placed, one before the other, at such distances as to give the
greatest possible amount of concentration of light. The back part of
the tube is closed, while near the end two large holes are cut in its
sides opposite to each other, through which the chimney of the lamp
projects. The whole is fastened by means of clamps to a stand, to which
is also attached a jointed arm bearing the reflector. This apparatus is
used either in connection with a student's lamp or with an argand
gas-lamp, and it will be found very convenient to have it mounted upon
a gas-bracket which can be raised and lowered and swung from side to
side.

Mackenzie's light concentrator consists of a cylinder of sheet iron
about 6 inches long by 2½ in diameter. Near one end a hole is cut in
the side of the cylinder, and a short piece of tube holding a
condensing lens is attached to the edge of the hole. This lens, which
is plano-convex with a spherical curve, and of 2½ inches diameter, is
placed with the plane side toward the light. {24} This concentrator is
intended to be slipped over the chimney of an argand burner, and should
be so adjusted that the centre of the flame corresponds with the centre
of the lens. It may, however, be used in connection with a student's
lamp, incandescent electric lamp, or even a candle, giving in all cases
a very satisfactory light, which, however, must be reflected from the
head mirror into the patient's mouth.

The best light, however, when the examinations are conducted in the
office of the physician, is the electric incandescent light, which
presents numerous advantages over the gas or oil lamp. It is more
brilliant and whiter than any other suitable artificial light, giving
off neither gases nor heat, nor does it consume the oxygen in the room;
and since the introduction and perfection of storage batteries it has
become available and convenient for use in private houses. Numerous
experiments which the author has carried on for some time have resulted
in the application of this form of light for laryngoscopy in two ways
which are both very satisfactory. The incandescent lamp is mounted upon
the universal gas-bracket in place of the argand burner, and either the
Tobold lamp or Mackenzie's light concentrator is slipped over it, so
that it comes opposite the centre of the lens. In fact, the electric
lamp is substituted for the gas-burner, and the whole apparatus is used
as described above. The arc light may also be used in the same manner,
but does not give as satisfactory results on account of its
unsteadiness.

[Illustration: FIG. 3. The Author's Electric Illuminator for the
Laryngoscope.]

The second method is to mount the electric lamp on the head mirror in
such a way that it projects a little from the surface and is a little
to one side of the centre of the reflector (Fig. 3). The light is then
thrown forward in a cone, and can be directed with great ease into the
mouth of the patient. Since thus the source of the light moves with the
mirror, the observer can follow the motions of the patient more easily;
and if, in the first place, an easy position of the head has been
assumed when adjusting the light, much less {25} fatigue is experienced
by the examiner with this apparatus than when the light is reflected
from a stationary source. Still another mode of using the incandescent
lamp, which was suggested by Trouvé, is to mount the lamp within a tube
one end of which is closed by a plano-convex lense, while the other end
is covered by a metal cap carrying in its centre a ball-and-socket
joint, by means of which it is fastened to the frontal plate of the
head band. In this way the light with its condensing apparatus is
carried on the forehead like the head mirror.

Sunlight is certainly the best source of light for the illumination of
the interior of the larynx and nasal cavities, but, unfortunately, it
is not available at all times and in all localities. When it can be
obtained, however, the student should not neglect the opportunity, and
should not be deterred from using it for examination by the little
extra apparatus and trouble necessary.

The most convenient plan is to place a small plane mirror mounted upon
a stand in such a manner that it can be turned in any direction, such
as a small toilet-glass, in the direct rays of the sun coming through a
southern window. Then turn the mirror until the reflection falls upon a
second plane mirror supported by a jointed arm and placed in a distant
corner of the room, and in front of the chair upon which the patient is
seated, with his back to the first mirror. The light from the second
mirror is then thrown into the patient's mouth in the same manner as
when a light concentrator is used. The second mirror may also be
mounted on the head band and used as a head reflector, but this latter
plan is not as satisfactory, because the reflected light from the first
mirror is apt to strike the observer's eye and temporarily blind him.

Sunlight, as well as the light from the oxyhydrogen and electric-arc
lamps, is white, and therefore shows us the parts in their natural
coloring, which is claimed as a great advantage over all other sources
of light. It is true that the yellow rays which are predominant in all
other artificial lights make the mucous membrane appear redder than it
really is, and the observer may be led to believe that a congestion
exists if the patient be examined by white light first, and then by
yellow light on different occasions. But as all our knowledge and
appreciation of shades of color depend upon a comparison with a
standard, it makes no difference whether this standard, as in the case
before us, is a little redder when viewed by yellow light or not so red
when seen by white light. This advantage of the white light is,
therefore, not of much practical value, and the expense and
difficulties connected with the use of the oxyhydrogen or electric
arc-light for laryngoscopy fully outweigh any advantage which can be
claimed for it.

THE ART OF LARYNGOSCOPY.--Before entering upon a description of the
details of the art it will be necessary to clearly understand the
optical principle upon which the use of the laryngoscope is based, and,
further, to remember that the object to be viewed is situated below the
straight path of light and vision. The optical law referred to is, that
"The angle of incidence is equal to the angle of reflection," and
consequently, in order to illuminate the cavity of the larynx and to
see its details, the laryngeal mirror must be placed in such a position
in the fauces that the light is reflected downward. The light rays
forming the laryngeal image will then be reflected from the surface of
the laryngeal mirror into the eye of the observer. It should always be
borne in mind that the image seen in the mirror is a reflected one,
like the image of one's self seen in a looking-glass, so that what
appears to be right is left, and vice versâ. On account of the
difference in height of the parts forming the image, and because the
mirror must be placed above and slightly behind the opening of the
larynx, the picture appears reversed in an antero-posterior direction.
The same holds good when viewing a drawing of a laryngeal image.

{26} POSITION OF PATIENT AND OBSERVER.--The relative positions of the
patient, observer, and the source of light are of very great
importance, especially to the beginner, and a want of proper adjustment
will often make it extremely difficult, if not impossible, to obtain
the desired view of the larynx. The patient having been seated upon a
chair, or better still upon a piano-stool, the source of light is
placed upon a table at his right, at such a height that the centre of
the flame is on a level with his eyes and a few inches behind. The
observer then takes a seat directly in front of the patient, and,
separating his knees, places his feet on either side of those of the
patient, thus being able to grasp the patient's knees with his own
should occasion require him to do so. This position is preferable to
the one in which the knees of the observer are either on one side or
the other of the patient's knees, because then the observer, in order
to throw the light from the head mirror into the mouth of the patient,
has to assume a constrained position which very soon becomes fatiguing.
Under no circumstances should the patient be allowed to grasp the
observer's knees, for then the latter is powerless to restrain the
struggles of his patient, and cannot quickly leave his seat should
vomiting occur. When the examination is made at the physician's office
or wherever it is practicable, it is of advantage to have a head-rest,
such as photographers use, for the patient's head.

The positions having been taken, the observer places the head reflector
upon his forehead a little above the left eye, and by rotating it upon
its ball-and-socket joint reflects the light from the lamp- or
gas-flame upon the patient's face so that the circle of light is
bounded above by the tip of the nose and below by the tip of the chin.
It is of great importance that the adjustment of the reflector should
be made by means of its joint, and not by rotating or inclining the
head, for it is necessary that the head should have an easy position
which can quickly be resumed should it become necessary to move the
head. It requires considerable practice to quickly reflect the light
from the head mirror in any desired direction, and it is therefore well
for the beginner to practise this by throwing the light upon a spot on
the wall before he attempts to examine a patient, as he will thus save
himself, as well as the patient, unnecessary annoyance. If a light
concentrator be used which supports the reflector on the jointed arm,
this of course is not necessary, but the practice with the head mirror
will even then be found advantageous, because when a patient is to be
examined in the sick room a light concentrator cannot usually be
employed, and the physician has to fall back upon the head mirror for
illuminating the laryngeal cavity.

When the reflector has thus been properly adjusted the patient is
required to incline his head backward and open his mouth as wide as
possible, when it will be found that the centre of the circle of light
falls upon the root of the uvula. A careful examination of the oral
cavity, the anterior and posterior pillars, the tonsils, and the wall
of the pharynx should be made before the laryngeal mirror is
introduced, not only because the condition of these parts often imparts
valuable information, but also in order to be sure that no infectious
sores be present which might contaminate the instruments to be
introduced. The laryngologist cannot be too careful to prevent the
carrying of infectious material from one patient to another; and if he
should by this preliminary examination discover a specific sore, he
should use only such instruments as are reserved for this class of
cases, and which are kept in a separate box or drawer of the
instrument-case.

Everything being in readiness, the laryngeal mirror is held over the
lamp, with the glass side down, for a few seconds until it is warm, so
as to prevent the condensation of moisture on its reflecting surface,
and is then introduced in the following manner: The handle is held
between the thumb and fore finger of the right hand like a pen-holder
(Fig. 4); the hand is bent {27} backward upon the wrist and held below
the chin of the patient. Meanwhile, the protruded tongue is grasped
between the folds of a napkin or towel held in the left hand, and
gently but firmly pulled out of the mouth. Great care should be
exercised to prevent the frænum of the tongue from coming in contact
with the sharp edge of the front teeth, for this soon becomes very
painful and may prevent a successful examination. Many laryngologists
are in the habit of letting the patient hold his tongue, which becomes
necessary when operations or applications are to be made to the larynx;
but for the purpose of examining only it is better for the observer to
hold the tongue, as he thus gains more control over the movements of
the head of the patient.

[Illustration: FIG. 4. Position of Hand in holding the Laryngeal
Mirror.]

The mirror is now rapidly introduced into the mouth of the patient,
without touching the tongue or the palate, and carried backward until
its rim touches the wall of the pharynx, when it is lifted upward,
carrying on its back the uvula, and the stem is brought into the angle
of the mouth, so as to be out of the line of vision (Fig. 5). In this
position the light of the reflector will fall upon the reflecting
surface of the laryngeal mirror, and will be reflected downward so as
to illuminate the laryngeal cavity and reflect the laryngeal image into
the eye of the observer.

[Illustration: FIG. 5. Diagram of Section of Head, showing the Position
of Laryngeal Mirror in the Pharynx.]

{28} There are, however, numerous obstacles and difficulties which must
be overcome to successfully practise laryngoscopy--obstacles which are
partly due to the want of skill on the part of the operator, and partly
to over-sensitiveness and want of control of the patient, or, finally,
to abnormal positions of the parts. Taking them up one by one, in the
order named above, the reader will soon learn to overcome these
obstacles by practice and careful attention to details.

As has already been pointed out, a satisfactory view of the laryngeal
image cannot be obtained if the position of the light, of the patient's
head, and of the observer is not properly arranged; further, if the
laryngeal mirror is either too cold or too hot. In the former case the
moisture of the breath will condense on its reflecting surface and
render it non-reflecting, and in the latter case the patient will feel
the heat and will object to the presence of the mirror in the fauces.
The examiner should therefore carefully test the temperature of the
mirror on the back of his hand before introducing it. Many
laryngologists are in the habit of testing the temperature by placing
the mirror against the cheek, but this is a dangerous practice, for a
slight scratch or abrasion of the skin from shaving may be inoculated
with infectious material from a specific sore, and the writer knows of
more than one instance in which such infection has occurred; while a
scratch on the hand is not so likely to be overlooked, and therefore
the danger is much less. Pulling too hard upon the tongue, so that the
frænum becomes injured by the edge of the teeth, is another obstacle,
for the patient will not bear the pain thus occasioned. Touching the
tongue or palate in the act of introducing the mirror, besides coating
the reflecting surface with the secretions of the mouth, causes in most
patients gagging, and should therefore be avoided. When the mirror has
been introduced it should be held very still, and if it becomes
necessary to rotate it, this should be done slowly and steadily,
because the slightest trembling motion of the rim of the mirror resting
against the wall of the pharynx produces gagging and cuts the
examination short at once. It is therefore advisable to steady the hand
holding the mirror by placing the third finger against the cheek of the
patient, or, better still, against the thumb of the hand holding the
tongue.

Undue irritability of the fauces is of very rare occurrence, and is
almost invariably produced by one or the other of the above-mentioned
mistakes of the examiner. When it does exist independently, it can in a
measure be overcome by letting the patient drink a large draught of
ice-water immediately before introducing the mirror, and by holding the
mirror so that it does not touch either the pharyngeal wall or the
palate. In this manner but a very unsatisfactory view of the larynx can
be obtained, and it is better to overcome the irritability by practice
on the part of the patient--_i.e._ by introducing the mirror frequently
and removing it before gagging sets in, and by directing the patient to
introduce a teaspoon into the fauces before a looking-glass several
times a day. Even the most obstinate cases can thus be educated to
allow of a lengthy examination. No matter how tolerant a patient may
be, however, the mirror should never be left in the fauces after the
first symptoms of gagging show themselves, but should at once be
removed. It is better in all cases to leave the mirror in the mouth but
a short time and to introduce it frequently, thus studying the
different parts of the image one after the other, than to attempt to
see everything at once. In laryngoscopy, as in many other arts, not
only the hand, but also the eye, must be educated to appreciate all the
details and the variations from the normal.

Among the malformations of the parts which present obstacles to
laryngoscopy are, in the first place, hypertrophied tonsils, which by
narrowing the space in the fauces make it impossible to introduce the
ordinary-sized mirror. A smaller mirror or one of oval shape can,
however, usually be slipped past the {29} enlarged glands and the
desired image obtained. An elongated uvula does not exactly prevent a
view of the larynx, but it materially interferes with a good image,
because its end by hanging below the rim of the mirror is seen in the
reflecting surface and obscures part of the image. Removal of the uvula
by surgical means is of course the best remedy.

The third and most serious obstacle presented by malformation or
malposition of parts is a pendent epiglottis--_i.e._ an epiglottis
which by being bent too far over covers the laryngeal opening and
prevents a view. This obstacle exists to a certain extent in most cases
that come under observation, but is easily overcome by letting the
patient sound the vowel sound of _eh_, which causes a rising of the
epiglottis and opens the laryngeal cavity to view. There are some
cases, however, in which this expedient does not sufficiently raise the
epiglottis to obtain a glimpse of the vocal cords, and only the
arytenoid cartilages are seen, from the motion and color of which we
can often obtain valuable information in regard to pathological
processes. In these cases, when it becomes absolutely necessary to see
the whole extent of the vocal cords, we may succeed by causing the
patient to laugh in a high key, but when this fails the only resource
left is to lift the epiglottis by grasping its upper margin with a pair
of curved forceps especially designed for this purpose and called
epiglottis forceps (Fig. 6). If this instrument is not at hand, the
same object may be attained by clasping the edge of the epiglottis with
a bull-nose forceps, to which is fastened a string weighted at the
other end by a small weight, such as a rifle-bullet. The string with
its weight hanging out of the mouth of the patient makes traction upon
the forceps, and thus the epiglottis is raised. In cases of operation
within the laryngeal cavity this method of raising the epiglottis is
even preferable to the epiglottis forceps, because it leaves the hands
of the operator free to use the mirror and the instrument to be used in
operating.

[Illustration: FIG. 6. Elsberg's Sponge-holder and Epiglottis Forceps.]

AUTO-LARYNGOSCOPY.--There is perhaps no better method for the beginner
to overcome the difficulties besetting laryngoscopy than to practise
the art on himself, for then only will he be able to appreciate to its
full extent the necessity of observing all the minute details described
above, as the pain and inconvenience which he inflicts upon himself by
his false movements will teach him better, and enable him to attain
proficiency in the use of his instruments quicker than any other method
of practice. Nothing need, for auto-laryngoscopy, be added to the stock
of instruments necessary for the examination of others, except a stand
to which the reflector is fastened and a small toilet-mirror. The
observer seats himself beside a table upon which, at his left, is
placed the lamp a little behind his head and the centre of the flame on
a level with his eyes. The stand, an ordinary retort-stand, is placed
in front of him, and to it is fastened at the proper height the
reflector. On the same stand, and immediately above the reflector, is
attached the plane mirror in such a manner that it can be inclined at
an angle. Inclining the head slightly backward, the observer then by
watching his face in the plane mirror directs the light upon his mouth
by moving the reflector upon its ball-and-socket joint until the circle
falls upon his mouth. He then opens his mouth as wide as possible,
grasps his protruded tongue between the folds of a towel or {30} napkin
held between the thumb and fore finger of the left hand, and introduces
the laryngeal mirror with the right hand in the manner described above.
The laryngeal image as it appears on the surface of the laryngeal
mirror is reflected by the toilet-glass above the reflector, and can be
seen in all its details by the person practising auto-laryngoscopy. By
substituting a perforated mirror for the toilet-glass the student can
demonstrate the image to others in his own person if the observers look
through the perforation in the mirror.

Before giving a description of the laryngeal image it will be well, for
the sake of completeness, to mention the fact that of late photography
has been employed to reproduce this image, both in this country by T.
R. French of Brooklyn[17] and by Lennox Browne of London, England, with
very gratifying results. The writer himself several years ago made
experiments in this direction, which, however, were not very
satisfactory in their results. The method employed by French is a very
simple one, and it will be best to give his own description of the
process:

"The camera consists of a box 4½ inches long, 1-7/8 inches wide, and ¾
of an inch in thickness. The back opens upon hinges, and admits of the
introduction of either the ground glass or the plate-holder. On the
anterior face a tube 1-1/8 inches long is attached, in the outer end of
which the lens is placed. This lens has a focus of 1¼ inches. At the
side of the tube a part of the handle of a throat mirror is fixed, and
into that the shank of the throat mirror is passed and fastened by a
thumb-screw. The shank of the mirror is somewhat curved, and is
attached to the side of the frame holding the mirror. The object of
this is to allow the lens being held opposite any part of the opening
of the mouth, and also to prevent the possibility of a shadow being
cast upon the mirror. In the front part of the box is a shutter made of
lead and perforated with a hole just the size of the lens. The shutter
is held in position by a lever acting as a key on the anterior face of
the camera.

"The apparatus is used in the following manner: A reflector, either
plane or concave, attached to a head band, is arranged over the left
eye so that the pencil of sunlight from the solar condenser is received
upon it and thrown into the mouth. The patient, with the head inclined
slightly backward, now protrudes the tongue and holds it well out
between the fore finger and thumb of the right hand. The throat mirror
with the camera attached, held in the right hand of the observer, is
placed in position in the fauces, and the light adjusted so that the
larynx can be seen with the observer's left eye to be well illuminated.
If, now, the tongue does not mount above the level of the lower edge of
the lens and the lower edge of the mirror, it may be taken for granted
that when the plate is exposed the picture received upon it will be
nearly the same as that seen with the left eye in the throat mirror.
The photograph is taken by pressing upon the key with the index finger;
this releases the shutter, which in falling makes an instantaneous
exposure amounting to perhaps one-seventh of a second.

"In using condensed sunlight with a small camera it is important to
throw the circle of light from the inner side of the reflector, that
nearest the nose; for in this way a part of the larynx exposed to the
lens of the camera may be illuminated which cannot be seen with the
eye. To ensure this it is best to cover the outer half of the reflector
with black silk. On account of the parallax or displacement of the
image due to the difference in point of view between the eye and the
camera, some skill is necessary in managing the illumination so that
the part which it is desired to bring out will be exposed to the lens
if not to the eye."

[Footnote 17: _Archives of Laryngology_, vol. iv. No. 4.]

THE LARYNGEAL IMAGE.--When the mirror is introduced and is held in the
proper place, and the light is reflected downward, the laryngeal image
{31} will appear on the surface of the mirror. As it is, however, so
different from what might be expected after having examined a larynx
removed from the body, it requires a detailed description, and the
student will do well to refer to the diagrams frequently while
examining patients, to make himself familiar with the details he sees,
and to recognize them when they are altered by disease or when they are
slightly different in shape in different individuals. Figs. 7 and 8
represent the image of the larynx in the act of respiration and of
phonation as it appears on the surface of the mirror, while Figs. 9 and
10 are diagrammatic, and are intended to represent the same.

[Illustration: FIG. 7. Laryngeal Image during Respiration.]

[Illustration: FIG. 8. Laryngeal Image during Phonation.]

[Illustration: FIG. 9. Laryngoscopic Diagram showing the vocal cords
widely drawn apart, and the position of the various parts above and
below the glottis during quiet breathing. _g. e._ Glosso-epiglottic
fold. _s. u._ Upper surface of epiglottis. _l._ Lip or arch of
epiglottis. _c._ Protuberance of epiglottis. _v._ Ventricle of the
larynx. _a. e._ Ary-epiglottic fold. _c. W._ Cartilage of Wrisberg.
_c. S._ Cartilage of Santorini. _com._ Arytenoid commissure. _v. c._
Vocal cord. _v. b._ Ventricular band. _p. v._ Processus vocalis.
_c. r._ Cricoid cartilage. _t._ Rings of trachea. (From Mackenzie.)]

[Illustration: FIG. 10. Laryngoscopic Diagram showing the approximation
of the vocal cords and arytenoid cartilages, and the position of the
various parts during vocalization. _f. i._ Fossa innominata. _h. f._
Hyoid fossa. _c. h._ Cornu of hyoid bone. _c. W._ Cartilage of
Wrisberg. _c. S._ Cartilage of Santorini. _a._ Arytenoid cartilages.
_com._ Arytenoid commissure. _p. v._ Processus vocalis and cartilages
of Seiler. (From Mackenzie.)]

The first detail to attract the eye is the epiglottis, which appears as
a yellowish-red arch reaching from side to side across the image. It is
thicker in the middle than at either end, and a protuberance is usually
seen in the centre pointing forward. This arch is the upper margin of
the epiglottis, and the protuberance is the tubercle, situated near the
insertion of the epiglottis into the thyroid cartilage. The shape as
well as the color of the epiglottis is very variable in different
individuals, being sometimes rounded as in the drawings, sometimes
rolled up like a dried leaf, sometimes notched in the centre, and
sometimes presenting a point at this place. However, all these
variations in shape have nothing to do with any pathological process,
and may therefore be termed normal. The color of the organ also varies
from a bluish-yellow to a pink-red, and these variations are also
normal, being due to a greater or less thickness of the tissue covering
the cartilage, which by shining through imparts its bluish color to the
tissue. The superficial blood-vessels also are more prominent in some
individuals than in others, and may not be noticeable in some cases.

{32} Immediately behind the epiglottis we see two pit-like depressions,
separated from each other in the middle by a fold of mucous membrane
and bounded on either side by similar folds less prominent. These folds
are the glosso-epiglottic ligaments, and serve to connect the tongue
with the epiglottis, while the depressions are the glosso-epiglottic
grooves, in which we usually find the foreign bodies which have
accidentally been swallowed.

The ends of the epiglottic arch are lost in folds of mucous membrane,
which run forward and inward to meet in the median line some distance
in front of the epiglottis. Along their course several nodules of
different size are noticed, which are symmetrically situated on either
side. The one nearest to the epiglottis is the cartilage of Wrisberg, a
small cartilaginous nodule imbedded in the tissue. The larger one,
situated at the end of the fold of mucous membrane, is the arytenoid
cartilage, and a third small nodule is noticed close to the arytenoid
cartilage between it and the cartilage of Wrisberg, which is called the
capitulum Santorini. The folds of mucous membrane are termed the
aryteno-epiglottidean or ary-epiglottic folds. Their color is normally
of a pinkish-red, and does not vary much in different individuals.

The arytenoid cartilages forming the ends of the ary-epiglottic folds
are movable, approaching and separating alternately during the act of
respiration, while during phonation they are pressed against each
other, thus obliterating the space between them which is seen when they
are separated. This space is the inter-arytenoid space or commissure,
and is formed by the lateral walls of the arytenoid cartilages and the
upper margin of the posterior portion of the cricoid cartilage. The
mucous membrane in this commissure is very loosely attached to the
deeper structures, and is thrown into folds by the approximation of the
arytenoid cartilages. Its color is much lighter than that of the
ary-epiglottic folds, due to the shining through of the cricoid
cartilage. Outside of the ary-epiglottic folds and the inter-arytenoid
commissure is the tissue forming the posterior and lateral walls of the
oesophagus (not shown in the diagrams), and near the epiglottis a space
called the pyriform sinus is noticed between the ary-epiglottic folds
and the wall of the oesophagus.

Running from the epiglottis to the ary-epiglottic folds are two broad
bands, one on either side, covered with mucous membrane and of a
pinkish-red color, which are lost on either side in the tissue forming
the walls of the laryngeal cavity, while toward the middle of the image
they present concave and tolerably sharp edges. These are the
ventricular bands, which were formerly termed the false vocal cords,
and which form the lip to the opening of the ventricle of the larynx.
Between the ventricular bands filling up the central portion of the
image are seen the vocal cords, two bands of a pearl-white color which
are attached to a cartilaginous process of the arytenoid cartilages,
and run from these parallel with each other to the angle of the thyroid
cartilage immediately below the tubercle of the epiglottis. These
present sharp edges toward each other, and follow the motions of the
arytenoid cartilages to which they are attached, so that when in
inspiration the cartilages are separated the edges of the vocal cords
are also some distance apart, forming, together with the
inter-arytenoid commissure, a triangular opening called the glottis.
That portion of the opening which is bounded on either side by the
edges of the vocal cords alone is called the membranous portion, while
the base of the triangle is termed the cartilaginous portion, being
bounded on either side by the vocal processes of the arytenoid
cartilages. This portion is readily distinguished from the membranous
portion by its slightly yellow color, and by the fact that a very
obtuse angle is formed at the junction of the two portions when the
glottis is wide open during respiration. Through the open glottis the
lower edge of the cricoid cartilage and several of the rings of the
trachea can usually be seen, and there are a few cases in which even
the bifurcation of the trachea can be dimly illuminated, showing in the
{33} laryngeal image the openings of the bronchi. The distance is,
however, too great for bright illumination, and nothing can be seen
distinctly, so that it is of little value in a diagnostic point of
view. During phonation the glottis is narrowed to a slit by the
approximation of the arytenoid cartilages and inner edges of the vocal
cords, and, as has already been stated, the inter-arytenoid space
becomes obliterated. In the higher notes of the female voice, the
so-called head tones, the cartilaginous portion of the glottis remains
closed entirely, while the membranous portion appears as an elliptical
opening which is diminished in its longitudinal diameter with each rise
in pitch. This becomes possible because of the presence in the vocal
cords of a slender rod-like cartilage attached to the end of the vocal
process, which can readily be seen in the female larynx, but which is
only rudimentary in the male.

This description, intentionally, has been made without reference to the
anatomical relation of the parts, but to give a clear idea of what is
seen in the laryngeal mirror. The reader should therefore always bear
in mind that the laryngeal image, being a reflected one, is reversed,
and that, on account of giving a bird's-eye view of the larynx from a
point above and behind the organ, distances are materially diminished;
and the image is also reversed in an antero-posterior direction, so
that the epiglottis appears to be posterior when in reality it is
anterior.

RHINOSCOPY.--Rhinoscopy, or the art of inspecting the nasal cavities
and the naso-pharyngeal space, is divided into two portions--viz.
anterior and posterior rhinoscopy; and it will be convenient to observe
this division in the following description of the methods employed. But
before proceeding with the description it will be well to briefly
review the topographic anatomy of the parts, because in most works on
general anatomy the nasal and naso-pharyngeal cavities are discussed in
a few sentences, and they are rarely if ever examined in the
dissecting-room, so that the student has but a very imperfect knowledge
of the relation of the parts belonging to these cavities. (See Fig.
11.) The nasal cavities, which are wedge-shaped, with a narrow arched
roof, extend from the nostrils to the upper portion of the vault of the
pharynx. Their outer walls are formed by the nasal process of the
superior maxillary and lachrymal bones in front; in the middle, by the
ethmoid and inner surface of the superior maxillary bones; behind, by
the vertical plate of the palate bone and the internal pterygoid
process of the sphenoid and the turbinated bones. These latter run
before backward, three on each side, and are designated as the
inferior, middle, and superior, the latter being the smallest of the
three. The sinuses or spaces between these turbinated bones are called
meatuses; so that the space between the floor of the nose and the lower
turbinated bone is called the inferior meatus, the one between the
lower and middle turbinated bones is the middle meatus, and the one
between the middle and superior turbinated bones is the superior
meatus.

[Illustration: FIG. 11. VERTICAL SECTION OF HEAD, SLIGHTLY
DIAGRAMMATIC. 1. Superior turbinated bone. 2. Middle turbinated bone.
3. Lower turbinated bone. 4. Floor of nasal cavity. 5. Vestibule. 6.
Section of hyoid bone. 7. Ventricular band. 8. Vocal cord. 9 and 23.
Section of thyroid cartilage. 10 and 24. Section of cricoid cartilage.
11. Section of first tracheal ring. 12. Frontal sinus. 13. Sphenoidal
cells. 14. Pharyngeal opening of Eustachian tube. 15. Rosenmüller's
groove. 16. Velum palati. 17. Tonsil. 18. Epiglottis. 19. Adipose
tissue behind tongue. 20. Arytenoid cartilage. 21. Tubercle of
epiglottis. 22. Section of arytenoid muscle.]

The nasal cavities are separated from each other by a septum or
division wall composed of the perpendicular plate of the ethmoid bone
and the vomer posteriorly and the cartilaginous septum anteriorly, thus
presenting a smooth surface as the inner wall of each cavity. The floor
is formed by the palatine process of the superior maxillary bone and by
the palate bone, and runs in a slanting, downward direction from before
backward. The roof is formed by the nasal bones and nasal spine of the
frontal in front, in the middle by the cribriform plate of the ethmoid,
and posteriorly by the under surface of the body of the sphenoid bone.
Directly communicating with the nasal cavities are other cavities
situated in the bones of the skull, the lining mucous membrane of which
no doubt is largely affected by the pathological processes in nasal
diseases: these are the antra of Highmore, large triangular cavities
situated in the body of the superior maxillary bone and communicating
with the nasal cavities by an irregularly-shaped opening in the middle
meatus; {34} then the frontal sinuses, two irregular cavities situated
between the two tables of the frontal bone. The communication between
them and the nasal cavities is established by the infundibulum, a round
opening in the middle meatus, and finally the sphenoidal cells or
sinuses, found in the body of the sphenoid bone, communicating with the
nasal cavities by small openings in the superior meatus. That portion
of the nasal cavities which projects beyond the end of the nasal bone
is surrounded by cartilages forming the alæ of the nose.

In the cartilaginous septum of the lower animals we find a small cavity
lined with mucous membrane, called after its discoverer Jacobson's
organ, the minute anatomy of which has lately been described by
Klein.[18] This {35} organ in man is, however, only rudimentary. The
nasal cavities are lined with mucous membrane, which varies greatly in
thickness in different localities, and which materially decreases the
size of the cavities in the living subject from that seen in the
denuded skull. This mucous membrane is covered by ciliated epithelium
in man, with the exception of that portion which lines the
vestibule--_i.e._ that portion of the cavity of the nose surrounded by
cartilage only--which is covered by pavement epithelium.

[Footnote 18: _Quarterly Journal of Mic. Science_, January, 1881.]

In the lower animals we find that in the olfactory region the ciliated
epithelium is either absent, or that ciliated and non-ciliated
epithelium alternates in patches.[19] The author has not been able to
find a statement in the literature on the subject as to the kind of
epithelium found in the accessory cavities in man, but it is very
probable that the mucous membrane of the frontal sinuses and the antra
of Highmore is covered with ciliated epithelium; otherwise it would be
difficult, if not impossible, for the secretions of that mucous
membrane to pass through the narrow channels into the nasal cavities.
The color of the normal nasal mucous membrane is of a light pink shade
in what is termed the respiratory portion, while it is of a yellowish
hue in the olfactory region, that portion of the mucous membrane which
covers the roof and the outer walls of the nasal cavities down to the
upper margin of the middle turbinated bone and the septum down to about
the same level. It is in this region that the nerve-ends of the
olfactory nerve are distributed. Immediately beneath the mucous
membrane, and between it and the periosteum of the bony walls and the
perichondrium of the cartilaginous portion of the septum, we find a
tissue which bears a striking resemblance to the erectile tissue of the
genital organs.[20] It is composed of a network of fibrous tissue, the
trabeculæ of which contain a few organic muscular fibres. Its meshes of
various sizes and shapes are occupied by venous sinuses lined with
endothelium. These are supplied with blood by small arterioles and
capillaries, which are quite numerous in the fibrous tissue and can
readily be demonstrated under the microscope. In this arrangement of
elements of the nasal mucous membrane we find a ready explanation of
the fact that liquids of greater or less density than the serum of the
blood when introduced into the nasal cavities produce pain, for we have
here the most favorable conditions for osmosis, which will cause either
a contraction or a distension of the sinuses. In the larger masses of
fibrous tissue between the sinuses or caverns we find imbedded the
glands, with their ducts opening out between the epithelial cells of
the mucous membrane. There are two kinds of glands in this region,
which have been described by Klein[21]--viz. serous and mucous glands.

[Footnote 19: Haenle, _Anatomy des Menschen_, vol. ii.]

[Footnote 20: Haenle, _loc. cit._]

[Footnote 21: _Loc. cit._]

This cavernous erectile tissue is most abundant at the lower portion of
the septum and of the lower turbinated bones; and, although it has been
recognized and described as true erectile tissue by Haenle, Virchow,
and others, yet to Bigelow of Boston belongs the honor of having first
called attention to the part which this tissue plays in nasal diseases.
He gave to it the name turbinated corpora cavernosa.[22] The expansion
of the nasal cavities formed by the alæ of the nose is termed the
vestibule, which is lined with pavement epithelium and forms the
entrance to the cavities proper. The naso-pharyngeal cavity extends
from the posterior ends of the turbinated bones and the edge of the
vomer to the line where the velum palati touches the pharyngeal wall
during the act of deglutition or phonation. In this cavity we find the
openings of the Eustachian tubes, two crater-like elevations, with a
pit-like depression of variable size and shape, one on either side; and
a collection of glands with a central duct-like opening disposed on the
roof and posterior wall of the cavity. This gland was named by
Luschka[23] the pharyngeal {36} tonsil. The openings between the edge
of the vomer and the lateral walls of the naso-pharyngeal cavity are
termed the posterior nares.

[Footnote 22: _Boston Med. and Surg. Journal_, April, 1875.]

[Footnote 23: _Der Schlundkopf des Menschen_.]

ANTERIOR RHINOSCOPY.--Anterior rhinoscopy is a very easy and simple
procedure, and is practised as follows: The patient is placed in
position as for laryngoscopy, and the light directed upon his face so
that the centre of the circle of reflection from the head mirror falls
upon the tip of the nose. The examiner then elevates the tip of the
nose with his left hand, resting the fingers on the forehead of the
patient, and lifts the ala away from the septum with a slightly bent
probe, when he will be enabled to see a considerable distance into the
nasal cavity. It is, however, better to employ a speculum instead of
the bent probe, because the parts then are seen in their usual relation
to each other, and are not distorted by the forcible traction necessary
when the probe or a dilator is employed. The nasal speculum (Fig. 12)
is best made of hard rubber and shaped like the ordinary ear speculum,
except that the narrow end is oval instead of round. This instrument is
to be introduced by a sort of rotatory motion until the end has passed
the edge of the vestibule, when it will remain in position, displaying
the interior of the nose. Great care should be exercised, when
introducing the speculum, not to scratch the mucous membrane of the
septum, for this will give rise to pain and start hemorrhage, both of
which are to be avoided as much as possible. When applications are to
be made to the mucous membrane of the septum or turbinated bones, or
when operations are to be performed within the cavity, it is best to
employ an instrument called a nasal dilator, of which there are a large
number of different forms, the most satisfactory of which is shown in
Fig. 13. The dilator is introduced by compressing the blades between
the thumb and fore finger, and pushing them into the nostril until
their ends have passed the edge of the vestibule. The pressure is then
removed, and the spring separating the blades holds the nostril open;
the handle or stem of the instrument, hanging down, need not be held or
supported, as the blades press sufficiently upon the tissues to retain
the instrument in position. If the pressure is too great, however, it
will soon produce pain, and the patient will object to the use of the
instrument.

[Illustration: FIG. 12. Nasal Speculum.]

[Illustration: FIG. 13. Bosworth's Nasal Dilator.]

The view obtained both by the speculum and the dilator is rather
limited, and usually comprises only the anterior portions of the lower
and middle turbinated bones, together with the cartilaginous portion of
the septum. In order to get a good view of the lower and middle meatus
and of the floor of the nose the patient's head should be inclined
forward or backward as occasion requires. The student should, however,
not be satisfied by simply inspecting the parts, but should aid the eye
by the sense of touch, for pathological changes are of common
occurrence, and their nature, whether soft and fleshy or hard and bony,
erosions of the mucous membrane, or deep ulcerations, can often only be
determined by the aid of the probe. In the same manner can the
permeability of the meatuses be determined better than by inspection
{37} only. In cases where it becomes necessary to determine whether the
anterior portion of the septum is of normal thickness, or whether a
projection seen through the speculum is due to localized deflection, an
instrument called the septometer is of great assistance (Fig. 14). This
instrument is similar to the one used by mechanics to determine the
diameter of a piece of wood or iron being turned on the lathe. In using
it the long straight shanks are introduced one in each nostril, and,
being closed upon the septum, the rounded points are gently moved up
and down and backward and forward over the bulging portion of the
septum. The motion of the index attached to the curved shanks of the
instrument accurately indicates the relative thickness of tissue
grasped between the points in the nose. By means of this instrument we
can thus ascertain whether we have to deal with a deviation or a
localized thickening of the septum; for if it is a deviation the index
will move but slightly, while it will travel a considerable distance
when the points pass over a thickened portion.

[Illustration: FIG. 14. Septometer for Measuring Thickness of Nasal
Septum.]

Although simple in its details, anterior rhinoscopy is often made
difficult or altogether prevented by obstacles which are mostly due to
malformation of the parts, such as deviation of the cartilaginous
portion of the septum, exostoses from the superior maxillary bones
reaching into the nasal cavity, adhesion between the anterior portion
of the lower turbinated bone and the septum, nasal polypi, anterior
hypertrophies of the mucous membrane, and so forth; or they may be due
to faulty instruments, as too much pressure in the spring of the
dilator; or, finally, they may be caused by want of care in the
handling of the instruments, as when the septum is scratched by the
edge of the speculum and hemorrhage ensues.

POSTERIOR RHINOSCOPY.--Posterior rhinoscopy is much more difficult than
laryngoscopy or anterior rhinoscopy, and requires more patience and
dexterity on the part of the examiner than either of the former,
because but very few persons have control over the movements of the
velum palati, and in most of these the upper portion of the pharyngeal
wall is so sensitive that the slightest touch with an instrument gives
rise to reflex cough and to gagging. In many cases, however, with
patience and skill the naso-pharyngeal cavity and the posterior portion
of the nasal cavities can be illuminated and inspected. To do this the
patient is placed in the same position as for laryngoscopy, except that
the head is not inclined backward, and after the mouth is opened as
wide as possible the light from the reflector is thrown into the oral
cavity. The tongue is then depressed with a tongue depressor. This
instrument in its simplest form in which it is daily used by the
practitioner for examining the fauces is the handle of a spoon. For
laryngoscopic or rhinoscopic purposes, however, the spoon is not to be
recommended, because the hand holding it must be on a level with the
mouth, thus obstructing the view and light. An instrument has therefore
been constructed which obviates this difficulty. It consists of a
leaf-shaped blade of silver or German silver bent at right angles and
inserted into a flat wooden handle. The lower surface of the blade is
slightly concave, and ribbed so as to take a better hold of the
slippery back of the tongue, and from the bend is about 3 inches in
length. It is introduced into the mouth as far back as possible, and
pressed upon the back of the tongue while the hand of the examiner is
below the chin of the patient. For the sake of convenience in carrying
the instrument the blade has been so hinged to the handle that it will
fold up against the latter and will {38} open at a right angle with it
(Fig. 15). A more elegant and lighter instrument of the same
description has lately been introduced in which the handle is also made
of metal, and, like the blade, is heavily nickel-plated, and which when
folded can be carried in a pocket-case. Soon, however, the metal tongue
depressor becomes tarnished by the secretions of the mouth or by the
substances used for applications to the throat, and then presents an
appearance disgusting to many patients, who will not on that account
submit to its use. For the sake of greater cleanliness, J. Solis Cohen
devised a tongue depressor made of hard rubber, which is known as
Cohen's tongue depressor (Fig. 16). It consists of a piece of ebonite
bent upon itself, either end being a little over 3 inches long. The
bend being more than at right angles, the hand holding the instrument
rests underneath the chin of the patient; but if a different curve be
desired for any particular case it can easily be obtained by placing
the instrument for a little while in hot water. When soft it can be
bent into any shape, which it will retain when cooled by immersion in
cold water. Great care should be exercised not to carry the blade of
the instrument too far back, as then gagging will at once set in. In
cases where the tongue resists the pressure of the tongue depressor, it
is better to exert but a gentle pressure upon the back of the organ,
under which it will slowly recede, than to try to subdue it by force,
for in the latter case it will unavoidably slip from under the blade of
the instrument, and the desired space in the fauces is not obtained.
With children the writer has found the fore finger of the left hand to
be the best means of depressing the tongue, for the little patients as
a rule have a horror of the formidable-looking instrument.

[Illustration: FIG. 15. Folding Tongue Depressor.]

[Illustration: FIG. 16. Cohen's Tongue Depressor.]

After the tongue has subsided into the floor of the mouth a small
laryngoscopic mirror is introduced into the pharyngeal space behind the
velum palati, with the reflecting surface upward, and is held there
without touching the wall of the pharynx. The handle of the mirror, as
in laryngoscopy, is brought into the angle of the mouth, so as to be
out of the line of vision. As is usually the case, the velum palati at
the approach of the mirror will rise and apply itself to the posterior
wall of the pharynx, when of course the naso-pharyngeal space, being
shut off, cannot be illuminated. Under these circumstances the velum
must be made to hang down as in the act of nasal respiration, which is
most easily accomplished by telling the patient to breathe through his
nose. It is of course impossible to do so when the mouth is open, but
the patient, not being cognizant of the fact, will make the attempt,
and the palate will come down, permitting illumination and inspection
of the naso-pharyngeal space and the posterior nares. In those cases in
which this {39} expedient fails it becomes necessary to forcibly pull
down the velum by means of a blunt hook made by bending a silver
laryngeal probe, or to tie it down by passing small elastic bands
through the anterior nares and bringing the ends through the mouth and
tying them over the upper lip. The smallest black rubber tubing is
admirably suited for this purpose, as it can be introduced without an
instrument. When the palate is pulled down with the palate hook, or
when operations in the naso-pharyngeal space are to be performed, the
patient must hold the tongue depressor himself, so as to leave the
other hand of the operator free. Few persons can do this, however,
satisfactorily, and it will be found more convenient to use Jarvis's
tongue depressor and rhinoscope, as modified by the writer (Fig. 17).
The instrument consists of a stout wire, which, after having been
forked or divided at some distance from its insertion into the handle,
forms the loop for the tongue depressor. The two branches then cross
each other, and are bent to form another loop at an angle to the larger
one. The ends of the wire are somewhat flattened and press against each
other, thus closing the smaller loop and forming a sort of pincette,
which can be opened by pressing the sides of the larger loop toward
each other. The ends of the pincette are perforated by a small hole,
which receives a pin attached at right angles to the short shaft of a
small mirror, thus forming a hinge, so that the mirror can be placed at
any desired angle with the handle or stem. The spring of the pincette
cannot be made strong enough to prevent a change of the angle of the
mirror by coming in contact with the pharyngeal wall, and therefore a
ratchet was placed at the shaft of the mirror where it hinged to the
end of the pincette, and a small steel spring, coming from one of the
branches of the wire where they cross each other to form the small
loop, by engaging in the teeth of the ratchet holds the mirror at the
angle given to it before introducing. The large loop acts as a tongue
depressor, so that with this admirable instrument the examination of
the post-nasal cavity can be made with one hand, leaving the other free
for the manipulation of other instruments. In order to be able to exert
more pressure upon the tongue and to bring the hand out of the line of
vision, the handle may be attached to the stem at an angle like the one
in the folding tongue depressor. Except in cases of cleft palate the
naso-pharyngeal cavity cannot be illuminated in its whole extent, and
must be studied in parts, which when placed together in the mind of the
examiner form the rhinoscopic image, a slightly diagrammatic drawing of
which is seen in Fig. 18.

[Illustration: FIG. 17. Jarvis's Rhinoscopic Mirror and Tongue
Depressor.]

[Illustration: FIG. 18. RHINOSCOPIC IMAGE. 1. Vomer or nasal septum. 2.
Floor of nose. 3. Superior meatus. 4. Middle meatus. 5. Superior
turbinated bone. 6. Middle turbinated bone. 7. Inferior turbinated
bone. 8. Pharyngeal orifice of Eustachian tube. 9. Upper portion of
Rosenmüller's groove. 11. Glandular tissue at the anterior portion of
vault of pharynx. 12. Posterior surface of velum.]

THE RHINOSCOPIC IMAGE.--In the middle of the drawing we see a
triangular plate with its apex downward; this is the posterior margin
of the vomer or nasal septum. On either side we notice curtain-like
folds projecting against the septum; these are the posterior aspects of
the turbinated bones. On either side of these and on the margin of the
drawing we notice pointed elevations projecting toward the interior of
the cavity, with a crater-like {40} depression on their apices; these
are the lateral pharyngeal walls with the orifices of the Eustachian
tubes. Above we see the vault of the pharynx, and below the posterior
surface of the velum palati with the uvula.

Another method of examining the laryngeal and naso-pharyngeal cavities,
which is especially valuable in cases where neoplasms or impacted
foreign bodies hide the parts forming the laryngoscopic and rhinoscopic
images, is by means of digital palpation. Even where no obstruction is
present the beginner will do well to resort to this method in all
cases, for he will thus become better acquainted with the topography of
the parts than by inspection only. The procedure is not as difficult
nor as disagreeable to the patient as might be imagined, and needs but
little description.

When the laryngeal cavity is to be examined by palpation, the head of
the patient is thrown back, and steadied in that position by the left
hand of the examiner while he introduces the index finger of the right
hand into the mouth and slides it along the back of the tongue until
the tip comes in contact with the upper margin of the epiglottis.
Passing downward along its lateral margin on either side, the
ary-epiglottic folds and the tips of the arytenoid cartilages can be
felt, and likewise the upper surfaces of the ventricular bands. The
vocal cords are, as a rule, too low down to be reached by the tip of
the finger. An examination of this kind should of course be made
quickly while the patient is holding his breath, so as not to obstruct
respiration too long, which in cases of narrowed glottis by neoplasms
might give rise to serious results. When the naso-pharyngeal space is
to be explored by the finger, the patient's head is bent forward, and
the index finger is gently pushed upward between the velum and the
pharyngeal wall. When this is accomplished, the velum is drawn forward
and the finger pushed along its posterior aspect until the different
portions forming the rhinoscopic image are reached and explored by the
sense of touch.




{41}

DISEASES OF THE NASAL PASSAGES.

BY HARRISON ALLEN, M.D.


Coryza.

Coryza is an acute inflammation of the mucous membrane of the nasal
chambers. The disease is ordinarily idiopathic, but may be produced by
irritative vapors, pollen, or dust. In the idiopathic form the symptoms
of coryza are often preceded by malaise, with chilly sensations, and in
severe attacks with headache. The attack itself is divided into two
stages: that of determination or congestion, and that of exudation. In
the first stage the excessive quantity of blood flowing into the
arterio-venous network and the capillaries of the nasal mucous membrane
distend them and obstruct the nasal chambers.

The symptoms are referable either to such obstruction of nasal
respiration--in which group are included oral respiration, sensations
of distension, and throbbing in the nose--or to reflexes, such as
frontal headache, attacks of sneezing, and dull aching pain in the
teeth.

The first stage lasts for a period varying from a few hours to several
days, and is followed by the stage of exudation. This is characterized
by a free watery or mucoid discharge from the nasal chambers, and by
the cessation of the symptoms due directly or indirectly to pressure of
the layers of swollen mucous membrane against each other. The discharge
at first is watery, and is doubtless composed of transuded liquor
sanguinis. It is followed by a mucoid fluid, which in severe or
neglected cases may assume a purulent character. In many instances,
even in mild cases, the discharge becomes muco-purulent toward
recovery. The second stage is associated in children and adults of
delicate constitution with excoriations of the nostrils.

Suppuration may take place in nurslings and in old people. It would
appear that in coryza, as it exists in the northern countries of
Europe, the beginning of the second stage is apt to be marked by free
suppuration.

Acute coryza may involve the sinuses of the face, particularly the
maxillary sinus. The involvement of the frontal and sphenoidal sinuses,
while possible, is infrequent. Pharyngitis, laryngitis, and
occasionally acute aural catarrh, often coexist with the disease.

The symptoms of coryza are so distinctive that the diagnosis is easily
made. But since any obstructive or catarrhal state of the nose is
described by patients as a cold in the head, it is necessary for the
medical attendant to distinguish the various diseases so denominated.
Acute coryza may be confounded with angiose hypertrophy; with the
obstruction to nasal respiration due to deflection of the nasal septum
or to an inflamed soft polypus; with catarrhal irritation affecting
surfaces which are already enlarged by hyperplasia or which are
undergoing atrophy; or with the effects of operative interference in
the nose.

In angiose hypertrophy the swollen membranes will contract under a mild
{42} current of electricity or by change in the position of the body.
Both chambers are rarely involved at the same time. Reflexes are of
infrequent occurrence. Obstruction to nasal respiration due to a
deflected septum arises from causes which are insignificant and do not
affect the constitution. The genuine influenzal or catarrhal element is
absent. In an inflamed soft nasal polypus an attempt at inspiration
will, as a rule, detect the presence of the growth. In diffuse multiple
polypi the case is different. Many persons who are reputed to take cold
readily, or who may be said never to be free from cold, are really
sufferers from neglected polypi. Persons suffering from atrophic
catarrh always speak of an exacerbation of their symptoms as a fresh
cold, and describe the disease itself as a cold. The sense of fulness,
the throbbing, the heat, and the characteristic discharge of coryza are
absent. A fresh cold in atrophic catarrh is an attack of inflammation
(often catarrhal in character, it is true) which affects the involved
surfaces, but is attended with an increase of plastic exudation and
accompanying fetor.

It is a common occurrence for patients who have had a cautery
application made or a polypus removed to return after a few days'
absence with the report that they have contracted a cold. While the
condition may be an attack of acute coryza, the chances are in favor of
the symptoms being excited by the manipulation or the reaction from the
operation. The symptoms are mild in character.

TREATMENT.--The treatment of coryza is both local and constitutional.
The local treatment consists in applications of agents which tend to
constrict the vessels of the nasal mucous membrane. In the first rank
of such agents may be named cocaine, which in a 2 per cent. or a 4 per
cent. solution will often give notable relief by overcoming the sense
of obstruction. Individuals will be found in whom the effect is of
short duration, and in some persons I found the medicine to have no
effect whatever. In more favorable subjects the relief will be
acknowledged for a period varying from four to six hours. Next in rank
may be named a current of constant electricity (say from six to ten
cells) passed through the cheeks. Should neither of the above-named
agents be available, inhalations of iodine vapor, a few drops of
chloroform rubbed upon the palms and inhaled, or the inhalation of the
spirits of ammonia may be recommended. Toward the later stages of the
disease detergents and mild astringents are well borne. The
constitutional treatment includes the administration of diaphoretics
and minute doses of opium, especially in the early stages of the
disease. Coryza is commonly self-limited, and by far the larger number
of cases do not come under the care of the physician.


Chronic Nasal Catarrh.

Chronic nasal catarrh embraces those more or less persistent affections
of the nasal chambers whose symptoms resemble those of acute coryza.
The term catarrh is inexact. It is used to include several diseases
associated by a single characteristic--namely, the existence of an
increased amount of mucous secretion upon the affected membranes.

In order to understand the varieties of nasal catarrh, it is necessary
to have clear conceptions of the uses of the nasal chambers. The normal
performance of the function of respiration demands that when the mouth
is closed the currents of air should pass through the nose. These
currents, however, do not sweep over the entire nasal surfaces, but are
confined to those portions which answer to the inferior meatus and the
space bounded within by the septum, without by the median surface of
the inferior turbinated bone, and above by the under surface of the
middle turbinated bone. In the lower mammals this space is separated
posteriorly by a transverse bony lamina which {43} effectively excludes
the upper portion of the nasal chambers from the tract just named.
Anteriorly, at the termination of the inferior meatus and the middle
turbinated bone, the tract is in freer communication with the upper
spaces. The passage thus briefly defined may be called the respiratory
tract, and when it remains patulous no serious interference with nasal
respiration can occur.

The transverse diameters of the tract are subject to frequent changes,
owing to the erectile character of the mucous membrane in its walls.
But as long as the surfaces do not touch one another obstruction cannot
exist. The passage, even when narrowed to a chink or line intervening
between the median and lateral walls of the tract or between the floor
and the roof of the inferior meatus, is sufficient evidence that there
is room for the transit of the currents of air. The membranes
themselves are subject to changes in form which are dependent upon the
degree of development of their erectile tissue.

There is doubtless a disposition on the part of the erectile tissue to
grow in the direction of the least resistance, and thus to occupy, by a
process of compensative hypertrophy, the spaces left as the result of
variations or defects in development in the bones composing the
framework of the nasal chambers. The greater development of the
erectile tissue may in this way be found on the side answering to the
larger respiratory tract, which may therefore be more apt to suffer
from changes in the conditions of nasal breathing than the chamber
having the smaller tract. The erectile tissue acts as a monitor to the
throat and lungs by presenting warm surfaces over which the air passes,
thereby having the temperature raised before it enters the throat and
lungs. It also acts by occluding the chamber, and thus aids in shutting
out irritant vapors and dust. The lower animals possess a higher degree
of development of the tissue at the point where the adducted ala
presses against the septum. This point answers to the position of the
organ of Jacobson. With man, the locality of the adduction corresponds
to the junction of the premaxillary with the maxillary portion of the
nasal chambers, and is often the seat of a delicate band of mucus
extending across from the inferior turbinated bone to the septum.

That portion of the nasal chamber above the respiratory tract may be
called the olfactory tract. It does not appear to be involved in the
diseases under consideration, or, if it is, no clinical signs or
symptoms are presented with which the author is acquainted. It will
therefore receive no attention in this article.

For convenience the varieties of chronic catarrh may be classified as
follows:

FIRST VARIETY--that dependent on defective nasal respiration.

This variety is caused by--

  _(a)_ Osseous obstruction in the nasal chamber.

  _(b)_ Membranous obstruction in the nasal chambers from compensatory
          hypertrophy of the erectile tissue, alone or with
          hyperplasia.

  _(c)_ Obstruction arising from hypertrophy of the adenoid tissue in
          the pharyngeal vault.

  _(d)_ Contracture of the levator palati muscles.

SECOND VARIETY--that dependent on structural changes in the component
parts of the nasal chamber.

This variety is associated with--

  _(a)_ Chronic inflammation of the nasal mucous membrane without
          hypertrophy of the erectile tissue.

  _(b)_ Atrophy of the turbinals and their associated mucous membrane.

  _(c)_ Necrosis of the bones which enter into the framework of the
          nasal chambers.

FIRST VARIETY.--Defects in nasal respiration induce hyperæmia,
distension of the erectile tissue, hyperplasia of the mucous membrane,
and {44} inevitable distress in the nose. A sense of fulness across the
bridge of the nose and at its sides is complained of. Frontal headache
may be present.

_(a, b)_ When the septum is deflected and the left nasal chamber is
narrowed, the labor of sustaining nasal respiration is thrown on the
right side. This arrangement invites a flow of blood to the already
large turbinals, and creates obstruction which is frequently referred
to the right side, although both are alike affected. Thus, subjects in
which the initial obstacle is osseous complain of distress caused by
cavernous-tissue hypertrophy of the lining membrane of the opposite
side. This represents a very common class of cases.

When the septum is not deflected, but projections from it impede the
current of air, there may be either unilateral or bilateral
obstruction, dependent upon the shape of the septum itself. Hypertrophy
of the cavernous layer of the mucous membrane usually coexists. These
cases are numerous, but less common than those last described.

Infrequently, cases are seen where the distress is occasioned by
defects of the osseous structures not accompanied by cavernous
hypertrophy.

Treatment of the above disorders consists in restoring nasal
respiration by removing obstructions, whether they be osseous or
membranous. The septal projections may be drilled or filed away, or, if
marked deflection of the anterior portion be present dependent upon a
malposition of the triangular cartilage, an operation simple in
character may be performed for its correction. This consists in
severing the connection of the lower margin of the cartilage with the
maxilla and slipping the partially free cartilage to a new position.
The details attendant upon the operation need not be here given. The
reduction of the hypertrophied membranes can be best accomplished by
cauterization. The most efficient method is by means of the electric
cautery. The electrode used should be flexible and of small size. The
points which most frequently require cauterization are the premaxillary
portion of the inferior turbinated bone, the under surface of the same,
and the septum at the maxillary spur. Rarely the inferior surface of
the inferior turbinated bone at the palatal region requires attention.
The applications are best made over small surfaces at a time, and
should be repeated at intervals of from two to three days until all
suspected points have been at least once cauterized. Not infrequently,
the effect of the cauterization at one spot will cause constriction to
take place in the vessels of the entire mucous surface, so that while
this condition lasts it is impossible to tell what additional points of
the membranous obstruction demand removal. At the following visit,
however, the vessels have become relaxed, the membranes are again
turgescent, and if obstruction now occurs it can easily be detected.

The galvano-cautery can only be used in the nasal chamber in patients
who are earnestly seeking relief and are willing to assist the
physician in all his efforts. With the tractable, intelligent subject
it can with proper care be limited exactly to the spot intended. It is
scarcely necessary to observe that any erratic or unexpected motion of
the head will sear unaffected and sensitive surfaces. The interior of
the vestibule is perhaps the most sensitive of these, and should always
be protected by the use of the nasal speculum. No additional protection
is needed, though in the judgment of others, among whom may be
mentioned E. Shurly of Detroit, Michigan, an ivory shield passed in the
nose parallel to the electrode is a necessary safeguard.

The pain of the application is generally slight, and can be in part
annulled by a previous application of a 4 per cent. solution of
cocaine. Some annoyance is acknowledged on the following day from the
pressure of the eschar. Traumatic congestion of the entire mucous
surface of the corresponding chamber is at the same time detected, and
is usually sufficiently decided to produce some of the effects of acute
coryza. This condition will spontaneously terminate in from thirty-six
to forty-eight hours. The most annoying features {45} following an
application of the galvano-cautery which has been too freely made do
not belong to the group just indicated, but rather to reflex
disturbances. Pains are occasionally excited in the teeth, in the
temple, eye, nape of the neck, and the middle ear. On one occasion in
the writer's experience a unilateral reflex excitation of the entire
opposite side of the body occurred, and a prickling sensation, followed
by numbness, ensued, which lasted for twenty-four hours. Very rarely a
congestion of the pharynx, of the larynx, and the larger bronchial
tubes ensues, which can scarcely be directly attributable to the
application, yet it has followed in a sufficient number of cases to
lead me to believe that the two are in some remote way associated.
Perhaps such a condition is analogous to the slight irritation of the
respiratory tract following excision of the tonsil. Careful use of the
galvano-cautery will obviate the conditions above described. They are
important to remember as serving as limitations to the use of this
valuable agent.

_(c)_ It will be seen that osseous obstruction in the nasal chamber and
hypertrophy of the cavernous nasal tissue often coexist. More rarely, a
third element occurs as a complication, or it may be found
independently of all other morbid processes. I allude to the presence
of hypertrophy of the adenoid tissue in the pharyngeal vault. When this
tissue is only moderately developed, it need not, and does not,
interfere with nasal respiration; but when it projects downward to such
a degree as to lie within the axis of the lower portion of the
posterior nares, it produces the same effect upon nasal breathing as
though obstruction existed within the chamber. The growths can be
easily detected, as a rule, from behind by the aid of the rhinal
mirror, but it should not be forgotten that they also can be seen from
in front, provided the chamber is free from obstruction along the
respiratory tract. In some individuals the ribbed or lobate structure
of the mass can be discerned, but more often its presence is revealed
by the minute points of light reflected from the lobules. If it be a
matter of doubt whether these points of reflection are within the nasal
chamber or beyond it in the pharyngeal vault, the patient may be
requested to swallow, or to pronounce the letter _e_; when, if the
point of reflection is within the nasal chamber, it will not change its
position, but if it be within the naso-pharynx, it will be moved
slightly from side to side, or it may for a moment disappear.

The symptoms of nasal catarrh which are provoked by the presence of
such a growth can be alone successfully treated by the removal of the
offending mass. In young individuals--say, from twelve to eighteen or
twenty years of age--the finger inserted into the naso-pharynx from
behind can often break down the growth. Slight hemorrhage follows this
procedure, and the tags of imperfectly-destroyed tissue can be
subsequently treated by caustics and powerful astringents. In the event
of the patient proving intractable, the growth may be reached from in
front through the nasal chamber, and the galvano-cautery can be used by
passing the electrode backward through the nostril until it meets with
resistance, which is invariably at the pharyngeal vault. Should this
method of treatment not be permitted by an undisciplined or nervous
person, the prolonged use of a glycerole of iodine may gradually reduce
them in size; but no definite result can be promised from such
treatment.

_(d)_ Very rarely, through inordinate elevation of the soft palate
owing to over-action of the levator palati muscles, the passage of
communication between the naso-pharynx and the oro-pharynx is
inadequate. Consequently, the nasal chamber is imperfectly ventilated,
and its secretions, not flowing backward or being displaced to the
normal extent, become semi-inspissated, and create obstruction by
lodging in the respiratory tract, either in the premaxillary or palatal
portions. To successfully combat this condition it is evident that no
local treatment is demanded, either in the nose or the naso-pharynx,
other than to increase the tonicity of the pharyngeal and palatal {46}
muscles. Very frequently in such cases there is a symmetrical atony in
the muscles last named, which demands the internal use of strychnia and
iron and the application of galvanism.

PROGNOSIS.--When nasal catarrh has proved to be dependent on defective
respiration, the removal of the causes entering into this condition may
with reason be expected to effect recovery. The prognosis, therefore,
is favorable. In young persons, in whom reparative power is present in
the highest degree, and in whom a secondary hypertrophy of the
cavernous tissues is least developed, a prompt cure may be obtained by
removal of the osseous or other forms of obstruction. In adults,
however, the prognosis is less favorable, especially with those who
have approached or passed middle life, and who have contracted vicious
habits of breathing, which are likely to persist even after the removal
of their causes. It is also tenable that in such subjects the mucous
lining of the cranio-facial sinuses has become involved. Should anosmia
persist after the capacity of the chambers has been augmented--in a
word, should this condition not be dependent upon obstruction, but upon
changes in the olfactory surfaces--the prognosis is less favorable than
in any of the cases of the above-named group.

Treatment will, however, always secure amelioration of the symptoms,
and few cases occur which cannot be greatly improved. The general
health is invariably benefited. Should a tendency to asthma exist, it
is apt to disappear, the complexion clears, and in adolescence the rate
of general development is accelerated.

SECOND VARIETY.--The group of nasal diseases included under this head
is not a natural one, since it embraces disorders characterized by a
negative feature--viz. absence of obstruction to nasal respiration.
Nevertheless, it is convenient to consider under a single head a number
of relatively infrequent disorders in which there is invariably an
underlying constitutional cause. Subjects of disorders herein embraced
are not merely sufferers from insufficient oxygenation of the tissues,
but have impaired general vitality or possess a decided constitutional
taint, whether specific or otherwise. The nasal condition is simply the
most prominent of the local manifestations.

Three distinct disorders are herein named: first, chronic inflammation
of the nasal mucous membrane; second, atrophy of the turbinals and
their associated mucous membrane; third, necrosis of the bones entering
into the framework of the nasal chambers.

_(a)_ Inflammatory thickening is a rare affection. It is more frequent
in males than in females, and in persons of a sedentary occupation than
in those who are actively employed. Those subject to it are apt to have
light-blue or gray eyes and auburn or sandy hair. On examination, the
chambers may be found free from peculiarities of bony structure,
capacious, and without hypertrophy of the cavernous tissues, yet the
membranes be of a deep-red color and of cushiony consistence, yield
bright reflexes, and the shank of the instrument introduced into the
nose is mirrored upon them. The most conspicuous alteration is not seen
on the turbinals, but on the septum. The parts are very vascular, and
the most moderate manipulation will often end in free capillary oozing.
The discharge, though moderate in quantity, is inclined to be purulent,
and resembles semi-coagulated albumen. Quite frequently, in the
examination of a neglected case, minute flecks of this modified
secretion are seen scattered over the septum and the inferior
turbinated bone. Rarely, the discharge is maintained by the presence of
a morbid growth or inflammatory products, either in the nasal chamber
or a chamber accessory to it. The discharge then appears to consist of
pure pus mixed with the normal secretion of the nose, and, thus
rendered viscid and tenacious, it excites by its presence a condition
of the lining mucous surface quite similar to that above described.

{47} Under excitement, as after an attack of coryza, the discharge
becomes more serous in character, and is occasionally of a chocolate
color from its admixture with blood. It is without odor. There is no
obstruction to respiration except during sleep, when, in aggravated
cases, mouth-breathing may be established. Thus, the patient will often
complain of an obstruction which is never present at the time of the
examination. He further complains of a sense of dryness in the nose,
with some pharyngeal irritation. The palato-pharyngeal and
palato-glossal muscles are weak and often asymmetrical; the tonsils are
small, but the adenoid tissues are generally unaffected. In a dry
atmosphere, especially if it be loaded with irritating particles, the
pharyngeal irritation is increased--a complication which is probably
due to the inspired air passing too rapidly through the capacious and
imperfectly-guarded nasal chambers and throat. Although I have
carefully searched for all indications of aural complications,
especially for the symptoms of progressive dry catarrh, I have never
detected them but in a single instance.

The prognosis is to be guarded, although a careful course of treatment
and proper care of the general health will greatly improve, if not
entirely cure, the disease.

TREATMENT.--This consists in the application of nitrate of silver,
either in strong solution or in the solid stick, to the under surface
of the inferior and middle turbinated bones, of washing the parts with
a dilute solution of carbolic acid, and of passing through the cheek
tissues a constant electrical current of a strength of from five to ten
cells. Tonics and alteratives should not be neglected, and an outdoor
life, as far as is practicable, should be enjoined. The galvano-cautery
may be used to destroy any nodules of tissue which resist other
treatment. All applications are well borne, if indeed we may not look
upon the condition of the surfaces as partially analgesic, and thus far
of unfavorable significance. It is certain that indurated tags of
oedematous and chronically inflamed mucous membrane overlying a bone,
such as the middle turbinated or the alveolar line about the necks of
the teeth, will never yield to anything but the most powerful
astringents. Upon such tissues the most concentrated solutions of
nitrate of silver are never caustic. The premaxillary portion of the
inferior turbinated bone is frequently seen hopelessly infiltrated, and
it must then be destroyed by the electro-cautery. When a discharge of a
pus-like character exists, careful search should be made for the cause.
If a tumor or foreign body be found, it should be removed, but if the
cause lie in one of the outlying spaces of the nasal chamber, it is
evident that the above treatment is palliative only.

_(b)_ In atrophy of the nasal mucous surfaces and turbinals we have, as
in the last-named group, spacious chambers, a purulent discharge,
pharyngeal irritation (in many cases), and always associated a thin and
relaxed, if not a paretic, condition of the velal muscles. These cases
might be looked upon as an advanced stage of the preceding affection,
since it may be surmised that the stage of infiltration has been
succeeded by one of atrophy. The mucous membranes are everywhere pale,
and closely bound to the underlying bony framework. The discharge is
purulent and confluent; where in contact with the air it is desiccated,
but where protected, as by crust-like surface-layers, it is semi-fluid
and tenacious. There is, consequently, no disposition for the discharge
to escape from the nose, and it accumulates until the sense of
obstruction induces the patient to remove it by artificial means. When
first seen, the nasal chambers are frequently so fully occupied with
discharge as to conceal the characteristic appearances of the mucous
surface. This prolonged retention induces incipient decomposition of
the mass, which gives rise to the odor so characteristic of this group
of cases.

The subjects of atrophic catarrh (ozæna) are never in robust health.
They are, as a rule, of spare habit, anæmic, and with family histories
which, while {48} not distinctive, indicate that the affection is, to
some degree at least, hereditary. A few cases have come under my notice
in which all the general features of atrophic catarrh were present, but
with very slight although confluent discharge, unaccompanied by fetor.
Such cases are, strictly speaking, examples of atrophic catarrh, while
they could not, under the old nomenclature, be included under the head
of ozæna.

The prognosis is unfavorable for entire recovery, but treatment
systematically pursued will make the patient entirely comfortable to
himself and others--will arrest the progress of the disease and vastly
improve the general health. As in other forms of nasal disease, should
anosmia be present the prognosis is less favorable.

[Illustration: FIG. 19. Antero-posterior section of the bones of the
face in position, showing the premaxillary portion of the floor of the
nose greatly elevated above the plane of the remaining portions. In
ozæna, as mentioned in the text, a disposition of parts may exist
similar to that delineated, and cause discharge to collect and undergo
offensive decomposition.]

TREATMENT.--The parts should be carefully cleansed--an act which, while
imperfectly accomplished by either the syringe or the douche, is, in my
judgment, best performed by the galvano-cautery. This instrument, the
one relied upon for the subsequent treatment of the case, is to be
selected for its initiation. The largest speculum which the nose will
admit being placed in position, a spiral-looped electrode is introduced
cold into the nose and held against one of the crusts. When heated it
will effect so firm an attachment to it as to enable the mass to be
withdrawn with great ease. In patients with {49} whom the palatal
portion of the floor of the nose is depressed below the level of the
maxillary a considerable quantity of discharge may lie concealed from
observation. When, after the removal of all visible crusts, the fetor
persists, it is reasonable to suppose that the palatal depression is
filled with decomposed pus and mucus. To test such a condition, the
electrode should be appropriately curved and introduced. I have been
surprised at the quantities of discharge which can in this way be
withdrawn from a locality which, as far as I know, cannot be cleansed
in any other way.

With the removal of the crust relief is at once experienced, and if the
discharge could be removed as fast as it forms the disease would not
really be a source of offence. The general health would also improve,
from the fact that an atmosphere tainted with a burden of decomposition
would no longer be breathed. But in practice this cannot be attained,
and it is imperative, after the chambers have been entirely cleansed,
to cauterize the lining membrane throughout. I have been in the habit
of beginning such cautery treatments with the middle turbinated bone,
passing thence to the inferior turbinated bone, then to the roof of the
nose in front of the sphenoidal sinus, and lastly to the septum. Small
surfaces only should be covered at a single treatment, so that it may
take a month or six weeks to finish a single series of applications.
This treatment is almost always well borne, nothing ever ensuing beyond
a slight headache or a temporary establishment of a serous discharge.
Notwithstanding that the condition in question is one of atrophy, the
reparative power of the mucous membrane remains apparently unaffected.
At all events, no danger from sloughing is to be dreaded after such
extensive destruction of tissue. The thin eschars separate within from
three days to a week, leaving a healthy mucous membrane beneath. In one
instance the cauterization had extended to a sufficient depth to expose
the bone, and yet from this denuded surface no exfoliation took place,
the parts healing rapidly and satisfactorily. No other local treatment
is relied upon for fetid atrophic catarrh than the one mentioned. No
disinfectant washes are required if the discharge is removed as
described. Should the patient be so situated as to be unable to report
regularly for its removal or treatment, a wash composed of one part of
Labarraque's solution to sixteen parts of water may be ordered with
advantage, or a solution of carbolic acid, gtt. j to fluidounce j, with
a little glycerin, may be snuffed up the nose twice a day, or
listerine, diluted one-half with water, may be used with advantage. The
general health, of course, should be cared for, and any complications
met. I have found that during the winter months arsenic and cod-liver
oil are well borne, associated with minute doses of Lugol's solution.
For adolescents earthy and the calcareous phosphates are indicated, and
for all abundant exercise and careful dieting. When the symptoms have
been relieved, the patient should be requested to report once a month,
for it is not to be expected that all symptoms will disappear, and some
point of advice can be advantageously offered at this interval.

_(c)_ Necrosis in the nasal chamber is a cause of catarrh, inasmuch as
the fragments of bone lying within the nose excite irritation and
induce discharge. I have never seen a case of this form of disease
which was not due to syphilis. The remains of syphilitic angina are apt
to be present, and the general manifestations of constitutional
syphilis are well developed. The septum is more frequently affected
than the turbinals.

Discharge due to necrosis can be readily distinguished from that
arising from any other cause by the presence of detached fragments of
denuded bone, by the characteristic fetor, and by the history of the
case.

The prognosis is favorable, for all symptoms will cease upon the
extraction of the fragments, or at least those which remain are of an
entirely different character, and are due to the resultant
imperfections of the septum, and consequent irritation arising from the
too free entrance of air into the {50} nose. I have seen in one case an
extensive tumefaction and infiltration of the tissues covering the
middle turbinated bone at the same time that the septum was breaking
down. These masses require treatment with the galvano-cautery and
astringents after the dead fragments have been removed.


A TABLE OF NASAL DISEASES GROUPED BY SYMPTOMS.

Cases in which interference with nasal respiration is a conspicuous
symptom:
  Due to deflection of nasal septum (common).
  Due to angiose hypertrophy of the mucous membrane (common).
  Due to tumors lodged in the nasal chamber.
  Due to adenoid hypertrophy in the naso-pharynx.
  Due to over-activity of the levator palati muscles (rare).

Cases in which discharge is a conspicuous symptom:
  Due to hyperplasia of the mucous membrane over the turbinated bones
    (common). The discharge when flowing backward is described as a
    dropping; when forward, as a running at the nose. The discharge is
    either mucoid or muco-purulent.
  Due to tumors lodged in the nasal chambers or appendages. The
    discharge is usually excessive. When due to myxomata (polypi) the
    discharge is mucoid (common). In inflammatory complications of the
    same the discharge is muco-purulent (common). When due to neoplasms
    other than myxomata the discharge is purulent, and rarely
    muco-hæmic (rare).

Cases in which retention of mucus in the nose or upper part of the
    throat is a conspicuous symptom:
  Due to retention of inspissated mucus at the roof of the naso-pharynx
    (common).
  Due to the mucous secretion of the nose and throat being excessively
    tenacious (rare).

Cases in which fetor is a conspicuous symptom:
  Odor putrid.
    Due to retention and decomposition of plasmic exudation from
      atrophied bone and mucous membrane (common).
    Due to necrosis of the bones within or bordering upon the nose
      (rare).
    Due to decomposition of muco-pus in the maxillary sinus (rare).
  Odor musty.
    Due to partial decomposition in small patches of desiccated mucous
      crusts (common).
    Due to morbid secretion unaccompanied by profound alteration in the
      structure of the nose (rare).
    Due to ulcerations of the mucous membrane (rare).

Cases in which a sense of dryness is a conspicuous symptom:
  Due to ineffective erectile tissue permitting air imperfectly warmed
    to enter the nose and the pharynx (often met with in neurosis). It
    is caused by temporary constriction of the erectile tissue or by
    the atrophy of the tissue.
  Due to neurosis. Neurotic patients will often complain of a sense of
    dryness in the nose and the naso-pharynx when all the conditions of
    excessive mucoid discharge are present.

Cases in which hyperæsthesia exists, so that slight lesions that in any
    way interfere with the nasal functions form the basis of persistent
    complaint (not infrequent).


Epistaxis.

Epistaxis, or nose-bleed, is a form of local hemorrhage perhaps of more
frequent occurrence than hemorrhage from any other mucous surface of
the body. This is doubtless owing to the extreme vascularity of the
lining membrane of the nose and the special arterio-venous (cavernous)
spaces of the turbinated bones; and the bleeding may be said to be of
grave character in proportion as these spaces are involved. In some
individuals a special disposition to nasal hemorrhage exists. From the
fact that the affection is transmitted from parent to offspring, and is
frequently found in all members of a given family, this form of
hæmophilia is probably dependent upon some structural peculiarities in
the cavernous spaces.

The causes of epistaxis are both local and general. Among the local
causes may be included traumatism, either from blows or other injuries,
attempts on the part of the patient to relieve irritation by picking
the nose, or from the {51} use of cutting or other instruments in the
hands of the surgeon. Septal ulcerations in this way are often
accompanied by moderate bleeding. In a case reported by R. G. Curtin
the nasal branch of the ophthalmic artery was thought to have been
ruptured. Among the general causes the most frequent is undoubtedly the
depressed state of the system preceding or accompanying typhoid and
other anæmic states. Thus, among the prodromes of typhoid fever
epistaxis holds a conspicuous position. It is also seen in chlorotic
females, especially in those suffering from that phase of anæmia known
as Grave's disease. It also occurs in vicarious menstruation and in
local facial or encranial congestions. In those disorders of nutrition
accompanied by a tendency to capillary extravasation, such as purpura
and scurvy, the nasal mucous surface participates in the general
disorder. In a case of the former disorder coming under the notice of
the writer the blood had forced its way out in large quantities by
every capillary avenue.

TREATMENT.--Epistaxis when a symptom of a dyscrasia is of course to be
treated as a local expression of a general condition. In typhoid fever,
scurvy, and purpura or anæmia the bleeding is a sign of the general
distress, and requires no special local method of treatment. Epistaxis
when of local character should be treated, first, by removing the
cause; second, by diminishing the flow of blood to the part; third, by
cold and astringent washes to the affected surface; and, fourth, by
compression.

First. Should the bleeding be kept up by fragments of bone impinging
upon or lacerating the mucous membrane, they should be restored as far
as possible to their natural position and retained there by appropriate
apparatus. If they are entirely denuded of their periosteum and mucous
membrane, they should be removed. Foreign bodies should be extracted,
and if septal ulceration be present it should be carefully treated, the
crusts removed, the ulcerated surfaces touched with nitrate of silver
in stick, and the nasal chamber plugged from in front to exclude the
outside air.--Second. The position of the body is of great importance
in treating epistaxis. The recumbent position is no doubt to be
preferred. The patient often holds one arm elevated or ties a cord
about the proximal end of a limb. These innocent accessories to
treatment may be permitted, since they are based upon well-known
physiological principles, although it must be said that the bleeding
can in all instances be checked without their aid. Cold applications to
the nape and sides of the neck are often of service. Various internal
remedies, such as ergot, gallic or sulphuric acid, and erigeron, may be
administered with good effect in addition to the local
measures.--Third. Astringent washes, such as a solution of alum--about
drachm j to the pint--will often check a moderate degree of capillary
bleeding without other aid. Tannic or gallic acid may also be used.
Should these measures fail, the Monsel solution may be used on pledgets
of cotton carried up to the bleeding spots. In Curtin's case, already
quoted, a pledget saturated with the solution of the perchloride of
iron placed over the nasal branch of the ophthalmic artery promptly
arrested the bleeding. In lieu of these styptics the platinum wire loop
of the galvano-cautery battery may be used. The writer has often
succeeded in checking bleeding after a removal of a polypus or the use
of the galvano-cautery when the exact position of the hemorrhage is
known by laying upon the affected spot a little square of patent lint.
It acts much as in checking the bleeding from a leech-bite.--Fourth.
Compression of the mucous lining of the nose and exclusion of these
surfaces from the air--a method familiarly known as plugging the
nose--is the dernier ressort in the treatment of epistaxis, and is to
be relied upon in the event of failure of other methods. This failure
is, however, relatively infrequent. Observers agree in describing the
procedure tedious and rather disagreeable, as much to the operator as
to the {52} patient, who has already been exhausted by loss of blood
and the previous measures resorted to for his relief.

[Illustration: FIG. 20. Bellocq's Canula.]

The instrument usually relied upon for this purpose is known as
Bellocq's canula (Fig. 20). This little instrument consists of a hollow
curved tube of metal fashioned somewhat like a Eustachian catheter, and
bearing within it a flexible and adjustable metallic band which carries
at its extremity an eyelet. Any one who has used the Eustachian
catheter will recall the number of instances in which it could not be
passed, or if passed the frequency in which great distress followed. If
this be true of the Eustachian catheter, it is also true of the Bellocq
canula, the difficulty in the case of the catheter, indeed, being the
lesser of the two, inasmuch as the physician has a number of sizes to
select from. Conceding, however, that the instrument (with a long stout
thread passed through the eyelet of the stylet) has been placed in
position in the nasal chamber, one end of the thread is seized within
the mouth and brought out between the lips, while the other, carried by
the instrument, is withdrawn through the nose and is allowed to hang
from the nostril. The two ends of the thread are now tied firmly
together, and a pledget of lint or cotton, fashioned somewhat after the
shape of the posterior naris, is tied to the thread. Traction is now
made upon the nasal portion of the thread until the plug is firmly
lodged against and within the posterior naris. The remaining portion of
the oral thread is now cut off close to the velum, and the free end of
the nasal thread secured by adhesive plaster to the integument. The
nostril should next be stopped from in front by pledgets of lint or
absorbent cotton. The size of the nasal chamber and naso-pharyngeal
varies so markedly that a rhinoscopic examination is of use in fixing
upon the size of the plug. If it be too small, it will be drawn
entirely within the nose, and possibly beyond the bleeding spot. If it
be too large, it will partially or entirely occlude the posterior naris
of the opposite side, and thus by interfering with nasal respiration
greatly increase the distress, or by pressure against the Eustachian
fossa and velum interfere with the hearing and with deglutition. The
plug should be retained in position until a purulent mucus appears
within the nose: this is usually about the third day. The plug now
usually becomes a little loose, and can readily be withdrawn by pushing
it back into the pharynx, where it is seized with forceps. Too long
retention of the plug in position is followed by great fetor and the
free formation of muco-pus--conditions which tend to debilitate the
patient.

D. Hayes Agnew informs me that he for a long time practised stopping
nasal hemorrhage by plugging the chamber from in front. Strips of
patent lint four inches long by half an inch wide are employed for this
purpose. They are gradually pushed into the chamber until the entire
space is filled as far as is practicable. An essentially similar method
is described by F. H. Bosworth in his _Manual of Diseases of the Throat
and Nose_.


Morbid Growths.

These may be said to include the myxoma, sarcoma, fibroma, carcinoma,
also the true hypertrophies and submucous inflammatory thickening.

{53} The myxoma, more commonly known by the name of soft or gelatinous
polyp, is the most prominent of the morbid nasal growths. It occurs
ordinarily in small pedunculated seed-like masses, ranging in size from
that of a grain of wheat to a grape. The most common seat is on the
anterior portion of the middle turbinated bone and on the median
surface of the inferior turbinated bone at the palatal portion. Instead
of being pedunculated, they may be sessile; that is, each tumor may
have a base equal to, if not exceeding, any diameter of the tumor.

The symptoms of nasal polypus are of three kinds: (1) those arising
from obstruction of the nasal respiration; (2) those arising from the
irritation excited by their presence; (3) the symptoms, reflex in
character, manifested at points beyond the limit of the nasal chambers.

(1) The polypi necessarily tend to obstruct the respiratory tract of
the nasal chamber. The first symptoms are of this character, and as a
rule furnish the first intimation to the patient that trouble exists.
Difficulty of nasal respiration is acknowledged, accompanied with a
sense of tension and fulness, which is found to be worse during damp
weather than when the air is dry and bracing. If the growths are freely
pendulous, the act of blowing the nose may change the position of the
mass and secure temporary freedom from distress. Incidental to
obstruction, an intonation of the voice is often present. Loss of
smelling and of taste is a frequent result of the mass interfering with
the movement of the odoriferous particles. The loss of the sense of
taste is dependent upon the loss of the sense of smelling.

(2) Polypi when large enough to press against the membranes of the nose
excite an increased flow of mucus. As a rule, this flows forward, and
is removed by the handkerchief. The quantity of fluid thus escaping is
often very great. Patients often report the necessity of carrying about
with them for a single day's use from eight to ten handkerchiefs. In
the turgesence excited by an attack of coryza the mucus becomes thicker
and of a yellowish color. Occasionally a sensation of dropping of mucus
from the nose into the throat is a source of complaint.

(3) The reflex symptoms belonging to the presence of nasal polypi are,
as a rule, referred to the forehead. This is especially the case if the
growths involve the middle turbinated bone. When the tumors are so
located, and have not impinged upon the respiratory tract, the symptoms
of obstruction may be absent, and those of mucus excitement so moderate
as not to excite attention, while the tension in the forehead,
especially over the frontal bos, is pronounced. This sensation is
intensified by prolonged inclination of the head forward, being
especially aggravated in the acts of writing at a desk, working at a
sewing-machine, kneeling at prayer, etc. Occasionally tinnitus aurium
and suffusion of the conjunctivæ are present.

Neglected polypus ends in deformity of the nasal chambers and bones of
the face. The face assumes a peculiar expression called by the older
observers frog face. This is rarely if ever seen in this country, owing
doubtless to the fact that the sufferers from nasal polypus seek
medical advice in the early stages of the affection. Moderate degrees,
however, of deformation of the turbinated bones are often seen.

Since the symptoms of soft nasal polypus are produced entirely by
mechanical means, they can be closely imitated if not replaced by other
morbid states of the mucous membrane. A hyperplastic state of the
membrane over the middle turbinated bone will give rise to all the
symptoms of a sessile polypus in the same situation. It is well to
remember that this condition of the membrane often coexists with
polypus, and of course will persist after the polypus has been removed.
It follows that a guarded prognosis should always be made in case of
sessile polypus. A tedious course of treatment of the indurated and
chronically inflamed membranes may be required after the {54} tumors
have been removed before a cure is effected. The prognosis of soft
polypus is more favorable as to the immediate results of treatment than
in sessile polypus. The liability to recurrence can be materially
lessened by carefully conducted after-treatment.

The diagnosis of soft pedunculated polypus is readily accomplished if
the examination is made by aid of an appropriate speculum, the rhinal
mirror, and a powerful light. Even without these aids the tumors can be
seen by direct sunlight within the nostril if they are entirely
occluding the chambers, and even in the event of nothing being visible
by such inspection the movement of the masses by the act of blowing the
nose will be noticed. The fact that the nasal obstruction is aggravated
by damp weather seems to assist the physician in framing a diagnosis.

The diagnosis of sessile polypus requires a careful use of all the aids
of rhinoscopy. They can be distinguished from hyperplasia of the mucous
membrane by their lobulated form, and from the fact that the probe can
move them slightly from their base. They can be distinguished from
adenoid growths at the root of the pharynx by the fact that they remain
unmoved during the act of swallowing.

The disease is not apt to recur if the treatment is thoroughly carried
out.

The treatment of soft polypus consists in their removal. All observers
are now agreed on this point. Injection by astringents and acetic
acid--a process that at one time held out much promise--has been
generally abandoned. In removal of the polypus one of two methods may
be resorted to: that by avulsion, and that by the use of the snare.
Avulsion is effected by forceps adapted for this special use. With such
an instrument the polyps can readily be seized and removed. The rule
that nothing should be seized which is not seen is subject to no
exception. In no other way can the operator be secure against
accidents. Incautious operators have frequently torn away strips of
mucous membrane or portions of the turbinated bones in their crude
attempts to remove these growths. Severe hemorrhage and death through
violent lacerations of the ethmoid bone near the cribriform plate, and
subsequent extension of the inflammation thereby excited to the
membranes of the brain, have been known to follow these crude surgical
procedures.

[Illustration: FIG. 21. The Author's Nasal Forceps.]

W. C. Jarvis of New York has modified the wire snare for application to
the nose for the removal of polypi and hypertrophied tissues, and
reports that it is a safer, more expeditious, and less painful method
of operation than the forceps, which he unqualifiedly condemns. His
instrument, while undoubtedly an ingenious adaptation of the principle
of the snare, and a valuable addition to our means of treating nasal
affections, cannot, in my judgment, take the place of the forceps in
removing nasal polypi. As the aurist finds both the forceps and the
snare useful in removing growths from the external meatus of the ear,
so I am sure the physician will need both in the treatment of nasal
polypi. In many cases the malformations of the nasal septum are such
that {55} I have been unable to use the snare where the forceps could
be used with relative ease. I find when the loop is quickly drawn the
same amount of bleeding follows as when the forceps are used. When it
is slowly drawn, the sitting is tedious, and both the patient and
attendant find the process wearying. The amount of blood lost when the
forceps are properly used is not considerable, and is always under
control. F. H. Bosworth[1] describes the operation as extremely
painful. So far from this being the case in my experience, I find the
patients complain greatly of the constriction of the wire loop on the
pedicle of the polypus, and invariably prefer the forceps. I must add
that this preference was in no way influenced by myself, for I was
disposed at one time to agree with the writers who have of late
criticised the method of removal of the polyps by avulsion.

[Footnote 1: _A Manual of Diseases of the Throat and Nose_, 1881, p.
241.]

No matter which of the methods be accepted, the treatment of polypus
resolves itself into two simple propositions. When one or two large
polypi are present in a capacious nasal chamber, the removal of the
growths either by avulsion or snaring is a simple matter, and can often
be accomplished in a single sitting. When numbers of small polypi are
scattered over a large surface, particularly if they grow from the
sides of the middle turbinated bone, the treatment is tedious, and even
after the growths are removed a series of applications are required to
cure the thickened and infiltrated mucous membrane.

Sarcoma, fibroma, and carcinoma are infrequent causes of nasal disease.
When located in the nasal chambers they do not present any characters
with which I am familiar which distinguish them from the expressions
they assume in other parts of the body. When involving the respiratory
tract they alike create symptoms by obstruction, by excitement of the
secretions, and by the reflexes due to the involvement of the branches
of the fifth pair of nerves. When situated in the olfactory track the
obstruction to nasal respiration is absent, but the reflex symptoms are
pronounced: the patient is liable to depression of spirits and to
frontal headache. Encroachment upon the orbital, pharyngeal, and
encranial spaces is common in the last stages.

Perhaps the most common way in which these morbid growths induce
symptoms referable to the nose is by obstruction of the respiratory
tract by the incursions of a mass originating at a point beyond the
limits of the nasal chambers. In this way a growth in the pharynx may
close one or both choanæ, or protrude into the nose from the
spheni-palatine space by breaking down the ascending plate of the
palatal bone as it forms the median wall of this space; or the growth
may project inward from the superior maxilla.

In one case under my care, of obscure growth high up within the nose,
which ended fatally by involvement of the membranes of the brain, a
tenacious mucus of a dark chocolate color was withdrawn from the nose
into the throat. The peculiar color of the mucus was found to be caused
by a mixture of blood. In my judgment, this peculiar mixture of blood
and pus was significant. The blood and mucus had not been mixed in the
nasal chamber to cause the chocolate or rusty hue, for then we would
have had the appearance customary in epistaxis of bright blood and
frothy mucus mechanically held together. The even dissemination of the
blood through the mucus would point to the conclusion that the blood
had escaped in small quantity at the time of the formation of the
mucus. Why such mucus does not constantly form in inflammatory states
of the mucous membrane of the nose, as it does from the pulmonary
mucous membrane in pneumonia, I am not prepared to say. But existing as
it did in a case where a deep-seated disease was present may be
accepted as a fact in some way connected with the invasion of a morbid
growth in and upon the nasal mucous surface.

The pharynx is always in a state of hyperæmia when morbid growths of
{56} the above groups are present in the nose. The front of the velum
is apt to be covered with a great number of minute papillæ, which,
however, are often seen in anæmic individuals, and are not therefore
pathognomonic.

The treatment of the growths enumerated and the general conduct of the
cases are subjects for the general surgeon, and a consideration of them
here would be out of place.

It may, however, be well to describe a few instruments which have been
found useful in the large group of cases where cauterization is the
principal treatment indicated. Foremost among these is the instrument
shown in Fig. 22, which combines advantageously the essential features
of the galvano-cautery and the wire snare.

[Illustration: FIG. 22. The Galvano-cautery Snare described in the
text: 1, the cable of the battery; 2, the canula (which is not shown in
full length); 3, the platinum wire; 4, the vulcanite carriage, with
screws holding the ends of the platinum wire in metallic contact with
the hinge-connections, by which the current is transmitted from the
battery; 5, a slotted barrel of aluminium; 6, a movable nut on the
screw; 7, a small portion of the screw disengaged from the slotted
barrel; 8, milled stationary screw-head.]

[Illustration: FIG. 23. The Double Battery employed by the Author: The
two sets of plates are seen united by a flat band of metal. The case
which encloses the two separate batteries opens in front, displaying
the cells, the plates (which are seen pendent over the cells), and the
treadle. Above the figure of the battery lies a figure of the Flemming
electrode handle and the electrode in position.]

It is well known that a loop of wire which is steadily narrowed has
great power in severing the attachment of tumors and other outgrowths.
When of a large size, it may be sufficiently powerful to pass through
bony structures, as well as the softer parts of the body. The principle
of the snare has been employed both in the throat, the ear, and the
nose; but when my attention was first directed to this subject the
forms available were too large and heavy for the delicacy of
manipulation demanded in removing small tumors lodged in the narrower
recesses of the nose. Moreover, no snare that I could then find would
permit the galvanic current to pass through the loop at the time it was
being narrowed. I was led, therefore, to inquire into the
practicability of an instrument which would at once be light, be of
small size, and yet be sufficiently powerful to remove that class of
hypertrophied tissues and polypoid growths which are of such frequent
occurrence in the nasal chambers. The instrument shown in Fig. 22
combines these qualifications, and satisfactorily performs the service
for which it was designed. The only feature of an essential character
which may be said to be novel is the fact that the platinum wire (3,
Fig. 22) forming the snare is covered with a uniform coat of copper,
excepting alone the portion forming the loop, which is bare. As a
consequence of this arrangement the current of electricity from the
battery is conducted through a double canula (2, Fig. 22) by means of
the copper. The length of the instrument being about 9½ inches, and its
weight less than ½ ounce, delicacy of manipulation is not interfered
with. Besides possessing all the features of the cold wire snare, it
has the additional advantage of securing a more rapid and painless
operation, without any hemorrhage. Sessile (pyramidal) or resilient
growths may be removed by first burning a groove of any depth into
them, after which the loop is drawn while the current is passing
through it. For this task the cold wire snare is obviously incompetent.
Growths of unusual size or hardness may be destroyed by the same
procedure, and nodules no larger than a grain of wheat may also be
excised with great nicety. {57} It will be seen that failure to remove
at least a portion of the growth attacked is an event exceedingly
unlikely to occur. I have been particularly struck with the facility
with which hypertrophies of the inferior turbinated bone can in this
way be treated; and if cocaine be freely applied before the operation,
it constitutes, in my judgment, the most speedy and the least painful
of any means by which such conditions can be reduced. By using a canula
with a curved end it is easy to snare growths situated on the posterior
portion of the inferior turbinated bone. The current passing through
the battery (Fig. 23, B) to the instrument can be interrupted by any of
the numerous devices with which the practical electrician is familiar;
or the treadle of the battery can be depressed and locked by the
lever-catch, and the interruption of the current be determined by the
pressure of the finger {58} on the knob in the handle (Fig. 23, A).
This is under all circumstances desirable, since the weight of the
cells is sufficient to demand considerable force to be exerted by the
foot--always enough to destroy the delicacy of the manipulation of the
instrument.

[Illustration: FIG. 24. Two Electrodes of peculiar shape in use by the
Author.]

An electrode which is wrapped nearly to its distal end (Fig. 24), and
used either in a straight or a curved form, is of great advantage in
reaching growths within the naso-pharynx. The straight form can be
thrust directly back through the nasal chamber, and the curved form can
be passed from the oro-pharynx to the naso-pharynx without danger of
burning the posterior border of the soft palate.




{59}

NEUROSES OF THE LARYNX.

BY HOSMER A. JOHNSON, M.D., LL.D.


DEFINITION.--Disorders of sensation or motion, or of both sensation and
motion, due to disease, first, of the centres from which the nerves of
the organ are derived; second, to disease along the track of the
nerves; third, to disease in the terminal distribution of the nerves;
fourth, to reflected irritation from neighboring or distant parts; and
fifth, to myopathic change. This last condition is not necessarily a
neurosis; it is nevertheless a cause of modification of the function of
the parts to which the nerves are distributed, often a result of
paresis or paralysis, and therefore inseparably associated with the
neuroses of the organ. Disorders of innervation, depending upon
structural disease of the larynx, such as ulceration or tumor, are not
included in this definition.

ANATOMICO-PHYSIOLOGICAL CONSIDERATIONS.--The framework of the larynx
consists of cartilages securely but rather loosely articulated with
each other. The movements of these cartilages produce changes in the
position and tension of the soft parts. The thyro-cricoid articulation
allows ginglymoid and sliding motion; the aryteno-cricoid, rotatory and
sliding motion; the hyo-thyroid, ginglymoid motion. The physiology of
the muscles of the larynx is quite complex, since nearly all have
fibres taking a number of different directions, and the changes in the
form and positions of the parts depend upon the combined action of
different muscles and parts of muscles which may be individually
brought into action to produce the required results. The muscles may,
however, be roughly divided into groups: 1. Constrictors of the
superior strait; 2. Dilators of the superior strait; 3. Adductors of
the vocal cords; 4. Tensors of the vocal cords, external, internal; 5.
Relaxers of the vocal cords; 6. Abductors of the vocal cords.

The superior strait of the larynx is closed by the action of the
oblique portions of the arytenoideus, acting in conjunction with the
ary-epiglottici, into which some of its fibres are continued, thus
drawing the cartilages of Santorini downward and inward and
approximating the ary-epiglottic folds and depressing the epiglottis;
while the thyro-epiglottici complete the closure by further depressing
the epiglottis. Fibres of the latter muscle, acting alone, may dilate
the superior strait by drawing apart the ary-epiglottic folds.

The transverse portion of the arytenoideus and the superior fibres of
the crico-arytenoidei postici approximate the arytenoid cartilages. The
crico-arytenoidei laterales, and also in a slight degree the external
fibres of the thyro-arytenoidei, rotate these cartilages, turning their
vocal processes inward: the action of the latter two muscles as
adductors is imperfect unless the arytenoids are drawn backward and
fixed by the arytenoidei postici.

The tensor group comprises a number both of the extrinsic and intrinsic
muscles of the larynx. The crico-arytenoidei postici draw the
arytenoids back, external rotation, and consequent abduction, being
prevented by other muscles. The anterior fibres of the crico-thyroid
and those fibres of the {60} sterno-thyroid inserted anterior to the
crico-thyroid articulation approximate the cricoid and thyroid
cartilages, and thus tighten the vocal bands. The posterior fibres of
the crico-thyroid slide the thyroid upon the cricoid, lengthening the
antero-posterior diameter of the larynx. This muscle, acting as a
whole, also compresses the alæ of the thyroid with the same effect. The
constrictors of the pharynx have a similar function. The hyo-thyroidei,
acting in conjunction with the elevators of the hyoid bone, draw the
thyroid forward and tilt it downward upon the cricoid. The form and
internal tension of the vocal bands are greatly influenced by the
thyro-arytenoidei, especially their inner fibres, while the ascending
fibres of the muscle draw the inferior portions of the vocal bands
upward and prevent the sagging of their edges. This muscle, acting
alone, has been thought to cause extreme relaxation of the vocal bands.
Modern research renders this statement of relaxation doubtful. The
contraction of those fibres of the sterno-thyroidei inserted
posteriorly to the crico-thyroid articulation tilts the thyroid upward,
and thus relaxes the tension of the bands.

The crico-arytenoidei postici rotate the arytenoid cartilages outward,
separating the vocal processes, and, acting in conjunction with the
posterior fibres of the crico-arytenoidei laterales, draw the
cartilages outward and downward.

In the cadaveric condition, which is one of relaxation of all the
laryngeal muscles, the glottis is neither closed nor widely open; the
epiglottis is erect against the dorsum of the tongue; the arytenoid
cartilages are slightly separated, so that the glottic opening is a
triangle with the base posteriorly, as in the act of inspiration, but
the separation is much less than in the act of breathing. This
condition is met with in paralysis affecting all the muscles of the
organ.

The nerves of the larynx are derived from the pneumogastrics. The
superior laryngeal is mainly a nerve of sensation for the parts above
the edges of the vocal bands. There are some notable exceptions to this
statement: a branch, external, descends to the crico-thyroid muscles
and is motor in its function. Filaments from the superior laryngeal
endowed with motor functions are also distributed to the folds
extending from the arytenoids to the epiglottis; these are the
ary-epiglottidean bands, and are concerned in the movements of the
epiglottis. It is probable that the arytenoids are also in part
supplied by the superior laryngeal; in other words, that both the
superior and inferior laryngeal nerves are mixed, branches from the
spinal accessory, as well as from the pneumogastric proper, entering to
each of these nerves. Beclard[1] states that the one, the spinal
accessory, is a nerve of phonation; the other, the pneumogastric, is a
nerve of respiration. The sensations of the mucous surfaces below the
glottis depend upon filaments from the pneumogastrics returned along
with the motor fibres from the spinal accessory. The two orders of
fibres go to make up the recurrents. The relations of the recurrents
themselves to the large vessels, as well as to the bronchial glands,
are of importance. At the point of their origin they are in close
relation with the aorta and right subclavian; they are also in close
relation with the top of the lungs. Disease of these organs and
structures, especially of the large blood-vessels, such as aneurism of
the aorta or subclavian, disease of the glands, tumors, abscess,
traumatism, etc., may modify or completely destroy the functions of the
laryngeal nerves. In short, anything or any condition by which pressure
may be made upon the pneumogastrics or recurrents may become a cause of
nervous disturbance in the larynx. In addition to this general source
of innervation, Elsberg[2] describes a special centre of sensation for
the throat in the medulla oblongata. He also describes three kinds of
sensibility in the larynx--tactile, dolorous, and reflex. Rossbach[3]
details experiments from which he concludes that there are nerve-cells
in {61} the mucous membrane of the larynx which preside over the
function of secretion. The larynx is endowed with at least two kinds of
sensibility: the one tactile--when exalted it becomes painful; the
other, reflex sensibility, is double. First, there is as a result of
excitement a contraction of the subjacent muscle, and there follows
closure of the glottis. This is seen in the application of irritants to
the parts, such as solutions of nitrate of silver or other escharotics.
There is no cough, but great difficulty of inspiration. Expiration is
free and easy. There may follow some degree of pain for several hours.
It will be seen that the phenomena are the same as those observed in
the irritation of other mucous surfaces. The irritation is immediately
translated into motion; this motion is probably reflex, but not
necessarily through the centres, such as the brain or cord. The motion
is of the subjacent muscles. Second, the mechanical irritation produced
by the presence of a drop of water or a morsel of food in the larynx
results in violent and explosive cough. The cough persists until the
offending drop or body has been removed. This kind of sensibility calls
into action distant muscles. There is no spasm of the adductors of the
glottis, as in the case of the application of caustics. It is probable
that the filaments of the nerves, the irritation of which gives rise to
spasm, are distributed more generally than those which preside over
reflex action at a distance and produce cough. The one set of functions
are designed probably to protect the organ from the intrusion of
foreign bodies; the other for their expulsion, as well as for the
removal of the secretions of the parts or of matter brought up from
below. The hypothesis of a third form of sensibility, as described by
Elsberg--namely, the dolorous--seems hardly to be demanded for the
larynx more than for all other mucous surfaces subject to pain. The
nerve-cells of Rossbach in the mucous membrane may be peculiar to the
larynx and trachea, as he claims, but further observations are required
for the demonstration of this as a special histological fact
distinguishing laryngeal from other mucous surfaces.

[Footnote 1: _Dic. Eng. des Sci. med._]

[Footnote 2: _Int. Med. Cong._, 1881.]

[Footnote 3: _Ibid._]


PERVERSION OF SENSATION OF THE LARYNX.

There is some difficulty in grouping the derangements of the
sensibility of the larynx, for the reason that in many cases the
perversion of this function is only a symptom of some other disease of
the organ. Probably in all cases the trouble is, in fact, an expression
either of disturbance in the structures of the larynx, involving more
than the sensory nerves, or it is the result of change in structure or
function of neighboring or distant parts. Various attempts have been
made to classify these disorders according to the kind of perversion
and also according to the cause of the trouble. Elsberg, in a paper
presented to the International Congress, London, 1881, p. 224. vol.
iii., makes an attempt at a scientific classification based upon
anatomico-physiological facts. That there is yet much to learn in
regard to these facts, especially the physiological facts, will be
admitted by every one at all familiar with the literature of the
subject. Elsberg, under the term of dysæsthesia, makes two principal
divisions--namely, first, disorders having reference to the quantity or
intensity of the sensation; this embraces simple hyperæsthesia and
simple anæsthesia. The second grand division relates to the quality of
the sensation, and includes only paræsthesia or sensory delusions.
These grand divisions are still further subdivided.

In fact, we have to do with exaltation of sensibility simply, with
sometimes pain; second, with delusion of sensation; and, third, with
lost or diminished {62} sensation. For all practical purposes,
therefore, we may adopt this arrangement, but should consider it as
only provisional, as has been well observed by Schnitzler. These
conditions are described under the terms hyperæsthesia, with or without
pain; paræsthesia; anæsthesia.


Hyperæsthesia.

DEFINITION.--Exalted sensibility of the larynx, not necessarily
associated with pain or other disorders of function. This condition is
rare, but it is nevertheless met with. We sometimes find that the
larynx is abnormally sensitive to touch or to an irritant, even though
there is no marked inflammation. The symptoms and history justify the
consideration of the condition apart.

ETIOLOGY.--Predisposing causes are probably to be found in the general
condition of the nervous system. Persons of a highly susceptible
nervous organization are, other things being equal, more prone to this
affection. Certain habits of life, such as confinement to the house or
want of exercise in the open air, excessive use of the voice in
singing, especially in unnatural keys or after unnatural methods, have
seemed to me to predispose to the exaltation of the sensibility of the
organ. It must be confessed, however, that so little is accurately
known of the history of the disease that we are left in much doubt as
to the rôle of these conditions in the production of the abnormal
state. The exciting causes of hyperæsthesia of the larynx are the
long-continued action of the predisposing causes--acute and chronic
inflammation, mechanical and chemical irritants, etc. So far as my own
experience goes, the use of the voice in an unnatural key, or perhaps
rather the strain upon the parts by efforts to force the organ to
perform the function of phonation in an abnormal manner, has more
frequently been assigned by the patient as the cause than any other one
thing. I have seen quite a number of singers who have by an effort of
the muscles, apparently, produced an intensified irritability of the
mucous surfaces. It is possible that in rare instances there may be an
exalted activity of the receptive centres, and that the local trouble
in the larynx is only a manifestation, in the distribution of the
nerves, of the central disease. In such cases, however, the disorder
should reach all the parts supplied by the pneumogastrics. Inflammation
of the pharynx, soft palate, posterior nares, and perhaps of the
structures of the ear, have an influence over the sensibility of the
parts below, probably through the relations of the glosso-pharyngeal
and other nerves to the laryngeal branches of the pneumogastrics. E. F.
Ingals of Chicago has seen a case of laryngeal hyperæsthesia produced
apparently by a varicose condition of the vessels about the base of the
tongue. Frankel, Tornwaldt, Bayer, Schnitzler, A. H. Smith, Glasgow,
and others have reported cases in which there were symptoms of
hyperæsthesia or of reflex motor disturbances due to trouble in the
nose or pharynx. The general health has much to do with the development
of the local trouble. Asthenia is associated so frequently with
hyperæsthesia of other parts that we should expect to find this
relation also in the larynx.

SYMPTOMS.--The symptoms of hyperæsthesia of the larynx are in part
involved in the definition of the affection--exalted susceptibility to
the touch, intolerance to the presence of mechanical irritants, a
sensation of discomfort in the presence of chemical agents, such as
gases or impure air, and, when the exaltation is excessive, positive
pain. This pain may be only a soreness or tenderness or it may amount
to neuralgia. This last form of exaltation is rare. When present it has
been considered a special disease and treated as a separate affection.
Von Ziemssen and Mackenzie regard it as a variety of hyperæsthesia.
Schnitzler, Jones, Wagner, and Mackenzie report cases. The {63} pain is
said to be not confined to the larynx, but to extend up toward the ear
and along the course of the superior laryngeal nerve. In two cases
observed by the writer the pain not only extended along the course of
this nerve, but into the pharynx and posterior nares as well. In these
cases the patients were both singers, and both had adopted with great
enthusiasm a new method by which the abdominal muscles were brought
into action at the expense of the muscles of the thorax. The pain was
always aggravated by any effort to sing, but more especially by any
return to the method noted. The pain not unfrequently extended to the
face as well as to the ear.

Neuralgia of hysterical origin, according to Thaon,[4] is more
frequently met with on the left side than on the right. Instead of
being general, it is not unfrequently limited to points or
circumscribed patches.

[Footnote 4: _Proceedings Laryng. Cong._, Milan.]

COURSE AND TERMINATION.--The course of the affection is very uncertain.
In the neuralgic variety the pain may be transient, passing away in a
few days or hours even, but generally there are frequent recurrences
extending through weeks or months. Simple exaltation of the common
sensibility is much more persistent and more uniform in its character.

Hyperæsthesia of the larynx is so largely dependent upon the general
health that not only is it very irregular in its course and duration,
but its termination is equally uncertain. It can hardly be said to be a
cause of death, as it does not involve structures necessary to life. It
disappears occasionally without treatment. When complicated with other
affections, such as acute or chronic inflammation, alterations of the
function of the pneumogastrics, with disease of the thoracic viscera or
with general derangements of the nervous system, its course and
termination must depend largely upon the persistence of these
complications.

PATHOLOGY.--So far as the pathology and morbid anatomy have been
studied, there is no appreciable change of structure. This is true, of
course, only of those cases which are not complicated. Whether the
primary lesion is in the mucous membrane, denuding, pinching, or
otherwise modifying the terminal portions of the nervous filaments, or
whether there is an alteration of the conducting portion of the sensory
nerves, or, in fine, whether there is some lesion of the receptive
centres, it is impossible in most instances to say. It is probable,
however, that in some cases the first morbid fact has been an
alteration in the nerves themselves. The cases induced by unnatural
methods of using the vocal organs are apparently of this character.

The diagnosis, prognosis, and treatment will be considered in
connection with Paræsthesia.


Paræsthesia.

Closely connected with hyperæsthesia of the larynx is a form of sensory
delusion consisting of the impression that some foreign substance is
lodged in the organ or that there is some alteration an the structure
of the parts. This is known as paræsthesia.

ETIOLOGY.--The first variety of sensory delusion depends on a primary
injury to the parts. A bone or pin or some other foreign body, perhaps
having lodged in the parts for a short time, has left a persistent
impression upon the mucous surfaces. It is possible that in some
instances there may have been no foreign body in the parts, as we have
in many cases only the statement of the patient. Local inflammations,
small in extent, may possibly have left the parts in a morbidly
sensitive condition justifying on the part of the subject the
hypothesis of a foreign body.

The second variety of paræsthesia is the expression of some disturbance
in {64} a distant part. It is usually hysterical in its character or a
variety of hysteria associated with neurasthenia. It belongs to the
same class of phenomena as the sensory delusions in other parts of the
body. The globus hystericus is one of its forms. Thaon[5] says that
hysteria may give rise to neuralgia as well as to other forms of
hyperæsthesia of the larynx. It also, according to this author,
produces that form of paræsthesia in which there is a sense of a bone
or pin or some foreign substance in the larynx. The general condition
of asthenia, and especially of neurasthenia, may be assigned as a
predisposing cause. The local injury in the one case and the general
hyperæsthetic condition in the other, with some determining fact, such
as the mental impression or an apprehension of trouble in the larynx,
constitute the exciting causes.

[Footnote 5: _Proceedings of the International Congress of
Laryngology_.]

SYMPTOMS.--It usually comes on after an injury or as a result of the
presence of a mechanical obstruction or irritation, the presence of a
bone or pin being frequently invoked as an explanation of the feeling.
In a few cases the sensation is suggestive of an alteration of the
structure of the parts. Patients are inclined to think that they have a
tumor or that there is some deformity. In the first class of cases
there is a sense of pricking or of scratching in the larynx. This is
not constant in locality or in intensity. There will be times,
occasionally days, in which the sensation may be entirely absent, after
which it returns with great severity, the patient insisting that the
cause of the trouble has simply changed its location--in other words,
that there is a migratory body in the throat. That form of paræsthesia
in which the sensation is that of a tumor or malformation is also
irregular in the mode of its manifestation or kind of disturbance. Like
the other forms, it comes and goes, changes its location, and undergoes
modification in its character. It may be associated with neuralgia.

DIAGNOSIS.--Hyperæsthesia and paræsthesia are recognized by the
symptoms already described and by the aid of the laryngoscope. The
mirror reveals the fact that the parts are normal in structure and that
there is no foreign body present. The mucous membrane may be hyperæmic
or anæmic, but is not the seat of any active inflammation. The
excessive sensibility and pain of the larynx in ulceration of the parts
will be excluded from this group of troubles by the revelation of the
laryngeal mirror. Cases of pain or perverted sensation dependent upon
the disorders of the nerve-centres usually involve the whole range of
functions supplied by the pneumogastrics, and will generally be
recognized by this fact. Such cases can hardly be called local, and do
not belong to the group of affections embraced in this article.

PROGNOSIS.--The prognosis of simple paræsthesia of the larynx is not
grave. Though it may exist for a long time, it, so far as we know, does
not terminate in death. While it sometimes results in recovery without
treatment, it in a large proportion of cases yields only to both local
and general treatment. Its duration is uncertain. Paræsthesia coming on
after the presence of a foreign body in the organ may last many months
and then gradually disappear. This result will be largely aided by the
moral support which is gained if we can convince the patient that the
sensation is entirely a delusion.

TREATMENT.--For the purpose of meeting local indications in
hyperæsthesia we may apply with a brush or by the means of the atomizer
a solution of morphine and alum of the strength of 15 centigrammes of
morphine and 2 grammes of alum to 50 grammes of water, or to this may
be added 20 centigrammes of carbolic acid and 10 grammes of glycerin.
Of this solution an application may be made each day with the
hand-atomizer. The hand-atomizer is preferable to the steam-atomizer,
for the reason that we know in the use of the former the strength of
the solution. In the use of the steam-atomizer the medicated solution
is diluted with the water of the steam, and we are {65} ignorant as to
the strength of the application. The method of application by the use
of the atomizer is to be preferred to the brush or sponge probang, for
the reason that we produce by it no mechanical irritation of the parts.
The brush or sponge can hardly be used without giving pain or
discomfort. In addition to the solution above indicated, solutions of
borax, of sulphate of zinc, of tannin and glycerin with chloroform, of
nitrate of silver not too concentrated--2 to 10 centigrammes to 30
grammes of distilled water--tincture of aconite, solutions of the
bromides, cocaine and other anæsthetics, may be used with benefit. In
many cases the administration of general tonics along with the local
treatment will be of the greatest value. The application of electricity
to the parts through the surfaces--that is, from one side of the larynx
to the other--will add to the efficacy of other local treatment. The
strength of the current should not be so great as to give rise to any
discomfort. The current should be continuous, and should be repeated
every day for several weeks if the disorder does not yield sooner. In
cases which have been induced by vicious habits of living or of
exercise of the organ there should of course be an entire change of the
habits. The producing cause should, if possible, be removed. The
exposure of the parts to anything which gives rise to pain is to be
avoided. If hyperæsthesia has been induced by unnatural methods of
singing or of speaking, these should be remedied.

In neuralgia the general treatment for that affection is indicated.
Quinine and iron have especially been found useful. In the hysterical
variety of both hyperæsthesia and paræsthesia general treatment is of
more value than local measures. General tonics, moral support, such as
will be secured if we can convince the patient that there is really no
serious trouble with the organ, but that it is only a morbid sensation,
will be of the greatest value. In these cases change of climate, change
of occupation, diversion by new associations, with expectation of
recovery on the part of the patient, often bring about the most
satisfactory results. The diagnosis should be certain and the physician
should be able to speak with confidence in the matter. This will go far
toward effecting a cure. For the purpose of diminishing the general
irritability of the system bromine in some of its combinations,
potassium, sodium, iron, quinine, etc., may be useful.


Anæsthesia.

DEFINITION.--Diminished sensibility of the mucous surfaces dependent
upon lesion of the nerve-centres, alteration of the conductivity of the
nerve-trunks, or upon disease in their terminal distributions. It is
usually bilateral, but may be limited to one side. This alteration of
the sensitive condition of the mucous membranes is usually observed
after diphtheria. It is also met with in bulbar paralysis. In this last
condition it is only one of the phenomena of paresis or paralysis
involving several different organs. It is not, therefore, properly a
disease of the larynx, and the consideration of it will not be embraced
in this article. It has been stated that hysteria is frequently
accompanied with anæsthesia of the larynx. Von Ziemssen, Chairou, and
Schnitzler have published cases. It seems very improbable that this
condition of the organ is so generally present in hysteria as is
claimed by Chairou. It is, however, certain that anæsthesia as well as
hyperæsthesia of the larynx exists as a complication of hysteria. In
the later stages of all exhaustive diseases, as cholera, etc., the
sensibility of this organ is either diminished or abolished. This is
not, however, a true paralysis in the sense in which we generally use
the term. It is only one of the manifestations of the general failure
of the life-forces. The special senses, the reflex functions, all share
in this paresis, this severing of the relationships of life. Anæsthesia
of the larynx is usually {66} confined to the parts supplied by the
superior laryngeal nerves, and is sharply limited by the edges of the
vocal bands. If there is anæsthesia of the parts below these bands, it
is of much less significance and hardly requires our consideration.

ETIOLOGY.--So far as we know, there are no predisposing causes. The
chief exciting cause of this affection is unquestionably diphtheria. It
is, in fact, a sequel of diphtheria. It will hardly be necessary to
repeat here what the reader will find fully discussed in the sections
devoted to diphtheritic inflammation of the fauces and adjacent parts:
we are mainly concerned with the phenomena. Just how this morbid
process produces paralysis is not known. It is believed by some
observers that the disease is produced by the alteration of the
nutrition of the parts during the progress of the diphtheria. It is
stated that the parts most nearly related to the seat of the exudation
are most likely to become involved. This is thought to sustain the
theory of the direct propagation of the morbid changes from the mucous
surfaces to the nerves and muscles. That the paralysis following
diphtheria is not, however, produced alone in this manner seems to be
made evident by the fact that distant parts, parts which have not been
at all involved in the disease, do nevertheless become affected with
paralysis. This paralysis develops when the general health and the
nutritive changes are all improving. It is quite evident, therefore,
that the loss of power in the laryngeal muscles, as well as the altered
sensibility, in part at least, must be due to some lesion of the
nerve-centres. In addition to the causes above noted, anything which
impairs or destroys the function of the superior laryngeal nerve may
produce this affection. In the anæsthesia from hysteria we know only
the fact, but do not know just how the derangements of the nerves in a
distant part, or in the nerve-centres perhaps, are so reflected as to
change the function of this organ. The hyperæsthesias, the
paræsthesias, and the anæsthesias of hysterical character are all
probably produced in the same manner. Anæsthesia in bulbar paralysis is
easily understood, but need not, for the reasons already given, engage
our attention.

SYMPTOMS.--This condition is usually associated with paresis or
paralysis of the muscles of the part. One of the first symptoms of loss
of sensibility is, therefore, a failure of the constrictors of the
larynx to protect the organ from the intrusion of foreign substances in
the form of food and drink. Particles swallowed find entrance into the
respiratory tube, and this with no sense of discomfort. If the
paralysis is complete both above and below the glottis, the intrusion
of these substances is not recognized. There may be no cough or spasm
to indicate the fact. In the mean time, the particles of food descend
into the bronchi, and may become the exciting causes of
broncho-pneumonia. It is often noticed after tracheotomy for diphtheria
that food and drinks gaining access to the respiratory tract are
discovered at the tracheal opening. In several cases within the
knowledge of the writer this fact has led the operator to fear that the
posterior wall of the trachea had been opened. In all cases in which
the pharynx is in a state of paresis a careful examination should be
made by means of the laryngeal mirror.

There are no subjective symptoms, and this fact makes it probable that
the affection is more common than has been supposed. The patient
complains neither of pain nor of any other discomfort. This statement
is only true, however, when there is simple loss of sensation. There
may be paræsthesia associated with partial anæsthesia. In such cases
there will be noted the usual symptoms of paræsthesia. In hysterical
forms of anæsthesia the appearance of the parts is often variable from
day to day. The location of the disordered function is well defined at
the time of one examination, while at the next the condition may be
quite different. It is stated by Thaon[6] that {67} in one-sixth of the
cases of hysteria the larynx is in some way affected. The epiglottis is
more usually the seat of the affection in the hysterical variety.
Several authors have noted that with the laryngeal disorder there is
often a zone of modified sensation beneath the chin and on each side of
the larynx. This sometimes amounts to absolute loss of cutaneous
sensibility.

[Footnote 6: _Loc. cit._]

COURSE AND TERMINATION.--According to Mackenzie, Von Ziemssen, and
others, the anæsthesias following diphtheria usually terminate in
recovery. It is quite possible, however, that the literature of the
subject does not give us elements on which to base an opinion. I am
inclined to think that cases die from this disorder in which the nature
of the affection is never recognized. It is quite certain that
paralysis of the fauces is not unattended with danger. It is also
probable that in many of these cases the real danger is not so much
from the loss of muscular power in the pharynx, and consequent
inability to swallow, as from the fact that the larynx is not protected
from the introduction of foreign substances, that the intrusion of
these substances is not recognized, and the consequent disorders of the
lungs become the cause of death more frequently than has been supposed.

DURATION.--Paralysis of the sensory nerves of the larynx usually lasts
only a few weeks. When a result of diphtheria it disappears with the
motor trouble with which it is associated. As a complication of
hysteria, or rather when hysterical in character, it may last
indefinitely. When dependent upon changes in the centres from which the
pneumogastrics are derived it has a history commensurate with that
affection.

The PATHOLOGY AND MORBID ANATOMY have been suggested in the discussion
of the cause and symptomatology of the disorder. The question of the
local or general changes in the diphtheritic variety is noted in the
history of the disease.

The DIAGNOSIS is made mainly by the examination with the laryngoscope.
The probe will at once determine the presence or absence of the
sensibility of the mucous membrane of the parts. In addition to touch,
electricity may be employed. In these cases the alteration involves
both the tactile and reflex sensory functions. There will therefore be
neither cough nor spasm resulting from a mechanical irritation. The
surfaces are usually quite normal in color and form. The epiglottis is
erect, abnormally so, and there will often be more or less paresis, or
even complete paralysis, of the other muscles of the organ. In some
cases the difficulty in deglutition due to derangement of the reflex
functions may be also suggestive of alterations of sensation in the
parts within the larynx, but it is only a suggestion.

The PROGNOSIS is usually favorable, but for the reasons given above
this should be accepted with some degree of reservation. The
diphtheritic varieties share in the uncertainty of other forms of
paralysis in that disorder. The hysterical forms are not dangerous, but
may continue so long as the primary affection persists.

TREATMENT.--This should be both local and general. The local treatment
consists almost entirely in the application of electricity. Both the
galvanic and faradic currents are recommended. In my own practice I
have been accustomed to resort to the galvanic, but modified by the
introduction of a shunt or switch, so as to produce a wave of
electricity. The manner in which this is accomplished is to connect in
the circuit a coil such as that used for the faradic current. This
takes out of the direct current, with each closure of the circuit in
the coil, a portion of the quantity of the current, and without
entirely interrupting the working circuit gives a wave of electricity,
producing, so far as I can judge, the results of both the primary and
secondary currents. There is not the shock of complete interruption,
while there is the stimulus of the irregular quantity. The electrode
which will be found most convenient is that devised by Mackenzie or
some modification of it. It {68} should be applied through the parts
from one side of the larynx to the other by placing the tip or point of
the instrument in one of the pyriform sinuses over the superior
laryngeal nerve. A double electrode will often answer better, placing
one point in one sulcus, while the other is in contact with the mucous
membrane of some other part of the organ or in the opposite sinus; that
is, on the other side of the larynx. The current then passes through
the parts and stimulates all the tissues between the two poles. The
application should be made every day, and for several minutes at each
sitting, interrupted, of course, as required by the variable condition
of the parts. The current should not be so strong as to produce
positive pain. This is not easily reached, however, for the reason that
the response is slow and uncertain. The strength of the current should
be tested upon the normal surfaces of the patient, or, better, upon the
mucous membranes of the operator, before applying it to the morbid
parts.

In case a reliable tangent galvanometer is used, much more certainty
can be reached than when the strength is determined solely by the sense
of touch. With this exhibition of electricity there should also be
administered such remedies as are best calculated to restore the
general strength of the patient--quinia and iron, with the bitter
tonics, and especially strychnia in what would be considered large
doses (.003-.005 grammes), two or three times a day, with interruptions
every few days. In the hysterical cases, as well as those following
diphtheria, electricity is often of great value.

Attention should also be given to the proper treatment of any local
trouble in the viscera of the abdomen or pelvis. Uterine disease, if
present, as it frequently is, demands attention. It is believed by some
authorities that the unilateral disorders of the larynx dependent upon
ovarian irritation generally manifest themselves upon the side
corresponding to the diseased ovary. It is, however, rare to meet with
complete unilateral anæsthesia. In addition to the use of these
measures, change of surroundings, especially in the hysterical variety,
diversion by new associations, new occupations, etc., are to be secured
whenever practicable.


DISORDERS OF MOTION.

Disorders of motion are perhaps more complex than those of sensation.
They may be divided into two general groups--1st, exalted action; 2d,
diminished or arrested action. The first group is susceptible of a
subdivision: first, those in which the sensory functions are exalted as
well as the motor. In some of these cases the real disturbance is very
probably hyperæsthesia rather than increased irritability of the nerves
going to the muscles. Generally, however, the morbid phenomena are
mixed; the two sets of nerves are both in a state of over-action.
Spasm, for instance, may be the result of excessive activity of the
sensory function coupled with the exaltation of the motor impulses, or
exaggerated irritability. Second, the spasm or exalted activity of the
muscles may be entirely independent of sensory impressions, possibly,
in some instances, dependent upon muscular conditions, but generally
only the local expression of some central nervous trouble. Chorea may
be cited as an example. The diminished action of the motor system may
also be due to either a want of the sensory common or special
impressions; or it may be due to failure of the motor centres or some
interruption of the continuity of the conducting media; or, lastly, it
may be for the reason that the muscles themselves are so changed that
they do not respond to the normal stimuli, such as the {69} commands of
the will or reflex impressions. It will be seen from this brief
statement that the subject of motor derangements is one of much
complexity. From the very nature of the complications it is often
impossible to satisfactorily analyze the symptoms and to determine with
certainty, in a given case, whether we have to deal with a simple or a
compound result. We may, it is true, in some instances arrive at
approximately correct conclusions by resorting to the physiological
methods of testing the muscle by galvanism and faradism. In other
instances we may by a careful study of the history of the disease reach
at least a provisional opinion. We must, after all, admit that much
will in many of these derangements remain to be conjectured.


Exalted Action.

There is quite a difference among authorities as to the place in the
classification of disease of the larynx which should be assigned to
spasm as met with in childhood, and which is also occasionally
encountered in adult life. It is not possible, perhaps, in the present
state of knowledge, to separate in every instance those cases in which
there is disorder of the circulation and nutrition of the larynx from
those in which the spasm is the result of disturbance simply of
innervation, or in other cases the reflex manifestations of nervous
irritation elsewhere. Generally, however, this can be done. I have for
a long time been accustomed to consider the affection known as
spasmodic croup to be a mild inflammation of the larynx, and that it
differs from the same affection in the adult for the reason that the
lumen of the tube is smaller, the cartilages are more yielding, and the
susceptibility of the parts is greater, and further for the reason that
the nervous system in childhood is always more prone to spasm than in
the adult. Stridulous laryngitis, however, is a real disease, and is
for the reasons above given a neurosis, even though it is an
inflammation. It is entitled to a separate description for the reason
that the symptoms are so well marked and differ in so many particulars
from those of ordinary inflammations. That there is, besides, a true
spasm of the muscles of the larynx, independent of inflammation, by
which the vocal cords and the constrictors are brought into action and
possibly kept in a state of tonic contraction, is possible.

In a majority of instances of laryngeal spasm there is a degree of
inflammation, as above stated, or at least a degree of congestion of
the mucous membranes. It is certainly true, however, that in
exceptional cases there are no indications of such a condition of the
parts, so far as we can determine by ante- or post-mortem study. It
seems to be evident, then, that under this name of spasm of the larynx
or of some synonym of it many careful observers have recorded facts and
have grouped them with the thought that the functional derangement was
the main trouble. The real difficulty appears to be that the spasm is
in fact a symptom--a symptom of perhaps several different disorders,
but so prominent and creating so much alarm that it has seemed for the
time being to be the disease itself; and yet in most cases there is a
mild form of inflammation, local in its extent, and producing, so long
as there is no interference with the function of respiration, no
general disturbance. It is perhaps appropriate to include in the
discussion not only the purely nervous cases, but also those conditions
in which, while there is hyperæmia, and probably always some
derangement of secretion, nevertheless the symptoms and dangers concern
mainly the motility of the muscles of the organ.

The disease occurs both in children and in adults. There is, however,
in its etiology, course, and terminations quite a marked difference, as
observed before and after puberty. We shall therefore consider, first,
spasm of the glottis in children; second, in adults.


{70} Spasm in Children.

SYNONYMS.--Laryngismus stridulus, False croup, etc.

ETIOLOGY.--Predisposing Causes.--The disease occurs most frequently in
children from a few months to two or three years old. It is
occasionally met with in those still older and up to puberty. It seems
to be more often encountered in patients of a strumous habit than in
those of a healthy constitution. Rickety children are especially liable
to the affection: the German pathologists especially insist upon this
factor. Patients of a nervous temperament predisposed to general spasms
are especially predisposed to this affection in the larynx. It is a
general law that muscles weakened either by disease or by fatigue or by
deficient nutrition are especially irritable. In them mechanical as
well as other forms of stimuli produce local contraction with great
readiness. These contractions are, it is true, rather the expression of
the condition of the muscles than of the nerves. The muscular condition
must, however, be regarded as a predisposing cause of the spasm. In the
same way, perhaps--namely, by the inherited tendency to lower forms of
vitality, weakened muscular power--we may account for the fact that
family history of similar conditions, such as false croup in other
members or in the parents, should be considered as among the evidences
of predisposing tendencies to spasm of the glottis.

Sex has in this affection, as well as in most laryngeal diseases of
children, a predisposing influence. Mackenzie has collected in all,
from different sources, 8248 cases. Of these, 5378 were boys and 2870
girls--a proportion of nearly 2 boys to 1 girl. In adults the reverse
holds good, females being much more frequently seized than males. It is
certain that season has something to do with the development of the
disease, but this influence should be regarded rather as a producing
than a predisposing cause.

Dentition, worms, weaning, or anything which produces an irritation of
the alimentary canal may also, by exciting the reflex irritability of
the nervous system, become predisposing causes of laryngismus. The
influence of dentition has, however, been probably over-estimated.

The exciting causes of spasm of the glottis are not well defined. In a
few cases we are able to definitely fix upon something as the occasion
of the attack. It is possible that there may be some central lesion,
and this may be well defined. This is rare, however. It is nevertheless
true that the onset is generally preceded by some derangement of the
general health. There has been for a day, or perhaps only for an hour
or two, a slight cold, a little hyperæmia of the respiratory mucous
surfaces, or disturbances of the digestive tract, or the child has been
unusually fatigued or excited from play or study. The secretions have
in other cases been deranged. No one of these causes has perhaps been
of sufficient gravity to attract the attention of the mother or nurse.
The indisposition, if it has been noticed at all, has been regarded as
only one of the many ephemeral troubles that so often occur in infancy,
and no anxiety has been felt. Of all these possible causes, the one
most frequently invoked after the attack is a cold, slight, it is true,
but nevertheless, in the light of the subsequent history, evidently a
mild form of inflammation of the laryngeal mucous membranes.

SYMPTOMS.--Spasm of the glottis usually takes place at night. It is
true that some authorities deny that this is the case. Stefen says
"that it is quite as likely to occur during the day as night." In a
great majority of instances, however, it will be found that the attack
occurs after the child has been asleep. During the day there has been
perhaps a slight disturbance of the general health, a little
inclination to cough, or there has been a catarrh of the fauces or
bronchial mucous surfaces; nothing, however, of a serious character has
been observed. At midnight or later the little one awakes with a
crowing or {71} whistling inspiration. It starts up in bed, and
evidently experiences great difficulty in breathing; this difficulty is
manifestly in inspiration; expiration is easy and free. The eyes are
prominent, the lips blue, the surface often bathed in perspiration;
pulse frequent, small, at times irregular; there is, if the child be
old enough to reason in the matter, great alarm; there is often cough,
and this cough is characteristic: it is a hoarse, metallic, barking,
peculiar cough, described as croupy. If the spasm is limited to the
larynx, the other muscles not being affected, the patient clutches at
whatever it can reach, and often seizes the throat as though there was
something there to tear away. The general surface becomes cyanotic and
all the symptoms of asphyxia are present. The voice, though not
generally extinct, is altered; it becomes hoarse, or husky, as it is
called; in a few minutes the severity of the attack is passed, and the
little sufferer sinks exhausted into a sleep more or less disturbed. A
second attack may occur the same night, or there may be nothing more to
alarm the attendants till the next night. The second attack, if it
occurs, as it generally does, on the succeeding night, is less severe
than the first; the third still more mild; and this generally ends the
case for the time being. During the intervals--that is, during the
day--the patient in a majority of cases is up, and seems to be but
slightly affected by the seizure of the night before. There will
perhaps be a slight cough, with some loss of appetite and indisposition
to engage in play. This is the most usual type of the disease. In a few
cases there is more marked derangement of the general health. The
spasms are more severe; the cramp is not confined to the laryngeal
muscles, but involves other parts, such as the muscles of the chest and
the extremities. During the intervals of the attack there is perhaps a
little fever, the digestive tract is disordered, the cough may be
marked during the day, there may be an increase in the secretions of
the respiratory surfaces. Attacks may recur during the day and for
several days; the cough may retain its croupy character, and the voice
may continue to be hoarse.

COURSE AND DURATION.--Spasm of the larynx is usually a transient
phenomenon, lasting only from a few seconds in the milder cases to
several minutes in the more severe forms of the disease. The attacks
are intermittent. The seizures are relieved by intervals of comparative
relaxation of the muscles of the parts. Even in the intervals there is,
however, a degree of contraction of the constrictors, so that the
relief is not absolute. Two or three days elapse before the attack may
be said to have entirely ceased. In the severer forms the consequences
of the spasm may continue even for a still longer time. There are
usually no sequelæ. When the patient has recovered there is nothing
left of the disease, though there is often a predisposition to a
recurrence; the same causes that produced the first attack, or even
slighter causes, may produce a second. These causes are generally
persistent; the seizures are therefore usually repeated.

PATHOLOGY.--In cases dependent on central disease the pathological
changes are to be sought for outside of the larynx. In rickets and
other morbid conditions which by reflection produce spasm of the
glottis the pathology proper is distant and not in the organ; there is
only an excess of motility in the nerves and muscular apparatus.
Efforts have been made to differentiate spasm and false croup, but the
confusion is only equalled by the disagreement as to the relation of
diphtheria to true croup. It is probably true that the cramp is
generally due to some excess of motility in the system at large, and
that the larynx is the seat of pathological changes that determine the
spasm in that organ. This is especially true in those cases associated
with rickets, derangement of the alimentary canal, etc. It seems to be
a fact, nevertheless, that in a majority of cases the mucous membranes
are, as already stated, the seat of a very mild inflammation. Or
perhaps we should say they are slightly hyperæmic. So far as we can
judge from {72} examination in cases which have terminated fatally, as
well as from ante-mortem observation, there is no structural change of
tissue to be recognized by the naked eye, unless it be, during life, a
slight fulness of the vessels. There is a change, however, in the form
of the organ, at least at the entrance to the larynx. The constrictors
are in a state of action, so as to partly close the superior opening to
the larynx, and the epiglottis is rolled so as, in some instances, to
become almost a tube. I have repeatedly recognized this in the image
seen in the laryngeal mirror. Cohn reports a case of impaction even of
the epiglottis in the vestibule of the larynx (p. 627). This fact is
also suggested by the difficult inspiration and the altered voice and
cough. In young children the yielding character of the cartilages
probably adds largely to the obstruction produced by spasm of the
muscles about the vestibule.

DIAGNOSIS.--The diseases with which spasm of the larynx is most likely
to be confounded are true croup, simple inflammation of the larynx,
foreign bodies in the larynx, and possibly, in the absence of the
history of the case, tumor situated in the glottis or along the vocal
cords.

It will readily be distinguished from true croup by the fact that in
the one case, true croup, the attack is insidious: the patient has been
sick some time, usually several days before spasm occurs; there is also
fever, with usually more cough; the voice is altered before the
appearance of spasm; the first seizure is slight, almost imperceptible,
and the subsequent attacks become more and more severe; dyspnoea is
continuous. All these facts are in marked contrast with the picture of
an attack of spasm of the glottis as we have attempted to describe it.
In the one case the most alarming symptoms are at the beginning. There
is an explosion of morbid phenomena, each recurrence less alarming till
complete convalescence is established. In the other disease the
symptoms and dangers are constantly increasing in severity, till at
last the spasms become as fearful as the initial seizure in
laryngismus. The morbid anatomy of the two diseases is also widely
different; and this difference can be recognized during life. Simple
ordinary inflammation of the larynx may give rise to hoarseness and
cough; the hoarseness is, however, different from that in laryngismus.
There is fever, and the hyperæmia of the organ can be readily
recognized. The disease is progressive, does not present its most
alarming symptoms at the beginning, and spasm, if it occurs, is a late
event.

It is possible that spasm of the larynx might be mistaken for a foreign
body in the organ. It will be remembered that the attacks of spasm
usually occur at night after the child has been asleep. The history of
foreign bodies in the larynx reveals what we should expect--namely,
that the accident almost always occurs during the day. In a great
majority of cases this history also furnishes reliable information of
some substance or object which was in possession of the child, and
which has disappeared. The dyspnoea is more continuous and the course
and symptoms more variable. There will therefore be no great difficulty
in any case, and in most cases no difficulty at all, in making a
certain diagnosis as between these two conditions. In a few cases of
laryngeal tumor the symptoms are very similar to those of the disease
under consideration. The attacks in the case of a pedunculated tumor on
the vocal cords may take place at night and may be intermittent. The
rarity of this affection in children in comparison with spasm of the
larynx, and the further fact that in the case of tumor there is a more
continuous disturbance of respiration, make the differentiation easy.
Paralysis of the adductors gives rise to more dyspnoea during sleep,
but the history and laryngeal mirror make the diagnosis easy and
certain.

PROGNOSIS.--The large majority of cases of spasm of the larynx recover.
Statistics show that there are deaths from this disease, but in
proportion to {73} the number attacked I think the mortality is small;
how small we do not know. The confusion in classification is so great
that we cannot place much dependence upon published statistics. In our
climate I think most observers will admit that a patient seldom dies
from this affection unless there be associated with it some morbid
condition of a serious nature.

TREATMENT.--The immediate and pressing indication in spasm of the
larynx is for something to relax the constrictors and allow the act of
inspiration to be accomplished without embarrassment. For the
accomplishment of this purpose three methods of treatment may be
resorted to: First, heat; second, emetics if there be time; third,
anæsthetics and antispasmodics. Of all these measures, the first is the
most easily applied, and will probably in a great majority of cases
prove efficient. It is usually within the reach of the attendant or
nurse. It can in any event do no harm. This fact is not to be
overlooked, as the symptoms are so alarming that friends and physicians
are often tempted to do too much. Heat may be applied by means of
cloths dipped in hot water (110° F., or even more) applied to the neck
and chest of the patient, or the child may be placed in a bath of 105°
F., while the head is kept cool by cloths wet with cold water. This
treatment may be continued till the spasms yield. The second of the
measures suggested is usually safe, and may be resorted to along with
the first. Those agents should be selected which act with most
promptness, and the doses should be adapted to the age and condition of
the patient. Alum, sulphate of zinc, sulphate of copper, are perhaps
the best, but by no means the only ones. Ipecacuanha, by the relaxing
effect which it has upon the muscular and nervous system, may be useful
not only in overcoming the spasm, but in preventing the recurrence of
the attack. Antimony is unsafe, and the other emetics are quite as
useful in relaxing the muscles. The third of the measures suggested
should be used with great caution. It may be doubtful whether, in fact,
anæsthesia is ever indicated in simple spasm of the muscles of the
larynx. The dyspnoea renders it very difficult to produce full
anæsthesia, and without this the relaxing effect is not reached. In
cases in which there is serious disease outside of the larynx there
should be appropriate treatment directed to the extrinsic trouble.
During the intermission--that is, during the day following the
spasm--attention should be directed to the condition of the digestive
and excreting organs as well as to the respiratory tract. In malarial
districts I have thought that quinia given in antiperiodic doses the
morning after the seizure has been of benefit in preventing or
diminishing the severity of the next spasm. In addition to these
measures, for the prevention of the subsequent attacks bromide of
potassium or bromide of sodium in 3 to 5 grain doses may be given once
in three to six hours after the spasm has ceased. Five grains of
chloral, as advised by Mackenzie, given at bedtime the night after the
attack, will also diminish in a certain number of cases the severity of
subsequent seizures, or possibly entirely prevent them. Musk, myrrh,
camphor, castor, and other similar antispasmodics are theoretically
indicated, but, in fact, are of but little if any value. If the disease
is central, involving the floor of the fourth ventricle, the local and
general spasms are only symptoms, and the treatment must be directed
entirely to the preservation of life. It should be remembered in this
connection that in the floor of the fourth ventricle the pneumogastric
and the glosso-pharyngeal, as well as filaments of the spinal
accessory, have their origin. The range of distribution of these nerves
marks to some extent the range of the morbid phenomena in disease of
central origin. It may of course be true in any given case that only a
small portion of the central gray matter is involved, but as a rule the
organic change in one of the nerves at the point of origin does give
rise to disorder of function of one or both of the others.

General tonics and attention to hygienic conditions are of great {74}
importance for the purpose of giving vigor and regularity to all forms
of nervous and muscular activity.


Spasm of the Glottis in the Adult.

The affection is usually bilateral; that is, all the muscles guarding
the vestibule of the larynx, and probably in most cases the adductors
of the vocal cords, are involved. That this is not always true,
however, I am convinced by a case now under observation in my own
practice. The patient is an adult, and I have been able to determine by
laryngoscopic examination that the muscles on the left side are the
seat of the spasm. The epiglottis is drawn downward and backward on
that side. The top of the left arytenoid cartilage is drawn forward,
while the similar parts of the right side remain in their normal
position except the change necessarily produced in the epiglottis. This
condition is not constant, and is not a paralysis of the opposite side.
This is the only case that I have seen, and I do not know of any
similar case on record. Nothnägel[7] reports a case of spasm of the
adductors upon making an effort to phonate. The cords were normally
separated in inspiration, but at the first effort to speak they closed
firmly, leaving no line of opening between them. The attack seemed to
have been produced by a powerful impression made upon the nervous
centres. It seems probable that it was hysteria. Krishaber describes a
form of what he calls spasm of the larynx in adults, which seems to be
rather a local manifestation of a central disease than a neurosis of
the larynx. It is in many respects similar to epilepsy. The danger,
even in cases in which life is threatened, is not from asphyxia, but
from the arrest of the functions of circulation and respiration--an
arrest of the effort even to breathe. It hardly seems proper to include
this among the troubles of which we are treating. He calls it ictus
laryngé.

[Footnote 7: _Deutsch. Arch. für klin. Med._]

ETIOLOGY.--It is certain that the same causes that produce spasm in
childhood are efficient in the adult, though there is an absence of
some of the conditions that render the disease so frequent in infancy.
The cartilages have become more firm, and consequently are not so
easily moved by the action of the constrictor of the vestibule of the
glottis; the size of the cavity in proportion to the necessities of the
body for air is larger; the control of the voluntary over the automatic
actions of the muscles of mixed function is greater; the reflex
irritability of the nervous apparatus is less. These facts all render
the probability of spasm in the adult much less than in the child. On
the other hand, the development of the generative organs, and the
widespread influence which they have upon the respiratory and
circulatory as well as upon the central nervous system, introduces a
new factor as a cause of motor disturbances of the larynx. This new
element is a reason for the fact that in adults the predisposing
influence of sex is reversed: after puberty the disease occurs more
frequently among females than among males. The hysterical character of
many of these cases may be inferred from this preponderance of one sex
over the other among the subjects attacked.

This fact has been seen and described by Charcot, Lefferts, and others.
Irritation along the track of the nerves, morbid conditions of the
mucous surfaces, or muscular irritability, may be each a cause of
spasm.

SYMPTOMS.--The symptomatology of spasm in the adult does not differ in
any material respect from the phenomena observed in children. It is in
the rarity and the comparatively milder character of these symptoms
that the difference is to be found. The attacks occur at night, as in
children, but, so far as I have observed them, they may also take place
during the day. When very severe they occasion great alarm to the
patient, and for this reason {75} produce a profound impression, not
only upon the physical, but also upon the mental and emotional, state.

The duration and termination of the affection are about the same as in
children. In the mortality-tables we find every year a certain number
of deaths from spasm of the larynx in adults. It is probable that among
these there are quite a number which should be placed elsewhere. A
patient may die from spasm of the larynx, which spasm is produced by an
ulceration, by a tumor, by the presence of a foreign body in the organ.
As in children it is quite certain that the deaths reported as from
spasm of the larynx include many that should be referred to central or
other diseases, so here the immediate cause of death is not
unfrequently given instead of the real and essential cause. This fact
makes it difficult to reach anything like a definite conclusion as to
the termination of the disease; only this can be said: the great
majority of cases recover.

PATHOLOGY.--With the exception of those cases in which there is disease
of the central nervous system or along the course of the nerves, we
know nothing of the morbid anatomy of this affection. In fact, there is
no appreciable alteration of the tissues or of the relations of parts;
the spasm is to be considered as a symptom of disease, and not as the
disease itself, or necessarily even as a sign of morbid structure in
the organ.

DIAGNOSIS.--In adults we can make the diagnosis certain by the aid of
the laryngoscope. This can be done in a certain number of cases in
childhood, it is true, but not with the same ease as in those who have
reached more mature years. Ulcerations, benign and malignant growths,
and foreign bodies may each or all produce spasm, but the existence of
such causes is revealed by the mirror, and excludes such cases from the
group under consideration.

TREATMENT.--This does not differ in any essential respect from that
suggested in spasm of the larynx in children. Attention to the
condition which has been instrumental in the production of the
affection, the use of antispasmodics, such as bromides, chloral, myrrh,
musk, camphor, ether, chloroform, etc., will meet the urgent symptoms,
while the use of tonics, such as vegetable bitters, quinine, iron,
cod-liver oil, with attention to a proper hygiene, constitutes the
general treatment.

The question of tracheotomy in spasm of the larynx should be
considered. It is sometimes stated that there is never in simple spasm
a justification for this operation, and that the other means at our
control are always adequate to meet the indication. Krishaber, Thaon,
and others are of this opinion. Gougenheim and Schnitzler think it is
sometimes required. While in a very large majority of cases of
uncomplicated spasm of the larynx the spasm will yield to the measures
recommended, it is nevertheless true that there are cases in which this
result is not realized. The slowness of the action of some of the
drugs, the difficulty in securing their introduction into the system,
their absence at the time of the attack, and the delay in their
administration,--all these facts may render it absolutely necessary to
resort to an operation for the purpose of saving the life of the
patient. It is, however, rare that this necessity will occur. In one
case recently in my own practice I think a life was lost for want of
the operation. The trouble was, as I thought, of hysterical origin, and
at the time of the consultation did not threaten life. There was free
movement of the vocal cords, and the vestibule of the larynx was not
obstructed. Spasm of the constrictors occurred at night, and did not
continue for a great length of time. There was certainly not paralysis
of the abductors of the glottis. I directed an antispasmodic, and
advised that if the spasm returned the next night a physician in the
neighborhood should be sent for. The spasm did recur, and the physician
was called, but before he reached the house the patient was dead. No
post-mortem was held, and {76} the question of the morbid anatomy could
not be determined with any degree of certainty. From the fact that
there had not been spasm till the night previous to the consultation,
that she was an adult female previously in good health, with no organic
disease, no tumor, no ulceration, no paralysis, and with a perfectly
healthy condition of all the parts of the organ as revealed by the
mirror, I am led to believe that the cause of death was simple spasm of
the larynx. It is possible that this was one of those cases described
by Krishaber and Charcot under the name of ictus laryngé or laryngeal
vertigo, and that the death was due to some central disease; but the
description given by the attendants was that of true spasm of the
muscles of the larynx, and it is more probable that, as in Cohen's
case, there was impaction of the epiglottis in the vestibule. The
question of the operation should be considered in severe spasm which
does not readily yield to the ordinary means. It is certain, I think,
that life may sometimes be saved by a timely opening of the trachea.

E. F. Ingals suggests tubage of the larynx in cases of spasm
threatening death. If the physician is present at the time of the
dangerous symptoms, this may be attempted. A large-sized catheter or
one of Schrötter's dilators may be used with no danger to the patient,
and possibly with the result of saving life.


Chorea of the Larynx.

There is a kind of disturbance of the motor function of the larynx
which has been described as chorea. The derangements of phonation and
of respiration are such as we should naturally expect from want of
co-ordination of the muscles concerned in speaking and breathing. There
may be a true chorea of the laryngeal muscles when there is no other
indication of the disease. Lefferts, in the first volume of the
_Transactions of the American Laryngological Association_, reports
three cases which he designates chorea of the larynx. They were all
characterized by spasm of the muscles concerned in phonation. It is to
be observed, however, that all three were women in early life, and that
there were no other choreic troubles mentioned. There were, so far as
the histories indicate, no hysterical phenomena present, if we assume
that the laryngeal trouble was not of that character. In the recital of
these cases the author seems to think that the evidence that the
patients were not simulating is a sufficient proof that the troubles
were not hysterical. This will not, I think, be accepted as adequate
proof of the absence of hysteria. It is certainly possible that the
patients were all three really choreic, but there is at least in the
fact of the sex, the absence of other manifestations of this disease,
and, so far as the author informs us, no antecedent history of
rheumatism or other morbid conditions so frequently preceding chorea, a
doubt as to the nature of the affection. Chorea affecting the muscles
of the throat and of respiration is, I think, not unfrequently met
with, but there is in these cases, so far as I know, such well-marked
symptoms of the origin and nature of the trouble as to leave no
reasonable room for doubt.

Cases of unmistakable chorea limited to the laryngeal muscles have been
seen by Knight, Roe, and others. Chorea or spasm of the expiratory
muscles alone may occur. I have the records of one such case, an adult
male. I was unable to say certainly that the larynx was the only part
involved. After a full inspiration there followed a series of short,
jerky, expiratory acts till the movable air in the thorax was all
expelled. For a few breaths the respiration was regular and full, when
the same phenomena were repeated. There was no organic disease. There
was forcible closing of the glottis during the {77} spasmodic
expiratory efforts. The patient recovered under treatment by
arsenic.[8]

[Footnote 8: It may not be easy in all cases to distinguish between the
true choreic cases and the hysterical affections. Knight of Boston has
given special study to choreic troubles of the larynx. He recognizes
three varieties: The first includes those cases in which the adductor
and expiratory muscles each side of the larynx are involved; second, in
which the laryngeal muscles alone are involved; third, in which the
expiratory muscles alone are involved.]

TREATMENT.--This should be the same as for other forms of chorea.


Nervous Cough.

Besides this ataxic condition we have hysterical disturbances of the
motor functions, which are of various kinds according to the muscles
involved. A constant effort to clear the throat, as it is called, is
sometimes met with--a scraping of the throat, by which there is
produced a rough, harsh sound similar to that which is heard in some of
the inflammations of the organ. At other times the form is that of
cough--a cough which is almost constant, and which is not associated
with disease of the mucous surfaces of the thoracic viscera. This cough
is sometimes almost continuous for days, and months even. It occurs at
intervals of a minute or more, with the same character of hoarseness
and roughness, without any interruption, except during sleep, when the
breathing is free and easy. I saw a few years ago a little patient who
had a cough of this nature which lasted several weeks, when it was
replaced by the peculiar rasping, scraping effort mentioned above. The
patient was a girl of fourteen years and had not developed. The moral
effect of a severe case of typhoid fever in a younger sister, followed
by the confinement of the mother, effected a cure. It is not at all
uncommon to find that certain patients suffering from uterine troubles
are also affected with laryngeal derangement of this character. A lady
was seen by the writer a few months ago who had a rough, harsh cough,
with attacks of asthma. There was no evidence of thoracic disease, and
I learned that she had had this cough from the time of her last
confinement. I advised her to consult a gynæcologist, who found that
she had a laceration of the cervix uteri. For this she was operated
upon, and from the time that she recovered from the immediate effects
of the operation she had no more asthma or cough. It had been purely
hysterical.

Cohen reports in his work _On Disease of the Throat_ (p. 627) an
epidemic of hysterical cough in a school for girls near Philadelphia.
The cough was peculiar in character. The neighbors called them the
barking girls. Cough of this character may be dependent upon other
conditions than hysteria. Irritations reflected from other parts, as
the ear and naso-pharynx, have been noticed.[9]

[Footnote 9: Cohen, p. 636.]

E. F. Ingals reports a case of an adult female whose voice had been
abnormal for several years. It had been preceded by measles. Upon
laryngoscopic examination the ventricular bands were seen to be
approximated during the effort of phonation, while the true or vocal
bands were, when last seen, moderately separated. The voice was not
extinct, but hoarse, low in pitch. The true cords could not be seen
during phonation on account of the closure of the false cords. This
could hardly be considered as chorea, but there must have been an
irregularity of muscular action, something between chorea and
hysterical ataxia. There were no other abnormal movements of the
larynx.

TREATMENT.--For these hysterical forms of trouble the treatment should
be such as to correct, if possible, the morbid conditions upon which
they {78} depend. Under the subjects of Anæsthesia, Hyperæsthesia, and
Paralysis this has been sufficiently discussed.


PARALYSIS AND PARESIS OF THE MUSCLES OF THE LARYNX.

The function of the muscular apparatus concerned in respiration and
phonation depends mainly upon the action of the recurrent nerves, as
stated in the paragraph devoted to the Anatomico-physiological Facts.
Disease of the centres in or near the floor of the fourth ventricle,
where, in close proximity, the pneumogastric fibres of the accessory
and the glosso-pharyngeal nerves take their origin, may be the sole
cause of a paralysis of these muscles. Disease along the course of the
nerves anywhere between this centre and the termination of the nerves
may give rise to the same result. Change in the structure or function
of the nerves at the point of their contact with the muscles in some
instances may possibly be the sole cause of the paralysis. Alteration
of the muscles themselves, such as atrophy or degeneration, produces a
like effect. In certain cases both the nerves and muscles are involved
in the morbid processes, but in some instances, even where there are
undoubted changes in the muscles, these changes are secondary, the
result of the long inactivity of the muscles. It is possible to group
these morbid conditions with reference to the nerves involved; but it
frequently happens that several different conditions are present at the
same time, and groups of muscles supplied by different nerves are
simultaneously involved. It is therefore difficult to classify these
troubles with reference to the nerves by which the parts are supplied.
The further fact that of individual muscles or parts of muscles
supplied by the same nerve-trunk some are affected, while others are
intact, renders this effort to make a physiological classification
still more unsatisfactory. As a rule, however, we may state in general
terms that diseases of the superior laryngeal nerves produce paralysis
or paresis of the external tensors of the vocal cords, the
crico-thyroids, and, to a certain extent, of the constrictors of the
larynx. Diseases of the recurrent nerves produce paralysis or paresis
of the other muscles of the organ. If the disease of the nerve is of
one side only, we have, as a rule admitting of only a very few
exceptions, a unilateral impairment of the motor functions of the
parts. In the case of the loss of power of individual muscles or parts
of muscles it is by no means easy to find a satisfactory explanation.
It seems probable that in some instances the reason is to be sought in
the centres, but in a great majority of cases the muscles are
degenerated or the nervous filaments of the particular parts are in a
morbid condition.

Notwithstanding this difficulty of classification, the troubles of
respiration and phonation due to the complete or partial paralysis of
the muscular apparatus are, for the convenience of study, divided into
groups. These groups are based either upon the seat of the primary
lesion or upon the kind of disturbance or the symptoms of the case.
Neither method of grouping is satisfactory. We must content ourselves
with a provisional arrangement. With the single exception of the
arytenoideus, the muscles are double and symmetrical; paralysis may
therefore be general or partial, unilateral or bilateral.

The causes, symptoms, or terminations vary with this general or
partial, double or single, character of the affection. We propose,
therefore, to consider these motor derangements under the following
heads, which in the main follow the classification of Mackenzie and
most other writers upon the subject:

1. Paralysis of the whole larynx--of one-half of the larynx; {79}

2. Paralysis of the constrictors of the larynx;

3. Paralysis of the adductors of the vocal cords: _(a)_ unilateral,
_(b)_ bilateral, _(c)_ central;

4. Paralysis of the tensors of the vocal cords: _(a)_ internal, _(b)_
external, _(c)_ unilateral, _(d)_ bilateral;

5. Paralysis of the abductors of the vocal cords, openers of the
glottis: _(a)_ unilateral, _(b)_ bilateral.


Paralysis of the Whole Larynx.

Paralysis of all of the muscles of the larynx gives rise to a position
of the parts which has, as before stated, been called the cadaveric
condition. The vocal cords are neither abducted nor adducted. The
opening of the glottis is sufficiently wide to admit of easy
respiration, but the cords are so far apart as to make phonation
impossible. The effort to articulate is not attended with any change in
the position of the vocal bands. In respiration there is no additional
widening of the glottic chink. The superior portion of the larynx is
also in a peculiar condition. The epiglottis is erect, standing against
the dorsum of the tongue; the vestibule of the larynx is widely open;
deglutition is difficult.

ETIOLOGY.--So far as we know, the causes are to be found either in
central disease or hysteria. When the cause is in the centres, there is
almost of necessity functional lesion of other parts of the muscular
apparatus, especially of the parts supplied by the glosso-pharyngeal
nerve. There will, therefore, be dysphagia. It is possible that the
central lesion may be very circumscribed; in such cases we may have
paralysis of individual laryngeal muscles or parts of muscles. These
cases are probably very rare, and the indication of more general
paralysis is, in fact, the point upon which the diagnosis of central
disease depends. Tumor or other disease along the track of the spinal
accessory before it unites with the pneumogastric may produce the same
effect. When the affection is upon one side only the paralysis is also
unilateral. There are, as before noted, exceptions to this statement.
In these instances it is probable that the innervation of the affected
part or side is supplied by branches from the opposite trunk. Such
cases have been reported by George Johnson, Lefferts, and others. It
has also been found that injury or paralysis of one recurrent nerve is
sometimes followed by bilateral paralysis. Schnitzler reports a case in
the _Wiener Med. Report_ for 1882. The left recurrent was compressed by
aneurism of the arch of the aorta; the right was normal. There was,
however, bilateral paralysis. Experiment by Tourgues[10] demonstrated
the fact that powerful excitation and consequent exhaustion of one of
the pneumogastrics may result in paralysis of the other. This result is
in accordance with facts seen occasionally in traumatism of one of the
pneumogastrics.

[Footnote 10: Reported in the _Gazette de Montpellier_, Nos. 35 and 36,
1882.]

A pure, uncomplicated paralysis, in which all of the muscles of the
larynx are implicated, and in which no other muscles are concerned,
will almost always be found to depend upon some lesion of the
pneumogastrics or the spinal accessories after they leave their point
of origin. Whether the paralysis is dependent upon the lesion at one
point or another, the symptoms are the same so far as the larynx is
concerned. The vocal cords are in a state of absolute rest between
abduction and adduction; the effort at phonation gives rise to no
contraction of the tensors; the arytenoids leave the cartilages
slightly separated; and the state of the organ is that of muscular
death.

When the lesion upon which a paralysis of the muscles of the larynx
depends is below the point at which the superior laryngeal nerves leave
the {80} pneumogastrics, the paralysis is limited to the phonators and
respirators. The muscular bands and fibres by which the glottis is
constricted are, in part at least, still capable of being thrown into
contraction. This condition of recurrent paralysis may be due to a
disease of the nerve-trunks, tumor pressing upon the nerves,
cicatricial tissue by which the nerves are compressed, aneurism of the
arch of the aorta or right subclavian artery, disease of the apex of
the lung, especially of the right side, pleuritic adhesions, or, in
fact, any injury or lesion along the trunks of the recurrents or
pneumogastrics. The paralysis may of course be partial or complete.

The SYMPTOMS vary according to the extent of the muscular disability.
In case of complete paralysis of one side there may be aphonia, but not
dyspnoea. The glottis admits a sufficiency of air, but does not close
so as to allow of the vibration of the cords. Where there is complete
paralysis on one side only, the voice is not necessarily entirely
suppressed, but it is changed in its quality; it becomes rough, weak,
and in its use gives rise to great fatigue. In long-continued cases
there is in part a compensation for the want of motion of one of the
vocal bands. The muscles of the sound side act with increased vigor, so
as to carry the sound cord at its posterior extremity beyond the median
line. The result is, that the two cords are brought so near each other
that phonation is possible. The arytenoid of the non-paralyzed side is
drawn forward beyond its fellow. The cord upon the affected side is
less tense than that on the healthy side. The vibrations are therefore
not equal; the pitch is different; the voice is therefore unnatural,
rattling, uncertain.

As we proceed to discuss the lesions in individual muscles or sets of
muscles we shall have occasion to refer to these etiological
considerations, as well as to some of the symptoms noted with partial
or complete loss of power of the whole group of muscles of the organ.


Paralysis of the Constrictors.

Complete paralysis of the muscles, by which the vestibule of the larynx
is closed, is rare. The partial paralysis of these muscles is, however,
by no means uncommon. As we have already endeavored to show, it is
probable that the motor functions of the muscular fibres in the
ary-epiglottic folds--the superior constrictors--are mixed. Probably
both the superior and inferior laryngeal nerves are concerned in their
movements. It is not, therefore, easy to group these disorders
according to the nerves involved, as has been done by Von Ziemssen,
Mackenzie, and others.

Partial paralysis of the constrictors may be due to deficient power of
one or both of the laryngeal nerves, superior or inferior. The parts
involved are the arytenoids, transverse and oblique, and the muscular
fibres in the folds going from the arytenoid and from the thyroid
cartilages to the epiglottis.

The ETIOLOGY of this form of paralysis associates itself with that of
anæsthesia of the parts--namely, the arrest of motor impression in the
centre, obstruction along the course of the nerve, disease in the nerve
itself, in its trunk or termination, or, lastly, myopathic changes
rendering the muscle incapable of responding to the nervous influences.
Disease in the centres may possibly affect only these muscles; the
disorders of motion may be well defined and local in extent, but
usually, in case of central disease, there is a complication of
external manifestations and we have a wider range of disturbances. The
most common cause of this loss of power is diphtheria.

SYMPTOMS.--The symptoms of paralysis of the constrictors of the larynx
are for the most part mechanical. The failure to close the vestibule of
the organ in the act of swallowing allows food or drink to pass into
the larynx, {81} and, as there is usually anæsthesia of the parts also,
the invasion of the larynx is not perceived; no reflex irritation is
produced, no cough for the extrusion of the offending matter, which may
descend into the trachea, and, reaching the bronchi, may become the
agent in the development of a bronchitis or a broncho-pneumonia. The
secretions of the mouth overflow the borders of the laryngeal opening
and fall into the tube below. Fluids are swallowed with greater
difficulty than solids. The voice is not altered except in cases where
the crico-thyroids, one or both, are involved, as in complete paralysis
of the superior laryngeal nerve. The effort to close the glottis, as in
the preliminary act of coughing, is accomplished with difficulty. The
sound of the cough is somewhat altered. This is for want of the
reinforcement to the adductors furnished by the closure of the
vestibule of the larynx. Upon laryngoscopic examination the epiglottis
is seen to stand erect against the dorsum of the tongue. The
ary-epiglottic folds are lax or wide apart. With this is loss or
diminished sensibility of the surfaces. There is little or no change in
the color of the membranes. The secretions are normal in quality, and
only slightly in excess in quantity.

The course of the disease is in cases of diphtheritic origin like that
of anæsthesia from the same cause. The termination, except in rare
instances, is recovery. In cases of central origin the local symptoms
in the larynx are almost necessarily associated with disorders of other
parts. The progress and termination will depend upon the nature and
extent of the central lesion.

The PATHOLOGY of this form of paralysis is probably multiple. When of
diphtheritic origin it has been believed to consist in a change of the
nerves along the trunk or in their distribution, or an alternation of
nutrition due to the local changes in the larynx or pharynx during the
progress of diphtheria, or to both of them. It is also probable that it
is in many cases as much a myopathic as a neuropathic trouble. In other
words, during the progress of the diphtheria the muscles, as well as
the nerves, have undergone a change in their nutrition; and this local
change in the peripheral portions of the nerves, along with this
degeneration of the muscles, goes to make up the pathological anatomy
and constitutes the essential local morbid condition.

There is, however, abundant reason to think that in some cases at least
the influence of the diphtheria in the production of paralysis reaches
far beyond the parts which are the seat of the local manifestations of
the trouble, or even the centres from which these nerves are derived.
It is well known that the extremities may be affected, and that other
muscles become involved which can have no direct and immediate relation
to the tissues which have been attacked with the diphtheria. It seems
therefore evident that there must, at least in certain cases, be a
general derangement of the centres, or that there must be some other
explanation for the impairment of the muscular power than that which
ascribes its loss solely to the local and poisonous action of the
morbid deposit or to the defective nutrition of the parts. It is
probable that there is in these cases a widespread influence, a
constitutional trouble, which, like the disease itself, is general and
not local except as to its manifestations.


Paralysis of the Adductors.

A pure, uncomplicated paralysis of the adductors of the vocal cords is
extremely rare. When present it is marked by symptoms and signs which
are easily recognized. A partial paralysis of an hysterical nature is,
however, not unfrequently encountered. The etiology of paralysis of the
lateral crico-arytenoid muscles is in most instances the same as that
of the other muscles of the larynx. There may be a morbid condition of
the centres in the fourth {82} ventricle, from which the spinal
accessory takes its origin. It is certainly possible in theory that
certain fibres ultimately distributed to these muscles may alone become
diseased in their course along the trunk of the nerve. There may be
change in the final distributions by which the function of the nerve is
arrested. There may be myopathic change in the muscle itself, rendering
it non-responsive even to normal nerve-impressions. All of these causes
are theoretically possible. In fact, however, we know but little of the
real causes which operate in any given case. Mackenzie, Von Ziemssen,
and others ascribe it in some instances to catarrh from exposure to
cold. There is developed a hyperæmia of the mucous surfaces of the
supraglottic space. The structures beneath are involved in the
tumefaction as a result. The voice is impaired or lost; the aphonia,
which was at first due to the mechanical difficulties in the way,
persists after the local inflammation has subsided. The vocal cords
remain permanently apart, even though there is no swelling to prevent
the arytenoids from approaching each other. Gerhardt attributes this
form of paralysis in certain cases to a rheumatic inflammation
affecting either the articulations or the muscles themselves. Trichina
have been found in one or both muscles, producing a paresis. Syphilis,
central or laryngeal, may account for a number of cases. When the loss
of power is due to local syphilitic trouble, there is, however, usually
a recognizable change in structure, something more than a simple
paralysis.

It would seem strange to find a rheumatism so localized as this
hypothesis implies. Mackenzie has met with a case in which the
paralysis was unilateral and toxic, due to lead-poisoning. He thinks
there may be other cases of similar origin, and suggests arsenic also
as a possible cause. In his case he compares this paralysis of the
lateral crico-arytenoids to the loss of power in the extensors of the
forearm in well-marked cases of lead-poisoning. The affection was
limited to the adductor muscles. Seifert and Lublinsk in _Berlin. klin.
Woch._ also report cases. The adductors only were affected. The very
few cases in which this form of paralysis has been carefully noted do
not supply us with the material for a more exact opinion as to the
causes of the trouble.

SYMPTOMS.--The symptoms of this form of paralysis are for the most part
such as depend upon the mechanical relation of the parts. There is no
pain; there is no dyspnoea, except in cases in which there is a catarrh
of the larynx; there is no cough. There is however, complete aphonia.
There may be an exception to this statement when the paralysis is
unilateral. It is possible that where one cord comes to the median
line, and the other is affected only with paresis, in the course of
time the cord on the sound side may pass beyond the median line and
render phonation possible. In such cases, however, the voice is not
normal in quality.

Upon inspection with the laryngoscope the glottis is seen to be widely
open. The cords approximate the lateral walls of the supraglottic
space. Upon an effort to phonate the cords remain immobile. If the
constrictors are unaffected, the act of laughing is still possible,
from the fact that a partial occlusion of the lumen of the tube is
accomplished by the action of the borders of the laryngeal opening and
by the approximation of the false cords. In case of unilateral
paralysis of course there is motion of the cord upon the sound side,
leaving one-half of the glottis open. It has been stated by Von
Ziemssen that there is sometimes an anæmic condition of the mucous
surfaces. When present, this is probably only a contingent phenomenon,
the evidence of a slight alteration of the circulation in the tissues.
It is true that the permanent immobility of the parts ought to diminish
the activity of the circulation in the muscles, and perhaps also in the
neighboring structures. On the other hand, the surfaces have been found
hyperæmic. Probably no importance should be attached to the surface
condition as a means of diagnosis.

{83} The course, duration, and termination of this form of paralysis
must depend largely upon the cause. When the disorder depends upon a
catarrh, we may expect that the trouble will disappear, or at least be
mitigated, as the local affection is relieved. If of syphilitic or
rheumatic origin, it should disappear pari passu with the primary
disease. So far as we know, there is no danger to life, the loss of
voice being the only important result.

The DIAGNOSIS is easy. The laryngoscope will enable the observer to
differentiate it from all other affections by which the voice is
destroyed. It is possible that disease affecting the articulation of
the arytenoids, and thus preventing their movement, might give rise to
a doubt. A careful examination in such cases will, however, generally
reveal the fact of tumefaction or other evidence of structural change.

Closely allied to the paralyses which we have just been considering are
the affections of the glottis of hysterical origin.

If the cases of true paralysis of the lateral crico-arytenoid muscles
are rare, it is equally true that a partial arrest of the action of
these muscles, and temporary for the most part in duration, is not
unfrequently met with. The etiology of these cases seems to be much
more within our knowledge than that of those of which we have just been
speaking; at least the conditions under which they occur are much
better known. For the most part they occur in females. They are met
with in patients of nervous temperament, generally adults, though I
have seen one case in which the subject was still undeveloped. There
are very generally the evidences of hysteria in some of its various
manifestations. We may therefore assume that the disease is functional
in its nature and that it is reflex in origin. It has been said that,
as it is not dependent upon any disease of the muscles or nerves of the
larynx, so far as we know, it should not be classed among the
paralyses. For the same reason it should not be considered as a
neurosis of the organ, but of the system in general. But it is a
neurosis of the larynx, and therefore ought to be placed here. In
addition to this, it is in its symptoms identical with or very similar
to the true paralyses dependent upon alteration of the nerves or of the
muscles of the part.

The etiology of the affection has already been suggested in the
definition. A disturbance of the functions of the uterus, or possibly
of other portions of the nervous system, may be so reflected as to
materially interfere with the action of the muscles of the larynx. It
is possible that the affection may occur in males, as other troubles
called hysterical sometimes do. That the uterus is not always the
source of the reflex disturbance is certain. I have very recently seen
a case in which there was unquestionably an intermittent partial
paralysis of the adductors of the muscles in an adult man. It seemed to
be dependent upon the condition of the stomach. Whenever there was
flatulence or an accumulation of gases in the stomach, the voice became
husky, requiring great effort and expenditure of air in phonation, and
then extinct. Examination with the laryngoscope showed the cords in the
condition of adduction. In the effort to speak there was a very slight
approximation of the vocal bands, but not enough to admit of their
vibration. With the recovery from the disorder of the stomach this
condition disappeared. I have seen one other case similar in character.
I think we may therefore assume that the trouble can be produced by any
affection which creates a disturbance of the pneumogastrics, and which
by reflex action interferes with the proper functions of the spinal
accessory.

The disease is always bilateral. Its advent is generally sudden. The
symptoms are first and almost solely loss of voice. The aphonia may
from the beginning be persistent, or there may be intervals when the
patient speaks with ease. In some cases the patient is able to whisper;
in others this power is also lost: in the effort to phonate there is
absolutely no sound. There is {84} no pain, but there is often cough:
this cough is hoarse, like that which has been described under a
previous heading. The general health is in some cases apparently
perfect, but in a majority of instances there will be found some
disturbance of the viscera of the abdomen. Perhaps in all cases this is
true, but so slight that we are obliged to look carefully in order to
find it. Upon inspection with the laryngoscope the cords are seen to be
separated, but not so widely as in complete paralysis of the adductors
from other causes. There is no marked morbid condition of the mucous
surfaces. The secretions are not affected. It is possible that there
may be at the same time a partial paralysis of the pharyngeal muscles,
so that there is also dysphagia. In a few instances there is a
paræsthesia of the parts above. The dysphonia or aphonia is then
associated with a feeling as though there was a foreign body in the
throat. In efforts at phonation the cords usually move slightly toward
the median line, but not enough to enter into vibration. When this
condition of things is observed, and there is no other cause for the
explanation of the loss of voice, we may with safety assume that we
have to do with an hysterical paralysis of the adductors.

The duration of this form of motor disturbance is uncertain. It may
terminate suddenly after a short duration or it may continue
indefinitely. It is a cause neither of dyspnoea nor asphyxia. It always
ends finally in recovery. This statement is possibly subject to an
exception in cases in which there are other diseases present and when
these diseases are of themselves dangerous to life.

The pathology and morbid anatomy are dependent upon the length of time
during which the muscles have been in a state of inaction. It is
possible that the muscles may degenerate or lose their power to act
with the normal vigor, or there may be a simple atrophy of the muscles,
as in a case reported by Mackenzie. So far as I know, this alteration
of the muscles is very seldom found in hysterical paralysis. When
degeneration or atrophy does exist, it is probably a result, and not a
cause, of the paralysis. So far as we know, there is no antecedent
change in the larynx. This must of necessity be the case, since the
disease is reflex, and not primarily in the organ of speech. Why the
morbid influences are manifested in this organ to the exclusion of
others we do not know. In fact, we do not know that this is the case.
So far as we can judge from the records of similar cases found in the
literature of the subject, we may safely believe that there is in
nearly all of the patients some other disorders of motility, but the
derangements of speech are so striking that these have masked all minor
troubles.

The intimate relation between the organs of expression, of which speech
is one of the most important, finds in these cases a striking
illustration. The quality of the voice is modified by emotion. The
evident relation of the generative functions to this psychical state is
well known. This fact explains the association of these troubles so
frequently encountered in the study of the morbid conditions of the
larynx. It is true that the disturbance is not always limited to the
phonators, but it is nevertheless more frequently met with in these
muscles than in the muscles of respiration. Emotion and the expression
of emotion go together. Their morbid conditions are therefore
associated.


Paralysis of the Arytenoideus--Central Adductor.

The function of this muscle is to approximate the arytenoid cartilages.
Its paralysis leaves the posterior borders of the cartilages separated,
even though the vocal processes are by the action of the lateral
crico-arytenoids made to approach the median line. There is left a
triangular opening at the base of the cartilages, through which the air
escapes in the act of speaking. This, the {85} cartilaginous portion of
the glottis, remains patent even though the anterior three-fourths of
the space be closed. The result is generally, but not always, a loss of
speech. The air whistles through this opening, but phonation is
difficult or absent. The causes are to be sought in the derangements
resulting in the loss of power of the other muscles. Upon examination
with the laryngoscope the triangular opening is readily seen. The
ligamentous portion of the glottis is seen to close in the effort to
speak, while the cartilaginous portion is widely open. There is no
other morbid condition necessarily present. The trouble is frequently
associated with paralysis of the adductors of the two sides--that is,
the lateral crico-arytenoids. In these cases there is complete
separation of the cords throughout the whole length.

The DIAGNOSIS is easy except in instances where there is ankylosis of
the articulation of the cartilages. Even in these cases a careful study
of the parts, as revealed by the mirror, will enable the observer in
most instances to recognize evidence of structural disease on the walls
of the larynx. There will also be a history of some antecedent
affection, such as syphilis or tuberculosis, or possibly arthritis. The
course and termination of this form of paralysis depend largely upon
the etiology in any given case.


Paralysis of the Tensors of the Vocal Cords.

It will be remembered that these are in two groups, the internal and
external.

The internal are the thyro-arytenoids. While their function is in part
still a matter of discussion, it is very generally conceded that they
have to do with the form and tension of the cords. Their paralysis
produces a very marked derangement of the functions of the larynx as
the organ of speech. They act ordinarily along with the crico-thyroids,
but from the fact of their separate innervation it would seem very
probable that they should be the seat of special functional
derangements. In fact, it is true that their paralysis in a limited
number of cases is found to be quite independent of any disturbances of
the external tensors.

ETIOLOGY.--In addition to the general causes of laryngeal paralysis,
the use of the voice in an unnatural or too high a key or the too
long-continued use of the organ may result in a temporary or even
permanent impairment of the power of these muscles. Their exposure to
the causes of inflammation, lying as they do so near the surface of the
mucous membranes, subjects them to the morbid influences of the
catarrhal troubles to which the glottis is liable. They are probably
more frequently affected than the literature of the subject would lead
us to suppose, as in many cases the disease is temporary.

SYMPTOMS.--These consist mainly in the alteration of the voice. It is
hoarse, the register is lower, the quality is uneven. Occasionally a
note is, if not lost, uttered with difficulty; some letters, such as
the aspirates, requiring the careful adjustment of the glottis, are
articulated with great uncertainty. There is what has been called a
rattling of the voice. It is quite impossible to sing or to speak long
in a high key; even prolonged ordinary conversation gives rise to
fatigue, for the reason that there is so great a waste of air in the
effort. The pressure upon the under surface of the cords in their
relaxed condition forces its way upward and through the glottis without
throwing them into normal vibration.

DIAGNOSIS.--The laryngeal mirror reveals the glottis only partly
closed. There is an oblong opening extending from the thyroids to the
base of the arytenoid cartilages. The vocal processes even are not
brought to the median line, but are so far apart as to leave a
noticeable slit between them. It seems from this fact that these
muscles are therefore the aids of the lateral {86} crico-arytenoids in
the rotation of the cartilages on their bases. In the effort at
phonation the cords are seen to move with difficulty. The disease may
be unilateral or bilateral.

This form of paralysis in course and termination does not in any
essential respect differ from other paralyses of the larynx. The
duration is therefore very uncertain, and will depend largely upon the
cause of the affection.


Paralysis of the External Tensors of the Cords.

This is a rare disease, but is present in complete paralysis of the
superior laryngeal nerve. It is then associated with anæsthesia of the
superior portion of the glottis, as well as paresis of the depressors
of the epiglottis, and generally of the constrictors of the vestibule
of the larynx.

ETIOLOGY.--It may be the result of injury to the external branch of the
superior laryngeal in its distribution to the muscles. It may be caused
by diphtheria. It is possible that the motor fibres of the superior
laryngeal nerve may be alone involved, while the sensitive portion is
still normal. Cases of partial paralysis are recorded by Von Ziemssen,
Gerhardt, and others.

The SYMPTOMS are such as we should expect in diminished tension of the
vocal bands: lowering of the pitch of the voice, with inability to
reach the higher notes. There ought to be, therefore, hoarseness. Acute
paralysis of this muscle has been known to produce aphonia (Ramon).

DIAGNOSIS.--It is said that this form of paralysis gives rise to a
well-recognized condition which may be seen in the laryngeal mirror.
The cords are described as wavy, irregular in their relation to each
other, like the position of two pieces of ribbon, which, having an
attachment at their extremities near to each other, are allowed to fall
into folds. This condition, if ever present, is, I am convinced, very
rare. It is probable that the descriptions have been given to
correspond with what ought to be seen, rather than what is actually
seen, in the mirror. There is said to be a slight depression of the
vocal processes in the act of inspiration, and a corresponding
elevation of them in the act of expiration and phonation. The
diminished tension should produce this change in position. The disease
may also be recognized by placing the finger upon the edge of the
crico-thyroid muscle during the effort to speak. The muscle acts so
strongly in the healthy condition that it may be easily felt; in
paralysis this contraction is wanting.

The course and duration of the disease must depend upon the cause and
complications. When the muscles suffer in common with the sensory
apparatus supplied by the superior laryngeal nerve, as in the case of
diphtheria, there is reason to expect that it will disappear with the
other morbid phenomena.


Paralysis of the Posterior Crico-Arytenoids.

The functions of these muscles render any loss of their power as
glottis-openers a matter of importance. It will be remembered that they
are so situated that they not only rotate the arytenoids, turning the
vocal processes away from each other, but they also serve to fix the
cartilages, giving them a firm support as points of attachment for the
vocal cords. The outer fibres tend also to draw the body of the
arytenoids away from each other, as well as to fix them in a
postero-lateral position. They are, more than any other of the muscles
of the larynx, organs of respiration. They are also in constant action:
with each inspiration they contract, and during expiration they {87}
fall into rest. In this respect they resemble the other muscles of
respiration and the central organ of the circulation. In some respects
they also resemble the muscles of the heart in the degenerative changes
to which they are subject. Their antagonists are the lateral
crico-arytenoids. When both sets of muscles are paralyzed, the glottis
is in what is known as the cadaveric condition; that is, the vocal
cords are neither widely separated nor parallel to each other. There is
an opening of a triangular shape as in the act of easy inspiration, not
sufficiently approximated to admit of speech, but sufficiently open to
admit of free inspiration. With this understanding of the physiology of
the parts, we can readily appreciate the results of the loss of power
of these muscles. As stated by Bosworth, the especial danger is in the
integrity of the adductors, tending for the want of antagonism to keep
the glottis closed. Of all the muscles of the larynx, these are
therefore the most important so far as life is concerned.

The disease is progressive (Lefferts, Semon, Bosworth).

The first symptom which attracts attention is generally inspiratory
dyspnoea while taking active exercise. The difficulty continues to
increase till there is constant difficulty in the act of inspiration,
usually with spasm. The dyspnoea is more marked during sleep than when
awake. Death may occur at this period of the disease before the gravity
of the trouble has been recognized. As a rule, tracheotomy will be
required to prolong life, after which the dangers to the patient are
passed.

The ETIOLOGY of this form of paralysis presents some peculiar problems.
In all paralyses of the individual muscles we are obliged to invoke
nerve-changes in special nerve-cells in the centres from which the
individual nerves have their origin--changes along the course of the
nerves; or, on the other hand, some myopathic change in the muscles
themselves. In the muscles now under consideration we have a special
function--namely, respiration--involved. The disorder is usually
limited to these muscles alone. If it becomes general, it commences
here. The phonators not being involved, it is probable that in a part
of the cases reported the essential cause of the paralysis must be
ascribed to disease in a centre in the brain, or at least along the
course of the nerve near its origin. Other cases are evidently due to
pressure on the pneumogastrics or recurrents. This view has been
proposed by Bosworth. Von Ziemssen and others have thought that
syphilis enters very largely into the pathology of this group of cases.
There has been noted, as confirmatory of this proposition, that other
symptoms of central disease have been in a few instances observed.
Diseases affecting the recurrents have been known to affect these
muscles alone: Ingals reports cases. On the other hand, it is quite
certain that in a large majority of the cases recorded there has been
no satisfactory cause assigned. In nearly all of the post-mortems there
has been found a degeneration of the muscles. This is as we should
expect to find it where the structures have been for a considerable
time in a state of inaction. The histological change may possibly be in
any case only the result of the paralysis, and not the cause of it. In
a few instances there has been discovered a degeneration of the
nerve-trunks by which the parts are supplied. As to the causes by which
the muscles may become affected, we can imagine that the exposed
position suggested by Mackenzie renders them peculiarly liable to
mechanical injuries from hard substances forced down the oesophagus.
They are subjected to changes of temperature produced by hot and cold
drinks and food. Their relation to the seat of local inflammation of a
specific as well as of a non-specific character renders them liable to
become involved in morbid processes. The fact that the disease
occasionally occurs after diphtheria, as I have in two instances
demonstrated, gives additional weight to this hypothesis. The fact
probably is that there are several varieties of the affection. The want
of more accurate information as to the {88} previous history, as well
as to the immediate antecedents of the attack, renders it impossible as
yet to differentiate the cases due to one or other of these causes. For
the present, then, we may conclude that paralysis of these muscles may
depend upon either disease of the centres, disease along the track of
the nerves, pneumogastric or recurrent, or to disease of the peripheral
branches or fibrils, or to disease of the muscles themselves.

SYMPTOMS.--These are at first so slight that the trouble is usually not
recognized till it has reached such a stage that the act of inspiration
is either attended with fatigue or there is stridor which annoys the
patient or alarms his friends. Soon afterward there begins to be a
dyspnoea, a difficulty in breathing, especially during any active
exertion and during sleep. The voice in the mean time remains normal.
Expiration is free. The general health is usually undisturbed. There
may be a catarrhal affection of the mucous surfaces, but if so it is
quite accidental. Spasm supervenes. There is at times great difficulty
of breathing, and, finally, the effort becomes so great that the
patient becomes alarmed. Upon examination with the laryngoscope the
vocal cords are seen in close proximity to each other even during the
inspiratory effort. In fact, they are, by the pressure of the air upon
their upper surfaces, brought closer together during inspiration than
during expiration. They seem to act as valves which are closed by the
weight of the atmosphere upon their wide, flat upper surfaces, pressing
them against each other. Hence the inspiratory stridor and dyspnoea.
The act of expiration is a passive one in health, and in this condition
the air is easily forced out by pressing the cords away. The order of
the movements of the cords is therefore changed--in the normal
condition wide in inspiration, narrow in expiration; in this disease
narrow in inspiration, and while not wide, at least wider, in
expiration than in inspiration. In other respects the parts are normal.
There is nothing to suggest the trouble except the closure of the
glottis during inspiration.

The course and duration of the disease are in a large majority of cases
chronic. Once established, it tends to persist. The cases of
diphtheritic origin should be excepted from this statement. In those
forms in which the trouble is entirely in the muscles of the part life
may, so far as we know, be continued indefinitely. Where the trouble is
central it is probable that the cause has a tendency to involve other
parts of the brain, and in this way to lead to other, and possibly
dangerous, complications. Of this, however, we know but little. The
paralysis is not directly the cause of death, except as it closes the
glottis. The dangers are therefore mechanical. When the patient has
once been placed in a condition of safety by the operation of
tracheotomy the local paralysis no longer endangers life.

Mackenzie, Von Ziemssen, Cohen, and in fact almost all writers upon the
diseases of the larynx cite and publish cases by the way of
illustration of the symptoms, course, and termination of this class of
troubles. They are now so numerous that it would seem to be hardly
necessary to do more than to give the conclusions which the recorded
instances suggest. Fortunately, this form of laryngeal disease is rare,
and when present it is easily recognized. The treatment is clearly
indicated. In all cases in which the inspiratory difficulty is marked
tracheotomy should be performed, even though suffocation does not seem
to be imminent. The treatment for the radical cure of the disease must
be in the main the same as that required in other forms of laryngeal
paralysis.

TREATMENT OF PARALYSIS OF THE LARYNX.--The grouping of these disorders
for the purpose of description has, for the reasons already given, been
based largely upon symptoms. For the purpose of treatment we may
properly divide them with reference to their causes. With these in
view, we have, first, those cases in which the cause of the affection
is within the {89} cranium--central disease; second, those in which the
loss of power is the result of disease or pressure along the course of
the nerves outside the cranium and before reaching the larynx; third,
those in which there is disease of the structure of the larynx itself,
nerves or muscles; fourth, those in which the cause is to be found in
some distant part--reflex paralysis; fifth, those of toxic origin. This
last includes paralysis after typhoid fever, diphtheria, etc., as well
as those produced by lead, arsenic, mercury, and possibly copper and
other toxic agents.

Diseases of the base of the brain or medulla are for the most part not
amenable to treatment. They are generally organic and progressive. The
exception to this statement, or at least the most notable exception, is
syphilis. The influence of this disorder in the production of paralysis
of central origin must be admitted, but it seems to have been by many
authorities overstated. The coincidence of paralysis with an earlier
infection does not by any means justify the inference that the one
disease has been produced by the other. When, however, there is reason
to think that this relation may exist, antisyphilitics should be
administered. In a few cases this treatment has been followed by marked
improvement of the laryngeal disease.

Cases dependent upon malignant growths within the cranium are
absolutely beyond the reach of treatment. Paralysis dependent upon bony
tumors, even though they are benign in character, are also for the most
part beyond the reach of surgical interference. If the paralysis is
complete--that is, if all the muscles are involved--there are no
indications for any operative procedure. If, however, only the nerves
that supply the posterior crico-arytenoids are involved, as
occasionally happens, tracheotomy should be resorted to even though the
dyspnoea is not urgent. This operation places the patient in a
condition of temporary safety, and gives time to resort to other means
if the indications for their use can be found.

The second group of cases includes all those in which the cause of the
paralysis is due to the presence of disease of the nerve-trunks, or to
pressure upon the nerves between their emergence from the cranium and
their terminations in the muscles of the larynx. Malignant growths and
benign tumors situated along the tract of the nerves, and pinching
them, are readily recognized, and when not contraindicated by other
facts they should be removed. Enlargement of the thyroid gland may in
some cases press upon the nerve and cause paralysis. This is
occasionally relieved by appropriate treatment directed to it. Among
those means which have occasionally been found efficacious for this
purpose iodine or some of its compounds, and especially electricity in
the form of galvanism, seem to be entitled to the most confidence. For
paralysis dependent upon cicatricial pinching of the recurrent
nerve-trunks relief may possibly be obtained by dissecting out the
bands by which the nerves are compressed. This is hardly indicated for
the partial derangements which do not endanger life, as in unilateral
paralysis of the recurrent. Where the trunk of the nerve is entirely
obliterated nothing can be done, and in many cases of injuries along
the trunk of the recurrent it will be impossible to know that the nerve
has not been destroyed in the mechanical lesion.

Paralysis caused by pressure upon the intra-thoracic portion of nerve
is beyond the reach of surgical interference. When this is aneurism,
disease of the apex of the lung, or pleuritis, as may possibly happen,
the paralysis or paresis must of course have a history coeval with the
thoracic disease. The causes themselves are unfortunately persistent
and tend to terminate in death; the paralyses are therefore persistent
and beyond the reach of medical or surgical relief. In cases where the
posterior crico-arytenoids are especially involved, tracheotomy, as in
the same condition from intra-cranial disease, should be performed. It
is certainly true that there may be a morbid {90} condition of one or
both of the pneumogastrics or recurrent nerves without macroscopic
changes in their structure; in such cases the use of the faradic
current together with general tonics is indicated.

The third group is made up of those cases in which there is disease of
the nerves or muscles of the larynx itself. It seems to be true that in
most of these patients there is a derangement of the general nutrition;
but this is not all: there is also a special morbid condition of these
special structures. For degeneration of the muscles of the larynx there
is probably no remedy; for atrophy there may be something done by
different methods of exercising the muscles. The use of electricity
when the muscles are still responsive to the current should be
attempted. Regular applications by which they are thrown into action
may result in the improvement of their nutrition. The use of them so
far as they are phonators, without carrying it to the extent of
producing fatigue, is also indicated. In addition to these local
measures, tonics for the purpose of improving the general condition may
be administered. Strychnia, with the purpose of stimulating the
centres, will also be found in some cases useful. When the disease is
partial, as in the case of the posterior crico-arytenoids, such
operative measures as have been already indicated must be resorted to.
The purpose is to prolong life, even though we cannot cure the disease.

The fourth group, the paralyses of reflex origin, are generally within
the reach of treatment; at least, they usually recover. They depend for
the most part, as will be remembered, upon some disorder of distant
organs. There is primarily no disease of the larynx, and not
necessarily even a secondary disorder of its structures. It is true
that long inaction may result in atrophy of the muscular structure, but
this is, I am convinced, a rare exception to the rule that in
hysterical paralysis there is maintained a complete integrity of the
muscles of the organ, even though the parts have been for years in a
state of inaction. For some reason, the nutrition is maintained much
better than in paralysis from other cases. The trophic nerves are
evidently not involved. The treatment should be both local and general.
It should be directed to the larynx and to the distant part upon which
the motor disorder of the larynx depends. So far as the larynx is
concerned, we know of nothing better than electricity. The faradic
current, by which the muscles are stimulated and the nervous energies
awakened, seems to be most useful. The method of applying electricity
to the larynx may be varied according to the nature of the case and the
age of the patient. In young children the current should be directed
through the walls of the larynx from side to side or from before
backward. It should be repeated every day if possible. In adults the
current may with advantage be passed through the larynx from within
outward or from one side to the other. This may be accomplished by the
use of Mackenzie's laryngeal electrode. The instrument is either single
or double. Armed with a sponge and bent to the proper curve, one pole
is introduced into the larynx, the other placed upon the neck, and then
by pressing a spring the circuit is closed, permitting the current to
pass through the parts from one pole to the other. In using the
instrument with two electrodes, as in paralysis of the arytenoids and
constrictors, the instrument with two branches, each armed with a
sponge, and to which the two poles are attached, is introduced with one
branch in one of the depressions in one side of the larynx, and the
other on the opposite side in the corresponding depression. The circuit
is now closed as before, with the muscles between the two poles as part
of the circuit. The electrodes may be carried down into the organ and
the stimulus applied directly to the vocal bands. In some cases the
first shock is followed by distinct phonation; in others repeated
applications are necessary; while in still others all efforts of this
kind fail entirely. Both the galvanic and the faradic current may be
used. When the object {91} is to stimulate the dormant energies of the
nerves or muscles, the faradic is probably the more useful; if it is
desired to modify the nutrition of the parts, the galvanic is
preferable. The strength of the current should be carefully tried upon
the surface of the hand of the operator before introducing it into the
larynx. The shock to the nervous system from the dread of the operation
has sometimes resulted in the recovery of the voice before anything has
been done. The morbid spell is broken and the patient speaks. This is
true in spasm even, as shown in a case reported by Lefferts, where it
was thought that tracheotomy was necessary for the purpose of saving
life. The patient, frightened at the thought of the operation,
recovered, and respiration became easy. There was no reason to think
that the case was one of simulation.

For the general condition, which is usually one of asthenia,
nerve-stimulants are indicated, and the bitter tonics, with iron and
strychnia, good generous diet, outdoor exercise, change of
surroundings, travel, moral impressions, in short everything that tends
to promote general good health,--these are among the most important
requirements. If there is local uterine trouble, this of course
requires attention, or if there is any other derangement which serves
as the point of departure for the morbid phenomena, this will also
demand consideration. In fact, no organ suffers alone. There is a
community of function and there is a community of suffering. This
subject has been perhaps sufficiently discussed in the consideration of
the treatment of hysterical disorders of sensation and of spasm, to
which the reader is referred.

The fifth group comprises paralyses toxic in their origin. When the
cause is typhoid fever or diphtheria, we may confidently expect the
paralysis to disappear with the other manifestations of adynamia. Time
and tonics, with attention to diet, and in the more protracted cases
electricity, will generally be all that is required. Cases depending
upon the toxic effects of lead or arsenic demand the treatment
appropriate for the other manifestations of these forms of paralyses.
The iodide of potassium internally, with attention to the general
health, and especially to the functions of the excreting organs,
constitute the most important measures. In addition, strychnia may be
administered, and the faradic current applied through the larynx. It is
certainly possible that laryngeal paralysis may be produced by arsenic,
as shown in the case reported by Mackenzie, and probably also by copper
or mercury. Such cases, however, must be exceedingly rare. The
potassium iodide, as suggested for lead-paralysis, may be resorted to
in case mercury is supposed to be the cause. For arsenic- and
copper-poisoning the reader is referred to articles upon these subjects
elsewhere. Cases in which there is evidence of a local lesion due to
syphilitic intoxication should receive both local and general
treatment.




{92}

ACUTE CATARRHAL LARYNGITIS (FALSE OR SPASMODIC CROUP).

BY A. JACOBI, M.D.


PATHOLOGY.--Catarrhal inflammations of the mucous membrane and the
submucous tissue of the larynx are of frequent occurrence. They are
either general or local; that is, confined to the epiglottis or the
vocal cords, etc. The affected parts are red (only less so where the
elastic fibres are developed to an unusual degree and capable of
compressing the dilating capillaries) and more or less tumefied.
Sometimes small hemorrhages occur. The secretion is either changed in
character or in quantity. It is either mucous or purulent, or (mainly
in passive congestions produced by interrupted venous circulation)
serous. The epithelium is either thrown off or accumulated in some
spots, particularly on the vocal cords, so as to form whitish
conglomerates which may become the abode of schizomycetæ. The
muciparous follicles are enlarged and dilated; to this condition is due
the granular form of laryngitis, with the nodulated condition of the
epiglottis or the fossæ Morgagni or the inferior vocal cords.[1]

[Footnote 1: Ziegler, _Pathol. Anat._]

When the catarrhal process is of longer duration, the capillaries and
small veins become permanently enlarged; round cells are deposited
between the epithelium and cellular tissue; the cellular tissue becomes
hypertrophied; papillary elevations are formed on the vocal cords. The
disintegration of the epithelium and the bursting of the tumefied
muciparous glands lead to the formation of erosions and ulcerations;
the chronic swelling and hypernutrition of the muciparous follicles to
their destruction by cicatrization or simple induration; and to atrophy
of the mucous membrane.

Many of the specific causes of inflammation of the larynx exhibit no
peculiar alterations of their own. Scarlatina, measles, and
exanthematic typhus are complicated with either a catarrhal (in most
cases) or a diphtheritic laryngitis. Variola, however, has a peculiar
form of its own, with red, pointed, whitish stains or nodules,
consisting of a cellular infiltration or of a deposit upon or into the
upper layers of the mucous membrane, composed of necrotic epithelia and
pus-corpuscles or of coherent membrane. Hemorrhages or abscesses are
but rare, and chondritis seldom results from it. Even syphilis has not
always changes which are characteristic. The laryngitis accompanying it
is often but catarrhal, without anything pathognomonic about it. But
whitish papules consisting of granulation-tissue (plaques muqueuses),
gummata often changing into sinuous ulcerations, particularly on the
epiglottis and posterior wall of the larynx, also perichondritis with
loss of cartilage and deep cicatrization, such as are not found in
either carcinosis or tuberculosis of the larynx, are frequently met
with. Typhoid fever shows different forms of laryngitis, from the
catarrhal to the ulcerous. Epithelium is thrown off at an early period
of the disease; erosions and ecchymoses follow; rhagades on {93}
the margins of the epiglottis, and a deposit on the anterior wall of
the larynx and the vocal cords, consisting of epithelium and round
cells, are frequent. That they should be mixed with micrococci and
bacteria is self-understood. Not so that these bacteria are to be
considered as the cause of the disintegration which is taking place,
the less so as no specific typhoid bacterium has been demonstrated, and
several varieties of them are found both in the mouth and in these
ulcerations. These changes are apt to terminate in ulceration of the
epiglottis and false vocal cords; these will extend in different
directions, and to the deeper tissue down to the cartilage.

In tuberculosis, laryngitis is a frequent occurrence. In most cases it
is secondary to the pulmonary affection, and due to the direct
influence of the contagious sputum--according to Heinze, however, not
to contagion, but to the influence of the infected blood. In other
cases it appears to develop spontaneously, before any pulmonary
affection is diagnosticated, and may then be due to some poison
circulating in either blood or lymph. Tubercular laryngitis, according
to Rindfleisch, commences in the excretory ducts of the muciparous
glands. That this is so in a great many cases is undoubted. The first
changes visible are small cellular subepithelial infiltrations or real
subepithelial tubercles, which, while growing, undergo gaseous
degenerations and ulcerate. These ulcerations are either flat and small
or deeper with an infiltrated edge, and are apt to terminate in
secondary nodulated infiltrations and abscesses. Large tumors are not
met with, but oedema and phlegmonous inflammations are by no means
rare.

ETIOLOGY.--The predisposition varies according to individuals, ages,
and seasons. Some mucous membranes appear to be more sensitive than
others. The hereditary transmission of peculiarities of structure of
all or some tissues or organs is apparent, in the case of laryngitis,
in the fact that many children in the same family or the children of
parents who were sufferers themselves are affected. Children are more
liable than adults, infants more than children: 20 per cent. of all the
cases are met with under a year, 25 from the first to the second, 15
from the second to the third. Not many occur after the twelfth year.
The narrowness of the infant larynx and the looseness of its mucous
membrane afford full play to injurious influences, such as dust, cold
and moist air, changing temperatures, hot vapors and beverages. Colds,
though their nature and effects can hardly be said to be understood,
are certainly amongst the main causes. Perspiring surfaces afford
frequent opportunities. One of the principal causes is insufficient
clothing--more amongst the well-to-do than amongst the poor. The latter
have this blessing in their misfortune, that they are protected
uniformly if at all, and have their skins hardened by exposure. The
bare necks and chests, the exposed knees, the low stockings and thin
shoes of the children of the rich, old and young, are just as many
inlets of laryngeal catarrh, inflammatory disease, and phthisis.
Persons suffering from nasal catarrh or pharyngeal catarrh are liable
to have laryngitis. Thus, not only rachitis, with its influence on
lymphatic glands and the neighboring mucous membranes, but also acute
infectious diseases, such as whooping cough, measles, influenza,
erysipelas, hay fever, tuberculosis, syphilis, typhoid fever, and
variola, are as many causes of laryngitis. That over-exertion of the
voice should produce laryngitis seems probable, but experience does not
teach that those babies who cry most are most subject to laryngeal
catarrh.

SYMPTOMS.--Acute laryngitis is a frequent disease, and has always been.
Still, in 1769, Millar mistook it for a sensitive neurosis, considering
it as identical with spasm of the glottis, and recommended
antispasmodic treatment. Guersant understood its nature better. He
first (1829) used the names false croup and stridulous laryngitis.
Acute laryngitis is attended with but little fever in the adult, but
with a high elevation of temperature in {94} the young. In all, it
yields a number of symptoms, part of which are uncomfortable only;
others are liable to become dangerous.

Seldom without any catarrhal premonitory symptoms of other parts of the
respiratory tract, sometimes, however, without any, there is a burning,
tickling, irritating sensation in the larynx--a sense of soreness in it
and the lower portion of the pharynx. Sometimes these sensations amount
to actual pain, to difficulty of deglutition, and to the sensation of
the presence of a foreign body. Speaking, coughing, cold air, increase
the discomfort and pain. Hoarseness, sometimes increasing into aphonia,
follows soon after, is seldom simultaneous with, the first appearance
of cough, but lasts longer than the latter, which is, according to the
severity of the case or the stage of the disease, changing between
loose and dry, hoarse and barking. Inspiration is apt to become
impeded, mainly in infants and children. In these it is often sibilant.
It is followed by a reflex paroxysm of cough, with interrupted and
brief expirations, during which the forcible compression of the thorax
may result in cyanosis. The principal attacks are met with at night
amongst children. Quite suddenly they wake up with a dry, barking
cough, interrupted by considerable dyspnoea, which is great enough
sometimes to give rise to much anxiety. They toss about or cling to a
solid body, raise themselves on their knees, breathe with great
difficulty, exhibit cyanosis in its different hues, perspire very
freely, and yield all the symptoms of the strangulating attacks of
membranous croup, its over-exertion of the sterno-cleido-mastoid
muscles and supraclavicular and diaphragmatic recessions not excepted.
These attacks occur but rarely during the day; on the contrary,
well-marked remissions are quite common in the morning. Their
occurrence during the night is best explained by the facility with
which mucus will enter the larynx from above during the reclining
posture, the increasing dryness of the pharynx during sleep, perhaps
also the nervous influence depending upon the relative diminution of
oxygen and increase of carbonic acid in the respiratory centre, leading
to spasmodic contractions.

Some of these grave attacks of sudden dyspnoea are explained by the
participation of the submucous tissue in the morbid process. When that
occurs, adults also, who as a rule do not suffer from dyspnoea in
laryngeal catarrh, are badly affected. The symptoms are rigor, high
temperature, pain, hoarseness or aphonia, a barking cough, labored
expectoration--which is sometimes bloody--dyspnoea, orthopnoea,
cyanosis. In some cases, to which the name of laryngitis gravis or
acutissima has been given, the symptoms grow urgent to such a degree
that tracheotomy alone is capable of saving life.

Otherwise, the severity of the symptoms does not go parallel with the
local lesions. Particularly in children, hoarseness, cough, and
dyspnoea are liable to be grave, while the local hyperæmia is not
intense at all. A pharyngeal catarrh is very apt to increase the
suffering. Complications with tracheitis or bronchitis are liable to
prolong the course of the disease and to render respiration--which is
not accelerated in laryngeal catarrh--more frequent. Otherwise, the
disease runs a favorable course. Remissions of the severe attacks which
may occur in several successive nights take place in the morning.
Expectoration, which in the beginning was either absent or scanty,
becomes soon more copious and mucous; the hard, barking, loud cough
grows looser with increasing secretion. In most cases the violence of
the affection is broken in from three to five days, and the disease
runs its full course in a week or two. But hoarseness may remain behind
for some time; in rare cases aphonia has become permanent and relapses
are frequent. Not infrequently children are presented who are reported
to have had croup five or ten or more times. In some families all the
children are subject to laryngeal catarrh, and hereditary influence
cannot be doubted.

The very worst complication of laryngitis is oedema of the glottis. It
{95} affects both the mucous membrane and the submucous tissue of the
larynx. It is met with on the inferior (posterior) surface of the
epiglottis, in the ary-epiglottic folds, and on the false (inferior)
vocal cords, the submucous tissue of which is of a very loose structure
normally. Amongst its causes--which may be various (foreign bodies in
the larynx, injuries, mechanical and chemical irritants of any kinds;
typhoid, tubercular, variolous, syphilitic ulcerations; erysipelas of
the neighborhood, inflammations of the parotids or tonsils, suppuration
in the pharynx, thyroid body, and cellular tissue of the neck)--both
catarrhal and croupous laryngitis are not at all uncommon. This is
particularly so when they are complicated with cardiac and renal
anomalies, pulmonary emphysema, and compression of the veins of the
neck by glandular swellings; also with changes in the structure of the
walls of the blood-vessels. The last-named pathological conditions are
alone capable of giving rise to chronic oedema of the larynx, which is
by no means so fatal, but still dangerous.

In glottic oedema the dyspnoea is both very great and very sudden.
First, it is inspiratory only, but soon becomes both inspiratory and
expiratory. The swelling is felt distinctly by the examining finger;
the laryngoscope is neither required nor advisable.

DIAGNOSIS.--It is by no means easy in all cases. When laryngeal
diphtheria (membranous croup) happens to be frequent, the most
experienced diagnostician will meet with occasional difficulties. The
sound of the barking, explosive, tickling cough locates its origin in
the larynx, but the affection may be very mild or very severe.
Expectoration in small children is not pathognomonic; even when it is
copious it is not brought up, but swallowed. Fibrinous expectoration
would settle the diagnosis of a croupous process. Depressing the tongue
with a spoon or spatula and producing the movements of vomiturition
often reveals the presence of a tough, viscid mucus rising from the
larynx. It renders the catarrhal nature of the laryngitis positively
clear. The frequency or volume of the pulse is of no account in
diagnosis; it is too variable. Of more importance is the temperature,
at least in children. Uncomplicated sporadic croup has no increase, or
very little; catarrhal laryngitis is mostly attended with high fever.
In very many cases this symptom has guided me safely, in spite of the
statements of the books. The stenosis of catarrhal laryngitis comes on
very suddenly, in diphtheritic laryngitis mostly slowly. In the former
it is not of long duration; remission sets in soon, and is more
complete than in membranous croup. An attack of stenosis occurs mostly
in the night, and is apt to return with the same vehemence after a fair
remission after twenty-four hours. The frequency of relapses in
catarrhal laryngitis in children who have been affected before must,
however, not prejudice in favor of the catarrhal nature of an
individual case, for not infrequently will those who have had many
attacks be taken with membranous croup some other time. In the latter
the main symptoms--viz. stenosis, hoarseness (or aphonia), and
cough--will mostly develop simultaneously and in equal proportion; the
unproportionality of these symptoms--for instance, much stenosis and
cough, but little hoarseness, or barking cough and hoarseness with
little stenosis--would speak for catarrh. The laryngoscope, when it can
be used--viz. in the adult and very docile children--reveals redness of
the mucous membrane of the pharynx and all or part of the larynx; also
tumefaction of the epiglottis or fossæ Morgagni or ary-epiglottic
folds. Sometimes the inferior part of the larynx only is affected;
Ziemssen has described a severe form under the name of hypoglottic
laryngitis. The vocal cords can be watched easily. Their proportionate
and parallel contraction is often interfered with.

Tubercular laryngitis, particularly when there is no pulmonary
tuberculosis, is not easily diagnosticated by the local changes only.
The long duration of {96} hoarseness and fever, increasing emaciation,
and the knowledge of the presence of tuberculosis in the family are
more conclusive than local examinations can be.

PROGNOSIS.--The termination of catarrhal laryngitis in the adult is
almost always favorable. Still, relapses are frequent, and it may
become chronic, with permanent tickling of the mucous membrane and
submucous tissue. In children it is mostly favorable; still, it is
doubtful, because of the frequency of complication with, or
transmutation into, bronchitis, pneumonia, or glottic oedema, and
because of the facility with which in a prevailing epidemic the
catarrhal laryngitis becomes diphtheritic. The elevation of temperature
is not a very significant symptom in regard to prognosis. The danger
does not increase with the temperature at all. On the contrary, those
cases which set in with a high temperature will, as a rule, terminate
soon and favorably. When, however, the temperature rises again after
having gone down to the normal or nearly normal standard, complications
or extension of the catarrhal or inflammatory process must be expected.
Catarrhal secretion from the nasal mucous membrane, which was dry in
the beginning, is a favorable symptom; so is the looser and moister
character of the cough.

TREATMENT.--Whatever plays an important part in the etiology of the
disease ought to be carefully avoided. The feet must be kept warm under
all circumstances, nothing being more injurious to health in general,
and to that of the respiratory organs in particular, than cold and
moist feet. Shoes and stockings must be kept dry, the latter changed
when wet, and of slowly-conducting material. No part of the body must
be kept uncovered, and the dresses of children made the particular
object of care on the part of the family physician. Linen must not be
in immediate contact with the skin, cotton--or, still better in all
seasons, wool--being required for the undergarment. At the same time,
the hygiene of the skin requires attention. Regular washing or bathing
need not be mentioned as a requisite, as it is self-understood. What,
however, cannot be insisted upon too much is this, that the skin must
get accustomed to cold water. The whole body must be exposed once a day
to cold water--washing or bathing--and well rubbed off afterward with a
thick towel. Young infants and those who are very susceptible to colds
begin with tepid water, the temperature being lowered from day to day.
Even children of three or four years enjoy, finally, a morning bath at
sixty or sixty-five degrees F. in winter. Such as do not get easily
warmed up under the succeeding friction may mix alcohol with the water
they use for washing and sponging purposes, in the proportion of 1:5-8.
Sea-bathing also makes the skin more enduring, to such an extent that
exposure to cold air has no longer any damaging influence. In fact,
cold air without wind is easily tolerated even by those who have a
tendency to respiratory disorders, while wind and draught must be
avoided. From this point of view the change of climate sometimes
required for such as suffer from catarrhal laryngitis must be
instituted. It is not always necessary to select a very warm climate;
undoubtedly, many of the winter resorts are badly selected, for the
very reason that they are too warm. On the other hand, great elevations
are not advisable. The sudden atmospheric changes and fogs of high
mountains are injurious.

Patients suffering from catarrhal laryngitis or a tendency in that
direction must avoid all irritation of the pharynx and larynx. They
must not smoke, or talk too much or too loud. Those few clergymen who
suffer from clergymen's sore throat in consequence of speaking only
will remember that they can speak just as forcibly when speaking less
vehemently. The use of alcoholic beverages, unless greatly diluted, is
prohibited. Catarrh of the nares and pharynx must get cured. The former
will get well in most cases under the use of salt water. A tepid
solution of 1 or ½ per cent. of table-salt {97} in water, snuffed up
copiously (a tumblerful) from the hand of an adult patient, or a
similar solution in a small quantity injected through each nostril of a
child, twice or three times a day for weeks and months in succession,
will often remove a laryngeal as well as a pharyngeal catarrh. Care
must be taken that the fluid passes the whole length of the nasal
canal. It must be applied in the fauces, and will then be ejected
through the mouth or a small portion of it swallowed. Many a severe
nasal catarrh requires no other treatment. Some chronic ones require
the use of a spray of nitrate of silver in a solution of ½-1 per cent.
every other day, or of a 2 per cent. solution of alum daily. Where both
the pharyngeal and nasal catarrh are complicated with, or kept up by,
enlarged or ulcerated tonsils, these organs must be resected. The
combination of these two measures, exsection of the tonsils and nasal
injections, has proved very beneficial in a great many cases.

The treatment of an acute case requires great care. Avoid injurious
influences. The patient must keep silent and quiet in bed. The
temperature of the room is to be about 70° F., the air moistened by
vapor, which must not be allowed to get cold before it reaches the
patient.

When swelling and dyspnoea are considerable, particularly in those
grave cases attended with swelling of the submucous tissue, the
application of an ice-bladder or ice-cloths will be found beneficial
and agreeable. But the cases in which these applications are
indispensable are but few. In most of them the necessity of subduing
intense inflammation is less urgent than the advisability of increasing
the secretion of the congested larynx. For that purpose warm poultices,
but of light weight, act very favorably. Inhalation of warm vapors
either constantly or at short intervals, or of muriate of ammonium or
spirits of turpentine, will prove beneficial. The latter is evaporated
from the surface of boiling water, on which a small quantity, from a
teaspoonful to a tablespoonful, may be poured every one or two hours.
The hydrochlorate of ammonium is evaporated, 10 or 20 grains (1.0
gramme), every one or two hours by heating it on a hot stove or
otherwise. The white cloud penetrates the air of the whole room, and,
while not uncomfortable to the well, serves a good purpose in
liquefying the viscid and tough secretion of the mucous membrane. The
internal administration of liquefying and resolvent remedies may
properly accompany the external applications and inhalations. Amongst
them I count the alkalies, mainly bicarbonate and chlorate of potassium
or sodium and the hydrochlorate of ammonium. A child of two years will
take daily a scruple (gramme 1.0-1.5). The iodide of potassium will
also have a good effect and counteract many a predisposition to
chronicity. A child may take from 8 to 15 grains a day (gramme
0.5-1.0). Hydrochlorate of apomorphine, gr. 1/50-1/30 (0.001-0.002),
dissolved in water, a dose to be given every two hours or every hour,
is quite sufficient to act as a fair expectorant without being enough
to produce emesis. Antimonii et potassii tartras has been used more
extensively in former times than at present. An adult would take gr.
1/20-1/15 every two hours. Children ought to be spared the drug, as it
is depressing, produces unnecessary vomiting now and then, even in
small doses, and, what is still worse, diarrhoea. The other antimonial
preparations, such as kermes mineral and the oxysulphuret of antimony,
are less depressing and less purging, but also less effective; and
there are but few cases where a good substitute could not be found. For
the purpose of increasing secretion the hydrochlorate of pilocarpine
has been recommended. It certainly has that effect, but its indications
become doubtful in many cases where the saving of strength is of
paramount importance. I shall return to this subject in my remarks on
the therapeutics of membranous laryngitis.

Derivation is of great service when well directed. Local depletion must
be avoided. A purgative in the beginning is beneficial--a dose of
calomel {98} as good as, or mostly better than, anything else.
Diaphoretics and diuretics act quite well; the best of them all are
warm beverages of any kind. They need not come from the apothecary's
nor be very unpleasant to take--water not too cold, Apollinaris,
Selters, or Vichy, hot milk, tepid lemonade in large quantities and
very often. Sinapisms have a good effect. When not kept on longer than
a few minutes--long enough to give the surface a pink hue--they may be
applied every hour or two.

Some urgent symptoms may require symptomatic treatment. When secretion
is copious, but too tough, and expectoration insufficient because of
both the character of the mucus and the incompetency of the respiratory
muscles, ipecac in small doses or camphor is indicated. A child's dose
of the latter would be gr. ¼-½(gramme 0.015-0.03) every one or two
hours. In these cases the hydrochlorate of ammonium may be combined
with the carbonate (ammon. chlorid. drachm ss. (2.0); ammon. carbonat.
scruple j (1.25); extr. glycyrrh. pur. scruple ij (2.5); aq. pur.
fluidounce iij (grammes 100.0)--teaspoonful every hour). When the
difficulty of expectoration is excessive an emetic may be resorted to.
It is true that infants and children vomit with less straining and
difficulty than adults, but, still, the practice of flinging emetics
around is too common. The unpleasantness of getting up in the night
because of a pseudo-croup in a distant patient's baby is not a correct
indication for encouraging the indiscriminate use of emetics. When they
are required, antimonials ought to be excluded from the list. Ipecac,
sulphate of zinc, sulphate of copper, turpeth mineral are preferable.

In urgent cases the hydrochlorate of apomorphia may be used
hypodermically (six or ten drops of a 1 per cent. solution in water).
Cases of such urgency, and so excessive dyspnoea coupled with cyanosis,
as to necessitate tracheotomy are but very rare. But once in thirty
years and in many more than four hundred tracheotomies have I been
compelled to operate for a case of catarrhal laryngitis. Still, a few
such cases are on record. The best-known amongst them is that of
Scoutetten, who operated successfully on his own daughter six weeks
old.

Narcotics prove quite beneficial, particularly in complications with
pharyngeal catarrh. A dose of gr. j-jss of Dover's powder (gramme
0.05-0.1) at night will secure rest for several or many hours to a
child of two or three years; an adult is welcome to a dose of 10 or 12
grains (0.6-0.75). When the irritation is great during the day, it is
advisable to add a narcotic (acid. hydrocyan. dil., min. j; vin opii,
min. viij-xij; codeine gr. 1/3-1/2, or extr. hyoscyam. gr.
ij-iij--daily) to whatever medicine was given. I am partial to the
latter, giving it up to gr. viij-x (0.5-0.6) to adults daily in their
mixture, retaining the single dose of opium or morphine to be taken for
the night. At that time a single larger dose is rather better than
several small ones. Narcotics cannot be dispensed with in all those
cases in which--as, for instance, in tubercular laryngitis--deglutition
is very painful because of the catarrhal and ulcerous pharyngitis.
Bromide of potassium has a fair effect, but frequently fails, and the
administration of morphia before each meal is sometimes an absolute
necessity.

That complications, such as bronchitis, have their own indications is
self-understood. The general rules controlling the treatment of
laryngitis are not interfered with by them. Oedema of the glottis,
however, when occurring during an attack of laryngitis, has its own
indications, and very urgent ones indeed in all acute cases. In chronic
cases a causal treatment is required according to the etiology of the
affection as specified above. In acute cases it is not permitted
because of want of time. The danger of immediate strangulation is often
averted only by a deep scarification or the performance of tracheotomy.

Chronic cases require all the preventive measures enumerated above and
{99} the internal use of iodide of potassium or sodium (scruple
j-scruple iiss = gramme 1.25-3.0 daily, for adults), and tincture of
pimpinella saxifraga three or four teaspoonfuls daily. When it is given
it ought to have an opportunity to develop its local effect on the
pharynx also by giving it but little diluted, and not washing it down
afterward (tinct. pimpinella saxif., glycerin. _aa_, teaspoonful every
two hours). In these cases, while the local salt-water treatment
recommended above is indispensable, the nitrate-of-silver spray
mentioned in that connection is here again referred to as very
beneficial indeed. But the solution of 1 per cent. is the highest
degree of concentration allowable. Conducted through the nose, it will
reach the larynx better than through the mouth. When both accesses are
rather difficult the application must be made directly to the larynx.




{100}

PSEUDO-MEMBRANOUS LARYNGITIS.

BY A. JACOBI, M.D.


PATHOLOGY.--Pseudo-membranous laryngitis is characterized by the
presence, on and in the mucous membrane, of a pseudo-membrane of a
whitish-gray color, various consistency, and different degrees of
attachment. It has been called croupous when it was lying on the mucous
membrane without changing much or at all the subjacent epithelium and
could be removed without any difficulty. It has been called
diphtheritic when it was imbedded into the mucous membrane and was
difficult to remove. This difference exists, but it does not justify a
difference of names except for the purpose of clinical discrimination;
for the histological elements of the two varieties are the same, and
the difference in their removability is explained by the anatomical
conditions of the territory in which they make their appearance. The
membrane consists of a net of fibrin studded with and covering
conglomerates of round cells, mixed with mucus-corpuscles, epithelial
cells more or less changed, and a few blood-cells. The fibrinous
deposit is either quite superficial or lies just over the basal
membrane or on layers of round cells originating from the basal
membrane. It is continued into the open ducts of the muciparous
follicles, filling them entirely in the worst cases, or meeting the
normal secretion of mucus in the interior of the duct. The principal
seat of the pseudo-membrane is that mucous membrane which is covered
with pavement epithelium; thus it is that the tonsils are the first,
usually, to exhibit symptoms of diphtheria. But cylindrical epithelium
is by no means excluded. However, while pavement epithelium is
generally destroyed by the diphtheritic process, the cylindrical
epithelium is frequently found unchanged, or but little changed, on top
of the mucous membrane under the pseudo-membrane.

The nature and consistency of the pseudo-membrane in the larynx is best
studied by the light of the study of its anatomy. There is a great deal
of elastic tissue in both epiglottis and larynx; the mucous membrane of
the latter is thin, and sometimes folded on the vocal cords. The
epithelium of the epiglottis is pavement; only at its insertion it is
cylindrical. In the larynx it is also pavement on the true vocal cords
and in the ary-epiglottic folds, and fimbriated toward the fossæ
Morgagni and trachea. Lymph-vessels are but scanty on the epiglottis,
still more so in the larynx. Of acinous muciparous glands there are
none on the epiglottis, none on the true vocal cords; they are more
frequent in and round the fossæ Morgagni, with cylindrical epithelium
in the glandular ducts. The trachea and bronchi contain a good many
elastic fibres, less connective tissue, fimbriated epithelium, some
lymph-vessels, but no lymph-glands, and acinous muciparous glands in
large numbers. Wherever the pavement epithelium membrane is abundant
the membrane is firmly adherent and imbedded into the mucous membrane.
Where it is cylindrical and plenty of acinous glands secrete their
mucus, they are loosely spread over the mucous membrane, from which
{101} they can be easily removed; while the histological condition of
both the imbedded and the loose membrane is exactly the same.

Before the membranous deposit takes place the surface is in a condition
of catarrh. Round the membrane the mucous membrane is red and slightly
swollen. Not always, however, is that so. Particularly, the epiglottis
may be covered on its inferior surface with a solid membrane or be
studded with tufts of membrane, without much or any hyperæmia. The same
can be said of the larynx, which is supplied with but a scanty
distribution of blood-vessels and a sufficient network of elastic
fibres to counteract the dilatation of blood-vessels peculiar to the
catarrhal and inflammatory processes.

In uncomplicated cases of membranous laryngitis the membrane is
confined to the larynx. Dozens of years ago--viz. before 1858, when
diphtheria began to settle amongst us, never, it appears, to give up
its conquest again--that took place in most cases. But since that
period we meet with few such simple cases. As a rule, the membrane
makes its appearance in the pharynx first, from there to descend into
the larynx, and not infrequently into the trachea and bronchi. In
other--fortunately, but few--cases the membrane is formed in the
bronchi and trachea first, and invades the larynx from below.

Other organs suffer but consecutively and from the results of impeded
circulation only. Thus, in post-mortem examination hyperæmia of the
brain, liver, and kidneys, and bronchitis, broncho-pneumonia, or
pulmonary oedema, are met with. Only those cases of membranous
laryngitis which are complicated with general diphtheria yield the
additional changes of the latter.

ETIOLOGY.--Intense irritants will produce an irritation on mucous
membranes. In the larynx the product is, according to the severity of
the irritation, either a catarrhal or a phlegmonous or a croupous
laryngitis. The irritating substances may be mechanical, chemical, or
thermical. Heubner produced diphtheria of the bladder by cutting off,
temporarily, the supply of circulation. Traumatic injury of the throat
and larynx will soon show a croupous deposit. Caustic potassium,
sulphuric acid, caustic ammonium, corrosive sublimate, arsenic,
chlorine, or oxygen, applied to the trachea or larynx, produce croupous
deposits.[1] Inhalations of heat, smoke, and chlorine have the same
effect. These, however, are not the usual causes of croup. Cold and
moist air is a more common cause, mainly during a prevailing epidemic
of diphtheria. In former times, which are unknown to the younger
generation of physicians, when no such epidemics existed, the only form
of diphtheria occurring now and then was the local laryngeal diphtheria
called pseudo-membranous croup. It was then a rare disease, while at
the present time it is of but too frequent occurrence. In my _Treatise_
I have explained at some length the relations of the two (p. 128).

[Footnote 1: A. Jacobi, _Treatise on Diphtheria_, p. 111.]

Age has some influence in its development. The disease is not frequent
in the first year of life; between the second and seventh years almost
all the cases are met with. There are families with what appears to be
a general tendency to croupous laryngitis. It may return. Even
tracheotomy has been performed twice on the same individual.[2] It is
contagious. In the same family, from a case of croup, either another
case of laryngeal croup may originate or another form of diphtheria
will develop in other members of the household. It is not so
contagious, it is true, as generalized diphtheria must be, for the
infecting surface is but small in uncomplicated membranous croup, and
the membrane not so apt to macerate and be communicated. Boys appear to
be affected more frequently than girls. But the previous constitution
makes no difference.

[Footnote 2: _Treatise_, p. 27.]

SYMPTOMS.--Membranous laryngitis begins sometimes with but slight
symptoms of catarrh, sometimes without them. Nasal, pharyngeal, and
laryngeal catarrh may precede it a few hours or a week, with or without
fever and with {102} a certain sensation of pain or uneasiness in the
throat and a moderate amount of cough and hoarseness. This condition
has been called the prodromal stage of membranous laryngitis, though it
is just as natural to presume that the changes in the mucous membrane
merely facilitated the deposit of false membrane. The latter is more
apt to develop on a morbid than on a healthy mucous membrane. The
membranous laryngitis proper dates from the time at which, with or
without an elevation of temperature, a paroxysmal cough makes its
appearance--first in long, afterward in shorter intervals--which is
increased by a reclining posture, mental emotions, or deglutition. At
an early period this cough, which is very labored and gives rise to
dilatation of the veins about the neck and head, is complicated with
hoarseness, which gradually increases into more or less complete
aphonia. Respiration becomes audible, sibilant, with the character of
increasing stenosis. Inspiration becomes long and drawn; expiration is
loud; head thrown back; the scaleni, sterno-cleido-mastoid, and serrati
muscles are over-exerted; above and below the clavicles and about the
ensiform process deep recessions take place in the direction of the
lungs, which are expanded with air, but incompletely; dyspnoea becomes
the prominent symptom, and occasional attacks of suffocation render the
situation very dangerous and exciting indeed. These sudden attacks of
suffocation are due--besides the permanent narrowing of the larynx by
the membranes, which gradually increase in thickness--to occasional
deposits of mucus upon the abnormal surface of the larynx and vocal
cords, by partly-loosened false membrane, which now and then become
audible, yielding a flapping sound, by oedema in the neighborhood, and
by secondary spasmodic contractions. They are mostly met with in the
evening and night; there is often a slight remission in the morning,
which rouses new hopes, which soon, however, prove unfounded.
Meanwhile, the pulse becomes more frequent in proportion with the
increase of dyspnoea, and finally irregular; the temperature rises but
little, and usually only when the throat or other organs, which are in
more intimate connection with the lymph circulation than the larynx,
are participating in the exudative process; and the laryngeal sounds
become so loud as to render the auscultation of the lungs impossible.
The glands of the neck are not swollen when the process is confined to
the larynx. Now and then small or larger, rarely cylindrical, pieces of
false membranes are expectorated, with or without any amelioration of
the condition. In this condition the patient may remain a few hours or
a few days.

Then the dyspnoea will rise into orthopnoea; the anxious expression and
bearing of the little patient--for the vast majority of the sufferers
are children--becomes appalling to behold; cyanosis increases; the head
is thrown back; the larynx makes violent excursions upward and
downward; the abdominal muscles work in rivalry with those of the
thorax and neck; the surface is bathed in perspiration; still,
consciousness is retained by the unhappy little creature tossing about
and fighting for breath, and in complete consciousness he is strangled
to death. Now and then the carbonic-acid poisoning renders the pitiful
sight a little less appalling to the powerless looker-on by giving rise
to convulsions or anæsthesia and sopor, which finally terminate the
most fearful sight, the like of which the most hardened man, the most
experienced medical attendant, prays never to behold again.

Besides the brain symptoms just mentioned, but few other organs give
rise to abnormal function. In the kidneys the stagnant circulation
results in albuminuria--in the bronchi and lungs, in hyperæmia,
inflammation, and oedema.

The symptoms described above are the same both in those cases which are
strictly localized and those which descend from the pharynx. In the
latter there is fever only when the pharyngeal diphtheria was attended
with it. The process descending into the trachea and bronchi changes
the symptoms {103} but little, as far as the laryngeal stenosis is
concerned, for it is the latter which destroys by suffocation. Only
when tracheotomy has been performed, and the immediate danger of
suffocation has been removed, the further progress in a downward
direction gives rise to a new series of symptoms. After the temporary
relief procured by the operation dyspnoea will set in anew, not always,
however, of that intense degree of the laryngeal stenosis; respiration
will become dry and loud again, and a little more frequent than in the
uncomplicated laryngeal cases. Death will finally also result, either
from suffocation or from the symptoms I enumerated above.

Lastly, when membranous laryngitis is but the terminating development
of extensive membranous bronchitis, the symptoms differ from those
described above in this, that the laryngeal symptoms last but a short
time. For days or weeks no symptoms but those of an ordinary bronchial
and tracheal catarrh were observed: all at once the process reaches the
larynx; in a few hours the very last stage of croupous stenosis is
reached; even tracheotomy does not relieve the symptoms. Or the
fibrinous bronchitis was extensive enough to give rise to a sufficient
number of symptoms before the larynx was reached. Amongst them is,
foremost, frequency of respiration, because of its insufficiency;
diminution of respiratory murmur over the area supplied with the
affected bronchi; sometimes localized absence of respiratory murmur,
while the percussion sound is sonorous. Another complication is
emphysema, either subpleural or pulmonary. It is not frequent, except
in combination with fibrinous bronchitis. The increase of respiratory
movements is quite sudden, percussion sound tympanitic, and
auscultation negative. Pulmonary oedema is quite frequent; it is the
result of the rarefaction of air in the bronchi, the consecutive
dilatation of the blood-vessels, and the effusion of serum by
intravascular pressure. Every severe case is accompanied with it; in
every tracheotomy it is met with coming up into the incision. Oedema of
the glottis is less common, but it is met with in the same manner and
with the same symptoms which characterize the glottic oedema of
catarrhal laryngitis.

PROGNOSIS.--It is not favorable even in the simple and uncomplicated
cases. Infants and children under two years almost invariably die. The
percentage of average mortality rates very high--from 80 to 90 and
more. It is probable that some recent therapeutical advances have
reduced it, will reduce it, considerably. Tracheotomy is known to do so
certainly, as from 20 to 45 out of 100 operations prove successful. The
previous condition of the patient is of very little account in regard
to the course and termination of the disease; no constitution protects
or saves. The more the disease is local the better the prognosis. When
fever makes its appearance, it means a complication, such as extending
diphtheria or bronchitis or bronchi-pneumonia, and impairs the chances
of recovery. The expectoration of membranous shreds or whole membranes
does not improve the prognosis much, as the new formation of membranes
may be very rapid indeed. I have seen new membranes rising to a
formidable extent in from two to seven hours. The prognosis is improved
when the cough becomes looser, expectoration more purulent, pulmonary
respiration become audible again after having been covered by the
laryngeal noises, rhonchi become moist, and portions of lungs which
before were inaccessible to air by clogging membranes are reopened.
Increasing debility, frequent and irregular pulse, are ominous
symptoms. Even more so is the failure on the part of emetics to take
effect.

DIAGNOSIS.--It may be quite difficult to diagnosticate croupous from
catarrhal laryngitis, particularly in those cases where the former is
not complicated with any visible exudative process in the fauces. In
membranous laryngitis stenosis begins gently (except in those cases
which ascend from the bronchi) and increases gradually; there are, it
is true, remissions in the {104} morning (mostly), but they are but
slight, and the subsequent evenings are worse than the previous ones.
It increases from day to day until a slight cyanotic hue of the lips is
followed with more general cyanosis. There is no fever or very little,
except in the cases of generalized diphtheria. The character of the
cough does not change; perhaps it becomes more dry and suppressed after
a while. Hoarseness does not improve, but increases steadily into
aphonia. Expectoration is but scanty; now and then a small portion of
mucus from the lower portion of the respiratory tract, now and then
shreds of membrane, are expelled.

In catarrhal laryngitis stenosis begins abruptly and suddenly, and is
often at its height a few minutes after the commencement of the attack.
Remission sets in soon, is more marked, sometimes complete, and a new
attack, just as sudden as the first, may occur in the next night. Real
cyanosis is but rarely developed; when it is, it changes soon into a
more normal condition. Catarrhal laryngitis in the child is a febrile
disease. In it the cough changes after a little time, some moisture
mixes with the expectoration and changes both cough and articulation;
also, the voice is not equally husky; now and then a clear note comes
in. Close inspection of the throat exhibits sometimes a thick, viscid
mucus floating up and down with the excursions of the larynx in
catarrh. It never has any membranous expectoration.

Local oedematous swelling of the ary-epiglottic folds, with or without
membranous deposits in some other parts of the larynx, yields all the
symptoms of membranous croup with its dangers and death-rate. The
effect of this oedema is partial paralysis of the vocal cords. Thus,
inspiration is impeded, as in membranous obstruction; expiration,
however, is free and the voice intact to a certain extent. This local
oedema may be detected by palpation.

General oedema of the larynx (glottis) is fortunately rare. The attack
is very sudden; there is no cold, no hoarseness, no choking cough, no
membrane; there is only dyspnoea, gasping, asphyxia, sopor, and death,
unless relief is given almost instantaneously.

The presence of a foreign body has been mistaken sometimes for
membranous laryngitis. The history is a different one; there was no
prodromal catarrh; the children were taken suddenly while playing or
eating.

The laryngoscope would be a great aid in diagnosis if it could be used
during the distress of a membranous laryngitis. Still, it has been
employed by Ziemssen, Rauchfuss, and others. But the opportunities are
rare.

TREATMENT.--The objects of treatment differ with the various stages of
the disease. The inflammatory symptoms of the commencement, the
completed exudation, the maceration and disintegration, and also the
expectoration of the pseudo-membranes, and, finally, the asphyctic
stage, have each their own indications. If there is anything which must
not be recommended, it is depletion. Fortunately, there are but few
practitioners left who still apply leeches or employ more general
depletion, but these few are still doing too much harm by their
practice and teaching. The application of ice, however, in bags over
and near the larynx, and of iced cloths frequently changed, combined
with the swallowing of small pieces of ice from time to time, is apt to
be beneficial in well-nourished, hearty children. Such as have been
anæmic, with thin muscles and pale mucous membranes, do not bear it so
well.

The most powerful and reliable preventive and solvent, thus far, is
hydrargyrum. It is true that many voices have been raised against it,
but from Bard, Bretonneau, and Billard to Rauchfuss, Ch. West, Lynn,
Pepper, and others, the remedy has had its admirers. Large single doses
of calomel have been given by some, amounting to 15-30 grains (gramme
1.0-2.0), but that treatment has not found many friends. In small and
frequent doses it has been of good service to me both in fibrinous
laryngitis and bronchitis, {105} particularly in the latter; gr. ¼-½
may be given every half hour or every hour. Tartar emetic is liable to
develop so many unfavorable effects that even doses--in combination
with calomel--of 1/100 of a grain require great caution. The most
reliable mercurial preparation, in my experience, and the least
hurtful, is the corrosive chloride. In the stomach it combines with the
chloride of sodium, is absorbed without being changed, and transmuted
into an albuminate during its circulation in the blood. Babies of
tender age bear one-half of a grain and more, daily, many days in
succession. Salivation and stomatitis are exceedingly rare after its
use. Gastro-intestinal disturbances are not at all frequent; diarrhoea,
if observed at all, is very moderate, and can be avoided or removed by
the administration of mucilaginous and farinaceous food or a mild dose
of an opiate. But the administration of the bichloride requires care in
regard to its solution. A fiftieth of a grain may be safely given to a
baby a year old every hour, but it must be dissolved in one-half of a
tablespoonful or a whole tablespoonful of water. The solution of a
grain in a pint of water is about correct. In those very rare cases in
which no preparation of mercury is borne internally the inunction of
sufficient and frequent doses of the oleate of mercury may take the
place of the internal administration or alternate or be combined with
it. The blue ointment is not so effective as the oleate. The
subcutaneous injection of the corrosive chloride may be added to the
modes of administration if no time must be lost in introducing as much
as possible of the drug into the system. Now and then, however, the
subcutaneous tissue of the child does not tolerate it well in that
form, though the solution may be not larger than 2 per cent.[3] The
cyanide of mercury, in doses of a hundredth of a grain every hour, has
been warmly praised by A. Erichsen and C. G. Rothe.

[Footnote 3: _The Medical Record_, May 24, 1884.]

The large mortality in croup and the inefficiency of remedial treatment
have been the reasons why the recommendations of remedies have been
very numerous. Alkalies were held in great favor during different
periods of our literature, mainly the carbonate and bicarbonate of
potassium (and sodium), in daily doses, to a child, of ½ drachm or 1
drachm or more; also the chlorate of potassium or sodium. As an
adjuvant it may be useful; as an antidiphtheritic or antimembranous
remedy it must not be regarded. What it can do is to heal or prevent a
catarrhal stomatitis and pharyngitis. The best and most reliable is
probably the iodide, in larger doses than are usually given. One or two
drachms daily (grammes 4.0-8.0) are well tolerated when sufficiently
diluted. Benzoate of sodium was recently recommended for its supposed
antifermentative and antibacteric effect; its practical utility is but
very limited; not even its antifebrile effect is anything but reliable.
Lime-water has not fulfilled in my hands the promises made by
others--neither its internal use nor spray nor inhalation. The most
certain mode of introducing lime particles into the larynx is, after
all, the inhalation of slaked lime, which allows a quantity sufficient
to be somewhat effective to enter the respiratory organs. Its
comparative inefficiency has been acknowledged by those who add 1 per
cent. of the liquor of caustic potassium or sodium to the lime-water.

Quinia, in doses of 15 or 30 grains (grammes 1.0-2.0) daily, has been
recommended by Monti for the same indications, mainly in the
commencement of febrile cases. It has been claimed that cold
applications, to be changed every hour or two according to the
Priessnitz or hydropathic plan, had a great power in macerating and
disintegrating mucous membrane. Many of the successful cases of these,
as of all other specialists, are undoubtedly the result of the
convenient substitution of a grave diagnosis for a milder one. The
effect of such applications in laryngeal catarrh, like that of warm
applications, is undoubted. Vesicatories applied to the neck over the
larynx are never {106} useful--frequently injurious by the sore surface
becoming the seat of a pseudo-membrane.

Inhalations of warm vapor are decidedly beneficial, but atomized water
is not of equal value. Thus, Richardson's atomizer is not so useful as
Siegle's inhaler or other apparatuses working on the same plan.

Lactic acid, in solutions of 1:10 or 25 (Monti's solution of 1:200 is
certainly too weak), has been applied by means of a sponge, inhaled, or
thrown in from an atomizer for the same purpose. Good results have been
reported, failures also; and still, recoveries are rushed into print
much more readily than failures. The same may be said of the local
applications of glycerin, boric acid, carbolic acid in solutions of 1
or 2 per cent., salicylic acid, iodoform, and hypermanganate of
potassium; also of bromine (bromine and potas. bromid. _aa_) 1:water
500, or a stronger solution.

Tannin, dry or with glycerin, is rather more injurious than it can be
useful. It is apt to coagulate the mucus contained in the pharynx and
the upper part of the larynx, and to render the dyspnoea graver than
before. Such an aggravation of symptoms must be carefully avoided,
though it be but temporary. The same must be said of alum, which has
been used solid, in finely-powdered condition, down to a 3 per cent.
solution in water.

Spirits of turpentine are inhaled either from an inhaling apparatus or
by saturating the air of the room. Water is kept boiling constantly on
a stove, oven, or alcohol lamp (not on gas, which consumes a larger
quantity of oxygen), and a tablespoonful of the spirits of turpentine
is poured hourly or in shorter intervals upon the boiling surface.

Hydrochlorate of ammonia can be used in the same manner as described in
the article on Catarrhal Laryngitis.

Hydrochlorate of pilocarpine was introduced into the treatment of
diphtheria and pseudo-membranous croup some years ago, and recommended
as no less than a specific. It increases, physiologically, the
secretion of the skin, the mucous membranes, the lachrymal and
muciparous glands, the kidneys. It also depresses the heart's action.
In all cases in which the latter effect is to be feared the drug is
contraindicated; thus in septic diphtheria, in pseudo-membranous croup
with great asthenia, in general debility and anæmia. By increasing the
secretion of the mucous membranes it is expected to macerate the
pseudo-membrane and raise it from its bed. This can be accomplished
wherever the membrane is deposited upon the mucous membrane--that is,
whenever the number of muciparous follicles is large and the epithelium
is cylindrical. This is not so on the vocal cords, and thus the
floating effect of pilocarpine cannot be obtained exactly where it is
most needed--that is, on the vocal cords, where the pseudo-membrane is
more intimately imbedded into the tissue than, for instance, on the
posterior wall of the fauces or the trachea and bronchi. Still,
pilocarpine may be tried, in combination with other modes of treatment,
as long as the heart's action is competent and the general condition
satisfactory. It is dissolved in water; its dose, for a child a year
old, 1/30 grain (2 milligrammes = 0.002) every hour. A subcutaneous
injection every four or six hours of 1/60 grain (three drops of a 2 per
cent. solution) will prove very effective for good and evil. I believe
it has rendered me good service in some well-marked but mild cases of
pseudo-membranous laryngitis, which it either aided in healing or
prevented from getting worse.

Emetics have their distinct indication. It is irrational to expect any
relief from them when the larynx is narrowed by firmly-adhering
pseudo-membranes. Their indication depends on the possibility of
removing something which acts as a foreign body. This something can be
either mucus or loose or partially loose membrane. The peculiar
flapping sound produced by the latter admits of or requires the
administration of an emetic. Above I have stated which {107} of them
ought to be selected. Turpeth mineral in a dose of from 3 to 5 grains,
repeated in six or eight minutes, acts quite well. Hypodermic
injections of apomorphine may be required in urgent cases.

The introduction of catheters into the larynx, according to the methods
of Horace Green, is a dangerous proceeding and ought not to be indulged
in. It gave the idea to Loiseau and Bouchut to force a tube into and
through the larynx, full of pseudo-membrane, for permanent use until
the pseudo-membrane would have disappeared. This tubage was rendered
ridiculous at once by the assertion of Bouchut (1858) that children
suffering from croup who were supplied with this laryngeal tube were
not only relieved at once, but expressed their gratitude in audible
oratory. Still, there are some cases on record of more recent date in
which tubage is reported to have been attended with success. It is not
very probable, however, that a larynx which admits of no air, because
of its being clogged with firm pseudo-membrane, should be willing to
admit and endure the presence of a tube.

Massage of the larynx has been recommended by Bela Weiss. It consists
in systematical gentle pressing and kneading of the larynx by the
physician while sitting behind the patient. He asserts its satisfactory
influence not only in catarrhal but also in diphtheritic (croupous)
laryngitis.

The inhalation of oxygen has proved rather advantageous in my hands in
a few instances. The most memorable case of the kind I have mentioned
elsewhere. It was that of a child on whom tracheotomy had been
performed. The pseudo-membranous process, however, invaded the bronchi,
with the result of producing dyspnoea, cyanosis, and convulsions.
Whenever a current of oxygen was introduced into the lungs through the
canula both cyanosis and convulsions would cease, and returned when its
supply was stopped.

But if no medication will have proved successful, the symptoms of
stenosis, dyspnoea, cyanosis, and the supra- and intraclavicular and
epigastric recension increase steadily to an alarming extent. When the
pulse becomes frequent and intermitting, even without the presence of
asphyxia and anæsthesia, air ought to be introduced into the lungs by
tracheotomy. No positive rules can be laid down as to the length of
time one ought to wait before performing it. No subdivision of the
disease into several stages is of any benefit in selecting the exact
period in which the trachea must or may be opened. No alleged
contraindication to the performance of tracheotomy, whether the tender
age of the patient or a complication with either an inflammatory or an
infectious disease, must be considered valid. The one strict indication
for the performance of tracheotomy is when the diagnosis of
pseudo-membranous laryngitis is undoubted, the increasing dyspnoea,
cyanosis, and approaching asphyxia, with the certainty that a
well-directed and sufficient medicinal treatment has been, and in all
probability will be, useless. Even under these circumstances there is
no mathematical certainty. The matured experience of a well-informed
and thoughtful physician will commit but few errors. If there be the
slightest doubt, the operation ought to be preferred to suffocation.

The operative procedure and the surgical treatment after the
performance of tracheotomy will form the subject of a special article
in this work. In this place a few remarks upon the medicinal and
dietetic treatment in that period of the disease must suffice.[4]

[Footnote 4: Cf. _The Med. Rec._, May 24, 1884.]

The nutrition of the patient has generally suffered much. Before the
operation but little food was taken, still less was digested, and the
operation itself and the anæsthetic have added to the previous weakness
or exhaustion. Moderate feeding and stimulation are therefore to be
commenced soon. Vomiting after chloroform I have seldom seen to last
long or to be embarrassing under these circumstances. Feeding and
stimulation are the more necessary {108} the more the hungry
lymph-vessels are liable to absorb injurious material when not supplied
with healthy food.

Is internal treatment required? The general treatment must be
continued. If it consisted in the administration of hydrargyrum, either
internally or externally, it must be continued. If its effect was not
sufficient to clear the larynx and to render the operation unnecessary,
it will or may be sufficient to complete its effect in the next day or
two, to prevent the process from descending or the membranes becoming
too many or too thick. No changes ought to be made in the treatment
unless there be changes in the symptoms. Not infrequently the first
symptoms of broncho-pneumonia come on within a few hours after the
operation, recognizable by frequent pulse, respiration frequent beyond
proportion, and physical symptoms. The stomach is not very reliable.
Quinine answers best hypodermically. From 6 to 10 grains may be
injected at once. The preparation which has served me best in the last
few years is a solution of the carbamid in five parts of water. If an
additional remedy is required, from 20 to 30 grains of sodium
salicylate may be given in the course of three or four hours, in hourly
doses, to reduce the temperature. Tincture of digitalis will prove
advisable at the same time when the heart appears to require it.
Strychniæ sulphas will act as a powerful nervine; 1/25 grain may be
given to a child two years of age every two hours, until four or five
doses shall have been taken. The rest of the treatment of the
complications depends on their nature and character. It is not the name
of the disease which has to be treated, here as in every case, but the
individual patient.

In regard to stimulants I have but little to say. I use alcohol in the
most pleasant shape, preferring brandy or whiskey. I use a great deal
of camphor, 10 to 40 grains daily, or in cases of urgency Siberian
musk, from 2 to 5 grains, every half hour or hour, until from 15 to 20
grains have been taken in cases of collapse or great prostration.




{109}

DISEASES OF THE LARYNX.

BY LOUIS ELSBERG, M.D.


Inflammation, Erosion, and Ulceration of the Epiglottis.

Of the diseases of particular portions of the larynx, those of the
epiglottis deserve especial attention in a work designed for general
practitioners, on account of the comparative ease of recognizing and
treating them if understood, and the promptness their management
requires. They occur more frequently than is generally supposed, their
symptoms are often erroneously ascribed to other affections, and they
may lead to extensive disease in the respiratory apparatus, sometimes
of a very serious character. Adjacent portions of the root of the
tongue and pharynx or of the larynx are apt to be coaffected. In
diseases which commence in the pharynx, usually the lingual surface,
and in such as spread upward from the larynx only the laryngeal
surface, of the epiglottis is involved mainly or exclusively.

Before describing the affections of the epiglottis a few words must be
said of the manner of using the tongue-spatula. Physicians almost
without an exception press the tongue from above downward and from
before backward; but in order to bring the epiglottis into view in the
majority of instances the proper method is just the opposite of
this--viz. from below upward and from behind forward. Place the spatula
far back, lift up the base of the tongue, and draw it forward. The
usual manner of depressing the tongue--no matter how good or bad an
instrument may be used, and an ordinary spoon-handle serves the purpose
better than most of the so-called tongue-depressors--pulls upon and
irritates the pharyngo-glossal fold, and often hides the epiglottis
instead of bringing it into view, besides producing intolerance and
intractability. The blade of the tongue-spatula should be long (at
least four, still better five, inches), slightly curved downward, not
more than from half an inch to one inch wide, and joined to the handle
at an obtuse angle.

1. Acute inflammation of the epiglottis is usually caused by taking
cold, exposure to draughts, wet, sudden changes of temperature, etc.
The symptoms are local pain and difficulty of swallowing; in severe
cases also some dyspnoea and dysphonia. Only occasionally there is a
hemming cough, and that a peculiar one, induced (usually voluntarily)
by a feeling of a foreign body at the root of the tongue. The diagnosis
is made by means of the tongue-spatula and laryngeal mirror, the
epiglottis being seen to be inflamed and swollen. When the lower
portion, the so-called cushion of the epiglottis, is affected, the
mirror is required for diagnosis. In this case suppuration is apt to
occur. The prognosis is good with attention; neglected epiglottitis may
cause great discomfort, and even death. Treatment must be
antiphlogistic and supporting. For mild cases systemic and dietetic
regulation suffices, with externally either hot fomentations or cold
applications as the patient can best bear. Severer cases require in
addition leeches and ice to the part; and cases of threatened
suppuration, medicated and unmedicated steam inhalation, and, when
necessary, lancing of the abscess through the {110} mouth under
guidance of the mirror. After the acute inflammation has subsided,
local treatment may become necessary to hasten or produce complete
restoration, as will be noticed in Chronic Epiglottitis.

Inflammatory oedema of the epiglottis will be considered under the head
of Laryngeal Oedema.

Chronic inflammation of the epiglottis is usually the result of uncured
acute epiglottitis or of laryngitis. The main symptom is dysphagia. The
epiglottis is found swollen and more or less discolored. Not only
tongue-spatula and laryngeal mirror, but also the finger carefully
introduced into the mouth, may ensure the diagnosis, especially if the
upper portion be affected: then the thickened epiglottis is seen and
felt as a peculiar rounded tumor at the base of the tongue. Oedema is
distinguishable from chronic inflammation by both sight and touch. As
to prognosis, it must be observed that the process of restoration is
slow and that there is always danger of acute exacerbation. The
treatment consists in attention to the general health and habits and in
local applications. The latter are indispensable, and should be made by
means of an instrument (Elsberg's applicator or the like) carrying a
little wad of cotton or sponge. Some prefer a brush: to such individual
preference no objection need be made, but powders and sprays are not
advisable. The remedies to be applied should be in liquid form, and
belong pharmacologically to the class of alteratives. Iodine, iodoform,
and silver nitrate in solution are most useful. In subacute
inflammation (see above) potassium bromide and chlorate, respectively,
in saturated aqueous solution, may be applied once a day, or a
saturated solution of iodoform in sulphuric ether, or ten grains of
crystallized silver nitrate dissolved in an ounce of water, every other
day. In chronic epiglottitis the tincture or compound solution of
iodine, the ethereal solution of iodoform, and the watery solution of
silver nitrate, in degrees of concentration varying according to the
severity of the case and the individuality of the patient (the choice
of either of the three agents, the repetition of the same, or the
change from one to the other depending upon the effect produced),
should be accurately applied to the part affected by means of the
laryngeal mirror or the tongue-spatula.

2. The most frequent, and at the same time the most neglected, morbid
condition of the larynx is erosion of the free edge of the epiglottis.
Louis has called attention to the epiglottic erosions in connection
with tubercular phthisis: he found them present in about one-sixth of
the patients who died of that disease, and they are caused, in his
opinion, by the constant passage of pus over the part. Horace Green was
the first who pointed out that they are also frequently met with
independently of tubercular disease. According to him, "These
instances, for the most part, have been found occurring in those cases
in which a persistent, teasing cough, following chronic follicular
disease or common catarrhal inflammation, has obstinately resisted all
the ordinary measures for its arrestment. On depressing the tongue in
such cases by means of the ordinary bent spatula or tongue-depressor,
so as to bring the epiglottis into view, this cartilage has been found
frequently inflamed, vascular, and its superior border marked at one or
more points by distinct erosions. In much the largest proportion of
cases these erosions make their first appearance on the left superior
edge of the epiglottis. Next in frequency they will be found occupying
its centre, and occasionally, but very rarely in comparison with the
two preceding locations, they have been observed upon its right border.
These erosions are not readily detected, at first, by the inattentive
observer, as they are quite small, are only slightly depressed, with a
pallid base, sometimes a little reddened, and with whitish, linear
edges. The surrounding mucous membrane is generally inflamed, its
delicate network of superficial vessels is red and injected, and the
epiglottis itself more or less thickened." Sometimes epiglottic
erosions exist without {111} much cough, and certainly a cough can
exist without erosions; but the two seem frequently to act
interchangeably as cause and effect; and certain it is that a cough,
from whatever cause, once firmly established, when such erosions have
supervened rarely if ever yields so long as the erosions continue, and
often stops when they are cured. According to my experience, the left
and right sides of the upper border are affected with about the same
frequency, and oftener than the centre. The erosions are catarrhal in
their nature, even in tubercular subjects; in non-specific cases they
degenerate exceedingly rarely into ulcers--_i.e._ they may exist for
years without involving any tissue below the epithelium unless the
patient is or becomes syphilitic or phthisical. They often produce
symptomatically, especially in the beginning, more hemming than cough.
The diagnosis is easy on thorough inspection of the epiglottis.
Prognosis is generally favorable, except in phthisical cases; in
others, although they sometimes prove exceedingly obstinate, they
usually yield with surprising promptness to topical treatment. In
specific cases, and even in chronic naso-laryngeal catarrh, they are
apt to recur, however. A cotton wad dipped in a strong solution (gr.
xxx-drachm j ad ounce j water) of either silver nitrate or gold
chloride must be brought accurately into contact with the eroded spots
once in twenty-four or forty-eight hours; ordinarily only a fortnight's
treatment is necessary, except for the frequently accompanying (or
underlying) catarrhal condition of a more or less large extent of the
upper respiratory mucous membrane. In very severe cases a few
applications at longer intervals of a still stronger solution (drachm
j-drachm ij), or even of the solid silver or gold preparation, may be
required.

3. Epiglottic ulcerations differ from erosions in the fact that the
latter are confined to the epithelium, while the former involve also
deeper structures. It has been asserted by some observers that an
erosion is always the first stage of an ulceration, and by others that
the one never passes into the other. I believe that both of these
extreme assertions are incorrect; but if it were possible to
distinguish, clinically or pathologically, every case of superficial
ulceration from erosion, I might incline to agree with the latter.
Histologically, epiglottic ulceration affects the mucous membrane,
glands, or cartilage. Most frequently it seems to originate in the
follicles. As Horace Green has long ago pointed out, "At first an
enlarged or pimple-like follicle appears on the border of the
epiglottis, surrounded by an inflamed and highly-injected portion of
mucous membrane. Soon the follicle softens, and degenerates into an
ulcer with irregular edges and an inflamed and reddened circumference.
In many instances these ulcers remain for some time superficial,
destroying only the mucous membrane; in others they penetrate deep into
the fibro-cartilage, and occasionally they result in the total
destruction of the epiglottis." Sometimes the ulcer seems to originate
in the superficial layer of the mucous membrane, the molecular death
proceeding from the surface downward; these are the cases which in the
beginning cannot be distinguished from erosions. Both these kinds of
ulceration of the epiglottis occur without, and with, grave
constitutional affections, but the cartilaginous tissue usually, though
not invariably, remains intact except in phthisis, syphilis, and
cancer. Lupus, lepra, and glanders also give rise to ulceration, and
sometimes to much accompanying thickening of the epiglottis. The seat
of the ulcers is, as a rule, on the upper border and laryngeal surface
of the epiglottis, only exceptionally on the lingual. Together with
ulcers on the laryngeal face those on the lingual face are found, but
not vice versâ. Ulcers of the epiglottis are usually small, but
numerous, worm-eaten in appearance, and frequently pass to other
laryngeal structures. Though occasionally resulting from tuberculosis,
syphilis, and other constitutional affections, they also occur as
primary disease due to catarrh and local injury, but may become the
antecedents, and in many instances the exciting cause, of other grave
maladies. Indeed, I quite agree {112} with Horace Green that they are
often "not only among the earliest manifestations of thoracic diseases,
but are themselves in many instances the true exciting cause of these
affections; and furthermore, this postulate once established, that we
have it in our power, by timely topical medication, to arrest,
positively, cases of disease which otherwise would, and in many
instances which do, terminate fatally."

The symptoms vary with the seat and extent of ulceration. Cough and the
sense of irritation in the throat are usually present. "In several
instances all the prominent rational signs, with some of the earlier
physical manifestations, of pulmonary disease have been observed to
follow long-continued ulceration of the epiglottis; all of which
symptoms have been seen to disappear after these lesions have been
healed." When the upper border is extensively affected, and still more
when either surface, especially the lower portion of the laryngeal
surface, be involved, there is difficulty of swallowing; the pain is
due often as much to surrounding inflammation as to the epiglottic
lesion. In some cases the voice also is affected.

The diagnosis of the existence of an ulcer is easily made when the
epiglottis can be seen not only with the spatula, but also with the
laryngeal mirror. Its origin and nature are, however, not always easily
recognized, and the patient's general condition and history, as well as
the appearance of the ulcer, must be taken into account. The diagnosis
of catarrhal epiglottic ulceration must be made only after other
underlying conditions, as phthisis, syphilis, malignant disease, lupus,
lepra, and glanders (see the articles on those subjects), have been
excluded. The prognosis is good, except in cases of phthisis, syphilis,
etc., or in which already a great deal of the cartilage has been
destroyed; and even in these cases appropriate treatment will often
give the patient much comfort. Appropriate constitutional treatment
must be instituted in all cases in which the constitution is affected.

Topical treatment consists in the application of alteratives,
astringents, stimulants, or sedatives, as the case may call for. Some
cases may require once or more times touching with solid silver
nitrate; watery solution of this remedy, varying in strength from gr. x
to drachm ij to the ounce; solution of gold chloride of similar
strength; of iron pernitrate and perchloride drachm ss-drachm j to the
ounce; of zinc chloride (gr. x-drachm ss to the ounce); a solution of
iodine in olive oil (gr. x-xxv ad ounce j with a few grains of
potassium iodide), or of iodoform in sulphuric ether (drachm i-drachm
ij ad ounce j); carbolic acid in glycerin (gr. v ad ounce j) or
Magendie's solution of morphine, or a mixture of morphine and syrup of
tolu (gr. 1/8-1/2 to a few drops),--have most frequently been
beneficial in my hands. In many cases in which the pain on swallowing
has been so great as to make deglutition almost impossible, I have
succeeded in temporarily anæsthetizing the parts before a meal by
applying, after cleansing them, a watery solution of cocaine
hydrochloride (gr. xx ad ounce j). If, in spite of all, the difficulty
of swallowing threatens the patient with starvation, feeding with the
oesophageal tube must be resorted to.


Laryngeal Oedema.

DEFINITION.--Infiltration of a fluid or semi-fluid into the submucous
connective tissue of the larynx.

SYNONYMS.--Oedema of the glottis (often incorrectly so called, as will
presently be seen), Oedematous laryngitis, Phlegmonous laryngitis,
Submucous laryngitis, Dropsy of the larynx, Angina laryngis infiltrata,
Angina laryngea oedematosa, Angine infiltro-laryngée, etc.

CLASSIFICATION.--Cases of laryngeal oedema are classified as to their
occurrence into acute and chronic, corresponding generally to
inflammatory {113} and non-inflammatory; as to the nature of the
infiltration, into serous, purulent, sanguineous, sero-purulent,
sero-sanguineous, etc.; as to the extent of the infiltration, into
diffuse and circumscribed (the latter often leading to
abscess-formation, and then called laryngeal abscess rather than
laryngeal oedema, differing, however, from perichondric abscess); and
as to the seat, into epiglottic, supraglottic, infraglottic, and
glottic. When epiglottic, it implicates, besides the upper border,
often the glossal, hardly ever the laryngeal, surface; in supraglottic,
the ary-epiglottic folds, arytenoid region, ventricular folds, or
ventricles are involved; in glottic, the interfibrillar connective
tissue of the thyro-arytenoid muscle is infiltrated, very
exceptionally, if ever, the submucous tissue of the vocal bands
themselves;[1] and in infraglottic, the submucous connective tissue
down to the first ring of the trachea. Glottic oedema occurs extremely
seldom, but the designation oedema glottidis is often used, no matter
what portion of the larynx is affected. Laryngeal oedema usually
affects both sides; occasionally one side more than the other, still
more rarely one side exclusively.

[Footnote 1: Such a case has been positively reported, or I would deny
the possibility of its occurrence.]

ETIOLOGY.--Laryngeal oedema is seldom, if ever, idiopathic. Usually it
accompanies or follows either some disease or injury of the larynx[2]
or neighboring structures or a constitutional affection. Acute oedema
may be caused by catarrhal or diphtherial pharyngo-laryngitis;
irritation from scalds, burns, caustics, foreign bodies (especially
sharp ones), or other trauma; laryngeal ulcers, especially syphilitic
and tuberculous; laryngeal perichondritis, tonsillitis, parotitis, or
inflammation of cervical tissues on the one hand, and pyæmia and
septicæmia, endocarditis, erysipelas, small-pox, scarlatina, measles,
typhoid fever, typhus, or acute Bright's disease of the kidneys on the
other. "It has ensued upon deglutition of very cold water and upon
prolonged vocal efforts" (Cohen). Perichondritis and chondritis,
tuberculous, syphilitic, carcinomatous, or typhoid ulcerations of the
larynx, especially when deep-seated or extensive, are sometimes
attended with acute, but more often with chronic, oedema.
Non-inflammatory or chronic laryngeal oedema is sometimes part and
parcel of general dropsy in consequence of heart, kidney, or lung
disease: Horace Green has reported a case occurring in a man who had
hydræmia from great losses of blood from hemorrhoidal tumors; and it is
sometimes due to some impediment to free venous circulation in the
laryngeal tissues, from paralysis of the walls of the vessels,
mechanical obstruction, tumors of the thyroid body or in the
mediastinum, etc. compressing the jugular veins, compression of the
superior vena cava, etc.

[Footnote 2: According to Sestier, who has written (in 1852) the most
elaborate treatise extant on the subject, four-fifths of all cases
occur in other laryngeal affections.]

Cohen mentions cases to show that acute iodism and mercurialization may
cause laryngeal oedema. He also says that although occurring in
individuals in good general health, it is more apt to take place in
those of impaired constitution or recently convalescent from acute
diseases; and in some instances there would appear to be some peculiar
predisposition toward its occurrence the nature of which is not
understood, for examples are on record of more than one attack in the
same individual. Under all these circumstances the immediate exciting
cause, when apparent, seems to be exposure to cold and moisture.

Laryngeal oedema is not a disease of childhood; exceptional under five
years, it is very rare until after ten. Most cases occur between
eighteen and thirty-five. After the sixtieth year it is again rare; and
it occurs more rarely in women than in men.

SYMPTOMATOLOGY.--The symptoms of laryngeal oedema vary with the seat
and degree--that is, according to the class to which the case belongs.
{114} Increasing interference with breathing is the most prominent
symptom. Interference with swallowing, though not always present, is
the next prominent. Sometimes the occurrence is so sudden, insidious,
or overwhelming that the patient dies before aid can be procured. Such
was Boerhaave's case of a man who during dinner suddenly spoke with a
changed voice, which his companions took as a joke, and in a few
minutes fell dead; Rühle's case of a servant-girl, who, a trifle
hoarse, went out lightly clad on a cold morning and suffocated while
going up stairs on her return; and the case of a patient of mine with
subacute catarrhal laryngitis, who rode out behind a fast horse on a
cold afternoon, and died, within ten minutes after entering his own
house, from serous infiltration of the upper aperture of the larynx. A
number of similar cases have been reported, but usually the disease
runs its course less rapidly. When the ary-epiglottic folds are the
seat of the oedema, the patient experiences either suddenly or
gradually a difficulty of inspiration, while the expiration may be at
first unimpaired, and with increasing sensation of constriction of the
throat or of the presence of a foreign body, hoarseness, and stridor,
but often without dysphagia, the most threatening paroxysms of
suffocation supervene. When the epiglottis is the main seat, while
respiration is also more or less impeded, swallowing is rendered
painful, difficult, and sometimes impossible without choking and
regurgitation through the nares, and the voice roughened and sometimes
extinguished. When the arytenoid region is also affected, respiration
and deglutition are still worse, aphonia is complete, the sense of
irritation at the upper aperture of the larynx often amounting to pain,
and the patient with great effort expectorates slightly. In oedema of
the ventricular folds there is early aphonia and gradually increasing
dyspnoea, which affects both expiration and inspiration, sometimes the
former even worse than the latter. This makes the sufferer's efforts to
breathe most frightful to witness, the feeble inspiration being
accompanied by a slow whistling sound, and the expiration, despite most
violent exertion, almost entirely shut off. Glottic oedema is, as
before said, exceptional; when it occurs to any great extent apnoea
ends the case unless operative relief is immediately afforded. In
infraglottic oedema, which is exceedingly rare and chronic in nature,
there is steadily increasing dyspnoea, wheezing, cough, and abundant
expectoration.

In acute cases of supraglottic and epiglottic oedema the suffocative
paroxysms may last several minutes, and recur at irregular intervals of
a few hours with increased intensity. If not relieved, patients become
wildly excited or terror-stricken; they may throw the chest forward,
open the mouth, grasp the throat outside or thrust their hands into it,
and make convulsive movements in their struggles for breath; with
protruding eyes and flushed face they become cyanotic, the extremities
cold, the pulse small and frequent; coma supervenes, and death. In
chronic cases the symptoms are not so violent, though they may steadily
progress to impending strangulation, but for a long time the dysphagia
gives the patient much more distress than the dyspnoea.

In circumscribed acute cases leading to the formation of an abscess
there is usually pain in a particular spot, and often general
feverishness, in addition to all the symptoms before mentioned,
according to the seat of the oedema. Sometimes the suffering in
laryngeal abscess at its height is very intense. Perforation into the
pharynx, oesophagus, or even externally, may take place, but usually
the pus points into the larynx. When the pus is evacuated either
spontaneously or by incision, violent choking, coughing, and hawking
may occur, but after it is evacuated all dangerous symptoms usually
rapidly subside.

In sanguineous infiltration the symptoms do not differ from serous or
purulent oedema under the same circumstances. Hemorrhagic infusion is
usually {115} sudden, and the resulting stenosis often fatal. Muscular
spasm or paralysis sometimes coexists with laryngeal oedema, and
greatly adds to the interference with respiration.

PATHOLOGY AND MORBID ANATOMY.--The seat of the morbid process being the
connective tissue, those localities of the larynx in which this tissue
is most abundantly interposed between the mucous membrane and the
cartilage are most liable to infiltration. I must say from my own
experience that the epiglottis--particularly the glosso-epiglottic
region--is most frequently affected,[3] next the ary-epiglottic folds,
then the arytenoid region, and then the ventricular folds. The
ventricles and the vocal bands are very rarely involved. Infraglottic
oedema is still more rare, and is never an extension of the
supraglottic. The disease is never a primary one, and, though seated in
the submucous connective tissue, it may have started with inflammation
of either the overlying mucous membrane or the underlying
perichondrium. Effusion of blood is generally limited to traumatic
cases, but has ensued from mercurialization, small-pox, and typhus;
purulent infiltration and abscess formation is the result of
phlegmonous inflammation and breaking down of the tissue, occurring
especially in the cushion of the epiglottis and in the ventricular and
ary-epiglottic folds; but as a rule the effusion in laryngeal oedema is
of a serous or sero-purulent character.[4] In infraglottic oedema it is
said to be fibrinous.

[Footnote 3: According to Sestier, the ary-epiglottic folds are
affected in nearly every case, either alone or together with other
parts.]

[Footnote 4: In 90 cases Sestier found the infiltration serous 60
times, sero-gelatinous 6, sero-purulent 9, sero-purulent with plastic
lymph 4, purulent 8 times, sero-sanguineous twice, and sanguineous
once.]

The mucous membrane covering the oedematous structures is tense and
discolored; except in very inflammatory conditions it is yellowish,
shimmering, and pallid. On cutting into the diseased parts often but
little exudation takes place, and sometimes even squeezing between the
fingers does not suffice to cause disgorgement.[5] After the fluid is
evacuated the parts collapse and the mucous membrane is left wrinkled
and folded.

[Footnote 5: In 23 autopsies Sestier found that incisions into the
oedematous structures made the liquid run out either without any or
with slight pressure 10 times; with repeated pressure, with difficulty
and only in small quantity, 6 times; and not at all, in spite of
repeated incisions and pressure, 7 times.]

DIAGNOSIS.--With the laryngoscope, the spatula, and the finger the
seat, the degree, and often the nature of the infiltration can be
determined. A successful laryngoscopical examination may sometimes
require in such cases more than ordinary skill, and there is often so
much tumefaction that the parts are not easily recognizable. The
epiglottis may appear as a thick roundish tumor, or be of a more or
less indistinct horse-shoe shape, overhanging the laryngeal aperture;
the ary-epiglottic folds may be converted into large lateral cushions
pressing against the arytenoid bodies, or be merged with the latter
into huge, irregularly pear-shaped, oval, or globular masses; and the
ventricular folds may be immensely tumefied, or else, by means of the
swelling and the being pushed into a horizontal position of the whole
lateral lining of the upper laryngeal cavity, may be obliterated
altogether. Glottic oedema never occurs except with supraglottic, and
the upper surface of the vocal bands may look elevated, arched, and
bladder-like, even if only the thyro-arytenoid muscles are infiltrated.
In infraglottic oedema there is usually neither epiglottic nor
supraglottic oedema; pads are seen underneath the vocal bands, either
ring-shaped or projecting from side to side toward the middle line, and
fill up to a greater or less degree the rima glottidis. The oedematous
parts have sometimes a pinkish, but usually a yellowish, translucent or
semi-translucent aspect. Accumulation of pus lessens the translucency
and sometimes makes the yellow more marked. Sanguineous {116}
infiltration shows a bluish-red or livid discoloration. In chronic
oedema the color is lighter, sometimes a dirty gray.

I have already explained the proper method of using the spatula. It
reveals in all cases, sometimes best during retching, the epiglottis,
and in many cases the ary-epiglottic folds. With the finger these parts
can be touched, and all the more easily when they are swollen; but
great care must be exercised to avoid provoking by digital examination
a suffocative paroxysm. When felt by the finger the peculiar elasticity
or fluctuation present is unmistakable.

PROGNOSIS.--Laryngeal oedema is always a very dangerous condition--in a
chronic case less so than in an acute one. The prognosis depends
largely upon the causative or accompanying disease. The more local the
oedema and the more promptly medical, and in most instances surgical,
aid can be had, the more favorable is the prognosis, though uncertain
even then. Sometimes a rapidly fatal attack supervenes in a mild,
chronic, or apparently convalescing case. In abscess formation it is
generally favorable unless the underlying disease makes it the reverse.

TREATMENT.--Antiphlogistic treatment of every sort has been recommended
against this dread disease. Its frequently rapid course usually
necessitates primarily topical measures. Even fifty years ago, when
bleeding and tartar emetic were in vogue, Ryland entirely
discountenanced these, and said: "Our chief reliance must be placed on
the local detraction of blood by means of a large number of leeches
applied in the vicinity of the larynx; on the use of blisters, which
should never be put on the front of the neck, as their operation will
interfere with the subsequent performance of tracheotomy should such a
step be necessary, but on the back of the neck or the upper part of the
chest; and on the internal administration of large doses of calomel,
which, either by their purgative effect or by their specific action on
the general system, tend to check the inflammation in the glottis and
to promote the absorption of the effused fluids. These remedies can
only be of use during the early stages of the disease, and experience
shows but too plainly that even then we have far more reason to
anticipate failure than success."

Many years ago it was proposed to catheterize the trachea for the
purpose of allowing air to reach the lungs in this and other diseases
in which the larynx is obstructed; and more recently Hack has shown the
great benefit of using, under sight by means of the laryngoscopic
mirror, Schrötter's dilating hard-rubber tubes in acute as well as
chronic laryngeal oedema. According to him, they do good not only
symptomatically, but also curatively.

Furthermore, we can employ, under the guidance of the mirror or of the
finger, scarifications of the infiltrated structures by means of the
laryngeal lancet, or in its absence of a long bent, sharp-pointed
bistoury covered, except for a quarter of an inch or so from its point,
with adhesive plaster. (For the epiglottis the ordinary gum lancet will
often do.) An abscess is opened in the same way. When the bleeding
following scarification is excessive we use ice internally or
externally, or both; when bleeding is insufficient, steam inhalation,
hot fomentations, etc. To promote absorption we make topical
applications, either before or certainly after the scarification, of a
saturated solution of iodoform in sulphuric ether (drachm ij ad ounce
j), or of a strong watery solution of silver nitrate (scruple ij-drachm
j ad ounce j). Astringents, especially tannin and alum, applied in the
form of spray to parts that cannot otherwise be reached, are advisable;
and antispasmodics and narcotics (potassium bromide and morphine)
should not be omitted in cases complicated with muscular spasm, etc.
The internal administration of fluid extract of jaborandi in drachm
doses or the hypodermic injection of pilocarpine is highly lauded as
promoting absorption; also diaphoretics, purgatives (salines and croton
oil), {117} etc. From the beginning the patient's general functions
must be regulated and his strength supported by tonics and nutritives,
and any underlying disease amenable to treatment must of course be
attended to. The slow swallowing of pieces of ice is often of great
benefit. In every case that does not visibly improve by the vigorous
carrying out of the treatment hitherto detailed, especially the
catheterization by means of Schrötter's tubular dilators, the ultima
ratio--viz. tracheotomy, particularly inter-crico-thyroid
laryngotomy--must be resorted to without waiting until the patient has
lost much ground by the impediment to respiration. One of the lessons
taught us by pathological investigation is that epiglottic,
supraglottic, and glottic oedema does not extend beyond the upper
surface of the vocal bands: therefore, while in infraglottic oedema,
and when the two conditions supraglottic oedema and infraglottic
coexist, tracheotomy should be performed, in the other cases the
air-passage should be opened by introducing a tube through the
inter-crico-thyroid membrane. This operation is, especially for the
general medical practitioner, much easier, safer, and quicker of
performance, and answers in those cases all purposes. This important
lesson is not heeded by any of the recent authors on the subject.
Indeed, Cohen expressly says: "The trachea is to be opened in
preference to the larynx, as being at a greater distance from the seat
of the disease and less liable to involvement, as well as for the
reason that the disease occasioning the oedema may be extending low
down in the larynx, and therefore exist at the very point usually
selected for laryngotomy." Supraglottic oedema does not extend to the
region of the inter-thyro-cricoid membrane, and the tube may therefore
safely be there introduced.


Perichondritis and Chondritis of the Larynx.

DEFINITION.--Inflammation of the laryngeal perichondrium and cartilage.

SYNONYMS.--Phthisis laryngea of the older authors, Laryngitis affecting
the cartilages, Deep-seated ulcerative laryngitis, Caries cartilaginum
laryngis, Vomica laryngis, Perichondric laryngeal abscess, Necrosis
laryngis. (Some of these names refer to the product or terminal stage
of the disease.)

ETIOLOGY.--Laryngeal perichondritis and chondritis occur either as
idiopathic or as symptomatic or secondary affections. Even the former,
caused by so-called catching cold or exposure to cold and wet while the
system is in a state of lowered vitality, may have a septicæmic basis;
it is much more rare than the secondary. Rühle has remarked that
arytenoid perichondritis may probably sometimes start in the
crico-arytenoid articulation, and in an instance which has come under
my observation this certainly seemed to have been the case. Authors
state that occasionally the inflammation commences in the cartilaginous
tissue itself, instead of in its investment; this is hardly
conceivable. Perichondritis must always precede chondritis, but it
always causes the cartilage to become involved in the morbid process.
Quite often perichondritis and chondritis constitute an extension of a
particular ulcerative disease of the mucous and elastic membranes. In
the great majority of cases the causes are tuberculosis, syphilis,
diphtheria, cancer, lupus, typhus and typhoid fever, small-pox, or else
traumatic occurrences, especially suicidal throat-cutting, decubitus or
other pressure upon the part--as, for instance, the frequent
introduction in an aged subject of the oesophageal sound observed by
Ziemssen, and overstrain of the voice alleged by Flormann. At least
three cases are reported (viz. by Porter, Lawrence, and Eppinger) in
which the disease has been ascribed to the administration of mercury,
and Graves and Stokes remark that in broken-down constitutions, {118}
where large quantities of mercury have been used, chronic laryngitis is
very apt to terminate in ulceration of the cartilages.

The disease occurs oftener in men than in women, and oftener between
the twentieth and fortieth years than at any other age.

SYMPTOMATOLOGY.--I distinguish three stages of laryngeal perichondritis
and chondritis--viz. the inflammatory, suppurative, and necrotic. The
symptoms of the first stage are obscure: the main one is pain, usually
of a boring, burning character, localized according to the precise
cartilage affected, which is increased by functional or other movement
of the part and by pressure from the outside. To the pain there are
gradually added--also depending somewhat upon the precise seat of the
inflammation--cough, dysphonia, and dysphagia. In cricoid
perichondritis--especially when, as is generally the case, the
posterior surface of the plate of the cricoid cartilage is
affected--there is sometimes inflammatory reddening of the pharyngeal
mucous membrane which may extend upward to the palate. Inflammatory
swelling of some part of the cartilaginous framework may be
recognizable in the first stage of the disease by means of the
laryngoscope.

The suppurative stage is attended with more swelling of the part
affected, due to accumulation of pus and to collateral oedema. Pain,
dysphagia, or dysphonia, and sometimes irritative, harsh cough may be
much augmented; but, above all, dyspnoea now appears, which sometimes
so rapidly increases that the patient dies asphyxiated unless
tracheotomy is performed.

During the necrotic stage the symptoms of laryngeal stenosis sometimes
persist, and sometimes cease with the expectoration of quantities of
pus containing possibly a part, and occasionally the altered whole, of
the affected cartilage: with continued purulent expectoration the
patient's strength fails, the breath becomes very fetid, and hectic
fever and death may supervene.

Swelling of cervical lymphatic glands, though by no means always
present, has been observed in the early and sometimes only in the later
stages of the disease.

The course of the disease, whether idiopathic or secondary, is either
acute or chronic. It tends either toward abscess-formation, which
predominates, or toward new growth of tissue; for a time sometimes the
one, sometimes the other occurs, and, as a rule, during the former the
process is more acute, and during the latter more chronic: the
proliferated tissue, after being produced, may break down and increase
the amount of pus. When acute, the three stages of the disease follow
each other rapidly, if, indeed, the third be not cut off by the death
of the patient. When chronic, the pus collected is very apt to burrow
and to make fistulous passages and openings internally and externally.
At various points also perichondric hypertrophies, ecchondroses, and
exostoses are apt to occur.

The inflammatory stage can terminate by more or less complete
resolution, though usually some enlargement of the cartilages
permanently remains; recovery can also take place in the later stages,
and leave deformities and produce cicatricial contractions.

PATHOLOGY AND MORBID ANATOMY.--The perichondrium of the larynx is
diseased comparatively oftener than that of any other region of the
body; which, aside from other causes, is partly due to the fact that
the laryngeal cartilages become with increasing age normally vascular
and ossified. The morbid process never affects at one time the whole of
the cartilaginous framework of the larynx, and usually only one
cartilage, or even only a limited portion of one cartilage, except in
the case of the cricoid and arytenoid, which are sometimes together
implicated. Perichondritis does not spread easily. The cricoid is most
frequently affected, next the arytenoid, far less often the thyroid,
and exceedingly rarely the epiglottis.

As already remarked, the inflammation of cartilage and perichondrium
{119} has a great tendency to suppuration--occasionally, though rarely,
proliferation and hypertrophy; or, on the other hand, and more
frequently if the inflammation is a slowly progressing one, the
processes leading to ossification take place. The suppurative stage
follows the inflammatory quickly unless the latter has been
comparatively very slight. A great abundance of pus collects between
the cartilage and its investing membrane. As the former is thereby
denuded and separated from its nutritive vessels, it must become
necrotic. Exfoliated pieces of cartilage are generally found in the
abscess. Caries of adjacent tissues is apt to take place, and oedema of
the surrounding connective tissue, and sometimes far-reaching
destruction, before the perichondrium bursts or becomes destroyed over
a large extent. In cricoid perichondritis, the plate mainly being
affected, the abscess projects mostly toward the oesophagus and the
trachea, or it points outwardly when the narrow portion is involved;
the opening when the abscess has burst is frequently large, and shows a
portion of the necrosed cartilage; sometimes there are a number of
perforations. In arytenoid perichondritis the abscess bulges either
into the interior of the larynx or into the adjacent pyriform sinus;
bursting usually occurs at the posterior portions of the ventricular
folds or near the posterior vocal process, and the undermined edges may
disclose the dead cartilage. In thyroid perichondritis either the
interior of the larynx, the pyriform sinus, or the outside of the neck
is encroached upon.

In the course of the necrotic stage of the disease the laryngeal
framework may cave in, and a stenosis be produced which may quickly put
an end to the patient's life unless tubage--as explained under the head
Oedema--or tracheotomy be performed. A loose piece of dead cartilage
getting into the rima can produce the same fatal effect. Smaller or
larger pieces of necrosed cartilage, sometimes partially or wholly
ossified, have been expectorated, or, post-mortem, found lying in the
respiratory passage, looking dirty-yellowish or blackish. Fistulous
openings may take place in the larynx, pharynx, and in the skin
covering these parts. Gaucher has reported an extraordinary case in
which a perichondritic abscess of the thyroid cartilage had opened into
the vertebral canal, as well as externally by the side of the
sterno-cleido-mastoid muscle. If the perichondritis has followed
deep-going ulcerative destruction of the mucous membrane, the
perichondritic abscess bursts more easily, and less burrowing of the
pus usually takes place.

In the rare termination of healing of the necrotic stage of
perichondritis the loss of cartilage-substance is supplied by
connective-tissue granulation emanating from the perichondrium. Cohen
has reported a case in which there was apparently a reproduction of the
whole cricoid cartilage, the necrosed original one remaining in the
interior of the larynx as a foreign body.

Just as laryngeal stenosis is the grave danger during the continuance
of the disease before the perichondritic abscess has opened from its
protrusion into the laryngeal cavity, together with the accompanying
oedema, and from the undermining of soft parts by burrowing pus, and
after the abscess has opened from exfoliated pieces of cartilage
blocking the interior, or, when eliminated, from caving in of the
laryngeal framework, so laryngeal stenosis is the grave consequence of
the disease from remaining deformity, cicatricial contraction,
ankylosis of the crico-arytenoid articulation, etc. An open
perichondritic abscess may also lead to extensive gangrenous
destruction, and occasionally to subcutaneous emphysema.

Under the microscope the first stage of perichondritis is marked by the
appearance in the fibrous basis-substance of the perichondrium of more
or less coarsely granular corpuscles, the so-called inflammatory
corpuscles. As to their origin, it is well known that Virchow taught
that they are produced by the enlargement, division, and subdivision of
the connective-tissue corpuscles, while Cohnheim claimed that they are
nothing but emigrated {120} colorless blood-corpuscles: in point of
fact, most of them arise from the liberation of the living matter
contained in the basis-substance, by the liquefaction or melting out of
the non-living ingredient, and the increase and division of this matter
into medullary or inflammatory corpuscles which constitute the
so-called inflammatory infiltration. So long as the corpuscles remain
connected by filaments of living matter, the inflammatory process may
terminate by a new formation of basis-substance in hyperplasia--_i.e._
in the new formation of connective tissue. When, on the contrary, the
inflammatory corpuscles are torn apart and become suspended in a liquid
exudate, they constitute pus, and then the termination of the
inflammatory process is in suppuration; that is to say, usually in an
abscess.

The perichondrium and cartilage are normally so closely connected that
the one tissue passes gradually into the other without definite
boundary-line, and the cartilage participates in the inflammatory
process by a liquefaction of its basis-substance, reappearance of the
living matter therein contained, and the formation of more inflammatory
corpuscles. So long as the inflamed perichondrium remains in living
connection with the cartilage, both tissues may participate in the new
formation of a dense connective tissue, and hyperplasia be the result
of the perichondritis and chondritis. Should, on account of suppuration
at the boundary of the cartilage, the vascularized portion of the
perichondrium become detached, the cartilage, being itself devoid of
blood-vessels, will become dead. Its corpuscles will shrivel, and
together with the lifeless basis-substance become disintegrated. Pieces
of necrotic cartilage may be found lying in the surrounding pus, and,
though usually chondritis has preceded the necrosis, the latter may
ensue without previous change of the cartilage tissue, especially if
the perichondritis runs its course to suppuration rapidly; but in every
case suppurative perichondritis precedes necrosis of the cartilage.

After the elimination of necrosed portions cartilage is as a rule
replaced by newly-formed dense fibrous connective tissue. Some
clinically-observed cases, aside from the remarkable case of Cohen
already mentioned, indicate, however, that, exceptionally, new
formation of cartilage may occur from hyperplastic perichondrium, in
the same manner as new bone is sometimes formed from hyperplastic
periosteum after osseous necrosis.

DIAGNOSIS.--The inflammatory stage may be suspected, rather than
positively recognized, from the peculiar pain if the laryngoscope (or,
in the rare case of thyroid perichondritis, palpation) reveals
enlargement of a part of the cartilaginous structure without much
injection of the mucous membrane. The presence of other symptoms
mentioned, and in the case of cricoid perichondritis the localized
pharyngeal reddening, make the diagnosis more probable. During the
suppurating and necrotic stages the diagnosis becomes certain from the
symptoms I have described, especially expectoration of fragments of
necrosed cartilage, together with direct examination. The laryngoscope
may show the abscess; sometimes the finger or a probe can detect
fluctuation, and frequently through an opening the probe detects the
necrosis. The movement of one or both vocal bands may be affected
either mechanically from purulent accumulation, or from articular
ankylosis, or from interference with muscular attachments or action, or
with innervation. In my hand, and in that of others, a probe introduced
through an external fistula has been seen in the larynx; others have
been able to inject colored fluid and find it in the interior.

PROGNOSIS.--Except in slight cases death is more apt to take place than
recovery. If tracheotomy has saved the patient from impending death,
ultimate prognosis is still unfavorable in severe cases. In idiopathic,
traumatic, and syphilitic cases the prognosis is of course better than
in others in which we have to face grave dangers of the underlying
disease as well. The {121} remaining laryngeal stenosis after recovery
makes the prognosis bad as to the doing away with the tracheotomy-tube,
although it is far more favorable at the present day than it was
previous to Schrötter's success with dilating measures.

TREATMENT.--Throughout the disease the patient's general health and
strength must be carefully attended to, tonics and stimulants used
according to circumstances, and the underlying condition of secondary
perichondritis, such as syphilis, etc., treated secundum artem.
Locally, the treatment during the first stage must be antiphlogistic,
by leeches, ice, etc., and soothing, especially by inhalations.
Afterward, abscesses must, if accessible by means of the laryngoscope,
be opened. Artificial feeding, through either an oesophageal or a
rectal tube, may become necessary. Schrötter's hard-rubber tubes may be
inserted to conduct air to the lungs, but tracheotomy, not laryngotomy,
must be performed if, in spite of this tubage, suffocation threatens.

The methodical dilatation of post-perichondritic laryngeal stenosis
requires special bougies, catheters, hard-rubber tubes, pewter plugs,
and dilators which are not to be found in the ordinary armamentarium of
a medical practitioner; but the proper and frequently successful use of
these can be acquired with patience and perseverance when a case of the
kind presents itself for treatment.


Chronic Laryngitis.

DEFINITION, SYNONYMS, AND CLASSIFICATION.--Under the name chronic
laryngitis are brought together a number of different diseases of the
larynx which have the character in common that they are more or less
inflammatory and chronic in their course. The various conditions of
chronic inflammation of the mucous membrane (chronic laryngeal catarrh)
prominently belong to this category, but the chronic inflammation of
every other constituent tissue of the larynx, except cartilage and
perichondrium, is included.

The synonyms refer mostly to individual etiological and other factors
not applicable to all cases, as clergymen's laryngitis, phthisical
laryngitis, and many of the designations of different classes.

Chronic laryngitis frequently involves more than one tissue, but
usually one prominently. Histologically, the following kinds of chronic
laryngitis have been distinguished: viz. catarrhal, when simply or
principally the mucous membrane is affected; granulous or glandular,
when the muciparous glands; submucous or parenchymatous, when the
connective tissues underneath the mucous membrane are prominently
implicated; and muscular, when there is chronic inflammation of the
muscular tissue. According to the seat, there will be supraglottic,
glottic, and infraglottic chronic laryngitis. There have also been
described atrophic, hypertrophic, and polypoid chronic laryngitis; dry
and blenorrhoeic or hypersecreting chronic laryngitis; simple, fetid or
ozænic, and ulcerative; phlebectasis laryngea, trachoma, etc.

ETIOLOGY.--Chronic laryngitis is caused in many ways. Frequently it
follows uncured or neglected acute laryngitis. It is apt to occur in
persons whose avocations or habits lead them to strain or otherwise
abuse their vocal organ, to work in an impure or irritating atmosphere,
or to use tobacco or alcohol excessively; and it may depend upon or be
an extension of chronic inflammation of either the naso-pharyngeal or
tracheo-bronchial mucous membrane. Secondarily, it accompanies all
long-continued laryngeal affections, such as phthisis, syphilis, lupus,
etc. Males suffer more often than females, and middle-aged persons more
often than either children or the very old. Boys at the time of puberty
are liable to become affected.

SYMPTOMATOLOGY.--The diseases comprised under the collective name of
chronic laryngitis give rise to various symptoms, of which the chief
are {122} morbid sensations in the region of the larynx and alteration
of the voice. Unless ulceration have occurred, the morbid sensations
hardly amount to pain, except on acute exacerbation from catching cold
or after long-continued use of the voice. They consist in a sense of
dryness or of pressure, in a tickling or in an unnatural feeling that
cannot be definitely described in words. Though not acute, they are
sufficient to make the patient constantly conscious of their existence
and to induce fruitless efforts at clearing the throat, etc. The
alteration of the voice varies from occasional unsteadiness or veiling,
or a loss of power or purity of tone, to different degrees of
hoarseness, dysphonia, and even aphonia. In singers and public speakers
the disease interferes sometimes with professional vocal efforts only,
ordinary conversation not being affected. The voice is best, sometimes
worst, after a night's rest, and in either instance changes after
moderate use for worse or better as the case may be; but long-continued
exercise is always harmful. The voice is comparatively easily fatigued,
and then the vocal organ becomes positively painful.

In addition to the two chief and constant symptoms there are others
that may or may not be present, and which sometimes assume even greater
prominence than the modification of the voice. Thus, secretion, which
in most cases is very slight, glassy grayish, and viscid, is
occasionally very abundant, yellowish, or darkish, or more rarely still
mixed with streaks of blood and in clumps, though not sticky or dried
into scabs, and is sometimes so fetid that the patient's breath is
exceedingly malodorous. Cough, which in most cases is either absent or
comparatively trifling, barking, or hacking, occasionally is the most
troublesome of all the symptoms. Dysphagia is sometimes present even in
simple or mild cases. In severer cases, in the later stages, especially
in syphilitic and phthisical chronic laryngitis, swallowing becomes
painful and difficult, or even impossible. Dyspnoea occurs only from
accumulations of phlegm in the larynx, and is then lessened after
expectoration, or it may depend upon the diminished lumen of the
laryngeal cavity on account of thickening of the walls, as it is
especially apt to do in subglottic chronic laryngitis, or on account of
so-called polypoid hypertrophies in simple cases, gummata or
cicatricial tissue in specific cases, etc. Dyspnoea may become so
urgent as to require tracheotomy.

PATHOLOGY AND MORBID ANATOMY.--In catarrhal chronic laryngitis there is
congestion of the mucous membrane, dilatation of the blood-vessels, and
altered secretion. The mucous membrane becomes, as a rule,
hypertrophied, tougher, and more firmly connected with the subjacent
tissues. Laryngeal venous congestion (so-called phlebectasis laryngea)
is occasionally, though rather rarely, met with; and still more rare is
a hemorrhage from the surcharged vessels in chronic cases. In granular
or glandular chronic laryngitis--_i.e._ when the muciparous glands are
prominently involved in the inflammatory process--they form elevations,
making the surface uneven, and the tissues become tenser and more
compact. When the submucous connective tissue takes much part in the
process the hypertrophy is still greater, and not only may the lumen of
the laryngeal cavity become greatly diminished, but projections of
various lengths (the so-called cellular polypi and papillary
excrescences) are apt to occur. The objective term tuberosa is
sometimes added to laryngitis or to the designation for inflammation of
a portion of the larynx; as, for example, that of the vocal bands--viz.
chorditis tuberosa, when small whitish, tumor-like elevations occur.
These, especially on the vocal bands, where they have been described by
Tuerck, Elsberg, Cohen, and others, are also called trachomata. In
cases to which the name muscular chronic laryngitis is given the
muscular tissue has been found prominently hypertrophied. Moura
Bourillou has recorded a case in which the striated fibres of the
posterior crico-arytenoid muscle were converted into fibrous tissue. In
many of {123} the common cases of catarrhal chronic laryngitis the
alteration of the voice depends upon paralysis of the
muscles--especially the thyroid arytenoid and the arytenoid--directly
caused by the transmitted inflammation and by thickening of the
overlying mucous membrane. In fetid chronic laryngitis there is usually
found excoriation of the mucous membrane, and atrophy. That
erosions--_i.e._ superficial ulcerations extending no deeper than the
epithelial layer--frequently occur in the course of catarrh is admitted
by everybody, but much unnecessary discussion has been indulged in
concerning the question whether deeper ulcerations of the mucous
membrane can ever take place under these circumstances. It has been
insisted upon that catarrhal ulcerations never occur. This is a
mistake, but it is true that catarrhal ulceration is rare unless the
patient is greatly debilitated or cachectic. Ulcerative chronic
laryngitis in the majority of cases depends upon some cachexia--_i.e._
tuberculosis, syphilis, lupus, lepra, etc.

Tuberculous chronic laryngitis--laryngeal phthisis proper--frequently
accompanies pulmonary consumption. Usually it follows, but occasionally
precedes, the latter. Unquestionably, it also occurs, though rarely,
without any disease in the lungs. Anæmia of the laryngeal mucous
membrane is present from the first, and usually persists throughout.
There is a low form of inflammation, swelling of the tissue, and then
ulceration, the ulcers being at first small, and afterward coalescing
to form larger ones. Much destruction may take place, and more or less
oedema is always present. Paralysis of some of the interior laryngeal
muscles may also occur, depending alike upon anæmia and oedematous
infiltration of the muscular substance, or upon compression of the
nerve-tracts by enlarged lymphatic glands (most frequently on the right
side) or upon involvement of the nerves--pleuritic adhesions,
tuberculous deposits, etc.

Syphilitic chronic laryngitis is a local manifestation occasionally of
hereditary, but usually of acquired, syphilis. It may vary from a
slight erythematous condition of the mucous membrane to intense
inflammatory thickening or destructive ulceration, may be accompanied
by laryngeal oedema and pericarditis, and may lead to dangerous
adhesions, cicatrizations, and stenosis. The chronic laryngitis
occurring in lupus and lepra and in malignant diseases of the larynx
partakes of the character of these processes, and is accompanied by
their peculiar thickenings, tuberosities, granulations, and
ulcerations.

DIAGNOSIS.--Chronic alteration of voice, local morbid sensation, and
other symptoms mentioned may lead us to suspect the presence of chronic
laryngitis, but are insufficient for diagnosis without mirror
examination. The diagnosis can be positively made only by means of the
laryngoscope, and even by this means requires care. It is of the utmost
importance that the physician make himself perfectly familiar with the
appearance of the healthy larynx by the particular illumination he uses
for examining patients.

A very able laryngoscopist, Carl Michel of Cologne, confesses[6] that
he has many times diagnosed chronic laryngitis when none existed, and
explains that with inadequate illumination the contours of the small
vessels run into one another and make the whole surface which they
traverse appear red. In simple chronic laryngitis the redness has a
somewhat livid look; in syphilitic chronic laryngitis it is darker and
more angry-looking; in phthisical cases it is duller, even though the
mucous membrane be congested, while usually it is pale. In both the
latter diseases the swelling is greater, the natural contour of the
parts more changed, and destruction more imminent than in the simple
chronic laryngitis. When oedema is present there is a peculiar
transparent or translucent appearance. In subglottic chronic
laryngitis, especially when {124} much hypertrophy has already taken
place, the color is often quite light grayish instead of red.

[Footnote 6: _Practische Beiträge zur Behandlung der Krankheiten des
Mundrachenhöhle und des Kehlkoffes_ (Leipzig, 1880).]

Phlegm found in the larynx may have come from the bronchial tubes or
the trachea; when it is cleared away by cough or otherwise, the larynx
may prove to be unaffected. In all cases of suspected secondary chronic
laryngitis, phthisical, syphilitic, etc., the state of the lungs and
whole respiratory tract, as well as the general health in every
respect, hereditary tendencies, and past diseases, must be carefully
inquired into.

PROGNOSIS.--The prognosis of chronic laryngitis is good as to life
except in broken-down constitutions, neglected exacerbations, and grave
underlying affections; but, even with these exceptions, it can be said
to be favorable as to cure only with expert local treatment and if no
severer tissue-alterations, usually hypertrophic, have as yet taken
place. If the latter have taken place--especially if the submucous
tissues are prominently involved--the organ can seldom be restored to
perfect integrity. For persons in ordinary vocations and situations in
life the recovery that can generally be secured may be entirely
satisfactory, but more exacting demands on the speaking and singing
voice require special measures, including hygienic precautions, to be
carried out carefully, and sometimes to be long continued.


BY J. SOLIS COHEN, M.D.

TREATMENT.--Whatever the grade or stage of a chronic laryngitis, the
constitutional condition or proclivity of the patient always requires
suitable hygienic, dietetic, and therapeutic management. The repair of
regional or local morbid conditions may often be confidently entrusted
to such constitutional measures; and it is only when these morbid
conditions resist the influence of systemic treatment, or are of some
special character obviously insusceptible to such influence, that
topical medication or actual surgical procedure becomes requisite in
addition. The accessibility of the interior of the larynx to
instrumental manipulation under laryngoscopic guidance offers great
temptations for topical interference. The result is, that the diseased
larynx is sometimes submitted to unnecessary, and even injurious,
direct attack at the hands of a dexterous manipulator untrained in
general practice, and consequently ignorant of the beneficial influence
of purely constitutional measures upon many local morbid conditions.
While it is highly proper, therefore, to utter a few words of caution,
it is equally proper to assert that many local conditions are entirely
beyond the control of systemic measures, and require topical treatment.

Constitutional Treatment.--Simple or catarrhal chronic laryngitis,
unassociated with special diathesis, is often admirably influenced by
the prolonged administration of some preparation of cubeb; the
oleoresin being preferred by the writer in doses of from fifteen to
twenty-five minims for the adult, three times a day on crushed sugar.
This drug being eliminated in part by the bronchial tract, it seems
especially adapted to exert upon chronic inflammatory conditions of the
aërial mucous membrane that healing process which it is known to exert
on mucous membrane elsewhere. Among other useful constitutional
remedies from which similar service can be expected may be enumerated
compound tincture of benzoin in doses of from thirty to sixty minims
for the adult, three or more times daily; fermented infusion of tar or
tar beer, several ounces daily; and petroleum mass, one to two grains
for the adult, three or four times daily, with pulverized extract of
glycyrrhiza in pill or capsule. In cases with deficient secretion
ammonium chloride is indicated. In cases associated with impaired
digestion, with excess of acidity, the {125} prolonged use of alkaline
mineral waters is advisable; preferably, if convenient, at their
sources. In cases associated with chronic diarrhoea the mineral acids
are indicated. Cod-liver oil, hydrated chloride of calcium, and
preparations of iodine and of arsenic are useful in patients of the
scrofulous diathesis. Iodoform, one grain for the adult, rubbed up with
glucose or some other excipient, in pill or capsule, three times a day,
is often useful in patients with the tuberculous diathesis. Specific
remedies are required for syphilis. In like manner, any constitutional
abnormality is to be systematically attacked.

The functions of skin, kidneys, and intestine are to be maintained as
nearly normal as may be, or even a little in excessive action from time
to time for derivative purposes. Abstinence is to be enjoined from all
exposures or indulgences deleterious to the parts diseased; with as
sparing a use of the voice as is compatible with ordinary domestic or
social demands, and absolute rest for prolonged periods of days at a
time whenever unusual demands have resulted in exacerbating the malady.
Under such treatment many cases of simple catarrhal or glandular
chronic laryngitis may get well, as has been intimated, without any
special local measures.

Topical Treatment.--The difficulty of impressing patients with the
necessity of submitting to these hygienic measures and to dietetic
restrictions, and for avoidance of occupations or habits which favor or
maintain the condition of chronic inflammation, renders topical
treatment necessary in many instances. Direct instrumental medication
requires the personal attention of the medical attendant. Medication by
inhalation or insufflation may be entrusted to the patient or the nurse
in most instances. In instituting a course of topical treatment several
things must be taken into consideration, such as the condition of
hyperæsthesia, hypersecretion, insufficient secretion, congestion,
hemorrhagic infiltration, hemorrhage, hypertrophy of tissue or
tissue-elements, erosion, fissure, ulceration, and excessive
granulation. The first three of these furnish the clue to the nature of
the home-treatment, the remainder to that required at the hands of the
physician. The home-treatment is to be directed to keeping the parts
clean and comfortable; the manipulation of the physician is to be
directed toward overcoming special pathological conditions.

Should secretion be defective, alkaline sprays inhaled at regular
intervals, for a few minutes at a time, tend to augment secretion and
to facilitate the detachment of adherent mucus. For the purpose choice
may be made of the following drugs in the proportion of about five
grains to the ounce for the adult, dissolved in distilled water or
tar-water, with the addition of a sedative when the parts are
hyperæsthetic, or an opiate when they are painful: ammonium chloride,
sodium borate, sodium bicarbonate, sodium chloride, sodium chlorate,
sodium iodide, potassium iodide, potassium chloride. The spray should
be propelled by means of compressed air, with what is known as the
hand-ball atomizer, in preference to steam, the effect of which is too
relaxing in most instances. A few drops of some aromatic or balsamic
product will render the spray more agreeable in many instances. Should
these agents fail, pyrethrum or jaborandi may be found more
serviceable, in the proportion of from one to five minims of the fluid
extract to the ounce of water.

Should secretion be excessive, astringents are indicated; and choice
may be made from alum, five grains to the ounce of rose-water; tannic
acid, two or three grains; zinc sulphate or zinc sulphocarbolate, two
grains; lead acetate, two grains; ferric chloride, one grain; and
silver nitrate, half a grain to the ounce. Personal supervision of the
initial inhalations is requisite to ensure proper use of the spray.
Whether the medicament is to be propelled directly into the larynx by
means of a tube with a vertical tip to be passed beyond the tongue, or
to be inhaled by efforts of inspiration from spray projected
horizontally, will depend upon the skill of the individual using it.
Hard-rubber {126} spray-producers are furnished with series of tips, so
that either method may be employed. When the horizontal tip is used,
the instrument should be held some distance from the mouth, so that the
spray may be deflected into the larynx by the act of inspiration. When
the tube is placed within the mouth most of the spray becomes condensed
upon the pharynx, and very little can be drawn down into the larynx. As
metallic tubes are liable to become reduced by certain
remedies--ammonium chloride, for instance--tubes of glass or of hard
rubber are to be preferred.

Should a steam apparatus be employed, the patient should remain housed
for half an hour after inhalation, except in very warm weather. In
cases of hyperæsthetic mucous membrane the home inhalation of volatile
remedies daily is often useful. Compound tincture of benzoin,
camphorated tincture of opium, oil of pine, oil of turpentine,
terebene, eucalyptol, creasote, carbolic acid, may be inhaled from a
bottle containing hot water or from a special inhaler, a few drops of
chloroform being advantageously added when there is a good deal of
irritative cough. A few drops of the more pungent volatile substances,
such as terebene, eucalyptol, and creasote, may be dropped on the
sponge supplied with the perforated zinc respirator of Yeo of London,
and the apparatus be worn for an hour or longer continuously. In cases
with excessive secretion and in syphilis, ethyl iodide is indicated as
a remedy appropriately administered by this method. When the parts are
very irritable, a respirator of this kind or some similar contrivance,
or a fold or two of woollen or silk gauze worn in front of the mouth
and nose while in the open air, will often protect the tissues from too
cool an atmosphere, and enable the patient to bear exposure with
comfort.

Topical treatment of a more decided character being required, the
physician usually chooses between powder and solution. Powders are
usually propelled by a puff of air through a properly curved tube,
whether from a rubber ball, a reservoir of compressed air, or the
mouth. The mouth allows the most delicate and accurate application, but
the mouthpiece should be protected by a valve from receiving a return
current when the patient coughs. Solutions may be applied by means of
pipette, syringe, brush, cotton wad, or sponge, according to
indications. A fragment of sponge securely fastened to a properly-bent
rod or pair of forceps is the safest and most effectual material for
positive contact against a limited surface, and a brush the best for
painting larger surfaces. The use of the cotton wad involves a slight
risk of leaving a detached shred of fibre in the larynx, but renders
the manipulation less unpleasant to the patient than the use of the
sponge, and is less irritating to the mucous membrane. Spasm of the
larynx is usually excited the first time that a medicinal application
is made within it, and even death by suffocation has followed the
incautious use of powerful agents. Hence strong solutions should not be
used until the tolerance of the parts has been sufficiently tested by
weak or innocuous ones. The remedies which have been employed topically
for intra-laryngeal medication seem to include every available
medicinal agent that could be mentioned, from rose-water to the
incandescent cautery. The list of really useful ones is not very long.
Those upon which the most reliance is placed by the writer comprise
tannic acid (a saturated glycerite), zinc sulphate (thirty grains to
the ounce of rose-water), and silver nitrate (forty to sixty grains to
the ounce) in obstinate and protracted cases of simple chronic
laryngitis; iodine and carbolic acid, singly or in combination (one
grain or more to the ounce of glycerin), and chinoline tartrate or
salicylate (five or more grains to the ounce), in cases attended with
infiltration; iodoform (finely pulverized or in recent saturation in
sulphuric ether) in ulcerative or proliferative tuberculosis; and
iodoform and acid solution of mercuric nitrate (one part to ten or
twelve of water) in progressive ulcerative syphilis resisting
appropriate constitutional treatment. Other {127} astringents in the
simple varieties; resorcin in the glandular, hypertrophic, polypoid,
and tuberculous varieties; chromic acid and incandescent metal in the
circumscribed hypertrophic and in the polypoid varieties; and zinc
chloride and copper sulphate in the syphilitic varieties,--proffer
additional resources. These applications are to be made at intervals of
one day or more, according to results. Hyperæsthesia and pain, whether
of the larynx or of parts adjacent, can usually be subdued by the local
anæsthetic effect of solutions of erythroxyline hydrochloride (2 per
cent. or stronger) applied at intervals of a few hours, or even by the
fluid extract or a strong aqueous infusion of the erythroxylon-leaves.
Before the anæsthetic effect of this drug was known, morphine powder
(one-eighth to one-fourth of a grain, alone or associated with tannin
or with iodoform) or aqueous solutions of morphine salts and of aconite
were employed to relieve pain and obtund sensitiveness. The oleate of
morphine (2 to 4 per cent. solution) and the oleate of aconitine (2 per
cent. solution) are similarly useful. Morphine, by its constitutional
influence, is preferable to erythroxyline in some instances, though
less prompt in its effects. Where ulcerative processes at the top of
the larynx or thereabouts entail odynphagia, these preparations should
be used before administering nourishment. The use of erythroxylon
products may be entrusted to the nurse or to the patient with
comparative safety. Morphine and aconite should be applied only by a
medical attendant or an exceptionally skilled nurse. Before any
medicinal curative or reparative agent is applied the parts should be
thoroughly cleansed of suppurative and secretory products. This may be
done with sprays of alkaline solutions--five or more grains of sodium
borate or bicarbonate, for example--dissolved in pure water, in
tar-water, or in an emulsion of coal tar. An excellent agent,
especially in the presence of pus, is hydrogen dioxide, usually
furnished in a 10-volume solution which should be diluted with two or
more parts of distilled water. It is likewise disinfectant and gently
stimulant to mucous membrane. The manipulations by the physician
preparatory and medicatory should be performed laryngoscopically,
otherwise the entire procedure must be haphazard.

Neoplasmata and fungous growths may require removal should they
interfere with respiration. In the presence of stricture, surgical
interference by tracheotomy may become requisite. Elsberg, according to
the testimony of his assistant, Schweig, seems to have been
particularly favorable to the performance of this operation in
obstinate cases of ulcerative laryngitis of whatever character, and
even in protracted non-ulcerative cases, for the purpose of securing
physiological rest to the parts, although the procedure might not be
indicated to relieve any embarrassment in respiration. The writer's
experience in tracheotomy as a factor in producing rest has not been
favorable, such a result being usually defeated by the cough so
frequently following a tracheotomy, no matter how well-adjusted a tube
may have been inserted. His recommendation, therefore, is limited to
cases of embarrassment to respiration due to stricture or constriction
unamenable to intra-laryngeal interference.


Morbid Growths of the Larynx.

DEFINITION.--Neoplastic formations, benign and malign, in the interior
of the larynx, in its cartilaginous framework, in its
investment-tissues, or upon the exterior of the organ.

ETIOLOGY.--Inflammation of the mucous membrane, local irritation or
injury, ulceration, cell-proliferation, and excessive granulation seem
to be the exciting causes of benign neoplasms. They follow on
laryngitis, whether catarrhal, syphilitic, tuberculous, exanthematic,
toxic, or traumatic. They {128} are quite common, so to speak, several
thousands of cases being on record, and as many or more probably being
unrecorded. Heredity does not seem to play any special part in their
production. They are occasionally congenital, and may be developed at
any age; but they are encountered the most frequently in subjects
between the ages of thirty and sixty years, probably because of the
greater exposure to laryngitis attending the activity incidental to the
prime of life. Males are affected far more frequently than females,
probably on account of greater exposure to sources of laryngitis.
Benign growths are sometimes followed by malign growths in recurrence,
and are sometimes converted into malignity by irritation, whether
physiological, mechanical, or instrumental. Malign growths are
attributed to cold, chronic laryngitis, and traumatism as the initial
exciting causes. Butlin suggests a cryptogamic origin. They are far
more common in males than in females, and occur chiefly between the
ages of twenty-five and seventy, but they have been noted as occurring
exceptionally much later, and even as early as the first year.

PATHOLOGY AND MORBID ANATOMY.--By far the greater number of laryngeal
morbid growths belong histologically to the category of benign
neoplasms, but the important location they occupy often renders them
clinically malign. By far the greater number of benign growths are
papillomas, perhaps fully two-thirds, although Elsberg has reported
that but 163 instances were papillomas out of 310 seen in his own
practice.[7] This has been an exceptional experience. Then we have
fibromas, myxomas, adenomas, lymphomas, angeiomas, cystomas,
ecchondromas, lipomas, and composite neoplasms. Laryngeal morbid
growths, too, occasionally undergo the fatty, colloid, or amyloid
degenerations. Papillomas are frequently multiple, and most frequently
sessile, but the other benign neoplasms are most frequently single and
are more often pedunculated. All this class of morbid growths affect
the anterior half of the larynx more than the posterior. They are most
frequent on the vocal bands or very near to them, although they may
occupy any portion of the larynx. They vary in size from the smallest
protuberance to a bulk sufficient to block up the cavity of the larynx
and even project above it. The dimensions of the greater number of
papillomas vary from the size of a pea to that of a small mulberry.
Other benign neoplasms rarely reach the bulk attained by papillomas.

[Footnote 7: _Archives of Laryngology_, p. 1, New York, 1880.]

Malign growths are far less common than benign ones. They comprise both
sarcomas and carcinomas. Sarcomas occur in the varieties of
spindle-celled, round-celled, giant-celled, mixed-celled, fibrosarcoma,
lymphosarcoma, and myxosarcoma. Some attain only the size of small
beans, and few exceed the size of a pigeon's egg. The majority of them
are primary growths. Most of them originate in the interior of the
larynx, whence they may extend by contiguous infiltration, even
penetrating the laryngeal walls. The vocal band and the ventricular
band are the most frequent seat. The epiglottis is a common seat. These
growths appear either in irregular, smooth, spheroid masses, or
nodulated, mamillated, and dendritic. They are much the more common in
males, and occur chiefly in subjects between the ages of twenty-five
and fifty. Their growth is slow for a year or more, and then becomes
more rapid.

Carcinoma is much more common than sarcoma. It is most frequently
primary, and primarily limited to the larynx, but occurs likewise in
extension of carcinoma of the tongue, palate, pharynx, oesophagus, or
thyroid gland. It rarely extends to the oesophagus or penetrates the
laryngeal walls.

Squamous-celled carcinoma or epithelioma is the commonest variety,
large spheroidal-celled or encephaloid being much less frequent, and
small spheroidal-celled and cylindrical-celled occurring still more
rarely. Intrinsic {129} laryngeal carcinoma is usually unilateral at
first, and most frequently in the left side. Its most frequent seat is
at the vocal band. It rarely occurs below this point, and when it does,
as in the five cases analyzed by Butlin,[8] it seems to be at some
point just beneath. Extrinsic laryngeal carcinoma usually begins in the
epiglottis, and sometimes occupies that structure only. It may begin in
a cicatrix in the skin.[9] Carcinoma is the more common in males,
chiefly in subjects between the ages of fifty and seventy. It has
occurred within the first year, at three years, and as late as at
eighty-three years. Carcinoma is liable to extend by infiltration of
tissue and destroy all the contiguous and overlying tissues, so that it
may extend into the pharynx or even externally; the large
spheroidal-celled variety presenting the most frequently progressive
ulceration into contiguous tissue, and the squamous-celled, intrinsic
ulceration. Hemorrhage is frequent. Perichondritis, abscess, necrosis,
and fistula take place in old cases.

[Footnote 8: _On Malignant Disease of the Larynx_, p. 36, London,
1883.]

[Footnote 9: Cohen, _Transactions American Laryngological Association_,
p. 113, 1883.]

SYMPTOMATOLOGY.--Small growths in localities where they neither provoke
cough nor interfere with voice or respiration may run their course for
a long time without giving rise to any symptoms at all. Growths of
larger size, pedunculated growths, and growths located upon important
structures give rise to interference with voice, respiration, or
deglutition as may be--to cough, and even to pain. Dysphonia is due to
mechanical interference with vibrations of the edges of the vocal
bands; aphonia, to mechanical interference with their approximation;
diphthonia, to mechanical interference at an acoustic node. These
manifestations may be permanent or intermittent. Dysphonia is one of
the earliest symptoms of carcinoma, and is usually continuous for a
number of months before any other indication. Aphonia in carcinoma is
often due to nerve-lesion. Dyspnoea is due to some considerable
mechanical occlusion of the respiratory tract, whether by the growth
itself or in consequence of oedema or of intercurrent tumefaction. It
is inspiratory rather than expiratory, and subject to aggravation at
night. As with the dysphonia, it varies with the size, location, and
mobility of the growth and the position of the head and neck. It may be
intermittent or permanent; be slight or severe; or it may terminate in
apnoea by spasm, by mechanical occlusion of the calibre of the larynx,
or by impaction of the growth at the chink of the glottis. Marked
encroachment on the breathing-space is not accompanied with as marked
dyspnoea as in acute processes, the parts seeming to acquire tolerance
during the slow growth of neoplasms.

Dysphagia is due to a growth at the top of the larynx or on some
portion of its pharyngeal surface. It is quite frequent in carcinoma,
preceding dysphonia in the extrinsic varieties. It may be associated
with regurgitation of food, drink, or saliva into the larynx,
provocative of paroxysms of suffocation. Cough is due to growths which
project from the vocal bands or press upon them, or to hemorrhage or
accumulation of secretory or suppurative products. Hemorrhage, cough,
and expectoration of bloody and fetid masses are indicative of
carcinoma. Pain is usually due to intercurrent conditions. Aches in the
part and sensations of the presence of a foreign substance are more
frequent. Intense pain is exceptional in benign neoplasmata; it is
often an early symptom in carcinoma, in which it is apt to radiate
toward the ears and along the neck. Epileptic seizures and vertigo are
sometimes occasioned by reflex influence. Exceptionally, large growths
may produce change in the external configuration of the larynx. The
general health is not much involved in benign growths, unless they
interfere seriously with important physiological functions. Impaired
health is far less manifest in sarcoma than in carcinoma. Emaciation,
pyresis, and marasmus eventually occur as constitutional manifestations
of malign growths.

{130} DIAGNOSIS.--Laryngoscopic inspection usually reveals the growth
and furnishes the best means of diagnosis. Intra-ventricular and
subglottic growths may elude detection. Palpation is sometimes
available, especially with children. Palpation with probes under
laryngoscopic inspection is sometimes requisite to determine the
mobility of a growth, its form and seat of attachment, and even its
size. It seems, too, to discriminate a neoplasm from an eversion of a
ventricle. While the histological character of a growth cannot be
definitively decided by laryngoscopic inspection, the varieties present
a series of characteristics sufficiently pronounced for approximative
discrimination. Papillomata are often multiple, usually sessile, and
usually racemose or dendritic. Some are white, but the majority are
red, and the tinge varies from one extreme of the tint to the other.
Some are as small as the smallest seeds; most of them have a bulk
varying from that of a pea to that of a berry; some of them are so
extensive as to appear to fill the larynx or even project above its
borders. They are far the most frequent in the anterior portion of the
larynx, and are often located upon a vocal band. Fibromata are most
frequently single, smooth and pedunculated, and red. Some are white or
gray. Some are vascular. When fully developed they vary in size from
small peas to large nuts. They are more frequent upon a vocal band.
Their development is slower than that of papillomata. Myxomata are
usually single, smooth, pyriform, and pedunculated. They are usually
red or reddish. Their ultimate size varies from that of grains of rice
to that of Lima beans. They are most frequent at the commissure of the
vocal bands. Angeiomata are usually single, reddish or bluish, vary in
size from that of small peas to that of berries, and are most frequent
on the vocal bands. Cystomata are usually globular, sessile,
translucent, and white or red. They are most frequent in a ventricle or
on the epiglottis. Their size varies from that of hempseed to that of
peas. Ecchondromata are usually developed in the posterior portion of
the larynx. Other benign growths are very rare, and do not seem to
present special features for recognition by laryngoscopic inspection.
Sarcomata are usually present as sessile, hard, well-circumscribed
growths, smooth or lobulated. Some are dendritic on the surface, but
not to the extent noticed in papillomata, and their location at the
posterior portion of the larynx would suggest their true character, for
papillomata rarely occupy this position except in tuberculosis.
Superficial ulceration occurs in some cases, but is not extensive.
There is no peculiarity in the color of the mucous membrane, which may
be paler or redder than is normal. The lymphatic glands are not
involved.[10] Carcinomata present first as diffuse tumefactions in
circumscribed localities, gradually undergoing transformation into
well-formed growths, then nodulation, and then ulceration. Meanwhile,
especially in extrinsic varieties, the submaxillary and the cervical
lymphatic glands become successively involved and tumefied.
Squamous-celled carcinoma becomes pale, wrinkled, and nodulated, and
sometimes dendritic. Large spheroidal-celled carcinoma becomes
nodulated, dark, and irregularly vascular, and finally ulcerated,
perhaps at a number of points. In the ulcerative stage of carcinoma of
the epiglottis and of the interior of the larynx discrimination is
requisite from syphilis and from tuberculosis. In all cases of doubt as
to malignancy, laryngoscopic inspection should be supplemented by
microscopic examination of fragments detached for the purpose. The
early detection of sarcoma may lead to surgical measures competent to
save life--a remark applicable, perhaps, in a far more limited degree
to intrinsic carcinoma.

[Footnote 10: Butlin, _op. cit._, p. 14.]

PROGNOSIS.--The prognosis is usually good in benign growths submitted
to proper surgical treatment. Left to themselves or treated
medicinally, the prognosis is bad both as to function and to life. Such
growths are occasionally expectorated after detachment during cough or
emesis. Some {131} occasionally undergo spontaneous absorption. Some
remain without change for years. Most of them enlarge and compromise
life as well as function. Recurrence occasionally follows thorough
removal, and this recurrence is occasionally malign in character.
Repullulation frequently follows incomplete removal. The prognosis is
favorable in sarcomata, provided thorough eradication can be
accomplished by surgical procedure. Incomplete removal is followed by
repullulation or recurrence. Unsubmitted to operation, sarcoma will
destroy life either mechanically by apnoea or physiologically by
asthenia.

The prognosis is unfavorable in carcinoma. Recurrence takes place as
the rule despite the best devised resources of surgery. Intrinsic
carcinoma offers some hope of success to the surgeon; extrinsic
carcinoma, little if any. Life is shortest in the large
spheroidal-celled, and longest in the small spheroidal-celled variety,
other conditions being equal. Death may take place by apnoea or
asthenia, as in sarcoma, or by hemorrhage, collapse, or pyæmia.
Submitted to tracheotomy at the proper moment in cases in which death
is threatened by occlusive dyspnoea, life is prolonged and suffering
mitigated. The fresh lease of life is longest in the squamous-celled
variety.

TREATMENT.--The essential treatment is surgical, and to surgical works
the reader must be referred for details. Suffice it to say that when a
benign growth is small and does not embarrass respiration, it need not
be attacked at all, unless its interference with the voice deprives the
patient of his means of livelihood. The majority of benign growths are
accessible to instruments passed through the mouth. Some require
external incision into the larynx, whether partial or complete. The
intra-laryngeal procedures in vogue include cauterization, both
chemical and by incandescence, incision, abscission, crushing,
brushing, scraping, and evulsion. According to the character and
location of the growth, direct access from the exterior is practised by
infra-hyoid pharyngotomy, by partial or complete thyroid laryngotomy,
mesochondric laryngotomy, cricoid laryngotomy, complete laryngotomy,
laryngo-tracheotomy, or tracheotomy, as may be indicated.

The thorough eradication of sarcomata usually requires a direct access
by section of the thyroid cartilage or even of the entire larynx. This
procedure failing or appearing insufficient, partial or even complete
laryngectomy may be necessary. Temporizing is of no avail.

The treatment of carcinoma is palliative, unless it be decided
advisable to attempt eradication, which may offer some chance of
success in intrinsic carcinoma still confined to the larynx.
Laryngectomy may be unilateral in some instances, and must be bilateral
in others. Unilateral laryngectomy is the more hopeful. Eradication
proffers no hope in cases of extrinsic carcinoma in which the growth
has passed the boundaries of the larynx. After recovery from the
laryngectomy an artificial appliance may be adjusted to the parts for
the purpose of supplying a mechanical method of producing sound in the
larynx for speaking purposes. Should no radical procedures be
instituted, treatment is relegated to general principles, with
prophylactic performance of tracheotomy in the presence of dangerous
occlusion of the larynx. The voice should be used but little. All
sources of laryngitis should be avoided. Ergot or hamamelis may be
given to restrain hemorrhage, and morphine to relieve pain and secure
sleep. Sprays can be used to keep the parts free from morbid products.
Erythroxyline may be applied to produce local anæsthesia as required.
Semi-detached portions of growth may be removed from time to time.
Nourishment may be given by the bowel when necessary, and so on as in
other diseases of the larynx in which the functions of respiration and
deglutition are seriously impaired. Medicinally, arsenic may be given
in the early stages, as that drug is conceded to possess some slight
retarding influence on the growth of carcinoma.


{132} Lupus of the Larynx.

Lupus is rare in the larynx. It usually occupies the structures above
the vocal bands. It is most frequent in females, and usually associated
with cutaneous lupus.

ETIOLOGY.--Scrofulosis and syphilis seem to be the predisposing causes.
Climate may have some influence. The reason of the special proclivity
of the female is undetermined. Of 9 reported cases, records of which
are before the writer, 8 were in females.

PATHOLOGY AND MORBID ANATOMY.--Laryngeal lupus is usually an extension
of the disease from the upper lip or the nose, extending along the
nasal passages, pharynx, and palate. Destructive ulceration takes
place, with irregular cicatrization and the formation of hard nodules
of hyperplastic tissue of irregular conformation, varying from the size
of hempseeds to that of small peas, similar to the cutaneous buccal and
pharyngeal nodules.

SYMPTOMS.--These include dysphonia, dyspnoea, dysphagia, and cough.
Pain is exceptional.

DIAGNOSIS.--Laryngoscopic inspection reveals the characteristic
nodulation, the nature of which is inferred from the coexistence of
external lupus. The disease may be confounded with lepra, syphilis,
tuberculosis, or carcinoma. Discrimination from syphilis is the most
difficult, and is predicated chiefly on its slow progress and on the
absence of constitutional manifestations.

PROGNOSIS.--This is unfavorable. The reported cures seem to have
occurred only under the influence of antisyphilitic treatment.

TREATMENT.--The prolonged use of cod-liver oil and of potassium iodide
seems to be more beneficial than any other systemic treatment.
Destruction of the nodules and ulcerated tissues is indicated when the
diseased structures are sufficiently circumscribed and accessible. This
may be done with the sharp spoon or with the electric cautery. Silver
nitrate and iodine have been lauded as topical remedies.


Lepra of the Larynx.

Lepra is rare in the larynx.

ETIOLOGY.--Its cause seems to be climatic. In Europe it is most
frequent in Norway and Sweden, and in America in Cuba and the West
Indies.

PATHOLOGY AND MORBID ANATOMY.--It is always associated with cutaneous
lepra, and usually with lepra of the nasal passages and the pharynx.
According to Schroetter's observations, laryngeal lepra occurs as small
connective-tissue nodules on the epiglottis or in the interior of the
larynx, or as uniform thickenings, general or circumscribed. These may
lead to stricture. Extensive ulceration may ensue.

SYMPTOMS.--Dysphonia, aphonia, dyspnoea, cough, and local anæsthesia
are the main symptoms. Pain is infrequent.

DIAGNOSIS.--This depends upon the external manifestations of lepra and
the laryngoscopic detection of the characteristic thickenings and
nodulations.

PROGNOSIS.--This is unfavorable.

TREATMENT.--This must be conducted on general principles. Elsberg
commended iodoform topically and gurgun oil internally.




{133}

DISEASES OF THE TRACHEA.

BY LOUIS ELSBERG, A.M., M.D.


Disease originating in or confined to the trachea is rare. It hardly
ever follows tracheotomy unless the shape of the canula or its relation
to the windpipe be improper; the normal tracheal mucous membrane
probably resists cadaveric disintegration longer than any other mucous
membrane of the body. But morbid processes of the larynx often extend
downward, and those of the bronchial tubes still more frequently
upward, so that the trachea is found affected in connection with both.
Indeed, in what is ordinarily simply called bronchitis (see article on
BRONCHITIS) the windpipe is seldom free from the inflammatory
condition.

We shall here consider Inflammation, Ulceration, Morbid Growths,
Stenosis, and Dilatation (hernia, fistula). Tracheotomy may have to be
performed in any of these diseases to prevent impending suffocation,
and in some to gain access to the part for further treatment. (See
article on TRACHEOTOMY.)


INFLAMMATION.

Tracheitis is either simple or complicated, and acute or chronic.


Simple Tracheitis.

DEFINITION.--Inflammation of the windpipe limited to the mucous
membrane.

SYNONYMS.--Catarrhal tracheitis, Tracheal catarrh.

Its ETIOLOGY may be gathered from the corresponding sections on
Catarrhal Laryngitis and Bronchitis.

SYMPTOMATOLOGY.--In acute catarrhal tracheitis local irritation is
complained of, varying according to the severity of the case from a
mere tickling sensation to soreness and pain. This morbid sensation is
increased by pressure on the part, and with it there is cough and
expectoration--the former either brassy and hacking, or paroxysmal and
violent; the latter at first scanty, but very soon more copious than
when the larynx alone is affected, although much less so than when the
inflammation involves the bronchial tubes at the same time. The
sero-mucous secretion gradually becomes muco-purulent or even purulent.
When inflammation is confined to the trachea there is no alteration of
the voice, and, except in children, in whom the calibre of the windpipe
is proportionately small, usually no or only very slight dyspnoea. In
mild cases there are no constitutional disturbances. Severe cases are
accompanied by {134} the febrile symptoms of a bad cold. The disease
runs its course in from a few days to a week or two.

Uncured or too frequently repeated attacks of acute catarrh of the
windpipe lead to chronic tracheitis, occasionally with considerable
hypertrophy of the mucous membrane. In mild cases the cough and
expectoration are less than in the acute disease, but persist, with
exacerbations in cold, damp weather; in other cases the cough is more
frequent, and the expectoration either thick, glutinous, and scanty, or
else thin, frothy, or glairy, semi-transparent, and abundant. The
separation by forcible paroxysmal coughing of accumulated adherent
tough secretion from the tracheal mucous membrane has been observed to
cause not only slight dyspnoea, but even the dangerous suffocating
attacks of foreign bodies in the larynx. In color the sputa vary from
gray to green and yellow; occasionally they are streaked with blood;
sometimes they are without taste or odor; sometimes they are nauseous
and fetid. Frequently patients with chronic tracheitis complain of "a
sort of tightness at the root of the neck." In some cases a sense of
dryness in the region of the trachea is the principal or the only
symptom complained of, and this may alternate with, or even actually
coexist with, occasional hypersecretion of tracheal or bronchial mucus.

In chronic bronchitis and senile pulmonary emphysema mucorrhrea and
cough usually depend to some extent upon the chronic tracheitis that is
present.

PATHOLOGY AND MORBID ANATOMY.--The pathological characteristics of
simple tracheitis are hyperæmia, active or passive, swelling, and
increased secretion of mucus. There is no fibrinous exudation.

Acute inflammation causes the mucous membrane to become softened,
swollen and red, either uniformly or in points or patches, frequently
with ecchymoses and catarrhal erosions, more perceptible in the lower
than in the upper portions of the trachea. Scanty secretion sometimes
lies upon the surface in pearl-like drops, which might be mistaken for
solid elevations only that they can be wiped off.

In chronic inflammation the redness is more dull, reddish-blue or
grayish; the secretion, sometimes more scanty and sometimes more
abundant, is puriform and usually spread out over larger portions of
the surface; and the glands are enlarged and prominent, with their
ducts so dilated that their mouths are readily visible, sometimes, to
the naked eye, and always with a low-power lens, and the rest of the
tissue is hypertrophied, especially at the back wall of the trachea.
Catarrhal tracheal ulcers are exceedingly rare, superficial, and of but
slight extent, but they do occur, and are usually situated on the
intercartilaginous membrane.

DIAGNOSIS.--Tracheoscopy, a modification of laryngoscopy, can alone
determine with certainty whether, and to what extent, the trachea is
inflamed. Unfortunately, very few practitioners have as yet mastered
this method of examination, which, though really not more difficult
than laryngoscopy, requires greater illumination (necessitating under
some circumstances a mirror of longer focal distance) and different
relative position of patient and operator. (See article by Seiler.)
Figs. 25 and 26 show the tracheoscopical images of a case in which
there was intense acute tracheitis. The anterior wall is seen in Fig.
25, and the posterior in Fig. 26; on both, but especially the latter,
clumps of phlegm and ramifying injected blood-vessels are distinctly
seen. In many cases, by means of the stethoscope, either dry sonorous
or mucous râles may be heard over the windpipe; at other times we may
be aided in coming to a conclusion by the presence of
dysphagia--increased when the chin is raised and diminished when the
chin is pressed on the chest, as pointed out by Hyde Salter--and by the
morbid sensations, increased by pressure, in the region of the windpipe
when there is cough and expectoration.

{135} [Illustration: FIG. 25. Acute Tracheitis: anterior wall.]

[Illustration: FIG. 26. Same case as Fig. 25: posterior wall.]

PROGNOSIS.--Simple tracheitis, though occasionally not without danger
in extremely young and very old patients, rarely if ever destroys life.
Under good hygienic circumstances it frequently gets well of itself,
and it does not usually produce sufficient swelling or hypertrophy to
cause stenosis. It is, however, when severe, an annoying disease, apt
to recur, and, unless properly managed, difficult to eradicate.

TREATMENT.--Tracheitis is treated very much like bronchitis confined to
the larger tubes, only that local measures are more prominently
applicable, especially in chronic cases. Frequently, when acute, the
disease may be arrested by a Dover's powder, a warm bath, and a
diaphoretic drink at night, with hygienic attention, regulation of
systemic functions, and soothing applications, such as inhaling simply
vapor of water or medicated water, or using warm-water poultices
externally. Expectorant mixtures, containing ipecacuanha, sanguinaria,
squills, or senega, may be given, according to the age and condition of
the patient, with matico and the like, when the secretion is abundant,
and with ammonium acetate or sodium bromide (potassium carbonate or
ammonium carbonate where there is depression) or tincture of aconite
(especially when fever is present), or a very minute quantity of
tincture of veratrum viride, when there is much dryness. Inhaling the
steam arising from a pint of hot water (160-170° F.) containing 10 grs.
of extract of conium, 1 drachm of compound tincture of benzoin, and
half a drachm of ammonium sesquicarbonate, or inhaling nebulized
solution of potassium bromide, 10 to 20 grains to the ounce, or fumes
of evolving ammonium chloride or of nitre-paper, is very serviceable,
as well as placing a mustard plaster or a hot poultice on the upper
part of the chest (not directly over the windpipe) and on the back of
the neck or between the shoulders. Some patients require for several
days to take daily from 8 to 10 grains of quinia sulphate, then a
smaller quantity, care being taken not to discontinue the remedy
suddenly. Smoking eucalyptus-leaves, with much inhalation of the smoke,
is useful in protracted cases. In chronic as well as acute tracheitis
not only balsamic, anodyne, and astringent inhalations either of
vapors, or of liquids nebulized by the various spray-producers are in
vogue, but also insufflations of powders, injections of liquids, and
touchings with the sponge or cotton-wad probang or tracheal applicator.
Powders should never or only rarely (as, _e.g._, morphia, 1/16-1/8 of a
grain, when the cough is troublesome, etc.) be blown into the trachea;
injections and touchings should be made use of only after the operator
has acquired the necessary skill to apply them by means of the mirror.
A few drops of a solution of silver nitrate, varying in strength
inversely as the chronicity of the case from 5 grains to 60 to the
ounce of water, thus accurately applied at proper intervals of time,
have proved successful in otherwise intractable cases. In chronic
tracheitis general tonic treatment must be combined with the local, and
attention be paid to possible coexistent cardiac and {136}
broncho-pulmonary affections or other morbid conditions. In some cases
it is advisable to administer potassium iodide; in rheumatism, sodium
salicylate; in gout, colchicum. The utility of producing alkalinity of
the blood (as by giving alkaline mineral waters to drink, etc.) has
received a new and direct support by Rossbach's recent observations of
diminution of the blood-supply and of the secretion in the tracheal
mucous membrane of cats whose blood was made alkaline by injecting
sodium carbonate into the femoral vein.

Patients subject to tracheitis should observe all the precautionary
measures of so-called bronchitics as to sponging, bathing, and friction
of the body, wearing a respirator, clothing, exercise, habits, etc.


Complicated Tracheitis.

Under this heading are here classed together all inflammatory
conditions of the windpipe differing from simple or catarrhal
tracheitis. In these, other tissues may be affected as well as the
mucous membrane. In exanthematous, erysipelatous, and exudative
tracheitis the mucous membrane is prominently involved; in oedematous
and phlegmonous tracheitis, the submucous connective tissue; and in
perichondritic and chondritic tracheitis, the cartilages and their
investing membrane. The latter forms are connected with suppurative and
ulcerative processes, and, unless traumatic, almost never occur, except
in phthisical and syphilitic tracheitis. I shall speak of them under
the head of Ulceration.

The tracheitis of measles and scarlatina consists in an acute catarrh,
with sometimes considerable desquamation of epithelium, erosion, and
capillary hemorrhage. In cases of small-pox in which the larynx is
affected, the same disease may extend into the trachea, varying in
severity from a congestion of the mucous membrane to an intense
pustular process. Erysipelas of the larynx may also involve the
windpipe, and when it does is exceedingly dangerous. More than half a
century ago Gibson observed in an epidemic of erysipelas that when it
spread to the trachea it generally proved fatal.[1] Tracheal oedema is
extremely rare even when the larynx is oedematous. Phlegmonous
inflammation and abscess have been observed in a few instances.
Tracheal diphtheria is usually an extension of diphtherial disease of
the larynx. Without entering into a discussion of the nature and cause
of diphtheria, as either a local or general disease, it is here
sufficient to refer to the fact that while in simple inflammation of
mucous membrane no fibrinous exudation takes place, certain poisonous
irritations lead to the exudation of lymph which infiltrates the tissue
and may form a pseudo-membranous deposit upon it: experiments have
proved that ammonia, chlorine, and, certainly, bacteria, are able to
produce this. In laryngo-tracheal diphtheria or croup the disease most
frequently commences in the pharynx, occasionally in the larynx, and
much more rarely in the trachea.

[Footnote 1: _Transactions of the Edinburgh Medico-Chirurgical
Society_, vol. iii., 1828.]

The treatment of each of these forms of complicated tracheitis is the
same as the treatment of the corresponding form of laryngitis.


ULCERATION.

Tracheal ulcers are just as multiform as laryngeal ulcers, but far more
rare. Like inflammation, they may occur by extension from above or
below, {137} and only those following localized morbid conditions are
certain to have arisen in the trachea. Under the head of Inflammation
it has been stated that simple catarrhal ulceration does occasionally
occur; of this there is really no doubt, but some writers have denied
it and thrown the whole subject into great confusion. It is true,
however, that a tracheal ulcer has usually a so-called dyscratic base,
and either is diphtherial or phthisical (tuberculous) or syphilitic or
lupoid or leprous or carcinomatous, or else comes from extraneous
causes; as, for instance, from traumatic ulceration or extension or
perforation from neighboring abscess, etc. There are two kinds of
ulcers--viz. one in which the molecular death of tissue proceeds from
the surface inward, and another in which it proceeds from within to the
surface. Catarrhal ulcers, as well as ulcers from decubitus after
tracheotomy, from pressure of the canula, belong to the first kind;
when involving only the epithelium or the epithelium and the layer
immediately underneath it the name erosions is given them; and if it
were true that catarrhal erosions never penetrate to the deeper
structures, it would be justifiable to say that there are no catarrhal
ulcers, but only erosions: they do, however, penetrate, and sometimes
to great depths. In the second kind of ulcers the epithelium is at
first normal or intact, and the loss of substance of underlying tissue
in consequence of inflammatory processes in the mucosa, submucosa, or
perichondrium affects the epithelium secondarily. This occurs whenever,
from any cause, there is primarily caries of cartilage or suppuration
of submucous tissue, especially in typhoid conditions, in phthisis, and
in syphilis.

[Illustration: FIG. 27. Tuberculous Ulceration of the Trachea, as seen
during life.]

[Illustration: FIG. 28. Same case as Fig. 27: post-mortem appearance.]

[Illustration: FIG. 29. Syphilitic Ulceration of Trachea, as seen
during life.]

{138} [Illustration: FIG. 30. Same case as Fig. 29: post-mortem
appearance.]

The seat of tracheal ulcers is usually the posterior wall and the lower
portion, unless the upper portion is affected by extension from the
larynx or by pressure from a tracheotomy-tube. They are found also in
other portions, and sometimes are so numerous that they give to the
membrane a sieve-like appearance. Occasionally they denude some of the
tracheal rings. In shape they vary, being mostly irregularly circular
or oval, and excavated or scooped out; in size they vary from that of a
pin's head to that of a marble. In tuberculosis they are generally
small and numerous, have a pale background, and are occasionally
confluent, while in syphilis they are usually isolated and large, very
destructive, and apt to cause contractions or other deformities by
{139} partial or extensive cicatrization. Such contracting ray-like
cicatrices have more than once produced fatal stenosis.

The SYMPTOMS are frequently obscure, but local pain and irritation are
usually, purulent or muco-purulent sputa are sometimes, present. The
diagnosis is difficult unless tracheoscopic examination reveals the
condition. Fig. 27 shows the tracheoscopical image, and Fig. 28 the
post-mortem appearance, of a case of tuberculous tracheal ulceration on
the upper portion of the front wall, while Figs. 29 and 30 show the
image during life and the appearance after death of a case of
syphilitic ulceration. In Fig. 30 the posterior wall is seen with the
ulcers, and below them a star-shaped cicatrix.

The PROGNOSIS generally depends upon the underlying disease, and is
grave because the latter is. Perforation may take place, as well as
cicatrization and hypertrophy, and either process may lead to a fatal
issue. In a number of instances post-mortem examination has shown that
tracheal ulceration may produce surprisingly great ravages before
destroying life.

TREATMENT, like the prognosis, depends somewhat upon the disease
underlying the ulceration. Pain is relieved by anodyne, and
cicatrization promoted by alterative inhalations, as of nebulized
glycerated solutions of morphine, ethereal solution of iodoform,
iodinic preparations, oil of solidago, citronella oil, etc. Catarrhal
ulcers heal without special treatment with the subsidence of the
catarrhal inflammation. In syphilitic ulceration, stenosis from
cicatrization is to be dreaded, and specific constitutional treatment
is the main reliance. The internal administration of cod-liver oil has
been found of service in nearly all cases of tracheal ulceration,
especially in phthisis, lupus, etc. Appropriate general treatment must
be combined with the local.


MORBID GROWTHS.

DEFINITION.--Tumors, benign or malignant, growing from the wall and
projecting into the interior of the windpipe. Inversion of the mucous
membrane forming a protrusion into the interior will be spoken of under
the head of Stenosis; and tumors of other organs extending into the
trachea, such as cancer of the oesophagus, lymphatic glands, thyroid
body, etc., are excluded from consideration under the present head.

FREQUENCY OF OCCURRENCE.--Aside from post-tracheotomic
granulation-tumors, which with careless tracheotomy or after-treatment
occur often, the disproportion in the frequency of laryngeal and
tracheal morbid growths is even greater than that of other laryngeal
and tracheal affections. I have met with only eight instances of
tracheal morbid growths, strictly so called, in a special practice
during more than twenty-five years. This is exclusive of
post-tracheotomic vegetations and tumors from contiguity.

ETIOLOGY.--Local irritations and chronic inflammatory conditions seem
often, if not always, to be the forerunners of tracheal tumors, but the
real cause of the latter is unknown. Recently it has been suggested
(see the article on LARYNGEAL TUMORS) that the ever-present bacilli
play a rôle in the production of morbid growths as well as in that of
other diseases. As it is known that some parasitical organisms on
plants use up their nidus very slowly, with the formation of peculiar
excrescences, while others very rapidly destroy the tissue of their
host, it would be easy to suppose that some such difference in the
micro-organism causing the tumor determines its benign or malignant
character.

Post-tracheotomic vegetations may arise from the irritating pressure of
a {140} tracheotomy-tube, especially from the use of a fenestrated tube
or a tube ill fitted to the patient. Some observers are of opinion that
such tumors existed before the performance of the operation, and,
indeed, led to it, even though the supposed reason may have been
laryngeal or some other tracheal disease. While it cannot be denied
that such may have been the case sometimes, there is no doubt that in
other instances--and not only in those in which the vegetations "always
grow from the cicatrix" (Petel)--they are truly caused by the
operation, or by the wearing of the tube, especially if it be in any
way unsuitable as to size, form, etc.

SYMPTOMATOLOGY.--The symptoms of tracheal tumors are local irritation;
tickling or other morbid sensation, sometimes inducing and sometimes
not inducing cough; and encroachment upon the
breathing-space--dyspnoea--depending on their precise seat, size, and
rapidity of growth. It is usually difficult for the patient to specify
the beginning of his trouble, because, on account of the large size of
the windpipe, dyspnoea generally comes on very gradually. An accidental
catarrhal condition of the tracheal mucous membrane from a cold usually
first arrests the patient's attention. The very great diminution of the
calibre of the tube that the patient can bear when the tumor enlarges
slowly is sometimes astonishing. Unless the tumor is pedunculated (so
that expiratory efforts can throw it up into the larynx), which is
generally not the case, expiration and inspiration are equally
affected, both becoming gradually more and more labored and noisy.
Sometimes the act of swallowing large morsels brings on an increased
dyspnoea; sometimes respiration is accompanied by a sort of valvular
sound. Cough is frequently, but not always, present, and depends,
together with expectoration, upon either coincidental catarrhal
condition or irritation from the tumor: in the latter case it is
essential, dry, and persistent, and may vary with the position of the
patient. Sputum may be bloody and even contain shreds of the tumor, as
in similar cases of laryngeal growth. With increase of the tumor the
voice becomes weak and suffers in extent of range, as in other cases of
tracheal stenosis; the same is true of the diminished rising and
falling of the larynx. The course and duration of the disease vary
considerably with its nature. I have observed a tracheal fibroma to
remain stationary for eight years, when the patient died from other
causes and the diagnosis was confirmed post-mortem; and, on the other
hand, a cancer to grow so rapidly that the patient died from
suffocation within five months of its first causing the slightest
symptom. If not relieved, suffocatory paroxysms, with or without
consequent bronchitis and pneumonia, lead to a fatal termination.

PATHOLOGY.--As in the larynx, so in the trachea, the pathological
character of neoplasmata is generally that of papilloma. Of my eight
cases, all observed during life, four were papillomatous (two examined
microscopically after successful extirpation, one post-mortem, and one
in situ macroscopically only), one was a fibroma, microscopically
examined, one an osteo-chondroma, one a sarcoma, and one a carcinoma,
the three last having been examined post-mortem.

Of non-malignant tracheal tumors observed by others, the large majority
were papillomata; next in number come fibromata. Aside from these two
kinds of tracheal tumor, the cases recorded in literature are the
following: Rokitansky more than thirty years ago described tracheal
enchondromata found after death; and Cohen discovered in the corpse of
a phthisical patient a number of small enchondromata on the central
portions of the tracheal cartilages. Steudener, Demme, Wilks, Chiara,
and Eppinger have observed, post-mortem, tracheal osteomata. Gibbs has
described a tracheal cystic tumor[2] seen with the laryngoscope;
Müller, under the guidance of Gerhardt, a myxo-adenoma observed
tracheoscopically and carefully studied {141} during life and after
death; and Eppinger has recorded a case of post-mortem tracheal
adenomata and cysts, Simon having previously found three similar tumors
on dissecting a new-born tigress. Virchow speaks of the occurrence of
retro-tracheal retention-cysts, and Gruber has observed several; but
there can be no doubt that at least some of the tumors thus described
are nothing but circumscribed dilatations of the tracheal mucous
membrane--practically, dilated mucous glands. As to malignant tumors,
in addition to my two cases Schrötter has reported two cases of
sarcoma, and Labus one of fibro-sarcoma, while Rokitansky, Klebs, Koch,
Schrötter, Langhans, and Mackenzie have described cases of carcinoma.

[Footnote 2: Cohen questions whether this was a cyst or an abscess. It
burst spontaneously.]

Cases of cancer of the oesophagus, which involve the trachea--excluded,
as before stated, from present consideration--are, comparatively
speaking, by no means rare, and are apt to establish a fistulous
communication between the two tubes.

DIAGNOSIS.--The symptoms mentioned are those common to nearly all cases
of tracheal stenosis, and will be referred to again under that head.
Tracheoscopy alone makes the diagnosis certain; unless when the seat of
the disease is ascertainable without, its nature is shown by the
expectoration of portions of the tumor. The first case of tracheal
tumor ever diagnosed during the patient's life was observed by means of
the mirror by Tuerck in 1861; but it is very difficult in the mirror to
estimate distances as to depth, and unless the number of tracheal rings
above a tumor can distinctly be counted, a growth in the lower cavity
of the larynx may readily be mistaken for one in the trachea, and vice
versâ. Catheterism of the trachea shows the distance at which the tumor
is situated, sometimes very accurately, but it is dangerous unless
performed under the guidance of the mirror, and even then requires
great care. The introduction without the mirror of a probe or sound for
the same purpose is still more dangerous and unjustifiable, while with
the mirror it is perfectly safe in proper hands. Localized protrusion
of the mucous membrane into the interior is the condition which most
simulates tracheal tumor. (Compare Fig. 32.)

[Illustration: FIG. 31. Papilloma of Trachea.]

The pathological nature of a tracheal tumor can sometimes be determined
in situ with more or less probability. Without microscopical
examination it is not always possible to say whether a growth is benign
or malignant unless the mass has advanced to ulceration, and then
specific disease must be excluded by the history and concomitant
symptoms. Papillomata have a peculiarly uneven surface; fibromata are
usually more smooth. With equally good illumination, tumors of the
trachea resemble tumors of the larynx, and may be similarly
differentiated. The former are almost always non-pedunculated, or at
least none of those hitherto observed have had a long pedicle. Their
seat is generally the posterior wall, or the cicatrix of the anterior
wall after tracheotomy. In Fig. 31 is seen the tracheoscopic appearance
of one of my cases of tracheal papilloma.

PROGNOSIS.--The prognosis is always unfavorable in malignant cases, and
also in non-malignant when the tumor grows rapidly or has already
attained a large size. The introduction of the laryngoscope has
bettered the prognosis, inasmuch as in many cases early recognition
enables us, by performing tracheotomy, to prevent sudden death from
suffocation, and also because by the aid of the mirror removal has been
accomplished through the natural passages.

TREATMENT.--Removal of a tracheal tumor through the natural passages
{142} by means of either cutting or cautery instruments requires so
much special ability on the part of the operator that it need not be
described in detail in a work designed for general medical
practitioners. When the tumor is situated above a point at which
tracheotomy can be judiciously performed, no physician worthy of the
name should hesitate to lay open the trachea in any case in which
suffocation is impending. Removal of the tumor by surgical operation
after opening the windpipe may be attempted or not according to
circumstances, but in all cases palliative measures by sedative
inhalation and otherwise may be resorted to, and the patient's general
health, especially in malignant cases, must be kept up as much and as
long as possible.


STENOSIS.

DEFINITION AND PROXIMATE ETIOLOGY.--Stenosis is narrowing or more or
less occlusion of the windpipe. It is either stricture or constriction
from within, or compression from without, or both combined.
Constriction within the trachea is due to swelling or thickening or
cicatricial displacement of the mucous membrane or other tissue,
inversion of its walls, or morbid growth or foreign body in its
interior. Compression from without is due to goitre (which has in some
cases prevented viability) or other disease of the thyroid body;
aneurism; abscess; enlarged bronchial glands or cervical lymphatics;
disease of the sternum, clavicle, or vertebræ; mediastinal tumor;
cystic, emphysematous, or other tumor of neighboring tissue; or foreign
body. According to Rose's observations of goitre,[3] compression of the
trachea leads to fatty degeneration of the cartilages and their
subsequent softening and absorption; after which, the windpipe having
become membranous throughout and no longer patulous, death can
easily--in some positions or flexion of the body, etc.--take place.

[Footnote 3: _Der Kropftod und die Radicalcur der Kröpfe_, Berlin,
1878.]

In acute tracheitis, though there is swelling of the mucous membrane,
the large size of the tube usually obviates stenotic symptoms, while
chronic tracheitis does occasionally lead to sufficient contraction to
interfere with respiration; but generally stenosis is the result of
syphilis, and frequently follows ulceration and cicatrization. In a
case recorded in the _Bullétin des Sciences médicales_ for January,
1829, the lumen of the trachea was reduced to two lines.

[Illustration: FIG. 32. Involution of Trachea, due to aneurism.]

SYMPTOMS AND DIAGNOSIS.--The main symptom is the peculiar, gradually
increasing dyspnoea; once observed, it is recognized without much
difficulty. There may also be mucous râles; cough rough and sibilant;
attempts at clearing the throat without expectoration, or occasionally
with some expectoration, which is at first light-colored, then streaked
with blood, and at last purulent, but never abundant (unless
accidentally complicated by catarrh), and always difficult to eject;
perhaps occasional pain, but constant disagreeable sensation
(tightness) in the trachea just  above the sternum. Tracheoscopy
settles the diagnosis. The tracheal rings are seen either as diminished
circles or arcs--sometimes concentrically placed, sometimes in two
different directions, as shown in a case of tracheal stenosis from
{143} compression causing protrusion of the mucous membrane into the
interior, represented in Fig. 32, or else constricting bands are
visible.

As to the dyspnoea, both inspiration and expiration are
affected--frequently, however, the former more than the latter, as is
shown by pneumatometry. The head is thrown forward and the chin up; the
larynx moves up and down less energetically than in health (while the
respiratory movements of the larynx are abnormally increased in
laryngeal dyspnoea); the thorax is less expanded than normally,
especially its upper portions.

As to catheterization and probing, see the remarks under the head of
Morbid Growths.

PATHOLOGY.--The pathological changes in cases of stenosis vary with its
cause. In the great majority of cases of stricture from within,
syphilis--antecedent ulceration followed by cicatrization--has produced
the stenosis; in compression thyroid disease, and next often aneurism,
is the cause. The stenosis is most frequently situated in the lower,
next in the upper, and least in the middle, portion; more often than
the latter alone the whole tube is affected.

PROGNOSIS.--This is rather favorable with timely and proper treatment
unless a continuing active cause be irremovable; without treatment,
however, the cases almost invariably terminate fatally from pneumonia,
tracheal spasm, apnoea as before explained, etc.

TREATMENT.--When the symptoms are urgent and the stenosis is not too
low down, tracheotomy must be performed. Sometimes a very long and
flexible tube may be introduced with success in case of very low
stenosis, but more often tracheotomy is disappointing on account of the
stenosis extending too low down even when its beginning is higher up.

Stricture, especially when the symptoms are not very urgent, may be
relieved by dilatation through the natural passages, with, or if
possible without, previous tracheotomy. The cure of compression implies
removal of the compressing tumor or disease. Soothing inhalations, such
as of hops, benzoin, etc., diminish irritation and give temporary
relief.


DILATATION (HERNIA, FISTULE).

Dilatation of the trachea is either confined to the tube (when the
synonym tracheaectasy is applied to it) or is diverticular. In the
former case it may involve only a part or else the whole extent of the
windpipe. Whenever free respiration, especially expiration, is
chronically impeded, some portion of the air-tract below the
obstruction is apt to become dilated; thus, a bottle-shaped dilatation
is sometimes found immediately below an annular contraction. On the
other hand, tracheaectasy may extend upward from bronchiectasy. It has
been observed post-mortem to a slight extent in public criers,
trumpeters, etc., and in old coughers from laryngeal disease, chronic
bronchitis, pulmonary emphysema, etc., but without giving rise to
distinct symptoms during life.

Diverticular dilatation forms an air-containing tumor which either
looks into the oesophagus or is discernible on the outside of the neck.
Though rarely met with, it ought to be thought of in all appropriate
cases, and when pointing externally ought always to be recognized by
the careful practitioner. It is either hernial, glandular, or
fistular--three pathological conditions which have hitherto been
confounded. On account of the construction and position of the trachea
there can be but little protrusion outward without previous {144}
dilatation. Unless there be a deficiency of the cartilaginous rings,
only the posterior wall, which is always unsupported, and to a slight
extent also the intercartilaginous membranous portions, are liable to
tracheal hernia. This is properly called tracheocele; but the various
terms aërial goitre, aërial bronchocele, pneumatocele, tracheal
air-cyst, tracheal retention-cyst, internal tracheal fistule,
subcutaneous or incomplete fistule of the trachea, have been
indiscriminately used as synonyms of tracheocele, and have added all
the more to the confusion, as some of them originated, no doubt, as
correct appellations of the particular cases to which they were
applied. Aside from the occasional occurrence, both congenital and
acquired, of tracheo-cutaneous fistule, complete and incomplete, and
the still more rare occurrence of hernia of entire portions of the
mucous membrane, the cases of diverticular dilatation of the
trachea--or saccular tracheaectasy, as it may be called--are glandular,
as found by Rokitansky more than fifty years ago. Virchow seems to
regard all such glandular dilatations as retention-cysts (see Morbid
Growths), but although retro-tracheal retention-cysts doubtless do
occur (Gruber has reported two unquestionable instances), and although
the tumors now under consideration do in fact sometimes contain a
little mucus in addition to air, they do not constitute cysts or
adenomatous new growths, but are simply distended portions of the
tracheal mucous membrane, respiratory glands, whether the dilatation be
caused, as Rokitansky thought, by traction (Zerrung) and hypertrophy of
the mucous glands, or, as Eppinger suggests--and which is more
likely--mainly by increased intra-tracheal air-pressure. There must,
however, I think, coexist some deficiency or weakness of the
cartilaginous or other tissue, either congenital or acquired.

When the dilatation is retro-tracheal only, the symptoms are very
obscure, and diagnosis during life is at best uncertain. In one such
case under my care, confirmed (death having occurred from another
cause) by post-mortem examination, there was some dysphagia and slight
alteration of the voice. In all other cases the characteristic and
unmistakable sign of the disease is the peculiar intermittent, or, at
all events variable, aërial cervical tumor. It increases and diminishes
with forcible expiration and inspiration, and attains its largest size
during violent coughing, hawking, blowing of the nose, or other
expiratory effort. Occasionally the voice is considerably affected. The
tumor, especially by the manner in which it can be made to temporarily
disappear and reappear, can usually be easily differentiated from
subcutaneous emphysema and goitre, the only two conditions with which
it might be confounded. In the fistular variety the opening into the
trachea can sometimes be seen by means of tracheoscopy.

Aside from the deformity which the tumor may cause, it sometimes
induces laryngeal spasm and dyspnoea; otherwise it is of no gravity.

As to TREATMENT, methodical and continued compression by applications
of astringent collodion or by mechanical means is the only palliative
measure applicable; when suffocatory attacks call for it, tracheotomy
must be performed.




{145}

TRACHEOTOMY.

BY GEORGE M. LEFFERTS, A.M., M.D.


The operation of tracheotomy, or the artificial opening of the
air-passage--using the term in its modern acceptation as including all
of the five incisions that are both anatomically and surgically
possible, either singly or in combination, between the lower border of
the thyroid cartilage and the upper edge of the sternum (incisura
jugularis sterni), and reserving the term laryngotomy to denote the
division of the thyroid cartilage alone--fulfils two important and
usually urgent indications: First, in allowing the respiratory current
free access to the lungs in cases where the laryngeal obstruction is of
such a sudden or of so progressive a character as to either immediately
or remotely threaten the life of the patient; and, secondly, in
affording a ready means of direct access to those portions of the
air-tract which lie below the level of the glottis, and thus permit not
only of the direct extraction of such foreign bodies as may
accidentally have found their way within the air-passage, but of
neoplasms here located and of occluding diphtheritic membranes.
Catheterization and aspiration of the trachea are likewise both
rendered not only possible, but easy of execution. Both general
indications mentioned often coexist, and are met by the operation in a
large class of cases; the first alone plays its important life-saving
rôle in many.

The disease or accident which renders the operation necessary varies
greatly, and upon this variation depends not only the surgeon's
decision as to the precise time at which the opening into the air-tube
must be made, but also the precise point at which the operation should
be performed. These general questions I treat of in detail. The special
indications may conveniently, but somewhat arbitrarily, be arranged as
follows, in groups, which I have attempted to make complete, although
some of the conditions, being purely surgical, do not strictly come
within the compass of this essay:

A. Acute inflammatory diseases of the larynx and trachea:
  1. Acute oedema of the larynx.
  2. Erysipelatous and exanthematous laryngitis.
  3. Acute perichondritis, with abscess.
  4. Diphtheritic croup.

B. Chronic affections of the larynx and trachea:
  1. Syphilitic laryngitis.
  2. Phthisical laryngitis.
  3. Chorditis vocalis inferior hypertrophica.
  4. Carcinoma of the larynx or trachea.
  5. Non-malignant growths of the larynx or trachea.
  6. Tumors overlying the superior aperture of the larynx.
  7. External compression of the trachea by tumors of the neck or
       chest.
  8. Strictures of the larynx or trachea.

C. Neurotic diseases:
  1. Paralysis of the abductors of the vocal cords.
  2. Spasm of the adductors of the vocal cords. {146}

D. Traumatic conditions:
  1. Foreign bodies in the larynx or trachea.
  2. Impaction of foreign bodies in the pharynx or oesophagus.
  3. Fracture of the larynx. Rupture of the trachea.
  4. Scalds and burns of the larynx.
  5. Incised and gunshot wounds of the throat.
  6. Poisonous bites inflicted by certain insects about the mouth or
       neck.
  7. Suffocation from the passage of blood, fluids, etc. into the
       air-passages (tracheotomy, with aspiration of the windpipe and
       artificial respiration).
  8. Suffocation from the acute collection of either mucus or serum in
       the bronchia (ditto).
  9. Suffocation from the inhalation or development of poisonous gases
       (tracheotomy, with artificial respiration).

Finally, although it pertains alone to the province of the surgeon, I
may allude to the temporary tracheotomy and "tamponing of the trachea"
which has been recommended--and certainly found efficient--in
preventing the entrance of blood to a dangerous degree into the lower
trachea and lungs during the performance of certain operations in the
neighborhood of or upon the air-passages, such as resection of the
upper jaw, the extirpation of large nasal and naso-pharyngeal polypi,
removal of the tongue, subhyoidean pharyngotomy, laryngotomy, and
extirpation of the larynx.[1]

[Footnote 1: For the details of this procedure consult Schüller, _Die
Tracheotomie, etc._, Stuttgart, 1880.]

All-important as a preliminary to the operation itself is a thorough
knowledge of the surgical anatomy of the region upon which it is
proposed to operate; and this not alone in the adult, but especially in
the child, where essential differences often exist. Possible anomalies
also are not to be forgotten.[2] The assurance of the surgeon depends
upon this knowledge: mere, manual skill will not compensate for its
want; the success, both immediate and remote, of the operation is in
great measure the reward of its possession.

[Footnote 2: See Pilcher, "The Anatomy of the Anterior Median Region of
the Neck," _Ann. of Anat. and Surgery_, Brooklyn, April, 1881.]

It will be remembered that the trachea commences at the inferior border
of the cricoid cartilage, directly opposite to the lower edge of the
fifth cervical vertebra, and reaches thence downward, in the median
line of the neck, until it bifurcates opposite to the third dorsal
vertebra. In its upper part it is nearly subcutaneous, and is
surmounted by the prominent ring of the cricoid cartilage (easily
identified, even in the young child), above which, in turn, lies a
slight depression (the crico-thyroid space) between the cricoid and
thyroid cartilages. As the trachea descends in the neck it recedes
gradually, lying at the episternal notch about one and three-eighths of
an inch from the surface. Throughout the whole of this course it is in
relation with important structures. In its cervical portion it is
covered by the sterno-hyoid and sterno-thyroid muscles, and in the
median space, which is usually distinct between them, by layers of the
deep cervical fascia. It is also crossed by the isthmus of the thyroid
gland, which lies between the second and fourth tracheal rings; by the
arteria-thyroidea ima, when present, and below by the plexus formed of
inferior thyroid veins with their tributary and communicating branches.
In the latter region, but more superficially, are some communicating
branches between the anterior jugular veins. The innominate and left
carotid arteries are also anterior to it in the episternal notch as
they diverge from their origin. Laterally, the trachea is in relation
with the common carotid artery, the lateral lobes of the thyroid body,
the inferior thyroid veins, and the recurrent laryngeal nerves. The
thoracic portion of the trachea is covered by the manubrium sterni,
with the origins of the sterno-hyoid and {147} sterno-thyroid muscles,
by the left innominate vein, and by the commencement of the innominate
and left carotid arteries. Still lower, the transverse portion of the
arch of the aorta crosses, and the deep cardiac plexus of nerves lies
in front of it. Posteriorly, throughout its length, it rests upon the
oesophagus.

In performing, then, either the superior or inferior operation of
tracheotomy, after cutting through the skin and superficial cervical
fascia--which is really loose areolar tissue containing fat--the
superficial layer of the deep cervical fascia is reached, and
immediately below it more or less adipose tissue and the two anterior
jugular veins lying in an inferior tracheotomy to either side of the
wound, which is always made in the median line. As a matter of fact,
these various layers are rarely demonstrable, and the surgeon proceeds
irrespective of them until he reaches this point in his operation--viz.
the muscles which overlie the trachea. These may overlap in the median
line, and have to be retracted after having been separated; or, again,
a thin line of connective tissue marks a slight interval between their
inner edges, and is readily seen and dissected through if the operator
has kept his incision vertical and strictly in the median line of the
neck--a matter so important to the success of his operation that I do
not hesitate to again allude to it. The muscles separated and gently
retracted, together with the overlying tissues, toward the sides of the
wound, the upper edge of the isthmus of the thyroid gland overlying the
second and third, perhaps fourth, rings of the trachea, is always seen
in a superior tracheotomy--its lower edge very frequently in the
inferior operation. The isthmus is adherent to the trachea and to the
larynx through the deep layer of the deep cervical fascia, but is
capable of being slightly displaced or pushed upward or downward as the
case may be, and thus kept from obscuring the operative field. This
being done, the deep layer of the deep cervical fascia is seen covering
and strongly adherent to the tracheal wall together with the thyroid
veins. A few touches of the knife, carefully avoiding the
blood-vessels, serve to clear it away, and the tracheal rings are
clearly exposed.

In carrying out this dissection, which has been described as occurring
in an ordinary and uncomplicated adult case, several matters must be
borne in mind; and especially is this true if the operation concerns
infants. In them, for instance, the thymus gland rises half an inch
above the level of the sternum, and is frequently to be found as late
as the sixth or seventh year. In both adults and children the
innominate artery occasionally comes into view in an inferior
tracheotomy, obliquely crossing the lower portion of the right half of
the trachea. It is relatively higher in the child than in the adult.
The left innominate vein is also often observed when the trachea is
opened low down.

Certain abnormalities of the blood-vessels have been alluded to above.
The commonest consists in the existence of a thyroidea ima artery,
which when present usually arises from the innominate trunk, but
sometimes from the right common carotid or the aorta: it passes to the
thyroid body directly in the median line of the neck and close to the
trachea; again, the place of the anterior jugular veins may be taken by
a single central vessel, almost sure to be wounded during the operation
if it exist (Mackenzie).

In performing the operation through the thyro-cricoid membrane
(thyro-cricotomy) or through the cricoid cartilage alone (cricotomy),
the same tissues are met with, and the same dissection is necessary in
the earlier stage of the operation, as have been described in the
operation of superior or inferior tracheotomy; but the parts are more
superficial, adipose and cellular tissue less abundant, blood-vessels
much less numerous, and the operation very much simpler. The thyroid
gland of course does not come into view, {148} and the crico-thyroid
artery, a very small vessel, needs no attention in the dissection.

I have here and elsewhere included under the general term tracheotomy
five distinct operations, having for their object the opening of the
air-passages, which are surgically possible between the lower border of
the thyroid cartilage and the upper edge of the sternum. In this
classification I have followed that of Schüller, and its simplicity,
but exactness, and the avoidance of the old confusion of different
terms which results from the use of one intelligently employed, seem to
me to commend it. These five operations are--1. Thyro-cricotomy, or the
opening made through the crico-thyroid membrane alone. 2. Cricotomy, or
the division of the cricoid cartilage alone. 3. Superior tracheotomy,
the incision being made above the point where the isthmus of the
thyroid gland crosses the trachea and below the cricoid cartilage. 4.
Median tracheotomy, when, the isthmus being displaced or torn through,
the trachea is opened immediately below its site. And 5. Inferior
tracheotomy, the incision being made below the point of crossing of the
isthmus of the thyroid gland, and at varying distances, dependent
mainly upon the age of the patient and size of the parts, above the
sternal notch.

Rarely, I am bound to admit, is the field of all of these operations as
distinctly limited in practice as is here indicated, and one, perhaps
two, are rarely selected. Thyro-cricotomy (old term laryngotomy) is
often indicated, and cricotomy and median tracheotomy are sometimes
performed as here described. Superior tracheotomy is commonly a
combination of at least two of the methods--viz. the division of the
upper rings of the trachea and the cricoid cartilage as well. It may
even, probably frequently does, trench also upon the thyro-cricoid
membrane (thyro-cricotomy) and upon the field of a median tracheotomy,
the isthmus being pushed downward or even cut or torn through. The
latter operation and cricotomy are, I believe, rarely if ever done from
choice. Finally, inferior tracheotomy is a common method. As here
described, it meets a large number of indications, and, despite its
superior difficulties over the higher operations, is therefore
necessarily often chosen; not infrequently, however, does it invade the
median region, the isthmus of the thyroid being pushed upward.

Which of these operations shall be selected in a given case depends
upon the particular conditions which render it necessary, and likewise,
to some extent, upon the age of the patient. Durham summarizes the
question very fairly. Thyro-cricotomy (old term laryngotomy) is by far
the easiest operation to perform, and its execution is attended by
least risk; therefore it is the operation to be preferred in any sudden
emergency when suffocation threatens, and especially where the surgeon
is alone with the patient. Generally, it is not as applicable as the
others, especially in early childhood, on account of the limited
dimensions of the thyro-cricoid space. It cannot be recommended in
cases of acute or extensive diseases or injuries of the larynx, nor is
it likely to be of much service if a foreign body is in the trachea or
bronchus. On the other hand, it is probably the best operation to adopt
in cases in which foreign bodies are impacted in the larynx, in cases
of limited chronic disease or contractions of the superior laryngeal
parts--usually the result of syphilitic ulceration--and in cases in
which respiration is impeded by intra-laryngeal growths which cannot be
removed by the natural passages.

Cricotomy, combined with superior tracheotomy (old term
laryngo-tracheotomy), is not a difficult operation, and may be
advantageously practised, especially in children; in the adult it meets
many indications. Holmes recommends it the more urgently, in preference
to an inferior tracheotomy, the earlier the age of the subject may be.

Inferior tracheotomy is comparatively difficult to perform, and during
its performance dangers may have to be encountered greater and more
numerous {149} than those met with in either of the other operations.
This is true certainly of children. As regards young children, Holmes
states that after the age of five or thereabouts the surgeon can, if he
prefer it, open the trachea below the isthmus of the thyroid gland. He
himself does not recommend the operation before puberty. In the case,
however, of a foreign body loose in the windpipe of a child, where a
large opening is required, it can hardly be obtained above the thyroid
body and below the cricoid. To cut through the isthmus of the thyroid
(median tracheotomy) is, in early life at least, a doubtful proceeding
when it is of large size, on account of its vascularity, and the
incision must be made below it--in other words, an inferior
tracheotomy.

When the operation of tracheotomy shall be performed is a question
which the experience and individual views of the surgeon, based on
experience, must decide in each case. The doubt always arises in the
mind of the inexperienced operator whether the symptoms are
sufficiently urgent to render the operation necessary. To him these
general rules may be given: The immediate indication for the operation
is to be looked for in the thorax. It is the recession of the lower
part of the sternum and contiguous ribs and the retraction of the
intercostal spaces and clavicular fossæ at each act of inspiration. He
must not wait until lividity of the lips and blueness of the
fingernails prove that the blood is being imperfectly oxygenated
(Mackenzie). Let him remember also that, aside from the immediate and
imminent danger of sudden suffocation, a remote one exists and
increases the longer he postpones his operation and allows the struggle
for air to continue--viz. vascular engorgement and oedema of the lungs,
especially in young children; the production of all those conditions
which allow, and even predispose, the lung after the operation to fall
an easy prey to the inflammatory processes.

The instruments necessary for the performance of the operation of
tracheotomy are few and simple, and are such as may ordinarily be found
in any small operating-case. A scalpel, a probe and sharp-pointed
bistoury, dissecting and artery forceps, a tenaculum, a grooved
director, two small retractors, scissors, and a dilator for the
tracheal wound, are necessary. To these may be added the needles and
thread, waxed ligatures, sponges, and tape. The tracheal tube is
elsewhere described. A faradic battery, good suction syringe, and a
large flexible catheter may render good and timely service if at hand.

It is true that many other and more or less complicated instruments
have been devised for the purpose of facilitating the operation; and
other methods, aside from that of the knife, have come of recent years
into vogue; but, still, simplest means, as above given, have in the
experience of most surgeons been proven to be the best. This statement,
undeniably true for all surgical measures, is especially so for the
operation under consideration, which is often necessarily undertaken
without opportunity for elaborate preparation and under the most
adverse and inconvenient circumstances. The more familiar, therefore,
the surgeon is with his instruments, the better and more certain will
be his work.

Holding this view, it is unnecessary for me to more than briefly
mention such instrumental aids as the grooved tenaculum of Chassaignac,
the groove serving to guide the operator's knife into the trachea; the
sharp double hooks of Langenbeck, which, after being caught in the
tracheal walls to either side of the site of the intended incision, are
sprung apart after the latter is made, thus dilating the wound and
rendering the introduction of the tube easy; the tracheotome of
Thompson, a pair of curved cutting forceps, the blades of which are
caused to open by a screw after they have been plunged through the
tracheal walls; that of Garin, a forceps with curved blades--one, the
longest and sharpest-pointed, being made to penetrate the trachea, the
instrument then opened, and both blades cut their way to the desired
extent of {150} incision; finally, the tracheotome of Maisonneuve, a
curved dilating hook with cutting inner edges. Its point is entered
between the first and second rings of the trachea and brought out again
between the fourth and fifth; the handle is then carried under the
chin, so that the blades are made to cut through the trachea and the
skin between the points of insertion and exit, after which, upon
pushing a spring, the two halves of the hook separate, and the canula
is introduced between them (Thornton). And the trachea-stretcher of
Marshall Hall, by means of which a portion of the trachea is cut out
and the opening kept patent.

None of these instruments have been proven to possess any practical
worth; on the contrary, their use, especially that of the latter forms,
has in more than one instance been attended with disastrous results.

To obviate the danger of serious hemorrhage during the performance of
tracheotomy, both the galvano-cautery knife and the thermo-cautery
instrument of Paquelin have been recommended within the past few years,
and a number of operations placed upon record. The procedure is the
same whichever means be used. The skin and soft parts overlying the
trachea are usually alone cut through by means of the cautery-knife,
the cartilaginous rings of the tube, when reached, being divided with
the ordinary knife. This fact alone speaks against the thoroughness
attainable by means of these methods; but, still more important,
neither has been found reliable in checking hemorrhage, and in several
instances the operator has been obliged in haste to lay aside his
cautery apparatus and turn to the ordinary and better-known means to
complete his operation. The healing of the tracheal wound made by the
cautery is slow: erysipelatous inflammation may attack the wound as the
result of the burn, and extensive sloughing of the edges is not
unknown, while the resulting cicatrix is large, strong, and
contractile, and has caused, in one case at least, a stenosis of the
trachea. In the face of these facts he must indeed be an enthusiastic
advocate who would recommend the procedure. Mackenzie justly remarks
that the use of the thermo-cautery for opening the air-passage merely
introduces an unnecessary complication into the operation.

The choice of a proper tube, one suited to meet the special indications
in a given case and specially adapted to the age of the patient and the
calibre and position of his trachea, is no unimportant matter, and may
do much not only to facilitate the immediate success of the operation,
but likewise prevent the occurrence of those possible unfortunate
results, ulceration, fatal hemorrhage, abscess, pneumonia, and pyæmia,
no lack of which are recorded in our literature.

Although the number and variety of mechanical devices and forms of
tracheal tubes that have from time to time been devised by the
inventive ingenuity of operators is large, the choice practically
centres upon one of two forms. The first, and the one most commonly
used, is but the original canula of Trousseau, modified by Roger, in
that the tracheal portion of the tube is detached from the collar or
neck-piece, and moves freely with the movements of the patient; and by
Obré, by the important device of an inner tube to prevent clogging of
the outer or original tube by mucus. Starting upon this essential
basis, the instrument-maker has perfected the instrument of to-day. It
is a silver tube, double throughout, the inner tube projecting at the
lower or tracheal end beyond the outer--an important point, as it
prevents any possible permanent occlusion by mucus or blood-crusts,
membranes, and the like at this point, removal of the inner tube at
once clearing the end of the outer one. The curve of both tubes should
correspond to the arc of a quadrant, and the outer is fastened to a
transverse collar or shield by means of two small projections or pins
upon its sides which lie under small wire bridges upon the shield after
it has passed through an opening in the {151} transverse neck-collar
large enough to permit of its free movement during the respiratory
movements of the trachea, as well as during the forcible action caused
by cough. The ends of this collar or shield curve slightly backward to
correspond with the curve of the neck, and are perforated by,
preferably, large oval openings, instead of the usual small,
inconvenient slit, through which the tapes are passed which hold the
tube in position by encircling the neck. To this same shield is
fastened, by means of a small turn-screw or a revolving collar, the end
of the inner tube, which is thus prevented from being forced out of the
outer tube by coughing or any motion of the patient. Upon the upper or
convex surface of the outer tube a small ovoid opening is usually made
for the purpose of permitting the expiratory current to pass upward
(the inner tube being removed) into the larynx and render phonation
possible; also, the free opening of the outer tube being closed, to
allow of respiration being carried on through the larynx and natural
passages--often an important matter, as the case progresses toward
recovery, in instances where the operation of tracheotomy has been
performed on account of laryngeal obstruction.

A set of these tubes, which can now be readily obtained, should consist
of four, with the following diameters: No. 1, one centimeter; No. 2,
nine millimeters; No. 3, seven millimeters; No. 4, five millimeters:
their length is of course in relative and fixed proportion to these
measurements. A tube should always be selected less in diameter than
the trachea operated upon: to seek to introduce one of the same calibre
is not only unnecessary, but cannot fail to be dangerous. Tubes
constructed upon the same principles as that just described (Lüer's)
are made of hard rubber instead of silver (Leiter): their lessened cost
is their principal recommendation, added to the one that they are more
easily kept clean and sweet than the silver tubes. The fact that they
are necessarily made much heavier and thicker than the latter is a
disadvantage, the lumen of a hard-rubber tube being smaller than that
of a silver tube of corresponding external diameter. The objection
urged against them, of their great danger of breakage, I have not found
borne out by experience. Tracheal tubes are also constructed of
platinum, and recommend themselves on the score of lightness.

The main objection to any of the forms of tube just described exists in
the nature and shape of their curve, which not infrequently causes the
lower or tracheal end to lie in contact with the anterior tracheal
wall, or its convexity with the posterior, and irritate, even ulcerate,
them. This misfortune is entirely obviated by the canula of Durham, the
second of the two forms to which I have called special attention, and
which is essentially a right-angled tube, made of four sizes, with a
long horizontal portion, varying from 7 to 4 centimeters, and short
vertical portion, of from ½ to ¾ of an inch in length and slanting
slightly backward. The former portion is capable of being lengthened or
shortened in any sized tube by means of a screw arrangement attached to
it as it passes through the usual neck-collar or shield; and the
vertical tube can thus be correctly adapted to the particular depth at
which the trachea naturally lies in a given case from the surface; and
not alone this, but also to the condition of the overlying parts,
whether thin or fat, swollen or otherwise. Once in position, the
vertical portion of the tube remains in the long axis of the trachea,
and does not touch its walls to any injurious degree. Owing to its
right-angled shape, the angular and descending portions of the inner
tube of this canula are necessarily made upon the lobster-tail
principle, with joints--a possible disadvantage, as they can become
clogged with mucus and may become detached. Other modifications and
improvements exist in this Durham canula over the older one first
described, which add to its utility, but need not here be dwelt upon.
Suffice it to say that the tube is an excellent one for its purpose,
and is deservedly highly {152} spoken of and recommended by those who
have had experience in its use. Its cost is an objection.

The other forms of tracheal tube need but passing mention. The bivalve
canula of Fuller is made in two lateral segments, fastened to a collar
and tapering when closed to a point, so that introduction of the
apparatus through the tracheal wound is made easy. Once introduced, an
inner complete canula is slid into its place, thus separating the two
outer halves and rendering the whole round and compact. It has been
criticised unfavorably on account of the danger of hemorrhage that it
is likely to cause through pressure on the tracheal walls by the sharp
edges of the outer canula. In Gendron's canula the same lateral blades
are separated after introduction by means of a screw fastened on a
transverse bar.

Soft-rubber canulas were introduced to the profession not long since by
Morrant Baker for subsequent use after the operation of tracheotomy,
the usual tube having been worn meanwhile for a few days. Being soft
and flexible, they are certainly safe and comfortable for the patient,
but their thickness and the absence of any inner tube are, especially
the latter, serious disadvantages. They are not, I believe, generally
used. Finally, the long, flexible tracheal tube of König was devised by
its author to meet the indications in cases where the trachea is
compressed from without by tumors, and where a long canula that is
flexible, but at the same time rigid enough to resist pressure, becomes
a necessity. It is made in the form of the ordinary tracheal canula,
only larger, some three or more inches of the centre of the descending
portion of the tube being constructed of spirally-twisted silver wire.

It may not be out of place to remind at this point that a tracheotomy
is not infrequently performed, of necessity, very hastily, and in the
absence not only of a tracheal tube, but likewise of other and even
more essential instruments. The lack of the former need never be a
barrier to the prompt performance of the operation, for the ready wit
of the true surgeon will show him various ways out of his temporary
difficulty. A thick goosequill fastened by threads passed through its
outer end makes an efficient improvised canula. A bit of elastic
catheter answers the same purpose. Retractors for the edges of the
tracheal wound, made of wire--silver if it be at hand, a couple of
hairpins if it be not--and connected together by an elastic tape which
passes around the neck, will not only answer a good temporary purpose
in holding the tracheal wound dilated, but have been recommended by
Martin--in a more elegant form, it is true--as a proper method of
treatment after opening the trachea. Finally, one or more stitches
passed through the cartilaginous edges of the wound, and attached to
the soft parts beyond it, will serve to secure its patency, at least
temporarily.

If a patient be doomed to wear a tube constantly in his trachea, the
instrument described above can be removed at a suitable interval after
the operation and its place supplied by a single tube of the same size
and form as has been found adapted in the case. In the convexity of
this permanent tube an ovoid opening should be made to allow of the
passage to the larynx of the respiratory current, in part at least, and
to its mouth a pea-valve may be fitted which shall admit air on
inspiration, and not allow it to escape on expiration, thus doing away
with the necessity of the patient's closing the opening of his tube
with his finger each time that he requires to speak. Several forms of
these valves have been devised, but practically they are of little use,
are annoying to the patients, and, as a rule, not tolerated by them.

How shall the operation of tracheotomy be performed? An answer to this
question necessitates a short description of the operative steps of the
different procedures that is given in the order in which, I believe,
the operations are, as a matter of experience, found to occur in
practice--viz. 1st, superior {153} tracheotomy, combined or not with
cricotomy; 2d, thyro-cricotomy and, 3d, inferior tracheotomy. Certain
preliminaries are common to all.

The patient should be extended upon a table covered with one or two
thicknesses of blanket and of suitable height, which has been placed
sideways in front of a window if the operation is done by daylight. (At
night several candles tied together afford a better and safer light
than a kerosene or oil lamp.) The surgeon stands at the right side of
his patient and facing the window. Of his two assistants--and the value
of trained assistance in this operation is inestimable--one faces him,
without obscuring the light, and is prepared to use the sponges, hand
the instruments, manipulate the retractors, and render such direct
assistance as may be required. The second sits at the head of the table
and holds the head of the patient steadily, the neck being well
extended and thrown backward over a small round pillow (or, better, a
wine-bottle wrapped in a towel) which has been placed beneath it. The
head must be held directly in the median line of the patient's body,
and even in that of the operating-table. The assistant's attention must
never waver from this important duty. In certain cases too great
inclination of the head backward serves to increase the urgent
dyspnoea, or even to check respiratory efforts. This effect he must
watch for, and be prepared to relieve instantly by raising the head.
His duties also include the preliminary administration of an
anæsthetic, and its use during the operation if required. That such use
is safe in this class of operations is now generally admitted, but it
is not always necessary. The operation is not an exceedingly painful
one, and I have often performed it, with the adult patient's consent,
without using any anæsthetic (sometimes freezing the skin over the site
of the incision before making it), he submitting rather than undergo
any addition to the sense of urgent dyspnoea from which he is already
suffering. In children anæsthetics--ether being more commonly employed,
although chloroform is often used--are much more necessary, often
indispensable. Their effects are speedily manifested when asphyxia is
present in any marked degree, and but little of the vapor need be
inhaled. The administration, always to be carefully watched and
profound anæsthesia avoided, renders breathing easier in many
instances, certainly lessens laryngeal spasm, and may be discontinued
early in the operation when the air-tube is or has been nearly reached
by dissection. Any slight risk attending their use is more than
outweighed by the safety and precision which they ensure in the more
difficult and delicate steps of the operation (Sands). If the patient
be already insensible or if death be imminent, their use, of course, is
contraindicated.

The operator having previously decided which operation he will perform,
and after carefully identifying the position of the various parts, the
larynx especially, marking them with ink upon the skin if he chooses,
now steadies the loose skin over the site of his intended incision, and
then makes it, freely, firmly, cleanly, and exactly in the median line.
If it be for a superior tracheotomy, combined or not with cricotomy,
the operation I shall first describe, it must extend from just at the
notch of the thyroid cartilage downward for about four inches. A free
external incision is very desirable in all cases. The subcutaneous
tissue now rapidly dissected through by the careful use of the knife,
the veins as met with either being pushed to one side or, if they cross
the line of incision, cut if small, then twisted or immediately
ligated, or if large doubly ligated and then cut between the ligatures,
the interval between the sterno-hyoid muscles is sought for and found,
then separated by the blade or handle of the knife and held apart by
retractors at the side of the wound. It is important that the faint
whitish line of connective tissue which marks the interval between the
muscles be recognized, otherwise it happens that the operator passes
through the body of one of them, deviates at once from the median line,
and approaches the side of the trachea {154} instead of the front. The
ring of the cricoid cartilage above and the upper edge of the isthmus
of the thyroid gland below can now be either seen or felt by the finger
in the wound between them; and about the latter lies more or less
connective tissue and numerous small veins. As a rule, careful touches
of the point of the knife, or, as some operators prefer at this stage,
its handle or the use of a blunt director, serves to dissect up
piecemeal or tear through and clear this away, the veins again being
pushed out of the way, or if necessary cut and tied, and all parts held
aside by removing and replacing freshly the retractors from time to
time as the dissection proceeds, until the ring of the cricoid and the
upper rings of the trachea come plainly into view; that is, are seen,
not alone felt. During this dissection, especially if the handle of the
scalpel be used, too much pressure must not be made upon the trachea.
More than once I have known it to cause sudden suspension of the
respiration, probably by exciting reflex spasm of the larynx. If the
isthmus of the thyroid gland extend far upward, it must be pressed
downward, its facial attachments to the cricoid and trachea cut or torn
through, and may require to be held downward in the lower angle of the
wound by an additional retractor. The upper rings of the trachea having
been thus well cleared of their overlying parts, the next step of the
operation follows. I am in the habit of now removing the retractors and
allowing the trachea, which may have become displaced by them, to
resume its normal position, the head of the patient being meanwhile
readjusted. All this takes but a few seconds. A tenaculum is then
implanted in the median line, either just below the edge of the thyroid
or the cricoid cartilage, if the latter is not to be severed, and held
firmly by the assistant at the head of the table, thus steadying and
elevating slightly the trachea and rendering the incision into it
certain. The retractors are now reintroduced at the sides of the wound,
and the operative field is clear and steady. A glance having shown that
all bleeding has ceased, another that the tracheal dilator and
tracheotomy-tube lie ready at hand, the operator plunges a
straight-pointed bistoury through the tracheal wall at the level of the
third or fourth ring in the median line, and cuts quickly upward until
the cricoid cartilage is reached, if he proposes, as in the adult can
usually be done, to limit his operation to a superior tracheotomy. If
not, as in the child, and the cricoid cartilage must be cut through to
gain sufficient space for the introduction of the tube, it also is
severed by prolonging the incision upward to the thyro-cricoid
membrane. A hissing of escaping air, with the bubbling of a little
blood and paroxysms of cough, follows the incision and shows that the
trachea has been fairly opened. The tracheal dilator is now introduced,
the lips of the tracheal wound separated, and the canula slipped neatly
into the windpipe (unless in the case of a foreign body), and secured a
moment or two later, when respiration is fairly established, by tapes
passing around the neck. The tenaculum and retractors are removed at
the same moment that the tube is slipped into place.

Many different methods have been recommended for the dilatation of the
tracheal wound and to assist the introduction of the canula. The
dilator (Trousseau) which has been mentioned surely answers all
purposes, and is simple and easily used. An ordinary dressing forceps
will likewise do the work if introduced closed and afterward opened.
More complicated procedures are unnecessary.

Thyro-cricotomy requires that the superficial incision be so made over
the larynx that the thyro-cricoid space shall lie in the centre of one,
about two inches long, made in the median line. Following now the
dissection just described, the thyro-cricoid membrane is easily reached
and quickly seen as soon as the sterno-hyoid muscles are retracted. It
should then be divided transversely close below the lower edge of the
thyroid cartilage, the wound dilated, and the tracheotomy-tube slipped
into place.

{155} Inferior tracheotomy demands that the external incision be free.
In children, and in adults with a short neck, it should extend from the
cricoid cartilage to just above the sternum. The subsequent steps of
the operation are as for superior tracheotomy, with but slight
differences. The anterior jugular veins may come into view, but can
generally be avoided. If they are joined by a transverse branch, this
is necessarily cut through after being doubly ligated. After the
thyro-hyoid muscles are separated, the rings of the trachea are much
less distinctly felt at first than in superior tracheotomy, being
covered by more connective tissue and numerous veins. These inferior
thyroid veins, especially if large, are the great obstacle in the way
of this operation, and much care is necessary in order to avoid them,
which should be done if possible. The lower edge of the isthmus of the
thyroid gland, which presents to a variable extent above in the wound,
does not, as a rule, offer any obstruction. The thymus gland present in
infants is easily pulled downward and out of the way. The trachea at
length fairly exposed and all bleeding controlled, the left fore finger
of the operator is placed in the lower angle of the wound to securely
protect the large blood-vessels here located, and the incision made
through some three tracheal rings from below upward.

It may happen that in either a superior or inferior tracheotomy no time
will be allowed for careful and slow dissection as here described. In
such instances Durham advises that the surgeon grasp the trachea
between the fore finger of his left hand on the left side and the thumb
on the right, and make uniform, steady, deep pressure, thus firmly
securing it and at the same time protecting the large vessels of the
neck. The fingers thus placed are not to be moved until the trachea is
reached, which is accomplished by rapid incisions confidently made. The
pressure of the fingers causes the wound to gape and the trachea to
advance. The latter reached, it is caught by the tenaculum and the
operation completed as before described.

The operation of median tracheotomy may require a word. As has been
stated, that part of the trachea covered by the isthmus of the thyroid
gland is very commonly encroached upon in performing either or both
superior and inferior tracheotomy, the isthmus being slightly displaced
from its site. Other than this the site here mentioned would rarely be
selected as the point for opening the trachea. Certain conditions, it
is true, might render it necessary, but they would be rare. The danger
lies in the hemorrhage which, theoretically at least, is to be expected
when the isthmus of the thyroid gland is either torn or cut through;
but opinions vary very greatly as regards this danger. With a thin,
narrow isthmus in children I have frequently, in performing superior
tracheotomy, cut my way through to a sufficient extent to clear a
suitable space upon the trachea through which to introduce a tube
without difficulty or danger. I should not recommend the procedure,
however, were the isthmus to be seen to be, when reached, thick, wide,
and exceedingly vascular, but at the same time believe that the danger
even here of cutting into it is much overestimated.[3] Roser's
recommendation to apply a ligature to the isthmus on either side of the
median line previous to its division is not generally applicable.
Hueter has shown that the fibrous capsule of the thyroid gland
enclosing it and its blood-vessels is firmly attached to the trachea
and sides of the larynx, and that from the isthmus this fascia extends
upward over the larynx (fascia laryngo-thyroidea), and thus prevents,
in a measure, attempts at displacing the gland downward. Bose[4]
recommends that this fascia be divided transversely over the anterior
convexity of the cricoid cartilage, when a director can be passed
behind the isthmus, to lift it from the trachea and depress it far
enough to expose three or four of the {156} rings: the capsule of the
gland thus remains unbroken and no hemorrhage occurs. The procedure
certainly merits trial; twice it has succeeded well in my hands.

[Footnote 3: See Foulis, "Some Points on Tracheotomy," _Glasgow Med.
Journ._, vol. xv. No. 2, p. 123.]

[Footnote 4: _Archiv für klin. Chirurgie_, vol. xiv. p. 137.]

Cricotomy, the division of the cricoid cartilage alone, is an operation
which, as far as I am aware, is rarely ever performed. The objection
urged against it, however, that in the adult the elasticity of the
cricoid cartilage is so great that a wound through its ring cannot be
made to gape sufficiently to allow of the introduction and retention of
a canula without discomfort and danger of necrosis of the cartilage, is
not borne out by experience. In children the objection cannot of course
be urged.

The description of the operative steps which has been given, and which
comprises the routine in an ordinary and easy cure, should not mislead.
The operation is not always as simple and safe as would appear from
what has been said. At times complicated and difficult, at times
dangerous in practice from the delay involved, it demands in all, but
especially in certain urgent cases, a trained hand and eye, sound
anatomical knowledge, coolness, self-reliance and presence of mind on
the part of the operator. Despite the greatest caution, and even in
apparently favorable cases where time for dissection and deliberation
is allowed, certain mishaps may occur which complicate the operation to
a serious, dangerous, or even fatal degree. Some of these, as will be
seen, are avoidable with care, but others may happen that are not only
unavoidable, but totally unforeseen, and from their very suddenness all
the more embarrassing.

Accidents may occur during the dissection of the soft parts overlying
the larynx and trachea, and the importance of carefully determining by
palpation the location of the various parts prior to making the
preliminary incision, and of studiously preserving their relation and
location during the dissection, cannot be overestimated. Neglect of
this precaution has in more than one instance led to the air-passages
being opened through the thyroid cartilage or thyro-hyoid membrane,
instead of at the intended point. It should not be forgotten also that
the natural laxity of the several layers of connective tissue of the
neck is much increased by their division, and that the trachea, being
naturally freely movable, is thus very easily displaced from its normal
position during the act of dissection; especially will this happen when
unskilful attempts are made to hook aside or retract the divided
structures during the operation. Thus it may easily occur that the
entire trachea is drawn to one side and entirely lost, or, more
commonly, is turned upon its vertical axis, and finally opened at the
side instead of anteriorly in the median line. It may not be opened at
all, either being altogether missed by the surgeon in his dissection,
which is continued past it, even down to the vertebral column, or the
tracheal tube may be passed into the tissues lying in front of the
trachea, under the mistaken idea that the latter has been incised.
Persistence in keeping to the median line during dissection--a golden
rule in the operation of tracheotomy--will render the first accident
impossible; the second may be avoided by hooking up the trachea, as has
been described, before incising it. If the opening into the trachea has
not been made large enough to receive the tube, as often happens to the
young operator, and even to the experienced when he fears to extend his
incision on account of the proximity of the thyroid isthmus, no
resource remains but to carefully enlarge it, pushing the thyroid
isthmus or veins from before the course of the knife. If the opening be
small, and be lost both to touch and sight, a second should at once be
made, especially in urgent cases, and no time lost in searching for the
first. This opening must be made directly in the median line, otherwise
the canula will stand awry in the wound and be easily dislodged from
its position in the trachea. If the first opening made is faulty in
this respect, it is better to at once make a second. It may seem
unnecessary to {157} warn the surgeon against thrusting his
sharp-pointed bistoury too far inward at the moment of incising the
trachea; but as a matter of fact it has been driven through both
anterior and posterior walls, and even through the oesophagus, until it
has struck the spine. The converse, or a too superficial incision, is
an accident more likely to occur, the point of the knife not being made
to penetrate the mucous membrane of the trachea, which is probably
swollen and thickened. No relief in such cases follows the incision,
and an attempt to introduce a tracheal tube may cause it to pass
between the mucous membrane and tracheal walls into the submucous
tissue, thus stopping up the tube as it progresses. The disastrous
result of such an accident can readily be foreseen unless the
complication be quickly appreciated as to its nature, the tube
withdrawn, and the incision completed. Much more frequently will a
somewhat similar accident occur in the operation of tracheotomy for
croup or diphtheria. The pseudo-membrane overlying the walls of the
air-passage is not penetrated, but pushed before the knife, which has
properly incised the walls of the tube; the introduction of the canula
now crowds this membrane still farther back toward the posterior
tracheal wall, and a complete tracheal stenosis is added to the
pre-existing laryngeal one; sudden and urgent dyspnoea follows, and
prompt relief alone wards off fatal suffocation. Fortunately, in such
instances the forcible efforts at respiration and struggles of the
patient are often sufficient to break through the occluding membrane
and allow the respiratory current to pass. Violent cough often follows,
and more or less of the membrane is forced out through the tube. Should
these events not come instantly to pass, the surgeon must not wait for
the efforts of the patient, he being often cyanosed and unconscious at
this point, but by passing an elastic catheter down through the
tracheal tube break through the occluding membrane forcibly. The
occurrence of such an accident is always denoted by absence of
respiration through the canula and by alarming asphyxia, and its cause
needs but little reflection to be appreciated.

Much the same train of events happens if during the introduction of the
canula large portions of the false membrane are completely detached and
drawn down into the lower trachea by the violent inspiratory efforts of
the patient, or stripped up from the mucous membrane and pushed
downward into the air-tube. No time should be lost in either case in
removing the tracheal tube, dilating the tracheal wound by forceps or
otherwise, and in endeavoring to clear the trachea by seizing the
obstructing membrane with forceps. If this be unavailing, the
suction-syringe must be adapted to the mouth of the canula and the
trachea cleared by aspiration. A large elastic catheter may take the
place of the canula. Sands recommends in such instances as the
foregoing that another opening should be freely made below the first
one in the trachea, when respiration will probably be re-established.
The success of this procedure of course depends upon the depth to which
the false membrane has been drawn in the trachea.

Schüller regards the moment at which the trachea is opened as the most
important and most dangerous of the whole operation. Certain of the
accidents which may occur at this period have been detailed; others
remain to be spoken of, one of which at least--viz.
hemorrhage--requires special mention. Even before the tube is cut into
it may cause an important question to arise for the surgeon's decision.
A bleeding, often copious and persistent, which arises during the
course of the operation from the accidental or unavoidable wounding of
the thyroid veins, especially when they are large and numerous, the
patient unruly, and perhaps with a short fat neck, and the fact that
having wounded one the blood flows so over the parts as to obscure and
increase the chance of wounding others, constitutes one of the
commonest difficulties met with in the operation of tracheotomy.
Hemorrhage arising from a wound of the thyroid isthmus is much rarer,
and neither, as a rule, need be {158} feared if due care and
promptitude be exercised. But should it occur in a case in which the
urgency of the dyspnoea allows of no time in which to employ the
ordinary methods by ligature, torsion, pressure, or otherwise of
checking it, shall the incision be made and the risk boldly incurred of
blood passing to a dangerous degree into the trachea, and this in the
face of the oft-repeated advice--the, in some quarters, absolutely
given rule--that the trachea is never to be opened until all hemorrhage
has ceased? I hold that it unquestionably should be, and that he who
waits in many instances until the former moment will have to wait until
his patient is dead. Durham truly says that it is useless to let the
patient die from suffocation while attempting to prevent death from
loss of blood; and yet this has been done.

In any case, then, where there is great venous congestion, marked
venous bleeding, and little time, the patient being on the point of
suffocation, the surgeon should carefully but boldly proceed and
complete his operation in spite of the hemorrhage, opening the trachea
and introducing the canula even though the entire field of his
operation be obscured by blood. The tracheal opening once made under
such circumstances, the patient, if the blood which enters the windpipe
be not coughed up again, may be turned upon his face, so that the blood
will gravitate toward the tracheal opening and the lips of the latter
compressed about the rigid tube; or the blood may be aspirated from the
trachea by means of the suction-syringe through an elastic catheter in
the wound or the tracheotomy-tube by the operator's mouth, according to
the urgency of the case. These measures answer for the slighter cases,
but where the patient has suffered from urgent impending suffocation
before the opening of the trachea, the entrance of the blood and its
suction downward by the first inspiration may make it complete, and the
danger is great. Still, the choice lies between the two evils, and the
advice given above holds good. To the treatment there recommended will
now have probably to be added artificial respiration and faradization.
Comfort in any case may be taken in the fact that the re-establishment
of respiration through the tracheotomy wound quickly relieves the
pulmonary capillaries and the right heart of their distension, the
venous circulation resumes its natural course, and the venous bleeding,
perhaps alarmingly free, ceases almost immediately or is readily
checked by pressure.

Where time is afforded and despatch in the operation is not a
necessity, the trachea should not be opened until all hemorrhage has
ceased. This, as a rule, is readily controlled by the usual measures,
and in a large percentage of operations is not excessive. A direct
fatal hemorrhage is very rare; likewise an arterial hemorrhage of any
extent, especially if the possible anomalous position of certain
arteries, such as the thyroidea ima, be borne in mind and care in
making the incision exercised. Nothing but gross carelessness on the
part of the surgeon and entire loss of presence of mind can account for
the opening of the carotid or innominate arteries, as has been done.
During the performance of the low operation of tracheotomy the finger
of the operator must more or less frequently be pressed into the lower
angle of the wound, and his anatomical sense constantly on the alert.

The entrance of air into a vein during the operation is a possible
accident, especially when it is much enlarged and imbedded in dense
tissue, as sometimes occurs in malignant disease of the throat or when
large tumors of the parts exist. Should such an unfortunate
complication occur, the proper treatment, according to Erichsen, should
be compression of the wounded vein with the finger and its immediate
ligation if possible; compression of the axillary and femoral arteries
and a recumbent position for the patient to favor cerebral circulation;
and, lastly, artificial respiration.

At the moment of opening the windpipe two conditions may suddenly {159}
supervene, both of which need, as may usually be easily done,
differentiation from the asphyxia produced by the entrance of blood
into the trachea. The first of these is the apnoea which not
unfrequently arises in children suffering from urgent dyspnoea the
moment that a free opening is made and the air-stream rushes unimpeded
into the lungs. The condition lasts but a moment or two, and need
excite no alarm. The second is based upon the fact that the operation
itself not seldom excites an alarming asphyxia, probably by provoking
laryngeal spasm. The introduction of the tube serves to promptly
relieve it.

Finally, I may refer to those rare but unfortunate and unpreventable
cases where the introduction of a tracheotomy-tube after a carefully
conducted operation fails to give relief. Such instances are reported
by several authors, and depend upon the existence of some unascertained
pathological lesion, such as the presence of a stricture of the trachea
below the site of the operation, compression of this tube from without
or a tumor within, stricture of the primary bronchi, or some similar
condition. A careful preliminary examination and study of the case will
in the majority of instances do much to fix the indications for the
operation and perhaps account for the surgeon's failure.

The operation itself having been practically completed with the
introduction of the canula, the after-treatment of the case now becomes
the important consideration. This naturally varies in accordance with
the accident or disease which has rendered the opening of the trachea
necessary. In the instance of a foreign body lodged in either larynx or
trachea the tube may at once be removed as soon as the former is
removed or expelled. Indeed, the introduction of the tube is often
unnecessary, as the offending article flies out through the wound as
soon as the trachea is opened. The only contraindication would be to
this rule when the foreign body is of a sharp and irritating character,
and has been impacted in the larynx, especially of a child, and
consequent inflammation and swelling of the parts may confidently be
looked for. Should the operation have been called for on account of
laryngeal or tracheal obstruction due to syphilis, both constitutional
and local treatment are indicated, the latter varying with the special
conditions presented, and being fully described in the section of this
work treating of that subject. The patient not infrequently is obliged
to wear the tracheal tube permanently. In croup and diphtheria the
first efforts of the surgeon after introduction of the tube should be
directed toward the removal of such shreds of the membrane as present
through the tube or may be reached by forceps introduced through it
into the air-passage. Large quantities may thus often be gotten away,
to the manifest relief of the patient. A pseudo-membrane covering the
vocal cords and causing glottic stenosis has thus also more than once
been removed through the wound. A feather carefully passed through the
tube into the trachea, by exciting cough and through its mechanical
effects, is of assistance in promoting the expulsion of membrane lodged
in the trachea below the wound. The use of an elastic catheter and
aspirating syringe for the same purpose is advised by Roux and Hueter.
In any case, constitutional treatment as well is indicated, and other
measures--viz. the inhalation of steam, direct local applications, and
the like--such as may meet the views of the particular operator.

Granted that the operation has been performed to meet the indication in
cases of sudden and urgent dyspnoea arising from the passage of blood
into the trachea or the accumulation of serous fluids in the lower
air-passages, as well as in cases of dangerous intoxication from the
effects of poisonous gases and narcotics, aspiration of the trachea in
the former instances, followed by artificial respiration in all, and
perhaps the catheterization of the trachea in the latter, as advised by
several recent writers, will tax the surgeon's energies as the primary
consideration after his operation. The catheter may be first used for
the purpose of aspiration in the former cases, if {160} necessary, then
for the injection of air, it here taking the place of the natural upper
air-passages.

In cases of acute laryngeal oedema, certain chronic inflammatory
processes, neoplasms in the larynx or trachea, and injuries or wounds
of the air-passages, the proper treatment, aside from that of the
necessary tracheotomy, will suggest itself on ordinary surgical
principles, or is elsewhere specially treated of in this work in
connection with the subjects themselves.

Aside from these special indications for after-treatment, which must be
met as they arise, there are certain general rules for the management
of any case after the tracheotomy-tube has once been inserted: they
relate mainly to the care of the patient, the dressing of the wound,
and the care of the canula.

A variable period of intense and exhausting suffering from dyspnoea
having probably preceded the operation, the sooner the patient is
allowed to seek refreshing sleep the better; and this may be allowed if
there be no danger of hemorrhage. Nourishment of a fluid character and
stimulants, if necessary, are to be allowed in quantities and at times
dictated by good judgment. The patient's first attempts at swallowing
must be watched and directed, as the fluids frequently pass in part for
a short time into the larynx, and may appear at the tracheal wound. If
the condition persist, it may be, no other apparent cause existing,
because the tracheal tube is too long and presses on the posterior wall
of the trachea, thus interfering with deglutition. For the first day or
two at least a competent nurse must be in attendance, and the care of
the tube entrusted, after explicit directions, to her. For the first
twenty-four hours the secretions usually need to be constantly cleared
from the mouth of the inner tube as they are coughed up by the patient,
and the tube itself occasionally removed and thoroughly cleaned in
carbolized water (or water to which a little borax or potash has been
added) by means of a bristle brush, such as is used for cleaning pipes.
As the case progresses, the secretions are not as profuse or annoying,
and the patient learns to assist himself, in caring for his tube and to
remove and replace the inner one. Attempts at using the voice are to be
abstained from, and a slate or pencil and paper used until, if the case
progress favorably, the third day, when he may be shown how to produce
it by closing the outer fenestrated tube (the inner being removed) with
the finger. The outer tube does not require usually to be removed,
except in diphtheria, for cleansing until the third or the fourth day,
prior to this it being done by means of a feather. The removal of the
tube should always be done by the surgeon himself, and the occasional
danger of its difficult reintroduction, caused by the swelling of the
parts, not forgotten. At the same date, the wound sutures may be cut
and removed. After its first removal the outer tube is taken out,
cleansed, and replaced at each daily dressing, which consists in the
washing of the wound with carbolized solutions, the application of
adhesive strips, if necessary, across it after the sutures have been
removed, and the insertion between the neck-plate or collar of the
tracheotomy-tube and the skin, upon which it presses, of a layer of
sheet lint covered by a little simple cerate or like dressing. The
tapes attached to the canula for fastening it about the neck need
changing, and care must be taken to regulate each day their degree of
tension about the neck in proportion to the amount of inflammatory
swelling attendant upon the wound through the soft parts overlying the
trachea.

The patient, during, especially, the first few days after the opening
into the trachea has been made, should be kept in a well-ventilated
room with a uniform temperature. There is rarely any occasion, except
in cases of croup and diphtheria, when it may be advisable, to envelop
him in steam. Some surgeons place a small wad, two or three layers of
gauze, wrung out frequently in hot water, over the mouth of the tube
for the first day or two. A {161} large, coarse sponge answers the same
purpose; and the precaution seems to me to be a good one, preventing,
as it does, air of a low temperature from entering the lungs, and
rendering it moist and free from adventitious particles. The difficulty
is in keeping it in place.

The question as to the final removal of the canula is a difficult one
to answer here, depending as it does upon the various causes for which
the operation was originally performed. In certain cases, as will be
seen from what has been said, its sojourn in the trachea will only be
from a few moments to a few hours; while, on the other hand, in cases,
for instance, of severe syphilitic disease of the larynx, with
cicatricial stenosis of its cavity, the tube, once introduced, has to
be worn during the lifetime of the patient. Between these extreme
limits the period varies greatly. As a general rule--perhaps from the
fourth or fifth day to the end of the first week--an attempt to cause
the patient to breathe through the natural passages, the outer end of
the outer fenestrated tracheal tube being closed, will partially
succeed. Each day will now make success greater; the voice in part
returns, and a period is soon reached when the outer tube may be closed
with a cork (at first during the daytime only) and respiration carried
on entirely through the larynx. The speedy removal of the tube and the
closure of the tracheal wound then follow as a matter of course. I have
never found it necessary to employ any of the various forms of
after-treatment canulas, and believe them to be unnecessary. The
original tube, preferably a fenestrated one, as heretofore described,
is to be worn until convalescence is established, then permanently
withdrawn.

The tube should be removed at the earliest safe and practicable moment.
Its lengthened sojourn is not devoid of danger, as will be shown; and
an atrophy of the laryngeal muscles, especially the abductors of the
vocal cords, may follow their prolonged disuse, or at least inactivity,
thus giving rise to a narrowing of the glottic opening perhaps
inconsistent with respiration.

The wound, covered by granulation-tissue if the tracheotomy-tube has
been worn for any length of time, quickly closes, when the latter is
removed, and needs to ensure this but a few narrow strips of adhesive
plaster to be passed across it and attached to the side of the neck, to
prevent the air being forced out through it during the first day or two
when the patient coughs or attempts to speak.

In cases where the tube has been worn for a long period, and the edges
of the opening have firmly cicatrized, their freshening by the knife or
scissors is a necessary preliminary to their being brought together by
means of a suture or two.

The wound in the trachea closes not by the formation of a
cartilaginous, but rather of a dense connective tissue, and the
cicatrix is so smooth and small as to be with difficulty discernible.
The cicatrix remaining externally upon the neck need be but slight and
linear, and cause no disfigurement, especially if the wound have been
properly treated and watched during the healing process.

Among the complications and accidents which may occur after a
tracheotomy successfully performed,[5] none is commoner, and none,
perhaps, is more to be feared, than the broncho-pneumonia which may
develop at any time within the first three or four days, and especially
in those cases where the operation has been rendered necessary by a
diphtheritic inflammation of the throat or air-passages. Bronchitis is
common when much blood has escaped into the trachea during the
operation. The periodical and careful auscultation of the chest is
therefore desirable, in order that the earliest physical signs of these
morbid conditions may be detected.

[Footnote 5: See Parker, "On Some Complications of Tracheotomy, with
Illustrative Cases," _Lancet_, Jan. 24, Jan. 31, and Feb. 7, 1885.]

{162} Secondary hemorrhage is rare: should it occur, the wound must be
opened, enlarged if necessary, and the bleeding vessel sought for and
secured. A slight hemorrhage may be checked by pressing the parts
firmly about the tracheal tube and the use of styptics locally.

When the pathological condition of the parts has demanded that the
canula be worn for a long time, and in cases where sufficient care has
not been taken to select one suited to the age of the patient or to the
particular form of operation that has been chosen, perhaps to the needs
of the special case, an ulceration of the anterior or posterior wall of
the trachea, the result of the pressure of the lower edge of the tube
or of its upper posterior and convex side, may occur. Usually, it
happens on the anterior wall, rarely on both, and the main trouble to
which they give rise lies in the repeated hemorrhages that proceed from
the laceration of granulation-tissue, in changing the canula, for
instance, and the descent of the blood into the trachea and lungs.
Cases of extensive ulceration, with erosion of the large vessels at the
root of the neck, and fatal hemorrhage, have been reported.
Considerable care should then be exercised in so adapting a canula to a
special case that it will lie as free as possible within the lumen of
the trachea. Ulceration of the tracheal walls, it is claimed, never
occurs with the right-angled canula of Durham. Occasional change of
form in the canula or the use of canulas with rounded extremities
(perforated with numerous slits) is often advisable when the tube is
worn for a length of time.

Another complication following the prolonged sojourn of a tracheal
tube--rare, it is true--is the development of a mass of
granulation-tissue, a veritable tumor, which may occlude the lumen of
the trachea and lead to serious disturbances of respiration. The growth
usually occurs about the inner edges of the tracheal wound, extending
thence inward and upward or downward, as the case may be, and is most
frequently met with, perhaps, after tracheotomies undertaken for
diphtheria, although it may occur as a result of the ulcerations
mentioned above, and develop even from the cicatrix in an old and
perfectly-closed tracheotomy wound. The size of the mass, its location,
and the amount and manner of its interference with the respiratory
current vary much, but the condition must ever be regarded as a
troublesome, even dangerous, one, and may always be suspected when
attempts at the removal of the canula temporarily or permanently are
followed by sudden and urgent dyspnoea.

The exuberant granulation-tissue which forms about the outer edges of
even a recent tracheotomy wound, and occasionally renders the
reintroduction of the tube difficult, as well as closing the wound
while it is out, is a much simpler matter, and is easily remedied by
cutting it away with the scissors or checking its formation by caustic
applications.

A subcutaneous emphysema not infrequently occurs as the result of poor
surgery and delay at the time of introducing the tube into the
windpipe, or may come on later when the tube fits the tracheal wound
incompletely. In either case it need excite no apprehension, and
usually quickly subsides. Cervical cellulitis is a more serious matter,
but is fortunately rare if unconnected with disease of the cartilages
of larynx or trachea. It probably depends upon injury to the tissues
and a too extensive opening up of the intermuscular strata at the time
of the operation. Should the complication arise, the tendency to the
burrowing of pus must be prevented by free drainage and, if necessary,
incisions. The other surgical indications are to be treated on general
principles.

When the incision necessary for the introduction of a tracheotomy-tube
has been made through healthy tissue, necrosis of the cartilage in
contact with the tube belongs to the rarest of the complications of the
operation. The simple traumatic perichondritis set up by the operation
shows no tendency to {163} eventuate in death of the parts. Equally
rare is cicatricial contraction of the trachea as the direct result of
the operation. That it may follow the healing of the extensive defects
sometimes left by the syphilitic and other processes can readily be
understood; and the same defects, involving as they occasionally do the
loss of large amounts of tissue and destruction of important parts, may
eventuate in the formation of an aërial fistula during or after the
healing process is completed. The occurrence of such a fistulous
opening as the result of a simple and uncomplicated tracheotomy wound
could only be regarded as the evidence of unskilful surgery and
after-treatment. The various plastic operations undertaken for the
repair of such defects are described in the works on general surgery,
notably in the able monograph of Schüller. Dislodgment of the canula
out of the trachea as the result of an insufficiently long tube, or of
neglect to fasten the tapes which hold it properly about the neck, so
that it slips during coughing or the movements of the patient, is an
accident which may not for the moment attract the attention of an
inexperienced surgeon unless laryngeal dyspnoea is urgent. The patient
breathes quietly, the air passing by the sides of the tube, which
apparently is correctly placed. The simple test of ascertaining whether
air be passing through the canula or not, or of making a trial whether
the patient breathe as well when the finger closes the opening of the
outer tube, as he will do if the tube is out of the trachea, will
decide the question. Should the tube have slipped, it is of course at
once to be replaced.

The breaking off of a portion of the inner canula, and the terminal
piece falling down the trachea--several instances of which have been
reported during recent years--is more apt to happen with the
right-angled canula of Durham, the inner tube of which is necessarily
made up of segments held by small rivets: these become in time loosened
and the piece that they held detached. The outer tube of the
hard-rubber canula also has become detached from its collar and dropped
into the trachea. An occasional inspection of the condition of the tube
is therefore desirable.




{164}

DISEASES OF THE BRONCHI.

BRONCHITIS, ACUTE AND CHRONIC; CATARRHAL; MECHANICAL; CAPILLARY; AND
PSEUDO-MEMBRANOUS.

BY N. S. DAVIS, M.D., LL.D.


DEFINITION.--Inflammation of some part or of the whole of the mucous
membrane lining the bronchial tubes between the bifurcation of the
trachea and the alveoli or air-cells of the lungs. The inflammation may
vary in grade from simple hyperæmia, with increased irritability, to
the most intense engorgement, exudation, and tumefaction of the
membrane, and in activity from the most acute and rapidly-progressive
to the most chronic and protracted in duration.

SYNONYMS.--By the earlier writers the disease was called Peri-pneumonia
notha, Angina bronchialis, and sometimes Erysipelas pulmonis. More
recently it has been called Catarrhus suffocativus, Catarrhus
pituitosus, Catarrhus bronchialis, Bronchial catarrh, and Bronchitis;
_Fr._ Bronchite; _Ger._ Bronchialentzundung. Adopting the simple name
of bronchitis, acute and chronic, in the further consideration of the
subject I shall group the cases as they occur in general practice under
the heads of Catarrhal, Mechanical, Capillary, and Pseudo-membranous
Bronchitis.

HISTORY.--During all the earlier periods of medical history bronchitis
was generally confounded with inflammation of the membrane lining the
larynx and trachea on the one side, and with pneumonia and pulmonary
phthisis on the other. Among the earliest writers who gave more
accurate descriptions of bronchitis as a distinct disease were Badham,
J. P. Frank, and Broussais, in the latter part of the eighteenth
century. Full and accurate descriptions of the disease, differentiating
it from inflammation of other parts of the respiratory organs, were not
given, however, until the discovery of auscultation by Laennec, and its
practical application aided by percussion to the physical examination
of the chest. This important addition to the previous means for
studying the exact location and extent of all diseases within the
chest, and the largely increased attention given about the same time to
the study of morbid anatomy, soon led to as accurate an appreciation of
the existence and extent of disease in any part of the organs of
respiration and circulation as in any of the structures of the human
body.

ETIOLOGY.--The causes of bronchitis, like those of all other acute
diseases, may be divided into two classes--namely, predisposing and
exciting. The first embraces all those influences that are capable of
rendering the mucous membrane of the air-passages more susceptible to
impressions, whether by direct increase of the irritability of the
structure or indirectly by altering the quality of the blood and the
tone of the smaller blood-vessels. The second embraces such influences
only as are capable of exciting a direct increase of irritability of
the lining membrane of the bronchial tubes, with congestion of {165}
blood in its capillaries. Among the most common predisposing causes may
be mentioned age, sex, occupation or modes of life, and climatic
influences. As a general rule, the several grades of bronchitis are
more prevalent during childhood and old age than during the active
period of adult life. The British Registrar-General's Report for 1868
contained 33,258 deaths attributed to bronchitis, being 1344 for every
million of inhabitants. Of the whole number, 10,550 died during the
first three years of life, and 18,485 over forty-five years of age,
leaving only 4223 to occur between the ages of three and forty-five
years. This, however, is very far from indicating correctly the
relative prevalence of the disease at the different periods of life,
for the reason that the disease is far more fatal both in early life
and in old age than in the early and middle periods of adult life.[1]
During the months of February, March, and April, 1882, in San
Francisco, there were 65 deaths reported from bronchitis, of which 37
were of children under five years of age, 25 adults over forty years,
and only 3 persons between five and forty years. During the same months
there were reported 154 deaths from bronchitis in the city of Chicago,
with about the same ratio in regard to age. In the city of
Philadelphia, during the seven years from 1862 to 1869, the deaths from
bronchitis at all periods of life aggregated 969, of which 495 were of
children under five years of age, 14 over five and under fifteen years,
and 460 of persons over fifteen years of age.[2] These and similar
mortuary statistics have led to the very general adoption of the
opinion that early childhood and old age are pre-eminently susceptible
to attacks of bronchitis. Yet my own clinical observations and records
relating to the time and number of acute and subacute cases of
bronchitis coming under my own care lead to a very different
conclusion. By reference to those records I find a larger number of
cases occurring between the ages of ten and thirty years than at any
other period of life. Thus, during the first six months of the present
year (1882) I recorded 59 cases of primary bronchitis; that is, cases
not arising secondarily as complications of other diseases. Of this
number, only 5 were children under ten years of age, 38 between ten and
thirty years, and 16 over forty. It is probable that similar results
will be obtained by all who will take the trouble to record the whole
number of cases, instead of simply the number of deaths. The statistics
of mortality in relation to this disease are deceptive, not only in
regard to relative susceptibility of the human system to attacks at the
different periods of life, but also in regard to the ratio of mortality
of the disease itself. It is generally conceded that the chief
mortality from this disease occurs during infancy or early childhood
and in old age, cases rarely terminating fatally in youth or the more
active period of adult life. Careful examination of cases will show
that this fatality at the extremes of life is owing mainly to the
greater tendency of the inflammation at those periods to extend
directly from the bronchioles into the lobules of the lungs, thereby
complicating the bronchitis with lobular pneumonia; and in more than
half the cases reported under the head of bronchitis the fatal result
was caused by the pneumonia instead of the bronchitis.

[Footnote 1: See _Reynolds's System of Medicine_, Amer. ed., vol. ii.
p. 318.]

[Footnote 2: See _A Practical Treatise on the Diseases of Children_, by
J. F. Meigs, M.D., and William Pepper, M.D., 4th ed., p. 189.]

Neither recorded facts nor my own clinical observations show any
decided difference in the susceptibility of the sexes to attacks of
bronchial inflammation.

Those occupations which confine the parties pursuing them much indoors,
and at a temperature either too warm or too cold, strongly predispose
to attacks of inflammation of the membrane lining the respiratory
passages. Habitual exposure to a warm, confined air invites free
exhalation from both the bronchial and cutaneous surfaces, with
increased susceptibility, and {166} consequently renders the individual
more susceptible to all external impressions. Habitual passive exposure
indoors to a low temperature represses the exhalations and causes the
retention of some of the products of tissue-change which by their
presence in the blood render the individual more liable to attacks of
inflammation on the supervention of any exciting cause. For the same
reasons the habitual wearing of too much warm clothing on the one hand,
or too little on the other, predisposes to attacks of bronchial
disease. Another error of importance is the unequal adjustment of
clothing to different parts of the cutaneous surface. In children
especially we often see an abundance of warm clothing over the whole
body, while the legs and feet and neck have but a single covering, and
sometimes none. And even adult women often go out loaded with warm
clothing, while their feet and ankles are protected only by thin shoes
and stockings. All those occupations that surround the workmen with an
atmosphere filled with irritating gases, floating particles of stone,
metal, or charcoal, or with the dust from grain and many vegetable
substances, increase the liability of such workmen to attacks of all
grades of bronchial inflammation.

It is universally conceded that bronchitis, as well as inflammation of
all other parts of the mucous membrane lining the air-passages,
prevails most in such countries as are characterized by a cold, damp,
and variable climate. This can be well illustrated by comparing the
prevalence of this class of diseases in that belt of our own country
lying north of the fortieth parallel of latitude and east of the Rocky
Mountains with the prevalence of the same class in the belt south of
the thirty-third parallel and bordering upon the Atlantic and Gulf of
Mexico. In the former the summers are comparatively short, with brief
periods of high temperature, the winters cold, and the transition
seasons, spring and autumn, long and exceedingly variable, with a
predominance of cold and dampness. In the latter all the conditions
just mentioned are substantially reversed. Perhaps the earliest
reliable statistics we have bearing upon this subject are those
collected by Samuel Forrey from the several military posts occupied by
the United States Army, and given in a series of articles in the
_American Journal of Medical Science_, and subsequently in an octavo
volume, on the climate of the United States and its influence over the
prevalence of diseases. The valuable facts presented by Forrey were
added to by Daniel Drake, and given in full in his large work on the
topography and diseases of the great interior valley of this continent.
From these sources we learn that the average annual number of attacks
of inflammation of the mucous membrane of the respiratory passages in
every 1000 soldiers at Fort Snelling, in Minnesota, latitude 44° 53'
N., was 600. At Fort King, fifty miles from the Gulf of Mexico,
latitude 28° 58' N., the annual number of attacks average only 101.2 in
every 1000 persons. Again, at Madison Barracks, near Sackett's Harbor,
New York, the average number of attacks for every 1000 persons was
637.2, while at Key West, Florida, the average number of attacks was
208.9, and at Baton Rouge, Louisiana, only 207.2. Lest it should be
thought that these five posts had been selected for the purpose of
showing the most extreme contrasts, it may be added that Drake, after a
laborious comparison of the statistics at all the military posts in the
great interior valley from Fort Snelling at the north to Fort Jessup in
Louisiana, the most southern, makes the "ratio of decrease in bronchial
inflammations" as we pass from the north to the south as 31.5 for each
degree of latitude.[3] A similar comparison of the statistics of all
the posts on the Atlantic Slope from Madison Barracks to Key West gives
nearly the same results. The general inference here drawn concerning
the much greater prevalence of bronchitis in the colder and more
variable climate of the northern belt of our country {167} than in the
southern is fully corroborated by all the facts to be gathered from
observations in civil life.

[Footnote 3: See _A Systematic Treatise on the Principal Diseases of
the Interior Valley of North America, etc., etc._, 2d Series, pp. 795,
796.]

A study of these same military statistics, representing the mean ratio
of the prevalence of diseases of the respiratory passages for a period
of ten years at nearly all the posts, will justify some other
inferences of interest besides the one just stated. According to this
general inference or rule, which is assented to by all the authors
within my reach, the three important factors in the climates most
favorable for producing bronchial inflammation are cold, variableness,
and dampness, the latter being emphasized by most writers as of
predominating influence. Yet the tables before us show that the highest
ratio of prevalence of inflammatory attacks of the mucous membrane of
the respiratory passages in the northern part of the interior valley
was at Fort Snelling, in the immediate vicinity of St. Paul, Minnesota,
being 600 attacks for every 1000 soldiers, while the lowest ratio was
at Fort Dearborn, on the site now occupied by the city of Chicago,
being only 102 for every 1000 soldiers. Looking at the posts in the
eastern part of the northern belt of country, Madison Barracks, at
Sackett's Harbor, at the eastern end of Lake Ontario, gives a ratio of
637 attacks for every 1000 soldiers, while Fort Niagara, at the mouth
of the Niagara River, near the western end of the same lake, gives a
ratio of only 355. Again turning to the posts in the southern belt of
country, the tables show at Fort Jessup, in the interior of Western
Louisiana, a ratio of 432.8, while at Fort Jackson the ratio was only
47.5 and at Fort King 101.2. As Fort Snelling is on the high rolling
prairie of the interior of Minnesota, noted for its cold and dry air,
and Fort Jessup on the elevated arid plateau between the head-waters of
the Sabine and the Red River, they cannot be noted for a high degree of
atmospheric moisture. On the other hand, Fort Dearborn was located on
the south-west shore of Lake Michigan, on the borders of a low and wet
prairie with a substratum of impervious clay, giving all the conditions
favorable for the prevalence of a high degree of atmospheric moisture.
And Forts Jackson and King are both on low alluvial lands only fifty
miles from the Gulf. Again, Fort Niagara is surrounded by all the
conditions favoring a high degree of atmospheric moisture, certainly
equal to those surrounding Madison Barracks in nearly the same
latitude, and yet the ratio of attacks in the latter was nearly double
those in the former. It is evident, therefore, that there exists some
important factor in the climatic relations of the inflammatory
affections of the respiratory passages besides temperature, humidity,
and changeableness. A glance at the topography of the whole country
will show that each of the posts giving a high ratio of
attacks--namely, Madison Barracks and Forts Snelling and Jessup, to
which may be added Forts Gratiot, Crawford, and Wood--are so located as
to be exposed to the prevalence of unusually severe winds or
atmospheric currents either from the north-east or the north-west and
west, with certain relations either to high mountain-ranges or
ocean-currents. For instance, from Madison Barracks the open valley of
the St. Lawrence River extends in a north-easterly direction to the
Atlantic Ocean, where the cold ocean-current is from the north,
favoring the pressure of cold atmospheric currents directly up the
valley from the north-east, reaching its termination at the eastern end
of Lake Ontario with but little diminution of force. The mountains of
Northern New York, Vermont, and New Hampshire seem to prevent the
deflection of these currents to the south, and help to keep them
directly in the line of the valley. That the high ratio of attacks of
bronchial and catarrhal affections at Madison Barracks is largely due
to the influences here described is corroborated by the fact that the
same class of diseases are much more prevalent in the province of
Quebec, through which the valley of the St. Lawrence extends, than in
the province of Ontario, as shown by the Registrar-General's Report in
reference to the several {168} military posts in the Canadas. Turning
to Forts Snelling and Crawford at the north and Jessup at the south, we
find them so situated in relation to the great mountain-chains to the
west as to be fully exposed to the cold and strong atmospheric currents
that sweep over the Plains from the north-west and west with such force
as to justify the popular title of blizzards. Without consuming more
time in details, it may be said that the force and direction of
atmospheric currents have quite as much to do with the development of
inflammations of the air-passages, including all grades of bronchitis,
as either temperature or humidity.

As might be inferred from what has already been said in relation to the
influence of climatic conditions, season of the year is also found to
exert a marked influence over the prevalence of bronchial affections.
Those parts of the year characterized by a low temperature, high winds,
and frequent thermometric changes are accompanied by the highest ratio
of prevalence of inflammations of the respiratory passages. Thus, the
statistics compiled from the records of all the military posts by Drake
show an average ratio for the four quarters of the calendar year of
119.8 for the first quarter, 72.7 for the second, 48.7 for the third,
and 99.6 for the fourth.[4] This corresponds closely with the results
of clinical records kept under my own observation through a series of
years.

[Footnote 4: See Drake on the _Principal Diseases of the Interior
Valley of North America_, p. 792.]

That tubercular deposits in the lungs, cancerous growths, emphysema,
and previous attacks of bronchitis, all strongly predispose the patient
to further attacks of the last-named disease, is proved by universal
clinical experience.

EXCITING CAUSES.--Exposure to sudden and extreme changes in atmospheric
temperature from warm to cold is almost universally regarded as the
chief exciting cause of inflammation of the bronchial as of all other
parts of the mucous membrane of the air-passages. More accurate and
detailed observations, however, show that such changes of temperature
are seldom productive of diseases of this class unless accompanied by
coincident high winds and humidity. My own studies concerning the
relations between special meteorological conditions and the prevalence
of particular diseases have led me to the following conclusions in
regard to bronchitis and inflammation of the mucous membrane of the
air-passages generally:

First. Many sporadic cases are caused, at any and all seasons of the
year, by exposure of limited portions of the cutaneous surface to cool
or cold currents of air while the rest of the body is well protected.
Females going out with thin shoes and stockings or sitting before open
windows with low-necked dresses, and children out on cold days with
naked legs from short trousers and defective stockings, afford many and
familiar examples of bronchitis from this cause.

Second. The sudden transition from a protracted period of intense dry
cold to a higher temperature with increased atmospheric humidity.
Almost every winter season, in the northern belt of the United States,
east of the Rocky Mountains, is characterized by several periods of
steady dry, cold air, varying from one to three weeks in duration,
during which the mercury in the thermometer often descends more than
20° C. (8-10° F.) below zero, and which generally ends in a sudden
change in the direction of the winds and a marked elevation of
temperature, constituting what is popularly called a thaw. Such changes
are very uniformly accompanied by a general prevalence of catarrhal
affections of the air-passages, including many cases of bronchitis.
This class of cases occur principally in the months of December,
January, and February.

Third. The occurrence of those cold north-east winds that during the
latter part of autumn and early part of spring so often sweep over the
whole extent of our Atlantic coast and press up the valley of the St.
Lawrence to {169} the great interior lakes, and the still more severe
currents that come during the same seasons from the north-west and
west, over all the wide plains that intervene between the great
mountain-chains to the west and the upper lakes and Mississippi River
to the east, are also accompanied by a high ratio of prevalence of
bronchial affections, as has been already shown from the records of the
several military posts. Most of these severe storms of wind are
accompanied by either snow or rain and a marked increase of ozone or
active oxidizers. In some of the severe snowstorms from the north-east,
occurring in the latter part of February and in March, I have found an
unusual amount of free ammonia. Whether either the ozone or the ammonia
has had anything to do with the production of the bronchitis cannot be
determined until the observations and records now being made under the
auspices of the American Medical Association have been continued for a
few years, by which adequate data will be furnished for reliable
deduction.

Besides ordinary meteorological conditions, bronchitis may be produced
by inhaling irritating substances, such as steam, irritating gases,
steel-dust, or minute particles of other metals or stone in workshops,
and the dust encountered in handling grain, etc. The disease has often
occurred in epidemic form without the presence of an obvious exciting
cause. It also frequently occurs in connection with certain general
fevers, more particularly with typhoid, measles, influenza, and
pertussis. It also sometimes, though more rarely, accompanies
rheumatism, constitutional syphilis, and erysipelas. The presence of
tuberculous and cancerous deposits in the lungs almost always provokes
more or less bronchial inflammation during some part of their progress.


Acute Bronchitis.

SYMPTOMATOLOGY.--The most common form of acute bronchitis, by many
writers styled catarrhal bronchitis, acute bronchial catarrh, etc.,
presents considerable variety of symptoms, according to the extent of
the membrane involved and the intensity of the inflammatory process. As
a general rule, the disease commences with slight chilliness or unusual
sensitiveness to slight changes of temperature, accompanied by a sense
of soreness and oppression behind the sternum and sometimes across the
whole chest, with a frequent and rather dry, harsh cough. In many cases
there is during the first day or two coincident congestion of the
membrane lining the nostrils, fauces, and larynx, causing sneezing,
with some feeling of soreness in the throat and hoarseness, also a
heavy dull pain in the head, much increased by coughing. By the second
day a moderate general fever has supervened, characterized by dryness
and moderate heat of the skin, flushed face, slight increased frequency
and fulness of the pulse, more sense of oppression and soreness in the
chest, with a continuance of harsh, dry cough, which often causes
soreness in the epigastrium, radiating laterally in the direction of
the attachments of the diaphragm to the inner surface of the ribs. On
the second or third day the inflamed membrane begins to be less dry and
the paroxysms of coughing bring up a scanty expectoration of a
tenacious, somewhat frothy mucus, which gradually increases until about
the fourth or fifth day, when it becomes more opaque, sometimes
yellowish, and much more easily expectorated. At the same time that the
expectoration changes to a more opaque condition, the general febrile
symptoms begin gradually to abate, and the cough is accompanied by less
sore pain both in the chest and head.

In the milder class of cases, the decline in all the general symptoms
is so rapid that by the seventh or ninth day, convalescence is
established. But in the more severe cases the more important symptoms
may continue through {170} two weeks, and convalescence not be complete
until the end of the third week. And in some of the cases the
inflammation does not disappear on the subsidence of the febrile
symptoms, but degenerates into a chronic form, causing a continuance of
cough, with some muco-purulent expectoration and slight soreness in the
chest, through an indefinite period of time. The disease is most likely
to take this course when it occurs in young persons having a scrofulous
diathesis, or in connection with eruptive fevers or pertussis, or in
the aged afflicted with rheumatism.

During the active stage of ordinary cases of bronchitis the urinary
secretion is diminished in quantity, redder than natural, and deficient
in chloride of sodium, and the bowels are inactive. But after the
crisis of the disease is passed, as indicated by the character of the
expectoration, the renal and intestinal discharges soon return to their
normal condition.

The results of auscultation and percussion in ordinary bronchitis,
limited to the membrane lining the larger bronchial tubes, are mostly
negative. In some instances during the first or dry stage, the
respiratory or vesicular murmur may be slightly harsher or more dry
than natural, and after the exudation or secretion of mucus, as
indicated by expectoration, there may be some coarse, moist râles,
which are removed temporarily by coughing, but return again in a little
time. These râles are heard much more in cases occurring either in
infancy or in old age than in youth or the middle period of adult life.
Percussion elicits only the natural degree of resonance throughout the
whole course of the disease, except in those rare cases in which
complete occlusion of the bronchial tube has taken place, causing
exclusion of air from certain lobules of the lungs, and consequently a
shade of dulness on percussion over such lobules.


Mechanical Bronchitis.

By mechanical bronchitis is meant those cases in which the inflammation
is caused by the direct action of mechanically irritating substances
floating in the inspired air, as fine particles of steel and other
metals, particles of stone, charcoal, and various vegetable powders and
fungi. Such substances, when inhaled, are liable to impinge on the
surface of the bronchial membrane and produce direct irritation and
inflammation, both acute and chronic.

Cases originating from this class of causes differ from ordinary acute
bronchitis chiefly in the mode of beginning and in the greater tendency
to continue in the chronic form. Instead of slight rigors, coryza, and
early development of moderate general fever, the patient generally
complains first, and for several days, of a sense of tickling or
fulness in the air-tubes, with occasional paroxysms of violent coughing
and little expectoration. Sometimes particles of the foreign substance
that is producing the inflammation may be seen mixed with the mucus or
matter expectorated. In many of these cases there is much soreness in
the chest and considerable dyspnoea, especially during the night,
followed by severe coughing in the morning, and a more free discharge
of mucus occasionally containing little streaks of blood, but which is
never intimately intermixed with the sputa as in pneumonia. If the
patient, by change of occupation or otherwise, ceases to be exposed to
the further action of the exciting cause, the symptoms soon begin to
abate, and a complete recovery may take place in from two to four
weeks. If exposure to the further action of the exciting cause is not
avoided, the disease will necessarily assume a chronic form, and in
many cases produce such changes as to materially shorten the life of
the patient.


{171} Capillary Bronchitis.

By this term is meant inflammation in the smaller bronchial tubes, but
not necessarily involving the true bronchioles as they terminate in the
air-cells. It may arise from all the causes that are capable of
exciting inflammation in the larger and medium-sized tubes. It may
occur at any period of life, but is most frequent in infancy and early
childhood, and next in persons past the middle period of life.

The chief differences in the clinical history of this and ordinary
catarrhal bronchitis arise from the greater obstruction to the ingress
and egress of air through the inflamed tubes. The same degree of
tumefaction of the membrane that occasions but little obstruction in
the larger tubes is capable of completely obstructing many of the
smaller ones, and thereby causing much dyspnoea and sense of
oppression, with frequency of respiration, accompanied at first by an
abundance of dry râles in all parts of the chest, followed later by the
complete intermixture of dry sounds and moist submucous râles, the
latter caused by more or less exudation or secretion of mucus from the
inflamed mucous membrane. The addition of the tenacious mucous
exudation to the previous tumefaction of the membrane, often so far
obstructs the ingress of air to the air-cells of the lungs that the
respirations become short, very frequent and noisy, with blueness of
the lips, coldness of the extremities, drowsiness, and soon death from
suffocation. This result, however, is seldom met with except in quite
young children and in persons enfeebled by age or by previous disease.

In cases which do not thus tend to an early fatal result from the
direct obstruction of the bronchi the respirations continue frequent,
in young children sometimes reaching 50 or 60 respirations per minute,
with much dyspnoea and restlessness; the pulse is quick, but not in
proportion to the respirations; the expression of countenance is
anxious and often slightly bloated, with a leaden hue of the prolabia;
the wings of the nose expand and the chest heaves with each
inspiration, giving a great variety of dry, whistling sounds generally
throughout the whole chest, which after the first two or three days
become mixed with sharply-defined submucous râles, and in the later
stages give place to the latter entirely. The cough is frequent and
inefficient, on account of the difficulty of getting sufficient air to
make it satisfactory. The temperature varies from 38° to 39.5° C.
(101-103° F.), seldom rising above the latter figure unless complicated
with lobular pneumonia. The urine is generally scanty and deficient in
the chlorine salts, and the bowels are inactive. The labored efforts of
breathing in many cases make the upper and anterior part of the chest
appear more prominent than natural, and even more resonant on
percussion on account of temporary emphysema from over-distension of
the air-cells in those parts, while in some parts of the lower and
posterior portions there is less expansion and less resonance than
natural from the occlusion of some of the bronchi and the partial
obstruction of others leading to those parts of the lungs.

Between the third and fifth days usually the mucous exudation, which up
to that time had been scanty and tenacious, becomes more abundant and
more opaque, and in two or three days more assumes a distinct
muco-purulent character and is much more easily expectorated. As that
which comes from the smaller bronchial tubes is less mixed with air,
and consequently less frothy than that which comes from the larger
tubes, the two qualities of matter may often be recognized in the same
mouthful of sputa; and if the whole be placed in water, that from the
smaller tubes will drop lower in the water, or sink to the bottom if
detached from the other, which floats freely upon the surface.

In acute cases, at the same time that the expectoration becomes more
opaque and more easily dislodged by coughing, all the more important
{172} symptoms begin slightly to improve, and by the end of the second
week convalescence is fairly established. Many cases, however, are less
acute, slower in progress, and do not reach convalescence in less than
two or four weeks; and many of this class manifest a strong tendency to
continue indefinitely in a chronic form, more especially in persons
past the middle period of life. In some of the cases that do not
continue in a chronic form, the bronchial membrane is left in a
condition of such susceptibility that the attack is renewed on the
slightest exposure to the exciting causes.


Rheumatic Bronchitis.

Although many systematic writers on practical medicine make no mention
of this form of bronchitis except as a complication of general
rheumatic fever, yet cases both of acute and chronic inflammation of
the bronchi, of unmistakable rheumatic character, have so often come
under my observation that I am constrained to recognize it as a
distinct form of disease. In regard to the relative frequency of the
occurrence of this class of cases, I find in a brief report concerning
965 cases of chronic pulmonary disease, read in the medical section of
the American Medical Association by F. H. Davis in 1877,[5] the
following classification of the cases:

  Chronic catarrhal bronchitis . . . . . . . . . . . . . . . . . .  403
  Chronic rheumatic bronchitis . . . . . . . . . . . . . . . . . .  283
  Chronic bronchitis accompanied by gastric derangement and
    spasmodic dyspnoea . . . . . . . . . . . . . . . . . . . . . .  119
  Chronic bronchitis, modified by syphilitic disease . . . . . . .   37
  Hereditary pulmonary tuberculosis  . . . . . . . . . . . . . . .   56
  Inflammatory pulmonary phthisis  . . . . . . . . . . . . . . . .   67
                                                                    ---
      Total  . . . . . . . . . . . . . . . . . . . . . . . . . . .  965

It will be seen that, of the 842 cases of chronic bronchitis included
in the table, the writer classes 283, or a trifle more than 33 per
cent., as of rheumatic character. That the relative proportion of acute
cases of a distinct rheumatic character is less than those of a chronic
grade I have no doubt, and yet their number is not so small as to be
insignificant or unworthy of careful attention.

[Footnote 5: See _Transactions of American Medical Association_, vol.
xxviii. p. 269, 1877.]

They differ in clinical history from ordinary acute bronchitis chiefly
in the following particulars: Etiologically, a large proportion of them
occur in persons of a rheumatic diathesis, either hereditary or
acquired, and at those seasons of the year characterized by a
predominance of cold and damp air with frequent changes of temperature.

Symptomatically, they are characterized from the beginning by more
continuous dull pain in the chest, often extending to the attachments
of the diaphragm, the shoulders, and the dorsal portion of the spine;
by more persistent dry, harsh cough, often exhibiting a marked
spasmodic character and accompanied by a great aggravation of the pains
in different parts of the chest. When the smaller bronchi are involved
the stage of dry râles is much more protracted, the dyspnoea and
suffocative paroxysms of coughing more uniformly aggravated at night;
and when mucous exudation does take place it remains scanty and viscid,
rarely presenting a distinct muco-purulent character unless the case is
protracted into a chronic form, and sometimes not then. During the
active stage the urine is less in quantity and more decidedly acid in
reaction than natural, and the bowels generally costive.

When not interfered with by appropriate treatment, these cases run a
much more protracted course, and more frequently degenerate into a
chronic form, {173} than those of an ordinary catarrhal character. When
they are thus allowed to run a protracted course or to continue in a
chronic form, they manifest another tendency of great
importance--namely, to have the inflammation extend by continuity from
the fibrous and muscular structures of the small bronchi into the
connective tissue of the pulmonary lobules, inducing sclerosis of the
latter tissue and consequent compression or obliteration of the alveoli
or air-cells, and permanent contraction of the chest. Much and careful
clinical observation has satisfied me that many of the cases now
classed by writers as fibrous and inflammatory phthisis began as simple
acute or subacute rheumatic bronchitis, which, being renewed at every
return of the cold, damp, and changeable part of the year, not only
ultimately caused permanent thickening of the bronchial structures, but
gradually invaded portions of the connective tissue of the lungs, and
induced similar pathological changes in it, constituting the sclerosis
just mentioned.


Pseudo-membranous Bronchitis.

This affection has been described by different writers under the
additional names of plastic, croupous or croupal, and diphtheritic
bronchitis. The extension of the inflammation and membranous exudation
to the bronchial tubes in cases of diphtheria and pseudo-membranous
tracheitis and laryngitis or croup, is of frequent occurrence. But as a
distinct disease limited to the bronchial membrane it is of
comparatively rare occurrence.

In 1854, T. B. Peacock noticed in the _Transactions of the London
Pathological Society_ 34 cases collected from European sources; Biermer
in 1867 increased the number to 58; Kretschy in 1874 added 10, and
Chevstok 4 more cases--making in all 72 cases in Europe. In 1879, W. C.
Glasgow of St. Louis read to the medical section of the American
Medical Association an interesting report on the subject of plastic
bronchitis, in which he notices 23 cases which had occurred in this
country, accounts of which were obtained from an extensive
correspondence with leading physicians in all parts of the United
States, as well as from reference to our periodical medical
literature.[6] These statistics are certainly sufficient to justify the
statement that the disease is of rare occurrence both in this country
and in Europe.

[Footnote 6: See _Transactions of the American Medical Association_,
vol. xxx. p. 177, 1879.]

The statistics thus far collected show a much greater prevalence of the
disease in males than in females, and that the larger number of cases
occur between the ages of fifteen and fifty years, although one case is
reported by T. G. Simons of Charleston, S. C., as quoted by Glasgow, at
four years of age, and Goumoens one at seventy-two. In a large
proportion of the cases reported the disease existed in a chronic form.
When acute, and affecting a large portion of the bronchial membrane, it
is liable to lead to an early fatal termination from obstruction to the
ingress of air to the air-cells of the lungs. But in many cases the
disease has extended to only a limited number of the bronchi, and
recovery has generally taken place in from two to three weeks.

The symptoms differ from those of ordinary bronchitis in only two
important particulars--namely, the more violent and suffocative
character of the cough, and the actual appearance of shreds, patches,
or casts of pseudo-membrane in the matters raised and ejected by
coughing. The latter is the only reliable diagnostic symptom by which
it can be certainly differentiated from all other forms of bronchial
inflammation. When the membranous exudation is discharged in shreds or
small pieces, it may readily escape the attention of the physician, and
even considerable casts when expectorated are in some cases so
surrounded with mucus and collapsed into a slightly yellowish mass in
the central part of the mouthful expectorated, that they might be
regarded as only {174} a more muco-purulent part of the mucous
secretion. If the whole is thrown into water, however, and agitated a
little, the membranous patches and casts will be quickly unfolded in
such a manner as to be easily recognized. It is distinguished from
mucus by placing it in a solution of acetic acid, which causes it to
swell, while mucus contracts in a similar solution. It has the
appearance of having been formed in concentric layers, and is sometimes
cast-off so complete as to present a continuous representation of one
or both primary and several of the secondary bronchial tubes. Under the
microscope it has the same fibrillated appearance as other
pseudo-membranous formations.


Chronic Bronchitis.

Cases of acute and subacute bronchitis belonging to either of the five
varieties just described may be protracted until they assume a chronic
form, and other cases of each variety are met with which have been
chronic from the beginning. This form of the disease is met with in
aged persons more frequently than at an earlier period of life. In
children it sometimes follows as a sequel of measles and whooping
cough, and in adults is often associated with tuberculosis, emphysema,
and cardiac diseases.

ETIOLOGY.--Chronic bronchitis is capable of originating from any and
all the causes that have been enumerated as capable of producing the
more acute forms of the disease, and consequently prevails most under
the same conditions of topography, climate, and social relations.

SYMPTOMATOLOGY.--The symptoms of ordinary chronic catarrhal bronchitis
differ from those accompanying the acute form of the disease, chiefly
in the absence of general fever and the existence of much less pain or
feeling of soreness and oppression in the chest. The patient generally
complains of a rather harsh, full cough, usually more severe on first
retiring to bed at night and on rising in the morning, but occurring at
intervals through the day, and accompanied by a mucous or muco-purulent
expectoration varying much in its amount and tenacity. In the great
majority of cases occurring in young persons and in the first part of
adult life, the expectoration is simply a whitish or slightly opaque
mucus, more or less frothy from the intermixture of minute bubbles of
air, and easily dislodged, especially in the mornings. In old persons
and in cases which have continued a long time, the expectoration often
becomes more copious and more decidedly purulent, with slight
feverishness at night and some loss of flesh.

In all the cases except those last mentioned the general health of the
patient is but little impaired, the appetite and secretions usually
remaining nearly natural. Those who pursue indoor occupations or are
sedentary in their habits will be prone to constipation and imperfect
digestion--more, however, from the circumstances just mentioned than
from the effects of the bronchial disease. All cases of chronic
bronchitis are subject to temporary aggravation by exposure to a cold
and damp atmosphere, whether indoors or out, and are also very
susceptible to increase from the inhalation of air containing dust or
floating particles of solid matter or of irritating gases.

Cases of ordinary chronic bronchitis rarely prove fatal without the
intercurrence of some other disease, and yet there is no natural limit
to their duration. In many cases the symptoms almost disappear during
the warm months of summer, but return with the first period of cold and
wet weather of autumn. Such patients usually find permanent relief by
changing their residence to a mild and dry climate.

The symptoms of the rheumatic grade of chronic bronchitis differ from
those just described mostly in the more severe paroxysmal character of
the {175} cough, with either no expectoration or only a scanty quantity
of a glairy, tenacious mucus; in the more soreness or dull pain in the
intercostal muscles and attachments of the diaphragm; and in the more
marked influence of sudden and severe meteorological changes. Perhaps
the most marked and distressing cases of this variety of bronchitis are
those we occasionally meet with in old persons whose joints, especially
those of the extremities, have long been stiffened and sometimes
enlarged from chronic rheumatism, and who are harassed and worn from a
harsh, suffocative cough, the worst paroxysms of which are almost
always during the latter part of the night and the early morning,
accompanied by the expectoration of considerable quantities of a thick,
viscid, and very tenacious mucus, which is dislodged with so much
difficulty that in the midst of the more violent paroxysms of coughing
the action of the stomach is reversed and its contents ejected by
vomiting. This is very liable to happen just after breakfast, and to
occasion the loss of the morning meal. The condition of these patients
is very generally ameliorated during the warm months of summer, but on
the whole they emaciate and grow more helpless from year to year, until
they die either from exhaustion or the supervention of pulmonary
sclerosis (fibroid phthisis), endocarditis, or chronic diarrhoea. There
is one grade of rheumatic irritation which is liable to attack the
fibrous texture of the smaller bronchi and to give rise to a very
persistent form of asthma, which increases with every returning cold
season of the year; but as asthma in all of its forms is treated in
other parts of this work, I only allude to it in this connection.


PATHOLOGY AND MORBID ANATOMY OF BRONCHITIS.--The special pathology of
inflammation involving the mucous membrane and other structures of the
bronchi does not differ from that of similar grades of inflammation in
any other structures of the body. It consists essentially of an
increase or disturbance of those properties of living organized matter
which regulate the molecular movements constituting nutrition,
disintegration, secretion, and cell-evolution to such a degree as to
cause accumulation of blood in the capillaries, followed by exudation
and increased cell-proliferation, which may organize into plastic
material or pseudo-membrane or degenerate into pus, according to the
coincident circumstances and condition of the patient.

Consequently, the anatomical changes resulting from acute catarrhal
bronchitis are, in the early stage, more or less intense congestion of
blood in the vessels, causing redness and tumefaction of the membrane,
soon followed by an increased flow of mucus, with increase or
proliferation of mucous corpuscles and epithelium-cells, while
leucocytes or white corpuscles are seen permeating the capillary walls
and penetrating the submucous tissue or mingling with the increased
epithelium upon the surface. These several inflammatory products are
seen adhering to the surface of the inflamed membrane and in the
smaller tubes, often so filling their calibre as to greatly interfere
with the ingress and egress of air through them, and of course adding
to the dyspnoea that characterizes the capillary form of bronchitis.
During the latter stage of the disease pus-corpuscles are seen freely
intermingled with the mucus, and, owing to the exfoliation of much of
the epithelium, the surface of the mucous membrane often appears
irregular, abraded, or ulcerated.

When the inflammation has been protracted into a chronic form, the
vessels appear less congested, but the cell-proliferations continue
both in the mucous and submucous structures, causing thickening and
increased density, with a still more purulent quality of secretion. The
bronchial glands are also {176} sometimes found enlarged, and either
softened, colored with pigment, or, more rarely, calcified.

In addition to the foregoing changes, in many cases of the capillary
form of bronchitis some lobules of the lungs are found collapsed from
the complete occlusion of the bronchi leading to them by the
accumulation of tenacious mucus with other inflammatory products. And
in the same cases the air-cells in other parts of the lungs, more
frequently the upper and anterior parts, are enlarged from
over-distension, constituting a degree of emphysema.

In very chronic cases, especially of the rheumatic variety,
considerable hypertrophy of the connective tissue of the bronchi has
been found, and in other cases atrophy of the same tissue, the latter
generally accompanied by more or less dilatation of the tubes.

In pseudo-membranous or croupous bronchitis the bronchial tubes are
found lined, and in some cases filled, with a plastic exudate. Usually,
only a limited number of the bronchi are affected. The tube-casts that
may be expelled are generally in the form of balls, which may be
unrolled, and which will then be found to be fragments or complete
cylindrical casts of the tubes. They are, when expelled, usually
yellowish and often sanious. When washed they are white. There are
frequently points of enlargement along the casts which are caused
either by the presence of air-bubbles within them, or by a more rapid
exudation from that point on the bronchus. The largest casts are
usually solid and laminated in structure; the smaller ones more
frequently are hollow, containing a greater or less number of
air-bubbles; the smallest consist of a single solid thread. Under the
microscope the casts seem to be composed of a structureless or
fibrinous substance holding numerous mucus and pus-cells, more or less
numerous globules of fat, and occasional epithelial cells; seldom red
blood-corpuscles, although these may be numerous on the surface. The
casts are usually moderately compact, firm, and elastic. Toward the end
of the disease, however, they may be less firm. In some cases toward
the close of life epithelial cells are abundant in them, but in other
cases on post-mortem examination the epithelial lining of the bronchi
is found nearly or quite entire. The mucous membrane may be much
reddened, or, on the other hand paler than normal. The submucous
tissues are also sometimes involved in the swelling, and occasionally
infiltrated with serum.[7]

[Footnote 7: For a representation of one of the most complete specimens
of pseudo-membranous casts from the bronchi the reader is referred to
the paper of Glasgow in the _Transactions of the American Medical
Association_, already referred to.]

DIAGNOSIS.--The principal diseases from which acute inflammation of any
part of the bronchial mucous membrane needs to be differentiated are
pneumonia, pleurisy, laryngitis, tracheitis, and asthma, while it is
still more important to keep a clear line of diagnosis between the
chronic grades of bronchial inflammation and the earlier stages of
pulmonary phthisis and of emphysema. From nearly all the diseases named
it is separated by negative evidence or the absence of symptoms and
physical signs characteristic of those affections. It neither presents
the rusty expectoration or high temperature or fine crepitant râle of
pneumonia, nor the acute pains or short stifled cough or
friction-sounds of pleurisy in the early stage, and still less is there
in the middle and later stages any of the dulness on percussion that
characterizes the corresponding stages of the other two diseases. In
true asthma the active symptoms are distinctly paroxysmal, without
fever or increase of temperature, and the respiration during the
paroxysms is slow, with marked prolongation of the expiratory act;
while in bronchitis, both catarrhal and capillary, the symptoms are
continuous, the temperature increased, and the respirations more
frequent than natural. All grades of bronchitis are easily
distinguished from laryngitis and tracheitis by auscultation, which
enables us {177} to trace all the morbid sounds to the chest in the
former, and to the front part of the neck in the two latter.

The great advantage of recognizing pulmonary tuberculosis and other
forms of phthisis in the early stage of the disease makes the diagnosis
between it and chronic bronchitis a matter of primary importance. This
can be readily done by all practitioners who have acquired a reasonable
degree of skill in the practice of auscultation and percussion. In all
forms and stages of pulmonary phthisis, whether from primary tubercular
deposits, pneumonic exudation followed by caseous degeneration, or from
interstitial fibroid sclerosis, there is increased vocal fremitus and
diminished resonance on percussion; neither of which is present in any
grade of uncomplicated bronchitis. It is true that in the advanced
stage of some very severe cases of capillary bronchitis there occurs
sufficient pulmonary oedema to increase the vocal fremitus and diminish
the resonance over some parts of the chest; but the accompanying
symptoms and immediately preceding history of such cases are sufficient
to separate them from any stage of phthisis. The same remark is
applicable to those rare cases in which an attack of pseudo-membranous
bronchitis results in the complete occlusion of one or more of the
bronchi and the permanent collapse of the pulmonary lobules to which
the occluded tubes lead. If in addition to the plain difference in the
physical signs already mentioned we remember that in all the forms of
phthisis there is progressive loss of flesh, some increase of
temperature and acceleration of pulse, with a contraction of the upper
and anterior part of the chest, while none of these changes result from
bronchitis alone, there should be no difficulty in keeping the line of
diagnosis clear between these two diseases. And yet there is probably
no more frequent or important error committed in diagnosis than that of
mistaking the early stage of pulmonary phthisis for bronchitis. This
may arise in part from the fact that bronchitis often supervenes and
continues coincidently with phthisis. But the practitioner should
remember that whenever there is increased vocal fremitus and diminished
resonance in any given case there is some altered condition of the
lung-structure, and consequently some form of disease besides
bronchitis, however plain the ordinary symptoms of the latter may be at
the same time.

From pulmonary emphysema, chronic bronchitis is distinguished chiefly
by the abnormally-increased resonance on percussion in the former,
especially over the upper and anterior parts of the chest, and the
peculiar depression of the spaces above the clavicles and between the
ribs at the beginning of the inspiratory act, and their return to
over-fulness near its close; while none of these changes accompany any
grade of simple bronchial inflammation.

PROGNOSIS.--In the ordinary form of acute and chronic bronchitis there
is very little tendency to terminate fatally except when it attacks
infants or persons infirm from age. And even when it occurs at these
extremes of life the fatal terminations are usually caused by the
supervention of lobular pneumonia as a complication, and not from the
bronchial inflammation alone. Severe cases of capillary bronchitis are
more dangerous, and in young children and aged or debilitated persons
often prove fatal before the end of the first week of their progress by
the direct obstruction to the entrance of air into the air-cells of the
lungs. The pseudo-membranous or plastic bronchitis is still more
dangerous. It has been estimated that one out of every five dies. But
the statistics concerning the number and character of cases are not
sufficient to furnish a reliable deduction of the ratio of mortality.

The duration of acute attacks of bronchitis of all varieties from which
recovery takes place is from one to three weeks. Uncomplicated cases of
chronic bronchitis seldom prove fatal, neither is there any self-limit
to their duration. Many cases undergo marked improvement during the
warm {178} months of summer, but suffer a renewal of all the more
severe symptoms on the return of the cold and wet weather of autumn. In
other cases the symptoms continue nearly the same through all the
seasons of the year and until an advanced period of life.

TREATMENT.--There are certain leading objects to be accomplished in the
treatment of all grades of inflammation affecting the mucous membrane
and connective tissue of the bronchial tubes--namely, _(a)_ to diminish
or overcome the morbid excitability of the inflamed part; _(b)_ to
relieve the vascular hyperæmia or fulness of blood in the vessels, and
thereby limit the amount of exudation or morbid secretion and
consequent dyspnoea; _(c)_ to counteract or relieve secondary
functional disturbances, such as increased heat and dryness of the
skin, diminished renal and intestinal activity, and nervous
restlessness; _(d)_ to hasten the removal of such plastic exudations as
may have caused thickening and induration of the inflamed structures or
formed layers or patches of false membrane on the bronchial surface,
and to lessen the tendency to establish a stage of purulent
degeneration or suppurative action in the inflamed part; _(e)_ to
regulate diet, drinks, exercise, and clothing in such a way as to
sustain healthy nutrition and prevent the further action of
predisposing and exciting causes.

The first three objects to be accomplished belong more particularly to
the early stage of acute and subacute attacks, but are present in some
degree throughout the whole course of the disease; while the last two
belong to the latter stages of the acute and to all stages of the
chronic grades of the inflammation. While the foregoing indications to
be fulfilled or objects to be accomplished are present in all the
various grades and stages of inflammation of the bronchi, the
particular means for accomplishing them will be modified by the age and
previous physical condition of the patient, the nature of the
predisposing and exciting causes, the extent of the disease, and the
stage of its advancement; or, in other words, the nature and extent of
the pathological changes already accomplished. For instance: the same
remedial agents that would be most efficient in relieving the morbid
excitability and the vascular fulness of the first stage of acute
inflammation in a young or middle-aged and previously healthy, vigorous
subject might be positively injurious, or even fatal, if used in the
same stage of inflammation in a subject previously anæmic and feeble or
debilitated from age or from causes capable of impairing the quality of
the blood and favoring a typhoid condition of the system. Consequently,
the practitioner who not only sees clearly the objects most desirable
to accomplish, but who most judiciously selects and adjusts the means
or agents he uses to the special conditions of each patient, will meet
with the highest degree of clinical success.

In the first stage of acute attacks involving the bronchi of both lungs
in vigorous adult persons, and especially if the inflammation extends
into the smaller tubes, causing much dyspnoea and dry râles, there is
no single remedy that will so certainly and speedily check the intense
engorgement of vessels in the bronchial membranes, and thereby gain
time for the action of other remedies, as one prompt and liberal
abstraction of blood by venesection. In cases of a little less
severity, and in children, the application of from two to twelve
leeches to the upper and anterior part of the chest, the number being
regulated by the age of the patient, will be a good substitute for the
venesection. And in case leeches are not at hand extensive dry cupping
over both the anterior and posterior parts of the chest may be applied
with much benefit. Immediately after the venesection, leeching, or
cupping, and without these in cases of only ordinary severity, the
whole chest may be enveloped in an emollient poultice or in folded
napkins wet in warm water and covered with oiled silk. At the same time
the following combination may be given internally: {179}

  No. 1. Rx. Liquoris ammonii acetatis, (60.0 c.c.) fluidounce ij;
             Tincturæ opii camphoratæ,  (75.0 c.c.) fluidounce iiss;
             Vini antimonii,            (15.0 c.c.) fluidounce ss;
             Tincturæ veratri viridis,   (6.0 c.c.) fluidrachm iss.

M.--Sig. Give to an adult 4 cubic centimeters or 1 teaspoonful in a
tablespoonful of water every two, three, or four hours, according to
the severity of the case. The same may be given to children, the dose
being properly adjusted to the age of the child.

If the tongue be coated, the bowels inactive, and urine high-colored,
from 6 to 30 centigrams (grs. j-v) of calomel, according to the age of
the patient, may be given, and followed in four or five hours by a
saline laxative sufficient to procure two or three evacuations from the
bowels. Under the influence of these remedies the high fever and great
sense of soreness and oppression in the chest which exist in the first
stage of the more acute cases in previously healthy subjects rapidly
diminish, giving place to more moist râles, easier breathing, and some
expectoration. As soon as such amelioration of symptoms has been
obtained, the mixture containing veratrum viride should be
discontinued, and the following formula substituted in its place:

  No. 2. Rx. Syrupi scillæ comp.       (45.0 c.c.) fluidounce iss;
             Tincturæ sanguinariæ,     (15.0 c.c.) ounce ss;
             Tincturæ opii camphoratæ, (60.0 c.c.) fluidounce ij.

M.--Sig. Give to an adult 4 cubic centimeters in a little additional
water every three or four hours.

If the patient suffers much from severe sore pain in the head,
aggravated by coughing, or from nervous restlessness, the addition of
bromide of potassium, 16 grams (drachm iv), to the above formula will
render it more efficient in relieving these symptoms and in promoting
rest. Under such quieting and expectorant influences, aided by a mild
laxative when needed, the cough, soreness, and oppression in the chest,
and all other active symptoms, diminish from day to day, and
convalescence ensues in from seven to nine days.

If after the first three or four days the temperature rises in the
evening and the cough becomes more troublesome, interfering with rest
during the first part of the night, followed by some sweating in the
early morning, a single dose composed of sulphate of quinia from 3 to 6
decigrams (gr. v-x), pulverized sanguinaria-root 3 centigrams (gr. ½),
and codeine 16 milligrams (gr. ¼) given between six and eight o'clock
each evening for three or four evenings, will often contribute to the
rest of the patient and hasten the establishment of convalescence.

Cases are sometimes met with, especially in patients debilitated by
previous ill-health or age, in which the fever subsides after the first
three or four days, leaving the patient with a feeling of unusual
weakness, a deep harassing cough, copious muco-purulent expectoration,
and little or no appetite. In such cases tonics and the more
stimulating class of expectorants are indicated. A mixture of equal
parts of the syrup of Prunus virginiana, syrup of senega, and
camphorated tincture of opium, given in doses of 4 cubic centimeters or
one teaspoonful every four or six hours, and 13 centigrams (gr. ij) of
quinia three times a day, will often cause a rapid improvement in all
the symptoms. In some of the cases last described there is added to the
other symptoms a troublesome nausea and disposition to vomit with the
paroxysms of coughing, in which I have found the following formula a
good substitute for the mixture containing the prunus virginiana and
senega:

  No. 3. Rx. Acidi carbolici,         (0.50 grams) gr. viij;
             Glycerinæ,                (30.0 c.c.) fluidounce j;
             Tincturæ opii camphoratæ, (60.0 c.c.) fluidounce ij;
             Aquæ,                     (60.0 c.c.) fluidounce ij.

{180} M.--Sig. Give 4 cubic centimeters (fluidrachm j) or 1 teaspoonful
before each mealtime and at bedtime, giving the quinia a little after
the meals.

If more anodyne influence is required to procure rest at night, 16
milligrams (gr. ¼) of codeine may be added to the teaspoonful of
carbolic acid mixture given at bedtime. If, as sometimes happens in
cases of acute bronchitis, both of the catarrhal and capillary
varieties, the inflammation invades some of the lobules of the lungs,
as indicated by undue rise of temperature, greater expansion of the
wings of the nose during inspiration, with short expiration, and
diminished resonance with fine crepitation over limited portions of the
chest, I have found the most certain and speedy relief to follow the
application of a blister over the seat of the pneumonia and the
internal use of the following formula:

  No. 4. Rx. Ammonii chloridi,          (12.00 grams) drachm iij;
             Antimonii et
               potassii tartratis,       (0.13 grams) gr. ij;
             Morphiæ sulphatis,          (0.20 grams) gr. iij;
             Extract, glycyrrhizæ fluidi, (30.0 c.c.) fluidounce j;
             Syrupi,                      (90.0 c.c.) fluidounce iij.

M.--Sig. Give to adults 4 cubic centimeters (fluidrachm j) or 1
teaspoonful, mixed with a tablespoonful of water, every three or four
hours until some relief is obtained, and then at longer intervals. For
children the doses must be diminished in proportion to the diminution
of age. Quinine and laxatives may be used in these cases under the same
indications as in uncomplicated bronchitis.

In the severe attacks of capillary bronchitis in young children many
writers recommend emetics, and subsequently nauseating doses of
antimony or ipecacuanha. But I have not seen sufficient benefit result
from emetic doses of these agents to compensate for the early
prostration, and sometimes continued gastric irritability, which they
induce. I prefer the proper application of leeches at the very
beginning, followed by emollient applications to the chest, and the
same remedies internally as already mentioned, aided, perhaps, by an
earlier use of quinine and digitalis if the cardiac action becomes weak
and frequent. In all this class of cases, however, much caution should
be exercised in regard to the use of opiates, either alone or in
combination with other remedial agents, lest their narcotizing
influence should diminish the force and frequency of the respiratory
movements too much, and encourage the accumulation of the inflammatory
products in the smaller bronchi to such a degree as to produce apnoea
or death by the exclusion of air from the alveoli or air-cells of the
lungs. And yet just enough of these quieting agents to diminish
excitability and allay excessive restlessness is as desirable in
children as in adults.

In the plastic or pseudo-membranous form of bronchitis it is an object
of much importance, in the first stage, to limit the amount of plastic
exudation, and later to hasten the loosening and disintegration or
discharge of such layers of false membrane as may have formed on the
bronchial mucous surface. For these purposes alterative doses of
calomel may be given alternately with the doses of the formula
containing the liquor ammonii acetatis already given (see Formula No.
1) during the first twenty-four hours, and subsequently pretty full
doses of the iodides of sodium or potassium or of the bicarbonates. In
acute cases in children, when the symptoms indicate that the false
membrane is loosening and the dyspnoea is great, an emetic that will
induce prompt and free vomiting may hasten its expulsion and afford
much relief.

In the cases which have been described as rheumatic bronchitis of the
more acute or active grade I have seen the most prompt and satisfactory
degree of relief follow the administration of the following combination
of remedies in the early stage: {181}

  No. 5. Rx. Sodii salicylatis,       (25.00 grams) drachm vj;
             Glycerinæ,                (15.00 c.c.) fluidrachm iv;
             Vini colchici radicis,    (25.00 c.c.) fluidrachm vj;
             Syrupi scillæ compositi,  (45.00 c.c.) fluidounce iss;
             Tincturæ opii camphoratæ, (60.00 c.c.) fluidounce ij.

M.--Sig. Give 4 cubic centimeters (fluidrachm j) every three or four
hours in a little additional water.

In several cases in which this grade of inflammation was located
chiefly in the smaller bronchi, causing very distressing and persistent
dyspnoea, I have found an equal mixture of the wine of colchicum-root
and the acetated tincture of opium, given in doses of 25 to 30 minims
every three hours at first, to afford more relief than any other
remedies I could use; and after some degree of relief had been
obtained, by lengthening the interval between the doses to four or six
hours and continuing it a few days, all the symptoms were removed. When
the disease occurs in old persons, accompanied by severe paroxysms of
coughing and only a scanty and very viscid mucous expectoration, much
benefit may sometimes be derived from the use of the carbonated
alkalies, such as the carbonate of ammonium or bicarbonate of sodium,
dissolved in an equal mixture of the fluid extract of the Phytolacca
decandra, liquor ammonii acetatis, and camphorated tincture of opium,
in such proportions that the patient will get 3 decigrams (gr. v) of
carbonate of ammonium in each dose of the mixture.

It is proper to remark that there are many mild attacks of bronchitis,
caused by exposure to sudden and severe meteorological changes, which
if seen during the first twenty-four hours can be speedily arrested by
a hot or stimulating foot-bath and a full dose of the compound powder
of opium and ipecacuanha (Dover's powder), taken in the evening, and
followed the next morning by a saline laxative and two or three
moderate doses of quinine during the day. Similar results can also be
obtained in some cases by the use of any agents that will allay
irritability and at the same time produce a free or copious elimination
from the skin and kidneys. An efficient diaphoretic dose of
pilocarpine, or a full warm bath, followed by two or three moderate
doses of quinine, will succeed well if employed in the initial stage of
the disease. Unfortunately, but few cases come under the care of the
physician until after this stage is past.

TREATMENT OF CHRONIC BRONCHITIS.--Most of the cases of chronic
bronchitis are treated satisfactorily by a more moderate use of the
same remedial agents that have been recommended in the acute and
subacute grades of the disease, aided by a judicious regulation of
diet, dress, and exercise. In the great majority of cases of the
ordinary chronic catarrhal variety of bronchitis the formula already
given, numbered 4, or the one numbered 2, if given to adults in doses
of 4 cubic centimeters (fluidrachm j) before each meal and at bedtime,
mixed with a tablespoonful of water, will afford the necessary relief
without confining the patient to the house. If the bowels become
constipated while using either of these prescriptions, the evil may be
obviated by taking one of the following pills every evening:

  No. 6. Rx. Extract. hyoscyami, (2.00 grams) gr. xxx;
             Ferri sulphatis,    (2.00 grams) gr. xxx;
             Pulveris aloës,     (2.00 grams) gr. xxx;
             Pilulæ hydrargyri,  (2.00 grams) gr. xxx.

M. et ft. pil. No. XXX. If one pill taken every evening does not prove
sufficient to prompt one natural intestinal evacuation each morning,
another can be taken after breakfast. The patient should adhere to a
plain, nutritious, and easily digestible diet, avoiding the use of all
varieties of alcoholic drinks, wear good warm underclothes of flannel
all the time, and take moderate daily outdoor exercise so long as the
strength will permit.

{182} In addition to the several remedies that have been mentioned as
applicable to the treatment of the different varieties of acute and
subacute bronchitis, there are many others that have been found more or
less beneficial in the treatment of chronic cases. Among the more
important of these are the iodide of potassium and sodium, the
grindelia robusta, eucalyptus globulus, oenothera biennis, cimicifuga
racemosa, asclepias tuberosa, balsams copaiba and tolu, gum benzoin,
turpentine, cod-liver oil, and the hypophosphites of sodium, calcium,
and iron; and a still larger number that have been used for inhalation.
As a general rule, when the cough is harsh and the expectoration
scanty, with the predominance of dry râles, such remedies as the
muriate and iodide of ammonium and the iodides of potassium and sodium,
given in conjunction with small doses of antimony and some mild
anodyne, will produce the best effects. On the other hand, if the
expectoration is abundant and of a muco-purulent character, the
balsamic and terebinthinate remedies, given in connection with such
tonics as the lacto-phosphate of calcium, phosphate of iron, sulphate
of quinia and strychnia with codia, hyoscyamia, or lupulin, at night to
procure rest, will afford the greatest relief. In some of these cases I
have obtained very good effects from a combination of two parts of the
syrup of iodide of calcium with one of the fluid extract of hops, given
in doses of 4 cubic centimeters (fluidrachm j) each morning, noon,
tea-time, and bedtime.

When chronic bronchitis is complicated with pharyngitis and
laryngo-tracheitis, much palliative influence may be obtained by
judiciously-directed inhalations, either in the form of vapor or
atomization. But when the disease is limited to the bronchi alone,
inhalations have much less influence over its progress or in relieving
the more distressing symptoms. And unless the nature of the material
used is judiciously selected with reference to the particular stage and
grade of the disease, the inhalations will be more likely to do harm
than good. There are two conditions of the bronchi met with in
different cases of chronic bronchial inflammation to which local
applications can be made in the form of vapor with much benefit. The
first is indicated by an abundant purulent or muco-purulent
expectoration, sometimes fetid and at other times not. For such the
full deep inhalation of aqueous vapor impregnated with some antiseptic
and anodyne will be of great service. One of the best combinations that
can be used for this purpose is that of carbolic acid with camphorated
tincture of opium in the proportion of 2 grams of the former (gr. xxx)
to 90 cubic centimeters (fluidounce iij) of the latter; 4 cubic
centimeters (fluidrachm j) of this mixture may be put into 250 cubic
centimeters (fluidounce viij) of hot water in an inhaling-bottle and
the vapor inhaled freely, five minutes at a time, two or three times
each day.

The second condition alluded to is characterized by a persistent,
harsh, irritating cough, with little or no expectoration, indicating a
sensitive and congested condition of the mucous membrane with
diminished secretion. Such cases may generally be much relieved by
adding to the antiseptic and anodyne mixture just given some one of the
oleo-resin or balsamic preparations, of which perhaps none are more
efficient than that which is known in the shops as oil of Scotch pine.
Four cubic centimeters (fluidrachm j) of this may be added directly to
the quantity of the other ingredients already given, and then used in
the same manner. The combination thus used appears to allay the morbid
sensitiveness and speedily establishes a better secretory action.

There is another important class of cases met with most frequently in
persons of both sexes between twelve and twenty years of age. They
present a narrow, imperfectly-developed chest, with so sensitive a
condition of the bronchial membrane that every trifling exposure to
cold and damp air renews the vascular hyperæmia and cough, until both
become permanent and the morbid process extends into the connective
tissue of the pulmonary lobules, {183} establishing what some call
interstitial pneumonia and others fibroid phthisis. In the earlier
stage of all this class of cases the systematic daily practice of full,
deep inhalations of pure atmospheric air, coupled with a judicious
exercise of the muscles of the chest and arms, will do more to remove
all symptoms of bronchial disease and preserve the general health of
the patient than all the medicines that have been hitherto devised.
There is much evidence in favor of using compressed air for inhalation
in these and some other cases of bronchial inflammation. The late F. H.
Davis of this city, who during his brief professional career gave much
attention to the treatment of diseases of the respiratory organs, and
had good opportunities for clinical observation, says, when speaking of
the same class of young subjects, that "the inhalation of compressed
air for from five to ten minutes once or twice a day produced marked
and rapid improvement in all the cases. The size of the chest on full
inspiration was increased from one-half inch to one inch in the first
month, and a habit of fuller, deeper breathing and a more erect
carriage was established."[8] But he adds, with proper emphasis, that
the inhalations to be permanently curative must be continued faithfully
for many months, and be accompanied by a judicious regulation of all
the habits of life.

[Footnote 8: See paper read before the Chicago Society of Physicians
and Surgeons, April, 1877, on "The Respiration of Compressed and
Rarefied Air in Pulmonary Diseases."]

Every physician of much practical experience knows, however, that, in
defiance of all the remedies and methods of treatment hitherto devised,
there are many cases of chronic bronchial inflammation which will
continue, and be aggravated at every returning cold season of the year,
so long as the patient lives in a climate characterized by a
predominance of cold and damp air with frequent and extreme
thermometric changes. And yet a large proportion of these, by changing
their residence to a mild and comparatively dry climate, either greatly
improve or entirely recover. Consequently, in all the more severe and
persistent cases such a change is of paramount importance, and should
be made whenever the pecuniary circumstances of the patient will
permit. Probably the best districts in our own country to which the
class of patients under consideration can resort are the southern half
of California, the more moderately elevated places in New Mexico and
the western part of Texas, Mobile in Alabama, Aiken in South Carolina,
and most of the interior parts of Georgia and Florida. My own
observations lead me to the conclusion that the unfortunate invalid,
suffering from any grade of chronic bronchial inflammation, can find in
some of the regions named all the relief that could be gained in the
most celebrated health-resorts on the other side of the Atlantic. But
adherence to strictly temperate and judicious habits of life, with
regular daily outdoor exercise, is essential to the welfare of the
invalid in whatever climate he may choose to reside.

In the foregoing pages I have said nothing concerning the management of
those cases of asthma, emphysema, interstitial pneumonia, etc. which
often occur either as complications during the progress of bronchial
inflammations or as sequelæ, simply because they will all be fully
considered in the articles embracing those topics in other parts of
this work.




{184}

BRONCHIAL ASTHMA.

BY W. H. GEDDINGS, M.D.


SYNONYMS.--Asthma convulsivum (Willis); Spasmus bronchialis (Romberg);
Asthma nervosum; Krampf der bronchien.

DEFINITION.--A violent form of paroxysmal dyspnoea, not dependent upon
structural lesion; characterized by wheezing respiration, with great
prolongation of the expiration, and by the absence of all symptoms of
the disease during the intervals between the attacks.

HISTORY.--Derived from the Greek [Greek: asthmatnô] to gasp for breath,
the term asthma was employed by the older writers to designate a
variety of affections of which embarrassed respiration was the most
prominent symptom, thus including a great number of diseases which a
more extended knowledge of pathology has since distributed among other
nosological groups. By the earlier authors simple embarrassment of
breathing was designated as dyspnoea; if attended with wheezing it was
called asthma; while those forms in which the difficulty in respiration
was so great as to prevent the patient from lying down were
appropriately styled orthopnoea (Celsus). Ignorant to a great extent of
pathological anatomy and unprovided with the improved methods of
physical diagnosis which we now possess, they described as asthma not
only the dyspnoea due to cardiac and pulmonary diseases, but also that
occasioned by affections of the pleura and greater vessels. Covering
such an extensive range of territory, it was found necessary to
subdivide the disease into a number of varieties, each author
classifying them according to his conception of the cause, seat, and
nature of the trouble. Some of these--_e.g._ a. dyspepticum--still find
a place in medical literature, but the vast majority of them, having
ceased to be of any practical significance, have been discarded, and
are now only interesting as examples of the crude and fanciful notions
which prevailed in an age during which science rather retrograded than
advanced.[1] Of the writers of this period, Willis in the seventeenth
century is especially worthy of notice as being the first to describe
the nervous character of asthma. Without discarding the accepted forms
of the disease, he mentions another variety, characterized by spasmodic
action of the muscles of the chest, to which he gave the name asthma
convulsivum.

[Footnote 1: "Van Helmont, discarding the ancient doctrine of the four
humors, attributed asthma to an error of the Archeus, which he
conceived to be enthroned in the stomach and to constitute the source
of all diseased as well as of all healthy phenomena. This principle, he
supposed, sent forth from the stomach a peculiar fluid, which, when it
became diseased, gives rise to a morbid state of the parts to which it
was conveyed. He moreover imagined that this fluid sometimes mixed
itself with the male semen, and thus formed a compound which, as one of
its constituents is the means provided by nature for the propagation of
the species, possesses the power of generating a disease of hereditary
character. Thus, when this compound was conveyed to the articulations,
he affirmed it produced gout, and when it took its direction to the
lungs it then occasioned asthma" (_Baltimore Med. and Surg. Journ. and
Review_, Baltimore, 1833, p. 300).]

The improvement in physical diagnosis resulting from the brilliant
discoveries of Auenbrugger and Laennec greatly curtailed the domain of
asthma. {185} With the aid of auscultation and percussion it was
discovered that most of the cases hitherto regarded as asthma were only
symptoms of some organic disease. Many distinguished authorities,
particularly of the French school, went so far as to declare that there
existed no such disease as asthma, and that in every case the dyspnoea
and other phenomena described under that name were merely symptoms of
some organic affection.

Although very generally received at first, it was not long before this
too-sweeping reform encountered opposition from various quarters. Cases
were observed with marked asthmatic symptoms in which, after death, the
most careful examination failed to reveal the slightest trace of
textural lesion. The discovery by Reisseisen of muscular fibres even in
the minutest bronchi, and the demonstration of their electric
contractility by Longet and Williams, afforded a ready explanation of
these cases, and led to the opinion--which has since been generally
received--that asthma in the modern acceptation of the term is simply a
neurosis. The more recent theories in regard to the nature of asthma
will be more fully discussed in the portion of our article devoted to
the pathology of the disease.

SYMPTOMS AND COURSE.--The following description of an attack of asthma
by Trousseau, who was himself an asthmatic, is perhaps the best that
has ever been written: "An individual in perfect health goes to bed
feeling as well as usual, and drops off quietly to sleep, but after an
hour or two he is suddenly awakened by a most distressing attack of
dyspnoea. He feels as though his chest were constricted or compressed,
and has a sense of considerable distress; he breathes with difficulty,
and his breathing is accompanied by a laryngo-tracheal whistling sound.
The dyspnoea and sense of anxiety increasing, he sits up, rests on his
hands, with his arms put back, while his face is turgid, occasionally
livid, red, or bluish, his eyes prominent, and his skin bedewed with
perspiration. He is soon obliged to jump from his bed, and if the room
in which he sleeps be not very lofty he hastens to throw his window
open in search of air. Fresh air, playing freely about, relieves him.
Yet the fit lasts one or two hours or more, and then terminates. The
face recovers its natural complexion and ceases to be turgid. The
urine, which was at first clear and was passed rather frequently, now
diminishes in quantity, becomes redder, and sometimes deposits a
sediment. At last the patient lies down and falls to sleep."

The next day the patient may feel well enough to pursue his accustomed
avocation, and may remain free from all symptoms of the disease until
another attack comes on; but more frequently he is confined to the
house, if not to bed, the slightest exertion being sufficient to cause
dyspnoea; and during the following night there is a repetition of the
paroxysm.

If unchecked by treatment, the disease may continue for days, weeks,
and in some instances even for months, the paroxysms often increasing
in severity until, as in other nervous affections, it ultimately wears
itself out.

There is no regularity in the occurrence of the attacks. In some cases
they recur every few days, while in others there may be an interval of
weeks or months between the seizures. Even in the same case, although
the individual paroxysms of the attack may come on at the same hour,
there is, except in rare instances, no regularity in the recurrence of
the attack itself; and when it does recur at a certain time it is
almost always due to some cause which, as in hay asthma, exerts its
influence only at that particular period.

In the great majority of cases asthma comes on without any warning
whatsoever, but occasionally it is preceded by certain sensations which
to the experienced asthmatic are a sure indication that an attack is
impending. With some it is only a feeling of ill-defined discomfort;
others complain of various disorders of the digestive system--a sense
of dryness of the mouth and pharynx, uncomfortable distension of the
epigastrium with eructation of {186} gases from the stomach, and more
or less obstinate constipation. A troublesome itching of the skin often
precedes the attack. Some experience a feeling of constriction around
the throat; a profuse secretion of clear urine is a symptom of this
stage. Frequent gaping, frontal and occipital headache, are mentioned;
but far more constant than all of these are certain symptoms indicative
of a mild grade of acute catarrh of the respiratory organs--coryza,
with swelling of the Schneiderian membrane and discharge from the
nostrils, sneezing, redness of the conjunctivæ with increased
lachrymation, and later, as the irritation extends downward, more or
less cough.

The attack almost always comes on after midnight, and, as a rule,
between the hours of two and six o'clock in the morning. Salter states
that nineteen out of twenty cases occur between two and four A.M. There
are, however, occasional exceptions to this rule; sometimes the patient
is attacked soon after retiring, and Trousseau cites the case of his
mother, who always had her attacks between eight and ten in the
forenoon, and also that of a tailor, whose paroxysms invariably came on
at three o'clock in the afternoon. Indeed, there is no hour of the
twenty-four during which the seizure may not take place. Various
attempts have been made to explain why it is that the paroxysms of
asthma almost invariably occur during the latter half of the night.
Many attribute it to a stasis of blood in the lungs caused by the
recumbent posture of the patient, while others claim that it is due to
a dulling of reflex impression, the patient during sleep failing to
perceive the necessity of breathing. Germain Sée, who discredits both
theories, inquires why, if the above explanations are correct, does the
attack not come on soon after retiring, as is the case with the
dyspnoea of cardiac diseases.

The paroxysm of asthma develops very rapidly, but not so suddenly as is
claimed by many authors, several minutes to half an hour or more
elapsing before it attains its full height.[2]

[Footnote 2: Germain Sée in _Nouveau Dictionnaire de Médecine et de
Chirurgie_, tome iii. p. 617, Paris, 1865.]

The patient, experiencing an urgent desire for breath, instinctively
places himself in the position most favorable for the ready admission
of air into the lungs. If in bed he sits up, and, resting on his hands
or grasping his knees with them, he so fixes the body that the muscles
of respiration may work to the greatest advantage. The shoulders are
drawn up and the head thrown back. The expression of the face is one of
great anxiety--pale at first, then red, and as the attack increases in
severity assumes a dusky, bluish tint; the mouth is partially opened,
the nostrils are dilated; the eyes, the conjunctivæ of which are much
injected, are prominent, with a wild, staring look; and the forehead is
moist with perspiration. Others in their desperate struggle for breath
spring from the bed, throw open the window, and, regardless of
everything save what they believe to be impending suffocation,
recklessly gasp in the cold night air. Sometimes the sufferer prefers
to kneel before a table or some other article of furniture, supporting
his head with his hands. Whatever posture he assumes, he is actuated by
the one impulse of placing himself in the position that will enable him
to use to the greatest advantage the muscles of respiration and their
auxiliaries. The sterno-cleido-mastoid muscles are contracted to the
utmost, and, projecting like hard cords, with the aid of other muscles
draw the chest upward. The patient instinctively avoids every
unnecessary exertion as having a tendency to aggravate his dyspnoea; he
speaks but little, and when questioned usually replies with a motion of
the head.

In ordinary respiration the inspiratory movement is twice as long as
the expirium, the latter, except in forced expiration, being a purely
passive act. In asthma this rule is reversed, the expiratory movement
being four or five times as long as the inspirium, and is often so slow
that it fills the whole of {187} the pause which usually intervenes
between the completion of one respiration and the beginning of another.
It is sometimes so slow "that it seems as though the lung would never
empty itself." In the desperate struggle for breath the respiratory
muscles are exerted to the utmost in futile endeavors to expand the
chest; with each inspiration there is an elongation of the thorax, but
no lateral movement. The chest moves up and down, but there is no
expansion; "the muscles tug at the ribs, but the ribs refuse to rise"
(Salter), the walls of the chest remaining immovable.

Notwithstanding the all but tetanic contraction of the diaphragm, there
is during each inspiration a sinking in of the epigastrium, and in
severe cases also of the spaces above and below the clavicles. During
expiration the abdominal muscles, especially the recti, are hard and
tense, the pressure thus exerted being sometimes sufficient to expel
the contents of the lower bowel and bladder.[3] The transversus is also
tightly contracted, and a cross furrow above the umbilicus indicates
that the contraction of its upper half is opposed to the contents of
the abdomen forced down by the distended lung (Biermer). Although the
dyspnoea is great, there is no increase in the frequency of the
respirations so long as the patient remains quiet, but, on the
contrary, they are often less frequent than in health. This slowing of
the respiration is also observed in the dyspnoea from laryngeal
stenosis in croup, etc.; but in these cases we do not have the
prolonged expiration which is so characteristic of asthma (Biermer). At
every breath which the patient takes there is a peculiar wheezing sound
which may be heard distinctly all over the room; it is usually heard
only during expiration, but some authors (Biermer) claim that it is
also audible during inspiration.

[Footnote 3: Bamberger's case, as quoted by Riegel, _Ziemssen's
Pathologie u. Therapie_, Leipzig, 1875, Band iv. 2, S. 282.]

On auscultating the chest it will be found that the ordinary vesicular
murmur is either entirely absent, or if heard it is only over very
limited areas. In the place of it we have an endless and ever-changing
variety of dry sounds, such as whistling, cooing, mewing, snoring,
etc., technically styled sibilant or sonorous ronchi. They are usually
equally diffused over both lungs, but are sometimes confined to one.
The sibilant râles afford an index of the degree of spasm, being in
mild cases equally audible during both inspiration and expiration,
while in severe attacks they are louder during expiration (Biermer).
That the vesicular murmur cannot be heard is due not only to its being
masked by the louder ronchi, but also to the absence of the condition
necessary for its production, the spasmodic constriction of the
bronchial tubes or their plugging with tough, viscid mucus preventing
the entrance of sufficient air to produce the sound. Sometimes a
hitherto occluded tube becomes pervious, and we have vesicular
respiration where a moment before only dry sibilant râles were heard.
Usually at the close of the attack, when cough sets in, there are
occasional moist râles. These become more frequent as the expectoration
becomes more abundant. Frequently, however, the paroxysm terminates
much more abruptly, the spasm relaxes, and the air rushing through the
tubes gives rise to puerile respiration.

During the paroxysm there is, even in the early stages of asthma, more
or less distension of the lungs, measurement of the chest showing that
its circumference is four to eight centimeters greater than before the
attack (Beau). This transitory emphysema, which must not be confounded
with that due to structural changes observed in old cases, disappears
with the attack, and the lung returns to its normal condition. This
distension causes the exaggerated resonance obtained by percussion
which is one of the most constant symptoms. At the base of the lung,
especially posteriorly and laterally, there is a peculiar modification
of the percussion sound to which Biermer has applied the name
Schachtelton, from its resemblance to the note produced by striking
{188} an empty pasteboard box. Besides this exaggerated resonance, it
will be found that the line of dulness on the right side, which marks
the upper border of the liver, is fully two inches lower during the
paroxysm than before, and that the area of cardiac dulness is somewhat
diminished by the overlapping of the distended lung-tissue (Riegel).
Another peculiarity elicited by percussion, and to which Bamberger was
the first to direct attention, is that in some rare cases instead of
moving vertically the line of hepatic dulness remains unchanged during
both acts of respiration.

Toward the close of the attack the congested mucous membrane of the
bronchi begins to secrete, and there is more or less cough. The matter
expectorated consists at first of little balls of tough,
semi-transparent mucus not much larger than a pea. It is exceedingly
tenacious, and is raised with great difficulty. Examined under the
microscope, the sputum is found to consist "of a great number of
corpuscles, some of which are polyhedral in form with rounded angles;
they are pale, homogeneous, and slightly granular. At first sight they
resemble pus-corpuscles, but they are much larger, less circular in
form, and have no nucleus. In addition to these corpuscles there are
others which are oval, elongated, fusiform, and sometimes linear in
shape, but all of them appear to be of the same nature and possess the
same refracting power as the corpuscles first mentioned. They are all
of them agglomerated in a sort of viscous matter."[4] The expectoration
often contains blood, and in some rare instances profuse hemorrhages
have been known to occur. Sometimes the matter has particles of soot
and coal-dust intermingled with it, the so-called carbonaceous sputum
(Sée). In addition to the cells above described, the sputa contains
small yellowish-green masses or threads in which are imbedded the
peculiar octahedral crystals which Leyden has ingeniously connected
with the etiology of asthma, and to which we shall again have occasion
to refer.[5] Ungar has recently also discovered crystals of oxalate of
lime in the sputa.

[Footnote 4: Germain Sée, _Nouveau Dictionnaire de Médecine et de
Chirurgie_, pp. 612, 613; also, Salter, _Asthma, its Pathology and
Treatment_, Am. ed., p. 944.]

[Footnote 5: Riegel, in _Ziemssen's Handbuch d. Pathologie u.
Therapie_, vol. iv. 2, pp. 268, 285.]

Laryngoscopic examination reveals more or less congestion of the
air-passages. "In ordinary respiration the glottis is widely open
during inspiration, and at each expiration the arytenoid cartilages
approach each other so as to narrow the glottis; but in the labored
respiration of asthma the glottis is fixed in the condition of
expiration; that is, the glottis is narrowed, and the air enters and is
expired through the same narrow space."[6]

[Footnote 6: Steavenson, _Spasmodic Asthma_, p. 23.]

The embarrassment of respiration and the pressure of the air in the
distended alveolæ by impeding the capillary circulation of the lungs
prevent the left auricle from receiving its full supply of blood; hence
the pulse is small and weak during the paroxysm, but regains its
natural volume as soon as its immediate effects are over. The action of
the heart, like every other phenomenon of asthma, is subject to
constant variation. At one moment it beats tumultuously, while at the
next its action may be so feeble as to cause temporary syncope (Sée).
The venous blood, unable to overcome the obstacles to its passage, is
forced back into the vessels, causing distension of the cervical veins
and the jugular pulse sometimes observed in severe attacks. The bluish
hue of the face in bad cases is due to cyanosis resulting from
insufficient aëration of the blood. The paroxysm is unattended with
fever, the temperature, if altered at all, being rather below than
above the normal. Coldness of the face and hands is quite a common
symptom in protracted cases.

In addition to the nervous sensations described among the premonitory
symptoms, patients have been known to suffer from disturbances of a
more {189} serious nature during the paroxysm. In some instances there
is complete loss of consciousness, and Riegel[7] states that such cases
have been known to have tetanic convulsions of the trunk and
extremities.

[Footnote 7: _Loc. cit._ p. 285.]

The course of an attack of asthma is in most cases quite typical, the
paroxysms recurring nightly for an indefinite period, and usually
increasing in severity until, as in epilepsy and other nervous
diseases, it finally exhausts itself. On awaking from the sleep which
usually succeeds the final paroxysm the patient, unless the attack has
been very mild and of short duration, feels weak and exhausted, but
there is no tendency to the recurrence of the dyspnoea; on the
contrary, he may expose himself with perfect impunity to the causes
which at other times would be certain to produce an attack. The chest
feels stiff and sore, the cough and expectoration diminish, and in a
few days disappear, and if the disease has produced no organic lesion
the patient returns to his usual state of health.

DURATION.--The duration of asthma, except in young persons and in those
rare cases in which the cause can be discovered and removed, is very
indefinite, the disease lasting for years, if not for life. As the
patient grows older the attacks become less severe, but are more
frequent. Sometimes a case which has recurred for years and defied the
most energetic treatment will all at once recover of itself.

SEQUELÆ.--Although bronchial asthma is essentially a neurosis, and
therefore purely functional in its character, it is rare for it to
continue for any great length of time without causing some organic
affection of the lungs or heart.

The most common sequel of asthma is emphysema. The bronchial tubes
being more or less completely closed, either by contraction of their
muscular fibres or by plugs of thick, viscid mucus, the air pent up in
the parts beyond the obstruction is subjected to the negative pressure
produced by the exaggerated inspiratory act, becomes rarefied, and, in
obedience to the diminished resistance induced by the partial vacuum in
the thorax, causes distension of the air-cells. This condition
continues until, the tubes having again become pervious, the natural
elasticity of the lung-tissue, aided by the expiratory muscles, forces
out the air and permits them to return to their natural size. This is
the transitory emphysema to which we have already alluded. Germain
Sée[8] regards it as analogous to the paralytic emphysema which occurs
the moment the pneumogastric is divided. With repeated attacks the
air-cells lose their elasticity and remain permanently dilated. Owing
to the constant distension, the walls of the alveolæ become more and
more attenuated, until, finally giving way, two or more of them
coalesce, forming one large cell. The symptoms of this condition are
the same as those of ordinary vesicular emphysema.

[Footnote 8: _Op. cit._, p. 637.]

Owing to partial occlusion of the afferent bronchi and the altered
conditions of pressure mentioned, the blood accumulates in the
capillaries during the paroxysm, the lung-cells do not receive their
adequate supply of air, and oxygenation is imperfect. In the early
stages of the disease this congestion is only temporary, and disappears
with the removal of the obstruction, but in those cases in which the
attacks are severe and frequent the vessels lose their contractility
and remain permanently congested.

The state of chronic congestion just mentioned is occasionally attended
with serous exudation into the interalveolar tissue, which by pressing
upon the adjacent air-cells causes their obliteration. This oedema,
with the remains of the compressed air-cells and the viscid mucus
stagnating in the finer tubes, forms the little islets of carnified
tissue known as lobular pneumonia.

The most frequent change observed in the bronchial tubes in old cases
of asthma is hypertrophy of their muscular fibres, causing thickening
of their {190} walls and diminished calibre. In other cases they are
dilated, but this condition is due more to the concomitant bronchial
catarrh than to the asthma.

Obstructed in its course through the lungs, the venous blood
accumulates in the pulmonary artery, and, pressing back upon the right
ventricle, excites it to increased action, which in the course of time
leads to hypertrophy of its muscular fibres and dilatation of its
cavity.

In the early stages of asthma, the face is usually pale during the
intervals between the paroxysms, but when the latter become more
frequent the impeded circulation causes stasis in the peripheral
vessels. The imperfectly-oxygenated blood gives the face a dusky hue,
and in severe cases it may become bluish or even violet-colored. The
eyes are prominent, owing to the enlargement of the orbital veins
(Sée), and the conjunctivæ congested and watery.[9]

[Footnote 9: For a description of symptoms of the above-mentioned
secondary affections the reader is referred to the articles on
EMPHYSEMA and HEART DISEASE.]

ETIOLOGY.--Predisposing Causes.--Every one is not liable to asthma, and
the fact that out of a large number exposed to its exciting causes only
a few are attacked justifies the assumption that there is an inherent
tendency to the disease. That this tendency is hereditary in its nature
is conceded by every prominent writer on asthma except Lebert, who
believes this to be only occasionally the case. Thus, of 35 cases
collected by Salter, heredity could be traced in 14, of whom 7
inherited the disease from the father, and the remainder from
grandparents and other relations. Ramadge gives an instance in which
the disease appeared in four generations: an asthmatic father had four
children, three of whom inherited the disease; one of the daughters
married, and of her two children one became asthmatic; the other
escaped, but the disease reappeared in one of her children.[10]

[Footnote 10: Germain Sée, _op. cit._, p. 668.]

The hereditary tendency may skip one generation, as is the case with
Steavenson,[11] who inherited asthma from his grandfather, his father's
generation having been entirely free from the disease. In other cases
it may alternate with some other neurosis or with gout or rheumatism;
for instance, the children of an asthmatic father may be epileptic or
gouty and the grandchildren asthmatic, or the asthmatic tendency may
develop in one child of an asthmatic family and the gouty diathesis in
another. It is by no means necessary for the hereditary transmission of
the disease that the father should be asthmatic when the child is
conceived, as there are many cases recorded in which asthma developed
in children whose fathers had completely recovered before they
contracted marriage and never had any subsequent return of the disease.

[Footnote 11: W. E. Steavenson, _Spasmodic Asthma_, London, 1882, p.
8.]

All authorities agree that asthma is much more frequent among males
than females. Of Théry's cases, 60 were females and 80 males. The more
recent statistics of Salter show that the males exceed the females in
the proportion of two to one. This undue frequency of a purely nervous
disease among males appears at first to be at variance with the
generally-received opinion that such affections pertain rather to the
female sex; but on investigating the ages at which the attacks first
come on it will be found that between the fifteenth and thirtieth
years--that is, during the period when sexual function is most
active--the proportion is reversed, females being attacked much oftener
than males.

Asthma occurs more frequently in childhood than at any subsequent
period--a fact which may be explained by the great susceptibility of
young children to catarrhal affections of the air-passages and to the
frequent occurrence at that age of measles and whooping cough (Salter).
Of 225 cases collected by Salter, 71 occurred before the tenth year,
and of these, 10 began during the first year, the youngest of them
being only fourteen days old at the time of {191} the attack. From ten
to twenty it occurs less frequently than at any other period of life,
but from that age to the fortieth year there is a steady increase in
the number of cases. During the next decade, from forty to fifty, the
disease diminishes in frequency, and from that period on the number of
cases continues to grow smaller and smaller with advancing years,
comparatively few commencing after the fiftieth year.

The following tabular statement, compiled by Salter, shows the
comparative frequency of asthma during the various periods of life:

  From  1 to 10 years, 71 cases. | From 40 to 50 years, 24 cases.
   "   10 to 20   "    30    "   |  "   50 to 60   "    12   "
   "   20 to 30   "    39    "   |  "   60 to 70   "     4   "
   "   30 to 40   "    44    "   |  "   70 to 80   "     1   "

These figures demonstrate the fallacy of the popular idea that old
people are especially liable to asthma. Its prevalence during the later
periods of life is due to the fact that while, on the one hand, the
affection rarely causes death, on the other it is scarcely ever curable
except during childhood, and thus the cases contracted at different
ages accumulate and form a large aggregate as life advances.

Those cases occurring in childhood and late in life are likely to be
associated with more or less bronchial catarrh, while those which come
on when the body has attained its fullest development are almost
invariably purely nervous in character.

The period of life at which asthma commences is an important element in
the prognosis of the disease, the cases occurring in early childhood
being likely to end in recovery, while those coming on later in life
are exceedingly protracted in their course and liable to lead to
organic diseases of the heart or lungs.

Asthma does not appear to be influenced by the seasons, some authors
claiming that it is most frequent in summer, while others maintain that
the greatest number of cases occur in winter.

Exciting Causes.--Bronchial asthma being a neurosis of the
pneumogastric nerve, its exciting causes may be divided into those
which act upon the nerve directly, and those which are reflected from
more remote parts or organs.

In the first class the irritant may act upon the nerve at its origin in
the medulla oblongata or upon some part of its continuity. Various
poisons, organic or inorganic, when introduced into the system may so
change the character and composition of the blood as to interfere with
the nutrition of the respiratory centre, and thus cause more or less
embarrassment of respiration; but the attacks of dyspnoea due to these
causes are more continuous than those of ordinary asthma, and are
wanting in many of the symptoms which we have described as
characteristic of that disease. These forms of dyspnoea are usually the
result either of some constitutional disease or of some poison
introduced into the system, both of which act by diminishing the
proportion of red corpuscles in the blood. Of this we have examples in
the dyspnoea sometimes observed in syphilis and malarial fever and in
lead and mercurial poisoning--the so-called a. saturninum and a.
mercuriale. It is true that there have been instances in which the
paroxysms of asthma have come on at regular intervals and have yielded
to quinine, but it is not regarded as proved that such cases were due
to malarial poisoning (Sée).

Enlarged bronchial glands pressing upon the pneumogastric nerve may
cause asthma, and this explains why it is so frequent in children after
attacks of measles and whooping cough (Williams and Biermer). Others
have remarked that asthma is often coincident with hypertrophied
tonsils (Schaeffer). In the great majority of cases the exciting cause
does not act directly upon {192} the pneumogastric nerve, but upon the
skin or some other remote organ, whence it is transmitted to the
nervous centre and reflected back through the nerves of respiration to
the bronchi.

Biermer believes that the irritant in many cases, instead of being
directly transmitted to the medulla oblongata, causes a fluxion to the
exposed mucous membrane. He thinks that the absence of catarrhal
symptoms is more apparent than real, the evidences of congestion being
unappreciable during the early stages of the disease. According to
Riegel,[12] the action of the irritant may be explained in one of three
different ways--viz. 1st, both the spasm and the fluxion may be the
common result of the irritant; 2d, the catarrh may cause the spasm; or,
3d, the spasm may secondarily produce catarrh.

[Footnote 12: _Op. cit._, p. 256.]

Although cold may not be so frequent a cause of asthma as was formerly
supposed, low temperature undoubtedly acts as an irritant upon the
terminal branches of the respiratory nerves, especially the
pneumogastric, and in the manner just described may produce spasmodic
contraction of the bronchi. The effect of cold is of course much more
deleterious when it is associated with sudden changes and diminished
barometric pressure, high winds from the east and north being
particularly prejudicial. Aside from its meteorological
characteristics, the locality itself exercises a potent influence in
the production of asthma; and here, again, we have an example of the
capricious character of the disease. A patient who for years has
suffered with asthma may change his residence and find immediate
relief, but of the special factors which engender the disease in one
place and cure it in another we know as yet but little. It is, however,
a generally acknowledged fact that removal from the country to a
crowded city will often diminish the severity and frequency of the
attacks, and English writers mention numbers of cases of asthma which
have been permanently cured by a prolonged residence in the foggy
atmosphere of London. A very slight change is often sufficient to
afford relief, and sometimes removal to another part of the same city
is all that is necessary. The town of Aiken in South Carolina is
divided by a ravine into two sections: the elevation, soil, and
exposure are alike in almost every respect, but persons have been known
to suffer severely with asthma on one side and to enjoy perfect
exemption from it on the other. A gentleman who resides at Bath in the
same neighborhood is perfectly free from asthma at his home, but
invariably has an attack as soon as the train begins to cross the
Savannah River at Augusta, which is only a few miles distant. More
remarkable still is the case mentioned by a French writer of a young
man who was unable to sleep in the front rooms of a house without
having a paroxysm, but who did not experience the slightest
inconvenience when he occupied the back rooms.

Although removal to the city frequently affords relief, there are
exceptions to the rule, and many cases are recorded where a change of
residence to the country has effected a cure. Ozone, of which but
little is as yet known, is supposed by some to be a cause of asthma,
and it is not unlikely that the relief afforded by removal to a large
city may be partly due to the relatively small proportion of this agent
in the atmosphere of crowded localities.

Dust of various kinds, the pollen of plants, certain vapors, gases,
smoke, and the emanations from many species of animals, have all been
known to excite attacks of asthma. Some persons are so sensitive that
the simple act of brushing their clothes is sufficient to bring on a
paroxysm. Others are unable to inhale the perfume of roses, lilies,
heliotropes, and many other flowers without suffering with an attack.
The dust of hay will often cause paroxysms even in those who are not
hay-fever subjects. Since Cullen first published the case of an
apothecary's wife who had asthma whenever ipecac was powdered in her
husband's shop numerous cases of a similar nature have {193} been
recorded. Ramadge relates the case of an employé in the East India
Company who was compelled to relinquish a lucrative appointment because
the smell of tea always provoked a paroxysm of asthma. Many persons are
unable to come into close proximity with horses, rabbits, cats, and
other animals without suffering, and Austin Flint of New York
experienced great inconvenience when absent from home from sleeping
upon feather pillows. In his case the asthmatic attack was not brought
on by all pillows, but what it was that made one kind more active than
another he was unable to determine.

In persons predisposed to bronchial asthma the eating of any
indigestible substance may of itself be sufficient to cause an attack,
and even an ordinarily full meal, if partaken of late in the day, may
have the same effect. Dyspepsia in its various forms and the presence
of irritating substances in the intestinal canal are such frequent
causes of asthma that they have led to the establishment of several
special varieties of the disease--_e.g._ a. dyspepticum, a. verminosum.

Asthma is frequently due to uterine and ovarian disorders, the
so-called a. uterinum.

Voltolini of Breslau has described cases which were evidently due to
the presence of naso-pharyngeal polypi, the attacks disappearing with
their removal and reappearing with their renewed growth. These
statements have been confirmed by subsequent cases observed by
Haenisch. Attention has lately been directed to a number of cases in
which the asthmatic paroxysm was found to be associated with catarrh of
the naso-pharyngeal and laryngo-tracheal mucous membrane. In such cases
it is thought that the irritation caused by the pressure of the swollen
mucous membrane upon the adjacent nerves is conveyed through them to
the pneumogastric, and thus provokes the bronchial spasm. Daly, Roe,
Harrison Allen, Hack, and others have traced the paroxysms of hay
asthma to an hypertrophied condition of the mucous membrane over the
turbinate bones and septum of the nose, which renders it peculiarly
susceptible to the action of the irritants which cause that troublesome
affection, and have succeeded in curing many cases by simply removing
the diseased tissue.

Mental emotion, if sufficiently powerful, may sometimes prevent the
occurrence of the asthmatic paroxysm; thus, Steavenson, referring to
his own case, states that although subject to frequent attacks he never
had one on going up for an examination; and the writer is acquainted
with a patient whose attack of hay asthma could frequently be checked
by an exciting game of cards.

Asthma, like other neuroses, is much more frequent among the educated
and refined than among the coarser and more ignorant classes of
society, and those leading luxurious lives are more liable to the
disease than those of simple and frugal habits. Of the various
professions, those which involve much exertion of the voice furnish the
largest contingent; hence it is common among public speakers,
clergymen, and lawyers.

In former days the retrocession of cutaneous eruptions was supposed to
play an important rôle in the production of asthma, but of late years
this theory of causation has found but few advocates among intelligent
physicians, the only author of any prominence who still adheres to it
being Waldenburg, who has proposed to designate such cases as a.
herpeticum.

PATHOLOGY.--We have elsewhere alluded to the various theories with
which the older writers endeavored to explain the phenomena of asthma,
and need not here refer to them again.

The first step toward a truly scientific theory of the pathology of
asthma was the discovery by Reisseisen of the smooth muscular fibres of
the bronchial tubes. These fibres are found not only in the large and
medium-sized bronchi, but even in those of the smallest calibre,
Kölliker having {194} demonstrated them in bronchioles 0.18 millimeter
in diameter. It was ascertained by Williams that by irritating the lung
he could cause contraction of these fibres, and Longet subsequently
proved that the same effect could be produced by galvanizing the
pneumogastric nerve. Guided by these important discoveries, most modern
pathologists have arrived at the conclusion that bronchial asthma is a
spasmodic contraction of the middle and finer bronchi, dependent upon
some derangement in the function of the pneumogastric nerve. This, the
so-called spasmodic theory, is not entirely new, Willis, as we have
before stated, having described as early as 1682 a variety of asthma
which he believed to be the result of a "spasmodic action of the
muscles and nerves of respiration," and to which he applied the term
"asthma convulsivum." Although revived from time to time, it was not
until some two hundred years later, and after Romberg had definitely
settled the question of the essential character of the disease, that
the spasmodic nature of asthma received general recognition. Bergson
adopted it in his prize essay in 1840, and ten years later it found a
warm supporter in the person of Hyde Salter, whose valuable
contributions have added so much to our knowledge of bronchial asthma.
The theory that asthma is due to spasm of the bronchial muscles met
with but little opposition until 1854, when Wintrich, after a series of
experiments, arrived at conclusions directly opposed to those of
Williams and Longet in regard to the contractility of the muscular
fibres of the bronchi, and refused to accept the spasm theory on the
ground that it afforded no rational explanation of the phenomena of
asthma. He believed that the various symptoms of that disease were due
to tonic spasm either of the diaphragm alone or of the diaphragm and
the other muscles of respiration. These experiments of Wintrich were so
carefully conducted, and his standing as a specialist in respiratory
diseases so high, that his theory found many supporters, and might
perhaps have been generally accepted had it not been for the
distinguished French physiologist, Paul Bert, who in 1870, with
improved methods of scientific research, succeeded in demonstrating
that Williams and Longet were after all correct in their statements as
to the contractility of the bronchial muscles.

One of the most zealous advocates of the spasm theory of asthma, and at
the same time its most learned expositor, is Biermer,[13] whose
classical lecture on that disease, which appeared a short time after
the publication of Bert's experiments, is perhaps the most satisfactory
work ever published on the subject. He defines bronchial asthma as a
"neurosis depending upon tonic spasm of the bronchial muscles and
caused by faulty innervation of the pneumogastric nerve." He claims
that this theory is confirmed by clinical experience--that the
suddenness with which the attack comes and disappears, and the long and
forced expiration with the sibilant râles and other evidences of
stenosis which accompany it, admit of no other explanation. In support
of this view he calls attention to the rapidity with which the paroxysm
yields to chloral, all of its symptoms disappearing within from five to
ten minutes after the administration of a moderate dose of that agent.
Wintrich and his supporters, besides denying the contractility of the
bronchial muscles, object to the spasm theory that the distension of
the thorax and descent of the diaphragm, both constant symptoms, are
incompatible with spasmodic closure of the bronchial tubes, and that
constriction from such cause by impeding the entrance of air into the
alveolæ would be more likely to cause diminution in the size of the
thorax than its enlargement, and that the diaphragm, instead of
descending, would be drawn upward. Biermer acknowledges that this to a
certain extent is true, and concedes that constriction of the tubes
would interfere with both acts of respiration, but claims that it does
not do so {195} to the same extent in the two movements. The spasmodic
constriction acts as a sphincter which is readily overcome during
inspiration, but prevents the escape of air during expiration, the
latter movement being slower and less complete than the former. Were
the expiratory pressure exerted upon the contents of the alveolæ alone,
it would readily overcome the spasmodic constriction of the bronchi,
but it also compresses at the same time the bronchioles. "When the
bronchi are spasmodically contracted, they are subjected during
expiration to the general pressure of that movement plus the pressure
of the spastic contraction of the bronchial muscles. The walls of the
bronchioles being soft and compressible, the expiratory pressure,
instead of overcoming the obstruction and opening them, would tend to
close them all the more tightly." He calls attention to an analogous
condition which obtains in capillary bronchitis, when, owing to
swelling of the mucous membrane and to the accumulation of secretion in
the tubes, the alveolæ are cut off. Here, too, the expiratory pressure
is often sufficiently powerful to overcome the obstruction, but if
under these circumstances it is too feeble, collapse of the lung
ensues. When, on the other hand, the inspiration is strong enough to
overcome this obstacle, air enters the alveolæ, and, being imprisoned
there, causes inflation of the air-cells as in asthma. That collapse of
the lung does not occur in the latter disease is due to the fact that
the inspiratory act is always sufficiently powerful to overcome the
spastic contraction of the bronchioles.

[Footnote 13: A. Biermer, "Ueber Bronchial Asthma," _Sammlung
klinischer Vorträge_, No. 12, Leipzig, 1870.]

The air entering the lung during inspiration is pent up by the spastic
constriction of the bronchi, which, acting as a valve, admits of its
passage in one direction, but impedes its escape during expiration, and
thus causes inflation of the air-cells and insufficient aëration. Owing
to the distension of the alveolæ the thorax is expanded and the
diaphragm forced downward. A tetanic spasm of the diaphragm lasting for
hours, such as that which Wintrich describes, and with which he
endeavors to explain the descent of that muscle as well as the other
symptoms of asthma, is not only improbable, but is contrary to clinical
experience. If the diaphragm were thus spasmodically contracted, it
would remain fixed in one position, but Biermer has demonstrated that
there is more or less rhythmic movement of that muscle even during the
paroxysm; but if no movement of the diaphragm were observed, it would
still be no proof of tonic spasm of that muscle, as its immobility
might be due to other causes. According to Biermer, the inflation of
the lungs and their insufficient ventilation afford a satisfactory
explanation of the most important symptoms of asthma, as Breuer[14] has
shown, in his paper on the automatic regulation of respiration through
the pneumogastric nerve, that various embarrassments of respiration
must be corrected by some suitable modification of the act itself;
hence when, as in asthma, the lung is unable to empty itself, the
expiratory act must be strengthened and prolonged to overcome the
obstruction occasioned by the spasmodic constriction of the bronchial
tubes; whereas incomplete filling of the lung would necessitate
increased inspiratory effort. According to Biermer, "expiratory
dyspnoea is as characteristic of obstruction of the finer tubes," be it
from spasm, as in asthma, or from stoppage with viscid mucus or from
swelling of their lining membrane, as in bronchitis, as the same
condition during inspiration is of narrowing of the larger
air-passages--an important point in differential diagnosis to which we
shall again have occasion to refer. He is unable to explain the
relationship between bronchial spasm and catarrhal hyperæmia of the
air-passages, but believes that it may be accounted for as follows:
"Either the bronchial fluxion causes the spasm--that is, that there
exists between them a causal connection--or the hyperæmia and the spasm
are the {196} joint effect of the exciting (centripetal) nerves; in
other words, both are due to reflex action."[15]

[Footnote 14: "Die Selbsterneurung der Athmen durch den N. vagus,"
_Sitzungsbericht der K. K. Akademie der Wissenschaften zu Wien_, Bd.
lviii. Abtheilung ii., Nov., 1868.]

[Footnote 15: In presenting Biermer's theory the writer has drawn
freely upon that author's well-known lecture on "Bronchial Asthma," as
published in _Volkmann's Sammlung klinischer Vorträge_, _loc. cit._]

Another explanation of the phenomena of asthma is that proposed by
Lebert,[16] who, although he concedes that bronchial spasm is an
all-important factor, denies that it of itself is sufficient to account
for the sudden and enormous inflation of the lungs observed in that
disease. He doubts the possibility of a valvular closure of the
bronchi, as claimed by Biermer, but believes that the bronchial spasm,
which he regards as primary, causes secondary spasmodic contractions of
the diaphragm and of the inspiratory muscles of the neck and chest. The
spasm of the diaphragm he believes to be tonic in its character, but
not continuous, thus meeting Biermer's objection to the Wintrich
theory, that tonic spasm of that muscle lasting longer than a few
minutes would inevitably cause fatal asphyxia.

[Footnote 16: _Klinik der Brustkrankheiten_, 1ster Band, 2te Hälfte, p.
438.]

Theodor Weber,[17] rejecting the above theories on the ground that
neither bronchial spasm nor tonic contraction of the diaphragm is
capable of explaining why catarrhal secretion should come on at the
close of an attack in which at the commencement there was no catarrh,
attributes the phenomena of asthma to sudden swelling of the bronchial
mucous membrane, the result of dilatation of its blood-vessels produced
through the agency of the vaso-motor nerves; thus reviving the
fluxionary theory of Traube. In support of this theory he cites the
result of Von Loven's[18] experiments, which prove that irritation of
the sensory nerves is followed by reflex engorgement of the territory
to which they are distributed. Weber considers that this engorgement of
the bronchial mucous membrane is somewhat similar to the acute swelling
and stoppage of the nostrils to which many persons are subject--a
closure which often does not last longer than a few moments, and which
is attended with increased redness and swelling of the Schneiderian
membrane. The mucous membrane of the nostril and that of the bronchi
being both parts of the respiratory tract, and somewhat similar in
structure, he concludes that the process in the nostrils is analogous
to that which occurs in the bronchi during the asthmatic paroxysm. As
additional proof of the correctness of his hypothesis he cites the fact
that such occlusion of the nostrils is often the precursor of the
asthmatic attack, and in some cases continues throughout the paroxysm.
See investigations of Daly, Roe, Allen, and Hack, further on.

[Footnote 17: "Ueber Asthma Nervosum," _Tageblatt der 45 Versammlung
deutscher Naturforscher u. Aertze in Leipzig, etc._, 1872, p. 159.]

[Footnote 18: _Naturforscher u. Aertze in Leipzig, etc._, 1872, p.
159.]

The idea that asthma is due to swelling and engorgement of the
bronchial mucous membrane appears to have been confirmed by the
tracheoscopic observations of Stoerk.[19] On examining the air-passages
with the laryngoscope, he could see the mucous membrane of the trachea
as far as visible (that is, to the bifurcation) grow red with the onset
of the paroxysm, and resume its normal appearance after the termination
of the attack. He opposes the spasm theory, denies the correctness of
Biermer's conclusions, and adopts Weber's explanation of the asthmatic
phenomena. He agrees with Wintrich that spasm of the diaphragm occurs,
but claims that it results from the tension to which it is subjected by
the inflated alveolæ: the diaphragm being forced downward by the
distended lung, its fibres are stretched, and the result is a tonic
spasm of that muscle. His objections, although well stated, are not
sufficiently conclusive to cause us to accept his opinion in preference
to that of Biermer and other supporters of the spasm theory.

[Footnote 19: _Mittheilungen über Asthma bronchiale, etc._, Stuttgart,
1875.]

{197} Max Schaeffer maintains that asthma is due to bronchial fluxion,
as advocated by Weber, but claims that the hyperæmia is followed by
spasm of the bronchial muscles, the former being primary and the latter
secondary. He also, with many other recent writers, believes that
asthmatic attacks are often associated with pathological conditions in
and about the upper air-passages, such as naso-pharyngeal and
laryngo-tracheal catarrh, polypi, hypertrophied tonsils, and enlarged
cervical glands; all of which act as irritants, which, being
transmitted through the neighboring nerves to the vagus, induce the
bronchial spasm.

Among the older and discarded theories is that of Bree, who in a work
published at the commencement of the present century expressed the
opinion that the dyspnoea of asthma was simply an effort on the part of
nature to rid the bronchial tubes of an irritating substance supposed
to have accumulated in them previous to the attack. He believed that
this materia peccans was thrown out with the expectoration which occurs
toward the close of the attack. He regarded the violent efforts made by
the respiratory organs to expel this offending substance from the
bronchial tubes as similar to the tenesmus of dysentery or the painful
contractions of the bladder when irritated by a rough calculus. Bree
was unable to define more clearly the nature of this offending
substance, but of late years another writer, Leyden,[20] has discovered
in the sputa of asthmatics certain peculiar crystals to the irritating
effects of which he attributes the various symptoms. These crystals had
been observed previously by Charcot in the blood of leukæmic patients,
and subsequently by Neumann in the medulla of the bones of patients who
had died of that disease. Leyden describes the expectoration in asthma
as tough, grayish-white, and very frothy. Imbedded in a transparent
hyaline mass are a number of small bodies, some thread-like, others in
the form of little plugs or flakes. Under the microscope these little
bodies are found to consist of a mass of brownish cellular detritus
containing large numbers of crystals. These are colorless, octahedral
in form, with sharp points, and vary greatly in size, some of them
visible at once, while others are seen only with the highest powers of
the microscope. Their composition has not been determined, but is
supposed to be a substance resembling mucin. Leyden's idea is that the
sharp points of these octahedral crystals irritate the terminal ends of
the pneumogastric nerve in the mucous membrane of the bronchi, and that
this irritation, being transmitted to the nervous centre, is reflected
back, and thus causes spasm of the bronchial muscles. It seems,
however, that these crystals are not peculiar to bronchial asthma,
having been also found in chronic catarrh and other affections of the
bronchi.[21]

[Footnote 20: "Zur Kentniss des Bronchial Asthmas," _Virchow's Archiv_,
Band liv., 1871.]

[Footnote 21: Not being able to obtain the original paper, the writer
is indebted for the greater part of what he has written in regard to
the Leyden theory to the treatises on asthma by Knauthe in _Eulenburg's
Encyclopædie der gesammten Heilkunde_, and by Riegel in the work
already quoted.]

Of the different theories of bronchial asthma which have just been
presented, that of Biermer, although unsatisfactory in many respects,
offers the best explanation of the pathology and symptoms of that
disease.

PATHOLOGICAL ANATOMY.--Bronchial asthma being a purely functional
neurosis, the organs involved present no anatomical changes specially
characteristic of that affection. It is true that in cases of long
standing, in which, owing to oft-repeated attacks, the air-cells have
become distended and their walls attenuated, we find the lungs in the
condition which will hereafter be described as emphysema, but these, as
well as the evidences of chronic catarrh observed in these cases, are
due to the secondary affections, and not to the primary disease.

As previously stated, a certain amount of hyperæmia of the mucous {198}
membrane of the larynx, trachea, and bronchi may be observed during
life with the aid of the laryngoscope; but whether this condition leads
to permanent tissue-changes observable after death is exceedingly
doubtful.

In the pneumogastric nerve pathologists have as yet been unable to
discover, either at its origin or along its course to the lungs, any
alteration in structure capable of explaining the phenomena of
bronchial asthma.

DIAGNOSIS.--The suddenness of the attacks; the occurrence of the
paroxysm usually in the latter half of the night; the slow, labored
expiration, with the whistling, wheezing sounds which accompany it; the
expectoration of catarrhal sputa toward the close of the attack; the
normal respiration and absence of all signs of disease during the
interval between the paroxysms,--are the features by which a case of
simple uncomplicated asthma may be readily recognized. When these
symptoms are present in their integrity in an otherwise healthy
subject, there is no difficulty in arriving at the diagnosis; but,
unfortunately, the picture is not always complete. The asthma may be
complicated with organic disease of the heart or lungs, while primary
disease of these organs, as well as certain affections of the nervous
system, may produce symptoms closely resembling those of bronchial
asthma, and from which it is very essential to distinguish them.

The following are some of the affections which may be mistaken for
bronchial asthma:

1. Bronchial catarrh may be accompanied with more or less difficult
respiration, but even in its worst forms it never causes the severe
attacks of dyspnoea observed in bronchial asthma, and, as Riegel justly
remarks, the severity of the symptoms in the latter disease are out of
all proportion to the insignificance of the physical changes.

The dyspnoea of bronchitis comes on more gradually, the attacks being
dependent upon a variety of accidental circumstances; whereas the
asthmatic paroxysm usually occurs quite suddenly in the night without
any apparent cause. The cough in bronchitis is severer and the
expectoration more abundant than in asthma; the latter is also
different in quality, becoming purulent as the disease advances,
whereas in asthma it seldom loses its mucous character. These points of
difference and the presence of the other symptoms of bronchitis are
sufficient to differentiate that disease.

2. Emphysema is frequently associated with asthma, either as a cause,
as is believed by many, or as an effect of that disease. It is often
exceedingly difficult to determine whether the emphysema when present
is the cause of the dyspnoea (symptomatic asthma), or whether the
inflation of the air-cells and other symptoms are not the result of the
bronchial spasm: a careful inquiry into the history of the case will
often decide the question. The points of difference between the two
diseases are very similar to those to which we have just called
attention as the distinguishing features between the dyspnoea of
bronchitis and the true asthmatic paroxysm. The suddenness with which
the attack comes and goes, the severity of the symptoms compared with
the insignificance of the local lesions, the absence of dyspnoea in the
intervals between the attacks (in uncomplicated cases), are all the
reverse of what is observed in emphysema. In that disease the attacks
develop more gradually; there is always more or less shortness of
breath, and the evidences of changes in the structure of the lung are
quite marked.

3. Dyspnoea resulting from cardiac disease is often very severe, but
may be distinguished from bronchial asthma by the presence of the
various murmurs and other physical signs by means of which that class
of diseases is recognized. The asthmatic paroxysm, as a rule, comes on
when the patient is most quiet, usually during sleep. The attack of
cardiac dyspnoea, on the contrary, is always brought on or aggravated
by physical exertion, mental excitement, or some other apparent cause.
In asthma the respiration during {199} the intervals between the
paroxysms is quite natural; in cardiac dyspnoea there is always more or
less embarrassment. Pain in the region of the heart, in many cases
quite severe and extending down the left arm, may direct attention to
that organ as the source of the dyspnoea.

4. Spasm of the glottis, croup, oedema of the glottis, tracheal
stenosis, are all attended with more or less violent attacks of
dyspnoea. We are indebted to Biermer for having directed attention to
an important symptom by means of which all these affections may be
distinguished from bronchial asthma. In the latter, and in all other
diseases causing narrowing or obstruction of the finer bronchi, the
dyspnoea is during the expiration, but if the impediment be in the
larger air-passages the dyspnoea will be during the inspiration.
"Dyspnoea during expiration is just as characteristic of narrowing of
the finer bronchi as the same condition during inspiration is of croup
and other forms of laryngeal stenosis." In croup the neck is extended
and the head thrown back. Notwithstanding the violent inspiratory
efforts of the patient, the lungs are but partially filled; the air in
them becomes rarefied, causing a yielding of the less-resisting parts
of the thorax--_e.g._ the supraclavicular space, the lower portion of
the sternum, and adjacent costal cartilages--and a sinking in of the
abdomen. During expiration, which is accomplished quickly and with
comparative ease, the thorax resumes its natural form. In bronchial
asthma, on the contrary, the head is thrown forward, and the shoulders
fixed in such a position as to enable the muscles of expiration to work
to the best advantage. The thorax, instead of sinking in, is expanded
and abnormally round, giving on percussion the peculiar pasteboard-box
sound (Schachtelton) which Biermer has described as characteristic of
inflation of the alveolæ. In croup the sibilant râles are heard during
inspiration, while in asthma they are more pronounced during
expiration.

5. Spasm of the diaphragm is another affection from which it may be
necessary to distinguish bronchial asthma. This rare disease, which is
almost always associated with hysteria, is characterized by a short
inspiratory movement, during which all the muscles of inspiration are
brought into action, and we have the same sinking in of the more
yielding portions of the thorax which has just been mentioned as one of
the distinguishing features of laryngeal stenosis. After this the
thorax remains fixed for a few seconds, the muscles of inspiration
remaining in a state of contraction. There then ensues a quick and
powerful expiratory effort, accompanied by a sound not unlike that of
hiccough; then another inspiration, with a repetition of the above
symptom; and so on until the attack is over. It will be seen from this
description that this affection resembles singultus more than asthma,
and that there is but little likelihood of its being mistaken for the
latter disease.

6. Paralysis of the posterior crico-arytenoid muscles, like croup,
spasm of the glottis, and all other affections which produce narrowing
of the larger air-passages, is distinguished by the dyspnoea being
inspiratory, and not expiratory. The function of the posterior
crico-arytenoid muscles being to enlarge the glottis, the result of
their being paralyzed would be to lessen the opening through which the
air passes to reach the lung; and in viewing the cords in such a case
with the laryngoscope it will be found that the opening is reduced to a
narrow chink. Another distinguishing feature is that the dyspnoea is
continuous, and, unlike bronchial asthma, does not come on in
paroxysms.

7. An affection which, like asthma, comes on in the night during sleep
is the condition known as nightmare, and, like the former disease, is
characterized by labored breathing. To distinguish it, it is only
necessary to awaken the patient, when the immediate cessation of all
symptoms will at once remove all doubt as to the nature of the
affection.

8. Through carelessness or ignorance intercostal neuralgia has been
{200} sometimes mistaken for asthma. Pain along the course of the nerve
and the presence of the points douloureux, which Valleix has described
as characteristic of neuralgic affections, are sufficient to establish
the diagnosis.

9. Embolism of one of the middle or larger branches of the pulmonary
artery is also characterized by great embarrassment of respiration, but
is not likely to be mistaken for asthma by any one at all familiar with
the two affections. The cachectic appearance of the patient, the
intense anxiety depicted on his countenance, the evidence of cardiac
disease or of some affection of the vessels, the weakened cardiac
impulse, the thready and at times irregular pulse, together with
evidences of more or less pulmonary oedema, are sufficient to
distinguish this form of dyspnoea from that of asthma.

PROGNOSIS.--As there is no well-authenticated case of death from
uncomplicated asthma, the prognosis quoad vitam may be regarded as
absolutely favorable. That death never occurs during the severe
paroxysms of asthma may be due to the action of the deficiently aërated
blood upon the respiratory centres, and bronchial spasm, causing
relaxation when the symptoms have become most threatening. The
asthmatic, if his case be incurable, may live for a number of years,
and even attain to extreme old age, but his life will be one of intense
suffering, which becomes more intolerable as he advances in years.
Sooner or later, bronchitis, emphysema, or heart disease is developed,
which in its turn may lead to renal disease and dropsy.

Such is the almost invariable result in middle-aged and elderly
persons; in the young, however, the chances of recovery are much more
favorable. Salter[22] states "that in youth the tendency is invariably
toward recovery, whereas in one attacked with it after forty-five the
tendency is generally toward a progressive severity of the disease and
the production and aggravation of those complications by which asthma
kills." The favorable result in childhood he attributes to the
recuperative power of youth: growth and change, being more rapid than
later in life, enable the system to repair during the intervals
whatever damage may have been sustained during the paroxysms.

[Footnote 22: _On Asthma_, Am. ed., p. 168.]

There is another class of cases in which, owing to our being able to
recognize and remove the cause, the prognosis is quite favorable: thus,
if it has been discovered that the disease is due to some local
influence, change will often effect a cure, and the patient will remain
well as long as he remains in the locality which agrees with him, but
generally relapses if he ventures to return to the place where he first
contracted the disease. The same may be said of that form of asthma in
which the disease is due to some trade or pursuit necessitating the
inhalation of irritating dust or gases: the indications are obvious.
Cases in which the paroxysms have been traced to the presence of nasal
polypi or to a tumor pressing upon the course of the pneumogastric
nerve have been promptly cured by the removal of these growths. In all
these cases it is presupposed that there is no organic disease, for the
presence of any one of the serious complications we have mentioned
would dissipate all hope of cure.

In arriving at a prognosis it is all-important to inquire into the
severity and frequency of the attacks, as violent paroxysms at short
intervals soon lead to incurable complications. It is also essential to
ascertain the condition of the patient during the intervals between the
paroxysms: if at that time he feels well and does not suffer with
shortness of breath, we may infer that as yet no organic change has
occurred; if, however, he complains of more or less dyspnoea during the
intervals, we may safely conclude that some organic disease has set in
and that the case is incurable. Salter attaches great importance to the
persistence of expectoration during the intermissions, regarding it as
indicative of bronchitis, and therefore as an unfavorable indication:
to use his own words, "Spitting is one of the worst signs in asthma."

{201} Briefly, those cases may be regarded as favorable in which the
patient is young and has no inherited tendency to the disease, is free
from the many complications of asthma, and in whom the attacks are
light and occur at long intervals. On the other hand, all cases may be
regarded as unfavorable in which the patient has reached or passed the
middle period of life, has inherited a tendency to asthma, if the
attacks are severe with short intervals, or if he has some one or more
of the secondary affections of the disease.

TREATMENT.--The treatment of bronchial asthma consists of measures to
mitigate and relieve the paroxysms and prevent their recurrence.

_A._ Of the Paroxysm.--A patient suffering with an attack of asthma
will generally instinctively assume the position in which he can use
the muscles of respiration to the greatest advantage, but if found in
the recumbent posture he should be advised to sit up in bed and grasp
the knees with his hands, so as to gain a position which admits of the
more ready entrance of air into the lungs. In severe cases it is better
to have him rise from the bed and support the head with the hands, the
elbows resting on a table in front of him. An ingenious
suspension-apparatus, intended to promote the comfort of persons
suffering with severe dyspnoea, was extensively advertised several
years ago, and may possibly still be furnished by the
instrument-makers. It consists of a cross-piece suspended from the
ceiling, to which straps are attached for supporting the shoulders
without in any way pressing upon the chest; it is also provided with a
band for the support of the head. In severe and protracted cases, when,
notwithstanding the patient's exhaustion, he is unable to rest upon
pillows, such an arrangement might afford great relief. If not
undressed, the clothing should be so arranged as to interfere as little
as possible with the respiratory movements. An abundant supply of fresh
air is essential, and to secure this one or more windows should be
thrown open.

Asthma being the most capricious of diseases, remedies often acting
differently in each individual case, it is well before commencing
treatment to follow Salter's advice and inquire of the patient what
remedy has usually afforded the most prompt relief in previous attacks,
and thus avoid the risk of prolonging suffering by using remedies
which, although apparently indicated, may in his case, owing to
peculiar idiosyncrasies, prove to be useless or even injurious.

We have seen that the disease is often due to some special cause, such
as the inhalation of an atmosphere laden with the perfumes of certain
flowers, with ipecac, dust, etc., the removal of which, if practicable,
should of course precede all attempts at treatment. The condition of
the stomach and bowels should be inquired into, and if found overloaded
they should at once be relieved, the one by an emetic and the other by
enema.

In the absence of any hint afforded by the previous experience of the
patient the choice of the remedial agent will depend upon the severity
of the attack. In the majority of cases, when severe, no remedy will
afford such prompt relief as the subcutaneous injection of morphia. To
be effective, the dose should be a full one, a fourth to a third of a
grain, either alone or, if there is likelihood of this occasioning
nausea, combined with one one-hundredth to one-eightieth of a grain of
sulphate of atropia. The writer is aware that the use of opium and
other hypnotics in bronchial asthma is discouraged by one of the most
distinguished authorities on that disease, Salter, who claims that they
are not only worthless, but often injurious. He believes that sleep
tends to promote the paroxysm, reflex action being much more active
then than during the waking hours, and that any agent which induces
such a condition is necessarily contraindicated--that, in his opinion,
in addition to exalting reflex action, it acts prejudicially, as "by
lowering sensibility it prevents that acute and prompt perception of
respiratory arrears which is the normal stimulus to those extraordinary
breathing efforts which are necessary to restore the balance." These
objections, although supported by {202} scientific evidence, are
insufficient to cause the abandonment of an agent which in the hands of
others has proved so prompt and efficacious in relieving the terrible
sufferings of asthma, and Salter himself admits that since writing the
above he has had cases in which it has been of signal service. A
serious objection to its use is that the dose has to be increased as
the patient becomes accustomed to its use. In confirmation of its
marked beneficent effects, I give the following extract from
Steavenson's treatise on asthma. Describing his own experience, he
says:[23] "Sedatives and antispasmodics I should consider most
serviceable drugs, but above all in value I should place the hypodermic
injection of morphia. This has never failed to relieve an attack in
myself, and I have never seen it fail in other patients. The objection
to it is that if often used the dose must be increased; but it is
better to increase the dose of morphia than suffer the agonies of
asthma and allow those organic changes in the constitution to take
place which I have described when speaking of the pathology of the
disease. I have now used morphia for five years, but my attacks are so
quickly relieved and so reduced in frequency that I have never yet had
to increase the dose I commenced with--namely, one-sixth of a grain."

[Footnote 23: _Op. cit._, p. 29.]

Having administered the morphia, other measures for the relief of the
patient should be resorted to. The feet and hands should be immersed in
hot water to which a small quantity of mustard has been added. Dry cups
between the shoulder-blades or sinapisms over the chest or epigastrium
often afford marked relief.

If, on account of the existence of an idiosyncrasy on the part of the
patient or from other causes, opium cannot be employed, we have in
chloral hydrate a substitute which is almost as efficacious and perhaps
even more prompt. Next to morphia, it is the most valuable remedy, and
many esteem it superior to that drug, over which it possesses the
advantage of not being followed by the disagreeable effects which so
often succeed the administration of opiates. It should be given in
doses of thirty or forty grains, and repeated if the paroxysm does not
yield.

The inhalation of chloroform has long been esteemed as a potent agent
in overcoming the bronchial spasm. One would naturally suppose that the
use of such a powerful sedative as chloroform would be a dangerous
proceeding in a disease which, like asthma, is attended with so much
embarrassment of respiration and circulation; but experience does not
justify this fear, and Salter, who has used it with good effect in 12
out of 13 cases, assures us that he has administered it "in the very
agony of the worst attacks; that, so far from fearing it under such
circumstances, it has been able to relieve the intensest asthma that
nothing else would reach; that he has given it, and that he has never
seen any bad effects from it." He goes on to state that as chloroform
relaxes the bronchial spasm, and thus removes the cause of the
"asphyxial stoppage, the intensity of the apnoea, so far from being a
reason against the administration of chloroform, is the great reason
for its immediate employment." He considers neither muscular weakness
of the heart nor valvular disease as any contraindication to its
administration, provided the circulation is not materially affected.
According to Stokes, the paroxysm is not entirely suppressed by
chloroform, but returns as soon as the patient passes from under its
influence; hence it must be repeated as occasion may require. It should
always, if possible, be given at the commencement of the paroxysm, and
should never be allowed to produce complete insensibility, nor should
so seductive a remedy be left in the hands of the patient. The danger
of the self-administration of chloroform is only too well attested by
the frequent accounts in the journals of persons found dead in their
beds from the effects of that agent, death in such cases being usually
due to the patient's {203} unconsciously leaving the handkerchief over
the mouth and continuing to inhale the chloroform after having become
insensible. When given sufficiently early, a few whiffs may be all that
is necessary to overcome the paroxysm; and this repeated as soon as it
threatens to return, will often enable us to control the symptoms
without resorting to larger quantities.

An old and still very popular treatment--said to have been introduced
by an American, Nicholas Frisi,[24] in 1843--consists of the inhalation
of the fumes of burning saltpetre or in smoking cigarettes made of
paper which has been soaked in a saturated solution of that substance.
Inhaled into the bronchi, it is supposed to act as an anæsthetic, and
produces relaxation of the constricted bronchial muscles. In point of
efficiency these inhalations rank quite high, and are probably more
generally used than any other remedy. Aside from the relief which they
undoubtedly afford, this method derives much of its popularity from
being within easy reach of the patient himself. The preparation of the
papers is exceedingly simple: A sheet of bibulous paper is dipped into
a saturated solution of the nitrate of potassa prepared with cold
water; after drying it is divided into strips of the size required.
These papers are burnt before the patient, the windows and doors of the
apartment having been previously closed to prevent the escape of the
fumes. Nitrate of potassa has been prepared in a variety of other ways
for the use of asthmatic patients, one of the most convenient of which
is the Kidder pastilles so extensively used in this country. Another
method is to roll the paper prepared as above into cigarettes, the
smoke of which is inhaled by the patient. The nitre is best used early
in the attack, but is also beneficial when the paroxysm is at its
height. The efficacy of this treatment is attributed by Germain Sée to
the formation of protoxide of nitrogen and carbonic acid gas, which act
as an anæsthetic, and perhaps also to the particles of carbon in the
smoke floating in the air, a smoky atmosphere being beneficial to many
asthmatics.

[Footnote 24: Germain Sée, _op. cit._, p. 709.]

The smoking of the Datura metel having been found efficacious in asthma
in India, Anderson of Madras in 1802 sent some of the leaves to Gen.
Gent, an English officer, by whom they were introduced into England.
Simms of Edinburgh, believing that the Datura stramonium might prove
equally good, tested it with such good results that it soon came into
general use, not only in asthma, but in other forms of dyspnoea. This
is the ordinary Jimson or Jamestown weed which is so widely distributed
over the Southern, Middle, and Northern States, and, like nitrate of
potassa, is much used, not only by the profession, but largely as a
household remedy for asthma. The dried leaves are either smoked in a
pipe or in the form of a cigarette. The effects, however, are quite
uncertain, sometimes acting like a charm, while at others it affords no
relief; its physiological action is that of a sedative. Of late years
another species of Datura has been introduced--the Datura tatula. Its
properties and uses are similar to those of stramonium, but it is
supposed to be less narcotic.

Belladonna and its alkaloid, atropia, are often used in the treatment
of asthma, but their action is uncertain and often unsatisfactory. The
three last-mentioned remedies are also used in combination, as in the
well-known Espic cigarettes, the formula for which, according to
Trousseau, is as follows, viz.:

  Rx. Fol. belladonnæ,          gr. vj;
      Fol. hyoscyami,           gr. iij;
      Fol. stramonii,           gr. iij;
      Fol. phillandrii aquatic. gr. j;
      Ext. opii,                gr. ¼;
      Aq. lauroceras,           q. s.

{204} The leaves, after being cut up, should be thoroughly mixed, after
which they are moistened with the cherry-laurel water, in which the
opium has been previously dissolved. The wrapper of the cigarette is
also soaked in the same solution and dried. One or two of these
cigarettes should be smoked during the attack. Abbott has been very
successful with belladonna applied as a spray (drachm j of the extract
to one ounce of water) when the spasm threatens.

Tobacco is a powerful depressant, and in those who are unaccustomed to
its use is an invaluable remedy in asthma. In the uninitiated it
excites nausea, vertigo, cold sweats, and other symptoms of relaxation
which Salter not inaptly compares to those of sea-sickness. "The moment
this condition can be induced the asthma ceases, as if stopped by a
charm." It may, however, be asked whether the remedy is not worse than
the disease. Those who retain a vivid recollection of the horrible
consequences of their first smoke will hesitate before prescribing
tobacco for one unaccustomed to its use. There are many who, not
wishing to lose the beneficial effect of tobacco in asthma, never smoke
unless a paroxysm threatens.

Lobelia, like the above also a depressant in its action, was formerly
much employed in asthma. It is still used, but its effects are
disagreeable and by no means certain.

The intimate nervous connection which exists between the lungs and
stomach would naturally lead us to anticipate good results from
emetics. In asthma, as in laryngismus stridulus, an emetic often
affords prompt relief and arrests the paroxysm. The nausea which
precedes the act of vomiting, acting as a depressant, causes relaxation
of the spasm, while the emesis by unloading the stomach removes an
important source of irritation. Like tobacco and lobelia, remedies of
this class are only beneficial when pushed far enough to produce the
symptoms of depression and collapse to which we have alluded; these
once established the relief is usually complete. Tartar emetic and
ipecacuanha are the representatives of this class most used in asthma.
Tartar emetic, owing to the excessive and long-continued depression
which it occasions, is now rarely employed, having been almost entirely
superseded by ipecacuanha, which is equally efficacious and more
prompt. Its effects also disappear more rapidly than those of antimony.
Like other remedies intended to cut short the paroxysm, ipecacuanha
should be given as early as possible. It should be taken in full doses
of at least twenty grains.

Bromide of potassium, as is well known, acts upon the vaso-motor
nerves, causing contraction of the arterioles of the brain and spinal
cord, and thus inducing a state of partial anæmia which results in a
lessening of the irritability of these organs, quieting muscular spasm
and inducing sleep. These effects would naturally lead to its
employment in spasmodic asthma. Although occasionally used with success
in shortening the paroxysm, it is better adapted, as suggested by
Riegel, for use during the intervals, when, if given continuously, it
sometimes diminishes the severity of the paroxysms and causes them to
recur less frequently.

Nitrite of amyl, a most valuable addition to our materia medica, has
been extensively used in the treatment of asthma, but the reports of
the results attained are too contradictory to admit of our forming any
just estimate of its merits. The general opinion is that it relieves
the dyspnoea and makes the patient for the time being more comfortable;
and this accords with my own experience. The usual method of
administration is to drop one or more minims upon a handkerchief and to
inhale the vapor. It is also used internally, and, in the single case
that has come under my observation, with benefit. The following case,
reported by Pick and cited by Riegel,[25] is instructive as showing the
favorable effects of nitrite of amyl: "The case was that of a medical
student who from his youth onward had suffered with {205} asthmatic
troubles, which increased as he grew older and had proved rebellious to
all remedies. Nothing except expectorants and narcotics afforded him
the slightest amelioration of his symptoms. On inhaling nitrite of amyl
he experienced immediate relief, which lasted for some time after the
inhalation. He was enabled to breathe deep and with comparative ease.
The relief afforded was but transitory, but, on the other hand, was so
sure that the patient resorted to it whenever the attack came on." The
same writer reports two other cases in which he succeeded by means of
nitrite of amyl in relieving the paroxysms and in increasing the
interval between them.

[Footnote 25: _Op. cit._, p. 295.]

More agreeable to the taste and at the same time more effectual than
the potassium iodide is hydriodic acid. It is best administered in the
form of a syrup, preferably that prepared by Gardener of New York.

Salter, who appears to have had more experience with alcohol than any
other writer, narrates the case of an elderly Scotch lady who, having
exhausted all the known medicines and other agents used in asthma, was
finally relieved by full doses of whiskey. This was invariably
successful, but the dose, of course, had to be increased as the disease
grew older. He also mentions another case in which nothing except
chloroform afforded any relief. This he describes as the severest he
has ever witnessed. "I have never seen or heard of spasms so violent or
that seemed so nearly to put life in peril. His most intense spasms he
calls 'screaming spasms,' from the strangling cries that the want of
breath compels him to make. At the time of which I am speaking he lived
on the same street with myself, and, although his house was half the
length of the street from mine, his nurse has often assured me that if
the doors had been open I could have heard his screams at my house at
night. All remedies except the chloroform had failed, when one day his
nurse advised him to try brandy. It afforded him almost instantaneous
relief. He took enormous quantities of it, the first day a quart, and
in the course of two months as much as twelve gallons. The spasm
invariably stopped as soon as he took it, and for the last five months
that he was under observation he had only what he called a 'thickness,
a tight, constricted breathing,' several times during the night."
Salter is particular in stating that the brandy should be given strong
and hot.

Another stimulant highly recommended by Salter is coffee. In stating
his objections to the use of opium it will be remembered that one of
his reasons for not availing himself of that remedy was that it caused
sleep, and that the exaltation of reflex action in that state favored
the asthmatic paroxysm. Coffee, being a strong excitant of the nervous
and vascular system, has the contrary effect and keeps the patient
awake. It should be prepared as a strong infusion without the addition
of either sugar or milk and given some time before the expected
paroxysm. Administered in this manner, he claims that coffee will
relieve two-thirds of all cases of asthma. The relief afforded is,
however, very unequal, being in some cases complete, while in others it
is only slight and transitory.

Quebracho in the form of an extract has been much used of late years in
the treatment of asthma and other affections attended with dyspnoea. It
has been found quite useful in mild cases.

The induced electrical current has been recommended by Schaeffer as a
means of cutting short the paroxysm. His method is to place one pole on
either side of the neck immediately below the angle of the jaw and in
front of the sterno-cleido-mastoid, so as to cover the course of the
pneumogastric and sympathetic nerves. The current should be
sufficiently strong to enable the patient to feel the passage from one
side of the throat to the other. It is applied for fifteen minutes
twice a day for six days, twelve sittings being usually sufficient to
afford relief. When the current is first applied it not {206}
infrequently causes dilatation of the pupils, but this is succeeded by
contraction when the treatment begins to manifest its beneficent
effects.

_B._ During the Intervals between the Paroxysms.--The diet and daily
regimen of the asthmatic should be most carefully regulated, the best
and most skilfully directed treatment being of little avail if these
important matters are neglected.

The asthmatic patient should be encouraged to pass much of his time in
the open air, but the amount of walking he should do will of course
depend upon his strength and freedom from secondary affections of the
heart and lungs. In a case of simple uncomplicated asthma the more the
patient walks the better he will feel; but this is not to be construed
to mean that he is to walk until exhausted; on the contrary, his walks
should at first be quite short, proportioned to his strength and wind,
and then gradually extended, but under no circumstances should he be
allowed to overfatigue himself. With a view to keeping the skin in the
best possible condition the body should every morning be sponged with
water, the temperature of which must be suited to the condition of the
patient. If he be feeble and anæmic, the water should be tepid, but
whenever admissible cold is to be preferred. After the bath it is
essential that the skin be thoroughly rubbed with a coarse towel until
it becomes slightly reddened. The cold bath properly used not only
invigorates the system generally, but by enabling the body to stand the
vicissitudes of temperature diminishes the risk of the patient's taking
cold.

The intimate relations existing between the lungs and stomach, and the
fact that asthmatics usually suffer at the same time with dyspepsia,
make the question of diet an all-important one. Their meals should
consist of good, nutritious food, rigidly excluding all heavy,
indigestible substances, such as cheese, nuts, dried fruits, etc. The
meals should be taken at regular hours, and, as asthma almost always
comes on at night, it is important that the principal repast should be
in the morning or early part of the afternoon, and that any food taken
between that and the hour for retiring should be of the lightest
possible description. The more empty the patient's stomach, the better
will be the chances of his passing a good night. Alcoholic drinks,
coffee, and other stimulants should only be allowed when prescribed as
medicines, as they have a tendency to aggravate the hyperæmia of the
air-passages, which is one of the prominent features of the disease.
Constipation should of course be carefully guarded against.

Aside from the apparently well-established fact that asthmatics do
well, and often remain so, in the damp, foggy air of crowded cities, we
have no means of determining beforehand what locality will suit a case
of asthma. Change of climate in such cases is a mere matter of
experiment, but when such change is determined upon the patient should
at first try a place which is in every respect the reverse of the one
he has previously lived in. If his former residence was in a city, he
should remove to the country; if the old place was dry, the new one
should be damp; if he has lived in a flat, low country, let him try the
mountains; and vice versâ. As already stated, removal from the pure air
of the country to the foul, smoky air of a city densely populated often
affords complete relief, but so soon as the patient returns to his old
home the asthma reappears and is as bad as ever.

As regards its capriciousness as to locality, I quote the following
interesting case from Salter's work on asthma: "G. C----, a confirmed
asthmatic, a native of a city in Scotland in which he resided, having
been a sufferer for many years, came to London in 1838 for the sake of
receiving the best medical advice. He took apartments in the centre of
the city of London, somewhere near St. Paul's. His intention was to
wait for an attack, and as soon as one came on to present himself to
his physician, that he might witness it and have a clear idea of the
state he was in. He waited six weeks, much to {207} his mortification,
not only without experiencing one, but without any difficulty of
breathing whatever. His health altogether improved; he slept well and
gained flesh. Being tired of waiting, he went back to Scotland without
having seen his physician at all, and, to his great disappointment, he
had not been in his native city many days when he was attacked in the
usual way, and continued to suffer just as before his visit to London.
Subsequently, finding it necessary on matters of professional business
frequently to visit London, he experienced the same result on all
occasions as at his first visit--perfect immunity from his disease. To
use his own expression, 'he felt in London like a renewed man.' On his
first arrival in town he was in a miserable state: he could not move
without feeling his shortness of breath distressingly; he got no rest
at night, and was seldom able to lie down in his bed. But in London he
could do anything--eat, drink, sleep. The consequence was he gained
flesh and strength, and went back to Scotland looking quite a different
man. This was the invariable result."

Having once found a place which agrees with him, the asthmatic should
remain there, as change of climate when no good is effected often does
harm.

Arsenic has long been a favorite remedy in asthma, and is undoubtedly
of great value in a number of cases. It was used in the form of a vapor
by Dioscorides, and, notwithstanding its poisonous properties, has
always occupied a prominent place in the therapeutics of diseases of
the air-passages. In Styria and other parts of Lower Austria arsenic is
habitually eaten by many of the peasants to enable them to breathe more
readily while climbing over their elevated mountains and to endure the
fatigue incidental to their long pedestrian journeys. The same habit is
said to prevail in China, where, however, it is not taken internally,
but is smoked mixed with tobacco. Its physiological effects are thought
to be due to the increased oxidation of the blood which it promotes, as
is proven by the great increase of urea observed after its
administration. The blood thus oxygenized stimulates the vital centre,
and thus the nerves and muscles of respiration are incited to increased
activity, as a result of which the respirations become freer and more
easy. Those who believe in the herpetic diathesis derive an additional
indication for its administration from the good effects which it
manifests in cutaneous diseases. It is best administered in the form of
liquor potassii arsenitis (Fowler's solution), giving at first only
three drops in a wine-glassful of water after each meal, and increasing
the dose one drop each day until the patient takes thirty drops in
twenty-four hours. Should any toxic symptoms supervene--pain in the
stomach or diarrhoea, puffiness of the lids or redness of the
conjunctiva--the arsenic should be at once suspended, and not resumed
until they shall have subsided. Thus given, it is quite safe. Trousseau
recommends its use in the form of cigarettes, which are prepared as
follows: "Twenty grains of the arsenite of potassium are dissolved in
half an ounce of water, and a sheet of bibulous paper soaked in this
solution until it is all taken up. The paper is then dried and divided
into twenty equal pieces, which therefore contain one grain arsenite of
potassium each. Each paper is then rolled in the form of a cigarette.
In smoking them the patient should endeavor to inhale the smoke into
the bronchi. He should take only four or five whiffs once a day."

Iodide of potassium often affords most satisfactory results in the
treatment of asthma, but in many cases it fails entirely. It is a drug
which must be given for a long period at a time, occasionally for
weeks, before it manifests its effects, and want of perseverance may
account for its failure in many cases. It forms one of the chief
ingredients in Aubrée's antiasthmatic elixir, the formula for which is
somewhat uncertain. According to Trousseau, it is as follows: {208}

  Rx. Rad. polygalæ,               gr. xl;
      Coque c. aqua fervida,       ounce iv _ad_ ounce ij;
      Filtrat, adde Potass. iodid. drachm iv;
      Syrup, opii,                 ounce iv;
      Spts. vin. gallic.           ounce ij;
      Tr. coccionellæ, q. s. _ad_ coloraud.
  Filtra.

Of this Trousseau states three tablespoonfuls are taken "in the morning
fasting, at noon, and in the evening, until the asthma disappears."
Each dose contains no less than forty-five grains of the iodide of
potassium and four-fifths grain of extract of opium. Aubrée himself
always insisted that each dose should be followed by a "tablespoonful
of chocolate pastille, which neutralizes the irritating action of the
iodide of potassium."[26]

[Footnote 26: Trousseau, _op. cit._, p. 656.]

A remedy resembling in its effects the one just mentioned is
nitro-glycerine. It is administered in the form of a one per cent.
alcoholic solution, in doses of half a drop, increased to three should
the smaller dose prove inefficient. Its effects manifest themselves in
from three or four minutes to a quarter of an hour, and disappear
within an hour after its administration. The dose should be increased
with great caution, as a single drop of the above solution has been
known to produce alarming symptoms. The euphorbia pilulifera, much
lauded by Australian physicians for its wonderful effects in bronchial
asthma, promises to rank as an invaluable remedy in the treatment of
that disease. It is best administered in the form of a decoction
prepared by steeping one ounce of the fresh, or half that quantity of
the dried plant, in two quarts of water, and simmering it down to one
quart. The dose of this decoction is three or four wineglassfuls during
the day, the last dose preferably in the evening, after supper.[27]

[Footnote 27: _Boston Medical and Surgical Journal_, 1885, p. 66.]

Leyden, whose theory has been mentioned elsewhere, has proposed a new
treatment based upon the solubility of the Charcot crystals in chloride
of sodium and carbonate of sodium. A solution of one part of these
salts in one hundred parts of water should be inhaled twice daily in
the form of a spray.

Oxygen has often been used in asthma, but is now seldom administered
except in cases associated with great anæmia.

Sée gives the following statistics of the results of the treatment with
compressed air in asthma and its secondary affections. Bertin used it
in 15 cases of emphysema, all of which he cured, and in 92 cases of
nervous and catarrhal asthma with emphysema, of which 67 were
completely and 22 partially cured, while it was only unsuccessful in 3
cases. Of Sandahl's 77 cases of asthma with emphysema and bronchitis,
57 were much relieved, and of 14 uncomplicated cases, all were
completely relieved. Compressed air may be applied either by placing
the patient in a pneumatic cabinet or by means of the portable
apparatus of Waldenburg. It must be remembered, however, that in the
cabinet the compressed air acts upon the whole body, while in the
portable apparatus only the air-passages and alveolæ are subjected to
pressure; hence if the latter is used the amount of pressure must be
considerably diminished. Notwithstanding the success claimed for this
method of treatment, it should be used with caution, and if the case is
complicated with emphysema it should either be regarded as
contraindicated, or, if employed, the pneumatic cabinet should be used
and not the portable apparatus. In the former, or "air-bath," the
exterior pressure of the compressed air acts as an auxiliary to "the
elasticity of the thorax and to the abdominal gases in" expiration, and
at the same time, by compressing the vessels outside the thorax, aids
the venous circulation. The same force exercised on the inner surface
of the {209} tubes tends to lessen the hyperæmia of the bronchial
mucous membrane (Moeller).[28] When the portable apparatus is used,
expiration in rarefied air causes retraction of the thorax, and thus in
a measure overcomes any tendency to emphysema. A better plan than to
use either singly is to combine the two--to expire into rarefied and
inspire compressed air--which may be readily accomplished with several
of the improved portable apparatuses.

[Footnote 28: _Thérapeutique locale des Maladies de l'Appareil
respiratoire_, Paris, 1882, p. 283.]

The inhalation of sulphuretted hydrogen as practised at Eaux Bonnes,
Cauterets, Aix-la-Chapelle, and other sulphur baths, is said to have
cured some cases, while in many others great benefit is claimed to have
been derived from its use; but allowance must be made for exaggeration
in many of the reports published.

In giving the treatment of asthma no allusion has been made to
Grindelia robusta and other recently-introduced remedies, partly
because the writer has had no experience with them, and again where he
has tried them they have given negative results.




{210}

HAY ASTHMA.

BY W. H. GEDDINGS, M.D.


SYNONYMS.--Hay fever; Hay cold; Summer catarrh; Catarrhus æstivus
(Bostock); Freuhsommer katarrh (Phoebus); Autumnal catarrh (Wyman);
Rose cold; June cold; Pollen fever; Pollen catarrh (Blackley). _Fr._
Catarrh de foin; Catarrh d'été; _Ger._ Roggen Asthma.

DEFINITION.--A form of catarrh caused by some irritant floating in the
atmosphere; appearing in the spring, early summer, or autumn; attacking
persons predisposed every year at the same time, the patient being at
other periods free from the disease; characterized by symptoms
resembling those of influenza, the chief of which are sneezing,
redness, swelling, and increased secretion of the conjunctivæ and of
the mucous membrane of the whole respiratory tract from its
commencement in the nostrils down to the finest bronchi; frequently
culminating in more or less severe attacks of asthma.

HISTORY.--Bostock, an English physician, is entitled to the credit of
having been the first to recognize and describe this peculiar
affection, for although, prior to his time, Heberden[1] had alluded to
symptoms which are now supposed to be referable to hay asthma, and
Cullen had noted the fact that some persons have asthma oftener in
summer than in winter, neither of these writers recognized the true
nature of the disease.

[Footnote 1: _Commentary on the History and Cure of Diseases_, 4th ed.,
London, 1816, chap. "Destillatio," p. 113.]

Bostock's first description of hay asthma appeared in the form of a
paper, "Case of a Periodical Affection of the Eyes and Chest," which he
read before the Medico-Chirurgical Society in London in 1819.[2] This
was a description of his own case. Nine years later he gave the details
of 18 additional cases and mentioned 10 others.[3] In the second paper,
having noticed that the disease as known to him, the American rose or
June cold, prevailed only in the late spring and early summer, he
styled it catarrhus æstivus. Rejecting the popular theory, that hay
asthma is due to the emanations from hay, flowers, etc., he maintained
that heat was the real cause of the disease.

[Footnote 2: _Medico-Chirurgical Transactions_, London, 1819, pp.
161-165.]

[Footnote 3: _Ibid._, London, 1828, pp. 437-446.]

It appears singular, in view of its frequency at the present time, that
notwithstanding the attention which had been directed to it only 18
cases should have been collected during the nine years which intervened
between the publication of the first and second articles by Bostock,
and tends to prove that in those days the disease could not have been
as common as at present. That this was indeed the case is rendered all
the more probable by the indisputable fact that, owing to the more
general education of the people and to the requirements of a so-called
advanced civilization, other nervous diseases are certainly much more
frequent than they were formerly. The great prevalence of hay asthma
among the educated is a further proof of the correctness {211} of this
conclusion. It must, however, be remembered that diagnosis did not then
occupy the position it now does, and it is not unlikely that it was
often overlooked or confounded with other diseases.

During the five years which succeeded the publication of Bostock's
second paper no less than five treatises on hay asthma appeared in
England, some of them by the most prominent medical men of that period.
They are remarkable as showing the great diversity of opinion
entertained at that early date as to the etiology of the disease. Thus,
Macculloch[4] (1828) attributed it to the air of hot-houses and
green-houses, while Gordon[5] (1829) attributed it to the flowers of
grasses, particularly those of the Anthroxanthum odoratum, and
suggested that grass asthma would be a more appropriate name than hay
asthma.

[Footnote 4: _An Essay on the Remittent and Intermittent Diseases_,
London, 1828, vol. i. pp. 394-397.]

[Footnote 5: _London Medical Gazette_, 1829, vol. iv. pp. 266-269.]

Even as late as 1859 the disease appears to have been scarcely known in
Germany, for Phoebus, who has since published a most excellent work on
the subject, on being consulted by a colleague suffering from hay
asthma frankly confessed that he was unacquainted even with the name of
the disease. This incident, and the belief that he had before him a
comparatively unworked field, stimulated him to investigate the
disease. By addressing circulars to the various medical societies and
hospitals, not only in his native country, but also in other parts of
Europe, as well as by personal interviews with patients and by
publishing requests for information in the various medical journals, he
collected a large number of cases and gained much valuable information
concerning the disease. The results of his assiduous and painstaking
labors were published in 1862 in the form of a valuable work,[6] which,
although over twenty years old, is still regarded the best authority on
the spring variety of hay fever.

[Footnote 6: P. Phoebus, _Der Typische Freuhsommer Katarrh_, Geissen,
1862.]

Previous to the year 1859, when Phoebus's circulars directed attention
to it, hay asthma seems to have been almost unknown in France, as, with
the exception of a single case by Cazenave of Bordeaux (1837), who
described it as a new disease, we find previous to that date no mention
of it in French literature.

The first case of hay asthma published in America, a typical one of the
autumnal form of the disease, is recorded by Drake in his work, _The
Principal Diseases of the Interior Valley of North America_, p. 803,
published in 1854.

It will be seen by this brief summary of the history of hay asthma that
the disease was first recognized in England in 1819, where in 1828 it
became generally known, and that at the time of the publication of
Phoebus's work (1862), with the exception of one or two isolated cases
in France and the United States, England was the only country in which
it was generally known and understood. Since the publication of
Phoebus's valuable work numerous additions have been made to the
literature of the disease, but with the limited space at my disposal I
can only refer to a few of the most important that have appeared in the
last two decades.

In no country has the subject of hay asthma attracted more attention
than in the United States, and in no other has its study been rewarded
by the discovery of so many new and interesting facts. To Morrill Wyman
of Cambridge, Mass., we are indebted for the first elaborate American
work on hay asthma, or rather the autumnal variety of that affection,
which Wyman believes to be a distinct disease in no way connected with
rose cold, June cold, and other forms which appear in the late spring
and early summer.[7] He had previously described the disease in his
lectures as early as 1854, and {212} also in a paper read before the
Massachusetts Medical Society in 1866. Being himself a sufferer from
it, he naturally devoted much time and attention to its study, and his
work may be justly considered the most valuable contribution to the
literature of the disease which has appeared since that of Phoebus.
Another American work on hay asthma is that of the late Beard of New
York.[8] He elaborates the nervous theory of the disease, and
establishes three varieties--the first appearing in the spring, the
second in midsummer, and the third in autumn. In 1877, Elias Marsh of
Paterson, N.J.,[9] read an exceedingly valuable paper before the New
Jersey State Medical Society, in which he describes a series of
experiments which led him to believe that hay asthma is caused by the
pollen of plants. In Europe the best treatise on the subject that has
been published of late years is undoubtedly that of Blackley of
Manchester, who by a series of ingenious and carefully-conducted
experiments claims to have found in the pollen of certain plants the
true cause of the disease. To all of these works we shall again have
occasion to refer in the course of this article.

[Footnote 7: _Autumnal Catarrh_, Cambridge.]

[Footnote 8: George M. Beard, M.D., _Hay Fever and Summer Catarrh_, New
York, 1876.]

[Footnote 9: "Hay Fever or Pollen-Poisoning," an essay read before the
New Jersey State Medical Society by Elias Marsh, M.D., Paterson, N.J.,
1877.]

ETIOLOGY.--In scarcely any other disease is there such a diversity of
opinion in regard to the cause as in hay asthma. We have seen how
Bostock and his contemporaries differed on this point, he attributing
it to heat, while of the others one claimed that it was caused by the
air of hot-houses and green-houses, and another insisted that it was
neither of these, but the flowers of certain grasses. Since that period
other theories of causation have been advanced, but the same diversity
of opinion as to its origin which marked its early history continues
even at the present day.

In treating of the etiology of hay fever the various causes may be
divided into two classes--viz.:

Predisposing Causes.--The fact that hay asthma is frequently
transmitted from one generation to another, so well established by
Wyman, is now very generally admitted, and will become more apparent in
the future, as in estimating this feature it must be remembered that we
have to deal with an affection which seventy years ago was entirely
unknown and which has only recently become generally recognized. That
the fact of the hereditary transmission of the predisposition is
becoming every year more generally accepted is made apparent by the
replies to two sets of circulars addressed to hay-fever patients in
different years. Thus, Wyman, whose circular was issued at least eight
years ago, received 18 affirmative replies out of 80, a little less
than 25 per cent.; while to the writer's circular, issued in 1882,
there are 25 affirmative replies out of 66. Numerous instances have
been recorded where the disease attacked not only two, but even three,
generations of the same family.

Hay asthma appears to be much more prevalent among males than females,
the proportion being 3 males to 2 females. There is no apparent reason
for this discrepancy other than that males are as a rule more exposed
to the vicissitudes of weather, and that the restless energy with which
many of them carry on their avocations predisposes to the disease.

The causes which produce hay fever act alike upon many thousands, an
infinitesimal percentage of whom are attacked. There must therefore be
some individual peculiarity which predisposes certain persons to the
affection, but, aside from the facts that those attacked are usually of
a nervous temperament, and that the respiratory mucous membrane of many
of them is extremely sensitive, and that the vascular erectile tissue
over the turbinated bones and lower portion of the septum is often
hypertrophied,[10] there are no {213} known peculiarities by which it
can be recognized. What races are subject is a question which thus far
has received but little attention. To the writer's knowledge, the only
well-established fact relative to race susceptibility is that negroes
are exempt from the disease, and that in India (Blackley) it does not
occur among the natives.

[Footnote 10: Roe, _The Pathology and Radical Cure of Hay Fever_, 1883,
p. 9.]

Statistics show that it is much more common in youth and middle age,
and that comparatively few are attacked after forty, as will be seen by
referring to the following table:

  Age when First Attacked. | Wyman's Cases. | My Own Cases. | Total.
  -------------------------+----------------+---------------+-------
  Under 10                 |       11       |      10       |   21
  10 to 20                 |       11       |      17       |   28
  20 to 30                 |       25       |      13       |   38
  30 to 40                 |        8       |      11       |   19
  40 to 50                 |       11       |       5       |   16
  After 50                 |        2       |       1       |    3
  -------------------------+----------------+---------------+-------

Wyman is of the opinion that females are attacked later in life than
males.

Without knowing the numerical proportion which the various professions
and occupations bear to each other, it is impossible, even with the aid
of statistics, to determine which of them is most subject to hay
asthma; but the annexed table shows conclusively that those who do
brain-work are much more frequently attacked than those who earn their
living by manual labor:

                                  | Wyman. | My Own. | Total.
  --------------------------------+--------+---------+-------
  Statesmen                       |   1    |    0    |   1
  Clergymen                       |   6    |    3    |   9
  Jurists and lawyers             |   6    |    2    |   8
  Physicians and medical teachers |   8    |    4    |  12
  Dentists                        |   1    |    0    |   1
  Pharmacists                     |   0    |    1    |   1
  School-teachers                 |   3    |    0    |   3
  Students                        |   6    |    1    |   7
  Military officers               |   3    |    0    |   3
  Authors, editors, etc.          |   0    |    1    |   1
  Mechanical engineers            |   0    |    1    |   1
  Bankers                         |   3    |    1    |   4
  Bank officers                   |   2    |    1    |   3
  Merchants                       |  11    |    7    |  18
  Brokers                         |   0    |    1    |   1
  Manufacturers                   |  12    |    3    |  15
  Clerks                          |   1    |    1    |   2
  Artisans                        |   1    |    1    |   2
  Farmers and gardeners           |   4    |    2[11]|   6
  Butchers                        |   1    |    0    |   1
  Laborers                        |   0    |    1    |   1
  --------------------------------+--------+---------+-------

It will be seen by the above that of 100 cases, only 12 were engaged in
outdoor pursuits, and that the remaining 88 followed occupations
necessitating confinement within doors and entailing more or less
intellectual effort; which proves conclusively that the earlier writers
on hay asthma were correct in regarding it as a disease of the more
cultured classes of society. The writer agrees with Wyman that the
large increase in the number of hay-fever sufferers may in a great
measure be attributed to the circumstance that many {214} who were
formerly pursuing agricultural and mechanical pursuits are now engaged
in occupations which require more or less intellectual effort.

[Footnote 11: One of these was an amateur and highly educated.]

To determine the value of temperament I have followed Beard's example,
and in my circular of inquiry propounded two questions: 1st, the
temperament of the patient's family; 2d, his own temperament. To the
first query I obtained replies which showed that the nervous
temperament predominated in 28 out of 37 cases; or, in other words, the
family temperament was more or less nervous in two-thirds of the cases.
As regards the patients themselves the temperament was as follows:

                      | My Own. | Beard. | Total.
  --------------------+---------+--------+-------
  Sanguine            |    8    |   18   |   26
  Nervo-bilious       |    5    |   23   |   28
  Nervous             |   23    |   67   |   90
  Nervo-sanguine      |    9    |   27   |   36
  Nervo-lymphatic     |    0    |    3   |    3
  Lymphatic           |    3    |    0   |    3
  Sanguino-bilious    |    4    |    5   |    9
  Bilious             |    7    |   29   |   36
  Sanguino-lymphatic  |    0    |    1   |    1
  Bilio-lymphatic     |    0    |    1   |    1
  --------------------+---------+--------+-------

It thus appears that the nervous element predominates in no less than
157 out of 233 cases.

Other diseases do not appear to predispose to hay asthma, nor, on the
other hand, is that affection a cause of any other disease. The
question whether naso-pharyngeal catarrh is more common among hay-fever
subjects has, after careful investigation, been decided in the
negative.

Exciting Causes.--It is generally conceded that the suggestion of a
large number of remedies in the treatment of a disease is good evidence
that no effective curative agent has as yet been discovered. This
observation regarding therapeutics equally applies to etiology, a long
array of causes usually developing the fact that great uncertainty
exists as to the real causative agent. Hay fever affords a most
striking proof of the truth of this remark. The simple enumeration of
the various agents which have been accused of causing the attacks would
cover several pages. An example of the multiplicity of its supposed
causes is afforded by the replies to the question in Beard's circular,
"What is the cause of your attacks?" no less than thirty-three agents
being accused of causing the disease. Of these I propose to confine
myself to a few of the most prominent.

Early in the history of hay asthma heat was considered its chief cause,
Bostock, its first describer, having held that view, as have also many
of his successors. It is now generally conceded that heat of itself is
not a cause, although by promoting vegetable growth and causing dust it
may still be regarded as an indirect factor in its etiology. That heat
of itself is not a cause is proved by the occurrence of the disease not
during the intensely hot weather of midsummer, but in the late spring
and early fall. It, however, undoubtedly produces a temporary
aggravation of many of the symptoms. This appears to be especially the
case in the autumnal variety, as those who have the disease in the
spring seldom complain of any ill effects from heat.

"Strong light, sunshine, especially when it falls upon the face, will
produce a violent paroxysm of sneezing, and the other symptoms then
follow in quick succession; and moving from shade to sunshine, even
when not otherwise annoying, will do the same." This is the opinion of
Wyman, and coincides with that of Phoebus, Abbott Smith, and others,
and is amply confirmed by {215} the experience of the writer. This
applies also, though in a less degree, to artificial light, especially
gas-light.

Dryness of the atmosphere, by promoting dust, may be regarded as an
indirect cause. Hay-fever patients agree almost unanimously that their
symptoms are aggravated on clear, bright, dry days, and that they feel
most comfortable in damp and cloudy weather.

There is no evidence to show that electricity is in any way connected
with the etiology of hay fever.

Ozone is certainly not a cause, as hay-fever patients feel best on the
sea-coast and ocean, where ozone is most abundant.

Long before hay fever was recognized by the medical profession hay was
supposed by the general public to be the cause of the disease. In
England especially, but also in the north of France and in Switzerland,
this opinion prevailed very generally. Some suppose that the dust which
it contains is the real cause, while others attribute it to its
peculiar odor. In those susceptible to its influence it appears to make
but little difference how they come in contact with it, whether in an
open field where it is mowed, by driving behind a wagon loaded with it,
or by entering a stable or loft where it is stowed away. It is not,
however, the cause of the autumnal variety, as it is harvested in the
temperate regions of North America, where this form of disease is most
common, in June or early in July, which is six or eight weeks earlier
than the period at which the attacks commence. That hay is a cause of
the earlier variety of the disease is evident from the experience of
numerous intelligent invalids, who trace it to that agent from the fact
that the outbreak coincides with the blooming or harvesting of hay, and
that removal from the locality in which they are exposed to its
emanations is followed by relief. It must be remembered, however, that
hay does not consist of dried grass alone, but that it contains other
plants and flowers, as well as a large amount of dust.

The flowers of grass, especially those of the Anthroxanthum odoratum,
may be regarded, like hay, as one of the causes of hay fever--a fact
that was early recognized by Gordon and others. Blackley[12] cites the
case of an Indian medical officer of high rank, whose statement is as
follows: "I have suffered from hay fever for about thirty-five years; I
have had it both in India and in England. The period at which the
attacks come on is not fixed, the date of the attacks depending more on
the grass ripening late or early than on any other circumstance. They
always begin toward the end of the hay season, when the grass is fully
in flower, and cease slowly and gradually--not directly--on gathering
in the grass."

[Footnote 12: _Hay Fever, its Causes, Treatment, etc._, p. 47, London,
1880.]

Rye, oats, and wheat in bloom may also be ranked among the exciting
causes of hay fever.

Indian corn in bloom often causes symptoms of hay fever, but that it
does so only in certain cases is evident from the fact that the disease
does not exist in some places where large quantities of corn are raised
(Wyman).

Geraniums, roses, heliotropes, and other sweet-scented flowers often
bring on attacks. The bean in bloom and elderflowers are also regarded
as causes.

Ragweed, also known as Roman wormwood, Ambrosia artemisiæfolia, a weed
which extends almost over the whole of the United States, is a powerful
cause of the autumnal variety, but, like all the other agents which
have been accused of causing hay fever, is by no means general in its
action, many patients being able to inhale the dust shaken from the
flowers with perfect impunity even during the critical period. On those
susceptible to its influence it will act not only during the hay-fever
season, but also at other periods of the year. Wishing to study the
plant, I procured during the fall several {216} specimens of it and
placed them between the leaves of a large quarto volume. During the
winter my wife, who is a sufferer with hay fever, accidentally opened
the book, and, seeing the plant, not knowing its nature, picked it up
and smelt it. She immediately began to sneeze, the eyes and nose itched
intensely, there was profuse lachrymation; in short, all the symptoms
of a mild attack of hay fever supervened, the effects of which lasted
until the following morning. The case is interesting from the fact that
in this instance the experiment was made unconsciously, and the effects
could not therefore be attributed to the imagination, the patient being
entirely ignorant of the nature of the plant. The prevalence of
autumnal hay fever appears to coincide with the blooming of the
ragweed, and conforms to the geographical distribution of that plant,
which grows wherever the disease prevails, while in exempted localities
it is seldom found or never seen. In Bethlehem, N.H., a diligent search
was made for it for two days by a botanical friend without his finding
a single specimen, although in the neighboring town of Littleton, which
is within sight of Bethlehem and is not exempt, the plant is quite
abundant. Marsh states that he saw none of it in New Brunswick nor at
Moosehead Lake.

Dust of various kinds is more frequently designated by invalids
themselves as the cause of their disease than any other agent. Thus, in
reply to his question as to the cause of hay fever, Beard received 104
replies assigning dust as the cause, while 540 attributed it to thirty
other agents. All kinds of dust, both in and out of doors, are accused,
but that of railway-cars is supposed to be the most potent.

There is but one case on record in which animal parasites were the
cause of an attack--that of Bastian, who while engaged in the spring
investigating the anatomy of the Ascaris megalocephala, one of the
parasites of the horse, noted that its emanations not only in the fresh
state, but after having been kept in spirits for two years, invariably
caused itching about the eyelids, irritation of the conjunctivæ, with
continuous sneezing and other symptoms resembling hay fever. These
symptoms ceased after two months, and did not return until the
following spring. He finally became so sensitive that the wearing of
the coat in which he had worked during the examinations was sufficient
to bring on the symptoms.[13]

[Footnote 13: Salisbury in _Infusorial Catarrh and Asthma_ attributes
hay asthma to an animalcular organism, the asthmatos, but his
assertions have not as yet been confirmed by other investigators.]

Helmholtz, himself a sufferer from hay fever, discovered that the
secretion of his nasal mucous membrane contained during the attack a
number of vibriones, and, never being able to find them there at other
times of the year, concluded that they were the cause of the disease.
Binz of Bonn having discovered that quinine was inimical to the
vibriones, Helmholtz supposed that that agent would be the proper one
to employ in the treatment. He used it with success, injecting a
saturated solution into the nostrils, the injection each time affording
marked relief.

THE POLLEN THEORY.--Believing from his own experience and that of
others that hay fever was due to the pollen of certain plants, Blackley
of Manchester instituted a series of ingenious and instructive
experiments to prove the correctness of his conclusions. In his first
set of experiments a very small quantity of the pollen of various
plants was applied to the lining membrane of the nostril. That of the
Lolium italicum produced at first a slight feeling of anæsthesia at the
point to which the pollen had been applied, followed "by a feeling of
heat which gradually diffused itself over the whole cavity of the
nostril and was accompanied by a slight itching of the part. After some
three or four minutes a discharge of serum came on and continued at
intervals for a couple of hours." The mucous membrane became so swollen
{217} as to partially occlude the nostrils and impede the entrance of
air. When rye was used the symptoms were much more violent, and were
attended by violent and long-continued fits of sneezing. With wheat and
oats the effect was equally decided. The same experiment was tried with
other orders of plants with varied success, some of them being very
active, while others were found to be quite inert. One grain of the
pollen of Alopecarus pratensis was applied to the fauces, causing
itching and diffused redness. That of the Lolium italicum rubbed into
the abraded skin of the forearm, as in vaccination, produced itching
and swelling.

Marsh,[14] who has repeated Blackley's experiments in America, gives
some very interesting facts in regard to the pollen of the Ambrosia
artemisiæfolia. On the 5th of August, 1874, he placed a few sprigs of
the ambrosia in full bud, but without open flowers, in a glass of water
in his office. The next day the flowers were open, and on handling the
plant for the purpose of preparing some microscopic specimens from it,
the pollen was freely scattered around. This caused in him severe
coryza of twenty-four hours' duration, with occlusion of the nostrils
and serous discharge. On August 13th he repeated the experiment, this
time intentionally applying some of the pollen to the nostrils. This
produced such severe symptoms that he had to have recourse to a
hypodermic injection of morphia for their relief. These, however,
continued into his regular attack, which should have been due a few
days later.

[Footnote 14: _Op. cit._, p. 14.]

Having proved that the pollen of certain plants was capable of
producing hay asthma, Blackley next turned his attention to the
determination of the amount of that substance floating in the
atmosphere of different places and at various periods of the year. The
plan which he found best adapted to his purpose was to expose slips of
glass to the open air for a given length of time, so as to allow any
solid matter the air might contain to deposit upon the glass. On each
of these slips a space of one centimeter square was made sticky by
covering it with a mixture of water, proof spirit, and glycerin. These
were exposed to the atmosphere for twenty-four hours, and then placed
under the microscope and the number of pollen-grains adhering to the
moistened square counted. These slides were exposed at the height of
four feet nine inches above the ground, "the average breathing-level,"
and were placed in a grass meadow four miles south-west of Manchester.
The experiment was begun early in April, 1866, and continued until the
1st of August. Only a small quantity of pollen was found during the
first month. On May 30th it appeared in much larger quantities, and
continued to appear on most of the days until August 1st. Barometric
pressure did not influence the deposit of pollen, but whenever the air
was drier the quantity was increased. A fall of rain, especially if
attended with lowering of temperature, had the effect of materially
lessening the number of grains. The largest quantity of pollen was
obtained on June 28th, the day after the highest temperature of the
season, showing that a large deposit of pollen coincides with, or
follows, a marked rise in temperature. Fully 95 per cent. of the pollen
collected belonged to the Graminaceæ, but this would not apply to other
localities and countries, in which that of other plants would naturally
predominate. These experiments were quite successful in demonstrating
that the rise and progress of the disease corresponded with the amount
of pollen present in the atmosphere. A third set of experiments was
made by attaching the glass slides to kites, to determine the amount of
pollen present in the air at different altitudes. These experiments
revealed the fact that grass pollen was much more abundant at
elevations of 500 to 1500 feet than near the surface of the ground.
Marsh also investigated this portion of the subject, only, instead of
attaching the slides to kites, they were placed in the attic windows:
he arrived {218} at conclusions in regard to the pollen of ambrosia
similar to those which Blackley had reached with reference to the
Graminaceæ.

The experiments of Blackley justify the belief that the cause of the
early form of hay fever, which prevails in England, is to be found in
the pollen of a number of plants, especially grasses and grains, which
bloom in the late spring and early summer, while those of Marsh prove
conclusively that the Ambrosia artemisiæfolia, or Roman wormwood, is
certainly one, and probably the chief, cause of the American or
autumnal variety of the disease.

GEOGRAPHICAL DISTRIBUTION.--Both varieties of hay fever prevail in the
United States, but the late variety is much more frequent, and may be
regarded as peculiar to this country. The distribution of the early
form of the disease is much more extensive. It is quite frequent in
Great Britain, and, according to our present knowledge, it extends over
France, Belgium, Holland, Switzerland, Italy, Russia, and in the plains
of India (but only among foreign residents). Further investigations
will probably show that it also extends over the other temperate
regions of Europe. As before stated, the autumnal form is confined to
the United States, where it prevails much more extensively than was
formerly supposed. Commencing in Florida, where it is quite rare, it
extends northward up to Eastport, Maine. Its northern border is defined
by Wyman[15] as follows: "From the St. Croix, south of Houlton in
Maine, or about the line of 600 feet elevation above the sea-level, the
line of exclusion turns eastward, following approximately the border of
the elevation just mentioned, excluding the interior lakes of Maine,
which are about 1000 feet above the sea, and, descending toward the
south, strikes the White Mountain region at its northern portion.
Thence, turning toward the St. Lawrence River and running along the
height of land which divides the waters falling into the Atlantic from
those falling into the St. Lawrence, parallel to the St. Lawrence, it
strikes that river north of Lake Champlain." Thence along the southern
border of the Great Lakes to the south of the island of Mackinaw,
between Lakes Huron and Michigan. "It then crosses the lake and runs
north of Lake Winnebago to St. Paul, Minn., leaving the Lake Superior
copper-regions beyond its influence." From this point the line is
undetermined, but there is evidence to show that the disease occurs in
Colorado. The statement of previous authors, that the disease does not
prevail in California, is confirmed by a statement recently made to the
writer by Hatch, secretary of the Board of Health of that State, who
adds that several parties have removed there to avoid the disease.
Southward, the line runs along the Mississippi River to New Orleans,
where the disease prevails. The southern and eastern borders are the
Gulf of Mexico and the Atlantic Ocean.

[Footnote 15: _Op. cit._, p. 63.]

SYMPTOMS AND COURSE.--No better description of an attack of the
autumnal form of hay fever has ever been written than that of Wyman,
who, being himself a sufferer from the disease, has had exceptional
opportunities for studying it in all its details. I therefore extract
the following from his work:[16]

"All the cases agree in the time of annual return, about the 20th of
August, varying but a few days from this date in different years. By
some individuals it is believed to be remarkably punctual, being first
noticed on precisely the same day of the month, and, it is even
asserted, at the same hour of the day. It is first perceived as a
slight itching in the palate and in all parts about the roof of the
mouth, soon followed by similar sensations, apparently in the
Eustachian tube, extending from the throat into the ears, and inducing
the sufferer to attempt relief by swallowing and by rubbing his tongue
against the back part of the hard palate, and by pressing and rubbing
the external orifice of the ear to give motion to the parts within.
There is often a sense of tension about the forehead, especially over
the eyes in the region of the {219} frontal sinuses. In a day or two
the nostrils are affected; there is irritation of the lining membrane,
sneezing, and a stuffing and obstruction of the nostrils. This
obstruction is peculiar; it occurs in paroxysms of short duration, one
or both nostrils becoming suddenly obstructed, and in two or three
minutes as suddenly relieved; at other times the obstruction is more
prolonged. But, however complete, it is in many individuals almost
immediately relieved by active exercise, rapid walking, leaping, or any
movement indeed which gives warmth to the extremities.

"At first these attacks occur only in the morning or on first rising;
as the disease advances they occur later in the day, but still in short
paroxysms. At this stage the discharge from the nostrils is limpid and
almost free from mucus; it is often very copious, especially during or
immediately following attacks of sneezing. Holding down the head is
often accompanied by a rapid dropping of the same fluid without
sneezing. With this trouble in the nostrils come watering of the eyes
and itching along the edge of the lids and in the conjunctivæ
generally, but most at the inner corners. This irritation occurs also
in paroxysms of a few minutes' duration. It is so intense that it is
difficult for the sufferer to refrain from rubbing the eyeballs
violently, which soon relieves them, notwithstanding that such
treatment increases the turgidity of the vessels until the whole
conjunctival surface is of a nearly uniform red. The eyelids are
swollen, their edges red and inflamed; the small glands are also
inflamed, and in some cases pustules or styes form and break, leaving
an excoriated surface which heals slowly. The whole face is often red
and swollen, especially in the morning. The senses of taste and smell
are much impaired, in some cases almost abolished; and at times there
is partial deafness, with a sense of obstruction of the internal ear.
The lining membrane of the external tube is sometimes much irritated,
even to the extent of producing a thin discharge, without evidence of
the irritation extending to the tissue beneath. Swallowing is
interfered with, especially when the nostrils are so obstructed as to
prevent the perfect motion of the parts necessary to this act. The
lining membrane of the mouth, tonsils, and pharynx partakes of the
general irritation, and becomes red; and sometimes there is soreness of
the throat. The lips become dry, cracked, and swollen. The skin is
easily irritated and excoriated, and the excoriations are not so
readily healed as in health. Many also suffer from itching of the skin,
especially of the scalp, back, and chest, at times accompanied by a
slight papular eruption. During some portion of this period there is
chilliness, or rather sensitiveness to cold; more or less pain or sense
of oppression in the head; the appetite diminishes; there is lassitude
and weakness, the skin hot and dry, with other signs of a febrile
movement.

"Toward the end of the second week to these symptoms are added
irritation of the membrane lining the air-tubes; a frequent and dry
cough, commencing with a sense of tickling in the upper part of the
windpipe, but little relieved by the cough or only after long coughing;
and the expectoration of a small quantity of transparent, glairy mucus.
The severity of these bronchial symptoms depends much upon the
condition of the atmosphere: if dry and dusty, the cough is much worse;
dampness and a rainstorm give relief.

"During the third week the affection of the lungs gradually increases;
the cough, still with very little expectoration, is more troublesome,
especially in the night, sometimes compelling the patient to spend an
hour or two sitting up, and not infrequently is spasmodic in its
character, producing convulsive retching or even vomiting.

"The disease may now be assumed to be at its height. It is in this
stage also that in some cases asthmatic symptoms appear, and, although
they are sometimes severe, are not long continued. At the end of the
third week the catarrhal symptoms diminish, the tickling of the fauces
ceases, the eyes and {220} nose improve; but the cough is apt to
continue longer, and the heart's action is easily accelerated by
exercise, and the pulse is sometimes intermitting. The skin is dry and
warmer than natural.

"During the fourth week in September these symptoms gradually diminish,
and by the end of September or the first frost are nearly gone, leaving
weakness and a more or less altered state of the mucous membrane of the
air-tubes, the effect of the prolonged irritation, from which the
patient, if otherwise in good health generally soon recovers."

[Footnote 16: _Op. cit._, p. 9.]

The spring form of the disease, known as June cold in the United States
and as hay fever in England, differs from the late variety in the time
of its occurrence, the attack coming on, as its name implies, in the
late spring, usually between the 15th of May and the 15th of June,
sometimes much earlier; one of my patients reporting that she commences
to sneeze as early as the middle of April. The attacks in this variety
usually cease during the first or second week in July, although a few
continue on into August--a fact which induced Beard to establish a
third or middle form of the disease. The symptoms are essentially the
same in both varieties, but are much less severe in the early form,
which is also of shorter duration. They differ as to cause, the spring
variety being usually due to newly-mown hay. It occasionally happens
that one person has both forms of the disease, or that a person who has
hitherto had the early form fails to have it in the spring and is
attacked in autumn.

INDIVIDUAL SYMPTOMS.--There is occasionally a stage of incubation,
lasting about a week, during which there is slight feverishness and
undue susceptibility to nervous impressions. The patient often
experiences a feeling of lassitude and weakness; the digestion is
disturbed, as indicated by a coated tongue, want of appetite, and
constipation; he is disposed to be wakeful, and when he does sleep his
rest is often disturbed by unpleasant dreams.

The first effect of exposure to the irritant is itching of the nose,
slight in the beginning, but increasing in severity as the disease
advances, until it at last becomes unbearable. The mucous membrane is
red and swollen, the swelling being often so great that it interferes
with the passage of air; a watery discharge sets in, which, although
slight in the early stages, soon becomes copious, and in severe cases
is so abundant that it actually streams from the nostrils. Sometimes,
when both nostrils are stopped, if the patient changes his position and
lies on the side the uppermost nostril will become free. These symptoms
are attended with sneezing--not the sneezing of an ordinary coryza, but
powerful sternutatory efforts repeated in quick succession and utterly
uncontrollable. In one case which has come under my observation the
sneezing invariably brought on menstruation in advance of the regular
period, and on some occasions caused abortion.

These symptoms just mentioned often appear and disappear with great
rapidity, especially in the early stages of the disease, and are
usually worse in the morning on awakening.

Itching of the eyes begins at the inner canthus and generally extends
over the greater portion of the conjunctiva, slight at first, but
becoming more troublesome as the disease progresses. There is also
redness of the conjunctiva, sometimes of the lids alone, at others
extending over the whole mucous membrane, and giving to the eyes a
bright-red appearance. The lids in severe cases are not infrequently
oedematous, lachrymation is greatly increased, and the tears, trickling
down the face, are liable to cause excoriation of the skin. Pustules
and styes often form on the lids. There is more or less photophobia,
according to the severity of the attack.

Owing to the occlusion of the nostrils the patient is often compelled
to breathe through the mouth, thus causing an uncomfortable drying of
the mucous membrane. There is a peculiar itching of the hard palate,
which {221} the patient attempts to relieve by rubbing the roof of the
mouth with the point of the tongue. This itching sensation extends over
the pharynx, posterior nares, and upward through the Eustachian tubes
to the ears, causing a disagreeable irritation, which the patient tries
to alleviate by thrusting the tip of the finger into the external
meatus. The mucous membrane of the pharynx is red and swollen. The
dryness observed early in the attack gives place later to increased
secretion, which is sometimes quite abundant. On the anterior surface
of the velum of one of my female patients I observed a hard papule
about the size of a lentil, which she assured me was always coincident
with the attack, and never appeared at any other time.

In addition to headache, which is quite common, patients frequently
complain of a heaviness and fulness, also of a peculiar sensation as
though the head were constricted by a band. This latter symptom I have
found present in about one-half of the cases investigated.

Itching of the skin is quite common, especially of the face, between
the shoulder-blades, and over the sternum, and is frequently
accompanied by a slight vesicular eruption and occasionally by
urticaria.

The whole respiratory tract is in a state of catarrh, but there is very
rarely any cough during the first week. This usually commences in the
second week, and at that time is short and dry, and becomes every day
more frequent until the third week, when it changes its type and
becomes paroxysmal. During the first three weeks there is little or no
expectoration, and what there is consists of small transparent
glutinous masses. About the fourth week the irritation reaches the
finer bronchi, and in many cases there is more or less asthma, which,
like ordinary bronchial asthma, usually comes on at night. The asthma
is sometimes quite severe and long-continued. Wyman states that very
few escape cough. This does not accord with the writer's experience, as
in 65 of his cases 15 had no cough.

Hay-fever patients suffer greatly from mental depression, complain of
lassitude, and their capacity for intellectual labor is diminished.
They are often troubled with insomnia, and when such patients do sleep
it is in a fitful way, and their rest is often broken by unpleasant
dreams.

NOMENCLATURE AND CLASSIFICATION.--The various terms used to designate
this disease are all misnomers, and up to the present time none has
been devised which conveys any idea of the true character of the
disease. Hay fever is incorrect, because hay is only a cause in a
limited number of cases, and fever is by no means a prominent symptom.
Hay asthma should be discarded, for asthma is far from being a constant
accompaniment of the affection. Autumnal catarrh or early spring
catarrh only serves to designate the time at which the two forms
usually appear, but conveys no idea of the disease in its entirety;
while the term pollen catarrh or pollen fever is objectionable on the
ground that, although the disease is most frequently produced by that
agent, there are causes other than pollen which may excite it.

Hay fever is variously classified by different authors, some, like
Thorowgood and Beard, regarding it as a neurosis, while others
(Bostock, Phoebus, and Wyman) appear to regard catarrh as its
distinguishing feature. Zuelzer has recently classed it among the acute
infectious diseases, but assigns no reason for placing it in that
group.

DIAGNOSIS.--To any one at all familiar with the symptoms of the disease
the diagnosis of hay fever is quite easy. Its distinctive features are:
It appears at the same time every year (the early form about the 1st of
June and the later about the 20th of August); the severity of the local
symptoms which usher in the disease--sneezing, stoppage of the
nostrils, the inflamed condition of the eyes, and above all the itching
of the nose, eyes, skin, and mucous membrane of the root of the mouth.
A detailed differential diagnosis {222} is not as important now as it
was formerly, when, as in the days of one of its early describers,
Phoebus, "Man sah sie nicht, wo sie war, und sie sah, wo sie nicht
war."

PROGNOSIS.--The number of elderly persons with hay fever, many of whom
have passed the allotted threescore years and ten, and the fact that no
one has ever been known to die from the disease, affords conclusive
evidence that it does not shorten life. On the other hand, when once
affected, except in those cases relieved by operative procedure, the
patient remains subject to it during the remainder of his life. A few
isolated cases are said to have recovered, but such a result is
extremely rare. It is thought by some that a prolonged residence in the
South may mitigate the disease, and eventually cure it, but this
assertion lacks confirmation. It does not, like bronchial asthma, lead
to secondary affections, the interval between the attacks giving the
organs time to recuperate, nor does it predispose to other diseases.

TREATMENT.--Aside from its surgical treatment, to which I shall refer
farther on, the only effectual remedy for hay fever consists in removal
to a region which is exempt from the disease. By going to such a
locality before the attack occurs, and remaining there throughout the
critical period, complete immunity from the disease may be secured. The
time of departure and return must be determined by the previous
experience of the invalid in regard to the date upon which his former
attacks have commenced. As the disease seldom comes on exactly on the
same day every year, but often varies three or four days, he should be
in his place of refuge at least a week before the usual time for the
attack, and should remain until he can return with perfect safety. This
is usually about the middle of July in the early variety, and after the
first frost severe enough to kill vegetation in the autumnal form.

In the milder form which occurs in the spring the seashore affords
considerable relief, except when the wind is from the land. It is
therefore uncertain, and is only indicated when the circumstances of
the patient prevent his visiting one of the exempt localities. On the
eastern coast of the United States there are several places of this
character, such as the Isles of Shoals, a group of rocky islands with
little or no vegetation off the coast of New Hampshire, the climate of
which is very like that of the ocean; and Fire Island, near New York.
Similar to the above, but much more exposed to land influences, are
Mount Desert and Nantucket.

The ocean itself affords complete exemption, and a sea-voyage is the
surest means of avoiding the disease. It is true that persons have been
known to be affected with hay fever even in mid-ocean, but in such
cases it is more than probable that the cause of the attack could have
been traced to the cargo. A case of this character came under the
writer's observation during a voyage from New York to Charleston during
the month of September, and was evidently caused by hay, a number of
bales of which were stowed on the forward deck of the vessel. It makes
comparatively little difference what particular voyage is undertaken,
provided the vessel's course does not bring her too near land; but for
most hay-fever patients a trip to Europe is to be preferred, especially
for those suffering with the autumnal form, as by going to that
country, where this variety does not exist, they avoid the necessity of
remaining nearly two months on the water. A voyage to California is
almost as good, and for the same reasons.

Whether this applies to the so-called June or rose cold, which is quite
common in Great Britain and prevails to some extent on the Continent,
has not as yet been definitely determined, but it is more than
probable. Whether patients who have contracted the disease in Europe
would escape in America is exceedingly doubtful. Two of the cases
reported to the writer, who were first attacked (with the early form)
in Europe--the one in Switzerland and the other at Florence--continued
to have the disease after their return to {223} this country; while, on
the other hand, an English lady who was subject to the disease at home
escaped entirely during her residence of three years in the Southern
States. Of the exempt regions in the United States, the one most
frequently resorted to, and which at the same time affords the surest
relief, is that of the White Mountains of New Hampshire--not the whole
of it, but a certain portion, which is bounded on the west by a line
drawn from Littleton to Lancaster (but not including the former place,
which is only partially exempt), on the north by Canada, on the south
by Franconia, Crawford House, and Jackson, while to the east it extends
as far as Bethel in Maine. Of the various places contained within this
territory, Bethlehem and Jefferson, Whitefield, White Mountain House,
Fabian's, Twin Mountain House, Crawford House, Glen, Gorham, and Mount
Washington, may be regarded as entirely exempt; Franconia Notch almost
equally so; while Dalton, Lancaster, and Bethel must be ranked as
uncertain. Another exempt region extends to the north and east of the
one just described, and comprises the lake region of Maine. Petoskey in
Northern Michigan, at the head of Little Traverse Bay, is said to
afford almost entire relief, and is resorted to by a large number of
patients from the Western and South-western States. There are also
several places in Vermont which offer more or less immunity, such as
Mounts Mansfield and Stow, both of which, however, are inferior to
those first mentioned. Canada, with the exception of a few cases
reported at Toronto, St. Catherine's, and at a few places near its
southern border, appears to be exempt. The same may be said of the
Adirondack Mountains and Pottersville on Schroon Lake and Marquette.
The Catskill Mountains and several places high up on the Alleghanies,
such as Cresson, Pa., Oakland and Deer Park in Maryland, afford relief
in many cases. Colorado is said to be exempt, but several patients who
have gone there failed to obtain relief. California is free from the
disease, and many hay-fever patients have escaped their attacks by
removal to that State. I know of no place in the Southern States which
affords relief except Florida, where the disease is rare; several cases
have been entirely relieved during their residence there. In others,
however, the experiment was unsuccessful.[17]

[Footnote 17: Two patients in their replies to the writer's circular
claimed to have been entirely exempt--the one (early form) at Beaufort,
and the other (autumnal) at Mount Airy, Habersham county, Ga. Wyman
mentions four cases that were relieved at or near Beaufort.]

The relief obtained by resorting to an exempt locality after the attack
has begun is very prompt, all symptoms of the disease disappearing
within a few days after the arrival of the patient. While residing at
Bethlehem, N.H., I was called one evening to see a German who had just
arrived on the train from Fall River. His condition was most pitiable:
his eyes were fiery red, the nose and face were terribly swollen, while
the water streamed from both eyes and nose. The asthma was at its
height, and his struggles for breath were fearful in the extreme. A
quarter of a grain of morphia was injected into the arm, and after
providing other means for his comfort I left him for the night. The
next morning, while preparing to pay him an early visit, the patient
himself appeared at my office, bright and cheerful, and so much changed
that I at first failed to recognize him. A single night had served to
dissipate all traces of his hay fever.

Unfortunately, a journey to the mountains, and a residence there of six
or eight weeks, are not within the reach of every one afflicted with
the disease; and for these unfortunates something must be done to
relieve, or at least mitigate, their sufferings. If unable to visit any
of the exempt localities, a sufferer may secure a certain degree of
comfort by exposing himself as little as possible to the exciting
causes of hay fever. As it is well known that heat and dust aggravate
the symptoms, the windows of the apartment occupied {224} by the
patient should be so arranged as to exclude the sunlight and every
precaution taken to avoid the presence of dust. He should eat good,
nutritious food, avoiding the use of all stimulants, except perhaps a
little light wine at dinner. Anything which induces dyspepsia must be
carefully guarded against, and care taken to keep the bowels regular.

Blackley[18] advises as a surer method of excluding the irritant
(pollen) the hanging of a curtain of thin calico before the door and
fitting into the lower portion of one of the windows a screen made of
two layers of thin black muslin enclosed in a square frame. When in use
both curtain and screen should be moistened with a solution of carbolic
acid, ten grains of the acid to one pint of water. For those who are
compelled to go out he has devised a very ingenious respirator. Having
taken an exact cast of the nasal passages from the margins of the alæ
and septum to the inferior turbinated bones, he constructed with the
aid of these, by means of the galvano-plastic process, cases of silver
fitting exactly all the folds and depressions of the cavity. Several
layers of platinum wire, 0.001" to 0.007", were arranged in the cases.
The sieve thus formed was moistened before using with a 1/10 per cent.
solution of carbolic acid. To prevent the pollen from coming in contact
with the eyes, they were protected with spectacles provided with
accurately-fitting gauze guards. The result of wearing this apparatus
was an almost perfect freedom from unpleasant symptoms.

[Footnote 18: _Op. cit._, p. 267.]

In the absence of any specific, the medicinal treatment of hay fever is
necessarily confined to palliative measures. Debility being one of the
prominent symptoms, tonics are indicated, and in this way quinine, at
times regarded almost as a specific, may be of use. It should be given
in doses of one or two grains three times a day before and during the
attack. Thus administered, it is undoubtedly of great utility in many
cases. Arsenic, whether in the form of Fowler's solution or the iodide
of arsenic, as suggested by Blackley, may also be used with advantage.
Galvanism, which was used successfully by Hutchinson of Rhode Island,
is strongly recommended by the late Beard. He advises that the negative
pole be placed at the epigastrium "and the positive applied a moment
over the forehead and on top of the moistened head, then over the front
and back of the neck, and down the upper and middle of the spine." The
current used should be mild and the sittings short. The writer has had
no personal experience with this method of treatment, nor has it been
generally adopted.

The injection into the nostrils of a saturated solution of quinine by
Helmholtz, although apparently useful in his case, has not met with
like success in the hands of others.

The troublesome itching and burning of the eyes and face are most
readily relieved by bathing the parts at first in tepid and then in
cold water, repeated several times a day, and with mild astringent
collyria, such as a strong infusion of tea or of one or two grains of
sulphate of zinc to an ounce of rosewater. If the lids be much inflamed
and the skin excoriated, the following ointment may be applied:

  Rx. Bismuth. subnit. drachm ss;
      Ungt. simpl.     ounce j.
   M. Ft. ungt.

The pharyngeal symptoms are best controlled by chlorate of potassium as
a gargle, or, better still, in the form of the compressed tablets now
prepared by many of our druggists. The treatment of the asthmatic
symptoms differs in no way from that which we have recommended for the
paroxysms of BRONCHIAL ASTHMA, the details of which were fully
described in the preceding article.

In 1880, Harrison Allen of Philadelphia published an article[19]
directing {225} the attention of the profession to the fact that many
cases of chronic nasal catarrh which had resisted the ordinary methods
of treatment could be readily cured by restoring the permeability of
the nasal passages.

[Footnote 19: _Am. Journal of Med. Sciences_, January, 1880,
Philadelphia.]

In April, 1882, William H. Daly of Pittsburgh, Pa., in a paper[20] read
before the American Laryngological Association, gave the histories of
three cases of hay fever which he had succeeded in curing by means of
operative procedure. In each of these cases the tissue over the
inferior and middle turbinated bones was hypertrophied, and in one case
it was so extremely sensitive that the slightest touch with the probe
was sufficient to excite a violent paroxysm of sneezing. In these the
diseased tissue was removed with the galvano-cautery or by the
application of glacial acetic acid.

[Footnote 20: "On the Relation of Hay Asthma and Chronic
Naso-pharyngeal Catarrh," _Archives of Laryngology_, vol. iii. No. 2.]

The following year (1883) a much more elaborate article[21] on the same
subject was published by John O. Roe of Rochester, N.Y. After
describing the highly vascular and somewhat erectile tissue covering
the inferior turbinated bones and lower portion of the septum, the
turbinated corpora cavernosa of Bigelow, he calls attention to its
great susceptibility to the action of irritants, whether applied
locally or to some remote portion of the body, citing as an example of
the latter the swelling, and sometimes almost complete closure, of the
nostrils supervening after exposure of the body to the action of a
current of cold air. In this situation the tissue is liable to become
hypertrophied, and in that state its susceptibility is greatly
increased. If, when in this condition, it is exposed to the action of
pollen, dust, or any other irritant, the substance produces a local
irritation which is reflected through the sympathetic nerves to other
parts of the respiratory tract; and it is to this reflected irritation
that Roe attributes most of the phenomena of hay fever. He regards it
as analogous to certain forms of laryngeal catarrh which, according to
the recent testimony of many distinguished laryngologists, are clearly
traceable to disease of the nasal cavity. Applying this theory to the
treatment of hay fever, he removed the hypertrophied tissue in five
cases, and in every instance succeeded in preventing a recurrence of
all symptoms of the disease. His operation consists in the removal of
the diseased tissue by means of Jarvis's wire écraseur and the
galvano-cautery, caustics having proved less effective. The wire snare
is best adapted for the removal of the tissue over the posterior
portion of the turbinated bone, where, owing to its being pedunculated,
it is readily caught in the wire loop. Over the anterior portion of the
turbinated bone, as well as over the septum, the growth is more
sessile, and is best destroyed by means of the galvano-cautery. To
avoid inflammatory reaction and to guard against other unpleasant
symptoms it is advisable to remove only a small portion of the growth
at a time. After each operation the part should be sprayed with warmed
vaseline to allay the irritation occasioned by the burning, and this
should be continued until the surface is sufficiently healed over to
admit of a repetition of the operation. The cauterization should be
repeated until every trace of the diseased tissue is removed.

[Footnote 21: _The Pathology and Radical Cure of Hay Fever_, New York,
1883.]

Prior to the publication of Roe's article Harrison Allen had operated
successfully on two cases, the histories of which he has not as yet
published, but has kindly communicated by letter to the writer,
together with a description of his method of operating. This latter
differs but little from that of Roe, except as regards the time at
which the operation should be performed, Roe maintaining that the
operation should never be performed when the patient is suffering from
an attack of hay fever, while Allen considers this immaterial, and does
not hesitate to operate even when the symptoms are at their height. If
symptoms of hay fever recur after the operation, the nares should be
{226} carefully examined, and if, as is usual in such cases, any
remnants of hypertrophied tissue be discovered, these should be at once
removed. The operation is not regarded as a very painful one, and a
patient of Allen's upon whom he had operated during an attack assures
me that he left the doctor's office feeling much better than when he
entered it. This is mentioned because hay-fever patients are
excessively nervous, and timidity on their part has hitherto prevented
many of them from availing themselves of this form of treatment.

It will be seen that, thus far, the operation has been performed in but
ten cases, but the results have been so uniformly successful as to
justify the belief that it is capable of relieving many cases of this
hitherto intractable disease. Whether this hypertrophied condition is
present in every case, as claimed by many, or in even the majority of
cases of hay fever, has not as yet been determined; and until further
observation shall have decided this question it will be impossible to
form an opinion in regard to the general application of this method of
treatment.




{227}

DILATATION OF THE BRONCHIAL TUBES, CIRCUMSCRIBED AND DIFFUSED.

BY SAMUEL C. CHEW, M.D.


DEFINITION.--Enlargement of the calibre of a bronchial tube or tubes,
whether confined to a limited portion of one tube, or reaching
throughout a great part of its extent, or involving several or many
tubes.

SYNONYM.--Bronchiectasis, from [Greek: bronchos], a bronchial tube, and
[Greek: echtasis], an expansion.

HISTORY.--The change in the physical condition and size of a bronchial
tube, designated as bronchial dilatation, never occurs as a primary
affection, but is always the result of some preceding disease,
especially of chronic bronchitis or fibroid phthisis. The full
consideration of its pathological origin belongs, therefore, to the
natural history of those causative affections.

Later writers have in general followed Laennec's description of the
different varieties of bronchial dilatation; which, indeed, can hardly
be improved upon, for such was the accuracy of that great clinician and
pathologist as an observer that nothing was likely to escape him as
regards physical conditions, though he may sometimes have been in error
as to the theoretical explanation of what he saw. Previously to
Laennec's observations dilatation of the bronchial tubes was, as he
remarked himself, almost entirely overlooked both by pathologists and
practitioners. The reason of this is evident from the considerations
that a smaller tube when dilated would, except to the most careful
examination, closely resemble a larger tube of normal size, and that a
large dilatation might be mistaken by the ear at the bedside and by the
eye at the necropsy for a pulmonary vomica.

Two principal forms of bronchial dilatation are met with. In the first,
or diffused bronchial dilatation, known also as the cylindrical form,
the tube is uniformly enlarged in calibre, so that, whereas in the
normal state it would have admitted only a fine probe, in its enlarged
condition it may be of the size of a goosequill. In this state it may
be readily mistaken, when seen by itself, for a larger tube; but the
alteration is conspicuous when the tube is seen to be larger than the
branch from which it is given off. In the second or circumscribed form,
which is also termed sacculated dilatation, a pouch-like or fusiform
distension occurs in the continuity of a tube. In a third form, which
is far less common, several successive enlargements are met with in the
course of one tube, which thus presents a beaded appearance. It happens
at times that all of these different varieties of dilatation may be
encountered in the bronchial tubes of the same lung. The second, or
sacculated, form is the most common, especially in young persons.

ETIOLOGY.--In both of the more common forms of bronchial dilatation the
previous existence of bronchitis is to be regarded as the chief
causative agency, though other conditions may serve to increase the
dilatation when it has once been established. Laennec's observations
led him to connect the {228} occurrence of bronchitis with the
production of dilatation of the bronchial tubes, though his explanation
of the mechanism of this production was erroneous, inasmuch as he
considered the accumulation of secretion in the affected tubes, and the
forcible inspiratory efforts made in coughing to dislodge this
accumulation, to be the direct causes of the enlargement. The part
played by bronchitis in producing dilatation is, however, less
immediate and mechanical than Laennec held it to be. It may, in a
general way, be considered the direct cause of the cylindrical and the
indirect cause of the saccular form of dilatation.

The long continuance of chronic bronchitis gives rise to weakness and
atony of the bronchial walls, so that they yield to the pressure
brought to bear upon them in the violent or protracted and repeated
respiratory efforts that are made in coughing. In such cases the tubes
which are themselves affected by the inflammatory process may yield
throughout a greater or less extent of their continuity, and thus the
cylindrical form of dilatation may be established. The same mechanism
may be supposed to give rise to the beaded variety of the disease if
the inflammatory action should be greater at several points along the
course of a tube, with intervals of tissue in a healthier or less
atonic state.

In the saccular form, on the other hand, the dilatation does not occur
in the portion of the tube which is chiefly affected with the
inflammatory process, but is the consequence of a local capillary
bronchitis involving the ultimate ramifications of the affected tube
and occasioning collapse of a portion of the lung. This collapse
operates in two ways in causing a pouch-like dilatation of an adjacent
bronchus--partly through the atmospheric pressure within the affected
tube, tending to fill the space created by the collapsed portion, and
partly by the traction of this collapsed lung-tissue outside of the
tube.

In addition to the part played by bronchitis and atelectasis of the
lung in occasioning bronchial dilatation, another important factor in
its production is to be found in the condition described by Corrigan in
1838 as cirrhosis of the lung, and since recognized as interstitial
pneumonia or fibroid phthisis. In this affection there is formed around
the blood-vessels and terminal bronchi, as well as around the
air-vesicles, a hyperplasia of the connective tissue, which, as is the
case with connective-tissue formations in other situations, ultimately
contracts, obliterating the air-cells, smaller bronchi, and
blood-vessels, and thus converts the lung-tissue into a tough, fibrous
mass. By the contraction thus produced the bronchial tubes of a larger
size, which have been previously weakened by bronchitis and have lost
their elasticity, are subjected to traction on all sides, and thus
become dilated. Dilatations of all forms may thus be produced,
cylindrical, sacculated, or beaded, according to the amount of lung
involved in the contracting process and to the degree and situation of
the bronchitis which favors the dilating action.

The determining causes, then, of bronchial dilatation are--1st, chronic
bronchitis; 2d, atelectasis; and, 3d, fibroid phthisis or cirrhosis of
the lung.

SYMPTOMATOLOGY.--The general symptoms of bronchial dilatation, as well
as the course and duration of the affection, are such as belong to the
pulmonary diseases favoring its production, especially chronic
bronchitis and fibroid phthisis. The cough and dyspnoea of these
diseases are aggravated by bronchial dilatation; but these symptoms,
together with the impairment of nutrition, are due rather to the
underlying affections than to the mere fact of dilatation. Increased
and fetid expectoration, which often occurs in bronchial dilatation
from retained and altered secretion, is by no means characteristic of
this condition, since it may occur where no sign of dilatation exists.

There is generally some degree of dulness on percussion over a dilated
{229} bronchial tube, due to the condensation of the lung-tissue
surrounding it, and varying in extent and degree with the amount of
that condensation, and also with the amount of secretion retained
within the tube. Sometimes, however, increased resonance of a
tympanitic character is observed, especially if the dilatation be of
the saccular form and near the surface of the lung. Such differences in
the percussion sound are analogous to what occurs over a pulmonary
vomica, which will generally give a dull sound, though, if the cavity
be superficial and thin-walled, it may yield a tympanitic resonance. On
auscultation bronchial respiration may be heard along the course of
tubes affected with cylindrical dilatation when they are free from
secretion; and this is more intense in proportion as the tube is more
dilated and the lung-tissue around it more condensed. Bronchophony and
increased vocal resonance also occur, and if mucus be present in the
dilated tubes coarse moist râles will be heard. In a saccular
dilatation there may be true amphoric breathing, with the gurgling
sounds heard in a vomica. In some cases there is an alteration in the
appearance of the chest-wall, which is retracted by the shrinking of
the condensed lung beneath.

Now, of the auscultatory signs that have been mentioned, the
bronchophony and increased vocal resonance, together with the
percussion dulness, belong also to pneumonia, which, however, at least
in its acute form, can be distinguished from bronchial dilatation by
the previous history, the febrile movement, and the general phenomena
of the case, and by the fact that the tubal breathing of pneumonia,
besides being less persistent, is most frequently met with in the lower
part of the lung, and that of bronchial dilatation in the upper part.

But the diagnosis between a dilated bronchus and pulmonary phthisis is
in some cases a very difficult problem, the signs of the cylindrical
form closely simulating those of the stage of deposit in phthisis,
because involving the same physical condition, and those of the
saccular variety corresponding often with the auscultatory signs of a
cavity. In the former case there may be the same localized dulness on
percussion, the same bronchial or broncho-vesicular breathing, and the
same sinking or contraction of the chest-wall apparent on inspection.
In the latter case there may be equally in saccular dilatation and in a
vomica amphoric breathing, gurgling, and pectoriloquy. In the
establishment of the diagnosis between these two conditions Austin
Flint, Sr.,[1] justly attaches importance to the circumstance that
there is in general a greater degree of percussion dulness over a
cavity than over a dilated bronchus, so that a relatively greater
prominence of the auscultatory signs as compared with the degree of
dulness makes the diagnosis of dilatation more probable. But the most
important evidence on the point is to be gotten from the history of the
case. If in a case where the auscultatory signs would leave the
examiner in doubt there were found loss of flesh, fever, night-sweats,
quickened pulse, and the other general phenomena belonging to phthisis,
the existence of this affection would be rendered probable in the
highest degree, and the auscultatory signs should be taken as
corroborating an opinion founded on the general symptoms.

[Footnote 1: _Dis. of Resp. Organs_, p. 353.]

Positive evidence, again, may be furnished by a microscopic examination
of the sputa; the discovery of particles of lung-tissue or the
so-called bacillus tuberculosis pointing clearly to phthisis.
Conversely, the absence of the general symptoms of phthisis would, in a
case presenting the above auscultatory signs, render it probable that
they are due to bronchial dilatation. Long-continued cough and abundant
expectoration are the chief symptoms common in both forms of disease.
There are, however, some cases in which even with the most careful
examination and weighing of evidence the physician will be left in
doubt, inasmuch as in some cases of otherwise {230} well-marked
phthisis the usual constitutional symptoms are absent or imperfectly
declared. In such exceptional cases the estimate of probabilities is to
be based on the fact that while bronchial dilatation is comparatively
rare, pulmonary phthisis is extremely common.

PATHOLOGY AND MORBID ANATOMY.--Enlargement of the bronchi may be met
with throughout almost the entire extent of a lung; when limited to a
part of the organ the change most frequently occurs, according to
Laennec, Rokitansky, and other observers, in the superior lobe and
toward the anterior border. The tubes of the third or fourth order in
respect to size are most frequently affected, the primary bronchi being
never involved except in association with tracheal dilatation.

In the different forms of dilatation the bronchial walls are found in
various states. In the cylindrical variety they are for the most part
thickened and hypertrophied, both as to the mucous and the fibrous
coats; the mucous membrane being in a catarrhal state, covered often
with muco-purulent discharge, and easily broken down and detached,
while underneath the white fibrous coat is sensibly thickened.

In the sacculated form, on the other hand, the bronchial wall generally
presents a thin and atrophied appearance, the mucous membrane
undergoing but little change, except that the stretching to which it
has been subjected gives it a smooth and shining look. This difference
in the degree of thickening of the bronchial walls in the two forms of
dilatation is in part due to the fact that in the saccular variety the
enlargement in calibre is far greater than it is in the cylindrical
form for a corresponding extent of a tube, so that its wall is much
more stretched and attenuated, and thus the tendency to hypertrophy
which has play in the cylindrical form is more than overcome in the
saccular. But the chief reason of the difference in the state of the
walls in the two forms of dilatation is found in the different modes in
which they are respectively brought about, as already described.

DIAGNOSIS.--It has been shown that the determination of the existence
of bronchial dilatation is at times one of the most difficult problems
in diagnosis, from the fact that the auscultatory signs belonging to it
may be equally met with in other affections, especially in pulmonary
phthisis. The diagnosis is to be established, when this is possible,
only by a careful consideration of the physical signs in connection
with the general symptoms, so that the sources of doubt arising from
the one set of phenomena may be as far as possible corrected by the
other. These signs and symptoms, and the various affections to be
discriminated by them, have been sufficiently set forth under the head
of Symptomatology. While in this way a clear conclusion may be reached
in many cases, yet there are others in which, notwithstanding the
utmost care, there may still be a doubt as to whether the symptoms and
signs indicate a dilated tube or a pulmonary cavity.

PROGNOSIS.--The prognosis of bronchial dilatation is directly connected
with that of the affections which chiefly give rise to it--viz. chronic
bronchitis and fibroid phthisis. When chronic bronchitis has lasted
long enough to cause dilatation, it is seldom if ever cured, and,
though improvement may take place from time to time in its symptoms,
yet the dilated bronchi can hardly undergo diminution in their size.
And in fibroid phthisis, while the progress of the disease is often
very slow, yet it is on a downward grade, and the connective-tissue
contraction giving rise to the dilatation increases with the advance of
the malady.

TREATMENT.--The treatment of cases of bronchial dilatation resolves
itself in great degree into that of the underlying and causal diseases
on which it depends. As regards methods specially directed to the areas
of dilatation, they consist of alterative, astringent, stimulant, and
antiseptic remedies, either administered by the stomach or used by the
process of inhalation. Cough {231} may be allayed with the syrup of
lettuce containing in each dose from one-eighth to one-fourth of a
grain of sulphate of codeia or 10 or 12 drops of the spirit of
chloroform. If expectoration is very profuse, sulphate of atropia, in
the dose of one-hundredth to one-eightieth of a grain, or the extract
or tincture of belladonna, may be used. Turpentine and eucalyptol have
a controlling influence over this symptom, and are specially beneficial
if the bronchial secretion is fetid. They may be given by the mouth in
the dose of minim v-xx in emulsion, and applied also by inhalation of
their vapor or by spray. Inhalations of solutions of carbolic acid,
minim j-x to an ounce of water, are more effective than anything else
in checking fetor of the expectoration and the breath. This agent may
also be administered by the mouth in the dose of fluidrachm j-iv of a 1
per cent. solution.




{232}

EMPHYSEMA.

BY SAMUEL C. CHEW, M.D.


DEFINITION.--The term emphysema is derived from [Greek: emphysaô], to
inflate, and signifies an increased amount of air in a part or the
whole of one or both lungs. Accordingly as the situation of this excess
of air is _(a)_ in the air-vesicles or _(b)_ in the connective tissue
between the lobules, emphysema is divided into Vesicular emphysema and
Interlobular or extra-vesicular emphysema.

HISTORY.--These two affections are different pathologically and
anatomically, vesicular emphysema being a much more common and
important affection than the interlobular form. The distinction between
the two forms was first drawn by Laennec. Previously to his time the
essential difference between them was unknown; and, as the accurate
diagnosis of the disease can be made only by auscultation, its
existence was no doubt very often entirely overlooked. It has been
remarked by Rokitansky[1] that "had Laennec done nothing else for
medical science, his discovery of this diseased condition, and of the
causes giving rise to it, would have sufficed to render his name
immortal."

[Footnote 1: _Path. Anat._, vol. iv. p. 53, Am. ed.]


VESICULAR EMPHYSEMA.

Vesicular emphysema may be defined as an absolute or relative increase
in the amount of air contained in the vesicles of a part or the whole
of one or both lungs. As a substantive disease it occurs in two
principal forms--hypertrophic and atrophic; but besides these it is met
with as a secondary affection due to other diseases and limited to
certain areas of the lungs, sometimes acute and sometimes chronic in
its production and duration. It will therefore be best to consider the
disease under the following different forms:

  1st. Acute lobular emphysema;
  2d. Chronic lobular emphysema;
  3d. Hypertrophic lobar emphysema;
  4th. Atrophic lobar emphysema.


1. Acute Lobular Emphysema.

This form of the disease is the result of the rapid distension beyond
their natural size of air-vesicles which had previously been healthy.
It is most frequently met with in children and as the consequence of
bronchitis or {233} whooping cough. The paroxysms of cough occurring in
these affections, especially in the latter, are attended by deep
inspirations, by which the vesicles are directly distended, and by
violent expiratory efforts, with closure of the glottis, so that the
air is forced into those portions of the lungs where there is least
resistance, particularly at the apex and along the margins. In a large
proportion of cases of acute lobular emphysema, when the distending
cause is removed by the cessation of the cough, the vesicles return to
their normal size through their natural elasticity, which has not been
destroyed. But in some cases, when the cough has been of unusual
violence or of very long duration, the change may be permanent through
loss of this elasticity, and thus a form of chronic lobular emphysema
is produced.

SYMPTOMS AND SIGNS.--Unless emphysema of this form is extensive and
extreme in degree, it is not attended with symptoms additional to those
of the affections giving rise to it. When very great it may occasion
increased percussion resonance.

TREATMENT.--The treatment is only what is required by the causal
affections.


2. Chronic Lobular Emphysema.

In many cases emphysema is confined to a limited number of lobules,
especially at the apices, the anterior borders, or about the base of
the lung; and being gradual in development and permanent in duration,
it is then termed chronic lobular emphysema. This is the form
frequently met with in the different varieties of pulmonary phthisis,
in which its development seems supplementary to the incapacitation of
other portions of the lung. The lobules nearest to the surface of the
lung or immediately beneath the pleura are found to be most distended,
so that they often project beyond the adjacent surface.

Chronic lobular emphysema is chiefly of interest in connection with the
other pulmonary diseases which give rise to it. The mechanism of its
production is like that of acute lobular emphysema, but the diseases
occasioning it being chronic the emphysema to which they give rise is
equally permanent. At the apex of the lung, its most common situation,
it is very often associated with tubercle in a calcareous state. The
changes accompanying this deposit of tubercle favor the loss of
elasticity in the vesicles of the apex, and the violent expiratory
efforts, with closure of the glottis, occurring in the attacks of cough
to which phthisical patients are subject, force the air into this part
especially, and also into other regions of less resistance, and thus
occasion permanent distension of the vesicles.

SYMPTOMS AND SIGNS.--The signs of this form of emphysema are so often
masked by those proper to phthisis that the detection of the former is
difficult or impossible. This, however, is of no practical importance
in respect to treatment. At times the distension of the vesicles at the
apex is so great as to produce bulging in the supra-clavicular region
and to overcome the dulness due to deposit by the resonance it
occasions.

TREATMENT.--No special treatment beyond that of the causative
affections is required.


3. Hypertrophic Lobar Emphysema.

This is a substantive affection, and is much the most important form of
the disease, both in its origin and development and in the consequences
to which it leads. Though sometimes limited to one lung, or even to a
single lobe of {234} one lung, yet it more commonly involves the
greater part of both lungs, which are increased in size, as shown by
the alteration of the contour of the chest during life and by the
appearance of the organs after death. This enlargement of a lobe or of
a whole lung is of course the aggregate of the increase in size of the
individual vesicles, the changes in which form the pathological units
of the disease.

ETIOLOGY.--In no disease is the study of etiology as throwing light on
treatment, both medicinal and hygienic, of more value than in
emphysema, the important question being as to whether it takes its
origin from some immediate mechanical cause acting upon the healthy
cell-walls, and thus distending them, or whether they suffer such
distension only when they have been previously weakened by some
degenerative process in their tissue. The importance of determining
this point correctly with reference to treatment is obvious.

In partial and lobular emphysema the change may have been wrought by
causes mechanical in their nature and directed specially to the
affected parts, such as have been already referred to; but in the
general diffused or lobar form of the disease, in which by degrees the
greater part or the whole of a lung is involved, we are almost
compelled to assume the existence of some degenerative process or
tendency coextensive with the malady and determining its existence.
That any one form of degeneration is present in all cases has never
been proved; indeed, it may be said to have been disproved. Rainey's
view, that the change in the air-cells is essentially dependent on
fatty degeneration of their walls, was based mainly on observations
made upon a single case, and, although favored by the eminent authority
of C. J. B. Williams, it has not been substantiated. The same thing
must be said of Sir William Jenner's teaching, that fibroid
degeneration is the essential lesion. Though both fibroid and fatty
changes are found in not a few cases, yet in others a careful
examination has failed to detect either the one or the other of them,
so that neither can be regarded as the essential condition explaining
all cases. Nevertheless, it is probable in the highest degree that a
degenerative change of some kind, due to imperfect or perverted
nutrition of the cell-walls, always exists in general lobar emphysema,
though its nature may sometimes elude observation.

In cases of well-marked emphysema there may be no discoverable
morphological changes in the walls of the alveoli, though, as remarked
by Hertz,[2] "a tissue-relaxation may be present in the lung without
our being able to recognize any corresponding microscopic abnormality."

[Footnote 2: _Ziemssen's Cyclop._, vol. v. p. 373.]

It may be said, then, that while in partial or local emphysema the
alteration in the air-vesicles may be effected by extraordinary efforts
brought to bear upon healthy cell-walls, in general or lobar emphysema,
on the other hand, it may be produced by ordinary efforts acting upon
weakened and diseased cell-walls. The morbid change is probably not in
all cases alike, being sometimes fatty, sometimes fibroid,
degeneration, and in other cases of a kind not ascertained.

In addition to other considerations, the markedly hereditary nature of
emphysema in not a few instances would of itself render the existence
of some constitutional predisposing cause highly probable. On this
point A. T. H. Waters[3] quotes the observations of Greenhow and
Jackson. Out of 42 cases collected by Greenhow, 23 showed an hereditary
tendency, and in 28 reported by Jackson, 18 were of emphysematous
parentage. In stating his belief that substantive or general emphysema
is the result of some degenerative process, Waters bases it on the
following considerations: 1st. The high degree of development which the
disease often reaches, without any {235} previous history of violent or
long-standing cough, in connection with either bronchitis, whooping
cough, or any similar affection. 2d. The frequency with which the
disease attacks the whole of both lungs, and the uniform character of
the morbid changes often observed throughout all parts of the lungs.
3d. The hereditary nature of the disease, as shown by observations.
4th. The manner in which the disease is influenced by certain remedial
measures which are known to act beneficially on other diseases attended
with degeneration of tissue.

[Footnote 3: _Diseases of the Chest_, pp. 122, 123.]

As to the nature of the immediate exciting cause of emphysema, whether
in the general or local form, different views have been maintained. The
most important of these are the inspiratory and expiratory theories.

The former of these theories, that in accordance with which the disease
is referred to inspiratory action, was maintained by Laennec, and under
the influence of his authority was at one time generally accepted. In
accordance with this view, the existence of bronchitis is an important
factor in the production of emphysema, as undoubtedly it often is in
the lobular form. The dilatation of the air-vesicles was attributed to
their over-distension by inspiratory efforts allowing the free entrance
of air, the escape of which was impeded by bronchial mucus. Inspiration
was thus regarded as a more powerful act than expiration, which was
considered too feeble to drive the air beyond the accumulated mucus. In
this way the air was supposed to accumulate in gradually increasing
amount within the cells, which thus became distended.

But in opposition to this view it has been shown by Hutchinson's
researches that Laennec was wrong in supposing inspiratory power to be
greater than that of expiration; and it is further opposed by the
researches of Mendelssohn and Traube, and those of Gairdner, which have
shown conclusively that the presence of a pledget of mucus in a
bronchial tube, so far from causing distension of the air-vesicles to
which it leads, must ultimately ensure their collapse. The collapse
thus occasioned, which is most common in the lower parts of the lungs,
may lead, partly perhaps through inspiratory pressure, to vicarious
emphysema in the upper portions, which receive a relatively larger
quantity of air, in accordance with Williams' theory of negative
inspiratory pressure.

It is true, then, as maintained by Laennec, that bronchitis may
occasion emphysema, but the emphysema does not occur in the vesicles to
which the affected tubes directly lead, nor from the force of
inspiration applied to these vesicles, as Laennec taught, but in other
portions of the lungs.

The expiratory theory affords a more satisfactory explanation of
emphysema than does the inspiratory theory, and one more completely in
accordance with the physiology of respiration and the anatomy of the
thorax.

In ordinary expiration, in which the lungs are uniformly and equably
compressed by the chest-walls, there is nothing tending to force air
into one part of these organs more than into another, and thus produce
emphysematous dilatation. But in forced expiration, such as occurs in
the act of coughing, it may be plainly seen, if the chest be uncovered,
that the air is driven upward to the top of the lungs, so as to produce
a perceptible bulging in the supra-clavicular region. This bulging is
notably increased in the coughing-spells of emphysematous subjects; and
this fact is urged by Sir William Jenner both as throwing light upon
the expiratory act as a principal factor in the disease, and as
accounting for the special frequency of emphysema in the upper parts of
the lungs. The explanation of this phenomenon is found in the
circumstance that in the strong expiratory efforts of coughing the
abdominal muscles force the diaphragm upward, and thus compress the
lungs from below; at the same time the strong lateral anterior and
posterior thoracic walls resist pressure, while the superior part of
the thorax, covered over {236} with fascia, but not completely
protected by a bony structure, offers least resistance. To this
unprotected part of the lungs and to the free margins and borders,
which contain normally the smallest amount of air, will the strong
currents produced by violent expiratory efforts be driven, so as to
cause distension of their vesicles. Thus, the frequent coughing-spells
of bronchial catarrh, so commonly associated with emphysema, give rise
to the expiratory efforts which are the immediate cause of the
emphysema.

While, therefore, it is probable that in some cases and to a certain
degree inspiration may have a share in occasioning emphysema, yet
expiration is to be regarded as a more important and more frequent
factor in its production. This, at least, is probably the case in
partial and lobular emphysema, and in some instances of the lobar form
where the disease gradually spreads throughout a lobe. But in
rapidly-diffused and extensive lobar emphysema such an explanation
cannot always be admitted, because sometimes the disease advances
steadily, so as to involve the greater part of one or both lungs
without the occurrence of any paroxysms of cough which could distend
the air-cells by their violent expiratory efforts. In such cases the
only distending force would seem to be that of ordinary inspiration,
which, while it might have no effect upon healthy lung-tissue, may
easily be supposed to exercise sufficient dilating power upon
air-cells, the walls of which are in a state of degeneration, and, thus
being unnaturally weak, yield to pressure.

SYMPTOMS AND SIGNS.--One of the earliest symptoms of emphysema is
shortness of breath; and, though at first it may not be very marked,
yet as the disease advances it becomes more and more urgent, especially
on going up stairs or walking up hill. Distension of the stomach by a
full meal is likely to induce it, and even a slight degree of bronchial
catarrh may render it extremely distressing. This symptom is due
chiefly to two causes: First, the obliteration of numerous capillaries
in the pulmonary system, occasioned by the thinning and destruction of
the cell-wells in which they ramify, interferes with oxygenation, so
that an increased number of inspiratory acts is required to supply the
deficiency, and thus respiration is hurried; and, secondly, the
impairment of the natural elasticity of the air-vesicles prevents the
expulsion of their contents; the residual air remains, therefore,
unchanged, and cannot supply oxygen to the blood; and thus increased
expiratory efforts are made in order to expel the stagnant air and
obtain a fresh supply. Notwithstanding this increase of both
inspiratory and expiratory action, the movements of the chest are but
slight. As far as bronchial catarrh is a cause of dyspnoea in
emphysematous patients, improvement may take place in the warm dry
weather of summer, when this symptom is often much mitigated.

Cough is a very constant symptom, varying in degree with the extent of
bronchial catarrh. The act of coughing is feeble and expectoration is
effected with difficulty--so much so that sometimes the retained
secretion threatens suffocation.

Asthma occurs in paroxysms, and as a distinct phenomenon from the
dyspnoea which is more or less constant. The asthmatic seizures often
come on in the night after the patient has been asleep; they are
characterized by orthopnoea and constriction in the chest, and
generally subside with free expectoration.

The physical signs of emphysema are highly characteristic and of great
importance. On inspection a peculiar conformation of the chest is
observed when the emphysema has lasted for some time, the departure
from the normal form gradually increasing in the progress of the
disease until, in advanced cases, a degree of deformity is produced
which is strikingly characteristic. In the earlier stages, or if the
emphysema is local and partial, the alteration in the chest-wall
consists only of a prominence corresponding with the dilated {237}
portion of the lung. But when the disease is general and occupies a
considerable portion of both lungs, a rounded, convex, or barrel-like
form of the thorax is produced, most noticeable in the upper part, and
due to increased prominence of the ribs. The thoracic portion of the
spine becomes more curved, and thus throws the shoulders forward,
producing a stooping attitude. The intercostal spaces at the upper part
of the chest are frequently effaced by the pressure of the enlarged
lung, while at the lower part the depression of these spaces may be
increased, especially during inspiration, by the action of the
diaphragm. The enlargement of the thorax as a whole is chiefly due to
the changes in its upper part, the lower part appearing sometimes by
contrast to have lessened in volume. This, however, is in most cases
apparent rather than real; but in some instances the dimensions in the
lower part of the chest are actually lessened.

The respiratory movements in well-marked emphysema are characteristic
and peculiar. The dilatation of the chest which is sought to be
accomplished by muscular action is small and disproportioned to the
amount of effort put forth, notwithstanding that the need for air keeps
the sterno-mastoid and scaleni muscles in constant action. The reason
of this is that, the lungs being distended nearly to their utmost
capacity, there is but little room for further expansion. As there is
only slight enlargement on inspiration, so with expiration the walls of
the thorax contract but little at their upper part.

The result, therefore, of their muscular efforts is that the ribs are
lifted and the sternum carried forward, so that the whole chest rises
and falls in respiration as if its walls formed a solid case. But the
character of respiration is by no means the same in all cases of
emphysema. More than forty years ago Stokes[4] called attention to the
different modes of breathing in different cases accordingly as there is
or is not displacement of the diaphragm; and his observations have more
recently been reaffirmed by Waters[5] and others. In the one class of
cases the diaphragm retains its normal position and the upper part of
the chest is very prominent, probably because the disease is chiefly in
the upper portion of the lungs. Here there is but little descending
movement of the diaphragm in inspiration and the abdomen remains flat.
In the other class the diaphragm has been displaced and pushed downward
by the enlarged lungs, which have probably been involved in the disease
throughout their whole extent. In these cases the abdomen is protruded
more or less with every inspiration. The difference between the two
types of breathing is important, as in the latter class of cases there
is more advanced and extensive disease than in the former, the symptoms
being more urgent, and especially the dyspnoea greater. Inspection of
the chest shows that the movement of inspiration is more quickly
accomplished than that of expiration, which is prolonged, labored, and
often wheezing in character.

[Footnote 4: _Diseases of Chest_, 2d ed., p. 173.]

[Footnote 5: _Diseases of Chest_, p. 140.]

Percussion and auscultation furnish signs of the utmost importance for
determining the existence of emphysema which are in direct accordance
with the physical conditions giving rise to them.

Increased resonance on percussion is observable over all portions of
the lungs when the disease is general, but it is most marked at the
upper part and along the anterior borders. When the disease is partial,
the increased resonance is limited to the portions of the chest-wall
over the affected areas. This sign is of course due to the greater
amount of air in the distended vesicles. In very marked cases the
resonance sometimes loses the vesicular and approaches the tympanitic
character. There is very little, if any, further increase of the
resonance on full inspiration. This is unlike what occurs in health,
and is due to the fact that the capacity of the distended lungs is not
relatively increased in emphysema, as it is in health, by the act of
inspiration.

{238} Over the cardiac region the normal dulness on percussion is
lessened or entirely superseded by resonance from the overlapping of
the heart by the distended lung. In partial emphysema the heart may
escape this encroachment and its area of dulness may not be lessened;
and even in some rare cases where the disease is general and far
advanced the same thing may be observed, from the lung being bound by
pleuritic adhesions, so that it cannot expand in the direction over the
heart. But, as a very general rule, it will be found in hypertrophic
emphysema that the normal præcordial dulness is lessened or absent.
When this is observed the heart is in some cases forced downward, its
beat being felt most distinctly in the epigastrium; and in other cases
it is carried directly backward, so that its impulse can hardly be
detected at all.

Over the posterior wall of the chest percussion gives a clear note at a
lower level than in health, because the dilated lung extends farther
down toward the bottom of the thorax.

The signs afforded by auscultation are highly characteristic of
emphysema, and, like those of percussion, in direct relation with the
physical condition of the lungs. The respiratory sounds are notably
feebler, because the amount of air entering and leaving the lungs at
each act of respiration is less than in health. The distended lungs can
admit only a small amount of air at each inspiration, and from their
diminished elasticity they can expel but a small amount at each
expiration. This feebleness is directly proportioned to the degree of
the disease, or, in other words, to the amount of distension; for the
greater the distension, the less movement of the lungs and the less
play of air. If the disease be unequally advanced on the two sides of
the chest, the respiratory murmur will correspondingly vary, being
feebler on the side where the disease is most advanced.

Besides this change in intensity, there is also an alteration in the
rhythm of the respiratory acts corresponding to what has been referred
to above as observable on inspecting the chest. The ratio of
inspiration and expiration is always changed in well-marked
emphysema--so much so as to be in many instances reversed, the
expiratory occupying more than double the time of the inspiratory act.
Inspiration is short and quick, because the air enters freely and the
limit of the possible expansion of the lungs is speedily reached.
Expiration is prolonged, because there is a loss of their normal
elasticity, and an effort is made by voluntary action of the expiratory
muscles to expel the stagnant residual air. This alteration in rhythm
is eminently characteristic of emphysema when the disease is far
advanced and occupies a considerable portion of the lungs. Feebleness
of respiratory murmur is an earlier sign than alteration in rhythm, and
may be observed before any marked prolongation of the expiratory act
occurs and before there is any very positive increase of resonance on
percussion. Hence it is of great importance if not otherwise
explicable, as it sometimes is by unusual thickness of the chest-walls,
because it indicates, taken by itself, an early stage of emphysema in
which treatment may be most likely to be beneficial. It is sometimes
found in very advanced stages of emphysema that the respiratory sounds
are almost totally inaudible; but in general, while both murmurs are
feeble, expiration is more appreciable than inspiration. If, however,
the disease is associated with bronchitis, either constantly or
intermittingly, the proper auscultatory signs of the accompanying
affection may be observed, though modified by the emphysema. Thus,
moist and dry râles according to the stage of the bronchitis, sibilant
or sonorous, subcrepitant or mucous râles according to the size of the
bronchial tube involved, may be heard, the abnormal sounds being
notably prolonged during expiration.

It can hardly be doubted that the sign referred to by Laennec as
"perfectly pathognomonic of emphysema," and described by him as "the
dry {239} crepitant râle with large bubbles" (râle crépitant sec à
grosses bulles), is in most cases, if not always, dependent upon
coexistent bronchitis. Certainly, many cases of emphysema are met with
in which, in the absence of bronchitis, no such sound is heard. The
signs or combination of signs which are indeed "perfectly pathognomonic
of emphysema" are increased resonance upon percussion, associated with
marked feebleness of respiration and prolonged expiration. This
association of signs is always indicative of emphysema, because it can
be explained only by the physical conditions involved in this disease.

Auscultation of the cardiac region gives results corresponding with
those afforded by percussion and palpation. When the lung is distended
sufficiently to overlap the heart, the sounds belonging to the latter
organ will be more or less indistinct and distant, and sometimes
scarcely audible. If the heart be pushed to the right or downward
instead of being driven backward, the sounds may still be distinct, but
they are out of place and have their greatest intensity under the
sternum or at the epigastrium. The proper signs of hypertrophy or
dilatation of the heart, which may be revealed on post-mortem
examination, and the mechanism of which will be referred to farther on,
are to a great degree masked during life; for the overlapping lung
prevents the detection of increased cardiac dulness by percussion or
increased impulse by auscultation.

Palpation of the chest serves to confirm the evidence supplied by
inspection. The effacement of the intercostal spaces, the lessened
mobility of the ribs, and the situation of the apex-beat of the heart
are signs of importance of which the sense of touch takes cognizance.

COMPLICATIONS AND SEQUELÆ.--Bronchitis is one of the most frequent of
the affections complicating emphysema. In the partial form of the
malady it often sustains, as has been already seen, a direct causal
relation to the emphysema. When the disease is diffused and general,
bronchitis is sooner or later almost always encountered, and is then of
a congestive rather than an inflammatory type, being often
unaccompanied by fever, and in part due to interference with the
circulation through the smaller bronchial arteries. For, as some
branches of these vessels are distributed in the interlobular areolar
tissue, and others ramify upon the walls of the smallest bronchial
tubes, a constant pressure may be made upon them by the dilated
air-vesicles, and this obstruction of the circulation through them may
occasion passive congestion. The bronchitis accompanying advanced
emphysema is generally attended with free secretion, amounting in some
cases to a bronchorrhoea so profuse as seriously to imperil life by
suffocation, the danger being increased by the difficulty in
expectorating that exists. The discharge from the bronchi is often in
such cases of a muco-purulent character. So urgent is the danger
sometimes arising from this complication that unless it be relieved
death may quickly ensue. The face and other portions of the surface
become livid or leaden, the whole body more or less cool, the pulse
weak and hurried, and copious râles are audible even without applying
the ear to the chest. Life is threatened both by the accumulation in
the respiratory passages obstructing the entrance of air, and by the
tendency to the formation of heart-clots from the embarrassment to the
pulmonary circulation and the consequent malaëration of the blood.

Another very common complication of emphysema is asthma, which, indeed,
is sure to occur in greater or less degree of violence and at longer or
shorter intervals in all cases where the disease has become extensive.
The attacks often come on in the night, arousing the patient from
sleep. The tendency to a nocturnal occurrence of asthma may be due to
the recumbent position favoring passive congestion of the lungs, and to
the diminished activity of the respiratory process during sleep when it
is not aided by {240} voluntary effort. From both these causes an
irritation may be set up determining reflex spasm of the bronchi.
Moreover, the paroxysmal occurrence of asthmatic attacks is an
illustration of the general law in accordance with which morbid
neurotic conditions frequently occur intermittingly, though the
eccentric cause of them is constantly existing, as witnessed in the
subjects of epilepsy or angina pectoris. The frequent recurrence of
these attacks of spasmodic asthma is in all probability the cause of
the hypertrophic state of the muscular tissue in the bronchial tubes
which is often met with as a part of the morbid anatomy of emphysema.

The structural alterations of the heart that occur in emphysema are the
results, more or less directly, of the mechanical conditions involved
in the disease. Earliest in the sequence of changes affecting this
organ are non-compensative hypertrophy and dilatation of its right
chambers; and by some writers it has been maintained that the
alterations due to emphysema are found only on this side of the organ.
This, however, has been completely disproved by extended observations,
and it has been shown that left hypertrophy and dilatation, while not
such direct consequences of emphysema as the corresponding changes on
the right side, are yet frequently encountered, and are plainly due to
the disease in the lungs.

The hypertrophy and dilatation of the right chambers of the heart are
easily understood when it is considered that the constant pressure of
the enlarged air-vesicles of the emphysematous lungs interferes more
and more with the circulation through the pulmonary capillaries, and
that there is thus a constant impediment to the onward course of the
blood from the pulmonary artery, and a continuous backward pressure
within the right ventricle and auricle. The effort to overcome this
pressure leads to hypertrophy, and ultimately, as this effort is less
and less effective, to dilatation of the right chambers.

It would appear as though the readiness with which the alterations on
the right side of the heart may be explained has led, if not to their
being more frequently observed, yet at any rate to their being more
emphasized, than are the corresponding changes on the left side. Some
writers have referred only to those on the right side, giving the
correct explanation of them, but making no mention of the similar
condition on the other side. Thus, Rokitansky[6] refers to the
obstruction to the circulation occasioned by the expansion of the
air-cells in pulmonary emphysema as one of the causes of dilatation of
the right ventricle and auricle, but says nothing of similar changes on
the left side. Other pathologists, however, as Lebert and Gairdner,
have shown that at least in long-standing emphysema the left side is
also not infrequently involved in disease.

[Footnote 6: _Path. Anat._, vol. iv. p. 130.]

What explanation, then, is to be given of those changes in the left
chambers which, if less frequent than hypertrophy and dilatation on the
right side, are yet certainly not uncommon? Evidently, they cannot be
referred to obstruction in the pulmonary circulation; for this, while
producing backward pressure into the right compartments, must, on the
contrary, lessen the amount of blood received by the left chambers,
which therefore have no excessive labor thrown upon them from this
cause, and so cannot become hypertrophied in such a manner.

The explanation is probably to be found partly, as suggested by
Waters,[7] in the altered position of the heart occasioned by the
emphysema, and partly in the remora of the venous circulation.

[Footnote 7: _Diseases of the Chest_, p. 152.]

There are thus two factors to be considered, the first of which applies
to the right heart as well as to the left. As to this first, the more
extensive the emphysema the greater is the degree of displacement that
the heart {241} undergoes; and as the normal position of the ventricles
with reference to the arteries emanating from them offers the easiest
course to the blood-currents, any departure from this position causes
an embarrassment, and consequently increased labor, in the left
chambers as well as the right; hence one explanation of the hypertrophy
on both sides. As to the second factor, the obstruction to the general
capillary circulation necessitates an increased effort of the left
ventricle to overcome it; and so, as far as it is concerned, another
cause of hypertrophy is in operation.

It is frequently observed in advanced emphysema that there is a marked
disproportion between the forcible heart-beat and the feeble radial
pulse, the former being due to the hypertrophy, and the latter to the
small amount of blood received and propelled by the heart.

Besides these changes in the size of the heart and the thickness of its
walls, constituting hypertrophy or dilatation as the case may be, a
displacement of the entire organ is a not uncommon consequence of
emphysema. The direction of this displacement may vary, so that it may
be either directly backward, the heart being overlapped by the
distended lung, or it may be downward or to the right of the sternum. A
much greater degree of displacement of the heart may result from the
pressure of pleural effusion than from emphysema of the lung; but when
due to pleurisy it is generally of shorter duration and admits of
perfect restoration, whereas when caused by emphysema it is usually
permanent. The writer has at present under his care a case of extreme
displacement of the heart to the right, the apex-beat being felt and
seen to the right of the sternum; but in this patient, while extensive
supplementary emphysema of the left lung, due to the almost complete
incapacitation of the right lung, has probably had a share in causing
the displacement, yet a more important cause of it has been contraction
of the right side of the chest, the result of absorption of an old
pleural effusion which has left the lung bound back and adherent. This
case closely resembles one reported by Stokes as presenting "the
singular phenomenon of the displacement of the heart to the right side,
consequent on the removal of an effusion of the right side."[8]

[Footnote 8: _Diseases of the Chest_, p. 467.]

Dropsy is to be regarded as one of the most notable complications and
consequences of emphysema; for when the disease is of long standing the
loss of balance between the arterial and venous circulation occasioned
by the obstruction to the passage of blood through the lungs gives rise
ultimately to effusion of the serum, which is first seen in the lower
extremities, and may subsequently become general.

In consequence of the disturbances in the circulation and respiration
which have been considered, it is not surprising that the nutritive
function should be impaired, as is found often to be the case in the
subjects of old emphysema, who present a cachectic and anæmic
appearance, partly due to malaëration of the blood, and partly to
imperfect performance of the assimilative functions occasioned by
passive congestion of the alimentary tract. Still another cause may be
found, as suggested by Hertz,[9] in the insufficient supply of the
elements received from the lymph through the imperfect emptying of the
thoracic duct into the distended left subclavian vein.

[Footnote 9: _Ziemssen's Cyclop._, vol. v. p. 382.]

There has been much discussion as to the connection between emphysema
and pulmonary phthisis, some pathologists having held that the two
affections are incompatible with each other, and that emphysema may
thus exercise a prophylactic influence against phthisis. Careful and
extensive observations furnish no valid grounds for such a belief. So
far as supplementary emphysema is concerned, it is a common thing to
find emphysematous patches at the bases and along the margins of lungs
the apices of which are tuberculous. In such cases the increased
inspiratory labor thrown upon some portions of the {242} lungs in
consequence of impaired function of other parts accounts for the
emphysema. But, besides this common condition, cases are met with in
which the emphysematous portions are themselves beset with tubercle.
Such a case is reported by Waters,[10] in which an emphysematous lung
was found studded with tuberculous matter, which on microscopic
examination was seen in the air-sacs and ultimate bronchial tubes.

[Footnote 10: _Diseases of the Chest_, p. 156.]

While emphysema ensures no absolute immunity from tuberculous diseases
of the lungs, yet the physical condition involved in it does lessen the
liability to tuberculous deposit, which is favored by active hyperæmia,
and active hyperæmia is not apt to occur in an emphysematous part of a
lung. It likewise lessens the liability to such pulmonary affections as
hæmoptysis, oedema, and perhaps pneumonia. The diminished pulmonary
circulation occasioned by the shrinking and obliteration of the
capillaries explains the infrequency of hæmoptysis. The same cause,
together with the smaller amount of interlobular areolar tissue that
the emphysematous lung contains, lessens the liability to oedema,
because there are both less blood from which the serum can be effused
and less of the tissue in which it can be collected and held. And the
infrequency of pneumonia in an emphysematous lung is owing to the
absence of conditions favoring hyperæmic changes.

DURATION AND TERMINATIONS.--No definite limit can be assigned to the
duration of emphysema, as the progress of the disease varies very much
in different persons according to the underlying cause, and according
also to the care taken in avoiding those influences which promote its
development, such as physical exertion or exposure to cold and damp.
Many persons with extensive emphysema, if they can secure favorable
climatic conditions, and thus escape attacks of bronchial catarrh, will
live on for years in comparative comfort, whereas in others the disease
may advance with rapidity to a fatal issue if their situation in life
necessitates hard work or exposure to causes that induce frequent
attacks of bronchitis. The immediate cause of a fatal termination is
generally either apnoea resulting from extensive bronchitis, or
asthenia from impaired action of the heart, or both of these conditions
together.

PATHOLOGY AND MORBID ANATOMY.--From examinations made at various stages
of the disease in those who have died of emphysema it is seen that the
earliest change is a dilatation of the air-sacs, which become gradually
more distended, their walls growing thinner, until they may yield at
some points and perforations occur. As the disease advances the
perforations become larger and more numerous, until the walls are so
far destroyed that several sacs or even lobules are blended together,
forming only one cavity. The alveoli may be dilated to the size of a
mustard-seed, or even a pea, without undergoing rupture, and may thus
become visible by the unaided eye; but when the emphysematous spaces
are as large as a hazelnut or small walnut they consist of numerous
air-sacs, or even of several lobules, fused together by the atrophy and
breaking down of the interalveolar and interlobular tissues. When the
cavities thus produced by the fusion of several sacs or lobules are in
the subpleural portion of the lung, they will sometimes project beyond
the adjacent surface, so as to form appendages of the size of a small
walnut which appear to be connected with the lung by a pedicle. It is
remarked by Waters that perforation of the cell-walls is much more
common in lobar than in lobular emphysema, even though the dilatation
of the sacs may be as great or greater in the latter than in the former
affection; which is due, no doubt, to the fact that the extensive and
diffused changes in the lobar form are dependent upon a degenerative
process, in consequence of which the walls are specially prone to give
way.

All the changes just referred to, from the earliest and slightest
degree of distension to extreme attenuation and perforation of the
walls, with final {243} coalescence of several sacs and the formation
of appendages, may be met with at the same time in different parts of
the same lung. The most advanced changes are found most commonly at the
apices and free margins of the lungs, while in the deeper parts an
earlier stage only may have been reached.

The blood-vessels in the cell-walls are diminished in calibre by the
atrophy of these walls and by the constantly-increasing air-pressure,
so as to admit only the watery part of the blood; and thus is explained
the pigmentary change in the surrounding tissues where the
blood-corpuscles collect. Ultimately, many of the vessels are
obliterated, and the backward pressure thus induced extends to the
pulmonary artery, and thus gives rise to hypertrophy and dilatation of
the right side of the heart, as already explained. It is this pressure
on the vessels in the alveolar walls that causes also passive hyperæmia
of the bronchial mucous membrane, and thus produces a tendency to
bronchitis, which so often occurs as a consequence of emphysema, while,
again, primary bronchitis is frequently a factor in the production of
the disease. The principal change in the bronchial tubes, in addition
to the hyperæmia and softening of their mucous membrane due to
coexisting bronchitis, is a hypertrophic thickening of their muscular
coat, the result probably of repeated spasmodic action in the asthmatic
attacks.

DIAGNOSIS.--The chief points by which the diagnosis of emphysema is
determined have already been referred to under the head of Symptoms and
Signs. The most important of these are the auscultatory signs; for,
although the general symptoms and history of the case may point with
probability to the nature of the malady, yet if these alone be regarded
other affections may easily be confounded with it.

The auscultatory signs proper to emphysema are increased resonance upon
percussion, feeble respiratory murmur, and prolonged expiration. Any
one of these physical signs may be met with in other affections than
emphysema, but when they occur conjointly they point only to this
disease. In addition to them the alteration in the form of the
chest-wall, so that it becomes rotund or barrel-shaped, and the
asthmatic character of the breathing, are important indications. The
diseases most likely to be mistaken for emphysema are phthisis,
bronchitis, pneumothorax, and pleural effusion.

In the early stage of phthisis feebleness of respiratory murmur with
prolonged expiration might suggest the existence of emphysema; but,
apart from the fact that these signs at any time when a doubt might be
felt are generally confined to the top of the lung in phthisis, the
diminished percussion resonance, the bronchial or broncho-vesicular
breathing, the bronchophony or bronchial whisper, and increased vocal
resonance and fremitus--all of them proper signs of phthisis and all
wanting in emphysema--would by their presence or absence clearly
establish the differential diagnosis between the two affections. In
more advanced phthisis, when softening has taken place and a cavity
exists, difficulty in discriminating between the two diseases could
hardly arise.

Emphysema is so frequently associated with chronic bronchitis and with
intercurrent attacks of acute bronchitis that it is often important to
determine whether these latter affections exist independently or are
complications of the emphysema. The question is in general settled by
the history of the case and by the conformation of the chest, showing
whether previous dilatation of the air-cells has taken place or not; as
also by the presence or absence of the special signs of emphysema when
those of the bronchial affection are encountered.

Capillary bronchitis, from the urgent dyspnoea attending it and the
vesiculo-tympanitic resonance which it sometimes presents, especially
in the upper and anterior parts of the chest, may possibly be mistaken
for emphysema, from {244} which, however, it may be distinguished by
the quickened pulse and high temperature that belong to this form of
bronchitis, as also by the rapid diffusion of the subcrepitant râle
over both sides of the chest in capillary bronchitis; whereas this sign
is absent or less marked in emphysema. Moreover, capillary bronchitis
is most common in childhood, when diffused emphysema is less frequently
met with.

Pneumothorax is characterized by distension of the chest and increased
percussion resonance--signs which belong also to emphysema; but the
possibility of error is avoided by the consideration that whereas in
emphysema the respiratory sound is feebler than natural, in
pneumothorax it is strongly exaggerated and amphoric in character; and
there are also the additional signs of metallic tinkling and the
plashing noise or "Hippocratic succussion sound" made by moving the
body backward and forward. Moreover, even as regards the sign in which
the affections would appear to resemble each other, a difference may be
observed on careful examination; for the percussion note of
pneumothorax is purely tympanitic, while in emphysema the increased
resonance has still a vesicular character to some degree. Pneumothorax,
again, is always a unilateral affection, and emphysema is almost as
constant in its occurrence on both sides of the chest.

It might appear that there would be little liability to confuse
emphysema with pleural effusion, in view of the very general presence
of dulness on percussion in the latter affection and of resonance in
the former. But in some cases of fluid effusion in the chest a degree
of tympanitic resonance is met with, more especially in children. J.
Lewis Smith remarks that "as a rule in the pleuritis of children, at a
certain stage of the effusion, percussion produces a sound which is
either decidedly tympanitic or which partakes of the tympanitic
character."[11] In both affections, moreover, there may be enlargement
of the chest. The doubt, if it arise, may be settled by the
consideration that in emphysema the altered resonance and the
enlargement are on both sides; whereas in pleurisy these signs are in
general on one side only; and, further, the enlargement is more marked
at the top of the chest in emphysema and at its base in pleural
effusion.

[Footnote 11: _Diseases of Children_, 5th ed., p. 607.]

In concluding the account of the diagnosis it may be said that when the
history of a case, the frequent or constant occurrence of dyspnoea, and
the more or less rounded conformation of the chest make the existence
of emphysema probable, this probability may be converted into a
certainty by the discovery of resonance on percussion, feeble
respiratory murmur, and prolonged expiration.

PROGNOSIS.--The circumstances, apart from treatment, which especially
affect the prognosis of emphysema are the form in which the disease
occurs and the ability of the patient to secure immunity from
influences which may increase the malady itself or the attendant
bronchitis, such as hard work, great exertion of the respiratory
organs, and exposure to cold and damp.

Acute supplementary emphysema, even when it affects considerable
portions of both lungs, may entirely disappear and the vesicles be
restored to their integrity on the removal of the underlying cause.
Thus, the vicarious dilatation of air-cells following acute bronchitis
or whooping cough in children may leave no sign of its previous
existence after recovery from these diseases. In general, the shorter
the duration of the causal diseases, the more likely is the emphysema
to disappear; for if it be maintained for a considerable time, the
elasticity of the cells may be so damaged that they may never return to
their natural size.

In hypertrophic lobar emphysema the prognosis in most cases is
unfavorable as regards perfect recovery; while yet the disease may not
materially shorten life, and with proper care may be compatible with a
fair degree of {245} comfortable existence. And, indeed, even in this
form of the disease, provided it do not affect a great extent of lung
and have not been of very long duration, there is in some cases ground
for hope of ultimate recovery, with restoration of the air-cells to
their normal condition. Modern methods of treatment have rendered the
prognosis in such cases somewhat less unfavorable than it was once held
to be.

TREATMENT.--The treatment of emphysema comprises several distinct
objects: 1st, the arrest of the degenerative changes which may be going
on in the walls of the air-vesicles, and which favor their dilatation;
2d, the restoration, as far as is possible, of the integrity of the
lungs, so that they may resume their natural size; 3d, the relief of
bronchitis, asthma, and dropsy, which are associated as secondary
affections with the primary disease.

To meet the first of these indications, the arrest of degenerative
change, iron is among medicinal agents the one most to be relied upon;
for, though neither it nor any other means has power to restore loss of
tissue or to reproduce integrity of structure when several alveoli are
fused into one cavity by the breaking down of their partition-walls,
yet by enriching the blood it may improve the nutrition of these
cell-walls so that the tendency to dilatation and rupture may be
checked. Iron steadily administered in small doses is the best means
for effecting this end, and if the patient object to one form of the
metal after using it for some time, it may be changed for another. The
best preparation of the drug is probably the tincture of the chloride,
and one of the best forms for administering this medicine is the
mixture of acetate of iron and ammonium (Basham's mixture) introduced
into the U. S. Pharmacopoeia of 1880. This is especially valuable, when
any dropsical effusion exists, on account of its gentle diuretic
action. In addition to iron, other agents promotive of nutrition, such
as cod-liver oil and the hypophosphites, may be used with the same
view. Stomachic tonics, such as the simple bitters and pepsin, may be
useful by aiding digestion and nutrition; and at the same time, by
preventing the formation of flatus, they may relieve the dyspnoea
caused by upward pressure on the diaphragm. That real benefit may be
derived from such measures is beyond doubt; and it is to be feared that
some practitioners, in their conviction that no cure can be wrought in
those parts of the lung which have actually undergone wasting and
rupture, have to too great an extent neglected the use of means which
may at least prevent the advance of similar changes in other parts, and
thus tend to stay the progress of the disease.

Deep and hurried respiration will increase the air-pressure within the
yielding vesicles; for this reason active exercise is objectionable,
especially walking up hill, and the use of wind instruments is to be
strictly prohibited. Indeed, as regards this last cause of respiratory
pressure the patient's inability to practise is in general warning
enough, but in the early stages of the affection a caution against it
may be necessary.

The suggestion of the use of strychnia against emphysema is not founded
on a correct knowledge of the mode of action of this drug; for,
although it may stimulate muscular contractility, it has no influence
upon the elasticity of the air-cells and no power to restore them to
their natural size. Whatever benefit may result from it is due solely
to its action on digestion and the improvement in nutrition to which it
may thus contribute.

The second indication of treatment, the restoration of the dilated
air-cells to their natural size, is possible, if at all, only at an
early period of the disease or in portions of the lung which have not
gone beyond a moderate degree of cell-dilatation. An enlarged space
formed by the fusion of several cells cannot be lessened in size by any
means, medical or mechanical, and the loss of respiratory power from
the destruction of the cell-walls in which oxygenation is effected does
not admit of permanent relief. Where, however, such {246} destruction
has not yet taken place and distension is not extreme, there is reason
to believe that a return of the cells to their natural size may in some
cases be accomplished. The inhalation of condensed air has been
recommended with this view; and no doubt good may result from it, due
chiefly to the retardation of the breathing and of the heart's action
which it occasions, while dyspnoea is relieved by the larger supply of
oxygen taken in at each inspiration. This improvement in respiration
causes more complete tissue-metamorphosis, and thus aids nutrition and
all the functions.

Still greater benefit is to be derived from the exhalation into
rarefied air--a measure which acts upon mechanical principles, and has
been found to give relief not only to the symptoms of emphysema, but to
the organic disease itself; for the retention and stasis of the
residual air, which is far larger in amount in emphysema than it is in
health, serve at once to keep up the dilatation of the cells and to
increase the dyspnoea; and therefore any means which will effect the
withdrawal of this air will favor the return of the cells to their
normal size, and at the same time relieve the dyspnoea. This benefit is
accomplished by the method of expiration into rarefied air, which acts
by suction--or pneumatic aspiration, as it may be termed--drawing out
the air from the distended vesicles, and relieving them of the
continual presence and pressure of this air. Better results would
appear to be gotten from the conjoint use of the two methods--the
inspiration of compressed air and expiration into rarefied air--than
from either one alone.

By the persistent use of these means in cases which have not advanced
so far as to defy all treatment not only may the symptoms of dyspnoea,
cough, asthma, and impaired nutrition be improved, but the size of the
chest may be diminished, as shown by measurement; and this can result
only from the return of the distended air-cells, in some degree at
least, to their normal capacity.

The apparatus best fitted to effect this double purpose is that of
Waldenburg, as modified by Tobold.[12] The method of using it is
simple, and can readily be understood by examining the instrument. It
must be said that the most valuable action of this apparatus consists
in the withdrawal of the air from the cells which it effects, for this
tends to produce an organic change for the better--viz. the diminution
of the enlarged cells by a sort of suction; while its other action, the
supply of condensed air, gives relief to symptoms mainly. In emphysema
the expiratory act is relatively more impaired than the inspiratory,
and the apparatus is best adapted to the relief of this greater
deficiency. Henry Saltzer, formerly of Germany and now of Baltimore,
has recently obtained very favorable results from its use in emphysema,
not only as regards the dyspnoea and other symptoms, but also in the
way of lessening the size of the chest as determined by
measurements.[13]

[Footnote 12: This instrument is made by Messrs. J. Reynders & Co. of
New York.]

[Footnote 13: A reference to Saltzer's observations and measurements
may be found in Weil's _Handbook of Topographical Percussion_, pp. 107,
108, Leipzig, 1880.]

The third indication of treatment has reference to the complications of
emphysema. Of these the most common, and one of the most important, is
bronchitis, which is to be treated in the same way as when it occurs as
an independent affection. Expectorants to promote and remove secretion
and agents to allay cough are very important means, because the
retention of secretion and the effort of cough to expel it cause a
strain upon the air-cells, and thus increase the emphysema. The local
use, by inhalation or spray, of opiates, belladonna, hyoscyamus, and
other agents of this class, is often most serviceable by giving relief
to the cough without disturbing digestion. As bronchitis is in many
emphysematous patients a very chronic affection, and is attended with
submucous thickening in the bronchial tubes and consequent diminution
of their calibre, the iodide of potassium is an agent of special {247}
value for its relief. Whether the influence of this remedy is due to a
sorbefacient power or to some other unexplained mode of action, there
is no doubt of its great value in chronic bronchitis, so that for this
complication of emphysema it claims a very high rank among medicines.
The rapidity with which relief is afforded to the cough and dyspnoea of
bronchitis, and to the asthmatic paroxysms attending it, by full doses
of 10 or 15 grains of iodide of potassium at intervals of four hours,
makes it probable that its action is partly neurotic in character. It
is remarked by Austin Flint, Sr., that when the iodide has effected a
marked improvement in the chronic bronchitis he has known the
characteristic deformity caused by the emphysema to be notably
diminished.[14]

[Footnote 14: _Clinical Medicine_, p. 131.]

A dangerous symptom which sometimes arises in the course of the chronic
bronchitis accompanying emphysema is profuse bronchial catarrh, which
may destroy life by producing apnoea, the surface becoming cold and the
pulse feeble and vanishing as the patient seems to be drowning in his
own secretion. In this condition the writer has in several instances
found prompt and unmistakable benefit from the hypodermic injection of
hydrobromate of quinia, and he would strongly advise the use of this
agent. The solution he has employed is of the strength of 4 grains of
the salt to 20 minims, and of this 15 to 20 minims has been the dose
given. Under the action of this remedy the pulmonary capillaries would
appear to be so toned that further effusion is checked, and the gasping
and cyanotic condition has been speedily succeeded by comfortable
breathing. For the same symptom Waters advises the use of moderately
large doses of turpentine (drachm doses in aromatic water every two
hours) on a plan suggested by Sir D. Corrigan of Dublin.[15]

[Footnote 15: _Diseases of the Chest_, p. 172.]

As bronchitis has so much power to produce emphysema when the
conditions favorable to its occurrence exist, and to increase it when
already established, everything tending to prevent it is of great
importance. With this view the avoidance of cold and wet, and, when
practicable, recourse to a mild climate in winter, are advisable.

The attacks of asthma to which emphysematous patients are subject are
to be treated in the same way as the purely spasmodic form occurring
independently of discoverable organic disease. If the difficult
breathing has come on suddenly and the patient is not laboring under
advanced dilatation of the heart, prompt relief may be given by a
hypodermic injection of morphia; but if the heart is much dilated, this
might endanger too great depression. Chloral is generally unsafe for
the same reason. The bromides in full doses may be serviceable in the
less severe attacks, and the tincture of lobelia in doses of 10-20
drops every fifteen minutes until slight nausea is felt is often of
great benefit, as is also the smoking of stramonium-leaves.

The dropsy met with in advanced stages of emphysema may be so prominent
a symptom as to require special treatment. Its cause is found in
dilatation and weakness of the right chambers of the heart, which
result from obstruction to the circulation through the lungs when
compensative hypertrophy is no longer efficient, for then these give
rise to passive congestion of the liver and kidneys and remora of the
general venous system, with dropsical leakage, seen first and chiefly
in the lower extremities. Treatment is therefore to be directed chiefly
to increasing the tone of the heart; and for this purpose digitalis is
most useful, as it is in other forms of cardiac dropsy. The chief
indication of its beneficial action is seen in the better action of the
kidneys consequent upon the increased impulsive force given to the
heart. When acting favorably, marked relief both of the dropsy and the
dyspnoea may be obtained from the use of this agent in the dose of 2 to
4 drachms of the infusion or 10 or 15 drops of the tincture every three
or four hours. If {248} the stomach should not bear the digitalis, as
is sometimes the case, or if it fail to act or lose its power, the
fluid extract of convallaria, recently introduced as synergistic with
foxglove, may be employed as a substitute for it.

Under similar circumstances, if the patient's strength will admit of
it, great benefit will sometimes result from a mercurial purge, by
which passive congestion of the portal system may be relieved and the
upward pressure of an engorged liver in some degree lessened.


4. Atrophic Lobar Emphysema.

This disease differs from the hypertrophic form of emphysema in the
circumstance that the bulk of the affected lungs has undergone
diminution from waste or atrophy of their tissue. Absolutely, the lungs
may contain no more air than they should in health--they may even
contain less--but, relatively, there is an increased amount of air in
them in consequence of the diminished amount of the lung-tissue. Such
relative increase of air in a given area of the lung may be very
considerable from the atrophy and destruction of the cell-walls, the
alveoli coalescing so as to form cavities, while the individual
air-cells are not dilated. The entire lung, however, is shrunken, the
chest-wall correspondingly depressed and contracted, and the thoracic
muscles atrophied. The function of the affected lungs is impaired in
consequence of their loss of size and the diminution of the respiratory
movements. This is of course especially noticeable when exertion is
made, while under other circumstances there may be little or no
embarrassment of breathing unless the disease is far advanced and has
involved a large amount of both lungs. But, in general, this form of
disease causes less distress and is a less formidable affection than
hypertrophic emphysema. In some cases a mingling of the two forms is
found, as when a person the subject of general atrophic emphysema has a
local vesicular dilatation developed at the top and margins of the
lungs.

The shrunken state of the lungs in atrophic emphysema prevents the
heart from being overlapped, so that the area of cardiac dulness is not
lessened, as it is in the hypertrophic form; and as the general waste
of the system is attended with a diminution of the amount of blood,
dilatation of the right ventricle, and consequent dropsy, are not apt
to occur, as they are in hypertrophic emphysema.

ETIOLOGY.--Atrophic emphysema is always due to constitutional causes.
It is found chiefly in old persons or in those in whom impaired
nutrition has produced the degenerative changes of old age. Hence it is
described by some writers as senile emphysema or senile atrophy of the
lungs.

SYMPTOMS.--Of the general symptoms of atrophic emphysema, apart from
those which belong also to the hypertrophic form, the most marked
are--first, the lessened size of the thorax; and, second, the character
of the dyspnoea, which is not urgent, and is not apt to occur except on
making exertion. The blood is lessened in amount from the general
impairment of nutrition, and is therefore adapted, so to speak, in
quantity to the diminished aërating space. Percussion in general gives
exaggerated resonance, from the relative increase of air in the lung
and the thinness of the thoracic wall, which thus vibrates more
perfectly. In some cases, however, from loss of elasticity in the
cartilages of the ribs, the resonance is even diminished. On
auscultation there are found somewhat prolonged expiration and, in
general, feeble inspiratory murmur--signs which belong also, but in
greater degree, to true hypertrophic emphysema, from which, however,
the atrophic form is to be distinguished by the contraction of the
chest that is seen throughout its entire contour.

In some cases of hypertrophic emphysema there may be, it is true, an
appearance of partial contraction of the chest-wall, since where the
{249} emphysema has produced a marked bulging of the upper portion of
the thorax the part below may seem by contrast to be contracted. But in
the atrophic form of the disease no distension is seen at any part of
the chest-wall, the whole surface being more or less sunken and
contracted. Even in hypertrophic emphysema with distension of the
thorax, when the disease has lasted a long time there may be some
degree of wasting of the lung-tissue; but this condition does not
constitute true atrophic emphysema, which is such from the beginning
without any preceding stage of hypertrophy.

DIAGNOSIS.--The diagnosis of atrophic emphysema is to be made by the
physical signs studied in connection with the conformation of the
chest.

PROGNOSIS.--The prognosis of this affection is hopeless as regards a
cure, since the organic change is due to the degeneration of age; yet
the disease may continue for years without materially or at all
affecting the duration of life.

TREATMENT.--The atrophied lungs can never be restored to their
integrity; treatment is therefore limited to the use of tonics and
nutriment in order to hold in check the process of waste; and to the
relief of bronchial catarrh, which is apt to be attended with profuse
purulent secretion. The agents best suited to these two purposes have
already been considered.


II. INTERLOBULAR OR EXTRA-VESICULAR EMPHYSEMA.

Interlobular or extra-vesicular emphysema is, as has been previously
stated, an affection differing anatomically and pathologically from the
form of disease already described. In the vesicular form air is present
where it normally belongs, but in undue amount; in the interlobular
form it is present where it ought not to be--that is, in the meshes of
the connective tissue between the lobules, beneath the pleura, and
around the bronchial tubes and pulmonary vessels. These situations may
be reached by the air through a rupture of the vesicles, and thus in
some cases vesicular may be associated with interlobular emphysema, the
rupture having occurred from violent cough; or the emphysematous
infiltration may be gaseous, as the result of gangrene occurring during
life or of decomposition after death.

DIAGNOSIS.--The presence of air in the connective tissue of the lungs
cannot be determined by any signs or symptoms; if, however, it should
be discovered in the subcutaneous tissue of the neck, face, or chest,
giving rise to puffiness and crackling of the integument, its presence
in the areolar tissue of the lungs may be suspected, especially if
there be coexisting vesicular emphysema, the air having passed into the
mediastinum and thence into the tissue beneath the skin.

The existence of interlobular emphysema is not, in general, of serious
significance, as the air commonly disappears from the subcutaneous
tissue in a few days; whence it may be inferred that it likewise
disappears from the connective tissue of the lung, the opening which
had admitted it there having become closed. If present in large amount
in the lung-substance, it may, however, increase the difficult
breathing of an emphysematous subject by compressing a number of the
air-vesicles. Or, again, if the interstitial emphysema be subpleural,
the bulla may burst, and the air, escaping into the cavity of the
chest, may occasion pneumothorax, or even hydro-pneumothorax, from the
resulting inflammation. Such an occurrence is, however, very uncommon.

Even when the diagnosis of interlobular emphysema is established, no
treatment is needed or practicable.




{250}

COLLAPSE OF THE LUNG (ATELECTASIS).

BY SAMUEL C. CHEW, M.D.


DEFINITION.--The term atelectasis is derived from [Greek: atelês],
incomplete, and [Greek: echtasis], expansion, and designates a
condition in which the lung has failed to expand or has returned in
part or throughout its whole extent to the state of non-expansion which
is normal in foetal life. In the former case the state is one of
congenital atelectasis, and is of course met with only in the new-born;
in the latter it is acquired atelectasis, or collapse of the lung, a
portion or portions of the organ which have once been expanded having
the air excluded from their alveoli, so that these collapse and return
to the pre-natal state. To this condition of acquired atelectasis the
term apneumatosis, from [Greek: a] negative, and [Greek: pneumatôsis],
filling with air, was applied by Fuchs in 1849, and it has since been
adopted by Graily Hewitt.

HISTORY.--For a long time this affection was regarded as a peculiar
form of pneumonia, for the reason that at post-mortem examinations
patches of collapsed lung-tissue were found which appeared to have
undergone solidification. Inasmuch as the condition was most frequently
met with in young children, and the supposed solidification was often
limited to certain lobules of the lung with intervening healthier
spaces, it was described as the lobular pneumonia of children.

The secondary nature of the affection, and the fact that it is very
generally preceded by bronchitis, and sometimes by catarrhal pneumonia,
were pointed out by Barthez and Rilliet in 1838. Some other important
distinctions between this affection and general or lobar pneumonia had
been referred to by various writers, but it was not until 1844 that its
true nature was satisfactorily elucidated by Bailly and Legendre, who
showed, by blowing air into the lungs after death, that the lobules
supposed to be hepatized were not really solidified by exudation, but
had simply collapsed for want of air.

ETIOLOGY.--The congenital atelectasis of new-born children may be due
to original feebleness, to protraction of labor interfering with the
blood-supply through the cord, or to obstruction of the air-passages by
mucus or other substances. In any case, it is the result of
non-expansion of the chest, so that the lungs are not unfolded. This
constitutes atelectasis in the strict sense.

Acquired atelectasis, apneumatosis or collapse of the lung, is an
affection most frequent in early infancy, though not limited to that
period of life, since bronchitis with defective innervation and great
impairment of strength, the essential factors in the production of the
disease, may occur at any period of life.

It is probably in almost every case secondary to bronchitis, and due to
the occlusion of the smaller bronchi by the presence of mucus allowing
the egress, but impeding the ingress, of air, so that the lobules to
which they lead are gradually evacuated of air, and thus finally
collapse.

Obstruction of a bronchial tube by a foreign body or by the pressure of
a {251} morbid growth within the lung may produce collapse of the
lobules to which such tube leads, a smaller or larger part of the lung
being involved in proportion to the size of the obstructed bronchus.
Such cases are, however, very rare, and they more closely resemble the
condition brought about by the pressure of a pleural effusion giving
rise to the state of carnification, which is, in effect, an atelectasis
involving the greater part or the whole of a lung, and not limited to
certain lobules nor taking place lobule by lobule.

The principal cause of lobular collapse is no doubt bronchial catarrh,
the action of which is aided by impairment of the general strength and
of muscular respiratory power; for the natural elasticity of the
lung-tissue would favor the exit and oppose the entrance of air unless
it were counterbalanced by muscular action in inspiration. If, then,
this inspiratory action is lessened, the requisite amount of air will
not enter the alveoli, and that which they already contain will be in
part driven out, and perhaps in part absorbed into the blood, by the
pressure to which it is subjected. Deficient innervation and lower
vital power are thus important elements in determining collapse, which
is most common in very young infants or in those who, though somewhat
older, have had their nutrition impaired by malhygienic influences or
by other diseases.

The mechanism of the production of lobular collapse by the presence of
mucus in the bronchial tubes has been well explained by the classical
observations and experiments of Gairdner and of Hutchinson. They showed
that the physical result of collapse is in part due to the force of
expiration being greater than that of inspiration, and in part to the
anatomical formation of the bronchial tree. As to the former of these
causes, it was shown by the experiments of Hutchinson, already alluded
to in the article on EMPHYSEMA, that the force of expiration capable of
being applied for the overcoming of obstruction in the bronchial tubes
is greater than that of inspiration--in opposition to the teaching of
Laennec, who regarded the inspiratory as the greater force. Repeated
efforts to clear the bronchial tubes of accumulated secretion by the
forced expiration of coughing must therefore remove air from the
alveoli in greater amount than it can be returned to them by
inspiration, and so they must ultimately be evacuated of their contents
and consequently collapse.

The second mechanical cause to which Gairdner refers is found in the
shape of the bronchial tubes, which taper in size as they advance
toward the air-cells. The mucus contained within a tube may in
consequence of this shape act as a ball-valve, being displaced forward
in the direction of the greater diameter by the expiratory efforts,
thus allowing the exit of air, the entrance of which will be impeded
because inspiratory action will at once close the valve. This
valve-action of a plug of mucus is well illustrated and proved by the
experiments of Mendelssohn and Traube. In one of these a shot was
introduced into the left bronchus of a dog, and in two days the left
lung was found collapsed and the right one in a state of supplementary
emphysema. The collapsed lung was afterward distended by inflation. In
a like manner pledgets of mucus may establish an air-pump action that
will empty the cells to which the obstructed tubes lead and cause them
to collapse. It is, moreover, not improbable that a portion of the
contained air is absorbed by the blood-vessels, as is maintained by
Fuchs.

As a predisposing cause age has a remarkable influence in producing
atelectasis, the condition being much more frequent under five or six
years of age than after that time. This is explained by two
considerations: The first is the greater prevalence of catarrhal
affections of the air-passages in young children than in other
subjects; the second is the fact that the chest-walls in a child are
more pliable and less firm and resistant than those of an adult, so
that when the diaphragm descends in inspiration a portion of the
chest-wall {252} may sink in, and the lung immediately beneath such
portion will not expand to meet the costal wall as it does in older
persons. According to Graily Hewitt, the part at which the chest-wall
is most depressed is "at the junction of the cartilages with the ribs,
and the ribs which more especially exhibit this want of power to resist
the atmospheric pressure are those just above and below the nipple, the
fourth to the seventh inclusive."[1]

[Footnote 1: _Reynolds's Syst. Med._, vol. iii. p. 872.]

The principal cause of collapse involving an entire lobe or the whole
lung is the presence of liquid in the thorax in the form either of
inflammatory serous effusion, empyema, or hydrothorax. The admission of
air into the cavity of the chest by perforation of the lung or by a
penetrating wound of the thorax may also lead to the same result by
allowing atmospheric pressure on the lung. In such cases the lung may
again expand on the absorption or withdrawal of the liquid or air, but
it sometimes remains permanently compressed and carnified.

SYMPTOMS.--It is probable that atelectasis in very limited degree may
exist without being discovered or suspected, the amount of lung
involved being insufficient to interfere by its loss of function with
respiration or to give rise to appreciable symptoms.

In congenital atelectasis the symptoms are obvious from the moment of
birth, and all point to obstructed or imperfect respiration; but they
vary in degree. Should expansion of the chest not take place at all,
the heart, which at first may be felt feebly beating, will soon stop,
and death will occur. In other cases, in which the atelectasis is not
absolute, but yet expansion is not accomplished sufficiently for
respiration to be kept up, the infant is more or less cyanotic,
especially about the lips and face and at the extremities. The
movements of the thorax are slight in degree, and the cry is weak and
suppressed, and at last inaudible. In such cases death usually occurs
in a few hours, but sometimes life is protracted for several days. The
symptoms then are like those of acquired atelectasis or collapse of the
lung.

In this condition--which, as already stated, is generally the result of
bronchitis occurring in debilitated children--the symptoms show
malaëration of the blood. Sometimes they are gradually developed, and
sometimes they occur quite suddenly, according to the rapidity with
which the collapse spreads through the lung and the number of lobules
involved in it.

The signs of bronchitis are present before the occurrence of collapse,
and are more or less mingled with those pointing to the collapsed
state. The hurried respiration so often met with in bronchitis is
increased by the collapse of any considerable numbers of lobules in the
lung. The evidences of imperfect oxygenation of the blood, which in
children are often apparent in bronchitis, are greatly augmented on the
occurrence of collapse, the breathing becoming more rapid and
oppressed, the working of the alæ nasi increased, and the dusky hue of
the surface spreading and becoming deeper. The character of the
respiration is modified in a very remarkable way, as pointed out by
George A. Rees of London, in consequence of the pliable and yielding
condition of the chest-walls in early childhood. When the upper part of
the chest is elevated in inspiration and the diaphragm descends, the
space thus produced cannot be filled by the lungs in consequence of
their partially collapsed state; and for this reason the intercostal
spaces and the lower end of the sternum are sunken by the atmospheric
pressure at each inspiratory act. This character of breathing may also
be observed in older subjects of collapse as regards the depression of
the intercostal spaces, though in less degree than in children, in
consequence of the greater rigidity of the thorax after childhood.

As collapse of the lung in very limited degree may be unattended with
general symptoms, so likewise it may have no positive auscultatory
signs. A {253} moderately extensive tract of the lungs must be affected
in order to produce these to an appreciable extent. This amount cannot
be stated exactly, but, according to Gerhardt, it is from an eighth to
a sixth of one lung.[2]

[Footnote 2: _Ziemssen's Cyclop._, vol. v. p. 332.]

Dulness on percussion, varying in degree and extent with the number of
affected lobules and their nearness to each other, is a very constant
sign of collapse; but it must be kept in mind that if the collapsed
lobules are disseminated or central the dulness may be hardly
observable. Sometimes there is difficulty in detecting dulness, because
from the bilateral character of the bronchitis the collapse of lobules
may take place in about equal degree on both sides, so that one side
cannot be contrasted with the other. Ordinarily, however, there is a
difference in the degree of dulness between the two sides, because the
affection is more extensive in one than in the other; and in general
the loss of resonance over the collapsed lobules is determinable
without comparison of the two sides. Not uncommonly, patches of dulness
are found with intervals of comparatively clear resonance.

On auscultation the respiratory sounds are feeble or entirely absent in
an area in which a number of adjacent lobules are involved together in
collapse.

When a considerable part of a lobe is affected, bronchial breathing may
sometimes be heard, but this is in general less marked than the degree
of dulness and the amount of condensation would lead the examiner to
expect, because the breathing is too feeble to give rise to the
vibrations necessary for the production of this sign.

An important indication of lobular collapse is the rapidity with which
the signs just described are developed; a part or parts of the lung
which had been clear on percussion and normal in respiratory character
becoming in a day, or sometimes in a few hours, dull and nearly silent
to the ear. This very suddenness with which the physical signs are
developed in a case of bronchitis or catarrhal pneumonia in a child
points very plainly to the occurrence of collapse of the lung.

PATHOLOGY.--The pathological appearances in collapse of the lung vary
according to the extent of tissue involved in the change, and also
according to the cause which has induced it. In the disseminated
lobular form which is due to bronchitis the collapsed portions are
chiefly seen on the surface and at the margins of the lung, and they
extend more deeply into the organ as it becomes more involved in the
atelectatic condition. On the surface or on a section the collapsed
patches are depressed somewhat below the surrounding parts and are of a
darker hue, so that they are readily seen as dark-red or purplish spots
surrounded by the lighter healthy tissue. The contrast is sometimes
enhanced by the fact that the non-collapsed parts are even paler than
natural from the vicarious emphysema that has been established in them.

The consistence of the affected part varies in different cases. If the
change has occurred without previous congestion, the texture may be
somewhat flaccid; but if there has been hyperæmia, the part will be
leathery, non-crepitant, and resisting pressure. If no crepitation can
be detected the part will sink in water from the complete expulsion of
air from the affected lobules. A cut surface is smooth and does not
present the granular appearance of a hepatized lung, nor can
exudation-matter be pressed or scraped from it.

The collapsed lobules may be made to swell up and resume their normal
appearance and rosy color by forcing air with a blowpipe into the
bronchus leading to them. This is so generally true, at least, that it
has been regarded as a certain test by which to discriminate between
atelectasis and pneumonic consolidation when there may be a doubt at a
post-mortem examination as to which condition exists. In general, the
attempt to inflate will succeed when the air is directed into a
collapsed lobule; but the test is of less value than it was once held
to be because it has been shown, on the one hand, that lobules {254}
which have been collapsed for some time will not always expand under
the inflating force, and, on the other, that in recent catarrhal
pneumonia the alveoli may for a time still be inflated with air.

Meigs and Pepper, while stating that in general the results of the
attempt to produce inflation are altogether different in the two
conditions, yet hold, in accordance with Gairdner's teaching, that
"partially pneumonic lung may be inflated when the affection is recent
and combined, as it frequently is, with bronchitic collapse; while in
the latter lesion--_i.e._ collapse of lobules--in its purest forms
complete inflation is often very difficult or impossible after the
collapsed state has been of some duration."[3]

[Footnote 3: _Diseases of Children_, p. 143, 4th ed.]

Nevertheless, the test is of value when applied along with others; for,
as stated by J. Lewis Smith, "the inflated pneumonic lung is more solid
and resisting when pressed between the thumb and fingers than is the
collapsed lung."[4]

[Footnote 4: _Diseases of Children_, p. 570, 5th ed.]

The chief differences between the two conditions are--1st, the color,
which in collapsed lobules is purplish or livid, and in pneumonia
reddish-brown; 2d, the microscopic appearance, showing the alveoli
filled with cell-proliferation in pneumonia and free from change in
collapse; and 3d, the state of the adjacent pleura, which is inflamed
and often covered with lymph in pneumonia, while it is entirely healthy
in non-complicated collapse.

The bronchial tubes present the appearances met with in bronchitis,
being more or less congested, showing a softened state of their lining
membrane, and containing liquid mucous secretion and sometimes firmer
pledgets which have caused the obstruction.

As regards changes in the heart, extensive atelectasis may prevent
closure both of the foramen ovale and of the ductus arteriosus. From
the obstruction to the flow of venous blood offered by the collapsed
portions of the lungs the right ventricle may become so distended that
a portion of its blood may still be forced through the ductus
arteriosus, and another portion backward into the auricle and through
the foramen ovale, so that both of these channels may be kept pervious.

DIAGNOSIS.--Congenital atelectasis, if complete, cannot be mistaken for
any other condition occurring at birth, and is sufficiently denoted by
the signs already described.

Imperfect expansion of the lungs continuing for some days after birth
might suggest patency of the foramen ovale from the purplish hue of the
surface common to both conditions. The expansion of the chest and the
resonance that it yields on percussion in the cardiac affection will be
sufficient to discriminate them except in those cases in which they
exist together.

Acquired atelectasis or collapse of the lung may require to be
distinguished from bronchitis, from pleural effusion, and from
catarrhal pneumonia.

Even uncomplicated bronchitis is in children sometimes accompanied with
so much dyspnoea as to cause apprehension that collapse of lobules has
taken place, but the absence of percussion dulness, either diffused or
in patches, will exclude the supposition.

From pleural effusion collapse of the lung may be distinguished by the
fact that the dulness due to pleurisy is generally on one side only,
that it is more intense and diffused than that of collapse, and that
its line of demarcation may often be made to shift with the position of
the patient.

Catarrhal pneumonia is in general distinguishable from collapse by the
history, course, and symptoms of the disease, especially the sudden
rise of temperature that belongs to pneumonia; as also by the
auscultatory signs. The percussion dulness of pneumonia is more
extensive than that of collapse, and is accompanied with bronchial
breathing; whereas in collapse the respiratory sounds are feeble and
mingled with moist râles.

{255} PROGNOSIS.--In congenital atelectasis, if there be no expansion
of the lungs within the first few minutes after birth, the prognosis is
generally bad. In some apparently hopeless cases, however, the
persistent employment of means tending to arouse the respiratory
function, and especially of those acting through a reflex influence, is
crowned with success. The prognosis varies according to the amount of
unexpanded lung; for even when some respiratory efforts have been made,
if the air enter only a limited extent of the lungs, the infant will
drag on a feeble existence for perhaps a few days, and then perish from
apnoea and exhaustion. When the lungs are once fully inflated the
danger from congenital atelectasis is past.

In acquired collapse of the lung the prognosis is dependent both upon
the number of lobules involved and upon the amount of strength
possessed by the patient. A larger amount of disease may be recovered
from if the nutrition and nervous system be not much depressed, while a
smaller amount may prove fatal in less favorable conditions of the
general system. Much also depends upon the extent and duration of the
coexisting bronchitis, and the degree to which it has affected the
constitutional powers.

TREATMENT.--In the treatment of congenital atelectasis the main
endeavor must be directed to arousing the respiratory function; and
this is best accomplished by means acting reflexively through the
centres of respiration. Sprinkling the chest and back with cold water,
the application of cold water to the spine by a sponge or by affusion,
or the alternate use of cold and hot water in the same way, will often
induce a deep inspiration by which the lungs will be unfolded and
respiration perfectly established. If this be not fully accomplished,
it is of the utmost importance that the child should be carefully
watched as long as the atelectasis continues in any degree, and that
the same means should be again resorted to when the failure of
respiration is threatened. The temperature of the surface should be
maintained by artificial heat and woollen wrappings, as a depression
below the normal standard easily takes place, and serves to lower all
the vital processes and increase the difficulty of keeping up
respiration.

In acquired atelectasis treatment must to a great degree be directed to
the superinducing bronchial catarrh. Counter-irritation of the chest
may be practised with Stokes's liniment, which consists of equal parts
of oil of turpentine, acetic acid, and camphor liniment, or with
mustard poultices prepared with special reference to the sensitiveness
of a child's skin by mixing the mustard with a double portion of flour
or Indian-corn meal. With the same view, dry cups may sometimes be
advantageously used.

Expectorants are serviceable by relieving the bronchitis, the best
being the syrup or wine of ipecacuanha in the dose of 5 to 10 drops, or
the muriate of ammonia in the dose of 1 to 3 grains in simple syrup or
syrup of liquorice, every two or three hours.[5] These agents may
modify the inflammatory state of the bronchial mucous membrane, and
thus prevent the extension of the collapse. If bronchial secretion be
profuse, the question of the use of emetics becomes very important.
When employed judiciously with reference to the real needs of the case,
they may be eminently beneficial, acting partly by removing the
accumulation in the bronchi which may have occasioned the {256}
collapse and may favor its further extension, and partly perhaps by the
deep inspiration which precedes emesis serving to expand the collapsed
lobules. It must be remembered, however, that there is always a
tendency to failure of the vital powers in acquired atelectasis, and
that this may be dangerously increased by emetics of a depressing
character. The best for the purpose are alum, sulphate of zinc, and
ipecacuanha. The repetition of the emetic must be determined by its
effect on the breathing and on the patient's strength.

[Footnote 5: One of the following formula may be used:

      Rx. Syr. ipecac.          drachm i-ij;
          Syr. prun. virginian. drachm vj;
          Ammon. muriat.        drachm ss;
          Aquæ,                 ounce j.  M.
Dose, teaspoonful for a child of three to six months.

Or,

      Rx. Ammon. muriat.        drachm ss-drachm j;
          Syr. glycyrrhiz.
          Aquæ,            _aa_ ounce j.  M.
Dose, as above.]

Tonics and supporting measures are always called for in the treatment
of atelectasis, in view of the fact that the condition is essentially
dependent on failure of constitutional strength. Milk, wine-whey, and
animal broths are appropriate articles of food; alcoholic stimulants
are generally required; and in emergencies, if sudden increase of
prostration occur, the carbonate of ammonia in the dose of 1 or 2
grains may be given.

During the whole course of the malady such tonics as quinia or the
compound tincture of cinchona or one of the soluble salts of iron may
be administered.


Brown Induration of the Lungs.

DEFINITION.--Increased density of certain portions of the lungs, which
are of a reddish color, with brown or yellowish-brown spots scattered
throughout the indurated tissue.

SYNONYMS.--Pigment induration; Congestive carnification.

HISTORY.--This affection is a form of passive congestion of the lungs,
in regard to which it is somewhat uncertain whether the morbid process
is simply one of congestion or whether along with this an inflammatory
element is likewise present. It is beyond question, however, that the
changed condition of the lung is primarily and chiefly congestive, and
that it originates from causes which produce congestion.

ETIOLOGY AND MORBID ANATOMY.--The etiology and morbid anatomy of this
affection are so closely related that they are best considered
together. The most important fact both in the etiology and pathology of
brown induration of the lungs is that it is gradually brought about as
the consequence of obstruction to the pulmonary circulation from
disease of the mitral valve, either constrictive or regurgitant in
character. Interference with the return of the blood to the left side
of the heart is in this way produced, with consequent stasis in greater
or less degree within the pulmonary capillaries.

The most marked changes observed in lungs which have undergone this
form of congestion are that they do not collapse when the chest is
opened, and that they are more compact and less elastic and crepitant
than healthy lungs. On section they present a reddish color
interspersed with spots of yellowish- or reddish-brown, which sometimes
are of a very dark hue.

Microscopic examination shows an increased size of the capillaries of
the lung, which seem to encroach upon the air-cells and thus lessen
their capacity. Whether the walls of the alveoli have themselves
undergone thickening is a question about which different opinions have
been entertained. Rokitansky states that "when stasis has continued for
a longer period the walls of the air-cells and the interstitial tissue
become swollen, so that the former may become perfectly impermeable to
air;"[6] and although, in the passage quoted, he is writing of
pulmonary congestion in general, and not of this form in particular,
yet, as he is describing a stasis which has continued for some time,
the observation would seem applicable to the affection under
consideration.

[Footnote 6: _Path. Anat._, vol. iv. p. 59.]

Wilson Fox affirms that he has found alveolar thickening in
considerable tracts in this affection, with a distinct increase of
fibrous tissue in the walls {257} of the alveoli; but this change, he
goes on to say, is not uniformly present, and in some places the
alveoli are found filled with epithelial products like those of
catarrhal pneumonia.

The true explanation of the condition is probably this: that, beginning
as a passive congestion, such as might be expected to result from the
mitral disease with which it is almost constantly associated, the
affection afterward assumes an inflammatory condition of a low type
with epithelial proliferation, and in some cases with thickening of the
alveolar walls and the interlobular connective tissue. Passive
hyperæmia is, however, always the basis of the disease. The brownish
spots visible in a section are caused by the leakage of blood from the
congested capillaries into the alveoli or interstitial tissue without
the occurrence of any large extravasation. The blood thus exuded
undergoes pigmentary change, with the production of hæmatoidin, the
shades of color varying accordingly as the exudation has been recent or
of longer duration.

The failure of the lungs to collapse is due to the encroachment of the
dilated capillaries on the air-cells, and perhaps to the thickening of
the cell-walls and the partial occupation of the cells themselves by
epithelial products.

SYMPTOMS.--The general symptoms and the physical signs of this
affection are of the same character as those that occur in other forms
of pulmonary congestion. Dyspnoea is felt, especially on making
exertion; and this may be attributable in part to the associated
cardiac disease as well as to the condition of the lungs. Loss of
resonance on percussion and feebleness of respiratory murmur are
observable; and when the condensation is great bronchial breathing may
be heard.

DIAGNOSIS.--It is evident that there is nothing in these signs
distinctive of this particular form of congestion, which is, in fact,
not diagnosticable with absolute certainty during life. The probability
of its existence may, however, be inferred if along with the above
symptoms and signs a presystolic or regurgitant mitral murmur is heard,
showing constriction or incompetency of the mitral valve.

PROGNOSIS.--The prognosis of this affection is of course always
unfavorable, because the condition depends upon mechanical disease of
the heart of an incurable nature. Temporary improvement may, however,
sometimes take place under proper treatment.

TREATMENT.--Such treatment must be used as serves to support the
weakened heart and hold in check the tendency to dilatation. With this
view digitalis or convallaria may be employed, with tonics and
alcoholic or ammoniacal stimulants as occasion may require.
Counter-irritation over the lungs may be used and expectorants may be
given. If dyspnoea be urgent, the preparations of ether, such as
Hoffman's anodyne, or the carbonate of ammonia, may be administered.




{258}

CONGESTION AND OEDEMA OF THE LUNGS (HYPOSTATIC PNEUMONIA).

BY SAMUEL C. CHEW, M.D.


Congestion and oedema of the lungs are often found together, but they
are different morbid conditions, and each may occur independently of
the other. It is best, however, to consider them in connection with
each other.

DEFINITION.--By congestion of the lungs is meant an active or passive
hyperæmia of the pulmonary vessels, which are surcharged with blood.

Oedema of the lungs signifies an effusion of fluid consisting mainly of
the serum of the blood into the air-vesicles and, to some extent, into
the pulmonary connective tissue. Congestion is at times the determining
cause of oedema, but the latter condition may arise from causes not
tending to produce the former.

HISTORY AND ETIOLOGY.--As pulmonary congestion and oedema are almost
always secondary and dependent affections, their etiology is an
essential part of their history, so that these subjects will be best
considered together.

Active congestion of the lungs may result from any cause producing an
increased afflux of blood to these organs, such as hypertrophy or
functional over-action of the heart, or the sudden recession of the
blood from the surface and perhaps from other internal organs, such as
may take place under the influence of cold. Violent exercise, rapid
walking up hill, or even mental excitement, may in some impressible
subjects suffice to produce it.

Why vascular congestion should occur in a greater degree and more
readily in the lungs than elsewhere from the effect of cold is
sufficiently evident when it is considered that the pulmonary
capillaries are not supported by surrounding tissue, as those of other
parts are. And for the same reason the direct action upon them of cold
air or of certain irritant gases, such as ammonia or chlorine, may
suffice to cause an undue afflux of blood to them.

How far a neurotic influence exercised reflexively through the
vaso-motor system may serve to produce active congestion has not yet
been fully determined; but it is probable that the sudden pulmonary
congestions which have been known to follow the drinking of a large
quantity of cold water when the body is heated may be attributed to
such an action.

Passive congestion may be occasioned by a retardation of the blood-flow
from the lungs; as, for example, by a hindrance to its onward passage
through the left chambers of the heart in consequence of obstructive
valvular disease, especially a great degree of mitral or aortic
stenosis. So also mitral or aortic incompetency, by allowing the blood
to be crowded backward in the pulmonary veins, may interfere with its
passage through the lungs, and in this way set up passive hyperæmia.

By some writers mere weakness of the heart is spoken of as a cause of
{259} passive congestion of the lungs; but it can hardly be regarded as
such apart from influences affecting the blood itself or the tonicity
of the pulmonary vessels; for it is to be considered that while
weakness of the left chambers of the heart might impede the onward
course of the blood received from the lungs, yet at the same time the
right chambers, if weakened in a corresponding degree, would send less
blood into those organs, and then the conditions of passive hyperæmia
would not exist. It is well known, moreover, that cardiac weakness
coming on suddenly as in syncope, or gradually as in various asthenic
diseases, may be present without the occurrence of any signs of
pulmonary congestion. Yet it is not impossible that there may be a
disturbance of the balance between the actions of the right and left
sides of the heart, and that thus passive congestion of the lungs may
result from a relatively greater weakness on the left than on the right
side of the heart, so that the left auricle and the pulmonary veins may
be obstructed, and backward pressure produced while the right ventricle
is still sending blood into the lungs.

It is probable, however, that, in addition to the propulsive power
exercised on the blood by the contraction of the heart, another agency
affecting its passage through the lungs is the interchange of gases in
respiration; and therefore any interference with the reception of
oxygen and the elimination of carbonic dioxide may tend to retard the
blood-flow, and thus favor stasis or passive congestion. In this way
the inhalation of impure air, especially air containing an undue amount
of carbonic dioxide, may occasion passive hyperæmia.

Pulmonary oedema is never a primary affection, but is always due to
some preceding disease. In the first place, it may, as already stated,
take its origin directly from congestion of the lungs, the walls of the
obstructed vessels allowing the transudation of serum, which will
collect in the air-cells and connective tissue and also in the mucous
membrane of the terminal bronchi. In an early stage it may be present
in the walls only of the alveoli without being effused into their
cavities.

Another cause of pulmonary oedema is obstruction of the circulation of
a part of a lung, such as may take place in pneumonia or miliary
tuberculosis, the vessels of other parts becoming distended by backward
pressure, so that the serum of the blood will exude into the air-cells
or interstitial tissue. When this occurs in pneumonia it may be a most
alarming and dangerous complication.

Still another and very frequent cause of pulmonary oedema is Bright's
disease in its different forms, in which the oedema occurs as a part of
the general dropsy incident to these affections. In acute congestive
nephritis it may come on very rapidly, constituting acute pulmonary
oedema. Hertz remarks that an acute oedema may take place in the course
of an acute nephritis, as has been reported by Lebert, but that such an
occurrence is not frequent.[1] The writer of this article has himself
seen several cases of acute pulmonary oedema occurring as a part of the
dropsy of scarlet fever.

[Footnote 1: _Ziemssen's Cyclop._, v. p. 279.]

More frequently it is met with in chronic albuminuria, and varies in
amount from time to time, as dropsical effusions elsewhere do in this
condition.

Attacks of asthmatic dyspnoea are not uncommon in the course of
Bright's disease, especially in cases of chronic contracted kidney.
They are described as uræmic asthma, and are referred by some writers
to the action of the depraved blood on the centres of respiration. This
explanation may be correct in some cases, but it seems likely that they
are due in part to dropsical oedema of the bronchial mucous membrane,
the connective tissue, or the air-cells. A weakened condition of the
heart, such as is apt to occur {260} in advanced periods of Bright's
disease, has probably some share in determining the oedema.

In any case of oedema, according to its situation, whether it is in the
connective tissue, the bronchial mucous membrane, or the air-cells, and
according also to the amount in which it is effused, it will interfere
more or less with breathing. If there be interstitial infiltration with
swelling of the bronchial mucous membrane, lessening the calibre of the
tubes, there may be merely some embarrassment of respiration; but if
the effusion invade any considerable number of the air-cells, urgent
dyspnoea will be produced. Oedema is generally most abundant at the
lower part of the lungs, and is not uncommonly associated with pleural
effusion, the two conditions being due to the same cause; and then the
interference with respiration is greater and more perilous.

SYMPTOMS.--It is possible that a slight degree of pulmonary congestion
may exist when the circulation is hurried without the occurrence of any
other symptoms except moderate acceleration of the breathing. Under
such circumstances, however, the existence of congestion cannot be
proved. When it is brought about in greater degree, either by
over-action of the heart or sudden recession of blood from other parts,
the earliest and most prominent symptoms are a sense of oppression in
the chest and quickened, laborious respiration, which may rapidly
increase until the dyspnoea becomes most urgent and distressing. The
heart's action grows more hurried, the pulsations in the carotid and
temporal arteries are strongly felt, and the face is deeply flushed.
Cough is always present, at first dry in character and afterward
accompanied with expectoration of frothy mucus, which may be tinged
with blood or may be even mingled with a considerable amount of
bright-red blood.

The different appearances of the expectoration are probably due to the
fact that in some cases the distended pulmonary capillaries allow the
transudation of blood-corpuscles, and in others they are actually
ruptured by the strain, so that pure blood escapes from them.

If the congestion is due to weakened action of the heart, with remora
of the venous circulation, and is passive in character, the symptoms
may be less acutely developed and less urgent than they are in the
active form; indeed, in some cases in which very considerable portions
of the lung are involved there may be no excessive dyspnoea while the
patient is quiet, in consequence of the organism having become
gradually accustomed to the imperfect respiration.

As the congestion increases, however, and the lungs become more
affected, the signs of malaëration are more conspicuous. Dyspnoea is
more oppressive, the face and surface generally, especially the lips
and extremities, become cyanotic and cold, and the patient perishes
from apnoea and from coma occasioned by oedema of the brain or medulla
or stasis of blood in the cerebral veins, the respiratory centres being
paralyzed. With the occurrence of somnolence the efforts to free the
air-passages from fluid by coughing and expectoration grow less and
less as the sensibility is obtunded.

When the congestion is not very extensive the amount of air in the
lungs is not lessened sufficiently to materially affect the percussion
note, which may remain resonant, though it may have a somewhat
tympanitic quality. The vesicular murmur is still heard, but it is
rather rough in character. When the general symptoms indicate a graver
degree of congestion there will be corresponding changes in the
physical signs; resonance will be lessened, or even replaced by
dulness, in consequence of the filling of the alveoli with serum or
blood; and the respiratory murmur will be completely masked by coarse
and fine mucous râles. If the dulness is very marked, bronchial
breathing and bronchophony may be observed. Elsewhere in parts not
{261} involved in the congestion exaggerated or puerile breathing may
be heard from the supplementary action that takes place there.

The physical signs may vary as to their situation with the patient's
position as the blood in the congested vessels and the serum in the
alveoli and connective tissue gravitate from side to side. But when the
change described as hypostatic pneumonia has taken place, and the
affected portion of the lung has become condensed in texture, position
has little or no influence on the physical signs, which will still
remain even when the affected side is kept uppermost.

When oedema of the lungs is produced by serous effusion invading the
air-cells, there is some degree of dulness on percussion, especially at
the lower part of the chest. Respiratory murmur is feeble or
suppressed, and fine moist râles are heard, with an intermixture at
times of the true crepitant râle. These signs are generally heard on
both sides, but when an area of oedema is due to pneumonia the signs
may be present only on the affected side.

COURSE AND TERMINATIONS.--Acute congestion of the lungs depending on
over-action of the heart or a sudden recession of blood may cause death
in a short time, or may disappear, either spontaneously or under
appropriate treatment, almost as suddenly as it has come on. The
abatement of the symptoms is generally attended with profuse serous
expectoration, and sometimes with hemorrhage, by which the congested
vessels are relieved, so that they return to their natural state.

When acute oedema of the lungs is due to Bright's disease in the acute
or one of the chronic forms, it is often quickly fatal, though if
properly treated it may disappear. When a consequence of chronic renal
disease it is apt sooner or later to return. Chronic passive hyperæmia
and chronic oedema of the lungs admit of only temporary relief, because
they are occasioned by such diseases of the heart or kidneys as are
themselves generally incurable; and they are very sure to recur, even
though they may be relieved for a time. It is not uncommon in cases of
this sort to see the symptoms of chronic oedema suddenly aggravated by
the occurrence of an acute attack, which is the immediate cause of
death.

PATHOLOGY AND MORBID ANATOMY.--The pathological appearance of a
congested lung varies according to the form of the congestion and the
manner in which it has been occasioned. Acute congestion may occur very
suddenly from some of the causes that have been mentioned, and may
disappear with equal rapidity, leaving no traces behind. But sometimes,
from the extent of the congestion, respiration is interrupted to such a
degree that life is quickly destroyed. In such cases the affected
portion of the lung is of a dark color from being engorged with blood,
which flows from it if an incision is made. The part is heavier and
crepitates less than normal lung-tissue. The bronchial mucous membrane
is apt to be hyperæmic, as might be expected from the communication
that exists between the pulmonary and bronchial vessels, and the tubes
themselves are filled with mucus and sometimes with frothy and bloody
serum.

Where the tonicity of the pulmonary vessels has been impaired by
sickness, age, or other debilitating influences, passive congestion of
the lungs is very likely to ensue if the heart become weakened; and as
the effect of gravity will aid in determining the stasis of the blood,
the resulting congestion is in life most marked in the lower and
posterior regions of the lungs, where the changes are chiefly found
after death. As gravity may thus determine the congestion to one part
of the lungs, so a change in the patient's position may cause it to
disappear from where it was first manifest and to appear in another
part which has become most dependent. The condition thus brought about
is known as hypostatic congestion. One of the consequences of passive
{262} hyperæmia thus induced is a transudation of the serum of the
blood into the air-cells and connective tissue of the lungs; and this
is one way in which pulmonary oedema may be occasioned. When hypostatic
congestion has lasted for some time, it may no longer be affected by
changing the patient's position; and when this is the case it may be
accompanied by exudation of fibrin into the air-cells and by
proliferation of epithelium, thus producing the condition termed
hypostatic pneumonia.

All three of these states may be present in one lung at the same time,
one portion being passively congested, another oedematous, while the
most dependent part may be the seat of hypostatic pneumonia.

The congested parts of the lungs are very dark in color, in some cases
almost black; blood flows freely from a section through them, and serum
exudes from the alveoli and interstitial tissue when oedema exists. If
the altered condition of the lung has lasted for some time, the texture
of the affected part may be so firm as to resemble that of the spleen;
whence this change is sometimes termed splenization. In this condition
dark-red points consisting of extravasated blood may be seen scattered
about. If the state already described as hypostatic pneumonia exists,
the affected part is still more firm and dense in texture, and presents
a granular appearance on section from the exudation of fibrin which has
probably taken place, so that it resembles a portion of a lung that has
been the seat of an inflammatory process from the first.

DIAGNOSIS.--The diagnosis of pulmonary congestion in its different
forms, and of pulmonary oedema, is in general not difficult if the
symptoms of the causative diseases are carefully observed. Acute
pulmonary congestion coming on suddenly, and not preceded by any other
affection, needs to be distinguished from the early congestive stage of
pneumonia, which it somewhat resembles from the slightly impaired
resonance on percussion and the dyspnoea that may occur in both
diseases. The chief points of distinction between the two affections
are the absence in congestion of initial chill, of pain in the side,
and of rise of temperature; all of which are in general present in
pneumonia. As the case advances the divergence between the two
affections will be wider.

The diagnosis of acute oedema and of chronic congestion and oedema is
based upon the physical signs belonging to them, taken in connection
with the symptoms of cardiac and renal disease with which they are
associated.

Capillary bronchitis bears some resemblance to pulmonary oedema, since
in both affections there are moist subcrepitant râles; but in capillary
bronchitis there is no such loss of percussion resonance as occurs in
pulmonary oedema, and, moreover, fever is not present in oedema, as it
is in the inflammatory affection. The character of the expectoration is
also different in the two diseases, being thicker and more tenacious in
bronchitis and serous or watery in oedema. From hydrothorax, oedema is
distinguishable by the shifting line of dulness and by the absence of
râles in hydrothorax.

PROGNOSIS.--Acute congestion of the lungs is always a serious
affection, and, as already stated, terminates fatally in some cases in
a short time. In the majority of instances, however, it disappears
spontaneously or under suitable treatment, and the lungs are in general
restored to their integrity. It may result in pulmonary hemorrhage,
from which recovery may take place, or which may give rise to
hemorrhagic infarction, the blood being drawn into the alveoli.

Passive congestion being a secondary affection, its prognosis depends
upon the diseases which occasion it.

In pulmonary oedema the prognosis is always very grave. When occurring
suddenly as a consequence of acute congestive nephritis, it may wholly
{263} disappear under proper treatment, and if the kidney affection is
likewise cured there will be no further return of the pulmonary
complication. When it comes on in the course of chronic renal disease,
it may disappear and recur from time to time, but it is apparently not
often the direct cause of death by itself. Sometimes, however, it is
associated with cerebral oedema and other conditions which together
occasion a fatal termination. When due to pneumonia, oedema adds very
much to the gravity of the affection, and may be the immediate cause of
death.

TREATMENT.--The treatment of acute pulmonary congestion consists in the
use of means to check the undue flow of blood into the engorged lungs.
Of these the best, if the patient be seen promptly and the strength of
the pulse admit of it, is general bloodletting, by which the mass of
the blood is lessened and the action of the heart and pressure within
the blood-vessels are lowered, so that both the amount of blood in the
hyperæmic vessels and the force with which it reaches them will be
diminished.

This measure may be also useful in the way of preventing or checking
acute pulmonary oedema by lessening the blood-pressure. Should
venesection be thought inadmissible, cups may be applied to the chest
in front or behind, and at the same time the volume of the blood may be
temporarily lessened by placing ligatures around the thighs, so as to
check the flow of blood in the veins near the surface. Revulsion from
the congested vessels of the lungs may also be effected by mustard
foot-baths or the application of mustard poultices to the chest.
Aconite may be serviceable by controlling over-action of the heart, and
may be given in the dose of 1 or 2 drops of the tincture of the root at
intervals of half an hour until some effect on the circulation is
produced.

It is of importance to remove any blood or serum that may be present in
the air-cells and smaller bronchi; and for this purpose one of the
quickly-acting and non-depressing emetics may be given, such as
apomorphia hypodermically or the sulphate of zinc or turpeth mineral by
the mouth. Respect must be had to the condition of the patient's
strength in ordering an emetic, since if there be much prostration, or
if the interference with respiration has seriously depressed the heart,
more harm than good might result from its use. Expectorants may
somewhat later supplement the action of emetics, or serve to keep up
the good effects gotten from them by helping to remove the residual
fluids from the air-passages. Among the best of these are the syrup of
senega and the carbonate or hydrochlorate of ammonium.

Passive congestion of the lungs, being dependent upon a weakened
condition of the circulation, requires the use of means to sustain and
reinforce the heart's action. The alcoholic and ammoniacal stimulants
are here of great importance, and digitalis may be of sovereign
efficacy, especially in cases where the congestion is associated with
dilatation and attenuation of the heart. The power possessed by this
drug of increasing arterial pressure, and thus producing diuretic
action, may render it further serviceable when the congestion is
accompanied with oedema, as in this way the serous infiltration may be
absorbed and removed. From 10 to 20 drops of the tincture or from 2 to
4 drachms of the infusion of digitalis may be given every two hours
until some effect on the pulse or the kidneys is noticed. If the
stomach should not bear digitalis well in either of these forms, as is
the case with some patients, the alkaloid digitalin in the dose of 1/60
grain may be given. The convallaria recently introduced as synergistic
with digitalis may be substituted for it, and in the dose of from 20
minims to 1 drachm of the fluid extract it will be found not uncommonly
to be an efficient heart-tonic. Like digitalis, too, it possesses
diuretic power from the increased arterial pressure that it occasions.

Passive pulmonary congestion may assume a chronic form in connection
with chronic cardiac and renal disease, and without presenting urgent
{264} symptoms may cause almost constant embarrassment of respiration
in greater or less degree. Under such circumstances the preparations of
iron are helpful by enriching the blood and increasing the tone of the
heart. One of the best preparations is the mixture of acetate of iron
and ammonium,[2] known as Basham's mixture, which combines diuretic
with chalybeate action. This may be given in the dose of from 1 to 4
drachms.

[Footnote 2: _U. S. Pharm._, 1882.]

It is of great importance in all cases of passive congestion and of
hypostatic pneumonia to change the patient's position from time to
time, so as to counteract the influence of gravity and relieve
dependent portions of the lungs.

Pulmonary oedema occurring in an acute form in the course of either
congestive nephritis or chronic renal disease may seriously imperil
life, and therefore it demands prompt and bold treatment. When it
results from acute nephritis, it is more immediately dangerous than
when dependent on chronic disease of the kidneys; yet in this acute
form it may admit of perfect cure if proper remedial measures be at
once instituted. Cups may be applied to the loins with the view of
relieving the engorged kidneys and enabling them to resume their work
of removing fluid from the body. In cases where the strength of the
pulse is sufficient, it may even be good practice to abstract blood by
the lancet to the amount of six to eight ounces. According to
Oppolzer,[3] this treatment may be proper even when somnolence
indicates oedema of the brain, provided there be no irregularity of
respiration or intermission in the pulse--signs which contraindicate
bloodletting.

[Footnote 3: _Ziemssen's Cyclop._, v. p. 285.]

Active diaphoretics are among the best medicinal agents to be employed,
their good effects being due to their derivative action and to the
large discharge of fluid from the skin which they occasion, thus
promoting the removal of what is effused in the lungs. The fluid
extract of jaborandi in the dose of from 20 minims to a drachm, or the
hypodermic injection of 1/8 to 1/6 grain of nitrate or muriate of
pilocarpine, frequently causes prompt and profuse perspiration. The
writer is confident that he has seen life saved by the use of this drug
when it has been in urgent peril from pulmonary oedema. In the absence
of this agent, or along with it, the hot-air bath, which can almost
always be extemporized in an efficient form, may serve to promote or
increase fluid discharge from the skin. If the patient's strength is
sufficient, one of the hydragogue cathartics may be given, and among
them the most prompt and active is elaterium in the dose of 1/12 to 1/8
grain every four hours. The action of this drug must be carefully
watched and its depressing tendency guarded against by the use of
alcoholic stimulants.

When pulmonary oedema results from weakness of the heart, as in
dilatation of that organ, or from chronic renal disease, all lowering
measures must be avoided. Bloodletting, whether general or local, would
still further depress the heart, and by increasing the hyperæmia of
chronic Bright's disease would favor the further effusion of serum into
the lungs. Dry cupping over the chest before and behind may be
serviceable as a revulsive measure. Stimulants and tonics are called
for, and digitalis or convallaria is directly indicated from the
special power possessed by these agents of improving the cardiac tone
and promoting the action of the kidneys by increasing blood-pressure.
Digitalis has been thought objectionable when there is much
irregularity of respiration, and perhaps it would be safest to postpone
its administration until this symptom is relieved by the use of
alcohol, ammonia, musk, or other prompt diffusible stimulants.

The writer has had repeated opportunities for observing the value of
quinia given hypodermically in checking effusion of serum into the
air-passages, and he would strongly recommend its use in the treatment
of pulmonary oedema in the form of the hypodermic injection of the
solution of hydrobromate of {265} quinia of the strength of 4 grains to
20 minims. Of this solution 10 to 20 minims may be injected at once. If
such a solution cannot be obtained, a full dose of 10 to 15 grains of
the sulphate of quinia may be given by the mouth.

As in the case of passive congestion of the lungs, so in oedema,
advantage may be gained by changing the patient's position from time to
time, so as to prevent the constant gravitation of fluid to the same
portion of the affected organs.




{266}

HÆMOPTYSIS.

BY WILLIAM CARSON, M.D.


The word means, literally, spitting of blood, from two words, [Greek:
haima], blood, and [Greek: ptyô], I spit.

SYNONYMS.--If we go back far in the history of medicine, we find many
synonyms, such as Hæmoptoe, Emptoe, Emptoica passio, Pneumorrhagia,
Hæmorrhagia pulmonis, Crachement de sang, etc., etc.

DEFINITION.--Bronchial hæmoptysis is the spitting or expectoration of
blood which has been effused into the bronchi or bronchioles from the
bronchial vessels. Pulmonary hæmoptysis is the spitting or
expectoration of blood which has been effused into the air-cells, the
inter-alveolar and interlobular tissues. This distinction is not always
practicable in diagnosis or practice. It may, however, serve for a
grouping of some well-known clinical forms of hæmoptysis.

It is not possible to give indications by which the origin of blood in
the lungs may be positively determined except by a reference to other
symptoms than the hæmoptysis. In general, bronchial hemorrhage is
characterized by a bright-red, fresh color, is aërated, unmixed, and
uncoagulated. In pulmonary or parenchymatous hæmoptysis the blood is
dark, non-aërated, and coagulated to some degree, and often alternates
with a mixed blood and mucus sputum. These distinctions are not
reliable, and must be supplemented by all of our clinical resources in
the case before us. The author maintains that in the hæmoptysis of
phthisis the hemorrhage in the large majority of cases is both
bronchial and pulmonary. The typical parenchymatous hemorrhage is found
in hemorrhagic infarction and pulmonary apoplexy, which, compared with
phthisis, are rare occasions for hæmoptysis. This general statement
will form the basis of what follows in this exposition.

HISTORY.--Historically, there are not many phases in the doctrine of
hæmoptysis. Controversy has been chiefly confined to its relations to
phthisis as cause or effect.

The simplicity and directness of observation of the ancients give a
special interest to their views of hæmoptysis. They believed that it
was oftener cause than effect. They found a warranty of that opinion in
what they thought was a direct conversion of blood into pus, and in the
irritating qualities of the latter. Hippocrates'[1] fundamental
statements are, "Ex sanguinis sputo, puris sputum malum;" "Ex sanguinis
vomitione tabes et puris purgatio per superiora purgatio;" "Ex
sanguinis sputo puris sputum et fluor, ubi autem sputum retinetur
moriuntur." Another statement of his is given in translation by
Peter:[2] "When some of the veins of the lung are ruptured the
hemorrhage is in proportion to the size of the vessel; a part, on the
contrary, unless the vein be very small, diffuses itself in the lung,
putrefies {267} there, and after having putrefied forms pus. As a
result, it is at one time true pus, at another pus mixed with blood,
and another time it is pure blood, which is rejected; and if the vein
was very full it is from it that the mass of the blood comes, and thick
pus, mixed with putrefied pituitous secretion, is expectorated."

[Footnote 1: Edition 1696, book 7, p. 1141, Aphorisms 15 and 16, 80 and
81.]

[Footnote 2: _Clinique médicale_, tome 112, p. 243. The precise
locality of this quotation is not given by Peter, but it is from
Hippocrates' _Opera_, ed. Kuhn, Leipsic, 1825, vol. ii. p. 178.]

Thomas Young[3] gives the following sentences from Hippocrates'
_Predictions and Aphorisms_: "The most dangerous consumptives are cured
by a rupture of the great vessel which corrodes the lungs;" "Purulent
expectoration after hæmoptysis is dangerous;" "In some cases
consumption originates from an effusion of blood into the lungs without
hæmoptysis, especially after a strain or accidental injury; a
collection of phlegmatic humors form around it by causing pain and
cough, with purulent and bloody expectoration." All of these quotations
show the Hippocratic doctrine distinctly, that the hæmoptysis where it
appeared in a case was mostly the cause of the subsequent phthisis, and
that phthisis ab hæmoptoe was not only one of the most common, but one
of the most dangerous forms.

[Footnote 3: _A Practical Historical Treatise on Consumption Diseases_,
London, 1815, p. 111.]

The doctrine that blood effused into the lungs became pus, and produced
corroding and ulcerating effects, appears in many other prominent
authors between the Hippocratic writings and the nineteenth century.
Celsus[4] (30-40 A.C.) says: "Hæmoptysis is one of the causes of
purulent expectoration." Galen[5] (131-201 A.C.) says: "Phthisis is
lung ulceration;" and he thinks "that in the greatest number of cases
it originates in a mechanical way, through tearing of the tissue by
means of an outpouring of blood in consequence of a catarrh or strain."
This extract would imply that he thought the hæmoptysis in many cases
secondary, but that when it did occur it had the effect which
Hippocrates attributed to it, that of producing "purulence of the
lungs." Sylvius[6] (1614-1672) says: "Hæmoptysis is one of the causes
of purulent expectoration."

[Footnote 4: Young, _op. cit._, p. 128.]

[Footnote 5: Waldenburg, _Die Tuberculose_, p. 19.]

[Footnote 6: Waldenburg, _op. cit._, p. 28.]

Morton's[7] (1689) language partly is: "Decantatum istud medicorum
adagium, quod pus sequitur sanguinem;" and then, translated, he says:
"It (the adage) appears to have originated in the fact that 'purulence'
of the lungs, or phthisis pulmonalis, usually follows hæmoptysis more
quickly and oftener than any other disease." In the sentence
immediately following he suggests this result may be due to a
putrefaction of clots that the hæmoptysis has left behind in the lungs,
or to a copious effusion of humors from the whole body to the tender
lungs, or to an erosion of some vessel.

[Footnote 7: _Phthisiological Ed._, 1727, lib. 111, chap. v. p. 95.]

Another theory appears in Hoffmann's language,[8] and was probably
suggested, directly or indirectly, by Sylvius's description of
tubercles: "The blood is easily extravasated into the pulmonary
vesicles, stagnates there and putrefies, corrodes the neighboring
parts, and finally destroys the air-passages or they are converted into
nodes or tubercles." The blood becomes tubercularized, and the phthisis
ab hæmoptoe is established. This idea is found at different periods,
and we find a recent French author arguing against this hypothesis.

[Footnote 8: Peter, _loc. cit._, p. 244; Young, p. 211, _Opera_;
Hoffmann, _Physico-medica_, Geneva, 1740.]

The reversal of these ideas is generally acknowledged as the results of
Laennec's energy and genius, yet similar opinions to his had been
expressed by French and English physicians. Bayle does not place
phthisis ab hæmoptoe in his classification. Desault,[9] one of
Laennec's countrymen, near a hundred years before him, "insists that
tubercles constitute the essence of consumption, being generally
anterior to hæmoptysis." Mudge[10] says that hæmoptysis is often the
consequence of the obstruction produced by tubercles. A {268}
preparation for the positive opinions of Laennec is discernible in
these and other authors. His views on this particular topic were
opposed by Andral. The latter modified his earliest expressions to some
extent.

[Footnote 9: Young, p. 220, _Desault sur les Maladies venériennes, la
Rage et la Phthisic_, Bordeaux, 1733.]

[Footnote 10: Young, _loc. cit._, _Radical Cure for a Recent Catarrhic
Cough_, London, 1779, 2d ed.]

The next important historical epoch in the causative relations of
hæmoptysis and phthisis is in the energetic protests of Niemeyer. They
were in some respects a return to the Hippocratic doctrine, in that he
asserted the predominance of hæmoptysis as cause; but he gave the
doctrine a basis better adjusted to a better pathology, in that he made
the important element of inflammatory lesions the medium between the
effusion of blood and the final purulence or ulceration (ulcus
pulmonum) of the ancients. He energetically advocated the doctrine of
the positive effect of effusion of blood in the bronchi or pulmonary
substance in producing disorganization of the lungs, without reference
to any hereditary or predisposing element or existence of tubercles.

Jaccoud[11] calls attention to the fact that Graves had anticipated
Niemeyer in the partial revival of the Hippocratic doctrine and the
teachings of Morton and Hoffmann on phthisis ab hæmoptoe.

[Footnote 11: _Clinique médicale_, vol. ii. p. 302, Graves.]

In a recent work[12] there is a general adhesion to the modern
modifications of the Hippocratic doctrine in regard to the pathogenetic
relations of hæmoptysis and phthisis. There is a decided rejection of
the causative influence of tubercle in producing hæmoptysis.[13] "The
connection between pulmonary hemorrhage and tubercle stands on no
pathological proof;" "From all the evidence I have been able to obtain
on this point, tubercle seems to have been very unjustly credited with
hemorrhage."[14] He differs from others in attributing much more to the
hæmophilic constitution in the production of hæmoptysis. Other phases
of the history of hæmoptysis might be given. We shall allude to two
only: one is the classification of the varieties. Alexander of Tralles
treats of hæmoptysis under three heads: 1, Hæmoptysis by rupture; 2, by
erosion; 3, by dilatation. Bricheteau[15] makes four divisions: 1,
constitutional; 2, accidental; 3, succedaneous; 4, critical and
symptomatic. These two classifications show in themselves their origin,
in that the one is representative of a local, and the other of a
constitutional, pathogenesis.

[Footnote 12: _On Pulmonary Hemorrhage_, Reginald E. Thompson, London,
1879.]

[Footnote 13: Page 32, _op. cit._]

[Footnote 14: Page 33, _op. cit._]

[Footnote 15: _Maladies chroniques de l'Appareil respiratoire_, Paris,
1851, p. 523.]

The last historical phase is the therapeutic one. We find in the
practice of the present day survivals from the ancient authors. Morton
recommended ligatures around the limbs to arrest hemorrhage, and bark
to prevent hæmoptysis from becoming phthisis.[16] Venesection, which to
some extent is a modern remedy, was frequently practised by the older
physicians. Erasistratus[17] recommended ligatures, applied to the
limbs in several places, to prevent the return of the blood to the
lungs; Asclepiades thought this practice founded on an erroneous
theory, but experience is in its favor. The head should be kept high,
the face wetted with water, the room cool, and the patient perfectly at
rest. Lietaud (1765) is cautious of employing astringents or
purgatives, but recommended ligatures to the limbs and cold to the
scrotum. A drachm of rhubarb was given by Fernelius in hæmoptysis.
Bryan Robinson[18] (1752) relates a case in which an emetic of
ipecacuanha, taken three times a week, kept off hæmoptysis for eight
years, while tar-water constantly brought it on. Marryat (1758, London)
"advises two grains of tartarized antimony, and as much of the sulphate
of copper, in half a spoonful of water." Ipecacuanha was frequently
employed in hæmoptysis by the practitioners of the centuries preceding
the nineteenth.

[Footnote 16: Young, pp. 201, 202.]

[Footnote 17: _Op. cit._, p. 128.]

[Footnote 18: _Op. cit._, p. 156, ed. 1660.]

As an important preface to the subjects considered in this article we
introduce an account of the vascular supply of the lungs.

{269} Before entering into a statement of the distribution of the
minute vessels to the lungs it is desirable, in view of the possible
diseased connections between the larger bronchial and vascular trunks,
to recall some points of the topographical anatomy of the latter. "The
root of the left lung passes below the arch of the aorta and in front
of the descending aorta. The bronchus, together with the bronchial
arteries and veins, the lymphatics and lymphatic glands, is placed on a
plane posterior to the great blood-vessels. The pulmonary artery lies
more forward than the bronchus, and to a great extent conceals it,
while the pulmonary veins are placed still farther in advance." The
left bronchus "in passing obliquely beneath the arch of the aorta is
depressed below the level of the pulmonary artery, which is the highest
vessel."[19] Practically, the chances of abnormal communications lie in
the relations of the aorta, more especially the different parts of the
arch, to the left bronchus and pulmonary artery, and to the trachea, of
the innominate artery to the trachea, and of the glandular structures
at the root of lung to the pulmonary artery.

[Footnote 19: Quain's _Anatomy_, vol. ii. pp. 897, 898.]

The encroachment of aneurism of the subclavian artery on the lung, and
consequent communication between it and the bronchus, is another form
of accidental or extraneous hæmoptysis.

A recognized classification of the vascular systems of the lungs is
into--1st, functional; 2d, nutritive. To the first belong the pulmonary
arteries and veins, and to the second the bronchial arteries and veins.
Both physiological and pathological experience justifies this division.

Notwithstanding the great attention and labor bestowed upon the
circulation of the lungs, there are still unsettled some important
points. We adopt from Küttner[20] some of the anatomical data
applicable to our subject. The branches of the pulmonary artery follow
uninterruptedly the bronchial ramifications. The mutual relations of
the artery and bronchus are such that the larger vessel lying in any
preparation of the lung directly next to the bronchus, and running in
the same direction, can be pronounced to be a branch of the pulmonary
artery. In the lungs of the embryo both lie in the same
connective-tissue sheath that originates at the root of the lung,
enters with them into the root of each lobule, and there spreads out.
In the lobules both run not only closely alongside of each other; there
appear also branches of the pulmonary artery on the bronchus itself,
and press on to the mucosa of the same.

[Footnote 20: "Beiträge zur Kentniss der Kreislaups-verhältnisse der
Saugethierlunge," _Virchow's Archiv_, vol. lxxiii. p. 476, etc.]

With the appearance of the terminal bronchiole this relation is
changed. The bronchial artery, as such, ceases; the pulmonary
artery--or rather its lateral branches--exclusively surround the
alveolar diverticulæ on their external surfaces. At the point where the
terminal bronchiole is developed into the infundibula the corresponding
trunk of the pulmonary artery divides into a number of
branches--"pinselförmig;" each infundibulum receives its stem, which
spreads itself after the manner of a feather on its external surface.
The terminal branches of the pulmonary artery cover the terminal
alveoli. On every lung in which the infundibula and lobules are well
distributed the terminal branches of the pulmonary artery extend beyond
the borders of the infundibula and lobules into the interlobular and
subpleural connective tissue, and here either lose themselves in a
capillary distribution or extend to the periphery of an adjoining
acinus, being lost in its capillaries.

One peculiarity of the pulmonary artery is that from a large trunk
relatively fine lateral branches come. From a vessel of 0.136 mm. come
branches of 0.033, 0.016, 0.011, 0.010 mm. The finest disappear
immediately as vasa vasorum; the larger pass to the perivascular or
peribronchial connective tissue {270} and become capillary, or they
appear on the surface of the immediately adjoining lobules and
disappear in the capillary paths of the alveoli.

The terminal branches of one and the same principal artery behave
differently according as they are distributed to the connective tissue
or to the alveoli. In the first case they form wide meshes and narrow
tubes, and are not different from the capillary terminations of the
body in general. In the other case the meshes are narrow; the vessels
in all of the pulmonary capillaries are wide. If these vessels are
followed from their origin to their final termination, it will be seen
that a considerable part of the pulmonary artery is spread in the
interlobular connective tissue; that it is not exclusively a secretory
vessel; that the capillary network of all the lobuli are in anastomotic
connection.

An anatomical investigation shows that between the branches of the
pulmonary artery no anastomoses exist. It is, however, proved that
under certain conditions connections between the larger branches of the
artery may occur. This artificial connection is favored through
peculiarities of terminal branching: wherever two parallel branches of
the pulmonary artery are followed, it will be seen that the terminal
branches lie alongside of each other without anastomosis. One can be
convinced of that, and, further, that the capillaries of only one or
two alveoli separate them. These unusually short capillaries between
two arteries are those in which differences of pressure in one or the
other artery produce wide connections. Küttner agrees so far with those
observers who think that between the larger branches of the pulmonary
artery no wide anastomoses exist already formed. In this sense the
pulmonary artery can be designated a terminal artery; on the other
side, however, it must not be forgotten that such connections can arise
at any time, and the artery there loses the type of a so-called
terminal artery.

He further remarks that the vascular-district supply of the pulmonary
artery is not so limited as Cohnheim and Litten believe; that, more
than that, some branches of it pass from one lobule to the adjoining
one; that others are distributed in the subpleural and interlobular
connective tissue and in the bronchial wall.

If the lung of an animal be injected from the pulmonary artery, there
is produced a complete filling of the vessels of the bronchial wall and
into the subepithelial layer--a fact the more interesting that a
similar event can scarcely be produced by a filling of the bronchial
artery.

Pulmonary Vein.--Only at the root of the lung do the bronchus,
pulmonary artery, and pulmonary vein lie close to each other. In the
continuance of the same the artery and the bronchus remain close by
each other, but the vein pursues its own course. The branches of the
same are, from the hilus to their capillary termination, situated in
the interlobular connective-tissue paths. They form on the external
margins of the lobules wide blutbuchten, in which the veins of the
infundibula enter with short stems. The artery lies intralobular--the
vein interlobular. The bronchial veins connect not only with branches
of the azygos and superior cava, but also with those of the pulmonary
vein.

Bronchial Vessels.--The variety of origin of the bronchial arteries is
notable. Whatever their origin, they follow with their chief trunk the
bronchus into the parenchyma of the lung, and give off insignificant
lateral branches to the connective-tissue layers. There is still
another kind of artery, which divides independently in the connective
tissue of the lungs, without resting on the bronchial walls; they come
from the oesophageal, mediastinal, and pericardial arteries, branch in
the mediastinal pleura, appear with these at the hilus of the lung, and
form partly an independent mesh of pleural arteries, and partly spread
themselves in the interlobular connective tissue.

All the vessels of the serous membranes of the diaphragm can contribute
{271} in many ways blood to the hilus of the lung: the unusually
fine-branched arteries appear in this way to be in condition to
compensate for obstructions (or lesser). The bronchial arteries in
comparison with the other vessels of the lungs give off sparingly
lateral branches; among the most interesting are the branches which
spring directly from the trunks of the bronchial artery, pass through
the peribronchial connective tissue, appear at the adjoining
infundibula, and lose themselves in capillary terminations.

The capillary districts of the bronchial arteries pass immediately into
those of the pulmonary. It is a fact that besides the pulmonary artery
the bronchial artery provides the infundibula and alveoli with blood.
If the bronchial artery springing from the intercostal and internal
mammary arteries be ligated or cut, leaving open the vessels of the
mediastinal pleura, and the lung be injected from the abdominal aorta,
a mere inspection will show a filling of the parenchyma of the lung;
anastomoses between the pleural arteries and the intra-acinous trunks
of the pulmonary arteries can be recognized. There is an anastomotic
connection between the pleural branches of the pulmonary and bronchial
arteries.

The bronchial, as also the pulmonary, artery can be filled by means of
the fine arterial branches from the mediastinal pleura.

The principal branches of the bronchial arteries go to the bronchi; at
the alveolar passage they here stop as such; their capillaries become
continuous with those of the pulmonary artery. The greater part of the
few collateral branches nourish the submucous peribronchial and
perivascular connective tissue, the nerves, the lymphatic vessels; the
smaller part enter the alveoli of other bronchial systems and become
capillary.

The branches going to the lung with the mediastinal pleura spread
themselves in the pleura and interlobular connective tissue, nourish
the large subpleural and interlobular lymphatic vessels, but lose
themselves in capillary distribution on the alveoli and infundibula.

The pleural and bronchial arteries anastomose partly with each other
and partly with branches of the pulmonary artery.

With reference to the branches of the pulmonary artery going to the
bronchi, it may be said that they, without giving special branches to
the external layer of the bronchi, press on to the basal membrane and
form a compact capillary network in common with the proportionately few
branches of the bronchial artery.

Amidst differences of opinion, as between Küttner, Lalesque, and
Cohnheim and Litten, there is a concurrence as to the chances of
supplementary function by anastomoses between channels that are
ordinarily separate. Küttner admits a modified form of terminal
arrangement in the pulmonary artery, but at the same time claims an
amount of potential connection that is liable to come into actual
operation and suspend, if not destroy, the terminal type.

The correlation of both functional and nutrient vessels is so intimate
that we believe there is no conclusive argument against the actual
transfer of office from one to the other in certain strained conditions
of disease; Virchow's experiment proves it.

The wonderful delicacy and distensibility of the enormous network of
pulmonary vessels (relation of uncovered space in the alveoli to that
covered by the vessels being 50 out of 200, Kuss); their capacity of
response to great variations of supply and tension; the prompt
supplementary function proven by Litten[21] to belong to the
tracheo-oesophageal, pericardial, phrenic, and pleuro-mediastinal
arteries, and their equilibrium under the sensitive changes of the
aortic system; the slower submission of the lesser circulation to the
peripheral impressions, which markedly affect the aortic system; the
facts {272} verified by Lichtheim[22] that on closure of any portion of
the pulmonary artery the same quantity of blood will pass through the
portion remaining open as before; that this is brought about through
increase of pressure in the sections still open, and through the
simultaneous increased rapidity of circulation and distension of the
vessel walls; and that this mechanism is able to compensate for
obstruction of three-fourths of the pulmonary artery,--are important
factors in the anatomical and physiological relations of hæmoptysis.

[Footnote 21: "Ueber den Hämorrhagischen Infarct," _Zeitschrift für
klinische Medicin_.]

[Footnote 22: _Die Störungen des Lungenkreislaufs_, by L. Lichtheim,
Berlin, 1876, p. 65.]

ETIOLOGY.--The natural history of hæmoptysis is practically that of
phthisis: exceptions to this will be noted hereafter. As heredity is
largely a determining influence in the latter, it may be assumed that
it qualifies its principal symptoms. More or less uniformity prevails
in the transmission of normal or abnormal conditions, and we seem to
find an illustration of the latter in the correspondence between the
percentages of hereditary phthisis and those of hæmoptysis in such
cases. Reginald Thompson[23] says that "out of 1064 cases of
well-marked inherited phthisis, 426 suffered from hæmoptysis." In his
calculation he omitted all those in which the disease began with
hæmoptysis. Had these then been included, they would have raised the
percentage over that shown by the figures, which is slightly above 40.
The rate would not then be much below that given as an average of cases
of hereditary phthisis. This percentage of cases of hæmoptysis in
hereditary phthisis is a sufficiently uniform transmission to prove the
influence of heredity. Its influence is shown not only in the number of
transmissions, but in the transmission of types; so that, as we have a
family type of phthisis, we may have a family type of hæmoptysis, such
as the cases where all the phthisical members of a family are subject
to hæmoptysis of uniform characteristics, instances where the same
uniformity in type is transmitted, and instances where the phthisical
heredity appears to have its survival in moderate and transient attacks
of hemorrhage.

[Footnote 23: _The Causes and Results of Pulmonary Hemorrhage_, p.
110.]

Atavism is also seen in some family histories. We have in view such an
instance, where the marked hæmoptysical tendencies of one generation
skipped the next to reappear in the third.

A special study of the relation of cases of copious hæmoptysis to
different forms of heredity has been made by Reginald Thompson. His
table is as follows:

                     COPIOUS HÆMOPTYSIS.
  +-------------------+----------------------------------+
  |                   |            Cases.                |
  +-------------------+--------+--------+----------------+
  | Age at which      | Mother | Father | Non-hereditary |
  | attack commenced. |   123  |   102  |      105       |
  +-------------------+--------+--------+----------------+
  |        5          |   ...  |     1  |      ...       |
  +-------------------+--------+--------+----------------+
  |       10          |   ...  |     4  |        2       |
  +-------------------+--------+--------+----------------+
  |       15          |    27  |    16  |       14       |
  +-------------------+--------+--------+----------------+
  |       20          |    30  |    22  |       20       |
  +-------------------+--------+--------+----------------+
  |       25          |    34  |    24  |       24       |
  +-------------------+--------+--------+----------------+
  |       30          |    18  |    19  |       16       |
  +-------------------+--------+--------+----------------+
  |       35          |     8  |     9  |       12       |
  +-------------------+--------+--------+----------------+
  |       40          |     2  |     4  |        8       |
  +-------------------+--------+--------+----------------+
  |       45          |     3  |     1  |        5       |
  +-------------------+--------+--------+----------------+
  |       50          |     1  |   ...  |        2       |
  +-------------------+--------+--------+----------------+
  |       55          |        |     1  |                |
  +-------------------+--------+--------+----------------+
  |       60          |        |     1  |                |
  +-------------------+--------+--------+----------------+
  |       65          |        |        |                |
  +-------------------+--------+--------+----------------+

He claims that this table shows that of the cases of direct heredity,
cross-heredity, and non-heredity, those who were the subjects of
cross-heredity--that is, those from the mother--were more liable to
copious hæmoptysis than either the cases of direct heredity or of
non-heredity; and the numbers of the two latter so closely correspond
as to show that heredity from the father has little influence as
regards hemorrhage. The conclusion he draws from the table is that "an
heredity is drawn from the mother which differs from that derived from
the father, and to this must be attributed the excess of cases of
copious hæmoptysis."

{273} This difference will be seen in the following table, which shows
the number of cases occurring before and after thirty:

  +-----------------+-----+-------------------+------------------+
  |    Cases.       |     | Before age of 30. | After age of 30. |
  +-----------------+-----+-------------------+------------------+
  | Mother          | 123 |        91         |       32         |
  +-----------------+-----+-------------------+------------------+
  | Father          | 102 |        65         |       37         |
  +-----------------+-----+-------------------+------------------+
  | Non-hereditary  | 105 |        60         |       45         |
  +-----------------+-----+-------------------+------------------+

He thinks the explanation is to be obtained from the statistics of
hæmophilia, which show a large proportion of transmissions from mothers
to sons, and that we have here a strong argument connecting copious
hæmoptysis, not with tubercle, but with hæmophilia.

His next table is one of 125 cases of double heredity, calculated upon
the same basis as the others, that of 400:

  +----------+-------------------------+
  |          |          Cases.         |
  +----------+------------+------------+
  |          |   Double   | Calculated |
  |          |  heredity  |     to     |
  +----------+------------+------------+
  |          |    125     |    400     |
  +----------+------------+------------+
  |    5     |    ...     |    ...     |
  +----------+------------+------------+
  |   10     |      3     |     10     |
  +----------+------------+------------+
  |   15     |     20     |     74     |
  +----------+------------+------------+
  |   20     |     40     |    128     |
  +----------+------------+------------+
  |   25     |     23     |     75     |
  +----------+------------+------------+
  |   30     |     15     |     48     |
  +----------+------------+------------+
  |   35     |     12     |     37     |
  +----------+------------+------------+
  |   40     |      9     |     29     |
  +----------+------------+------------+
  |   45     |      1     |      3     |
  +----------+------------+------------+
  |   55     |      1     |      3     |
  +----------+------------+------------+
  |   60     |      1     |      3     |
  +----------+------------+------------+
  |   65     |            |            |
  +----------+------------+------------+

which shows a close approximation to the table of cases of
cross-heredity from the mother, and that the calculated number for 400
cases of double heredity are almost identical with that of the actual
number of 400 cases of cross-heredity between the ages of fifteen and
twenty-five--in the first case being 202, in the second 203--and the
calculated number of cases before thirty amount to 287, not quite equal
to actual number for cases of cross-heredity, which is 294. He
concludes that these cases do not show a greater tendency to hemorrhage
than is shown in cases of direct and non-heredity. We may accept these
figures and calculations as important without endorsing the conclusion
which they are intended to sustain--viz. that such hæmoptyses are
essentially of hæmophilic origin. It may be stated as a general opinion
that hæmophilia does not especially manifest itself in pulmonary
hemorrhages, and that hæmophilic families are not specially liable to
phthisis.

The hemorrhagic diathesis, as distinguished from the specific bleeders'
heredity, does not often manifest its activity through the lungs, and,
as correlative, phthisis does not often show hemorrhages in other
organs than the lungs.[24] Leudet has met in 244 cases of phthisis 9
times hemorrhages in other organs than the lungs; oftenest by the
intestine, the skin, the nasal mucous membrane; more rarely by the
brain and urinary organs; 10 times between the muscles of the abdominal
walls. These considerations suggest that the phthisical hæmoptysis is
distinct from that of hæmophilia or the hemorrhagic diathesis, and has
an independent origin.

[Footnote 24: "Rémarques sur la Diathese hémorrhagique," _Mém. Soc. de
la Biologie_, 1859, p. 179.]

Some facts in regard to the previous diseases of patients admitted into
the Brompton Hospital with phthisis are given in the second medical
report of that institution, which may have a bearing on the special
features, such as hæmoptysis. Among 1973 patients admitted, 275 were
found to have suffered with well-marked attacks of rheumatism, and 16
had acute symptoms of it while in the hospital, making a larger number
than of any other disease, fevers coming next with 238. The connection
of forms of hemorrhage with {274} so-called rheumatism suggests a
possible influence of that kind in favoring hæmoptyses during the
evolution of phthisis. We know of no facts collected with the view of
studying this relation. If such a conclusion were sustained, it would
tend to confirm the view connecting hæmoptysis with hæmophilia or the
hemorrhagic diathesis.

Williams[25] gives a statement qualifying the assumption that the
hemorrhagic variety of consumption specially originates in family
predisposition, for in 72 cases out of 1000 tabulated cases of phthisis
family predisposition was present in only 25 instances. This percentage
is scarcely small enough to exclude a predisposition.

[Footnote 25: _Pulmonary Consumption_, p. 157.]

Considering hæmoptysis in this aspect, as a result of heredity, does
not account for all the cases with which we meet. We are surprised
occasionally by the appearance of pulmonary hemorrhage where heredity
of phthisis cannot be traced. Such persons present the aspect of a
vulnerable state; they yield readily to a phthisical invasion. Some of
the so-called cases of phthisis ab hæmoptoe are found in this class,
yet they may have inherited a phthisical predisposition, brought about
by various degenerating influences acting on their ancestors, such as
antihygienic surroundings, bad air, insufficient food, frequent
childbearing, and excessive nursing. The heredity is not in special
symptoms, but in a predisposition which needs only some exciting cause
for a specific symptomatology that may be carried forward to the next
generation.

One individual may himself yield to the same degenerating influences,
and live with more or less of an acquired predisposition until similar
exciting causes reveal his specific weakness. Another may find that he
has a phthisis directly acquired from a single attack of severe illness
without the aid of any element of heredity or of the acquired
predisposition. The gradation would then be inherited predisposition,
acquired predisposition, and acquired phthisis. Hæmoptysis may find its
origin in these several relations of heredity. Combined, they represent
the law of uniformity and the law of variation in hereditary
transmissions. If these general observations be correct, they show that
the ordinarily stated percentage of transmission of hæmoptysis in
inherited phthisis does not express the totality of influence operating
in the production of hæmoptysis. Something must be subtracted from the
so-called non-inherited phthisis and added to the inherited form.

When we attempt to express the relation of acquired or non-inherited
phthisis to hæmoptysis, we find no sufficient data. Thompson's table
above given is assumed by him as showing that the influences
superinducing hæmoptysis in the non-hereditary class are equivalent to
the heredity operating through the father, which is quite subordinate.

R. Thompson[26] states that out of 1064 of his cases of well-marked
inherited phthisis, 426 had hæmoptysis; of 1016 when phthisis was not
known to be inherited, 558 had hæmoptysis.

[Footnote 26: _Loc. cit._, p. 110. In a later work Thompson (_Family
Phthisis_, London, 1884) states that the general effect of the paternal
inheritance is to reduce the number of cases of copious bleeding for
the total period of life, but an excess is observed for the special
period between twenty and twenty-five; that in the inheritance of the
females from the father the number of cases of bleeding is large, the
number of the copious cases being twice as many as the moderate. The
effect of double heredity upon males was to make the cases of copious
bleeding numerous, and that nearly half the total number of cases were
disposed to bleed. In females there was an increase in the number of
cases of moderate amount. As regards acquired phthisis among males,
that hæmoptysis is a well-marked feature, and nearly three-fourths are
cases of copious bleeding; as to acquired phthisis among females, that
the number of cases is considerably smaller, the reduction being marked
in the cases of copious bleeding.]

{275} In a collection of cases of phthisis taken from the Cincinnati
Hospital records, amounting to 1266, there were of

  Cases of hæmoptysis                          475, or 37.51 per cent.
      "    phthisis,
             with family history of same       332
      "    hæmoptysis in same                  127, or 38.25    "
      "    acquired or non-inherited phthisis  934
      "    hæmoptysis in same                  348, or 37.25    "

In 10 cases there was a family history of hæmoptysis; that is, of a
general family peculiarity in that direction. These percentages show no
great difference between the relations of inherited and non-inherited
phthisis to hæmoptysis, the inherited exceeding by 1 per cent. that of
the non-inherited form.

Without here attempting a comprehensive statement of what the
predisposition, transmitted or acquired, is, we may mention two
influences of important force--a tendency to fragility of vessels and
to the catarrhal disposition. It is sufficient to speak of the fact
that in no other disease of the lungs than phthisis have we as a common
feature this vascular fragility. It differentiates the disease and the
symptoms. If it appear in any of them, it should at once excite a
suspicion of the phthisical constitution. That it does appear in some
such cases without ulterior effects does not invalidate the general
statement. It may be put down as a part of the phthisical habit
directly concerned in the liability to hæmoptysis. The proof of this
proposition is more clinical than anatomical.

The attempt to prove that it is hæmophilic rests upon the application
of a few histological examinations of hæmophilic vessels to the
phenomena of phthisical hæmoptysis. The assumption of identity has only
the doubtful force of analogy. Histological examinations of the vessels
in the earliest stages of phthisis and hæmoptysis are too rare to
afford sufficient data. In the latter stages the condition is too
complex, because of positive inflammatory and ulcerative processes.

Although alterations in the vessels in the early stage of simple
inflammation cannot be histologically demonstrated, yet they must exist
in order to allow diapedesis. So with early phthisis: in the
pre-hæmoptoic stage the alterations are not demonstrated, yet that such
disorder of function must have accompanying structural change
underlying the phenomena of the initial hæmoptysis is in accordance
with physiological and pathological doctrines, and has much consistent
clinical force. When we presuppose a delicacy of, or injury to, the
blood-vessels of a part, there is the imminence of not only a rupture,
and consequent hemorrhage, but of those changes which, leading through
stasis and congestion, come to be inflammatory, and which affect still
further the vascular structures and adjoining parenchyma.

Besides these changes initiated in the blood-vessels, there are others
of close relation to the phthisical constitution, which begin in the
vulnerable epithelial elements of the bronchial mucous membrane and of
the air-cells. They are the evidences of the dispositio catarrhalis,
which received its name from the old observers, and the validity of
which has been confirmed by modern pathological and clinical
researches.

It is responsible for the great susceptibility to catarrhal affections
of the bronchi and air-cells which lays the foundation for chronic
catarrhal pneumonia.

These two elements, of fragility of vessels and of the catarrhal
tendency, are the tangible instruments of heredity. They are also the
factors of the acquired predisposition.

The Vienna Hospital reports, running through more than fifteen years,
and embracing more than 20,000 cases, give as the ages most liable to
hæmoptysis those between eighteen and twenty-nine years. No statistics
as to sex are given.

{276} Of 1266 cases of phthisis[27] taken without selection from the
records of the Cincinnati Hospital, there were

  Between 10 and 20 years,  81; in this class, hæmoptysis  20
     "    20  "  30   "    459;   "      "         "      208
     "    30  "  40   "    363;   "      "         "      143
     "    40  "  50   "    191;   "      "         "       62
     "    50  "  60   "    110;   "      "         "       28
     "    60  "  70   "     45;   "      "         "        9
  Over           70   "      7;   "      "         "        1
  Age not stated            10;   "      "         "        4
                          ----                            ---
                          1266                            475

[Footnote 27: We desire to acknowledge the services of Walter A. Dun,
then a resident physician at the Cincinnati Hospital, in collecting
these cases from the hospital books.]

Ware in _Mass. Med. Soc. Proc._ gives ages in 317 cases:

   43 up to          20
  139 between 20 and 30
   77    "    30  "  40

Of Pollock's[28] 351 cases of profuse hæmoptysis,

   43 were under     20 years of age.
  168 between 20 and 30   "       "
  100    "    30  "  40   "       "
   40 over           40   "       "

These figures from widely-different sources testify to the fact that
the greatest number of cases of hæmoptysis occurs between twenty and
thirty years of age, or at least with a variation of only about a year
from those extremes. The possibility of hæmoptysis, if we may judge by
cases reported, lies anywhere between sixteen days of age and the limit
of life. A case of hæmoptysis in a child sixteen days old is alluded to
in _Nouv. Dict. de Méd. et de Chirurg_.[29] The oldest on the list of
the Vienna Hospital reports is seventy-two. In our Cincinnati Hospital
list we have 7 over seventy years. Others have reported cases beyond
these figures.

[Footnote 28: _Prognosis in Consumption_, p. 311.]

[Footnote 29: Vol. xxix. p. 391.]

A case of death from pulmonary aneurism and hæmoptysis in a child aged
two and a half years is reported in _London Path. Soc. Trans._;[30]
also one by Powell[31] of a child seven months old from a similar
rupture--illustrations of the remark that children are subject not so
much to initial as to terminal hæmoptysis.

[Footnote 30: Vol. ii. p. 35.]

[Footnote 31: _Med. Times and Gaz._, June, 1874.]

As to the relations of sex to the amount of hæmoptysis, we have the
Table XI. from the second medical report of the Brompton Hospital:

  +------------------+-------------------+--------+----------+--------+
  |                  | Males. | Females. | Males. | Females. | Total. |
  +------------------+--------+----------+--------+----------+--------+
  | Below drachm j   |        |          |        |          |        |
  |   in quantity    |  843   |    700   |   55   |    83    |  1681  |
  | From drachm j    |        |          |        |          |        |
  |   to drachm iv   |  616   |    482   |   34   |    69    |  1201  |
  | From ½ oz.       |        |          |        |          |        |
  |   to 4 oz.       |  429   |    268   |   13   |    21    |   731  |
  | Above 4 oz.      |  343   |    153   |    9   |     7    |   512  |
  | Entirely absent  |  588   |    193   |   74   |    65    |   920  |
  |                  | ----   |    ---   |  ---   |   ---    |  ----  |
  |                  | 2819   |   1796   |  185   |   245    |  5045  |
  +------------------+--------+----------+--------+----------+--------+

These results correspond with the general one stated by Williams,[32]
that large hemorrhages occurred in 34.76 per cent. of males, and in
only 17.67 per {277} cent. of females. In the above table, where
quantities of blood above four ounces were noted, the male figure is
more than double that of the female. As regards exemption, it is stated
that of the cases of decided phthisis which had been free from
hæmoptysis, about five-sevenths were males, and under two-sevenths
females. In general it may be said that females are more liable to
small and males to the larger hemorrhages.

[Footnote 32: _Treatise on Consumption_, p. 156.]

Of 268 females in our Cincinnati Hospital list, 44 had
hæmoptysis--about 13 per cent. Of 998 males, 431 had hæmoptysis, or
about 43 per cent.

In the second Brompton Hospital report[33] it is stated that "many of
the most violent attacks of this nature (sudden fatal terminations)
have depended on a sudden rise in the temperature." The peculiar
prevalence of hæmoptysis on the coasts of some warm countries has long
since been noted. Archibald Smith,[34] in giving his practical
observations on the diseases of Peru, says: "There appears to be a
general predisposition to this disease, hæmoptysis." An intelligent
individual, himself a sufferer while then a resident on the lower
portion of the North American south-western coast, has given me the
same statement. Pasley[35] says at least 10 per cent. of the cases of
phthisis in Trinidad which die in the hospital terminate in a profuse
hæmoptysis; the quantity of blood varies from 15 to 70 or 80 ounces,
and the duration of life from the beginning of the hæmoptysis till the
end five to fifteen minutes. Of Ware's cases,[36] 83 were in winter,
101 in spring, 69 in summer, 102 in autumn, or 185 in autumn and
winter, 170 in spring and summer. In four months of warm weather, June,
July, August, and September, 97 cases; in October, November, December,
and January, 134; in February, March, April, and May, 124--an average
of 129 for the eight cold months, an excess of 32 cases, or about 33
per cent.; in the transition seasons, spring and autumn, 101 and 102.
The highest numbers were in March and November, 38 and 39; lowest
number in June, 18. These are the only figures obtainable as to our
climate, and they do not agree with those given by R. E. Thompson's
table,[37] showing the prevalence of hæmoptysis as to months in 1000
well-marked cases:

 Jan., Feb., Mar., Apr., May, June, July, Aug., Sept., Oct., Nov., Dec.
  67    61    90    95   112   130   128   64    64     55    81    63

The summer months of June and July show the largest numbers, and the
months of December, January, and February lesser numbers. The decrease
in August is explained in great measure by the diminution in
attendance. It is possible that other elements of climate besides
temperature may account for this difference between American and
English figures.

[Footnote 33: Page 17.]

[Footnote 34: _Edinburgh Med. and Surg. Journ._, vol. liv., 1840.]

[Footnote 35: _Brit. Med. Journ._, Jan. 10, 1880, p. 53.]

[Footnote 36: _Mass. Med. Soc._, 1860.]

[Footnote 37: _On Pulmonary Hemorrhages_, p. 114.]

A more correct opinion as to the effect of altitude is developing.
Archibald Smith[38] more than forty years ago testified to the good
effects of removal from the coast to the high sierras of Peru in cases
of phthisis with hæmoptysis. His own instances of great improvement
following removal to high levels, 5000 to 8000 feet, are conclusive. He
also gives instances where renewals of hemorrhagic attacks followed the
return to the coast. It was the custom for physicians to send their
consumptive patients to the sierras without reference to their
hemorrhagic attacks.

[Footnote 38: _Loc. cit._]

Similar testimony is accumulating in this country. The Colorado regions
are supplying, through their physicians, much material bearing upon the
effect of altitudes on hæmoptysis. H. K. Steele of Denver, Col.,
writes, June, 1883, that "it is the opinion in the profession
generally, and I endorse it, that this country acts beneficially in the
hæmoptysis of phthisical patients." Jacob {278} Reed, Jr., says[39]
that not only does the ascent to this altitude (6000 feet) not
predispose to pneumorrhagia in consumptives, but that "hemorrhagic
cases do well here; in most cases the bleedings becoming less frequent,
in many cases ceasing altogether." By letter May, 1883, he says these
cases number between 500 and 600, and he feels justified in the
positive statement that not only does altitude not precipitate
hæmoptysis, but that "those suffering from this symptom are benefited
here, their bleeding becoming less frequent and less in quantity." He
makes an exception of florid cases in active progress or old cavities
waking up to new action.

[Footnote 39: "Altitude in Reference to Pneumorrhagia," an analysis of
70 cases, read at the eighth annual convention of the Colorado Med.
Soc., 1878, p. 66.]

Denison,[40] after an analysis of 90 cases of hæmoptysis out of 202 of
phthisis, says: "The advantages of high altitudes are pre-eminently for
hemorrhagic cases in the first stage, while hemorrhagic cases with
excavations, especially if the bleeding has been recent and softening
is in progress, should be interdicted from going to great elevations."

[Footnote 40: _Rocky Mountain Health Reports_, p. 140.]

He also quotes Herman Weber[41] as recommending "alpine climates, not
only as a prophylactic measure against hæmoptysis, but also as a means
to promote the cure of the effects of the inflammatory processes
resulting from pulmonary hemorrhage."

[Footnote 41: _Hæmoptysis as a Cure of Inflammatory Processes and
Phthisis, with Remarks on Treatment_.]

These statements are sufficient to show that the view formerly
prevalent, and still more or less so, that high altitudes have the
effect of prolonging or favoring hæmoptysis, is not altogether correct.
It should be understood as applying to the extreme heights of 10,000 or
15,000 feet, and that rapidity of transfer and unusual exertion are
necessary and qualifying considerations. Jourdanet[42] places the
region of safety in phthisis about the mid-point between the level of
the sea and the snow-line. The preservative level is lower in Alpine
than in American regions. The line of perpetual snow in Mexico being
about 4500 meters, the preservative zone would be 2250 meters. In
Switzerland, where the line of snow marks 2700 meters, the same zone
would be 1350 meters. No such definite limitations are attainable as
regards hæmoptysis, but a correspondence of zones might be conjectured.

[Footnote 42: _Influence de la Pression de l'Air_, vol. ii. pp. 183,
184, 213.]

The belief that pregnancy in some way favors hæmoptysis is a very old
one. It has been more or less accepted by modern writers. Trousseau[43]
gives his observations to the effect that there are women who during
pregnancy, and others who during nursing, spit blood. His belief was
that such hæmoptyses were not symptomatic of pulmonary tubercle nor of
cardiac disease, but he classifies them as cases of hemorrhagic
deviation. Peter[44] speaks of a gravid pulmonary hyperæmia, proven in
part by his determination of increased local temperatures in the lower
intercostal spaces. Some of his cases do not sustain his theories, and
can properly be referred to puerperal accidents, such as emboli in
phlegmasia alba dolens. Such cases as we have met with in connection
with pregnancy or lactation have had hereditary or acquired tendencies
to phthisis. We have under view a case where hæmoptysis always recurs
during pregnancy and where there is a family history of phthisis. A
brother has pulmonary hemorrhages preceded by inflammatory attacks,
which stand in a relation to him corresponding to the pregnant
hyperæmia of the sister. The well-known effects of pregnancy or
prolonged lactation in developing phthisis are a sufficient explanation
of this class of cases.

[Footnote 43: _Clinique Medic. Trans._, vol. i. p. 531.]

[Footnote 44: _Leçons de Clinique médicale_, vol. ii. p. 664, 2d ed.]

Many exciting causes are assigned by patients in explanation of a
dreaded {279} event, and some are otherwise misinterpreted. Their mode
of action is not intelligible unless we keep in view the anatomical,
physiological, and pathological data heretofore given. Numerous cases
occur where no exciting causes can be found, such as those coming on in
the quietude of sleep. The insidious agencies of the predisposing
causes must be responsible. A study of many cases will show that the
alleged causes have become operative only after a considerable time has
elapsed, during which a congestive or inflammatory condition has
appeared, the expression of a latent tendency. Dancing in a warm room
or speaking long in the open air, followed in twenty-four hours by
bleeding, are such instances. The physical effort was only so far
instrumental as it gave a chance for the development of a potential
diathetic condition. It was not the direct cause. Falls, frights, blows
on the chest, heavy lifting, playing on wind instruments, and emotional
excitement are sufficient to bring on a hemorrhage by direct influence,
and by so increasing arterial tension as to overcome the resistance of
vessels already weak. It is not intended to maintain the impossibility
of rupture of healthy vessels under some circumstances, but the large
provision made in the great distensibility of the pulmonary vessels and
in the supplementary functions already alluded to make it necessary to
be cautious in such admissions. The fact that hemorrhages from the
direct causes are sometimes not followed by phthisical effects does not
necessarily disprove their diathetic origin.

The effect of blows on the chest in producing hæmoptysis and phthisis
has been the subject of medico-legal examinations in suits for damages.
In all of such cases within our knowledge there has been the element of
fright or great emotional excitement, and hence a complexity of
causation. An hereditary tendency to phthisis was also present--a fact
which diminished the force of the plea that the blow was alone
responsible for the injuries to the health of the parties concerned.

Diseases or injuries of the brain may be mentioned as causes of
pulmonary hemorrhage, which may occasionally be shown by hæmoptysis.
Experimental pathology has recently thrown much light on these cases.
(See PULMONARY APOPLEXY, _infra_.)

It may be worth while, in view of recent researches, to refer to a form
of hæmoptysis closely associated with a newly-discovered parasite,
named Distoma Ringeri,[45] after Ringer of Tamsui, Formosa, who
discovered the parasite, but did not at once recognize its etiological
relation to the endemic hæmoptysis. In a post-mortem of a man dead from
rupture of an aortic aneurism he found the parasite lying on the
lung-tissue, probably escaped from a bronchus. There were some small
deposits of tubercle, no cavities, and slight congestion of the lungs.
Manson found that these parasites were associated with a
frequently-recurring hæmoptysis. Baely of Tokio[46] discovered the
parasite, probably before any others. It is quite common in North
Formosa and through Japan. Manson says:[47] "Endemic hæmoptysis can be
readily diagnosed. There is a history of irregular, intermitting
hæmoptysis, associated with a slight cough, and in the intervals of
more active bleeding the expectoration once or several times a day of
small pellets of viscid, brownish mucus. Examination of a small portion
of the sputum with the microscope at once settles the diagnosis,
sometimes as many as twenty parasites being found in a single field."
Further examination is necessary to determine the manner in which this
parasite produces the hæmoptysis.

[Footnote 45: _The Filaria sanguinis hominis and certain New Forms of
Parasitic Disease in India, China, and Warm Countries_, p. 134, by
Patrick Manson, Amoy, China.]

[Footnote 46: _London Lancet_, Oct. 2, 1880.]

[Footnote 47: _Ibid._, p. 143.]

The association of bacilli tuberculosis with hæmoptysis is proven by a
number of examinations. These will be referred to in their diagnostic
relations at another page. It is not intended here to imply an
etiological relation, {280} because as yet our knowledge does not point
to the blood-vessels as being the special or usual habitat of bacilli
or the place of their most destructive efforts.

Hydatids of the lung are a cause of hæmoptysis which may come from
congestion accompanying their growth, or from their rupture and
consequent opening of blood-vessels.

Before proceeding farther we shall refer more fully than before to the
conditions prepared by heredity, age and sex, etc. for the action of
the exciting causes. The agencies were stated to be the peculiar
vulnerability of the vascular and epithelial structures of the lungs.
When the morbid imminence is reinforced by an infective element, as in
phthisis, certain results follow which make easy the action of the
incidental causes. Because of the enormous vascularity and great
delicacy of structure of the lungs, and their liability to external
influences, slight external irritants in such constitutions produce
more than what follows in other cases. Instead of a transient hyperæmia
or mild catarrhal inflammation, we may have that fluxionary hyperæmia
of which an early outcome is hæmoptysis. Experimental pathology
explains such occurrences by demonstrating that while a normal vessel,
as in the mesentery, will require a pressure of seventy millimeters of
mercury to produce extravasation of its contents, an inflamed one will
not stand more than twenty-five millimeters. If catarrhal pneumonia
proceed in its phthisical form, it adds its elements of danger.

After its early stage of congestion we have the initiative processes
extending from the epithelial structures of the bronchi and alveoli to
the alveolar wall, which becomes thickened. By means of the double
pressure of abundant epithelial and fibrinous products retained within
the alveolar cells, and of the increased growth in the alveolar walls,
obliterative endarteritis and obstruction of blood-supply follow, the
final result of which may be destructive changes opening the way for
softening and ulceration, and consequent hemorrhage.

The same early hyperæmia accompanies the development and growth of
tubercle, whether it come from the bronchioles, the blood-vessels, or
alveolar walls. Trasbot[48] says: "A tubercle is found to be developed
along a small artery, most frequently at the angle formed by a terminal
division of the vessel--some around a capillary, around which it forms
a kind of bead, or in the network of an anastomosis, which envelops it
on every side. Vessels are more numerous in the tissues round the
nodules and in the septa or interstices of the large masses than in the
healthy connective tissue: there the vascularity is often so great as
to be mistaken for inflammation."

[Footnote 48: Quoted by Creighton Bevine, _Tuberculosis in Man_, p.
133.]

Hamilton,[49] speaking of the formation of tubercle in the alveolar
wall and cavity, says: "Capillary blood-vessels, filled with
blood-corpuscles, are drawn into it, and in this stage are distinctly
visible. They are all much engorged, and occasionally minute
extravasations are visible, the blood-corpuscles being thrown into the
alveolar cavity." The chance of an earlier obliteration of vessels is
greater under these circumstances than where the process begins in any
other structure. The final result is that combination of catarrhal and
tubercular products characteristic of mixed phthisis.

[Footnote 49: _The Pathology of Bronchitis, Catarrhal Pneumonia,
Tubercle, etc._, 1883.]

As increased vascularity accompanies and surrounds the nascent
tubercle, so vascular neo-formations accompany or are intermixed with
the obliterated zone of vessels, as long since described by Guillot and
recently substantially confirmed by Ewart. The former says:[50] "There
result numerous and inextricable anastomoses, which extend incessantly,
and of which the whole forms a mass of vessels proportional in extent
to the age of the tubercles and cavities that they entirely surround."

[Footnote 50: _L'Expérience_, vol. i. p. 553.]

{281} There ensues a connection between this system and that forming on
the false pleural membranes, and a supplementary function of supply for
regions outside of the area of obliterated vessels and for walls of
cavities is established. Considering the want of vitality of new
formations generally, it is quite probable that these become sources of
hemorrhage occasionally. Successive extensions of the diseased regions
reduce the amount of this supply, so that the converse
follows--comparative anæmia of the lung involved and diminished
tendency to hæmoptysis in some of its forms.

These observations, involving considerations of predisposition and its
tangible forms, do not apply to the important class of cardiac
hæmoptysis. The factors here are increased venous tension, pulmonary
hyperæmia of mechanical rather than vital origin, sclerosed or
atheromatous vessels, capillary ectasis, and embolic obstruction of the
pulmonary artery with resultant infarction, etc.

SYMPTOMS.--The definition requires that the blood be pure or unmixed,
yet the coarse physical appearances may vary a good deal. The color is
usually a bright red, but may be dark or venous in hue. There is
sufficient inconstancy in color to prevent its being reliable in
distinguishing the special source of the bleeding, though usually the
bright color is of bronchial and the dark of pulmonary origin. If
bright red at the onset, it loses some if not the whole of its
brightness as the attack progresses or is subsiding, sometimes because
of retention in the air-passages. The mass is more or less frothy, and
varies in density and specific gravity, in diffluence or adhesiveness,
the latter quality increasing in proportion to congestive or
inflammatory conditions, whether in the early or later stages. This is
dependent on the increase of the plastic, fibrinous, or reactive
elements in the blood and adjoining tissues. The mass may lie in a
circumscribed or in a splashy form in the bottom of the vessel,
circumstances of distance and force of ejection, as well as of physical
quality, producing the variations. The quantity varies greatly, both as
to the amount at each act of expectoration and as to the amount during
all of them. The whole amount throughout an average attack of initial
hæmoptysis might be placed at about one and a half to two ounces. Such
would be called moderate but decided hemorrhage. The extremes would
range between a teaspoonful and several pounds, and the time consumed
in the attack may vary between the time taken up by one or two
ejections and several months. The intervals between the successive
ejections will vary from a few minutes to twenty-four hours or more in
a case lasting a week. The manner of ejection is sometimes by a single
effort of hawking or throat-scraping or clearing, sometimes by a slight
hacking cough or by a vigorous effort of expulsion; at other times the
outflow is so rapid through the mouth and nostrils that it resembles
vomiting and may suggest a hemorrhage of the stomach.

The effect which a severe attack may have on the patient is often
notable. He becomes pale out of proportion to the amount of blood that
he has lost; the pulse is full, bounding, and corresponds to what is
called the hemorrhagic pulse. This is sometimes due to the mental
shock, but again it is independent of any excitement on the part of the
patient, or of even any sort of constitutional disturbance, as fever.
We have seen it in full development in connection with a profuse
hæmoptysis and a temperature of 105°. It has been noted also as part of
the phenomena of hemorrhage produced by septic influences upon the
vaso-motor system. Walshe's dictum is no doubt true, that there is a
calm and excited variety quoad cardiac action.[51] In the former there
is little vascular or mental excitement or debility, and the patient
does not willingly yield to the necessary restraint.

[Footnote 51: _Diseases of the Lungs_, p. 330.]

Feebleness is an accompaniment, sometimes to a degree disproportionate
to the amount of blood lost, and is an element in the shock which the
patient {282} feels at so unexpected an event. The early part of the
attack is usually without fever. This comes on later as a part of the
reaction phenomena, and becomes then a very important prognostic
symptom. We have known it, however, to range as high as 105° before the
hemorrhage appeared, and without any reduction by a most obstinate
continuance of the depletion.

Many cases occur without premonition. In a proportion there are
symptoms precedent to the outbreak. The significance of these is often
not perceived until the hæmoptysis appears. Certain subjective symptoms
are common. A sense of burning, which is substernal or unilateral,
corresponding to that lung which is then or shall afterward show itself
affected; soreness within the same bounds; dyspnoea, rarely grossly
objective; slight hacking cough for variable periods, and, more
immediately antecedent, a salty taste in the mouth,--are some of these.
They have their origin in a state of hyperæmia or irritation which has
its outcome in catarrhal processes or hemorrhage. Which it may be will
depend on certain predisposing as well as the immediately operative
causes already mentioned.

Of the objective states, some importance may be attached to
characteristics of the individual, such as the brunette complexion,
dark hair and eyes, or to external correspondences with others of the
family known to have been similarly affected.

More than the usual care is necessary in the physical examination,
particularly in the use of percussion. Palpation and auscultation can
be safely applied, but there might be greater difficulty in getting the
patient into a good position for the actual examination. In the
hæmoptysis of incipient phthisis the physical signs most usually found
are deficient expansion and resonance and vesicular murmur at either
apex. These are evidences of causes that had been in operation before
the hæmoptysis, and indicate important physical changes at the region
where they may be found. Yet they do not necessarily indicate that the
bleeding has its origin at that place. Add moist bubbling râles, and
the presumption becomes almost a certainty that you have found the
locality of the hemorrhage. If these subside as the amount of blood
expectorated gets smaller, the inference is still stronger. Successive
increments of physical signs would indicate that the bleeding had been
correctly located and that the lesion which gave origin to it was
progressing. A proportion of cases occur where no physical sign can be
found even after careful examination, so that it happens sometimes that
at the period of most importance for diagnosis physical signs are not
available, and when they are most distinct in the advanced cases the
diagnosis is already established. They may even become embarrassing by
their abundance. The true significance of the physical signs cannot be
determined until the attack has subsided entirely. The termination of
an attack is usually by disappearance of the congestion of which the
symptoms related were the expression. The soreness and oppression
beneath the sternum, the dyspnoea and fever, are relieved. The
persistence of cough would not necessarily augur badly, because there
is apt to be some catarrhal secretion which necessitates it. The
general result is relief. If the termination is to be unfavorable,
there will be an evident increase of constitutional symptoms,
especially of fever, as in the case alluded to above with the high
temperature. There will be a slower return to the pre-hæmoptic state
and an increase of the physical signs, and you may have apparently a
case of phthisis ab hæmoptoe. The impetus in a large majority of cases
is from the constitutional elements which initiated the symptoms,
rather than from the local cause, blood within the air-passages.
Clinical experience proves that there are cases where serious and rapid
injury to the lungs has followed closely upon an hæmoptysis. It is
admissible to classify such as phthisis ab hæmoptoe only, in the sense
that the effusion of blood in the remote parts of the lungs has brought
about catarrhal pneumonia, which in those predisposed {283} ends in
phthisis. Sommerbrodt's[52] experiments proved that the healthy animals
recovered from the catarrhal pneumonia.

[Footnote 52: _Virchow's Archiv_, vol. lv. p. 192.]

To determine the genuineness of any such special case, we should be
able to include inherited or acquired predisposition; to prove priority
of the hæmoptysis to cough, dyspnoea, and fever, and that these
followed soon after the bleeding; and to show that the age at the time
of the occurrence was not the phthisical age. If a direct or mechanical
cause can be found for the bleeding, the proof would be still stronger.
Most of the cases depended on to prove phthisis ab hæmoptoe or
hemorrhagic phthisis (Powell) do not answer to these requirements. In
the 8 cases reported by Sokolowski[53] are summarized these features,
and they give strong support to the conception of a phthisis ab
hæmoptoe. The mode of termination by sudden death is by syncope, and
suffocation cannot be said to be very frequent. There have not been
more than 3 suddenly fatal cases (within a half hour) in the Cincinnati
Hospital records in a period of fifteen years: 22 cases are given in
the second medical report of Brompton Hospital, where the cases of
phthisis are very numerous; Powell's table[54] has 15 cases, which
happened at the Brompton Hospital between February, 1868, and November,
1870. The cases which we have collected as occurring since that amount
to about 20. T. Williams[55] says that of 198 patients who died, 4 died
of profuse hæmoptysis. Thompson[56] says that of 383 deaths occurring
in the hospital (Brompton) during three years, 26 were from fatal
bleeding--a percentage ranging between 2 and 6 in the two series.

[Footnote 53: _Berlin. klin. Wochenschrift_, 30 Sept., 1878.]

[Footnote 54: Vol. xxii., _Lond. Path. Soc. Tr._]

[Footnote 55: _Med.-Chir. Trans._, vol. liv.]

[Footnote 56: _Loc. cit._, p. 115.]

The symptomatology given above is a general one. Looked at with
reference to the varieties of hæmoptysis, the assignment would be to
the earliest or initial attacks. Assuming five varieties--1, the simple
or idiopathic; 2, the congestive; 3, the ulcerative; 4, the cavernous;
5, the extra-pulmonary--it would belong to the simple or to the
congestive form.

Under the first may be included those cases which occur without any
heredity or traceable cause, are not accompanied by fever, soreness,
dyspnoea, or physical signs, and which further observation shows are
not followed by pulmonary disease. Such cases are rare, yet clinical
records afford them. Time is so important an element in the diagnosis
that the presumption would be against such a classification at the time
of the call for treatment. They have probably developed the hemorrhagic
element of phthisis, and by otherwise vigorous constitutions are
protected from its further evolution.

The congestive form is the one with which we most often meet, and is
essentially the expression of the predisposing element mentioned as one
of the agencies of heredity. Unlike the idiopathic variety, it has its
positive symptoms, so familiar to the practitioner. Special clinical
forms, as the hæmoptysis of pregnancy, the so-called vicarious cases,
the earliest attacks in the hemorrhagic variety of phthisis, the
hæmoptysis of plastic bronchitis (which has a phthisical element in
it), that of hydatids of the lung preliminary to the opening of the
hydatid, and probably others, such as cancer of the lung, may be placed
in this category. Hysterical hæmoptysis is a term of doubtful
propriety, because facts show that the tubercular diathesis has close
affinities with the neuropathic heredity,[57] and hence that the
hæmoptysis arises from the tubercular and not the neuropathic element.
From this point of view it has its congestive origin, and can be
properly classified under this head.

[Footnote 57: J. Grasset, _Brain_, vols. vi. and vii.]

The ulcerative form is familiar to us in the second stage of phthisis.
It is more subordinated to the constitutional features, fever, hectic,
and debility, to the purulent expectoration, and to the
easily-determined physical signs. {284} Notwithstanding the apparently
increased chance of profuse hemorrhage, the quantity of blood is often
quite small and apt to be accompanied with a mixed sputum. It is not so
florid as in the congestive form. Some of the most copious hemorrhages
in this stage arise from the presence of the hemorrhagic diathesis or
are found in persons of full and plethoric habit. They will recur at
intervals of once or twice a year for many years, and some of them
finally cease, with a remainder of physical signs. The physical signs
usually indicate nothing more than consolidation of the lung for a long
time. They are dulness, bronchophony, bronchial breathing, and mucus or
crackling sounds over a limited area in the upper part of the chest. In
the slow cases of pulmonary fibrosis there is now and then a small
amount of ulcerative action to produce hæmoptysis. We have seen cases
fatal by a suffocating quantity without discovery of the actual source.

In cavernous hæmoptysis there are striking facts which give this class
a great interest. It includes most of the suddenly fatal cases which
shock families or hospital inmates. It comes from rupture of small
aneurisms in the walls of old cavities. A less dangerous form is that
from small granulations or vessels in the walls of recent cavities or
from small vessels in their trabeculæ. The elucidation of hemorrhage
and death from pulmonary aneurism is of the later acquisitions in our
knowledge.[58] A distinction between the ulcerative and pulmonary
aneurism forms is not always practicable. A detection of the aneurism
by auscultation has not been recorded, though it is at times quite
large. In the latter form you may have, as in the former, repeated
attacks of hemorrhage before this fatal one. The most decisive
indication in favor of the aneurismal source of the bleeding, besides
frequent and abundant hemorrhage, would be the proofs of a chronic
cavity. In Powell's[59] 15 cases of fatal hæmoptysis 3 were without
discoverable source; of the other 12, 3 were immediately fatal; in the
remaining 9 the previous attacks of hæmoptysis occurred at periods
varying from eighteen months to two days. The aneurisms were all in the
left lung except 2: 6 occurred in individuals with family histories of
phthisis; 3 with such histories; 2 are negative or doubtful of fatal
hæmoptysis.

[Footnote 58: Williams says that Peacock and Fearn of Derby were the
first to record instances of pulmonary aneurism in England. Stark in
his works edited by J. C. Smyth, 4th Lond. ed., 1788, p. 31 (quoted by
Young, _loc. cit._, p. 331), relates a case of diseased lungs in which
sudden death took place from the bursting of an aneurism of the
pulmonary artery.]

[Footnote 59: Vol. xxii., _Path. Soc. Trans._, London.]

We have a table of cases collected from reports made since Powell's--in
all 21. In 10 the aneurisms were in the left lung, 8 were in the right,
and in 3 the place of the aneurism was not designated; 16 were in
males, 4 in females, and 2 not noted. The relation of heredity to
phthisis was not noted, except in 1, which was affirmative. In 2 there
was no previous attack of hæmoptysis. The longest interval between the
first and fatal attack was four years: 7 were immediately fatal. From
both collections we have 33 aneurisms of the pulmonary artery in
cavities, 20 being in the left lung; 10 were in the right. Most of the
aneurisms were situated in the upper lobes, as might naturally be
expected. Powell's opinion was that there were good grounds for saying
that the more chronic and quiescent the cavity, and the more unilateral
the disease--the more nearly, in short, it approached the type of
fibroid phthisis--the more probable it was that the hemorrhage, if it
occurred in any quantity, proceeded from a pulmonary aneurism. Taking
15 cases from our list the duration of which could be fairly named, the
average was about seventeen months. The average duration of Powell's
cases was about twenty-four months. Most of our cases were bilaterally
affected, and only 2 were positively stated to have been of the fibroid
variety. Yet, practically, {285} the clinical features enumerated by
Powell form the best standard by which to determine the source of the
fatal hemorrhage. Copious hæmoptysis, with great chronicity and
quiescence of phthisis and cavernous physical signs, points to aneurism
of the pulmonary artery within the cavity.

In the class of extra-pulmonary hæmoptysis are included those cases of
ulceration and rupture of aneurisms of the aorta and its branches into
some portion of the air-passages, and the necessary discharge of blood
therefrom. Experience justifies a classification of this kind. Cases
have occurred where the pulmonary symptoms and signs have been so
prominent as to have obscured those of the coexistent and causal aortic
aneurism until the fatal hæmoptysis revealed the mistake. Still others
of simultaneous tubercular disease of the lungs and aortic aneurism are
reported. J. W. Ogle[60] reports a case where the patient had had cough
for seven years, at first attended with hæmoptysis, dyspnoea, and
palpitation, and afterward consolidation of the left lung, and where
death was produced by rupture of aortic aneurism into the right
bronchus. Bronchitis and pneumonia have been treated without suspecting
the real cause until a similar event occurred. Janeway and Loomis[61]
also give instances of aortic aneurism and phthisical deposits with
doubtful diagnoses in the same persons. We have seen an instance where
illness began with cough, frothy and then purulent expectoration, then
loss of flesh and strength and pain in side, fever to 102, dulness
below right clavicle, and then a number of large hemorrhages, and
finally a fatal one, all of the hemorrhages depending on an aneurism of
the internal carotid artery discharging into the mouth. The chances of
these irregular clinical associations must, then, be borne in mind.
Careful examination only will enable us to eliminate the doubtful
features.

[Footnote 60: _Lond. Path. Soc. Trans._, vol. xvii. p. 104.]

[Footnote 61: _N.Y. Med. Rec._, vol. vii. p. 304.]

In a collection of 33 aortic aneurisms discharged through the
air-passages, 9 had histories of hæmoptysis previous to the last one.
These discharges were more or less copious, and, considering the
physical signs of phthisis obvious in some, and recollecting that
aneurisms were not recognized, the clinical features were such as to
produce if not justify a diagnosis of intrapulmonary hæmoptysis. Of the
33, 16 opened into the left bronchus, 14 into the trachea, 2 into the
right bronchus, and 1 is given without special designation of the point
of communication. Of 2 aneurisms of the arteria innominata, both opened
into the trachea. Aneurisms of the subclavian have also been known to
have discharged through the apex of the lung. These clinical and
anatomical facts point to a large predominance of symptoms and lesions
connected with the left lung where the pulmonary organs are at all
affected. In our own table, while 18 had marked lesions and symptoms
pertaining to the left, only 6 had them connected with the right lung.
These figures are too limited to be decided, but so far as they go they
tend to prove a greater amount of left-lung lesion in extra-pulmonary
than in cavernous hæmoptysis.

So far we have considered the symptoms and classification of phthisical
hæmoptysis. There remain those other forms of pulmonary hæmoptysis
connected with cardiac disease and hemorrhagic infarction. Practically,
these are reduced to the first variety, as cardiac disease is the
question we have most frequently to consider in this connection. We are
justified in assuming the parenchymatous origin of cardiac hæmoptysis,
because it rarely appears until chronic valvular disease has prepared
the way for its occurrence by its well-known degenerative effects on
the pulmonary circulation whereby thrombosis appears, and because at
those advanced periods emboli are often injected into the pulmonary
artery capable of producing hemorrhagic infarction and consequent
hæmoptysis. This latter is accompanied by aggravation of symptoms
already serious--increase of dyspnoea, cardiac perturbation, and
probably cough. If the hemorrhage be copious, shock may appear, and
varies {286} according to the size of the obstructed vessel and the
amount of hemorrhage. The patient may have some premonitions, but not
of the kind noted in the initial hæmoptysis of phthisis, such as the
superficial soreness, burning, or pain localized in the substernal
regions. The hæmoptysis, after it has begun, continues more regularly,
at shorter intervals, and for a longer time, with the coarse appearance
of the blood already mentioned, such as dark, non-aërated, coagulated
sputum. The quantity may equal that from the most typical bronchial or
broncho-pulmonary hæmoptysis in phthisis; usually it is not copious.
Fever is not an ordinary accompaniment, but may develop in consequence
of increased structural lesion, as from pneumonic infiltration around a
large infarction. It has not then the typical range of ordinary
pneumonia, seldom going beyond 100 or 101. The physical signs exclusive
of the primary cardiac lesion are those pointing to limited
infiltration of lung-tissue about the middle or lower region of the
lung. We have limited areas where percussion is dull, almost as much so
as over pleuritic effusion, and where the respiration is very feeble or
suppressed, and later a bronchial breathing adjoining as a consequence
of pneumonic complication. There may be several of these areas, varying
in size. Sometimes the localization by physical signs is impossible
because of the hemorrhage or infarction being small and deep-seated.
Pain becomes a localizing symptom when the infarction is superficial
and the pleura becomes involved. The form of valvular disease most
likely to produce hæmoptysis is mitral disease, especially mitral
obstruction disease.

Beside infarctions originating in cardiac disease there are others of
peripheral origin, as in the puerperal condition from phlegmasia
dolens. Hæmoptysis is a rare symptom in such cases, but when it does
appear it has the same basis. It is seldom severe, and soon merges into
an expectoration of pneumonic character, with the clinical forms of
embolic pneumonia, or possibly of abscess or gangrene of the lung.

PATHOLOGY.--Incidentally, the pathological relations of hæmoptysis have
been already indicated as being connected with phthisis and cardiac
disease--principally with the former. If phthisis be an infectious or
specific disease, as a large and growing professional opinion claims,
hæmoptysis has its specific relations with it. Few symptoms have
greater differentiating force than it has. Its occurrence, outside of
well-known cardiac or dyscrasic disease, removes any case of primary
pulmonary disease from the category of simple inflammation. There may
be much more congestion in bronchitis, more catarrhal products in
simple catarrhal pneumonia, and more fibrinous or croupous exudation in
pneumonia, than in the primary stages of phthisis, and yet no
hæmoptysis appear. The mechanical conditions are present in greater
degree, but the infective element is wanting. Its closest affinity is
with apex pneumonia or alveolar catarrh, yet probably most of such
cases occur without it. A blood-dyscrasia contributes an important
element in the pathogenesis of hæmoptysis.

In cardiac hæmoptysis the pathology is more simple. Extreme mechanical
conditions of obstruction and reversal of the circulation are
reinforced by nutritive changes of the vessels and heart, until the
so-called cardiac cachexia is established. There is no infective
element, and such cases are seldom if ever followed by phthisical
destruction.

MORBID ANATOMY.--Reference has already been made to anatomical changes
having direct or indirect relation to hæmoptysis, such as those in the
blood-vessels. The anatomical basis of the slight hemorrhages of the
early stage of phthisis is seldom if ever discoverable. The belief in
vascular fragility and congestion with special origin rests much more
upon clinical reasoning than demonstration. The large hemorrhages are
now and then fatal within short periods of time or instantly, and we
then have the opportunity of noting the general appearance of the
lungs.

{287} It is notable that cases are not very frequent where the source
of the bleeding has not been found by the most careful search. The
general appearance varies according to the length of time that has
elapsed since the bleeding which preceded death.

In the cases immediately fatal the tubes are filled with fresh blood,
which has stained the mucous membrane and has changed the general
surface of the sections of lung into a dark, mottled, or patchy color.
The greater amount of blood is to be found in the lung from which it
has primarily come, but in the more profuse hemorrhages, and
particularly where there has been time for the struggles of the
threatening suffocation, much blood may either overflow or be inhaled
into the other lung and carried into the extreme portions of the
air-sacs. If the flow be not overwhelming, the patient may survive long
enough to allow other effects from the blood, which has by gravitation
or insufflation been carried into certain parts of the lung. We are
indebted to Reginald E. Thompson[62] for the most important study of
the secondary effects of the blood thus remaining. He says that the
relics of blood are to be found in the presence of hard nodules, often
deeply, though not always, pigmented. They are mostly found at the
summit and middle part of the upper lobe, the middle axillary region,
between the third and fifth ribs, close to the pleura, the anterior
inferior border, and the middle part of the base corresponding to the
summit of the arch of the diaphragm. "Absorption, decoloration, and
fibrination go on; the outlying portions of the blood disappear; the
central nodules become hard and white, and alone remain to show what
has taken place." They are in some cases of varying color, slight red
or of an ivory white, mottled with old blood-pigment, around the
bronchioles especially, and in the shape of small black granules.
Microscopically, they consist of "a group of alveola firmly packed with
a semi-opaque, homogeneous fibrinous material, and there is some
thickening of the alveolar tissue and also of the interlobular tissue,
which thickened tissue forms the limiting capsule."

[Footnote 62: _Op. cit._, p. 46, etc. These researches are an important
epoch in the history of hæmoptysis.]

The ultimate fate of these nodules is variable. Sometimes they go on to
formation of cavities, or softening occurs around the periphery or in
the centre, and leads to general liquefaction of the nodule, or they
may separate from the surrounding tissue by traction. Sometimes the
effect of retention of the blood in the air-passages is a catarrhal
pneumonia, with the ordinary anatomical proofs of it referred to in the
paragraph on modes of termination of hæmoptysis.

Accepting the observations, we have the demonstration of a phthisis ab
hæmoptoe.

The morbid anatomy of cases fatal from rupture of aneurisms of the
branches of the pulmonary artery has been made prominent by the
researches of Rokitansky and Rasmussen.[63] He describes small sac-like
aneurisms and ectasias situated in the vessels running along the wall
of the cavity. The aneurisms have the shape of a bag and an even
surface. The walls of the unbroken aneurisms are of great thickness,
and those of the broken ones thin. The opening is always found on the
most protruding part of the sac; the edges are thin; their size varies
from a pea to a small orange. Powell[64] says a microscopic section
taken from a specimen in an early stage shows new connective-tissue
elements, causing induration affecting the whole thickness of the wall
and obscuring the distinction between the coats. The wall is brittle,
becomes thinner from want of support, and yields to an inciting cause,
with rupture and death as the result.

[Footnote 63: _Edinburgh Med. Journal_, 1868-69.]

[Footnote 64: _Trans. London Pathological Society_, vol. xxii. pp. 54,
55.]

{288} The morbid anatomy of cardiac hæmoptysis is found mostly in two
conditions--that of degenerated, atheromatous, varicose blood-vessels,
brought about by the condition of chronic obstruction and increased
venous tension in valvular disease; and in that of pulmonary
infarction.

The first prepares the way for diapedesis or rupture, and consequent
hæmoptysis. The rupture takes place in the parenchyma, or, as the
anatomical details formerly given make probable, from the blood-vessels
of the bronchial mucous membrane also.

Pulmonary infarction is recognized by a dark, dense, pyramidal or
wedge-shaped area of varying size situated at the surface of the lung,
with the base of the pyramid coming to the pleura. It is found oftener
in the lower lobes and in multiple form. It is caused by an embolic
obstruction of a terminal branch of the pulmonary artery; sometimes by
a thrombosis or by both. A venous reflux from the neighboring districts
is supposed to fill the empty vessel, and after a certain time has
elapsed changes are supposed to have occurred in their walls by which
the blood escapes into the air-cells and interstitial tissue.
Litten's[65] explanation, sustained by his experiments, is that the
venous reflux, after a closure of the pulmonary artery, is by no means
necessary to the formation of an infarction. The infarction fails if
the pulmonary artery and the bronchial artery, and those arteries lying
outside the lungs, but in circulatory connection with them--the
pleural--are simultaneously shut off. If the whole arterial supply be
thus taken away, but a living connection be maintained by means of the
veins, an infarction does not follow, while it immediately follows if,
at the same time with the open veins and closed pulmonary arteries, the
collateral or supplementary circulation be kept free. A venous reflux
cannot occur so long as a circulation in the capillaries of the lung is
sustained by collateral arterial branches. The explanation is that in
an unobstructed circulation the entire resistance which is offered to
the blood-stream in the capillaries of the lung is overcome by the
pressure existing in the pulmonary artery, which, corresponding to the
greater width of the capillaries, is much less than the pressure in the
corporeal arteries. If the pulmonary artery becomes suddenly
impermeable, the pressure in the collateral arteries, which originates
partly from the bronchial artery, and partly from those outside of, but
in connection with, the lungs, as the pleural, etc., is sufficient to
prevent a venous reflux, but not sufficient to overcome the entire
resistance in the lungs and to drive the blood beyond the capillaries
into the left auricle. Then follows an accumulation and stasis of the
blood in the capillaries and smaller veins, and hence results at first
a hyperæmia and later a diapedesis. Litten makes another important
change in Cohnheim's doctrine: he maintains that the hemorrhage appears
before the integrity of the vessel-walls is impaired.

[Footnote 65: _Zeitschrift für klin. Med._, vol. i. p. 148, Berlin,
1880.]

Other fatal cases find their anatomical basis in the softening and
ulcerating processes, which while forming cavities are liable to open
vessels of greater or less size in their walls or trabeculæ.

The condition of the heart in phthisis is one which has an effect in
influencing the occurrence of hæmoptysis. The general statement by
Peacock, that the weight of the heart in phthisis, though less than in
acute diseases, is greater than that in other chronic diseases, needs
to be modified somewhat, as he did not make a distinction between
different forms of phthisis. The more the case approaches the fibroid
variety the more likelihood of some increase of size, particularly in
the right ventricle. Spatz,[66] a later authority, gives as the result
of his examination that phthisis diminishes the size of the left
ventricle--that an absolutely compensatory hypertrophy of the right
ventricle, which is apparent in special cases, does not as a rule
exist, although {289} the resultant decrease does not throughout stand
in relation to the decreased weight and volume of the whole body in
phthisis. The ratio between the depth of the left ventricle and
circumference of the aorta is diminished; and, as this is not
compensated for by hypertrophy of the walls of the ventricle, arterial
tension diminishes and the pulse becomes soft and small. The chance of
rupture of weak vessels by relatively excessive tension is thus much
weakened in the later stages of phthisis.

[Footnote 66: _Deutsches Archiv für klinisch Med._, vol. xxx. p. 154.]

Another element capable of modifying the hæmoptysical features of
phthisis is claimed by Jaccoud[67] as existing in the insufficiency of
the tricuspid valve, which compensates the increased tension in the
field of the pulmonary artery arising from obstruction of a
considerable part of it. The amount of blood passing from the right
ventricle is thus, by a reflux, proportioned to the area of obstruction
in the artery, and the tension is reduced so as to prevent rupture of
the weak vessels. His conclusions are based on 18 cases of measurements
of the tricuspid orifice. They varied from 111 to 130 millimeters. The
evidence obtainable during life was a systolic murmur heard at the
ensiform cartilage and cervical venous reflux.

[Footnote 67: _Clinique médicale_, vol. ii. p. 346, etc.]

DIAGNOSIS is mostly called for with regard to the chances of
hæmatemesis. Inspection of the blood is naturally an early point for
attention. Its bright-red color, frothy look, freedom from extraneous
matter, and its coming up by coughing are strong evidences easily
acquired of its pulmonary origin. Corroborative circumstances are the
family history of phthisis or hæmoptysis, the presence of pulmonary, or
in fewer instances of cardiac, physical signs, the immediately
premonitory symptoms spoken of before. Fever, the age of the patient,
and the continuance of the discharge of blood in its later gradations
of color and mixture of catarrhal elements, inspection of the mouth,
fauces, and larynx, would exclude those possible sources. Each has its
limitations, but together they are conclusive as against hæmatemesis.
Recent and accumulating experience attributes some diagnostic value to
the presence of bacilli tuberculosis in the expectorated blood.
Hiller[68] reports 6 cases of hæmoptysis in which the blood showed in
bacilli: 3 were completely initial. The bacilli were easily
demonstrated by preparations and also by inoculation on guinea-pigs.
They have also been found in the blood of cases of acute tuberculosis
by Weichselbaum.[69] Resort may be had to the well-known tests for the
presence of the elastic tissue of the lung in sputum.

[Footnote 68: _Centralblatt für die med. Wissenschaft_, March 24,
1883.]

[Footnote 69: _Wiener med. Wochenschrift_, No. 13, 1884.]

As positive data for hæmatemesis we have the dark color of the blood,
its firmer clotting, greater density and want of aëration, acid
reaction, the presence of extraneous matters of food and drink, their
ejection by vomiting, and pain or uneasiness at the epigastrium. As
corroborative we have the less frequent occurrence of hæmatemesis, the
individual history of gastric disease, such as ulcer of the stomach or
presence of hepatic cirrhosis from intemperate habits, and the history
of a blow on the abdominal surface: discharges of blood from the bowels
are more likely to occur in hæmatemesis.

Hæmoptysis may be simulated, as by scratches or cuts on some part of
the internal surface of the throat or mouth. The blood is then likely
to be thinned by secretion from the mouth. Inspection would detect the
imposture. The chance of blood from an epistaxis being swallowed and
afterward ejected by vomiting is to be remembered. Cardiac hæmoptysis
is distinguished in most cases by the presence of symptoms and physical
signs of valvular, usually mitral, disease in a considerable degree of
advancement. These are so pronounced as to exclude phthisical disease.
Other and fewer cases occur where the hæmoptysis is the first evidence
of the cardiac disease, and they require a careful exclusion of all the
features of tubercular disease, so as to be able to {290} arrive at a
correct conclusion. There are no conclusive considerations pertaining
to the amount and character of the blood. In the severe and copious
hemorrhages there is likely to be present a marked shock.

PROGNOSIS.--Hæmoptysis usually implies phthisis existing or imminent,
and yet it has in general a favorable effect on its course. This
applies more to its first stage than subsequently, and more to the
small than to the large hemorrhages. The gravity of the small ones
increases in proportion to their frequency. The family and personal
equation is of more importance than the mere quantity. We may have a
slight hæmoptysis and a large increase of the morbid condition
following it, and the reverse, the result depending on the individual
tolerance of and susceptibility to reaction. As in the second stage the
reactive elements are more potent, the small hemorrhages then are less
beneficial. They are the index of activity in the destructive lesions,
and yet may relieve the accompanying congestion. The easiest
appreciable symptom of the progress of the disease is the fever. We may
fail to properly interpret physical signs because of want of
familiarity with the individual case before us. If besides more fever
there be more cough, dyspnoea, and debility, the prognosis increases in
gravity. These remarks will apply with more force to the large
hemorrhages than the smaller ones, and are guides for prognosis in all
the clinical forms of hæmoptysis. In the special clinical form, the
hemorrhagic variety of phthisis, bleedings recur often and in large
quantities during years, and some of the cases end with final recovery.
The fever and constitutional irritation give way under seemingly very
unfavorable conditions. The fact that a great part of them have no
history of heredity, and that they come on at a late period of life,
may account for this, because they thus escape the influences which
heredity and age are known to impose upon the other classes of
phthisical subjects. Some interesting conclusions have been drawn from
the history of cases of profuse hemorrhages. Pollock[70] thinks that
they shorten the duration of the first stage and lengthen the duration
of the second and third. Out of his 351 cases, 204 occurred in the
first three months of illness: 45 had remained in the first stage when
examined, 142 having undergone softening, while 164 had cavities. Of
286 cases of profuse hæmoptysis classified by Williams,[71] the number
of cases in the first stage was 187, and the percentage of deaths was
13.95; 65 cases were in the second stage, and the percentage of deaths
was 24.61; 31 were in the third stage, and the percentage of deaths was
67.74, showing increased effect of hemorrhages upon pulmonary
structures advancing in destructive processes and upon constitutions
being progressively undermined by them. In other clinical varieties the
symptom is so clearly subordinated to the general process that it loses
its prognostic importance in the established disease. There is an
imminence of fatal hemorrhage in many of them, as in fibroid phthisis,
cancer, abscess, gangrene, and hemorrhagic infarction of the lungs. In
extra-pulmonary hæmoptysis or in that from rupture of pulmonary
aneurism there is seldom opportunity for prognosis.

[Footnote 70: _Elements of Prognosis in Consumption_, p. 139.]

[Footnote 71: _Pulmonary Consumption_, p. 150.]

If the condition be recognized, we can but say that the fatal attack is
liable to come at any moment. In cardiac hæmoptysis the hemorrhage is
an event coming toward the close of organic and obstructive changes
which are not much within our control. There are minor degrees, as
shown by expectoration of single small masses of dark coagulated blood
and by the absence of marked aggravation of the symptoms, which do not
prognosticate unfavorably for the immediate, but do show impending
dangers of a future, attack. Morbid anatomy shows traces of a recovery
from a number of premonitory threatenings. The elements of a serious
prognosis are the appearance of a shock, increased dyspnoea, a large
amount of hæmoptysis, increased perturbations in the heart-action, and
increased areas of dulness or râles at certain parts of {291} the lung
other than the usual sites of consumptive disease. These and other
evidences of constitutional initiation are not as available as in the
other varieties mentioned.

TREATMENT.--In the cases of the mildest form very little more need be
done than to keep the patient quiet. His apprehensions may require
attention. They may be allayed by assuring him that the hemorrhage will
be more of a security than a danger, because it is the expression of a
local congestion that will be relieved by the discharge. We have found
that a large dose of quinine (ten or fifteen grains) will answer the
double purpose of a nervous sedative and of controlling the congestion
and hemorrhage if the latter object be necessary. This suggestion
becomes still more applicable in the severe forms of hæmoptysis. The
dose may be repeated within twenty-four hours if needed. If congestion
be manifested by its symptoms of substernal heat, soreness, oppression,
dyspnoea, and cough to a greater degree, and if the hemorrhage is
becoming copious and the hemorrhagic pulse developed, and the
temperature elevated, the necessity of a more active interference is
evident. Absolute quiet in bed, fresh air, a calm and equable behavior
on the part of the family or friends in attendance so that no
excitement may be reflected to the patient, are essential. The
medicines selected should be such as may control the vascular
excitement, and hæmostatics. Ergot will fulfil such indications. It has
its limitations in its unpleasant taste, but it should be pushed to the
points of tolerance. Of the fluid extract one teaspoonful should be
given every hour or two until some effect is observed in slowing the
pulse or checking the hemorrhage. If the stomach rebel, ergotin pills
may be substituted in doses of three to five grains at the same
interval. Should all the resources of ergot medication be required or
the above mode of use fail or disagree, hypodermic injections may be
added. Two to three grains of the extract of ergotin would form a
proper dose, to be repeated every one or two hours. It has been quite
the exception in our experience to have serious irritation follow the
use of it in this way. Failure in this and other uses of ergot will
follow because we do not administer it with sufficient freedom.[72]
Another most valuable hæmostatic is turpentine. It should also be given
freely. From ten to thirty drops in an emulsion or in sugar may be
given every two to four hours, according to tolerance and to the
threatening character of the case. The ergot and turpentine are best
alternated at intervals of one to three hours, according to the
requirements of the attack. Some preparation of opium is often required
to quiet cough--morphine or codeine, one-fourth grain of the former and
one-half grain of the latter, repeated at intervals until their effects
are obvious. By adding the use of broken ice and the external
application of cold compresses frequently repeated, and, if time and
strength permit, the inhalation of persulphate of iron spray twenty or
thirty minims in half an ounce of water, we get a plan of treatment
adapted to the urgent cases. Some recent reports have confirmed the
confidence of the ancients in the use of ligatures. They may be applied
to both lower limbs. A dozen dry cups may be applied to the chest.
There is no occasion or time for the use of many medicines, but if a
general plan, such as the above, must be changed, acetate of lead in
doses of two grains every two hours would be an excellent substitute,
due regard being had to the possible toxic effects from too long
continuance of it in such doses; it is usual to add a little opium to
it. Gallic acid is an effectual remedy for the control of different
kinds of hemorrhages. Like ergot, it is usually given in too small
quantities. Twenty to thirty grains must be given every two to four
hours. {292} It is better borne by the stomach, and can often be
continued longer, than the medicines above mentioned.

[Footnote 72: A medical friend, T. C. Minor of Cincinnati, has in his
own case used three or four drachms of the fluid at a dose, with the
effect of reducing his pulse twenty beats in a few hours.]

We have already noted ipecacuanha as one of the survivals of ancient
practice. It has had warm advocates among modern physicians. Graves
places vivisection first and ipecacuanha next in his plan of treatment.
Trousseau strongly recommended it. Peter and the French practitioners
also strongly endorse its use in the severe forms. We have no doubt of
its efficacy. It is important to exclude if possible the existence of a
pulmonary aneurism or any such source of blooding, as there are no
special means by which this can be done. It is a good rule to use the
ipecacuanha in the cases of early or first-stage hæmoptyses. We would
give it as it is given in dysentery. Precede its administration half an
hour with thirty drops of laudanum, then give ten grains in water. If
vomiting comes on, repeat it in an hour, and again, if hemorrhage
continue, in two hours. The usual experience is that tolerance is
established after two or three doses. It has also an application in
small doses of one-quarter to one-half a grain in the milder forms,
with irritative cough and slight fever.

Graves calls attention especially to the excellent effect of opium in
all kinds of passive hemorrhage, hæmoptysis as well, but insists that
it should be given only after vivisection has been performed or when
the hæmoptysis has become rather passive, or in scorbutic and similar
cases. His direction on one occasion to a physician, in a case of
protracted bleeding of the gums, was, "Go home and give two grains of
opium immediately, and then half a grain every hour until the bleeding
stops." A combination applicable to the persistent bleeding recurring
day by day is the sulphate of magnesia made soluble in rose-water by
the free use of dilute sulphuric acid--one teaspoonful of the former,
fifteen drops of the acid, one-half to one ounce of the rose or plain
water. Many other remedies might be mentioned, and among them atropia.
After the bleeding has ceased it is necessary to be assured as to the
condition in which the lung has been left, and to counteract, if
needed, any persistence of irritation. Fever is the most valuable
evidence as to this point. If it exist, the use of quinia and ergot had
better be continued freely. A three-grain ergotin pill about three
times daily, and five grains of quinia morning and evening, can be
tolerated two or three weeks. Local irritation should be applied if
physical signs or pain warrants it.




{293}

PULMONARY APOPLEXY.

BY WILLIAM CARSON, M.D.


DEFINITION.--Escape of blood into the pulmonary parenchyma, with
laceration of its substance.

SYNONYMS.--Hemorrhage (pulmonaire) foyer (Jaccoud); Diffuse pulmonary
apoplexy or Diffuse pneumorrhagia (Fleich); Diffuse pulmonary apoplexy
(Loomis); Pneumo-hemorrhagie (Gendrin), etc.

HISTORY.--Latour[1] is quoted as being the first to use the words,
"apoplexie du poumon."[2] Yet Duguet[3] also quotes from Frank that
Dolocus had a long time before employed it. It is known that cases had
been described long before this, as by Corvisart in 1808, Allan Burnes
in 1809, among those of this century, and by Prosper Martiano, Bonet,
Morgagni, Haller, etc., among the more ancient authors.[4] Again,
Laennec gives the weight of his authority, and establishes Latour's use
of the name, until, as the synonyms show, modern usage has almost
abandoned it. Among the multitude of those who have treated of
pulmonary apoplexy, we will have filled the requirements of this brief
historical statement by mentioning Virchow and his pathological
investigations into embolism, and also Cohnheim,[5] and later
Litten's[6] studies on infarction, which have some indirect connection
with pulmonary apoplexy.

[Footnote 1: _Histoire philosophique et médicale des Hémorrhagies_,
1815, passage misquoted in _L'apoplexie pulmonaire_ by Duguet.]

[Footnote 2: _Op. cit._, pp. 220, 222, and 224.]

[Footnote 3: _Op. cit._, p. 11.]

[Footnote 4: Duguet, p. 10, etc.]

[Footnote 5: _Untersuchungen über die Embolischen processe_, 1872.]

[Footnote 6: _Zeitschrift für klinisch Medicin_, Erster Band, 131.]

ETIOLOGY.--Predisposing Causes.--The male sex affords predominance of
cases, because of greater liability to accidents, to the various forms
of ulcerative destruction of lung-tissue, and to aneurisms of the aorta
and pulmonary artery.

The adult age is most exposed for similar reasons. Ogston's
statistics[7] support in a general way, but not with strictly technical
force, their quotation by Herz.[8] Omitting the last 4 of his 20 cases
(2 of which were from poisoning, 1 from fracture of skull by a fall
down stairs, and 1 from drowning), the average for males (12) was 56.4,
and 55.3 for females (4).

[Footnote 7: _Brit. and For. Med.-Chir. Rev._, vol. xxxvii., 1866, p.
459.]

[Footnote 8: _Ziemssen's Handbook_, vol. v. p. 298. Ogston says (p.
465) it did not appear, however, that any distinct rent of their
substance had taken place--to any extent, at least. "When we consider
that the area of the extravasation was sufficient to involve often one
or two entire lobes, and that death was in most of them very sudden,
the cases may be adopted as showing the action of causes similar in
kind, if not in degree, to those operative in undoubted pulmonary
apoplexy."]

As more efficient predisposing causes than either age or sex, may be
mentioned aneurisms of the aorta and pulmonary artery, amyloid
degeneration of bronchial and pulmonary vessels, the influence of
Bright's disease in producing disease of blood-vessels, and
atheromatous diseases of the pulmonary artery.

Exciting Causes.--Penetrating and contused wounds of the chest by their
{294} direct mechanical effect, and diseases and injuries of the brain
through the medium of the nervous system, may produce pulmonary
apoplexy, the result in the latter case being usually an infiltration
or small infarction.

SYMPTOMATOLOGY.--Pulmonary apoplexy is the least common of the two
forms of distinctive pulmonary hemorrhage, the other being pulmonary
infarction, already treated of under HÆMOPTYSIS. A proportion of cases
is associated with mitral disease in its most advanced stages. At that
time we may expect pneumorrhagia, but whether from infarction or
apoplectic laceration even the event can only occasionally determine.
In the latter, if hemorrhage makes its appearance it will be copious
and generally overwhelming; at other times the hemorrhage may not
appear, and the patient dies suddenly with possibly other indications
of the internal flow. The physical signs cannot be relied on, for often
the pulmonary tissue is already changed by the long-continued
obstruction of circulation. Rupture of aneurism, particularly of aorta,
in the great majority of cases takes place into a bronchus, and not
into the parenchyma. In case of wounds of the contused variety a
laceration of parenchyma occurs at times sufficient to produce marked
hæmoptysis. If the blood be not ejected, there are no certain
indications of what has happened. If the case be seen immediately after
the accident, such physical signs as moist bubbling râles on the margin
of an area of feeble or suppressed vesicular murmur, possibly attended
with a dull, high-pitched percussion note over that area, would afford
a strong presumption in favor of ruptured lung and consequent
hemorrhage.

The same signs later might be due to a limited traumatic pneumonia. If
the internal hemorrhage, whether traumatic or spontaneous, has made its
way through the pleura, then, if the patient live long enough for
examination, besides such symptoms as great oppression and exhaustion,
the physical signs peculiar to pleural effusion may appear to a limited
degree. This opportunity seldom occurs, as such a rupture produces
almost invariably a fulminant and rapidly fatal result.

COURSE, DURATION, AND TERMINATION.--The course of the lighter cases is
much like that of pulmonary infarction, and that of the severe forms
too brief for observation. As to termination, it is quite possible
there are cases of laceration so limited as to allow complete recovery,
but clinical experience shows that pulmonary apoplexy is usually fatal.

PATHOLOGY AND MORBID ANATOMY.--With branches of the pulmonary vessels
weakened by long-continued heart disease, or with such vessels as are
found with chronic nephritis, a sudden increase of tension in them from
unusual effort or excitement will precipitate a fatal rupture.
Sometimes the progress of the degeneration is so insidious and complete
that a rupture may occur without obvious exciting cause. This is also
the natural history of aortic aneurism. An examination soon after the
laceration will show a mass of blood, usually coagulated, sometimes
partly fluid, lying in an irregular cavity with walls of the lacerated
lung-tissue. After a longer time the lung-tissue beyond the walls of
the hemorrhagic focus becomes oedematous to a certain extent. A
contraction of the cavity, with change of contents, may proceed to the
extent that an encapsuled mass of very small size will remain as the
final result (Rokitansky).

DIAGNOSIS from bronchial hemorrhage by the probable existence of
phthisical conditions and history. The quantity of blood ejected may be
profuse in either case, and therefore be no criterion. From pulmonary
infarction, as the other form of pulmonary hemorrhage, by the larger
amount of hæmoptysis. If there be no hæmoptysis, a presumption would
exist in favor of apoplexy in case of extreme dyspnoea or a fatal
result. The associated diseases or causes being similar, no inference
from the medical history would be reliable except in case of injuries.

{295} PROGNOSIS.--As we meet with it in recognizable form, the result
is almost invariably fatal. A qualification is allowed because of the
experience of such a pathologist as Rokitansky, who describes a process
of cure in a few cases. The prognosis in such would be determined
partly by the severity of the antecedent or accompanying disease, as in
heart lesions, and partly by the increased respiratory distress, pain,
exhaustion, and hemorrhage.

TREATMENT.--As has been before intimated, a case of pulmonary apoplexy
distinctive enough to be diagnosed is usually one that is beyond the
reach of treatment. Remedies that may relieve dyspnoea, exhaustion, and
hemorrhage are those to be relied on. External irritants, as
turpentine-stupe stimulants, ergot, turpentine internally, and such
other remedies as are of known effect in the treatment of the
associated heart troubles and of the incidental pulmonary infarctions.




{296}

ABSCESS OF THE LUNG.

BY WILLIAM CARSON, M.D.


DEFINITION.--A circumscribed suppuration of the lung, resulting in a
cavity.

SYNONYMS.--Abcés du poumon; Lungenabscess.

HISTORY.--The ancients described abscess of the lung, and placed it
among the terminations of the inflammation of that organ. They believed
that if the inflammation did not resolve itself by the fourteenth or
twenty-first day its termination was to be by suppuration. Hippocrates,
Van Swieten, and others are mentioned among those who maintained these
views and consequent frequency of such cases which prevailed until
physical methods and pathological investigation proved their
incorrectness. J. P. Frank, Bayle, and Cayol[1] are given credit for a
partial reversal of this opinion. Avenbrugger,[2] a pupil of Van
Swieten, in describing vomicæ, divides them into two kinds--the
ichorous and the purulent. By the purulent vomica he means an encysted
abscess of the chest resulting from the conversion of an inflamed spot
into a white, thick, glutinous, fatty matter. When these communicate
with the bronchi and discharge any of their contents by expectoration,
they are called open; otherwise, close or shut. He gives symptoms and
signs belonging to the respective varieties. Corvisart, in his comments
on these propositions, says: "In fact, the purulent vomica is always
the result of an inflammation, more or less acute, of the lung." He
makes distinctions between the various kinds of purulent vomica and the
ichorous vomica. Laennec, as in many other subjects of which he
treated, has the credit of placing this one on its modern basis, at
least so far as the frequent termination of pneumonia in abscess is
concerned. Among English writers Stokes deserves especial mention.
Abscess was the fifth and the last of the stages of pneumonia,
according to his classification. He treated largely of the perforating
abscess. Traube, Trousseau, and Leyden are among those who have
contributed largely to the elucidation of the subject. The latter has
especially claimed for this subject a more prominent place in the
literature of practical medicine, and has strongly enforced his views.

[Footnote 1: _Nouv. Dict. de Méd. et de Chirurgie_, tome xxix. p. 394;
and Leyden, "Ueber Lungenabscess," _Sammlung klinische Vorträge_, von
Richard Volkmann, Nos. 114, 115.]

[Footnote 2: _On Percussion of the Chest_, a translation of
Avenbrugger's original treatise by John Forbes, with comment by
Corvisart, 1761-1808, pp. 38, 43, etc.]

ETIOLOGY.--Predisposing Causes.--Everything tending to debilitate the
constitution may become a factor in the production of abscess of the
lung. Senile constitutions, Bright's disease, chronic alcoholism,
diabetes mellitus, and insanity are some of the predisposing causes.

Exciting Causes.--These may be divided, as in the case of gangrene,
into the pulmonary, or those originating in the lung or pleura, and the
intra-pulmonary, or those originating outside of the lung or pleura.
Among the former are included pneumonia and empyema, perforating and
discharging into the {297} lung, or one variety of Stokes's perforating
abscess, pulmonary apoplexy, and suppurating bronchial glands, opening
up a passage through the lung and bronchial tube. Either croupous or
catarrhal pneumonia may be associated with or terminate in pneumonia.
Among the latter, or extra-pulmonary class are included cases of
embolism from the right heart, producing infarction, or from the
systemic veins. These emboli carry with them the productive capacity of
suppuration. Abscess external to thoracic walls, as in deep-seated
mastitis, will at times perforate the walls and enter the lung.
Abscesses of the liver not infrequently perforate the diaphragm, and
are discharged through the lung.

Foreign bodies in the bronchi may ulcerate through them and produce
suppuration of the lung, which may finally open a way externally
through the chest-walls.

SYMPTOMATOLOGY.--The symptoms of abscess of the lung, as may be
inferred from the enumeration of causes, are divisible into two
categories--one including those symptoms with which the abscess may be
associated, but which do not necessarily prognosticate it; and the
other including the symptoms which indicate the abscess as a fact
accomplished. In the simplest and most frequent clinical form, that
following pneumonia, the early symptoms would be those of a severe and
irregular form, as shown by very troublesome and uncontrollable cough
or unusual pain or respiratory embarrassment, high fever, but at that
time fairly typical pneumonic temperature, great prostration, etc.
These may all diminish in due time, and mostly do without suppuration
following. A return of pain, dyspnoea, fever, and general distress
should awaken suspicion, yet they may be the result of an extension of
pneumonia to other portions of the lungs. Rigors and sweats and
increased depression would point to a suppurative process and under
such circumstances to the lung as the locality. We cannot, then,
positively predict an abscess. It is suspected when a more or less
copious eruption of purulent discharge occurs suddenly, and sometimes
the discharge is so abundant and pus-like that any other alternative
than abscess is very remote; at other times the discharge is small in
quantity. The proof of physical cavernous signs is the final step. This
is often difficult. A slightly greater increase of lung-density,
probably at the middle or upper part, with imperfect bronchial
breathing, the appearance of a few moist râles or crepitus, the gradual
increase of these and merging into coarser crepitus, and revelation of
more or less of the cavity signs, is the physical history of many cases
of abscess of the lung. Others have a much more pronounced course, such
as the cases of so-called gangrenous abscess--a sort of connecting link
between gangrene and abscess of the lung. The breaking down of tissue
is ostensibly very sudden, and the cavernous signs are very soon
unmistakable. Other clinical forms are the pyæmia, to be distinguished
by the antecedent history, which will reveal a source for infectious
emboli. The abscesses are usually multiple and small, so that their
precise locality cannot be made out. The proof of infectious
transportation is sudden pneumonic symptoms, as pain, tinged and
finally purulent expectoration. Rupture into pleura may occur and
produce empyema. Rupture of hepatic abscess and discharge through the
lungs is also a clinical form shown by this antecedent event, pointing
to hepatic inflammation. The egress of the pus is sometimes through a
narrow track, and not by a reservoir within the pulmonary tissue; at
other times the lung is really excavated. The discharge of pus is
usually copious and paroxysmal. Leyden recognizes as his third class a
form of chronic abscess, or one coming on during a case of chronic
pneumonia and bearing great resemblance to a variety of phthisis. Its
general symptoms are much the same as in the acute variety,
differentiated by the element of time.

COURSE.--It may be said, in a general way, that the etiology has much
to {298} do with its course. If the cause be pneumonia, the course will
be such as the detail of symptoms already given shows. In some unknown
way the natural course of the disease is interrupted, and what promises
to be an average case is followed by the characteristic features of
abscess. If pyæmia be the precedent condition, a peculiar form of
pneumonia, embolic in origin, appears, and abscesses again follow.
Greater septicity and rapidity of destruction are probable sequences.
The perforating abscesses are subject to modifying influences of
mechanical effect, such as gravitation and the resistance of tissues,
and have their peculiar course, which is often marked by great
chronicity.

TERMINATION.--In the course of seventeen years the reports of the
Cincinnati Hospital show that there have been 6 cases of abscess of the
lung treated there. Of these 4 died and 2 were discharged as improved.
These figures show the infrequency of such cases, and also represent a
greater mortality than probably occurs in the non-hospital class. We
know of no large statistics which show what is the percentage of
recoveries. Our own experience in private practice gives a majority of
recoveries. They were cases following typhoid fever, croupous and
catarrhal pneumonia, and hepatic abscess. A termination in a chronic
cavity now and then happens: perforation of the pleural cavity, with
subsequent pyo-pneumothorax, discharge externally through an
intercostal space, or even extension into the abdominal cavity, are
among the actual events of such abscesses.

DURATION.--The duration of an ordinary case is subject to wide
variations between one and six months. A few cases are recorded of
several years' duration. Previous constitutional condition has much to
do with this element. The degree of infectiousness in the pyæmic class
is important as to time. The abscesses become a subordinate condition
in the fate of the case. In this connection we may also refer to
Leyden's third variety, a so-called chronic abscess.

PATHOLOGY.--A close parallelism, etiologically and otherwise, is
observable up to certain points between gangrene and abscess of the
lung. Both are products of, or associated with, pneumonia. That which
finally determines whether the result shall be gangrene or abscess is
unknown to us. In the article on GANGRENE OF THE LUNG some
investigations are referred to which point to a probable solution in
the existence of specific forms having special pathogenetic force. The
tendency of experimental and clinical investigations is to connect the
suppurative process closely with the product of specific germs. Ogston
in 65 cases of acute abscess found micrococci present in all of them.
Obstruction of blood-vessels in the centre of the pneumonic area or on
the margin of the abscess walls is an important anatomical element in
the production of abscess, and it is claimed that it is often due to
colonies of micrococci within their calibre; so that it is probable
that there are both mechanical and biological or chemical influences at
work. If the view of the zymotic and infectious character of pneumonia
be tenable, the contingency of an abscess developing in its course
would seem not very remote. Yet the proportion of cases of abscess from
pneumonia is not more than 2 per cent. Leyden's high authority supports
the idea of the essential and specific differences in the chemical and
morphological peculiarities of gangrene and abscess of the lung, but
the subject is as yet on a hypothetical basis.

MORBID ANATOMY.--The fresh cavity, generally in the upper lobe, has
rough, ragged, and irregular walls, and may have bridles of the more
resistant structures, as bronchi and vessels, crossing it. Such a
cavity is quite likely to contain portions of undissolved parenchyma or
more or less malodorous pus. The older cavity becomes smoother walled,
and of more regular limits and cleaner contents. A gradation from
granular hepatization through congested to crepitant tissue is almost
uniform in the varieties of abscess, {299} whether simple or pyæmic. In
addition, some peculiarities are observable in the latter. These are
usually several, varying in size from a pea or less to a walnut, some
round and others wedge-shaped; others lying superficially and forming
slight elevations on the pleural surface. In proportion to the curative
progress the cavity will contract and disappear, occasionally leaving
behind a cicatricial mark. A lining pus-secreting membrane will
sometimes form, resulting in such a limitation of morbid action and
such a disappearance of reactionary symptoms as to make the disease
entirely local, but quite chronic.

DIAGNOSIS.--The more or less sudden and copious expectoration of pus,
without a specially offensive odor, in the course of a case having up
to that time the history of a pneumonia, would be considered as due to
the development of an abscess in the lung. Some degree of fetor in
breath and expectoration is observed, but it is far different from that
of gangrene. The detection of the débris of lung-structure in coarse
particles, and the microscopic discovery of elastic lung-tissue, are
important diagnostic points in contradistinction from the solution of
tissue that gangrene usually effects upon the parenchyma of the lung.
According to Leyden's[3] very complete investigations, the microscope
reveals fatty crystals, mostly in roundish fragments, of the size of
the epithelium of the lung and of a brilliant structure; pigment-débris
of a yellowish-brown or brownish-red color; hæmatoidin and bilirubin,
which Traube thought were due to hemorrhagic infarction, but which
Leyden has observed in all of his cases; and, lastly, micrococci, in
the well-known form of the round, granular micrococci colonies, which
differ from those in gangrenous fragments in that they show very little
movement and do not give the iodine reaction.

[Footnote 3: "Ueber Lungenabscess," _Volkmann's klin. Vorträge_, p.
994.]

Difficulties of diagnosis arise in the case of an empyema discharging
through the bronchi, or of an encysted empyema discharging through the
third or fourth intercostal space in front; also, between abscess of
the superior portion of the liver and one in the base of the lung, or
between the latter and a pyo-pneumothorax. Very careful study of the
history in each case is of the first importance. Where this is not
attainable the difficulty is often much increased. In the case of the
empyema the discharge is more profuse at each time, the whole amount in
a given period is much greater, and the time of opening is much delayed
beyond that of the pneumonic abscess. Trousseau gives the case of a
child who brought up for more than six months 200 grammes of pus daily.
He makes children an exception to the rule as to the late opening of
the pleural abscesses. In the encysted empyema discharging either
internally or externally the difficulties are greater. A portion of the
lung-tissue may be so near behind the deposit of matter as to make the
physical signs confusing if the pus has opened externally. Some of
these and of the interlobular deposits it is almost impossible to
diagnose.

In hepatic abscess opening into the lung and bronchi the discharge is
copious, dirty brown, paroxysmal, and will generally, on careful
observation, show the bile color or its chemical reactions or some
microscopic débris of the liver. In Leyden's third class, or the
chronic abscess arising in the course of chronic pneumonia, the history
is so much like that of some forms of phthisis as scarcely to serve in
diagnosis. He thinks there are some macroscopic and microscopic
appearances which may serve for diagnosis. There are in the
expectoration dark and compact pieces of greenish-black color, not
unlike plugs of pus, and larger, black-pigmented fragments of
parenchyma, from a pin's head to a hempseed in size. Microscopically,
they consist of a close and strongly-pigmented parenchyma, which seldom
reveals alveolar structure. They show fatty degeneration and
cholesterin plates. This class of cases is mostly without fever. The
application of the bacilli-tuberculosis test would seem to offer some
assistance in diagnosis.

{300} PROGNOSIS.--A grave prognosis may be formulated if there be a
history of feeble constitution, and especially if it be further
impaired by habits of intemperance, if the patient belong to either
extreme of age, if there has been a recent debauch, or if there be wide
variation from the typical form of pneumonia. Variations will be shown
in such a complexus of symptoms as follows: fever of low grade, subject
to extremes in range; feeble and frequent pulse, but not so marked as
in gangrene of the lung; dyspnoea, objective and subjective; typhoid
depression; tongue dryish; delirium; copious and fetid or difficult
expectoration; physical signs of extensive lesion, such as a large
cavity with a large outlying pneumonic area. A favorable prognosis
would be conditioned on the appearance of a fewer number of these
symptoms or on their evolution in a milder form.

The capacity of the patient to endure a long-continued suppurative
discharge is principally determined by his natural vigor and his
ability to assimilate food, other elements, such as extent of injury to
the lung, being the same. A well-defined superficial cavity would be
more favorable, because within surgical relief.

In the pyæmic variety the force of the infectious element will
determine largely the result. Chills and sweats are important
prognostic elements in such a case.

In the secondary abscesses of either the empyematous or hepatic variety
prognosis is grave--more so in the latter than in the former, because
surgical procedure would be more promising in the former, and because
of the implication of an organ so liable to destructive inflammation as
the liver. A long and tedious course of suppuration is possible in
either. The dangers in an established abscess arise from liabilities to
septic infection and exhaustion consequent on want of reparative power
and persistent suppuration.

TREATMENT.--The treatment of abscess differs little if at all from that
of gangrene of the lung. The tendencies of the two diseases toward
exhaustion and infection are similar, but are less pronounced in the
former. The same remedies are necessary in both, such as stimulants,
tonics, antiseptics, anodynes, and expectorants internally, inhalations
and drainage externally; brandy and malt liquors as stimulants;
nourishing and concentrated food at frequent intervals; quinine as
tonic and antiseptic; carbolic acid and turpentine as most valuable
antiseptics (the latter being also an excellent stimulant); eucalyptus
in cases of profuse as well as fetid discharge; carbonate of ammonia,
senega, as expectorants; morphine and codeine or anodynes to control
cough; carbolic acid for inhalation; and in cases of definitely
localized cavities a free opening to be made with antiseptic
injections.

Successful cases of surgical interference are reported, and such
treatment is now recognized as proper when the system is giving way
under septic poison, evinced in chills, sweats, and great prostration,
where the purulent discharge is fitful and imperfect, and where the
physical signs are clear enough to show the locality of the abscess.




{301}

GANGRENE OF THE LUNG.

BY WILLIAM CARSON, M.D.


DEFINITION.--Putrid necrosis of the lung-tissue.

SYNONYMS.--Lungenbrand, Gangrene du poumon, Gangræna pulmonum.

HISTORY.--By common consent, Laennec has the credit of first
identifying, naming, and classifying gangrene of the lung as a distinct
disease; yet Lieutaud[1] in 1707 describes imperfectly a case of
gangrene of the lung in a child: "the right lung, within and without,
appeared entirely putrid." Bayle[2] is considered, in his section on
his fourth variety of phthisis (phthisis ulcereuse), to have described
a rather chronic form of gangrene of the lung. Morgagni, Boerhaave,
Stoll, J. Frank, and Cullen considered gangrene as one of the
terminations of peripneumonia.[3] Laennec's development of the subject
has only in a few directions been enlarged. His classification is
universally adopted. His description is adopted generally as the most
complete. There have been, however, controversies on different points,
such as the relation of pneumonia and of the obstruction of the vessels
to gangrene of the lung.

[Footnote 1: _Historia Anatomica Medica_, 1787, Obs. 329, cited by
Louisa Atkins, 1872.]

[Footnote 2: Bayle, G. L., _Recherches sur la Phthisis pulmonaire_,
1809-10, p. 30.]

[Footnote 3: I. Straus, _Nouv. Dict. de Méd. et de Chir._, p. 403,
etc.]

In the pathology and etiology of gangrene Virchow's investigations on
embolism and thrombosis opened up important relations; in diagnosis,
Traube and Leyden and Jaffee; in medical treatment, also Traube; and in
surgical treatment, Haley and Lawson (1879),[4] S. C. Smith (1880), E.
Bull (1881), Fengar and Hollister (1881), Mosler and Voght (1882). The
antecedent development of pulmonary surgery, through important work
done by Mosler, Pepper, and others, had prepared the way for special
applications of it to gangrene and abscess of the lung. Spencer Wells
claims to have suggested similar proceedings nearly forty years ago.

[Footnote 4: _Lungen Chirurgie_, Mosler, xx. p. 67.]

ETIOLOGY.--Predisposing Causes.--Constitutional weakness is a common
predisposing influence: it may be a primary condition, but is more
often secondary or dependent on some recently-acting debilitating
cause, as typhoid fever, chronic lung disease, diabetes, etc. Chronic
alcoholism is a cause which, besides its effect on the system at large,
may add a special one on the lungs in producing hyperæmia or drunkard's
pneumonia.

Of 46 cases we have collected mostly from the Vienna Hospital report,
the youngest was nineteen years old and the oldest was forty-seven
years. Lebert[5] has collected altogether 60 cases, 32 of his own and
28 of others: 19 occurred between twenty and thirty years, and 1
between thirty and forty. Huntington[6] gives 32 cases from the
Massachusetts General Hospital Record between 1857 and 1875: 9 were
between twenty and thirty years, and 12 between thirty and forty; the
youngest was ten years old and the oldest sixty-four. It is noticeable
that these figures coincide largely with those {302} showing the
incidence of phthisis. Louisa Atkins[7] gives, as the youngest ages
among all the varieties, one of three months and another of two months.

[Footnote 5: _Klinik der Brustkrankheiten_, vol. i. p. 827.]

[Footnote 6: _Boston Med. and Surg. Journal_, vol. xcv. p. 486.]

[Footnote 7: _Gangræna Pulmonum bei Kindern_, 1872.]

Of the 46 Vienna Hospital cases, 43 were male and 3 female.
Huntington's cases were males 24, females 8. Of Lebert's own 32 cases,
22 were males; of the 32 others summarized by him, in 4 sex was not
mentioned, and of the remainder 17 were males and 11 females. These
figures show the large predominance of males in the liability to
attack.

Exciting Causes.--They may be classified as pulmonary and
extra-pulmonary. The influence of the alcoholic habit has been referred
to above among predisposing causes: debauches are a frequent
antecedent, especially in hospital cases, by means of resulting
pulmonary hyperæmia and drunkard's pneumonia. Its association with
croupous pneumonia may be assumed as settled after some warm disputes.
The pneumonia of Bright's disease and putrid bronchitis are
occasionally causative; bronchiectasies result in it not unfrequently.
Extension of diphtheritic inflammation from the tracheal and bronchial
mucous membrane is another form. The catarrhal pneumonia secondary to
measles may produce it in children.

Embolism is the most frequent cause in the class of extra-pulmonary
causes. It may be mechanical or infecting. A bronchial artery may be
plugged so as to produce a gangrenous slough from mechanical cutting
off of nutrition. Embolism of the pulmonary artery branches is more
frequent, and by bringing about infarction and apoplexy may produce
gangrene. Of the infecting variety may be mentioned emboli from the
peripheral veins, as in surgical or uterine phlebitis, or from cerebral
sinuses secondarily involved from otitis. Other causes acting from
without on the lungs are foreign bodies, as particles of food passing
beyond the trachea into the lungs, as in case of the insane or
drunkards, and blows on the walls of the chest. These latter are
capable of producing not only the ordinary phenomena of
contusion-pneumonia[8] but gangrene, and without evidence of external
injury or fracture of the ribs.

[Footnote 8: M. Litten, p. 26, vol. v., _Zeitschrift für klinische
Medicin_.]

SYMPTOMATOLOGY.--Gangrene of the lung is the termination of a process
the beginning and progress of which are not declared or cannot be
followed through characteristic symptoms. Even its final occurrence may
remain unknown if a communication be not established with a bronchus,
which event is followed by the true symptoms, the expectoration and its
odor. Whatever symptoms occur previous to that event may occur
independent of it. Adopting Lebert's dictum,[9] gangrene of the lung is
not a pathological unit. As its pathogenesis varies, so does its
symptomatology. A feature common to its several varieties is marked
constitutional depression and variations from the typical form of the
disease in which it occurs. If pneumonia, croupous or catarrhal, be the
precedent or associated disease, it will be marked by soft and feeble
and frequent pulse, restlessness, dulness or distress of countenance,
more or less cyanosis, cool and relaxed skin, possibly delirium, dry
tongue, unusual dyspnoea and pleuritic pain, copious prune-juice
expectoration, irregular or non-typical temperatures. Along with these
functional variations occur some in physical signs, as a lesser amount
of dulness or of bronchial breathing, indicative of less structural
density and corresponding exudation. A case with such an evolution may
afford a presumption of an outcome in gangrene, but appearance of the
characteristic expectoration and fetor is necessary to exclude it from
irregular forms of pneumonia, which have no such termination. The same
general remark applies to the cases of gangrene in bronchiectasic
cavities. Perhaps some aggravation of the general condition may excite
apprehension, but the characteristic phenomena of expectoration, odor,
etc. must decide. If the cause be of embolic origin, we {303} may
expect some suddenness and perhaps shock in the beginning, and later
the evidences of a more limited inflammation of the lung-tissue, such
as circumscribed dulness and modified respiratory sound, which finally
end in those indicating destruction of lung-tissue.

[Footnote 9: _Op. cit._, p. 803.]

The macroscopic characters of the expectoration are those of a putrid
or fetid liquid of varying shades of color, ashy gray, dirty green, or
greenish-yellow, prune-juice, or more or less hemorrhagic. The odor,
which is at first so fetid and penetrating, often disappears after the
expectoration has been standing a while. It is separable, as first
described by Traube,[10] into three principal layers. The uppermost,
covered with a layer of foam, consists of, first, dirty green,
crumbling, confluent lumps; second, of larger, homogeneous, green
muco-purulent masses; and, third, of whitish-gray, transparent, mucous
masses. The second layer is formed of a colorless fluid. At the bottom
is a fine yellowish-white sediment. Microscopically are found fat-acid
crystals, many large fat-drops, and finely granular débris, masses of
free, black pigment. It is said elastic tissue is nowhere to be found,
but to this statement there are no doubt exceptions. Other bodies have
been found by Leyden and Jaffee,[11] which they named Leptothrix
pulmonalis. Kannenberg,[12] besides the above forms, found constantly
infusoria of the family of monads in the sputa of 11 out of 14 cases of
pulmonary gangrene. He considers them peculiar to the processes of
decomposition in the lungs.

[Footnote 10: _Gesammte Beiträge zur Pathologie und Physiologie_,
Zweiter Band, p. 452, etc.]

[Footnote 11: _Deutsches Archiv für klin. Med._, Band ii. pp. 488,
etc., "Ueber putride Sputa."]

[Footnote 12: _Virchow's Archiv_, Band lxxv.; _Zeitschrift für
klinische Med._, Band i. p. 228.]

PROGNOSIS in general is unfavorable. Individually, the gravity of the
case is determined by the evidence bearing on previous habits and
constitution; by the violence of the onset, as shown in prostration,
severe pain in the chest, dyspnoea, persistent and violent cough,
delirium, feebleness and softness of the pulse; by the variations from
the typical standards of croupous, or especially catarrhal, pneumonia,
such as greater amount of septic or infectious or typhoidal element,
non-typical and low temperatures in the early stages and also in the
stage of disintegration; by the amount of the latter as shown in the
physical signs of extensive lesion and in the amount of gangrenous
sputum; and by the irritant effect of this in producing bronchial
catarrh, and consequent catarrhal secretion, which may of itself become
an element of danger in a system already much prostrated. Favorable
prognosis is allowable when these conditions are being gradually
reversed.

PATHOLOGY.--The pathology of gangrene of the lung is scarcely more
settled than it was forty years ago, when Stokes[13] published his
eighteen propositions, embodying his experience. Obstruction of vessels
and inflammatory exudations are present as important pathological
conditions, but of themselves are not pathogenetic of gangrene. Other,
as yet unknown, elements of putrefactive agency are present. Leyden and
Jaffee's observations and those of Kannenberg have been mentioned[14]
as efforts to throw light upon the pathogenesis of gangrene of lung,
but how far the bodies described by them precede, coincide, or follow
the familiar clinical phenomena are undetermined questions.
Filehne,[15] in his experiments to determine the reason of the almost
universal absence of elastic fibres in the expectoration of patients
with gangrene of lung, comes to the conclusion that there is a ferment
which, acting under alkaline conditions, destroys the fibres. The
agents of this ferment he does not try to determine. Stokes anticipates
the tendency of modern experimental pathology by announcing as an
alternative proposition that "a process of putrefactive secretion
precedes in many cases the death of lung." The constitutional debility
which is so early a symptom prepares the way for such {304} an
invasion. In reference to the relation between the septic material and
thrombosis in gangrene, Kohler[16] affirms that the septic material
produces the fibrin-ferment, and thereby capillary thrombosis.
Recklinghausen thinks that a special material capable of exciting
coagulation has not yet been found in gangrenous substances, but that
there may be several factors, such as anæmia, changes in the
vessel-wall, imbibition with foreign substances, etc. Other
experiments[17] and views point toward the conclusion that there are
substances formed in various diseased conditions which have the power
of ferments and of producing coagulation of blood in the lesser
circulation.

[Footnote 13: _Dublin Quarterly Journal Med. Science_, Feb. 1, 1850.]

[Footnote 14: _Op. cit._]

[Footnote 15: "Sitzungsbericht der Phys. Med. Soc." in _Erlangen
Schmidt's Jahrbucher_, 1877, No. 7.]

[Footnote 16: _Recklinghausen's Handbuch der Pathologie_, p. 136.]

[Footnote 17: Wooldridge, Du Bois-Reymond, _Archiv Centralblatt für
med. Wissenschaften_, No. 41, vol. xi. 1874, p. 734.]

MORBID ANATOMY.--The circumscribed variety, as it usually appears, is a
cavity irregular in outline, with ragged walls, made so by the unequal
invasion of the lung-tissue by the gangrenous process. Sometimes the
cavity itself contains loose fragments of lung-tissue, or the contents
may be of a dirty, greenish, or brownish color, with some of the odor
of the expectorated matters. If the case has been a chronic one, the
walls are smoother, with a more or less formed lining membrane and the
contents of a less characteristic color or odor. The cavity is usually
in the right lung, and in the middle or lower portion. There is much
variety of statement on this point. The tissue immediately adjacent to
the gangrenous walls shows more or less of the products of catarrhal
pneumonia. The vessels terminating in the walls are obstructed by
coagula. If the gangrenous part come to the pleural surface, belonging
to what Fournet calls the superficial variety, it may produce adhesions
there, or it may result in perforation, with the result that we have
the products of pleuritic inflammation united with the contents of the
gangrenous cavity. In multiple foci, some will show the less advanced
stages of disease, such as incomplete softening and local inflammatory
lesions. In the diffused variety the lesions are sometimes described as
being the same except in extent. The demarcations, however, from
surrounding tissue are not as well marked; the tissue is soft, breaking
easily under pressure, sometimes oedematous, dark or dirty black on
surface or on section of lung; at other times the surface is mottled
with lighter-colored patches. A secondary result is the production of
bronchitis by the contact of the irritant expectoration from the
gangrenous cavity.

DIAGNOSIS.--Abscess of the lung is the disease most likely to be
confounded with gangrene of the lung. In the former you do not have the
same amount of profound constitutional depression; the symptoms have a
more frank expression, as it were, because of better precedent
conditions usually; the first eruption of matter from the abscess is
more copious and sudden than the usual manner of expectoration of
gangrenous sputum; the appearance of the contents of the abscess is
that more nearly of healthy pus, though the latter has at times a dark
dirty brown or hemorrhagic look; the separation into layers is not apt
to occur; the odor is usually not so fetid; microscopically, elastic
fibres are much more abundant in abscess than in gangrene of the lung.
The cavernous physical signs are not reliable in either disease. There
are cases in which it is impossible, and in which it is of no practical
importance, to make a diagnosis between gangrenous abscess and
pulmonary gangrene. Gangrene supervening in phthisical cavities is
distinguished by the history of a chronic pulmonary disease in which a
cavity has been previously marked. It is phthisis advanced to the
destruction of tissue plus the unknown gangrenous element which has
found a lodgment in a favorable place. Stagnation of cavity contents,
depression of system, etc. are favoring conditions. The same remarks
apply to bronchiectasic cavities and putrid bronchitis, physical signs
in the latter being additional points of difference.

{305} Our experience proves that the essential SYMPTOMATOLOGY of
gangrene of lung, except the débris of lung-structure in the sputum,
can occur where there was no gangrenous destruction, either
circumscribed or diffuse, no bronchiectasic cavities or bronchial
dilatations, and no phthisical cavity. In the case alluded to the
gangrenous odor and general characters of the sputum and the separation
into layers and the consolidation of tissue were present, but the
post-mortem afforded no explanation of the fetid expectoration. It was
a case of debauch and alcoholic excesses and exposure.

COURSE, DURATION, AND TERMINATION.--The course of this disease is
essentially an acute one. Whatever the early condition be, the
gangrenous element hastens its progress, as in cases beginning with the
phenomena of acute pleuro-pneumonia. A pre-existing phthisical cavity
will take on acute phases, also the septic element will be reinforced,
and, as indicated in the enumeration of symptoms, clinical
irregularities will be introduced. The early prostration is increased,
and the patient dies from exhaustion after a period varying from three
days to six weeks from the time the gangrene became manifest. Various
complications, such as pleuritis and perforation of pleura and
pneumothorax, hemorrhage, or extensive, diffused gangrene may cut short
the patient's life within the average period. Occasionally the
gangrenous cavity becomes chronic and the patient may live for months
in imperfect health. The termination of the circumscribed variety is
usually death. Diffuse gangrene is invariably fatal.

TREATMENT should be directed, first, to the known precedent states of
constitutional weakness, bad habits, etc., which lay a foundation for
unhealthy inflammatory processes, and for the pathogenetic elements
that bring about the gangrenous and septic and exhausting conditions;
second, to the special symptoms, such as severe pain in the side,
harassing cough, dyspnoea, etc. Remedies of the first class are quinia,
turpentine, early alcoholic stimulation, carbonate of ammonium,
antiseptics, as carbolic acid, etc. An anticipation from the beginning
of any irregular form of acute pulmonary disease of its termination in
gangrene is impossible, and hence early treatment is necessarily
general. It would be properly confined to the use of quinia, which
would be useful, either before or after the gangrenous element had
developed, in small doses frequently given, unless high temperature or
the septic process indicate the use of large ones. Turpentine
internally is desirable in proportion to the infectious or typhoidal
character of the attack. Its use by inhalation is beneficial when
gangrenous destruction has already taken place. Brandy or whiskey in
moderate and frequent quantities, one-half to one tablespoonful every
three hours, and carbonate of ammonium, meet the requirements which the
tendencies to debility indicate. Milk, milk-punch, beef and chicken
extracts should be given in the intervals between the administration of
medicines. This general plan is applicable throughout the pre- and
post-gangrenous stages. In the symptomatic treatment pain and a general
respiratory distress often demand attention. Opium is then useful, both
in relieving pain and moderating dyspnoea and cough. As these symptoms
are often urgent in the later stages of gangrene of the lung, the
treatment of the disease harmonizes both in its constitutional and
symptomatic aspects. Prescriptions can also be readily prepared which
contain remedies that have a decided effect in correcting the fetor of
the breath and expectoration, and thus evincing an influence on the
putrefactive process or ferment, which has become the prominent feature
of the disease. The author recommends that carbolic acid, in the dose
of one grain every four hours, be given for that purpose, and also its
use by inhalation. Assistance can sometimes be given by putting the
patient in such a position on the side as to promote the emptying of
the cavity.

Tapping a gangrenous cavity and the introduction of drainage-tubes may
be successfully resorted to. The cases suitable for such surgical
treatment have {306} been described by Fenger and Hollister[18] as
those where, "the presence of a gangrenous or ichorous cavity having
been ascertained, it is found that notwithstanding an outlet through
the bronchi for a portion of the contents of the cavity, it steadily
fills up again; the partial evacuation does not relieve the patient;
the infection of the healthy portions of the lung from the decomposed
contents of the cavity has commenced or is evidently about to take
place; the breath and expectoration continue fetid; absence of
appetite; increasing weakness, with or without fever, etc." For the
steps of the operative procedure reference may be made to the complete
directions given by the same authors or to works on surgery. The double
opening advised by the above authors would be the most efficient plan.

[Footnote 18: _Amer. Journ. Med. Sci._, Oct., 1881, p. 385.]




{307}

CROUPOUS PNEUMONIA.

BY ALFRED L. LOOMIS, M.D.


SYNONYMS.--English and American: Acute sthenic exudative pneumonia;
Primary lobar pneumonia; Vera peripneumonia; and Pneumonitis. _Fr._
Fluxion du poitine and Fièvre pneumonique; _Ger._ Pneumonia lobaris and
Lobäre Lungenentzündung.

DEFINITION.--Croupous pneumonia is an acute general disease with a
characteristic local pulmonary lesion. Anatomically considered, it is
an acute inflammation of the vesicular structure of the lungs,
resulting in infiltration of the alveoli, with inflammatory products,
which renders them impervious to air. This condition is known as
hepatization.

HISTORY.--Until the time of Laennec, pneumonia and pleurisy were
described as one disease. Hippocrates said that pleurisy was "a disease
quickly fatal, and characterized by sputa of various colors." Although
these two diseases were undifferentiated, accurate descriptions of the
lesions and objective signs of pneumonia have come to us from the
earliest medical writers.[1]

[Footnote 1: Thucydides, _The Plague at Athens_, B.C. 430.]

Much of the early history of this disease is interwoven with the
detailed accounts of a great variety of pulmonary symptoms which
occurred in the epidemics and plagues which prevailed in Eastern Europe
in the centuries just preceding the Christian era, and in Western and
Southern Europe during the sixteenth and seventeenth centuries. The
black death has been regarded by some as an epidemic of pneumonia.
While it is probable that in most of these epidemics the lung was early
involved, and that its implication hastened death, yet no proof exists
to sustain the belief that they were other than epidemics of typhus
fever, dysentery, and those (as yet unknown) fevers which collectively
were named plagues. That many of these plagues were complicated by
pneumonia there is scarcely room for doubt.

French investigators were the first to separate the pneumonic process
from all other morbid processes which occur in the thoracic organs.
Valsalva, Morgagni, and Boerhaave gave accurate descriptions of
pneumonia, but they did not sharply distinguish it from pleurisy.
Bichat and Pinel separated collapse of the lung attending pleuritic
effusion from inflammation of the lung-substance.[2] Laennec was the
first to draw the line sharply between pneumonia and pleurisy, and to
him, more than to any other observer, is due the credit of describing
pneumonia as a distinct disease. With his labors begins a new era in
the history of pulmonary inflammations.

[Footnote 2: _Nos. phil._, ii., Pinel.]

Grisolle's work[3] is especially valuable in statistics relating to the
climatic element in the development of pneumonia and its comparative
frequency among different races. The elaborate treatise on the
geographical distribution of pneumonia by Ziemssen has furnished data
for a more accurate knowledge of its geographical boundaries. Following
in the footsteps of Laennec, {308} Chomel, Stokes, Addison, and many
laborers of our own day have furnished the material from which the
clinical and pathological history of pneumonia is now being
constructed.

[Footnote 3: _Traité de la Pneumonie_.]

Recently, Jürgensen has strongly advocated the infection theory of
pneumonia, and has presented strong arguments in support of his
opinions. Sturges of London and Cohnheim[4] advocate the use of the
term pneumonic fever, and the former gives a most interesting general
comparison between it and the affections which he regards analogous to
it. Careful pathological experiments have recently been made by
Heidenhain, Sommerbrodt, Schuppel, and Klebs[5] with a view to
establish the germ-theory of pneumonia.

[Footnote 4: _Leçons de Chir. méd._, 1877, p. 17.]

[Footnote 5: _Arch. für experiment. Pathol._, p. 420.]

The literature of the past ten years is richer in the development of
facts and experimental investigations than all the centuries that have
preceded; and these recent experiments, combined with modern statistics
and the results of the microscope in pathological histology, have given
to croupous pneumonia a separate and distinct place in the list of
pulmonary diseases.

MORBID ANATOMY.--Anatomically as well as clinically, there are three
recognized stages in croupous pneumonia: 1, Stage of engorgement or
congestion; 2, Stage of red hepatization; 3, Stage of gray
hepatization, resolution, or purulent infiltration (suppuration).

It has been claimed that the stage of engorgement is preceded by a dry
stage, or "stage of arterial injection," in which the lung-tissue is
dry and of a bright-red color. It is evident that congestion of the
minute branches of the pulmonary artery would not give to the
lung-tissue a bright-red color, and if such a condition exists it must
be due to injection of the bronchial vessels. It is by no means proven
that such injection ever precedes pneumonic engorgement. In the stage
of engorgement that portion of the lung which is involved in the
pneumonic process does not collapse when the thoracic cavity is opened.
The affected portion of lung is distended and firmer than normal
lung-tissue, and when pressed upon crepitates less, often remaining
indented after the pressure is removed. The lung is not entirely
airless, for by pressure the air can be forced from one portion of it
to another. Its color is darker than normal, usually being of a
brownish-red or purple. There is an increase not only in its actual
weight, but in its specific gravity. On section a thin, frothy,
blood-stained serum exudes, and sometimes on pressure flows freely from
the cut surface; occasionally this exudation is tenacious. When alcohol
is added to this fluid, it coagulates into a granular, amorphous mass.

The capillaries around the air-cells are distended, and dark blood
oozes from their divided ends. Occasionally, upon close examination,
there may be seen beneath the pleura and between the air-sacs small
points of blood-extravasation. A portion of lung in this stage, when
placed in water, does not float as near the surface as healthy
lung-tissue.

When examined with the microscope, the lumen of the alveoli are seen to
be diminished by the encroachment of the varicosed and tortuous
capillary vessels. As a rule, the air-sacs are uniformly dilated; some,
however, may be collapsed--a condition probably due to pressure during
the early period of the pneumonic process. The epithelia of the alveoli
are swollen, and contain a granular protoplasm with free nuclei. The
air-vesicles also contain exfoliated epithelial cells and white and red
blood-corpuscles. The serum which escapes into the alveoli from the
distended capillary vessels is the fluid in which these cell-elements
float. Since the enlarged epithelia often suffer a division of their
protoplasm, embryonic mono-nucleated cells are intermingled with the
other elements. It is still a disputed question whether the bronchial
or the pulmonary capillaries are the chief source of the pneumonic
exudation.

Physiology teaches that lung-tissue is nourished by the blood in the
{309} ramifications of the bronchial arteries, and that the pulmonary
capillaries are the passive media for the interchange of gases. Hence
it is claimed that the bronchial capillaries only are implicated in the
inflammatory process. Virchow has shown that the pneumonic process can
be completely established in places where pulmonic capillaries cannot
be traced on account of the plugging of a large branch of the pulmonary
artery;[6] yet even he admits that secondarily the pulmonary vessels
have much to do in the inflammatory process.

[Footnote 6: _Ges. Abhang._, p. 369, Virchow.]

On the other hand, it is claimed that in the early stages of the
pneumonic process the parts that are supplied by the bronchial
capillaries are not reddened or injected, as they would be were these
vessels primarily concerned in the inflammatory process. Reasoning from
the above, it would seem that both sets of vessels are involved, but
that usually one set is implicated at the very commencement to a
greater extent than the other.

It is often difficult, and sometimes impossible, to differentiate
between the anatomical appearances produced by pulmonary congestion and
oedema and the first stage of pneumonia. In pulmonary congestion and
oedema the fluid in the alveoli is serum, and contains none of the
pathological cell-elements found in the first stage of pneumonia. The
alveolar capillaries are turgid, and in this respect resemble the
capillaries in pneumonic congestion, but when a stream of water flows
over a portion of lung in the first stage of pneumonia its dark color
remains, while in hyperæmia of a non-inflammatory character this is not
the case.

On account of its color and its resemblance to liver-tissue the name
red hepatization has been given to the second stage of croupous
pneumonia. The lung in this stage has a dark liver or mahogany color,
and is slightly mottled, the mottling becoming more marked the farther
advanced is the hepatization. The color is of a brighter red when the
lung is first removed from the body than after it has been exposed to
the air.

The volume of the lung is increased--at times so as to bear the impress
of the ribs. It is solid and firmer than normal; pressure does not
indent but tears it; it is very friable, and its torn surface presents
a granular appearance. Its specific gravity is increased. It is
airless, and there is an entire loss of crepitation.

Upon section it is seen that the granular appearance of the cut surface
is due to the pneumonic exudation which fills the alveoli. This
granular appearance is not so well shown on the cut as on the torn
surface. The granules can be readily removed from the air-cells by
means of a fine needle. A dirty, red, viscid fluid slowly oozes from
its cut surface, which is more apparent after the lung has been exposed
to the air for twelve or twenty-four hours and has undergone
post-mortem changes. At any time this viscid, rusty-looking material
may be scraped from the cut surface, or it exudes when a portion of the
lung is firmly compressed. A portion of the inflamed lung quickly sinks
in water, and small spots of blood-extravasations may be seen scattered
here and there throughout its substance. When a stream of water is
poured over the cut surface of the implicated lung the color changes
from a maroon to a gray or yellow-gray, the usual color of fibrillated
fibrin.

Not infrequently the material in the infundibula and air-cells extends
into the minute bronchi, but these tubes are rarely completely filled
with the pneumonic exudation. When examined under the microscope the
alveoli are found filled with a solid material composed of a network of
fibrillated fibrin, in whose meshes are leucocytes, red blood-globules,
and changed epithelia. These latter are in various forms, usually round
or oval. They may, however, become quadrangular, triangular, or
irregular. They are granular, and may contain a single nucleus, a
nucleolus, or multiple nuclei. These cells finally become granular, and
fat-globules accumulate in them. {310} They also become discolored from
imbibition of blood-coloring matter, so that in the latter part of the
process there is quite an accumulation of pigment-granules, not only in
the free cells, but in the fixed epithelia. The larger cells discharge
their nuclei into the accumulation of corpuscular elements, and the
whole contents of an alveolus present a more or less round shape. The
alveolar walls remain unchanged, or are slightly thickened by the
capillary turgescence. All of these different cell-elements have been
regarded by different observers as characteristic of pneumonia. The red
globules give the color to the consolidated lung. The pus-cells are
always numerous.

The transition from red to gray hepatization is never well defined. The
mottling gradually becomes more marked, so that the affected portion of
lung assumes a marbled or granite appearance. As the deep-red color of
the second stage fades the density of the pneumonic consolidation
becomes less and less, until it is a mere pulp, breaking down under
slight pressure. The decoloration is due to the pressure on the
blood-vessels, to decoloration of the blood-corpuscles that were
present in the second stage, and to fatty degeneration of the other
cell-elements which occupied the air-sacs.

The weight and density of the affected lung-tissue are diminished, and
toward the end of this stage the lung crepitates. On section a nearly
uniform dirty-gray, bloodless surface is exhibited, from which flows
spontaneously or upon slight pressure a dirty-white or reddish-gray
puruloid fluid. The granular red hepatized look has disappeared or is
very indistinct. The amount of oedema in the affected portion of the
lung varies in different cases. When it is excessive a large quantity
of serum exudes from the cut surface, which then exhibits a smooth,
non-granular, glistening appearance, and it does not so readily break
down when pressed upon as do other forms of gray hepatization. When
examined under the microscope, the alveoli are seen to be filled with
numerous round mono-nucleated cells, the intercellular fibrils that
bound the elements together having disappeared; in other words (the
fibrillated having become granular fibrin), the alveoli are filled with
a fluid or semi-fluid mass in which numbers of discrete oil-globules
and protein granules are freely mingled.

The granular and fatty elements are due to the rapid degenerative
changes that occur in the cell-elements. In this stage leucocytes still
emigrate from the blood-vessels. The masses that occupy the alveoli are
now shrunken, and between them and the alveolar wall is a layer of
fluid, so that in a thin section the contents of the air-sacs are
readily lifted out by a camel's-hair brush. All of the affected portion
of the lung is rarely in the same stage of the inflammatory process,
and to distinguish red from gray hepatization, or the latter from the
beginning of some of the conditions next to be mentioned, is often
impossible.

The changes which take place subsequent to the stage of gray
hepatization, and the modifications due to age, remain to be
considered.

Croupous pneumonia may terminate--1, in resolution [recovery]; 2, in
suppuration, purulent infiltration; 3, in abscess; 4, in gangrene; 5,
and very rarely, in chronic (fibroid) pneumonia.

1. During resolution the lung is moist, lighter than in the stage of
hepatization, has a yellow or yellowish-green color, and still shows a
marked loss in elasticity. On section, the lung appears to be
non-granular, and a tenacious, puruloid fluid escapes when the section
is pressed upon. Some oedema may still remain. When examined under the
microscope the alveolar capillary vessels are seen to have returned to
their normal calibre; the alveolar epithelium is restored; the cells in
the air-sacs are degenerated, broken down, and resolved into a
detritus. The degeneration of these cells is both fatty and mucoid, and
the coloring matter of the blood gives origin to the granular {311}
pigment which is scattered throughout the disintegrated and liquefied
mass. Some of the pigment is supposed to come from the connective
tissue between the alveoli. In this condition the alveolar contents are
either expelled by expectoration or undergo absorption, the lung being
finally restored to its normal condition.

2. When purulent infiltration or suppuration of the lung occurs, its
surface becomes yellow--more so than in any of the preceding
conditions; it is soft, moist, and friable, and gives somewhat the
sensation of an abscess. It is well described as miry.[7]

[Footnote 7: _Pneumonia_, Sturges, 1876, pp. 110, 113.]

On section, a diffluent, purulent fluid exudes from a surface whose
yellow color is due both to the large number of cells which are
undergoing fatty degeneration, and to the anæmia which results from
over-distension of the alveoli with these cell-elements.

When examined under the microscope, the cells are found not only
crowding the alveoli, but infiltrating the inter-alveolar tissue. This
corpuscular infiltration of the alveolar walls may so interfere with
their nutrition that they will undergo softening and degeneration.
Whether these cells (in all respects resembling pus-cells) have
emigrated from the blood-vessels or are the result of epithelial
changes is still unsettled. Reason and analogy seem to point to a dual
origin. Now and then these cells are pigmented. Occasionally the
alveolar walls become thinned, indistinct, and finally rupture.

There has been much discussion over the term suppuration of the lung,
but the appearances reported by those who uphold, as well as by those
who protest against, the term are identically the same, all agreeing
that the "lung is filled with pus."

3. Abscess of the lung, as a termination of croupous pneumonia, is
exceedingly rare, and is always preceded by extensive cellular or
interstitial oedema; small abscesses are formed by the rupture of
several of the alveolar septa. It may follow purulent infiltration.
These abscesses vary in size from that of a pea to one which may occupy
the greater part of a lobe. They may have a thick, well-defined,
irregular wall, their interior being crossed by shaggy shreds of
broken-down lung-tissue, or they may form irregular excavations in
softened lung-tissue. They may be single or multiple. Several abscesses
are often found in the same lobe. They increase in size by peripheral
growth or by fusion of several small abscesses.

Abscesses are more common in the upper than in the lower lobes; their
frequency is variously estimated as 1 in 30 or 60 cases. These
pus-cavities, if of small size, may ultimately close by cicatrization,
in which case they may open into a bronchus of sufficient size to allow
of the discharge of their contents. Under such circumstances the
contents of the abscess are expectorated; interstitial inflammation is
set up around their site, which after a time encloses them in a firm
connective-tissue wall; contraction ensues, and finally only a line of
cicatricial tissue marks their former situation. Or if no such
bronchial opening occurs, the abscess becomes encapsulated in firm
cicatricial tissue, and the contents undergo cheesy and calcareous
transformation. Sometimes these abscesses perforate the pleura and
discharge their contents into the pleural cavity, causing
pyo-pneumothorax. External fistulous openings have occurred, but they
are a rare termination of pulmonary abscess.

4. Gangrene is said to be a termination of croupous pneumonia in about
2 per cent. of cases, but this estimate is based on too few statistics
to be wholly reliable. It is met with in bad constitutions where there
is very great vital depression, in chronic alcoholismus, and in cases
of intense septic poisoning. Interference with the blood-supply,
causing the formation of pulmonary or bronchial thrombi, leads to its
development.[8] While usually limited to a {312} small area of
lung-tissue, it may invade large tracts, and be either circumscribed or
diffuse.

[Footnote 8: Huss, _Pneumonia_; Carswell, _Ill. El. Forms of Disease_.]

The gangrenous portion of the lung is changed to a dark, dirty, pulpy
mass, sometimes wanting the fetor of gangrene. When the mass has become
diffluent, a sort of cavity is formed, in which are found fetid fluid
and shreds of gangrenous lung-tissue. Around the gangrenous mass there
is a zone of gray hepatized, friable tissue, which in turn is bounded
by a zone of red hepatized tissue. When the above-named zones are not
present in diffused gangrene, the cavities are large, and shreds of
tissue and vascular bands traverse the cavity, which swarms with
bacteria. Such a gangrenous mass may lead to sloughing of the pleuræ.
It has been denied that a croupous pneumonia can terminate in gangrene,
but modern pathologists all support the opposite view. It may be
mentioned that gangrene in croupous pneumonia of the horse is of
frequent occurrence.

5. Chronic (interstitial fibroid) pneumonia may result when the process
of resolution in croupous pneumonia is delayed and the inflammatory
process does not advance beyond the stage of gray hepatization. In such
cases the walls of the alveoli, and finally the inter-alveolar tissue,
become the site of new connective-tissue developments.

The peculiarly hard and oedematous condition that sometimes marks gray
hepatization is, by some observers, regarded as an intermediate stage
between croupous and interstitial pneumonia. An abundant
cell-production in the second or third stage of croupous pneumonia may
be followed by shrivelling of the alveolar contents, and subsequent
cheesy changes may bring about one form of phthisis. Whether this can
ever occur independent of tubercle is still a mooted question. This is
called (by those who believe in such an origin of phthisis) cheesy
infiltration, and is to be differentiated from tubercular infiltration.

In childhood croupous pneumonia is not of so frequent occurrence as
catarrhal. In its anatomical changes it does not differ from croupous
pneumonia in adults. In old age the pneumonic changes usually begin in
the upper lobes of the lung, and extend downward--the reverse of what
occurs in adult life. In the stage of engorgement crepitation is
usually wholly absent, and when the stage of red hepatization is
reached the color is found much darker than in adults, sometimes being
blue or black; the lung is much more strikingly marbled, and on section
the granules, in those cases where they are present, are much larger
than in adult life. Frequently in senile pneumonia the granular look is
absent. Gangrene is a far more frequent termination of croupous
pneumonia in old age than at any other period. The highly-rarefied
condition of the lungs at this period seems to favor the development of
small abscesses.

Croupous pneumonia involves either the whole lobe or a whole lung. Its
most frequent seat is the lower lobe of the right lung. Its next most
frequent seat is the lower lobe of the left lung, then the upper lobe
of the right, the middle lobe of this lung being least frequently
involved. Double pneumonia has been variously estimated as occurring in
from 5 to 50 per cent. of cases, but in all probability the percentage
rarely, even in epidemics, exceeds 12 or 15 (Huss, Grisolle, Barth,
Ziemssen). In old age the difference in point of frequency of attack
between the two sides is very slight, and some affirm that sthenic is
more frequent on the right and typhoid pneumonia on the left side.
Double pneumonia is more frequent in the senile period than during
adult life.

The average duration of the different stages is as follows: The stage
of engorgement lasts from two to three days; the stage of red
hepatization, from three to five days; and the stage of gray
hepatization, from two to six days. In old age the stages rapidly merge
into each other, and suppuration of the {313} lung may occur within
thirty-six or forty-eight hours from the onset of the pneumonia, while
it is not at all infrequent for complete red hepatization to occur
within the first six or eight hours.

The changes in the pleura over a pneumonic lung are quite
characteristic. An uneven, thin, downy-looking layer of plastic lymph
is spread over the pleural surface, which presents a fine arborescent
vascularity. At times this plastic layer may partially conceal the
liver-brown color of the pneumonic lung. As the stage of gray
hepatization is reached, pleuritic adhesions are apt to be formed,
which subsequently undergo absorption, and thus the pleuritic changes
follow, to a certain extent, those which are taking place within the
lung. The cell-elements in this fibrinous meshwork are chiefly pus- and
large endothelial-cells. The pleura itself is opaque, congested, and
ecchymotic, and may be so thickened as to give rise to a dull note on
percussion after the pneumonia has undergone resolution. If there are
adhesions from previous pleurisies, or pleuritic changes that have
occurred prior to the lighting up of a pneumonia, they will modify its
course and termination.

The right heart is dilated, and on inspection immediately after death
it is not unusual to find both ventricles filled with pale, firm clots
that insinuate themselves between the columnæ carneæ and sometimes
extend into the vessels. The pulmonary vessels running to the affected
portion of the lung may be the seat of thrombosis. Pericarditis is so
frequently found at the post-mortem of those who die of pneumonia that
its occurrence must be regarded as something more than either accident
or complication.

The blood is hyperinotic in croupous pneumonia, and, while the amount
of fibrin is only slightly increased at the very onset, the amount
obtainable goes on increasing until the eighth or ninth day; _i.e._ as
the amount of fibrinous exudation within the alveoli augments, so does
the same factor appear in greater quantity in the blood--a circumstance
whose opposite condition we should expect to observe. In infectious
diseases--_e.g._ variola--as the temperature rises the hyperinosis
increases. In pneumonia, however, the pyrexia and fibrin increase in
the blood and bear no relationship to each other. The amount varies
greatly in every case; it has reached 10.5 in 1000.

Around the zone of pneumonic inflammation it is not infrequent to
discover pulmonary oedema; and in many fatal cases extensive oedema
seems to be the direct mode of death.

Temporary compensatory emphysema may occur in the neighborhood of the
inflamed lobe or lobes. It may be mentioned that when emphysema has
previously existed the pulmonic granules observable in the second stage
are of unusually large size.

The bronchial glands are enlarged and congested, and in rare instances
they may suppurate. The lymphatics of the lung are choked with fibrin
and with red and white blood-corpuscles, and the deeper lymphatics
contain products identical with those in the pulmonary alveoli. In both
lymphatic vessels and in the lymph-glands (bronchial) at the root of
the lung there are always well-marked evidences of inflammation.

The liver and spleen are congested, the latter organ especially
presenting the characteristics which are found in it in cases of death
from fevers.

Finally, gastro-intestinal catarrh is occasionally observed, and in
rare cases it is attended by ulceration and hemorrhage. But there seems
no good reason for believing that there is any connection between
pneumonia and these intestinal changes. Indeed, most of the
observations bearing on this point were made during cholera epidemics.
Still, analogous influences might induce both at the same time.

No change in the brain accompanies pneumonia, except congestion. Pus
and inflammatory products when found in the meshes of the pia-mater are
in {314} all probability due to coexisting meningitis or cerebro-spinal
meningitis of an epidemic character.

ETIOLOGY.--The specific cause of croupous pneumonia is as yet
undetermined, and the very existence of such a cause is still a matter
of conjecture.

Among the predisposing causes age ranks first. There are three distinct
periods of life in which the liability to pneumonia is greatest--viz.
in early childhood, between the ages of twenty and forty, and after
sixty.

Notwithstanding the fact that catarrhal pneumonia is a very common
disease in childhood,[9] the statement that croupous pneumonia is rare
at this period cannot be received.[10] From a number of statistical
tables it appears that it is five times more frequent during the first
two years of life than in the succeeding eighteen.[11] It is met with
most frequently between the ages of twenty and forty, and after a lapse
of twenty years the predisposition to it increases, pneumonia being the
most fatal of all acute diseases after the sixtieth year. Nine-tenths
of the deaths from acute diseases after the age of sixty-five are from
pneumonia. Each year after sixty the liability to it is greatly
increased.

[Footnote 9: "Die lobuläre pneumonie ist im Sänglingsalter eine
ausserordenich häufige Krankheit" (Vogel, _Kinderkrankheiten_, p.
222).]

[Footnote 10: "Lobäre pneumonie kommt viel seltener vor" (Vogel, _loc.
cit._).]

[Footnote 11: _Klinik der Kreislaufs u. Athms. org._, Breslau, 1856.]

In early life, in what may be denominated the first period, anterior to
the second year, males and females are very nearly equally affected.
Between twenty and forty, the time when the condition of males and
females is most diverse, the proportion is 3 males to 1 female, or at
least 2 to 1. After sixty, when the hygienic condition of both sexes
again differs very slightly, this proportion is less striking, and the
disease is pretty evenly divided between old men and old women; still,
the male sex always furnishes more cases than the female. When women
work as men do, or when both sexes are huddled together (as in
prisons), then the difference between them is lost.

The puerperal state does not seem to increase the predisposition, but
pneumonia is more apt to occur at the time of the catamenia.

The general condition of the individual at and before the pneumonic
seizure seems to have some predisposing influence, although opinion is
divided as to whether the strong and robust or the feeble and sickly
are the more predisposed to it. Those who are convalescing from acute
and severe illnesses, those who are habitual alcohol-drinkers, and
those who are under the influence of malarial poison are far more
liable to pneumonia than those who are free from such taints.
Enervating habits, poverty, antihygienic surroundings and dyscrasiæ
(especially cancerous), and chronic nervous diseases act as
predisposing causes. Difficult dentition in children seems to act in a
similar manner. Diphtheria, erysipelas, measles, small-pox, and other
acute infectious diseases must be ranked as causes predisposing to
pneumonia.

Chronic and acute uræmia, pyæmia, septicæmia, and all that class of
diseases which depend upon the retention of excrementitious substances
in the blood, are also powerful predisposing causes. It is also of
frequent occurrence in chronic blood diseases, such as chronic
alcoholismus. Suppuration in the abdominal cavity, which opens into the
thorax, may lead to a pneumonia. Long-continued, passive pulmonary
hyperæmia from any cause becomes a predisposing cause to pneumonia. The
pneumonia which frequently occurs during acute articular rheumatism has
been regarded by some as metastatic from the joints; but the more
reasonable explanation is that the blood-changes in rheumatism
predispose to pneumonia.

One attack predisposes to others; as many as twenty-eight attacks have
been noted in the same individual, the time between the attacks and the
{315} number of them being governed by no rule and subject to the
widest variations.

When pneumonia follows a severe blow or injury to the chest or shock
from any traumatic cause, the injury (or the shock) must be regarded as
a predisposing cause. It is noteworthy to observe how often in the aged
fracture of the hip-joint is followed by pneumonia. Within four hours
after this injury croupous pneumonia has been established.

The influence of prolonged exposure to intense cold and sudden chilling
of the surface of the body as a predisposing cause of pneumonia is
still undetermined. Cold does not markedly affect the pneumonia-rate,
except in the very old. Nearly nine-tenths of the cases of senile
pneumonia occur between November and May. The January and February
statistics seldom exhibit the highest pneumonia-rate, as they would
were there any direct relationship between pneumonia and cold. In
elevated regions north-east winds favor the development of pneumonia,
and it is most prevalent in any locality during those periods of the
year when there are the greatest extremes of temperature. A
continuously low or a continuously high temperature has much less
influence in its production than great vicissitudes of temperature. In
New York City early spring and winter seem to be the periods when it is
most prevalent.

A glance at its etiology shows that it is a disease to which all things
predispose that depress the general vitality: this is evidenced by the
fact that children and old people are greatly depressed by the intense
cold of winter and the chilling winds of March and April. Almost
unknown in the polar regions, pneumonia is not an infrequent disease
along the Mediterranean coast; and one peculiarity is to be noted here,
that in cold as well as in warm climates moderate elevation above the
sea-level predisposes to its occurrence.

Rainy seasons or moist districts do not influence the pneumonia-rate to
any appreciable degree. Both these conditions have a direct effect in
increasing the prevalence of bronchial catarrh, but they do not
increase the pneumonia-rate.

The well-established facts that pneumonia occurs oftener among the poor
than the wealthy; in the sailor when on shore oftener than when he is
on shipboard; in soldiers oftener than among civilians at the same
military post,--these are explained on the ground of better hygienic
surroundings, better mode of life, nourishment, etc., of the one class
as compared with the other. And in studying the predisposing causes of
pneumonia one is led more and more to observe that it is the more
liable to occur the less resistance individuals are able to offer to
some (as yet unknown) specific pneumonic influence, and that depressing
influences of whatever kind unquestionably predispose to croupous
pneumonia.

The more dense the population in a district, the greater the
pneumonia-rate. Hirsch says: "The amount of the mean fluctuation in the
mortality from pneumonia is in inverse ratio to the density of the
population." When a city has attained a certain size, wind, weather,
seasons, and races have but a slight influence in varying the
pneumonia-rate. Thus, in New York City from 1840 to 1858 (eighteen
years) the mortality from pneumonia was 5.85 per cent., while from 1859
to 1877, inclusive, it was 6.2 per cent.

Before considering the exciting causes of croupous pneumonia, or their
relation to its predisposing causes, the question meets us, Is croupous
pneumonia an acute specific constitutional (infectious) disease or a
local inflammation?[12]

[Footnote 12: _Virchow's Archiv_, Bd. lxx., Heidenhain.]

That it is not a simple local inflammation appears from the following
facts: the experiments with the inhalation of hot air, moist warm air,
icy-cold air, {316} vapors of various noxious acids and gases;[13] the
tracheal injection of caustic ammonia[14] and mercury; and
traumatism,--have all resulted negatively as exciting causes. And these
experiments have all the more weight since they have been conducted not
only at different times, and in countries distant from each other, but
also because they have been repeated by various pathologists, and
always with a similar result--viz. the development of lobular or
catarrhal, and not of croupous, pneumonia. Section of the vagi
certainly produces hepatization of the lungs, but it is not the
hepatization of croupous pneumonia. Its distinctive microscopical
characteristics are always wanting in the part of the lung consolidated
by such experiments. A strong argument of those who adhere to the local
theory of pneumonia is, that cold occupies a prominent place in its
production. As exposure to cold and to draughts is a common experience,
it is easy to ascribe the origin of any disease to cold.

[Footnote 13: Sityl, _K. K. Akad. zu Wien_, 867, Reitz.]

[Footnote 14: Gendrin, _Hist. Anat. des Inflam._]

"Close rooms and bad air," says Squire, "more predispose than does
outdoor exposure, unless that be prolonged or the individual resistance
weakened by fatigue or intemperance." Both wet and cold invariably
heighten the bronchitis-rate and exacerbate catarrhal processes, but
neither of these can be proven to influence the pneumonia-rate.
Statistics show that croupous pneumonia is more prevalent in our
Southern States than in our Northern States. The epidemics in the West
Indies are as well known as, and have been more devastating than, those
in Iceland and in the Norse countries. The prevalence of pneumonia in
this continent progressively increases from the pole to the equator.

Hirsch's statistics and statement, that "the amount of the mean
fluctuation in the mortality from pneumonia is in inverse ratio to the
density of the population," is a strong argument in favor of the view
that croupous pneumonia is due to some specific pneumonic infection,
for all acute general diseases increase where there is over-crowding.

It is often stated that pneumonia is a far more frequent disease now
than it was twenty years ago. That I might arrive at something definite
on this point, I have carefully examined the death-reports of England
from 1840, also those of New York City, dividing them into two periods
of eighteen years each; and I find that the average mortality from
pneumonia in England from 1840 to 1858 was 5.57 per cent.; from 1859 to
1877, 4.77 per cent., an actual decrease of 14.3 per cent. In New York
City from 1840 to 1858 the average ratio of mortality from pneumonia to
all other diseases was 5.85 per cent., and from 1859 to 1877 it was
6.20 per cent., showing an increase in New York of 15.2 per cent. Thus
it is shown that while in England pneumonia is on the decrease, in New
York City it is on the increase.

Those who advocate cold as a cause of pneumonia base their argument on
the seasons of the year when it is most prevalent. The winter and
spring are pre-eminently the seasons of pneumonia, but cerebro-spinal
meningitis, diphtheria, influenza, measles, and other diseases of
similar general character occur with greatest frequency in the winter
months, yet it is not now claimed that cold causes them. While it is
not to be denied that cold is to a limited extent an exciting cause of
pneumonia, the belief that it is the primary or principal cause must be
held in abeyance if not altogether rejected. Again, the symptomatology
of pneumonia seems to militate against its being a local disorder.

There is no relationship between the amount of lung-tissue involved and
the intensity of the symptoms; high fever, delirium or convulsions, and
rapid heart-failure are often as well marked when a post-mortem reveals
only one lobe to be involved as when a double pneumonia exists. "The
local inflammation in its gradual extension and composite character
offers no sort of {317} parallelism to the fever which for a while
accompanies it." In local phlegmasiæ there is a direct ratio between
the amount of surface involved and the attendant constitutional
disturbances.

Rarely does a second chill occur when there is an extension of the
pneumonic process. "Small consolidations with high fever and severe
constitutional symptoms, and extensive infiltrations with a
comparatively slight fever and general disturbance, are the rule and
not the exception."[15]

[Footnote 15: _Ziemssen's Cyclop. Prac. Med._, vol. v. p. 146.]

The absence of regular and constant prodromata, the absence of a known
period of incubation, of a typical temperature-range, and of
characteristic surface phenomena, and the fact that it is not
contagious,--these must not be overlooked when we are tempted to regard
croupous pneumonia as an acute infectious disease.

The points of resemblance between croupous pneumonia and the acute
general diseases are the following: It has an initiatory chill, an
orderly pyrexia, and a somewhat typical course, inasmuch as there are
in many cases a day of abrupt crisis and a definite duration. The
symptoms follow in regular sequence.

There is a peculiar countenance, and here we note a resemblance to
typhus and typhoid; there are usually herpetic eruptions; the kidneys
are not infrequently the seat of a nephritis; and catarrhal pyelitis is
a common condition. The cerebral symptoms greatly resemble the
condition that accompanies the exanthems. The peculiarity of its
commencement in the very young and old--convulsions in the former and
coma and collapse in the latter--serves to point to an alliance with
those diseases where a specific morbific agent acts primarily and
principally on the nervous system. Etiologically, it often arises under
precisely similar circumstances as those which give origin to
cerebro-spinal meningitis and diphtheria, to both of which diseases it
is also allied, since the pathological changes are distinct from those
of any other inflammation.

Again, the influence of septic, miasmatic, and atmospheric conditions
is certainly almost universally acknowledged. A good example of this is
the sewer-gas pneumonia so often occurring in New York City, and of
which frequent mention is made by English writers. Again, there have
been frequent epidemics of pneumonia in certain districts in garrisons
and on board ship, where over-crowding, bad ventilation, and general
antihygienic surroundings prevailed.[16]

[Footnote 16: In the _U. S. Sanitary Commission Memoirs_, Russel
reports: "The surgeons on duty with the regiments in the barracks
(Benton, Mo., 1864) report that men occupying the same bunks with those
affected were very much more liable to be attacked than those more
remote. Some of the most intelligent surgeons were led to believe that
the disease was actually contagious."]

During the winter of 1881-82 I remember three instances where two
individuals in the same house were simultaneously attacked with
croupous pneumonia.

Pythogenic pneumonia is a form which arises under miasmatic influences,
and is contagious.[17]

[Footnote 17: _Dub. Med. Journal_, 1874, vol. i., Grimshaw and Moore.]

"The epidemic form of croupous pneumonia at certain times bears the
distinct characteristics of a specific infectious disease."[18]
Miasmatic and zymotic pneumonia are names which have also been given to
this form; and indeed it is now generally acknowledged that croupous
pneumonia does occur as an epidemic disease when it is, seemingly,
dependent upon a specific contagion. Huss thinks that during a typhus
epidemic pneumonia is apt to assume the low typhoid form.

[Footnote 18: _Berliner klinische Wochensch._, 1879, No. 37, A. Kühn.]

Moreover, as in typhoid and cerebro-spinal meningitis, so in pneumonia,
we {318} have abortive cases, and forms which are distinguished by the
names sthenic, asthenic, malignant typhoid, icteric, etc. Still, a
pneumonia epidemic is different from a typhoid or cholera epidemic: it
does not sweep over large districts and affect all ages and classes
indiscriminately.

Every acute general disease has its complications, and the occurrence
in pneumonia of peri- and endocarditis, as well as its cerebral and
renal complications, allies it to other acute general diseases.

Cerebro-spinal fever has its characteristic lesion in the membranes at
the base of the brain and about the cord; typhoid fever, in the
lymph-structures of the intestinal tract; diphtheria commences in and
chiefly involves the epithelia; and pneumonia has its characteristic
local lesions in the vesicular structure of the lungs. Croupous
pneumonia is occasionally met with in intrauterine life, and it is to
be remembered that acute general diseases occur far oftener in the
foetus than local inflammations. Again, the accepted treatment of
pneumonia at the present day is an indication of its specific
character. Thus the weight of evidence leads to the opinion that
pneumonia is an acute specific general disease caused by a specific
poison. The nature and action of the pneumonia-poison may be indicated
by the following facts and experiments: Hyperinosis does not seem
capable of causing croupous pneumonia; the fibrin increases as the
consolidation is completed, and does not antedate either the pyrexia or
the hepatization. Excessive bleeding increases the amount of fibrin
obtainable from the blood; and when, in pneumonia, we find one lung
weighing three pounds more than the other, may not the blood-elements
effused into the alveoli have much to do with the hyperinosis?

Pneumonia resembles quinsy[19] in its pyrexia, temperature-curves,
duration, its constitutional as compared with its local symptoms, and
its rapid and abrupt decline. Both have a similar herpetic eruption,
and in both the amount of chlorides in the urine is subnormal, the urea
(in both) being increased.

[Footnote 19: Sturges, _Pneumonia_, _loc. cit._]

An analogy has been noted by some observers between pneumonia and acute
rheumatism. Trousseau sees an analogy between erysipelas and
pneumonia.[20] But apart from their etiology it is difficult to
recognize any constant resemblances between them. Sturges places
"pneumonia in a middle place between the specific fevers, so called,
and the local inflammations," and adds that it has something in common
with both. Cohnheim classes croupous pneumonia among the miasmatic
contagious diseases.

[Footnote 20: _Clinical Lectures_, vol. iii. p. 353.]

The idea of its being a specific disease dates from the latter part of
the eighteenth century:[21] it is not by any means a modern thought,
although it has within the last ten years received a new impulse and
given rise to extended discussions.

[Footnote 21: C. Strackius in _Nov. Theo. Morg._, 1786.]

It seems to me that the resemblance of pneumonia to the acute general
diseases is to be found for the most part in its nervous phenomena, and
that the complications which render pneumonia dangerous are those which
interfere directly with the muscular power of the heart or diminish its
nerve-supply.

In order that the influence exerted by an abnormal nerve-supply upon
the contractility of the cardiac muscles may be more apparent, let us
glance at a few modern physiological facts. When the inhibitory nerve
of the heart, the pneumogastric, is cut, the heart beats wildly. When
the peripheral cut end is stimulated, the heart stops in diastole. But
neither of these phenomena instantly follows the operations, on account
of the intervening cardiac ganglia, the part of the vaso-motor system
which has its centre in the medulla oblongata. Afferent inhibitory
filaments (the depressor branch) of the vaso-motor centre are also in
the vagus. Now, by injecting atropine into the blood we so influence
these cardiac ganglia (which intervene between the conditions of the
vagus and the resulting action upon the heart-beat) that the inhibitory
{319} action is entirely checked. Thus an intimate connection is
apparent between the local heart-mechanisms, the general vaso-motor
system, and some filaments of the vagus. Again, we know that the
natural explosive decompositions of the nerve-cells of the respiratory
centre may be either augmented or enfeebled according to the condition
of the blood supplying this ganglion. Now divide the cervical portion
of the pneumogastric, and there results, after a more or less prolonged
period, an extensive pulmonary consolidation (hepatization), which is
not accompanied by the least sign of heart-failure. It is to be
remembered that such pulmonary consolidation has none of the essential
pathological characteristics of croupous pneumonia.[22]

[Footnote 22: Michael Foster, Wagner, Goetz, Heidenhain, Du
Bois-Reymond, Ludwig, and Pflüger.]

From these experiments the following deductions seem at least
reasonable: The tonic influence normally held by the vaso-motor system
of nerves over the vascular system is either lessened or destroyed by
an altered blood-state or by some morbific agent in the blood
introduced from without. The large quantity of blood which would then
be retained in the arterioles throughout the body, and which could not
be returned to the heart, may cause so great a diminution in the
blood-pressure as in itself to cause heart-failure. But in addition,
and in connection with this, may not the action of a morbific material
in the blood upon the intrinsic cardiac ganglia so interfere with their
function, or so act upon the medullary vaso-motor centre itself, that
the movements of the heart are deranged and its power is more or less
diminished?

It would seem that this materies morbi in the blood may as well act
upon both the medullary centre of the vaso-motor system and the ganglia
in the wall of the heart as upon either alone. The phenomena of
asphyxia are brought about by influences acting solely on the medullary
centre. Again, the large amount of urea excreted, the result of
excessive tissue-change throughout the body, may also be due to
deranged nerve-function.

Klebs[23] even claims that he has found the infectious agent--a monas
pulmonale--which can be inoculated, with the result of developing
croupous pneumonia. This has been credited so far as to lead to the
subcutaneous injection of carbolic acid to destroy the pneumonic germ.
Incidentally, it may be remarked that it has been shown that the
contagion of the pleuro-pneumonia of cattle, according to Parkes, "has
been found in the pus- and epithelium-cells of the sputa." The true
nature of the pneumonia poison, if one exists, is as little determined
as that of the other acute contagious general diseases. But, whatever
its nature may be, its primary action seems to be on the nerve-centres.

[Footnote 23: _Arch. für exper. Path. u. Pharm._, vol. iv., 1875.]

SYMPTOMS.--The symptoms of croupous pneumonia may be considered under
two heads--Subjective, or rational symptoms; and Objective, or physical
signs.

Subjective Symptoms.--In only a small proportion of cases are there
prodromata. Grisolle found that prodromata occurred in 50 out of 205
adult cases, or in about 25 per cent.; and Fox says that he finds the
proportion to be about 28 per cent. In old age they seem to be more
frequent, the proportion being about 60 per cent.[24]

[Footnote 24: Durand-Fardel, _Mal. des Viellards_.]

There may be for a day or two, or even for a week, preceding a
pneumonic seizure a feeling of general malaise, accompanied by
anorexia, headache, dull pains in the limbs, back, and lumbar region,
vertigo, epistaxis, or slight diarrhoea. Sometimes the skin assumes a
slightly jaundiced hue, and there may be flashes of heat accompanied
by, or alternating with, slight rigors. Flying pains in the limbs and
chest and epistaxis are common in senile croupous pneumonia. When
prodromes have existed more than three or four days, they will be vague
and undefined.

{320} Rise in temperature as a prodrome is by some thought to be caused
by a deep-seated and undiscoverable hepatization. But let us take one
example from many in support of a contrary view--viz. the case of an
inmate of Bellevue Hospital during the winter of 1880-81. For three
days preceding the first appearance of consolidation the temperature
ranged at 102° and 103° F. During this time there were several slight
rigors followed by flashes of heat.

Wilson Fox[25] states that he knows of but one case--the one referred
to by Monthus in his _Essai sur la Pneumonie double_.

[Footnote 25: _Reynolds's System_, art. "Pneumonia."]

In epidemics febrile symptoms and diarrhoea often precede for some two
or three days the first sign of consolidation.[26]

[Footnote 26: _The Lancet_, vol. ii., 1878, p. 701, Couldrey.]

In the great majority of cases croupous pneumonia is ushered in by a
distinct chill. Huss and Grisolle found a chill in 80 per cent. of
their cases; Fismer and Louis in about 77 per cent. of theirs; and
Lebert in over 92 per cent. of his. In 84 out of 100 cases admitted to
my ward in Bellevue Hospital, a distinct chill marked the invasion of
the disease.

Generally, the patient retires in his usual health, to be seized with a
severe chill during the night. The chill lasts from half an hour to two
or three hours. Its abruptness and severity are almost characteristic
of the pneumonia.

In children, headache, nausea, vomiting, delirium, and convulsions may
take the place of the chill; its onset then closely resembles that of
the exanthemata, indicating the action of some irritating poison upon
the nerve-centres. When these symptoms are not present there will be
more or less anorexia, thirst, and a tendency to stupor. The child will
awake in the middle of the night with a burning skin, a bounding pulse,
flushed face, and hacking cough. When there are convulsions, followed
by a loss of consciousness, the pneumonia is usually at the apex of the
lung.[27]

[Footnote 27: Rilliet and Barthez.]

If an old person is seized with a severe chill during the night, it is
almost a certain indication that pneumonia is developing. Although the
chill of invasion is of less frequent occurrence, it is more
significant than in adult life. A protracted fit of shivering and pain
in the side are the two diagnostic symptoms of acute sthenic senile
pneumonia. They occur in about 50 per cent. of all cases, and from
statistics taken from the Salpêtrière it seems that in March and April
these two symptoms are almost always present.

In the other half of the cases of senile pneumonia the onset is marked
by a frequent, irregular respiration, slight rise in temperature, short
hacking cough, and signs of great exhaustion. Nausea, vomiting,
diarrhoea, and collapse or a semi-comatose condition may usher in a
senile croupous pneumonia.

Durand and Fardel give the following statistics of the mode of advent
in 35 cases of senile pneumonia: 7 began with distinct rigors; 8 with
rigors and pain in the side; 6 with rigors and vomiting; 8 with pain in
side alone; and 6 with vomiting only. When a chill is the initial
symptom, either in childhood, adult life, or at the senile period, it
is rarely repeated.

In adults, following the chill there is usually pain underneath the
nipple of the affected side; sometimes the earliest symptoms following
the chill are headache, vomiting, and diarrhoea, dyspnoea, a hacking
cough, and pain that simulates that of lumbago. Within twenty-four
hours after the invasion the aspect of the patient becomes
characteristic: there is a rapid rise in temperature, attended with
great prostration; the pain in the side is aggravated by coughing and
deep inspirations; and the respiratory movements are accelerated. The
countenance assumes a dull or anxious expression, with a tendency to
lividity; the pulse is accelerated, full, and soft; there is complete
anorexia and great thirst; speech is difficult, and often there is
great restlessness. The urine becomes scanty and high-colored, the
bowels are constipated, and the tongue is dry and covered with a white
coating.

{321} These symptoms either increase in severity or are attended by
exacerbations and remissions until the day of crisis, which usually
occurs between the third and the ninth day; when, if recovery is to
take place, there is a sudden remission of all the pneumonic symptoms;
the temperature falls abruptly; the surface becomes moist; the flush of
the countenance disappears; the pulse and respiration become normal;
and the patient rapidly passes on to complete convalescence.

In some cases the decline in the symptoms is gradual and the disease
terminates by lysis and not by crisis. In unfavorable cases signs of
heart-failure appear within the first few days, and the patient sinks
rapidly into collapse and dies.

With this brief outline of the disease I will pass to an analysis of
its prominent symptoms.

Respiration.--The respirations are more constantly increased in
frequency in croupous pneumonia than in any other acute disease. In
most febrile diseases the respirations increase in frequency with the
pulse-rate. In pneumonia there is no uniform ratio between pulse and
respiration; this is regarded by some as an important diagnostic
sign.[28] In some cases the respirations will be 80, and the pulse only
90, per minute. The acceleration in the respiration is not in
proportion to the amount of lung-tissue involved, but seems to be due
to a peculiar condition of the nervous system which existed prior to
the pneumonic seizure or is caused by a poison acting upon the
nerve-centres. Traube[29] thinks that it is due to the pain and to the
high temperature. This theory would not explain its occurrence in those
cases where the pleura is not involved--_i.e._ when no pain is
present--and yet the shallow, panting, rapid breathing is well marked.

[Footnote 28: _Dis. of Lungs_, Walshe, 1860, p. 366.]

[Footnote 29: _Annal. de Charité_]

In other pulmonary diseases, when there is high temperature, as in
acute phthisis, the respirations are not so much accelerated as in
pneumonia. The character of the respiratory acts is also peculiar: they
resemble the panting of a dog. Accelerated breathing may or may not be
accompanied by dyspnoea; in many cases the dyspnoea seems to be
independent of it, for extreme dyspnoea is often present where the
respirations are but slightly increased in frequency.

In children the acceleration of respiration is more marked than in
adults, and the ascent of the chest occurs during expiration, and not,
as normally, with the inspiration. The diaphragm is markedly contracted
with each expiratory act, and the diagnosis will as often be made by
the character of the respiration as by the physical exploration of the
chest, for in children the early physical signs of pneumonia are often
unsatisfactory.

The hurried breathing prevents a young child from nursing; it takes the
mother's nipple for an instant, nurses greedily, and then drops back,
gasping for breath.

It is to be remembered that in pneumonia in children the pulse and
respiration discrepancy will not be so well marked as in adults: the
pulse may be 150 to 160 per minute, while the respirations are 80 or
90. In children there will early be noticed the peculiar expansion of
the nostrils which comes on late in adults. In senile pneumonia the
chest enlarges vertically during inspiration. The whole act has a
panting character, and the expiration is prolonged.

In perfectly healthy old people the inspiratory movements are jerky in
character. The lungs become fully expanded only after a succession of
interrupted efforts. An exaggeration of what is physiological in old
age--_i.e._ catchy breathing--is the most frequent form of abnormal
respiration in senile pneumonia.

Dyspnoea, although frequently accompanying accelerated respiration, is
by {322} no means a constant attendant of it. When urgent it is not in
proportion to the amount of lung involved, since double pneumonia may
be accompanied by less dyspnoea than when but one lobe is involved. It
can be due only in small degree either to the diminution in the total
breathing capacity, to the pain, or to the rapid and destructive
tissue-metamorphosis; for on the day of crisis it ceases, although the
lung at this time is not relieved of its obstructive exudation. The
most intense dyspnoea usually occurs in those cases where there is
extensive nervous prostration, and must always be regarded as a symptom
of great gravity.

In secondary pneumonias, especially where there is coexistent disease
in any part of the respiratory tract, the dyspnoea is usually more
marked than in primary and uncomplicated pneumonia. It differs from the
labored dyspnoea of general capillary bronchitis. A diagnosis between
these two diseases can often be made by the character of the dyspnoea.

When the summit of the lung is involved, the dyspnoea is always greater
than when the pneumonia is at the base. In pneumonia of the apex in
children the dyspnoea is so great that the nostrils are widely dilated,
the mouth is open, and its corners are drawn downward and outward. In
senile pneumonia, even when the respirations are 70 per minute,
patients do not complain of difficulty in breathing.

When persons over seventy who have been asthmatic or are the subjects
of chronic bronchitis develop a pneumonia, they often suffer less from
dyspnoea than before the pneumonic attack. They feel exhausted, are
unable to move about, and on lying down to rest often suddenly expire.

Immediately after the initial chill pain is present in over 85 per
cent. of the cases. It is of a sharp stabbing character, and is usually
located over the seat of the pneumonia; it is intensified by coughing,
sneezing, and deep inspirations. In some cases there is tenderness on
pressure over the seat of the pain. The pain usually disappears after
the third or fourth day of the disease; if it continues until the
eighth day, it may be regarded as evidence of pleuro-pneumonia. If the
pneumonia is central there will be no pain. In old age, even in a
pleuro-pneumonia, pain is never severe. It is rather a dull, uneasy
sensation referred to the whole chest, or if localized by the aged
patient is referred to the pit of the stomach, the nipple, the loins,
the hypochondrium, or even to the side opposite to the one involved.

Cough is generally present within twenty-four hours after the accession
of croupous pneumonia. At first it is short, ringing, or hacking in
character, and increases the pain in the side. It sometimes entirely
ceases just before a fatal termination. In children a hacking cough is
more constant than in adults. Within a few hours it becomes painful and
urgent, and occasionally assumes a paroxysmal character, resembling
whooping cough.

Old people with pneumonia often have no cough. When present it is
slight, and may escape the notice of the patient as well as of the
physician. When an aged person suffering from chronic bronchitis or
asthma, who has had a chronic cough, develops a pneumonia, the cough
generally becomes less severe, and may entirely cease.

Expectoration.--The sputum in pneumonia is characteristic. During the
first forty-eight hours it is simply frothy mucus; then it becomes
semi-transparent, viscid, gelatinous, and tenacious, but never opaque.
Streaks of blood often appear early, mixed with the sputa. So tenacious
is it that the cup which contains it may be inverted without spilling
the mass. It can be drawn out between the thumb and finger into thin
strings, and its tenacity undoubtedly is one cause of the difficulty in
its expectoration. Its color varies: generally on the second day the
brick-dust or rusty sputa are observed; still, there are numerous
exceptions. The color is due to admixture of blood which extravasates
from the capillaries of the alveoli. The rusty sputa are preceded {323}
in some cases by a transient brighter red expectoration. In other cases
it is of a creamy-yellow color, resembling in this respect ordinary
catarrhal sputa; or, again, it becomes dark and of a prune-juice color.
A severe pneumonia may have none other than a purulent sputum.

Prune-juice sputa of an offensive odor are indicative of a depraved
state, and occur only in grave forms of pneumonia. In alcoholismus and
in those markedly septic forms of pneumonia which are to end fatally,
the prune-juice or burnt-sienna sputum is usually present. In some
instances prune-juice sputa appear before the physical evidences of
hepatization.

A watery and blood-stained expectoration indicates pulmonary oedema and
congestion, and is an unfavorable symptom. When a case is tending to a
fatal termination, the sputa become scanty, less tenacious, more
diffluent, and often of a greenish color. But a greenish color may be
present during the stage of resolution, and may temporarily occur in
the middle period of a pneumonia, without being indicative of serious
changes. It is usually present in the so-called bilious pneumonia when
there is jaundice.

Pre-existing or complicating lung diseases may mask or alter the
ordinary rusty pneumonic sputa. On the day of crisis, when resolution
occurs, the sputa usually become abundant and of a creamy-yellow color.
But purulent creamy sputa may occur with a complicating abscess and in
some cases of purulent infiltration. During the whole course of the
disease there may not be a single characteristic sputum, or it may not
be present until the fifth, sixth, or even the twelfth day of the
pneumonia. Again, the sputa may continue of a brick-dust hue until the
ninth or tenth day. There is frequently an entire absence of
expectoration in the pneumonia of acute articular rheumatism and in
pneumonia of the apex.

Lastly, the sputa may be more or less pigmented, or when venesection or
purgation has been extensively practised expectoration may suddenly
cease.

In children expectoration is rarely present, but the brick-dust masses
may often be detected in the ejected matter after an attack of
vomiting. In senile pneumonia expectoration is never an early symptom,
and it is liable during any period of the disease to suddenly cease.
Rusty sputa occur in only about 33 per cent. of senile pneumonias. They
are at first scanty, gray, and frothy, then yellow or catarrhal (sputa
cocta). In severe and fatal cases profuse bloody expectoration may be
present at the onset. The reason why the viscid (pathognomonic) sputum
of pneumonia is so often absent in senile pneumonia is that the stages
pass rapidly into each other, and purulent infiltration takes place
very early. The day of crisis is not marked by the same changes in the
expectoration that mark the crisis in pneumonia of adult life.

A chocolate-looking serous expectoration usually accompanies the
so-called typhoid pneumonia.

When examined under the microscope, the sputum is found to contain
swollen epithelia, both spheroidal and columnar, red and white
blood-globules, minute spherules of fat, and the other elements which
were described as filling the alveoli during the stage of red
hepatization. (See Morbid Anatomy.)

Walshe affirms that pus-cells are not found in the brick-dust
expectoration of pneumonia. The mucoid cells will often be stained by
the liberated coloring matter of the blood, and pigment-granules may be
found mingled with the granular débris of its resolving stage. In about
75 per cent. of the cases there will be found in the sputa, when
floated in water, casts of the alveoli and bronchioles.[30]

[Footnote 30: _Diagnost. u. Pathognos. Untersuch._, 1845, Remak.]

The chemical constituents of the sputa are albumen, mucus, and mucin.
Different observers have found the sputa to contain tyrosin and sugar.
There are two explanations of the acid reaction of pneumonic sputa.[31]
{324} Verdeil thought it due to the excess of pneumic acid in the
inflamed lung. Bamberger claims that it is due to the deficiency in
alkaline phosphates.[32]

[Footnote 31: _Gaz. méd._, 1851, p. 777, Robin et Verdeil; _Chem. Anat.
Phys._, vol. ii. p. 460 _et seq._]

[Footnote 32: _Wurtzburg Med. Zeitschr._, ii., No. 506.]

It may be noticed that the following differences exist between
pneumonic and catarrhal sputa: catarrhal sputa contain 10 to 14 per
cent. of alkaline earths; pneumonic sputa contain no alkaline
phosphates. In catarrh the ratio of the soda to the potash is 31 to 20;
in pneumonia the ratio is 15 to 41. There is 3 per cent. of sulphuric
acid in catarrhal and 8 per cent. in pneumonic sputa.

Early in pneumonia there is an increase of the fixed salts, notably
chloride of sodium, in the serum of the blood. It has been thought that
from the rapid and excessive cell-transformation in the lung the
chloride of sodium is attracted to that organ. In one case where no
sodium chloride was found in the urine 10 per cent. of the solid
material of the sputa consisted of that salt. Still, the presence of it
in the sputa and blood, and its absence from the urine, are facts that
still need elucidation.[33]

[Footnote 33: Beale gives the following analytical table of a case of
acute pneumonia:

  Chloride of Sodium.  Per cent. of Solids.
    Urine                      0.
    Blood from heart           0.68
    Hepatized lung             2.59
    Healthy lung               1.43]

The expired air in croupous pneumonia is colder than normal, and, as in
many acute general diseases, there is a diminution in the amount of
carbonic acid excreted.

Temperature.--The temperature-range of a typical case of croupous
pneumonia shows it to belong to the remittent or subremittent type of
diseases rather than to the class of febrile disorders marked by a
continuous pyrexia. In rare instances it is intermittent.

As in most acute general diseases which are ushered in by a distinct
chill, the temperature rises rapidly during the chill. In two or three
hours after the chill it may range from 102° to 105° F. After
twenty-four hours it is subject to evening exacerbations and morning
remissions, but the morning temperature is rarely more than 2° F. lower
than the evening. Indeed, the difference in the subremittent type may
amount to only ½° F., and in the remittent type to only 1° F. At
midnight a second exacerbation may occur, but not so marked as that
occurring early in the evening. Occasionally the remissions occur in
the evening and the exacerbations in the morning.

[Illustration: FIG. 33. A Typical Case of Lobar Pneumonia in the Adult:
Recovery by Crisis.]

The temperature is usually highest on the evening of the third day. In
some cases the maximum range may not be reached until a few hours
before the crisis, on the fifth or sixth day. {325} In fatal cases,
just preceding death, the temperature may reach 107° or even 109° F.

An (average) typical temperature-curve is shown on the preceding page
(Fig. 33).

If after the fourth day of a pneumonia an unusual remission is followed
by a high temperature-range, either an extension of the pneumonia or
the occurrence of some active complication is indicated. If in an
otherwise mild pneumonia the temperature suddenly rises to a high
point, a grave complication is indicated. The sudden fall of
temperature on the fifth or sixth day indicates a crisis and the
beginning of convalescence; it may occur in the morning or after the
evening exacerbation.

In a typical case it is usual to find the temperature on the morning of
the fifth, sixth, or seventh day two or more degrees lower than on the
preceding night, and subsequently it falls until a normal, or not
infrequently a subnormal, temperature is reached. The crisis may occur
by successive and increasing remissions, while the exacerbating
temperature remains constant (Fig. 34); and indeed it is common for the
remissions to be excessive immediately preceding the crisis.

[Illustration: FIG. 34. Lobar Pneumonia, where the Crisis was marked
with Evening Exacerbations, reaching nearly the highest pyrexia of the
second stage: Recovery.]

Just before the final fall the fever may be greater than at any time
preceding.[34] When the decline in temperature is gradual (lysis), the
normal temperature is usually reached by the ninth day, but it may be
delayed until the twelfth or fourteenth day. A very slow or protracted
lowering of the temperature is attended by a coincident slow
disappearance of the physical signs of consolidation. There is no
explanation for this, except that it is met with oftenest in the weak,
debilitated, and dissipated where venesection has been practised or a
depressing plan of treatment has been resorted to.

[Footnote 34: See Fig. 33, where a temperature of nearly 105° F. is
followed on the evening of the fifth day by the final fall.]

A high temperature persisting after the tenth day indicates purulent
infiltration (see Fig. 38).

Pneumonia involving the apex of the lung is usually marked by a higher
average range of temperature than when it is confined to the lower
lobes. Statistics show that the fifth and seventh days are the days of
crisis in the majority of uncomplicated pneumonias. Of 867 cases
terminating by crisis, in 677 the crisis occurred before the eighth
day. Neither the height of the temperature-range nor the amount of lung
involved affects the critical day.

In the form of pneumonia sometimes called bilious--a form that prevails
in miasmatic regions--the temperature is markedly paroxysmal.

In children the temperature rises very rapidly, sometimes reaching 106°
F. within the first twelve hours. The highest recorded temperature in
the pneumonia of children, with recovery, is 106°-107° F. The average
temperature {326} of pneumonia at this period of life is 104° F., the
range being higher than in adult pneumonia.

In children the day of crisis is oftener the seventh than the fifth
day. The fall of temperature during the crisis is somewhat remarkable;
it often falls two and a half degrees below the normal, and this
exceedingly low temperature may be maintained for two or three days,
and yet the child recover.

The accompanying charts show ordinary temperature-curves from children
with pneumonia (see Figs. 35, 36).

[Illustration: FIG. 35. A Typical Case of Lobar Pneumonia in a Child:
Recovery.]

[Illustration: FIG. 36. A Case of Lobar Pneumonia in a Boy ten years
old, in which thermometrical observations were made every four hours:
Crisis on the sixth day.]

In old age it is often difficult to determine the exact day of the
invasion of pneumonia except by the temperature. The rectal temperature
rises to 103° or 104° F., or even higher, on the first days, and
continues at about the initial point for three or four days, with daily
morning and evening oscillations of a degree or a degree and a half.
The temperature-rise does not begin for several hours after the initial
chill, if a chill occur (see Fig. 37).

[Illustration: FIG. 37. A Typical Case of Senile Lobar Pneumonia:
Recovery.]

Relapse in pneumonia is a rare event; it is quite phenomenal for it to
occur four days after the crisis. The temperature suddenly rises, but
usually returns to normal in three or four days.

Pulse.--The pulse in pneumonia varies with the type and extent, as well
as with the stage, of the disease. In an ordinary mild case the
pulse-rate is usually between 90 and 120 per minute. When the
pulse-rate for any length of time is above 120, the case must be
regarded as an exceedingly grave one.

{327} The pulse at the onset of croupous pneumonia is usually full and
soft. As the disease progresses it becomes small and feeble. In severe
cases, and when the nervous system is markedly implicated, it is rapid,
and may be 130 to 140, or even 160, at the onset of the disease. In
such cases it will also be small and feeble.

A high temperature is usually accompanied by a rapid pulse, and a low
temperature by a moderately frequent, full pulse. At the day of crisis,
when the temperature falls, the pulse will fall; and this occurs in the
severe as well as in the mild cases.

Subsequent to the third or fourth day in severe cases the pulse, in
addition to its frequency and feebleness, may exhibit dicrotism, or it
may be jerky, very compressible, and intermittent. Sometimes just
before death the pulse becomes markedly slow. The feebleness of the
pulse is ascribed by some to cardiac depression, the result of the high
temperature; by others it is claimed that the afflux of blood to the
left ventricle obstructs, and causes a deficiency in, the aortic
circulation. In other words, hepatization is adduced as a cause of the
feeble pulse. In chronic wasting diseases, in feeble, weak individuals,
or in those already suffering from cardiac disease, weakness of the
pulse is a very marked symptom.

I cannot regard a feeble pulse in pneumonia as due to the pulmonary
hepatization, for it is not that pneumonia which is most extensive that
is accompanied by the greatest heart-flagging. Heart-failure may exist
before, or just as, consolidation is beginning. In many pulmonary
affections the obstruction to the pulmonary circulation is greater than
in pneumonia, and yet there is no heart-failure. The pneumonia with the
highest temperature-range is not necessarily the pneumonia in which
heart-failure is most marked {328} or earliest to develop. There are
many diseases in which there is a much higher range of temperature and
yet no evidence of heart-failure occurs.

If a prolonged high temperature is the cause of feeble heart-power by
the parenchymatous changes which it induces in its muscular fibres,
such a high fever is not met with in pneumonia, and the heart is rarely
found at post-mortem to exhibit such changes. May not the
heart-failure, as indicated by a rapid, feeble, and intermittent pulse
in pneumonia, be due to the presence in the blood of a morbific agent
(as in certain infectious diseases) which so affects the nerve-centres
which supply the heart that its contractile power is diminished and its
rhythm disturbed? The pulse early shows commencing heart-failure by
each cardiac pulsation producing a variable filling of the arteries
with blood; hence the beats first vary in force, then waves occur, then
true intermissions. I have been able to detect this heart-insufficiency
by these variations of the pulse within twenty-four hours after the
onset of a pneumonia, and occasionally during the initiatory chill.

In children the pulse-rate is greatly increased; it may reach 200 in a
minute. It is very small, unequal and irregular, but never
intermittent.

In senile pneumonia the pulse is not a reliable indication. The pulse
may be only 50, and yet this would be a rapid pulse for the particular
case in which it occurs.

In old age, both in health and in disease, the pulse has a fictitious
hardness on account of arterial changes. The pulse may not be
intermittent or irregular, yet the heart may be very irregular and
intermittent in its action. Again, the pulse may be feeble and
intermittent and the heart be acting regularly.

Remittence of the pulse is quite common in senile pneumonia independent
of cardiac changes. The action of cold upon the surface in the aged is
very quickly indicated by the radial pulse lessening its volume and
strength, so that if the pulse at the wrist is taken it should be from
the arm which has been covered. To avoid error, the pulse in senile
pneumonia must be counted at the heart.

The surface of the body may be pungently hot and dry until the crisis
is reached, or it may be bathed in perspiration from the onset of the
disease. A moist surface has been regarded as a very favorable sign,
but when in the height of the disease the parched skin becomes moist
and the patient is not relieved, it is an unfavorable rather than a
favorable symptom, and is met with more often in fatal cases than in
those that recover.

In most cases of croupous pneumonia the expression of the countenance
is characteristic. It is one of anxiety, and over the malar bones is a
mahogany flush--not, as in typhus fever, diffused, but well defined and
circumscribed, so that it is sometimes called the pneumonic spot. While
the cheeks exhibit a spot of this dusky hue, the rest of the face may
have an earthy pallor. Bouillard states that the pneumonic flush on the
cheek is most marked when the pneumonia has its seat at the apex of the
lung. Some authorities state that the cheek flushes most or solely on
the affected side, while others[35] have shown that the cheek on the
side opposite to that affected is the one that is usually flushed. In
this connection it is interesting to mention the case of Jaccoud, who,
suffering from an attack of pneumonia himself, noticed for twenty-four
hours preceding the pneumonia signs a flush and a burning sensation in
the cheek opposite to the side affected. Usually one cheek is more
flushed than the other, and this is undoubtedly due to disturbance of
the vaso-motor system.

[Footnote 35: Barthez and Rilliet.]

When the impediment to the circulation is excessive, or when vaso-motor
disturbance is marked, the lips become cyanosed. At the time of crisis
the face becomes paler.

In about one-half the cases pneumonia is attended by an herpetic {329}
eruption upon the lips, nose, cheeks, or eyelids. It rarely appears
before the second or third day. It may not appear until the crisis is
reached. Herpes occurs with varying frequency in different years, but
is more commonly met in pneumonia than in any other febrile state. One
winter nearly every case of pneumonia in Bellevue Hospital was
accompanied by herpes labialis. When sweating exists and involves the
entire body, it is very frequently accompanied by sudamina, which are
either abundant or sparse, and seem to have a critical significance.

In children, while the surface of the body is hot and dry the
extremities are cool. The pneumonic flush instead of having a mahogany
tint assumes a bluish-white tint. Cyanosis of the extremities is more
frequent than in adults, and herpes labialis more common. All the
cutaneous symptoms are exaggerated in children.

In old age the pneumonic flush is often the first objective sign of
pneumonia. The eyelids alone are cyanotic. If the face is dusky at
first, it subsequently assumes a sallow hue, and the surface-heat,
which is greatest in the morning, is succeeded by a cold, clammy
perspiration.

Cerebral Symptoms.--The cerebral symptoms in the early stage of
pneumonia are not very significant. Headache is usually present at the
onset, and may continue throughout the disease. It usually steadily
diminishes after the third day. If it is severe in the evening, there
will be slight delirium at night--so slight as often to escape notice.
Delirium and convulsions rarely occur except in debilitated subjects
and in persons of enervating habits. It is most frequently met with in
alcoholic subjects, and then it assumes the character of delirium
tremens. It is an active, busy, restless delirium: the patient is
constantly talking, but seldom in a coherent manner. Sometimes, in
those who are not alcoholic subjects, the delirium may assume an active
and violent character. Whenever active delirium is present, it is
important to make careful and diligent search into the previous habits
of the patient.

Pneumonia of the apex is more apt to be accompanied by severe cerebral
symptoms than when it has its seat at the base.

Delirium may pass into coma. When delirium and headache are marked
symptoms, muscular tremors (subsultus tendinum) are very apt to occur,
with insomnia and frightful hallucinations. Indeed, these cerebral
symptoms are often so prominent in alcoholic pneumonia, and occur so
early, that the pneumonia may be wholly masked, and will only be
discovered by the temperature-range and by a careful physical
exploration of the chest.

When delirium is present in feeble patients, it assumes a low muttering
typhoid type, and a state of stupor is soon reached.

Among the rare nervous symptoms met with in pneumonia may be mentioned
photophobia, disturbances of vision, and deafness.

In children the cerebral symptoms are more prominent than in adults,
and they do not seem to be influenced by the extent of lung involved.
Stupor and restlessness on the one hand, or headache, delirium, and
convulsions on the other, may usher in pneumonia in children without
any prodromata.

Sometimes children pass rapidly into a semi-comatose condition which
has not been preceded by delirium or convulsions. Convulsions are as
common in children as they are rare in adults, and occur with greatest
frequency and severity during dentition. The convulsions may be general
and resemble those of epilepsy (pneumonie éclamptique of Barthez and
Rilliet), or they may attack single muscles or groups of muscles, the
child occasionally passing into a tetanic or opisthotonic condition.

If convulsions do not occur until late they are quickly followed by a
deep and fatal coma. A very rare occurrence is partial paralysis of the
muscles which were involved during the convulsive period. Such
paralysis is often {330} permanent. Again, the cerebral symptoms may
closely resemble those which attend cerebro-spinal meningitis--viz.
headache, constipation, great prostration, delirium, convulsions,
opisthotonos, and strabismus. As in meningitis, there is a peculiar
cry, and all the symptoms may point directly to the brain. These
symptoms are most likely to be present in the pneumonia of the apex in
children from five to seven years of age.[36]

[Footnote 36: This form is the pneumonie méninges of Barthez and
Rilliet.]

In senile pneumonia headache may persist throughout the entire attack;
it is usually accompanied by delirium of a mild type, especially when
the apex of the lung is involved. These patients are very loquacious
and have a constant desire to get out of bed.

Alimentary Tract.--The symptoms referable to the digestive apparatus
are neither diagnostic nor important. Nausea and vomiting are not
infrequent, and in about 15 per cent. of all cases are among the
initial symptoms. Gastric symptoms, when severe and persistent, greatly
endanger life. There is no characteristic appearance of the tongue: it
may be normal throughout, or covered with a creamy-white fur, which
becomes dry and brown as the disease advances. In severe cases and
toward the end of the disease the lips and tongue become brown, dry,
and cracked, and sordes collect on the teeth. Anorexia is marked at the
onset, and the thirst is intense. When convalescence commences the
tongue becomes clean and the appetite returns. Occasionally there is a
catarrh of the oral mucous membrane. Diarrhoea may occur as one of the
initial symptoms. It is most apt to be present when there are nausea
and vomiting. As a rule, the bowels are constipated and the stools dry.
In young children nausea and vomiting are more common, and in 50 per
cent. of the cases usher in the disease. They usually cease on the
second day, although they may persist until the crisis occurs.
Excessive and violent diarrhoea may precede a fatal termination.

In senile croupous pneumonia the tongue early becomes dry, shrivelled,
and covered with a thick brown coating, and is protruded with
difficulty. Although these patients do not complain of thirst, they
take with avidity fluids that are placed to their lips. As the period
of crisis is reached critical diarrhoea is of frequent occurrence.

Loss of strength occurs earlier and is more marked in pneumonia than in
any other acute disease except typhus fever. Pneumonia patients become
very weak within the first five days. The recovery of strength during
convalescence is rapid.

Urine.--The urine at the onset of pneumonia is scanty, high-colored,
and of high specific gravity. The amount of urea excreted is twice or
three times more than the normal. The excess of urea increases until
the crisis, and then suddenly diminishes with the fall in temperature,
often below the normal standard.[37]

[Footnote 37: The daily amount of urea normally excreted is subject to
great variations: it ranges between 355 and 460 grains. Parkes gives
the result of 25 different observations: the lowest estimate was 286.1
gr. and the highest 688.4 gr.]

Uric acid is also increased, and follows the same course as that of the
urea. The inorganic salts of the urine, especially the sodium chloride,
are diminished, and during the height of the pneumonia may be wholly
absent. Much has been written concerning this diminution, which is by
no means peculiar to pneumonia, but in no other acute disease is its
diminution so constant and marked a symptom. Sodium chloride is
probably retained in the system, for when the salt has been
administered in large quantities none has appeared in the urine. The
reappearance of the chlorides in the urine marks the approach of
convalescence, and when the crisis occurs they appear in excess,
following an opposite course to the urea and uric acid.

Although these last two ingredients are in very rare cases retained,
the {331} same as the chlorides, to appear when the crisis occurs,
their retention is usually accompanied by a critical diarrhoea, which
is followed by a prolonged convalescence. The diarrhoea is undoubtedly
due to the irritation caused by the urea.

Parkes[38] states that sulphuric acid is increased and phosphoric acid
is diminished, but Huss affirms that both acids are diminished. With
the increase of the urea and uric acid, and diminution of chlorides,
biliary pigment will appear in the urine, and occasionally the biliary
acids.

[Footnote 38: _On the Urine._]

Slight albuminuria is an ordinary phenomenon of pneumonia, and, though
usually met with in the second stage, it may appear at any time. This
symptom is present in 35 per cent. of all cases. Its presence is a
point of resemblance between pneumonia and other acute blood diseases.
The more severe the pneumonia, the more marked is the albuminuria. Some
have ascribed its presence to passive hyperæmia the result of the
pulmonary obstruction. This is questionable, except in those rare cases
where venous engorgement is indicated by cyanosis, enlargement of the
liver, jugular pulsation, etc.

In children the amount of urine corresponds to the quantity of fluid
taken.

Critical Phenomena.--At the end of the first week, during which all the
symptoms have increased in severity, the continued fall of temperature
tells us that convalescence is established. As the temperature falls,
profuse (critical) sweating occurs. Both of these phenomena may occur
to such an extent that for hours the condition of the patient is one of
collapse.

In rare cases death has occurred in the midst of these symptoms. The
respirations and pulse-rate are diminished in frequency, the pulse
being small and frequently exhibiting dicrotism. The cough becomes
loose, the dyspnoea abates, the flush disappears from the cheek, the
sputum is more copious, and is expectorated with less difficulty; it
loses the rusty color from metamorphosis of its hæmoglobin, diminishes
in viscosity, and no longer adheres to the side of the vessel, but
becomes more opaque, of a creamy consistency, and resembles that of
simple bronchial catarrh. When resolution is retarded, the
creamy-yellow tint may give place to an almost black hue, on account of
the excessive amount of pigment present. As convalescence advances, the
sputa become scantier, more mucous, watery, transparent and colorless.
At the time of crisis the intense thirst diminishes, the appetite
returns, pain in the side subsides, and the patient passes into a
quiet, natural sleep, to waken fully convalescent, suffering only from
extreme exhaustion.

Epistaxis, hæmaturia, and hemorrhage from the bowels sometimes occur at
the critical period, and may be regarded either as accidents or as the
result of the defervescence. After the crisis the amount of urea in the
urine (which during the height of the disease was augmented) falls to
normal or nearly to normal. Sodium chloride appears in the urine as
soon as the crisis occurs.

The critical phenomena in children are the same as in adults, and
frequently the fall in temperature is so great that for hours after the
crisis they lie half unconscious, with a cold surface covered with a
colliquative sweat. With the critical sweat there is often a catarrhal
flow from the nose. When children have been extremely restless or
delirious the crisis is marked by the patient passing into quiet sleep.

In old age, when recovery occurs, it is generally by crisis, and a
critical diarrhoea is much more frequent than a critical sweat.

In adults and in children the recovery of strength and flesh is rapid;
in the aged the period of convalescence is very prolonged, and often
does not begin (when the pneumonia is of the asthenic--typhoid--type)
until the fourteenth or fifteenth day; still, complete recovery may be
reached.

Symptoms indicating Danger.--When croupous pneumonia is to terminate
fatally, dyspnoea is greatly increased; the patient suddenly sinks; the
pulse {332} becomes extremely small, rapid, irregular, intermittent,
and dicrotic. Large moist râles are heard over the larger bronchi and
trachea, while the auscultatory signs of pulmonary oedema become more
and more apparent. The sputa become frothy, liquid, and blood-stained,
or are entirely suppressed. The respirations become more and more
hurried, the face is sunken and livid, the extremities are cold, and
the superficial capillary circulation is more and more interfered with,
as is indicated by the cyanosis. The body is bathed in a profuse cold
perspiration. The fatal issue is usually preceded by coma.

The temperature may steadily rise up to the time of death, or death may
occur in the defervescence. In alcoholic pneumonia death is preceded by
cerebral symptoms, such as somnolence, numbness of the limbs, a sense
of formication, and slight convulsive attacks.

In children death is often preceded by convulsions or coma. If the
disease is protracted, death may be preceded by extreme exhaustion and
collapse. Cyanosis and extreme rapidity of the pulse are usually
present in children just before the fatal issue.

Senile pneumonia may end fatally within a few hours after its onset in
a most unexpected manner. The aged patient walks apathetically about,
totters to the bed, lies down, and dies. If the pneumonia has existed
for a number of days, the signs of a fatal termination are sallowness
of the face, a cold clammy skin, expansion of the alæ nasi, and a
sudden rise or fall of the temperature. The inspirations become mere
gasps, and, following the apathy, the patient gradually lapses into
complete coma.

Symptoms which attend the Termination of Pneumonia in Abscess.--Acute
pneumonia terminates in abscess in from 1 to 2 per cent. of all the
cases. It is therefore a rare termination. It is most frequent in
debilitated, weak subjects and in those who have received a depressing
plan of treatment. The expectoration is exceedingly copious and fetid,
and the sputa are yellowish or yellowish-gray in color, consisting
almost wholly of purulent matter. Pigment is usually found in the
expectorated masses, and when shreds of pulmonary tissue are present
the diagnosis is established. The fever assumes a hectic type and is
accompanied by rigors and sweats.

After these symptoms have continued for a time, the patient grows
weaker and emaciated, and death results from exhaustion, from asphyxia
(when a large bronchus is plugged with pus), or from the discharge of
the abscess into a neighboring cavity.

DaCosta states that "pulmonary pneumonic abscesses are at the base of
the lung;" Fox locates them "at the apex;" Green, "on the upper lobe;"
I have found them in both situations.

The physical evidences of a lung-cavity are the most reliable signs of
pneumonic abscess. Abscess is a very rare termination of croupous
pneumonia in children. In old age the formation of abscesses is never
evinced by any well-marked symptoms. The finding of elastic fibres in
the sputa with the physical signs of a cavity are the only diagnostic
signs.

Symptoms which attend the Termination of Pneumonia in
Gangrene.--Gangrene as a termination of pneumonia has been found in
about 14 per cent. of cases.[39] This must be regarded as an
exceptionally high percentage. Its occurrence is usually accompanied by
symptoms of sudden collapse. The pulse becomes rapid, feeble, and
intermittent, the face is pale and of a deathly hue, and there is a
profuse expectoration of blackish-green masses containing shreds of
decomposed and decomposing lung-substance of an exceedingly fetid odor.
The breath is fetid and the whole body emits a cadaverous smell. The
rapidly-increasing prostration is sometimes accompanied by hemorrhage.

[Footnote 39: In 28 out of 200 cases (_Guy's Hospital Reports_, Sec.
vii., 1848).]

The sickening and indescribable odor of pulmonary gangrene is most
perceptible after an attack of coughing. Gangrene has its most frequent
site in {333} the lower lobes of the lung, and it is here that a
careful search must be made for the rather ill-defined physical signs
which attend its development. In old age, when a pneumonia is to
terminate in a gangrene, typhoid symptoms appear very early, and death
occurs with symptoms of the profoundest collapse within five days from
the initial chill.

Symptoms which attend the Termination of Pneumonia in Purulent
Infiltration.--The symptoms of purulent infiltration differ but
slightly from those of the third stage of pneumonia. When resolution
does not take place at the period of crisis, and the temperature
remains high, accompanied by symptoms of prostration and profuse putrid
expectoration, with none of the physical signs of resolution, purulent
infiltration is to be suspected. Death may result from exhaustion, or
recovery take place after a prolonged convalescence (see Fig. 38).

[Illustration: FIG. 38. Croupous Pneumonia in the Adult, terminating in
Purulent Infiltration: Death on fourteenth day.]

Mild delirium is a frequent symptom during the stage of purulent
infiltration. The sputa contain a large number of cells in various
stages of fatty degeneration. The temperature has regular evening
exacerbations, and often ranges higher than during any preceding period
of the disease. The tongue becomes brown and dry, sordes collect upon
the teeth, and the patient passes into a typhoid state.

Typhoid pneumonia is a term which has been applied to a variety of
croupous pneumonia which is attended by typhoid symptoms. It has also
been called asthenic, low, or nervous pneumonia. There are symptoms of
extreme prostration from its onset. After well-marked pneumonic
symptoms have been present for a few days, the patient passes into a
condition of extreme prostration.

There is little or no expectoration, no dyspnoea, no pain, no cough.
Sordes collect on the teeth and gums; the tongue becomes thickly coated
with black crusts; the pulse becomes small, feeble, and rapid, and
there is a tendency to the formation of bed-sores; and then occur
stupor, somnolence, and a continuous low muttering delirium. This form
of pneumonia is met with most frequently in the aged. In some cases
there is marked disturbance of the special senses.

Tremors and subsultus tendinum frequently coexist. It may be
accompanied by glandular swellings, by sharp and darting muscular
pains, by arthritic symptoms, or by great gastric disturbance. It is
not infrequent in epidemics, {334} and it may follow or accompany
erysipelas, Bright's disease, alcoholismus, or phlebitis. It is always
a grave condition, but recovery is possible. Convalescence, which is
very tedious, may commence as early as the twelfth or fourteenth day.
Sometimes a modification of typhoid pneumonia accompanies dysentery,
intestinal catarrh, or a phlegmonous gastritis. There are great
sweating, profuse diarrhoea (colliquative), and high fever. The odor of
the sputa resembles that of gangrene of the lungs. Such cases commonly
end fatally.[40]

[Footnote 40: _Cyclo. Pract. Med._, iii., art. "Gastritis."]

Bilious or Gastric Pneumonia.--Croupous pneumonia occurring in malarial
districts, accompanied by gastro-enteric or hepatic symptoms, is known
as malarial or bilious pneumonia. It has all the characteristic
symptoms of pneumonia of a very severe type, but the fever is
paroxysmal. The tongue is heavily coated; nausea and vomiting are
common, and may persist throughout its entire course; the epigastrium
is distended and tender; the skin is jaundiced; the liver is enlarged,
and there is usually an exhausting diarrhoea, attended by greenish,
black, viscid, and inodorous stools. The hepatic congestion and
jaundice are due to a coincident gastro-duodenal catarrh.

Bilious pneumonia may be of a sthenic or asthenic type. The theory that
the liver becomes inflamed by extension from the lung is untenable.

The symptoms of bilious pneumonia have frequently led to a diagnosis of
typhoid gastric fever or some severe acute affection of the intestinal
tract. But a reference to the physical signs will remove all doubts.

Bilious pneumonia runs a more protracted course and has a much longer
period of convalescence than ordinary croupous pneumonia. In old age
this form is not infrequent. The vomiting is distinctly bilious in
character, and at this period of life somnolence and stupor are quite
common, and are exceedingly unfavorable symptoms.

Latent Pneumonia.--Pneumonia in adults is seldom latent unless it
complicates some disease whose symptoms are so severe, and the
attending prostration is so great, as to obscure the characteristic
signs of the pneumonia. Intercurrent senile pneumonia is always latent,
and Grisolle says that an exploration of the thoracic organs in the
majority of such cases gives negative results. If, then, an
intercurrent senile pneumonia runs its course without expectoration,
without dyspnoea, without the pneumonic flush, and without any of the
physical signs of pneumonia, its diagnosis must rest--first, on the
extreme frequency of pneumonia in old age; secondly, on the fact that
of all the phlegmasiæ of advanced life pneumonia is the one which is
oftenest latent; thirdly, that of all the acute diseases in old age
pneumonia is attended by the highest range of temperature and the
greatest prostration. When an old person has a slight rigor followed by
febrile movement, with great prostration, for which no explanation can
be found, pneumonia may be suspected, even though all its diagnostic
signs are absent.

Intermittent or remittent pneumonia, which is described by some authors
as a distinct type, is a form of acute pneumonia in which a malarial
element is so pronounced that all the pneumonic symptoms, even the
physical signs, undergo distinct intermission, returning each day with
increasing severity. Occasionally, instead of the quotidian it assumes
the tertian type. During the intermission the temperature may fall to
normal. Severe chills and sweating are often present, and the pneumonia
is not infrequently double.

The malarial conditions which give rise to this type of pneumonia occur
more frequently in our Southern and Western States than in any other
part of the world.

PHYSICAL SIGNS.--By studying the physical signs of croupous pneumonia
in connection with the different stages of its morbid anatomy, their
importance as elements in diagnosis and prognosis can best be
appreciated.

{335} Stage of Engorgement.--The physical signs indicative of the first
stage of croupous pneumonia are usually present within twenty-four
hours after its invasion. If the pneumonia is central, their appearance
may be delayed until the third day.

Inspection.--On inspection the movements of the affected side are
noticed to be more or less restricted, while the unaffected side moves
as in health. In double pneumonia the respiratory movements will assume
a costal type, attended by an increase in the abdominal breathing.

Palpation.--On palpation there is more or less increase in the vocal
fremitus on the affected side. The degree of increase corresponds to
the extent of the engorgement. It must always be remembered that
normally the vocal fremitus is more marked on the right side than on
the left.

Percussion.--There is slight dulness over that portion of the
chest-wall which corresponds to the affected portion of lung: its
extent varies with the amount of lung involved. It is never well marked
until the end of the first stage, although the pulmonary capillaries
are engorged with blood from the commencement. Even at the end of this
stage the intensity of the percussion sound, although diminished and
muffled, has a slightly tympanitic quality, due to the fact that the
exudation has not completely displaced the air in the distended
alveoli. Very extensive central pneumonia may fail to give either
increase in vocal fremitus or dulness on percussion until the second
stage is well advanced. Absolute dulness during this stage is of rare
occurrence.

Auscultation.--During the dry stage, which according to some[41] is
said to precede the exudation stage, there will be noticed a feebleness
and unnatural dryness of the respiratory murmur. Sometimes it is harsh,
at others feeble and loses the peculiar breezy, rustling quality of the
normal respiratory sound. If it is less intense over the affected
portion of the lung, it is exaggerated over the unaffected portion.
These changes are apt to pass unrecognized unless auscultation is
practised frequently and early in the disease. As soon as the
engorgement is well marked and exudation takes place into the
air-cells, fine crackling sounds are heard at the end of inspiration.
These sounds are called crepitant râles, and are regarded as the
characteristic sign of the first stage of pneumonia. They resemble
those produced by throwing salt on live coals or rubbing the hair in
the neighborhood of the ear between the fingers. These râles do not
necessarily depend upon the presence of fluid in the alveoli, but may
arise from the sudden separation of the alveolar walls at the end of
inspiration when they have been agglutinated by a tenacious exudation.
They are as numerous as they are minute, are unaffected by coughing,
and remain audible over a circumscribed space from twelve to
twenty-four hours. Whenever the pneumonic stages follow each other in
rapid succession, the crepitant râle may not be heard. It is rarely
present in a pneumonia which is developed during an attack of acute
articular rheumatism. With the crepitant râle the respiratory murmur is
feeble or assumes a broncho-vesicular character.

[Footnote 41: Stokes.]

When, as often happens, pneumonia has been preceded by or complicates
any other thoracic affection, the crepitant râle will be mingled with
the sounds arising from that particular condition. It is said[42] that
bronchial breathing is sometimes heard in this stage of pneumonia. The
voice-sounds undergo slight increase in their intensity over the seat
of the pneumonic engorgement.

[Footnote 42: Traube, _Annal. der Charité_, i. 286.]

In children the crepitant râle is frequently absent, and, though it may
be heard at the end of a full inspiration after coughing, it is never
so fine or distinct as in adults. In children there will be no increase
in vocal fremitus if, as often happens, a large bronchus leading to the
inflamed spot is plugged with mucus.

{336} In old age the physical signs of adult pneumonia are modified by
certain physiological changes which occur in the lungs and chest-cavity
of the aged. The more complete bony union of the chest-walls, the
curvature of the spine, the rigidity of the bronchial tubes, the
rounded form of the chest, and the senile rarefaction of the lungs,
give rise to extra resonance on percussion as compared with an adult
chest. On account of the great arching of the sternum and the
deposition of carbonaceous material at the apex of the lung, the
clavicular region near the median line gives a dull percussion sound.
The scapular and supra-scapular regions are less resonant than in the
adult, on account of the tilting of the scapulæ due to curvature of the
spine. There is a loss in the vesicular element of the respiratory
murmur, and it resembles the sound produced by a forceful expulsion of
air from the compressed lips. When the septa or the alveoli are torn
and greatly distended, it has a bronchial character. Its intensity
varies: at one moment it is loud, at another hardly perceptible; the
variation occurs not only in the same individual, but in different
individuals of the same age. The vocal sounds are loud and
bronchophonic in character, and have a vibration closely resembling
oegophony. It is also to be mentioned that it is almost a physiological
condition for old people to have bronchorrhoea; hence mucous râles may
be present during the whole period of advanced life, and if one relies
on the usual crepitating râles of adult pneumonia for a diagnosis he
will be misled.

Inspection and palpation in the first stage of senile pneumonia furnish
little positive information. Percussion will give little dulness until
the lung has reached the stage of red hepatization, and even then it
may be so slight as to pass unnoticed. Very early in the disease the
respiratory murmur is feeble and indistinct over the affected portion,
while the portion of lung that is not involved assumes, for the time,
all the characters of a normal adult respiratory murmur. Again, the
breathing over the pneumonia may be intensely puerile and interrupted.

The crepitant râle is rarely present in the first stage of senile
pneumonia, but subcrepitant râles and large moist râles resembling
those of bronchitis are heard during the whole of this stage. The
explanation of the absence of the crepitant râle is to be found in the
physiological condition of the air-cells just referred to. Sometimes,
on a deep inspiration after violent coughing, fine crepitation is
heard, but upon careful examination it will not be found to differ from
the râles of capillary bronchitis. It may be stated as a general rule
that the feebler and more superficial the respirations the less
distinct will be the adventitious sounds.

The physiological rigidity of the bronchi in old age favors the early
development of bronchial breathing, which is often the first physical
sign of senile pneumonia. One of its peculiarities, when occurring in
the stage of engorgement, is that it is most distinct at the root of
the inflamed lung.

Stage of Red Hepatization.--The physical signs of the second stage of
croupous pneumonia are more diagnostic than those of either of the
other stages.

Inspection shows the expansive movements of the affected side to be
more markedly diminished than in the first stage, while those of the
healthy side are increased. Frequently there is absolute loss of motion
over the inflamed lung.

Palpation.--By palpation the vocal fremitus is usually increased on the
affected side over the consolidated lung-tissue. In some instances it
may be only slightly increased, and in rare instances it will be found
less marked upon the affected side than upon the healthy. Palpation may
also reveal slight displacement of the heart from the pressure of the
distended lung; and in rare cases well-marked pulsation is felt over
the affected lung.[43]

[Footnote 43: Skoda, Stokes, and Graves regard this as the result of
increased pulsation of the arteries in the inflamed spot; and Walshe
and Fox rather admit it, but Grisolle denies it.]

{337} It is evident that the vibrations of the vocal cords can be
transmitted from the trachea through the bronchi and lung to the
chest-wall, and there is no reason why the cardiac impulse may not
likewise be transmitted through a solidified lung to the chest-wall.

If the pneumonia is central, the vocal fremitus may not be increased.
It is diminished when there is an abundant pleuritic exudation over the
pneumonic lung.

Percussion.--On percussion there will be marked dulness over that
portion of the lung which is the seat of the pneumonia, while over the
healthy portion, as well as over the opposite lung, there will be
exaggerated resonance. The nearer the hepatization approaches the
surface of the lung, the more marked will be the dulness. There is a
peculiar sense of resistance on percussion over a completely airless
hepatized lung which is not present in solidification from other
causes. The exact outline of an hepatized lobe can often be traced on
the chest-wall.

The tympanitic quality which is sometimes present during the stage of
engorgement may continue anteriorly during the second stage, and yet
posteriorly the dulness will be complete. A tympanitic percussion sound
is sometimes elicited over that portion of lung which is adjacent to
the consolidated lobe. When an upper lobe is consolidated, forcible
percussion may elicit a tympanitic sound, for the column of air in a
large bronchus will vibrate under forcible percussion. The cracked-pot
sound (bruit de pot fêlé) is occasionally met with over those relaxed
and permeable parts of the lung in the immediate vicinity of the
consolidation. When this sound is present over the consolidated
portion, it is due to the sudden expulsion of air from one of the
larger bronchi. It is most frequent in young persons with thin, elastic
chest-walls. The cracked-pot sound in pneumonia is not increased in
intensity when the patient's mouth is open.

In basic pneumonia the subclavicular percussion note may be distinctly
amphoric in character. Dulness may appear within twelve or twenty-four
hours after the onset of a pneumonia, or it may be delayed until the
fourth day.

Auscultation.--As soon as the air-cells are completely filled by the
pneumonic exudation, the crepitant râle ceases and bronchial
respiration is heard over the affected lung. The bronchial breathing is
due to the fact that the vesicular element of the respiratory sound
disappears on account of the complete consolidation of the vesicular
structure, and the tracheal element of the respiration is conveyed to
the chest-walls through the consolidated lung. It often has a metallic
element, or may sound like the tearing of a piece of linen. Bronchial
respiration is more intense in pneumonia than in any other disease.

Laennec taught that bronchial respiration was due to the superior
conducting power of condensed lung. Skoda combats this view, and says
that bronchial respiration is generated or magnified in caverns and in
the bronchi of condensed lung-substance by the air in these cavities
and in the bronchi vibrating in consonance with that within the
trachea. The condition necessary for this consonance is provided in the
circumstance that the air is pent up in confined spaces whose walls
reflect the sonorous undulations.

The more complete the consolidation, the more intense is the bronchial
respiration. At the commencement of this stage the tubular breathing
only attends expiration, while later it accompanies both acts.
Pleuritic exudation may mask or render this sound very indistinct. It
may in rare instances be absent even when extensive consolidation
exists and the pleura is perfectly normal. This can be accounted for in
most cases by the plugging of a large bronchus. There are cases in
which its absence is inexplicable.

The vocal sounds are increased in intensity and bronchophony is heard
{338} over the consolidated lung. The physical conditions of the lung
which give rise to bronchophony have the same diagnostic significance
as the bronchial respiration, and in all instances its occurrence, its
distinctness, its temporary disappearance, and its reappearance are
dependent upon precisely the same conditions as are the changes in the
bronchial respiration. If the pleural cavity is partially filled with
fluid, bronchophony will be indistinct or absent below the level of the
fluid, while at its level the voice-sounds will be either bronchophonic
or oegophonic.

During this stage the heart-sounds are transmitted to the surface over
the hepatized lung with greater intensity than normal.

In children dulness is especially marked in the infra-scapular region
of the affected side. Some authors[44] speak of a feeling of greater
solidity below than above the scapula, which can be detected before the
ear can detect actual dulness on percussion. Vocal fremitus may be
increased, but it is not reliable on account of the changes in the
voice.

[Footnote 44: West.]

In old age, inspection and palpation give negative results. Dulness on
percussion in old age would be regarded as normal resonance in the
adult; hence the percussion sound in senile pneumonia may be only
relatively dull. The tubular or bronchial breathing in the second stage
of senile pneumonia is more intense than in adult pneumonia. Small
gurgles or mucus râles generally persist throughout this stage.
Bronchophony is not well marked. On causing the aged patient to cough
and expire violently, tubular breathing may be heard where it was
before absent.

Stage of Gray Hepatization.--There is no abrupt transition from the
second to the third stage of pneumonia, so that the physical signs of
the early part of gray hepatization are the same as those of the second
stage.

Inspection.--As resolution progresses, expansive motion on the affected
side becomes more and more apparent.

Palpation.--On palpation the vocal fremitus will be found approaching
normal, its intensity diminishing as resolution occurs.

Percussion.--Dulness on percussion becomes less and less marked, but of
all the signs this is the last to disappear. Rare cases are mentioned
where it has disappeared in twenty-four hours after the commencement of
resolution by crisis. As the percussion sound approaches the normal, a
tympanic note is again present in circumscribed spots.

Auscultation.--The bronchial respiration that was present in the second
stage gives place to broncho-vesicular breathing. This soon becomes
blowing, then indeterminate, and finally approximates to, and merges
into, normal vesicular breathing. Bronchophony gives place to
exaggerated vocal resonance in connection with the changes in the
respiratory and vocal sounds. The crepitant râle returns, but is soon
obscured by larger and moister crepitating sounds, "the resolving
subcrepitant râle of pneumonia," called also the râle redux. Large and
small mucus râles, sibilant and sonorous, accompany the subcrepitant
râles, to disappear only when resolution is complete. Not infrequently
the bronchial râles that are developed during the stage of resolution
are of that character called consonant[45] or ringing.[46]

[Footnote 45: Skoda.]

[Footnote 46: Traube.]

The physical signs of this stage are all retrogressive, and they
disappear in the opposite order to that in which they appeared. In rare
instances resolution is so rapid that the subcrepitant râle is not
heard. In this class of cases dulness on percussion and bronchial
breathing continue for some time after the crisis.

In children, bronchial breathing rarely disappears before the seventh
day. It is often accompanied by the subcrepitant râle. When resolution
takes place, bronchial breathing and the subcrepitant râle will
disappear at the same time.

{339} In old age, inspection, palpation, and percussion give similar
results as in adult pneumonia. On auscultation coarse crepitating
sounds and loud gurgles are often heard at a distance from the site of
the pneumonia. The râle redux is not distinctive of or peculiar to the
third stage of senile pneumonia. The sounds heard during this stage are
called mucous crepitations, by which is meant liquid crepitating râles
produced in tubes intermediate between the bronchioles and the larger
bronchi.

If pneumonia terminates in purulent infiltration, the temperature
remains high and symptoms of great prostration are developed. The
bronchial breathing continues, and becomes more intense, dulness on
percussion persists, and sharp, high-pitched râles resembling fine
gurgles are abundant.

The occurrence of abscess or gangrene is indicated by the physical
signs which attend the formation of cavities in consolidated
lung-substance.

No one of the physical signs which is present in the different stages
of pneumonia is sufficient for a diagnosis, but the manner and order of
their occurrence, and their relation to the symptoms which mark the
different stages of the disease, enable one to reach a positive
diagnosis in all typical cases. The only symptom of croupous pneumonia
which can be regarded as diagnosticated is the sputum.

The physical signs of pulmonary abscess in the aged are very generally
wanting. Distinctly localized gurgling and cavernous respiration may,
when taken in connection with the rational signs, suffice for an
approximate diagnosis, but the great rarity of abscess in old age
should make one cautious in its diagnosis. The sputa will greatly aid
in such cases.

The physical signs of senile pneumonia are subject to greater
variations than ever occur in pneumonia in the adult, and often they do
not even follow the course, irregular as it is, which has just been
described.

Gray hepatization or abscess may be reached without any distinctive
auscultatory signs, even after repeated and careful examination. The
râle redux of resolution may be absent, dulness and bronchial breathing
being immediately followed by normal (senile) resonance without
crepitation. This occurs most frequently in the typhoid variety.

DIFFERENTIAL DIAGNOSIS.--In typical cases of croupous pneumonia (except
in childhood and old age) the diagnosis is not difficult. The prolonged
chill of invasion, the rapid rise of temperature, the accelerated,
panting respiration, pain, cough, characteristic sputum, increase in
vocal fremitus, dulness on percussion, the crepitant râle, bronchial
breathing, and bronchophony are sufficient to establish the diagnosis.

Croupous pneumonia may be confounded with acute pulmonary congestion
and oedema, capillary bronchitis, pleurisy, hypostatic congestion,
catarrhal pneumonia (in children), pulmonary apoplexy, meningitis, and
typhoid fever.

Pneumonia begins with a chill, while pulmonary oedema has no chill.
Pneumonia is a febrile disease, while in pulmonary oedema there is no
rise in temperature. In pneumonia there is pain in the side; there is
no pain in pulmonary oedema. The sputum in pneumonia is viscid, rusty,
and microscopically pathognomonic; pulmonary oedema is accompanied by a
profuse watery expectoration. Pneumonia is commonly unilateral, and can
occur in any part of the lung, while pulmonary oedema is bilateral, and
usually occurs in the most dependent portion of the lung. In pneumonia
we have the crepitant, dry râle, while in pulmonary oedema we have
subcrepitant râles, larger and more liquid than those in pneumonia.
Bronchial breathing and bronchophony occur in pneumonia, and are absent
in pulmonary oedema. Percussion dulness is more marked in pneumonia
than in pulmonary oedema, and the diseases with which the latter
condition is apt to arise will aid us very much in the diagnosis.
Urinary symptoms are negative in pulmonary oedema, while in pneumonia
the chlorides are diminished or absent.

{340} The stage of resolution in pneumonia is not infrequently mistaken
for general capillary bronchitis, but, though the subcrepitant râle is
present in both, it is heard all over the chest in capillary
bronchitis, while it is confined to a comparatively small space in
pneumonia. The expectoration is muco-purulent in bronchitis, and viscid
and fibrinous in pneumonia. The temperature is lower in bronchitis
(100°-103°) than in pneumonia (104°-106°). Capillary bronchitis is
bilateral, pneumonia usually unilateral. Capillary bronchitis does not
commonly begin with a chill, like that which occurs in pneumonia, but
comes on more insidiously and without pain. Capillary bronchitis gives
an exaggerated percussion note, while there is dulness on percussion in
pneumonia. There is bronchial breathing in pneumonia, and a feeble
vesicular murmur in capillary bronchitis. In capillary bronchitis the
cyanotic appearances are very much more marked than in pneumonia, and
there is no perversion of the pulse-respiration ratio. The breathing is
labored in capillary bronchitis, and panting in pneumonia. In capillary
bronchitis there are several slight attacks of chilliness; in pneumonia
there is usually only one chill, at the onset.

The chief points in making the diagnosis between pneumonia and pleurisy
are the pain, sputum, and percussion note. Pneumonia is ushered in by a
distinct chill, followed by a rise in temperature to 104° to 105°,
while pleurisy begins with chilliness or a number of slight rigors, and
the temperature is lower, rarely above 100°. The dry hacking cough of
pleurisy may be accompanied by slight mucous expectoration, while in
pneumonia the expectoration is characteristic. In pleurisy the
breathing is catching; in pneumonia it is panting. In pleurisy the face
is pale and anxious; in pneumonia the cheek bears a dull
mahogany-colored flush. In pleurisy the pulse is firm, small, tense,
and wiry; in pneumonia it is full and bounding. The amount of chlorides
in the urine is not altered in pleurisy, but in pneumonia they are
diminished or absent. The pulse-respiration ratio is not affected in
pleurisy, while in pneumonia it may fall as low as 2:1. There are no
critical days in pleurisy, while in pneumonia crisis occurs about the
fifth or seventh day. In pleurisy with effusion there may be bulging of
the intercostal spaces, and the heart may be displaced; these phenomena
never occur in pneumonia. The vocal fremitus is feeble or absent in
pleurisy, while in pneumonia it is much increased. In pneumonia there
is dulness on percussion, while percussion over a pleuritic effusion
elicits flatness, which changes with the position of the patient. In
pleurisy the grazing, rubbing, or sticky friction-sound may be heard
with both respiratory acts; in pneumonia we hear the crepitant râle. In
pleurisy the respiratory sounds are feeble or absent, as are the vocal
sounds, while bronchial breathing and bronchophony are marked in
pneumonia. It may be remembered, however, that if adhesions from an old
pleurisy bind the lung to the chest, vocal fremitus may be increased in
pleurisy. Again, bronchophony and bronchial breathing may exist in
pleurisy, but they are always diffuse, never sharp and tubular, as in
pneumonia, and are usually confined to the scapular region.

Hypostatic congestion of the lungs is accompanied by copious, watery,
blood-stained expectoration. In pneumonia the sputa, though bloody, are
rarely watery. Pneumonia occurs anywhere in the lung, and has
well-marked rational symptoms; hypostatic congestion occurs in the most
dependent portion of the lung, disappears when the patient sits up, is
accompanied by no rational symptoms except dyspnoea and expectoration,
and usually can be traced to a long-continued recumbent posture in
those who are suffering from extensive blood-changes.

It is often difficult to decide whether a child has catarrhal or
croupous pneumonia. It is to be remembered that catarrhal pneumonia is
always secondary, while croupous is primary. Catarrhal pneumonia
usually follows {341} a bronchitis, croupous pneumonia rarely. In
catarrhal pneumonia both lungs are involved; in croupous but one, and
often only a single lobe. Catarrhal pneumonia is accompanied by a
catarrhal sputum, while croupous pneumonia has a viscid, rusty,
fibrinous expectoration. There is no day of crisis in catarrhal
pneumonia, while croupous pneumonia in children almost always ends in
well-marked crisis. In catarrhal pneumonia dulness on percussion is
generally confined to the posterior dorsal region, and does not extend
so far forward as in lobar pneumonia. Again, the extent of the physical
signs and the rapidity of their development in catarrhal pneumonia are
in contrast with those of croupous.

The range of the temperature is a most valuable guide in their
differential diagnosis, since not only the height of the fever is
greater in croupous, but the temperature-curve is different, as seen in
the accompanying tracings:

[Illustration: FIG. 39. Acute Lobar (croupous) Pneumonia in a Child:
Recovery.]

[Illustration: FIG. 40. Acute Lobular (catarrhal) Pneumonia in a Child:
Recovery.]

Pulmonary apoplexy is rarely met with independent of valvular disease
of the heart or pyæmia. It is a non-febrile disease, while pneumonia
has marked pyrexia at the onset. In pulmonary apoplexy dyspnoea is very
intense and comes on abruptly; in pneumonia it comes on slowly and
progressively increases. The expectoration in pulmonary apoplexy
consists of small, black sooty-looking coagula, while in pneumonia the
viscid fibrinous mass contains numerous cell-elements other than
blood-corpuscles. In apoplexy the dulness is distinctly circumscribed,
and around it moist râles are heard, while in pneumonia the area of
dulness is more extended and râles are heard over the seat of the
dulness. The urinary symptoms are negative in pulmonary apoplexy; in
acute pneumonia the chlorides are diminished or absent. There is a
peculiar acid odor to the breath--an odor like that of tincture of
horseradish--in pulmonary apoplexy, never found in pneumonia.[47]

[Footnote 47: Guéneau de Mussey.]

When croupous pneumonia has its seat at the apex of the lung, it may be
{342} confounded with the first stage of phthisis. But the history of a
chill followed by the characteristic pneumonic symptoms will generally
enable one to make the differential diagnosis. Besides, the fever in
phthisis is irregular and is subject to irregular exacerbations and
remissions. If the signs of consolidation persist with little or no
change, if the temperature at no time falls to normal, if there are
night-sweats, if emaciation is progressive,--then the case is to be
regarded as one of phthisis, even though there may have been pneumonic
consolidation complicating it.

In children pneumonia is so frequently accompanied by marked nervous
symptoms that it may be mistaken for meningitis. Meningitis is
developed insidiously; has but slight febrile symptoms (102-103° F.),
which remit with comparatively great regularity; has a pulse which is
often slower than normal; has no thoracic symptoms, no dyspnoea nor
accelerated breathing; the face is pale and anxious; and the physical
signs of pneumonia are absent.

Sometimes a latent pneumonia with typhoid symptoms is mistaken for
typhus fever: especially is this the case when the latter is
prevailing. I frequently saw cases where such a mistake had been made
while in charge of the typhus-fever patients on Blackwell's Island
during a typhus epidemic. In these cases there will be active typhoid
symptoms, such as dry tongue, delirium, high temperature, etc. The
countenance in this pneumonia, although the cheeks may have a purplish
hue, does not exhibit that dull, heavy leaden expression so commonly
seen in typhus fever. Although there may be delirium in both instances,
the delirium in the former disease is of a milder type than in the
latter. The characteristic pneumonic expectoration is often absent in
this class of cases; therefore it cannot be relied upon as a point in
the differential diagnosis. If pulmonary consolidation is a
complication of typhus fever, it will not be developed until after the
sixth day of the fever, the time when the eruption is visible. If no
eruption is present, the pneumonic consolidation may be regarded as the
primary affection, and the symptoms which simulated those of typhus
fever may be regarded as secondary.

Pneumonia with typhoid symptoms is sometimes mistaken for typhoid
fever. It is called typhoid pneumonia. The differential diagnosis is
not difficult if one remembers that the pneumonia which complicates
typhoid fever does not come on until late in the fever, and the regular
history of typhoid fever precedes its development. On the other hand,
when the typhoid symptoms are present from the beginning or come on at
the end of the second stage of pneumonia, the physical signs of
pneumonia will attend or precede the typhoid symptoms. If a patient
over sixty years of age with this type of pneumonia is not seen until
the second or third week of his sickness, although evidences of
lung-consolidation may be found, it will be very difficult to decide
whether the pneumonia is or is not complicating a typhoid fever; and
under such circumstances a differential diagnosis may be impossible.

PROGNOSIS.--The mortality-rate of pneumonia is shown by the following
statistics: Of 12,421 cases treated in the hospitals at Stockholm, 11
per cent. died. In the Vienna hospitals 24 per cent. died. The Basle
hospital's report for thirty-two years gives 23 per cent. of deaths,
Grisolle reports 59 per cent. of deaths in those over sixty years of
age. In the United States medical reports from May 1, 1861, to July,
1866, of 61,202 cases which occurred among the white troops, 14,738
died, or a little more than 24 per cent.; and of 16,133 among the
colored troops (for the same period) 5233 died, or nearly 33 per cent.
The deaths from all other inflammatory diseases of the respiratory
organs for the same period were only one-seventh as many as from
pneumonia. The Confederate hospital reports give the rate of mortality
from pneumonia for twenty-five months of the same period as 33-1/3 per
cent. Of 255 cases treated in my wards in Bellevue Hospital during a
period of four years, the rate of mortality was 34 per cent.

{343} The statistics given of private practice differ remarkably from
those of hospital reports, and are somewhat contradictory. Of Lebert's
205 cases, 7-3/10 per cent. died. Ziemssen lost only 3-1/3 per cent. of
his cases. Bennett (mentioning, however, that no complication existed)
lost none of his 105 cases. Brundes of Copenhagen lost more than 21 per
cent. of his 142 cases. Wilson Fox gives to pneumonia the fifth, and
Walsh the third, place among fatal diseases. The mortality-average from
all the published reports to which I have had access gives 20.1 per
cent. of deaths.

From such facts it must be admitted that a disease in which death
occurs in 1 out of every 5 cases should be classed among the very fatal
diseases. But the death-rate varies very much at different times: it is
to-day the same as when Andral wrote, nearly fifty years ago. He stated
that it varied from 33 to 2 per cent. There can be no doubt but that
treatment somewhat influences the variations in the
mortality-statistics, but not to such an extent as to account for the
great differences in the reports of different observers.

The prognosis depends more upon the age of the patient than upon any
other single element. In infancy the mortality is greater than in early
childhood, in which period statistics give from 4 to 6 per cent. as the
ratio. The period of dentition seems to influence the prognosis in
children. Between the ages of forty and sixty the death-rate is from 10
to 25 per cent.; uncomplicated cases will recover. After sixty the
prognosis is exceedingly grave, and the greater the age of the patient
the less are the chances of recovery.

Statistics do not give pneumonia its proper place among the fatal
diseases of old age. My own experience leads me to believe that it is
the most fatal of all acute diseases at this period of life, for the
large number of autopsies in which it has been found to be the cause of
sudden death in individuals of advanced years, and the frequency with
which red or gray hepatization is found at the autopsy when pulmonary
disease was not suspected during life, must greatly increase the
statistical rate of mortality. Many modern authorities, who have had
large experience in the hospital practice of the aged, state that
nearly nine-tenths of those who die over sixty-five die of pneumonia.
Pneumonia is more fatal in females than in males, in the proportion of
about 3 to 2.

Statistics vary in regard to the influence of seasons on the prognosis
in pneumonia. In some years the proportion of deaths is far greater in
summer than in either the spring or winter. And it must be acknowledged
that certain as yet unknown atmospheric influences are of the utmost
importance in determining the death-rate in different years. Statistics
do not show that the mortality-rate is greatest during cold weather.

The prognosis is greatly influenced by the extent of the pneumonia.
Double pneumonia is not often recovered from, and pneumonia of an
entire lung is more dangerous than when only a single lobe is involved.
In pneumonia at the apex in infancy and old age the prognosis is
unfavorable. The more feeble the patient at the time of the attack, the
less are his chances of recovery. Previous attacks have no influence
over the prognosis.

Most authors make mention of certain diseases that complicate
pneumonia. Few give condensed statements of their influence on the
death-rate. In 255 cases of my own, 87 were fatal and 168 recovered. Of
these 255 cases, 124 were complicated and 131 were uncomplicated. Of
the complicated cases, 75 died; of the uncomplicated, 12. Of these
complications, alcoholism was present in 30 cases, pleurisy in 17,
Bright's disease in 13, pericarditis in 9, hypertrophy and dilatation
of the heart in 3, peritonitis in 2, fibrinous bronchitis in 1, and
rubeola in 1. Lebert in his statistical report on pneumonia states that
he lost only 5½ per cent. of his uncomplicated cases and all of his
complicated cases. Huss of Stockholm lost 6 per cent. of his
uncomplicated {344} and 20 per cent. of his complicated cases. Wilson
Fox says that, according to the reports of English physicians,
pneumonia complicated by endocarditis is fatal in 75 per cent. of the
cases; complicated by pericarditis, in 54 per cent.; by Bright's
disease, in 50 per cent.; and by alcoholism, in 25 per cent. Brundes of
Copenhagen in 120 uncomplicated cases lost only 6-2/3 per cent., while
of 22 complicated cases he lost all, or 100 per cent. Thus it is
evident from my own records, as well as from those of others which I
have given, that the rate of mortality in complicated pneumonia is much
greater than in uncomplicated.

By a careful study of these complications it is apparent that they all
exert a direct influence upon the heart, diminishing its power and
crippling its action by obstructing the blood-current from the right
ventricle toward the lungs. It is unnecessary to discuss these
complications in detail; it is sufficient to state that weakening of
the contractile power of the cardiac muscle is an essential feature of
endocarditis, pericarditis, Bright's disease, and alcoholismus. In all
acute infectious diseases such complications are regarded as dangerous,
because they increase the liability of heart-failure when such failure
is especially to be feared.

Other complications in addition to those already mentioned which
increase the mortality-rate in pneumonia are chlorosis, phthisis,
emphysema, laryngitis, oedema glottidis, bronchitis, pleurisy,
parotitis, pregnancy, erysipelas, and rheumatism. Bronchitis,
pleuritis, and jaundice do not seem to increase the mortality-rate very
much, although they certainly influence it; while pregnancy, parotitis,
and affections of the joints are very serious complications. Excepting
small-pox and cholera, abortion is more apt to occur during the course
of pneumonia than in any other acute disease.

A case of pneumonia may be called mild so long as the temperature does
not rise above 104° F.; an elevation of temperature above 106° F. for
two days renders the prognosis unfavorable. Wunderlich[48] says that a
gradual rise in temperature after the fourth day is always an
unfavorable symptom. A low temperature is dangerous only when the
respirations are very much accelerated.

[Footnote 48: In _Die Eigenwärme in Krankheiten_.]

When the pulse is 120 or 130 for two or three days, the prognosis is
bad; if the pulse reach 150 per minute, a pneumonia patient rarely
recovers. An irregular and intermittent pulse, and one whose tracing
exhibits dicrotism, has a most unfavorable prognosis. In children the
rapidity of the pulse is not of so much importance, while in old age
the pulse is seldom or never a reliable element in prognosis. A feeble,
irregular, and intermitted pulse is always an unfavorable symptom.

Prune-juice expectoration is also an unfavorable sign, as it indicates
extensive blood-changes or a depraved condition of the patient. If
there is an entire absence of expectoration in the second or third
stage of a pneumonia, or if it becomes scanty and difficult, the
prognosis is unfavorable. Any sudden suppression of the expectoration,
with coincident tracheal râles, in any period of the disease, indicates
impending death.

In adults delirium is an unfavorable symptom, except when it occurs at
the onset of the pneumonia. When delirium occurs late in one who is the
subject of chronic alcoholismus, it generally indicates a fatal
termination. Convulsions in children with great jactitation, and in old
age subsultus tendinum and a tendency to coma, are unfavorable signs.
Great exhaustion and signs of prostration, accompanied by a sunken,
pallid countenance and cold, clammy perspiration, are always attended
with danger. In children bronchial breathing after the seventh day,
numerous subcrepitant râles, copious and persistent diarrhoea, and
swelling of the veins of the hands, are unfavorable.

In old age a sudden rise or fall in temperature, apathy, somnolence,
and a {345} sallow countenance, are all symptoms indicative of great
danger. Any complication renders the prognosis unfavorable, and the
occurrence of pulmonary oedema or congestion in the unaffected parts of
the lung is to be regarded as a forerunner of death.

Purulent infiltration, the formation of an abscess, and the development
of gangrene are all attended with danger. Recovery from gangrene is
very rare.

Death does not result from heart-clot, for the conditions which favor
the forming of the clot precede its formation. The fibrin factors in
pneumonia are increased--often 400 per cent. more than normal. The
heart is so enfeebled that the right ventricle cannot empty itself; the
columnæ carneæ and the chordæ tendineæ whip up the residual blood
(already prepared for clotting). Heart-clot, it is well known, is the
rule when the death struggle is prolonged and the cardiac contractions
gradually become weaker and weaker. Such heart-failure is always the
beginning of death.

In seeking for the causes of death in pneumonia, observers have taken
the results of their post-mortems as a standard of their observations.
One finds oedema of the lungs at the majority of his autopsies, another
finds a clot in the heart in most of his fatal cases; hence the
conclusion is reached that pulmonary oedema and heart-clot are causes
of death in pneumonia. But it must be remembered that in every disease
there is a great difference between the cause and the mode of death.
If, as a result of the failure of heart-power during the last hours of
life, pulmonary congestion and oedema are developed and clots are found
in the heart-cavities, it ought not to be assumed that these conditions
are the cause of death. Jürgensen states that in fatal cases of
pneumonia oedema of the lungs is always present, and heart-clots are
frequently met with.

Death may occur, then, from heart-insufficiency, from some of the
complicating diseases (cardiac especially), or from asphyxia. In some
cases death seems to come from the overwhelming of the system with a
poison which acts primarily and principally upon the nervous system. In
a few cases fatal collapse has followed an apparently regular,
well-marked crisis.

TREATMENT.--The treatment of croupous pneumonia involves not only many
unsettled questions in modern therapeutics, but it embraces a history
of the therapeutics of inflammation. An heroic, antiphlogistic plan of
one period gave place to the rational plan of another, and that in turn
to the expectant plan of a later period, while to-day an antiseptic
method finds many advocates.

Regarding it as a general disease with characteristic local lesions,
and not a local inflammation with constitutional symptoms, its
treatment must vary with the constitutional condition of the patient
and the type of the disease. When uncomplicated and occurring at
certain periods and in certain conditions of life, it will terminate
spontaneously in recovery. But when certain complications exist and
certain conditions are present, and at certain ages, it is almost
necessarily fatal. Any plan of treatment in such a disease, if resorted
to indiscriminately, must needs be unreliable and unsatisfactory.

Although there is no doubt that a large percentage of cases of croupous
pneumonia will recover without treatment, there is also little doubt
but that well-directed therapeutical efforts can save lives and render
convalescence less tedious. If it is remembered in the treatment of
pneumonia that the pneumonic lung no more requires treatment than do
the intestinal ulcers in typhoid fever, and that we are to be governed
by the patient's general condition, and not by the physical changes in
the lung as indicated by the physical signs, it is evident that all
those measures which have been employed for the arrest of a local
inflammatory process have no place in our therapeutics. It is for this
reason that venesection, which at one time had its stronghold in {346}
the treatment of pneumonia, has now fallen into disuse. A summary of
the arguments against its practice seems to be conclusive, and the
numerous discussions that have so often distracted the most careful and
truthful observers are well expressed in the following terms:[49] 1st.
That indiscriminate bleeding immensely increases the mortality of the
disease. 2d. That it is specially fatal in old people and in young
children, in patients of exhausted constitutions, and in those
suffering from chronic diseases, and particularly from Bright's
disease. 3d. That it is absolutely unnecessary in the majority of cases
of young adults and also young children. 4th. That in the majority of
cases it has no influence whatever either in cutting short the disease,
in lessening its duration, or in diminishing the pyrexia, but that
occasionally these results appear to follow from its use when practised
early. 5th. That in the majority of cases it hinders the critical fall
of temperature and delays convalescence. 6th. That in the majority of
cases, as shown especially by Bennett's and Didel's data, recovery is
equally if not more rapid when it is not practised as when it is
resorted to. 7th. That in a few cases a moderate venesection may be
necessary in the early stages to avert immediate danger of death from
asphyxia.

[Footnote 49: Wilson Fox, _Reynolds's System of Medicine_.]

Not only does indiscriminate bleeding increase the death-rate and have
no influence over the progress, course, or severity of pneumonia, but
it postpones crisis and convalescence, and in the old, young, and
enfeebled is very often nothing less than a fatal procedure. In a
robust, vigorous individual, in spite of the fact that a free bleeding
at the very onset will temporarily relieve the urgency of some
symptoms, it nevertheless diminishes by so much the chances of
recovery, lessens the power to fight against the disease, and makes the
patient far more pregnable to subsequent dangers and complications.

Venesection has no influence upon the temperature. It may sometimes
postpone imminent death from asphyxia; and the fact that there is one
condition in which bleeding may be practised is no contradiction to the
foregoing statements, for venesection is then resorted to on account of
conditions that must be treated independently of the coexistent
pneumonia, such as sudden engorgement of the heart with blood, attended
with all the signs of sudden and extensive pulmonary oedema and
congestion. When the patient is vigorous and the above-mentioned
emergencies exist, free bleeding gives prompt relief. In no case should
more than ten ounces of blood be taken.

A careful study of the pathology of pneumonia not only leads one to the
conviction that venesection must do harm, but it strongly
contraindicates the employment of all those remedial agents which have
been used to arrest a simple pulmonary inflammation. Hence tartar
emetic, veratrum viride, aconite, and all other cardiac sedatives which
at one time were used so extensively have now fallen almost entirely
into disuse, as by their effects they can only add to the burden of a
heart already overtaxed by the venous stasis and the lack of arterial
blood. They may for a time lower the temperature and diminish the
pulse-rate, but they will accomplish this at the expense of
heart-power, and will almost certainly favor the earlier and more
certain development of that heart-insufficiency which must be regarded
as the most powerful death-producing agent in pneumonia. Dangerous
collapse has frequently followed the free use of these drugs.

Veratria is claimed to be a cardiac depressant; and this fact should
make us hesitate before we administer it in pneumonia. It acts promptly
in slowing the pulse, but its effects are only temporary, and when used
for a couple of days the larger doses that are necessary to bring about
the desired results interfere with the nutrition of the patient, often
causing vomiting and diarrhoea. Aconite is also a cardiac sedative, but
my experience with it has {347} convinced me that it is in all respects
inferior to veratria. Digitalis, which may be regarded as a cardiac
stimulant, is to be preferred to either veratria or aconite. It not
only lowers the temperature, but lessens the frequency of the pulse,
steadies it, and produces in the majority of cases its well-known tonic
action upon the heart. Its use in children is sometimes followed by an
intermittent pulse, but it is a symptom of no dangerous import.

Calomel and antimony have been almost entirely discarded from the
therapeutics of pneumonia: there is no evidence that the former has any
influence either upon the progress of the disease or the absorption of
the pneumonic exudation. Those who advocated its use believed it to be
most advantageous after the patient had been freely bled and large
doses of tartar emetic had been given. The latter was also a part of
the treatment where bleeding was practised. It exercises a depressant
effect upon the heart, and hence, although it may diminish the
frequency of the pulse and lower the temperature temporarily, it is an
exceedingly dangerous relief, as it is obtained at the expense of vital
power. It is absurd, with our present knowledge of the pneumonic
process, to discuss what was once claimed for tartar emetic--namely,
that it had the power of arresting the pneumonic process as well as
preventing pulmonary congestion in the unaffected portion of lung.
These drugs, while they at best afford only temporary relief, require
most careful watching to guard against their dangerous and prostrating
effects.

Expectorants have no place in the treatment of pneumonia, as only a
very small portion of the exudative matter in the lung is removed by
expectoration. If mucus or other secretions accumulate in the bronchial
tubes in sufficient quantities to cause inconvenience, it is in
consequence of the exhaustion and a loss of muscular power which attend
the disease, for which expectorants will afford no relief.

Counter-irritation, by blisters or other irritants applied to the
surface of the chest in the earlier stages of pneumonia, is of
questionable utility. Occasionally, blisters may be applied during the
third stage to hasten the process of resolution and promote the
absorption of plastic exudation. The application of leeches, followed
by a linseed poultice or some other soothing fomentation, will often
relieve the pain in the side which is so urgent at the onset of a
pneumonia. If extensive pulmonary oedema occurs, dry cups applied to
the chest will afford relief to the dyspnoea and temporarily remove the
oedema.

It has come to be a quite universal practice in this city to encase the
chest in a layer of cotton batting or flannel covered with an oil-silk
jacket. While this procedure has no direct influence on the course of
the pneumonia, it promotes diaphoresis and protects the surface from
sudden changes of temperature, and is always grateful to the patient.
It is especially serviceable in children.

A pneumonic patient should be kept in bed, as nearly as possible in a
horizontal position. Every appliance for promoting rest should be
employed. He should be cautiously moved for the necessary examinations
of the chest, and should be kept as short a time as possible in a
constrained position. If there are evidences of heart-failure, the
sitting posture should be avoided and talking should be prohibited. The
sick-room should be large, cheerful, and well ventilated, and its
temperature should range between 65° and 70° F. In acute febrile
disease there is no danger of catching cold from draughts, and the idea
of the laity that the moment a person is sick or has a fever he must be
put in a dark, close room is one of the superstitions of ignorance.
Pneumonic patients always demand air, and the cooler the more grateful
it is. Pure fresh air has a marked antipyretic power. It is a good rule
to allow adults to regulate the temperature of the sick-room to suit
their feelings.

One of the most important things in the successful treatment of
pneumonia is a carefully-regulated diet. The food should be fluid or
semi-fluid and {348} highly nutritious, such as milk, eggs, beef-tea,
and concentrated meat-broths. Milk is to be preferred to all other
forms of nutrition. It should be given in small quantities at short
intervals.

When not contraindicated wine may always be administered with milk.
Such administration of wine is not a part of the stimulating plan of
treatment hereafter to be considered, but it is a means of increasing
the digestive power of a feeble stomach.

If expectoration becomes difficult, it may be from a loss of muscular
power in the bronchial tubes, when stimulants are indicated; or from
extreme viscidity of the sputa, when alkalies will be of service. Just
here it may be mentioned that alkalies and neutral salines possess a
diuretic and diaphoretic power which often affords relief from the
pungently hot skin, and may aid the elimination of effete material by
the kidneys.

It should be remembered that in the treatment of croupous pneumonia we
have to do with a self-limited, acute febrile disease, which usually
runs a cyclical course.[50] Routine treatment is therefore always
harmful.

[Footnote 50: Fernet ("De la Pneumo. franche aigue," etc. _Arch. gén.
de Méd._, 1881, pp. 5-155) has demonstrated the regular and cyclical
course of pneumonia. The evolution of the malady is represented by the
march of the fever and is figured by the thermometric curve.]

The nervous shock which attends the ushering in of a severe croupous
pneumonia is greater than in any other acute disease, unless it may be
peritonitis, and the important question presents itself at its very
onset, What measures shall be employed to overcome or mitigate the
impression made upon the nerve-centres by the morbific agent which is
operating to produce the pneumonia? The experience of the last few
years leads me to the conclusion that during the developing period of
the disease, when the pneumonic blow is first struck, and until the
pneumonic infiltration is completed (usually for the first four days of
the disease), if the patient is brought under the full influence of
opium, and held in a condition of comparative comfort by hypodermic
injections of morphia repeated at regular intervals, he is placed in
the best condition not only for resisting the shock, but also for
combating the activity of the pneumonia. Opium does not, when thus
administered, interfere with a stimulating or antipyretic plan of
treatment which may be demanded, but it does very greatly diminish the
chances of heart-failure, cases often recovering under its use which
from age and condition of life seemed hopeless. Then the great relief
and comfort which it gives to the sufferer in the first four days of
his struggles are sufficient to commend it, especially in those cases
where pain is severe and the restlessness of the patient is exhausting.

After the pneumonic infiltration is completed opium should be
administered with great caution, for paralysis of the bronchi (which it
induces), and the consequent accumulation of secretion in the bronchial
tubes, may greatly increase the already existing difficulty of
respiration.

In all severe types of croupous pneumonia there are two prominent
sources of danger: heart-insufficiency and high temperature. There are
consequently two prominent indications for treatment--viz. to sustain
the heart and reduce temperature.

A large proportion of deaths from pneumonia result directly or
indirectly from heart-failure. Alcoholic stimulants, judiciously
employed, are the most efficient means which we possess for sustaining
a flagging heart, but their indiscriminate use is more dangerous than
indiscriminate venesection. It may be that only a few ounces of brandy
will be required to carry a pneumonia patient through a critical
period, or it may be that its free administration will be required to
save life. In the old and feeble, and in those who have been accustomed
to the use of alcohol, stimulants may be indicated from the
commencement of the attack, and their free use required throughout the
whole course of the disease. Each case demands careful study. In no
{349} other disease is so much discretion and judgment required in the
administration of stimulants as in croupous pneumonia. The pulse, being
the indicator of the condition of the heart, must be carefully studied.
A frequent, feeble, irregular, or intermittent pulse always indicates
heart-insufficiency. The quantity of stimulants to be administered in
any case must be determined by their effect upon the pulse. It is
advisable to commence their use in small quantities, and carefully
watch their effects. If the effect is beneficial, a favorable result
will follow within a few hours, and then the quantity to be
administered can be increased according to the necessities of each
case. It is seldom necessary to give more than six or eight ounces of
brandy in twenty-four hours, yet if the necessity of the case demands
it may be given in much larger quantity, twelve or twenty-four ounces
often being required in twenty-four hours. A dicrotic pulse is a
certain indication for the administration of stimulants.

The period immediately following the crisis is the one in which
stimulants are usually most serviceable. Delirium is a symptom which
calls for their administration, whether it is due to asthenia, pyrexia,
or is an expression of blood-poisoning. When muscular tremor and
subsultus tendinum are present, alcohol may usually be freely given. A
critical collapse in the aged and weak, attended by great prostration
and a subnormal temperature, is a condition in which alcohol shows its
best effects, and the amount of asthenia will determine the amount of
stimulation required.

It has been claimed that carbonate of ammonium in large doses
stimulates the heart and prevents the formation of heart-clots by its
action on the blood. The cause of heart-clot is the heart-failure, and
there is no evidence that carbonate of ammonium prevents the
coagulation of the blood when the blood-current is slowed. Besides,
large doses of carbonate of ammonium irritate the stomach, and on this
account interfere with nutrition, and thus diminish the chances of
recovery. As a diffusible stimulant it is inferior to champagne.
Moreover, champagne can be administered for a much longer period
without causing gastric disturbances.

Camphor and musk have been highly recommended as cardiac stimulants,
but they are inferior to alcohol.

Digitalis of late years has been extensively used to counteract
heart-insufficiency, but it is very uncertain in its action in the
heart-insufficiency of pneumonia, and has seemed to me more frequently
to do harm than good. The nervous element of the heart-failure
contraindicates its use.

The second important indication in the treatment of croupous pneumonia
is to lower the temperature. The plan of applying cold compresses to
the chest in pneumonia, though far from being a new one, still has its
strongest advocates in the modern school of therapeutics. It is
proposed to apply thick compresses wet in ice-water over the seat of
the inflammation, changed every five minutes. Some use the Esmarch
ice-bag for the same purpose. Patients who were moribund have, it is
said, been revived by immersion in a cold bath. The advocates of this
treatment claim that the temperature is lowered; that the patient
experiences a feeling of relief during the bath; that the pain,
dyspnoea, pulse-rate, restlessness, and severity of the attack are all
ameliorated; and that the duration of the disease has been cut short by
the continued use of cold baths or cold packs.[51]

[Footnote 51: Rules for the employment of cold as an antipyretic in
pneumonia:

Cold Bath.--As soon as the axillary temperature in the evening rises
above 103° F., place the patient at full length in a bath with a
temperature of 70° F. or 80° F. Gradually lower the temperature of the
bath by the addition of cold water or ice until the temperature of the
patient begins to fall. It may be necessary to lower the temperature of
the bath to 60° F. before the temperature of the patient is affected.
After the temperature begins to fall, thermometrical observations must
be taken every two or three minutes; the rectal temperature only can be
relied upon. If the temperature falls {350} rapidly--that is, two or
three degrees in five or six minutes--as soon as the fall reaches 102°
F. the patient should be removed from the bath; if it falls slowly, as
soon as it reaches 101° F. he should be removed and immediately placed
in bed. The patient should never be kept in the bath until the
temperature reaches the normal, for it continues to fall for some time
after his removal from the bath, and he may pass from a condition of
fever into a state of collapse. The duration of the bath should rarely
exceed fifteen minutes. While the patient is in the bath cold should be
applied to the head by means of a sponge or by an ice-bag.

In the young, the feeble, and the aged the duration of the bath should
never exceed five minutes. Once commenced, the baths must be persisted
in until the crisis is reached.

Cold Pack.--This is much less effective than the bath, but if the
patient is too feeble to be moved it may be employed. The patient
should be wrapped in a sheet wrung out of tepid water, and over this a
sheet should be applied wrung out of ice-cold water; the latter may be
removed as often as it becomes warm. Its application and removal may be
continued until the desired fall in temperature shall be obtained.

Cold Compresses.--The method of applying cold compresses in pneumonia
is as follows: A cloth of some thickness is to be wrung from ice-cold
water and applied every five minutes to the affected side, or an
ice-bag is employed instead of the compresses. It is claimed for this
method that it not only relieves the local symptoms, but lowers the
temperature and hastens the day of crisis.

If cold is to be applied to the chest, either moist or dry, all the
disadvantages arising from repeated exposure and frequent changes of
temperature can be avoided by the use of the rubber coil, and it should
always be employed in preference to wet compresses.]

The experience of American practitioners, so far as I have learned, is
against this plan of treatment. It is found that under it pneumonia is
more liable to extend; that the shock of the cold to the surface causes
a nervous depression from which the old and feeble do not rally; that
although a reduction of temperature may be effected,
heart-insufficiency is more rapidly reached and is more difficult to
overcome. Besides, the statistical results of this plan of treatment
are decidedly against its use. The above statements do not prohibit
cold sponging of the limbs and face if it is grateful to the patient.

If the high temperature in pneumonia is due to rapid
tissue-metamorphosis, the result of the action of some morbific agent
in the blood, it follows that we must look for an antipyretic which can
check this rapid tissue-change. It is claimed with reason that the
sulphate of quinia is a sedative to the arterial system, and has a
stimulating effect, sui generis, upon the capillary circulation; that
it can arrest cell-development, and also check the amoeboid movements
of the white corpuscles. Theoretically, therefore, it is a remedy par
excellence for the lowering of the temperature in this disease; and
clinically and empirically it has been found to reduce temperature more
permanently and with greater certainty than any other agent. None of
the objections brought against the other antipyretics can be urged
against this one, for it possesses the twofold power of reducing
temperature and sustaining the heart-power from its action on the
nervous system. To act antipyretically, quinia must be given in large
doses. From twenty to forty grains must be given within two hours, or
the whole quantity may be given at a single dose. The greatest
reduction of temperature will be reached in about seven hours after the
quinia is taken.[52]

[Footnote 52: When quinia is employed as an antipyretic in pneumonia it
must be given in large doses. The administration of two grains every
two hours, or a larger quantity administered in divided doses within a
period of twenty-four hours, will not act as an antipyretic; but from
twenty to forty grains must be administered within a period of two
hours. If the stomach is irritable, ten grains may be given every half
hour until the desired quantity has been administered. Usually in from
four to six hours after the antipyretic dose has been taken the fall of
temperature will begin, and in about twelve hours it will reach its
minimum height; then it will remain stationary from twelve to
twenty-four hours. After the temperature has once been reduced by the
quinia, its administration may be discontinued until the temperature
shall again rise to 105°. As a rule, the temperature does not reach as
high a point as before the quinia was administered. This mode of
administering quinia rarely produces any symptom of cinchonism {351}
other than transient deafness after the first dose. In a large
proportion of cases the temperature by this method can readily be kept
below 103° F.

In Ringer and Gill's experiments with quinia on temperature it took at
least twenty grains to produce a fall of a degree. From fifty to eighty
minutes were required before the fall occurred, and the effects lasted
from forty-five minutes to three hours. Ringer states that in pneumonia
the quinia does not readily pass out with the urine, but is delayed in
the system for a considerable time.

Lately, antipyrine has been brought before the profession as a valuable
and powerful antipyretic. I have used it in both private and hospital
practice, and have found it a prompt and efficient means of reducing
temperature. It has not seemed to me, however, to have any other
beneficial effect either in mitigating the severity or shortening the
course of the disease. In two cases its use was followed by collapse,
which in one case terminated fatally. My experience has seemed to bear
out the belief that this drug is a decided cardiac depressant, and I
should for this reason consider it much less desirable as an
antipyretic than quinia.]

During convalescence tonics and restoratives--iron, quinia, the mineral
acids, cod-liver oil, or strychnia--should be administered, and the
highest degree of nutrition should be maintained. If bronchitis
complicates pneumonia, it may be treated with muriate of ammonium,
ipecacuanha, and senega. If severe gastric catarrh occurs, hot
fomentations may be applied to the abdomen, and calomel, followed by a
saline purgative, may be administered.

Diarrhoea is rarely so severe as to require treatment; five grains of
Dover's powder usually suffices to control it.

In the delirium which occurs in alcoholic patients small doses of the
tartrate of antimony and potassium are said to be useful. I have
controlled this form of delirium best with small doses of hydrate of
chloral.

By some, camphor, musk, and turpentine are recommended during the stage
of gray hepatization, but it seems to me that the requirements are far
better fulfilled by alcoholic stimulants.

In the first stage of senile pneumonia an emetic, when not specially
contraindicated, is given in the Salpétrière Hospital. The physicians
of the Montpellier General Hospital regard ipecacuanha as an heroic
remedy in senile pneumonia. The English regard nitrate of potassium as
the most efficacious, while the Germans prefer hydrochlorate of
ammonium. Antipyretics are rarely necessary in senile pneumonia; the
most important thing is to sustain the heart by stimulants and
concentrated fluid nutriment combined with iron and quinia. In senile
pneumonia the diarrhoea occurring with the typhoid form must be
promptly checked by vegetable astringents.

In children, as in old age, leeches and blisters should never be used.
The whole chest should be enveloped in a linseed-meal poultice, to
which some anodyne may be added (opium, aconite, or belladonna) if
there is severe pain.

In asthenic pneumonia, in addition to the nutritious diet, burgundy,
port wine, or brandy should be used, and stimulant embrocations should
be applied to the chest. In children the state of the bowels must be
most carefully watched. Stimulating expectorants are more frequently
necessary than at any other period of life.

In conclusion, I would urge that all remedial measures which tend to
paralyze the heart should be excluded from the treatment of pneumonia,
and great care should be exercised not to over-stimulate the heart, for
over-stimulation often results in paralysis. It must always be
remembered that in the milder cases there is necessity for no treatment
except a regulated diet and attention to those general hygienic
measures which have already been referred to.

I shall not attempt to discuss the treatment of the complications which
may occur in the course of a pneumonia, for it is impossible to even
mention every contingency that may arise. The rule is to treat the
pneumonia so long {352} as it is the controlling disease, and the
complication when it shall have become the most prominent and dangerous
element in any given case. In prolonged convalescence it is of the
utmost advantage that the pneumonic patient shall have a change of
scene and climate.

Antiseptics.--The use of antiseptics in the treatment of pneumonia has
as yet given no definite results. I have employed hypodermically phenic
acid after Declat's method in several well-marked cases of simple
pneumonia, without being able to determine that the temperature or
course of the disease was at all influenced by its use.

F. Schwarz[53] states that the very favorable results which he has
obtained in croupous pneumonia can only be due to one thing--_i.e._ the
specific action of iodine, which renders inert the exciting cause of
the disease, which he regards as an organism, and that its efficacy is
limited exclusively to the very early stage of the pneumonia. He
believes that its action in acute lobar pneumonia is the same as Von
Willebrandt claimed for it in typhus, typhoid, and in malarial fevers.
He even states that he regards iodine as a genuine specific in pure
uncomplicated croupous pneumonia if employed within twenty-four or
thirty-six hours after the ushering-in chill, that hinders its
development and arrests its progress.

[Footnote 53: _Deutsche medicinische Wochenschrift_, January, 1881, No.
2.]

After using benzoate of soda in diphtheria, scarlet and puerperal
fever--drachm ij in the twenty-four hours--E. B. Cady[54] states that
when an epidemic of pneumonia visited his town in Wisconsin he had
equally good results from the similar use of this salt in pneumonia,
cases recovering which had a temperature of 106° F. and 107° F.

[Footnote 54: _N.Y. Med. Record_, 1880, July, 3, "Benzoate of Soda in
Pneumonia."]

Orth[55] has recently written an interesting account of the treatment
of pneumonia (lobar) with iodine.

[Footnote 55: _Allg. med. Centr. Zeitschr._, Berlin, 1881, i. p. 181.]

T. H. Buckler strongly recommends its treatment with salicylate of
sodium and fresh lemon-juice.[56]

[Footnote 56: _Phila. Med. News_, 1882, xl. p. 652.]

Phenic acid, boracic acid, and the salicylates are highly recommended
by many as the best drugs in the antiseptic treatment.




{353}

CATARRHAL PNEUMONIA.

BY WILLIAM PEPPER, M.D., LL.D.


SYNONYMS.--Broncho-pneumonia; Lobular pneumonia. Although numerous
other names have been used to designate this affection, it is
undesirable to perpetuate them.

DEFINITION.--Catarrhal pneumonia is an inflammation of the parenchyma
of the lungs, frequently bilateral, and affecting scattered groups of
lobules, which may, however, coalesce, so that considerable areas of
lung-tissue become continuously involved. This anatomical distribution
explains the name lobular as opposed to that of the lobar or croupous
form. As implied by its other titles, it has close associations with
bronchial catarrh, and occurs nearly always either as an extension of
inflammation from the larger tubes or in connection with capillary
bronchitis. In consequence, it is often combined with pulmonary
collapse, with which latter condition it was until recently confounded.
The affected areas show lesions of the bronchioles, together with a
morbid product filling the alveoli, and consisting in varying
proportion of altered epithelial cells from the alveolar walls, of
cells drawn by aspiration from the bronchioles, and of exudation from
the blood-vessels. Catarrhal pneumonia may be circumscribed or diffuse,
and acute, subacute, or chronic. Its course and duration vary greatly:
at times it terminates fatally in a few days, or runs a lingering
chronic course, while recovery rarely occurs in less than fourteen
days. The mortality is always considerable, and it acquires additional
gravity from its tendency to leave behind it organic lesions of the
lungs or even to induce phthisis.

ETIOLOGY.--As catarrhal pneumonia is so closely associated with
bronchitis, and so commonly preceded by it, it may be premised that all
the causes of bronchial catarrh must be considered as liable to induce
this form of pulmonary inflammation, whether they do so by exciting
bronchitis, which subsequently extends to the alveoli, or whether, as
more rarely happens, they affect simultaneously the lining membrane of
the bronchi and of the lobules.

There are, however, several influences which must here be carefully
considered, since they have a special tendency to determine the
production of the more grave form of disease.

The effect of age in predisposing to catarrhal pneumonia is undoubtedly
great, and yet it seems to have been often over-estimated, since by
many this has been regarded almost as a disease peculiar to childhood.
The great frequency with which young children were formerly held to be
affected by this form of pneumonia has, however, been found to be due
in part to the fact that many cases of pulmonary collapse were included
with it; while, on the other hand, there is strong reason to believe
that the frequency with which adults are attacked has been greatly
under-estimated in consequence of the failure on the part of the
profession at large to clearly recognize this affection. It seems in
the highest degree important that more {354} correct views on this
subject should be generally received. While it is probable that the
more severe and widely-disseminated pneumonias of catarrhal type are
commonly recognized now-a-days, it appears undoubted that in very many
instances of apparently mild sickness, of acute or subacute character,
which are regarded as simple febrile colds or as the result of malaria,
the true condition is one of circumscribed catarrhal pneumonia, which,
while threatening no immediate danger to life, may if neglected leave
lesions of grave significance. Still, it is undoubted that it is during
the early years of childhood, and particularly the first five years,
that catarrhal pneumonia, and more especially its grave and fatal form,
is of frequent occurrence; while the period of next greatest liability
is at the other extreme of life, among aged and debilitated subjects.

Under the head of Pathology we shall have occasion to dwell on the
relations between defective respiratory power, pulmonary collapse, and
catarrhal pneumonia; and it is evident that this connection helps to
explain the relative frequency of the latter in early childhood, when
conditions of debility are so common, and when rickets not rarely is
superadded as an important factor. Another potent cause of the
liability of young children to catarrhal pneumonia is the prevalence at
that period of life of the infectious diseases, which are apt to be
complicated with bronchitis, and which then present a combination of
conditions favoring its development. This is especially true of
measles, of whooping cough, and of diphtheria, while influenza, which
is also frequently complicated with this form of pneumonia, is
operative at all ages. Among predisposing causes which operate chiefly
at a later period of life must be mentioned organic diseases of the
heart and vesicular emphysema. The latter especially has shown itself
important in our experience, both as predisposing to the occurrence of
catarrhal pneumonia and as adding to the gravity of the attack.

Unquestionably, all states of bad nutrition and depressed vitality
render the system much more liable to attacks of catarrhal pneumonia.
The bad air of crowded houses or of ill-ventilated public institutions,
especially if conjoined with the effect of improper food and of other
defects of hygiene, plays an important part in inducing the fatal forms
of this disease which are common among children exposed to such
conditions. It is equally evident that among adults the effect of
overwork, with insufficient sleep and outdoor exercise, is to develop a
peculiar sensitiveness and weakness of system which make the ordinary
causes of bronchitis capable of exciting a deeper and more serious
catarrh. Finally, there are many individuals who possess a catarrhal
diathesis--that is, in whom the epithelial layers are especially
vulnerable, and when attacked are especially prone to take on cellular
proliferation of a deep-seated and obstinate character. Such
constitutions, which are frequently found in the subjects of phthisical
heredity, furnish a ready soil for the development of catarrhal
pneumonia.

Nor must the practical lesson be here overlooked that when acute or
subacute bronchitis exists, an additional motive for prompt and
thorough treatment is to be found in the fact that undue fatigue or
exposure may be followed by an extension of the inflammation and by the
onset of catarrhal pneumonia.

PATHOLOGY AND MORBID ANATOMY.--Allusion has already been made to the
relation existing between catarrhal pneumonia and collapse of the lung;
and the present seems to be the proper place to speak more fully of it,
since in order to appreciate the lesions in any case it is necessary to
distinguish between those which are the result of the inflammatory
process and those which can be explained by simple collapse of the
lung-tissue. It is indeed true that in some cases the development of
catarrhal pneumonia takes place in areas already the seat of collapse.
This is only what would {355} naturally be expected. For the production
of both conditions the existence of preceding bronchial catarrh is, if
not necessary, at least highly favorable. The folds of the swollen
mucous membrane of the smaller tubes come into contact with each other,
or else the diminished lumen of the tubes is occluded by the viscid
mucus formed as the result of the catarrh. The normal activity and
rhythm of respiration is disturbed by the fever and the lowered
innervation. During expiration more and more of the air escapes from
the alveoli of the affected area through these partly-obstructed tubes,
while during inspiration, owing to the less force of that part of the
respiratory act and to the shape of the bronchial tree, air cannot
enter to replace it. Thus, or by the action of a plug of mucus in a
conical bronchial tube, serving as a ball-valve, a condition of
airlessness or of collapse is induced in a more or less extensive area.
It is not, indeed, to be supposed that the mere occurrence of such
collapse serves in any way to excite inflammation of the alveoli. But
at the same time it is evident that there will be a strong likelihood
that the catarrh which has advanced so deeply into the finer tubes will
extend in some spots to the alveoli, and consequently that in a
collapsed area of some extent there will be one or more foci of
pneumonia developed. Moreover, it must be remembered that the collapsed
lung-tissue becomes more or less hyperæmic and disposed to take on
inflammatory action, and that the irritating bronchial secretions, the
suction of which into the alveoli plays an important part in these
affections, would necessarily be less apt to be dislodged by cough and
expectoration from areas which had become collapsed. On the other hand,
it is evident that when areas of catarrhal pneumonia have occurred
directly from extension or establishment of catarrh in air-containing
alveoli, the conditions will exist which favor the development of
collapse in the surrounding zones of lung-tissue. Thus it happens that
while the lesions either of collapse or of catarrhal pneumonia are
found separately, it is common to find more or less evidences of
alveolar inflammation in connection with collapse, especially if it has
lasted any length of time; and still more common to find a considerable
proportion of collapse coexisting with catarrhal pneumonia.

A simple practical rule must therefore be here insisted upon: that in
all post-mortem examinations of the lungs in cases of catarrhal
pneumonia, after careful study of the external appearances, a moderate
inflation by means of a blowpipe must be practised, and the effects of
this upon the consolidated areas be carefully studied before the lung
be incised, in order that any element of collapse may be recognized and
eliminated.

The external appearance of the lungs usually presents evident lesions.
There are patches or layers of soft lymph on the pleura over the
affected areas, and when the former are removed the serous membrane is
found roughened, congested, and ecchymosed. On the other hand, while
the pleura over a collapsed patch usually presents small ecchymoses,
there is rarely any evidence of inflammation. More or less evident
signs of vesicular emphysema are also usually present, bearing some
proportion to the extent of the pulmonary collapse. When the areas
affected are small and scattered, the emphysema is limited to their
neighborhood; but when, for instance, both lower lobes are extremely
involved, the upper lobes may present a high degree of emphysematous
distension. In rare instances subpleural emphysema, from separation of
the membrane over a pneumonic focus, may be observed; and even, as in a
case published by me some years ago,[1] perforation of the separated
pleura may occur, leading to pneumothorax.

[Footnote 1: _Philada. Med. Times_, Aug. 15, 1872, p. 425.]

After section of the lungs there will always be found lesions of the
bronchial mucous membrane, which presents evidences of catarrh
extending as high as the trachea or larynx in some cases, but
habitually growing more {356} intense in the finer tubes, where the
membrane is reddened and swollen. Frequently the infiltration extends
throughout the structure of the bronchial walls, so that the tubes
stand out prominently above the surface of the section. Delafield[2]
has insisted with especial emphasis upon these alterations in the
bronchial walls, and on the view that the inflammation extends from the
bronchi, not to the group of air-vesicles into which they lead, but
directly outward to the peribronchial zones of lung-tissue. In severe
cases of longer standing the bronchial tubes often present in addition
dilatations, either cylindrical or more rarely globular.

[Footnote 2: "The Pathology of Broncho-pneumonia," _Medical News_, Nov.
15, 1884, p. 534.]

The bronchi contain morbid secretions in the form of clear viscid mucus
in the early stage, while later they are filled with creamy pus. In
some cases there are also found small subpleural collections of more or
less inspissated yellowish secretion contained in dilated alveoli or in
small globular dilatations of terminal bronchioles. The most plausible
explanation of their nature is, as suggested by Fauvel, that they are
caused by the suction of particles of bronchial secretion into the
alveoli in the forcible inspiratory effects which follow paroxysms of
cough, and especially such paroxysms as occur when whooping cough is
complicated with catarrhal pneumonia.

The lung-tissue itself exhibits, associated in varying degrees,
congestion, oedema, emphysema, collapse, and pneumonic consolidation.
The patches of simple collapse are to be easily recognized by their
familiar appearance, being depressed below the surrounding tissue,
bluish in color, non-crepitant and solid to the touch, and on section
smooth, airless, firm, and not friable. They sink in water. As already
stated, they can, when recent, be readily inflated, and thus restored
to their normal condition. Such patches are most common at the
postero-inferior parts of the lungs. They are mostly pyramidal in
shape, and vary in size from a few lines to one or two inches in
diameter, though in severe cases an entire lobe, or even an entire
lung, may pass into this state of collapse. On the other hand, the
areas of pneumonic consolidation appear as slightly prominent nodules,
varying in size from that of a pea to that of a hazelnut, which may be
distinctly felt with the finger, if occurring in the midst of a
collapsed patch, by their elevation above the surrounding depressed
tissue. They are usually scattered throughout both lungs, often with
some symmetry of disposition, especially in the postero-inferior
portions. The surrounding zone of tissue is more or less congested and
oedematous, and when the nodules are closely adjacent they may become
confluent, so that large portions of a lobe or an entire lobe may
become infiltrated. Vigorous inflation will usually show in such cases,
however, that the consolidation is not uniform or complete. Section of
the lung will show that the most varied stages of the inflammatory
process are represented in the different nodules; and this is a highly
characteristic feature of the disease. The recent nodules are
brownish-red or grayish-red, faintly granular, smooth, friable, and
yield on scraping a small quantity of thick reddish secretion. Later
they become reddish-gray and yellowish-gray in color, yield a thick,
airless, milky substance, and finally grow more firm and dry: the
inflammatory product undergoes fatty degeneration, is gradually removed
by absorption or by expectoration, and the affected area of lung-tissue
is slowly restored to its normal state. This is the course in favorable
cases, while in those which run into a chronic form or which terminate
fatally at an early period the lesions undergo various modifications.
In some instances the inflammatory product undergoes more acute
degeneration, with destruction of the pulmonary tissue in the affected
area, and the subsequent formation of abscesses, which are not to be
confounded with the minute aspiration-abscesses above described. I have
notes of autopsies in which the lungs have presented every stage of the
process of catarrhal pneumonia, from the nodules of incomplete
consolidation to {357} circumscribed abscesses. In other cases the
thickening of the walls of the alveoli and of the bronchi, together
with dilatation of the tubes, has become marked, and the interstitial
changes in the zones of peribronchitic pneumonia extend and induce a
slow process of fibroid thickening which results in that form of
chronic pneumonia which has been called cirrhosis of the lung and
fibroid phthisis. In still other cases the morbid products in the
alveoli, with or without an antecedent process of suppuration, undergo
caseation; and the presence of the degenerate cheesy foci, associated
with alveolar and peribronchial thickening, may lead to catarrhal
phthisis with or without true tuberculous formations.

The microscopic examination of the pneumonic nodules shows that the
essential condition consists in a morbid accumulation within the
alveoli, together with changes in the walls of the vesicles, which
become infiltrated with cells in the same way as the bronchial walls.
These changes become more marked after the disease has lasted some
time. The epithelium lining the alveolar walls is the seat of cloudy
swelling, becomes less closely attached, and undergoes proliferation,
with the formation of large epithelial elements. The morbid product
filling the alveoli is composed in varying proportions of these latter
elements, of the richly cellular bronchial secretion which has been
sucked in from the bronchioles, of leucocytes, and much more rarely of
red blood-corpuscles which have escaped from the pulmonary capillaries,
and finally of fibrillated exudation. In contrasting these minute
appearances of catarrhal pneumonia with those of the croupous form it
is to be noted that in the former the fibrinous element is not
constant, or is at most scanty, and that the results of diapedesis,
leucocytes, and especially red corpuscles, are much less prominent. At
a later period of the process fatty infiltration and degeneration of
the alveolar contents usually occur, which is the most favorable
change, since it disposes toward evacuation with restitution of the
lung to its normal state; but at times a larger proportion of pyoid
cells appears, and the alveolar walls become involved and break down,
so that small abscesses are formed, or, again, the contents may become
inspissated and caseous, associated with nuclear growth in the walls of
alveoli and bronchioles.

An account has thus been given of the lesions in fully-developed and
disseminated catarrhal pneumonia; but I would again ask attention to
the existence of a mild and circumscribed form of the disease, which
rarely if ever causes death of itself. In these mild attacks, which
occur frequently in adults, the part affected may be the base of the
lung, but more commonly it is the root, the apex, or the lower anterior
portion of the upper lobe. The anatomical condition is probably one of
congestion, with extension of catarrhal inflammation into the alveoli
without any preceding collapse, and with a varying degree of
implication of the walls of the vesicles and of epithelial accumulation
in the alveoli, though the process may not always go on to the
production of fully-formed pneumonic nodules, such as above described.
Yet it seems to me not only illogical, but eminently unsafe, to regard
such cases otherwise than as catarrhal pneumonia, since while under
proper treatment and in fairly healthy constitutions they uniformly
terminate in resolution, on the other hand, they will, if neglected or
if occurring in highly-vulnerable constitutions, run into a subacute
form, with more extensive implication of the alveolar walls and
peribronchial tissue, and will induce catarrhal phthisis. Allusion will
be made again to these cases when speaking of the symptoms and
diagnosis of catarrhal pneumonia.

In addition to the pulmonary lesions, the bronchial glands are, with
rare exceptions, swollen and congested. In cases of longer standing
foci of suppuration have been occasionally noted in them (Steiner),
though cheesy nodules are more common. Acute miliary tuberculosis is a
comparatively frequent complication. Oedema and congestion of the brain
and meninges occur {358} frequently, but are to be regarded as
secondary lesions without special significance. It is probable,
however, that more numerous examinations, in cases where death has been
preceded by grave cerebral symptoms, would reveal the occasional
occurrence of circumscribed areas of meningitis, with or without
miliary tubercles. The liver is congested in acute cases, while in
older ones there is apt to be fatty degeneration, which we have seen
occur in irregularly distributed patches, imparting a peculiar mottled
appearance to the organ. The kidneys also may be congested, but serious
changes in the epithelium are rarely met with. Vastly more common are
the lesions of catarrhal inflammation of the mucous membrane of the
stomach and intestine. While in acute cases they may be superficial and
slight, in those which have run a longer course Peyer's patches are
prominent, and the solitary glands are enlarged, and not rarely oval
ulcerations exist which may coalesce, so that I have seen quite
extensive destruction of the mucous membrane of the colon simulating
the effects of dysentery.

SYMPTOMS.--Before entering on a detailed description of the symptoms of
catarrhal pneumonia it must be premised that this disease presents a
far greater range in its degrees of severity than does croupous
pneumonia. In this latter disease, although clinical evidence shows
that its extent and course are less uniform than is often assumed,
there is a remarkable uniformity in the stages through which the
inflammatory exudation passes; but in catarrhal pneumonia, as in all
forms of catarrhal disease, it is a marked characteristic that the
process varies almost infinitely in different cases, both in the
location, the extent, and the degree of development of the lesions. It
is difficult to avoid the conclusion that a corresponding variety is
presented by the symptoms, and that a complete clinical picture of
catarrhal pneumonia must include cases of very mild character and of
short duration, as well as those of a more severe and fully-developed
type. I propose, therefore, to describe a mild form, an acute form of
the ordinary well-developed disease, and also a subacute and chronic
form.

The mild form is undoubtedly often overlooked, the attack being
regarded merely as a feverish cold or as an ordinary bronchitis. Yet
certain peculiarities in the symptoms, the course, and the tendencies
of the cases I refer to serve to distinguish them, and enable them to
be recognized as of more serious nature. More commonly the attacks
occur in young adults whose systems are abnormally sensitive either
from original weakness or in consequence of overwork, previous
sickness, or the action of other depressing and exhausting causes.
After some imprudent exposure there is a slight rigor, followed by
headache, flushed, feverish feeling, soreness in the chest, aching in
the limbs, and tight, dry, painful cough. A careful examination soon
after the onset would reveal the familiar signs of a bronchial catarrh,
though even now there might be noted a tendency for the affection to be
less diffused than is usual in ordinary bronchitis.

If the patient is not prudent and solicitous about his health, no
physician is summoned at once, and not rarely in the course of
forty-eight or seventy-two hours the general symptoms have subsided so
considerably that the patient feels able to move about, and may be led
by pressure of business claims to resume his occupation. He finds
himself so weak, however, and the cough is so much aggravated, that
medical advice is sought. Distinct fever of remittent type is found,
the morning temperature not exceeding 100° or 100½°, while in the
evening it rises to 102° or 103°. There is a tendency to perspiration,
especially on exertion, while exposure to a cool wind or draught causes
a chilly feeling; exertion soon fatigues; sleep is restless; appetite
is impaired; the tongue coated; the bowels irregular; and the urine
high-colored. Cough is troublesome and somewhat painful, and the chest
feels sore and weak. Physical examination will reveal, in the first
place, bronchitic {359} râles, dry and moist (sonorous, sibilant, and
mucous), on both sides of the chest, though not rarely much more
markedly on one side than on the other, or even limited to a portion of
one side.

In addition to this, careful auscultation, especially if conducted not
only during ordinary respiration, but during the strong inspirations
which follow cough, will detect in certain localities subcrepitant
râles, associated with feeble respiratory murmur and slightly prolonged
and blowing expiration. The percussion resonance or the vocal fremitus
or resonance may be only slightly impaired. These signs, which are
connected with an extension of catarrhal inflammation into the alveoli
and the consequent partial occlusion of certain lobules, may be met
with in the subclavicular spaces, at the lower anterior margin of the
upper lobes, at the roots of the lungs, or elsewhere. If the patient be
confined to bed and suitable treatment be employed, the local and
general symptoms will pass away in five to ten days. The cough grows
looser, and the sputa, which were at first very scanty and mucoid, grow
muco-purulent, and then diminish in amount. There follows a greater
degree of anæmia and of weakness than would have been expected from
what is apparently so slight an ailment, and especially there remains a
marked sensitiveness of the throat and chest, so that after any slight
recurrence of catarrh there may be a temporary return of râles at the
affected spot, until gradually the general health and the healthy tone
of the lungs are restored. But if, on the other hand, the patient
persists in keeping about and exposing himself, the febrile process of
remittent type will be prolonged, and though the disturbance of general
health will gradually subside, repeated renewals of catarrhal
irritation will occur, and the local disease will become more deeply
seated, will be attended with increased infiltration of the lobules,
and if the reaction of the system be greatly depressed will end by
becoming chronic. According to my observation, it is in this way--and
this fact confers its great importance upon the mild circumscribed form
of catarrhal pneumonia now under discussion--that very many cases of
pulmonary phthisis begin; and according to the power of resistance of
the tissues, and to the tendency of the system to become infected by
the products of unhealthy inflammation will be the disposition for the
disease to assume this unfavorable development. It is true that the
precise anatomical conditions present in the early stages of such cases
cannot be demonstrated, since death rarely if ever occurs at that
period; but it seems difficult to regard them as differing from those
found in partially developed patches of consolidation in more severe
and typical cases of catarrhal pneumonia. The constitutional symptoms,
the local signs, and the course and results of the affection all
indicate that it is not an ordinary bronchial catarrh, but that it is
properly to be regarded as a mild type of catarrhal pneumonia. Without
pretending to describe minutely all the clinical features of these
interesting cases, it may suffice to have called attention to their
frequent occurrence and great actual importance, and to the fact that
owing to the indifference of the patient or to the hasty examination of
the physician their true nature is often overlooked and the disease is
allowed to pass far beyond its original character of a local catarrhal
trouble.

Acute catarrhal pneumonia in its fully-developed form occurs most
commonly in children, especially as a complication of measles or in the
course of capillary bronchitis. It is evident, therefore, that the
passage from the stage of severe bronchial catarrh to that of alveolar
inflammation may be barely perceptible at first. This is especially
true because in such cases the development of the pneumonia is usually
preceded by a considerable amount of pulmonary collapse. The child is
already suffering with fever, rapid shallow breathing accompanied with
movements of the nostrils and possibly with inspiratory retraction of
the thorax, and with frequent painful cough. No rigor, as a rule,
occurs to mark the inception of the pneumonic complication. {360} The
fever, however, nearly always rises rapidly, and from 102° or 103°,
which has been the maximum during the preceding catarrh, it quickly
reaches 104° or 105°, or even higher. It will be promptly noticed also
that the respirations become even more accelerated, shallow, and
imperfect; in some cases they reach 100 in the minute. The alæ nasi
play violently; the elevation movement of the thorax is marked, while
expansion is but slight; there is retraction of the base of the chest
during inspiration, which is short and quick, while expiration is
prolonged and labored. Severe suffocative paroxysms occur from time to
time. The cough is frequent and painful, so that adults complain
severely of it, while in children it causes moaning or crying. Later,
when the nervous symptoms grow more prominent, the cough grows much
less frequent and severe, or even ceases. Sputa are rarely raised by
children unless with the act of vomiting; they are tenacious, but not
rusty colored, though they may be slightly streaked with blood. The
pulse soon grows very rapid, 160, 180, or even 200 in young children,
and loses force and volume. The appetite is lost, but thirst is
extreme. The tongue becomes brown and parched from deficient secretion
and from mouth-breathing. Diarrhoea is not uncommon, owing to the
frequent presence of intestinal catarrh as a complication. The urine
occasionally contains a small amount of albumen; and it is stated
(Bednär) that the chlorides persist. The nervous symptoms are
prominent. As the dyspnoea increases there is extreme restlessness, the
child tossing about incessantly, with slight delirium. Soon the flush
on the face yields to a distinct cyanotic appearance, with coolness of
the extremities. The restlessness subsides, and there is a tendency to
stupor, alternating with spells of active and restless delirium, and
finally deepening into coma, at times with rolling of the head, so that
there may be a close resemblance to the later stage of tuberculous
meningitis.

During the development of these symptoms the physical signs are for the
most part unsatisfactory and require great care to determine and to
interpret them. As already intimated, inspection shows inspiratory
retraction of the base of the chest, increased movement of elevation,
with defective expansion. Percussion does not usually give definite
results, owing to the fact that the lesions may be symmetrical in the
two lungs, and because the pneumonic process is complicated to a very
variable extent with the results of pulmonary collapse. In children
especially the most gentle and careful percussion is requisite to
detect and map out the affected areas. Some assistance may be rendered
by the fact that the dulness dependent on collapse is often found in
the form of symmetrical elongated areas in either intervertebral
groove. The results of palpation are even less satisfactory than those
of percussion. If the patches of consolidation are not extensive and
are scattered, no change will be detected; and it is only when
superficial areas of considerable extent are consolidated that distinct
increase of vocal fremitus can be determined. It may be remarked here
that, on the contrary, there is impairment of fremitus over areas of
pulmonary collapse.

Auscultation usually shows the continuance of the râles due to the
preceding bronchitis. In addition to these coarser dry and moist râles
there is also heard fine moist crackling over the area of pulmonary
consolidation; these fine subcrepitant râles are heard both during
inspiration and expiration. Pure bronchial breathing, such as is heard
in croupous pneumonia, is by no means constantly present. Over large
areas of catarrhal pneumonia, when the small bronchial tubes are
comparatively unobstructed, it may exist; but, on the other hand, there
may merely be weak diffused blowing breathing.

In adults an equally grave type of acute catarrhal pneumonia is not of
such common occurrence. Cases are met with, however, occurring
especially in subjects whose systems are depressed--as, for instance,
by overwork--in old or feeble persons, or in connection with
diphtheria, typhoid fever, or influenza. The {361} disease may then run
a course closely resembling that described above as found in children,
the rapidly developing interference with aëration of the blood, the
speedy failure of cardiac power, and the appearance of grave nervous
symptoms all being strongly marked. Such cases constitute a notable
proportion of what is commonly styled typhoid pneumonia, especially in
the aged, the disease being often in reality catarrhal instead of
croupous. I have also met with rapidly fatal catarrhal pneumonia
developed during the course of typhoid fever, particularly during the
later stages of cases marked by considerable bronchitis and great
nervous depression. In one instance the patient, a young man of
twenty-six years, who had been much exhausted by mental worry and
anxiety, passed through a well-marked attack of typhoid fever with
moderate pyrexia, but with decided nervous symptoms. Convalescence
seemed established on the twenty-first day, when he was carelessly
allowed to sit up in a chair, and while there was exposed to a draught
of air; he felt chilly, fever reappeared with cough, but no rusty
sputa; centres of catarrhal pneumonia developed in the lower lobe of
the right lung, then in the middle lobe; the fever varied from 101½° or
102° in the mornings to 103½° or 104° in the evenings. On the seventh
day there was a sudden fall to 99°, with a rise in the afternoon to
106°; centres of inflammation appeared in the left lung. For the next
five days there were remarkable fluctuations of temperature, the range
being from 100½° or 101° in the morning to 106° and 106½° in the
evening. The variations in the pulse-rate were not so marked.
Respiration was hurried and imperfect. Nervous symptoms of a typhoid
and ataxic nature developed, and death occurred on the twelfth day.
Considerable daily fluctuations in temperature, though rarely so
regular and extreme as in this case, are often noted in catarrhal
pneumonia, and are of some diagnostic importance. I have many tracings
to show the remittent though atypical course of the pyrexia of this
disease. Such grave cases of acute catarrhal pneumonia are very fatal,
even in adults, scarcely less so indeed than in children; and when
recovery occurs the convalescence is protracted, and often interrupted
by more or less serious renewals of catarrhal inflammation with
constitutional disturbance.

As already remarked, the pulse-rate, which soon becomes rapid, 110 to
124, does not vary as much as the temperature; and even during marked
remissions of the pyrexia the pulse usually continues rapid. The
appetite is greatly diminished or lost; the tongue is coated, often
heavily so; vomiting is not often present spontaneously, but may be
excited by the spasmodic attacks of cough. The respirations are hurried
and superficial, frequently rising to 40, 50, or 60 in the minute in
adults, and this rapidity persists during remissions of the fever just
as does the rapidity of the pulse. As a rule, it is not possible to
observe any marked difference in the movements of the two sides, owing
to the irregular distribution of the foci of disease. The cough is
frequent and may be painful. It is apt to occur in paroxysms, and the
spells may be so severe as to cause alarming interference with
respiration, and also to induce serious exhaustion.

The sputa are at first scanty and consist of tenacious mucus, which may
possibly show fine blood-points, but which are quite different from the
rusty-colored sputa of croupous pneumonia. Later the sputa become more
abundant and less consistent, being much affected by the amount of
bronchitis attendant.

The results of physical examination are much more satisfactory in
adults than in children, owing partly to the less frequency of
pulmonary collapse as a complication, and partly to the assistance
obtained from the more careful study of the vocal fremitus and
resonance possible in the former. Inspection will not show inspiratory
retraction of the base of the chest to anything like the extent seen in
children, owing to the greater rigidity of the thoracic walls. {362} In
the later stage of the disease, however, when considerable infiltration
and obstruction of the lungs has developed, such retraction and also an
inspiratory depression of the suprasternal space may be noted.
Palpation does not give such clear results as in croupous pneumonia,
yet careful observation will show relative increase of fremitus over
the affected areas. Auscultation of the voice usually gives valuable
results. They are not constant, however, nor is it common, even when a
considerable area is consolidated, to meet with such bronchophony as in
the second stage of croupous pneumonia. Still, it is nearly always
possible to detect some alteration of the vocal resonance by comparing
corresponding portions of the two sides; and this, as contrasted with
the negative results in bronchitis, possesses high value. The
respiratory murmur is usually feeble and blowing over the patches of
catarrhal infiltration. In some cases it is as intensely bronchial as
in the croupous form; but more commonly the greater or less obstruction
of the bronchioles renders it weaker and more distant and diffused. I
have observed considerable areas of consolidation due to catarrhal
pneumonia, over which the respiratory murmur was so feeble as to
suggest the presence of moderate pleuritic exudation. Râles are apt to
be present at all stages of the disease. Usually they are fine
subcrepitant or fine dry crackling râles, audible in both inspiration
and expiration; and even over consolidated areas these may be audible,
being doubtless transmitted from the fine bronchioles.

As the case progresses toward resolution the râles become larger and
looser. It often happens that the râles are variable, changing in
character, extent, and position from day to day vastly more than occurs
in croupous pneumonia.

Percussion gives valuable data if practised with care over symmetrical
areas of the two lungs. From such comparative study alone can
satisfactory results be obtained, since in many cases the areas of
disease are too small or not sufficiently superficial to yield more
than relative dulness. But it must happen rarely that spots are not
found where resonance is at least relatively impaired, while of course
in some cases actual dulness is readily detected. It has been stated
that collapse of the lung is a comparatively rare complication in
adults, yet careful study of the physical signs from day to day will
occasionally show its existence in a marked degree. It may occur in a
striking manner in the subacute catarrhal pneumonia of emphysematous
subjects; but in acute cases also considerable areas of the affected
lung may quickly pass into a state of collapse. In a fatal case of the
acute form in a young man I observed the abrupt development of the
signs of pulmonary collapse over the whole lower lobe of the right
lung, requiring care to avoid the error of supposing a considerable
pleuritic exudation to have supervened, but passing away in the course
of thirty-six hours with renewed expansion of the lobe and restoration
of the previously existing physical signs.

It is not necessary to give any detailed discussion of the other
symptoms of acute catarrhal pneumonia as occurring in adults--the
atypical remittent type of fever; the rapid pulse and breathing; the
digestive symptoms, anorexia, thirst, occasional nausea, and a
comparatively frequent tendency to diarrhoea; the nervous restlessness
and depression, with delirium supervening, at first slight, later more
active, and toward the close of fatal cases of such violence as to
require restraint, alternately with deepening stupor from exhaustion
and defective aëration of the blood. Albuminuria may be present in a
slight degree toward the close of severe cases. When death occurs in
these acute cases it usually does so from the tenth to the sixteenth
day. In children it may occur suddenly during or after a violent
paroxysm of cough, or an attack of convulsions may be the immediate
cause of death. More commonly death is preceded by evidences of
increasing intensity of interference with the aëration of the blood,
and with deepening stupor and nervous {363} disturbances such as have
been described. The degree of cardiac failure present is to be ascribed
rather to nervous exhaustion than, as in many cases of croupous
pneumonia, to the action of hyperpyrexia on the muscle of the heart.
The extreme interference with respiration in catarrhal pneumonia is
readily accounted for, not only by the extent of lung-tissue actually
involved in the process, but by the associated bronchitis with swelling
of the mucous membrane, by the accumulated bronchial secretions, and by
the frequent complication with collapse. When recovery is to follow,
the disease declines gradually and irregularly, slight recurrences of
fever and renewed catarrhal irritation being observed from time to
time. These exacerbations may not rarely be traced to atmospheric
influences or to trifling indiscretions on the part of the patient. The
pain declines gradually; and the pulse-rate also falls, but even after
the temperature has become normal some degree of rapidity of the pulse
is apt to remain for a considerable time. The physical signs gradually
disappear: the respirations, like the pulse, remain somewhat rapid, or
at least are for some time readily accelerated; and there is apt to be
some cough remaining, with gradually decreasing muco-purulent
expectoration. The digestive functions are also apt to be left in an
enfeebled condition, and the recovery of full nutrition and health is
often slow. A peculiar sensitiveness of the general system is
frequently noted after this disease, so that morbid processes,
especially of catarrhal type, are readily excited.

As would be expected, catarrhal pneumonia frequently presents much less
violent symptoms and runs a much less acute course than above
described, so that it may be said to assume a subacute or chronic form.

In children this may occur as the result of an acute attack, the severe
symptoms gradually subsiding, and passing into a less violent but
persistent type. In other cases the disease assumes this form from the
beginning, and such instances are more commonly noted after ordinary
bronchitis of moderate severity or after whooping cough. In adults this
form also is less common than in children. It is met with as an
intercurrent affection in certain cases of phthisis; and not rarely the
exacerbations of that disease are due to the development of centres of
catarrhal pneumonia which too often become later the seat of an
extension of the tuberculous process. It occurs in this form also in
the old and cachectic, and doubtless proves the undetected source of
death in many cases where the end is preceded by irregular pains and by
some signs of hypostatic infiltration of the lungs. In a feeble and
exhausted state of the system at all ages it is liable to be induced.
At times this is brought about by a series of recurring slight
catarrhal attacks, gradually deepening into a subacute process of
catarrhal pneumonia; while in other cases a more powerful disturbing
cause will in such states of system directly induce this type of the
disease. It develops insidiously. There is little or no pain. The fever
is highly irregular; the maxima usually occur in the evening and reach
102° or 103°, but there may be such marked remissions as to make the
case closely simulate one of intermittent malarial fever complicated
with bronchitis, and I have known such an error to be made in repeated
instances. In some cases, especially in the old and feeble, there may
be very little fever, at least until the disease is more fully
developed. The dyspnoea is not urgent; the pulse is not extremely
rapid; and cough may actually seem diminished if the disease has
originated in the course of severe bronchitis. The physical signs
develop slowly, but may eventually appear over considerable areas of
lung-tissue. In this way with an irregular fluctuating pyrexia,
presenting from time to time marked exacerbations, with an equally
varying amount of cough and muco-purulent expectoration, and with
marked and progressive debility and emaciation, these forms of
catarrhal pneumonia pursue a course extending over many weeks or
months. Complete recovery is still possible, after a tedious
convalescence. Commonly, {364} however, some permanent lesion of the
lungs, as emphysema, dilatation of the bronchial tubes, or
circumscribed induration of the lung, will remain as sequels. In a
large proportion of cases a fatal result finally follows, more commonly
from the passage of the morbid process into pulmonary phthisis usually
associated with true tuberculosis; while in some cases acute miliary
tuberculosis supervenes and proves rapidly fatal. Undoubtedly, however,
cases of chronic catarrhal pneumonia may continue purely as such, with
recurring exacerbations at irregular intervals from the development of
new centres of disease, until death is finally induced by exhaustion.

COMPLICATIONS AND SEQUELS.--It is needless to repeat what has been said
as to the essential connection between catarrhal pneumonia and
bronchitis, so that the latter is to be regarded as an invariable
symptom and attendant rather than as a complication. As might be
expected also, catarrhal laryngitis of varying degrees of severity is
of comparatively common occurrence. Especially in cases occurring in
connection with measles, where the upper respiratory tract is already
inflamed, the increased intensity of the laryngitis may induce so much
swelling as to cause some mechanical obstruction to respiration which
will arouse fears of pseudo-membranous formation, and which, during the
spasms of cough and dyspnoea which are apt to occur occasionally, will
closely simulate true croup. Pleurisy rarely appears in such a high
degree as to constitute a serious complication. When the areas affected
are superficial, there is apt to be circumscribed plastic exudation on
the corresponding portions of the pleura. Less frequently quite
extensive plastic pleurisy occurs, with layers of exudation
sufficiently thick to modify the physical signs; and in still more rare
instances does fibro-serous effusion occur. I have noted the occurrence
of purulent pleurisy, as has Jürgensen; and in two cases it was found
to be associated with subpleural purulent foci, one at least of which
had ruptured. In the other cases the purulent character of the pleurisy
was presumably due to the constitutional dyscrasia. Allusion has
already been made to the occurrence of emphysema and bronchiectasis in
connection with catarrhal pneumonia, especially of the subacute and
chronic varieties. The observations of Delafield on the tendency of the
catarrhal inflammatory process to extend laterally through the
bronchial wall into the peribronchial zones of lung-tissue are of
special interest in their bearing on the liability to dilatation of the
bronchial tubes and to deep-seated circumscribed indurations of
lung-tissue as sequels of catarrhal pneumonia.

Gangrene of the lung I have known to occur as a complication in one
case of extraordinary severity, but in which recovery ultimately
followed a very tedious process of reparation. It was attended with
recurring attacks of hæmoptysis. The case occurred in a young man of
twenty-four years of age: the lesions existed chiefly over the right
back, though there were smaller centres elsewhere; and the spot of
gangrene and from which the hemorrhages occurred was near the right
root. He was four months in bed; his convalescence extended over a
year; evidences of induration at the above spot lasted five years; and
now, eight years after the attack, he is in vigorous health, though
still with slight cough.

Pneumothorax may occur as a sequel in protracted cases in consequence
of the rupture of a subpleural abscess. I have elsewhere reported cases
of this, and Steffen has also reported two instances.

Tuberculosis occurs in various ways in connection with catarrhal
pneumonia. There may be a development of acute general miliary
tuberculosis, owing to the depressing and irritating effect of the
disease upon a constitution strongly predisposed to tuberculosis. Or
tuberculous pulmonary phthisis may ensue, either directly as a
complication or as a sequel to ulcerative changes of inflammatory
nature in the lung. Finally, those who have passed through {365} an
attack of catarrhal pneumonia are usually left with such vulnerability
of system that any predisposition to phthisis or to tuberculosis is
very apt to be readily called into activity. It seems highly important
to note this close and complicated connection between catarrhal
pneumonia, in its various types and even in its mild and circumscribed
form, and subsequent organic disease.

Further evidence of the profound disturbance of nutrition often
effected by an attack of this disease may be found in the occasional
development of marked rachitis, and in the much more frequent
establishment of subsequent anæmia and debility, which prove obstinate
and are associated with a high degree of susceptibility of the system
to morbid influences, and which are doubtless, in some instances at
least, dependent upon impaired primary assimilation due to lesions of
the intestinal canal, which existed as complications of the original
attack of catarrhal pneumonia. It has been mentioned that
gastro-intestinal irritation is often present, both in the acute and in
the more chronic forms, and this may reach such a high degree as to
justify the name of a complication. It has seemed to be especially in
these cases, or in those where, owing to the subsequent vulnerability
of the system, gastro-intestinal catarrh occurs as a sequel, that the
serious impairment of nutrition above mentioned is most likely to
ensue.

Lastly, allusion must be made to the frequency with which severe
nervous symptoms appear, especially during the later stage of the
attack. As has been seen, convulsions are not rare in children, while
at all ages active delirium and extreme restlessness, often requiring
restraint, are of frequent occurrence. These cannot be attributed, as a
rule, to uræmic intoxication, but are to be referred to the high
systemic irritation, the great nervous exhaustion, and the marked
interference with respiration and aëration of the blood. It is probable
also that circumscribed areas of lepto-meningitis, or even of
tuberculous meningitis, are of occasional occurrence in these cases.

DIAGNOSIS.--The direct recognition of catarrhal pneumonia in its acute
stage is not always free from difficulty, while both in the acute and
chronic forms there are certain conditions with which care must be used
not to confound it.

In the first place, it is important to recognize at the earliest moment
the development of the pneumonic process during acute bronchitis of the
finer tubes. In all cases of the latter, especially in children and in
patients of debilitated system, this occurrence must be constantly
apprehended. Its occurrence may be strongly suspected if sudden rise in
the fever and in the rate of respiration and pulse is noted, though if
the areas affected are small, scattered, or deeply seated it may not at
first be possible to demonstrate it. It must be remembered also that in
the capillary bronchitis of children the fever and disturbance of pulse
and respiration may be aggravated quite abruptly from extensions of the
disease, so that actually it must be recognized that in such cases the
presence of small pneumonic centres can only be assumed, but can
neither be proved nor disproved. The course of the pyrexia may afford
some assistance, since I believe more marked diurnal variations,
amounting at times to distinct remissions, will be noted in cases of
catarrhal pneumonia than in those of severe bronchitis not so
complicated. In adults less hesitation need be felt in admitting the
development of pneumonic foci under such circumstances, even though the
physical signs are negative. Usually, however, carefully repeated
examination will soon reveal the signs of infiltration in irregularly
disposed areas; and I suspect it must be infrequent that the close
study of the relative physical signs afforded by examination of the
corresponding areas on the two sides of the chest will not afford
substantial ground for diagnosis.

It must always be remembered that areas of consolidation arising in the
{366} course of severe bronchitis of the finer tubes may be from
collapse, and not from pneumonia. This is especially apt to be the case
in children, but occurs not rarely in feeble adults. The diagnosis of
catarrhal pneumonia from mere collapse must therefore be carefully
considered. The occurrence of collapse, though it may be marked by
sudden and severe increase of dyspnoea, pulse-rate, and distress, is
not accompanied by a corresponding rise of temperature; and this is a
point of capital importance. Again, the development of the physical
signs is usually much more abrupt than where catarrhal pneumonia is
occurring. Considerable areas of dulness on percussion appear in the
course of twelve or twenty-four hours, between the successive visits of
the physician, without corresponding increase of fever; and these areas
may subsequently present marked peculiarities, at times disappearing
almost as abruptly, to be succeeded by similar areas in other portions
of the lungs, though at times also they persist and pass through the
changes already described. The physical signs furnish further
assistance. Retraction of the base of the chest during inspiration is
much more common in collapse, especially when the areas are at all
extensive and when they occur in the lower lobes, since there is
necessarily a reduction in the volume of the lungs; and this, added to
the inability to inflate the affected lobules, induces this important
sign, which should always be carefully looked for. The dulness over
collapsed lung-tissue is rarely as marked as over extensive areas of
catarrhal pneumonia; the vocal resonance and fremitus are diminished;
râles are wanting or are feeble and transmitted; and again, it must be
mentioned that the physical signs present remarkable variations within
short periods of time. It is, however, necessary to suspect the
existence of pneumonic areas in cases of severe bronchitis where
portions of lung become collapsed, and continue so, while the general
symptoms indicate persistence of inflammatory action. The differential
diagnosis is therefore in many instances rather as to the relative
proportion of these factors than as to the total absence of either.

Catarrhal may be confounded with croupous pneumonia. This error may
most readily be made if the case be not seen until a consolidated area
of considerable extent is present, since, as we have seen, in some
instances the foci of catarrhal pneumonia may chiefly occupy one lung
and may coalesce. Even then, however, the dulness of percussion rarely
corresponds with the outline of the lobe, and is rarely as complete as
in croupous pneumonia, nor are the bronchial respiration, the
bronchophony, and the exaggerated vocal fremitus as pronounced, for the
simple reason that the consolidation is not so uniform, and that many
of the smaller bronchial tubes are more or less obstructed by swelling
of the mucous membrane or by the accumulation of viscid secretions. It
will rarely happen, moreover, that strong efforts at
respiration--induced, if necessary, by having the patient cough during
the auscultation, so as to ensure a full inspiration--will fail to
develop subcrepitant râles at some point of the catarrhal
consolidation. To this must be added the information drawn from the
history of the case; the character of the cough and sputa; and, above
all, the atypical course of the pyrexia, and the fact that
carefully-repeated examinations will show frequent and abrupt
variations in the physical signs around the margins of the affected
area. If the case is observed during its development, there will be
less difficulty in making a correct diagnosis. The process is very
rarely unilateral throughout its development; and the evident
bronchitis, the development of irregularly scattered foci of partial
consolidation in both lungs, and the frequent coexistence of collapse,
combined with the absence of the characteristic symptoms and course of
the croupous form, make the nature of the case apparent.

The diagnosis of ordinary pleurisy with effusion from catarrhal
pneumonia presents no difficulty. But, on the other hand, it is not
easy to recognize the {367} occurrence of a moderate pleuritic effusion
complicating a catarrhal pneumonia. The fact that the lower lobes of
both lungs are apt to be involved in the pneumonic process interferes
with the displacement of the heart, and the enfeebling of the
respiratory and vocal phenomena may be attributed to bronchial
obstruction or to collapse. A careful study of the outline of the dull
area, and of the effect upon it of changes in the position of the
patient's body, has proved of service. After all, this is a rare
complication; but not so rare is the coexistence of plastic pleurisy
with catarrhal pneumonia, and this also may give rise to doubt in the
diagnosis. An area of dulness appearing near the base and extending
with moderate rapidity, attended with bronchial irritation, with
irregular fever of slight or of moderate degree, and with some
evidences of engorgement of the lower part of the opposite lung, and
presenting over the affected area, in addition to marked percussion
dulness, bronchial respiration not of intense concentrated type,
distant bronchophony, no increase of vocal fremitus, and crackling
râles irregularly scattered over the affected area, represent a
clinical condition, occasionally met with in adults, which requires
care to ensure its proper interpretation. I have observed crackling
râles in particular in such cases, which might have been regarded
either as intrapleural or as developed in the finest bronchioles. It
will be observed, however, that the degree of dulness is excessive for
a mere plastic pleurisy; that the respiratory and vocal signs, while
not typical of croupous consolidation, are yet far more developed than
would be consistent with the presence of a quantity of plastic pleural
exudation sufficient to cause such dulness; that any such grade of
plastic pleurisy is very rare; and that the general symptoms and the
course of the disease are indicative of much more gravity than would
attach to such a pleuritic process if it were to exist. It is
altogether probable that there has been here a coexistence of catarrhal
pneumonia with a moderate degree of plastic exudation on the
corresponding part of the pleura.

Again, it is essential to distinguish catarrhal pneumonia from acute
miliary tuberculosis with special localization in the lungs and
meninges. This diagnosis may present marked difficulties both in
children and in adults, but of course chiefly in the former, and
especially at a late period of the case, when cerebral symptoms,
closely simulating those characteristic of tubercular meningitis, may
have appeared. The irregular fever, the marked disturbance of pulse and
respiration, with evidence of diffuse bronchial irritation, but out of
proportion to the physical signs of consolidation, the occasional
vomiting in the early stage, and the appearance of nervous symptoms,
are present in both conditions. But in tuberculosis there may be high
fever before any marked evidences even of bronchial irritation appear;
there is not so much bronchitis to aid in explaining the dyspnoea;
there is not so much tendency to pulmonary collapse, and the physical
signs present are more persistent; the pulse presents the
characteristic successive stages of alteration; vomiting is apt to be
more frequent, while the diarrhoea which is often present in catarrhal
pneumonia is replaced by constipation; the Cheyne-Stokes respiration is
more apt to appear; and, finally, an ophthalmoscopic examination may
reveal retinal tubercles. It remains true, however, that in some cases
it must evidently be wellnigh impossible to decide whether the case is
one of acute tuberculosis, with a high grade of bronchitis, and very
probably with some centres of pneumonic infiltration associated, or one
of catarrhal pneumonia developing out of a severe bronchitis. It must
be remembered, moreover, that even when the case has begun as one of
catarrhal pneumonia there is a tendency to the development of
tuberculosis, both pulmonary and general; so that it may be found after
death that the nervous symptoms, which were reasonably ascribed to
congestion, to high temperature, to prolonged and exhausting nervous
irritation, and to the effect of imperfectly aërated blood, are in
reality connected with the {368} presence of miliary tubercles in the
meninges, while at the same time these have also been developing around
the pneumonic foci in the lungs.

It is no less important to bear in mind the necessity for close study
in distinguishing between chronic catarrhal pneumonia and phthisis.
There are not a few cases of the former where the protracted irregular
fever of hectic type, the progressive debility and emaciation, the
moist râles, the areas of altered percussion resonance, possibly the
signs of a dilated bronchus, and the purulent sputa, may closely
simulate true phthisis, but yet which microscopic examination of the
sputa for bacilli and elastic fibre, and the effect of treatment and
climatic change, prove to be merely inflammatory. On the other hand, it
appears undoubted, from the standpoint of clinical observation, that in
many cases, especially where a predisposition exists, catarrhal
pneumonia terminates in phthisis.

DURATION, TERMINATIONS, PROGNOSIS.--The duration of this disease is
highly irregular, and care must be taken not to confound the subsidence
of the marked general symptoms with a full restoration of the affected
areas. A considerable period is required for this latter process to be
effected, and during this interval the lung-tissue continues in a
highly sensitive and vulnerable state. Speaking with reference to the
obvious symptoms, however, it may be said that mild acute cases may
terminate in seven to ten days; fully-developed acute cases, in fifteen
to twenty-five days; while the subacute and chronic forms may last
several or many months.

Death may occur in from two to four days, especially in weak young
children, while more commonly the fatal result occurs from the seventh
to the tenth day. Of course in the chronic form death may occur after
many weeks or months.

The various terminations are in complete recovery; in apparent
recovery, but with vulnerable lungs or general system; in partial
recovery, but with residual lesions, such as bronchial dilatation or
emphysema; or the disease may pass into the chronic form, associated
with chronic bronchitis, or it may lead to the development of acute
tuberculosis or of chronic phthisis.

The rate of mortality of catarrhal is much higher than that of croupous
pneumonia. Excluding the mild circumscribed form, if such is admitted
to exist, as I believe it does, the mortality varies from 30 to 60 per
cent. It is apparently less fatal when occurring in the course of
measles than in connection with some other diseases, as diphtheria or
whooping cough. The nature and tendencies of this disease make it
evident that debility and frailty of the patient would render catarrhal
pneumonia much more fatal. So it is found that in infants within the
year death almost constantly follows, and in older children of bad
constitution, especially in those who are scrofulous or rachitic and
subjected to malhygienic influences, it is almost equally fatal. After
puberty the mortality is chiefly influenced by the constitutional state
of the subject and by the extent of the pneumonic process.

The greater tendency to pulmonary collapse and to severe capillary
bronchitis in young children justifies Jürgensen's generalization, that
before the age of puberty the danger from catarrhal pneumonia grows
greater in proportion to the youth of the individual. Partly because
the disease is more apt to assume the subacute form in feeble and
sickly individuals, partly because in this form the pneumonic process
is more apt to run into destructive lesions of the lung-tissue or to
induce tuberculosis, it is found that the mortality from the subacute
is even greater than from the ordinary acute form.

It is needless to detail the special symptoms of unfavorable
significance. The most important considerations to guide us in
prognosis are, therefore, the age, constitution, and vital resistance
of the individual; the extent of the pneumonia and of the associated
pulmonary collapse and capillary bronchitis; the degree of
gastro-intestinal irritation; the vigor of the circulation {369} and
respiration, and the manner in which aëration of the blood is
maintained; and, finally, the grade of the fever and the character of
the nervous symptoms.

TREATMENT.--It is difficult to lay down definite rules for the
treatment of catarrhal pneumonia, as the indications are extremely
variable and complicated.

In the first place, it is scarcely necessary to call attention to the
importance of guarding against the development of this disease in all
cases of bronchitis occurring in children or in delicate adults. This
care is essential not only in idiopathic bronchitis, but in those
general diseases, such as measles and whooping cough, in which
bronchitis is constantly present. As children of bad constitution and
those exposed to depressing hygienic conditions, such as over-crowding,
bad air, and the like, are most liable to become attacked with this
form of pneumonia during the course of a bronchitis, it is especially
in such cases that our precautions must be most stringent. They should
include a strict attention to the condition of the sick-room, which
should be well ventilated, but free from drafts, the temperature not
being allowed to rise above 68° or 70°, and the air being kept moist by
the generation of steam. The diet must be carefully regulated, so that
the child's strength shall be as far as possible maintained, and
stimulants must be used if indicated by weakness of the pulse or by a
tendency to failure of respiratory power. Stimulating applications
should be made to the chest, both to serve as counter-irritants and
because they stimulate respiration. It would be manifestly unsuitable
to enter here into the details of the treatment of such cases of
bronchitis, and the above remarks have been made chiefly for the
purpose of calling attention in an emphatic manner to the great
importance and value of strict and thorough treatment of all severe
cases of bronchitis, especially in children, not only with a view to
the prompt cure of the primary disease, but because thus also will the
development of the more serious conditions of pulmonary collapse and of
pneumonia most surely be prevented.

So soon, however, as the coexistence of catarrhal pneumonia is
established the gravity of the disease should be promptly recognized,
and the closest attention should be paid to every detail of treatment.
The condition of the sick-room as to temperature, ventilation, the
absence of drafts, and the suitable moisture of the air must be even
more carefully watched. The clothing of the child and the bed-covers
must be adapted to the season, the weather, and the patient's habit and
strength. It is certainly true that aggravations of the disease are
often induced by apparently slight indiscretions in the above respects.
It is rarely desirable to employ poultices. Unless skilfully made and
dexterously applied, they fatigue by their weight; dangerous exposure
is incurred in the frequent changing necessary; and, especially in the
case of children, they do not keep their position well. A layer of
cotton batting stitched inside of a merino shirt of suitable weight,
upon the outside of which oiled silk may be stitched, forms an equally
efficient and vastly more comfortable and convenient protection. This
should be directed when the bronchitis assumes a severe type, or
certainly as soon as pneumonia is suspected. It will not be necessary
to change this for a week or ten days, unless copious sweating calls
for its more frequent renewal. Among the advantages of this application
must be reckoned the fact that it allows us to employ at any part of
the chest, and as often as desired, local stimulants or
counter-irritants, such as turpentine liniment, mustard plasters, or,
what is one of the most valuable, the repeated application of tincture
of iodine of suitable strength so as not to cause too severe
irritation.

The next most important part of the treatment relates to the
restoration and maintenance of the digestive function, which is so
commonly disturbed in this disease. No one factor contributes more
powerfully to produce vital {370} debility, which in turn rapidly
increases the gravity of the lung disease by the failure of respiration
and the development of collapse, than does gastro-intestinal disorder.
Not only the diet, but the entire medication, must therefore be
rendered subordinate to the conditions of the digestive tract. It has
been seen that, at the onset of the attack, vomiting and diarrhoea are
not rare symptoms, and that throughout the course of the disease the
condition of the tongue, of the appetite, and of digestion often shows
that a catarrhal process exists in the gastro-intestinal as well as in
the bronchial mucous membrane. It is therefore frequently advisable for
a day or two to avoid all remedies directed to the condition of the
lung, and to address the treatment, dietetic and medicinal, solely to
the state of the alimentary canal. Thus it will often be of service to
employ minute doses of calomel and bicarbonate of soda or of Dover's
powder, as in the following formulas, adapted for children of five
years of age:

  Rx. Hydrargyri chloridi mitis, gr. j;
      Sodii bicarb.              gr. xxiv;
      M. et div. in Chart No. xij or No. xvj.

S. One every two or three hours until the bowels are moved once or
twice.

  Or, Rx. Hydrargyri chloridi mitis, gr. j;
          Pulv. ipecac. composit.    gr. x;
          M. et div. in Chart No. xij or No. xvj.

S. One every three or four hours.

During this early stage of cases attended with marked gastro-intestinal
irritation it may be desirable to use remedies to allay high fever, for
which purpose fractional doses of tincture of aconite by the mouth and
quinia by enema or suppository are efficient, while avoiding all risk
of injuring the stomach. The diet at first should be carefully
restricted: it is not at this time that prostration is to be feared,
while by a thorough allaying of gastric irritation and by the
establishment of fair digestion an ally of immense value for the later
and more dangerous stages is secured. But at all periods of this
disease the occurrence of vomiting or of diarrhoea should be the signal
for instant revision of the diet and for the omission of any remedy, no
matter how strongly indicated on other grounds, which could be regarded
as the cause of the disturbance.

Milk, skimmed or whole; gruel, light broths, or beef-tea; junket,
arrowroot, or similar light yet nourishing articles, are most suitable.
Stimulants are frequently indicated on account of the tendency to
failure of the respiration and heart, and owing to the typhoid nervous
symptoms. They are required at all ages, especially by young children
and by the aged. Children in particular bear relatively large amounts,
and respond to their use well and promptly. The form and strength of
the stimulant must be adapted to the state of the stomach. Wine-whey
and weak milk-punch are often serviceable. Many children will take
brandy or whiskey in water, but will refuse the former preparations.
Dry champagne has proved highly valuable in many serious cases,
especially in older persons, for young children will rarely take it.

Other important indications are to favor expectoration and to stimulate
the respiratory forces. These are closely associated, and are of prime
importance, since in catarrhal pneumonia the principal danger to life
undoubtedly comes from the progressive diminution of the pulmonary area
open to respiration, and from the increasing failure of the respiratory
muscles to overcome the obstruction to full inflation. It is through
this agency that pulmonary collapse extends, that heart failure
subsequently occurs, and that carbonic acid poisoning, with its
attendant nervous symptoms, is finally developed.

The preparations of ammonia seem to be the most valuable remedies to
meet these indications. In adults, where the disease is attended with
high fever, the following may be ordered: {371}

  Rx. Ammonii chloridi,               gr. lxxx;
      Syr. scillæ vel syr. senegæ,    fluidrachm iij;
      Liq. ammoniæ acetatis, q. s. ad fluidounce iv.

Ft. sol. S. A dessertspoonful in water every three hours. To this may
be added one or two drops of tincture of aconite in each dose, watching
carefully for the appearance of its effects; or small doses of morphia
or of deodorized tincture of opium may be added, according to the
severity of cough or of nervous restlessness. But to children in nearly
all cases, and frequently to adults, it is best to give carbonate of
ammonia at once, as follows:

  Rx. Ammoniæ carbonatis,       gr. xlviij;
      Pulv. acaciæ et sacchari, _aa_ q. s.
      Sp. lavandulæ comp.       fluidrachm ij;
      Aquæ,            q. s. ad fluidounce iv.

Ft. mist. S. One teaspoonful in water every two or three hours for a
child five years old.

It may occasionally be necessary, owing to the abundance and the
viscidity of the bronchial secretions, to administer an emetic, but
this should be avoided if possible. If required, choice should be made
of one which will act promptly and decisively without subsequent nausea
or relaxation. Such is a combination of alum and ipecacuanha, or of
sulphate of zinc and ipecacuanha, which have proved very satisfactory
in my hands. Jürgensen recommends apomorphine, administered
hypodermically, as the agent which he has found most efficient. The
dose of this substance is about gr. 1/12 for an adult, whilst for a
child of five years it should not be more than gr. 1/30 or gr. 1/25.
The dose may be repeated in 15 or 30 minutes if no emetic action is
secured.

I attach great importance to the use of strychnia in catarrhal
pneumonia after symptoms of respiratory failure appear. Its value as a
stimulus to the muscles of respiration, and possibly directly to the
respiratory nervous centre, is established. It may be given alternating
with the ammonia mixture, thus:

  Rx. Quiniæ sulph.           gr. xxiv;
      Strychniæ,              gr. ¼;
      Acid. muriatici diluti, gtt. xvj;
      Glycerinæ,              fluidrachm iij;
      Liq. pepsinæ,  q. s. ad fluidounce iv.

Ft. sol. S. Teaspoonful in water every three or four hours, for a child
of five years of age.

But when urgent symptoms arise it may be given in much larger doses and
hypodermically, so as to ensure its full absorption and effect. I have
thus given in many severe cases, and at times with unquestionably good
results, as much to an adult as gr. 1/24 every four hours, day and
night, for seventy-two or ninety-six hours.

The fever in catarrhal pneumonia does not demand special treatment
nearly so often as in the croupous form. Though the evening maxima may
be quite high, yet the occurrence of the morning remissions brings some
relief and obviates the necessity for vigorous antipyretic treatment.
The nervous system and the heart do not therefore suffer severely and
constantly from this cause in this disease. Still, there are not a few
cases when hyperpyrexia occurs and demands prompt treatment. If the
nervous symptoms are not threatening, and if the respirations are still
fairly well performed, it will be proper to try the effect of a few
full doses of quinia, or, if that fails, of antipyrine. But if, despite
these remedies, or in the event of the stomach rejecting them, or,
finally, if more urgent symptoms of nervous and respiratory failure are
impending, recourse should be had to cold effusion, particularly if the
highly laudatory statements of Bartels, Ziemssen, and Jürgensen be
confirmed by further observation. I have not found it necessary, or may
have failed to {372} appreciate the necessity, to resort to the
external use of cold in catarrhal pneumonia; but the remarks of
Jürgensen as to the remarkable influence of cold water dashed upon the
surface of the chest or directed against the cervical spine in
stimulating deep respirations accord with general observation, and
suggest this mode of treatment, especially in cases of sustained high
temperature with rapid, shallow, imperfect respirations and defective
aëration of the blood.

The nervous symptoms frequently are so severe as to require the
administration of sedatives. Remedies of this class must, however, be
used cautiously and sparingly. It were unwise to give those which
depress the heart and respiration, or, on the other hand, to administer
opium in such doses as would blunt perception and lessen cough to an
injurious degree. By the use of small doses of opium from the beginning
of the attack, however, combined with strict attention to the other
details of treatment, it is often possible to prevent the development
of severe nervous symptoms which would require powerful sedatives. In
cases of extreme restlessness and sleeplessness benefit may be found
from the use of such a suppository as the following:

  Rx. Pulv. assafoetidæ, drachm j;
      Quiniæ sulph.      gr. xxx;
      Ol. theobromæ,     q. s.

To be made into twelve suppositories of small size, suitable for a
child of five years of age, one of which may be used and repeated in
three or four hours.

Enemas of chloral hydrate, from five grains for a child of five years
to twenty grains for an adult, may be used without fear of depressing
the heart or checking the secretions, and with great relief to the
nervous symptoms, especially if tending toward convulsions. In cases of
extremely active and restless delirium, where prompt sedative action is
demanded, and yet where the use of opiates is forbidden, the hypodermic
use of hyoscyamia in doses of gr. 1/80 to 1/100 for an adult may give
gratifying results.

In cases which pass into a subacute form a continuance is demanded of
every precaution as to the diet, the hygiene of the sick-room, and the
use of general tonic remedies. Advantage may then be found from the use
of oil of turpentine, which has seemed to me the most valuable
alterative and stimulating expectorant under such circumstances.

As the case progresses into the chronic form it becomes necessary to
gradually substitute for the more strict and special method of
treatment previously employed one in which the maintenance of the
general health shall be the prime object. The regulation of the diet,
care in dress, the cautious resumption of gentle exercise, and the use
of carefully-regulated pulmonary gymnastics so as to favor the full
inflation of the lungs and the invigoration of the respiratory muscles,
are to be closely attended to.

The condition of the skin demands careful attention also, and dry
friction, inunction, and suitable stimulating sponge-baths followed by
friction, according to the constitutional condition of each patient,
may be cautiously directed with great advantage.

The remedies suitable for the more acute stages may now be replaced by
cod-liver oil, arsenic, or iodide of iron. Occasionally alterative
expectorants, such as copaiba or yerba santa, with or without an
alkali, as muriate of ammonia, will still be found desirable.

Most signal benefit will also be obtained from suitable change of
climate, associated with a continuance of careful regimen and
treatment; and, indeed, we may be gratified by witnessing a complete
restoration to health, with the exception of unimportant residual lung
lesions, of cases in which the general symptoms and the physical signs
strongly indicated hopelessly incurable organic disease. Not only in
the acute, but in the most tedious chronic, cases of catarrhal
pneumonia must our efforts be continued to the very close.




{373}

PULMONARY EMBOLISM.

BY BEVERLEY ROBINSON, M.D.


DEFINITION.--Pulmonary embolism signifies the transport during life of
clots, or of other solid substances appearing within the right heart or
systemic veins, from these parts to the trunk or divisions of the
pulmonary artery.

SYNONYMS.--_Fr._ Embolie pulmonaire; _Ger._ Embolie der Lungenarterie;
_It._ Embolia pulmonare.

CLASSIFICATION.--A rigorous classification of the different kinds of
pulmonary emboli or a clear separation of them into distinct orders is
very difficult on account of the rôle in producing them, partly
mechanical, partly dyscrasic, of some of the affections in which they
are likely to occur. This is particularly true of the puerperal state,
uterine affections, and fractures.[1] Bertin, however, has made of them
four divisions, according as the cause is mechanical, dyscrasic, mixed,
or undetermined; but these are objected to by Luzzato on the ground of
their inadequacy, and he deems it preferable to regard them from the
point of view of their medical, surgical, or obstetrical origin. From
this latter point of view we also consider it best to consider them
until a more satisfactory separation shall be established.

HISTORY.--Latterly, the subject of pulmonary embolism, or the
obstruction of this artery by means of a clot which has had its origin
in the right heart or one of the systemic veins, has been very
carefully studied. Many cases of sudden death are properly and readily
explained in this manner, where formerly they would have been doubtful
or inexplicable. Sometimes the previous existence of a fibrinous
coagulum in the right heart or in the crural vein has been recognized
previous to the symptoms indicating plugging of the pulmonary artery;
occasionally these coagula have been wholly overlooked, and the sudden
cry with intense dyspnoea, pointing to obstruction of the blood-supply
to the lungs, is a matter of dread surprise to the beholder. According
to Trousseau,[2] our knowledge of embolism is due mainly to Legroux.
This is not, however, the view of Ball[3] nor of Walshe, who attribute
the clearest insight into this process to the clinical and experimental
observations of Van Swieten, who, half a century before Legroux's time,
had injected different coagulating materials into the veins of animals
and produced the characteristic symptoms of pulmonary embolism. To
Virchow's[4] exhaustive researches, however, we are principally
indebted for a great deal of what is actually known upon this subject
to-day. True it is that contemporaneous writers have added many new
facts to those he so well elaborated, but the greater part of credit in
this line of study should be awarded to him. After Van Swieten's time
the doctrine of pulmonary embolism fell somewhat into disrepute, owing
to the lukewarmness of Hunter and {374} Morgagni. Cruveilhier (1842)
recognized their existence, but was so much impressed by his doctrine
of phlebitis that he believed the majority of pulmonary coagula were
autochthonous (formed on the spot), and not the consequence of
transport or migration in the venous current. This opinion was strongly
combated by Virchow, who held that pulmonary coagula formed some time
before death were not the result of an inflammation of this arterial
vein (Galien), but always had for origin a migratory clot which came
from some part of the venous system.[5] This doctrine of Virchow's is
certainly too exclusive, and although primary or secondary inflammation
of the pulmonary artery is certainly rare, it is certainly not unknown,
and when it exists will sufficiently explain the formation of a
fibrinous clot. Facts of this kind have been reported by Bumann,
Bouillaud, Andral, and more recently still by Lancereaux, who has shown
to the Anatomical Society of Paris[6] distinct new formations in the
pulmonary artery. Until further investigations are made on this point
it seems wise to abstain from having an opinion too categoric on one
side or the other. Virchow's first studies on pulmonary embolism were
published in 1846, and were based upon 11 cases of this disease. All
these cases were caused by migratory clots from the heart or one of the
systemic veins. In this first publication, and later on (1854-56),
Virchow gave the results of numerous experiments in which he had
injected bits of fibrin of diverse origin, particles of flesh, and
fragments of rubber into the jugular veins, and showed in an admirable
description the immediate effects of embolic plugs upon the blood, the
arterial coats, and the surrounding pulmonary tissues.[7]

[Footnote 1: _Étude critique de l'Embolie_, Paris, 1869.]

[Footnote 2: _Clinical Lectures_, Sydenham Society's ed., vol. iii. p.
414.]

[Footnote 3: _Des Embolies pulmonaire_, Thèse de Paris, 1862.]

[Footnote 4: _Froniep's Neue Notizen_, 1846, p. 910.]

[Footnote 5: Bucquoy, _Des Concrétions sanguines_, Paris, 1863, p.
138.]

[Footnote 6: _Bullétin_, 1861, p. 377.]

[Footnote 7: _Dict. de Médecine et de Chirurgie_, vol. xxix. p. 334.]

In 1852, Senhouse Kirkes[8] also studied very carefully different cases
of embolism, and showed how they were connected with organic disease.
Most of these cases, however, showed rather the effects on the brain
and the production of right or left hemiplegia than the asphyxic
sequelæ of obstruction of the trunk or divisions of the pulmonary
artery. In France the doctrine of embolism was at first received
doubtingly, and was the subject of animated discussions at the Medical
Society of the Hospitals in 1857. In this year Charcot and Ball
published the first case of pulmonary embolism which had been observed
in that country. Five years later (1862) pulmonary embolisms formed the
subject of a remarkable inaugural thesis by Ball, and articles of
considerable value were also written in regard to it by Velpeau,
Lancereaux, Lemarchand, Trousseau, etc. Spontaneous coagulation of the
blood in the right heart and pulmonary artery was considered by Meigs
in 1855 to be a frequent cause of death in the puerperal state.
Analogous cases, although none of them occurred after childbirth, had
five years previously been carefully studied by Paget.[9] The cases of
sudden death subsequent to confinement are now generally considered to
be due to pulmonary embolism.[10] Amongst the later sources of
information on the subject of pulmonary embolism or its consequences we
would direct special attention to the work of Luzzato[11] and the
theses of Duguet[12] and Levrat.[13] These and numerous other writers
have made researches as to the different varieties of pulmonary
embolism, such as the fatty (Flournoy), atmospheric, specific, those
following confinement, or traumatism.

[Footnote 8: _Med.-Chir. Trans._, vol. xxxv.]

[Footnote 9: _Ibid._, vol. xxvii. p. 162, and vol. xxviii. p. 352.]

[Footnote 10: Playfair, _A Treatise on the Science and Practice of
Midwifery_, Philada., 1882.]

[Footnote 11: "Embolia dell' Arteria pulmonale," _Annali Univers. di
Med. e Chir._, Milano, 1877-79.]

[Footnote 12: _De l'Apoplexie pulmonaire_, Paris, 1872.]

[Footnote 13: _Des Embolies veineuses d'Origine traumatique_, Paris,
1880.]

ETIOLOGY.--The great majority of emboli which are found in the
pulmonary artery after death come from the systemic veins. They may
also be {375} transferred from the right heart. According to
Hayden,[14] in fact, the migratory clot is usually derived from cardiac
thrombosis of the right heart. This opinion, however, is not generally
accepted as correct. Of all the veins of the economy, those of the
lower extremities give the largest number of emboli. This statement is
notably true of the femoral and internal saphena veins. According to
Lancereaux,[15] the reason why coagula form in the veins of the lower
limbs high up and in the cerebral sinuses is the fact that in these
locations the action of the vis-a-tergo and thoracic aspiration is
scarcely or at all felt. Besides, we know that coagula of these veins
are very frequently found in cachectic conditions (tubercle, cancer)
and in the puerperal state (phlegmasia alba dolens). As we shall have
reason to remark further on, embolism of the pulmonary artery is often
due to fragments of cancer, of pus, of a valve, etc., which have made
their way into the return blood-current, or indeed have formed there in
the first place. The direct cause of the separation of a portion of
thrombus is either some mechanical cause or the influence of regressive
changes affecting the clot. We are called upon, however, to consider
briefly--1, the causes in a general way which predispose to the
formation of thrombi; 2, the diseases, dyscrasic and local, in which
emboli occur most frequently. Virchow, Richardson, and others have
shown conclusively that the blood is prone to coagulate in the
vessels--1, whenever it stagnates or is arrested in its course; 2, if
there be, by reason of morbid alteration of vascular wall or presence
of an embolus, a mechanical obstacle present; 3, if the blood be
modified by septic conditions or increase of fibrin. Now, then, in the
veins of the lower extremities we have a considerable tendency to
stasis--greater indeed than exists elsewhere in the economy--because
these veins have to contend against the weight of the blood in the
iliac veins, the venæ cavæ, and the right heart. Further, they are
often obliged to resist the effects of accidental pressure in the
abdominal cavity, or that which takes place in lungs altered by some
chronic diseases[16] (emphysema, pneumonia, bronchitis). Usually in
these veins, as elsewhere, when a thrombus exists there is local
inflammation at its level of the walls of the vein. This inflammatory
condition itself is dependent upon mechanical injury, change of the
blood (gout),[17] or the introduction of septic material. At times
septic material is introduced into the blood and absorbs from
disintegration of a clot. Hence arise typhoid or pyæmic symptoms.

[Footnote 14: _Dis. of the Heart and Aorta_, Part ii. p. 1029.]

[Footnote 15: _Gaz. hébdom._, 1862, quoted by Bucquoy.]

[Footnote 16: Hayden, _Diseases of the Heart and Aorta_, Part ii. p.
1023.]

[Footnote 17: Tuckwell, _St. Bartholomew's Hosp. Reports_, vol. x.,
1874.]

I. Amongst the medical causes which frequently occasion pulmonary
embolism we should mention diseases of the heart,[18] of the lungs, the
stomach, the kidneys, and the uterus. Mitral affections which have
reached their ultimate period are a fruitful source of pulmonary
embolism on account of the effect produced on the right heart. The
slowing of the circulation in this condition by digitalis has been
wrongly accused by some writers of favoring the production of emboli.
Evidently, digitalis does not promote this formation when given with
circumspection, as it increases the force of the heart-beats. Sometimes
constitutional disease precedes the formation of emboli. This is
particularly true of leucocythæmia, which is an efficient cause of it,
at times, when sudden death has followed plugging of the trunk and both
branches of the pulmonary artery.[19] In the convalescence of typhoid
fever pulmonary embolism is quite frequent, and follows upon the
formation of thrombi in the veins. Such a specimen was presented by
Fagge at the meeting of the London Pathological Society on Nov. 16,
1876. The patient died suddenly in the fourth week of an attack of
typhoid fever following an attempt to get {376} out of bed. The marked
symptom of the case was intense dyspnoea.[20] It would appear that
emboli are more apt to take place in acute than chronic disorders,
because in the former they grow more rapidly, are less intimately
attached to the vascular walls, and in consequence are prone to become
detached and carried in the current of the circulation.[21] Chlorosis
has been invoked as a cause of venous thrombosis of the lower
extremities,[22] but rarely under these circumstances has pulmonary
embolism been due to its existence. Hayden[23] reports a case of
similar formation in advanced pulmonary phthisis. In this instance
death occurred, but no symptoms of pulmonary embolism were at any time
present. At the autopsy a firm, decolorized clot was discovered in
either femoral vein. Although phthisis is a frequent cause of
phlegmasia alba dolens, owing to the compression of enlarged lymphatic
ganglia or the blood-dyscrasia, it is not often the source of pulmonary
embolism (9 cases out of 160 of all kinds, according to Luzzato). A
probable explanation of this fact is that the fibrinous coagulum does
not form in the veins until a late period of the disease, and death
results before it has had time to soften and disintegrate.[24]

[Footnote 18: _Am. Journ. Med. Sci._, Oct., 1876.]

[Footnote 19: Hayden, Case 124, p. 1030.]

[Footnote 20: _Lancet_, Nov. 24, 1876.]

[Footnote 21: At times septic material is introduced into the blood and
absorbed from disintegration of a clot. Hence arise typhoid or pyæmic
symptoms.]

[Footnote 22: _Reports of Pathol. Soc. of London_, vol. xvi.]

[Footnote 23: _Op. cit._, p. 1024.]

[Footnote 24: _Dict. de Méd. et de Chirurgie_, vol. xxix. pp. 336,
337.]

II. Surgical affections are frequently the efficient cause of pulmonary
embolism. Thus, out of 160 cases of the latter disease collated by
Luzzato, 66 owed their origin to conditions embraced in this division.
Wounds, contusions, compressions, diseases of, and all surgical
operations upon, the veins are specially liable to be followed by
pulmonary embolism. Sometimes the thrombus formed originally in the
implicated vein takes place there spontaneously; sometimes it is the
direct consequence of a localized phlebitis. Several times the
injection of tincture of iron into varicose veins of the inferior
extremity[25] or into a nævus[26] has been the occasion of symptoms
indicating sudden obstruction of the pulmonary artery; again, it is an
accident, more frequent than is generally admitted, of the operation of
transfusion (Vulpian). According to Le Dentu,[27] the varicose veins
tend to cause stasis of the blood, and thus to favor coagulation. They
are, therefore, a predisposing cause of the formation of thrombi, and
hence of pulmonary embolism. Extensive burns and frostbite are also
efficient causes of venous thrombus, and after this manner predispose
to pulmonary embolism. The separation of the placenta after delivery
leaves an open condition of the uterine sinuses which is a real
traumatism, and which occasions the formation of sanguineous coagula.
The irritation of the sinuses may extend to the large extra-uterine
veins (iliacs), and lead to further deposits of fibrin which may give
rise to pulmonary embolism. In these latter cases the inflammation of
the veins, if it occurs, is apt to follow the formation of the
coagulum. Cases of pulmonary embolism have sometimes been occasioned by
the compression of the lower extremities with Esmarch's elastic
bandage.[28] Massari indeed cautions his readers against the use of
elastic bandages for varicose subjects. Even if their use be deemed
advisable, never should the limbs be permitted to remain bandaged
during several consecutive hours, for fear lest fibrinous clots be
formed. Azam cites a case of cyst into which an injection of iodine was
made, and quickly followed by obliteration of the pulmonary artery.
Hélie (1837), Gütterbock, and Marjolin (1837) have each related a case
of pulmonary embolism following a sprain. The most frequent cause, in
this division, of pulmonary embolism is {377} without question
fractures. The first case reported is probably one by Virchow in 1846
of an extra-capsular fracture of the thigh which led to a fatal
termination by a pulmonary embolism.[29] Sixteen years later (1862) a
second fact of pulmonary embolism following upon a fracture was
communicated to the Institute by Velpeau.[30] In 1864, Azam[31] read
two memoirs--the first before the French Academy of Medicine, the
second before the Congress of Bordeaux--in which not only the relation
of fractures, but all kinds of traumatisms, to pulmonary embolism was
fully considered. In these two articles several illustrative cases were
recorded as being seen by Gosselin, Richet, and Labat. In the following
years several articles of value appeared on the subject of emboli and
of their relations with contusions and fractures. Among authors we
should cite the names of Bertin (1868), Durodié (1874), and Besson
(1878) as workers in this direction. It has been noted not only that
the fractures amongst traumatisms cause a large proportion of cases of
pulmonary embolism (16 times in 30 cases), but also that the number of
instances of fracture of the leg largely predominate (11 cases).[32]
The explanation given to the latter circumstance is in part the near
proximity of the bones with large veins (Verneuil), and second the
dilatation of the veins themselves (Le Dentu). Occasionally the
embolism of the pulmonary artery has consisted mainly of fat: in one
instance there was fracture of the thigh consequent upon a fall;[33] in
the other the patient was suffering from a gunshot wound of the left
knee.[34] In both specimens examined after death under the microscope
fatty matter was found in the capillaries and pulmonary arteries. It
was probable that the fat had been transported by the veins--in part
from the lacerated marrow, in part from the subcutaneous adipose
tissue.

[Footnote 25: _Soc. Méd. Bordeaux_, 15 Nov., 1867.]

[Footnote 26: _Annales d'Oculistique_, 1864.]

[Footnote 27: _Discussion à la Soc. de Chirurgie_, 14 Avril, 1875.]

[Footnote 28: _Annali Universali di Medicina_, Milano, May, 1877;
_Wiener Med. Woch._, 1875, No. 48, quoted from Dr. Dobell's report on
_Diseases of the Chest_, vols. ii. and iii.]

[Footnote 29: _Traube's Beiträge sur experimentalen Path. und Phys._,
1846, Heft 551, quoted by Levrat.]

[Footnote 30: _Comptes rend. de l'Académie des Sci._, 7 et 14 Avril,
1862.]

[Footnote 31: _Gaz. hébd. de Méd. et Chirurg._, 1864.]

[Footnote 32: Levrat, _Des Embolies veineuses d'Origine traumatique_,
p. 54, Paris, 1880.]

[Footnote 33: Hesch, _Anzeiger d. K. K. Gesellschaft der Aerzte in
Wien_, 1876, No. 3, quoted in _Dobell's Reports_, vol. cxi., 1877.]

[Footnote 34: _Dorpater Medicin. Zeitschrift_, Bd. vi., Heft iii. and
iv., 1877, pp. 326-338, cited by Dobell.]

III. The puerperal state has been considered by Behier, Dubreuilh, and
others with some degree of reason as one closely resembling a condition
of traumatism. In fact, the raw surface with widely-open uterine veins
and sinuses which exists so soon as the placenta is fairly separated is
analogous to that of a limb which has just been amputated. The
differences which present themselves are those which arise from the
special state of the patient herself. During gestation, and
particularly toward its terminal period, the relative quantity of
fibrin to the mass of the blood is greatly augmented. According to
Andral and Gavarret, this excess of fibrin may become so great as to
reach a third more than the normal quantity. After delivery of the
foetus and placenta involution of the uterus begins. This process lasts
several weeks, and during this period the blood is filled with effete
material. Besides these favoring causes of thrombosis which are special
to the puerperal state and mark its blood-dyscrasia, we have the fact
of loss of blood, both during and after confinement, as an efficient
and well-known cause of this accident. According to Leishman,[35] who
cites Merriam, this is doubtless the reason why after placenta prævia
cases of phlegmasia alba dolens are so frequently observed. Not only
does Richardson consider the loss of blood as predisposing toward
pulmonary thrombosis, but also syncope or exhaustion in other depressed
states of the system. In some such instances, however, we must not
ignore possible disease of the myocardium or compression from an
abscess of the broad ligament (Charcot and Ball). The coagula formed in
the femoral or saphena veins may {378} sometimes extend into the
iliacs, venæ cavæ, and become a frequent source of pulmonary embolism.
Owing to the rapid softening of clots formed in the uterine veins
during septic endometritis, we have a special cause of pulmonary
embolism accompanied by toxic phenomena (Virchow). Several of the
operations necessary in certain complications of this condition, such
as application of the forceps, detachment of the placenta, etc., have
been followed by pulmonary embolism (Massari). It is not remarkable
that with so many predisposing causes of thrombosis blood-clot should
be of frequent formation in the puerperal state.

[Footnote 35: _System of Obstetrics_, p. 710.]

Phlegmasia and pulmonary embolism have been well studied on account of
their gravity; the other situations of fibrinous deposit are very
imperfectly known. Playfair[36] believes that clots may form in the
right heart and pulmonary artery, just as they may be produced in other
portions of the venous system and under the influence of the same
causes. This conviction is opposed to that of Virchow and Bertin,[37]
who hold that an embolus must be the starting-point of a blood-clot,
and that without its presence it cannot form. Virchow, indeed,
considers stagnation of the blood as the most essential condition of
the formation of a coagulum. It would seem, however, that the action of
the heart is so feeble in certain debilitated persons, or in diseases
in which there is strong tendency to adynamia, that this objection is
at least partially met. Certainly, as Humphrey[38] has shown, the
pulmonary artery, owing to its numerous divisions and the prominent
angles it offers, is favorable to coagulation by its anatomical
formation. Moreover, if coagulation may form around an embolus, why
cannot similar causes which bring this about also occasion a
spontaneous deposit of fibrin? The greater number of cases of pulmonary
embolism in the puerperal state occur in young women not many days
after confinement (Hennig, Luzzato). Occasionally a case is seen as
late as the fifth week. Cases also occur, though exceptionally, during
pregnancy. Playfair[39] has endeavored to show, partly by post-mortem
appearances, partly by the date of the accidents, the distinctions to
be drawn between pulmonary embolism and pulmonary thrombosis. After the
nineteenth day from the date of delivery the accidents are usually due
to embolism, before this date to thrombosis. This would appear to be
rationally explained when we consider that the degenerative changes
which alter the vascular clot sufficiently to permit its transport from
the place of its formation to a distant organ take a certain time to
become effected. The causes of the pulmonary thrombosis are those which
produce coagulation elsewhere in the vascular circuit during the
puerperal state. Pulmonary embolisms are more frequent with women than
men on account of affections of the uterus and the puerperal condition
(80 to 66, Luzzato). In children pulmonary embolisms generally come
from clots first formed in some one of the peripheral veins (renal,
umbilical, diploe, etc.). Autochthonous clots in the pulmonary artery
may be due to direct pressure from enlarged ganglia of the neck. The
great number of pulmonary embolisms form in the vessels of the lower
extremities. Thus far, thrombi have not been shown in the larger
lymphatic trunks of the body.

[Footnote 36: "The Puerperal State," being Part V. from a _Treatise on
Midwifery_, p. 50, Philada., 1882.]

[Footnote 37: _Des Embolies_.]

[Footnote 38: _On the Coagulation of the Blood in the Venous System
during Life_, quoted by Playfair.]

[Footnote 39: _Lancet_, 1867.]

SYMPTOMATOLOGY.--The symptoms thus far observed of pulmonary embolism
are not usually very full or accurate. Many of the cases occur so
suddenly and fill the beholders with such dismay that clinical
observations are imperfect. Opposed to this statement we note the fact
that what pertains to pathology and morbid anatomy of pulmonary
embolism is particularly complete. Nevertheless, for the sake of
clearness and in view of accidents really {379} observed, we may divide
the cases into--1st, sudden, fatal form; 2d, grave form; 3d, benign
form.

1st. Sudden, Fatal Form.--In this category should be placed those
instances in which the main trunk or both primary divisions of the
pulmonary artery have become wholly obstructed in a sudden, almost
instantaneous, manner. Immediately the patient is a prey to the most
intense dyspnoea and anxiety; the chest-walls rise and fall in an
exaggerated degree and with great rapidity; the heart-pulsations are
tumultuous and irregular; there is intense pallor of the face; a groan
or cry is heard; there is a vain and brief struggle for breath; and
death may occur before aid can be offered, with symptoms resembling
those of asphyxia. These rapidly fatal accidents are always deeply
impressive, but never so appalling as when they take place in
convalescence, when everything appears to be going on well, and there
is no reason to apprehend such an occurrence had not numerous recorded
facts affirmed their verity. Such cases have been observed[40]
particularly after fractures of the lower extremities and during
recovery after confinement.[41] The accidents are not always asphyxic
in character, even though they be equally sudden and destructive.
According to Trousseau,[42] this is true where the embolus is arrested
in the right ventricle and is of sufficient size to cause stoppage of
cardiac contractions and an attack of fatal syncope. In instances which
are not mortal in a few moments, and where the gasping and struggling
for breath continue during half an hour, an hour, or more, the
excessive pallor gives way to a deeply cyanosed tint of the face. When
the face assumes a livid purple hue it has been considered as proof of
a condition of spontaneous thrombosis rather than embolism.[43]

[Footnote 40: Azam, 1re Mémoire, _Gaz. hébd. de Méd. et Chirurgie_,
1864; Observ. II., reported by Levrat.]

[Footnote 41: _British Medical Journal_, March 27, 1869.]

[Footnote 42: _Clinique méd._, t. iii. p. 715.]

[Footnote 43: Such a case is reported by Playfair in Part V. of his
_Treatise on Midwifery_, and is also recorded in _Obst. Trans._, vol.
xii. p. 194.]

Although the heart-beats are vigorous at first, they soon become weak,
intermittent, and irregular. Similar characters may be noted in the
pulse, which is very soon compressible, thready, and at times almost
imperceptible. These latter conditions of the cardiac movements may
exist from the beginning of the accidents, and may be accompanied by
coldness of the extremities and chilly sensations (Cohn). Frequently we
observe convulsive movements and foam at the mouth just before death.
When these symptoms have been remarked, the question has been raised as
to whether the patient was suffering from an epileptic seizure.[44] The
first impressive effects of pulmonary embolism undoubtedly attach
themselves to the respiration and circulation. The nervous system is
not always so visibly affected. Frequently the patients preserve
complete mastery of their intelligence to the end, and cry out in no
doubtful accents, "I am stifling! I am dying!" Occasionally they even
point with their fingers to the exact seat of the sudden obstruction in
the chest. In a case of Vidal[45] the peculiar and painful sensations
indicated by the patient in the precise location of the embolus had
considerable diagnostic importance. This indication, however, is not
always valuable, and may be misleading, as in the case reported by
Ormerod, when the patient, a young girl, paraplegic, was attacked
suddenly with intense feelings of suffocation and pointed to the throat
as being the seat of the obstruction.[46] Frequently these suddenly
fatal cases occur in the course of an acute or chronic disorder, and
usually the terrible phenomena manifest themselves after some movement
or effort, as one makes in sitting up in bed or reaching for a desired
object. Under these latter circumstances sudden pallor may overspread
the features, the heart {380} cease to beat, and the patient expire in
a true syncopal attack, without any of the asphyxic appearance
previously referred to. Usually, however, the need of air is most
acutely felt, the muscles of the neck and thorax are violently
contracted, whilst the patient suffers from intense anxiety and
oppression. Meanwhile, air enters the lungs freely with each successive
inspiration. Percussion and auscultation of the chest do not reveal any
notable change in the pulmonary structure, and the peculiar asphyxia
which is present results rather from the want of blood to be oxygenated
than from the lack of air or sanguineous stagnation. Indeed, Lancereaux
affirms that death in all cases of fatal pulmonary embolism follows
upon these progressive asphyxic features. Never, according to him, does
it occur from a real attack of syncope.[47]

[Footnote 44: Picot, _Les grands Processus morbides_, 1876.]

[Footnote 45: Ball, _Des Embolies pulmonaires_, Observ. xxvii., Thèse,
Paris, 1862.]

[Footnote 46: _London Med. Gazette_, vol. ix. p. 788, quoted by Hayden,
p. 1029.]

[Footnote 47: "Comptes rendus de la Société de Biologie," 1861, _Dict.
de Méd. et de Chirurgie_, vol. xxix. p. 365.]

The immediate cause of death in these cases is differently regarded by
eminent authorities. Virchow[48] holds that the heart-beats suddenly
stop and death is caused by syncope. Picot and Panum claim that
inasmuch as the left heart does not receive any blood from the lungs,
the brain cannot be supplied, and thus anæmia of the brain becomes the
immediate source of a fatal termination. True it is that owing to the
complete obstruction of the pulmonary trunk or its bifurcation no blood
can reach the brain, but for a similar reason the coronary arteries
cannot be supplied, and indeed the whole arterial system remains empty,
whilst the surface of the body becomes livid, owing to marked venous
distension. Paget holds to a conservative view, believing that death
results at times from anæmia and on other occasions from syncope. It is
the belief of the writer that most of the phenomena preceding death are
in the majority of cases those of asphyxia, and he recognizes with
Bertin[49] and Lancereaux that deficient oxygenation of blood is, after
all, the essential cause of death. In all cases of very rapid death,
Lancereaux believes that the embolic clot must have originated in, and
been transported from, one of the large veins of the lower extremities
or the pelvis, and that the prolongation of clots formed elsewhere in
the venous system, when broken off and carried in the blood-current,
are insufficient by reason of their small size to block up completely
the pulmonary artery.[50]

[Footnote 48: _Gesamm., Abhandl._, 1862, p. 316, quoted by Playfair.]

[Footnote 49: _Étude critique de l'Embolie_, Paris, 1869.]

[Footnote 50: Bucquoy, _Des Concrétions sanguines_, Paris, 1863, p.
147.]

2d. Grave Form.--In this form neither the pulmonary trunk nor one or
both of its primary divisions had become obstructed. The embolic clot
or clots have been carried farther into the pulmonary structure and
filled up one or more of the secondary bronchial divisions.
Nevertheless, the accidents declare themselves with the same remarkable
suddenness, and are accompanied by chilly feelings and pallor of the
face, just as we have for a brief period after all great shocks to the
system (Levrat). In spite of the rapid occurrence of the accidents,
they last a considerable time, and hence we are able to study more
carefully the respiratory and circulatory symptoms proceeding from the
pulmonary obstruction. The pallor of the face soon passes away, and we
have in its place cyanosis of the features and a livid hue of the
extremities, and in fact of the entire surface. Sometimes, owing to
tricuspid regurgitation, we have a venous pulse rapidly produced in the
veins of the neck. The patient constantly suffers from oppression and
anxiety, and sighs and utters complaints, whilst he makes powerful and
ineffectual efforts to diminish his uneasy sensations by deep and rapid
inspirations. Occasionally partial convulsions are noted. At times,
also, the patient complains of cephalalgia and vertigo, but rarely
shows signs of delirium. After a time the accidents narrated become
less, and there is relative ease. Soon, however, there is a
recrudescence of the attack, and the anxiety and oppression are even
{381} greater than before. A succession of such occurrences may take
place, and are attributable to a change of location of the clots. If we
examine the chest by our physical means of exploration, the result is
little better than negative. Percussion shows no abnormal dulness.
There are no abnormal râles, and at most there is only a certain rough
timbre of the respiratory murmur. After a short time the heart-beats
become irregular and feeble, the temperature falls one or two degrees
(Cohn), the body is covered with abundant clammy perspiration, and the
patient succumbs. Sometimes death is due, where the accidents are
prolonged, as much to the secondary effects in the lungs of the embolus
as to the embolic plug itself. The accidents commence, indeed, by
intense dyspnoea and oppression, but are soon followed by sanguinolent
sputa. Luzzato has mentioned one case where the hæmoptysis was an
initial symptom of pulmonary embolism, but it is very probably
explained by concomitant chronic cardiac disorder. Whenever we find the
local signs of an infarctus, the general condition is apt to become
more and more serious, new clots reach the lungs, and death occurs in a
few days from asphyxia. Frequently albuminuria and oedema of the
extremities are observed. In those instances where the patient recovers
the mucous râles and localized dulness caused by the infarctus remain
for a while, but the sanguinolent sputa diminish, and little by little
respiration becomes more vesicular. The patient is now only exposed to
dangers due to ulterior transformations of the infarctus. Occasionally
new infarctions may form several times and produce accidents similar to
those referred to. If there is no hæmoptysis, an infarctus can only be
suspected, and often after death this condition is discovered when
during life it was wholly overlooked. Sometimes the pulmonary
embolisms, although quite numerous, affect vessels of very small
calibre, and remain latent during life or occasion no characteristic
symptoms. In those examples in which some of the secondary divisions of
the pulmonary artery are filled with embolic plugs there is of course a
diminished supply of oxygenated blood sent by the left heart to the
brain, and there is likewise an accumulation of carbonic acid in the
nerve-centres. The lack of oxygen is not enough to cause rapid death,
and the accumulation of carbonic acid produces, no doubt, the symptoms
of temporary excitability and the local convulsions which are so often
present under these and analogous conditions. Whenever after this
period of excitement symptoms of slow asphyxia become apparent, they
are due either to an excessive afflux of blood into the free arteries
of the lung and the passage of the plasma through their walls into the
pulmonary vesicles, or they are caused by a succession of emboli
blocking up the remaining vascular twigs. Upon the mechanism of death
resulting from pulmonary embolism Jacquemet[51] has made a careful
study, showing the cases of death attributable to syncope and those
solely explained by asphyxia. The only physical sign observed in the
region of the chest in fatal cases which would appear without question
to be caused by a pulmonary clot is a prolonged basic murmur extending
itself to the right and left of the sternum in the direction of the
primary divisions of the pulmonary artery. "This sign," says
Walshe,[52] "I most certainly heard in an old gentleman whose life was
brought to a sudden close in the course of an acute affection by
coagulation in the pulmonary artery."

[Footnote 51: _Congrès médicale de France_, 2ème session, Lyon, 1864,
quoted by Levrat.]

[Footnote 52: _Diseases of the Heart_, 4th ed., 1873.]

Whilst authors have usually insisted with much emphasis upon the
habitual fatal termination of pulmonary embolism, especially where the
plug fills one or both of the large divisions of the pulmonary artery,
they have not referred as a rule to the possibility of the patient's
recovery. Now, if the arteries be only partially filled by the plugs,
and a current of blood can pass around them, the lungs may be
sufficiently supplied with oxygenated blood to sustain {382} life for a
while and until the clot can be reabsorbed. That this clot can be
reabsorbed in the pulmonary artery is shown by what has been frequently
observed in regard to clots which have been contained in other vessels
of the body.[53] Not infrequently, simultaneous with or following
upon[54] obstructed pulmonary circulation, the phenomena due to
peripheral thrombosis have been observed (phlegmasia dolens). In a
somewhat analogous manner, after anxious respiration had occurred,
obviously due to pulmonary embolism, a peripheral thrombus previously
present has been known to have disappeared.

[Footnote 53: Humphrey, _Med.-Chir. Trans._, vol. xxvii. p. 14.]

[Footnote 54: Case reported by Playfair in _Treatise on Midwifery_,
Part V., amongst those illustrative of recovery after symptoms of
pulmonary obstruction.]

3d. Benign Form.--This form occurs frequently after the traumatisms as
described by Besson.[55] Habitually we have few or no symptoms which
are at all characteristic. The embolisms are capillary and remain
latent. Now and then there may be a sudden attack of difficulty of
breathing, accompanied by constriction of the thorax which shall
probably be explained in this manner. Sometimes the sputa are slightly
covered with blood, and this fact lends additional authority to the
diagnosis. According to Ball, the physical evidences of the embolisms
in the chest are wholly disappointing. Besson, however, finds distinct
evidences of their presence in crepitant and subcrepitant râles and
dulness on percussion. Levrat[56] believes we may have probable signs
of the existence of capillary emboli, and cites as an example a case of
traumatism in which there might be present a thrombus, and where there
would be sudden hæmoptysis followed by sanguinolent sputa, and yet the
examination of the chest remained negative. There are cases reported by
Paget, Colin, and Feltz in which fatal terminations, caused by a
succession of asphyxic paroxysms, took place just as they do after
sudden plugging of the large pulmonary divisions. This is true only
when the capillary embolisms are very numerous.

[Footnote 55: Paris, 1878.]

[Footnote 56: _Thèse_, Paris, 1880.]

It has been noted that secondary changes of capillary embolisms are not
apt to occur in the anæmic and cachectic; in the plethoric and those
affected with chronic cardiac disorders the contrary is true. According
to the condition of the nervous system, to its greater or less tendency
to react, there will be more or fewer chances of the capillary
embolisms making their existence known by an attack of suffocation
(Luzzato).

PATHOLOGY AND MORBID ANATOMY.--Pulmonary embolism gives rise to
different morbid lesions. The nature of these and their extent depend
in great measure upon the size, situation, and character of the plug
which fills the main trunk of the pulmonary artery or one or more of
its divisions. The changes of tissue which take place are of course in
close relationship with the length of time which has elapsed since the
embolus first migrated. They are also influenced greatly by accidents
or complications which have arisen. It shall be our effort first to
narrate the important considerations which pertain to simple embolus,
and whether it affect a large artery or only a small vessel. After
speaking of the simple variety we will refer briefly to septic and
fatty emboli and also to those of other nature.

The pulmonary artery may be blocked up by a clot formed in situ. This
fact has been shown to be true by many writers--_i.e._ Lancereaux,
Duguet, etc. When a thrombus is present it may be occasioned by an
inflammatory condition of the artery (rare), or by a dyscrasic
blood-condition, or again by localized compression in the vicinity of
the coagulum, as from a tumor. We may find arterial thrombosis during
pulmonary phthisis, in pneumonia, in pleurisy, and in cases of cardiac
dilatation or degeneration.[57] Endocarditis of the pulmonary valve and
compression of the neck by enlarged ganglia have been mentioned as
causes of these thrombi.

[Footnote 57: Here it is due to relative stasis of the blood.]

{383} Ordinarily, a pulmonary embolus is fixed at the point of division
of the main vascular trunk. It more or less completely blocks up the
calibre of the artery, and is usually situated in the midst of a soft
new clot, which also covers it in front and behind. The embolus often
manifests its origin from a clot contained in one of the large veins of
the lower extremities. One end is rough and excavated, and fits into
the coagulum we find lodged there. It is often twisted like a
corkscrew, or has on its surface the mark of the valves of the vein
from which it has migrated. It is white or yellow in color. If we
examine the interior of an ordinary autochthonous clot, we find it
softer relatively than the clot of an embolus, and, moreover, no
prolongations proceed from it which fail to correspond with any
vascular division. The suddenness of the accidents and the
disappearance of a previous peripheric clot are strong reasons in favor
of the existence of the embolus.

More emboli are carried into the right lung than into the left, on
account of the larger size of the artery. The median and lower lobes
are also the ones most usually affected. When the right lung is
diseased the emboli are then more frequently transported on the left
side. After a time an embolus goes through certain transformations. It
softens at its centre, owing to degeneration of the white
blood-corpuscles. The hematies disappear soon, and the fibrin also
changes in structure, becoming soft and granular. This softening at the
centre of the embolus must not be confounded with a purulent change
which affects certain thrombi which come from or are carried to a focus
of suppuration. Whenever an embolus has been a long while in the
artery, a neo-membrane forms between it and the arterial wall. This
neo-membrane is mainly constituted by fibrillous tissue and here and
there some developed vascular twigs. As a whole, it forms a sort of cap
or covering for the embolus, and finally it takes up by absorption the
granular detritus which forms in the interior of the clot. We perceive
from the foregoing statement that a pulmonary embolism may heal, and
that the process of its cure differs in no respect from what occurs in
the case of a coagulum which disappears by absorption from some other
portion of the vascular system, or indeed from the surface of the
serous membrane. When the embolic plug comes from a focus of
suppuration or gangrene the vascular walls will probably be affected
with similar alterations.

In consequence of the obstruction of the main trunk, or of the
important branches of the pulmonary artery by embolic plugs, certain
effects are directly produced. These are--1st, mechanical; 2d,
nutritive; 3d, irritative.

Perhaps, however, before describing these effects in detail it would be
well to mention certain anatomical facts with respect of the
circulation of the lung which have considerable importance in view of
certain morbid lesions to which we shall refer presently. It has now
been proven experimentally, by the researches of Cohnheim, Litten, and
Küttner, that there are no vascular communications between the
pulmonary and bronchial arteries, and, further, that there are no
branches coming off from the small divisions of the pulmonary artery by
which a collateral circulation can be carried on when the arteries of
the third order are obstructed by embolic plugs. It is also further
corroborated by the investigations of the authors named that the
pulmonary artery is mainly instrumental in keeping up the function of
the lungs, whilst the bronchial artery is the artery of nutrition. If
the latter were obstructed in any manner, gangrene of the pulmonary
structure must surely follow; if the latter be ever so thoroughly
closed, no death of tissue will ever result.

The mechanical effects caused by the obstruction of the main artery or
of a primary division of it are much less considerable than when a
smaller artery is plugged. In the first case the only observable
condition is that of anæmia of pulmonary tissue. Occasionally
Lancereaux has noticed atelectasis of certain lobules. The pathogeny of
this condition is difficult to {384} explain, as air enters the bronchi
freely, and it should not be produced without effusion taking place. If
life lasts a few hours hyperæmia and oedema of lung-tissue may be
caused. The latter conditions are aided if there be existing organic
disease of the heart. If, now, the smaller arteries be obstructed by
embolic plugs, there is a strong tendency to the formation of
hemorrhagic effusions, to which the name infarctus has been very
properly given by Virchow. These infarctions vary in size from that of
a small nut to that of a pullet's egg, just as they implicate one or
more pulmonary lobules. They are situated at the periphery of the lung
underneath the pleura. They are conoid in shape, with the apex turned
toward the root of the lung. They seem like hard nuts under the surface
of the lung when felt with the fingers. Their color is dark-brown or
black; their cut surface is granular, even more so than the surface of
a lobule solidified by broncho-pneumonia. The capillaries in and around
these masses are filled with red blood-corpuscles. The same is true
also of the alveoli, in which we find degenerated epithelial cells in
large numbers containing granules of pigment. The connective tissue
about the alveoli becomes thickened, the alveolar cavities contract,
and finally the infarctions are changed into a real fibrous cicatrix,
in the same way as they are transformed in other viscera of the body.
Prior to this stage, however, we notice that the color of the
infarction has gradually changed, and that it has become pale and
yellow. This is due to the fatty degeneration of the fibrin contained
in the alveoli, and the same affection of the enclosed cells. May any
infarctions be restored to a condition of perfect integrity? It is more
than doubtful, even if the obstructing plug of the pulmonary artery
disappeared very soon, because the pulmonary parenchyma beyond the clot
has suffered so much from fatty changes and hemorrhage that the vessels
are unequal to their function. At times, owing to the stoppage of the
nutritive action of the bronchial artery, the infarction may become a
cheesy mass, which soon softens and is expectorated. This leaves a
cavernous opening in the lungs. Sometimes the infarction becomes
infiltrated with calcareous salts. It cannot be confounded readily with
other lesions, especially pulmonary apoplexy, on account of its
distinct limitations. Sometimes a lobule affected with
broncho-pneumonia and hemorrhage may simulate it closely. The pathogeny
or mode of production of the hemorrhage in a more or less limited area
of the lung which is concomitant with an embolic plug in one of the
branches of the pulmonary artery is difficult to present. This fact may
be explained by the different solutions afforded by various authors as
to the manner in which the apoplectic condition and the embolus are
correlated. Certain writers have affirmed that the embolus itself is
but a secondary phenomenon, and the surrounding hyperæmic state is the
real cause of its production (Laennec). Later authorities have
established that this statement is rarely true, and that the embolus
always occurs first and the localized congestion follows closely
afterward.

Precisely the way in which the congestion or hemorrhage was occasioned
has not been elucidated in a similar manner by all. Virchow years ago
(1856) recognized that one or other was due to vascular stasis and
reflux of venous blood from neighboring vessels; in other words, the
explanation here given was the same as for infarctus of the kidney or
spleen. Jürgensen regards infarctus as being similar in structure to
lobular pneumonia. It has been also affirmed that owing to incomplete
obstruction tissue supplied by the artery was at first anæmiated, and
later, by reason of excess of backward pressure from venous trunks, it
became congested or hemorrhage was effected. Duguet states that the
arterial walls beyond the embolic plug become inflamed, and thus act as
a cause of hemorrhage. The first effect, then, of an embolic clot being
arrested in the lung is that of anæmia. Soon this state is followed by
hemorrhage occasioned in the way I have mentioned. In the lung the
{385} hemorrhage means of necessity rupture of a vessel; in the spleen
and brain this is not so invariable. Whilst the smaller bronchi are
sometimes congested, they are rarely infiltrated with blood. For this
reason gangrene is not a frequent sequela of pulmonary infarctus. It is
not admissible that hemorrhage should occur without rupture of the
vessel in many instances, for the reason that the sanguineous effusion
is not always limited to the area supplied by a given vascular division
obstructed, nor is it in the centre of the lung conoid in shape. The
catarrhal changes in the lungs are very constant, although usually
superficial in character and only affecting the epithelium. As
Cohnheim[58] has pointed out, there is a proneness to degeneration
rather than to inflammatory action.

[Footnote 58: _Untersuchungen über die Embolischen Processe_, Berlin,
1872.]

Due consideration being given to the changes of tissue effected by an
arrested embolus, we can more fully understand the clinical phenomena
connected with them. True it is, however, that the troubles of
innervation and respiration thus brought on may pass unperceived, and
for the simple reason that the pathological lesion follows, as a rule,
only the transport of an embolus into a small arterial division. In a
similar way the intensity of the venous reflux is in direct
relationship with the functions of the heart and lungs, and if either
the diseased hemorrhagic effusion is rendered more certain.

It is probable that a simple embolus cannot be followed by a gangrenous
focus in the lung. This result is recognized frequently when the
embolus originates in a purulent deposit, whether it be the consequence
of an abscess, of puerperal fever,[59] of a compound fracture, etc. The
gangrenous cavity finally softens, its contents are expectorated, and
the pulmonary tissue becomes indurated and cicatrizes around the
excavation.

[Footnote 59: _Dublin Journ. of Med. Science_, May, 1875.]

Pulmonary embolism may at times be the occasion of a pneumonic
consolidation limited to the area of distribution of an obstructed
pulmonary division. Sometimes the consolidation extends beyond this
limit, and is seemingly the immediate effect of neighboring irritation.
When the consolidation exists near the surface of the lung, it may
extend to the pleura, producing considerable effusion and
pseudo-membranous deposit upon the visceral layer. Both sides of the
chest may occasionally be thus affected.

Capillary emboli of simple nature have long been described. Unless they
obstruct a great many vessels simultaneously, they rarely cause death
(Feltz). They do not, moreover, produce hemorrhages or infarctus,
inasmuch as a collateral circulation is so easily established. The
principal sources of these emboli exist outside of the vascular system,
and in this variety we find emboli of air, fat, of the débris of new
growths, etc.

Since 1866, the period at which Zenker first directed attention to
fatty emboli in the pulmonary capillaries as a complication of an
accident in which a patient was crushed between two wagons, many
observers have noted accidents due to these obstructing bodies. Fatty
emboli may follow numerous causes (contusions, suppurations,
osteomyelitis, etc.), but are more frequent and fatal after comminuted
fractures of the limbs than from any other single cause (Flournoy).

Occasionally the patient will have recovered from the shock following
the fracture, when he is suddenly attacked with intense dyspnoea and
expires within a few hours. The only effectual remedy would seem to be
immediate amputation of the limb above the seat of the fracture. When
the vessels of the lungs have been examined in these instances, they
have been found to contain elongated masses, several millimeters in
length, possessing a particular brilliancy, "disappearing under the
action of ether, and becoming a deep, black color with osmic acid."[60]

[Footnote 60: Déjerine, _Le Progrès médical; Med. Record_, Jan. 15,
1879.]

{386} Specific emboli may be followed by the mechanical effects of
simple emboli, but they are also accompanied by specific phenomena
which are in relation with the particular focus in which they took
origin--_i.e._ purulent or septic focus, gangrenous cavity, cancerous
tumor, etc.

In the region where the embolus is arrested, local alterations of
tissue become developed which correspond with the nature of the changes
which exist in the spot from which the embolus was derived. Very often
these morbid effects are produced without any mechanical results of
emboli being occasioned.

Septic emboli are observed in infectious diseases, such as pyæmia and
puerperal fever, and are prone to occasion not merely mechanical
effects, but equally the suppuration, liquefaction, and finally the
absolute destruction of tissue. Cruveilhier has seen pulmonary embolism
followed by metastatic abscesses. The formation of these was attributed
by him to suppurative phlebitis affecting the capillaries.[61]

[Footnote 61: _Dict. de Méd. et de Chirurgie pratique_, vol. xxix. p.
360.]

It is admitted to-day that infectious germs causing metastatic
abscesses may be transported in the pulmonary vessels without being
accompanied by pulmonary emboli. It is equally true, however, that the
usual means of transport for these infectious bacteria or micrococci is
an embolic plug (Jeannel).

The effects produced by the septic emboli are pneumonic consolidations
involving the lobules and going on rapidly to suppuration, and
sometimes to gangrene. The coloration of the lobules is red, gray,
tending toward yellow as the tissue shows signs of softening. The
contents of the abscess are yellow or brown and contain particles of
the pulmonary structure. The tissue in the vicinity is gray and
infiltrated with pus.

The number of metastatic abscesses is often very considerable. Their
size is usually smaller than the infarctus due to simple emboli. The
smaller abscesses are found usually near the surface of the lung. When
several abscesses unite into one they may attain the size of the fist.

Whenever there exists a gangrenous lesion in some portion of the body,
sphacelated débris may be carried from this focus into the venous
system, and finally into the lungs. Arrested in some spot of the
pulmonary tissue, the embolus will give rise to gangrenous changes
similar to those of the region from which it started.[62] The infarctus
thus produced will assume a dark color, then become gray toward the
centre, where it shows signs of softening. Later, under the form of a
thick semi-fluid mixture of extreme fetid odor and dark-brownish color,
it is expectorated by degrees, and leaves behind a gangrenous cavity.
The process of change in this case is due to the proliferation of
infectious germs. It may be, however, that the gangrenous particles
transported into the lungs have the power in themselves to decompose
the tissues by chemical action into more simple elements.[63] According
to the later researches of Doleris, septic bacteria have been found by
him in these putrid infarctions.[64]

[Footnote 62: This process was first pointed out by Cruveilhier in his
work on _Phlebitis_. It remained, however, for Virchow in his _Cellular
Pathology_ (p. 235, ed. Strauss), and later for Billroth in his
_Surgical Pathology_, 1868, p. 395, to give greater development to this
belief.]

[Footnote 63: Lancereaux, _Traité d'Anatomie pathologique_, vol. i.,
1875-77, p. 14 _et seq._]

[Footnote 64: Quoted by Levrat, p. 78.]

The infecting power of cancer is certainly not equal to that of
gangrene. Nevertheless, Lancereaux has shown that cancerous nodules may
be produced by metastasis. This belief in the possibility of a simple
embolus taking on a cancerous change, and carrying this disease to
far-removed parts, has been strongly combated by Cohn. Neither
experimental nor human pathology has thus far decided the subject in an
absolute manner. Certain it is, {387} however, that the power of emboli
from cancerous foci to carry similar disease elsewhere depends partly
upon the vitality of the cancerous particles, partly upon the power of
receptivity as shown by certain constitutions for developing special
diseases, and which relates, after all, to the general question of
dyscrasia. Langenbeck has shown that certain animals will die within a
few hours after the injection of cancerous juice. On the other hand, it
is known that the infective power of the juice only lasts a very brief
period. Weber, Luzzato, and others have reported numerous examples of
secondary tumors of similar nature developed in the lungs when
epithelioma, enchondroma, sarcoma, or carcinoma existed somewhere in
the body. Finally, it would appear that emboli containing hydatids in
embryo have been the means of transporting these parasites into the
pulmonary structure.

DIAGNOSIS.--The sudden commencement of the accidents, especially when a
peripheral thrombus has existed previously in one of the large veins of
the extremities, renders the diagnosis almost certain. If the patient
has been suffering from the effects of a traumatism (contusion,
fractures, operation on the veins of the limbs or rectum, etc.), and is
almost instantaneously attacked with intense dyspnoea and a feeling of
anguish which he refers to the thoracic region, we shall be able
usually to eliminate other intercurrent affections and to diagnosticate
the existence of pulmonary embolism.

This accident is often confounded with cardiac thrombosis. It may
usually be separated from it by the following differential symptoms:
Cardiac obstruction from a clot usually comes on insidiously, by
degrees; the heart-beats are irregular, tumultuous, muffled, and
distant; there may be a murmur from one or other of the cardiac
orifices; there is no initial chill; peripheral thrombosis is not
present as a rule; there is no sensation of localized obstruction in
the chest.

In pulmonary embolism the début may be instantaneous and death follow
in a few seconds; or, again, the beginning may be rapid, ushered in by
stifling in the chest, a chill, cyanosed face, followed soon by
excessive pallor, a distinct sensation of obstacle to breathing in a
particular region. Percussion and auscultation may remain negative. The
patient may have a succession of similar accidents, and yet finally
recover. According to Ball, pulmonary embolism and pulmonary thrombosis
cannot be distinguished during life. In one case which he reports where
pulmonary embolism should have been present without question the
autopsy showed the presence of a thrombus in the pulmonary artery. A
succession of chills, general malaise, febrile excitement, the
localized phenomena of pneumonia or gangrene of the lung, point
indubitably to the existence of septic emboli.

The differential diagnosis between pulmonary embolism and other
affections, such as angina pectoris, a foreign body in the
air-passages, pneumothorax, etc., may usually be reached without much
difficulty. Sometimes the paroxysmal dyspnoea with sensations of great
oppression which accompanies mitral stenosis may be mistaken for
pulmonary embolism. In these instances the absence of a discoverable
cause of the attack in pre-existing emboli, and the presystolic murmur
with marked general anæmia, may surely lead to an accurate diagnosis.
It must, however, always be remembered that in mitral stenosis it is
not infrequent to have cardiac coagula formed in the right auricle,
which may become detached and give rise to pulmonary emboli. Under
these circumstances a severe localized pain in the side of the chest
has considerable diagnostic importance as pointing to the presence of a
pulmonary embolus (Cohn).

When there is pre-existing cardiac disease of organic nature a syncopal
attack may sometimes occasion doubt with respect of a correct
diagnosis. The sudden loss of consciousness, excessive pallor, and
absence of pulse will ordinarily, however, confirm the diagnosis of
syncope. Rupture of the heart {388} is accompanied with symptoms of
syncope rather than those of suffocation (Balzer). Emboli of the
bronchial arteries are not accompanied by any characteristic symptoms
which will enable us to make a differential diagnosis. There is the
same sudden dyspnoea, the initial chill and hæmoptysis, as in pulmonary
embolism (Penzold).

PROGNOSIS.--As will be readily understood, the prognosis is sometimes
difficult to estimate and varies with many circumstances. Certain
emboli, even among those which have occasioned severe symptoms, have
never been recognized. Other pulmonary emboli always remain
comparatively latent. In this connection we should mention those which
take place in the lungs of tuberculous patients. Again, the size and
seat of the embolus will always have great importance in regard to the
prognosis. If the trunk or primary divisions of the pulmonary artery be
suddenly and completely obstructed by emboli, sudden death will surely
follow. If secondary divisions of the pulmonary artery are filled up,
more or less grave symptoms will usually follow. When emboli are
carried into the tertiary or still smaller branches of the artery, they
may not occasion any appreciable phenomena other than a moderate and
passing dyspnoea. If, however, there be a large number of small emboli
carried into both lungs at the same time, it is possible that rapid
death may follow their presence. It is true, however, according to
certain authors, that even a large embolus blocking up the main trunk
of the pulmonary artery may be followed by recovery. Such a case is
that of Jacquemier, reported by Ball. Even in this case, whilst the
presence of the embolus cannot perhaps be doubted, still the exact size
and location may be called in question. And here we may add that in all
cases of reported cure of this nature there will naturally and
inevitably exist an atmosphere of legitimate doubt about the correct
observations and diagnosis of the narrated facts.

What precedes relates exclusively to the existence of simple emboli. Of
course if the embolus be of septic origin, it will be followed by the
appearance in the lungs of foci of purulent pneumonia or of gangrenous
changes of tissue which will finally produce such structural
destruction as almost certainly to terminate in death.

TREATMENT.--The majority of those who have studied this subject have
recognized how vain are our efforts of treatment in many instances.
Pulmonary embolism is one of those accidents which we should always be
prepared to admit, however, when its characteristic symptoms show
themselves, and should endeavor rationally to combat by the therapeutic
means in our power. Even before we have any signs present which
indicate obstruction of the pulmonary circulation, we may have those
which point in a very certain manner to the existence of a peripheral
thrombus. This thrombus may block up completely one of the large veins
of the lower extremities, and may, owing to its possible detachment and
transport, be a constant menace to life. At times these peripheral
thrombi are accompanied by local inflammatory symptoms which belong to
phlebitis. This condition of things is not uncommon after fractures or
other traumatisms. Frequently there is no evidence of any inflammatory
state, and we recognize the thrombus solely by the signs which result
directly from obstructed venous circulation and by the existence of a
hard, indurated cord which fills the vein at a given level. Now, what
are the means we have at our command to prevent the transport of this
coagulum, or indeed to dissolve it, or absorb it in its place?

First, if inflammatory signs are present we should endeavor to subdue
these by local applications of an emollient character, for the reason
that excessive inflammation is apt to produce such changes as cause the
disaggregation of the clot, and hence its detachment. In either case,
whether there be or be not any local inflammatory condition, we should
insist upon absolute repose and quiet. We should not permit the limb to
be moved: we should be {389} extremely careful in all our manipulations
of it, and only employ those which are absolutely essential. The
patient should not be permitted to raise himself in bed, nor even eat
or drink without assistance. These counsels are very important, since
we know how frequently a very slight movement or exertion has been
followed immediately by the transport of the clot, pulmonary embolism,
and sudden death. In cases of fractures or severe wounds where such a
peripheral clot is discovered the surgeon should be particularly
careful in applying bandages and retentive apparatus. The risk of
displacement of the clot is greater after several days from the time of
the fracture or wound than it is at first, and it is at this period
that the most careful attention should be exercised. Instances are on
record in which so late as the fifty-seventh day after a fracture of
the lower extremity a peripheral thrombus was transported from its
original site and caused a fatal termination (Bouchard).

Some eminent writers have thought by employing a suitable medication we
might hasten the solution of the peripheral thrombi and thus prevent
their migration. With this view Legroux has given the acetate of lead
internally and applied it in solution over the seat of the thrombus.
Richardson has vaunted the use of the carbonate of ammonium in large
and frequently-repeated doses as a solvent of the fibrin. By its means
he believes he prevents the fibrin from precipitating from the blood,
and further helps it to resorb when it has already become solid.
Prevost, Dumas, and Schutzenberger recommend specially the bicarbonate
of sodium, taken internally, with a view of rendering the blood more
fluid and also hastening the retrogressive changes in the clot by its
oxidizing power. According to Boyer, the very object which is thus
sought if it were accomplished would result injuriously to the patient,
since it would favor the detachment of the clot. Further, the continued
use of large and frequent doses of ammonia or soda is prone to lower
the general system very much, and in this manner to act to the
prejudice of the patient. According to Azam, it would appear that what
we most desire to effect is the organization and adhesion of the
thrombus to the walls of the vessel. This can best be accomplished by
fortifying the patient in every possible way and raising his nutrition
to the highest attainable point. Iron, cinchona, the most nutritious
food, should be freely given. Further, the greatest attention should be
paid to the hygienic surroundings. The air should be purified, and if
by chance the patient is suffering from a wound close attention should
be given to the renewal of the dressings and the employment of a
disinfectant locally applied. One of the reasons for this last counsel
is because if the thrombus were detached it is important that it should
be free of any septic taint and not lead to specific accidents
(purulent pneumonia, gangrenous abscess). In the above enumeration we
include the means usually to be employed as preventive measures against
the migration of clots.

Is there any other method which can be adopted with any chance of
success? Of the surgical attempts we should mention favorably in
certain cases, and especially in those where the affected vein is
superficial, the adoption of persistent compression between the clot
and the heart. This means has been alluded to by J. Hunter[65] as far
back as 1773. Ligature and section of the vein have also been supported
by some writers as suitable operations to bring into use with a like
intent. Unfortunately, we are obliged to make a second traumatism in
order to carry out this object, and, further, we make by the ligature
at least a second coagulation, which may be the origin of the very
accident we seek to avoid. Nevertheless, J. Teissier[66] of Lyons
reports a case {390} observed by himself in the service of Noël Guéneau
de Mussey, in which a ligature was instrumental in arresting the onward
progress of the clot, which otherwise would have given rise to the
accidents of pulmonary embolism.

[Footnote 65: _Observations of the Inflammation of the Internal Coats
of the Veins_, quoted in thesis of Levrat, p. 108.]

[Footnote 66: _Nouveaux Éléments de Pathologie et de Clinique
médicale_, t. ii. p. 931, quoted by Balzer.]

In the event of pulmonary embolism taking place in spite of all
preventive means employed, what shall we do in order to combat this
terrible accident? According to Ball,[67] there are three indications
to be observed: 1. To establish collateral circulation in the lungs; 2.
To diminish local congestions; 3. To favor the resorption of the
obstacle.

[Footnote 67: _Thèse_ quoted, Paris, 1862.]

The first indication cannot be effectually responded to, by reason of
the fact that there is no way in which a collateral circulation can be
promoted in the lung, owing to its anatomical structure.

The second indication is best observed by the application to the
chest-walls of dry cups in large number, mustard poultices, turpentine,
blisters. In this place we must consider the propriety of bleeding. As
a result of the embolism there is arterial anæmia and venous plethora.
This latter condition can be temporarily relieved by venesection. In
this method, indeed, we have an immediate help for the distended and
burdened heart, and we give time to the system to recuperate somewhat.
We should, however, remember that bloodletting establishes a greater
tendency in the system to the formation of emboli, and is therefore to
be avoided. Moreover, sometimes it is decidedly objectionable on
account of cardiac degeneration, anæmia, or great weakness.

When this method is contraindicated we should not hesitate to recur to
the use of drastic purgatives (Jaccoud). Digitalis has been
recommended, so as to regulate the cardiac action and to increase its
power. Bertin has gone so far as to praise emetics and the use of the
faradic current over the thoracic parietes. It seems as if these were
dangerous methods to employ, since if a portion of the clot is still
undetached the efforts caused by these agents would be apt to separate
whatever portion remained in its original site. In order that a
quantity of oxygen should be inhaled in a given time sufficient to
supply the needs of the economy until a greater power of oxygenating
the blood is established, the inhalation of compressed air has been
vaunted. The objection to this means is merely the one which arises as
we reflect how improbable it is that this agent would be at hand in a
serviceable form when the sudden accidents of pulmonary embolism take
place.

The third indication, to favor the resorption of the obstacle, must be
virtually attended to by giving the alkalies in large doses internally.
The advantages and objections to this sort of treatment we have already
referred to.

After this exposition of the different means to be employed, both as
preventive and curative agents of pulmonary embolism, we are obliged to
recognize that very frequently they remain ineffectual. Usually the
accident takes place in a very sudden manner and when we are least
suspecting its advent. When the phenomena do occur which are caused by
its presence, they take place so suddenly, and terminate fatally in
such a brief period, that we scarcely have the time to employ the
remedial agents referred to. Finally, we must admit that in presence of
this complication, especially when there is complete obstruction of the
trunk or primary divisions of the pulmonary artery, all our therapeutic
means are without avail, and we are indeed almost powerless.




{391}

PULMONARY PHTHISIS (FIBROID PHTHISIS OR CHRONIC INTERSTITIAL
PNEUMONIA).

BY AUSTIN FLINT, M.D.


DEFINITION.--Pulmonary phthisis is a chronic disease, characterized in
its common form, anatomically, by a morbid product within the
air-cells, in a large majority of cases progressively increasing and
extending, having a tendency to cheesy degeneration and liquefaction
forming collections of puriform liquid which, evacuating by ulceration
into the bronchial tubes, are followed by cavities, these pathological
conditions accompanied by more or less induration from interstitial
morbid growth and by small granules called miliary tubercles. A
comparatively rare form of the disease is characterized by the great
predominance of interstitial growth, leading to notable diminution of
the volume of lung by atrophy and to dilatation of the bronchial tubes.
The latter form is now commonly distinguished as fibroid phthisis. This
will claim separate consideration after having considered the form
generally understood by the name pulmonary or pneumonic phthisis.

SYNONYMS.--Classification.--Much confusion, as regards nomenclature and
classification, followed the adoption by many of the theory of Virchow
that the sole characteristic of tuberculous disease is the presence of
the so-called miliary tubercles. According to this theory, the morbid
product which constitutes the most marked anatomical feature of the
common form of phthisis is simply an inflammatory exudation.
Heretofore, pulmonary phthisis and pulmonary tuberculosis were
considered as convertible terms, but, adopting Virchow's theory, in a
certain proportion of cases pulmonary phthisis is not a tuberculous
disease. Hence arose a variety of names denoting non-tuberculous
phthisis, such as chronic broncho-pneumonia, chronic lobular pneumonia,
catarrhal pneumonia, cheesy pneumonia, etc. These names have shared the
fate of the theory from which they originated, the latter, at the
present time, having but few supporters in any country. It is
convenient to distinguish the morbid product which is characteristic of
pulmonary phthisis as a tuberculous product, and it will be so
distinguished in this article.

The name acute pulmonary tuberculosis denotes an affection which may be
sharply separated from the chronic forms of pulmonary phthisis. The
acute affection is characterized by the presence, exclusively or in
great abundance, of miliary tubercles. It runs a rapid course and the
symptoms are those of an acute disease. The name phthisis implies a
chronic affection. In a small proportion of the cases of pulmonary
phthisis miliary tubercles become developed in great abundance. In
these cases acute pulmonary tuberculosis supervenes upon chronic
phthisis. These cases, by those who regarded phthisis in its ordinary
form as a non-tuberculous affection, were designated cases of
tuberculous phthisis. The fact that in cases {392} of phthisis there is
a liability to the supervention of miliary tubercles as abundantly as
in cases of acute tuberculosis, is to be borne in mind, but it does not
seem necessary to make a distinct variety of the disease on the basis
of this fact. In some cases of pulmonary phthisis the tuberculous
product is notably large at the outset, and destructive changes in the
lungs go on continuously with unusual rapidity. To these cases the
names phthisis florida and galloping consumption have been applied.

In view of what has been stated, the classification in this article
will not extend beyond a division into the common form of pulmonary
phthisis and the form distinguished as fibroid phthisis. The latter
form has been designated chronic interstitial pneumonia, chronic
pneumonia, and cirrhosis of lung. It is to be understood that reference
is had to the common form of pulmonary phthisis, except in that portion
of this article which has for its heading Fibroid Phthisis.

HISTORY.--Pulmonary phthisis, in typical cases, is developed so
imperceptibly that it might with propriety be included among the
so-called insidious diseases. A slight dry cough is the first local
symptom. This increases, and after a variable period is accompanied by
the expectoration of a small quantity of mucus. The latter becomes
gradually more abundant, and has the characters of the sputa in cases
of bronchitis. So slow is the increase of those symptoms before they
are regarded as of sufficient importance to require attention that not
infrequently the patient is unable to state precisely how long they
have existed. They are generally attributed to a slight cold which will
take care of itself or call for only popular remedies, and the
existence of a grave disease may not have been suspected until a
physical examination of the chest discloses the fact that the
phthisical affection has already made considerable progress. Coincident
with or preceding the commencement of cough is often some obvious
impairment of the general health, as indicated by diminished muscular
strength and endurance, decrease in weight, pallor of the complexion,
and lessened appetite. The impairment, however, may not interfere with
customary occupations, and may be evident to others when the patient
takes no cognizance of it.

In not a few instances hæmoptysis is the event which first awakens
suspicion of an important disease. The hemorrhage generally takes place
without any apparent causation, and often in the night. It may be
either slight or profuse. It may occur but once, or there may be
recurrences after intervals of hours, days, or weeks. The cough in some
cases dates from the occurrence of hæmoptysis. In other cases the
hemorrhage or hemorrhages antedate the cough for a variable period.

From the time when the symptoms and physical signs render the diagnosis
of the disease positive the history in different cases presents notable
variations. Comparatively, the course of the disease is continuously
progressive and rapid in cases of so-called galloping consumption. The
characteristics of the disease in these cases are--an unusual degree of
cough with abundant expectoration, rapid breathing, frequency of the
pulse, persistent pyrexia, chills or chilly sensations followed by
exacerbations of fever, profuse perspirations, anorexia, rapid
emaciation with decreasing muscular strength, and a fatal termination
after a few months. The physical signs in these cases show a large and
progressively increasing amount of solidification from the morbid
product, followed quickly by destructive changes.

The disease pursues a rapid course, and ends fatally whenever acute
tuberculosis supervenes. This may occur in the early part of the
chronic phthisical affection or at any period during its course. The
supervention of the acute disease sometimes follows a profuse
hæmoptysis. The characteristics are high fever, frequency of the pulse,
cyanosis, prostration, and death within a few weeks or even a few days.
The physical signs which denote a large {393} extent of solidification
of lung and the consequent destructive changes are wanting in these
cases.

A small proportion only of cases of pulmonary phthisis fall in the
category either of galloping consumption or of the supervention of
acute tuberculosis. In by far the larger proportion the disease is
chronic from the beginning to the end, and a fatal termination takes
place after a period averaging from two to three years, the period
sometimes extending to many years.

An important distinction, as regards the history of the disease, is
expressed by the terms progressive and non-progressive. The disease is
progressive when the local and the general symptoms denote more or less
activity in the tuberculous process, the physical signs generally
showing progressive extension of the pulmonary affection. It is
non-progressive when symptoms and signs having the significance just
stated are wanting. The disease may become non-progressive early or
late, and at any period during its continuance. A stationary condition
may continue indefinitely. The symptoms and signs may show processes of
restoration--namely, disappearance of the tuberculous product,
diminution in size, and the cicatrization of cavities. The disease is
then said to be regressive. A regressive course is not extremely
infrequent. It is more or less slow and may or may not end in recovery.
A stationary condition, regression having taken place to a greater or
less extent, is not infrequently observed. This condition may remain
because the pulmonary lesions are too great to admit of restoration. In
most cases the disease is not steadily progressive. It ceases from time
to time to progress, the periods of non-progression varying much in
duration. With each renewal of progress the physical signs generally
show an addition to the tuberculous product. As a rule, this product
does not increase continuously, but, as it were, by successive
eruptions after intervals of time which may be either short or long.

Pulmonary phthisis in some cases ceases to progress, and regression
continues, recovery taking place from an intrinsic tendency--that is,
irrespective of any measures of treatment. This highly important fact
has not hitherto been distinctly recognized by medical writers and
practitioners. I have established it by having recorded a series of
cases in which recovery took place without medicinal or other treatment
and without any material change in habits of life.[1] In these cases
the disease may be said with propriety to be self-limited.[2] The
weight of this fact in its bearing on prognosis and treatment is
obvious. That non-progression and regression ending in recovery may be
brought about by judicious measures of management cannot be doubted; in
other words, the disease may be arrested in a certain proportion of
cases when non-progression and recovery would not have resulted from an
intrinsic tendency or self-limitation.

[Footnote 1: _Phthisis, in a Series of Clinical Studies_, by Austin
Flint, M.D., 1875.]

[Footnote 2: Vide "Self-limitation in Cases of Phthisis," by Austin
Flint, M.D., N.Y., _Archives of Medicine_, June, 1879.]

Pulmonary phthisis proves fatal by undermining more or less slowly the
powers of life. The appetite and digestion fail. There is progressive
loss of weight and of muscular strength. A greater or less degree of
pyrexia is persistent, with diurnal exacerbations and night
perspirations, forming what is known as hectic fever. Muco-purulent
matter is expectorated in abundance, with fatiguing cough. The
respirations are accelerated, and there is often suffering from
dyspnoea. The pulse becomes more and more frequent and weak. Oedema of
the lower limbs is of frequent occurrence. The patient dies by slow
asthenia, the mental faculties usually remaining intact and the patient
hopeful of recovery to the last.

The history of the disease in many cases embraces tuberculous
affections elsewhere than in the lungs, and other complications. The
duration is often {394} shortened by some of these. The more important
are tuberculosis of the intestines, tuberculous peritonitis,
perforation of lung giving rise to pneumo-hydrothorax, pneumorrhagia,
pulmonary gangrene, tuberculous meningitis, and chronic laryngitis
affecting deglutition. The less important affections are pleurisy with
effusion, thrombosis of the femoral or the iliac vein, a circumscribed
non-tuberculous acute pneumonia, chronic laryngitis not affecting
deglutition, intercostal neuralgia, and perineal fistula. Profuse
hæmoptysis is sometimes a grave event, and may prove the immediate
cause of death.

It is impossible to divide the course of pulmonary phthisis into
sharply-defined stages based on anatomical changes. Often after death
the lungs present in different situations all the changes which
intervene between a fresh tuberculous product and cavities. The
division into a stage of crudity of the product and a stage of
softening is of no practical utility. There are no symptoms nor signs
which are reliable for determining when softening has taken place. The
existence of cavities can generally be determined by means of the
cavernous physical signs, and the disease may be considered as advanced
phthisis when cavities are discovered. The term incipient phthisis is
used to designate an early period of the disease. Having passed the
incipient or early period, and before reaching the advanced stage or
stage of excavation, cases may be conveniently grouped according to the
amount of the tuberculous affection. In different cases and at
different periods in the same case the affection is either small,
moderate, considerable, or large. Exact chronological divisions are
impracticable.

ETIOLOGY.--Pulmonary phthisis, as a rule, is developed irrespective of
any antecedent affection of the lungs. The researches of Louis
established the fact that the phthisical affection is very rarely
preceded by bronchitis, either acute or chronic.[3] My clinical studies
have led to the same result.[4] That a neglected cold may eventuate in
phthisis is a traditional popular error, unfortunately held also by
some medical writers and practitioners. The error is to be regretted
because it often interferes with hygienic management in cases of
phthisis. The name chronic catarrhal phthisis proposed by Niemeyer was
based upon this etiological error. It is a matter of common clinical
observation that persistent bronchial inflammation leading to pulmonary
emphysema, and often accompanied by asthma, involves no liability to
phthisis. The long-continued inhalation of coal- and stone-dust, of the
oxide of iron, and particles of other substances gives rise to
bronchitis and interstitial pneumonia (pneumonokoniosis, anthracosis,
siderosis, etc.), but is rarely followed by the common form of
pulmonary phthisis. It is common for phthisical patients to suppose, as
a matter of course, that their disease originated in a cold. In giving
the previous history they often say that they took cold at a certain
time. The analysis of carefully-recorded cases shows that very rarely
does the disease follow directly upon an attack of bronchitis,
notwithstanding that the frequency of the latter, from the law of
chances, would involve an accidental concurrence in a certain
proportion of cases. Acute lobar pneumonia or pneumonic fever has
little or no tendency to eventuate in phthisis. This statement is
sustained by the researches of Louis and by my clinical studies. In the
rare instances in which phthisis follows either acute pneumonia or
bronchitis, the latter diseases act only as auxiliary causes of the
phthisical affection if the sequence be more than an accidental
connection. This statement applies also to pleurisy with effusion. In
certain of the few instances of phthisis apparently having been
preceded by pleurisy it is probable that the former was the antecedent
disease, occurring early in the history of the phthisical affection and
retarding or arresting the progress of the latter. It may be added that
there is no ground for supposing that phthisis is ever produced solely
by traumatic causes acting upon the chest.

[Footnote 3: _Recherches sur la Phthisie_, 1825.]

[Footnote 4: _Phthisis, in a Series of Clinical Studies_.]

{395} It is an old doctrine that bronchial hemorrhage may be causative
of phthisis. This doctrine has been recently revived by Niemeyer and
some others. It is disproved by the following clinical facts: in
two-thirds of the cases in which hæmoptysis antedates phthisis the
development of the latter is after the lapse of a considerable
period--weeks, months, or years. The instances are few in which
phthisis immediately follows the hemorrhage. The occurrence of
hæmoptysis during the course of phthisis, as a rule, is not followed by
any increase of the phthisical affection. On the contrary, the local
symptoms are not infrequently relieved by the hemorrhage. It is,
however, to be remarked that hæmoptysis as a forerunner of phthisis is
of much significance. In the larger proportion of cases phthisis
follows its occurrence sooner or later. It is to be added, in view of
the recent discovery by Koch, that bronchial hemorrhage may proceed
from the same local cause which afterward leads to the development of
phthisis--namely, the presence of a special micro-organism.

The etiology of pulmonary phthisis not involving any antecedent
affections of the lungs nor any appreciable local causes, it would seem
to follow that the disease involves either a predisposing or a
causative agency elsewhere within the organism; and as, with our
present knowledge, the source of this intrinsic agency cannot be
localized, it is customary to say that the disease has a constitutional
origin. This use of the term constitutional here, as in other
instances, expresses an important fact--namely, that the disease is not
purely local; that is, attributable solely to extrinsic or any
appreciable causes acting on the affected part. At the same time, the
term is a confession of the imperfection of our knowledge, inasmuch as
it does not specify the nature of the causative or predisposing agency,
nor its origin, beyond the statement that it is not local. That the
constitutional agency has a special character is a logical inference
from the fact that the disease may be said to have such a character.
The term vulnerability does not fully express the special character of
the constitutional agency. The condition of the constitution which
stands in a causative relation to the disease is something more than an
undue susceptibility to morbific influences of any kind--a
susceptibility giving rise to diseases the nature and seat of which are
accidental. The condition is one which has relation both to the
character and the situation of the pulmonary affection. Such a
condition is expressed by the term cachexia.

It remains to inquire whence arises this phthisical or tuberculous
cachexia.

A congenital predisposition or diathesis exists in a certain proportion
of cases. This is to be inferred from the number of instances in which
several or many members of a household, brothers and sisters, become
affected with phthisis. There may or may not be evidence that this
predisposition is inherited. An inherited predisposition is to be
inferred from the number of the cases in which parents or grandparents
were phthisical. While statistical facts show undoubtedly heredity as
involving a causative agency, making due allowance for the law of
chances, it is important for the physician to bear in mind that a
tuberculous parentage involves only a certain measure of liability to
phthisis in the offspring. The progenitors of many healthy men and
women have been phthisical. There are instances of large families of
children in which many have died with phthisis, leaving, however, some
who escape this disease and are in all respects healthy.[5] The
question arises whether in cases of phthisis where there is lack of
evidence of a congenital predisposition the diathesis may not be
innate. The affirmative answer seems probable in view of the inability
oftentimes to find any rational explanation on the supposition that the
diathesis has been acquired. Positive data bearing on this question are
of course not available.

[Footnote 5: For data on which these statements are based, vide
_Phthisis, in a Series of Clinical Studies_, by the author.]

{396} Age has a decided influence on the development of phthisis. Cases
in which the ages of patients are between twenty and thirty years
greatly preponderate over the number in any other decade of life. Next
in order as to the number of cases are the ages between thirty and
forty years. The form of tuberculous disease under present
consideration is rare under ten years and also in advanced life. All
that can be said with our present knowledge in explanation of the
influence of age is, that either an existing diathetic condition tends
intrinsically to the development of the disease or that the diathesis
is likely to be acquired at certain periods of life more than at other
periods. Of these two explanations the former is the more rational.

Statistics show that occupations which involve sedentary habits,
confinement within doors, especially in small, illy-ventilated rooms,
poor or insufficient food, and prolonged mental depression, increase
the liability to phthisis. The disease is developed either during or
shortly after gestation in a sufficient number of cases to show that
pregnancy has a causative agency. Facts appear to show a less degree of
prevalence of the disease in most cold and tropical climates than
within the temperate zone. It is, however, true, as stated by Ruehle,
that "there are regions in all zones which are free from the disease,
and, on the other hand, there is no zone in which it is not very
prevalent." The prevalence is less in high than in low altitudes.
Humidity of the soil has been shown by Bowditch, Buchanan, and others
to enter into the etiology. In order to determine how far purely
climatic agencies exert an influence either for or against the
prevalence of the disease, it is necessary to take into account other
associated agencies, together with an innate predisposition; and the
latter especially does not admit an exact estimation.

Certain general diseases seem to involve a liability to phthisis as a
sequel. This is true of rubeola and pertussis. In cases of diabetes
mellitus, phthisis is considered as occurring sufficiently often to
show a causative connection. In my own clinical experience, however,
phthisis has not been of frequent occurrence in that disease. Typhoid
fever in some cases appears to favor the development of phthisis. Some,
however, have contended for the reverse of this statement. Certain
affections are apparently antagonistic in their influence. In this
category are pulmonary emphysema and obstructive or regurgitant
valvular lesions at the mitral orifice of the heart. The disease is
rarely developed in chlorotic patients. Facts go to show that
alcoholism opposes its development. In opposition to current belief, my
clinical studies lead me to conclude that they who have had scrofulous
disease of the cervical glands in early life are not likely to become
phthisical in after years. Contraction of the chest from deformity
diminishes the liability to the disease.

The communicability of phthisis is a doctrine dating as far backward as
the history of medicine extends. Distinguished physicians in every age
have held that the disease may be communicated under circumstances
which involve close proximity, as from husband to wife or vice versâ,
and from patients to nurses or attendants. The contagion is supposed to
be contained in the expired breath. The clinical evidence in behalf of
this doctrine is the number of instances which seem to be striking
examples of communicability. It is easy to collect a considerable
number of such examples. But in order to constitute clinical proof of
the doctrine of communicability the number must be so large as not to
be accounted for on the ground of mere coincidence. A collection of
isolated instances gathered from medical literature or reports from
different physicians does not establish the doctrine. Owing to the
great frequency of phthisis, mere coincidence suffices to account for a
certain number of instances. Moreover, long-continued proximity to
cases of phthisis generally involves causative agencies other than a
contagium--namely, confinement within doors and mental anxiety. In my
collection of 670 recorded cases of phthisis, the number of instances
in which there was {397} room for the suspicion of the disease having
been communicated either from the husband to the wife or from the wife
to the husband amounted only to 5. In one of these instances, a wife,
who became phthisical after her husband, had lost two sisters, one of
whom was a twin sister, by the disease. It must be admitted that the
analysis of these cases, without disproving the doctrine of
communicability, fails to lend to it support, for the reason that in
such a large collection of cases the number of examples of apparent
communicability are so few.

A new and strong impetus was given to the discussion of the doctrine by
the discovery of the inoculability of tuberculous disease. Villemin in
1865 demonstrated the fact that this disease could be communicated to
rabbits and guinea-pigs by inserting beneath the skin portions of the
tuberculous product. The experiments of Villemin and many others have
shown conclusively that the insertion of fresh undecomposed tuberculous
matter beneath the skin or within the pleural and the peritoneal
cavity, or in the anterior chamber of the eye, is followed by an
eruption of tubercles in these animals within two or three weeks. If
tuberculous matter taken from an animal in which the disease has been
produced by inoculation be inserted in another animal, the disease is
transmitted to the latter. These results of inoculation, which have
been abundantly confirmed in all countries, prove indisputably the
communicability, by that mode, of tuberculous disease in certain
animals which have a peculiar susceptibility thereto. The fact that the
disease is not readily communicated to dogs, cats, and other animals
shows a peculiar susceptibility to be an important factor in the
successful results of inoculation. The conclusion drawn by Villemin and
others from these experiments is that the disease is communicated by
means of a specific virus, a term implying the existence of a
contagium.

Opposed to this conclusion are experiments which appear to prove that
tubercles may be produced in rabbits by inoculating them with various
kinds of non-tuberculous matter. By those who adopt the doctrine of a
specific virus it is contended either that true tubercles are not
produced in these experiments, or that, if followed by the development
of true tubercles, the production of the latter is attributable to the
derivation of the virus from the laboratories in which tuberculous
animals had been confined or to a contagium received directly from
these animals. The introduction of non-tuberculous matter was found by
Cohnheim and Fraenkel never to be followed by tuberculous disease when
the experiments were repeated in places where tuberculous animals had
not been confined and the animals on whom the experiments were made
were isolated from those affected with tuberculosis. Cohnheim states
that inoculation with portions of indurated lung, or of the nodules
resulting from peribronchitis, or of the contents of bronchiectasic
cavities, will not give rise to true tubercles, for the reason that,
although taken from phthisical lungs, they do not contain the
tuberculous virus. This distinguished pathologist, at first an opponent
of the doctrine of a specific virus, afterward became a strong advocate
therefor. He was led to regard a successful inoculation as affording
the only criterion and reliable test of tuberculous disease; that the
etiology of tuberculous disease invariably involves the presence in the
system of this virus; that it exists in a latent form whenever there is
an innate predisposition to phthisis; and that it may enter the system
in different directions--namely, with the inspired air into the lungs,
and even within the skull through the foramen of the ethmoid bone, into
the small intestine by deglutition, and into the uterus with the semen.
Becoming developed in any situation, the virus may remain localized, or
it may be disseminated more or less extensively by means of the lymph
and blood. The behavior of the tuberculous virus, according to
Cohnheim, corresponds closely to that of syphilis.

Experiments made by Gerlach, Bollinger, Aufrecht, Chaveau, Leisering,
{398} Harms, Gunthern and others, have shown that the disease may be
communicated by incorporating tuberculous matter with food. Rabbits,
guinea-pigs, dogs, calves, swine, sheep, and goats have been rendered
tuberculous by these experiments. Klebs, Tappeiner, Parrot, and Puech
claim to have communicated the disease by combining with the food the
matter of expectoration from phthisical patients. Gerlach and Klebs
have seen the disease in animals fed with milk from cows affected with
the so-called pearl disease (perlsucht), which is considered to be
identical with phthisis. Finally, the disease appears to have been
produced by exposing animals to an atmosphere impregnated with fine
particles of tuberculous matter by means of an atomizer, and by blowing
into the trachea this matter reduced to a fine powder.[6]

[Footnote 6: For a summary of the experiments relating to the
communicability of tuberculous disease by inoculation, by the ingestion
of tuberculous matter, and by its inhalation, and for reference, the
reader is referred to an article by Wm. P. Whitney in the _Boston
Medical and Surgical Journal_, July 28, 1881; to the article on
"Tuberculosis" by Frederick C. Shattuck in supplement to _Ziemssen's
Cyclopædia of the Practice of Medicine_, 1881; to the "Cartwright
Lectures," by William T. Belfield, M.D., published in the _New York
Medical Record_ in February and March, 1883; and to an article by
Surgeon George M. Stemberg, U. S. Army, in the _American Journal of
Medical Sciences_, January, 1885.]

It is noteworthy that tuberculous disease may be produced by
inoculating with the infiltrated product, with matter from miliary
tubercles, or from scrofulous glands in the neck. The identity of these
morbid products is thus made evident, assuming that the fact of
communicability involves the existence of a specific virus.

The practical importance of the facts already ascertained respecting
the communicability of phthisis is obvious. They constitute the
foundation for a reasonable supposition that the disease may be
communicated to man by means of the meat of tuberculous animals, by
milk, and by breathing an atmosphere charged with particles of
tubercle. That the instances in which the disease is communicated,
however, are rare seems to be a rational inference from the difficulty
of obtaining clinical proof of communicability. That susceptibility is
an essential factor is made evident by the well-known predisposition
pertaining to certain periods of life. It is to be considered that
while the communicability of the disease to certain animals is
abundantly shown by the experiments to which reference has been made,
the existence of a special virus or a contagium is not as certainly
established by these experiments. They leave to be settled, by further
investigation, the question whether or not the communicability of the
disease involves only the agency of a septic matter devoid of the
special character expressed by the terms virus and contagium. Without
waiting for data sufficient to settle this important question, prudence
would dictate the propriety of all practicable precautionary measures.

Still more recently, and since the foregoing remarks on the
communicability of phthisis were written, have appeared the remarkable
experimental researches of Koch of Berlin. Koch claims to have
demonstrated the constant presence in tuberculous products of a
specific organism which he calls the bacillus tuberculosis, and that it
is not found in non-tuberculous products. This parasite he has
isolated, and by cultivation carried through several successive
generations. By its introduction, after, as well as before,
cultivation, into the pleural cavity, the peritoneal cavity, the
anterior chamber of the eye, and in other situations, he produced
tuberculous disease, not only in rabbits and guinea-pigs, but in dogs
and rats, the latter animals being less susceptible than the former to
tuberculous infection. In his experimental observations, animals not
inoculated, placed under the same external conditions as those
inoculated, did not become tuberculous. The same parasite, alike
capable of infecting healthy animals, he found in miliary tubercles, in
the cheesy tuberculous deposit, in scrofulous glands, and in the sputa
from {399} tuberculous patients. The parasite was found not to have
lost its vitality in dried sputa.[7]

[Footnote 7: For the details of Koch's researches vide his report in
the _Berliner klinische Wochenschrift_, April 10, 1882; vide, also,
_Verhandlungen des Congresses für Innere Medicin_, Erster Congress
gehalten zu Weisbaden, 20-22 April, 1882.]

The researches of Koch had been continued for two years before the
publication of the results in March, 1882. Moreover, his ability as a
skilled experimental observer in the study of micro-organisms, and his
sincerity as a truth-seeker, are universally admitted. Naturally, the
publication of the results of his researches excited at once great
interest in all countries. At the present moment (April, 1885)
questions connected with the bacillus tuberculosis are more considered
than any others relating to medical pathology and etiology. Thus far,
the observations of competent medical mycologists are confirmatory of
the results of the researches by Koch. It seems to be established that
the so-called bacillus tuberculosis is uniformly present in tuberculous
products, and as uniformly absent in other morbid products; that it is
generally present in the sputa of phthisical patients, and never
present in the sputa of non-phthisical patients; and that tuberculous
disease in animals may be produced by inoculation with this organism
after cultivation has been sufficiently continued to eliminate all else
pertaining to the tuberculous product. On these data are based the
conclusions that phthisis is an infectious disease--in other words,
that it involves in its causation a specific agent capable of
self-multiplication; that it is a communicable disease, and that the
agent of the communication is the bacillus tuberculosis--that is, this
agent is the contagium. The supposition that the presence of the
bacillus is secondary to the tuberculous affection is not tenable in
view of the fact that the affection is produced by the introduction of
this organism after it has passed through several generations by
culture out of the body.

As has been already seen, clinical experience fails to furnish positive
proof of the communicability of phthisis. There are many striking
instances which, taken by themselves, render it probable that the
disease was communicated; but, on the other hand, there are so many
cases of its development under circumstances not pointing to contagion,
and of the number of persons in close proximity to tuberculous patients
the proportion of those who become affected is so small, that it has
seemed impossible to establish the doctrine of contagion by clinical
evidence.

The insufficiency of clinical proof, however, cannot invalidate the
demonstration by inoculation. Assuming it to be demonstrated that the
disease involves a specific agent, and that this agent is proven to be
a contagium by its capability of producing the disease when introduced
into a healthy body, the conclusion as to communicability is not to be
shaken by the lack of corroborative clinical evidence or by inability
to explain certain facts which seem to be inconsistent with that
conclusion. Having accepted a demonstrated truth, the endeavor should
be to reconcile therewith facts which do not sustain it and which may
appear to be opposed to it. It remains to inquire in what way the
communicability of phthisis by means of a contagium vivum is to be
reconciled with facts furnished by clinical experience.

If we accept the conclusion that a particular parasitical organism is
the primary and efficient causative agent in the production of
phthisis, the development and multiplication of this organism must
require certain local conditions. Without these the parasite is
innocuous. The conditions are to its development and multiplication
what the peculiarities of soil are to the production of different
vegetables. Of the nature of these conditions we are at present
ignorant. When they exist the bacillus develops and multiplies; when
they are wanting the parasite is incapable of development and
multiplication. This dependence of specific morbific agents upon
particular {400} conditions is exemplified in other infectious
diseases. For example, the contagium of the eruptive fevers, received
into the system ever so abundantly, is inoperative in some persons,
and, as a rule with rare exceptions, it is never operative after the
disease which it occasions has been once experienced. In these
instances it is not the contagium itself which has lost the capability
of producing the disease, but the conditions for its activity are
wanting. Of the nature of these conditions we know as little as of
those which are essential to the development and multiplication of the
bacillus tuberculosis. The inoculation of animals with tuberculous
matter shows that the disease is produced in some species of animals
much more readily than in other species, and some animals of the same
species much more than others are susceptible to this contagium. These
facts are to be explained by variations in different species of
animals, and in different animals of the same species, as regards the
conditions required for the efficiency of the morbific agent.

The facts in the clinical history of phthisis which denote a
constitutional predisposition thereto or a tuberculous cachexia are
explicable by reference to the conditions requisite for the development
and multiplication of the parasite. A predisposition which may be
innate, inherited, or acquired involves the existence of these
conditions. The latter may be greater or less in degree. The causative
agencies of confinement within doors, humidity of soil, pregnancy, etc.
operate by either giving rise to or increasing these conditions. If
this view be correct, it is evident that the curative influence of
climatic changes, alteration of the habits of life, and other hygienic
agencies must be by means of an effect exerted upon these conditions;
and probably it is in this way chiefly that remedies are useful. Of the
essential nature of these conditions we know neither more nor less than
of what consists the tuberculous cachexia. We are, of course, as
ignorant of the one as of the other if it be assumed that they are
identical--that, in other words, the different expressions have the
same meaning. The only difference is this: If phthisis be an infectious
and a communicable disease, a contagium enters into its etiology;
whereas if the existence of a contagium be denied, it follows that the
cachexia is itself sufficient for the causation of the disease.

In connection with the etiology of phthisis a theory which of late
years has found favor with many should be referred to. It is, that this
disease may be a result of the absorption of caseated non-tuberculous
morbid products in different parts of the body. This theory of
autochthonous infection derives but little support from clinical
observation. In much the larger proportion of the cases of phthisis it
is impossible to discover anywhere caseated morbid products which may
be supposed to have a causative connection with the disease. To assume
that, when not discovered, foci of infection nevertheless are concealed
somewhere within the organism is evidently begging the question. On the
other hand, how often do suppurations, necroses, and degenerated morbid
products occur in different situations without being followed by
phthisis!

SYMPTOMATOLOGY AND COMPLICATIONS.--Giving under this head a fuller
account of the symptomatology and complications than has been already
given in sketching the history of the disease, it will be a convenient
arrangement to consider these topics in their relations to the
different anatomical systems of the body--namely, the respiratory,
circulatory (including temperature), hæmatopoietic, digestive, nervous,
and genito-urinary systems.

Symptoms, etc. referable to the Respiratory System.--The dry cough
which is the earliest pulmonary symptom in typical cases is to be
regarded as an effect of the local irritation caused by the presence of
the tuberculous product. This product, increasing and extending, gives
rise to circumscribed bronchitis which causes increase of cough with
expectoration. The expectoration represents this secondary bronchitis
prior to the occurrence of {401} ulceration, the escape of liquefied
tuberculous product, and the existence of cavities. The quantity and
the characters of the matter expectorated depend on the degree and the
extent of the bronchial inflammation, the latter depending on the
extent of the phthisical affection. Different cases present wide
variations in these respects. The frequency and severity of the cough
depend in a great measure on the quantity of the matter of
expectoration and its adhesiveness. The matter expectorated, at first
semi-transparent mucus, becomes muco-purulent, the characters
pertaining to mucus and pus being combined in varying proportions, as
in cases of chronic bronchitis. Nummular sputa--so called from the
resemblance in form to a coin when lying on a flat surface, the edges
often serrated--are considered as casts of small cavities formed by
dilated bronchi. A microscopical examination of the sputa may show
elastic yellow fibres. The presence of these is almost pathognomonic of
phthisis, and denotes either the process of ulceration or exfoliation
of tissue from within cavities.[8] Liquefied tuberculous product
appears in the matter of expectoration as a puriform fluid. It
sometimes contains small semi-solid tuberculous masses. The lining
membrane of tuberculous cavities furnishes a veritable purulent matter
of expectoration. It is stated by Buhl that the presence of alveolar
epithelium in the sputa is distinctive of phthisis; hence the name
proposed by him, desquamative pneumonia. It is, however, stated by
Frischl that the alveolar epithelium is found in the matter
expectorated in cases of oedema and congestion of the lungs.[9] There
is sometimes notable fetor of the matter of expectoration, due to
putrescent decomposition of the purulent contents of cavities or to
small sloughing portions of pulmonary tissue. The varieties of sputa
which have been mentioned may be accompanied by a serous liquid in more
or less abundance. Calcareous masses varying in size from a pin's head
to a pea are expectorated in some cases. I have known several hundred
to be expectorated in a single case. In the instances which have fallen
under my observation these pulmonary calculi have been expectorated
when the symptoms have denoted arrest and regression of the disease;
and it is consistent with this fact to regard them as obsolete
tubercles. They are not to be confounded with the small solid bodies
sometimes formed in the follicles of the tonsils, the latter consisting
of a sebaceous-like product, which is crushed, without crumbling, by
pressure, and emits a fetid odor. Since the discovery of the bacillus
tuberculosis by Koch microscopical examinations of sputa in a large
number of cases by different observers have shown that this parasite is
generally, but not invariably, present. Its abundance in the sputa
appears to correspond to the rapidity with which the tuberculous
affection is progressing, and examinations with reference to its
presence and its abundance are of much practical utility in diagnosis
and prognosis.

[Footnote 8: In order to discover the elastic fibres readily, Fenwick
advises as follows: "Prepare a solution of caustic soda, about twenty
grains to an ounce of distilled water. Collect all the patient has
expectorated in twelve or twenty-four hours, from ten at night to ten
the next morning being the best period. Pour this, previously mixed and
well shaken with an equal quantity of the soda solution, into a glass
beaker, and boil it over a gas or spirit-lamp, stirring it occasionally
with a glass rod. A test-tube does not warm as well as a beaker. As
soon as it boils pour it into a conical glass, and add four or five
times the amount of cold distilled water. If the mucus is still
gelatinous after boiling, you have either added too little soda or not
boiled it sufficiently. The cold water carries down to the bottom of
the glass any lung-tissues that may be present, where they form a
slight deposit in about a quarter of an hour; if no deposit is visible,
put the glass aside for two or three hours. Remove the deposit with a
dipping-tube, place it in a glass cell, cover it with a piece of thin
glass, and examine with a one-inch object-glass. The lung-structures
will be often found clinging to hairs and other foreign bodies present
in the sputa" (_Guide to Medical Diagnosis_).]

[Footnote 9: Vide Niemeyer by Seitz, tenth ed.]

Hæmoptysis occurs in a large proportion of the cases of pulmonary
phthisis. {402} It occurs much oftener in the early than in a later
period of the disease. As regards the number of attacks, their
duration, the intervals between them, and the amount of hemorrhage,
there are wide variations. Prior to the formation of cavities the
hemorrhage is from the bronchial tubes (bronchorrhagia). After cavities
are formed the blood comes from the interior of these. As a rule,
bronchial hemorrhage is not followed by the evidence of any increase of
the phthisical affection. Not infrequently a sense of relief follows.
The analytical study of a large collection of cases shows that the
occurrence of bronchial hemorrhage does not diminish, but apparently
increases, the chances of arrest and of tolerance of the disease. This
statement holds true with regard to cases in which the hemorrhage is
often repeated and profuse, as well as to those in which it is slight
and infrequent.[10]

[Footnote 10: Vide _Phthisis, in a Series of Clinical Studies_, by the
author.]

Cavernous hemorrhage may be due to rupture or ulceration of
parenchymatous bands which traverse cavities, but often it is caused by
the bursting of small aneurisms in their walls. It may be so profuse as
to prove fatal. Cavities sometimes become filled with coagulated blood,
which, if life continue, becomes decomposed and gives rise to a
grumous, fetid matter of expectoration. Bronchial hemorrhage is
supposed to be caused by a circumscribed hyperæmia at the situation
where the blood escapes. In a case under my observation in which death
took place shortly after a profuse hæmoptysis, there was congestion
limited to the middle lobe of the right lung, and the bronchial tubes
in this situation contained bloody mucus, none being found elsewhere. A
circumscribed hyperæmia, however, must depend upon some local cause.
Probably in most instances this anterior local cause is the tuberculous
product. That the escape of blood involves a change in the coats of the
vessels from which it escapes is probable.

A rare event occurring in connection with hæmoptysis is the coagulation
within the bronchial tubes of fibrin which may be expectorated in the
form of casts of the tubes, analogous to those which characterize
fibrinous or plastic bronchitis. I have met with an instance, and also
with a case in which after death the bronchial tubes of an entire lobe
were found to be filled with solidified fibrin. The death in this
instance followed quickly a profuse hæmoptysis. There is not the danger
connected with the gradual disintegration and expectoration of the
coagulated fibrin which was surmised by Niemeyer.

The presence of the tuberculous product in the lungs and the processes
to which it gives rise, inclusive of the secondary bronchitis, occasion
no pain. Patients often strike the chest with violence, as affording to
them evidence that the organs are sound. But in most cases, from time
to time during the course of the disease, sharp stitch-like pains
occur. They are sometimes slight or moderately severe, but they may be
sufficiently intense to confine to the house or even to the bed. They
last, usually, but a few days, and recur at variable intervals. They
are referred generally to the upper part of the chest, often beneath
the scapula. Patients are apt to imagine that the pains are rheumatic.
They are symptomatic of successive, circumscribed, dry pleurisies,
which are very rarely wanting in cases of phthisis, leading to the
pleuritic adhesions constantly found after death. These pleurisies are
secondary to the phthisical affection, and recur at epochs when new
developments of the latter take place. There is no reason to suppose
that they contribute in any way to the increase of the phthisical
affection. On the other hand, they protect against one important event
at least--namely, perforation of lung, and, as consequent thereon,
pneumo-hydrothorax. In this point of view they are conservative. These
pleuritic pains are to be discriminated from those of intercostal
neuralgia. The neuralgic pains generally are situated lower, and the
diagnostic criterion of intercostal neuralgia is {403}
available--namely, the tenderness on pressure in the intercostal spaces
near the median line in front, the axillary line, and the spinal
column.

The respirations are more or less frequent in different cases and at
different periods in the same case according to the impairment of the
function of hæmatosis by the pulmonary affection and the increased
frequency of the heart's action. A sense of the want of breath as
implied in the term dyspnoea is, however, seldom sufficient to occasion
much suffering. Even when the respirations are considerably increased
in number it is rare for the patient to complain of the want of breath
when at rest. A degree of muscular weakness which prevents the patient
from freeing the bronchial tubes and cavities of morbid products may
give rise to distressing dyspnoea. A sudden increase in the frequency
of the respirations, with dyspnoea and cyanosis, when not attributable
to filling of the bronchial tubes nor to pneumothorax nor pleuritic
effusion, points to the development of miliary tubercles in
abundance--in other words, to the supervention of acute tuberculosis.

Important complications referable to the respiratory system are
laryngitis, non-tuberculous pneumonia, pleurisy with effusion,
perforation of lung with pneumo-hydrothorax, pneumorrhagia, and
pulmonary gangrene.

Dysphonia and aphonia, the voice being husky or hoarse and the whisper
stridulous, denote laryngitis. These diagnostic symptoms are never
wanting, and the laryngeal complication may be excluded if they be
absent; but the extent to which the larynx is affected is of course
determinable by means of the laryngoscope. The affection in some cases
extending to the epiglottis, paroxysms of cough and spasm of the
glottis are produced by the act of swallowing food and drinks. The
interference with deglutition may be so great as to restrict seriously
alimentation, and in this way may hasten a fatal termination of the
disease. In the majority of cases, however, deglutition is not
interfered with. There is very rarely laryngeal obstruction to
respiration. The affection involves little if any liability to the
supervention of acute laryngitis or oedema of the glottis.

In most cases the laryngitis occurs at a considerable period after the
commencement of the pulmonary affection, this period, in a proportion
of more than one-third, being from two to four years. In some instances
it seems to occur coincidently with, and in some to precede, the
pulmonary affection. In the latter instances it is probable that latent
tuberculous disease of the lungs preceded the laryngitis. The diversity
as regards the interval of time between the date of the pulmonary
affection and of the occurrence of the laryngitis, the apparent
coincidence in the occurrence of both in some instances, and the want
of any uniformity in different cases as regards the amount of pulmonary
disease and the stage of its progress when the laryngitis occurs,
render it a rational conclusion that laryngitis is not dependent on the
disease of the lungs, but that it proceeds from the same cause which
determines the latter.

Excluding the instances in which the laryngitis involves the epiglottis
and interferes with alimentation, clinical experience teaches that this
complication does not diminish the chances of arrest or recovery from
the pulmonary affection, and that it has no untoward influence on the
duration of the disease in the cases which sooner or later end
fatally.[11] As a rule, in cases which recover the voice remains
permanently more or less affected.

[Footnote 11: Vide _Phthisis, in a Series of Clinical Studies_, by the
author.]

Acute lobar pneumonia or pneumonic fever is sometimes an intercurrent
affection in cases of phthisis. The cases are so rare as to show
absence of any predisposition to that disease derived from the
phthisical affection. The pneumonia ends in recovery in a proportion of
cases sufficiently large to show that, as a rule, the prognosis is not
unfavorably influenced by phthisis, and, as a rule also, the course of
the latter is not influenced unfavorably by the {404} pneumonia. A
circumscribed pneumonia is an occasional complication of phthisis. Its
non-tuberculous character is shown by the rapidity and completeness of
the absorption of the intra-vesicular product. This circumscribed
pneumonia gives rise to physical signs which appear to denote a rapid
and considerable increase of the phthisical affection. The
disappearance within a short period of the added dulness on percussion,
bronchial respiration, and bronchophony, is the evidence that these
signs represent a circumscribed pneumonia occurring as a complication.

Pleurisy with serous effusion is not an infrequent complication at an
early period in the course of the disease. There is very little if any
liability to its occurrence at an advanced period, except as associated
with pneumothorax from perforation of lung. It is probably secondary in
certain of the cases in which the phthisical affection appears to
follow the pleurisy. The pleuritic effusion appears to retard the
progress of the phthisical affection. Clinical experience shows that
this complication, if it be unilateral, is not an untoward event. A
double pleurisy with effusion is evidence of the existence of phthisis.

Perforation of lung, giving rise to pleurisy with effusion and
pneumothorax, is an event which belongs, with some exceptions, to an
advanced period of the disease. The perforation is caused by rupture of
the wall of a cavity superficially situated where pleuritic adhesion
from circumscribed dry pleurisy had not taken place. In most instances
the occurrence of the perforation is quickly followed by acute pain and
orthopnoea, with notable disturbance of the circulation, fever, and
prostration, these symptoms being due to the sudden entrance of air
into the pleural sac, the development of acute inflammation, and rapid
serous effusion. The recognition of the pneumo-hydrothorax by means of
physical signs is easy. The suffering of the patient becomes less after
twenty-four or forty-eight hours. In the great majority of cases death
takes place within a short period; that is, within a few days or weeks.
The duration of life depends on the amount of phthisical disease,
together with the condition of the patient as regards strength, etc. In
some instances, the perforation taking place when the phthisical
affection is small and accompanied by favorable symptoms, the
pneumo-hydrothorax is tolerated for a long period. The accumulation of
liquid within the pleural sac sometimes causes the air to disappear,
and the pneumo-hydrothorax is converted into simple pleurisy with large
effusion.

Pneumorrhagia and pulmonary gangrene are very rare complications of
pulmonary phthisis. The analytical study of nearly 700 recorded cases
furnished but a single example of each of these complications.

Symptoms and Complications referable to the Circulatory System,
including Temperature.--More or less acceleration of the pulse and
elevation of the temperature of the body belong to the clinical history
of pulmonary phthisis. It may be stated that the pulse and temperature
are never normal if the disease be progressive. A persistent normal
pulse and no elevation of temperature therefore denote arrest or
non-progression of the disease. It may also be stated that the
acceleration of the pulse and the increase of temperature form a good
criterion of the rapidity or otherwise of the progress of the
tuberculous disease, provided inflammatory complications be excluded.
The disease is progressing rapidly in proportion to the frequency of
the pulse and the increase of temperature.

If the disease be progressive daily exacerbations of fever take place.
They occur in the afternoon usually, and continue into the evening or
the nighttime, ending in perspiration which is more or less profuse.
The exacerbations are often, but not always, preceded by chilly
sensations, and sometimes by a well-pronounced chill which may be
accompanied by rigors. During the febrile exacerbations the cheeks
frequently present a circumscribed flush {405} and the eyes have a
glistening appearance. The term hectic fever has long been applied to
the febrile exacerbations which characterize progressive phthisis.

The febrile exacerbations sometimes occurring prior to the development
of marked pulmonary symptoms may be supposed to be malarial
manifestations. Recurring daily at or near the same hour, they may
simulate closely the paroxysms of intermittent fever. A differential
point is the existence of more or less fever between the exacerbations
in cases of phthisis, whereas after a paroxysm of intermittent fever
there is apyrexia. Another point is, the occurrence of exacerbations in
cases of phthisis is generally after mid-day, whereas in the majority
of cases of intermittent fever the paroxysms occur earlier. But of
course the existence of phthisis is to be ascertained by means of the
diagnostic symptoms and the physical signs. It is, however, to be borne
in mind that phthisis and intermittent fever may be associated.

The profuse night-sweating which is a source of great discomfort in
cases of phthisis has no fixed relation to the intensity of the fever
which precedes it. The fever may be high and very little perspiration
follow, and vice versâ.

Acceleration of the pulse and elevation of temperature may arise from
an inflammatory complication, such as pleurisy, pneumonia, or
peritonitis, and from the supervention of acute miliary tuberculosis.

To endeavor to explain the rationale of the acceleration of the pulse
and the rise of temperature would require the consideration of the
general pathology of the febrile state. The absorption of septic matter
is probably a factor, but is hardly sufficient for a full explanation,
and it would not be easy, with our existing knowledge, to explain the
modus operandi of this morbific agent. The difficulty here, however, is
not greater than in explaining the phenomena of fever when occurring in
other pathological conditions. Here, as in other instances, there is no
uniformity in the relative degree of acceleration of the pulse and the
increase of temperature. The latter may be high without a proportionate
disturbance of the circulation, and the reverse. Clinical experience
shows a connection between a persistent high temperature and the waste
of the body, and in proportion as the vital powers decrease the action
of the heart is enfeebled, and a notably small and weak pulse denotes
that death by asthenia is not far distant.

Thrombosis of the iliac vein on one side or on both sides is an
occasional event in cases of advanced phthisis (marantic thrombosis).
The effect is a considerable oedema of the lower limb or limbs. Oedema
of both lower limbs, however, occurs as an effect of feebleness of the
systemic circulation. If, as is sometimes observed, there be general
dropsy, it denotes a renal complication, which is generally the waxy
variety of chronic Bright's disease. Under these circumstances the
urine is found to be albuminous.

Symptoms and Complications referable to the Hæmatopoietic
System.--Pallor of the face is generally more or less marked from an
early period in the history of phthisis, and it becomes, as a rule,
more and more marked as the disease progresses. There is considerable
variation in this respect in different cases. Impoverishment of the
blood is in a great measure to be explained by the diminished ability
to ingest and assimilate food. It is not, however, in all cases
proportionate to defective alimentation, and therefore it is a fair
inference that the disease in some other unknown way interferes with
the blood-forming processes. Exceptionally, in some cases in which the
disease is progressing, pallor is wanting. The complexion sometimes
retains for a long time a rosy color. This is probably due to the
condition of the vessels, and is not evidence of a normal condition of
the blood. It is a noteworthy fact that notwithstanding the appearances
denoting anæmia in cases of phthisis the venous hum in the cervical
veins is, as a rule, wanting.

That the impoverishment of the blood is an effect of the disease, and
that {406} it does not contribute to the progress of the tuberculous
affection, may be inferred from the fact that anæmic patients are not
likely to become phthisical. This fact, which has already been stated,
is established by clinical observation. Nor do the diseases relating to
the hæmatopoietic system, anæmia being a prominent feature in
all--namely, leucocythæmia, Hodgkin's disease, pernicious anæmia, and
Addison's disease--involve any special liability to phthisis. Other
intercurrent affections occasion death in these diseases when it is not
due exclusively to the latter.

Symptoms and Complications referable to the Digestive System.--The
opinion has been held that the development of phthisis is preceded and
accompanied by appreciable disorder of the digestive system. This
opinion is not sustained by the analysis of carefully-recorded cases.
In many, and perhaps the majority of, cases at the time of the
commencement of the phthisical affection the appetite is not notably
impaired and the digestive functions appear to be well performed.
Sooner or later, however, the appetite fails. This symptom may be
marked when the food which can be taken does not occasion evidence of
indigestion. Different cases differ very much as regards the degree of
anorexia. It is marked in the cases in which there is notable increase
of temperature and acceleration of the pulse. It is often invincible;
that is, not only is the desire for food wanting, but there is a degree
of repugnance which renders it impossible for the patient to take it.
It is intelligible that in these cases emaciation and exhaustion must
be progressive. It is not more easy to give a pathological explanation
of anorexia as an effect of phthisis than when the symptom occurs in
connection with other diseases not involving either inflammation or any
ascertained structural affection of the digestive organs. The symptom
is probably connected with morbid changes within the gastro-intestinal
or peptic glands.

Vomiting is a rare symptom in cases of phthisis, except it be produced
sympathetically in paroxysms of coughing. As thus produced it is not
rare. It is of importance from its interference with alimentation.

Diarrhoea is a frequent symptom. It may be due either to intestinal
indigestion or to a subacute enteritis or colo-enteritis thereby
induced. A waxy or fatty affection of the liver may conduce to
diarrhoea by interference with the digestion of certain alimentary
principles. If, however, the diarrhoea be persistent, it points to
intestinal ulcerations. These are usually seated in the Peyerian and
solitary glands within the small intestine, but not infrequently they
are found after death in the large intestine, and in the small
intestine above the portion in which the Peyerian glands are situated.
The number and extent of the intestinal ulcers found after death do not
always correspond to the prominence of diarrhoea as a symptom. They
cannot be excluded by the fact that this symptom is not prominent. The
presence of pus and blood in the dejections is evidence of ulcerations.
If the ulcers be situated high up in the intestinal tract, the pus and
blood may have undergone changes which render them unrecognizable by
the naked eye, and the microscope is necessary to demonstrate their
presence. The diarrhoea is often accompanied by griping or colic-like
pains. In proportion as diarrhoea is prominent it contributes to
emaciation and exhaustion. These effects are expressed by the term
colliquative, which has long been applied by medical writers to
exhausting diarrhoea and perspirations occurring in cases of phthisis.

Peritonitis occurs in phthisis as an acute and as a chronic affection.
When acute, it is caused by intestinal perforation incident to
ulcerations; this is a rare accident. It is to be inferred whenever the
symptoms denote rapidly-developed acute peritoneal inflammation. The
peritoneal sac contains intestinal gas. Perforation is excluded if
percussion shows dulness or flatness over the site of the liver. The
normal hepatic dulness or flatness on percussion is always abolished if
the peritoneal cavity contains gas. A tympanitic resonance {407} over
the liver, on the other hand, is not evidence of the presence of gas
within the peritoneal cavity, inasmuch as this resonance may be
conducted from the transverse colon distended with gas. Peritonitis
from perforation is speedily fatal. In a chronic form the peritonitis
may be preceded by an eruption of miliary tubercles in this situation,
or the inflammation may have proceeded from intestinal ulcerations,
perforation not having taken place. The local symptoms of chronic
peritonitis are often not marked. The diagnosis is to be based on pain,
tenderness, muscular rigidity, and the signs denoting liquid within the
peritoneal sac. A chronic peritonitis may be associated with a small
pulmonary affection which may not actively progress, and under these
circumstances the peritoneal complication may be tolerated for a
considerable period.

Peritoneal fistula may be reckoned among the complications referable to
the digestive system. It occurs sufficiently often in cases of phthisis
to show some pathological connection. Analysis of cases in which it
occurs affords no evidence of its having an untoward influence on the
course of the phthisical disease. On the other hand, there is ground
for the opinion generally held that it either occasions or betokens
slowness in the progress of the pulmonary affection. It follows that it
is unwise to attempt to effect a cure by surgical interference. The
characteristic bacilli have been found in the matter derived from
peritoneal fistula, showing that this affection is tuberculous in
character.

Symptoms and Complications referable to the Nervous System.--The
symptoms referable to the nervous system relate to the mind. The mental
faculties in most respects remain intact, except that in proportion to
the general feebleness there is diminished ability to continue their
exercise. The integrity of the intellect, with one exception, often
remains up to the last moment of life. A marked characteristic of the
disease, however, is a delusion in respect to improvement and recovery.
In spite of the progressive emaciation and debility, which are obvious
to every one, patients are apt to believe that their condition is
becoming more and more favorable and to feel confident of restoration
to health. Even medical men affected with phthisis manifest the same
delusive ideas. So strong is the determination in some cases to keep up
the delusion that the statements of patients in regard to their
symptoms cannot be relied upon. They are sometimes offended if the
physician feels it to be his duty to intimate danger. On the other
hand, when patients are convinced of the nature of the disease, and
that they have not long to live, as a rule they become quickly and
completely reconciled thereto. Perhaps there is no other chronic
disease in which the near approach of death is generally regarded with
greater complacency.

Cephalalgia, delirium, and coma are symptoms which are developed in a
few cases. They denote tuberculous meningitis. This is a very rare
complication in the adult. When it has given rise to the symptoms just
mentioned a speedy fatal termination is to be expected.

Symptoms and Complications referable to the Genito-urinary
System.--Tuberculous disease of the kidneys, testicles, ureters and the
prostate gland is sometimes secondary to pulmonary phthisis. The local
symptoms will depend on the situation and amount of the tuberculous
product, together with the destructive changes to which it gives rise.
The consideration of the anatomical conditions and the symptomatology
falls properly under the head of diseases of the genito-urinary system.

As already stated, the variety of chronic Bright's disease known as the
amyloid or waxy is an occasional complication in cases of phthisis. The
other varieties may coexist, but the coexistence is rare. There is no
tendency in phthisis to these affections, and, on the other hand, they
do not involve any predisposition to phthisis.

{408} As regards functional disorders of the genito-urinary system,
there is nothing noteworthy which pertains to the urine. From the
readiness with which often phthisical patients of either sex enter into
the marital relation it may be inferred that the disease does not for a
considerable period extinguish the sexual instinct. By interrogating a
considerable number of patients Louis was led to conclude that in men
the disease has an erotic influence.[12] Phthisical women do not
readily conceive, but pregnancy is not extremely infrequent. They may
give birth to healthy children. During the course of phthisis the
menses, as a rule, cease, but they continue in some cases up to a late
period in the history of the disease. When suspended early they may
return if the disease become non-progressive. That the cessation of the
menses has an unfavorable influence on the tuberculous affection is a
popular error. Nothing is gained by efforts to bring about their
return. Their cessation, however, is not a good omen, and their return
has a favorable significance.

[Footnote 12: _Recherches sur la Phthisie_.]

MORBID ANATOMY AND PATHOLOGY.--In the definition of the common form of
pulmonary phthisis were embraced the leading anatomical characteristics
of the disease. For a full account of these, together with the changes
referable to peribronchitis, periarteritis, endoarteritis, secondary
pleuritis, and bronchitis, as well as for histological appearances, the
reader is referred to treatises on morbid anatomy. The practical
objects of this article will be fulfilled by stating the abnormal
physical conditions incident to the morbid changes in different cases
and at different periods in the same case, and by a statement of the
anatomical points involved in the general pathology. Knowledge of the
abnormal physical conditions is essential with reference to physical
signs and the diagnosis. It has also an important bearing on the
prognosis, and is not without importance in its relations to the
treatment.

Certain anatomical facts may be premised, as follows: The pulmonary
affection begins at or near the apex of one lung in the vast majority
of cases; exceptionally it begins at the base of one lung. The
affection extends from the apex downward. The extension is not
continuous in respect of time, but a series of tuberculous deposits or
eruptions takes place at different epochs after variable intervals.
Hence it is that different sections of one lung may show all the
changes which intervene between a fresh deposit and tuberculous
cavities. As a rule, not long after the affection begins in one lung
the other lung is affected. This rule is so constant that, although
both lungs are not affected simultaneously, the affection may be said
with propriety to be bilateral. The constant occurrence of secondary
circumscribed pleurisies and bronchitis has been stated under the head
of Pulmonary Complications.

At an early period of the disease the marked changes appreciable by
physical signs usually consist of a few hardened patches or nodules
varying in size from that of a pea to that of a filbert, situated at or
near the apex of one lung. The physical signs are those of slight
solidification--namely, some dulness on percussion, increase of vocal
resonance, and broncho-vesicular respiration. The presence of the
morbid deposit causes circumscribed bronchitis affecting the smaller
tubes, and this complication may give rise to subcrepitant râles within
the area of the tuberculous affection. The disease may end with no
further increase or extension of the local affection, this termination
resulting either from self-limitation or from the agency of treatment.
Of this fact I have proof from cases not only studied during life, but
in which appearances were noted after death. The ending of the disease
and recovery after a small tuberculous deposit occur oftener than is
generally supposed.

An increase and an extension of the phthisical affection occasion
larger {409} areas and also a greater degree of solidification. As the
amount of increase and extension within a given period varies very much
in different cases, it follows that there is nothing like uniformity in
these respects. Generally, the solidified portions of the lung form
islands between which the tuberculous deposit is wanting. Between these
islands the lung not infrequently becomes emphysematous. This vicarious
emphysema explains the existence of a vesiculo-tympanitic resonance in
some cases notwithstanding the solidification. Exclusive of that sign,
as thus accounted for, the solidification causes a dulness on
percussion proportional in degree and extent to the solidified portion
of lung. The auscultatory signs of solidification are generally
present--namely, either bronchial or broncho-vesicular respiration, and
bronchophony or increased vocal resonance, according to the degree of
solidification. The existence of bronchitis over a larger extent is
represented by more abundant and coarser moist bronchial or bubbling
râles. These râles do not, as has been supposed, necessarily denote
that softening of the tuberculous deposit has taken place. Dry
circumscribed pleurisies occurring from time to time, even from the
very commencement of the phthisical affection, may give rise to a
pleuritic friction murmur. The escape of the liquefied tuberculous
deposit into the bronchial tubes by ulceration, added to the products
of the bronchial inflammation, occasions an increase of the bubbling
râles. Moreover, the liquefied tuberculous deposit is better suited for
the production of bubbling sounds than the products of bronchial
inflammation. Hence the abundance of the bubbling râles, taken in
connection with the characters of the matter of expectoration, is
evidence of the escape of liquefied tuberculous deposit.

If phthisis be progressive, the physical conditions already
enumerated--namely, solidification, liquid in the bronchial tubes,
pleuritic exudation--continue. They are present in both lungs.
Associated with these conditions are cavities. The cavities formed in
different cases differ greatly in size and number. They differ also as
regards the number and the size of the openings by which they
communicate with the bronchial tubes. The latter conditions are of
importance with reference to the free discharge of the contents of
cavities and the production of certain physical signs. Enumerating here
the cavernous signs, they are--tympanitic resonance within a
circumscribed space, frequently with amphoric or cracked-metal
intonation, cavernous and sometimes amphoric respiration, increased
vocal resonance, cavernous whisper, pectoriloquy in some instances,
and, as a rare sign, metallic tinkling. An accumulation of liquid
within a cavity which has free communication with the bronchial tubes
gives rise to the cavernous sign called gurgling. I have met with an
instance in which a loud splashing sound was produced within a cavity
synchronous with the impulse of the heart, and due to the agitation of
the cavity by the cardiac movements. Owing to the association of
cavities with solidified portions of lung, the latter varying greatly
in different cases in the extent and the degree of solidification, with
the cavernous signs are combined those which represent varying degrees
of solidification--namely, either dulness or flatness on percussion,
either bronchial or broncho-vesicular respiration, and either
bronchophony or increased vocal resonance.

In the physical conditions incident to pulmonary complications of
phthisis--namely, pleurisy with effusion, perforation of lung with
pneumo-hydrothorax--the reader is referred to the article on DISEASES
OF THE PLEURÆ.

With reference to the general pathology of phthisis, points relating to
the morbid anatomy are to be considered. There are two distinct
varieties of morbid product in cases of phthisis--namely, the miliary
granulations and the infiltrated deposit formerly distinguished as
crude tubercle. Laennec taught that these are only varieties of
essentially the same morbid product, the former being preliminary in
their occurrence to the latter. Following {410} Virchow, some late
writers have restricted the application of the term tubercle to the
miliary granulations, regarding the infiltrated deposit as a
non-tuberculous inflammatory product. Histological investigations have
failed to establish an essential distinction between the two varieties.
The fact that they are so constantly associated shows some close
pathological connection. Both varieties undergo the same degenerative
changes. Each is found by inoculation to produce tuberculous disease in
certain animals. Moreover, according to the late researches of Koch and
others, each contains the characteristic parasite, the bacillus
tuberculosis. In view of these considerations, the doctrine of Virchow,
advocated by Niemeyer and others, is not tenable, and, as already
stated under the head of the Definition and Classification of pulmonary
phthisis, the term tuberculous is properly applied to both varieties.
There is no such affection as a non-tuberculous pulmonary phthisis. The
terms pulmonary phthisis and pulmonary tuberculosis are now, as
heretofore, to be regarded as synonymous.

That the pathology of pulmonary phthisis involves a predisposition or a
tuberculous diathesis has been already shown by facts pertaining to the
etiology. It does not in the least invalidate this logical conclusion
that in the present state of our knowledge pathologists are unable to
explain this diathetic condition; that is to say, in what it consists.
Its recognition is not merely a matter of speculative or theoretical
interest; it has an important bearing upon a rational prophylaxis and
on the treatment of phthisis.

Up to a very recent date the opinion has generally been held by
pathologists that the local phthisical affection may be determined
entirely by a tuberculous cachexia--that the latter, in other words,
may produce the affection exclusive of any local extrinsic cause; and
the question has been much discussed whether or not at the outset the
phthisical affection is an inflammation. But if the parasitic doctrine
be accepted, a local causative agent derived from without--namely, the
bacillus tuberculosis--is essential, the predisposition or the cachexia
consisting of certain unknown conditions which are required for the
development and the multiplication of the parasite. According to this
doctrine, the extension of the local affection is due to invasions
successively of different portions of the lungs, and the development of
tuberculous disease in other situations is due to the migrations of
this parasite. Without the presence of the bacillus, no matter in how
great degree the required conditions may exist, phthisis will not
occur.

Inflammatory processes, however, accompany and follow the development
of the tuberculous affection. Bronchitis, peribronchitis,
periarteritis, endoarteritis, interstitial pneumonia, and pleurisy are
terms which denote inflammation. To these are to be added ulceration
and suppuration within cavities. The infiltrated tuberculous deposit is
to be regarded as an inflammatory exudation. There is an intrinsic
propriety, therefore, in calling it a pneumonia. But the behavior of
this deposit differs widely from that of the exudation in lobar
pneumonia. In the latter affection it is readily absorbed and
disappears, leaving the pulmonary structure intact, whereas in phthisis
it is absorbed with difficulty, and in most cases leads to more or less
destruction of the pulmonary structure. For these reasons, irrespective
of histological points of difference, the term tuberculous should be
used to distinguish the exudative pneumonia which is characteristic of
phthisis. The term desquamative pneumonia was proposed by Buhl. The
so-called cheesy degeneration of the tuberculous products--a necrotic,
not an inflammatory, process--was considered by Laennec as a
distinctive mark of the products. This doctrine has been disproved.
Other morbid exudations and growths may undergo similar degenerative
changes.

DIAGNOSIS.--It is evidently very desirable to recognize the existence
of phthisis at as early a period as possible with reference to the
adoption of {411} measures with a view to prevent the further
development and progress of the disease. It is also very desirable, if
practicable, to determine that phthisis does not exist; that is, by the
absence of diagnostic points to exclude it. Difficulty of diagnosis
relates almost exclusively to an early period when the phthisical
affection is small. The diagnostic points pertaining to the symptoms
and the physical signs in the incipiency of the disease therefore
especially claim attention.

A cough of more or less duration, which was at first slight and dry,
gradually increasing and accompanied by the expectoration of mucus,
should always excite a suspicion of phthisis, especially if the
patient's age be between twenty and thirty years. This is not the
history of a chronic primary bronchitis. A cough as just described
should never be considered as nervous or sympathetic without due
investigation. It should not be attributed to pharyngitis, although the
latter affection is found to exist. Want of breath on exercise is a
symptom pointing to something more than a bronchial or pharyngeal
affection. The import of these symptoms is still greater if, after the
commencement of the cough or from an earlier date, there has been
decrease in weight and strength. Their significance is much increased
by the occurrence of hæmoptysis. Hæmoptysis followed by a persistent
cough, and still more if cough preceded its occurrence, is always
presumptive evidence of a phthisical affection. Occurring without
having been preceded by cough, and when cough does not immediately
follow, it should suggest the probability of phthisis. In the larger
proportion of cases under these circumstances it is a forerunner of the
diagnostic symptoms and signs of the disease. In connection with the
cough a persistent increase of the temperature of the body is an
important diagnostic symptom. Chilly sensations and flashes of heat are
symptoms of some importance. Especially significant are pleuritic
stitch-pains referable to the upper part of the chest or beneath the
scapula, these being symptomatic of the circumscribed dry pleurisies
which may occur at an early period of the disease. Impaired appetite,
pallor of the face, and a tendency to perspire during sleep have much
significance taken in connection with the pulmonary and other symptoms.

A positive diagnosis must rest on physical signs, together with more or
less of the foregoing symptoms. The physical conditions which furnish
the diagnostic signs are solidification of a small portion or of small
portions of lung, usually at or near the apex, the presence of mucus in
the small-sized bronchial tubes, and perhaps fibrinous exudation on the
pleural surface within a circumscribed area corresponding to the
solidified portion or portions of lung. The signs furnished by these
conditions are slight dulness on percussion, a broncho-vesicular
(formerly called rude or harsh) respiration, some increase of vocal
resonance and of the whispered voice, subcrepitant râles, and perhaps a
grazing friction murmur. It may be important to consider the physical
signs of phthisis with some detail. Aside from their importance, a
reason for this is that terms by which some signs are designated are
not used in precisely the same sense by all medical writers.

A small phthisical affection gives rise to slight or moderate dulness
on percussion. In order to appreciate this sign if the dulness be
slight, attention should be paid to the pitch of the resonance as well
as to the lessened intensity of resonance. The pitch is always raised.
By attention to the latter character, in conjunction with the
diminution of intensity, a degree of dulness may be sometimes
appreciated which, without attention to the pitch, might not be
determinable.[13] In determining abnormal dulness in the
infra-clavicular region on one side, the normal disparity between the
two sides of the chest {412} in this region must be taken into account.
The resonance at the right summit, as compared with that of the left
summit, is, normally, somewhat dull. Hence it is not as easy to make
out an abnormal dulness at the right as at the left summit. If the
relative abnormal dulness at the right summit be but slight, the
question is whether there be more than a normal disparity. This
question is rendered difficult by the fact that the degree of normal
disparity varies somewhat in different healthy persons. In cases of
doubt little reliance is to be placed on this sign alone, but it is to
be taken in connection with auscultatory signs.

[Footnote 13: The author was the first to indicate the fact that
dulness is always associated with elevation of pitch. Vide "Prize Essay
on Variations of Pitch in the Sounds obtained by Percussion and
Auscultation," _Transactions of the American Medical Association_,
1852.]

With reference to the auscultatory signs in cases of phthisis, it is to
be premised that often, owing to the importance of studying the sounds
derived from a limited area and of localizing morbid conditions, the
use of the stethoscope is indispensable. It is impossible to meet all
the requirements of physical diagnosis by immediate auscultation. After
an experience of more than a quarter of a century the writer would
advise the binaural stethoscope in preference to any other. For the
benefit of those who are not practically familiar with this instrument,
it should be added that in order to appreciate its advantages, the
instrument, in the first place, must be properly constructed, and, in
the second place, some practice is necessary. A sound produced within
the instrument is at first an obstacle, but it is speedily overcome by
use.[14]

[Footnote 14: The dissatisfaction with the binaural stethoscope so
often comes from defects in its construction that it seems proper to
refer to Tiemann & Co., and to Ford & Co., of New York as reliable
makers of this instrument.]

A small tuberculous solidification is represented by a
broncho-vesicular respiration. This sign was named and described by me
in 1856. The name takes the place of the terms rudeness, harshness, and
hardness--terms which are not only inadequate, but convey an erroneous
idea. Quoting from another work, the characters of the
broncho-vesicular respiration and its comprehensive signification are
as follows: "The sign represents the different degrees of
solidification of lung between an amount so slight as to occasion only
the smallest appreciable modification of the respiratory sounds, and an
amount so great as to approximate closely to the degree giving rise to
bronchial or tubular respiration. In other words, all the gradations of
respiratory modifications caused by incomplete or an inconsiderable
solidification are embraced under the name broncho-vesicular. The
gradations correspond to the amount of solidification; that is, they
show the solidification to be either very slight, moderate, or nearly
sufficient to be regarded as considerable or complete. The sign is
therefore important as evidence, first, of the existence of
solidification, and, second, of the degree of solidification. Analyzing
this sign, the most distinctive feature is the combination of the
vesicular and the tubular quality in the inspiratory sound. These two
qualities may be combined in variable proportions. The pitch of the
sound is raised in proportion as the tubular predominates over the
vesicular quality. The expiratory sound is more or less prolonged,
tubular in quality, and the pitch raised. The prolongation of this
sound, its tubular quality, and the raised pitch are proportionate to
the predominance of the tubular over the vesicular quality in the
inspiratory sound. If the solidification be slight, the characters of
the normal vesicular respiration predominate; that is, the inspiratory
sound has but a small proportion of the tubular quality, and is but
little raised in pitch, the expiratory sound being not much prolonged,
its tubularity not marked, the pitch not high. If, on the other hand,
the solidification be almost enough to give a bronchial respiration,
the inspiratory sound has only a little vesicular quality, the tubular
quality predominating, the pitch proportionately raised, and the
expiratory sound is prolonged, high, and tubular, nearly to the same
extent as in bronchial respiration. The less the solidification the
more the characters {413} of the normal vesicular respiration
predominate over those of the bronchial respiration; and, per contra,
the greater the solidification the more the characters of the bronchial
predominate over those of the normal vesicular respiration."[15] By
means of the broncho-vesicular respiration a slight morbid
solidification may be recognized in one of the infra-clavicular regions
or over the scapula. Here, however, as with regard to percussion, an
allowance is to made on the right side for a normal disparity. The
respiratory sounds on the right side at the summit, as compared with
those at the left, have normally the characters more or less marked of
a broncho-vesicular respiration. These characters are more marked as
the stethoscope is brought toward the sternum. Hence a small
solidification of lung is more easily ascertained by auscultation at
the left than at the right summit.

[Footnote 15: Vide _Manual of Auscultation and Percussion_, by the
author; also, paper contained in the _Transactions of the International
Medical Congress_, London, 1882. The broncho-vesicular respiration was
called by Skoda indeterminate (unbestimmt), and this term is still used
by German writers. These sounds are not indeterminate if the characters
derived from pitch and quality be analytically studied; they are sounds
intermediate between the normal respiratory murmur and bronchial
respiration.]

Not infrequently in cases of incipient phthisis the respiratory sounds
at the summit on the affected side are so weakened that their
characters cannot be studied. Weakness of the respiratory murmur in
these cases becomes a diagnostic sign taken in connection with other
signs.

A small tuberculous deposit may increase the vocal resonance. But,
again, a normal disparity between the two sides must be allowed for.
The normal vocal resonance is always greater on the right side. If,
therefore, it be a question as to the existence of a small tuberculous
affection at the right summit, it is to be decided whether the
disparity be greater than normal. A small tuberculous deposit at the
apex of the left lung, on the other hand, may not increase the
resonance to an equality with that at the right summit.

Attention should be paid to the whispered voice, and, still again, the
two sides show a normal disparity. The sound heard with the whispered
voice, which may be distinguished as the normal bronchial whisper, is
louder on the right than on the left side, and somewhat higher in pitch
on the left side, at the summit of the chest. If at the right summit it
exceed the normal disparity, and the pitch be higher than at the left
summit, the sign may be distinguished as increased bronchial whisper,
and it denotes solidification. If, on the other hand, the sound at the
left summit be louder than that of the right summit, there is increased
bronchial whisper, representing the solidification at the apex of the
left lung.[16]

[Footnote 16: The different abnormal modifications of sounds produced
by the whispered voice were first named and described by the author.
Vide _Manual of Auscultation and Percussion_.]

The normal points of disparity at the summit of the chest render the
diagnosis of incipient phthisis by means of alterations in the
resonance on percussion, the respiratory sounds, the vocal resonance,
and the whispered voice a problem in some cases of not a little
difficulty. In these cases an examination of the sputa for the presence
of the tuberculous parasite may furnish proof of the existence of the
disease. This proof may in some instances be obtained when the physical
signs, together with the symptoms, do not render the diagnosis
positive, and it may be sought for in order to corroborate the evidence
derived from other sources. The author can testify from considerable
experience to the value of an examination of sputa for bacilli in cases
in which the diagnosis is not rendered positive by other signs and by
symptoms. It must, however, be borne in mind that the absence of
bacilli in the sputa is not sufficient to exclude phthisis, especially
if but a single examination be made. In doubtful cases, if an
examination of the sputa be negative, the examination should be
repeated. The weight of evidence against the {414} existence of
phthisis is, of course, greater in proportion to the number of
examinations with negative results.[17]

[Footnote 17: The following method of staining the bacilli tuberculosis
in the sputum is essentially that recommended by Ehrlich in the
_Deutsche medicinische Wochenschrift_, Mai 6, 1882:

It is important that the sputum to be examined should be derived from
the lungs, and should not be solely that from the upper air-passages. A
small opaque particle from the sputum is to be pressed between two
cover-glasses, so that when these are drawn apart a thin film will
remain upon each. Each cover-glass, as soon as the film is dry, is to
be passed, with the preparation upward, rather rapidly three times
through the flame of a Bunsen's burner or of an alcohol lamp. The
preparation is now ready for staining.

A small quantity of water in a test-tube or flask is now shaken with an
excess of aniline oil (which need be only in small amount), and after a
few moments is filtered through moistened filter-paper. To the clear
filtrate thus obtained is to be added, drop by drop, a saturated
alcoholic solution of fuchsin (gentian-violet, methyl-violet, and
several other aniline colors may be substituted) until the fluid begins
to be opalescent, showing that it is saturated with the coloring agent.
In this manner an alkaline-aniline staining solution is prepared.

Into this staining solution the cover-glasses, having the dried films
of sputum prepared as above described, are dropped, preferably so that
they will float with the preparation downward. Here they remain from a
half hour to twenty-four hours. If taken out in a short time, the
fluid, at least for a time during the staining process, should be
heated moderately over a water-bath, and in any case the process of
staining is accelerated and rendered more certain by heating.

After removal from the staining fluid the cover-glass is washed for a
few moments in water, and is then dipped into a mixture of one part of
pure nitric acid (it should contain no nitrous acid) to about three or
four parts of water. Here it remains only a few moments, when it will
be found that the preparation has lost its color, although a part will
be restored by the subsequent washing in water, which should be done at
once. If the preparation has not been sufficiently decolorized, it may
be placed again in nitric acid, but it is not necessary or desirable
that it should remain there many minutes. The object of the nitric acid
is to extract the color from all but the tubercle bacilli.

The preparation may now be at once examined either in glycerin or
(after drying or after treatment with alcohol and oil of cloves) in
balsam. Ehrlich recommends, previous to this, a staining of the
background with some color other than that of the bacilli; thus, with
methyline blue if the organisms are stained red with fuchsin. This
staining of the background, however, is not necessary. While the ideal
method of studying the stained bacilli is by means of Leis's
oil-immersion lenses and Abbé's illuminating apparatus, they can
usually be seen readily enough with the high powers in ordinary use,
such as the one-fifth or one-sixth inch objectives of our American
microscope. After staining with fuchsin the bacilli appear as short
rods of a red color, frequently curved or bent.]

The adventitious sounds which have been mentioned--namely, the
subcrepitant râle and the pleural friction murmur--sometimes afford
valuable aid in the diagnosis. Taken in connection with the direct
signs obtained by auscultation and percussion, these accessory signs
when present make the diagnosis positive: they are by no means
uniformly present, and therefore their absence is not proof against the
existence of a phthisical affection. To these accessory signs another
sign may be added--namely, an abnormal transmission of the heart-sounds
within one of the infra-clavicular regions. In the middle of this
region there is nearly an equal transmission of these sounds normally.
Comparing the two sides as regards the two sounds respectively, the
first sound is a little louder on the left, and the second sound a
little louder on the right side. Now, with a little solidification the
sounds may be better transmitted, so that they are abnormally loud on
the affected side.

A decision that there is no physical proof of phthisis must rest on the
absence of all the foregoing signs after repeated examinations of the
chest.

It is not to be concluded that for a positive diagnosis of incipient
phthisis all or most of the foregoing diagnostic signs must be
recognized. They are not all present in all cases. Two or three of
these signs, and even a single one if well marked and associated with
diagnostic points pertaining to the symptoms and history, may suffice
for a positive diagnosis.

It is an interesting question how small a portion of solidification may
furnish signs sufficient for a diagnosis. I have the records of two
cases bearing {415} on this question. A patient came under my
observation at Bellevue Hospital in 1867. In the right infra-clavicular
region the respiration was abnormally broncho-vesicular, the vocal
resonance was increased, and there was increase of the bronchial
whisper within a small circumscribed space. On these signs was based
the diagnosis of a small tuberculous deposit. The case served to
illustrate the signs just named to classes for practical instruction in
auscultation and percussion. The patient, who was employed as a helper
in the apothecary's shop, died suddenly from taking by mistake an
overdose of the fluid extract of aconite. The autopsy showed at the
apex of the right lung a nodule of the size of a filbert, no
tuberculous deposit being elsewhere found.

A recent medical graduate, twenty-two years of age, had cough and two
attacks of hæmoptysis. His father and a sister had died with phthisis.
There was slight dulness on percussion on the summit of the chest on
the left side, with crepitation at both summits. These were the only
signs noted. This case was included among the cases of recovery
reported in my work on phthisis published in 1875. He enjoyed excellent
health and was notably vigorous for twenty-eight years. Death took
place in 1880 from disease of the heart and kidneys. The autopsy showed
at the apex of each lung a small indurated portion somewhat larger on
the left than on the right side. Elsewhere there was no appearance
denoting present or past pulmonary disease.

It is in only a small proportion of cases that, when patients first
come under medical observation, the phthisical affection is so small as
to render the diagnosis difficult. The tuberculous solidification is
generally sufficient to give rise to well-marked signs. The shrinkage
of the lung at the apex from interstitial growth and diminished
capability of expansion may have caused a small infra-clavicular
depression and restricted respiratory movements in this region. The
dulness on percussion is readily recognized. The characters of the
broncho-vesicular respiration are easily determined. The increase of
vocal resonance and increased bronchial whisper admit of no doubt. With
these signs, oftener than at an earlier period, are associated
accessory signs--namely, subcrepitant râles and bubbling in larger
tubes, pleuritic friction murmur, and undue transmission of the
heart-sounds.

At a somewhat later period, and sometimes even when cases are first
observed, the physical signs denote a still greater degree of
solidification. Infra-clavicular depression and restricted movements on
one side are marked. The respiration is bronchial and the voice
bronchophonic. There may be pectoriloquy with the bronchophonic
characters, showing that the speech is transmitted through solidified
lung.[18]

[Footnote 18: Bronchophony is to be understood as a sign distinct from
increased vocal resonance. In bronchophony the resonance may or may not
be increased. Intensity is not a character of this sign. Its
distinctive characters are concentration of the voice sound, nearness
to the ear, and elevation of pitch. The terms concentration and
nearness to the ear properly express what was intended by Laennec in
the words "la transmission évidente de la voix à travers le
stethoscope." Pectoriloquy is to be distinguished from bronchophony.
These two terms are sometimes confounded. Bronchophony is transmission
of the voice, pectoriloquy the transmission of speech--that is,
articulate words.]

Exceptional cases are to be referred to in which over lung containing
solidified portions from tuberculous deposit dulness on percussion is
wanting. Not only is dulness wanting, but the resonance is greater than
normal. The resonance is altered in character. With an increase of
intensity the quality is in part tympanitic and the pitch is raised.
This is the sign described by me many years ago under the name
vesiculo-tympanitic resonance. The distinctive characters are those
just mentioned--namely, increase of intensity, the quality a
combination of the vesicular and the tympanitic, and more or less
elevation of pitch. The name vesiculo-tympanitic expresses these
characters. It is the sign of pulmonary emphysema. It denotes that
portions of {416} lung situated between islands of solidification have
become emphysematous. The emphysema is vicarious; that is,
supplementary to the shrinkage of the portions solidified, and, added
thereto, probably collapsed lobules. Were one to be governed by
percussion alone in the physical diagnosis, this sign would in some
cases mislead. The liability to error is avoided by taking due
cognizance of the associated signs furnished by auscultation.

In cases of advanced phthisis cavities are added to tuberculous
solidification. It is desirable to recognize the existence of these. In
most instances the signs which may be distinguished as cavernous
suffice for the recognition of cavities. The cavernous signs are
furnished by percussion and by auscultation of the respiration and of
the voice.

A purely tympanitic resonance within a circumscribed space points to a
cavity, but a tympanitic resonance with either an amphoric or a
cracked-metal intonation is more especially a cavernous sign. An
amphoric or a cracked-metal resonance over a cavity may often be
obtained by observing certain rules in percussion--namely, percussing
with a single and rather forcible blow, the mouth of the patient being
open and brought close to the ear. These signs may be rendered still
more distinct by means of the binaural stethoscope, the pectoral
extremity being close to the patient's opened mouth, an assistant
making the percussion. These cavernous signs are not present when
cavities contain much liquid or when communication with the bronchial
tubes is temporarily obstructed; hence the signs are sometimes present
and sometimes absent.

There is a distinctive cavernous respiratory sign. This assertion is
called for by the fact that the existence of the sign is not as yet
recognized by all medical writers. According to Laennec, the
respiratory sounds derived from cavities resemble the bronchial
respiration. From his description it would be impossible to distinguish
the former from the latter. Skoda considered the cavernous and the
bronchial respiration as absolutely identical; and this view is held by
German writers at the present time. Walshe indicated an essential
differential point pertaining to the inspiratory sound in cavernous
respiration--namely, its low pitch. The fact that in purely cavernous
respiration the pitch of the expiratory is lower than that of the
inspiratory sound was stated by me in 1852.[19] The distinctive
characters of the cavernous respiratory sign as then indicated were as
follows: An inspiratory sound low in pitch and non-tubular in quality,
followed by an expiratory sound still lower in pitch and non-tubular.
The quality of the sound in inspiration and in expiration may be said
to be blowing, after the term soufflante used by Laennec, but applied
by him to a sound either bronchial or from a cavity, when the air seems
to be drawn from the ear of the auscultator.

[Footnote 19: Vide "Prize Essay."]

Appreciating clearly the characters which are distinctive of cavernous
respiration, it is impossible to confound this sign with bronchial
respiration, both the inspiratory and the expiratory sound in the
latter sign being high in pitch and tubular in quality. This cavernous
sign approaches much nearer to the normal vesicular respiration. The
only distinction between these two signs is the presence of the
vesicular quality in the latter and its absence in the former. Hence,
the only liability to error is in confounding the two. This error can
only be committed when the respiratory murmur is so feeble that the
vesicular quality is not readily appreciable. In order to avoid the
error, the respiration should not be pronounced cavernous when the
sounds are quite weak, except there be present other correlative
cavernous signs.

Cavities are often situated in close proximity to lung solidified by
tuberculous deposit or interstitial pneumonia: cavernous respiration
and bronchial respiration are then in juxtaposition, and their
differential characters are {417} rendered very distinct by contrast.
Under these circumstances, however, the cavernous respiration is
sometimes modified by combination with the characters of the bronchial
respiration. Not infrequently a cavernous inspiration is joined to a
bronchial expiration, the more intense expiratory sound representing
adjacent solidification extending over the site of the cavity and
drowning the weaker cavernous expiration. In another mode of
combination the inspiratory sound is bronchial at the beginning and
cavernous at the end. Here the cavernous sound occurs a little later
than the bronchial, and the latter is supplanted by the former. This
variety of broncho-cavernous respiration has been recently described by
Seitz under the name metamorphosing respiratory murmur
(metamorphosirendes athmungs geräusch). In like manner, the characters
of the cavernous and of the normal vesicular respiration may be
combined. This combination may be expressed by the term
vesiculo-cavernous respiration.

The effect of a cavity upon vocal resonance is to increase its
intensity without giving rise to the characters distinctive of
bronchophony--namely, nearness to the ear, concentration, and elevation
of pitch. Increased vocal resonance, and not bronchophony, is therefore
a cavernous sign. If bronchophony be present over a cavity, it denotes
adjacent solidification of lung. With the vocal resonance more or less
increased the vocal fremitus appreciable on auscultation is often
intensified.

A cavernous whisper has the characters of the expiratory sound in the
cavernous respiration; that is, it is low in pitch and blowing or
non-tubular in quality, being in contrast, as regards these characters,
with a high-pitched tubular sound in whispering bronchophony. The
latter sign is often found near a cavity, showing the proximity of
solidified lung.

Amphoric respiration, amphoric voice, and amphoric whisper are
pathognomonic signs of a cavity, provided pneumothorax be excluded. The
same is to be said of metallic tinkling, a very rare cavernous sign.
Gurgling within a circumscribed space is a cavernous sign of some
value. Pectoriloquy--that is, the transmission of articulated words--is
not, per se, a cavernous sign; that is to say, the speech may be
transmitted by solidified lung as well as through a cavity. This is
true alike of words spoken with the loud and with the whispered voice.
It is, however, easy to determine whether pectoriloquy be or be not due
to a cavity. If with the loud voice the transmitted speech be
unaccompanied by the characters of bronchophony, it denotes a cavity.
So, if transmitted whispered words be unaccompanied by the characters
of the bronchophonic whisper, they denote a cavity. On the other hand,
the transmission is by solidified lung if bronchophony and pectoriloquy
be conjoined in either the loud or the whispered voice.

The shrinkage of lung incident to the formation of tuberculous cavities
increases the depression apparent on inspection in the infra-clavicular
region. The site of a cavity is sometimes indicated by a circumscribed
bulging of intercostal spaces, within a localized area, on forced
expiration or an act of coughing. A sharply-defined circumscribed
depression corresponding to the area of a cavity is visible in some
cases. Another effect of shrinkage of lung is to uncover the aorta in
the second intercostal space on the right side, or the pulmonary artery
in a corresponding situation on the left side. The pulsation of these
arteries may then be perceived by the touch, and perhaps, also, by the
eye. This effect should not lead to the error of inferring the
existence of aneurism. Shrinkage of the upper lobe of the left lung may
cause considerable elevation of the heart, also enlarging considerably
the space within which is felt the cardiac impulse.

With a practical knowledge of the physical signs of which a concise
account has been given, it is practicable to determine, first, the
existence of phthisis in its incipiency when the tuberculous affection
is small; second, during the {418} progress of the disease to ascertain
the degree and the extent of the tuberculous solidification; and,
third, to recognize the existence of, and to localize, cavities.

Recapitulating the signs belonging to the foregoing phases of the
disease, in incipient phthisis they are slight dulness on percussion,
broncho-vesicular respiration approximating to the normal vesicular or
a respiratory murmur too weak for its characters to be studied, some
increase of vocal resonance, increased bronchial whisper, and, as
occasional accompanying signs, subcrepitant râles, pleuritic friction
murmur, and abnormal transmission of the heart-sounds, more or less of
these signs being limited to the summit of the chest on one side. After
further progress of the phthisical affection the signs are, dulness on
percussion more or less marked, either a broncho-vesicular respiration
approximating to the bronchial or a purely bronchial respiration,
either notable increase of vocal resonance or bronchophony, either
increase of the bronchial whisper or whispering bronchophony, and moist
bronchial or bubbling râles which may be either coarse or fine, or both
may be combined. After the affection has advanced to the formation of
cavities the cavernous signs are added to those of
solidification--namely, circumscribed tympanitic resonance on
percussion, cracked-metal and amphoric resonance, cavernous
respiration, cavernous whisper, increased vocal resonance and gurgling.
Pectoriloquy may be present before and after the formation of cavities;
in the former instance the transmission of speech being by solidified
lung, and in the latter through a cavity, the two modes of transmission
being easily differentiated by means of the characters associated with
the pectoriloquy.

An intercurrent pneumonia, not tuberculous, may lead to the error of
supposing the tuberculous affection to be much greater than it is.
Especially is there liability to this error if the patient have not
been under observation prior to the intercurrent pneumonia. The latter
may give rise to bronchial respiration and bronchophony, with notable
dulness on percussion over a considerable space. If the patient have
been under observation, the rapidity with which the solidification
denoted by these signs has been developed is a diagnostic point. A
notable diminution of the solidification within a few weeks or days is
evidence that it was due to an intercurrent pneumonia. The tuberculous
deposit is never absorbed with such rapidity. The following case may
serve as an illustration of this complication: A man aged thirty had
had for some time slight cough and want of breath on active exercise,
but he had kept about, actively engaged in business, until within a few
days of the date of my visit. He was then up and dressed, his chief
complaint being want of breath on any exertion. The physical signs gave
evidence of considerable solidification of the upper lobe of the right
lung. The question was, whether the solidification was due exclusively
to phthisis, or whether with this disease was associated an
intercurrent pneumonia. The question was settled definitively by an
examination of the chest six weeks afterward. At the time of this
examination the solidification had in a great measure disappeared;
there was only slight dulness on percussion, with increase of vocal
resonance and feeble respiratory murmur. Meanwhile, the symptoms had
denoted progressive improvement; the cough was now slight; he no longer
suffered from want of breath on exertion, and he had improved as
regards appetite, strength, etc. This patient consulted me seven years
and four months afterward. In the mean time he had considered himself
in fair health, but he had been subject to cough, and for the preceding
six months the cough had been persistent. There was now dulness at the
summit of the chest on the right side, with feeble broncho-vesicular
respiration, increase of vocal resonance, abnormal transmission of the
heart-sounds, and subcrepitant râles. He had held his weight and
strength, and his appetite and digestion were good.

{419} An occasional event in cases of phthisis is obstruction of a
primary bronchus from the pressure of an enlarged bronchial gland. This
event may explain a degree of embarrassment of respiration out of
proportion to the changes which have taken place in the lungs. The
bronchial obstruction is shown by notable feebleness or by suppression
of the respiratory murmur on the side of the obstruction, and an
increase of the murmur on the other side of the chest. Obstruction of a
primary bronchus may prevent the appreciation of morbid respiratory
signs on the obstructed side.

During the progress of phthisis the symptoms concur with the physical
signs in showing the progressive inroads of the disease upon the
pulmonary organs. They show, more than the physical signs, the inroad
upon the powers of life. They also afford evidence, in conjunction with
the physical signs, of arrest of the disease. More reliance is to be
placed on the symptoms than on the signs in judging of the rapidity on
the one hand, or on the other hand of the slowness, of the progress of
the disease. In these several points of view the consideration of
symptoms comes more properly under the head of the prognosis.

The symptoms pertaining to complications of phthisis may be the first
to lead patients to consult a physician. Not infrequently advice is
sought for harshness or hoarseness of the voice, arising from chronic
laryngitis, the cough and other symptoms which preceded this affection
not having been regarded as of sufficient consequence to require
medical aid. It is to be borne in mind that chronic laryngitis, when
not of syphilitic origin, is generally secondary to phthisis. The chest
is therefore to be examined carefully with reference to the signs of
the latter.

Pleurisy with effusion may be a complication which the physician is
called upon to treat. A lung compressed by liquid which fills the
affected side of the chest cannot be interrogated by means of physical
signs. Under these circumstances subcrepitant râles may denote a
phthisical affection on the summit of the chest on the opposite side.
The existence of cough and expectoration prior to the pleurisy is
strong evidence of an antecedent phthisical affection. The occurrence
of hæmoptysis adds greatly to the evidence.

A tuberculous patient who has not been under any treatment may apply to
a surgeon to be relieved of the inconvenience of a perineal fistula.
Operative interference for this affection should never be resorted to
without a careful examination of the chest.

PROGNOSIS.--Whether pulmonary phthisis is ever a curable disease has
hitherto been a mooted question. Prior to the time of Laennec instances
of apparent cure were open to doubt on the score of diagnosis. Laennec
did not admit the probability of a cure before the formation of
cavities, but he gave the histories in a number of cases in which the
cicatrization of cavities had taken place.[20] If by the term
curability be meant a complete restoration of the portions of lung
affected by tuberculous disease to the normal condition which existed
prior to the disease, the doctrine of Laennec is probably true. A
moderate or even a small phthisical affection leads to changes which
are permanent. There remains more or less impairment of the integrity
of the pulmonary organs. But if by the term be meant that all pulmonary
symptoms cease, that the patient has good general health, and that the
{420} damage to the lungs is not sufficient to prevent an adequate
exercise of their functions, a cure may take place before as well as
after the formation of cavities. Accepting the latter sense of the term
curability, no one at the present time will deny the statement just
made--a fact which is due, at least in a measure, to the different
views in regard to the treatment of phthisis now as compared with the
time of Laennec.

[Footnote 20: "Les observations contenues dans l'ouvrage de M. Bayle,
ainsi que ce que nous avons dit nous-mêmes ci-dessus du dévelloppement
des tubercles, prouvent suffisamment que l'idée de la possibilité de
guérir la phthisie au prémier degré est une illusion. Les tubercles
crus tendent essentiellement à grossir et à se ramollir. Il est peut
être au pouvoir de l'art de ralentir leur dévelloppement, d'en
suspendre la marche rapide, mais non pas de lui faire un pas
rétrograde. Mais s'il est impossible de guérir la phthisie au premier
degré, un assez grand nombre de faits mont prouvé que dans quelques cas
un malade peut guérir après avoir eu dans les poumons des tubercles qui
se sont ramollis et ont formé une cavité ulcéreuse" (_Traité de
l'Auscultation médiate_).]

The appearances found after death in cases which may be considered as
exemplifying, practically, recovery from phthisis vary according to the
extent of the tuberculous affection and the stage to which it had
advanced. In a case referred to in connection with the diagnosis (vide
p. 407) an examination after death, nearly thirty years having elapsed
from the date of recovery, showed within small circumscribed spaces at
the apex of both lungs a condensed pulmonary tissue. In the following
case there was a similar condition within larger spaces: The patient, a
man aged about forty, was attacked with hæmoptysis in April, 1846. Soon
afterward the symptoms and signs of tuberculous disease became
manifest, and death took place in the following June. On examination
after death the lungs were found to contain infiltrated tuberculous
deposits, some of which had undergone softening, and miliary tubercles
in abundance. In addition to these appearances, at the apex of each
lung was a solid mass nearly as large as a hen's egg, that on the right
side being somewhat larger than that on the left. The surface over
these masses presented a marked depression and a puckered appearance.
On dividing the masses they appeared to consist of condensed
parenchyma: they were of a reddish color, friable, and contained an
abundance of minute calcareous particles. They were surrounded by a
thick, firm wall isolating them from the adjacent pulmonary structure.
Eighteen years before his death this patient had cough and other
symptoms which were regarded at the time as denoting pulmonary
phthisis. He recovered, and had good health up to the fatal illness.
The only exception to this statement of his previous good health was
the occurrence of a perineal fistula, which was nearly cured by
division of the gut nine months before the hæmoptysis.

No one can doubt that tuberculous cavities may completely cicatrize.
Instances in abundance have been observed since the publication of
Laennec's treatise. The gradual contraction and final closure of a
cavity may be observed during life, the cavernous signs becoming less
marked, and at length disappearing. At the present time I see
frequently two persons who have recovered from phthisis, recovery in
one taking place nearly twenty, and in the other nearly ten, years ago.
In these cases the cavernous respiration was well marked in situations
in which now there is a feeble vesicular murmur. In both cases there is
a circumscribed depression of the chest in these situations.

Recovery may be said to take place when cavities do not cicatrize, but
remain, being lined by a membraniform structure and free from morbid
products. Under these circumstances cavities are innocuous. There is an
approximation to recovery when cavities furnish more or less matter of
expectoration, the lungs elsewhere being free from tubercles or
tuberculous products.

Recovery with calcification of tubercles is illustrated by the
following case: A farmer from Illinois, aged forty, consulted me in
June, 1843. Within the preceding four months he had from time to time
expectorated calculi, some of which were of the size of a small pea, in
great numbers. A hacking cough had existed for several months before he
began to expectorate the calculi. At the time of the expectoration of
these the cough was severe and he raised some bloody mucus. In the
intervals the cough was slight and without expectoration. The
examination of the chest was negative as regards any signs of disease.
Thirteen years afterward this patient came to report his condition of
health. The expectoration of calculi had continued for some {421} time
after his former visit; then his cough ceased, and meanwhile he had
been perfectly well.

It is a question whether the tuberculous product is ever absorbed. The
fact that in some instances the physical signs in life and the
appearances after death give no evidence of either tuberculous deposit
or cavities, and the fact that tuberculous solidification is observed
to diminish or disappear when apparently the deposit has not been
expectorated, render it probable that under some circumstances
absorption does take place to a greater or less extent. It is doubtless
true that, as a rule, the deposit is not absorbed; the tuberculous
affection in this respect affords a striking contrast to
non-tuberculous pneumonia.

Cases of recovery from phthisis are cited by medical writers as proving
the curability of the disease. The term curability implies that
recovery is due to remedial agencies. It does not therefore embrace a
truth of great importance in its bearing on the prognosis and the
treatment--namely, the disease in certain cases ends in recovery purely
from an intrinsic tendency. My clinical studies have furnished facts
which conclusively establish this important truth. Out of a large
number of cases (640) recorded during a period of thirty-four years,
recovery took place in 44. In 23 of these 44 cases there were no
measures of treatment to which the recovery could be attributed. The
disease ended favorably in these 23 cases from self-limitation. This
assertion does not express a conjecture or a theory, but a logical
conclusion. Self-limitation, therefore, is a highly important element
in prognosis; it is a highly important factor in the treatment. The
claim in behalf of phthisis of self-limitation, based on the analysis
of cases of recovery, was made by me nearly a quarter of a century
ago.[21] It has not as yet received that recognition in medical
literature which it is desirable that it should receive in view of the
importance of its practical bearings. It will enter here into
considerations connected with treatment and prognosis.

[Footnote 21: Vide _American Journal of the Medical Sciences_, January,
1858.]

Recovery from phthisis involves, of course, cessation of the progress
of the disease. This cessation of progress may be due either to an
intrinsic tendency or to arrest by measures of management, or to both
combined. Recovery may or may not follow the cessation of progress.
Owing to the disposition and the extent of the tuberculous affection,
reparation of the lesions does not take place. It is a useful grouping
of cases into--first, those which become non-progressive and end in
recovery; and, second, those in which the cessation of progress is not
followed by complete recovery. It is also useful to consider as forming
a third group cases in which the progress of the disease is extremely
slow. The cases in the latter group are the opposite to those in which
the progress of the disease is continuous and rapid, giving rise to the
name galloping consumption.

There is much significance in the fact that in cases of progressive
phthisis the disease does not, as a rule, advance by a steady increase,
but by a series of invasions. Successive eruptions of the tuberculous
affection occur. In these eruptions the affection may be either small
or moderate or considerable in amount. The intervals between them may
be brief or long. The disease may end with a single eruption. This may
be small or even slight, and followed quickly by recovery. There is
reason to believe that instances of this kind are not infrequent. The
phthisical affection may have been overlooked, or it is inferred from
the recovery that there was an error in diagnosis. In the great
majority of cases a series of eruptions occurs, and it is in this way
that the disease is generally progressive. These clinical facts,
regarded from the standpoint of the parasitic origin of phthisis, are
to be explained by supposing that bacterial colonies invade at
successive epochs different portions of the lungs, but that in a
certain number of instances there is neither invasion nor migration of
the parasite. {422} The occurrence of successive eruptions is made
manifest by the symptoms and the physical signs. After the occurrence
of a single eruption or a series, if there be no recurrence the
recovery will depend, cæteris paribus, on the amount of the tuberculous
affection.

The prognosis in individual cases involves clinical points which
pertain to the symptoms and signs of the pulmonary affection, and to
the symptomatic phenomena referable to other of the anatomical systems
of the body. The latter are of importance as representing the
constitutional condition or the cachexia, and as indicating either, on
the one hand, self-limitation, or, on the other hand, a progressive
tendency of the disease.

Other things being equal, the smaller the pulmonary affection the
better the prognosis. But assuming that the first tuberculous eruption
is small, it does not follow that other eruptions may not occur more or
less speedily, and, assuming a considerable or a large eruption,
another may not occur. The prognosis in the latter case is of course
much the more favorable. In forming a judgment in respect of the
prognosis, the amount of the pulmonary affection is less to be
considered than the symptoms which relate to the progressive tendency
of the disease and to its tolerance by the system. An unfavorable
prognosis, however, is to be based on the existence of an amount of the
pulmonary affection sufficient to compromise the respiratory function,
as shown by notable increase of the frequency of the respirations and
by dyspnoea. Hæmoptysis, as has been seen, if unaccompanied by other
symptoms which are untoward, even if the hemorrhage be profuse, is not
an unfavorable event. Microscopical examinations of the sputa afford
important information bearing on the prognosis. Examinations, thus far,
made by different observers, show that in proportion to the abundance
of the parasite in the sputa the disease may be considered as actively
progressing.

Important prognostics derived elsewhere than from symptoms referable to
the pulmonary organs relate especially to the circulatory system,
inclusive of the temperature of the body, to the digestive system, to
the hæmatopoietic system, and to nutrition. Acceleration of the pulse
is an unfavorable symptom. In proportion to the degree of acceleration,
either activity of the progress or a want of tolerance of the
tuberculous affection, or of both combined, is to be inferred. It is of
course important, if practicable, to know the patient's normal pulse as
the standard for comparison in individual cases, inasmuch as the
frequency in health varies considerably in different persons. A febrile
temperature is especially significant as a symptom of progressive
phthisis. It is the best criterion of the activity of progress. There
is no constant proportionate relation between the amount of the
pulmonary affection, as shown by the local symptoms and the signs, and
the elevation of temperature. Nor does the degree of fever correspond
always with the acceleration of the pulse. Diurnal exacerbations of
fever, with more or less profuse sweating, are evidences that the
disease is progressive. Both fever and the rapid action of the heart
not only have symptomatic significance, but they contribute to
progressive exhaustion.

Impaired power of digestion and anorexia are bad prognostics.
Especially bad is a degree of anorexia in which not only no desire for
food is felt, but it is so loathed as to render adequate alimentation
impossible. Diarrhoea, although not dependent on tuberculous disease of
the intestine, is a bad prognostic, as denoting impairment of the
digestive processes. Notable pallor, whether an effect of deficient
alimentation or referable to the hæmatopoietic system, weighs heavily
against the expectation of improvement. A considerable emaciation has
even greater weight. Whenever in the progress of the disease the
patient becomes notably pale and emaciated, there is little ground for
hope, especially if there be conjoined muscular debility, a rapid
pulse, and a high temperature. It is unnecessary to attempt a clinical
picture of the {423} disease as it is presented toward the close of
life. The reality is unhappily too familiar to every observer.

The picture just referred to has another side. The disease is not
always progressive. There is reason to believe that its progress is
sometimes arrested. It ceases to progress in some cases from
self-limitation. In a certain proportion of cases recovery takes place.
What, then, is the basis for a favorable prognosis? In general terms,
it is the absence of the unfavorable prognostics which have been
mentioned. The prognosis is favorable in proportion as the action of
the heart is but little disturbed, the temperature of the body
non-febrile, the appetite and digestion but little affected, the
complexion not much changed, and the nutrition of the body fairly
maintained. The inference under these circumstances is that the disease
does not tend to progress, and that the existing pulmonary affection is
well tolerated. The ground for encouragement is greater the less in
amount the pulmonary affection; but even if the symptoms and signs show
the latter to be considerable or even large, encouragement is
warrantable so long as there is evidence of non-progression and
tolerance. It is not, however, to be forgotten that there is always
more or less danger of a renewed tuberculous eruption.

The suspension of menstruation belongs among the unfavorable events,
but alone it has not great significance. Its occurrence as respects the
previous duration of the disease varies much in different cases. In
some cases menstruation continues nearly to the close of life. The
return of menstruation after its suspension for a greater or less
period is a favorable prognostic.

The occurrence of certain complications is of marked importance with
reference to the prognosis. Perforation of lung followed by pleurisy
and pneumothorax is in most instances speedily fatal. On the other
hand, simple pleurisy with effusion, in some instances at least, seems
to have a favorable effect upon the pulmonary affection. Tuberculous
ulcerations of the intestine preclude the expectation of improvement
and hasten the fatal termination. Tuberculous peritonitis is a fatal
prognostic. Chronic laryngitis, if it interfere with alimentation, is a
serious complication, but if that effect be wanting it is not
unfavorable as regards its significance in prognosis. Perineal fistula
is not unfavorable, to say the least. Renal disease, and any accidental
complication sufficient in itself to tell more or less against the
powers of life, must be regarded as telling proportionately upon the
prognosis.

What influence has the evidence of a congenital tendency and heredity
upon the prognosis? It is commonly believed that the chances of arrest
and recovery are less in proportion to this evidence. There is
doubtless truth in this belief, but it has sometimes too much weight in
the minds of both patients and physicians in individual cases. The
disease is by no means always progressive even when the antecedents of
the patient afford the strongest evidence of an innate predisposition.
The following instance is given by way of illustration: In 1861 a young
woman, eighteen years of age, affected with phthisis, came under my
care. The disease had existed for two years, and she had tried various
climates--namely, Cuba, Florida, Minnesota, Kentucky, and Ohio. The
case ended fatally in 1863. The mother of this patient and two sisters
had died of tuberculous disease. The father was tuberculous at the time
of her death, and he died soon afterward with an intestinal
complication. There remained two sisters and two brothers. The elder of
the brothers, aged seventeen, was attacked in 1861 and died in 1863.
The climate of Minnesota was resorted to in this case with no benefit.
The younger brother, aged sixteen, in 1861 had a dry cough, which after
a short time ceased, and he became apparently well and robust. The
physical signs at that time showed a small tuberculous affection at the
summit of the left lung. In the winter of 1863 the cough returned, and
the signs now showed a tuberculous affection of the summit of the right
lung. He was immediately {424} sent to Europe, and he passed the winter
and spring at Nice. He returned and went to South America in 1864. He
passed the winter of 1865-66 in New Orleans and France, making the
voyage in sailing ships. He passed the winter of 1866-67 in St. Paul,
and died in the following spring. Of the two remaining sisters, the
previous history in the case of the elder, aged thirty, seemed to
warrant a retrospective diagnosis of a small phthisical affection which
had ceased to progress and from which she had recovered. There were
slight dulness of the summit of the chest on the left side and
broncho-vesicular respiration. This one of the sisters has been well
for the twenty-three years which have elapsed since the date of the
supposed phthisical affection. The younger of the two sisters at the
age of twenty-two had a cough with small expectoration and a moderate
bronchial hemorrhage in the winter of 1862. There was abnormal dulness
on percussion at the summit of the chest on the right side, with
weakened respiratory murmur, some crepitation, and increase of vocal
resonance. After a few weeks the pulmonary symptoms ceased. In this
case there was no treatment, medicinal nor hygienic; she had passed the
winters in the city and summers at attractive places of resort,
entering with zest into social enjoyments, and she has been in all
respects well up to the time when I last saw her, in the spring of
1881, twenty years after the phthisical disease.[22]

[Footnote 22: Since that date a recurrence of the affection has taken
place, but without being progressive.]

The last two cases are instances of recovery from phthisis irrespective
of any medicinal or hygienic agencies; that is, a recovery by
self-limitation. Considering the evidence of a family predisposition, a
favorable prognosis at the outset would hardly have been justifiable.
From my records of cases other instances might be selected illustrative
of the caution not to allow too much weight in the prognosis, in
individual cases, to the evidence of an innate predisposition.

It might be supposed, from the greater liability to phthisis between
the ages of twenty and thirty years, that its occurrence at this period
of life affects unfavorably the prognosis. Facts, however, do not
appear to sustain this supposition. So far as the ratio of recoveries
bears upon the point, the study of a limited number of cases shows it
to be not larger after than before the age of thirty.[23]

[Footnote 23: Vide _Phthisis, in a Series of Clinical Studies_.]

The liability to a recurrence of the disease after recovery is
important to be considered in connection with the prognosis. Of 44
cases of recovery among those which I have recorded and analyzed,
recurrence had taken place in 6 up to the time of the analysis. In one
of these 6 cases the disease had recurred twice. The patient recovered
from the second recurrence, and is now well, more than ten years having
elapsed. In all the other cases the recurrence proved fatal. The
recurrence took place after periods ranging from one and a half to over
six years from the date of the recovery. So far as these cases warrant
a conclusion, it is that in cases of recurrent phthisis the prognosis
is very unfavorable. This conclusion might be materially modified by
the study of a large number of cases. The fact that after recovery
there is considerable liability to a recurrence of the disease has an
obvious bearing upon the prophylactic management.

Facts pertaining to the duration of phthisis come properly under the
head of prognosis. Of 44 cases of recovery which I have recorded and
studied, the duration varied from six months to ten years. In more than
one-half of these cases the pulmonary affection was small; in 4 cases
it was moderate in amount; in 10 cases it was considerable; and in 1
case it was large and advanced.[24] These facts show that the prospect
of recovery is much better {425} when the tuberculous affection is
small or moderate, but that a considerable and large affection does not
preclude recovery.

[Footnote 24: Vide _Phthisis, in a Series of Clinical Studies_, for
abstracts of the histories of these cases. Absence of all pulmonary
symptoms was known to have existed in the different cases for periods
between six months and twenty-seven years. Throwing out two cases in
which the period was six months, and one case in which it was eight
months, the average period was six years.]

Next to recovery, the course of the disease is favorable when it ceases
to be progressive and life with fair health is continued for a long
period. Out of the cases which I have analyzed, there were 28 in which
the disease was known to have existed for periods ranging from one year
and three months to twenty-five years. The duration was reckoned up to
the time of the analysis or of the last information obtained. The
number of years noted does not express the duration of life. The
average period during which the disease was known to have been
non-progressive is a fraction over eight years. The histories in these
cases exemplify the fact that phthisis, when it ceases to be
progressive, although recovery does not take place, is not incompatible
with fair and even good general health and long life. That recovery
does not take place is owing to the persistence of pulmonary lesions,
such as cavities which do not cicatrize or an interstitial pneumonia
with dilatation of bronchial tubes. The tuberculous disease no longer
continues, but the local effects of the disease remain. Slowness of
progress and prolonged tolerance are to be hoped for when the disease
neither ends in recovery nor becomes non-progressive. In some cases the
disease ends fatally, having existed for many years where at no time
could it be said that its progress had ceased. The prolongation of life
under these circumstances depends on the slowness with which the
disease progresses and the ability of the system to tolerate it.

The extremes of the duration of the disease in a large collection of
fatal cases are so far apart that the average period is of little
practical value as bearing on the prognosis in individual cases. In the
collection of recorded cases which I have studied analytically, there
were 112 the duration of which from the commencement of the disease to
its fatal termination was ascertained. The mean duration was about
twenty-three months. Laennec found the average duration twenty-four
months; Louis and Bayle, twenty-three months; Andral, twenty-four
months; Sir James Clark, thirty-six months; and Williams of London,
forty-eight months.

TREATMENT.--The author premises the consideration of the treatment by
stating that this article was written before sufficient time had
elapsed after the publication of the researches by Koch for their
confirmation by other competent observers. At the present time (May,
1885) the doctrine that phthisis depends on the presence of a special
micro-organism is to be considered as probably established. The grounds
for this statement have been presented under the head of the Etiology,
and reference to the practical bearings of the doctrine have been
introduced in connection with the Diagnosis and Prognosis. It is
evident that the doctrine is likely to have important bearings on the
treatment. If it be true that the origin, the extension, and the
diffusion of the disease within the body require the presence and the
multiplication of a particular parasite, it is evidently a rational
object of treatment to effect its destruction. For this object an
efficient parasiticide is to be sought after, to be administered either
by inhalation or by its introduction into the blood-vessels. Already,
within the short time which has elapsed since Koch's discovery,
extended observations have been made with various substances which are
destructive to bacteria outside of the body, but thus far without
success. A difficulty as regards inhalation is in the way of a
destructive agent in the form of either an impalpable powder or a vapor
or a gas reaching the colonies of bacilli in sufficient quantity to
effect the object, without doing injury to the tissues or inducing
toxæmia. As regards the introduction of {426} parasiticides into the
blood, it seems hardly probable that a toxic agent can be safely
introduced in sufficient quantity to effect the object. It remains to
be determined by clinical observation whether or not these difficulties
are insuperable.

Efforts to destroy the parasite in another direction promise to be more
effectual--namely, by the removal of the co-operating conditions on
which their multiplication depends. It is to be borne in mind that the
development and continuance of phthisis involves two factors, one which
is the presence of the parasite, and the other the existence of those
unknown conditions constituting the tuberculous predisposition or
cachexia. The removal of the latter may effect the destruction of the
parasite indirectly, but not less certainly than by bringing into
direct contact with it a destructive agent. It is in this indirect way
that the measures of treatment which experience has shown to be more or
less effective may be supposed to operate. And it is to be added that
those measures of treatment the usefulness of which rests on clinical
observation are in no wise disproved or modified by the parasitic
doctrine. At the present time the treatment of the disease is to be
governed by principles which, based on reason and experience, are
independent of that doctrine.

The intrinsic tendency of phthisis to be either progressive or
non-progressive underlies the treatment. In a certain proportion of
cases the disease tends to advance steadily and actively, as shown by
the symptoms and the physical signs. In these cases treatment cannot be
expected to do more than to palliate symptoms, and perhaps prolong the
duration of life. These are cases of so-called galloping consumption.
In a larger proportion of cases the disease does not steadily or
actively advance. Remissions occur. The pulmonary affection increases,
and extends by successive tuberculous invasions or eruptions after
intervals variable in duration. These cases offer more encouragement
for treatment. There is room to hope after each invasion that another
will not take place, and that the affection which exists may be
tolerated indefinitely if the cases do not end in recovery. In a
minority of cases when a certain amount of pulmonary affection has
taken place there is no further increase or extension. In this respect
the disease ceases to progress. In some of these cases after the lapse
of weeks or months all pulmonary symptoms disappear, and the patient
may be said to have recovered. The probabilities of the recovery and
the time required therefor vary, other things being equal, according to
the amount of the pulmonary affection. In other cases recovery does not
take place. More or less of pulmonary symptoms remain. The existing
lesions which these symptoms represent, however, may be well tolerated,
and their existence may not interfere with fair or even good general
health and long life.

Whenever the disease ceases to be progressive, with or without
recovery, an intrinsic tendency has more or less agency in the
cessation of progress. In some instances it is certain that this result
is wholly due to self-limitation. Expressing the fact in other language
than that of personification, the disease may become non-progressive
because the unknown, special, constitutional morbid conditions which it
is customary to embrace under the name tuberculous cachexia no longer
exist; or, assuming that a particular parasite is essential to the
progress of the disease, this organism may cease to multiply in
consequence of the non-continuance of conditions which are necessary
for its multiplication. Whatever be the explanation of the tendency of
the disease--to be, on the one hand, progressive, or, on the other
hand, non-progressive--it must be taken into account in estimating the
influence of measures of treatment. How largely an intrinsic tendency
to be non-progressive is accountable for apparent success in treatment
cannot be determined with precision. The evidence of its agency can
only be derived from the accumulation of cases of non-progressive
phthisis in which no active measures of treatment were pursued.
Reference has been made to a few such cases {427} among those which I
recorded during a period of thirty-four years. Some cases in addition
have come under my observation since the analysis of my cases recorded
up to 1875. It is evident that a large collection of such cases cannot
be made by a single observer.

From what has been stated, it follows that the treatment in case of
phthisis has reference especially to the constitutional conditions
which stand in a proximate causative relation to the pulmonary
affection. The chief objects are to arrest the disease and to keep the
cachexia in abeyance. In the present state of our knowledge measures of
treatment addressed directly to the pulmonary affection, albeit
important, are of secondary importance when compared with those which
either co-operate with or oppose the underlying intrinsic tendency of
the disease as manifested in individual cases.

Proceeding to consider the treatment in cases of phthisis, a convenient
division of topics is into those relating to the climatic treatment,
the dietetic and regiminal treatment, and the medicinal treatment.

Climatic Treatment.--It would be impossible within the limits of this
article to enter into a discussion of the various questions connected
with climatic influences or to consider the relative advantages of
different climates. Nor, were it possible, would this be desirable as
regarded from a practical standpoint. I shall confine myself to the
general considerations which bear upon the climatic treatment.[25]

[Footnote 25: For an account of the characteristics of different places
of resort in different countries, and a full consideration of the
subject of climate in relation to phthisis and other diseases, the
reader is referred to the article entitled "Klimatstherapie" by H.
Weber of London in _Handbuch der Allgemeinen Therapie_, von H. v.
Ziemssen, Zweiter Band, Leipzig, 1880.]

In the analytical study of the cases of phthisis I had recorded up to
the year 1875, I endeavored to draw some conclusions respecting
climatic treatment from the facts contained in the histories. Temporary
changes of climate entered into the treatment in 74 cases. The
histories were interrogated with reference to the number of cases in
which recovery took place, the number in which the disease ceased to be
progressive without recovery, and the number in which the disease
progressed slowly, with reference to the apparent influence exerted by
climate. The changes of climate in the 74 cases were various. In a
considerable number the patients traveled in Europe, visiting different
places. The foreign resorts in which they sojourned for greater or less
periods were Nice, Algiers, Mentone, Egypt, Nassau, Lima, Rio Janeiro,
Cuba, and the West India islands. In this country the different resorts
were in Minnesota, California, New Mexico, Florida, Georgia, South
Carolina, Louisiana, Virginia, Kentucky, the District of Columbia,
Michigan, and the Adirondacks. Colorado as a place of resort had not
excited much attention prior to my making abstracts of my histories for
analytical study, and for this reason it does not appear in the
foregoing list. I have notes of not a few cases in which the latter
climate was resorted to. It is at once evident that 74 cases
distributed over so many places of resort cannot furnish adequate data
for judging of the relative advantages of different climates.
Nevertheless, the analysis of these cases led to an important
conclusion as respects, in general, the usefulness of a temporary
change of climate. Of the 74 cases, 9 ended in recovery, 13 were in the
list of cases of arrested or non-progressive phthisis, and 5 were in
the list of cases in which the disease was slowly progressive. In 33
cases the disease ended fatally, and in 14 cases neither the duration
nor the termination of the disease appears in the histories. Moreover,
of the 33 fatal cases, in 23 the histories afforded evidence of more or
less benefit from the changes of climate.[26] From these facts it
seemed warrantable to deduce, as a positive conclusion, that in a
considerable proportion of cases a {428} change of climate has a
favorable influence on phthisis. It follows also, as a corollary, that
a favorable influence is exerted by a variety of climates. Indeed, it
would seem, judging from these facts, that the favorable influence
pertains to the change rather than to the particular climate selected.
If this be true, it follows that the agencies by which a favorable
influence is exerted relate to accessory or incidental circumstances
more than to purely climatic conditions.

[Footnote 26: For further details vide _Phthisis, in a Series of
Clinical Studies_.]

It is an absurd supposition that any climate exerts a specific
influence in arresting phthisis. This statement is not in the least
inconsistent with the fact that certain climatic conditions are much
more favorable than others for an arrest of the disease. Dryness,
equability, and purity of the atmosphere are essential elements of a
favorable climate. Within late years a high altitude (4000 to 8000 feet
above the ocean-level) has been deemed by many of much importance.
Aside from the purity of the air incident thereto, the rarefaction is
supposed to have a salutary effect by increasing the expansion of the
lungs.[27] Few at the present time regard a tropical temperature as
advantageous. The choice is usually regarded as lying between a cold
and a warm climate, each having favorable elements aside from
temperature. There is abundant testimony in behalf of each.
Circumstances pertaining to cases individually must determine which to
choose. A patient who in health has found cold weather more favorable
to vigor and well-being than warm weather will be likely to find a cold
climate more beneficial than a warm climate, and vice versâ. In order
to derive benefit from a cold climate a patient must have preserved
sufficient vigor to endure out-of-door life in such a climate.
Confinement much of the time within doors must deprive patients of the
benefit to be hoped for from a cold climate. For obvious reasons a cold
climate is better suited to men than to women. With reference to the
superior excellence of particular health-resorts, caution is to be
exercised in weighing not only testimony either for or against their
superiority, but the value of reported cases. Putting aside the chances
of error in diagnosis, it is to be considered that among those who
elect a particular place of resort an arrest of the disease or
improvement to a greater or less extent would probably have taken place
had any one of many places been selected, and perhaps if no change had
been made. On the other hand, in a certain proportion of cases the
disease will be progressive anywhere. A limited number of cases must
not be relied upon to establish the relative advantages of particular
places, especially if there be not data enough to judge of the
condition of the patient in each case as regards the amount of the
pulmonary affection, the temperature, pulse, and other symptoms. A few
cases which have been selected to illustrate either the favorable or
unfavorable influence of a particular climate are not entitled to any
weight in the formation of an opinion. To gather clinical facts
sufficient to determine by analytical study the actual advantage
severally of different climates is a work attended by so many
difficulties that it must be long before it can be accomplished.
Meanwhile, in discriminating between different places of resort the
physician is to be governed by rational considerations. In reality,
custom and fashion have much to do in this matter. Places which were
formerly in vogue as health-resorts have now fallen into disrepute. It
is almost inevitable that sooner or {429} later this will be the fate
of any place which becomes so popular as to attract very largely
phthisical patients, owing to the aggregation of the instances in which
no benefit could have been expected from climatic treatment.

[Footnote 27: On this topic the reader is referred to an article by C.
Theodore Williams, entitled "The Treatment of Phthisis by Residence at
High Altitudes," in the _Transactions of the International Medical
Congress_, London, 1881; also to a work entitled _Rocky Mountain
Health-Resorts, an Analytical Study of High Altitudes in Relation to
the Arrest of Chronic Pulmonary Disease_, by Charles Denison, M.D., 2d
ed., 1880.

There is much reason in the suggestion that the immunity from phthisis
in situations which are sparsely settled may be due not so much to
climatic influences as to the fact that these situations are free from
non-climatic causes contributing to the prevalence of the
disease--namely, in-door occupations, overcrowded dwellings, etc.]

There is reason to believe that the benefit derived from climatic
treatment is often in a great measure due to accessory circumstances.
As already intimated, this seems to be a fair inference from the number
of instances of arrest of the disease, of cessation of its progress,
and of notable improvement in a collection of cases in which many and
varied climates had been resorted to. Under the name accessory are
embraced a variety of circumstances--in fact, everything not pertaining
purely to climatic agencies. The opportunity of living in the open air
and freedom from the cares of business, together with relaxation and
mental diversion, are in the category of accessory circumstances. These
contribute largely in some cases to the benefit derived from change of
climate. Patients at a health-resort are apt to carry out hygienic
regulations more faithfully than when at home. In contrast to the
accessory circumstances which are favorable there are those which have
an unfavorable effect, such as home-sickness, ennui from lack of usual
occupations, anxiety lest affairs should suffer for want of personal
supervision, interruption of fixed habits, and the want of home
comforts. These in some cases may go far toward counteracting the
benefit from climatic influences.

All these accessory circumstances, as bearing upon individual cases,
are to be taken into account in deciding the question as to the
importance of climatic treatment. Of course a change of climate is
important, other things being equal, in proportion as the climate in
which the patient resides is humid, variable, and the atmosphere
impure. So far as purely climatic influences are concerned, it may be
important only that the patient escape the more trying seasons of the
year--namely, the spring and the hot summer months. A malarial climate
should certainly be exchanged, if practicable, for another during the
season when there is danger of being infected with the malarial miasm.
To avoid this cause of disease, as well as the changes of temperature,
etc. incident to the spring and summer months, it may not be necessary
to go very far from home. It is probably better not to go to a distant
climate for a few weeks, in order that the double acclimatation caused
by going and returning within such a brief period may be avoided.

It is of essential importance to take fully into account the condition
of the patient as regards the pulmonary affection and the general
symptoms before advising or sanctioning a change of climate which
involves long journeys and separation at a distance from home and
friends. There is more reason to expect benefit from a change the
stronger the evidence against an intrinsic tendency of the disease to
progress actively. Whenever the temperature and circulation denote
activity of progress the propriety of a change is doubtful. Whenever
there is great emaciation with muscular feebleness there is little
ground to expect material benefit from any climate. The experiment is
allowable at an advanced period of the disease only with a view to
satisfy the wishes of the patient and the friends, having a full
understanding with the latter in respect of the danger of dying away
from home. It should be added that sometimes in cases which offer no
ground for the expectation of any essential benefit journeys or voyages
are well borne, and life is apparently prolonged by a change from an
inclement to a genial climate.

Distance is a point to be considered in the selection of places of
resort. It is often an objection to crossing the ocean that
communication with relatives or friends is attended with delay and
difficulty. The voyages, as a rule, are not objectionable. Our own
country embraces almost every possible variety of climate, and
therefore, so far as purely climatic influences are concerned, it is
not necessary to resort to foreign countries. The latter, however, have
for many the advantage of being made more attractive by novelty and
{430} historical associations. Moreover, there are often better
arrangements for comfort and enjoyment. The accessory advantages are
always to be considered with reference to the particular tastes and
needs in individual cases. Good food in abundance and well cooked,
large and well-ventilated rooms, facilities for walking, riding, and
driving, opportunities for hunting, fishing, and other out-of-door
sports, ample provisions for in-door exercise in bowling, etc.,
agreeable society,--these are among the accessory advantages without
which often the best climatic influences will prove inoperative. To
these is to be added available judicious medical advice.[28]

[Footnote 28: For details concerning the health-resorts of the Riviera,
Hyères, Cannes, Nice, Mentone, and others which are much esteemed in
Europe, the reader is referred to a work entitled _The Riviera_, by
Edward I. Sparks, London, 1879.]

A mistake often made by those who find benefit from a change of climate
is to continue the change for too short a period. The benefit speedily
obtained may be speedily lost when the patient is again placed under
the climatic and other circumstances attending the development of the
disease. It is to be borne in mind that the benefit from a change of
climate does not depend on any special remedial agency, but on a
combination of favorable circumstances, and that the salutary
influences connected with climate are exerted not so much directly upon
the lungs as upon the general system. It follows that the beneficial
effect may be manifested more by increase of appetite, better
digestion, greater endurance of muscular exercise, and especially gain
in weight, than by immediate improvement in the pulmonary symptoms.
Many patients cannot afford the loss of time and the expense of
lengthened absence, and therefore are unable to make trial of change of
climate. These may be consoled by the fact that not a few cases of
phthisis do well without any climatic treatment. In some of the most
striking of the instances of arrest of the disease which have come
under my observation change of climate did not enter into the
treatment. Important as is this fact, it does not conflict with the
belief that additional chances of arrest and the prospect of more or
less improvement are often secured by climatic treatment. It is a wise
precaution for patients to reside permanently in a climate in which an
arrest of the disease has taken place. Of course this is not always
practicable. Its importance is attested by reason and experience, and
it is the duty of the physician, according to his discretion, to
suggest it. The many obstacles which are often in the way of its
adoption are sufficiently obvious.

Sanitaria for phthisical patients at health-resorts are doubtless
serviceable in many cases, because hygienic measures are enforced which
would not under other circumstances be thoroughly carried out. An
offset to this advantage is the depressing effect upon some minds of
association with other patients. Owing to this moral effect it is
sometimes judicious to advise patients not to go to places which, for
the nonce, are especially popular, in order that they may not have
before their eyes cases exemplifying all the phases of the disease, and
be led to talk over symptoms with other patients affected with
phthisis. As regards sanitaria, those in which the chief object is to
enforce measures of hygiene are perhaps most likely to be serviceable.
If these measures be secondary to some system of medication, there is
room for distrust.

It is hardly necessary to say that the treatment of patients in such
institutions should be under the charge of competent physicians who
have not originated or adopted any peculiar notions respecting the
pathology and therapeutics of the disease. As a matter of course, there
cannot and should not be any restriction in either originating or
adopting ideas and methods of practice, however much they may be at
variance with commonly-received opinions; but a physician who
appreciates his obligation to his patients will hardly feel willing
that they should be made subjects for testing pathological and
therapeutical novelties in behalf of which his own belief is not
committed.

{431} Dietetic and Regiminal Treatment.--The dietetic treatment
resolves itself into a few simple principles. It may be assumed that as
much assimilation of aliment as is possible is desirable. No one
probably will contend for the propriety of any restriction of diet with
a view to limiting the amount of the nutritive constituents of the
blood. The difficulty in this part of the treatment lies in the
impairment or loss of appetite and in lack of digestive or assimilative
ability. It is useless to consider whether such or such articles of
food are suitable or not for phthisical patients. All wholesome
articles which can be taken with any relish and digested are suitable.
Nothing could be more ill advised than to direct kinds of nutriment
which a patient does not like, and to enjoin avoidance of those which
the patient's appetite would dictate. Pains should be taken to
ascertain the articles of diet most acceptable or against which there
is the least repugnance, and to excite the appetite by variety and
culinary attractions. It is important not to judge too hastily of the
ability to digest the food which can be ingested. The evidences of
indigestion are nausea, vomiting, flatulence, acidity, and diarrhoea:
whenever these symptoms are wanting it is fair to assume digestive
ability. Nor should evidence of indigestion deter at once from
continuing articles which appear to have occasioned it. The processes
of digestion are so apt to be disturbed by extrinsic accidental
circumstances that a meal which will occasion indigestion to-day may
not do so to-morrow. In short, so far as regulation of the diet is
concerned the patient is to be encouraged to take all kinds of
wholesome food according to appetite and taste, giving to each and all
a fair trial as regards digestibility. Fully aware that these views may
not commend themselves to the approval of many who think that the diet
should be regulated on scientific principles rather than by the
instincts of the patient, I do not any the less adhere to them,
believing that they are based on experience and common sense. As
regards the liability, where the instincts are followed, to the
over-ingestion of food and to the ingestion of food indigestible from
its quality or modes of preparation, it is far better to incur whatever
inconvenience may therefrom arise than the evils of inadequate
nourishment. In short, the dietetic instructions to a phthisical
patient may be summed up as follows: Eat of wholesome articles of food
whatever the appetite may dictate; endeavor to maintain and develop
appetite and relish for food by the excitement of variety in kind and
in preparation; eat whenever hungry; satisfy the appetite; eat without
any expectation of harm; do not hastily attribute an indigestion to any
particular articles of diet; incur the risk of over-feeding rather than
of the greater evil of under-feeding.

Anorexia in a degree which I have characterized as invincible--that is,
an almost complete inability to take food--is one of the most
discouraging of symptoms in cases of phthisis. Of course if the symptom
continue the duration of life is simply a question of time and
tolerance. Milk is an invaluable form of food when appetite is
completely lost. The advantage sometimes of substituting for simple
cow's milk buttermilk, koumiss, or milk made sour by fermentation with
yeast is due wholly to these being taken more readily and more easily
digested. The same is true of the substitution for the milk of the cow
that of other animals--the goat, the ass, and the mare. Eggs may be
given in a liquid form with milk or other fluids. Very little reliance
is to be placed on the various meat-extracts (Liebig's, Valentine's,
and others) as representing any considerable amount of nutriment. Meats
artificially digested--that is, in the form of peptones, as in Leube's
meat solution--form a valuable addition to beef-tea. Rectal
alimentation may be resorted to. A. H. Smith has reported marked
benefit from defibrinated blood as a form of rectal diet.[29] A French
writer, Debove, has lately reported notable benefit from forced
alimentation, food being injected through a tube introduced into {432}
the stomach.[30] If in any way food can be introduced, in spite of the
anorexia, and assimilated, there may be room to hope that a return of
appetite will be among the beneficial effects. Cod-liver oil and
alcoholics will be considered in connection with the medicinal
treatment.

[Footnote 29: Vide _N.Y. Med. Record_, 1881, No. xix.]

[Footnote 30: Vide _Bullétin générale Report_, Paris, 1881. Another
French writer more recently in the same journal, Desnos, has pointed
out a source of danger in forced alimentation--namely, the occurrence
of violent acts of vomiting, during which portions of food ejected from
the stomach are inhaled. The danger is from asphyxia and pneumonic
inflammation excited by the presence of particles of food within the
smaller bronchi. In order to avoid this source of danger, food should
be introduced slowly and not in too large a quantity at a time.
Intolerance of the presence of the tube within the stomach is an
obstacle which may be overcome by use, but in some cases it is
insuperable (vide article in _Philadelphia Med. Times_, March, 1882).]

The regiminal treatment embraces changes relating to out-of-door life,
exercise, occupation, clothing, etc.

Of all the changes in this category, those relating to out-of-door life
and exercise are of greatest importance. In-door life and sedentary
habits, if not factors in an acquired cachexia, undoubtedly favor it.
This is shown by the place which these hold in the etiology and by
their agency in the arrest of the disease. With respect to the latter
point, the result of my analysis of recorded cases has much
significance. In 44 cases change of habits from those more or less
sedentary and confining within doors to those involving out-of-door
life and activity entered into the treatment. In all but 4 of these
cases the hygienic treatment consisted chiefly or exclusively of the
change of habits mentioned. Of the 4 excepted cases, in 1 the patient
passed several months in Europe; in 1 the patient passed a summer in
Minnesota; in 1 the patient made several voyages to Europe; and in 1
the patient travelled in Europe. Of these 44 cases, 15 are in the list
of cases of unknown duration and termination. Deducting these, the
remaining number is 29. Now, of these 29 cases, 11 are in the list of
cases ending in recovery; 7 are in the list of cases in which the
disease was arrested or became non-progressive; and 3 are in the list
of cases of slowly-progressive phthisis. Thus, only 8 out of the 29
cases were not included among those in which the course of the disease
was favorable in the three aspects just named, and in more than
one-third of the cases recovery took place. Of the 8 fatal cases, in
all save 1 case the change of habits appeared to be beneficial. The
benefit was marked in 2 of the cases, there being in 1 of them no
evidence of progress of the disease for several months.[31] Moreover,
the majority of the histories of the 15 cases of uncertain duration and
termination show more or less improvement. In 7 of the 11 cases ending
in recovery the change in habits constituted all the treatment. Making
the fullest allowances for an intrinsic tendency in the disease to end
in recovery, and in some instances purely from self-limitation, the
foregoing facts afford ample proof that changes of habits from those
more or less sedentary and confining within doors to those involving
out-of-door life and activity have considerable agency in the arrest of
phthisis and exert a favorable influence upon the disease when it is
not arrested. There is reason to believe that the favorable influence
is greater than any other class of hygienic measures, and it is
probable that to this source much of the benefit derived from change of
climate is to be referred.

[Footnote 31: For details of the changes of habits in these cases vide
_Phthisis, in a Series of Clinical Studies_.]

The particular changes to be made in order to secure as much
out-of-door life as practicable with a certain amount of exercise must
of course vary in different cases. Clerks, school-teachers, mechanics
whose business requires in-door life, etc., should, if possible, adopt
some other occupation securing the desired objects. Students,
clergymen, and men of leisure should systematically devote a fair
proportion of time to exercise in the open air, and as far as {433}
practicable the exercise should involve recreation. It is needless to
say that the importance of change is as applicable to women as to men.
Caution is sometimes necessary not to carry muscular exercise to an
injurious extreme. If carried to the extent of producing great fatigue
or exhaustion, it is debilitating instead of invigorating. Exercise
within doors, although much less useful than when taken in the open
air, is nevertheless useful. Gymnastic exercises may be recommended
when other measures which are to be preferred are not available. They
are inferior to rowing, horseback riding, hunting, etc. An increased
expansion of the chest is apparently a desirable effect of exercise.
Forced efforts of expiration to overcome a mechanical resistance, the
lungs being fully inflated, constituted a method of treatment formerly
in vogue, and I have met with instances in which it seemed to have been
useful. In taking exercise patients are apt to imagine that in order to
avoid catching cold they should go out of doors only when the weather
is in all respects favorable. Precautions in this regard are often
carried so far as to interfere materially with the amount of life in
the open air which is desirable. It should be understood that
phthisical patients are no more--and perhaps less--liable to catch cold
than persons in health, and that a cold, as a rule, does not affect the
progress of the tuberculous disease. These excessive precautions have
arisen from the error of considering phthisis as a sequel of
bronchitis. There is no ground for the great scrupulousness with which
phthisical patients avoid the night air, although out-of-door life in
the daytime is to be preferred.

Every practitioner has known of cases in which some remarkable changes
of habits as regards out-of-door life and exercise have led to
recovery, such as performing long journeys on horseback or on foot,
accompanying expeditions which involved camping in the open air with
hardships, etc. Several instances of this kind have come within my
knowledge. In one of these the patient, a young physician who consulted
me, on being told that he had incipient phthisis gave up his practice
and joined a tribe of Indians in the Far West. He remained with them
for more than a year, adopting all their customs, and returned in
vigorous health. But in order to rough it a patient need not go to a
distance from home and friends. This fact is lost sight of when
physicians sanction the exposures and hardships of travel without the
limits of civilization, but enjoin upon patients great care in taking
exercise out-of-doors so long as they remain in their places of
residence.

All who have had the opportunity of observing the effect of sea-voyages
in cases of phthisis are agreed as to their utility. A long sea-voyage
or a series of voyages entered prominently into the treatment of 20 of
the cases which I have analyzed. In a large proportion of these cases
the favorable influence was marked. This is an accessory circumstance
which contributes to the benefit in many cases derived from a change of
climate. It is evident that a certain proportion only of phthisical
patients can avail themselves of this measure. It is to be advised
especially for those who can leave home and business without anxiety,
who are fond of ocean-life, and who as a matter of course are good
sailors.

The supposed liability to, and danger of, catching cold often leads
phthisical patients to wear an overplus of clothing. When they strip
for an examination of the chest not infrequently they remove two or
three undershirts, a woollen or fur chest-protector, and sometimes in
addition an oiled-silk jacket. The body is kept in constant
perspiration by these articles. They occasion not only discomfort, but
debility. A single word expresses the governing principle in
clothing--namely, comfort. Articles of dress should be so adapted to
the seasons and to changes of temperature as to secure comfort. This
maxim applies to persons affected with phthisis as well as to those in
health. In some instances, from an erroneous theoretical notion,
patients {434} make themselves uncomfortable in an opposite way. They
dispense with woollen or silk underwear throughout cold seasons with
the idea that the system is thereby hardened. A good non-conductor of
heat next to the surface protects against changes of temperature and
promotes the functions of the skin. Attention to the sense of comfort
will enable the patient to avoid error in this direction as well as an
overplus of clothing.

Other regiminal observances relate to ventilation and the sponge bath.
The apartment in which the patient is expected to pass at least
one-third of the twenty-four hours should be sufficiently large and
well ventilated. Fresh, cool air in abundance is not deleterious, as it
would seem to be regarded when the utmost care is taken to exclude it.
It is essential to healthful sleep and invigoration. Here, again, the
supposed danger of catching cold antagonizes hygienic treatment. Air
should have free access to sleeping apartments in cases of disease as
in health. As a measure for invigoration the sponge bath is often
useful in cases of phthisis. The water used may be cool or tepid
according to the sensations of the patient and the effect. It should be
followed by a glow with a feeling of invigoration. The water may with
advantage be made stimulating by the addition of salt or of alcohol.

Medicinal Treatment.--The medicinal treatment in cases of phthisis
embraces no known remedies having a special influence over the disease;
in other words, no drug has as yet been found to be an antidote to the
tuberculous cachexia. Nevertheless, medicines in many cases form an
important part of the treatment. They have for their objects
improvement of appetite, digestion, assimilation, and nutrition, relief
from complications or associated affections, and the palliation of
symptoms.

Cod-liver oil is considered in this article, as is customary, in
connection with the medicinal treatment. It has, however, little or no
claim to be regarded as a medicine. It is a nutrient. It is a form of
fat which patients often digest readily, and which evidently increases
the weight of the body. That it does more than simply increase the
amount of fat in the body is shown by the fact that frequently under
its use the appetite, the digestion, the condition of the blood, and
the nutrition of the tissues manifest improvement. These effects are
not inconsistent with the statement that it is simply an article of
diet. Although the claims in its behalf as a special remedy which were
made forty years ago have long since been disproved, clinical
experience has continued to furnish proof of its usefulness in the
treatment of cases of phthisis. It should enter into the treatment
wherever it is well tolerated and digested. If it occasion nausea or
diminish the appetite or give rise to eructations, its use should not
be persisted in. In the choice among the different varieties of the oil
experience in each case is to be the guide. Some patients find the
brown varieties more acceptable than the pale, and vice versâ. I have
known in several instances the unrefined, coarse oil obtained at the
fish-markets to be preferred. Patients should not give up this part of
the treatment until the different varieties have been tried. The
popular preparations in which the oil is combined with salts of lime or
with some flavoring extract are sometimes tolerated by those who are,
or who fancy that they are, unable to tolerate the pure oil. They have
probably no advantage for those who are able or who are willing to take
the pure oil. The oil should never be given in doses larger than are
readily digested, and, following this rule, the doses will rarely
exceed half an ounce. They are best given shortly after meals. It is a
popular notion that the oil should not be continued in hot weather. The
weather should have no influence on its continuance, provided it be
well tolerated and digested. The addition of fifteen minims of ether to
a half-ounce dose of the oil has been found to promote its digestion,
and by means of this addition persons with whom the oil disagrees may
be able to take it without difficulty. The ether is to be given {435}
half an hour after the oil has been taken.[32] Salad oil, cream,
butter, and the extracts of malt may be made to supply, in a measure,
the place of the cod-liver oil in the cases in which the latter is not
tolerated.

[Footnote 32: Vide report by Dr. Andrew H. Smith, chairman of Committee
on Restoratives of the New York Therapeutical Society in the _N.Y.
Medical Journal_, April 20, 1879.]

Embracing the varieties of spirits, wine, and malt liquors under the
name alcoholics, these are to be regarded as alimentary, but also as
medicines. That they are useful in certain cases of phthisis is as well
established on the basis of clinical experience as any fact in
practical medicine. Their usefulness in this disease, as well as in
other diseases, is to be considered irrespective of questions relating
to their use and abuse in health. But as bearing on the very important
subject of intemperance it may be stated that, administered purely as
remedies in cases of phthisis, patients do not become so addicted to
them as to make it difficult to relinquish their use whenever this is
advisable. This statement is based on a large experience.

Alcoholics are useful in some and not so in other cases. The question
as to their usefulness is to be decided in each case by trial. If they
produce a sense of comfort without any excitation of the circulation or
of the nervous system, they are likely to be useful. If in lieu of a
cordial effect they occasion flushing, weariness, or indisposition to
exertion or discomfort of any kind, they are not likely to be useful.
The quantity to be given is to be regulated by the immediate effects.
There is sometimes a notably increased tolerance of alcohol. This is to
be ascertained by experimental observation. The quantity of alcohol
given should never occasion the least approach to alcoholic
intoxication. It should be given at or near the times of taking food,
or in combination with food, as in milk-punch or egg-nog.

As to the choice of an alcoholic, this is to be determined by the past
and present experience in each case. Each of the many varieties of
spirits, malt liquors, and wines is best suited to some cases and not
to other cases. There is no rule of choice applicable to all patients.
Changes in the form of alcoholics from time to time are often advisable
in the same case. In the majority of cases some forms of spirits will
be found best to agree. Malt liquors, either the strong or mild
varieties, agree best in some cases. Of wine, some patients take with
most comfort the light and some the stronger varieties. The effect upon
the pulse, respiration, and other symptoms should be observed with
reference to the employment of any of the alcoholics, and of the
particular ones best suited in individual cases, but much reliance must
be placed on the subjective symptoms. It has been proposed to
substitute pure alcohol for any and all the alcoholics used as
beverages, in order to give to the treatment more distinctly a
medicinal character and to avoid risk of the formation of a habit which
may lead to intemperance. Since, however, of the many varieties of
alcoholics, some agree in certain cases and not in other cases, it is
doubtful whether alcohol is able to take the place of all. This is a
point to be decided by clinical observation.

Phosphorus in the form of the hypophosphite of soda and of lime was
recommended about forty years ago on the theoretical ground that it
favored cell-formation and retarded the rapid waste of the tissues.
More recently it has been supposed to have a specific influence over
tuberculous disease. It has been employed pretty largely in different
countries, but without effects sustaining the claim of having a
specific action. It seems to be useful, and many physicians attach
considerable importance to its use.

The preparations of iodine, from their evident utility in certain
scrofulous affections, and in view of the identity of scrofula and
tuberculous affections, have heretofore entered largely into the
treatment of cases of phthisis. From the fact that they are now but
little employed in phthisical cases it may be {436} inferred that in
this instance, as in many other instances, theoretical considerations
have failed to find support from clinical experience.

Of arsenic it can be said that many able observers have borne testimony
to its great usefulness in some cases, as manifested by improvement in
appetite, nutrition, and in the powers of life generally, together with
the cough and expectoration. Here, as in other instances in which it is
desirable to continue the remedy for a considerable period, the doses
should be small and not increased. Noël Guéneau de Mussey testifies to
a remarkable efficiency in some cases of the mineral water of Bourbole,
either exported or taken at the spring.

Sulphur, especially as contained in the Sulphur Springs water, has long
been considered a useful remedy in phthisis as in other chronic
diseases. The Sulphur Springs of our country, however, although much
resorted to for other diseases, have not in phthisical cases with us
the celebrity which those in Europe (of which Des Eaux Bonnes are a
famous type) have with European physicians.

The symptomatic indications for medicinal treatment in cases of
phthisis are many and varied. Among the most important are those
relating to appetite and digestion. For the improvement of these
functions the preparations of cinchona, salicin, gentian, quassia, and
other of the vegetable bitter tonics, including nux vomica, may be
selected, according to the choice of the physician, or given in
succession. They have more or less efficiency in conjunction with the
more potential hygienic measures considered in connection with the
climatic, the dietetic, and the regiminal treatment. Pepsin and dilute
hydrochloric acid, taken after a meal, promote its digestion, their
medicinal action being, however, limited to the meal in connection with
which they are administered. The tincture of the hydrochlorate of iron
and other ferruginous tonics which are much used in cases of dyspepsia
and indigestion are useful in cases of phthisis. The anæmia which
exists so constantly in phthisical cases is an indication for their
use, and there does not seem to be ground for the conjecture which has
been entertained that they promote the occurrence of bronchial
hemorrhage. If they had this effect it would not disprove their
utility.

Pulmonary symptoms which may furnish therapeutic indications are cough
and expectoration, hæmoptysis, pain in the chest, and dyspnoea. Cough
is of course necessary for the removal of the morbid products within
the bronchial tubes and cavities. If the act of coughing be accompanied
by expectoration, palliation is not required. But often there is what
may be called a superfluous cough--that is, not accompanied by
expectoration. This superfluous cough may be frequent, and occur in
violent paroxysms which occasion fatigue and exhaustion. Frequently the
cough prevents sleep. Palliative remedies are then indicated. It is
desirable, if possible, to palliate cough with remedies which do not
contain an opiate, owing to the impairment of appetite and digestion
caused by the latter. Simple remedies, such as the balsam of tolu, the
syrup of wild-cherry bark, Turlington's balsam, etc., may suffice. If
not, other narcotics than opium should be tried--namely, hyoscyamus,
lactucarium, and belladonna. Fothergill recommends hydrobromic acid and
the spirits of chloroform. The addition, however, of some form of
opiate is often required. The paregoric elixir is the simplest form,
and therefore the best if it suffice. Of other forms, perhaps codeia is
in general to be preferred. Patients should be enjoined not to prolong
voluntarily ineffectual coughing efforts. The disposition to cough may
in a considerable degree be controlled by the will until the morbid
products are in a situation to be readily expectorated. The stimulant
expectorants and those which act by causing nausea are not indicated in
cases of phthisis, and are objectionable in so far as they impair
appetite and digestion. Stimulating medicinal {437} inhalations are of
doubtful propriety, but a superfluous cough is sometimes relieved by
breathing some vapor, a little laudanum or paregoric elixir having been
added to the water vaporized. The continuous breathing of an atmosphere
charged with carbolic acid, either by diffusing it in an apartment or
the use of a respirator, is advisable if there be fetor of the
expectoration.

It has been seen that bronchial hemorrhage is not, as a rule, an
unfavorable event in cases of phthisis. It does not follow from this
fact that the loss of blood is desirable, and therefore that the
hemorrhage should not be arrested. Moreover, the loss of blood in some
instances involves immediate danger. A first attack of hæmoptysis
occasions great alarm and anxiety. The prostration which appears is a
moral effect rather than the exhaustion caused by the loss of blood. In
repeated instances after attacks of hæmoptysis have several times
recurred, I have known patients to keep about as usual during an
attack, giving little or no heed to it.

The internal remedies which may be employed for the arrest of
hemorrhage are: Ergot or ergotin, acetate of lead, tannic or gallic
acid, and the astringent preparations of iron. Ergotin has been given
with good effect by subcutaneous injection, from five to ten grains in
water, with or without glycerin, being injected and repeated pro re
nata. Opium in some form should be conjoined in order to allay nervous
excitement. A teaspoonful of table-salt taken into the mouth and
repeated after intervals of a few moments is a well-known remedy during
the hemorrhage. The hemorrhage is sometimes so profuse and rapid that
much blood is swallowed, and may be afterward vomited. Under these
circumstances, and whenever the persistence of the hæmoptysis calls for
more prompt measures, cold may be applied to the part of the chest
which corresponds to the seat of the hemorrhage. This may be found by
means of a localized subcrepitant râle. Another measure is the
inhalation of a vaporized solution of the liquid persulphate of iron.
Still another and more potential measure is the temporary ligation of
one or more of the members of the body, the pressure being sufficient
to interrupt the flow of blood in the veins and not in the arteries.
This measure must be resorted to and continued only when the physician
is present. The effect is sometimes almost magical. The measure is a
substitute for venesection, which was formerly employed for the arrest
of bronchial hemorrhage. Cavernous hemorrhage, occurring usually late
in the disease, if profuse calls for prompt measures, and the topical
employment of cold will be likely to be the most promptly effective.

Pain in the chest denotes either pleurisy or intercostal neuralgia.
Mild counter-irritant applications by sinapisms or stimulating
liniments, with anodynes graduated to the degree of pain, are
indicated. Dyspnoea, if not caused by restrained movements of the chest
from pain, or by pleuritic effusion, or by an intercurrent pneumonia,
may denote either rapidity and extent of the tuberculous deposit or an
accumulation of morbid products within the bronchial tubes: if the
latter be the explanation, acts of expectoration are to be promoted.
This is not easily done if the difficulty of expectoration proceed from
great general debility. The ethereal stimulants, Hoffmann's anodyne,
chloric ether, and the compound spirits of lavender are advisable under
these circumstances as palliatives.

Pyrexia and increased frequency of the heart's action are symptoms
indicative of an active tuberculous cachexia. How far these are purely
symptomatic, and how far they may conduce to the progress of the
disease, cannot be determined with our present knowledge. It may be
assumed that they represent something more than is represented
generally by the fever which is secondary to a local inflammation. That
the febrile temperature is itself causative of changes in the tissues,
as well as in the functions of the body, is probable; and the muscular
power of the heart must be weakened by the {438} persistent frequency
of its action. A rational object in therapeutics is either the removal
or the neutralization of the morbid conditions on which the pyrexia and
the increased frequency of the heart's action depend. The means of
effecting this object are to be determined in the future, when more is
known of the morbid conditions giving rise to pyrexia; meanwhile, there
are certain medicines which, as experience shows, diminish the
temperature, and febrile temperature can be reduced by external means
which abstract heat from the body.

At the present time data are wanting for determining the importance of
antipyretic treatment in cases of phthisis. Hyperpyrexia, however, may
be considered as furnishing an indication for a trial of antipyretic
medication, and the most reliable of the drugs employed for that
purpose is quinia. It should be given for this object in full doses, as
in other instances in which it is given for an antipyretic effect.
These doses should not be continued long enough to disorder the
stomach. Diurnal exacerbations of fever, especially if ushered in by a
chill, may sometimes be arrested, or, if not arrested, materially
modified, by full doses of quinia, although there may be no ground for
the suspicion of malaria.

When the skin is hot and dry, with a high axillary temperature,
sponging the body may be employed and continued until the pyrexia is
diminished. I am not prepared to say whether the cold bath or the wet
sheet is admissible or allowable. As having some antipyretic effect,
and as diminishing the frequency of the heart's action, digitalis might
be expected to prove a valuable remedy to fulfil the symptomatic
indications under consideration. This drug was formerly much employed
in cases of phthisis. The fact that it has in a great measure fallen
into disuse may be taken as evidence that the theoretical
recommendations are not sustained by clinical experience. The liability
to disturbance of the stomach from its use is perhaps a sufficient
reason for considering it inapplicable.

The profuse night-sweating which so often occurs in the course of
phthisis claims treatment. Belladonna or atropia, the oxide or sulphate
of zinc, gallic acid, the acetate of lead, and aromatic sulphuric acid
are internal remedies for the palliation of this symptom. Sponging the
surface before bedtime with diluted alcohol, diluted acetic acid, or
with spirit in which alum is dissolved should be tried. Hot vinegar
largely charged with capsicum has been found to be an efficient
application. The covering at night should be as light as is consistent
with comfort. Brunton has found strychnine and nux vomica, given at
bedtime, useful. Another remedy, recommended by Murrell, is picrotoxin.
This is given in the form of a solution (1 part to 240 parts water),
the doses of from one to four minims daily, the last dose given late at
night.[33] Agaricus, or the common toadstool, is recommended as an
efficient remedy by Wolfenden of London and J. M. Young of Glasgow.
From ten to twenty grains may be given in the form of an electuary with
honey, or it may be given in the form of a tincture. In both these
modes it is apt to cause nausea. This objection does not apply to the
isolated medicinal principle, a crystallized substance which it is
proposed to designate agaracine. Of this one-twelfth of a grain is a
dose, which may be repeated if required. Young is of the opinion that
it is not less effective than atropia as an antihydrotic remedy, and
not open to the same degree of danger from an overdose as the latter.
He has found it to act also as a soporific remedy, to relieve cough,
and to diminish the temperature of the body.[34] A popular remedy is
cold sage tea taken at bedtime.

[Footnote 33: Vide _Supplement to Ziemssen's Cyclopædia_, 1881, p.
325.]

[Footnote 34: _Glasgow Medical Journal_, March, 1882.]

Of complications and associated diseases, one of the most frequent is
disease of the intestine. Of diarrhoea not thus connected the treatment
is that {439} of indigestion. As incident to tuberculous ulcerations
opium and astringents are indicated. Full doses of the carbonate of
bismuth, with a salt of morphia, will often prove an efficient
palliative. Peritonitis, acute and chronic, pleurisy with effusion,
chronic laryngitis, pneumo-hydrothorax, and cerebral meningitis are to
be treated according to indications which are considered in the
articles treating of these affections, making of course proper
allowances for their occurrence as secondary to the phthisical disease.
Intermittent fever associated with phthisis should be arrested as
promptly as possible. There is no foundation for the opinion which some
have held that malaria retards the progress of tuberculous disease.
Clinical facts show directly the reverse. If a perineal fistula occurs
in a phthisical patient, the safest policy is not to interfere with it
except so far as to make it as endurable as practicable. The idea that
a fistula has a salutary effect by way of revulsion has been one of the
reasons for making artificially an issue in the arm or elsewhere. This
was formerly much in vogue, but it has mostly, and probably deservedly,
fallen into disuse.

Medical opinion is sometimes asked concerning the propriety of marriage
with a phthisical man or woman. As an abstract question there need be
no hesitation as to the answer. If men went about deliberately
selecting wives, or vice versâ--as, for example, horses are
selected--there could be no doubt that phthisis should be considered a
disqualification. Husbands and wives, however, are not mated in such a
way. A marriage engagement has been entered into, and afterward one of
the parties becomes phthisical. The friends of the non-phthisical
party, not the parties themselves, come for advice, and the adviser is
sometimes placed in an awkward situation. With respect to the effect of
marriage on the tuberculous party, my analysis of 17 cases, 2 only
being women, did not show that it was unfavorable. Were it unfavorable,
considerations of sentiment and sense of duty generally outweigh all
others. A more important point relates to offspring. A hereditary
tendency is entailed in some, but not in all cases. The risk incurred
in this point of view having been fairly stated, the responsibility of
the medical adviser is ended.

After recovery from phthisis measures for the prevention of a relapse
should receive due attention. The hygienic influences which were
brought to bear on the disease, and which, as it is fair to conclude,
had more or less agency in effecting the recovery, are as far as
practicable to remain in operation. This important injunction applies
alike to cases in which an arrest of the disease has taken place, so
long as it ceases to be progressive. To prevent a renewal of its
progress is an object having a similar importance as the prevention of
a relapse after recovery.

In concluding the consideration of the treatment of pulmonary phthisis
reference is to be made to a measure to which one of our countrymen has
recently given much attention--namely, the injection of tuberculous
cavities. More than thirty years ago the late Brainerd of Chicago
related to me a case in which he made an opening through the chest-wall
into a tuberculous cavity. He had the idea that cavities might in this
way be treated by local applications with advantage. Of the result in
that case it is only recollected that no bad consequences followed.
Probably Brainerd did not prosecute further experimental observations,
as I am not aware of any publication by him on the subject. In 1873,
Mosler of Germany advocated making a free opening in tuberculous
cavities with a view to drainage and topical treatment. He reported 3
cases in which a drainage-tube was introduced and kept in the cavity.
The practicability of the operation and the absence of any evil result
were shown by his cases. The operation had been advocated and performed
prior to Mosler's publication, but without exciting consideration. To
William Pepper belongs the credit of injecting medicated liquids by
means {440} of a small syringe and hollow needles. Pepper has reported
12 cases in which cavities were thus injected. In these 12 cases two
hundred and ten injections were made. In no instance did any harm
result therefrom. The injected liquid in most of the cases was a very
weak solution of iodine. In some instances a weak solution of carbolic
acid was used. The objects are "the disinfection of the cavities, the
relief of cough, the diminution of secretion, and the modification of
the morbid action of the lining surface of the cavity, so as to favor
cicatrization and contraction and the prevention of infection of the
constitution." The results of the treatment in the cases reported by
Pepper go to show that it may contribute to these objects. His
observations have opened up a new and important department in the
therapeutics of pulmonary phthisis.[35]

[Footnote 35: For reports of Pepper's cases and other details vide
article in the _Transactions of the American Medical Association_, vol.
xxxi., 1880; also article in the _American Journal of Medical
Sciences_, October, 1874.]


Fibroid Phthisis, Chronic Interstitial Pneumonia, Cirrhosis of Lung.

The characteristic anatomical feature of this variety of phthisis is
the predominant growth of the pulmonary connective tissue. If, as is
generally held, this hyperplasia be due to a chronic inflammatory
process, the name chronic interstitial pneumonia is not inappropriate.
From an analogy to the structural affection of the liver characterized
by an abnormal development of Glisson's capsule, the affection was
called by Corrigan cirrhosis of the lung. The propriety of regarding it
as a distinct form of pulmonary phthisis is based on points pertaining
to the morbid anatomy and to the clinical history.

An abnormal interstitial growth enters more or less largely as an
element into the morbid anatomy in cases of the ordinary form of
phthisis. It is the chief element in typical cases of fibroid phthisis.
The affected lung-structure is condensed and indurated, owing to
obliteration of alveoli and bronchial tubes. The affection leads to
notable diminution in volume. Resulting therefrom is a compensatory
dilatation of bronchial tubes. Sacculated dilatations may reach the
size of an English walnut or even a hen's egg. These are known as
bronchiectasic cavities. The pleura is thickened and the opposed
surfaces closely adherent to each other. With these distinctive changes
are usually found small cheesy tuberculous deposits or true tuberculous
cavities and miliary tubercles. The latter anatomical points show
relationship to the ordinary form of phthisis. Exceptional cases are
those in which the interstitial pneumonia is the result purely of the
local action of inhaled irritating particles (vide PNEUMONOKONIOSIS).
In these cases the tuberculous characteristics may be wanting. In cases
of fibroid phthisis both lungs are often affected. But the affection is
apt to be confined to, or much more extensive in, one lung, so that
during life it either is, or appears to be, unilateral. Exceptionally,
both lungs are extensively affected. It may originate in and be limited
to a lower lobe. It is stated by Trojanowsky that when the affection is
unilateral it oftener begins in the upper lobe, and when bilateral the
lower lobes are first affected. A series of bronchiectasic dilatations
may be so closely situated as to resemble an anfractuous cavity
resulting from the discharge of liquefied tuberculous deposits.

It is customary to consider this affection as occurring consecutively
to acute lobar and broncho-pneumonia, to chronic bronchitis, and to
pleurisy. Taking into view, however, the slow, insidious development of
the affection, the infrequency of its occurrence, and the frequency of
the diseases just named, a more rational conclusion perhaps is that
when these diseases are associated {441} with the phthisical affection
they are secondary to it. The affection occurs oftener after than
during the decade in which the ordinary form of phthisis is most apt to
occur--that is, after thirty years of age.

The course of the affection as regards activity of progress is
strikingly different from that of ordinary phthisis in a large
proportion of cases. Commencing imperceptibly, after it has advanced to
a certain extent it may remain apparently stationary, or it progresses
very slowly during a long period. Its duration may extend over many
years. In a case for a long time under my observation it existed
probably for forty years. If the lesions be not extensive enough to
interfere notably with the respiratory function, it may be tolerated
indefinitely. The appetite, digestion, and nutrition may be well
maintained. The muscular strength may not be much impaired. The
circulation, temperature of the body, and other functions may be but
little disturbed. A fatal termination, if not caused by some
intercurrent disease, takes place after a very gradually progressive
general debility and exhaustion.

As regards the different anatomical systems of the body other than the
respiratory system, it is not important to add to the foregoing sketch
details of symptomatology. The important symptoms referable to the
respiratory system relate to cough, expectoration, and disturbance of
respiration. The cough varies according to the quantity and character
of the matter to be expectorated, the difficulty of its expulsion, and
the susceptibility of the patient to the reflex influences on which
cough depends. The matter expectorated is muco-purulent, and in many
instances it is at times extremely fetid. This is due to the
putrescency of morbid products detained within the bronchiectasic
cavities and bronchial tubes, owing to difficulty in effecting their
expulsion. The fetor may be suggestive of gangrene. The matter
expectorated, however, if examined microscopically, will not be found
to contain the débris of pulmonary structure. There may be sloughing of
small portions of mucous membrane, but this is probably rare. The
expectoration after certain intervals of putrid sputa in considerable
or great abundance, the expectorated matter during the intervals having
the characters of muco-pus without fetor, is almost pathognomonic of
this variety of phthisis. The repeated occurrence of the putrid sputa,
the clinical history, and the physical signs render it easy to exclude
abscess of the lung. The detention of morbid products within
bronchiectasic cavities, and the consequent putrescent decomposition,
depend of course on the difficulty with which the contents of the
cavity are expelled. This difficulty is greater if the cavities be in
the lower than in the upper lobe. In a case which came under my
observation the affection had been known by the attending physician to
have existed for fifteen years. There was more or less habitual
expectoration of ordinary muco-purulent matter, but after intervals of
several days a considerable quantity of intolerably fetid matter was
expelled. In this case the physical signs showed the affection to be
limited to the lower lobe of the left lung. There was notable
retraction of the lower and lateral portions of the chest on this side;
solidification of lung was denoted by bronchial respiration and
bronchophony over the posterior aspect; and the cavernous respiration
was perceived over a circumscribed area in the latero-posterior aspect.
This patient's general condition of health was fair; he had not a
morbid aspect, and he was able to perform the duties of a clerkship in
one of the municipal departments.

The respirations are more or less increased in frequency, the increase,
other things being equal, being in proportion to the amount of damage
of the pulmonary organs, or, in other words, the extent to which the
respiratory function is compromised by the lesions. These may be
sufficient to give rise to much suffering from dyspnoea. This was true
of a case under my observation in which both lungs were extensively
affected, while the muscular {442} strength and the functions generally
of the body were not greatly impaired. The embarrassment of breathing
is increased by an accumulation of muco-pus within the bronchial tubes,
and notable relief follows expectoration of the accumulated products.
Hæmoptysis occurs in some cases, but much less frequently than in the
ordinary form of phthisis. The hemorrhage is sometimes profuse. It
proceeds from erosion of the walls of vessels or the bursting of small
aneurisms within bronchiectasic cavities.

Cyanosis is marked in some cases. This symptom is not always in
proportion to the dyspnoea; that is, the cyanotic appearance of the
prolabia and face may be present when the patient does not manifest
suffering from a sense of the want of breath. The cyanosis is
symptomatic of distension of the cavities of the right side of the
heart, this being an effect of the obstruction of the pulmonary
circulation. The obstruction may lead at length to dilatation of the
right ventricle and auricle. Thence arises the general dropsy which may
take place at an advanced period of the history of fibroid phthisis. A
tricuspid regurgitant murmur may be perceived with or before the
occurrence of dropsy; also visible pulsation of the cervical veins. A
frequent physical sign under these circumstances is bulbous enlargement
of the ends of the fingers and sometimes of the toes. The clubbed
fingers, as they are called, are symptomatic of disturbance of the
circulation. They are observed in some cases of disease of the heart,
phthisis not existing.

The physical conditions giving rise to physical signs are as follows:
Notable shrinkage of lung; solidification, which, if the lung be much
diminished in volume, may be considerable or complete in degree and
extensive; dilated tubes and bronchiectasic cavities varying in size,
number, and relative situations; the presence of muco-pus in more or
less abundance, the quantity variable at different times within the
bronchial tubes and cavities. Vicarious emphysema is more frequent than
in the ordinary form of phthisis.

In typical cases of extensive and advanced unilateral fibroid phthisis
the affected side is much contracted. The appearance is like that
presented in some cases after recovery from chronic pleurisy. The range
of respiratory movements is much diminished, the two sides presenting a
marked contrast in this regard. With this one-sided contraction of the
chest there may be lateral curvature of the spine, the concavity
looking toward the affected side. The supposition that the contraction
is in reality a sequel of chronic pleurisy is at once disproved by
finding the evidence of a degree of solidification notably greater than
would be incident to the mere diminution of the volume of the lung. If
the affection be limited to a lobe, either the upper or lower, there
may be contraction more or less marked over the portion of the chest
corresponding to the affected lobe. If the two lungs be much affected,
the evidence of contraction is apparent to the eye on both sides. It is
rarely if ever that the two lungs are equally affected.

The signs furnished by percussion and auscultation which represent
solidification of lung, the presence of air in dilated tubes or
bronchiectasic cavities and emphysematous lobules, are present either
separately or in various degrees of combination. Solidification from
induration without dilatation, sacculated or otherwise, of tubes, or if
these be filled with morbid products and without vicarious emphysema of
adjacent lobules, will give dulness on percussion more or less marked
and over an area corresponding to the degree and the extent of the
solidification. There may be flatness over the greater part or the
whole of an entire lobe. Often, however, dulness is found in some
situation, and either tympanitic or vesiculo-tympanitic resonance in
other situations. Over bronchiectasic dilatations a tympanitic
resonance may have the amphoric or the cracked-metal intonation. On
auscultation the respiration over a space more or less extensive or
within separate spaces of variable extent is either bronchial or
broncho-vesicular. With these respiratory signs {443} representing
solidification of lung are associated either bronchophony or increased
vocal resonance, and the corresponding whispering signs--namely,
whispering bronchophony and increased bronchial whisper. Over
bronchiectasic cavities, may be heard the cavernous respiration and
whisper. These signs of cavity may be combined with those of adjacent
solidification of lung, giving rise to the several varieties of
broncho-cavernous respiration. Coarse mucous or bubbling râles are of
frequent occurrence, and the accumulation of muco-pus within the
cavities may be represented by gurgling.

By means of the foregoing signs furnished by percussion and
auscultation the character of the lesions, their situation, their
extent, and the physical conditions as regards the presence of morbid
products within the air-cavities, are determinable. These lesions are
sometimes in striking contrast to the symptoms which represent the
general conditions of the patient--the pulse, temperature, emaciation,
etc. The symptoms and the physical signs may seem to conflict with each
other, owing to the remarkable tolerance of the disease in some cases.
To the physical changes which have been stated is to be added removal
of the heart from its normal situation. If the seat of the affection be
the left lung, its shrinkage may be such that the heart rises into the
infra-clavicular region, and the space within which it is in contact
with the chest-wall is larger than when the organ is in its normal
situation. The latter circumstance is to be borne in mind with
reference to the error of inferring therefrom enlargement of the heart.
Not only is the area of notable dulness on percussion over the heart
greater than in health, but the movements of the organ are remarkably
apparent to the eye and touch. If the right lung be affected, the heart
may be removed to the right of the sternum, the heart-sounds being
heard here with their maximum of intensity. In this abnormal situation
the presence of the heart may give rise to a notable dulness on
percussion, and its impulses may be both seen and felt.

The differentiation of fibroid phthisis from the ordinary forms of the
disease cannot be made with positiveness so long as the anatomical
changes are small or moderate in degree and extent. The chief
differential point is a greater degree of depression at the summit of
the chest than would be likely to occur at an early period if the
affection were of the ordinary form. If the affection begin at the base
of the chest, it is more likely to be the fibroid variety. In typical
cases, when the affection is unilateral and has led to notable
shrinkage of the entire lung, taking the physical signs in connection
with the evidence of tolerance afforded by the symptoms, it may be
differentiated with confidence. Age is to be taken into account in the
diagnosis; patients are rarely under forty. The expectoration from time
to time of fetid mucus has considerable diagnostic significance.

With reference to the diagnosis, it is to be considered that between
the ordinary form of phthisis and typical cases of fibroid phthisis
there is every degree of gradation as regards the combination of the
anatomical characters of both. There is no sharp line of demarcation
between the two varieties. In these intermediate cases to determine by
means of the symptoms and physical signs the relative proportion of
each variety is not practicable, nor is this a matter of much practical
importance. It may be added that the coexistence of chronic laryngitis
and of tuberculous disease of the intestine is proof against fibroid
phthisis. There is no possibility of the restoration of a lung affected
with fibroid phthisis to its normal condition; but the prognosis as
regards tolerance, arrest of progress or slowness of progress, and
consequently duration of life, is much better than in the ordinary form
of phthisis. On this account the diagnosis is of importance. The
prognosis is better the nearer the approach to the affection in typical
cases. Per contra, the prognosis is less favorable in proportion as the
changes characteristic of the disease in its ordinary form are
associated with those characterizing fibroid phthisis. If the affection
be {444} confined to a lower lobe, it may not extend beyond this limit,
and the persistence of solidification of the affected lobe may not be
incompatible with good general health. Of these facts the following
case is an illustration: Phoebe, aged five years, came under my
observation in 1864. There was at that time notable dulness on
percussion over the lower lobe of the left lung, with bronchial
respiration and bronchophony. She had cough and expectoration, but had
not been confined to the bed or house, and her general condition of
health was then fair. The treatment consisted of tonic remedies and
out-of-door life. I saw her repeatedly during the next two or three
years, the physical signs remaining the same, and the general health
fair. In 1869 she had chorea and was treated with Fowler's solution. I
did not see her again until October, 1871; she had then, and had never
been free from, some cough and expectoration, but her general health
had been maintained. The signs of the solidification of the lower lobe
of the left lung were then present, the upper lobe remaining
unaffected. In November, 1874, I noted that I had again seen her and
examined the chest. The dulness on percussion over the lower lobe of
the left lung continued; there was at this time absence of respiratory
sound over this lobe, but the vocal resonance was greater than on the
opposite side. The left side was considerably contracted. She had still
some cough and expectoration, and there was some deficiency of breath
on active exercise. Her aspect was healthful, and she was well
developed for her age (fifteen years). Menstruation was irregular. She
consulted me for this irregularity, not regarding herself as ill in
other respects. About six years afterward I met her in the street, and
she accosted me. Her appearance was healthful.[36]

[Footnote 36: This patient remains in fair health at the present time,
May, 1883, nearly twenty years after she first came under my
observation.]

The treatment in cases of fibroid phthisis differs in no essential
points from that in cases of the ordinary form of the disease. The
slowness of progress and the long duration show less activity of the
tuberculous cachexia. Nevertheless, the cachexia either exists or has
existed, and the measures relating thereto which have been considered
as belonging to the dietetic and regiminal treatment are alike
applicable to both varieties of phthisis. The circumstances which
render changes of climate admissible, if not advisable, are much
oftener present in the fibroid variety, and there is greater
probability of the disease being either arrested or retarded. Medicinal
treatment is to be employed with reference to therapeutic indications
alike in both varieties of the disease.

The treatment by inhalations to prevent putrefactive changes in the
contents of bronchial tubes and in cavities is oftener indicated by
fetid sputa in cases of fibroid phthisis. The continuous breathing of
the atmosphere of a room containing an antiseptic vapor requires the
patient to remain within doors. A more effective method is to make use
of a respirator inhaler. A portable and convenient instrument, worn
over the mouth like an ordinary respirator, has been devised by W.
Roberts and improved upon by H. Curschmann. In this instrument the air
which is breathed passes through layers of tow moistened with the
antiseptic liquid. The disinfecting agents which have been found
efficient are carbolic acid, creasote, oil of turpentine, a mixture of
the tincture of iodine and the compound tincture of benzoin and
thymol.[37]

[Footnote 37: Vide article by William Pepper in _Transactions of the
American Medical Association_, vol. xxxi., 1880.]


Prevention of Phthisis.

The number of deaths throughout the globe which are caused by pulmonary
phthisis vastly exceeds the number caused by any other disease. {445}
The etiology of pulmonary phthisis embraces largely causes which can be
removed. Hence the disease is to a great extent preventable. Are any
comments on these simple statements needed in order that the prevention
of phthisis may be regarded as among the most important of the subjects
belonging to preventive medicine?

It has been assumed that phthisis involves a predisposition which is in
most, and perhaps in all, cases innate. Putting aside all questions
relating to an acquired tuberculous diathesis, it may be assumed that
the development of the phthisical affection depends in many or perhaps
in most cases, more or less, and probably often in a great measure,
upon causes which promote the diathetic condition. Now, many of these
causes are removable, and if removed phthisis is prevented, and the
prevention of a disease which may properly be called a scourge of the
human family will be diminished.

Of removable causes may be mentioned humidity of the soil in places of
residence; living in small unventilated dwellings; confinement within
doors; breathing in close workshops or factories, and in overcrowded
rooms at night, an atmosphere deficient in oxygen and contaminated with
pulmonary and cutaneous emanations; working underground in mines from
which light as well as pure air is excluded; a deficiency of food
sufficiently wholesome and varied; impairment of the cutaneous
functions from uncleanliness; and want of a proper adaptation of
clothing to the climate or season. These are obvious violations of the
hygienic requirements for health. It is unnecessary to cite facts to
show to what extent these violations prevail in different countries.
They are causes which admit of removal, however difficult may be the
task. Connected with their removal are other considerations than the
prevention of phthisis. But confining the attention exclusively to the
latter object, how incalculable would be the saving of life and health
were these causes to be removed! Much has been done within the last
half century toward diminishing the mortality from phthisis by
advancement in pathological and therapeutical knowledge; how much more
remains to be done by preventive measures!

The prophylaxis against phthisis must date from birth. An infant should
not nurse a mother who is consumptive or whose milk is of poor quality.
Care is to be observed in the selection of wet-nurses. All the various
articles which are sold under the name of infants' food should be
discarded. Many of these are fraudulent; that is, they are not what
they purport to be. But admitting that, if properly prepared, they are
safe substitutes for milk and the simple farinaceous foods, there can
be no guarantee for their proper preparation; and the risk is too great
to rely upon articles which cannot be readily tested and for the
genuineness of which dependence must be placed on irresponsible
dealers.[38] There is need of much caution respecting the purity of
milk, especially in cities. Much harm is not infrequently done by
over-care in children's diet--that is, by denying articles which they
crave, and restricting them to those which they do not like. In this
matter the instincts are not to be set aside, especially in early life,
when perversions of appetite and taste have not been acquired. Not
infrequently from undue caution the quantity of food is restricted, and
children suffer from insufficient alimentation; this is more likely to
occur in our country among the wealthy than among the poorer classes.
Other prophylactic provisions pertaining to exercise, out-of-door life,
clothing, etc. need not here be considered.

[Footnote 38: Vide "Address by A. Jacobi on Infant Diet," _Transactions
of the New York State Medical Society_, 1882.]

In order to combat the various causes which have been named, knowledge
of hygienic laws must be diffused among all classes. There is a
lamentable lack of information and of interest as regards matters of
hygiene among the more intelligent classes. But it is not sufficient to
enlighten these: the {446} knowledge must be extended, as far as
practicable, to those who, in this point of view, are lower in the
scale. Many persons of wealth fall in this category. The causes which
are purely personal can be reached only by information diffused by
means of publications, lectures, and intercourse with medical men and
others. Here is a rich field for missionary labors. To overcome certain
of the causes, however, the intervention of legislative authority is
necessary. With reference thereto health boards, properly constituted
and invested with adequate powers, should be organized in States,
counties, and cities. In this way it is practicable by the prevention
of phthisis to lessen greatly the rate of mortality.

Protection against the communication of the disease requires to be
specially noticed. Occupying the same bed with phthisical patients and
sleeping in the same room, if the latter be not enjoined by the
dictates of humanity, are objectionable. They are to be objected to on
the score of unhygienic influences, physical and moral, irrespective of
the doctrine of a tuberculous contagium, and of course still more in
view of the probabilities in favor of this doctrine. Care should be
taken to exclude from the table the meat of tuberculous animals. In
addition to the purity of milk in other regards, it should be
ascertained that the supply is not from cows affected with tuberculous
disease. Obviously, this is especially of importance with reference to
infants who are bottle-fed and in childhood, when generally milk forms
a much larger proportion of the diet than in after years. The
ventilation of apartments occupied by phthisical patients should be
attended to with reference to the possibility of the disease being
communicated by the inhalation of particles of tubercle; and it may not
be a needless precaution to introduce a disinfectant into the vessels
which receive the matter expectorated.




{447}

SYPHILITIC DISEASE OF THE LUNG.

BY EDWARD T. BRUEN, M.D.


DEFINITION.--Lesions of the lungs with a syphilitic impress include
catarrhal inflammation of the bronchial mucous membranes, chronic
inflammatory new formations, which affect especially the connective
tissue, producing sclerosis or else gummatous growths.

HISTORY.--From the early part of the eighteenth century attempts have
been made to create a word-portraiture representing the peculiar
features of syphilitic pulmonary disease as a separate entity. It has
been defined histologically and clinically from simple and from fibroid
phthisis, or from cases of syphilis in which a damaged state of the
general health has fostered the development of phthisis. But the
question, Is there a peculiar microscopic and macroscopic anatomy, or a
special symptomatology by the aid of which the cause, seat, and
dissemination of pulmonary syphilis can be recognized? remains even now
but partially removed from the field of debate and conjecture, although
unquestionably the syphilitic poison bears intimate relation with
various pulmonary processes.

ETIOLOGY.--Predisposing and Exciting Causes.--Syphilis of the lungs is
a rare disease as compared with the forms of specific laryngitis, but
even here Leman asserts that there is an early simple catarrh of the
larynx indistinguishable from the specific catarrhs. Whistler, in
recording his observations upon 88 cases of the lesions found in
syphilis of the larynx, observes that catarrhal congestions in early
laryngeal syphilis simulate the same lesions from ordinary causes.
Schnitzler lays particular stress on the association of pulmonary
syphilis with affections of the larynx and a specific bronchitis which
may occur in the first two months after inoculation. Many other writers
on this subject assert that laryngeal and bronchial catarrh attend the
period of early skin eruptions, disappearing in consequence of an
antisyphilitic treatment.

The rarity of pulmonary syphilis has been further attested by the
observations of Greenfield, who states that out of 22 cases of visceral
syphilis, only 1 occurred in the lung and 4 in the larynx and trachea:
in these cases, while the dura mater and cerebral vessels were
extensively diseased, no trace of skin affection could be found.
Goodhart has collected from the post-mortem records in Guy's Hospital
during twenty-two years 189 cases of visceral syphilis, but in only 38
of these chronic lung disease occurred. Phthisis associated with
syphilis is usually a late secondary or tertiary process, which appears
from two to five years after the infection; in rare cases ten--even
twenty--years have been said to elapse before the supervention of
pulmonary trouble. Cases of phthisis associated with syphilis have,
however, been described as occurring within the first twelve months
after infection. Further investigation may establish these cases of
early pulmonary syphilis as attributable to violent systemic infection,
or their etiology may be involved in the deterioration of the general
health which sometimes occurs. Moreover, one {448} must remember that
simple phthisis may more readily be developed in the scrofulous
syphilitic, owing to the predisposition of such persons to catarrhal
forms of inflammation. In the progress of syphilis there is also a
tendency to catarrhal processes through anæmia and damaged general
health, which may predispose certain cases to an ordinary type of
phthisis. The origin of the new formation in both tubercular and
syphilitic phthisis is similar--viz. the arterial, lymphatic, and the
peribronchial sheaths, spreading thence to the interlobular connective
tissues. It is therefore not surprising that it has been difficult to
differentiate the tubercular from the specific forms of phthisis, and
Goodhart asserts that there is no histological difference between
syphilitic and tubercular phthisis, except that the former is more
vascular.

We may assume that true pulmonary tuberculosis may be associated with
syphilis, but preserves its own pathological characters; that, although
we are ignorant of the exact differential histological changes, there
is sufficient evidence to show that there is a distinct association
between syphilis and pulmonary disease; and that syphilitic phthisis is
commonly interstitial. Whether the relation be one of cause and effect,
or whether the process is simply a modification of ordinary tubercular
phthisis, it is impossible at present to determine. The final
adjustment of the theories concerning the specific etiology of
tubercular phthisis may throw further light upon the etiology of
syphilitic phthisis. That gummata may be found in the lungs is a
well-established fact, and by some authorities is not considered rare.

The discussion of the etiology has already indicated the relation of
the predisposing and exciting causes to pulmonary processes in
connection with syphilis. In certain cases of syphilis the antecedent
of pulmonary changes is a laryngeal or bronchial catarrh. The relation
which an active virus in the blood sustains to the process is still
subject to debate. Hutchinson writes as follows: "If the infected blood
were the cause of the local phenomena, it is almost certain that such
phenomena will be symmetrical, because the blood is equally supplied to
both sides; such is the case during the secondary stage. If, however,
the symptoms result from tissue-conditions, and the blood is at the
time of the outbreak free, then there is a considerable probability
that local influences may take a large share in evoking them, and they
will be asymmetrical--evoked by some local cause."

The existence of gummata, then, does not necessarily show that there is
any active virus in the blood, because their formation is sometimes
symmetrical, sometimes asymmetrical.

PATHOLOGY AND CLASSIFICATION.--The lesions of pulmonary syphilis may be
divided into four classes: _(a)_ early phthisis, associated with
principal interlobular proliferation; _(b)_ advanced syphilis, in which
gummatous or allied formation exists; _(c)_ simple phthisis, developing
in consequence of impaired general health induced by syphilis; _(d)_
inherited or congenital syphilis, occurring in infants.

_(a)_ The pathological process in the majority of cases in the adult is
interstitial new formation, very often evoked by antecedent catarrhal
inflammation. At first small spindle-shaped and round cells appear and
develop into connective tissue, among the fibres of which blood-vessels
are freely produced; the septa of the alveoli are thickened and the
alveoli themselves compressed. In any morbid process in the lungs, such
as tubercle, sarcoma, or cancer, the alveoli act as the
inter-fascicular spaces of the connective tissue. In the same manner in
syphilis the alveoli of the lungs are always in the later stages, and
sometimes primarily, more or less filled with small cells, which,
surrounded by the newly-formed connective-tissue fibrous framework,
gives the appearance of some of the forms of simple phthisis. The
smaller bronchi become narrowed, and perhaps occluded, by the pressure
of the new growth which develops along their lumen. Occlusion of the
bronchi may also be caused {449} by enlargement of the bronchial
glands, which is one of the incidents of the syphilitic pulmonary
process.

If we endeavor to nucleate the peculiar impress attributed to early
syphilitic pulmonary processes, we find much that is vague. The
vascularity and advanced grade of organization of the new growth are
considered by Greenfield and Goodhart to be characteristic when
compared with tubercular consumption, in which the original growth is
bloodless and the tendency is to retrograde metamorphosis. Green and
Virchow suggest that the origin of syphilitic diseases of the lungs is
distinctive in this respect, that while in the ordinary forms of
phthisis the fibroid is secondary or coequal in its development with
changes in the alveoli and alveolar wall, in syphilis there are
primarily interstitial changes. In chronic bronchitis the fibroid
thickening proceeds from the bronchi. Wagner, however, maintains that
implication of the alveolar wall is as common in syphilis as in
ordinary phthisis.

In the general pathology of syphilis the change in the intima of the
blood-vessels is characteristic: this has not yet been demonstrated in
the lung, but merely the general thickening of the external coat of the
vessels. When entire vesicular consolidation and breaking down occurs,
the process is similar to ordinary phthisis, and indistinguishable from
it.

_(b)_ In the gummatous stage the same formation of cellular and
connective tissue is found as in the diffused form, with which gummata
are often associated. Gummata may originate anywhere in the
intervesicular tissue, usually near the visceral pleura. Sometimes they
are formed near the roots of the lungs, intimately connected with the
blood-vessels and bronchial sheaths. They may also be formed in the
deeper layers of the costal pleura or upon the periosteum of the ribs.
Owing to the peculiar anatomical formation of gummata, their subsequent
history is one of combined caseous and fatty degeneration. These
centres of softening may communicate with a bronchus, more or less
rapid evacuation of the mass may occur, and a cavity be formed which
often enlarges as the gummata break down. Contraction may ensue,
leaving a small fibrous scar with cheesy cretaceous deposit, or the
gummata may point externally, with or without the appearance of
inflammation in the adjacent tissues, or they may remain stationary for
an indefinite period. In some cases the pulmonary new formation may be
a combined interstitial, gummatous, and catarrhal process; but, as a
rule, the fibroid process of syphilis in the earlier stages is not
accompanied by the filling of the alveoli with catarrhal cells. Gummata
developed in or near the pleural sac may increase in size, and by
compressing the lung simulate pleural effusions.

_(c)_ The morbid anatomy of cases in which simple phthisis develops in
consequence of the vulnerability of the pulmonary tissues to the
exciting causes of bronchial inflammation requires no special
consideration.

_(d)_ Interstitial inflammation, gummata, and enlargement of the
bronchial glands have been found in the syphilitic foetus and in very
young children. It is also claimed that syphilitic disease of the lung
may be one of the forms of tertiary disease which develop in children
between the second dentition and maturity. Virchow and Lebert have
described pulmonary gummata in children suffering from inherited
syphilis. Depaul gives the cases of two children with pemphigus who had
soft puriform nodules or collections scattered through the lungs. In
the infant lung the highly cellular character and ready reversion to
the embryonic type of structure would naturally lead to exuberant
growth and rapid diffusion of the morbid process, which could not occur
in the more fibrous, less cellular lung of the adult. Hence the slower
growth in the latter establishes the more fibrous and limited extent of
disease: in other respects the origin and distribution of the growth
are identical in both cases. In the infant enlargement of the bronchial
glands {450} and bronchitis leading to broncho-pneumonia, or an unusual
proliferation of epithelium in the alveoli, is more frequent than in
the adult.

MORBID ANATOMY.--In the earlier stages of pulmonary syphilis the
macroscopic appearance of the lung is firmer at the seat of deposit
than elsewhere. It is also heavier and has a smoother surface. The
infiltrated parts are grayish-red or grayish-yellow, smooth, and
homogeneous. Sometimes the appearance resembles pale-whitish patches
invading districts of the lung. The hyperplastic material becomes
converted into a tough, contracting, fibrous tissue, which radiates
through the lung, drawing together the bronchial tubes and flattening
them, possibly even to obliteration. The entire lung may be involved,
but the changes most frequently proceed from the hilus of the organ
into the interior, following the track of the bronchial radicles and
the bronchial and pulmonary arteries. The lesions frequently develop
near the visceral pleura, where there is more connective tissue. This
accounts for the depressed puckered scars which are found on the
pleural surface.

The macroscopic appearances in specific pulmonary disease differ,
according to Goodhart, "both from a chronic pneumonia and from that
solidification ensuing after contraction of the lung from old pleurisy,
in that it is less evenly distributed, and generally less widely spread
over the lobe, than they. It is nodular, rather diffused, and more
symmetrical than unilateral. From miners' phthisis the appearance
differs in the absence of the extreme dilatation of the bronchial tubes
and more solidity from greater growth. The tissues involved are more
tough and less granular than red or gray hepatization." It is possible
to differentiate other forms of fibroid phthisis by noting, in addition
to the above points, the presence of the syphilitic process in other
viscera, and by comparing the clinical records with the post-mortem
examination.

Syphilitic lesions may be found in any part of one or both lungs, but
their localization at definite points in the lungs, leaving the balance
free even when the lesion has proceeded to formation of cavities, may
be characteristic. There is, however, a wide division of professional
opinion upon the subject of the localization of the process in
syphilitic pulmonary disease; some claiming the middle lobe, some a
symmetrical lesion at the apices, others lesions at a definite point
elsewhere than at the apices. If the pulmonary lesions are introduced
by an attack of pleurisy, the process in the lungs is usually located
at one or both bases. Some, however, locate the disease at the base,
without mentioning an antecedent pleurisy.

Gummata are more frequently situated in the middle or lower lobes of
one or both lungs, and are defined by a boundary layer of fibrous
tissue. Fibroid development may ensure their adhesion to the visceral
and costal pleura. They are gray or yellowish-gray, hard, well-defined
nodules, of varying size and number, occurring as single large masses
surrounded by normal or compressed lung. In the centre is found a
diffluent material, not unlike the centre of a scirrhous nodule,
similarly enclosed in a limiting fibrous investment from an inch to
many inches thick. In the condition of the neighboring pulmonary
substance a difference may be observed between gummatous and
tuberculous nodules: the latter occur in more numerous masses, usually
small, and the entire lung is more or less diseased; while in syphilis
extended districts of non-affected lung occur in the neighborhood of
gummata. Whenever gummatous lesions in the lungs exist a history of
pustular eruptions, laryngitis, arterial lesions--in fine, some
indication of general systemic syphilitic poisoning--can always be
found. Fournier thinks there are five anatomical points of distinction
between syphilitic gummata and tubercle: "1. Tubercle involves the
upper part of both lungs; gummata one lung, and may be limited to a
portion. 2. Gummata are few as a rule, solitary; tubercles sooner or
later become confluent. 3. Gummata are larger than tubercles, never
{451} miliary in form. 4. Gummata are always yellow or white, never
transparent like miliary tubercle. 5. Until softening takes place
gummata are of more equal consistence than tubercles, and if they
soften do not break down, wholly owing to the capsule. Histologically,
there is no difference in structure." Gummatous formations may be found
on the pericardium and heart and in the thoracic and abdominal walls.
Clinically, the most important pathological feature is that large
districts of healthy lung are interposed between the affected
districts; this is not so in ordinary phthisis.

Bronchial Lesions.--The syphilitic like the scrofulous are predisposed
to catarrhal inflammation, and this may spread down the bronchial
tubes, giving rise to a general bronchitis; a coexistent laryngitis may
or may not exist. Enlargement of the bronchial glands is frequently
combined with the syphilitic pulmonary process. When the glands are
enlarged they present a firm pigmented character, varying in size from
a hazelnut to an egg, and the connective tissue surrounding them is
usually infiltrated. Subsequently, owing to the pressure of the
mediastinal growths, the bronchi are narrowed and more or less
occluded; the same effects are occasioned in the smaller bronchi by the
pressure of the new growth which develops along their lumen. The
effects of bronchial narrowing or occlusion produce serious mischief in
the lungs proportioned to the degree of obstruction. By the retention
of the bronchial secretions the air-supply to the vesicles is
interfered with; emphysema with or without asthmatic symptoms or
atelectasis may ensue. Further, the results of bronchial narrowing
affect the circulation through the lungs, and in combination with
atelectasis very intractable local bronchitis may be developed; and,
with or without atheroma, hemorrhagic infarctions may occur, with a
form of pneumonia which has been described by Fuchs as apneumatosis.
The narrowing of the bronchial tubes in specific fibroid phthisis
affords a means of differentiating this disease from non-syphilitic
fibroid phthisis, in which the tubes are widened. Cases have been
reported of nodules of syphilitic new formations in the mucous membrane
of the superior and inferior extremities of the trachea and larger
bronchi. The nodules ulcerate, and in healing cicatricial bands of
fibrous tissue are formed which cause contraction of the tracheal tube
transversely or diminish its length. These lesions resemble tuberculous
ulceration, but they differ in the nature of the initial neoplasm by
the formation of cicatricial tissue and by the tendency to stenosis of
the tracheal tube. The cutaneous syphilides, mucous patches, the
exostoses of the bones of the cranium help to demonstrate the
connection of the marked cachexia with syphilis rather than scrofula.

SYMPTOMATOLOGY.--As the pathology of syphilitic pulmonary processes is
intertwined with the pathology of many other forms of phthisis
pulmonalis, so the symptoms must be common to those obtaining in other
forms of pulmonary disease. They are insidious and gradual in their
development, and may be classified as the subjective, the physical
signs, and the objective phenomena. The subjective symptoms may be
present without noticeable departure from an appearance of health.
There may be difficult respiration with more or less dyspnoea,
especially in the mornings and evenings, besides a sense of heaviness
and oppression in the chest, with a feeling of inability to inflate the
lungs. These symptoms may be increased on exertion, respiration
becoming wheezing, with imperfectly-developed asthmatic attacks.
Hoarseness, with varying degrees of aphonia, more or less dysphagia or
unequal pupils, may be present. Nearly all of these symptoms may be
accounted for as indicative of mediastinal pressure or irritation of
the pneumogastric nerve by the enlargement of the bronchial glands. The
catalogue of phenomena may be present in whole or in part, and the
intensity of their manifestations may vary from time to time in the
history of a single case. If the bronchial glands are much enlarged, a
sense of discomfort, oppression, and uneasiness {452} at the root of
the neck may be experienced, which increases until actual pain is felt,
located in the back between the scapulæ, but sometimes radiating
through the intercostal nerves around the chest. Cough, as a rule, is
an early symptom, usually dry, paroxysmal, and associated with
dyspnoea, or there may be bronchial catarrh, with a relative amount of
expectoration. Syphilitic disease of the larynx may occur coequal with
the pulmonary trouble, and some of the above symptoms may be thus
explained and many others added. Rheumatic and nervous symptoms,
including sleeplessness and deterioration of the blood-crasis, may
testify to the syphilitic infection of the blood.

When a physical examination of the chest is instituted, thickening of
the head of the periosteum of one or both clavicles, substernal
tenderness, thickening of the tibial periosteum, are usually detected.
Prominent among the physical signs are the evidences of enlargement of
the bronchial glands. According to Guéneau de Mussey, percussion over
the spinous processes of the cervical vertebræ in the course of the
trachea reveals in a healthy subject a distinct tubular sound down to
the point of bifurcation of the trachea at the level of the fourth
dorsal vertebra. Opposite the fifth and downward we get the
lower-pitched pulmonary resonance. When the tracheal and bronchial
glands are enlarged, the tubular sound over the upper dorsal vertebra
is replaced by dulness, which may contrast sharply above with the
tracheal and below with the vesicular resonance.

The respiratory murmur will be feeble in volume and limited to
inspiration, especially over the interscapular region. Over one or the
other bronchus the respiratory murmur may be more high pitched than in
health, and slightly exaggerated on one side or at the base of the
chest. The rhythm is often jerky and paroxysmal; the paroxysms are more
or less constant, but are liable at times to increase.

The additional physical signs in syphilitic phthisis, unassociated with
gummata, are those shared by other forms of fibroid phthisis, and do
not require particular description here, as increasing dulness, varying
degrees of bronchial breathing, and bronchophony. A peculiar alveolar
rustle, resembling the sound produced by the rumpling of wall-paper,
has been alluded to as characteristic.

Inspection or palpation sometimes reveals changes in the contour of the
chest, with displacement of the movable thoracic viscera, as in fibroid
phthisis. When cavities occur, the physical signs necessarily
correspond to those of other varieties of phthisis at this stage.

When a gumma is large enough to be recognized by physical examination,
one finds dulness or flatness on percussion, confined to a section of
the chest, and not occupying its semi-circumference, as in pleural
effusions. The vocal fremitus is suppressed in proportion to the size
of the gumma. The respiratory murmur is abruptly cut off over the area
of flatness, but it may be only distant bronchial breathing. The vocal
resonance is absent or is distant bronchophony. Around the gumma the
respiratory murmur is usually very feeble or scarcely audible,
generally without râles unless they are due to neighboring congestion.
The percussion resonance is good or exaggerated. Proportionate
vicarious functional activity prevails in the opposite lung. If the
gumma be large, the heart's impulse may be displaced to the left or
right, and dyspnoea may occur as in case of pleural effusions. In this
stage, owing to irritation of the bronchial mucous membrane, there may
be expectoration of a tough, glairy mucus, or as a gumma softens the
expectoration may become purulent.

The objective phenomena vary: the chest is often well developed, the
body fairly nourished, and constitutional symptoms of a severe
character may be wanting. The patient may be capable of hard physical
labor, even though a {453} considerable part of the lung be affected.
Moxon relates a case of a man "employed in carrying sacks of grain who
was suddenly killed, and who had fibroid infiltration of a great part
of the left lung and part of the right, and besides scars in his liver
and testes." But in some cases the complexion is pallid and waxy,
indicative of cachexia associated with digestive disorders, with
night-sweats, and a variable but low thermometrical record. Usually,
the progress of the disease is slower in syphilitic than in tubercular
phthisis, but when the systemic poisoning is grave and many other
organs are coincidently involved, the progress is more rapid; but the
process peculiar to syphilis is often past, and the patient suffers
from simple catarrhal phthisis with formation of cavities and softening
gummata. Diarrhoea and night-sweats are said to be less frequent than
in ordinary phthisis, and the pulse is slower. Hæmoptysis occurs
infrequently, because the process in the lungs is chiefly fibroid; but
it is possible through the rupture of newly-developed blood-vessels in
the new formation in the lung or hemorrhagic infarction through the
rupture of atheromatous vessels.

DIAGNOSIS.--This depends mainly on the history of the cases, the prior
or coexisting syphilitic lesions, especially laryngeal processes,
cutaneous syphilides, exostoses, perforation of the palate, substernal
tenderness, and the thickening of the tibial periosteum or that of the
head of one or both clavicles. Family immunity from phthisical
tendency, recovery from lesions usually incurable if they have any
other than a specific origin, are suggestive of pulmonary syphilis. If
a patient retains flesh and strength beyond the natural expectation
considering the serious lesions of the lungs, the fact is of relative
importance when considered in connection with the other diagnostic
features. The distribution of specific lesions is variously located by
different authors. Grandidier found induration affecting the middle
lobe of the right lung in 27 out of 30 cases believed by him to be
specific phthisis; the surrounding lung contained large areas free from
disease. This tendency to localization in portions of the lungs,
leaving large areas free from disease, is of value in diagnosis.

PROGNOSIS.--The prognosis is involved in the discovery of syphilis as
the cause of the disease and on the subsequent appropriate treatment.
Grave and important specific lesions, according to some authors, have
yielded to the resources of art. Fournier has recorded a case where
"dulness at the summit of the left lung was extensive and signs of a
cavity distinct. After six weeks of antisyphilitic treatment recovery
was almost complete. In this case the presence of a phagedenic ulcer of
the foot was the only sign that suggested syphilis, the symptoms of the
pulmonary affection being identical with those of tubercular phthisis."
The principles presiding over the prognosis of the various stages of
pulmonary diseases in general are applicable to syphilitic pulmonary
processes.

TREATMENT.--When a case of pulmonary lesion presents itself, unless the
existence of tuberculosis be demonstrated, we must ascertain if the
symptoms can possibly be due to syphilis, and the line of treatment
indicated in any single case must be based upon an estimate of the
prominence of the specific process. The ravages of syphilis, however,
often produce such loss of substance in the lung that the lesions are
irreparable, and therefore we cannot always accomplish the brilliant
results which usually attend an antisyphilitic treatment. If there is
evidence of enlarged bronchial glands, in addition to other measures
local counter-irritation is useful by means of the biniodide of mercury
ointment, 16 grains to the ounce, and applied for a continued period,
or a preparation of iodine with croton oil may be tried. In the main,
the general principles of treatment correspond with those recognized in
similar forms of pulmonary disease of a non-specific etiology.




{454}

PNEUMONOKONIOSIS.

BY EDWARD T. BRUEN, M.D.


DEFINITION.--A generic term applied to pulmonary diseases due to the
inhalation of particles of irritating dust.

SYNONYMS AND CLASSIFICATION.--The synonyms and classification of
pneumonokoniosis have been based upon the character of the dust
inhaled, using such terms as anthracosis ([Greek: anthrax], coal),
disease due to coal-dust; siderosis ([Greek: sidêros], iron), due to
metallic dust; chalicosis ([Greek: chalix], gravel or pebbles), due to
mineral dust; tabacosis, due to tobacco-dust; and byssinosis ([Greek:
byssos], cotton), due to cotton fibre and dust. A more imperfect
classification has been derived from the avocations of the sufferers;
for example, miners' phthisis, Sheffield grinders' rot, potters'
consumption and asthma, freestone-hewers', masons', or millers' lung.

HISTORY.--From the early experiments of Cruveilhier, who injected
mercury into the system and subsequently noted the pulmonary changes,
down to the experiments of the present day, evidence has accumulated to
show that inorganic irritant materials are capable of exciting
inflammatory new formation in the lungs. The difference between the
changes produced in the lungs by experimental processes and those
occurring after the inhalation by artisans of inorganic materials
consists in degree rather than in essential character. In
pneumonokoniosis the pulmonary processes are gradually developed, and
consequently the ensuing changes in the tissues represent those usually
associated with the more chronic forms of pulmonary lesions, and may
not only occasion phthisis, but during years of life may cripple the
sufferer by engendering chronic catarrhal processes in the mucous
membranes, complicated by emphysema or asthma.

ETIOLOGY.--Predisposing Influences.--Atmospheric dust is composed of
organic and inorganic matter, and both have been demonstrated by many
admirable experiments to be very widely diffused in the air we breathe.
In most instances the injurious action of inorganic dust is augmented
by the conditions of imperfect ventilation under which it is inhaled,
because the amount of dust deposited in the lungs is thereby increased.
Illustrations of this fact can be found in various avocations,
particularly among miners. The injurious action of dust inhaled when
there is imperfect ventilation is increased in proportion as there is
deprivation of sunlight, both conditions tending to lower the vitality
of the artisan. Again, the rigor of confinement of parents engenders a
sickly or scrofulous constitution which is transmitted to their
offspring, causing great mortality among the children of artisans,
especially where they, in turn, are subjected to unfavorable
environment.

When work is performed in constrained or stooping positions, or when
proper inflation of the chest is not secured, the liability to
pulmonary disease is increased.

The foregoing conditions having been considered, the injurious action
of dust upon the lungs is in proportion to the quantity deposited in
them. The {455} entrance of dust is, however, physiologically opposed
by the action of the pulmonary cilia, although the resistance is
frequently ineffectual. This inefficiency may be owing to the quantity
of dust inspired or to deficient tissue-integrity in general upon which
the ciliary action depends in inverse ratio.

Exciting Causes.--These vary materially in different avocations. The
most injurious industries are those in which the various forms of
grindstones are used, or those trades which necessitate labor in an
atmosphere loaded with particles of steel, iron, or flint. In London,
where millstones are made from French burr, a peculiarly hard flint
quarried on the Marne to the east of Paris, and more liable to chip
from its hardness and dryness than flint quarried in other places, the
mortality among the artisans is said to be very much increased.
Peacock, who has investigated this subject, asserts that in certain
manufactories of this class the average age of those engaged is very
low: of 23 apprentices the average age was twenty-four, and the longest
period during which the occupation could be followed was thirteen
years. The same author has also demonstrated the presence of silicious
particles in the lung-tissues. In the pottery districts of England the
death-rate from pulmonary diseases is greater among those who work at
that avocation than among the other inhabitants.

The study of the effect upon the lungs of the inhalation of coal-dust
is very important. In the coal-mining region of Cornwall the deaths
from chest diseases among miners is double that of males in the
community at large; the mortality of those working in lead-mines is
also very great.

The black spit of pitmen, examined under the microscope, is seen to
consist of mucus enclosing finely-divided particles of coal, frequently
presenting the special bands of the particular coal in which the
subject of the disease may have worked. The fact that coal-dust may
enter the lungs in the act of breathing is corroborated by Rindfleisch,
who, reporting for Traube a post-mortem made in 1860, found in the
fluid expressed from the parenchyma of the lung "one of the dotted
cells of coniferous wood entirely carbonized, in which he was able to
count seven pores close together. This particle of charcoal-dust
equalled half the diameter of an alveolus." Inhaled particles of dust
first penetrate the bronchial tubes and infundibula, and, entering the
alveolar parenchyma, mix with the general current of extravascular
fluid, together with which they ultimately tend to reach the lymphatic
vessels. On their way they must occasionally meet with corpuscular
elements which have the power of permanently adopting small solid
particles into their protoplasm: foremost among such elements are the
stellate corpuscles of the connective tissue, next the migratory
amoeboid cells, which are found in the connective tissue of the lungs
as well as elsewhere, and which carry the black pigment with them
wherever they go. The residual portion which escapes, being arrested by
cells on its way through the lymphatic system, is carried to the root
of the lung and enters the lymphatic glands of the mediastinum; here
the granules meet an obstacle to their further progress, for the
countless lymph-corpuscles with which the glands are stored are ready
to take up as many of the charcoal particles as can by any possibility
be accommodated in their protoplasm. We may conclude that the influence
of inhalations of coal-dust varies in different cases, but may be
considered as prominent among the exciting causes of pneumonokoniosis.

The charcoal-grinders and carriers, chimney-sweeps, moulders, iron and
glass polishers, and the workers in mother-of-pearl, all suffer more or
less from destruction of lung-function. Deposits of oxide of iron have
been found in the lungs of operators who have for years used this
substance as a polishing pigment. Merkel reports the case of a man who
was employed to clean the surface of oxidized iron by scrubbing it with
sand: his expectoration was grayish-black, and was found to contain
small grains of magnetic {456} oxide of iron; the lungs were found to
be indurated with cavities at the apices.

Many other instances of dusty avocations may be mentioned as exciting
causes. The polishing of brass is sometimes effected by rollers made of
canton flannel which revolve with great velocity, filling the air with
fibres of cotton which are capable of acting as mechanical irritants.

In the sizing process in some cotton manufactories the material is
often adulterated with clays or some sort of salt to lessen the
glutinous qualities of the flour or tallow, and although the process is
carried on in damp rooms to lessen the brittleness of the size, dust
prevails, causing irritation of the nose, eyes, and throat. Some
interesting observations have been made on this subject by James Y.
Simpson, who has especially investigated the hygiene of woollen
manufactories. He suggests that these artisans are comparatively
healthy because of the oil absorbed while running the machines. In the
manufacture of cotton it has been found that in mills where cotton
containing dust and dirt is used, as the East India varieties employed
in England during the American War, the respiration was affected, and
the expectoration of numbers of operatives contained slaty-colored
matters, found, on microscopic examination, to contain cotton fibres.

Bakers who have to deal with highly-dried biscuit flour suffer more
than those using ordinary brands of flour. But when all has been said,
when we consider how many persons live permanently in an atmosphere
specially surcharged with dust without showing a symptom of a morbid
state of the respiratory organs, and since the epithelial cells of the
lungs can contain particles of coal, it demonstrates that foreign
bodies may penetrate the lungs without always inducing serious changes.
Mineral matter has been found by Riegel in the form of silica in the
lungs of a boy aged four, constituting 2 per cent. of the ash left
after incineration. In those of a day-laborer aged forty-seven it
amounted to 13 per cent., and in those of a woman cook sixty-nine years
old it reached 16 per cent. Accepting these figures as accurate, they
show a progressive accumulation in proportion to age among individuals
breathing dusty atmosphere. Traube thinks that the changes in the lungs
of coal-miners may not be produced by the accumulated particles of
coal, but by the chemicals contained in coal, and not found in
charcoal. In a discussion of this question in London in 1869, Wilson
Fox thought it remarkable that in proportion to the number of persons
exposed to the inhalation of irritating substances the cases of
phthisis were comparatively few, and suggested that a diathetic
condition might underlie the entire pathology.

In summing up the evidence bearing on the predisposing and exciting
causes of pneumonokoniosis we cannot overlook the recent discoveries of
Koch and his collaborators, but may conclude that although there is
increasing evidence tending to show that the bacillus tuberculosis is
always present in tuberculous pulmonary processes, yet its exact
etiological relation cannot be considered as established. We may still
hold that when large amounts of inorganic materials are taken into the
lungs, particularly if the ventilation or hygienic conditions under
which the dust is inhaled are imperfect, certain diverse pulmonary
processes are apt to ensue. That phthisis can be thus produced is
undoubted, but the nature of the irritant has less to do with the type
of the resulting disease than has an inferior or scrofulous
constitution, inherited or acquired, or the indulgence in habits
directly damaging to the health; since an unvarying specific cause
would be more destructive than has been proven, large numbers of
individuals escaping any serious effects when equally exposed.

PATHOLOGY AND MORBID ANATOMY.--Whatever be the dust inhaled, the
pathological processes set up by it partake of the same essential
character, though differing in intensity and in the division of
pulmonary tissue {457} principally involved, while the combined
inhalation of organic particles may essentially modify the results
produced. Examination of the lungs has revealed deposits of various
inorganic materials which have been inhaled, such as oxide of iron,
indigo, snuff, silica, coal, carbon, etc. A black discoloration of the
pulmonary tissue, with or without induration, enlargement, and
blackening of the bronchial glands, may, however, have its origin in
morbid changes independent of inhaled matter, such as defective
elimination of carbon and carbonic acid, with a sort of precipitation
of carbon within the tissues.

The black coloration of the lungs, especially in miners, is also partly
due to the deposition of a true hæmatoidin pigment in granular form,
caused by the irritating particles inhaled setting up changes in the
bronchial or pulmonary tissues, resulting in the escape of the coloring
matter of the blood either by rupture of capillaries or from
transudation of serum. Similar discoloration is often found in cases of
chronic bronchial processes independent of a dusty etiology. The most
penetrating form of dust is the silicious, on account of its hard,
vitreous character. German authors comment on the difference in the
power of penetration of mineral coal-dust as compared with
charcoal-dust, because the spiculæ of the former are elongated,
sharpened splinters. The coloration of the lung from clay-dust does not
diffuse itself so readily as coal-dust, yet it possesses more
irritating properties and creates more damage.

The morbid anatomy of pneumonokoniosis includes nearly all the
pathological processes incident to the pulmonary tissues. The bronchial
lesions are those of chronic bronchitis, with thickening of the
bronchial mucous membrane, associated with possible ulceration and
bronchial dilatations, forming bronchiectasic cavities. These cavities
are caused by combined softening of the bronchial tissues with traction
from without by the newly-formed fibrous tissue. The bronchial glands
may be enlarged to the size of walnuts, and are often perfectly black
and gritty on section. These enlarged glands may occasion, through
pressure, many changes in the pulmonary tissues. The effect of this
pressure is especially manifest in the lymphatic system. The
lymph-circulation is further crippled by the accumulation in the
lymph-channels of the inhaled inorganic materials. These interferences
with the lymph-circulation may be followed by exudation or lobular and
interlobular formation of tissue; secondary to these changes the
pressure upon the vesicles may cause local congestions, exudations, and
even hæmoptysis. By one or all of these processes the expansile power
and elasticity of the lung are slowly depreciated, emphysema develops,
intertwined with the lesions of acute, subacute, or chronic bronchitis,
fibroid phthisis, and atrophic emphysema. Nodules of cretaceous matter
can be recognized through the lungs, which are black in anthracosis or
gray in silicosis. These nodules occur from the size of a pin's head to
that of a pea, and are especially found in the lungs of glass-cutters,
sandstone-workers, and grinders. In these cases they consist in part of
iron and in part of stone. In sandstone-workers they are composed of
silica; the organ feels nodulated, very fibrous, and in some cases
actually gritty. The predominant form of pulmonary change is fibroid;
hardened districts of advanced cirrhosis occur measuring two inches and
upward in length and width, and in depth and thickness nearly as much.
These may be rounded, but are not separable from the adjacent
structures, the condensation of the tissues lessening without a
defining line. On section they appear tough and leathery, most
pronounced along the anterior edges of the lungs, and are apt to be
covered in by thickened pleura. If the nodules previously alluded to
are encysted, fibrous prolongations extend from these cysts into the
substance of the lung, the thickening of the lung being greatest in the
septa, on the pleural surfaces, and along the course of the bronchial
tubes. Sometimes subacute or chronic pleural processes coexist. The
caseous masses found in tubercular fibroid phthisis are infrequent in
pneumonokoniosis, but in the latter process the {458} pathological
changes may be identical with the ordinary forms of phthisis,
especially in those individuals who are predisposed to pulmonary
affections and those in whom the pathological processes are rapid.

In anthracosis the lung is large and increased in weight; the surface
of the pleura has a bluish-black color, contrasting with the coal-black
color of the lungs, which are universally pigmented and contain nodules
of pigment. When only small quantities of pigment are present, it
presents the appearance of dark lines running between the lobules; on
section these are very hard and distinct, being about the size of a
millet-seed. They are universally distributed throughout the lung, and
in some places appear like small masses of charcoal. Upon squeezing the
organ a blackish fluid exudes which stains the hands, but the discharge
which is found lying in the bronchial tubes is often yellow and
muco-purulent, although the sputa during life is more or less
discolored. When the distribution of the discoloration of anthracosis
is investigated, it is found to closely correspond with the lymphatic
distribution of the lung, and the conclusion is probably well founded
that all other irritating particles pursue the same course through the
pulmonary tissues. When particles of coal or pigment enter the bronchi
with the air, they cannot pass through its mucous membrane, because the
basement membrane and fibrous coat underlying it present an obstacle to
their lodgment, whilst the cilia of the epithelium tend to prevent
their retention in the bronchi; they therefore enter the vesicles, and
may be found sticking to the walls. In this way the exemption of the
bronchi from pigmentation, even down to the smallest ramifications, can
be explained. The interlobular septa ate also the seat of great
pigmentation. The germinating epithelium elevates the cells slightly
above the surface, and in the interspaces between them the pigment
insinuates itself, and thus enters the underlying plasmatic or
lymphatic spaces; or the pigment may be incorporated into the
epithelial cells, which transfer it to the underlying lymph-space. Once
the pigment has found entrance to these lymphatic channels, it is
carried by them through the lymphatic vessels in the sheath surrounding
the bronchial tubes and the small branches of the pulmonary artery, and
in the interlobular septa to the bronchial glands. In this manner the
special distribution of the coloring matter in these situations is
explained. The special deposit around the small branches of the
pulmonary artery is owing to the double set of lymphatics, the
peribronchial and the perivascular, which form an anastomosis. The
perivascular set is the larger; consequently the pigment passes into
them more readily, forming the nodules. Pigment is also found in small
quantities around the bronchi, which can be accounted for by the
anastomosis of the lymphatics. The bluish-black appearance of the
pleura and the distribution of the pigment only in the deeper layers of
the visceral pleura are susceptible of a similar explanation, because
the deeper layers of the pleura contain lymphatic vessels which are
directly continuous by means of the lobular septa with the large
perivascular branches of the lymphatic system.

The consequences of the obstruction to the lymphatic and
pulmonary-artery circulation may be very serious. In grave cases the
lung breaks down, forming a gangrenous-like cavity, which differs from
an ordinary cavity in not being rounded; it is more like a gangrene or
slough. In a few cases the pathological appearances indicate phthisis,
chiefly interstitial, with formation of cavities; sometimes traces of
cavities are found which have cicatrized. More commonly oedema is
developed in the lung and the bronchial passages. As a consequence of
combined bronchial irritation from continuous inhalation of inorganic
particles, and the consequent oedema, a continuous germination and
shedding of the bronchial epithelium--a chronic bronchitis--associated
with emphysema, is maintained. The mechanical cause of this
bronchitis--more or less impediment to the vascular and lymphatic
circulations by the {459} pigment deposit--is capable of explaining the
persistence of various forms of bronchial processes in anthracosis and
in other forms of pneumonokoniosis after the patient has ceased working
in a dusty atmosphere.

SYMPTOMATOLOGY.--Pneumonokoniosis does not present a special
symptomatology. The course of the various morbid processes is insidious
and slowly progressive: the development of any of the forms of
pulmonary disease depends largely upon the degree of exposure to the
exciting causes, or the inherited tendencies, or the susceptibility to
influences liable to diminish general vitality or affect the personal
hygiene.

The earliest objective symptom of pulmonary lesion is cough, especially
recurrent in winter, accompanied by expectoration, which is whitish,
frothy, or stringy in character. Gradually the physical signs, taken
together with the symptoms, indicate the various forms of bronchitis,
acute, subacute, or chronic, sometimes associated with emphysema,
bronchorrhoea, or bronchial dilatation. In other cases the
symptomatology is that of asthma, either purely spasmodic or secondary
to emphysema or cardiac degeneration. In true anthracosis dyspnoea is a
marked symptom, and perhaps the accumulation of pigment may interfere
with the oxygenation of the blood, or dyspnoea may be due only to an
emphysematous pulmonary tissue. The sputa will be black so long as the
subject is working in an atmosphere loaded with pigment.

Fibroid phthisis is frequently associated with atrophic emphysema, and
the clinical history corresponds with that which is commonly observed
in these diseases. Hæmoptysis is rare, but if it occurs it suggests the
addition of some tubercular element; a purulent nummular sputa is a
suspicious sign of similar import. The symptoms and physical signs of
dry pleurisy are to be expected whenever any form of the phthisical
process supervenes. The cavities in the lungs are usually
bronchiectasic, unless tubercular phthisis occurs as a complication,
and the physical signs need no comment. Subacute and chronic laryngitis
with ulceration complicate certain cases, particularly those which have
inherited or acquired a tubercular tendency.

DIAGNOSIS.--The diagnosis involves a comparative examination of the
etiology and the physical signs.

PROGNOSIS.--The prognosis depends very largely upon the withdrawal of
the sufferer from an unhealthy environment. In each single case the
inherited tendencies, the personal constitution and habits, must be the
basis for an opinion upon the gravity of the pulmonary processes and
the possibilities of restoration to health. The progress of the disease
may be materially retarded or arrested by withdrawal from the
occupation involving the inspiration of dust, and restoration to
comparative health after years of invalidism is possible for these
victims of dusty avocations, even after serious damage has taken place
in the lung, if suitable hygienic conditions can be obtained.

TREATMENT.--The treatment of pneumonokoniosis divides itself into the
prophylactive and the curative. In works devoted to the hygiene of
occupation careful directions are given in reference to methods
designed to prevent the dust from entering the respiratory passages.
This is partly accomplished by the use of masks or respirators, which
possess the obvious disadvantages of clumsiness and interference with
respiration. Various devices may be employed in different avocations to
prevent the generation of dust, but the most practical plans consist in
thoroughly ventilating the atmosphere, and thus preventing the dust
from reaching the artisan. Aside from these, the management of the
various pathological conditions must be based upon the general
principles which govern the treatment of pulmonary processes.




{460}

CANCER OF THE LUNGS.

BY EDWARD T. BRUEN, M.D.


DEFINITION.--A malignant disease affecting the pulmonary tissues. (Vide
also MEDIASTINAL DISEASE.)

SYNONYMS.--_Fr._ Carcinome du poumon; _Ger._ Lungenkrebs.

ETIOLOGY.--Carcinomatous disease affecting the lung-tissue is
exceedingly rare as a primary process, and exhibits only a feeble
inclination to inoculate other portions of the body. In the majority of
cases the mediastinal glands are first affected, or it appears in the
lungs as secondary to disease elsewhere in the system. Metastasis is
probably effected by means of particles of living cellular material
which are transferred through the blood-vessels or lymphatics.

Cancer of the lung often reverses the rule that carcinoma occurs most
frequently in the female, Hasse, Kohler, and Cockle giving a majority
of cases among males. It has been met with in childhood and in extreme
old age, but is more common in the middle periods of life, from twenty
to sixty years.

PREDISPOSING AND EXCITING CAUSES.--The predisposing and exciting causes
of malignant pulmonary disease are involved in the obscurity that
surrounds the development of all neoplasms.

PATHOLOGICAL ANATOMY.--Clinically speaking, cancer in the pulmonary
tissues includes the scirrhous or encephaloid neoplasms. The colloid,
enchondromatous, or fibromatous growths have been recorded as possible
tumors, but possess only a pathological interest.

Malignant disease may commence in, or ultimately implicate, one or all
of the pulmonary tissues; secondary neoplasms have been experimentally
produced by lodgment in the lung of living cellular particles which
grew centrally by virtue of inherent cell-proliferation, independently
of changes produced in the surrounding tissues. Cancer of the lungs,
whether primary or secondary, usually originates near the roots of the
lungs, implicating the mucous and submucous membranes of the bronchi,
sometimes commencing in its small mucous follicles. The bronchial
passages and the lymph-channels become the viaducts along which the
growth proceeds in its march of invasion, involving most frequently the
posterior portion of the middle lobe. The apices of the lungs may be
implicated, but not primarily, as in tuberculosis. The mediastinal
lymphatics are originally involved in an unestimated number of cases,
or enlargement of these glands is coexistent with the development of
pulmonary cancer. The enlargement of the mediastinal glands is
sometimes moderate, but an enormous mass may be formed. (Vide
MEDIASTINAL TUMORS.)

Carcinoma is found in masses varying in size from a hempseed to an
orange or larger, and since its distribution follows the lymph-channels
in their circuitous route through the lung, we can account for the wide
distribution of the nodular masses of secondary cancer. The isolated
nodules present an {461} ovoid outline, sometimes situated near the
pleural surface, in contrast with the larger formations which affect
the roots of the lungs.

The primary malignant formation presents a single large mass of
infiltration, possibly associated with a few small nodules scattered
throughout the lungs; the right lung is conceded to be the most
frequently affected, but secondary cancer usually implicates both
organs.

Cancer in the parenchyma of the lung may diminish or occlude the lumen
of the bronchial tubes, or they may be filled with cancerous matter and
their walls perforated. The development of cancer along the
distribution of the bronchial passages shows us how readily chronic
bronchitis may occur as a complication and form a confusing element in
the diagnosis. The remaining pulmonary tissues may escape anatomical
change, or from pressure atrophic or hypertrophic emphysema or collapse
may ensue. These changes, together with the similarity to a fibroid
phthisical process which many cases suggest, must be borne in mind in
making a diagnosis. Pulmonary apoplexy, or even gangrene, is an
incident in some of the clinical pictures of this disease, and embolism
or thrombosis in other parts of the system may occur. The terminations
of intra-thoracic cancer vary in accordance with the history of these
growths elsewhere. Infiltration with blood or melanic deposition has
been noticed; evacuation of the new growth through the bronchi may
induce the development of cavities in the lungs, preceded or
accompanied by suppuration, ulceration, or gangrene. In addition,
hydro- or pyo-pneumothorax may occur by perforation or invasion of the
pulmonary pleura.

Carcinoma of the pleura is usually secondary to its development in the
lung, but it may be communicated from a similar process in the mammary
gland by infection through the pectoral and intercostal muscles to the
parietal pleura. Carcinomatous formations on the pleura are small and
hard in scirrhous, but are larger in encephaloid, cancer. The minute
spots of early formation are found scattered over the pleura like drops
of wax. The thickened tissues, when they coalesce, undergo
degeneration, and may form plaques of cartilaginous hardness. Large
pleural growths may compress or nearly efface the lung, but are among
the curiosities of medical literature.

Neuralgia may be occasioned when nodules impinge upon the intercostal
nerves. Similar pressure is the cause of the pain in pulmonary cancer,
except that induced by the pressure of mediastinal enlargement. Chronic
pleural inflammation may be frequently developed by the new growth, and
the diseased lung may become adherent to the inner surface of the
sternum and ribs. The lung in other cases may be compressed or
retracted, uncovering the heart and rendering the chest-walls smaller.
The chest may be enlarged, especially if there is pleural effusion;
usually the contour is unchanged.

Pleural effusions are frequent in the history of this disease: they may
be passive, resulting from pressure on the azygos or hemiazygos veins,
preventing the return of the blood from the pleural veins, or from
mediastinal pressure. An inflammatory hydrothorax may be excited by the
deposit of cancerous material in the pleura; and it is possible for
these effusions to undergo purulent transformation or to become
hemorrhagic. A hemorrhagic effusion when grouped with other symptoms
may be considered an important evidence of malignant formation. The
further history of pleural effusions in this association is usually an
increase of such an amount as to necessitate removal by thoracentesis,
but reabsorption is possible.

SYMPTOMATOLOGY.--The interest of the clinical observer nucleates itself
around the symptomatology and diagnosis. The frequent negative results
of physical examination indubitably prove that its teachings alone are
insufficient for the purposes of diagnosis, so that any study of a case
would be partial which did not unite the evidence yielded by physical
signs with the general symptoms. The clinical evidences are more
definite when the {462} neoplasms are multiple and associated with some
mediastinal process than when single or absolutely primary growths. The
development of the disease is insidious. Gradually the facies and
general surface of a patient indicate the true nature of the malady by
the characteristic cachexia. Cough is an early symptom, unimportant
save that it cannot be assigned to any definite cause. It may be dry
and hard, attended only by expectoration of glairy mucus, or the sputa
may be purulent. Usually the amount is in ratio with the degree of
coexistent bronchitis. In the latter stages of the disease the sputa
may contain blood, resembling prune-juice or black-currant jelly, due
to erosion of some of the blood-vessels. In this stage of softening
cells characteristic of the new growth, with portions of the pulmonary
structure, may be found on microscopic examination of the sputa; the
appearance of the expectoration sometimes suggests fibrinous
bronchitis.

When there is elevation of temperature it may present a hectic type,
with night-sweats, which are stated by Walsh to be sometimes confined
to the affected side. The presence of an abnormal temperature-curve is
indicative of associated inflammation of the bronchial mucous membrane,
the development of a pleural process or of phthisis, especially the
fibroid form. The pulse becomes accelerated in ratio to the degree of
these inflammations and the failure of the sufferer's strength.

The new growth determines some mechanical symptoms cognate to all
intra-thoracic tumors, especially those which involve the mediastinum.
Lancinating pain would presumably be a constant symptom, but is, in
fact, infrequent, unless the growth or growths enlarge so as to cause
pressure on the nerve-trunks, in which event pain may become a
distressing symptom. Characteristic pains complicate those cases in
which the pleural tissues are involved in the morbid process. Dyspnoea
is a pressure-symptom of considerable import if other conditions
capable of producing it, especially uncomplicated emphysema, are
rigidly excluded. When the new formation is infiltrated throughout the
lungs, the growth may, as in miliary tubercle, impair the aërating
power of the lungs by diminishing their elasticity and increasing their
density. When, however, the process is local and restricted, the
dyspnoea may be due to irritation of the terminal filaments of the
vagus; this being a mixed nerve composed of accelerator and inhibitory
filaments, the balance of innervating power may be readily destroyed
and partial or incomplete respiratory effort follow. Dyspnoea may also
result from pleural adhesions or effusions, or may be secondary to
direct cardial or pericardial involvement in the cancerous process.
Palpitation or increased pulse-rate may be referred to irritation of
the vagi, or to some of the foregoing pathological processes.

Kindred to these symptoms are the changes in the voice, which sometimes
undergoes frequent variations due to irritation or pressure on the
trachea or on the branches of the pneumogastric nerve, especially when
mediastinal disease is present. Aphonia, huskiness, a bass voice, or
high treble, one or all, may be constant or alternating harbingers of
the concealed mischief. The laryngoscope will inform one whether there
is direct involvement of the larynx with morbid growth. Dysphagia is to
be expected if the new formation involves the regions through which the
oesophagus passes, and a sacculated pouch may be formed above the
compressed spot. Changes of posture may increase or diminish the
pressure, and thus the dysphagia or dyspnoea may at times be more
pronounced than at others. Dysphagia may also be due to swelling of the
oesophagus near the location of pressure. Reflex irritation of the
sympathetic ganglia may induce pupillary contractions in one or both
eyes: this symptom is chiefly present when the mediastinum is involved.

The physical signs contingent on pulmonary cancer include those
ordinarily indicative of bronchitis with or without atrophic emphysema,
simple pleural effusion, or chronic pleurisy with retraction. By
inspection a study {463} should be made of the contour of the thorax,
the respiratory movement, and displacements of the intra-thoracic
viscera. The thorax may appear enlarged, either from the new formation
or from associated pleural effusions. It is often retracted, owing to
the atrophic changes, and collapse brought about by the new formation
or induced by pleural adhesions. The movements of the chest, unless
there is a pleural complication, possess no distinctive character in
this disease. Displacements of the heart or trachea may be expected on
mechanical principles if there is mediastinal disease. General
inspection may detect in the clubbed fingers evidences of venous
obstruction, and sometimes an asphyxial hue of the upper portion of the
body. Nearly always a general emaciation with anxious expression
exists, and a tawny or lemon-hued skin indicative of the cancerous
cachexia.

By palpation of the substernal or supra-clavicular spaces one may reach
masses of painless, movable, glandular enlargement, but these may be
easily overlooked unless a careful study be pursued. Circumscribed
swellings of the thoracic walls may be detected, though not often, and
the glands of the axillæ and neck may enlarge. Palpation may also
reveal an inequality in volume between the radial pulses, but not so
commonly as in purely mediastinal tumors or in aneurisms. Percussion
and auscultation are negative or yield an area of dulness or flatness
with restricted or absent respiratory murmur. When there is a single
large growth the boundaries of these signs are local. If the tumors are
diffused the respiratory murmur varies. In tiers of lung it is feeble
or absent; elsewhere it is harsh, puerile, or bronchial. Chiefly
remarkable is the fact that the character of the respiratory murmur
cannot be harmonized with any other pulmonary states when the entire
clinical evidence is taken. Vocal resonance corresponds with the
respiratory murmur according to accepted laws. When there is pressure
on the principal bronchus on one or both sides, one can detect either a
snoring, increased bronchial respiration, or else, if the pressure
decidedly narrows the calibre of the bronchus, the breathing becomes
feeble or wheezing. Expiration may be prolonged and sonorous in
character, with or without râles. The pressure is rarely equal on the
two sides. The vocal resonance in these cases is ringing and brazen.
Mensuration corroborates inspection. Pleural effusion from whatever
cause is revealed by the ordinary signs. Enlargement of the bronchial
glands, either primary or coexistent with the development of cancer in
the lung, reveals itself by pressure-symptoms proportionate in their
severity to the degree of bronchial enlargement. Pain, laryngeal
irritation, differences in the radical pulses, tumor if the enlargement
is anterior, one or all, may be present. The aorta itself may be
compressed by the enlarged glands; and by the narrowing of its lumen
thrill, and even systolic, murmur can appear, making a differential
diagnosis from aortic aneurism very difficult. (Vide MEDIASTINAL
TUMORS.) Embolism and thrombosis, with the ordinary symptoms, may
complicate the course of pulmonary cancer and obscure the diagnosis.

The duration of cancer of the lung is fixed by Walsh at 13.2 months,
mean average, maximum, at 27 months; minimum, at 3.5 months; but this
is based on a confessedly small contingent of cases. The first
symptoms, dry cough, pain in the chest, difficulty of breathing, may
last for some years without alarming the patient. After the more
dangerous phenomena appear the course is often more rapid. The history
of cancer in the lung in the main corresponds with cases of similar
types of cancer elsewhere. The grave symptoms appear earlier in cases
of mediastinal cancer than in cancer of the lungs proper. Death may
result from asphyxia; from bronchial obstruction; from pulmonary oedema
occurring suddenly, as in chronic alcoholism; from embolism of the
pulmonary artery; or from pleural effusion. Life may gradually ebb away
through general asthenia with malnutrition; in some {464} remarkable
cases the same result is accompanied by hectic fever and the typhoid
phenomena, with evidences of tissue-disintegration.

COMPLICATIONS.--The complications of pulmonary cancer have been already
outlined. They are chiefly the bronchial, pleural, and mediastinal
processes. Primary cancer of the lungs possesses a feeble tendency to
metastasis.

DIAGNOSIS.--The most valuable assistance is derived from a close study
of the personal and hereditary history. Whenever a new growth has been
extirpated, the possibility of its reappearance in the lungs should
always be remembered. The most disciplined comparative analysis of
physical signs may be fruitless. The origin of a primary growth from
the roots of the lungs may help to interpret the physical signs, and
examination of the sputa should never be omitted. In secondary cancer
the history of the case may include the removal or development of
morbid growths from other parts of the body. Any pulmonary symptoms in
these cases become more suspicious than they would in persons in whom
no signs of cancerous diathesis have ever made their appearance. This
rule must not be pressed too far, for forms of pleurisy, bronchitis,
and pneumonia or phthisis may be the explanation of the symptoms.

In the differential diagnosis it is a matter of universal experience
that some form of chronic pleurisy is the most frequent source of doubt
to the clinician. It has been said by Wintrich that vocal fremitus in
cancer is more often present than absent. If there is much pleural
effusion, paracentesis will be helpful in two ways. When the fluid is
turbid, highly albuminous, with a large proportion of coagulable
fibrin, it is an evidence of its inflammatory origin; but if it is
clear and limpid, and upon standing gives but a delicate veil of
pseudo-fibrin, it indicates a passive or mechanical cause. If the fluid
evacuated should contain any considerable amount of blood, such a
peculiarity in association with the other symptoms already indicated is
to be regarded as probable evidence of the existence of cancer of the
pleura. If the external veins of the thorax are enlarged, they indicate
a deep-seated cause of pressure. In malignant disease with retraction
there may be less deepening and narrowing of the intercostal spaces on
full respiratory movement than is associated with chronic pleurisy:
there is usually greater volume and nearness of the respiratory murmur,
although this is more noticeable on the left than on the right side,
since the liver is present in the latter. The greater severity of the
local symptoms and the increase in gravity of the disease must be
contrasted with the features of a disease in the decline, as is the
case in chronic pleurisy. Walsh considers that "the normal position of
shoulder, spine, and scapulæ distinguishes cancer from the results of
simple pleurisy." In addition, we have the shorter duration of cancer,
which is never over two and a half years, often less. The lemon-hued
cachexia is so frequently absent that the inference from general
inspection of the features is marred. From fibroid forms of pulmonary
disease we have the pressure-signs, giving evidences of mediastinal new
formation; also the possible prune-juice expectoration of cancer. The
retraction and displacements of the intra-thoracic organs, chiefly the
heart, are greater in fibroid disease than in either pleurisy or
cancer.

In addition, the history of phthisis includes a higher thermometrical
record, frequent hæmoptysis, and abundant sputa. Physical diagnosis in
cases of phthisis reveals a destructive process involving extensive
areas of pulmonary tissue in a comparatively regular sequence. The
cancerous process is more local or involves the tissues in an irregular
order. Moreover, the asphyxial hue and the pressure-symptoms
preponderate in malignant disease. To distinguish the cancerous process
from simple forms of bronchitis we may observe the frequency with which
the symptoms of bronchitis recur in cancer {465} without exposure to an
adequate cause; by the absence of marked tendency to hypertrophic
emphysema; by the resistance to treatment; by the persistence of
dyspnoea as a prominent symptom; and by the gradual development of
patches of hypostatic congestion. To differentiate from aneurism we
should consider the occupation of the patient, the absence of syphilis
or other causes of arterial disease, the history, the location of the
tumor, and the absence of the murmur. Hydatid cysts may simulate
cancer, but this disease is rare in America. (Vide PULMONARY HYDATIDS.)
In cancer of the liver, as that organ enlarges pulmonary symptoms may
occur from irritation, and congestion or oedema be produced. We must be
content to mention the possibility of error, and decide in each case
after a crucial analysis of the abdominal or thoracic symptoms.

PROGNOSIS; TREATMENT.--The prognosis is fatal; the treatment purely
palliative. It is quite justifiable to relieve pain by the hypodermic
use of morphia, cough by chloral or the usual narcotics, and fetor of
the breath may be palliated by inhalation of carbolic acid or other
disinfectants. Dyspnoea may be alleviated by the use of strychnia as a
respiratory stimulant--by inhalation of nitrate of amyl or small
allowances of chloroform or digitalis. Paracentesis thoracis must often
be resorted to in cases of pleural effusion, even although the relief
it affords be temporary.




{466}

PULMONARY HYDATIDS.

BY EDWARD T. BRUEN, M.D.


DEFINITION.--A disease in the lungs consequent upon the entrance into
the human system of the eggs of a small tape-worm, whose usual habitat
is the upper half of the small intestine of the dog.

SYNONYMS.--Tænia echinococcus; Acephalocyst. _Fr._ Kystes hydatiques du
poumon; _Ger._ Lungenechinococcus.

HISTORY.--Unmistakable references to this disease are found in the
writings of Hippocrates, Aretæus, Galen, and other early writers. For a
long time, however, the animal character of the hydatid cyst was not
recognized, but confounded with slowly-developed local dropsies of
various orders and with lymphatic dilatations. Their animal nature was
suspected by Hartman in 1685, but their origin was not separated from
the cysticercus. In 1766, Pallas clearly distinguished the two species,
and this author was followed in a more positive way by Groeze in 1782.
Laennec in 1804 carefully studied the hydatid cyst as found in the
sheep, recognizing even the mode of reproduction, but he erroneously
described the same parasite, when existing in man, as a distinct
animal, which he termed acephalocyst. Since 1821, Bremsen, Davaine,
Küchenmeister, and others have definitely settled the true mode of the
entrance of the Tænia echinococcus into the human system, and the
subsequent development of the hydatid cysts. The development of the
parasite resembles that of the cysticercus. Like the latter, the larvæ
infest the bowels of certain animals, and take their further
development in a different animal or species, forming vesicles which
are distributed in the parenchyma of the different organs, and in this
way more or less seriously compromising the functional life of the part
in which they occur.

ETIOLOGY. (See article on INTESTINAL WORMS, by Leidy.)--Hydatids have
been found in the human subject in all countries, but especially in
France, Germany, and in the north of Europe. They are rarely found in
North America, and the fact that the majority of cases seen here have
occurred in foreigners favors the probability of the hydatid disease
having been imported. But there are two countries where it may be said
to be endemic--Iceland and Australia. Finsen found 1 out of every 43
inhabitants affected with this disease in the district of Ofjord in
Iceland. Hydatids are communicated to the human race through the system
of the dog, and in Iceland the proportion of these animals to the
population is probably more than 1 to 3, a recent census recording
20,000 dogs to 70,000 inhabitants. Hydatids usually enter the system
through the digestive and respiratory organs. The Icelanders are
excessively uncleanly and careless of the laws of ventilation. In the
winter season both men and women are confined to the house in company
with their dogs, and in consequence the air is impregnated, and
oftentimes the drinking-water contaminated, through their dejecta,
which contain thousands of the eggs of the echinococci. The largest
{467} number of cases occur in the agricultural districts, since the
dogs are more required there than on the sea-coast.

In Australia large numbers of dogs are maintained to guard the sheep.
The droppings of these animals, dried by the hot winds, are inhaled as
dust. It is curious to note that in Australia, where the high winds
prevail, the proportion of pulmonary hydatids is very large, while in
Iceland, where the drinking-water is the principal medium of
communication, the lungs are less often affected than other viscera.
Finsen's records in the latter country show 255 cases; of these, 176
occurred in the liver, and only 7 in the lungs. In both Iceland and
Australia women are more subject to echinococci than men. This is
possibly accounted for by the facts that the women take care of the
dogs and wash the vessels from which they eat, and are also less
protected by hair about the mouth and nose than men.

The disease occurs most often between the ages of twenty and thirty
years, but it has been found in children of four years of age. Before
ten and after sixty the proportion of cases in both sexes is equal. The
malady is not hereditary, but uniformity of environment accounts for
the propagation in communities. Pulmonary hydatids occur as primary
formations in the lungs, but may be secondary to similar growths
elsewhere, especially in the liver. There is, however, scarcely a
tissue in the body in which hydatids have not been found.

MORBID ANATOMY.--Hydatid cysts consist of sacs of various sizes, from
that of a pea to an orange or even an adult head. They are usually
globular in shape, and attached by a vascular membrane to the organ in
which they are situated. The walls of the cysts are composed of a few
laminæ of indeterminate membrane of varying thicknesses, commonly
depending on the age of the cyst. In young cysts they occur in direct
contact with the lung, but as they grow larger a thicker investment is
formed, and large old cysts which have generally undergone spontaneous
rupture often have a dense leathery sac. Walsh asserts that the parent
cyst lies in direct contact with the lung-tissue, and, unlike that of
the liver, is rarely surrounded with a thick shell or cyst-wall of
pseudo-areolar tissue. The interior of the pouch is smooth and of the
aspect of serous membrane without epithelial covering. The parent cyst
contains daughter cysts which are single or multiple, and a liquid the
proportion of which is variable. This liquid is nearly limpid, and
non-coagulable by heat or acids; it deposits by evaporation crystals of
chloride of sodium.

Commonly, only one hydatid tumor is found in the human lungs, although
in animals multiplicity of cysts is the rule. They are usually located
in the base of the lungs, and are thought to be more common on the
right side, but they may occupy any portion of one or both lungs. They
have been found in the pleura, the bronchi, the pericardium, and the
thyroid gland. In the pleural cavity they may be attached to both the
costal and the visceral pleura; in the latter case they may form an
outgrowth from the lung into the pleural cavity. Authorities differ as
to the condition of the neighboring lung-tissue, some stating that the
cysts are rarely surrounded by healthy lung-substance, while others
assert the contrary. Since the growth of the cysts is often very slow,
the accommodating power of the lung is remarkable when no
constitutional mischief exists. In some instances the rapid enlargement
of a cyst has been accompanied by certain forms of pneumonia, secondary
inflammatory lesions, congestion of the neighboring tissue,
splenification, or even gangrene.

Hydatids situated either in the lung or pleura may rupture into the
bronchial tubes, and thence be discharged by cough and expectoration,
or they may open externally like a pleural empyema, or even rupture
through the diaphragm into the intestines or peritoneum. None of the
above accidents are necessarily fatal, not even the latter, unless the
fluid be puriform. {468} Empyema with pneumothorax usually follows
rupture into the pleura. Finsen observes that a general urticaria may
follow the rupture of a cyst into a serous cavity. In old cases, after
rupture of cysts, pulmonary changes may almost always be found. The
ruptured cyst may become a suppurating cavity, suggesting the possible
development of phthisis. In some cases hydatid formations have been
described with coexisting catarrhal or tubercular disease, or these
processes may occur as a complication without rupture of the cyst.

SYMPTOMS.--The symptoms of hydatid cysts are obscure, and the physical
signs difficult to analyze when the cysts are small. They are more
suggestive when the cyst becomes large enough to contain a pint or more
of fluid. The outline of the cyst is usually globular, and is imbedded
in healthy or nearly healthy lung-tissue. According to Bird, the
physical signs correspond with those familiar to us in pleural
effusions: absolute dulness or flatness on percussion, with absence of
respiratory murmur over a space of the chest-wall not smaller than the
palm of the hand; vocal fremitus and resonance are also abolished. The
expansion of the chest is more or less deficient upon the affected
side, but seldom with any change on mensuration.

The area of the above physical signs usually presents a rounded
outline, limited by a line of demarcation so exact that it can be
mapped out with pen and ink, but is unaltered by position. Their
location is generally in the lateral or infra-clavicular regions;
beyond the boundary-line percussion is vesiculo-tympanitic resonant or
normal, and the respiratory sounds begin at the very margin of the
pen-and-ink line, and, though probably harsh and puerile in character,
are indicative of healthy lung-tissue.

Pulmonary hydatids can seldom be examined by palpation, but all authors
allude to a frémissement or peripheral fluctuation which may sometimes,
but not invariably, be detected by palpation over the intercostal
spaces. Davaine directs palpation as one would palpate an abdominal
cyst. The sensation of fluctuation is as though the fluid were
gelatinous; when the quantity of liquid is excessive this movement is
not perceptible. It is most recognizable when there is but a single
hydatid in the parent cyst (Jobert). The frémissement cannot be felt
when the sac has undergone atheromatous degeneration, because there is
then no liquid, and the cysts are withered, agglutinated to one
another, and the tumor is inelastic and hard. By auscultating the tumor
while practising percussion one may hear more or less positive
vibrations resembling those produced by a bass string (Briançon).

The general symptoms of pulmonary hydatids are of mechanical origin:
pain, dyspnoea, cough, with duskiness of the surface, all of which are
more or less marked according to the size and location of the tumor and
its rapidity of growth. A phthisical appearance is possible, with
deterioration of the blood-crasis and progressive loss of flesh. Marked
clubbing of the finger-ends and incurvation of the nails have been
noticed, all of which symptoms have disappeared after the hydatid cyst
has been tapped or expectorated. Cough nearly always accompanies this
disease, as it does a large pleural effusion. The expectoration is a
glairy mucus, sometimes stained with blood; when local bronchitis
occurs as a complication, it may become muco-purulent. There is much
diversity of opinion as to the frequency of hæmoptysis, many authors
looking on it as a rare symptom. According to Bird, there is seldom or
never profuse hæmoptysis, though several ounces have been expectorated
at a time in an aggravated case where tapping had been long delayed.
The cause of hæmoptysis is usually pressure of the growing cyst upon
the pulmonary veins, leading to extravasations of blood.

If dyspnoea with deficient aëration of the blood, wasting, clubbed
fingers, and expectoration persist after the expulsion or death of the
hydatid, the probability is in favor of some associated pulmonary
inflammation. When {469} a hydatid cyst ruptures into the bronchial
passages, there is serious likelihood that the patient may choke or
suffocative dyspnoea supervene. The quantity of entozoal substance
voided at any one time varies from a few microscopical fragments up to
a pint or more of unbroken acephalocysts. The expectoration of
acephalocysts may continue several months. Serious general pulmonary
symptoms precede and follow this accident. When rupture has taken place
into a bronchial tube, there are the usual physical signs of a
pulmonary abscess or large vomica. The sac usually suppurates, and
there is a constant expectoration of blood, pus, and half-putrid
acephalocysts of excessive fetor, and often portions of gangrenous
lung-tissue. With these symptoms the temperature is sometimes of a low,
remittent type, with hectic and sweats. The symptoms resemble those of
empyema or advanced phthisis, and may continue for months, until the
patient, in most cases, sinks from exhaustion, unless relieved by the
evacuation of the sac and its contents. When hydatids develop in the
pleural cavity the signs are identical with a localized pleural
effusion.

Nothing has been said to differentiate pulmonary-hydatid expectoration
from cases where an hepatic hydatid cyst has burst into the lungs, and
the diagnosis may be very difficult. The physical signs of enlarged
liver are present, also the antecedent symptoms of disordered hepatic
action, especially intestinal indigestion and the staining of the sputa
with bile. If the cyst has undergone suppuration, the symptoms may be
allied to those of hepatic abscess.

The nucleation of testimony favors the view that a latent or slow
growth is by far the most common history of hydatids. Their duration is
very variable: patients may harbor them for a long time unconsciously,
even over a period of sixty years. This is corroborated by Finsen, who
reports cases in which the disease lasted sixteen, eighteen, and
fifty-two years, proving this by stating that these individuals had
left the country where the disease was endemic, and were residing
during these periods where the malady was rare.

TERMINATIONS.--30 or 40 per cent. of cases terminate in recovery if the
cysts spontaneously burst, death being caused in others by suppuration
and exhaustion. There is, in addition, the risk of sudden death from
the rupture of a large cyst in the lung, and consequent filling up of
the air-passages by its contents. The cysts may sometimes undergo
atheromatous changes in which the hydatids resemble crushed
grape-seeds. Microscopically, one finds a puriform fluid, plates of
cholesterin, crystals of hæmatoidin, hooklets of echinococci, and
débris of membranes. Again, the cysts may resemble a caseous or
cretaceous tubercle without special characteristics. This may be looked
on as a species of spontaneous cure. The growth of hydatid cysts may
bring about by pressure such a state of chronic pulmonary engorgement
that it affords a predisposing condition favoring the development of
tubercular phthisis.

DIAGNOSIS.--The differential diagnosis is necessarily difficult. The
nationality of the subject and the presence of a predisposing
environment should always be remembered. If the disease progresses
rapidly without interference, the diagnosis may be complicated by the
development of patches of bronchitis or pneumonia with rusty sputa. The
bronchitis is, however, local, which, taken with the physical signs of
a cyst, may be suggestive. The only absolute evidence of the existence
of hydatids in the lungs, whether primary or secondary, is the
appearance in the sputa of the characteristic cysts or portions of
them, such as fragments of the hooklets of the echinococci. This,
unfortunately, occurs as a late accident in their history. If the
boundaries of the cyst can be recognized, it is justifiable to resort
to paracentesis, and thereby withdraw some fluid for examination. The
physical signs of local serous effusion, globular in shape, not evenly
{470} distributed around the circumference of the chest, is one of the
best differential evidences between hydatids and pleural effusion.
Moreover, there is no fever in hydatids unless after rupture, or with
extensive phthisical complication, while there is a history of fever in
some stage of most cases of pleurisy. Hydrothorax is differentiated
through its being bilateral and by its etiology. From local encysted
pleurisy the only resort is exploratory puncture and the question of
the probabilities in each case. In the same way paracentesis removes
doubt whether there be mediastinal tumor, solid tumor of the lung, or
circumscribed pneumonic abscess; in the latter the general history of
each case is helpful. From phthisis we must have recourse to the
physical diagnosis already mentioned as belonging to hydatids. An
unbroken cyst in the liver, high up and far back on its convex surface,
may not be distinguishable from one in the base of the lung immediately
over the liver or one in the cavity of the pleura.

PROGNOSIS.--According to Reynaud, this depends on--1, whether the
hydatid is single or multiple; 2, whether the pressure is exercised on
blood-vessels or bronchi; 3, if hydatids are discovered elsewhere; 4,
size of cyst; 5, alterations in the walls of cysts; 6, whether
complicated with any other disease or independent.

If there is a tendency to pulmonary phthisis, inherited or acquired, or
if this disease exists as a complication, it forms an unfavorable
element in the prognosis. Persons once affected with hydatids are more
susceptible to a second invasion of the parasite. The practicability of
treatment by tapping is also an element in the prognosis.

TREATMENT.--Naturally, the preventive treatment rationally deduced from
the now distinctly-understood causes should be practised. The
water-supply should be protected from sources of contamination, and in
addition the inhabitants of countries where the disease is prevalent
should, as far as practicable, use boiled or stone-filtered water and
refrain from eating water-cresses or plants of like character wherever
these are liable to be contaminated.

Many drugs have been administered, among them the bromide and iodide of
potassium; solutions of salt are also said to be deleterious to the
life of the echinococcus; Laennec even prescribed salt baths. Tincture
of kamela has been recommended by Hjaltelin, a physician in the employ
of the Danish government in Iceland. He administered it in doses of
thirty drops daily to adults, continuing its use during a month or
more. It has a distinctly irritating and destructive effect on the
acephalocyst (Bird). Turpentine, from its well-known anthelmintic
powers and ready diffusibility, has naturally suggested itself as a
remedy, and according to some has proved of great service in many
instances, while in others it has signally failed.

Paracentesis is generally regarded as the most efficacious treatment,
and may be carried out upon the principles usually applied in the
treatment of hydrothorax. Bird recommends that the trocar should be not
less than six inches long and of the smallest diameter that is made,
always providing that it is strong enough to bear the strain of a firm
pressure. Cysts can be tapped in this manner even when they are
separated from the chest-wall by quite a deep layer of lung-substance.
This treatment should be practised at the earliest possible period in
the life of the cyst. Speaking of the aspirator, he says that cases
always do so well if tapped early enough with the simple trocar and
canula that aspiration is not required. The gradual expansion of the
lung as the cyst is emptied is sufficient to expel all the fluid,
especially if aided by the effects of coughing. In exceptional cases of
old standing, where there is a thick adventitious external wall to the
cyst, which is generally closely adherent to the ribs, or again in
cysts of the pleura, a free antecedent incision of the external tissues
is sometimes required. It has been suggested by different authors that
tincture of iodine should be injected after {471} aspiration to secure
the obliteration of the cyst by inflammation. The injection of carbolic
or salicylic acid under the same conditions has been practised with
success by Mosler and others.

The treatment of old suppurating cysts is rather different. The centre
of the sac, as nearly as can be judged, is fixed upon, and an incision
is then made through the skin and muscles, and the largest-sized trocar
and canula that will pass between the ribs is introduced into the sac.
This gives exit to a quantity of pus, even chalky substances and
fragments of cysts of different sizes. The opening must be free and
kept patulous for some weeks, and the sac should be daily washed out
with some disinfecting solution through the drainage-tube. Some delay
is always necessary to allow of the separation of the parent cyst from
its nidus and the gradual expansion of the lung. Immediate attempts at
its removal by forceps are generally unsuccessful, and portions are
very apt to be left behind. Several complications may interfere with
the success of the operation. One is the unavoidable piercing of a
small bronchus by the trocar. After the operation the wound of the
bronchus may remain patulous and a violent paroxysmal cough comes on,
with subsequent possible evacuation of the cyst through this channel.
The bronchial tubes, however, have been opened in operative treatment
of pulmonary cavities without serious result. When the parent cyst has
progressed to maturity quite unhindered, and is stuffed full of
daughter cysts, it has been recommended in such cases to introduce the
stylet and endeavor with its sharp point to stir up and break down the
smaller cysts as much as possible. The thermo-cautery has recently been
used successfully by Mosler to afford a means of penetrating the cyst
in the treatment of pulmonary hydatids. The tissues of the thoracic
wall must be first divided down to the pleura, as recommended in the
opening of pulmonary vomica by the thermo-cautery. Resection of the
ribs should be practised in case sufficient drainage cannot be
accomplished through an interspace.

Before applying to these operative measures it is desirable that
adhesions should have occurred between the visceral and the parietal
pleura. Fenger and Hollister recommend the introduction of a needle as
a means of diagnosis: if there be adhesions, it is unaffected by
respiration; if no adhesions exist, it is moved synchronously with the
breathing. There are, however, no absolutely reliable signs by which
this adhesion can be determined. Paracentesis of suppurating sacs has
been performed in cases in which the pleural surfaces have not been
adherent. In some instances the lung has been stitched to the opening
in the pleura, and after partial adhesion has occurred the purulent
collection has been punctured. In certain other cases, when pleural
adhesions have been absent, paracentesis has not been followed by
serious pneumothorax, possibly because the apposition of the pleural
surfaces is maintained by the tendency to cohesion which exists, and
after operative interference these surfaces are united by adhesive
inflammation.




{472}

ACUTE MILIARY TUBERCULOSIS.

BY JOHN S. LYNCH, M.D.


Acute miliary tuberculosis may be defined to be an acute disease
characterized by an eruption in one or all of the organs of the body of
small nodular or granular masses called tubercles, attended with fever
and various other functional disturbances.

The fact which Villemin and Klebs were the first to show,[1] and which
hundreds of others have since verified, that tuberculosis can be
conveyed by inoculation to certain animals, and the additional fact
that Koch and his followers seem to have identified the infective
material in the micro-organism which he has named bacillus
tuberculosis, would seem to justify our placing tuberculosis, along
with variola, measles, etc., among the acute contagious infectious
diseases. But since some able pathologists still deny the correctness
of Koch's conclusions; since in certain animals indifferent irritants
have excited a disease which could not be distinguished from
tuberculosis by the ablest pathologists of Europe and America; since to
some species of animals even more nearly allied to man by their
organism than rabbits and guinea-pigs the disease cannot be conveyed at
all, and that even to some of the latter inoculation fails to transmit
it; and, above all, since there is, as far as we know, not one single
case on record in which the disease has been clearly and unmistakably
traced from man to man in the order of infection,--we do not think that
as yet we are justified in defining it as a contagious infectious
disease purely and only. Everybody will take small-pox if not protected
by vaccination or inoculation, and this disease may be transmitted in a
modified form to many of the lower animals. The same may be said of
measles, scarlatina, and nearly all other diseases known to be
contagious and infectious. Since, then, so few persons take
tuberculosis that the evidence of its contagiousness rests upon a vague
popular belief, and since even some animals of a species known to be
peculiarly susceptible to the disease fail to take it even by
inoculation, we think that we are justified in assuming that there must
be something else besides a contagium required to produce the disease.
This is evidently a predisposition which depends upon some peculiar
diathesis, cachexia, or dyscrasia, congenital or acquired. It has been
assumed that scrofula constitutes the particular diathetic condition
which predisposes to tuberculosis, and it is common for scrofulosis and
tuberculosis to be spoken of as convertible terms. In the article on
SCROFULA in this work we have already given our reasons for dissent
from this view, and to that article the reader is referred. Farther on
we shall give our views as to what constitutes the tubercular diathesis
when we shall speak of the mode of formation of tubercle.

[Footnote 1: But Buhl had long before advanced the doctrine that
tuberculosis was a resorption disease.]

While, then, we cannot as yet admit that acute miliary tuberculosis is
always and only set up by a contagium, it is unquestionably true that
it is in a large majority of instances caused by an infective material,
which, however, {473} does not come from without, but is produced
within the system. This material is the purulent detritus resulting
from the softening and breaking down of the inflammatory and other
cellular hyperplasias which have undergone the caseous degeneration. It
seems to make little difference whether the caseous product was derived
from scrofulous glandular hyperplasia, catarrho-pneumonia, inflammation
of serous membranes with a cellular exudation, or ordinary cellular
inflammation; the only essential prerequisites being that there shall
exist a cellular exudation or proliferation, and that these cells shall
undergo the caseous degeneration.

The inoculation of this material into certain species of the lower
animals or its absorption into the blood of a human being predisposed
to tuberculosis will, as a rule, produce tuberculosis. Koch and his
disciples add to the foregoing another prerequisite--viz. that the
caseous matter must contain the bacillus tuberculosis. But as the
bacillus is generally found in all the cheesy inflammatory products we
have mentioned, they have (ignoring Virchow's definition of tubercle)
declared that all these are tubercle, thus very much enlarging the
hitherto accepted doctrine upon this subject. But if any of the cheesy
products are found not to contain the bacillus, then such product is
not tubercle, whatever may be the apparent identity or dissimilarity in
their etiology, microscopical appearances, or clinical history. This
seems to us to be a begging of the whole question of the relation of
the bacillus to tubercle, and in the absence of fuller experimentation
and investigation involves an assumption which cannot yet be admitted.

While the absorption of caseous pus is undoubtedly by far the most
frequent cause of miliary tuberculosis, it cannot be inferred that all
who may happen to have foci of caseous degenerations will necessarily
be attacked by tuberculosis. On the contrary, a vast majority escape,
and it is almost surprising how few of those who suffer from scrofulous
inflammation of glands, joints, etc. become the subjects of miliary
tuberculosis. Many cases of pulmonary phthisis also, originating as a
cheesy pneumonia, run their course without any distinct tubercular
complication. We can only explain these exemptions from the tubercular
process by supposing that in such cases the predisposition to
tuberculosis does not exist--they do not have the tubercular
diathesis--or that such persons possess a peculiar means of resistance
to the entrance of the infecting material into their blood.

Other diseases are supposed to favor the tubercular process, either by
directly exciting or increasing the predisposition to it. Among others,
measles, whooping cough, and typhoid fever have been regarded as
specially liable to be followed by tuberculosis. Bad air, poor or
insufficient food, onanism or other forms of sexual excess, severe
study with insufficient exercise, and, in short, anything which impairs
the strength or lowers the vitality, have been heretofore considered as
excitants or predisposers of the disease. Admitting all these causes as
effective in either exciting it or increasing the predisposition to it,
there still remains quite a large residuum of cases in which the
disease can be traced to none of these causes, and which, for the want
of more accurate knowledge, we are compelled to call idiopathic or
spontaneous. Such are those cases of tubercular meningitis occurring in
young children heretofore in apparent good health, and in whom no
traces of caseous degeneration can anywhere be found. It is true that
it may be asserted that these children may have been infected through
kissing by persons suffering from pulmonary consumption; but if this
were so the disease ought to be far more frequent than it is, since the
habit of kissing babies is universal and consumption the most
prevailing of all diseases. In the absence of any proof to the
contrary, we think that we are justified in believing that these are
cases of spontaneous tuberculosis, occurring in consequence of
intensity of the diathesis, either inherited or acquired.

{474} Miliary tubercles are found in the form of small roundish nodules
ranging in size from 1/500 to 1/250 inch (submiliary tubercles), up to
the size of a millet-seed or even of a pea. When of the latter size
they are always made up of a number of submiliary tubercles. Much
larger masses are found usually in the lungs and in the mesentery, but
these will generally be found to consist not of miliary or submiliary
tubercles alone, but of cellular new formations derived from
endothelial or lymphatic proliferations excited by the presence of
tubercles, and therefore mixed with them. When first formed they are
grayish in color, somewhat translucent, and tolerably firm to the touch
(gray granulations). They soon, however, undergo partial fatty
degeneration (this degeneration usually commencing in the centre of the
mass), and subsequently are converted into a dry, yellowish-white, and
somewhat crumbly mass which from its resemblance to cheese is called
caseous. This sooner or later softens (the softening process beginning
also in the centre), and the mass breaks down into a fluid
detritus--tubercular pus. In some situations they never reach the
caseous and purulent stage (notably in the cerebral meninges), because
the interference with the organs or nerve-centres of animal life
excited by their presence destroys the patient before there is time for
the accomplishment of these changes. The subsequent history of tubercle
depends upon the condition of the patient, his powers of resistance,
the intensity of the tubercular diathesis, the injury inflicted by the
first eruption, and the appearance of secondary eruptions. If all
conditions are favorable, the patient placed under proper hygienic
conditions and properly treated, the first eruption will also be the
last, and the tubercle dries up into an earthy mass (calcareous
degeneration), or it may remain for months, and even years, in its
caseous stage without undergoing the softening process.

If we examine a fresh tubercle under the microscope, we find, according
to Woodward[2] and Zeigler,[3] that it is usually made up of three
different kinds of cells: first and most abundantly, lymphoid cells
(Woodward) or white blood-cells (Zeigler); second, endothelioid cells;
and third, embryonic cells. In addition to these there is often found
(but not always) a few so-called giant-cells, generally occupying the
centre or circumference of the tubercle, and sometimes both. These
cells, which usually contain two or more nuclei and are much larger
than the ordinary lymphoid cell, were thought at one time to constitute
an essential histological feature of tubercle, and have been named
tubercular cells. But the frequent absence of these cells in genuine
tubercle has led to the conclusion that they do not possess any special
significance and are purely accidental. Each submiliary tubercle is
usually surrounded by a proliferating zone in which multinuclear
(giant) cells and fibro-plastic or spindle-form elements can be
distinguished (Cornil and Ranvier[4]). According to Rindfleisch,[5]
Woodward,[6] and Zeigler,[7] the cellular elements of tubercle are
always found included in a trabeculum of fine fibrillar (connective)
tissue, while Cornil and Ranvier deny the existence of any such
trabeculum, maintaining that its appearance is due to the action of
hardening agents used for preparing it for microscopic examination.
Virchow and Woodward believed that tubercle always takes its origin in
a lymphatic vessel, while Rindfleisch, partially agreeing with this
view, maintains that they most generally occur in the lymphatic sheaths
of the blood-vessels and follow the course of the latter, and that the
cells which compose the tubercle are formed by proliferation of the
endothelia of the lymphatics.

[Footnote 2: _Medical and Surgical History of the War of the
Rebellion_, Part 2, Medical Volume, p. 593.]

[Footnote 3: _General Pathological Anatomy_, London, 1883, p. 171.]

[Footnote 4: _Pathological Histology_, Philadelphia, p. 116.]

[Footnote 5: _Textbook of Pathological Histology_, Philadelphia, 1872,
p. 125.]

[Footnote 6: _Op. cit._]

[Footnote 7: _Op. cit._, p. 168.]

{475} Zeigler has not been able to demonstrate this relation of the
tubercle to a blood-vessel--that is, to an artery--but leaves us to
infer that they always arise from a capillary vessel, since he
maintains that the tubercle is primarily and principally made up of
emigrated leucocytes.

Such is a brief résumé of our knowledge as to the histology and mode of
formation of tubercle, and such are the opinions--in some particulars
agreeing, in others discordant--of those whose investigations and
observations the world regards as most complete and accurate. This
résumé is doubtless unnecessary and out of place in this article, since
this question (the histology and mode of formation of tubercle) has
been already discussed in the first volume of this work; but, as in the
explanation which is to follow of our views as to what constitutes the
tubercular diathesis and what is the mode of formation of tubercle we
shall have to frequently refer to the facts above stated, we have
thought it best, in order to save repetition and too frequent reference
to authorities, to give the above résumé of the present state of the
views of pathologists upon the histology of tubercle.

A careful consideration of the foregoing facts ought, it seems to us,
to enable us to arrive at a rational and probably correct conclusion as
to the mode of formation, as well as the principal etiological factors
concerned in the causation, of the miliary tubercle; and we venture to
offer the following explanation of the subject as more in consonance
with the facts above related than any view which we have seen upon this
question:

1. Miliary tubercles always occupy a lymph-space surrounding a
capillary blood-vessel. When found, as they quite often are, occupying
the wall of a larger vessel, artery or vein, it is still in the
lymph-sheath of a capillary of the vasa vasorum that they primarily
originated. And it may be said that this is the most dangerous site a
tubercle can occupy, because when softening takes place it is so apt to
burst into the lumen of the vessel and so produce a general infection.

2. The tubercular process consists at first of an undue or excessive
emigration of leucocytes through the walls of a capillary which runs
through a lymph-space, and where, of course, the walls of the vessel
are less firmly supported. Those cells whose vitality is lowered by the
causes which have preceded and excited the process can neither undergo
any process of differentiation nor wander on through the lymphatics;
they remain in the lymph-space, which they crowd and block up, and
finally by their pressure occlude, the capillary vessel from which they
emigrated. Until this event occurs they still retain a feeble vitality,
and even abortive attempts at proliferation are seen, which, however,
only reach the stage of division of the nucleus, the body of the cell
meanwhile swelling up by imbibition and thus forming the so-called
giant-cell. As soon as the capillary vessel becomes occluded further
addition to the incipient tubercle from this source ceases; nutrition
is now entirely cut off, and the cells, dying, become a foreign
substance, and soon undergo the caseous degeneration. But by their
presence they now excite a quasi-inflammatory process in the endothelia
lining the lymph-space, and hence we have a secondary addition to the
tubercle derived from the proliferating endothelia. Lastly, the
inflammatory process extends to the connective-tissue cells around the
lymph-space, and embryonic cells (the only cells capable of resulting
from connective-tissue inflammation) are added to the mass. This
constitutes the proliferating zone, consisting of many nucleated cells
and fibro-plastic and spindle-form elements, described by Cornil and
Ranvier.[8]

[Footnote 8: _Loc. cit._]

As soon as one capillary vessel becomes entirely occluded, the
neighboring ones become distended by a collateral hyperæmia, and the
same process of cell-exudation or emigration begins; and thus the
process goes on until all the capillaries supplied by a single arterial
twig take part in the process, and {476} one of the larger tubercles is
thus formed by an almost innumerable number of smaller (submiliary)
ones. It would seem to be quite probable that the trabeculum which
Rindfleisch, Woodward, and Zeigler described, and which Cornil and
Ranvier denied, consists of the remains of the connective-tissue fibres
which originally existed between the capillaries successively attacked
by the tubercular process.

In the lungs this process is usually complicated by a true
catarrho-pneumonic inflammation. The tubercle deposited beneath the
lining membrane of the air-sacs sets up inflammation in that membrane,
giving rise to abundant proliferation of the endothelia as well as
emigration of leucocytes, so that the air-sac becomes packed with cells
which may finally undergo caseation, and then cannot be distinguished
from the original tubercle which started the process. If the eruption
of tubercles should be very abundant, life may be destroyed by the
pneumonic process before caseation has even begun in the inflammatory
products. We have quite recently observed a case of this kind. A man
came to the city hospital (Baltimore, Md.) who presented all the
rational and physical signs of tuberculosis of the lungs. After about
three weeks, during which there was only moderate fever, no notable
dulness, and only a few scattered crepitant râles, the temperature
suddenly rose to 104° F.; dulness appeared first over the lower third
of the right lung, which rapidly extended over that side, and
subsequently to the left side, and the man speedily died, comatose and
cyanotic. The autopsy showed the most extensive miliary tuberculosis we
had ever seen in the human lung; but in addition to the tubercles,
which were found in almost every lobule of the right lung, the air-sacs
were almost universally filled with a soft, purulent-like matter which
oozed from the cut surface, and which could be squeezed out in enormous
quantities; myriads of Koch's bacilli were found. It was interesting to
note that the apparent starting-point of this tuberculosis was two
small cavities in the apex of the left lung surrounded by
firmly-indurated walls. Neither of these cavities was larger than the
kernel of an ordinary-sized almond, and, as the induration surrounding
them did not extend to the surface of the lung, their existence was not
recognized before death. The man gave a history of cough and fever,
which had lasted several weeks, about three years before his admission
to the hospital.

More frequently, however, the reverse of the process above described
takes place. That is, a catarrho-pneumonia terminating in caseation and
softening sets up tuberculosis through absorption of the caseous pus.
Indeed, in the case above related the order of pathological processes
was, first, a catarrho-pneumonia of limited extent, a cavity or rather
cavities; second, general tuberculosis; and lastly, a secondary
catarrho-pneumonia caused by the tubercles. We believe, therefore, that
Niemeyer's remark, that "the greatest danger for the majority of
consumptives is that they are apt to become tuberculous," is not so
absurd as a distinguished American author would have us believe.

The formation, then, of tubercle we believe to be an inflammatory
process, in which we have--1st, an exudation of lymphoid cells
(leucocytes) into the lymph-spaces, and occlusion by pressure of the
capillary vessel from which the cells have escaped; 2d, inflammation
and proliferation of the endothelium lining the lymph-space; and 3d,
inflammation of the tissues nearest adjacent to the space. If this is
simple areolar connective tissue, we have a "proliferating zone
consisting of many-nucleated cells and fibro-plastic and spindle-form
elements;" if a mucous or serous membrane, the usual products of
inflammation of such membrane in other and ordinary cases.

But behind these processes there must exist something else which stands
in the relation to them of predisposing and exciting causes. This we
believe to be some anatomical and histological peculiarity, congenital
or acquired, which gives to the individual that defective organization
which is denominated the {477} tubercular diathesis. It seems probable
that this diathesis comprises two factors--viz.: 1st, an unusual
thinness, and consequently weakness, of the walls of the capillary
blood-vessels, which permits and favors a too facile emigration of the
leucocytes; and 2d, a diminished or lowered vitality of the leucocytes
themselves.

Both of these factors may exist at the birth of the individual as an
inheritance from his progenitors, or both may be produced by causes
which impair the general nutrition during either intra-uterine life or
during the earlier infancy of the subject. Or one of them may exist
without the other, and the animal thus escape for a long time, though
exposed to the exciting causes of the disease. Sternburg's guinea-pigs
(animals peculiarly susceptible to tuberculosis) remained healthy while
enjoying the freedom of grassy fields, although inoculated with Koch's
bacilli, which were found in their blood and tissues when killed, while
those that were confined in cages under bad hygienic conditions
speedily succumbed after a similar inoculation.[9] If the first of
these factors exist, any exhausting disease producing a dyscrasia,
habits or hygienic conditions which tend to impair the nutritive
functions, even psychological and emotional influences which take away
the appetite for food or impair the functions of digestion--anything,
in fact, which tends to degrade the quality of the blood and diminish
the functional activity of the white blood-cell--may furnish the second
factor constituting the tubercular diathesis. Both factors being
present, it only requires an uncertain increase of the blood-pressure,
causing a dilatation of the capillaries, to ensure that increased
leucopedesis which constitutes the first step in the tubercular
process.[10] A protracted fever, therefore, of any kind, may furnish
both the second factor in the tubercular diathesis and the exciting
cause of the tubercular process itself; while any fever or any irritant
capable of exciting fever or reaction against its presence occurring in
man or other animal that happens to have the complete tubercular
diathesis may excite tuberculosis. Koch's bacillus will undoubtedly
excite tuberculosis in animals (and probably also in man) that have the
tubercular diathesis complete; but it does so only by exciting that
inflammatory and febrile reaction against its presence in the blood
which other and perhaps indifferent irritants may also excite. In
rabbits and guinea-pigs confined in cages, and therefore under
unnatural and unhygienic conditions, it suffices to excite the disease
only to introduce the bacillus into any part of their tissues: that it
will not do so in guinea-pigs that are healthy and kept under natural
conditions and surroundings Sternburg's experiments, alluded to above,
clearly prove. It is true that other animals that are regarded as
ordinarily non-tuberculous can also be inoculated with the bacillus
with affirmative results, provided the bacillus is introduced into the
eye or other serous membranes; but we must not forget that the pain and
injury of such an operation will almost inevitably produce that
deterioration of the health and impairment of cell-vitality which we
maintain constitutes so essential a part of the tubercular diathesis.
That the bacillus tuberculosis is always found in tubercle is
undoubtedly true; but it is there because tubercle furnishes the most
favorable and congenial breeding-place for it. Some special microbe is
found in almost every special inflammatory product--vibriones in the
pus of abscess, gonococcus in urethral inflammation, micrococcus in
diphtheria, etc.--but no one, we believe, now holds that these various
microbes are the causes of these diseases, since inoculation with pure
cultures have given entirely negative results. While we believe,
therefore, that the bacillus of Koch can excite tuberculosis in man or
animal having the tubercular diathesis, we {478} also believe that it
does so because of its property of exciting that amount of irritation
and reaction necessary to initiate the tubercular process--a property,
however, possessed by many other irritants; and while it is probable
that a few cases may be thus produced in man, a vast majority of the
cases arise independently of its presence. And hence we maintain that
tuberculosis is not a specific contagious disease in the sense that it
is only produced by a special contagion, as small-pox and other similar
diseases are.

[Footnote 9: _Journal of the American Medical Association_, vol. iv.
No. 12, p. 314.]

[Footnote 10: We hold that leucopedesis is a normal physiological
process that is always going on during the period of active growth of
the individual, as well as during the process of repair.]

Primary acute miliary tuberculosis occurs only in the young or early
adult period of life, for the reason, perhaps, that persons of the
tubercular diathesis can hardly long escape the exciting causes of the
disease, and so are attacked early. Persons possessing what may be
called the incomplete or partial diathesis may be attacked by a
secondary miliary tuberculosis at any, even the most advanced, age; but
it will be found that in all such cases of late tubercularization there
has occurred a direct infection of the blood by absorption of caseous
detritus from a softening cheesy pneumonia or cavity. "In 28 out of 52
cases collected by Litten, it was associated with pulmonary phthisis,
and this accords with general experience" (Roberts[11]).

[Footnote 11: _Practice of Medicine_, 5th ed., p. 301.]

Acute primary general miliary tuberculosis--that is, in which all or
nearly all the vascular tissues are attacked at once--must be one of
the rarest diseases. Such cases can only occur when the tubercular
diathesis is strongly marked and exciting causes of the most active
character have been applied. As a rule, tubercular eruptions occur in
successive crops, attacking the more vascular organs, as the lungs,
cerebral meninges, spleen, liver, serous and mucous membranes, and
bones, first and usually in the order given. Laennec's law, that if
tubercle is found in any other organ it will also be found in the lung,
is undoubtedly true, with the single exception perhaps of tubercular
meningitis. If our explanation of the causes and mode of formation of
tubercle is correct, we must a priori expect to find that a tissue so
soft and spongy as the lung, and which is so vascular and subject to
such great and sudden alterations of pressure and relaxation, would
naturally be the site of the first formation of tubercle.

SYMPTOMS AND COURSE.--It is impossible to give a clear or lucid
description of acute miliary tuberculosis, since there cannot be said
to be any constant or pathognomonic symptoms produced by the disease
per se. The symptoms present in any given case depend upon the organs
involved, and may be said to consist merely of those furnished by such
organs when invaded by inflammation. Fever is present in all cases. The
grade or height of this fever will depend upon the number and extent of
tubercular formations, and to some extent upon the organs involved. It
will generally be highest in tubercle of the serous membranes, and of
the lungs next. In general miliary tuberculosis the fever is highest,
and can be distinguished with difficulty from enteric fever. If the
intestinal mucous membranes are involved, and diarrhoea consequently
exist, the differential diagnosis will be almost impossible. The fever,
following the law of nearly all inflammatory and symptomatic fevers, is
usually remittent, and the remissions and exacerbations correspond to
the normal diurnal variations of temperature--lowest in the morning,
highest in the evening. The remissions are also usually attended with
perspiration, sometimes profuse, at others moderate. The patient early
falls into that condition of prostration and general exhaustion which
speedily comes on in all fevers of high temperature and protracted
duration expressed by the term typhoidal state. Even the pains
ordinarily complained of in inflammation of various organs are not
felt, or if felt at all are seldom mentioned; which perhaps helps to
render the diagnosis more difficult. Almost the only exception to this
is when the cerebral meninges are early affected, in which case
unusually severe headache may be complained of. Cough may be present,
{479} but is not more troublesome than in many cases of enteric fever,
and is quite out of proportion to the lesions found in the lungs and
pulmonary mucous and serous membranes. The expectoration varies, and is
sometimes entirely absent. Generally, it is moderate and consists of
frothy serum, occasionally streaked with blood. Hæmoptysis is said to
be occasionally present, but must be extremely rare. Respiration is
notably frequent early in the disease, and in the absence of pronounced
physical signs of pulmonary lesions is perhaps one of the most reliable
and pathognomonic signs present. Respirations are often as frequent as
60, seldom less than 30, per minute. The pulse is usually rapid,
generally hard at first, but soon becoming soft and weak. The rate
varies between 110 to 120 to 160 or more late in the disease.

The disease runs a rapid and invariably fatal course, often ending
within the first fortnight, seldom lasting as long as two months.

Tubercles, miliary and submiliary, are found after death in almost all
the vascular organs, varying much, however, in number in various
organs, and often presenting different stages of development. In some,
and especially in the lungs, tubercles will be found already in a state
of incipient softening, others still firm and yellow (caseous), and
others still grayish and semi-translucent, showing, we think, a
different period of eruption, and demonstrating the correctness of our
observation that miliary tubercles are always formed in successive
crops.

If the tuberculosis is associated with inflammatory phthisis, and, as
is the case in a majority of instances, has been caused by absorption
of caseous detritus, large masses of caseous matter may be found in the
lung, either in a softening condition, or cavities will be met with
empty or partially filled with pus, and surrounded by indurated walls
the result of interstitial pneumonia. These caseous masses and cavities
are, in our view, the result of precedent catarrhs or croupous
pneumonias, and not a result of the tubercular process.

Partial or local miliary tuberculosis is a much more frequent
occurrence than the general disease above described. It occurs most
frequently in persons under twenty-five years of age, and in a very
large majority of cases between the ages of two and twenty. It occurs
also most generally in the lungs first in point of frequency, in the
mesentery next, and last in the cerebral meninges. Of course a
secondary general tuberculosis may result in any of these cases from
resorption, except in the meningeal variety, which generally destroys
life before there is time for secondary infection.

Acute miliary tuberculosis may occur in the young as a consequence of
measles and other exanthematous fevers, whooping cough, typhoid fever,
and various other affections which seriously impair nutrition.
According to our own observation, it is most likely to attack boys and
girls soon after puberty who are pursuing too severe a course of study
in school with insufficient exercise in the open air, and perhaps also
those evil practices unfortunately too common in both sexes. Tubercular
meningitis as an idiopathic affection (that is, without the previous or
concurrent deposit of tubercles elsewhere) is almost exclusively met
with in children between two and seven years, but secondary
tuberculosis of the meninges may occur at any age. We have seen two
cases of pulmonary phthisis, one of three and one of three and a half
years' duration, and who bid fair to live for a long time, suddenly
carried off by tubercular meningitis. Both of these persons were past
thirty years of age.

Tuberculosis of the mesentery, peritoneum, and liver (for they are
sometimes found in all three of these organs) is invariably either
coincident with a general tuberculosis or the secondary consequence of
scrofulous inflammation of the intestinal glands. Quite often here the
tubercular process is associated with the scrofulous process, and large
masses of caseous material will be found in the mesenteric system of
glands.

{480} As in general miliary tuberculosis there are no symptoms by which
the disease can be positively recognized, so too in the partial or
local disease there are absolutely no pathognomonic signs. We may say
in general terms that if a person who is known to have had a pneumonia
which has ended in a permanent consolidation of any considerable
portion of one or both lungs, and who has for some time presented the
symptoms, however slight, of chronic pulmonary phthisis, is suddenly
attacked with fever and night-sweats; or, if fever has already existed,
the temperature rises considerably above the previous average, with
increase of cough; or if an uncontrollable diarrhoea sets in; or if
headache and delirium should suddenly occur--delirium out of proportion
to the fever,--then we are justified in believing that tuberculosis of
the lungs, mucous membrane of the bowels, or arachnoid has occurred. Or
if a young person of either sex, such as above described, should, after
becoming pale and anæmic, begin to have slight fever with a dry,
hacking cough, at first without expectoration or with a frothy
muco-serous expectoration, which for an unusual length of time
continues to retain this characteristic, and this fever and cough
cannot be otherwise accounted for, then the existence of pulmonary
tuberculosis is rendered extremely probable, although there is neither
history nor evidence of preceding pneumonia or scrofulous glandular
degeneration. If a few scattered and slight crepitant râles can be
heard over one or both lungs without alteration of pulmonary resonance,
and the respiratory rate is much too frequent for the temperature and
pulse, then the diagnosis becomes almost absolutely certain.
Unfortunately, this scattered or diffuse crepitant râle is often
absent, and there are absolutely no physical signs whatever of the
deadly mischief going on in the lungs.

Prolonged expiratory movement is spoken of by some as one of the
reliable signs of tuberculosis, but as this sign is usually present in
almost all forms of chronic pulmonary disease, its significance cannot
be relied upon. Or if a child over two and under ten years of age,
after showing evidences of malnutrition, should suddenly be attacked
with fever of moderate temperature, become restless and fretful, should
frequently vomit and retch even when the stomach is empty, and begin to
have convulsions, with squinting and trismus, and if old enough
complain of severe pain in the head, have a rapid, frequent, but
irregular or slow and intermitting pulse,--if these symptoms become
exaggerated at night and somewhat mitigated in the daytime, the
diagnosis of tubercular meningitis may be made with tolerable
certainty.

It would take more space than is allotted to this article to describe
all the phases of tuberculosis: we shall therefore summarize the
symptoms of this disease by saying again that the signs and symptoms of
tuberculosis are simply those of inflammation with fever and such
derangements of function and other local disorders as would be
furnished by inflammation of any given organ under other circumstances,
except that the pain produced by tubercular inflammation is not usually
so severe as in other inflammations, and hence diagnosis is not always
so easy as in the latter. For it is a remarkable fact that in tubercle
of the peritoneum--an organ which in a state of inflammation usually
gives such excruciating pain--this symptom is often not complained of,
and the existence of tuberculosis not suspected until after a
post-mortem. The same may be said of tubercle of the meninges. Pain is
often not complained of, and is never so severe as in ordinary
meningitis.

TREATMENT.--In acute general tuberculosis no treatment will be of any
avail. All that can be done is to moderate the fever and support
nutrition by appropriate food. For the first, quinia in large doses is
undoubtedly the best remedy. It should be given in one or at most two
doses daily. Twenty grains should be given early in the morning, and
this dose repeated at 1 o'clock P.M., or thirty to forty grains may be
given in a single dose about 8 or 9 o'clock A.M. Antipyrine should
prove a valuable antipyretic in these {481} cases, and, being probably
equally effective, produces less disorder of the nervous system and
digestive functions than the salt of cinchona. Judging from what we
have seen of its effects in other fevers and inflammations, fifteen to
twenty grains repeated about four times in the twenty-four hours should
keep the temperature very near normal.

For the second indication milk and raw eggs constitute the best diet.
Brandy or whiskey in the form of eggnog or milk-punch is useful, and in
the latter stages indispensable. It should not be forgotten that
according to the latest observations muriatic acid disappears from the
gastric juice of fever patients, and that its power to digest animal
food is therefore very much impaired. This should be supplied,
therefore, by giving after every ingestion of milk, eggs, or other
animal food ten to fifteen drops of dilute hydrochloric acid in a
sufficient quantity of water. Peptone will also aid in the proper
digestion of protein substances, and should therefore be added to the
acid. Some of the liquid peptone sold by manufacturing chemists
contains hydrochloric acid, and would therefore meet both these
indications.

By these means we may doubtless prolong the life of the patient and
promote his comfort or at least diminish his suffering, and if a cure
is possible secure it. Tuberculosis of the mesentery and peritoneum, as
well as tuberculosis of the cerebral meninges, will generally prove
fatal, the one by impairing the chylo- and hæmatopoietic functions, the
other by injury to the central nervous system, though Hartshorne of
Philadelphia reports one case of the latter in which temporary recovery
lasting one month took place, and quotes two cases by Guersant in the
_Dictionnaire de Médecine_ (1839) in which also partial recovery,
lasting five weeks and two months respectively, occurred. "May we not
imagine, however," says Hartshorne, "that if such convalescence could
last two months, it might in a case affected with nearly similar
lesions be prolonged indefinitely?"[12] I am informed that a case of
permanent recovery has been reported in England, but I have not been
able to obtain the reference. To these I have to add a case of my own
in which recovery has been maintained for a little more than nine
months. In this case, a boy of twenty-six months, the convulsions were
controlled for many days by hypodermic injections of morphia, while
quinia was given by the mouth when possible, and otherwise by the
rectum; and, though he had left hemiplegia and was for a time both
blind and deaf, he recovered entirely in about six weeks, and has
remained well.

[Footnote 12: _Reynolds's System of Medicine_, Am. ed., Philadelphia,
1880, vol. i. pp. 826, 827.]

In pulmonary miliary tuberculosis the treatment is by no means so
hopeless if the disease is promptly recognized and actively treated.
The thing to be accomplished in this case is to prevent secondary
eruptions and the softening of the tubercles already formed. We know
that this last can be done in caseous deposits resulting from
catarrho-pneumonia, and we also know that tubercle can be maintained in
a quiet state or be made to dry up by calcareous impregnation or
degeneration for an indefinite time, since post-mortems often show old
tubercles in one or the other of these conditions. We know of one man
who carried a caseous lung for nineteen years, coughing more or less
during all that time, but in a sufficiently good state of health and
strength to follow his occupation of ship-carpenter, but who died at
last from phthisis; while another, a farmer living in one of the
Southern States, has lived in fair health, with his left lung indurated
from top to bottom, for twenty-four years. There cannot be a doubt,
therefore, that if secondary crops of tubercles are prevented, and a
perfect state of health and general nutrition maintained, the tubercles
may remain quiescent in their cheesy condition or may undergo
calcareous degeneration and dry up into inert and innocuous masses
incapable of further harm.

The first and most important indication, therefore, in the treatment of
{482} tuberculosis is to suppress the fever; for as long as this
continues new tubercles will continue to form, since the fever is both
a predisposing and exciting cause. Quinia, therefore, or antipyrine,
should be given as directed in general tuberculosis. The patient should
be put to bed and not permitted to go about until the arrest of fever
seems permanent. Nutrition should be supported and promoted also by the
same means already indicated. As soon as the fever is permanently
arrested (but not before) the patient should be permitted to take
gentle exercise in the open air, and should be encouraged to spend as
much time as possible out of doors, and if able to do so should be sent
during the winter to that climate or place where, on account of its
warmth and dryness, the most time can be spent in the open air.

Hypophosphites of lime and soda should be given constantly, and
cod-liver oil also if the stomach can tolerate it. Large doses of the
oil are useless, and often hurtful, a dessert-spoonful being quite as
much as most stomachs can bear without exciting unpleasant eructations
and nausea. The appetite and digestion are best excited by tincture or
extract of cinchona and nux vomica. Iron we have found to be of little
use, and often hurtful. We much prefer small doses of arsenic (two to
five drops of Fowler's solution), and if there is much bronchitis this
will be found especially useful. Some persons, however, cannot tolerate
arsenic in any dose. The patient should carry a clinical thermometer,
and as soon as the slightest fever is detected he should go to bed and
active antipyretic treatment should be instituted, the tonics and
alteratives being meanwhile suspended. If cough is troublesome (but not
otherwise), one to two grains of codeia should be given two or three
times a day or as often as may be found necessary. This is much
preferable to morphia or other preparations of opium, which constipate
the bowels, dry the mouth, impair the appetite, and so stupefy the
patient that all inclination or even ability to take exercise in the
open air is destroyed. Codeia is amenable to none of these objections.

Guided by these principles, we think we have successfully treated many
cases of primary pulmonary tuberculosis--many in which the hereditary
predisposition was strongly marked and the diagnosis unquestionable. It
is true that many of these cases have relapsed and died after a
variable period, but others have remained well for several years, and
still others permanently.




{483}

DISEASES OF THE PLEURA.

BY FRANK DONALDSON, M.D.


Pleurisy.

DEFINITION.--Inflammation, partial or general, of one or both pleuræ.

SYNONYMS. Pleuritis ([Greek: pleuritis]) morbus lateralis; Morbus
pleuriticus (Celsus); Pneumona pleuritis (Cullen). _Fr._ Pleurésie;
_Ger._ Seitenstich.

HISTORY.--Pleurisy derives its name from the accompanying pain in the
side, usually its most prominent symptom. In the sense in which
Hippocrates used the word [Greek: pleuritis], it meant all kinds of
pain in the side, especially such as are of a violent character.
Pleurisy was mentioned by Celsus, and was still better defined by
Galen. Æctæus, however, was the first to describe it with precision and
to speak of its treatment. These ancient authors viewed the disease as
seated in the layer of the pleura lining the ribs or external parietes
of the chest. More modern writers contended that the disease was more
frequently in the expansion of the pleura over the lungs and other
parts. Boerhaave and Van Swieten contended for the separate and
distinct affection of the pleura. Sydenham, Hoffman, and Morgagni
believed that the pleura and the substance of the lung were generally
both implicated. Pinel was the first to definitely establish the
difference between pleurisy and pneumonia from the anatomical lesions.
Laennec laid the foundation of our present knowledge. He was followed
by Andral, Chomel, Louis, and Cruveilhier in Paris, and by Forbes and
Williams of London and Stokes of Dublin. They demonstrated, by the
physical signs and general symptoms during life and by the post-mortem
lesions, that inflammation may commence in and be limited to the pleura
in some cases, and in others that it may extend to and involve the
lungs. Again, they showed that in some instances the lung may be
inflamed without involving the pleura generally, yet that in the large
proportion of cases the disease may originate in one organ and extend
in a greater or less degree to the other, thus implicating both of
them. Previous to Laennec the incomplete anatomical knowledge of the
nature of the serous membrane, the pleura, as a capsule of the lungs,
and the thoracic organs and walls, as well as the theoretical views of
the nature of inflammation as a morbid process, led to erroneous views.
Their diagnoses were made from general symptoms only. Pleurisy was
considered the more common disease. Avenbrugger, Corvisart, and
Laennec, by their discoveries of the accurate physical modes of
exploration of chest diseases, gave far more reliable data for
differential diagnosis. Now we have, in addition to the general
symptoms, the modern refinements in auscultation and percussion, the
delicate measurements of Woillez's cyrtometer, Ransome's stethometer,
and Pravaz's and Alex. Wood's hypodermic exploring-needles to enable us
to attain great accuracy in the diagnosis.

CLASSIFICATION.--Pleurisy is one of the most common diseases of the
{484} respiratory apparatus. Though apparently simple, careful study
shows it to be extremely complex. It occurs in very different forms and
in a great many modifications, according to the producing causes and
the numerous lesions which follow its course. We might classify the
forms of pleurisy, according to their causes, as primary or secondary,
tubercular, traumatic, etc.; or we could designate them according to
their anatomical lesions, as dry pleurisy, pleurisy with effusion,
general or parietal pleurisy, encysted, multilocular, purulent,
hemorrhagic, etc. A methodical classification of all these forms is
difficult if we attempt to base it upon the prominent characteristics
or the lesions. We prefer a classification which enables us to study
separately the clinical varieties which are most frequently met with,
and therefore the most important. The symptomatology shows that the
inflammatory process in pleurisy is of different degrees of intensity.
We propose for our study to divide them into two main groups, according
to the nature of the exudation:

  Fibro-serous pleurisy, Acute,
                         Chronic.

  Purulent pleurisy,     Acute,
                         Chronic.

They may be local or general. When they result from disease of
neighboring parts, they are generally local. Each of these groups
comprehends primary and secondary varieties.

In the first, we have an exudation resembling the plasma of the blood.
The effusion is not serous, for the fluid is spontaneously coagulable,
whereas serum is not. It is not properly termed fibrinous, for it
contains more albumen than fibrin. Fibro-serous is the most accurate
term by which to designate it. The watery portion gravitates to the
lowest part of the cavity, while the plastic deposit is thrown out over
the two surfaces of the pleura. In the most acute forms the general
symptoms, especially the pain and fever, are well marked. The exudation
is at first largely fibrinous, but it is afterward more fluid in its
character. In milder cases, the latent variety of the older authors,
frequently designated as the subacute form, the subjective symptoms are
so slight that the individual is not aware of his condition until the
exudation, which is largely sero-fibrinous, mechanically interferes
with his respiration. When first recognized these cases are really
often chronic. They frequently remain sero-fibrinous in their character
for a long time. Sometimes they become sero-purulent (the intermediary
variety), and later purulent. Purulent pleurisies (empyema) are those
where pus is the product of the inflammatory action. They may be acute
(empyema d'emblée) or the result of transformation of acute or chronic
fibro-serous pleurisies.

By this division we shall be able to take into consideration the
fundamental causes of all the forms of pleurisy. Starting from the
simple primary form, we shall be able to study special varieties of
secondary pleurisies, such as tubercular and rheumatic.

Next, we shall examine separately the hemorrhagic variety as distinct
from hæmothorax. The localized forms, such as the interlobular,
diaphragmatic, and mediastinal, will be studied as varieties caused by
their development in different localities.

The simplest plan to elucidate the whole subject of pleurisy is to
analyze carefully, in the first place, the unquestionably acute
disease, primary pleurisy, and afterward to connect with it the study
of the several forms and varieties. Acute primary pleurisy has a
sero-fibrinous exudation, and is the most common form of the disease.
In it are best defined the usual characteristics of this inflammation.
We consider this the principal type of this class, and with it shall
study the development and character common to all the varieties of
inflammation of the serous membrane of the thoracic cavity.

PATHOLOGICAL ANATOMY OF FIBRO-SEROUS PLEURISY.--The anatomical {485}
changes in all forms of pleurisy begin by hyperæmia of the vessels of
the serous membrane and of the subserous connective tissue. This is
followed by an exudation of a liquid, a pseudo-membranous deposit. In
acute primary cases this is first noticed on the costal pleura. The
pleura itself shows, by puffiness and oedema with red points and small
ecchymosed spots, that the inflammatory process has affected it. In a
few hours, in acute cases, there is found a thin deposit of fibrinous
lymph of a reddish-yellow tinge, with more ecchymosed spots, resulting
from the rupture of fine capillary vessels. The pleura is somewhat
thickened and loses its transparency, and is studded with very fine
granulations. Under the microscope it is shown that the epithelial
cells are swollen, that their number has been largely increased by
proliferation, and that they have been detached in great quantities.
The granulations are scattered over the pleural surfaces, and separate
the pleura from the fibrinous deposit. The connective tissue is loaded
with liquid, in which are found in increased quantity leucocytes which
have migrated through the walls of the blood-vessels.

Over the surface of the pleura there is a tissue of granulations
composed of embryonic cells, which are derived from the proliferation
of the elements of the connective tissue. In this tissue of new
formation we find new blood-vessels coming from those belonging to the
subserous tissue, which advances through small points, even to the free
surface of the granulations. These vessels are very thin and brittle.
They sometimes rupture and cause ecchymoses of the pleura and of the
false fibrinous membranes--sometimes effusions of blood, which,
becoming mixed with the serum in the pleural cavity, cause hemorrhagic
pleurisies. This new tissue is susceptible of organization, and of
transformation progressively into a tissue analogous to that of a
cicatrix. Under the plastic exudation we find abundance of embryonic
cells, which become elongated and spindle-shaped in the formation of
new connective tissue. This is at first tender, but may become dense
and fine over circumscribed points, so as to produce bands which
enclose and touch the effusion. This is the origin of the organized
neo-membranes which are found on the surface of the pleura. It is,
moreover, this tissue of granulations which constitutes the bands which
unite the parietal to the visceral pleura, the adhesions being produced
by the contact and the union of vegetations or neo-membranes developed
on the two opposed layers of the pleura. The membranes form the
filamentous thin bands which draw obliquely together portions of the
pleural sac. These lesions are very often slight and rudimentary in
simple acute pleurisy, but are found well developed in purulent
pleurisy, especially when it is chronic. These are hyperplastic
parenchymatous lesions of the pleura. Acute inflammation of the pleura
gives rise to two distinct forms of exudation--the plastic, deposited
on the free surface of the serous layers or formed in flakes in the
fluid; and the serous, which falls into the dependent portions of the
cavity. The plastic may exceptionally exist alone. Their formation
together is the rule. Anstie questions whether the serous effusion ever
occurs without the fibrinous. The plastic exudation takes the form of
granulations more or less prominent, constituting a bed of very
irregular rough points. So long as the period of inflammation
continues, new plastic deposits are formed over the old ones. They thus
increase in thickness. The neo-membranes which play such an important
rôle in the natural history of pleurisies increase very rapidly. Little
by little, they are transformed into firm, very resisting tissues. They
may become fibrous, cartilaginous, or even calcareous in their
structure. These false membranes develop more freely at first when the
opposing surfaces are kept apart by the effused liquids. The rubbing of
the two pleuræ together seems to impede the process of organization.
According to Wagner, the lymphatics are dilated and contain a liquid
poor in corpuscles. The newly-organized and vascular {486} tissues
often become the starting-points of fresh inflammatory processes and of
new products.

Exudations are of two kinds--liquid and pseudo-membranous. When the
inflammation extends over a limited surface, the fibro-plastic
exudation may be the only one; in which case the disease soon
terminates with local adhesions. This is dry pleurisy, which is rarely
primary in its origin. Ordinarily, the principal lesion of acute
pleurisy consists in a sero-fibrinous effusion which collects in the
cavity of the pleura; almost always the liquid effusion exists in
decided quantity. In it there are suspended fibrinous flocculi, and on
the surface of the pleura are found false membranes. The nature of the
effused liquids has been thoroughly studied, ample opportunities having
been furnished since thoracentesis has been so extensively used. The
quantity of liquid is very variable, from a few grammes up to several
liters. The terms small, moderate, and abundant are used to designate
the quantity--one-half of a liter is considered a small quantity;
moderate, one to one and a half liters; abundant effusion, two to two
and a half liters; very abundant, when the effusion goes beyond three
liters. The liquid is transparent and of yellowish-amber color. It is
darker when the fluid has been some time in the chest, and resembles
that of bouillon. Sometimes it has a rose tint when the liquid contains
a sufficient quantity of red globules, or it may be somewhat opaque
when it encloses a large proportion of leucocytes.

The presence of a few red globules does not constitute a hemorrhagic
pleurisy, nor does the presence of a small quantity of leucocytes make
a purulent pleurisy. It is only when they are very abundant that they
severally give those characters to the effused fluid. Dieulafoy
states,[1] after frequent examinations of aspirated serous fluid of
acute pleurisy, simple and frank, that it contains the smallest
quantity, from 500 to 600 red globules to the cubic millimeter, while
the white globules were from fifteen to twenty times more numerous. In
some instances he counted 1500, 2000, and even 3000, red globules to
the cubic millimeter without the coloration of the liquid being
sensibly modified. He adds that the liquid from the pleura has not a
perceptible rose tint unless it contains from 5000 to 6000 red globules
to the cubic millimeter. He concludes that there is no tendency to
transformation into purulent pleurisy unless the number of red globules
reaches 4000 or 5000 to the cubic millimeter. Rindfleisch (ed. 1869,
Leipzig) states also that upon their number and that of the
proliferated epithelial cells, with the floating flocculi, depends the
convertibility of the serous into purulent effusions.

[Footnote 1: _De la Thoracentèse par Aspiration dans la Pleurisie
aigue_, p. 42, Paris, 1878.]

Chemical Character of Effused Fluid.--Mehu[2] gives the composition of
the fluid as closely resembling that of the serum of the blood. He
found in it the same elements--water, albumen, fibrinogenous matter,
salts, red globules, and leucocytes. The proportion of these principal
constituents of the blood was greatly modified in the pleuritic liquid.
The quantity of water was always increased. On the other hand, the
quantity of substances in solution was greatly diminished. The
exudation was really blood-plasma, more or less diluted, in which the
relative proportion of the constituent elements varied according to the
intensity of the inflammation. It has the same alkaline reaction, and
it is spontaneously coagulable, owing to the presence of the fibrin
which is in solution in the serum, the proportion of fibrin making it
coagulate more or less rapidly. Mehu found the quantity of fibrin to
vary from 09.073 to 19.276 to the kilogramme. The same mineral
substances were found, but in less quantity, than in plasma of blood.
The intensity of the inflammation causes alterations in the composition
of the exudations. The more acute the inflammation, the greater is the
quantity of albumen and of fibrinogen. The fibrinogenous matter
contained in the {487} exudation is coagulated only by contact with the
air. One portion of it becomes concrete in the interior of the body in
the form of fibrinous flocculi, which float in the fluid, and in the
false membranes, which are deposited in successive layers on the
surface of the inflamed pleuræ. This coagulation takes place in a
manner analogous to that of the coagulation of the fibrin in a drop of
blood. These false membranes are almost always found in acute
pleurisies, but their development is very variable. Sometimes they are
very thin, friable, and readily disappear; again, when the inflammation
is intense, they last a long time and cover thickly both pleuræ.
Occasionally they envelop the effusion and produce veritable cysts and
localized pleurisies. Their color is opaline or semi-transparent when
recently formed, but opaque when old. Their consistence varies
according to the duration of the disease. At first they are soft,
impregnated with fluid, easy to tear or break; later on they become
resistant and almost dry. The microscope shows these false membranes to
be formed of crossed fibrillæ, with intervals containing white
blood-corpuscles, with voluminous, swollen epithelial cells of serous
membrane, proliferated and detached.

[Footnote 2: _Arch. général de Méd._, 1872.]

When the pleural inflammation subsides, the exudation is destined to
disappear. Usually the cure is produced by the reabsorption of the
effused products. The liquid part of the exudation, the serosity, is
absorbed by the lymphatics, which are found frequently dilated, and
some of them are filled with fibrinous coagulations and the leucocytes.
The solid parts, the false membranes, concrete fibrin, and cells
disappear with more difficulty. They undergo granulo-fatty
metamorphosis, and are then taken up by the lymphatics.

These fibrinous false membranes are not, as was formerly supposed,
susceptible of organization. It is only the neo-membranes, formed by
the proliferation of the elements of the pleura, which are organized or
organizable. It is these that form bridles or ligaments which attach
the lung to the thoracic wall, and are susceptible of transformation
into cartilage or even into bone. In chronic cases these new membranes
bind the lung down, impair its expansive powers, and inflict great
damage upon the respiratory force.

Care must be taken to distinguish between the neo-membranes and the
plastic and liquid exudations. These last contain transitory-formed
elements entangled in the fibrinous layers. They are principally
lymph-corpuscles, containing solitary nuclei, together with a few
epithelial cells, almost always in process of disintegration, and
isolated blood-corpuscles (Fraentzel).

Distribution of Fluid.--The situation and form in which the effusions
are found in the pleural cavity furnish important data for study as
applicable especially to diagnosis. At the commencement of the disease
the effused plastic products form a thin covering to the pleural
surface--a slight cushion interposed between the lung and the thoracic
wall. Later, the fluid products gravitate by their weight to the lowest
portion of the cavity of the pleura; then, as they increase in
quantity, they gradually rise or are drawn to the superior portion of
the thorax. Once formed, these effusions are but slightly movable and
but little displaced by the varying positions of the patient, unless
the quantity be very great and no adhesions or bands have been made. If
the effusions be of viscid consistence, or if false membranes exist,
they are mechanically prevented from moving. The serous transudations
of hydrothorax always occupy the most dependent portion of the cavity,
but observation shows how frequently the pleuritic effusions are
immovable, being maintained and suspended between the diaphragm and the
lungs, and imprisoned in the situation where they form by the false
membranes.

Previous to 1843 the authorities universally taught that the effused
fluids in the pleural cavity obeyed, as they would in an open vessel or
in a vacuum, the law of gravity. They never appeared to question but
that the fluid {488} would necessarily assume its hydrostatic level,
and consequently that it would reach a horizontal line in all parts of
the chest. The distribution and the form which the effusions take were
first studied by Damoiseau.[3] Fernet and D'Heilly[4] maintain that
Damoiseau perfectly established the form and disposition which the
effusions take in pleurisy. To study them well we must bear in mind,
they say, three facts: the irregularly conical form of the pleural
cavity; the effect of gravity; and the habitual position of the patient
when lying down. Damoiseau and these authors utterly ignored the
retractile force of the lung, as well as that of the diaphragm, and the
resiliency of the thoracic walls, as effecting the position of the
fluids in the pleural sac. If we observe that the patient at the
commencement lies ordinarily on his back, the thorax being raised and
more or less inclined to the horizontal position, we easily appreciate
that the effusion ought to accumulate, at first, behind, in the most
dependent portion of the costo-vertebral gutter, below the inferior
angle of the scapula; then, as it increases in quantity, it rises and
obliquely strikes the conoidal cavity, which encloses it, and makes on
its surface curves resembling those of an oblique conic section
(Damoiseau). As Damoiseau described the pleuritic line of flatness as a
parabola, it was highest in the axillary region, where it first
appears; thence, as its summit rises, its branches advance downward and
outward to the sternum and the vertebral column.

[Footnote 3: _Thèse de Paris_, 1845.]

[Footnote 4: _Nouveau Dict. de Méd. et Chir._, Paris, tome xxviii.,
1880.]

Since Damoiseau's first paper[5] it has been generally acknowledged
that the line of flatness over the upper surface of a moderate effusion
is not horizontal when the patient is in the sitting or erect posture.
There has been considerable difference of opinion among the English[6]
and continental writers as to the exact disposition of the fluid: some
partially assent to Damoiseau's views; others, again, very materially
modify them. Wintrich,[7] who was one of the first among the Germans to
emphasize the percussion line of demarcation between a pleuritic
effusion and a contracted lung, says: "As the exudation gradually
increases, the level of the fluid does not present a line which is
horizontal or parallel to the ground, but one which descends toward the
ground at a more or less acute angle." Fraentzel says that the line is
never horizontal. Leichtenstein and Ferber[8] maintain that the line
depends upon the position of the patient early in the disease. Gee[9]
holds very much to this opinion. He states that the upper limit of the
surface of liquid, when it reaches as high as two inches above the
nipple, is horizontal. When lower than this, the dulness forms
irregular parabolic curves, which become smaller and smaller as they
descend. Austin Flint[10] says, in his more recent edition: "The upper
limit of the dulness or flatness, the position of the body being
vertical, is not in a continuous horizontal line extending over the
posterior, lateral, and anterior aspects of the chest." Flint,
Wintrich, and Fraentzel speak of the line being highest behind. Calvin
Ellis of Boston in two very suggestive papers[11] described a
curve-line made by the upper line of the effused fluid, which radically
differed from any one previously mentioned. "This curve begins, with
medium effusions, relatively low down on the back, passes outward from
the vertebral column, and soon turns upward and proceeds obliquely
across the back to the axillary region, where it reaches its highest
point. Thence it advances in a straight line, but with a slight
descent, to the sternum." Powell, however, does not find {489} that the
curve invariably commences at a lower level behind. G. M. Garland,[12]
in consequence of the resemblance of this curve to the italic letter
_S_, has named it, very appropriately, the letter _S_ curve. He adds
that, according to his experience, "this curve, as described first by
Ellis, may be traced, by proper percussion, in any case of free,
uncomplicated pleurisy when the patient's body is erect and the amount
of fluid present is not excessive. As any effusion increases in amount,
the curve of its distribution gradually rises and tends to flatten out,
so that it no longer presents its characteristic _S_ feature after it
reaches the second rib. At this point, when the fluid occupies nearly
the entire side, the curve comes quite near to the horizontal, but if
some of the fluid be withdrawn by aspiration or absorption the letter
_S_ curve will reappear and retreat downward in the inverse order of
its advance, until with entire absorption it becomes merged into the
normal boundary of the lung."[13] Garland quotes from two recent German
authorities--Heitler of Vienna and Rosenbach of Breslau--to the effect
that the line of flatness of the effusion extends lower on the back
than it does on the side, and that there is a triangle bounded by the
vertebral column, the upper curve from the bottom, and a line drawn
from the summit of the curve, where there is impaired resonance over
the lung from adhesions and oedema of the lung, but where there is no
fluid and no flatness. Garland had previously called attention to this
space, and had named it the dull triangle. He had warned all who sought
to trace the true line of pleuritic flatness to be careful not to
overlook this region. Heitler had likened it to a monk's hood cut
longitudinally through the centre and hanging apex down. Rosenbach made
this dull space, clearing up in exercise and deep breathing, as
distinctive between pleurisy and pneumonia. We must expect impaired
resonance on the posterior wall above the fluid, for the fibrinous
deposits from exudation collect there when the patient is in the
recumbent position. Garland[14] calls attention to the confused views
caused by confounding the two physical signs of dulness (or impaired
resonance) and flatness (absence of resonance), the latter only
indicating the presence of fluid. If the differential diagnosis between
the dulness on percussion over the dull triangle and the flatness over
the fluid be not carefully made by delicate, light percussion, the two
may easily be confounded and the fluid be thought to have arisen to a
much higher level than it has. In some cases, owing to greater
thickness in the walls and coverings of the chest and adhesions, it may
be more difficult to draw nice distinctions in percussion sounds. This
distinction can, however, be made if the percussion-stroke is used with
proper delicacy and lightness, and a comparison made between the two
signs, and not between them and vesicular resonance. If the percussion
be strong, the vibrations are communicated from the resonant lung above
the fluid, and deceive the examiner. The most effective manner of
percussing is at right angles to the general direction of the curve,
which is transverse across the chest. Thus examining, we have had ample
opportunities of confirming the statement of Ellis and Garland that the
curve line is never highest behind, even with the largest effusion.
Wintrich and his German followers hold a different view. In moderate
effusions it is highest in the axilla, from which point it turns
downward posteriorly to touch the vertebral column at the interscapular
region. In front it extends downward toward the sternum. R. Douglass
Powell[15] reports cases with drawings, showing that in typical cases
the fluid does not take a water-level, "but a curve, having its
convexity upward in the lateral region." When the effusion becomes
excessive and fills the whole cavity, there is flatness on percussion
everywhere. As the fluid subsides, however, from absorption or from
mechanical removal, the distribution again resumes, to a greater or
less degree, its previous shape. {490} In moderate effusions there is,
ordinarily, the dull triangle posteriorly, and Skodaic resonance under
the clavicle in front in the anterior triangle. On the left side the
lower limit of the effusion can be recognized by the flatness being in
the shape of the arch of the diaphragm. In cases complicated by
adhesions or by pathological changes in the lung itself the curve is
changed, and in some the Ellis curve is straighter than in others.
Adhesions form sometimes early in the disease. They mechanically
interfere with the usual distribution of the fluid, as do catarrhal,
tubercular, or pneumonic consolidations, and, indeed, emphysematous
conditions. All these physical alterations of structure modify the
elastic force of the lungs. According to Mohr's statistics, adhesions
were wanting in 47 per cent. of the cases analyzed by himself.
Garland's experiment of injecting glue and plaster of Paris, and
subsequently cocoa-butter, into the pleura of living and dead dogs, and
by moulds testing the curves formed, showed that if the dogs were
suspended by the head the curve of flatness on percussion was very
similar to the Ellis curve. On removing the casts after they had
solidified, he found they closely corresponded to the shape and
position indicated by the physical signs elicited before opening the
chest.

[Footnote 5: _Archives générale de Méd._, 1843.]

[Footnote 6: See Hyde Salter, _Lancet_, 1865; Powell, _Trans. Roy. Med.
and Chir. Soc._, vol. lix.; W. N. Stone, _Lancet_, 1877; Le Gros
Clarke, _Roy. Soc. Med. and Chir._, 1872.]

[Footnote 7: Quoted by Garland, _N.Y. Med. Journal_, 1879.]

[Footnote 8: _Ibid._]

[Footnote 9: _Auscultation and Percussion_, 1877.]

[Footnote 10: _Practice of Medicine_, 1880, p. 130.]

[Footnote 11: _Boston Med. and Surg. Journ._, 1874 and 1876.]

[Footnote 12: _Pneumono-Dynamics_, New York, 1878.]

[Footnote 13: _N.Y. Med. Journal_, Nov., 1879.]

[Footnote 14: _Pneumono-Dynamics_.]

[Footnote 15: _Med. Times and Gazette_, Oct., 1882.]

Ellis's observations, and those of Garland with his experiments, have
given us the most accurate views as regards the form of the curved line
of flatness.

Nearly all modern authorities, including Peter, Gerhardt, and Paul
Niemeyer, admit that fluids in the pleural sac assume more or less
irregular curves, and not a hydrostatic, horizontal level. Whatever may
be the nature and consistence of the effusion, fibro-serous,
sero-purulent, or purulent, it does not behave in its distribution as
if it were in an open vessel. But few writers, however, have troubled
themselves to ascertain the causes of this apparently abnormal
condition. They appear to have completely overlooked the facts that had
been discovered in regard to the mechanics of the chest in connection
with respiration and the circulation. Physiology had shown, especially
by Marry's researches, the negative force of the lungs in aspirating
the blood from the large venous trunks into the right side of the
heart, and thus assisting the whole venous circulation. John
Hutchinson[16] drew attention to the antagonism existing between the
expansion of the chest by muscular action and that of the lungs and the
chest-walls. Hyde Salter[17] showed that at the commencement of
inspiration thoracic elasticity was favorable to inspiration, but as it
advanced it became an expiratory force with lung-tension against
further expansion. R. Douglass Powell[18] drew further attention to
these facts in connection with respiration and its modification by
disease. Le Gros Clarke[19] showed that atmospheric pressure over the
abdomen kept the diaphragm in a condition of arched passive tension. He
claimed that this negative force resisted the elasticity of the lung,
and was the means of retaining the supplemental air in the lung and
limiting the encroachment of abdominal organs.

[Footnote 16: _Trans. Med. and Clin. Soc._, 1846.]

[Footnote 17: _Lancet_, Aug., 1865.]

[Footnote 18: _Trans. Clin. Soc._, 1870.]

[Footnote 19: _Trans. Roy. Soc._, 1872.]

Douglass Powell in March, 1876,[20] in an elaborate and very suggestive
paper on "Some Effects of Lung Elasticity," gives the practical bearing
of these physiological facts in clinical medicine, as indicating a
better insight as to the true mechanism and relative value in diagnosis
of some signs of chest diseases, especially as to the importance of
thoracic resilience as a force in respiration.

[Footnote 20: _Trans. Roy. Med. and Clin. Soc._, vol. lix.]

W. H. Stone early in 1877[21] reported his experiments on sheep as to
the amount of negative pressure exerted by the lungs, and concluded
that it was equal to four to five inches of water. He moreover showed
that even when the effusion was considerable in the pleural cavity, the
lung still had contractile force sufficient to support two inches of
water, so that to evacuate the {491} fluid it was necessary to use
external suction sufficient to overcome this lung-traction. In
December, 1877, G. M. Garland[22] gave to the public the results of his
observations and experiments in regard to the form of the curve of
distribution assumed by the pleural fluid, and its causes. He
demonstrated that "the lung, by virtue of the strength of its
contractility, takes the effusion along with it in its retraction, and
that thereby assumes a pneumono-dynamic instead of a hydrostatic
level," and that the Ellis curve was the true line of the upper level
of the fluid in free, uncomplicated pleuritic effusion. Thus the
physical cause of this condition was the retractile force of the lung
lifting up the fluid. This is aided by the elastic resistance of
thoracic walls and the negative pressure exercised by the effused
liquid. The normal line on right side of demarcation between lung and
liver is the letter _S_ curve drawn out, the summit being high and the
anterior branch correspondingly depressed. The modifications of this
normal line in pleuritic effusions represent the effect of the negative
pressure of the fluid. The decline in the Ellis curve toward the
sternum shows that the elastic energy of the anterior part of the lung
is feeble compared with that in the axillary region. "The layer of
fluid is of less thickness above than at the base of the lung against
the diaphragm. The upper surface takes its shape from the lung, which
lifts it up by its retractility, and the effusion by its weight exerts
a negative pressure upon the lung. The mass of the fluid is held when
in moderate quantity in the supplemental space between the lower border
of the lung and the diaphragm" (Garland). The atmospheric pressure from
the interior of the lungs and from the exterior of the chest-wall keeps
the costal and parietal surfaces of pleura together. Skoda, Powell,
Stone, Homolle, and Quincke have shown the retractile energy of the
lung, but the credit of drawing especial public attention to it, and of
afterward elucidating the subject in its practical application to the
study of pleurisy and in putting the whole subject upon a scientific
basis, is unquestionably due to G. M. Garland of Boston.

[Footnote 21: _London Lancet_.]

[Footnote 22: _Pneumono-Dynamics_, Boston, 1878.]

ETIOLOGY OF FIBRO-SEROUS PLEURISY.--The etiology of acute primary
pleurisy is frequently obscure. It may be hæmatic in origin, or it may
be secondary, arising from pathological causes or antecedent disease.
It is difficult to state with certainty whether it occurs in perfectly
healthy persons, because there may be occult pathological conditions
which cannot be appreciated. However, individuals are attacked with
acute pleurisy who to all appearance, both to themselves and to those
around them, are healthy. Authors differ very widely as to the disease
being ever caused in healthy persons by exposure to cold. The older
writers bring many proofs that such is the case. Ziemssen states that
he could not trace the disease to exposure to cold in a single instance
in 54 cases. Anstie holds the same view. Loomis states that in all
instances where it (pleuritis) has followed upon exposure he has been
able to find some predisposing cause. It is undeniable that pleuritis
very frequently indicates the existence of some constitutional
cachexia. Vital statistics show that it is more frequent in winter and
spring than at other seasons. The vicissitudes of the weather, of
temperature, and other atmospheric conditions have unquestionably a
marked influence on the prevalence of the disease. Drafts of air
passing over the chest or over other parts of the body, particularly
when the subject is surrounded in-doors with a warmer atmosphere, wet
clothing, intensely cold or a raw, damp atmosphere inhaled by persons
coming out of a comparatively high temperature, especially if they are
improperly protected by clothing, appear to be direct causes of primary
pleuritis. If individuals thus exposed are debilitated by fasting, by
such medicines as mercury, iodine, iodide of potassium, by
over-exertion, by free perspiration, or by previous disease, they will
be still more liable to contract the disease. Overheated apartments,
especially at night during the {492} sleeping hours, frequently are the
direct cause of acute pleurisies or of croupal pneumonias. These cases
are of such frequency that we are obliged to differ from the high
authorities who consider the pleura as free from acute idiopathic
inflammations as is the peritoneum.

There are numerous predisposing causes which, when examined, are found
to lessen the power of resistance of the organism. Senility is an
important one; so is childhood. Formerly it was supposed that pleurisy
rarely attacked children. This view was prevalent because the disease
often escaped detection. Of all chest diseases in children, mistakes in
diagnosis are most frequently made with pleuritis.

We might suppose that this disease would be frequently met with in
children, because they are oftentimes ill protected against the
vicissitudes of the weather; besides, their feebleness predisposes them
to feel keenly such shocks to their powers of endurance. The disease
may occur at any age, and is more common under two years than was
formerly supposed (Eustace Smith). Empyema is the form most frequently
found in children, the effusion soon becoming purulent in them.
Ziemssen tabulates the ages of 54 children whom he treated for primary
pleuritis: first year of life, 3; second, 1; third, 7; fourth, 4; the
remaining 39 between the ages of five and sixteen years.

Pleurisies are more frequent in males than in females, in the
proportion of 5 to 3, owing to the greater exposure of the former to
the exciting causes, and notwithstanding their stronger organisms.
Among the predisposing causes we must not fail to give due importance
to the malhygienic conditions which so powerfully impair the forces of
the body. Prominent among these are sedentary occupations, imperfect
alimentation, city lives, overwork of mind and body, deficient
sunlight, overcrowded houses, and dampness of soil. These and many
others interfere with the formative forces and lessen the power of
resistance to exciting causes of pleurisy.

Traumatic pleurisies are caused by injuries or other mechanical causes.
Injuries to the walls of the chest, contusions, burns, scalds, and
lacerations which are superficial, frequently give rise to primary
traumatic pleurisies. If the ribs are fractured, or blood, air, or pus
gets into the pleural cavity, we have what has been termed secondary
traumatic pleurisies.

Secondary Pleurisies.--The exciting causes of secondary pleurisies are
numerous. They are pathological, and more readily appreciated than the
causes of primary pleurisies. Owing to the anatomical connection
between the lungs and the pleura, diseases, acute and chronic, of the
former frequently give rise to pleurisies.

Among acute affections of the lungs, the several forms of pneumonia are
the most frequent causes of pleurisies. Fraentzel states that we always
find fibroid pneumonia associated with pleurisy as pleuro-pneumonia,
even when the inflammation of the lung-tissue itself does not reach the
pulmonary pleura. There is an intimate connection also between caseous
pneumonia and pleurisy. This is sometimes quite circumscribed, and
leads to adhesion of the pleural layers at the affected spot; sometimes
it is diffused over a great part of the pleura, and it is then not
infrequently associated with a considerable outpouring of different
kinds of effusions. Catarrhal pneumonia rarely occurs without secondary
pleuritis (Fraentzel). Pleurisies may also be caused by violent
bronchial catarrhs or by hemorrhagic infarctions.

There are cases where, from the presence of tubercles under the
parietal pleura, inflammatory action is set up and pleuritis ensues.
Vomicæ bursting into the pleural cavity or tubercular perforation in
pulmonary phthisis gives rise to pleurisies. Inflammation of the liver,
cellular abscesses, and pericarditis may cause secondary pleurisies.
Diffuse peritonitis is often complicated with pleurisy, the
inflammatory process extending from the {493} peritoneum to the pleura,
through the diaphragm, by means of the serous canaliculi. This
frequently occurs in puerperal peritonitis, and is almost invariably
fatal (Fraentzel). The author had a case of fatal peritonitis in a man
sixty-five years of age, which originated from an empyema. There was no
rupture nor perforation of the diaphragm, so that the inflammatory
process must have extended from the pleura to the peritoneum by means
of these canals. Malignant diseases of the mammæ, oesophagus, lungs,
and hydatids produce secondary pleurisies. Eruptive fevers, especially
scarlatina, variola, typhoid fevers, are among the most frequent
pathological causes of secondary pleurisies. It is doubtful whether
their germs pass through the circulation or through the lymph-canals,
and produce local inflammation of the same nature as their own, or
whether they render the pleura more sensitive to shocks of various
kinds. Rheumatism, gout, and nephritic diseases are frequently followed
by pleurisies. As we have rheumatic endocarditis and pericarditis, in
like manner there are rheumatic and uræmic pleurisies. Alcoholism and
pyæmia, septicæmia and the puerperal state, especially during the first
month after parturition, are powerful predisposing causes of
pleurisies, as are also any morbid conditions of the skin, kidneys, or
intestinal canal which interfere with their eliminating or depurating
functions. This includes all forms of blood-poisoning. Hutchinson says
that children suffering from congenital syphilis are especially liable
to serous inflammations, and that pleurisy is in them a not uncommon
cause of death. Niemeyer denounces the impropriety of giving the name
of secondary pleurisy to all cases of pleurisy occurring in subjects
with broken-down constitutions or weakened by other diseases. We often
meet with such cases when Bright's disease exists. Niemeyer holds that
it is not dependent upon renal disease, but upon the increased
predisposition for all kinds of inflammatory disease. A trifling cause
will sometimes excite a pleurisy when the resistance of the organism is
materially lessened by previous disease.

SYMPTOMATOLOGY.--Rational Symptoms.--These vary according to the
severity of the disease. Ordinarily, attacks of acute pleurisy come on
suddenly, and it rarely happens that there is any appreciable feeling
of malaise. Usually the first symptom is an acute pain in the side,
which alarms the patient. The significance of this severe stitch is
generally appreciated, as the subject at once calls attention to his
sufferings. The pain is sharp, cutting, stabbing, that causes him to
hold his breath as long as possible. When he is forced to breathe, it
is by the action of the superficial intercostal muscles. He endeavors
to fix his diaphragm and hold it rigid in order to prevent the surfaces
from coming in contact and thus increasing his agony. This causes him,
necessarily, to breathe frequently in order to get sufficient air. The
greater the intensity of the pain, the more frequent and shorter are
the respiratory acts. The dyspnoea and the effort to lessen the pain
give the patient an expression of great suffering. Usually, the pain is
felt over a circumscribed spot under the nipple of the affected side.
Sometimes it is experienced as low as the sixth or seventh intercostal
space, but rarely posteriorly below or under the scapula or in the
axilla. In children the seat of pain is not always in the chest. Their
lower intercostal nerves are often affected, and the sensation being
referred to the ends of these nerves where they ramify on the abdominal
wall, the pain is often seated in the abdomen. Such being the case in
children, care must be taken not to confound pleurisies in them with
epigastric or hypochondriac irritations. In adults, the pain is rarely
located in the abdomen when it is caused by pleuritis in the lower
portion of the pleural surface or in that part covering the diaphragm.
In children there is also much tenderness on pressure. In what has been
termed subacute or latent pleurisy the stitch may be entirely absent.
Valleix found pain in 40 cases out of 46. Sometimes it is absent {494}
in ordinary breathing, but is brought on by sneezing or violent
coughing or strong percussion. In severe cases, the effusion coming on
rapidly, the pain may subside by the second day. If the effusion comes
on slowly, the pain may keep up for six or eight days. The continuance
of the pain always shows that the inflammatory process in the pleura is
continuing, although the pulse and the temperature may be normal. The
renewal of the sensation of pain after the pleurisy has passed away
justifies us in the conclusion that there is a return of the
inflammation. When the pain is agonizing, with signs of collapse, it is
indicative of a secondary pleuritis arising in the course of a chronic
caseous pneumonia. Tubercular and purulent exudations are distinguished
from the sero-fibrinous by the longer duration and the greater
intensity of the pain--two circumstances which afford a reliable basis
for the diagnosis of such cases. The severe pain in pleuritis is
probably caused by the inflammation extending to the sheaths of the
nerves and to the nerve-texture itself (neuritis), as well as by
inflammation of the pleura itself.

Severe attacks of acute exudative pleurisy may commence with a severe
initiatory chill, followed by high fever, but ordinarily there are in
pleurisy slight rigors, initial in their character. Some authors
question whether they are not caused by the limited points of pneumonia
connected with the pleuritis. If the rigors occur at regular intervals
for days, we have reason to suspect tubercular trouble or empyema. The
temperature does not run any regular course in pleurisy, nor does it
bear any fixed relation to the pulse and the respiration. It usually
varies from 100° to 102° F. In violent, acute cases it may reach 105°
F.

Careful observations with the thermometer give us important indications
by which to diagnose the nature of the pleurisies. In those of a
tubercular nature the temperature continues high, from 100° to 104° F.,
for weeks. When the effusion becomes purulent the temperature becomes
like that of hectic fever--in the morning normal, and in the evening
rising to 102°, or even 103½° or 104° F. Sometimes the temperature is
one or two degrees higher on the diseased side than it is on the
healthy side.

As in other inflammations, the pulse in this disease varies
considerably. The researches of H. Newell Martin show that there is
ordinarily a constant ratio between the pulse-rate and the temperature.
If the temperature be high (over 102° F.), we must expect the pulse to
be as frequent as 115 or even 120 per minute. In mild cases, where the
temperature does not go beyond 99.5° or 100° F., the pulse will not
exceed 90 to 96. In slight cases, where the fibrinous exudation is very
limited, the pulse may not exceed 80. In tubercular and purulent
pleurisies the pulse may vary between 100 and 120. When there is a
relapse the pulse advances as the temperature rises. Anstie has called
attention to the quality of the pulse, which follows a uniform course
on the whole, regard being had to the general vital condition of the
patient. In the first stage of acute pains, with more or less tendency
to shivering, the pulse, as tested with the sphygmograph, presents the
algid form--_i.e._ the pulse-waves are very small and nearly devoid of
secondary markings. As soon, however, as flushing of the face occurs,
and a general sense of burning heat of the skin, the pulse passes to
the true pyrexial type; the waves become large and dicrotic. The
sphygmograph uniformly shows that the large and somewhat bounding pulse
is always less resistant than that of health.

Jaffé-Duval[23] states that he found the temperature of the diseased
side raised above that of the healthy chest. Subsequently, Peter,[24]
after a long series of researches, reported some very important results
as to the localized parietal temperature in cases of pleuritic
effusions: (1) He found that the {495} parietal temperature, as tested
by the thermometer, is always higher on the side of the pleurisy than
that of the body as tested in the axilla; (2) that the elevation of the
temperature increases as the effusion augments, the highest local
temperature corresponding to the period of secretory activity of the
inflamed pleura; (3) the rise affects both sides, but is greater over
the diseased pleura; (4) the temperature falls by degrees as the
effusion is reabsorbed--less on morbid side; (5) the absolute elevation
of local temperature is greatest in the sixth intercostal space; (6)
after paracentesis the parietal temperature is increased: this falls in
a few hours where the effusion is not re-formed, but when such is the
case it continues for some days. This local rise of temperature, he
considers, is from hyperæmia and cell-production, caused by the
traumatism from the needle added to the already-existing hyperæmia.
This excessive congestion, caused by the accumulation of blood
occurring when a large quantity of fluid is rapidly withdrawn, produces
the syncope, pulmonary congestion, consecutive albuminous
expectoration, the pain, and the oppression amounting sometimes to
suffocation, and occasionally ending in death.

[Footnote 23: _Thèse de Paris_, 1875.]

[Footnote 24: _La France médicale_, 4th May, 1878.]

At the commencement in acute cases the respiratory acts become very
frequent, even going to 40 or 50 per minute. They are short,
interrupted, and superficial. Their frequency makes up for their
incompleteness in furnishing sufficient air. The painfulness of each
act forces the individual not to expand the walls of his chest more
than he can avoid. Moreover, the high fever in itself produces frequent
respiration. As the temperature falls the respiration becomes less
abnormal. If the effusion forms rapidly, the patient may become
oppressed, even when the quantity is not large. If it is thrown out
gradually, the breathing is not so much interfered with until a large
quantity forms, the organism becoming accustomed to the interference
with the play of the lungs. The strength of the individual and the
activity of his nutritive functions are materially lowered. Sometimes
he breathes with difficulty, especially when he takes active exercise.
The dyspnoea is very painful and alarming. The aëration of the blood is
so materially interfered with that there results a large quantity of
carbonic acid, which irritates excessively the respiratory
nerve-centres.

During the acute stage the patient sometimes lies on his back, but more
frequently on the well side, and exceptionally on the diseased side. He
avoids lying on the side where the inflammation exists, because the
weight of his body increases the pain. I have, however, seen patients
who would persist in lying on the painful side and supporting it with
their hand. It sometimes happens that a patient lies on the affected
side, and will not move, because the movement gives him such acute
pain. Ordinarily, he prefers to lie on the healthy side, even after the
fluid has been poured out to a moderate degree, because his pain is
less. When, however, the effusion has become great enough to deprive
him of the use of the diseased side, he instinctively turns on that
side, so as to avoid the weight of the fluid pressing upon the lung on
the sound side. Moreover, he wishes to expand as much as possible the
side whose respiratory force now needs to do double work. This change
of position in patients has an unmistakable significance. It shows that
the sufferer is aware that he is more comfortable lying on the diseased
side. His physician's attention is drawn to the condition of the chest
as influenced by the increased quantity of fluid pressing the air out
of the lung.

Cough is not a constant symptom in pleurisy, but ordinarily it occurs
at some stage of the disease. It is short, dry, and suppressed in
character. It is painful, and therefore is avoided when possible,
especially previous to the effusion. It disappears generally about the
fourth or fifth day, when the effusion has attained a considerable
amount. The cause of the cough has been generally supposed to be the
exalted sensibility of the inflamed {496} pleura, but Nothnägel
maintains that such is not the case. Fraentzel holds that the cough is
caused by the strain on the lung-tissue and the finer bronchi when
there is a slight effusion. Cough brought on by change of position is
one of the characteristic symptoms of large effusions into the pleura.
If the lung is completely compressed by the pleuritic effusion, then no
actual strain on the alveoli or the bronchi can exist. In such cases
there is no cough, but it returns when the effusion decreases in
quantity, and quite violently, if this occurs suddenly, as, for
instance, in puncture of the chest (Fraentzel). In the latter case the
cough is probably caused by the rush of blood and the sudden expansion
of the chest.

Slight frothy expectoration may exist, but ordinarily there is none
whatever, unless from bronchial catarrhal complications. In that case
sero-mucous fluid is expectorated in small quantity. If it becomes
viscid and tinged with blood, it is caused by pulmonic involvement.

In empyema, if the expectoration becomes purulent, we ought at once to
suspect the presence of some circumscribed spots of necrosis of the
pleuritic covering of the lung, which have allowed the pus from the
pleural cavity to filter through the lung-tissue. By careful physical
examination of the chest we can ascertain whether there has been any
diminution in the quantity of fluid. When, as sometimes occurs, there
is actual perforation of the lung, the pus from an empyema comes in
quantity, through the bronchial tubes, out of the mouth. Patients may
sink from exhaustion following this discharge, or if the discharge be
excessive it may fill up the bronchial tubes too rapidly for its
removal by expectoration, thus causing suffocation. This danger is
increased if the discharge takes place during sleep.

Cyanosis is a symptom which should cause serious alarm, for it shows
that the effusion is so great as to interfere very materially with the
due arterialization of the blood. When the cyanosis is accompanied by
pallor, coming on suddenly in the course of a pleurisy, we may infer
with considerable probability that there is a hemorrhagic exudation.
But if the paleness comes on slowly during weeks or months, it may also
be dependent on a simple sero-fibrinous effusion (Fraentzel).
Protracted cases of effusion, especially if purulent, are associated
with emaciation and loss of strength. There may exist more or less
oedema of the lower extremities and of parts of the body where the
patient lies down, as we have in the chronic diseases of the chest.
When this oedema is limited to the affected side of the chest, whether
it be extensively developed and spread over the entire half of the
chest or confined to certain spots, it almost invariably justifies the
diagnosis that the effusion is purulent. The effusion may, however, be
purulent without the presence of this localized oedema. Occasionally,
cases are met with of effusion in the left pleura where there are
visible and palpable systolic pulsations in the intercostal spaces
arising from the impulse of the heart or of the larger blood-vessels
passing through the fluid.

Physical Signs.--Perhaps in no other disease of the chest are physical
signs so important for purposes of diagnosis as they are in pleurisy.
Even at the very beginning of the attack they give us valuable
information. In later stages, when the effusion is in the pleural sac,
they furnish, as we shall hereafter show, trustworthy data for
diagnosis, prognosis, and also very valuable indications for treatment.
There is no other disease of the chest where the physical changes made
by the inflammatory process are so pronounced and so accessible to the
senses of hearing, sight, and touch. The physical signs are so marked
that, almost by themselves, they give us the pathological condition.
They have been so carefully studied, and their correlative value
insisted upon, that they are readily interpreted. One is often tempted
to rely too much upon them to the exclusion of the proper consideration
of the general symptoms.

{497} As the physical condition of the pleuræ varies much in the
several stages of the disease, the physical signs must necessarily vary
accordingly.

At the very beginning of the attack the sensibility of the pleuræ is
augmented by the inflammation. Consequently, on inspection, it will be
observed that the patient is careful to avoid the pain caused by the
inflamed pleuræ rubbing together. He not only tries to avoid using the
ordinary muscles (especially the intercostals) for enlarging the
capacity of the lower portion of the chest, where the disease is
generally found, but he retracts his chest and keeps the pleuritic side
almost motionless. The well side has double work to do, and is seen to
expand more fully. The patient will frequently press the lower ribs in,
on the affected side, with his hand, or he will lie on that side, so as
to control the expansion of the chest, or he will lie on the healthy
side and bend his body over.

The respiratory movements are marked by an irregular and jerking
rhythm, and are quickly made. The pain felt on inspiration is of a
catching or stabbing character, and produces dyspnoea, the subject
struggling for air. The diaphragm is held as fixed as possible, so as
to prevent the movement of the inflamed surfaces over each other. The
patient restrains as far as possible the respiratory movements,
especially those of expansion and retraction. This is the condition not
only at the initiation of the disease, but at the next stage, that of
effusion. We meet with the same painful respiration also in dry
tubercular pleurisy. Mensuration shows that the sound side of the
thoracic cavity is slightly enlarged by the extra work it has to
perform in the first stage. The elevation movement is noticed to be
restrained when the effusion has increased to the extent of overcoming
the retractility of the lung, for the diaphragm is no longer drawn up
by the lung, and the effusion rises and separates the parietal and
pulmonary pleuræ. The diaphragm bags from the quantity of fluid, and
contracts but feebly. This condition forces the liver and the spleen
down in the abdominal cavity. Gradually the jerking rhythm ceases as
the effusion advances, and the characteristic stitch in the side
disappears. If the effusion increases until it reaches as high as the
second rib, the respiratory movements are scarcely perceptible to the
eye. When it reaches its maximum, the clavicle, they appear to be
arrested, but the vertical diameter is slightly altered by the action
of the intercostal muscles as they endeavor to elevate the ribs, and of
the diaphragm as it feebly contracts and relaxes. The pleural cavity,
which in health is lubricated by about two drachms of moist serous
secretion, is frequently filled to the extent of seventy, eighty, or
more--even to one hundred and twenty--ounces. We cannot wonder that it
should be changed in shape and diameter. All available space is filled
with the fluid, and yet the serous membranes continue to throw out the
secretions. The lung must lose in size by its retractile force, and
when that is overcome the fluid must press in all directions. The fluid
gradually rises from the surface of the pleura over the diaphragm, and
the lung, by negative pressure, draws it and the fluid upward. As long
as the diaphragm is arched, although the lung recedes before the
effusion, it is not really compressed. When, however, the diaphragm
yields and falls from the large quantity of fluid, then the fluid
conquers the lung. Ordinarily, the fluid, when in excessive quantities,
presses upon the lung and the bronchi until it forcibly expels the air;
the lung is compressed against the vertebral column, occupying a very
small space corresponding to the surface under the scapula, often not
larger than from three and a half to four inches square. Inspection
shows that the spaces between the ribs become flattened out, that the
ribs are more widely separated, and that the spaces themselves
frequently bulge. The first observable indication of great distension
of the pleural cavity, sufficient to cause intra-thoracic pressure, is
the depression of the diaphragm, and next the flattening of the spaces
between {498} the ribs. This last is followed by increased pressure,
which causes more general and marked enlargement. "This levelling of
the intercostal spaces is due partly to paralysis of the intercostal
muscles from serous inflammatory infiltration, and partly to the
limited range of movement now possessed by the lung, which is reduced
in volume by the effusion, and is no longer in contact with the
thoracic parietes" (Guttman). This is especially noticed in children
and young persons before the ribs become firm and resisting, the
negative pressure exerted by the lung being in part annulled by the
presence of the fluid. The diaphragm is notably depressed, and pushes
the liver, the spleen, and the stomach below their usual point. So
great is this centrifugal force that the heart's impulse may be felt in
the epigastrium. The heart, when the effusion is on the left side, is
frequently found over to the right of the sternum, and, in extreme
cases, even in the right axilla. When the effusion is on the right
side, the mediastinum is drawn over with it, and the heart is forced to
the left until the apex-beat is perceived as far as one and a half
inches to the left of the line drawn through the nipple, or, in some
cases, to the left axilla. This rarely occurs unless we have fluid
intra-thoracic pressure on the diseased side in addition to
lung-traction of the healthy side. Even the costal pleura, projecting
above the clavicle, may yield to pressure. Inspection reveals to the
observer these striking physical alterations. Hippocrates did not fail
to notice them.

1st. Mensuration shows that the semicircular, antero-posterior, and
vertical measurements of the side are generally increased. According to
Douglass Powell, the total circumference of the chest is always
increased in effusion. 2d. Except in children, the bulging of the
intercostal spaces does not occur until after the adjacent organs have
been displaced by the fluid. When the effusion is large, it becomes
evident, by inspection and by pressing the hand over the sides of the
chest below the armpits, that there is almost immobility of the
diseased side. We insist upon the importance of daily and repeated
comparative measurements of the two sides as aids to diagnosis and
prognosis in pleurisy. A full inspiration or a prolonged expiration
will sometimes show a marked difference by measurement when it is not
discovered during ordinary breathing. Woillez's cyrtometer, as
perfected by Samuel Gee, is the best instrument for testing the
circumference of the chest, and a pair of callipers for the diameter.
The cyrtometer tracings give us the altered shape as well as
circumference. It is especially valuable in the diagnosis of local
empyema from basic pulmonary cavities. Care should be taken not to
confound congenital deformities in the shape of the chest, such as the
alar, flat or pigeon-breasted, or rachitic, with alterations produced
by internal disease. It must also be borne in mind that the
semi-circumference of the right side is normally greater by one-quarter
to half an inch than that of the left side. By inspection of cases
where large effusions have remained for long periods of time slowly
absorbing--often, perhaps, not recognized--we discover marked
unilateral retraction of the chest-walls, with torsion of the spine and
shoulders. The adhesions preventing the lung from expanding, the
alveoli become obliterated, and we have, in fact, atelectasis of the
lungs. This is particularly the case in children, where the disease
prevents the proper development of the side, the healthy side becoming,
from supplementary work, more enlarged. Care must be taken not to
confound with these the anatomical depressions met with sometimes in
the anterior wall of the chest, especially at the lower portion of the
sternum. The amplification of the chest takes place, to a greater or
less degree, at its lower portion as soon as an appreciable quantity of
liquid collects, long before it is possible to have any intra-thoracic
pressure. The lung by its elasticity collapses, and the fluid is drawn
upward in contact with the lung. The thoracic wall, consequently, has
not, at that point, the retractile force of the lung to {499}
counteract its excentric resilience. It is not then drawn in in
expiration by the lungs, while it is continually being drawn outward in
inspiration. The lung-traction of the parietes of the chest is feeble
from the diminished size of the lung. The greater the amount of fluid,
the less lung-tension; consequently, the greater the enlargement of the
chest, as shown by the cyrtometer. If the lung is contracted to its
utmost limit (one-third of its size, according to Powell; one-eighth,
according to Rokitansky), then there could be no suction force
exercised by it upon the parietes of the chest, for, being disabled in
its elasticity, it literally has no power. The whole parietes of the
chest on the diseased side have nothing to antagonize their elasticity,
so it is kept enlarged. In addition, at this stage the fluid of itself
presses against the walls of the chest in all directions.

The elastic pulmonary tissue is always, to a certain extent, on the
stretch. It is striving to pull asunder the pulmonary from the parietal
pleura; but this it cannot do, because the air can have no access to
the pleural cavity. The five mm. of mercury elasticity of the lungs can
be increased by a distension of the chest from a forcible inspiration
to thirty mm. of mercury. Anything which lessens this elasticity of the
lungs takes off so much from the force which interferes with the
rebound of the thoracic resilience, and consequently increases the
circumference of the chest. Such is the case in emphysema, oedema of
the lungs, pulmonary congestion, and, curious to relate, at the outset
during the pyrexial stage of acute diseases, such as pneumonia,
variola, bronchitis. The enlargement of the thoracic circumference is
appreciable. It, however, gradually decreases and becomes normal. This
yielding of the thoracic walls is attributable to temporary engorgement
of the lungs, lessening their retractile force.

At the very commencement immediate results of percussion are negative,
but by delicate taps over a pleximeter there is a sound at the margins,
owing to the deficient expansion, of impaired resonance and of higher
pitch, and the vibrations are less full. There is also a sense of pain,
owing to the increased sensibility of the costal pleuræ. As the
fibrinous coatings form, the sound becomes less and less full and the
normal vibrations of sound are less diffused, more circumscribed,
giving to the finger, used as a pleximeter, a sense of resistance from
the diminished elasticity of the lung. This is especially the case at
the base over the attachment of the diaphragm. As the effusion rises
from the base, the sound on percussion becomes flat. The fluid being a
non-resonant body, the vibrations of the percussion taps do not extend.
The sound is of high pitch, but not resonant. It has been properly
designated by Skoda an empty sound, for it conveys to the ear the
condition beneath, which is one of perfect airlessness. It is not
simply a dull sound or one where there is not the normal resonance, but
it is destitute of all resonance: it is absolutely flat. The confusion
of dulness with flatness has in the past led to erroneous conclusions
as to the line showing the level of the fluid in pleurisy. As high an
authority as Woillez, in reference to fluid flatness, speaks of dulness
as complete, absolute, or very incomplete sub-dulness! The muscular
coverings of the walls of the chest or unusual amount of adipose tissue
or pleuritic coatings or bands produce impairment of resonance, and
sometimes marked dulness on percussion. But when the percussion wave
penetrates to the lungs, there is more or less resonance. When the lung
is solid from pneumonia or tubercular deposits, the sound is often very
dull, but rarely flat, because it seldom happens that all of the
alveoli are filled up, and even when they are the vibrations are
communicated to the bronchial tubes which contain air, and in this way
there is some resonance. We call particular attention to the importance
of these distinctions and to the necessity of light and delicate
percussion in order to test the resonance or non-resonance of the
thoracic cavities. If the percussion be strong, the vibrations are
conveyed {500} by the thoracic walls to the portions where there is no
fluid, and thus we have impaired air-resonance, and not flatness. We
have frequently seen errors of diagnosis in cases of pleurisy owing to
the physician percussing with too much force. To secure accuracy,
Garland[25] lays down the simple rule of percussing with great care and
always in straight lines, and of percussing each line to its terminus
before taking up another. Powell[26] compares the peculiar flat
percussion sound of pleuritic effusion to that elicited on striking
against a brick wall. The flatness is characteristic and more marked
than the dulness of lung-consolidation. If we are not careful to make
the distinction between impaired resonance and non-resonance, we may
easily draw erroneous conclusions as to the rise and extent of the
fluid in the chest. We have shown elsewhere (Pathological Anatomy of
Pleurisy--Distribution of Fluid) that, as the fluid collects in the
cavity, the lung contracts before it. The border above the level of the
liquid contains less air, the capillary circulation is less active, and
frequently there is more or less oedema, owing to its being the most
dependent portion. These physical conditions impair, to a greater or
less extent, the pulmonary resonance. Thus at the base above the fluid
we might, on reflection, naturally expect some dulness on percussion,
lessening as we recede from the fluid. Several observers have called
attention to the impaired resonance over the lowest portion of lung
posteriorly when the person is standing. Garland[27] termed it the dull
triangle. Heitler[28] of Vienna observed this same condition in that
locality, and likened it to a monk's hood cut longitudinally through
the centre and hanging apex down. Rosenbach[29] of Breslau noticed that
this non-resonant triangle in pleurisy would often clear up on exercise
or by breathing; this fact he considered distinctive between pleurisy
and pneumonia.

[Footnote 25: _Loc. cit._]

[Footnote 26: _Med. Times and Gazette_.]

[Footnote 27: _Ziemssen's Supplement_.]

[Footnote 28: _Wien. med. Wochenschr._, 1878, quoted by Garland.]

[Footnote 29: "Ein Beitrag zur phy. Diag. der Pleur.," _Berlin klin.
Wochenschrift_, 1878, No. xii.]

Although the fluid first collects over the posterior portion of the
diaphragm, flatness on percussion is first observed over the axillary
portion of the diaphragm, because, as explained by Calvin Ellis, the
conditions there are more favorable for percussion. As the effusion
increases the line of flatness, when the patient is in the upright
position, advances, not directly up the back and horizontally across
the chest, as was formerly supposed, but across the back in a curve
reaching its highest point in the axilla, from which it descends toward
the sternum.[30] R. Douglass Powell[31] says the upper margin of the
effusion in typical cases is not a water-level, but presents a curve
having its convexity upward and in the lateral region. Since the
attention of the author was first called to a careful examination of
the curve of flatness as ascertained by light and delicate percussion
(in the erect position), he has found it to be more or less of an Ellis
curve at an early stage of the effusion. The line is sometimes better
defined than at others. All observers, however, must acknowledge that
at the stage of the disease when cases of chronic fibro-serous pleurisy
are first seen the letter _S_ curve is not well marked. Mason states
that although in some of his 200 cases this peculiarity was observed,
in others the line was horizontal. When fluid fills the chest to excess
and overcomes the elasticity of the lung, it gives flatness on
percussion high up, even to the clavicle, and behind to the
supra-spinous fossa. The fluid filling the cavity, the line of flatness
becomes nearly horizontal. Then it is that percussion reveals the
displacement of the diaphragm and abdominal organs. On removing the
excess of fluid by aspiration or by absorption, this curved line
reappears, and continues as previously.

[Footnote 30: See section on Pathological Anatomy of Pleurisy,
distribution line.]

[Footnote 31: _London Med. Times and Gazette_, Oct., 1882.]

{501} Contrary to the general belief, when the fluid is moderate in
quantity change of position of the patient modifies but little the area
of flatness, owing to its being retained between the lung and
diaphragm. Woillez[32] noticed slight mobility (never more than to the
extent of one intercostal space) only in 5 of his 82 cases. He
concluded that the conditions were very different from what they were
in ordinary vessels outside the body. Woillez does not attempt to
explain what these conditions are. Skoda acknowledged that in the
majority of cases the fluid does not change its position as the patient
moves. Skoda and Wintrich attribute the non-movement of fluid to
adhesions. Garland, and subsequently W. H. Stone and Douglass Powell,
showed that the effusions were immovable when in moderate amounts,
because they were kept so by the retractility of the lung, and that the
large amounts were movable because the retractility had been overcome
by them. When in large quantities the fluid accumulates in depending
positions of the chest. Later on in the disease, adhesions and bands
mechanically interfere with the line of flatness; or if there be any
disease of the lung interfering with its retractive force, the fluid
may not take its usual line. These peripheral adhesions frequently
occur at the upper margin, and are sometimes wavy and irregular. They
often occur early in the disease, and prevent in a marked degree the
fluid from yielding to the negative lung-traction.

[Footnote 32: _Mal. Aigues des Org. Resp._, Paris, 1872.]

By these bands the pleuritic fluids become sacculated in different
parts of the thorax--between the lungs and the walls of the chest,
between the diaphragm and lungs and the pericardium, the mediastinum,
the vertebral column, and actually between the lobes of the lung.
Fraentzel holds that the percussion sound is dull over the thorax
whenever the effusion attains the depth of from one inch and a half to
two inches between the lung and the chest wall. Garland by his
experiments on dogs shows that the fluid does not thus rise between the
lung and parietes, except a very thin layer, by capillary attraction,
not sufficient to cause flatness on percussion or to interfere with the
expansion of the lung unless the amount is very excessive, and not
until the lifting power of the lung is completely overpowered. When the
effusion is very large, it fills up the posterior portion of the
thorax, compressing the lung against the uppermost portion of the spine
or the mediastinum. The percussion sound is absolutely flat, provided
the force of the blow be not too great; in that case the ribs are
thrown into vibration or the vibrations extend to the sound lung. This
materially impairs the dulness and may lead to error of diagnosis.

The lung may be prevented from contracting by reason of various kinds
of adhesions or by means of widespread infiltrations, by emphysema, and
by laryngeal stenosis. In such cases, as the effusion increases, it
quickly rises in the thinner layers without displacing the organs.
Fraentzel warns us that sometimes, in left-sided effusions, the lung
having become adherent to the heart, the heart is drawn back with the
lung away from the wall of the chest, and then it cannot be felt
anywhere: the absence of the apex-beat and the feebleness of the
heart-sounds may lead us to assume, incorrectly, that there is effusion
in the pericardium. If the fluid collects between the external layer of
the pericardium and the mediastinum, the heart is surrounded and
pressed by the pleuritic effusion.

The Skodaic resonance is a remarkable tubular quality of resonance
heard on percussion when the effusion extends up to the fourth rib or
beyond it, nearly filling the pleural cavity. It is a high-pitched,
long vibration, semi-tympanitic sound, rarely absent when, from an
effusion, the lung is retracted to a very small size, but still
contains some air. It is most frequently found anteriorly under the
clavicle, near the sternum, because to that point the lung withdraws as
long as it has any retractility left. If the air be forced {502} out of
the lung by pressure, this sound is no longer heard. Flint called this
peculiar tympanitic sound, heard above the level of the fluid in
pleurisy, by the descriptive name vesiculo-tympanitic resonance. The
vesicular, though feeble, is combined with the tympanitic quality, and
the intensity of the resonance is abnormally increased. This
subclavicular tympanitic sound is not peculiar to pleurisy. It exists
in pneumonia preceding hepatization, and was noticed by Hudson, Graves,
and Williams before Skoda called attention to it in pleurisy. Skoda's
explanation of this phenomenon is now generally accepted--namely, that
it comes from diminished tension of the lung-tissue, caused by
diminution in the quantity of air, and consequently relaxation of
lung-tension. The residuary air in the alveoli does not mix properly
with the tidal column: it is indeed pent up by the narrowed diameter of
the minute bronchi. Thus it becomes surcharged with carbonic-acid gas;
this relaxes the air-sacs and lessens their tension. In fact, the
percussion sounds are invariably tympanitic when the parietes of the
organ which contains air are not stretched. When they are firmly
stretched, the sound elicited by percussion becomes less and less
tympanitic, and finally dull: such, we know, is the case in striking a
drumhead. The chief characteristic of the sign relates to the quality
of the sound; the resonance is nearly devoid of vesicular quality. A
resonance absolutely non-vesicular is always tympanitic (Flint). This
tympanitic sound is so constant under the clavicle that although it may
be from other causes, its appearance would lead us to suspect effusion,
especially in children. It is not only at the apex, but wherever the
lung shrinks from pleuritic exudation and loses in tension, the
percussion sound has the tympanitic quality. We find it occasionally
near the sternum, and sometimes in sacculated effusions we observe it
in different parts of the thorax. Traube, and subsequently Fraentzel
(_Ziemssen's Cyc._), called attention to the fact that sometimes a long
expiration would cause a temporary abolition of this tympanitic sound
at the apex. Their explanation is that the sound is heard over the
compressed lung. Garland urges that this explanation cannot be a
satisfactory one, for a certain amount of pulmonary expansion is
essential to the production of tympanitic resonance.

This exaggerated resonance elicited by percussion has received its name
from the eminent German who wrote so much about it; but it did not
escape the accurate ear of the discoverer of percussion, Avenbrugger,
who clearly defined the subclavicular tympanitic resonance in
pleurisy.[33] Skoda's sign, however, is not unique, for observation
proves, when the lung is contracted with fluid below, that there are
several varieties of resonance. Notta,[34] who was not aware of Skoda's
ideas, describes the sound as hydroaérique where the lung is above the
level of the fluid. Roger,[35] who called especial attention to Skoda's
views, admitted that there were several varieties of tympanitic
resonance heard above the fluid. He compares them to those heard on
percussing over the stomach of the cadaver. Woillez[36] describes five
varieties or types of sonorousness, according to their intensity, their
tone, and their quality. He noticed these under the clavicle at
different points above the liquid--ordinarily on the level of the
second or the third rib. (1) The most common and the best defined was a
short sound, dry and superficial; the tone of this was acute, with
exaggeration of intensity. Williams[37] in 1841 called attention to
these peculiarities. With this variety we frequently have a
reverberation, pointed out by Stokes in 1837--a cracked-jar sound more
or less marked. Woillez noticed this variety in 11 of his 82 cases; of
this number 9 were in pleurisy of left side. (2) There was exaggeration
of intensity or tympanism with a grave tone: 7 of Woillez's cases
showed {503} this variety, of which 6 were on left side. (3) A
subclavicular resonance, unnaturally acute, but with exaggerated
intensity. (4) Exaggeration of intensity, with equal tone on both
sides; only 2 patients out of 82 showed this variety. (5) Exaggerated
abnormal resonance, more acute than healthy side, and with normal
fulness of sound. These are all modifications of percussion sounds
elicited in pleurisy and other pathological physical conditions
resembling it, where there are variations of tension together with
other modification of the structure of the lung. The bruit de pôt fêlé
is sometimes clearly marked, as it is also in hepatization of lung.

[Footnote 33: Avenbrugger, _Ouv._, ed. de Corvisart, 1808, Paris.]

[Footnote 34: _Arch. gén. de Méd._, 1850, t. xxii.]

[Footnote 35: _Ibid._, 1852, t. xxix.]

[Footnote 36: _Mal. Aig. des Org. Resp._, Paris, 1872.]

[Footnote 37: _The Path. and Diagnosis of Dis. of the Resp. Organs_,
1841.]

Traube's Semi-lunar Space.--There is a point on the left side where we
find normally a vesiculo-tympanitic sound, first pointed out by Traube
and enforced by Fraentzel. It is situated at the anterior base of the
left side, and is of a half-moon shape. It is bounded inferiorly by the
margin of the thorax, and superiorly by a curved line whose concavity
is turned downward. It begins in front, below the fifth or sixth costal
cartilage, and extends backward along the margin of the chest as far as
the top of the ninth or tenth rib. Its greatest breadth is from four to
four and a half inches. This tympanitic sound is caused by the air in
the stomach, which lies well up against the diaphragm. When the stomach
is pushed down by the falling of the diaphragm, from excessive fluid,
the tympanitic sound disappears. The value of this semi-lunar space in
the diagnosis of pleuritic effusions has been variously estimated.
Fraentzel considers it of great significance in the differential
diagnosis between pleurisy and pneumonia; Ferber and Garland do not.
Weil suggests that the area of this space may be diminished by filling
the stomach and colon with solid or fluid food. Garland shows that as
the diaphragm's depression depends upon the excess of fluid overcoming
the lifting force of the lung, we may have, with a vigorous, unimpaired
lung, a large amount of effusion in the pleural cavity, yet the
resonance of the semi-lunar space may remain tympanitic. The condition
of this semi-lunar space is of most diagnostic value in extensive
left-sided effusions. The more the diaphragm is pressed down by the
effusion, the smaller becomes the space of tympanitic resonance. It may
gradually disappear altogether.

Auscultatory percussion may sometimes be advantageously employed to
detect fluid in the pleura, especially in the younger subjects, for
intercostal fluctuation may frequently be appreciated when we press
carefully with the palm or surface of the finger between the ribs while
the percussion shock is applied to another part of the same side. If we
auscultate with a stethoscope, the chest extremity of which is made to
fit in between the ribs, while another person percusses the chest, we
can sometimes detect the fluctuation within the cavity of the chest.

We thus see that in the diagnosis of pleuritic effusions percussion is
very valuable, perhaps the most valuable of the physical signs. We must
not, however, forget that its significance may deceive us if the fluid
is prevented from gravitating by pre-existing adhesions, or if it is
encapsuled between the diaphragm and lung or between the lobes. Cases
occasionally occur where, from fibrinous bands, the fluid is kept in
the posterior part of the thorax, consequently there is pronounced
clearness and fulness in front. Percussion does not enable us to
diagnose the consistence of the contents of the pleura, or its nature,
whether it be fibro-serous or purulent. To do this we must resort to
Bacelli's method, or, still better, to exploratory punctures by the
hypodermic syringe.

Palpation.--The sense of touch gives valuable physical signs in
pleurisy. At the commencement, before there is any effusion of fluid,
even of fibrinous deposit, we notice by palpation the decreased
movement of the walls of the chest, and also the sensitiveness of the
walls. When the eye cannot {504} notice modifications of the expansion
and elevation movements or movements of the ribs, correct views may be
formed by palpation, especially in regard to the amount of local
expansion in the upper part of the chest. In the lower part, by
inserting a finger in the intercostal space we notice the modification
of local expansion, also the convergence of the ribs taking place
coincidently with the continuance of the elevation movement. We are
thus furnished with additional presumptive proofs of the impermeability
of the pulmonary tissue. When fibrinous effusion exists, the hand,
early in the disease, recognizes the pleuritic friction or grazing.
Later on, palpation perceives the rubbing when the muscles have
recovered from their temporary paresis.

As soon as the effusion begins to form we detect a lessening of the
delicate vibrations of the voice as communicated to our hands, always
guarding ourselves against error by remembering that the normal sound
is greater in the infra-clavicular region of the right side, and that
it is always weaker in children and women, unless they have shrill,
weak voices, in which case it may be entirely absent. It, indeed,
requires a certain sonority of voice to be felt through the walls of
the chest. When we find that both sides convey the vocal vibrations to
our touch, we may be sure there is no effusion of fluid. Errors are
often made by applying palpation over too extensive a surface, thus
reaching beyond the fluid. It is important to use light, delicate
palpation, employing the finger-tips instead of the whole hand, in
order to exclude the vibrations from above as we approach the confines
of the effusion. This vocal fremitus is entirely lost from the base up
to the point to which the fluid reaches, and later on when it separates
the two pleural surfaces. This absence of vocal fremitus is one of the
most valuable physical signs of pleuritic effusion. It enables us to
diagnose it from nearly all cases of lung-consolidation except when
caused by malignant disease. When there are considerable pleuritic
adhesive bands, they interfere with the complete absence of fremitus;
but in children this sign is not so reliable. With them vocal fremitus
is often scarcely perceptible in health. In dry tubercular pleurisy
palpation gives us the characteristic friction. Palpation detects also
the rubbing of the two lymph-covered surfaces after the absorption of
the fluid. When there are thick fibrinous bands extending between the
parietal and pulmonary pleuræ, there may be a vocal fremitus
notwithstanding the presence of a quantity of fluid in the pleural
cavity.

Displacement of Adjacent Organs.--The displacement of the heart as a
physical sign indicating the presence of fluid in pleurisy is one of
great significance. It is indeed a cardinal sign, second only in value
to percussion flatness. It is almost invariably met with. Stokes[38]
stated that it was observed at an early period, and was one of the very
first signs of effusion; "that it may exist even before the upper
portions of the chest have become dull, and is a circumstance of
constant occurrence long before any yielding of the muscular portions
of the thoracic walls." The heart is displaced at the very commencement
of the effusion, and its dislocation increases pari passu with the
effusion. The absence of the displacement, unless it can be explained
by some special circumstance which rarely occurs, such as the retention
of the pericardium by old adhesions or consolidation of the opposite
lung, would negative the diagnosis of unilateral effusion. In this
condition there is a marked contrast with the displacement and
depression of the diaphragm and the resulting alterations of position
of liver, spleen, and stomach. These only occur when the effusion is in
great excess--not until from the large quantity of fluid the
retractility of the lung is overcome, and it is consequently unable to
lift up the fluid and the diaphragm. This altered position of the
diaphragm drags the heart {505} downward by means of the ligamentous
attachment of the pericardial sac to its tendinous portion. The
deviations from the normal positions of the heart in slight effusions
can always be noticed if the exact point of the apex-beat is sought for
by palpation and listened for with the stethoscope. Careful percussion
will show the shifting area of flatness.

[Footnote 38: _Dis. of Heart and Aorta_, 1854, Dublin.]

Powell calls attention to a fallacy with reference to cardiac
displacements in the earlier stages of effusion--that, as the base of
the lung retracts, the left or the right margin of the heart, as the
case may be, becomes uncovered. This may lead to an apparent delay in
the displacement of the organ, the more extreme left or right boundary
being now within reach of palpation. The axis of the heart is not
greatly changed by an ordinary degree of effusion. It becomes a little
more vertical, and in extreme cases it may become slightly twisted.
Only in rare and extreme cases does the axis of the heart become
altered in direction beyond the vertical line. Powell[39] found at a
post-mortem a heart that had become so twisted as to present itself
obliquely edgeways in front. Sibson had previously pointed out this
disposition of the heart to turn over and to present its posterior
surface forward in cases of effusion.

[Footnote 39: _Consumption and Dis. of Lung_, London, 1878.]

In examining into the cause and significance of the displacement of the
heart in pleurisy we find that until within a few years, it was, and
indeed very generally now it is, believed that the sole cause was from
direct pressure of the fluid actually pushing the heart away from its
normal position. Skoda, Traube, Stokes, Powell, and Garland were, we
believe, the first authors to show that such was not the case,
certainly in moderate effusions. The displacements take place when the
amount is very small--too small to exert any positive pressure. It is
true that nature places the heart in such a position that it can yield
readily to slight forces. It hangs in the pericardial sac, which is
suspended by the aorta, and which is bound by ligaments to the body of
the third dorsal vertebra. Every change of position of the body causes
certain anatomical alterations of the heart's position. Wintrich,
Skoda, and Braune think that the heart swings like a pendulum from its
base, and that its apex is therefore elevated with every deviation to
the right or left. Lebert says the heart is first depressed by the
sinking of the diaphragm, and then elevated by being pushed to the
right. Fraentzel says that in displacements to the right the heart is
simply pushed over, and is never elevated as Wintrich describes it. The
mediastinum offers but slight resistance, and is very easily pushed to
the right side, where there is no compact organ to resist, and where
the cavity is larger; whereas it is with more difficulty pushed to the
left, where the heart occupies so large a space.

It has been satisfactorily demonstrated that until the pleura is about
two-thirds full of fluid no positive pressure is exercised upon the
lungs or heart. According to Rokitansky, the lung cannot be compressed
until seven-eighths of the pleural cavity is occupied by fluid. The
fluid cannot be drawn off by a canula unless air enters to replace the
fluid. Unless the pressure on the fluid from within the cavity is
greater than that of the atmosphere we cannot draw off a large
quantity: if the pressure balances that of the atmospheric air, only a
few drops of fluid are discharged externally, except by forced
expirations and coughs. This is the case even when the quantity reached
several liters. The feebler the expiratory force the less fluid
escaped. Yet the heart is displaced as soon as the effusion appears.
The significance of the displacement is that it shows the presence of
fluid, but does not show the measure of intra-thoracic pressure
(Powell).

Garland's explanation is that the heart, with the sac and its
connections, "is placed between two highly elastic bodies (the lungs)
which are striving to retract in opposite directions. The heart,
therefore, being acted upon on {506} either side by opposing forces,
occupies a position where these forces just balance each other; and
this is the status of physiological repose in the vertical position of
the body. Now, when an effusion is poured into either chest, the lung
of that side contracts, and thereby exhausts a certain amount of its
retractile energy. The opposing lung, however, still remaining normal,
immediately begins to draw the heart toward itself, and the degree of
displacement thereby induced will be proportional to the diminution of
energy in the compromised lung." Stokes divided displacements of the
heart into excentric and concentric. The former he considered due to
direct pressure of the fluid, and the latter, when from any cause there
was diminution in volume of one lung, the other lung, by its increased
volume, forced it over. The concentric displacements, he thought, were
generally the result of some chronic disease producing atrophy of lung.

Thus we see that displacements of the heart occur at three distinct
periods in the course of pleurisy, and from different causes in each
case: (1st) As soon as fluid forms in the pleural sac. At this period
the displacement is caused by the presence of the fluid which occupies
part of the pleural cavity. The lung by its elasticity retracts. It is,
consequently, of less volume and exerts less negative force upon the
mediastinum and its contents than the healthy lung. The two lungs
having by their equal tractile energy previously kept the heart in
situ, the healthy lung draws the mediastinum out of its position in a
transverse direction. Necessarily, the displacement of the heart from
this cause is in proportion to the amount of fluid effused. This is the
most frequent mode of displacement of the heart. It can be said to be
almost always present. (2d) When the quantity of fluid is great enough
to overcome the retractility of the lung and exert intra-thoracic
pressure, it forcibly expels the air from the alveoli of the lung and
by direct positive pressure pushes the heart aside. The displacement of
the heart in this case can only be produced when the pleural sac is
two-thirds or more filled by fluid. When this condition is met with,
the displacement is very great, because the heart has been already
displaced by lung-traction. Previous to the researches of Garland,
Stone, and Powell, this was supposed to be the only manner of
explaining the displacement of the heart from pleurisy. (3) Where, as
illustrated by Stokes',[40] Hunt's,[41] and Chew's[42] cases, the heart
is displaced toward the diseased side. This occurs more as a sequel of
pleurisy in the course of the absorption of chronic or suppurative
pleurisy, where by non-expansion of lung a partial vacuum is produced.
The external atmosphere presses in the thoracic walls of the diseased
side, and the internal atmospheric pressure from the healthy side is
exerted against the mediastinum and presses the heart in that
direction. Marked displacements from this cause are rare; slight
displacements are more frequent. Cicatrices from healing of large
cavities would have this effect. Mere consolidation of lung could not
cause it.

[Footnote 40: _Dis. of Resp. Organs_.]

[Footnote 41: J. W. Hunt, _Dub. Med. Journ._, _loc. cit._]

[Footnote 42: S. C. Chew, case reported to Med. and Chi. Soc. of Md.,
1883.]

Displacement of Lung.--The lung in cases of effusion is drawn up by its
own retractile energy. It has been demonstrated that this force is
considerable. As the effusion advances the lung recedes to a certain
point, when the fluid, having overcome the retractility of the lung and
having a fixed point below, actually exerts positive pressure upon the
lung (Garland), and compresses the air out of the alveoli and the
compressible bronchi. This compression cannot take place until the
diaphragm is no longer elevated into the thorax, but is bagged down by
the excessive weight of the fluid. There can be no compression of lung
until its elasticity has been exhausted. The gradual effect of the
continued contraction of the lung is to straighten out the letter _S_
curve. The force of lung necessarily diminishes gradually as it
contracts in volume. On the other hand, the immediate effect of
compression is to {507} obliterate that curve. So long, therefore, as
we are able to trace a well-marked letter _S_ on the chest, we may be
certain that the lung is well out of reach of compression (Garland).
Peyrot[43] showed by plaster-of-Paris injections into the chests of
cadavers, and then making cross-sections, that deformities of the chest
are not due to a development of one side, the other remaining normal,
but that they consist of a mutual adjustment of all parts. The
simultaneous movement of the sternum toward the left in left-sided
effusions makes the displacement of the heart appear greater than it
actually is.

[Footnote 43: _Arch. gén._, Juill., 1876.]

The Diaphragm and Intercostal Spaces.--The diaphragm is not depressed
below the edges of the ribs, nor do the intercostal spaces bulge until
the weight of the fluid exceeds the lifting force of the lung. The
admission of air into the pleural sac produces the same result. The
depression of the diaphragm is due in part to the weight of the fluid,
but chiefly to the diminished contractile energy of the retracted and
diminished lung. The displacement of the mediastinum depends upon
similar conditions. Since the traction of the lungs always affects both
sides of the thorax, the movable mediastinum must follow the lung,
which is still capable of contracting, and therefore with right-sided
exudations the left lung will draw the parts over to itself. Only with
excessive effusions in the pleural cavity does the pressure of the
fluid come into activity.

The liver and spleen may be pushed below their normal position by
excessive effusion after the diaphragm yields to the weight of the
fluid. Woillez found the liver displaced downward in the abdominal
cavity in one-fourth of the right pleurisies and only once in left-side
pleurisies. The extent on the right side was from two or three
centimeters to three fingers' breadth, even as far as the umbilicus.

The stomach, when the diaphragm sinks, may be pushed downward; thus the
so-called semi-lunar space of Traube may be obliterated. Ferber noticed
a peculiar displacement of the stomach in two cases where he had
produced an artificial hydrothorax of the left side. The fundus was
pushed to the right, and the stomach was folded over on itself to a
certain extent. A second and marked folding-in of the greater curvature
occurred near the pylorus. This condition of stomach, with left-sided
pleural exudations, has been hitherto entirely neglected by authors.
May not the vomiting which is often observed with excessive effusion,
and which has been attributed to violent acts of coughing, be due to
this doubling over of the stomach?

Auscultation.--At the commencement of acute pleurisy, when hyperæmia
exists with dryness of the pleural surfaces, auscultation shows a
respiratory murmur lessened in intensity and duration. There is also a
jerking unevenness in the rhythm of respiration, and weakness or
indistinctness of the vesicular murmur consequent upon the imperfect
and irregular expansion of the lung. On the healthy side the
respiratory murmur is hypervesicular, and becomes puerile and noisy in
character. In from twelve to eighteen hours the plastic fibrinous
deposit on one or both pleuræ causes us sometimes to hear, over
circumscribed spots, at the end of inspiration and the beginning of
expiration, a fine friction sound, which varies in intensity over the
points of contact of the surfaces. This is especially the case in the
infra-mammary, infra-axillary, and infra-scapula regions. Woillez heard
friction sounds in 52 of his 82 cases. The pain in respiration makes it
very jerking and irregular. The contact of the surfaces pushes aside
the lymph, and thus we hear the sound at a given point at one
inspiration and not at another. It is heard more distinctly during
inspiration than expiration. The reason of our not hearing the friction
sound at the early stage of pleurisy continuously, but with
interruptions in inspiration and expiration, is because the opposed
rough pleural surfaces do not continuously rub against one {508}
another, but remain adherent for a few moments, until a deeper
inspiration tears them asunder. The effusive stage comes on so rapidly
in acute pleurisy that often when patients are examined the friction
sound of the first stage has disappeared. It has been generally taught
that the cause of the disappearance of the friction sound, and its
subsequent reappearance as convalescence commences, are owing to the
fluid separating the surfaces and its reabsorption. We have seen, from
Garland's experiments and from careful clinical percussion
explorations, that the fluid does not come between the two surfaces
unless in very great effusion, but that it occupies the cavity between
the lung and diaphragm. Stokes long since showed that there was
temporary paresis of respiratory muscles, and consequently loss of
movement of the surfaces over each other, which movement was necessary
to produce friction sound. The reappearance of friction sounds
indicates recovery of this muscular power. When heard, the friction is
of the grazing variety--the most delicate form. Walshe designates it as
the attrition species, and says it is audible over a limited extent of
surface, occurring with occasional respirations, dry, and limited
strictly to inspiration. As the effusion appears, we find, beginning
with the lower border, that the respiratory murmur disappears, becoming
less distinct as the effusion advances in the pleural cavity.
Ordinarily, we hear no breath sounds. The absence, however, of breath
sounds as a sign of pleuritic effusion is by no means a constant one.
When the fluid contains many fibrinous bands, binding the lung down to
the costal pleura, or when the effusion is very large and forces the
air nearly out of the pulmonary tissue, pressing it into a firm mass
against the vertebral column (at a point corresponding to the spine of
the scapula), or when the lung is solid simply from the residual air
being pressed out of it, diffused bronchial tubular breathing is heard.
The tubular sound is conveyed, not ordinarily through the fluid, but by
the parietes of the chest and by the solid plastic linings and
adhesions. The fluid, if in large quantity and filled with fibrinous
bands, may also feebly conduct the sound, which, being produced on
solid surfaces, is best conducted by solids. We hear, in fact, a
respiratory sound of low pitch, but tubular in quality. It is
bronchial, but it differs widely from the familiar bronchial
respiration observed when the lung is consolidated in pneumonia. It is
a diffused distant tubular sound unaccompanied by moist sounds, soft in
its quality and muffled. It has not the brazen, harsh character of
pneumonic bronchial respiration. In pneumonia this sound is immediately
under the ear, the lung being in contact with the inner surface of the
ribs, and rendered a good conductor by its solidity, and the sound
rendered louder by the increased consonating properties of the walls of
the bronchi; whereas, in pleurisy, the lung is contracted above the
level of the fluid, or, when the effusion is excessive, is removed from
the walls by an indifferent conductor of its sounds, and the sounds are
conveyed from the compressed lungs at their base by the walls of the
chest, and, in a degree, by the deposits on the pleural surfaces. The
bronchial breath sound which we hear over the lung, compressed by
fluid, near the vertebra continues sometimes a long time after the
absorption of the fluid, because the lung, deprived of air, expands
slowly. If the effusion be small, we do not hear bronchial respiration,
because there is sufficient air in the alveoli to prevent the
conduction of the sound, the air not being compressed out by the
effusion, but the whole lung being lessened in volume. If, again, the
mass of fluid be very large, it prevents the free transmission of the
waves of sound, and we do not hear them.

The auscultatory phenomena necessarily vary according to the amount of
fluid in the cavity, the extent of the adhesions, the retraction, and
the compression of the lung-parenchyma. If the compression be
sufficient to prevent the air from passing down the bronchi, we do not
hear bronchial respiration, {509} because where, as in health, it is
not communicated to the ear (owing to its non-conduction by the
lung-tissue), it cannot be produced. Douglass Powell[44] calls
attention to another unusual pressure effect--altered quality of voice
and cough, a husky voice, and a laryngeal quality of cough
undistinguishable from that so often heard in cases of mediastinal
tumor or aneurism. These disappear after paracentesis.

[Footnote 44: _Consumption and Dis. of Lungs and Pleura_, 1878.]

Above the level of the fluid, and again as absorption of fluid takes
place, we have a return of the characteristic friction sound as the
muscles of the chest recover their normal power. With care this sound
will not be confounded with intra-pulmonary râles, which are moist
sounds removed or modified by cough or expectoration. These convey to
the ear the sound of bubbles of air as they pass through the mucus and
the secretions of the bronchi; whereas the friction sounds are
superficial noises from rough surfaces moving over each other. The
mucous râles which are sometimes heard are not from the pleurisy, but
from bronchial catarrh. The friction sounds heard in the stage of
absorption are ordinarily coarser and more abrupt. They are unequally
jerking in character, and in quality resemble osseous crepitation. In
chronic pleurisy, and for a long time after the fluid is gone in acute
pleurisies, we have pleuritic rubbing sounds when the walls of the
chest are drawn out in full respiration. At the absorption stage we
ordinarily hear the lung gradually expanding. The respiratory sounds
are feeble, and frequently moist subcrepitant râles are heard in the
bronchial tubes. If the effusion has been of long duration, we find the
pleural surfaces so thoroughly coated with fibrinous deposit, and the
lung so separated by bands from the costal pleura, that the expansion
of the lung is very much impaired and the percussion dulness does not
subside. Leaming and Camman of New York give numerous cases where there
might well be difference of opinion as to whether the signs heard were
intra-pulmonary or pleuritic. In cases where the intra-pulmonary
adventitious râles resemble the extra-pulmonary frictions, the
diagnosis is assisted by considering the length of the sound. The
character and intensity of the friction murmur varies very much. It may
be a slight grazing sound or a coarse, sharp creaking-of-leather noise.
Walshe gives no less than six modifications of the friction sound,
ranging from a feeble, scarcely audible noise to one of extreme
loudness. Friction sound is mostly an isolated phenomenon--that is, it
is not accompanied by any unnatural quality of respiratory or vocal
sound. Advanced type friction consists of a series of jerking sounds,
rarely exceeding three or four in number.

We must remember that sometimes, notwithstanding a considerable
quantity of fluid, the lung expands, and, pushing the fluid aside,
causes the rubbing of the pleural surfaces together. When unmistakable,
these respiratory friction phenomena are pathognomonic of the results
of pleurisy. Thus they are properly considered of great value in the
diagnosis.

Pneumo-pericardial Friction Sounds.--On the left side the uneven
pleural surfaces are sometimes forced together by the impulse of the
heart; of course, the resulting friction sounds are cardiac in their
rhythm. Then, again, fibrinous deposits on the outer surface of the
pericardium are forced against those of the covering pleural layers,
both by respiratory and heart impulses. Close attention to the rhythm
and the positions where these sounds are heard will prevent their being
considered pericardial in their nature.

The fluid may be nearly removed and yet the condensation of the
superficial strata be sufficient to produce extensive and marked
dulness. Under such circumstances the production of friction phenomena
is inevitable. The retention of some portion of the lung surface in
tolerably close proximity to the costal pleura by means of adhesions
also renders the production of {510} friction sound possible, although
a considerable quantity of fluid be present in the pleura. It is common
to find effusion signs in the back and friction signs in front. We most
frequently have friction at the base when there is absolute flatness.
If the walls be separated by fluid, there can be no friction from
contact. But it rarely happens that the fluid rises between the
surfaces. To produce friction sounds we must have motion of rough
surfaces which are in contact.

If the patient talks while we are listening in cases of small effusion
we hear over the scapula, toward the spine, and between the scapula and
the spine, bronchophony, as we do also when the lung is nearly deprived
of air, in which case the sound sometimes has the bleating, nasal
resonance designated by Laennec ægophony. In his opinion this was of
constant occurrence and of great diagnostic value, but now it has been
demonstrated that this sound can be heard when there is no fluid
whatever, but consolidated lung. Anstie calls it one of the fancy signs
of pleurisy. Ægophony is an unimportant variety of bronchophony, and
not a characteristic phenomenon of pleuritic effusions. Of itself, it
is not diagnostic of effusion, yet it is none the less true that it is
a modification of bronchophony, and is commonly met with in cases of
moderate pleuritic effusion, usually toward the upper margin of the
fluid. It is difficult to state definitely the amount of fluid which
usually produces it. Guttman thinks it is probably produced by the
vibration of the walls of the flattened, compressed bronchi; this
vibration is excited by the voice and transmitted to the thin layer of
fluid which, at the upper part of the exudation, lies between the lung
and the chest-wall. This tremulous movement of the sides of the bronchi
gives the voice sounds a quavering, interrupted character; and, as they
have to pass through a fluid medium to reach the surface, they lose in
clearness and precision and acquire a nasal twang.

When the effusion is large, and we have full dilatation of the chest,
all vocal resonance ceases, because the vocal vibrations go through
media of such different kinds that they are lost before they reach the
ear. During absorption, before the lung recovers its normal volume, we
again hear bronchophony. Pleural adhesions and thickening cause the
sound to be heard through the effusion when we least expect it. It is
not unusual to find ægophony and bronchophony in the same lung. They
are also found in some cases of pneumonia, and in some individuals,
especially in children, we have between the scapula a normal resonance
of the voice, with an ægophonic resonance.

Bacelli's Sign (Pectoriloquie aphonique).--This, the reverberation of
the whispered voice through the fluid, is a sign of considerable value.
If well marked it indicates fibro-serous fluid; its absence, however,
does not show that the fluid is not of this character. (See Purulent
Pleurisy.)

Auscultation is of great value as indicating with definiteness the
position occupied by the effusion as it is being reabsorbed.

Heart Murmur.--From excessive accumulation of fluid in the pleural sac
a systolic murmur over the base of the heart is very often heard. That
it is produced by pressure or twisting of the aorta is evident from the
fact that it ceases when the fluid is withdrawn.

Phonometry we have found of but little value in the diagnosis of
pleurisy.

COURSE AND DURATION. Acute pleurisy is essentially a unilateral
disease. It does not pursue a regularly-defined course, nor have we any
critical stages, as in pneumonia. In mild cases of acute primary
pleuritis the disease advances slowly and recovery is tardy. The
febrile movement may be four or five days in reaching its height. It
remains at this point for several days--from four to seven days; in
rare instances as long as ten days.

The effusion sometimes comes on very rapidly, but ordinarily is one or
two days in forming. When it appears it may be divided into (1) the
stage of {511} progress, (2) stationary period, and (3) resolution. For
the examination of both of these we must employ percussion, and
mensuration by means of the cyrtometer, which give us exact results.
Woillez in a large number of observations found that the first period
lasted from eleven to twenty-four days, most frequently from fifteen to
twenty days. The stationary period he found varied from twenty-four
hours to several days. Frequently the reabsorption commences suddenly
without any interval. Resolution is initiated from the eleventh to the
twenty-fifth day, and lasts over fifteen days.

As the effusion advances the acute symptoms--rapid pulse, the elevated
temperature, acute pain, and superficial dyspnoea--are materially
lessened. If, however, the effusion be very great, we shall have at
first painful dyspnoea, especially when the patient makes unusual
exertions. This dyspnoea is ordinarily in proportion to the amount of
the effusion. If there is much displacement of heart or distortion of
larger blood-vessels, there is imminent danger to life. After the first
few days we are often surprised at the tolerance of the whole system of
the excessive amount of fluid. Absorption, after the effusion has been
thrown out, is at first rapid, then it occurs more gradually; part of
the liquid portion disappears, and the fibrinous portion undergoes
fatty degeneration previous to absorption. The physical signs of
flatness, vocal fremitus, together with the return of the displaced
organs, the heart, liver, and diaphragm, to their normal positions,
give us accurate means of judging of the progress toward cure. The
general health shows unmistakable signs of improvement. The appetite is
better, as are also the color and strength. If the effusion remains
undiminished in quantity, or if it becomes purulent in character, the
general appearance will show evidences of weakness and lowered
vitality.

The average duration of acute primary pleurisies varies, when the
effusion has not reached any considerable height, from two to four
weeks. It may continue thirty or thirty-eight days--minimum duration
twenty days. The absorption requires many weeks if the effusion is
large or if it becomes chronic. Two months may elapse before the fluid
entirely disappears. In some cases it continues, unless thoracentesis
be performed, for many months. We have given the symptoms manifested
when there is any renewal of the inflammatory process. In pleuritis
acutissimus death may occur in ten days or two weeks from syncope, or
from thrombosis caused by pressure upon the large venous trunks and
consequent twisting, especially of the ascending cava, where it
perforates the central tendon of the diaphragm to reach the
pericardium, or by torsion of the aorta. When the effusion remains for
a long time, the lung may be permanently prevented from expanding by
pleuritic thickenings resulting from inflammatory products. In acute
primary pleurisy the tendency is toward resolution. Louis went so far
as to state that pleurisies never caused death. Trousseau, Lacaze, and
others give cases where sudden deaths were produced by the quantity of
fluid pressing upon the heart and blood-vessels. In subacute pleurisy
(latent pleurisy of the older writers) the course of the disease is so
gradual, so unattended by pain or even discomfort to the patient, that
he goes perhaps weeks with considerable fluid in the cavity without
being aware of it. He has probably been able to continue his occupation
without intermission. It is only when he begins to feel weak and to
lose flesh, and finds that his respiratory force is impaired, that he
consults a physician. The rational symptoms scarcely point to pleurisy,
but the physical signs of the presence of fluid are very distinctive.
In this form the effusion is ordinarily greater in quantity than in the
acute variety, and unless some of the fluid be taken away by
aspiration, absorption is very sluggish. In these cases, if the fluid
remains long in the cavity, the lung may become permanently disabled by
the long continuance of the compression.

{512} In chronic pleurisy the effusions from the acute or subacute
pleurisies remain unabsorbed. They ordinarily are purulent in
character, but sometimes they remain sero-fibrinous many months.
Purulent pleurisies may be primary as well as secondary. (See Purulent
Pleurisy.)

TERMINATIONS.--Pleurisy of a fibro-serous nature terminates in (1)
convalescence, (2) becomes chronic, or (3) ends fatally. Among those
who are cured there are some instances where the disease is of short
duration and the recovery prompt and complete. With others the disease
itself is of a severer type and lasts longer. If the attack of pleurisy
be secondary to another disease, especially if the latter be of a
nature to profoundly affect the nutrition, convalescence is very
tedious.

Acute pleurisies which are primary but rarely become chronic, but when
secondary they frequently are chronic from the beginning. Heyfelder
states that chronic pleurisies are three times more frequent on the
left side than on the right side.

Trousseau, Bowditch, Lacaze, Behier, and others have reported sudden
and unexpected deaths in cases of fibro-serous pleurisies. Not only has
this resulted in cases where the fluid was excessive in quantity, but
also in cases where the amount was moderate. Wilson Fox (_Brit. Med.
Journ._, Dec., 1877) gathered from medical literature between 50 and 60
sudden deaths from effusions of all kinds. Syncope has been the usually
assigned cause of death. Négrié[45] collected 12 cases of unexpected
deaths from pleurisy, and there were but 2 of them where syncope could
be assigned as the cause of the fatal termination. Of the remaining 10
cases, 3 were caused by what is invariably a grave complication,
pericarditis, and 7 by clots formed in the heart or pulmonary artery.
In the cases where pericarditis existed the deaths occurred as early as
the eleventh or twelfth day. In the other cases death occurred as late
as from the twentieth to the forty-fifth day. Woillez[46] reports 2
cases where death was produced by supervening congestion of healthy
lung.

[Footnote 45: _Thèse de Paris_, 1864.]

[Footnote 46: _Loc. cit._]

COMPLICATIONS AND SEQUELÆ.--The inflammation may extend by contiguity
to the lung-parenchyma, pneumonia supervening after a few days, or it
may appear to come on simultaneously. It is, however, a rare
complication. Lacaze[47] reported one case, and that followed
thoracentesis; Lugrol reported a similar case.

[Footnote 47: _Loc. cit._]

Pneumonia does not appear to commence after the effusion has reached
the point of compressing the lung. The inflammations frequently are
peribronchitic and broncho-pneumonic. The mediastinum may become
involved. Fraentzel states that it can never be clearly proved that
simple croupous pneumonia exists as a complication of primary pleuritis
on the side affected; on the sound side it occurs occasionally. Laennec
taught that the compression by the fluid always tended to prevent the
occurrence of pneumonia. Anstie's opinion was that when the lung is
compressed to carnification it is incapable of inflammation. The most
formidable way in which pneumonia may complicate pleurisy is where,
considerable effusion existing in one pleura, inflammation attacks the
opposite lung. It may be doubted whether this ever occurs in truly
primary pleurisies: kidney disease, specific fevers, pyæmia, etc.
nearly always precede it. Hyperæmia or congestion of the opposite lung,
without its amounting to pneumonia, does occur, and is a very grave
complication. The same may be said of double pleurisy and peritonitis
as resulting from blood-poisoning. It rarely happens in primary acute
pleurisy that both pleuræ become involved. When such is the case,
however, it is generally tubercular in its nature, and necessarily a
very grave if not a fatal complication. Walshe reports having seen 4
cases of idiopathic bilateral pleurisy in persons thoroughly healthy
and perfectly free from constitutional taint of {513} any kind. In all
the pericardium was involved, and in 1 the peritoneum. They were all
fatal. Acute pericarditis from extension of the inflammatory process is
a frequently-occurring complication. When the inflammation extends to
the pericardium, the effusion is of the same character as that of the
pleurisy, whether it be sero-fibrinous, purulent, or hemorrhagic. It is
a complication of great gravity and is sometimes the cause of a fatal
termination of the pleurisy. We have never met with endocarditis as a
complication, but Fraentzel speaks of having seen it in acute pleurisy
in children. Before complete carnification occurs oedema of the lungs
may be produced on the diseased side or in the healthy lung. This
pulmonary oedema, when it attacks the sound side, is acute, being
produced by rapid pulmonary congestion, which causes free, albuminoid,
and frothy expectoration, often ending in asphyxia. The serum and
albumen of the blood by transudation pass into the bronchi and the
alveoli, and fill them more rapidly than they can be expectorated: the
subject dies by suffocation. Auscultation reveals fine vesicular râles,
characteristic of oedema of the lungs, closely resembling the fine
crepitation of pneumonia. Traube has named this oedema pneumonia
serosa. Engorgement it certainly is, but it can scarcely be designated
a pneumonia. It closely resembles the oedema we meet with after
thoracentesis, which has been named by Hérard expectoration
albumineuse.

Bronchial catarrhs, when complicating pleurisies, cause dyspnoea, add
much to the discomfort, and protract the duration of the disease.
Barth[48] speaks of dilatation of bronchi as a complication of
pleurisy. Woillez[49] calls attention to a complication which has been
generally overlooked by the authorities--a persistent pain which some
patients suffer in the side of the chest a long time after the disease
has been cured. The most dangerous complications are syncope, formation
of clots, venous emboli, and exaggerated distension of the thoracic
walls by the effusion.

[Footnote 48: _Mém. de la Soc. Méd. d'Obs._, Paris, 1856.]

[Footnote 49: Article "Pleurisy," _Mal. Aigu. Resp._, 1872.]

Sequelæ.--The connection of pleurisies, especially chronic, with
subsequent tuberculosis, is very generally admitted. Bartholow says:
"The importance of pleuritis as a cause of phthisis is hardly
sufficiently recognized in inducing tubercular deposit, and by adhesion
limiting the movements of the organs, and thus inducing diseases."
Anstie says: "It is now well established not merely that pleurisy often
occurs in phthisical lung disease, but that pleurisy itself is capable
of setting up true tuberculosis even in previously healthy persons.
This is specially apt to occur where purulent effusion has been allowed
to remain too long in the pleura, or where paracentesis has been
performed repeatedly for empyema, the wound being closed in the
interval." Modern authors thus consider that a productive field is
offered for the bacillus tuberculosis.

Flint states that "in an analysis of 47 cases, in 3 the subsequent
development of phthisis was probable, although not demonstrated, and in
1 case only the occurrence of this disease as a sequel was certain." Of
53 cases reported by Blakiston, not one became phthisical during
several years after recovery from the pleurisy. Flint says the effect
of chronic pleurisy with effusion in a person already phthisical is to
arrest or retard for a time the progress of phthisis. We have mentioned
the retraction of the chest-walls with deformity of shoulders and
spine, and the permanent dislocation of the heart and larger
blood-vessels, as serious results, as also the orifices produced by the
bursting of the empyemas outwardly. These may all in time, with
judicious care and treatment, be very materially lessened, and even
cured. Empyema sometimes causes destruction of the periosteum of the
ribs and subsequent necrosis. It is questionable whether there are any
cases of pleurisy which do not leave more or less extensive adhesions
{514} between the two pleural surfaces. In many cases they do not, it
is true, seem to injure seriously the general health, yet they must
impair the full functions of the lungs. How frequently this is the case
is shown at autopsies of persons dying of other diseases, where we find
extensive adhesions when we had no reason during life to suspect that
such would be the case. Adhesive bands may interfere with the expansion
of the lungs and cause chronic bronchial catarrhs, ending in death.
Caseous pneumonias are among the sequelæ of pleurisy. When the false
membranes are thick and numerous, the lung remains impervious to air
and useless. This condition sometimes produces bronchiectasis. While it
is true that the lungs, when the effusion is not great enough to
actually compress them, sometimes retain their expansibility for three,
six, or even eight months, yet there are cases where they do not expand
after being bound down for months, and then we have depression of the
walls of the chest. Woillez met with 6 such cases.

DIAGNOSIS AND PROGNOSIS.--The diagnosis of the several varieties of
pleurisy ought easily to be made by the due appreciation of the general
symptoms and physical signs we have enumerated. Cases occur where the
differential diagnosis is not free from difficulties, even to the most
careful of observers. Pleurisies on the left side are more easily
diagnosed than those on the right side. Most of the signs are much more
frequently observed on the left than on the opposite side: some of them
are rarely met with except on the left. Before the discovery of the
science of auscultation and percussion pleurisy and pneumonia were
frequently confounded. By their aid the two diseases may ordinarily be
diagnosed with precision. In both there are chilliness, fever, cough,
and dyspnoea. At the initiation of acute pleurisies, we expect for
several days more or less of chilliness, but in pneumonia one, or at
most two, decided rigors. The temperature in primary pleurisy rarely
goes beyond 100° F. in the first twenty-four hours, whereas in croupous
pneumonia, in the same length of time, it not unfrequently rises to
103° F. or 104° F. In consequence of this high temperature in pneumonia
the skin becomes hot and dry, with frequently a bright spot on the
cheek corresponding to the side of the diseased lung. This is not the
case in pleurisies, where, on the contrary, we have a pale, anxious
expression of face. The comparatively mild fever of pleurisy is
continuous. We have not, as in pneumonia, the marked changes, often of
two or three degrees, between the morning and evening temperatures, nor
have we critical days (between the fifth and eleventh) where the fever
breaks with rapid defervescence.

Pleurisy is a more prolonged disease, and is not self-limited. The
cough of pleurisy is short and quick, with no expectoration, unless it
is thin, frothy mucus. In pneumonia the cough is longer, and is
accompanied by a tenacious expectoration, more or less free, and
generally (not always) tinged with blood. The rusty-colored sputa is
almost characteristic of pneumonia. At first there is a marked
difference in the dyspnoea in the two diseases. In pleurisy it is
superficial, because the lungs are not freely expanded in consequence
of the accompanying pain. In pneumonia it is deeper and the oppression
is greater. The struggle for breath in the first stage of pneumonia is
frequently alarming to witness. The relative frequency of pulse and
respiration is more modified in pneumonia. The stitch-like, cutting
pain in pleurisy is characteristic and very circumscribed, whereas in
pneumonia, unless the pleura is involved, there is little or nothing
beyond a dull soreness. We have in pleurisy the restrained movement of
the side affected, and corresponding increase of movement of the
healthy side. Not so in pneumonia. At the beginning of croupous
pneumonia we generally have the crepitant râle heard in inspiration,
but not observed in pleurisy. The friction sound, if present, heard in
inspiration and expiration, is equally characteristic of pleurisy. If,
as sometimes happens, we do not hear either {515} the crepitant râle or
the friction sound, we must be cautious in our diagnosis until we have
the more definite symptoms of the next stage.

Later on in the clinical course of the diseases, in their second
stage--consolidation in pneumonia and effusion in pleurisy--the
physical signs enable us to make the differential diagnosis. We expect
dulness in both diseases, but it is more absolute in pleuritic
effusions, and to the finger, as a pleximeter, the resistance is
greater. In pneumonia there is very seldom complete dulness over the
whole side of the chest, for there are frequently lobules not
consolidated, or spots where the solid deposit has been partially
absorbed. Moreover, the area of dulness is not bounded by that peculiar
curved line, with its concavity at the base behind, facing the
vertebra, gradually becoming convex as it turns upward and forward
toward the axilla, again descending toward the sternum, as is the case
in pleuritic effusions. Changes of position of the patient may cause
the fluid, when in large quantity, in pleurisy, unless prevented by
fibrinous adhesions of the two surfaces, to gravitate to a greater or
less degree, and thus alter the points where we have flatness on
percussion. The enlargement of the thorax, the bulging of the
intercostal spaces, the marked displacement of the organs, and the
frequently complete obliteration of the semi-lunar space, are
characteristic of excessive pleuritic effusions. The displacement of
the neighboring organs, especially of the heart, is a very valuable
diagnostic sign of pleurisy.

There are, however, other conditions besides the presence of fluid,
such as new growths and pneumothorax, which, by increasing the contents
of the chest, may produce the same result. We may also meet with cases
of congenital malposition of heart or instances where infantile
disease, or constrained position, necessitated by occupation, have
caused malformation of the contents of the chest.

The most characteristic percussion sign of effusion in pleurisy is the
semi-tympanitic (Skodaic) or amphoric resonance high up in front. In
rare cases it is found in pneumonia, but it is most pronounced over the
consolidated lung, whereas in pleurisy it is above the level of the
fluid. The vesicular murmur is not heard below the level of the fluid,
unless very feebly at its upper surface, nor indeed is the passage of
the tidal column of air up and down the bronchial tubes. In pneumonia
bronchial respiration and increased resonance of voice rapidly
supervene; whereas in pleurisy the voice is obliterated. In pneumonia
we find the characteristic loud, high-pitched, brazen bronchial
respiration over the whole of the consolidated portion. When a tubular
quality is given to the inspiratory murmur in pleurisy, it is a
diffused, distant, and low-pitched sound from the compressed lung.
There is a marked contrast between the increased vocal fremitus of
pneumonia and its entire absence in pleurisy. In pneumonia there is
strong bronchophony with a jarring thrill to the ear, but there is not
the displacement of the adjacent organs, the increased volume of the
affected side, nor the widening and bulging of the intercostal spaces,
with sometimes fluctuations, perceived on auscultatory percussion, as
in pleurisy.

Although both diseases are ordinarily unilateral, yet we more
frequently meet with double pneumonia than with double pleurisy. It
must be borne in mind that we may discover the coexistence of pneumonia
and pleurisy. When this does occur special care must be taken in the
diagnosis. In cases of pleurisy on the left side, sometimes the impulse
of the heart forces the two surfaces of the pleura together, and causes
us to hear a pleural, cardiac friction sound. It has the rhythm of the
heart, and is heard when respiratory movements have been suspended.
This sound is limited to the left border of the heart. Care is needed
to prevent the error of diagnosing pericarditis.

The diagnosis of pleurisy from hydrothorax, or passive transudation of
fluid into the cavity of the pleura from mechanical causes or
blood-poisoning, depends upon the recognition of the fact that
ordinarily the latter is not {516} ushered in by fever--that it is
bilateral, and is frequently accompanied with dropsy in other parts of
the body. Transudations being slowly developed, the lung gradually
contracts, and the presence of the fluid is tolerated for a
considerable time; indeed, it is not until it is excessive that it
compresses the lung. Thus, dyspnoea is not ordinarily produced until
the accumulation is very great.

Sometimes the diagnosis between pleurisy and intercostal myalgia, or
pleurodynia, is confused and uncertain. The pain may be as intense and
the respiration as jerky where there is no pleurisy, if there is great
soreness of the muscles between the ribs. The pain is, moreover,
accompanied by more or less rise of temperature. Oftentimes the
respiration is as painful as in pleurisy, for the individual
instinctively refrains from causing the muscles to contract. Usually
there is greater tenderness on pressure over the walls of the chest,
less fever, and the area of pain is larger in this form of muscular
rheumatism. The friction sound, if present, makes the diagnosis clear.
We sometimes remain in doubt for twenty-four hours.

Intercostal neuralgia less closely resembles pleurisy. It occurs
without fever, generally in anæmic subjects or in those debilitated by
chronic general diseases, especially uterine. The tenderness is limited
to several points along the course of a nerve, at the exit of the nerve
from the spinal cord, in the axillary region, and near the sternum.

Pericardial effusions and aneurisms can ordinarily be readily diagnosed
from pleurisies. Their positions in the cavity are so well defined, and
the accompanying physical signs are so characteristic, that they ought
not to be confounded with pleuritic effusions.

Solid tumors and cysts occupying a considerable portion of the pleura
or bulging into it from the mediastinum may deceive us into thinking
that there is an effusion. They displace organs, press upon the lungs,
or intervene between the lung-texture and the walls of the chest, thus
preventing us from hearing the entrance and exit of air and the
vibrations of the voice. Not containing air, we have flatness on
percussion. Being solid conductors, we have with them increased vocal
fremitus, whereas in pleuritic effusions it is not perceived.
Ordinarily, tumors are found at the superior or central portion of the
chest, and cause an irregular bulging of the walls instead of the
general enlargement caused by liquid effusions. Before the discovery of
the present modes of physical diagnosis intra-thoracic growths,
especially cancerous ones, were frequently confounded with pleurisies
by even the most careful observers. Now such errors are only
occasionally committed. The history of the case, the general symptoms,
absence of fever, etc. will assist us in making the differential
diagnosis. A careful examination by physical exploration will give us
valuable aids. The bulging produced by malignant growths is not so
marked nor is it so uniform. The dulness on percussion is not so
pronounced. It does not vary from changes of position of patient. The
displacement of heart and other organs is not so marked. Hunt[50] calls
attention to the considerable blood-stained expectoration from cancer.
He calls it currant-jelly expectoration. We must look also for the
characteristic signs of cancerous cachexia and enlargement of glands in
the axilla and in the supra-clavicular fossa. The exploring
aspirator-needle will generally enable us to arrive at an accurate
diagnosis, with the assistance of a microscope to examine the fluid or
solid matter withdrawn. The fluid thus obtained from cancer is
generally blood-stained.

[Footnote 50: _Loc. cit._]

Inflammations of the pleuræ are sometimes caused by the presence of
intra-thoracic tumors. Abscesses of the liver and echinococci cysts may
ascend, and, pushing the diaphragm before them, occupy the pleural
sacs, and thus simulate pleuritic effusions.

{517} Pulmonary atelectasis, caseous inflammation of the tissue of the
lung, aneurisms of the large thoracic blood-vessels, may, without care,
be mistaken for pleurisies. It is very important to ascertain the
nature of the fluid effused into the pleural cavity, whether or not it
is serous, sero-fibrinous, purulent, or hemorrhagic. Generally this can
be done by careful study of the accompanying general symptoms and the
clinical history of the case. If there are repeated irregular rigors
from the beginning, followed by high fever and free perspirations,
there is every reason to fear that the fluid is purulent. If symptoms
of blood-poisoning develop, we are still more confident that there is
pus. Its hemorrhagic character may be inferred when great pallor,
weakness, and lowered temperature suddenly appear during an acute
attack.

Bacelli's physical sign known as pectoriloquie aphonique, or the
passage through the effused fluid of the whispered voice, has
considerable significance as a means of testing the nature and
character of the fluid. His conclusion was that, when heard, it showed
the fluid was fibro-serous; when not heard, it revealed to us that the
effusion was purulent or sero-purulent. Laennec had noticed that in
voiceless consumptives the whispers would sometimes resound as if the
patient shouted in the ear of the auscultator. R. Douglass Powell
reported[51] 10 cases bearing upon the value of this sign. In 6 of
these, in which the fluid was clear, 5 yielded the sign, the sixth did
not. In 2 acute cases, when the effusion was purulent, the sign was
heard. He adds that he has heard the sign to perfection in fetid
sero-purulent effusion. Mercadie[52] claims that when pectoriloquie
aphonique is heard in purulent effusions it is only at the uppermost
part of the fluid near its limit, where it has become very thin from
the weightier portion, the flocculi, and the leucocytes falling to the
dependent portion of the sac. Care must be taken in listening for this
sign. The patient must be ordered to speak each syllable slowly and in
a whisper, distinctly counting up to twenty or thirty. If it be present
we ought to be able to perceive that the syllables sound, to the ear,
clearly articulated along the height of the effusion. The sound is
caused by the transmission of the whisper without any buzzing and
without continuous murmur. The maximum of intensity of this sound is
heard along the vertebral gutters and along the posterior base of the
pleural cavity. It becomes feeble in its distinctive character as we
approach the axillary region and also immediately under the angle of
the scapula. The theoretical objection has been made to this sign that
its production is contrary to well-known physical laws of the
conduction of sound-waves. It is said because the sound originates in
the air it must be indifferently conducted by fluid; moreover, that its
transmission ought to be in proportion to the density of the fluid,
whereas this sound is best conducted by a thin fluid. Walshe's
explanation of the greatly-increased sound-conducting power of a
consolidated lung in croupous pneumonia was that it was owing to its
homogeneity of structure. Bacelli avails himself of this principle to
account for our hearing through a fibro-serous fluid the whispered
sonorous waves, and our not hearing them when the fluid was
sero-purulent or purulent. In the latter case the fluid is excessively
heterogeneous, containing leucocytes in abundance, besides layers of
membranes, flocculi, and blood-discs. The sound-waves are lost as they
pass through these media of different density. We have found it to be a
physical sign of value in the differential diagnosis of the nature of
the fluid, yet its presence is not pathognomonic of serous effusions.
In thin fluids it is generally heard, and ordinarily it is not found in
purulent pleurisies. If well marked, it indicates a fibro-serous
effusion. Its absence does not necessarily show purulent pleurisy. Its
greatest value is as indicating the purulent transformation of a
fibro-serous effusion.

[Footnote 51: _Trans. Int. Med. Cong._, 1881, vol. ii.]

[Footnote 52: _Thèse de Paris_, 1876.]

Thanks to modern investigations, we have in the very fine needle of the
{518} aspirator, or that of the hypodermic syringe, a delicate and sure
means of accurate diagnosis, not only as to the nature of the fluids,
but as to that of tumors and growths which may be confounded with them.
We would not use for exploration a trocar and canula. We consider it
best to employ a short needle in aspiration, for fear that a delicate
hypodermic needle might break. Flint states that he has known several
instances of this accident. Aspiration can be performed with perfect
safety, and, indeed, without any fears of unpleasant results even if we
perforate an aneurism. The orifice made is so small that the tissues
close the moment the needle is withdrawn after making the exploratory
puncture. If care be taken to cleanse the instrument and to use
Listerism that no deleterious germ be introduced, the operation is
harmless. (See Purulent Pleurisy.)

Blunders in diagnosis, however, will rarely occur if an examination is
conducted with great accuracy, and if we follow the course of the
disease with care.

PROGNOSIS.--The prognosis of simple primary pleurisy is generally
favorable, unless it is complicated with other diseases or occurs in
enfeebled persons. The intrinsic tendency of the disease is to
recovery. Laennec considered that the prognosis in acute pleurisy was
always favorable. Pleurisy with scanty sero-fibrinous effusion is not
in itself serious. Dry pleurisy is free from danger. Subacute pleurisy
with large effusions, where the course of the disease is insidious and
slow, is more apt to be followed by tuberculosis than the more acute
cases. Louis's law, deduced from 150 cases, that patients never died
from the effusion in acute pleurisies, was long since disproved by
Trousseau. Lacaze du Thiers published in 1873, in his thesis, a number
of cases of sudden death from large accumulation of fluid. These deaths
were caused by a large amount of effusion being thrown out rapidly, and
suddenly compressing the lung before the system had time to accommodate
itself to the presence of the effusion. These cases, termed foudroyant,
should be very carefully watched. There is danger of death from
orthopnoea when the pleural cavity is completely filled, especially in
latent pleurisies, where the patient, unaware of the risk, makes,
perhaps, unusual physical exertions. Some deaths have been caused by
oedema of the lungs and some by syncope; others, again, from thrombosis
of the pulmonary artery. We must bear in mind the grave prognostic
value of attacks of orthopnoea and severe dyspnoea, because they, more
than the mere quantity of the fluid, show the want of tolerance in the
organism. These cases demand prompt mechanical interference with the
aspirator. The very rapid accumulation of the effused liquid, even if
unattended by dyspnoea, is an unfavorable sign, for observation has
proved that in such a case its absorption is attended with more
difficulty. Bilateral pleurisies attended with considerable effusion
are commonly fatal.

If there are complications with other acute diseases, such as
pericarditis or pneumonia, the prognosis may be far from favorable,
more particularly if pleurisies supervene when the organism has been
exhausted by a long continuance of the primary disease.

If absorption begins soon after the acute symptoms subside (and we
expect it to do so where the general health and strength are good), and
goes on vigorously, we can with confidence predict a favorable result,
especially if there be no contraction of the walls. The earlier the
reabsorption takes place the more favorable the prognosis. If, however,
four or five weeks pass without any perceptible diminution in the
extent of the effusion, there is cause for uneasiness. Especially is it
dangerous if, in addition, we have those ugly symptoms, emaciation,
weakness, and hectic fever, which point to the conversion of the fluid
into pus. There is the prospect of protracted formation of pus with its
dangerous sequelæ, including tuberculosis from infective absorption.

{519} That these dangers can in a great measure be obviated by prompt
thoracentesis ought now to be universally admitted. Anstie predicts
that the experience of the next twenty years will enable us to ensure
an absolute immunity from fatal results from either of these serious
complications. Symptoms of oedema of the lungs or of cyanosis are bad
prognostic signs; so is diminution in the amount of urine secreted,
which indicates that the arteries are incompletely filled. Still worse
are the symptoms of over-distension of the veins, dropsy, and the
appearance of albumen, casts, and blood in the urine.

The prognosis in secondary pleurisies is much more serious. In cases
where the effusion is purulent at their commencement, the prognosis is
graver than when it becomes purulent after remaining some time in the
cavity. This is because they are often pyæmic in their origin.

With modern treatment, however, the percentage of recovery is greater
than it formerly was. When we have to contend with chronic purulent
cases occurring in cachectic constitutions or in those debilitated by
other illnesses, especially tubercular, the prognosis is necessarily
unfavorable. The most fatal of all secondary pleurisies are those
supervening in the course of pyæmia or puerperal infection. Here death
is the rule, recovery the rare exception.

Pleurisies supervening on Bright's disease or nephritis, following
scarlatina and idiopathic fevers, have a high rate of mortality. The
modern employment of the thermometer is of the greatest assistance to
us in forming our prognosis. Marked variations of temperature, whether
they be below the normal or constantly high or advancingly high, have
grave significance. Anstie's valuable results from the use of the
sphygmograph, as giving us the favorable and the unfavorable pyrexial
pulse-forms, cannot be over-estimated. We fully concur with him, "that
in the dangerous secondary pleurisies the combined use, for prognostic
purposes, of the thermometer and the sphygmograph is more valuable than
all the other modes of observation put together." It is so because they
give us accurate physical data by which we can estimate the exact
condition of the patients.

Relapses, with a rapid increase in the amount of fluid after
reabsorption has been active and convalescence apparent, are frequently
attended with danger, because they often denote a tubercular or
hemorrhagic development. A very unfavorable sign is the rapid increase
in the effusion after spontaneous or artificial discharges, especially
if the fluid has become fetid in its character and has the dark
appearance of unhealthy, purulent matter.

TREATMENT.--The study of the natural history of acute fibrino-genic
pleurisy teaches us that there is always in it a tendency toward
recovery unless there is some constitutional weakness behind the
disease or a large fibro-serous effusion resulting from it. We have all
met with cases where patients have recovered in the course of a month
or six weeks spontaneously, without any treatment. Of A. L. Mason's 200
cases, 132 recovered without having to resort to thoracentesis. It is
often a harmless disease when left, as far as medical treatment is
concerned, entirely to itself. Of course the body-temperature and the
physical evidence of the effusion ought always to be carefully
observed. The hygienic treatment ought never to be neglected. We should
insist upon rest in bed in the most comfortable position to the
patient. The temperature of the room should be from 65° F. to 68° F.,
the approximate in-door winter degree for healthy adults.[53] The body,
especially the chest, should be kept quiet; all unnecessary movement
should be avoided. The food ought to be nourishing in quality, easy of
digestion, and in quantity sufficient to keep up healthy nutrition.
Stimulants are unnecessary, but it is a mistake to withdraw water,
which contributes so much to the comfort of the patient and {520}
cannot injure him in the first stage. We should take care that the
patient has enough sleep. If necessary, mild hypnotics should be used.
The effusion results from the inflammatory process, and not from simple
transudation. If the pain is very severe, we must resort to the
administration of opium by mouth or to hypodermics of from one-eighth
to one-sixth of a grain of morphia; this, however, should be avoided
when possible, as preparations of opium impair the appetite and depress
the patient. The pain ordinarily passes off in 48 hours, and can often
be relieved by application of hot-water bags, turpentine stupes, or
anodyne liniments. Bloodletting, general or local, is rarely necessary.
Leeches will give relief to the acute pain, but opium does that more
effectively. Depletory remedies are hurtful and retard convalescence,
and do not control the amount of the effusion, which in itself is
depletory. If the patient is seen at the initiation of the disease, a
large dose of quinia (from ten to fifteen grains), especially if the
temperature goes to 101° F., often has a marked effect in controlling
the temperature and also the tendency to effusion. Smaller doses may be
repeated every few hours. Liq. ammonii acetatis, in fluidrachm j to
fluidrachm ij doses every two hours, and Apollinaris or other alkaline
drinks, relieve vascular tension and promote the action of the skin and
kidneys. During the pyrexia, with the effusion increasing, we endeavor
to lower arterial pressure within the pleural vessels by aconite,
diaphoretics, mild salines, diuretics, with complete rest of the body.
Hot applications (not heavy poultices, however) may sometimes be used
at short intervals, with a view of dilating the superficial vessels and
thus relieving those of the interior.

[Footnote 53: _Boston City Hosp. Reports_, 3d Series, 1882.]

Under this simple treatment many patients are sufficiently well in a
few weeks' time to sit up. They ought not to be permitted to move about
unless there is a very small amount of effusion. Roberts[54] of
University College Hospital applies adhesive strips over the chest in
all cases from the beginning. Mason prefers Martin's india-rubber
bandage, three or four inches wide, extending from the lower border of
the ribs to the axilla, as it adapts itself better to the chest-walls
and supplies an easily-regulated elastic pressure. He considers it also
useful in promoting absorption after tapping. Generally in three or
four weeks, in favorable cases, the effusion has been absorbed and the
patient is able to resume his ordinary duties. The writer cordially
endorses Anstie and Bartholow's protests against the employment of
mercury for any supposed aplastic properties. It really exhausts the
recuperative forces of the organism, and probably injures instead of
benefiting in pleurisy.

[Footnote 54: Quain's _Medical Dictionary_.]

If the exudation be in considerable quantity, three or four weeks may
be required for its absorption. If this process is sluggish, can we by
medicines promote it? Mercury has lost its old reputation as a remedy
for this purpose. Iodine externally, and iodide of potassium in decided
doses, still retain, to a limited extent, the confidence of
practitioners. Preparations of iron, especially the muriatic tincture,
have had better effects in the hands of the writer than any other
remedy. Large blisters cause great discomfort, and their utility is
very questionable. Alkalies possess the power of dissolving exudation,
and of these the most efficient is ammonia, especially carbonate of
ammonium in doses of from five to ten grains. Saline laxatives, by
producing watery stools, have some power in reducing the amount of
fluid. Some authors recommend highly the acetate and citrate of
potassium dissolved in a decoction of scoparium. J. W. Hunt[55] places
most reliance upon pilocarpus pinnatus, which has given him most marked
and successful results, even where other remedies have failed. He
pushes it to the extent of producing extreme diaphoresis. He commences
with thirty minims of the fluid extract four times daily, rapidly
increasing {521} the quantity and the frequency of the doses to the
extent of fluidrachm j every two hours. The one-eighth of a grain of
its alkaloid, pilocarpine, given hypodermically, acts very promptly. He
admits that the vital forces are so exhausted by this treatment as to
require at once the administration of tonics, especially of iron with
strong food. Grasset[56] reported 5 cases of effusion treated by
jaborandi. They were cases of pleurisy without fever or sign of
inflammation--cases which ordinarily require several blisters to
produce an effect.

[Footnote 55: _Dublin Journal Med. Sci._, Dec., 1882.]

[Footnote 56: _Journal de Thérapeutique_, Avril, 1876.]

Ernest Wernaere[57] reported 7 cases of acute pleurisy where there was
considerable febrile reaction. Jaborandi was effectual in every case,
and the effusion rapidly disappeared after two doses of the infusion.
The fever at the same time was diminished, and there was no return of
it, as frequently occurs in non-inflammatory cases. It has less effect
upon children than upon adults. In a case of Wernaere's only one dose
was given.

[Footnote 57: _Thèse de Paris_, 1876.]

The value of counter-irritants has been frequently questioned of late
years. Fly blisters give relief in limited dry pleurisy. Many
practitioners have great confidence in large blisters used over the
chest after the febrile stage has subsided. Woillez, in tabulating the
results of the various means of promoting absorption, puts purgatives
first in utility, and blisters last. Blisters, he claims, had no effect
in 90 per cent. of cases. The iodide of iron, in pills, or the compound
syrup of the iodide of iron and manganese, with improved digestive
powers, are the best means of promoting absorption. At this period of
the disease it is an advantage to lessen, within certain limits, the
amount of fluid taken into the stomach, forcing the blood to abstract
water by absorption from the chest. Jaborandi has the same effect by
withdrawing water from the blood.

There are cases of excessive quantity of fluid, and others which resist
all drugs given to promote absorption. Among these are some acute
cases, but many of a subacute and chronic nature, where the effusion
remains stationary, injuring respiration and often mechanically
endangering life. This occurred in nearly one-third of Mason's cases.

Thoracentesis.--In studying the history of this operation we have seen
how frequently, since the time of Hippocrates, it has been in favor
with practitioners, and then has fallen into discredit. During the past
thirty years, thanks especially to Bowditch and Trousseau, its
unquestionable value has been established, and is now universally
recognized. Improved knowledge of pathology, safe and easily-applied
instruments, together with the discovery, by Lister, of the means of
securing the operation from septic dangers, have perfected this
surgical treatment. Observation in hundreds of cases has proved that,
properly used, it is almost without risk. As a means of diagnosis it is
the most accurate we possess; as a treatment for affording positive
relief it is a boon to suffering humanity; as a method of cure it has
been most successful.

Such being the estimate of its value, let us study, 1st, the
indications for its use; 2d, the manner of operating; 3d, and finally,
the objections founded upon the accidents that have followed its
application.

The indications are met with in two conditions--that of excessive
accumulation of fluid, and where there is non-absorption of the effused
liquid. In going over the symptoms we have seen the effects of large
collections of fluid in the pleura--how the heart is pushed out of its
normal position, and how the large blood-vessels are distorted. We have
called attention to the retraction and compression of the lung until in
many cases it is airless, and thus not able to perform its functions.
We have shown that all the adjoining organs and cavities are sometimes
forcibly thrown out of the position nature placed them in. The liver is
pressed forward into the abdominal cavity, and {522} the diaphragm is
unable, from mechanical pressure, to ascend and contract. The
mediastinum, with its contents, is materially interfered with.
Observation has shown that such a state is a very dangerous one. Not
only does it cause great dyspnoea, pain, and oppression, but the risk
to life is imminent. In a number of instances it has caused death.
Trousseau tells us of 3 deaths; Lacaze reports others. Bowditch, having
seen several fatal cases produced by the quantity of fluid, worked with
energy and perseverance until he was furnished by Wyman with his
ingenious aspirator, of which he promptly availed himself,
notwithstanding the objections he met with from others. "Ridicule," he
says, "was pointed at me by some high in surgery: at first the whole
medical profession was against me." He could not stand still and see
men die whose lives could be saved. Chew had a patient die suddenly
from this cause. Many authors mention cases of death from the large
amount of fluid. Wilson Fox summed up from the records between 50 and
60 deaths from effusion in the pleural sac. Moreover, many patients
have died where the disease was not recognized. The condition of the
circulatory apparatus is such that we can readily understand that
emboli would form in the heart, in the large blood-vessels, and in the
parenchyma of the lung itself. These clots produce grave results. If
they form in the pulmonary veins or in the left heart, they determine
an embolic obstruction of the central artery, with all its
consequences--apoplexy, hemiplegia, etc. If it forms in the right heart
or in the pulmonary artery, it may produce rapid aphasia and death
(Paget). Louis was certainly wrong when from his 150 cases of pleurisy
he deduced the law that none died of this disease per se. It is thus a
matter of the utmost importance that we should be able to recognize
that there is a quantity of fluid capable of producing such serious
results. The call for relief and diminution of the amount of fluid by
thoracentesis is urgent. What amount is dangerous to life, and how can
we arrive at an accurate estimate? To what extent can we judge by the
subjective symptoms, especially by the dyspnoea? Andral and Trousseau
both speak of it as a very fallacious and uncertain symptom, and by
itself may be unimportant as an indication. In the beginning of the
disease we find suffocating dyspnoea for a time when there is very
little fluid. Diffusible stimulants and anodynes give relief. On the
other hand, there are patients who with large amounts of fluid, even
two quarts, walk about with but little difficulty in breathing, and
attend to their pursuits unconscious of being in danger of sudden
death. Bowditch[58] speaks of several fatal cases in simple pleurisy
from excessive amounts, "from sudden failure of the power of the heart,
with or without more or less dyspnoea." This is especially the case
where the fluid forms insidiously, without marked general symptoms.
When, however, we meet with dyspnoea, together with other and more
reliable symptoms, it is very significant of danger, and ought to force
us to resort to thoracentesis to afford mechanical relief. If we rely
upon general symptoms, we may be deceived as to the amount of fluid,
and serious results may follow. However, we must bear in mind that the
most imperative reasons for thoracentesis are the signs of threatened
failure of cardiac power. Bowditch lays down the rule that "if the
dyspnoea is excessive, so as to amount to permanent orthopnoea, or if I
learn that within a few hours previous to my visit there has been even
one attack of momentary orthopnoea during which the patient felt as if
the breath would be wholly lost, I tap immediately, provided I am sure
that there is even a small quantity of fluid in the pleural cavity, and
that it is apparently the chief or perhaps only cause of the
orthopnoea. I fear," he says, "death may occur before my next visit."
This eminent American authority on this subject lays down as the result
of his vast experience the rule that "when a patient comes under {523}
notice in whom a large quantity of fluid has been long effused, I
advise thoracentesis as the first remedy." The author ventures to
assert that where the amount is excessive there is imminent danger to
life from the mechanical results of the presence of the fluid, even
during the febrile stages; consequently thoracentesis is urgently
necessary. I am confirmed in this view by Dieulafoy, Fernet, Clifford
Allbutt, Marshall, and Cross. Barnes[59] says in all cases where the
effusion is large and where dyspnoea is urgent it is better to operate
at once. "It is my practice to operate at once when the chest is two
parts filled with water, without waiting for urgent dyspnoea."
Dieulafoy, in discussing these questions, states,[60] after consulting
all the authorities accessible to him, that death has never been caused
by less than two liters (equivalent to 62½ fluidounces), except in one
instance reported by Blackey, where after death there was found 1500
grammes (47 fluidounces). In adults with well-formed chests he
considers 1800 or 2000 grammes as the amount demanding surgical
interference. He candidly acknowledges that he cannot make this an
absolute rule, because the capacity of the pleural sacs must
necessarily vary in different individuals according to their height,
breadth, development of thoracic muscles, sex, etc.; consequently, the
inconveniences and functional disturbances produced by a given quantity
of fluid in the chest must be different in different persons. But how
can we arrive at an accurate estimate of the amount in the chest?
Dieulafoy,[61] in calculating the quantity, states that if it amounts
to 1200 grammes when it reaches the sixth intercostal space, it ought
to be valued at 2000 grammes when it is found at the third intercostal
space. This is only approximative and unreliable. The height of liquid
is not always proportional to quantity. It varies with size of chest,
resistance of organs and walls, and condition of lungs. Potain insisted
upon the difficulties that the pulmonary hyperæmia caused in the
diagnosis, the abundance of fluid, the variable degree of yielding of
the lung, and the adhesions which have drawn the walls to the lung. The
true way of judging of the necessity for the operation is from the
grave functional disturbances and by the definite positive physical
signs which give us unmistakable indications which we dare not neglect.
We can calculate the amount of the effusion by the level of the
flatness on percussion, by mensuration with the cyrtometer, and of the
impaired thoracic movements by the stethometer. Physical examination
reveals the extent of the displacement of the heart and other viscera.
The displacement of the abdominal viscera, the liver, the spleen, and
the stomach shows that there must be excessive amount of effused fluid
in pleura--enough to produce serious intra-thoracic pressure. This is a
condition demanding surgical interference. The Skodaic resonance under
the clavicle, the complete flatness being horizontal instead of giving
us the Ellis curve, impaired resonance over the posterior triangle
becoming absolute dulness, the presence of cavernous or amphoric
respiration near the sternal-clavicular articulation, and, in rare
instances, subclavian murmur from pressure upon the subclavian
artery,--all these signs give unmistakable evidences that the pleural
cavity is full of fluid. It is important, in considering the treatment,
to form a correct estimate of the degree of intra-thoracic pressure,
for Erichson has shown that the mere collapse of a lung affects but
little the facility of the circulation through it; its compression or
forcible collapse necessarily retards the circulation and throws extra
work upon the already overburdened heart. The more precise our physical
diagnosis, the more appropriate will be our treatment. Douglass Powell
found the intra-thoracic pressure to vary from a -- pressure to ½ and
1½ inches of mercury at the commencement, and from -1/8 to -½, and even
-1, inch mercury at the termination of paracentesis, there being in all
cases a more or less considerable amount of fluid still remaining in
the pleura. He states, {524} as the result of his own observations,
that in recent cases the period of effusion at which the intra-thoracic
pressure is converted from a -- pressure or zero to a positive pressure
upon the lung and heart is marked clinically (1) by the flatness
mounting up above the third cartilage (patient in sitting position),
and (2) by the Skodaic resonance becoming changed from the full note to
a more tubular quality. The extent of Skodaic resonance is a very
valuable indication of the amount of fluid, and consequently of the
propriety of operating. If this tympanitic resonance be down to the
third rib, and the cyrtometer shows no decided enlargement, we had
better not interfere. On the other hand, if the Skodaic sign is not
heard, and instead there is flatness, we will be sure to find decided
increased measurements and tubular breathing behind. Under such
circumstances we may feel confident of positive intra-thoracic pressure
of from one inch to one inch and a half of mercury--an amount
sufficient to compress the lung and interfere with the heart's action.
There is some danger of syncope, even if the patient remains motionless
in bed, but if he moves about he is in imminent danger. The subject is
annoyed by a straining retching cough with frothy, viscid sputa with
perhaps some discolored points. The heart and the lung of the healthy
side give warning of the danger, which ought never to pass unheeded. A
murmur may be heard over the displaced heart, and over the lung on the
unaffected side we may hear a fine crepitant râle, showing pulmonary
hyperæmia and resulting oedema. The syphon or aspirator will afford, by
withdrawing perhaps a quart, the necessary relief. Nature will do the
rest in a large proportion of cases.

[Footnote 58: Unpublished MSS.]

[Footnote 59: _Brit. Med. Journal_, Dec., 1877.]

[Footnote 60: _Nouveau Dict. Méd._, vol. xxviii., art.
"Thoracentesis."]

[Footnote 61: _Loc. cit._]

We cannot always estimate accurately the quantity of fluid by the
displacement of the heart and other organs. The retractile energy of
the lung is a very important factor in producing this result. A very
large effusion, associated with a very powerful lung, will produce but
slight displacements, while small effusions, when the lung of the
affected side has lost its elasticity, will cause relatively great
displacements (Garland). If there be no adhesions present, the letter
_S_ curve of flatness becomes a sign of the greatest value. It marks
accurately the height of the effusion. Knowing this, as well as the
position of the heart and diaphragm, and the capacity of the chest, we
can estimate the quantity of fluid in the pleural cavity. If in left
pleurisies the heart be so pressed out of position that its apex beats
to the right of sternum it is very diagnostic. With these signs,
whether accompanied by dyspnoea or not, we must regard thoracentesis as
imperatively called for. The presence of the febrile movement is not a
counter-indication under these circumstances. The presence of a basic
murmur, caused by the heart or aorta displacement, is an urgent
indication for surgical interference.

There are attacks of fainting and syncope, suffocative paroxysms, with
irregular and painful palpitations of the heart, with sometimes
alarming threatenings of asphyxia--especially in pleurisy of the left
side. These symptoms are probably due to the twisting of the inferior
cava as it passes through the quadrilateral foramen of the diaphragm.
The danger is necessarily increased by long continuance of the
effusion. Prompt surgical treatment is indicated when we detect
evidences of embarrassed circulation in the opposite lung, with a
blowing quality of respiration and subcrepitant and oedemic râles.

In all cases of double pleurisy, where the total amount is sufficient
to fill one whole cavity, we ought not to postpone operating. Even when
the effusion is not very large, if there are other diseases of the
respiratory or circulatory systems to cause grave complications, and
danger of increased impairment of their functions, thoracentesis is
rendered necessary. That these conditions justify thoracentesis we
believe no one who has any practical experience will question. But two
conditions exist where there is considerable {525} difference of
opinion in regard to the propriety of operating: 1st, during the
febrile stage, and, 2d, where moderate effusion remains unabsorbed.

In regard to the first of these, many authorities, even among the most
enthusiastic advocates of the operation, have contended that unless
there is imminent danger to life from the excessive collection of
fluid, it should not be withdrawn, as it would at once re-form, and
additional inflammatory action might be excited by surgical treatment.
Castiaux,[62] however, strongly advocates the view that the operation
by aspiration will hasten the cure of acute pleurisy and prevent the
formation of the fibrinous deposits and bands which to a greater or
less degree, even in moderate effusions, impair the expansion of the
lungs. He relates 37 cases, almost all of which were operated upon by
himself. He was successful in all of them, and the patients suffered no
inconvenience or discomfort in consequence. In most of his cases the
pulse and body-temperature fell (perhaps the same day, certainly the
next morning), and even became normal after the operation, and the
patients improved rapidly. He aspirated as soon as he detected the
presence of fluid by exploratory punctures, believing that from the
moment we have at our disposition sure means of relief which are
harmless, it is useless to leave to nature the duty of removal--useless
to leave to untrustworthy medication the relief which we can promptly
give. He operated at the height of the first or inflammatory stage of
the disease. He assigned as reasons for operating that he thereby
relieved the lung of the compression which impairs expansion; that he
removed a liquid rich in fibrin and capable of increasing the thickness
of the neo-membranes; that by restoring the power to dilate he further
prevented the lung from being compressed by the false membranes. These
membranes cannot become organized unless they are separated by fluid.
He states that he removed the fluid as completely as possible. As soon
as the cavity was emptied respiration was made easy and the patient was
relieved. Auscultation showed, by the vesicular murmur, that the lung
had resumed its place without difficulty from top to bottom. The
effusion returned, only in a few cases, with high temperature and
frequent pulse, but another operation effectually arrested them. The
pleurisy was cut short and puncture was considered the means of
aborting the disease. The duration of the disease treated by this means
was much shorter. Thus the patients were not forced to retain for
months the liquid and false membranes in their chest. He states
emphatically that there never supervened any accident, and especially
that he never witnessed as a result the transformation of the serosity
into pus, although it might appear theoretically likely to occur, as
the serous membranes, already inflamed, ought to be more sensitive to
injury.

[Footnote 62: _Thèse de Paris_, 1873.]

This testimony is very strong. Moutard-Martin operated upon 12 patients
with fibro-serous effusions where they had existed less than ten days,
and where there was more or less of fever. Out of this number, 8 had no
reproduction whatever of fluid, and in 4 there was only a slight
re-formation, and there was no degeneration into purulent fluid in any
of them. In the other cases operated upon, where the effusions dated
from twenty to sixty days, the fluid was almost always reproduced,
though ordinarily to a moderate extent. He urges the prompt withdrawal
of the fluid as the most successful method, especially if there is
reason to suspect the formation of false membranes.

Wedal's[63] results confirm this view of the harmlessness of punctures
during the febrile stage; and, more than this, they show that they
hasten the cure. He operated on 17 patients from the second to the
fifth day, and three times from the eighth to the tenth day. In cases
of acute disease, where the patients were exempt from pulmonary or
bronchial complications, the cure was not protracted beyond the twelfth
day. Some were cured by the sixth day. His patients were, for the most
part, vigorous men, young {526} soldiers--very favorable subjects.
Ordinarily, however, as shown by J. L. Mason's[64] report of 132 cases
where the operation was not performed, the duration of the attacks was
weeks, and in some cases months. He considers the operation more apt to
be successful if performed early in the disease, and that the existence
of fever is no contraindication. The author has always pursued a more
conservative course, and abstained from operating in the febrile stage
unless, as in three instances, the effusion was so rapid in its
formation that there was danger of serious consequences from the amount
of the fluid. In these three instances the result was successful and
without unpleasant sequelæ. Moutard-Martin[65] states that aspiration
made during the febrile stage is in no way prejudicial to the patient.
Dieulafoy[66] advises us to wait until the fever falls.

[Footnote 63: _Étude clin. des épanchments pleurit._, 1877.]

[Footnote 64: _Boston City Hospital Reports_, 3d Series, 1882.]

[Footnote 65: _Loc. cit._]

[Footnote 66: _De la Thoracéntèse dans la Pleur. Aigue_, 1878.]

To remove the effusion during the inflammatory stage does not appear to
be rational treatment unless the quantity is so excessive as to
endanger the life of the patient. The fluid remains limpid unless
exposed to air or contact with foreign substance. When, after a time,
there is some coagulation, it is only of a thin layer which covers and
protects the roughened surface of the pleura. A certain amount of
effusion is useful; it separates and bathes in a bland fluid the tender
and inflamed surfaces, and keeps at rest the affected portion of the
lung. The lung in health exercises a constant traction upon the pleural
sac, the vessels of which have therefore to sustain a negative or
aspiratory pressure: this being so, it is physiological that if these
vessels become temporarily weakened and congested by the inflammatory
process, increased exudation proceeds from them. The effect of this
exudation is to neutralize lung-traction, and therefore to lessen the
afflux of blood to the weakened vessels. "Fluid effusion being thus
both natural and salutary, in acute pleurisy we must be watchful, but
not meddlesome" (Powell). We must not hurry, but we must try if nature
will not by spontaneous absorption cause it to subside. We can
ordinarily do this up to the end of two or even three weeks before
resorting to artificial means.

The defervescence in pleurisy, we have seen, has no fixed period, as in
pneumonia. In favorable acute cases the absorption begins as soon as
the temperature begins to fall. Moreover, the liquid may be absorbed,
notwithstanding the continuance of fever, and the effusion may continue
notwithstanding the defervescence. In the subacute form the febrile
period passes by unnoticed, although the effusion is often in large
quantity.

When not urgent, how long should we wait for absorption of fluid? This
is a question much discussed, and not yet settled. What becomes of the
effusion in the acute pleurisies?

In the first days of its formation the liquid portions of the effusion
are reabsorbed by the normal vessels of the serous membranes at the
points left intact and the recent vessels of the neo-membranes, but the
organization of these last demands, to be complete, from two to three
weeks; it is not until the end of that time that they will be most
favorable to reabsorption. Dybkowsky points to the anatomical fact that
the lymph-vessels are found only in those parts of the costal pleura
which cover the intercostal muscles, while the portions which are
reflected over the ribs are destitute of such vessels.

On the other hand, the eccentric pressure made by a considerable
effusion on the pleuræ may retard their vascularization and lengthen
out the work of absorption. Moreover, during the time necessary for
that organization a certain quantity of coagulable fibrin is deposited
on the surface of the serous membranes. The pseudo-membranous bridles
are not slow in forming, and cause the adhesions which press the lung
against the costal wall, the {527} vertebral gutter, and the superior
parts of the thoracic cage, toward which the effusion tends to force
them.

In very favorable cases the effusion may disappear by the twentieth day
of the disease. In many cases, however, it lasts with the false
membranes for several weeks, and not infrequently for many months.
Cases are recorded by Powell and others where the effusion remained of
a sero-fibrinous character for eighteen months and two years. Flint
mentions two cases where the effusion was permanent, having lasted for
years. Wilson Fox[67] thinks that there is but slight danger of the
fluid becoming purulent from mere lapse of time unless the patient
should have another fresh inflammatory attack. It must be noted,
however, that such is not the case in children. Voyet[68] says that
simple pleurisy in infants is transformed into purulent pleurisy with
facility and extreme rapidity--so much so that when with these a serous
effusion is slowly absorbed there is great danger of suppuration taking
place. M. Vertiac[69] states that chronic serous pleurisy may not exist
among children. In 13,000 sick children in eleven years Barthez did not
have a single case. Pathological anatomy has demonstrated to us that
this fluid in separating these neo-membranes on the parietal and
pulmonary pleuræ increases their development. The plastic rugosities
collect the fibrils of fibrin on their surface, in the same manner as
they are found on the twigs in whipping the blood, and as the
atheromatous deposits on the interior of blood-vessels favor the
formation of emboli. These false membranes may cause a number of
complications by surrounding the lung with a thick, inelastic shell.
The collapse of one part of the lung diminishes necessarily the field
of hæmatosis, and consequently causes a compensatory congestion of that
lung, and even of the lung of the other side. This occurring in an
individual predisposed to tuberculosis or in a condition to develop and
cultivate the bacillus tuberculosis may start the disease. Formad[70]
maintains that pleurisy is a very frequent cause of pulmonary
tuberculosis. These imperfectly organized embryonic membranes cause
deformities of the thorax; they are good ground for the growth of
pathological products, such as cancer or tubercle; their fragile
capillary vessels are the principal cause of a most troublesome form of
hemorrhagic pleurisy. (See HEMORRHAGIC PLEURISY.) If the lung be
compressed but a short time, it does not undergo irreparable injury,
but if for a considerable time, the thickened organized membrane, with
the effusion, causes a more or less considerable atelectasis, binding
down the lung and preventing its expansion. The author holds that the
effusion, after the fever has subsided, is, in itself, a foreign and
troublesome element; for even with a medium effusion we are not exempt
from unpleasant results.

[Footnote 67: _Brit. Med. Journ._, Dec., 1877.]

[Footnote 68: _Thèse de Paris_, 1870.]

[Footnote 69: _Ibid._, 1865.]

[Footnote 70: Paper read before the Baltimore Clinical Society,
February, 1883.]

Although, in moderate effusions, there is no compression of the lung,
yet there is necessarily collapse of it pari passu with the amount of
fluid. This interferes with its retractive power--the aspiration force,
as it has been called--by which the venous blood is drawn into the
right side of the heart. T. B. Curtis of Boston calls attention to this
very important fact, and shows that the result must be disturbance of
circulation, with imperfect blood-supply to the heart, interrupted
cardiac action, feeble arterial tension, together with venous repletion
and stagnation. In consequence of this condition there is a diminution
of the quantity of urine, and, as generally occurs where there is
venous congestion, a small quantity of albumen, cyanosis, etc.
Fraentzel, Traube, and Lichtheim attribute the venous stagnation, etc.
to obstruction in the pulmonary circulation resulting from pressure
exercised by the effusion. Curtis and Garland hold that these bad
symptoms are not caused by pressure, but by the diminished pulmonic
retractility which exercises the negative pressure of emptying the
large venous trunks.

{528} Such being the ill-effects of the retracted lungs, is it well to
allow even a moderate amount of fluid to remain in the pleural sac
after Nature has failed to remove it? Besides, the presence of liquid
alone displaces the organs, especially the heart and lungs; adhesions
form and keep them in an abnormal condition. The retracted lung, bound
down by bands, becomes enfeebled, loses its suppleness, and is rendered
rigid, seriously impairing respiration. There exist three
factors--false membranes, adhesions,[71] and interstitial
pneumonia--which tend to seriously disable the lung and even to produce
complete atelectasis pulmonum. We must bear in mind that there is some
danger of the fluid becoming purulent, especially if a fresh
inflammatory attack should occur. The less time a pleurisitic effusion
lasts, the sooner the patient will be placed beyond the probability of
these serious injuries to the process of hæmatosis. It is but right to
give Nature an opportunity, assisted by iron, salines, diuretics,
iodine, and even blisters, in cases of moderate effusion. The rapidity
of Nature's work in many cases in removing large quantities of fluid
here and elsewhere is wonderful. But if she does not act, we ought not
to let our patient become feeble and depressed in his nutrition, or
perhaps maimed for life, by not withdrawing the fluid. Sometimes the
absorbents only half do their work of removing the fluid, and leave a
quantity in the chest. Under these circumstances tonics, good diet, and
change of air will complete the absorption.

[Footnote 71: According to Wilson Fox, the density of the adhesions and
false membranes is determined within the first fortnight of the
effusion.]

The question arises, How long shall we wait for absorption? Test first,
by exploratory puncture, the nature of the fluid: if it is fibro-serous
day after day, try by the cyrtometer the size of chest and by
percussion the exact amount of flatness. If there is no evidence of any
decline of the effusion in two weeks, slowly withdraw some of the
fluid. This will start the absorbents into activity, for the natural
absorbing power of the pleura is diminished when it has been unduly
stretched for some time. The layer of lymphatics subjacent to the
pleura and communicating by stomata with the pulmonary lymphatics,
together with the other absorbent vessels, appear to be unable to
remove the fluid. We maintain that the pressure on the orifices of the
lymphatics is often too great for absorption to take place, and that by
removing the pressure we can start the absorbents into activity.
Aspiration under these circumstances shortens the duration by several
weeks and hastens convalescence. J. W. Hunt[72] advises that we should
wait two or three weeks before operating. Loomis[73] says if the fluid
remains stationary for one week, or is increasing when the cavity is
half filled, we must operate. Barnes[74] would only wait a few days if
the chest is half full, to see if absorption will begin to remove it.
When the chest is two-thirds full, he advises immediate surgical
interference. Oxley[75] advises a delay of three or four weeks before
operating. Anstie's[76] rule is to postpone operating for one month. T.
Clifford Allbutt's[77] general rule is, if an effusion rises above the
angle of the scapula, and abides in that quantity or increases for two
or three weeks in spite of adequate treatment, it must be drawn off,
whether the patient be embarrassed by it or not. Bowditch[78] says: "If
the effusion does not subside under the medical treatment, and the
symptoms have not lessened after two or at the utmost four weeks, I
have, after long experience, been led to the following general rules
for my own guidance: 1st. I never allow any time to elapse before
performing thoracentesis after a decided and prominent dyspnoea
appears, or if a sudden and very threatening orthopnoea occur, or if I
find the chest has become full or more than half full of fluid in a
perfectly latent manner {529} during a month of illness. 2d. After
there is dulness to the angle of the scapula, with the other rational
and physical signs of pleuritic effusions, I tap within four weeks,
even if the patient seems quite comfortable, if the line of dulness
does not get lower and seem to subside under the treatment. I think
fatal mistakes are made by delaying too long before tapping." The
author prefers ordinarily to wait for the subsidence of the fever in
acute cases, unless the effusion is in dangerous quantity. The
practitioner must continually use the thermometer as well as observe
physical phenomena and general symptoms. Cyrtometric tracings give very
valuable indications as to the activity or non-activity of the
absorbent vessels. After the fever subsides the fluid may be regarded
as a foreign body doing harm to the two principal organic functions
upon which the nutrition of the animal frame is dependent--respiration
and circulation. It is from this standpoint that Dieulafoy[79] advises,
if absorption is slow or difficult after two or three days, that the
fluid should be aspirated. The greatest success has been obtained in
cases where the fluid has been present but a short time. The number of
fatal cases is increased by delay of operation. Toussaint's cases show
this:

  4 deaths in 176 cases operated upon between  1st and  20th day.
  6    "       80   "      "      "      "    20th and  60th  "
  1    "        7   "      "      "      "    60th and 120th  "

In the quiet kind of pleurisy, formerly designated the subacute or
latent, thoracentesis is especially applicable. Ordinarily, when the
practitioner is consulted, there is considerable fluid, without any
febrile movement. Here we are in duty bound to assist nature. Iron in
the form of the tincture of the chloride and the syrup of the iodide
are our best remedies. We cannot give the patients the tonic influence
of outdoor air with exercise, because there is danger in their moving
about; but they should have an abundant supply of nourishing food, with
light wines. Absorption is very inactive and sluggish. Even with
moderate effusion to the extent of one-third of the pleural cavity, we
cannot let the fluid remain too long. Pidoux designated this form of
pleurisy as the thoracentesis variety.

[Footnote 72: _Loc. cit._]

[Footnote 73: _Dis. Resp. Org., etc._, 1875.]

[Footnote 74: _Loc. cit._]

[Footnote 75: _N.Y. Med. Ex._, Sept., 1882.]

[Footnote 76: _Syst. Med._]

[Footnote 77: Quain's _Dict. Med._]

[Footnote 78: Unpublished MSS.]

[Footnote 79: _La Thoracent. par Asp. dans les Pleur. Aigues_, 1878.]

Conclusions.--1st. The author wishes to be distinctly understood as not
advocating aspiration simply because there is an effusion, as a mere
matter of routine, for its indiscriminate employment is undoubtedly
attended with risk. He does claim that its performance is imperatively
called for when the pleural cavity is full or nearly so; when there is
much displacement of the heart or other viscera; when the patient is
suffering from serious dyspnoea and danger of syncope, and when there
are complications of disease of any kind of the other side or of the
heart; finally, when there is double pleurisy. Bowditch states that he
has seen thoracentesis give great relief in effusions following
Bright's disease and cardiac diseases.

2d. He thinks that in acute cases, after the subsidence of the fever,
if the pleura is one-third full of fibro-serous fluid, Nature will
probably do her work of removal promptly. If she shows no sign of doing
so, we should come to her assistance in about ten days or two weeks,
and draw off a portion of the fluid--enough to relieve pressure and to
encourage the absorption of what is left in the sac.

3d. In the subacute or chronic fibro-serous effusions it is not well to
wait over three weeks before operating. As he shall show in the study
of the dangers and objections, he considers the operation a perfectly
safe one if the simple rules now generally observed by operators are
faithfully carried out.

In studying the advisability of operating where there are not urgent
indications we must ever bear in mind that while it takes a large
quantity of {530} fluid to compress the lung, the retracted lung may,
by neo-membranes, be kept to its diminished volume. As long as the lung
is able to lift up the fluid and the diaphragm it is in no danger of
atelectasis. It is in a state of physiological rest. In a subject of
bad constitution interstitial changes may indicate an earlier
operation, but, if an effusion exists on the side on which there is
already lung disease of a phthisical nature, we should be loath to
interfere; for "experience has shown that an effusion checks, and
sometimes arrests, the tubercular process" (Powell).

Contraindications.--These are principally in connection with the
general condition of the patient. If it is such that there is no hope
of his rallying, if he is very old, or if he has intervening croupal
pneumonia, the operation is not justifiable. If the quantity of fluid
is not large and does not interfere with organic functions, we can wait
for some time.

Mode of Operating.--The old trocar method of operation is now
abandoned. It was not always an easy one, was painful, and there was
more or less danger of cutting the intercostal artery, of introducing
air, and of establishing, by the size of the puncture, a fistulous
orifice. If, perchance, the lung was perforated by the trocar,
pneumothorax was established. In some cases of sacculated and limited
effusions, and in chronic cases where the membranes were thick, it was
not effectual, and if the fluid was not reached, the operator hesitated
to introduce the trocar elsewhere. When the fluid flowed through the
trocar, it came frequently in jets with painful coughs. The above
operation was quite a formidable one. Now thoracentesis is always
performed with very fine perforated needles attached to aspirators of
some modern pattern, and guarded by Fitch's dome-trocar or Castiaux's
protected point. We employ Dieulafoy's Potain's bottle-aspirator,
Castiaux's of Paris, or Raumussen's of Copenhagen. Flint recommends the
use of Davison's syringe. We fear it would be found too rough an
instrument for so delicate an operation. The points of attachment of
the bulb with the tubing are not sufficiently air-tight. The valves are
very imperfect, and easily get out of order. In our efforts to pump out
the fluid we might throw air in, and with it particles of organic
matter.

The operator has his choice among no less than thirty-odd instruments
similar to Dieulafoy's. They all work upon the same principle--the
close operation, the withdrawal of the fluid by aspiration. The needle
or trocar must be capillary: the smallest that is effective is the
best--say a half millimeter in diameter--in order to make the orifice
as minute as possible.

If we prefer the syphon, we must use a larger canula than we employ for
aspiration--one of four millimeters in diameter. It should have two
outlets--one straight, for the trocar, and one at an angle, for the
attachment of the tubing. It should also be guarded by an air-tight
collar. Into the syphon tubing a T-tube may be inserted for the purpose
of attaching a side tube to be connected with a mercurial manometer, by
means of which the exact intra-thoracic pressure may be observed during
the operation. The syphon tube should be long enough to provide a fall
of one, two, or three feet, as may be necessary. A fall of twelve to
eighteen inches is usually enough, as we wish to remove the fluid
slowly. We can easily increase the force by lengthening the tube. If
the canula should become obstructed, lowering the basin suddenly will
probably remove the piece of lymph. The trocar can be pushed again
through the canula if necessary. In case the aspirator should be
needed, the end should have a metallic joint affixed to it. In all the
instruments used, absolute cleanliness should be observed. The tubing
previous to operation should be filled with a solution of carbolic acid
(1:40).

In cases of rapid effusion, especially during the febrile stage and
when the intra-thoracic pressure of fluid is great, some prefer using
the feeblest form of aspiration. Southey's capillary trocar, with
drainage-tubes attached, is used as a syphon for this purpose. The
fluid is drained off {531} through a narrow india-rubber tubing which
is placed under water to prevent air being drawn into it. Ordinarily,
the use of the fine aspirating-needle without much force, and slowly
drawing off the fluid, answers the same purpose. The fear some have
expressed, of the danger of injuring the lung by the force of the
rarefied space, is more theoretical than real. Even with a canula of
the size that Southey employs there is some danger of leaving a
fistulous orifice, for it has to be kept in for hours. If the smallest
tube is used, from which the fluid simply comes in drops, the operation
consumes five or even ten hours. Southey speaks of cases where the flow
was kept up for twenty-four hours. Unless aspiration is resorted to,
flocculi may easily stop up the canula, and then we are compelled to
reintroduce the trocar, and afterward to reattach the tubing. Oxley,
who thinks that the best results are obtained by the use of these
tubes, acknowledges that so much time was consumed that he inserts four
canulas, drawing off 44 fluidounces of fluid in one hour and ten
minutes, thus defeating the object of using this method, which was to
draw off the fluid very slowly, so as to enable the lung to expand
gradually and healthfully.

There are cases where, to withdraw the fluid, more suction force than
is usually employed with the syphon has to be used in order to
antagonize the negative force exercised by the traction of the lung and
the passive tension of the diaphragm. The author recently had a case
where, notwithstanding the presence within the right pleural sac of a
quantity of fluid large enough to obliterate the Skodaic resonance
under the clavicle, not a drop could be drawn out by a syphon attached
to a canula of 2 mm. in diameter. Having no additional tubing to
increase the force of the syphon at hand, he used Dieulafoy's rack
aspirator, ½ mm. in diameter, and drew off a quart of fluid--enough to
relieve the symptoms of oppression. Stone reports a case of the kind
where, although there were two quarts of fluid in the pleural sac, no
fluid could be drawn out with a syphon exerting a force of 1½ pounds to
the square inch, or one-tenth of an atmosphere. In the same case there
was actually, in inspiration, a negative pressure exercised by the lung
of two inches of water. Stone mentions another case where a boy fifteen
years of age died from the quantity of fluid, which would not flow out
when tapped. If he had had an instrument by which he could have used
aspiration he would have saved the life.

The value of this syphon method has within a few years grown much in
favor. It is simple and inexpensive. It allows the fluid to be drawn
out with a uniform and feeble aspiratory force. The flow is very slow,
which gives the lung time to expand gently, and the displaced organs to
return gradually to their normal position. With the manometer attached
we can judge accurately as to the intra-thoracic pressure. The size of
the canula has to be larger than when we employ the aspirator--4
mm.--whereas with the latter we use ½ mm. or 1 mm. in diameter. If by
any accident the lung should be perforated, the larger orifice would
not be as harmless and insignificant as the smaller one. It must be
borne in mind, especially in cases of long standing, that the
neo-membranes are very vascular, and that with a 4 mm. perforator we
may rupture the blood-vessels and complicate matters by the escape of
blood into the pleural cavity. It is claimed that when the canula and
syphon tubes have been introduced the patient can be left in charge of
the nurse. This, the author thinks, should never be done, for nurses
are rarely competent to judge whether a sufficient amount has been
withdrawn, nor are they fit to assume the responsibility of acting in
cases where promptness of treatment may be of the utmost importance.
The operator or a competent substitute must remain until the operation
is over. The withdrawal of fluid must, moreover, be slow, for slowness
contributes in a great degree to lessen the dangers. Fraentzel
recommends testing the force of the {532} aspirator in the palm of the
hand. Garland[80] employs needles which are 1-2 mm. in diameter and
remove only 50 to 100 grammes per minute. The thoracic pressure must be
relieved by the withdrawal of only enough fluid to effect that purpose.
It has been objected that the negative force of the aspirator is
uncertain. It is a well-founded objection, yet we can employ with it a
feeble force by exhausting only a portion of the air from the cylinder
or bottle, and thus remove the fluid cautiously and very deliberately.
It is admitted that if there is no intra-thoracic pressure the fluid
will not flow out unless we introduce air or negative force. We claim
that the syphon and the aspirator with capillary needles, employed with
the precautions dictated by modern experience, are both safe and
effective. Ordinarily, we prefer the bottle aspirator of Potain, or
Dieulafoy's instrument with the manometer attachment.

[Footnote 80: "Dis. of Pleura," in _Ziemmsen's Appendix_.]

Modern aspirators, if in perfectly good order, completely prevent the
possibility of septic contamination by admission of air. Unclean
needles and canulæ can--and we fear formerly often did--convert
sero-fibrinous into purulent pleurisies. A case came under Powell's
observation in which carelessness in this respect apparently led to
decomposition of the fluid, suppurative pleurisy, and ultimately to the
death of the patient. Before operating we ought always to test the
instrument, and see that it works well by passing carbolized water
through it. The points should be put in the flame of a spirit-lamp, and
then dipped in carbolized water and glycerin--not in oil, which may be
rancid. The hands and clothes of the operator should not be overlooked
in this regard. The atmosphere of the room should previously be
completely cleansed by ventilation, and afterward purified by
atomization of disinfectants. We must not, in a word, incur the
slightest risk of converting a simple inflammatory effusion of
fibro-serous fluid, a mild disease, into a suppurative inflammation, a
very troublesome, dangerous one.

A needle of not larger diameter than 1 millimeter (No. 2) should be
connected with the end of the tubing. Next turn the stopcocks which
shut off the barrel from the tubing on both sides, producing a vacuum
in the receiver. The patient should then be placed in the recumbent
position in bed, with his head and chest raised. We prefer this
position, as the easiest for the patient at the time of operation and
less apt to produce syncope or faintness. He can, without being moved,
lie down in the horizontal position, which he should maintain for at
least two hours. Bowditch has, without any accident, had his patients
to sit during operation sidewise in a chair, with one arm resting upon
a pillow placed upon the top of the back. The operation is accompanied
with so little pain that it is not necessary to use either general or
local anæsthesia. Some surgeons advise before operating the
administration of a small dose of morphia hypodermically, or a
stimulating drink of whiskey. We are not in the habit of using either.
We have generally allowed patients to take a good meal of
easily-digested food (milk if they consent) about two hours previous to
the operation. Whiskey and ammonia we have ready in case of need. If we
find it necessary to use a 4-mm. canula for syphon, it may be best to
spare the pain of its introduction by local anæsthesia by ether, or by
rhigoline in Richardson's spray, or by applying a piece of ice
surrounded by salt, as suggested by Powell.

The point of puncture should vary according to the quantity of fluid.
If the fluid is excessive, we can operate as high up as the fifth
intercostal space on the right side and the seventh on the left. We can
choose a lower intercostal, but as it is not proposed to draw off all
the fluid, the higher operation is preferable. If the chest is
two-thirds full, we can take the seventh or sixth intercostal space on
the right side and eighth on the left. If only one-third of the cavity
is occupied by fluid, we can go as low as the eighth intercostal {533}
on right and left sides, on a level with the angle of the scapula in
the axillary line. If the quantity of liquid is so great as to force
the abdominal viscera, especially the liver and the spleen, below their
normal position, we may be safe in puncturing below the seventh
intercostal space. But if such is not the case, the diaphragm may
easily be touched on a level with even the seventh intercostal space.
Aran plunged a trocar into the liver when operating through the seventh
intercostal space. Ch. Bernard impinged upon the peritoneum at the same
point. Woillez and Paul Barbille recommend the fifth intercostal space.
Cruveilhier advises the third or fourth as being the point of the
spontaneous openings. The author usually inserts the needle in the
sixth intercostal space in the mid-axillary line: it is out of reach of
the diaphragm and is accessible when the patient lies in the position
in which he prefers placing him. The space is sufficiently wide and the
parietes thin. Before operating the point must be examined carefully by
percussion, auscultation, and palpation, so as to be accurate in the
diagnosis that there is fluid at that point, and that nothing can be
injured--lung, heart, or diaphragm.

Before inserting the needle the skin should be wiped over with an
antiseptic solution. The skin being drawn up, the nail of the left
index finger serving as a director, the point, having been first made
aseptic, is introduced along the upper margin of the lower rib, taking
care not to injure the periosteum--not by a boring motion, but by a
sharp push, giving it a downward direction instead of a perfectly
straight one, so as to avoid striking the lung. When the fluid is
reached the stopcock is turned, so as to convert the needle into an
aspirator. The index tells us whether we have struck the fluid, and its
nature is shown. In chronic cases, where the bands are thick and
partitions are firm, we may not find the fluid the first time. In such
cases the needle is withdrawn and another point selected. The author
had a case where he made no less than eight punctures before getting
the fluid. At the last insertion of the needle he found it, and drew
off a large quantity. The patient feels relieved in a very short time.
As the fluid flows out the aspirating force should be only sufficient
to draw it out slowly and gently. It is well to stop for a few minutes
after aspirating about 4 fluidounces to watch the effects. The fluid
running in a very small stream, we give the lung time to accommodate
itself to its altered condition. The lung by this process is led,
rather than forced, to resume its normal position. It is a difficult
matter to fix the quantity that ought to be drawn off at one time. This
must vary according to the circumstances of each case. Our rule has
been to draw off more when the pleurisy is acute than when it is
chronic. The long continuance of the fluid in the cavity has so
impaired the lung's capability of expansion by the adhesive bands or
compresses that the sudden withdrawal of a large quantity is attended
with risk. If the patient bears the operation well, we may remove much
more than if the contrary is the case. The amount withdrawn at the
first operation should vary from 8 fluidounces to 16 fluidounces in a
child, and 12 fluidounces to 24 fluidounces for an adult. We must bear
in mind, as to the quantity to be removed, that ordinarily there is
more or less danger of producing fresh engorgement of the capillaries
and hyperæmia of the lung in removing a large quantity; and, moreover,
it is unnecessary. We wish to remove the intra-thoracic pressure upon
the lung and to promote the absorption of the fluid. The manometer will
tell us accurately whether it is necessary to take out one, two, or
three pints. If nature does not in due time remove what is left, the
operation can be again resorted to. Slowness in the withdrawal of the
fluid, as well as the small quantity drawn, lessens the probability of
any unpleasant effects. Bowditch says: "I always draw with great
deliberation. I pull so lightly upon the handle of the piston that it
seems as if the fluid itself were pressing out from the chest and
pushed the piston upward, my hand simply following that impulse. The
instant that the patient becomes {534} restless, especially if he have
any constriction or sharp pain in the chest, I withdraw the tube, even
if a large quantity of fluid remains. If I do this, I find the patient
is soon relieved, and in most cases nature appears stimulated even by
the withdrawal of a very small part of the effusion. The absorbents
begin to act well, and the fluid that is left is speedily removed."

One point is of the utmost importance: the needle should be instantly
withdrawn at the onset of dyspnoea, constriction, much cough, or any
tendency to syncope. These symptoms are warnings we should never
neglect. This is the time to administer stimulants, and ordinarily the
patient soon recovers from these effects. We must not, especially in
cases of long duration, expect to find much expansion of the lung until
next day. The greatest success has followed cases treated by early
operation and partial removals, repeated, if necessary, every day or
two until absorption is commenced.

The needle should be taken out suddenly, the operator having previously
turned the stopcock, and the skin allowed at once to fall over the
orifice, which is so small that no air can enter. It is indeed
obliterated at once. It may be well, however, to put some collodion
over it, with a small compress. The patient ought not to be permitted
to move for twenty-four hours after the operation. He should lie
quietly in bed and partake of simple nourishment. The removal of fluid
causes the return of friction sounds and of pleuritic pain. Nature
slowly does her work of absorbing the fibrinous bands. The
breath-sounds in some cases are not heard for weeks, or even months,
after the operation. Complete recovery being slow, and the shock to the
organism very serious, the patient should thoroughly re-establish his
health and strength before reassuming his active duties. A protracted
rest in an invigorating climate or a sea-voyage should be advised. If
the lung is slow to expand, the patient should frequently practise
long, deep inspirations.

Dangers of and Objections to the Operation.--Thoracentesis as a means
of relieving suffering humanity has from time to time been praised and
proscribed, even in this century. Boyer operated several times, and
never saved a single case. Dupuytren had only 2 successful cases in 50.
He said he preferred that his patients should die by the hand of God
rather than by the hand of man. Sir Astley Cooper had only 1 successful
case, Gendrin not 1 out of 20 cases. Davis saved two-thirds of his
cases. The eminent W. W. Gerhard of Philadelphia looked upon the
operation as nearly always attended by fatal results. What a contrast
to modern views and clinical results! Since Bowditch and Trousseau
popularized the operation, and Dieulafoy improved the aspirating
instruments, there is now no difference of opinion as to the imperative
necessity of operating in cases where there is, from the quantity of
fluid, imminent danger to life. Up to Nov., 1882, Bowditch[81] had
operated 386 times in 245 cases, without a single fatal result, and
with only 1 case in which alarming symptoms supervened. Dieulafoy's[82]
cases in 1878 amounted to 150, without the shadow of an accident. My
colleague, S. C. Chew, has never met with any unpleasant result from
his operations. The author has had 84 cases, with 138 operations,
without any unpleasant result beyond temporary cough and slight
dyspnoea. Fraentzel[83] had 85 different cases, with 164 operations. A.
L. Mason[84] performed 122 operations in 70 cases, with no unfavorable
result which could be attributed to the operation in any instance, but
usually with great and permanent relief. In 42 of his cases 1 operation
was all that was necessary. So common is the operation that cases are
not reported unless there is something to attract attention to them. As
illustrative of the great interest taken in the operation see the
number of writers on the subject and the numberless articles in medical
journals, and the modifications of instruments of all kinds connected
with aspiration {535} and drainage. Such being the case, we ought not
to be surprised that some operators may have used the aspirator-needle
when they ought not to have done so--that some should have neglected
the simple rules now insisted upon as the result of experience.

[Footnote 81: Unpublished MSS.]

[Footnote 82: _Tho. Pleu. Aig._, 1878.]

[Footnote 83: _Ziemssen's Cyc._, vol. iv.]

[Footnote 84: _Loc. cit._]

Although thoracentesis by aspiration is always a harmless operation in
itself, there are dangers and accidents which may follow. They may be
slight, serious, and sometimes even fatal. The number of deaths which
have been the result of the operation, however, is small compared to
that of persons dying from the effusion whose lives might have been
saved by the withdrawal of fluid. Thoracentesis was frequently made use
of without accident, and was considered a perfectly safe operation
until Terrillon[85] called attention to an accident which occurred
sometimes after operating, a complication which Pinault[86] had
mentioned in 1853--the albuminoid expectoration. Terrillon reported 2
cases of sudden and rapid death with that symptom. Several similar
cases, resulting in death, had been previously reported. Dieulafoy has
collected from different sources reports of 6 deaths with albuminous
expectoration, caused by acute oedema of the lungs brought on
apparently by the operation of thoracentesis in twenty-four to
thirty-six hours. In one of these cases (Gérard's) death occurred in
ten minutes; in another (Gombault's) in fifteen minutes; in another
(Bouveret's) in two hours; in Behier's in four hours. Terrillon's
cases, where there was this frothy, albuminoid, and sometimes bloody
expectoration, numbered 16, of which 6 were fatal. The patient is
attacked with cough and oppression, with the characteristic
expectoration. Auscultation shows the fine subcrepitant râles of oedema
of the lungs, mingled with tubular quality and ægophony. Gradually, in
favorable cases, the cough subsides, respiration is re-established, and
in one hour the danger has passed. In fatal cases the cough becomes
irregular and jerky, the agony increases, and the patient throws up the
yellowish and albuminous expectoration in quantity varying from 50
grammes to (in one case reported by Moutard-Martin) 1 liter. The
intensity of the dyspnoea and its duration vary very much--from twelve
to twenty-four hours.

[Footnote 85: _Thèse de Paris_, 1872.]

[Footnote 86: _Ibid._, 1853.]

There has been considerable discussion among different authors as to
what produce this serious condition. The view sustained by Hérard[87]
is the one generally admitted to be correct--viz. that it is from rapid
congestion and acute oedema of the lung, and not from the passage of
serous effusions of the pleura through the bronchi. Foucart[88] relates
a similar case of albuminous expectoration occurring in heart disease.
This condition could not be produced by perforation of the lung, for
the pre-existing vacuum renders the aspirator-needles the safest to
introduce, because if there is fluid present it at once flows out and
warns the operator not to push the implement farther in. In no autopsy
has the orifice made by the needle been found, nor has it ever been
known to produce pneumothorax. The quantity of albuminous sputa is out
of all proportion to the orifice made. In several cases of reported
perforation these symptoms did not occur. After the lung has been a
long time compressed by an effusion, and when, in consequence of the
expulsion of the liquid, it retakes its normal proportions, there
occurs a rush of serum which is expelled by the bronchi. Hérard has
seen patients in whom he could not find more than traces of liquid
after the puncture, and who at the end of a half hour or an hour
expectorated 500 to 1000 grammes of fluid which did not come from the
pleura. That oedema of the lungs, or serous exudation from the
capillaries into the walls and on the free surface of the alveoli, is a
result of hyperæmia and pulmonary congestion is admitted by Robin,
Bernard, Niemeyer, Jaccoud, and others. We have first congestion of the
lung, then oedema resulting from it, ending in free albuminous
expectoration, {536} which comes not only sometimes from the diseased
side, but from the healthy side, owing to pressure against the
mediastinum and the other lung. This is an accident the possibility of
which should be always before us in operating. No precaution ought to
be neglected which will ward it off. It is instructive to analyze
Terrillon's cases as to the cause of the oedema. As he considers that
the aspirator, by draining out the lung, is likely to produce this
unfortunate result, it is satisfactory to find that of the 16 cases
where this unpleasant symptom was found, 12 were where the old trocar
(Reybard's) was used without aspiration, and 4 where aspirators were
used. Of the 6 fatal cases collected by Terrillon, 3 were with the
trocar and 3 with the aspirator. Five out of the 6 fatal cases are
found to have been not simple pleurisies, but pleurisies with
complications, such as heart disease, bronchitis, tuberculosis,
numerous adhesions, double pleurisy. The same may be said of the benign
cases. In addition to these complications, large quantities of fluid
had been drawn out at one time. Dieulafoy challenges his confrères to
produce an instance of death from this cause when the fluid removed did
not exceed 1200 grammes. His rule now is never to withdraw more than
1000 grammes of liquid at one time, and in large effusions to empty the
sac by several operations. The older and more complicated the effusion,
the more rigorous should be the rule, because there is great danger in
thoracentesis when the fluid has existed long enough to have compressed
the lung to a serious extent by bands. All careful operators now follow
this rule. It is dangerous, and withal unnecessary, to draw off large
quantities at a time. The gradual removal of fluid diminishes the risk
of syncope where a sudden withdrawal may be serious in its effects. The
effect is to suddenly deprive the lung of pressure which has for weeks
perhaps made it anæmic. The blood rushes into the empty vessels, the
air into the alveoli, and violent congestion and consequent oedema
result. If, on the contrary, we draw out moderate quantities at
different times with the capillary needle, which is so small that its
introduction is harmless, the lung resumes progressively the functions
it has lost, and the circulation gradually enters. Thus there is no
risk of congestion.

[Footnote 87: _Acad. Méd._, 30 Juillet, 1872.]

[Footnote 88: _Thèse de Paris_, 1875.]

In examining the fatal cases reported by different authors, Foucart,
Dieulafoy, Mercier, Lerebenthel, and Gagnet, we find other modes of
death in addition to those by oedema of the lung, such as asphyxia and
pulmonary emboli, and, as connected with the heart, syncope and cardiac
thrombosis. In most of the cases these accidents resulted indirectly
from the operation in twenty-four hours or a longer time. In a case
reported by Guyot it occurred three days afterward. Congestion by
itself may cause sudden and rapid death by determining asphyxia.

There are other lung causes which produce sudden death following
thoracentesis, such as atelectasis, consecutive to effusion; secondary
pneumonia, caseous or not; pulmonary tubercles. Besnier reports a case
of gangrene of the lung following paracentesis. Of the 8 cases
collected by Dieulafoy which may be put into this category, we find
death from pericarditis, cardiac clot, and from thrombosis of the
pulmonary artery. Death from the heart may be due to old lesions, to
syncope, or to the presence of clots in the heart or small circulation.
Stokes has given fatty degeneration of the heart as a cause of death in
simple pleurisy without operation. Syncope, with death after operation,
is caused by the sudden return of the heart to its normal position. The
heart being pushed out of position, the larger blood-vessels are
distorted, and the course of the circulation is severely interfered
with. A very slight cause will arrest the circulation. By aspiration
the mechanical cause is removed, but a small embolus, may, by the
increased force of blood, be carried into the pulmonary circulation.
Death by emboli in the capillaries of the lungs is very similar to
death {537} from clots in the right side of the heart and at the origin
of the pulmonary artery. These clots may be formed in the pulmonary
vessels, or may be transported in the small circulation to points more
or less distant. Potain in 1861, and Vallin in 1869, reported sudden
deaths from effusion in the pleural sac, causing embolism of the
cerebral artery. How far aspiration is responsible for accidents of
this kind it is difficult to decide. Were they caused by thoracentesis
or notwithstanding the operation? They are unquestionably the cause of
death without the operation in excessive effusions. The conditions
which produce these results ought to be well considered previous to
operation. We notice that in most of these cases large quantities of
fluid were withdrawn--2000 grammes (Legroux), 3 liters (Vallin), 3500
grammes (Guyot), 1500 grammes (Chaillon and Goquel). The withdrawal in
cases of long standing of such large quantities had, beyond a doubt,
considerable influence in producing the fatal result. Bowditch[89]
addressed letters to 60 physicians, living in 31 of the States and 2 in
Canada--representative men--asking if they had ever seen or heard of
fatal results following thoracentesis by aspiration. Of this number, 53
replied in the negative, and 7 in the affirmative. "Upon an analysis,
however," he states,[89] "of the circumstances under which death
occurred in these last, I found nothing to shake my confidence in the
operation, provided it be performed with proper precautions during and
subsequent to the tapping. In no one of these cases had the operation
been the sole cause of the fatal result." "In 4 there was extra motion
on the part of the patient after operation, and in the other 3 the
disease had been allowed to continue without aid from a surgeon long
after the operation was needed. In 1 the operation was a forlorn hope.
One patient died on the table from anæsthetics." Bowditch adds: "These
cases should not lessen our confidence in the operation, but simply
teach us caution on three points--namely: do not delay too long; be
very careful to direct the patient not to move, if possible, for
twenty-four hours after operation; be cautious of using anæsthetics."
Bowditch, from 29 fatal cases collected from Otto Leichtenstein,[90]
from his own knowledge, and from European literature, tabulates the
causes of death in American and European practice: 7 of these cases
were caused by extra-exertion after operation; 3 from cyanosis and
coma; 4 from spray injections; only 1 from syncope; and 2 from
albuminoid sputa. He quotes the final remark of Leichtenstein: "Death
or any serious symptoms are so rare that they ought not to have the
least influence upon our estimate of this most benign and blessed
operation." Bowditch states that there were only 7 deaths in this
country (as far as he could ascertain), and 29, or four times as many,
in Europe, although the operation has been done much more frequently
here and for a much longer time. Does not this show that in this
country, in following Bowditch's precepts of great care and
deliberation, the operation has been more successful? He never ceased
in his lectures and writings to caution us to suspend the withdrawal of
fluid the moment the patient begins to suffer in breathing, even in the
slightest degree. Of course there may have been other cases occurring
in American practice of fatal results, of which no reports were made to
Bowditch.

[Footnote 89: Unpublished MSS., 1882.]

[Footnote 90: _Deutsches Arch. für klin. Med._, vol. xxv., 1880.]

The author has carefully gone over Leichtenstein's collected cases, and
he finds a number of deaths mentioned by other European authors which
are not included in his list. (The reader is referred to the theses of
Terrillon,[91] Foucart,[92] Foster,[93] Dieulafoy,[94] Mercier,[95]
Pinault,[96] Wilson Fox,[97] and others.) Terrillon alone reports 6
deaths with symptoms of oedema of the lungs following thoracentesis.
Leichtenstein does not mention any deaths from embolism, {538} such as
are quoted by Goquel, Chaillon, and Woillez. In his collection he gives
only 1 death by syncope, whereas Dieulafoy comments upon 4 as found
recorded by Trousseau and other French authorities. Toussaint's[98]
statistical tables of 300 cases, collected from other sources, give 14
deaths. Wilson Fox collected between 30 and 40 deaths connected with
thoracentesis. Besnier stated in 1876 that the mortality from pleurisy
in the French hospitals had greatly increased since the practice of
thoracentesis had been largely followed. It is difficult to account for
this in the face of the statements made by so many of its innocuousness
when properly guarded: it may be explained by the fact that suppurative
pleurisies are often confounded with those of a fibro-serous nature and
treated by simple aspiration. Many fatal cases of empyema are
complicated with phthisis; formerly these were added to the mortality
for phthisis; where paracentesis was performed upon them they were
added to the pleurisy column. Bearing in mind that chronic pleurisies,
serous and purulent, are frequently consecutive to diabetes, Bright's
disease, chronic alcoholism, cirrhosis of the liver, and other organic
diseases, patients die of the primary lesions, though they have been
relieved of the secondary ones. These statistics may record the deaths
as resulting from pleurisy, for which there was operative interference,
instead of from the organic diseases.

[Footnote 91: _Loc. cit._]

[Footnote 92: _Loc. cit._]

[Footnote 93: _Clin. Obs._]

[Footnote 94: _Loc. cit._]

[Footnote 95: _Thèse de Paris_, 1876.]

[Footnote 96: _Ibid._, 1855.]

[Footnote 97: _Brit. Med. Journ._, Dec., 1877.]

[Footnote 98: _Thèse de Paris_, 1878.]

Formerly, when trocars and canulas of considerable diameters were used,
only extreme necessity from peril to life made surgeons consent to
operate. We claim that by capillary needles, gentle force, and
protected points all the old objections are obviated. As Anstie says,
there is no opposition to the modern operation by men who have fairly
tried Bowditch's practice. Only theorists who are afraid of its
imaginary results and men too timid to act hesitate to make use of it.
We have discussed elsewhere (Purulent Pleurisy) the danger of admitting
air into the pleural cavity, but we insist that in the close method,
with capillary needles, there is no danger whatever of air entering.
The puncture is so very small that it closes at once by the elasticity
of the structure of the chest, just as the knuckle of the intestine in
hernia closes after the needle has drawn gases and fluid out of it.

Another objection urged against puncture of the pleura in such cases is
the possibility of perforating the lung by fine needles, thus letting
air into the cavity and causing cough.[99] Marotte read a memoir on the
subject to the Academy in 1872. He reported 4 cases, in all of which
there were only temporary effects, no serious ones. Dieulafoy[100]
says: "I have been witness to the puncturing of the lung several times,
and I have never seen any accident supervene under any circumstances. I
have thoroughly convinced myself that punctures performed with a No. 1
needle, diameter half a millimeter, are harmless, and experiments on
animals have given me the same results." He even suggests aspirating a
few grammes of blood from a congested lung in the first stage of
pneumonia, and thus practising local bloodletting. The author has 3
times pricked the lung in aspirating--twice with a No. 2 needle,
diameter 1 millimeter, where a few drops of blood were drawn into the
instrument, and they did not even produce a cough or the slightest
inconvenience. The third time was with a No. 4 needle (2 millimeters).
From this puncture some air escaped into the pleura, and for a few days
there was evidence of pneumothorax. It then disappeared entirely, the
air being absorbed. The case was a circumscribed empyema, which
entirely recovered.

[Footnote 99: Allbutt, _Quain's Dict. Med._, 1883.]

[Footnote 100: _Treatise on Pneumatic Aspiration_, Eng. trans., p.
256.]

It will be noted that throughout the discussion of this important
subject liberal use has been made of a valuable communication specially
prepared by Henry I. Bowditch for this purpose, and embodying the
mature results of his study and experience of thoracentesis. It seems
not only to establish conclusively the claim that to him, in
conjunction with Wyman, is due the {539} great credit of introducing
the principle of aspiration, but also to how great an extent it was
through his persevering and skilful advocacy and performance of the
operation that it became so firmly established in America upon a true
scientific basis.


Purulent Pleurisy.

DEFINITION.--Purulent pleurisy is that disease in which the pleura
secretes pus instead of fibro-serous fluid, as in simple pleurisy.

SYNONYMS.--Pyothorax; Empyema; Suppurative pleurisy.

HISTORY.--The term empyema was applied originally to any internal
collection of pus--[Greek: en] and [Greek: pyon]. It is now restricted
to pus in the pleural sac. The ancients, from the time of Hippocrates,
diagnosed and treated empyema by thoracentesis and pleurotomy. They
were familiar with the fact that it would sometimes discharge through
the bronchi and make an orifice through the walls of the chest, and
discharge outwardly. Their views of its pathology and its connection
with other forms of pleurisy were necessarily crude and indefinite. Of
late years, owing to the aids given by exploratory punctures, purulent
pleurisies have been thoroughly investigated. Townsend[101] divided the
disease into four varieties, all of which are from degenerations of
acute serous pleurisies, from increase of intensity of the inflammatory
phenomena, or from modification of the secretion of the serous
membrane. More modern researches have shown that frequently such is the
case, and that purulent pleurisies often succeed serous pleurisies. The
liquid when first thrown out is serous and limpid in character, and
afterward becomes cloudy, opaline, then more and more opaque and
purulent, owing to the pus being freely secreted and mixing with the
fibro-serous effusion. In a certain number of cases, however, the
effused liquid has from the first the appearance and anatomical
composition of purulent fluid--d'emblée purulente. This has been shown
by autopsies in cases of women who died in childbed from suppurating
pleurisies, and in persons attacked with pyogenic fever, not simply
from deposits of pus, but where an inflammatory period, of longer or
shorter duration, preceded the deposit.[102] Dieulafoy[103] showed that
in all effused liquids in the pleural sac there were present red
globules and leucocytes.[104] Laboulbène[105] has established the fact
that the exuded fluid in all pleurisies, even those apparently serous,
contained, from the time of their formation, purulent globules. All
cases, then, are historically purulent; but clinically serous and
purulent pleurisies are distinct in their progress, termination, and
treatment. Purulence is not always the sign of chronicity of pleural
inflammation. It may, and does, show itself in many instances from the
very commencement of the attack. Wilson Fox[106] shows there is but
little natural tendency in serous effusions to undergo purulent
transformations. He thinks in the vast majority of cases suppurative
pleurisies are so at early periods of disease. He states the proportion
of primary suppurative pleurisies as from 14 to 20 per cent. It is when
the number of leucocytes, from the intensity of the inflammation or
modification of the process, discolors the fluid and gives to it its
distinctive properties, that we use the name of purulent pleurisy.
Verliac[107] states that all chronic cases in infants become purulent.

[Footnote 101: Article "Empyema," _Cyc. Prac. Med._, vol. ii.]

[Footnote 102: _Pleurisie purulente_, (Moutard-Martin), Paris, 1872.]

[Footnote 103: "De l'Examen histologique des Liquides, etc.," _Soc.
Méd. des Hôp._, 1878.]

[Footnote 104: See section on Hemorrhagic Pleurisies.]

[Footnote 105: _Traité d'Anatomie path._, Paris, 1872.]

[Footnote 106: _Brit. Med. Journ._, Dec., 1877.]

[Footnote 107: _Thèse de Paris_, 1865.]

ETIOLOGY.--The causes of purulent pleurisies are divided into local or
traumatic, which are well ascertained and defined; and the general, the
{540} action of which is uncertain. Among the first are wounds of the
chest, fractures or caries of the ribs, phlegmonous abscesses of the
walls of the chest, effusions of blood, pathological liquids, pulmonary
gangrene, rupture of tubercular cavities, and other injuries from
adjacent organs, especially of those where pus is discharged into the
cavity, for the presence of pus engenders pus. Thoracentesis has been
accused of converting serous into purulent pleurisies by the admission
of air into the pleural cavity. If the atmosphere admitted is
contaminated by germs, we must acknowledge that such a result is
possible. By the older methods, previous to the adoption of Reybard's
protected canula, such a result may have been produced. We can thus, in
a measure at least, account for the great mortality in cases operated
upon. But since the adoption of the protected orifices of the small
aspirating trocar of Wyman and the capillary perforating needles of
Dieulafoy, we question whether, with such an insignificant puncture and
the complete exclusion of air, thoracentesis can be justly accused of
producing such serious mischief. Trousseau[108] earnestly denied such a
deleterious effect of the operation in his day. We have now not only
the results obtained by Demarquay, Leconte, and Manotte of injecting
air into the pleural cavities of inferior animals, but we have the bold
experiments of Matice, who, convinced that air could not have any bad
influence, actually had the audacity to perform the operation a number
of times, allowing the air to enter freely through the canula. From
numerous observations there resulted the fact, unsuspected by many,
that air, penetrating freely to replace the liquid extracted, never
gave rise to purulence in pleurisy; that, owing to its rapid
absorption, it did not in the least interfere with the expansion of the
lungs; in short, that it produced no accident whatever. While admitting
the force of Matice's conclusions, we think it preferable to avoid the
possibility of doing harm.

[Footnote 108: _Loc. cit._]

GENERAL CAUSES.--We have shown that secondary pleurisies frequently
occur in the course of convalescence from eruptive diseases, measles,
small-pox, and especially scarlet fever, and that they are purulent in
their nature. The puerperal condition predisposes to suppurative
inflammations of the serous membranes, and pleurisies in lying-in women
are almost always purulent. In rheumatism, gout, and delirium tremens,
and albuminuria as a rule, the pleuritic effusion is serous. It is
purulent in persons suffering from severe injuries and among men
exhausted by over-work or by alcoholic excesses, or protracted obscure
diseases, such as typhoid fever and pyæmia. Analyses of the cases in
which purulent transformation has occurred show that tubercles of the
lung have only a minor influence in its production--only 34 per cent.
of the whole number. Attimont's[109] observations were founded upon 130
cases, 80 of which recovered; of the remaining 50 that died, he found
tubercle in only 9 cases. Sometimes malhygienic conditions and
insufficient alimentation may account for them. Men are more subject to
this disease than women in the proportion of 8 to 1,[110] and young
children oftener suffer from purulent pleurisy than adults. It is not
easy to explain the transformation of serum into pus in pleuritic
effusions that have existed for some time where there have been no
grave symptoms. Imprudent exposure, affecting the general health, may
thus produce disastrous results. This occurs so frequently that
purulent pleurisies are generally called chronic pleurisies. There are
cases where neither local nor general conditions explain the
transformation of serous into purulent effusions in the chest.

[Footnote 109: _Thèse de Paris_, 1869.]

[Footnote 110: E. Moutard-Martin.]

PATHOLOGICAL ANATOMY.--This is shown by an examination of the effused
liquid, the different solid detritus that it contains, the false
membranes, the pleura, the lung, and the thoracic wall itself. The
liquid effused is purulent in character. It contains a greater or less
number of leucocytes, {541} some red globules, and voluminous granular
cells, besides crystals of the fatty acids and plates of cholesterin.
The pus is mixed with the serosity in varying quantities. The liquid
may be slightly opaline or greenish-yellow, and sometimes gray. It may
be thin or thick, with heavy flocculi, so as to pass with difficulty
through a canula. The liquid is, ordinarily, inodorous, but it may be
strong, and even fetid, where it has been in contact with air. In very
few cases of old standing can the pus be regarded as active, the
corpuscles being, as a rule, dead or having undergone fatty
degeneration. Active suppuration is also more readily set up in a
pleura which has already yielded pus.

Purulent effusions, independent of contact with air, may become in a
short time the seat of putrid transformations. False membranes undergo
alterations which produce fetid gases. The air, with its germs, its
humidity, and heat, the three grand factors in putrefaction, is thrown
in contact with substances of a putrescible composition. Marshall[111]
holds that sero-fibrinous effusions appear to have a greater tendency
to quick decomposition when air is admitted into the pleural sac than
the sero-purulent or purulent products. Pus, he considers, is more
stable and less inclined to rapid putrefaction than sero-albuminous
fluid. In quantity it varies from a very small number of grammes to
five or even six liters. By examining the fluid first drawn out we can
predict, by the number of leucocytes present, whether the pleurisy will
continue to be serous or will become purulent. If subjected to the
influence of ammonia, it will become thready, just as happens when pus
is suspended in water, if the fluid contains many of these
pus-elements. The purulent fluid may fill the whole or occupy but a
small part of the cavity, or again the interlobular spaces only may
contain the fluid, the cavity itself being empty. False membranes are
almost constantly present and adherent to the parietal or pulmonary
pleura; we find them also floating in the liquid. These false membranes
may be more or less voluminous. The flocculi, which may be as large as
an egg, undergo transformation when air is admitted, and become
horribly fetid. They may give rise to septicæmic symptoms. When we see
these enormous masses in the cavity, and are unable to get rid of them
by suction, we do not wonder that their presence should poison the
patient and the case become incurable. Pleurotomy is the only effective
mode of getting rid of these dangerous masses, with sometimes
gangrenous portions of pleural or lung-tissue. These false membranes
frequently form pouches and divisions for isolated quantities of fluid.
The false membranes are partly adherent and partly free, especially in
cases where there are pulmonary or thoracic fistula. These false
membranes differ in acute purulent pleurisies from those found in
pleurisies of long standing. They are but feebly adherent to the
pleura, and have a slight rose coloration. In old pleurisies the false
membranes are of greater density, sometimes from 6 to 8 mm. in
thickness. They are more adherent, and cannot be separated, and have a
grayish color. The physical state and position of the lung and
disposition of the adjoining structures are very similar to what they
are in serous effusions. In but few cases do the false membranes
envelop the whole of the lung. They pass over one part, and on to the
costal pleura. The pulmonary tissue is condensed, sometimes absolutely
impermeable to air, so that it will actually sink when dropped in
water, being in a state of atelectasis. In cases of shorter duration it
is found crepitant throughout its structure. Brouardet[112] called
attention to the inflammation in the under-pleural cellular tissue, as
well as in the interlobular connective tissue, forming interstitial
pneumonia, which determines condensation of this tissue and its
retraction after the manner of cicatrices, and afterward its
inextensibility. These explain the retraction of the thoracic walls and
the narrowing of the chest.

[Footnote 111: _Loc. cit._]

[Footnote 112: "Interstitielle Pneumonie," _Soc. Méd. des Hôp.
Bullétin_, 1872.]

{542} The most serious complication of this disease is the
pleuro-bronchial fistula[113] by which the fluid escapes through the
lung. The firm adhesions between the lungs and walls, forming enclosed
pockets, contribute in no small degree to the incurability of purulent
pleurisy. These pockets cannot be emptied thoroughly, nor can the
washings be made to penetrate them. The purulent secretion exercises a
destructive action over the tissues surrounding it, as well as upon the
viscera and walls of the chest: the soft parts become inflamed and
abscesses form; the intercostal muscles suffer atrophy and undergo
fatty degeneration, external openings occurring from ulceration. The
latter are found less frequently than pleuro-bronchial fistula. This
external perforation is habitually in front, in the upper intercostal
spaces, which, near the sternum, are very wide and not protected by
external intercostal muscles. The fifth intercostal is the most
frequent locality. There may be one or several openings. They may be
caused by the pus ulcerating through the parietal walls, or abscesses
may be produced in the walls and burst externally. Exceptionally, the
emptying of the liquid is by ulceration of the diaphragm into the
abdomen, causing fatal peritonitis. Some years since the author saw, in
consultation, a patient where the autopsy proved this condition. Rare
cases have been reported where the fluid escaped into the pericardium,
into the mediastinum, and into the opposite pleural cavity
(Fernet[114]). Bouveret[115] relates a number of cases in which the
discharge of pus took place through such unusual channels as the
oesophagus, the stomach, the intestines, and the pelvis of kidneys;
also where the pus perforated the posterior cul-de-sac of the pleura
and appeared in the posterior walls of the abdomen. In the last cases,
he states, it may point in the groin, the lumbar region, the buttocks,
or even in the thigh.

[Footnote 113: See section on Pneumothorax.]

[Footnote 114: _Loc. cit._]

[Footnote 115: _Journal de Méd._, Dec. 16, 1882; _N.Y. Med. Rec._,
March, 1883.]

SYMPTOMS.--In a large number of cases of purulent pleurisy the general
symptoms do not differ materially from those of fibro-serous
pleurisies. Sometimes, however, they do. This is according to whether
they are acute purulent or chronic purulent pleurisies.

In acute purulent pleurisy the disease commences in the same way as the
ordinary acute fibro-serous pleurisy. Indeed, the first effusion is
ordinarily serous in appearance, and afterward it becomes purulent. We
have the initial chilliness more or less marked, accompanied by the
characteristic pain in the side and dry cough, the fever keeping up,
even as high as 103° to 104° F.; and soon the signs of an effusion
supervene. In a few days, ordinarily, in acute fibro-serous pleurisies,
the febrile exacerbation disappears. Graves[116] states that the extent
of a pleurisy is not augmented after twenty-four hours. In acute
purulent pleurisy the fever persists in spite of treatment; the
effusion increases, sometimes less rapidly than in the serous variety,
but in a continuous manner. If thoracentesis is performed about the
eighth or tenth day, we notice that the fluid is opaline and contains a
large quantity of pus. After this the fluid is reproduced, and as it
forms the fever continues; the skin is hot and dry, the appetite
impaired, and sweats appear during the night. In examining carefully
the thoracic walls we find oedema of the diseased side. Later on there
will probably be oedema of the lower extremities.

[Footnote 116: _Clin. Méd._, edited by Neligan.]

Chronic purulent pleurisy is marked by symptoms somewhat different. It
commences in a similar manner to that of acute pleurisy, with fever,
but in a few days the fever disappears. In the evenings there may be
some febrile action with slight chills. It is remarkable that
frequently vast collections of purulent fluid do not give rise to
chills. The fluid augments progressively, but sometimes very slowly,
and often it appears to remain stationary for a long time. This
condition continues sometimes for many months. The {543} patients are
pale and feeble, although they may get up and walk until the quantity
is increased to such an extent as to impair their breathing capacity.
Then the forces of the body by degrees diminish, and the appetite is
impaired to a serious extent. The face becomes pale and the lips
discolored. From time to time diarrhoea supervenes and oedema of the
chest-walls is noticed, and general anasarca comes on without albumen
in the urine. If nature does not open an orifice through the parietes
of the chest or through the bronchi for the discharge, the patients
finally succumb in the last degree of wasting with profuse sweats and
fetid colliquative diarrhoea.

PHYSICAL SIGNS.--These, with some modifications, are very similar to
those of ordinary sero-fibrinous pleurisy. We have the same dilatation
of the chest, but it is more frequently localized. The oedema of the
thoracic walls is almost characteristic of the presence of pus in the
pleural cavity. We may, however, meet with it in fibro-serous pleurisy
and in cachectic subjects on the side of decubitus. Then, again, there
are cases of purulent pleurisy where it does not occur. It must be
looked for with care, especially at the lateral portion beneath the
armpit.

Mensuration and percussion afford especial evidences of purulent
pleurisy, and frequently they discover encysted points.

The tubular quality of respiratory sounds is more pronounced, as are
also the amphoric characters at the apex, caused by long-continued
pressure of the compressed lung around the large bronchi. Ægophony is
less frequently heard, the bronchophony is distant and less distinct,
and vocal fremitus is more completely abolished. The non-transmission
to the ear of the whispered voice through the walls of the chest
(Bacelli's sound) in purulent pleurisy is a sign of considerable
significance in tracing the transformation from serous fluid into pus.
We must, however, bear in mind that when the sero-fibrinous effusion
contains fibrinous flocculi, it has the same effect as a purulent fluid
in interfering with the passage of the voice. (See article ACUTE
PLEURISY.)

DIFFERENTIAL DIAGNOSIS can be but indifferently reached by considering
the points mentioned. An exploratory puncture enables us to decide with
certainty as to the nature of the fluid. Without this the diagnosis is
often very difficult. In acute purulent pleurisy the diagnosis is most
difficult, especially at an early period, because the general symptoms
and the local signs resemble closely those of ordinary pleurisy. When,
however, the disease is further advanced, and we have the earthy aspect
of countenance with oedema of the thoracic walls, we can be nearly
positive in our opinion. Moutard-Martin[117] speaks of this localized
oedema at the level of the fluid as a certain indication of the
purulent character of the fluid. But this oedema, as he admits, does
not always exist. It is wanting in many cases, and it may be found in
cases of sero-fibrinous effusion where the patient has been lying on
the side, and in other cases of advanced cachectic disease. Formerly,
there were many more errors of diagnosis, which were only discovered at
autopsies, but now, thanks to aspiratory punctures, the diagnosis is
much more accurate, and indicates to us the rational treatment. In both
varieties of purulent pleurisy there is a tendency to discharge by
making orifices through the walls of the chest or through the lung.
This is nature's mode of spontaneous cure. The most common is the
pleuro-bronchial fistula, and the period of the disease at which this
accident may occur is very variable. Woillez[118] cites a case where it
occurred as early as the twenty-eighth day; ordinarily it occurs at a
much later period, sometimes as late as the eightieth day. It comes on
early in purulent pleurisy. In infants the perforations take place as
early as in fifteen or twenty days, and are favorable to the cure in
one-half of the cases. Saussier in 29 {544} perforations of this kind
counted 15 cures. The symptoms of this accident are easy of
recognition. They vary according as the pleuritic effusion is diffused
through the whole pleural cavity or is limited, encysted, or
interlobular. In the first variety, where we have the physical
evidences of the presence of pus, suddenly, during a paroxysm of
coughing, the pus is forced up through the bronchi, and the patient in
a very short time expectorates a considerable quantity, varying from a
few grammes to a liter or more. The quantity thus thrown off depends
upon the diameter of the fistula. It may be excessive, as in a case
recently observed by the author where suffocation was produced, causing
syncope, asphyxia, and death, the flow being so rapid as to fill up the
bronchi to such an extent that the patient could not get rid of it. In
many cases the pus is brought up more gradually, with successive coughs
or with changes of position. Frequently vomiting is produced by the
flow from the vomica. After the first instantaneous evacuation of pus
(ordinarily continuous, sometimes intermitting) purulent expectoration
takes place. The patient may pass hours without any discharge, when
suddenly a severe cough brings up a quantity of pus, and again may
spend days without further expectoration. Pleuro-bronchial fistulæ may
have a valvular character, so that air may or may not be admitted into
the pleural sac as the pus is discharged. With or without the formation
of pneumothorax there is a tendency to cause putridity of pus. In cases
of children, who swallow their expectoration, it often produces a very
troublesome diarrhoea. The course of the disease and its prognosis are
necessarily altered according to conditions met with. When the air does
not penetrate, we observe that the diseased side becomes depressed and
the swelling, previously noticed, disappears. The flatness on
percussion diminishes or disappears entirely. On auscultation we have
coarse râles, sometimes just inside the fistulous orifices, sometimes
at a considerable distance. The general symptoms, as well as the
physical signs, improve, and the case advances slowly toward cure.
Ordinarily, the pus expectorated from the pleura, when free from
contact with the air, is odorless, but it is rarely as unpleasant as in
bronchial dilatations, unless it is long retained in the cavity, when
putrefaction ensues. When the air enters from the bronchi, it
frequently acquires a disgusting odor. If the air enters the pleura and
takes the place of the pus, the chest remains enlarged. Indeed, it
sometimes increases in size to such an extent as to cause suffocation
unless the pus and gas are withdrawn. The valve made by the false
membrane allowing the air to enter the cavity, but not to escape from
it, causes the fluid to accumulate rapidly, and we have pneumothorax to
a very painful degree. The diaphragm is pushed down, and, if the
disease is on the right side, the liver is forced down, and descends to
a level with the umbilicus.

[Footnote 117: _Purulent Pleurisy_, 1872.]

[Footnote 118: _Traité Clin. des Mal. Aigues des Organes Resp._, 1872.]

The collection of gas and fluid may be in such excess as to produce a
concavity of the upper surface of the liver, while the organ is forced
down into the abdomen. E. Moutard-Martin[119] explains this extreme
condition by the fact that the fistulous orifice being at the superior
portion of the lung, the air having equalized the interior pressure
with the exterior pressure, the liquid obeys the laws of gravity, and
depresses the diaphragm. The fluid thus does not reach the level of the
pulmonary fistula. Under these circumstances the expectoration may
cease altogether unless the patient, by change of position, allows it
to flow outward through the orifice.

[Footnote 119: _Loc. cit._]

The physical signs of this condition of pyo-pneumothorax are very
marked and characteristic. Above the level of the fluid there is
ordinarily a great exaggeration of resonance on percussion, especially
at first. At the end of a few days, however, this resonance is
sometimes materially modified, and we have obscurity of the percussion
vibrations. Percussion, by itself, may lead {545} us into error of
diagnosis which the other modes of physical exploration will correct.

On auscultation we hear the amphoric murmur, which is sometimes of
great intensity, and at others so feeble and distant as to require
great attention on the part of the auscultator. These varieties of the
amphoric respiratory sound appear to depend more upon the position of
the pleuro-bronchial fistula, and upon the greater or less free
circulation of air through the fistula, than upon the extent of the
cavity (E. Moutard-Martin). This sound and the amphoric voice are the
two principal auscultatory phenomena. There is also the vibrating
metallic tinkling produced always in expiration. Although the physical
cause may exist, this latter is by no means a constant sign. It may
disappear for hours, and even days together, and then be heard for a
short time. Sometimes it is only heard when the patient coughs suddenly
and violently. When heard it is a very valuable indication of the
presence of a pleuro-bronchial fistula. Auscultatory percussion gives
us a still more valuable diagnostic phenomenon--the metallic amphoric
reverberation--especially if we percuss with a metallic percussor over
a metallic pleximeter. The Hippocratian splashing caused by succussion
is a more characteristic sign of pyo-pneumothorax than any other we
have mentioned. Other signs may fail, and often this is the only sign
present. Almost all the symptoms and signs that have been considered
characteristic of the presence of pus may coexist with a perfectly
limpid sero-fibrinous effusion. We may even have in serous effusions a
high, fluctuating temperature, profuse sweats, and quick pulse lasting
several weeks. On the other hand, purulent effusions may be associated
with symptoms of so mild a character as to lull suspicion. Previous to
the application of exploratory punctures for purposes of accurate
diagnosis, purulent pleurisies were confounded with the milder disease
until so far advanced as to be too late for effective treatment. Now we
can without risk discover purulent pleurisies at their very
commencement, and before they reach the point of great danger to the
subject we can relieve them by thoracentesis, and afterward pursue the
treatment for a radical cure.

Limited, circumscribed pleurisies, such as are found at the base of the
surface of the diaphragm and in the interlobular fissures, as well as
those involving the pleural cavity itself, may empty their contents
through the bronchi. As we have shown, the diagnosis of these forms is
often very obscure and difficult. The fine capillary exploring-needle
is a safe, and often a reliable, means of diagnosis. It may happen that
we can only guess at the nature of the disease until, after a
protracted cough, there is ejected by the mouth a quantity of pus, and
the diagnosis is made clear. We may perhaps discover a point of
flatness at the base or about the centre of the lung, but often this
flatness is very incomplete, because the collection of pus does not
always reach the thoracic wall. It may, indeed, be separated from it by
healthy lung-texture. Auscultation may discover coarse râles or even
gurgling with cavernous respiration. The voice sometimes has the
character of pectoriloquy, at other times of bronchophony: the cavity
is rarely large enough or the walls sufficiently firm to give the
amphoric tone. Under these circumstances there is neither metallic
tinkling nor Hippocratian succussion. The diagnosis of bronchial
fistulas caused by encysted pleurisies may be confounded with
tubercular cavities or with dilated bronchi. The exact position,
however, of the lesion, the rapid manner of the first purulent
expectoration, and the nature of the pus expectorated, will enable us
always to arrive at an accurate diagnosis. We must remember that in
bronchial dilatation the disease is developed by degrees, and the
patients do not expectorate suddenly a notable quantity of pus;
tubercular caverns are ordinarily at the summit. The mode of
expectoration is different, and the matter expectorated does not
present the same purulent and homogeneous characters. {546} The general
health is very different where encysted pleurisies exist from what it
is in patients suffering from tubercular cavities. In the former case
it is comparatively good; there are no profuse night-sweats, diarrhoea,
etc. Perforation through the thoracic walls may take place at a period
more or less remote from the commencement of the disease. The first
indication of this result is, ordinarily, a pain over a limited point
of one or two of the intercostal spaces, followed, in a few days or a
week, by a raised sensitive point on the surface, without change of
color of the covering skin. This may remain a long time in an unchanged
condition, but generally it increases gradually until it becomes soft
and fluctuating, reducible by pressure, but increased in size by
efforts to cough or by forcible expectorations. The skin over the
raised point becomes thin with a purplish tinge; suddenly, from some
effort to cough or unusual exertion requiring suspension of breath, it
bursts and gives exit to a quantity of pus far out of proportion to the
size of the small tumor. Sometimes there are several such points in the
same subject, appearing simultaneously or consecutively, especially if
the discharge is not free through the first one. Ordinarily, there is
but one which appears on the anterior portion of the chest about the
fifth intercostal space or in the intra-mamillary line. These orifices
sometimes close and then reopen. Of 18 cases of empyema necessitatis
collected by John Marshall,[120] 1 occurred in the sixth intercostal
space and 17 in the fifth, and 6 of his own cases in the fifth, beneath
the nipple. This is, as he states, the weak point of the chest,
relatively unprotected by the adjacent muscles. The internal
intercostal muscle, the weakest portion of the great pectoral, and the
thin fascia, are the only coverings at that point. There is valid
reason why special bulging and spontaneous perforation should occur
there. The spot also corresponds nearly with the middle of the pleural
cavity when distended. The fifth intercostal space is wider than those
below, and its limiting ribs, held to the sternum, give firmness to its
borders--conditions which help the thinness of the walls in determining
the place of perforation. In children perforation often takes place in
the very wide second intercostal space. The perforation, although it
may contract in size, persists and remains a fistulous canal,
permitting air to enter and to escape. The fluid rarely becomes fetid
unless there is a pleuro-bronchitic fistula or air is otherwise freely
admitted. Sometimes when the orifice is oblique, the air does not enter
at all. When the purulent effusion escapes through the thoracic walls,
the patient experiences at once manifest relief. The respiration
becomes better, the fever decreases, the sweats disappear, the appetite
improves, and the general condition is decidedly ameliorated. This
improvement persists as long as there is free discharge, but if from
any cause it ceases, we have a return of serious symptoms. If no air
enters, percussion and auscultation show the gradual disappearance of
the evidences of disease; but if air enters we have the signs of
pyo-pneumothorax, amphoric breathing, metallic and succussion sounds.
The diagnosis of parietal openings is comparatively easy: the quantity
of pus, its odor, with the physical signs, show its nature. With care
this form of pleural opening is distinguishable from a fistula made by
caries of the ribs or by vertebral abscesses, and not communicating
with the pleura. The existence of a thoracic fistula does not prevent
the formation of pleuro-pulmonary fistula, and reciprocally a parietal
fistula can be found where the other has been previously formed. The
abscesses following purulent pleurisies and empyema have been long
recognized. Hippocrates mentioned them as contributing to a favorable
prognosis in empyema.

[Footnote 120: _London Lancet_, March, 1882.]

Pulsating empyema is where the lesion is situated in the neighborhood
of the heart or of the aorta, which transmit their impulse. They are
also sometimes called pulsating tumors, rising and falling with
alternate movements of {547} inspiration and expiration (Stokes,
Graves, and Aran). These cases strongly simulate aneurisms. According
to Fraentzel, the fluid is always purulent. In 1 case reported by him,
and in 2 cases seen by Traube, pericarditis with effusion was present.
Douglass Powell mentions two well-marked cases of pulsation in the left
supra-mammary region where the diagnosis between effusion and aneurism
was very difficult, but where paracentesis removed a large quantity of
fluid and the signs of pulsation ceased. In these cases there was
present neither pus nor pericarditis.

TERMINATIONS.--If allowed to take its natural course, pulsating empyema
almost always ends in death from exhaustion or syncope, or by
discharging through the lungs or through the intercostal spaces.
Formerly, it was oftener fatal than now, but it is still justly
considered the gravest form of pleurisy. We have seen that
exceptionally it is cured by becoming encysted. It may be cured by
spontaneous openings into the lungs, and more rarely by fistulous
orifices[121] through the walls of the chest. Is it possible for the
disease to be cured by the absorption of the pus? The bearing of this
inquiry upon the treatment cannot be over-estimated. If absorption can
remove the pus, we may safely leave it in the pleural cavity. If the
pus cannot be taken up by the absorbent vessels, we ought promptly to
make use of radical measures and evacuate it. The literature on this
point gives us few reliable cases. Spontaneous cure can rarely be
produced by absorption. Douglass Powell[122] writes that "the
spontaneous disappearance of such effusions is too uncommon to be
expected, and the process of reabsorption is one too full of peril to
be anticipated with anything but dread. It is indeed an attempt at such
absorption that occasions the most characteristic hectic symptoms."
Surgical intervention is the rule. The writers previous to the
introduction of exploratory punctures speak of cases where purulent
pleurisies were diagnosed and the effusions were absorbed. We have
shown that the differential diagnosis between serous and purulent
effusions is very uncertain when made from the general symptoms and
physical signs. Even Trousseau, with all his skill and vast experience,
made the mistake of diagnosis, and performed the operation of
pleurotomy in a case of serous effusion, and his patient died. There
are well-authenticated cases where, after thoracentesis, small
quantities of pus left behind have been absorbed, especially in
children. That purulent pleurisies have been effectively cured by the
pus becoming encapsuled has been demonstrated by autopsies of persons
dying from other causes. E. Moutard-Martin reports a case where, after
withdrawing with an exploratory trocar a few drops of pus, and thereby
establishing the diagnosis of purulent pleurisy, he was unavoidably
prevented from opening the chest. Two months afterward he found the
effusion had entirely disappeared. He states that this was the only
case he had ever seen of a spontaneous cure without evacuation.
Douglass Powell has seen one case which has satisfied him as to the
possibility of a local empyema becoming absorbed. Wilson Fox reports
another similar case. Chronic pleurisies in childhood are almost
invariably suppurative, yet Barthez and Rilliet report 7 out of 13
recovered. It must be, and generally is, admitted that cure by pus
undergoing retrogressive fatty degeneration, and then being absorbed,
is possible, but it rarely occurs. Should the more fluid portion be
absorbed, the inspissated pus remaining on the pleural surface may at
some future time, upon softening, give rise to secondary tubercular or
purulent collections. It is also true that cure is quite often effected
by spontaneous evacuation through the lungs and through the walls of
the chest. This is especially the case {548} in interlobular effusions
and in cases sacculated by adhesions. Such cure is explained by the
fact that adhesive inflammation, assisted by the elasticity of the lung
on both sides, glues together the walls, isolates the fluid, and
prevents air from entering, thus preventing the pus from putrefying.

[Footnote 121: In Andral's 8 cases of bronchial perforation there were
only 3 deaths--a mortality less than by artificial opening previous to
the application of Listerism.]

[Footnote 122: _Dis. of the Lungs and Pleura_, London, 1878.]

In cases of pulmonary perforations the probabilities of a favorable
termination by absorption of gas, evacuation of fluid and the contents
of the chest, are greater where air does not enter the cavity. The
presence of air, especially if stagnant, in contact with the pus, makes
a serious complication, causing putrefaction of the pus and consequent
septicæmia, with all its dangers. The discharge of the purulent
collection, through the parietes of the chest, after the manner of an
ordinary abscess, is ordinarily made through the anterior part of the
thorax, but it may take place in any part. At first this mode of
evacuation, empyema necessitatis, is a great relief, but cures rarely
result from it. Most frequently, owing to the imperfect evacuation
through the tortuous canal and the entrance of air mingling with the
pus, death supervenes unless the surgeon enlarges the orifice or
produces a new one, and thoroughly empties the sac and persistently
washes it out. From statistics collected by Wilson Fox, the mortality
is not so great from spontaneous parietal openings as was formerly
supposed. Of Andral's cases there were 2 deaths in 25. Goodhart had 11
cases, all of which recovered. Ewald lost 3 of his 6 cases. Cases of
empyema necessitatis should be treated as artificial openings with
every possible antiseptic precaution. The mortality would thus be
decreased. The chances of cure by absorption are so small that when
nature shows no tendency to either of the two spontaneous modes of
cure, there is great danger of a fatal termination through hectic
fever. The time for this result varies from a few weeks to months. When
in empyema we have fistulous orifices they sometimes remain open for
years. Near them are local points of depression, caused by external
atmospheric pressure. When acute purulent pleurisy follows a low fever,
such as typhoid or scarlet, a fatal termination may result in a short
time; in other cases it is many months before the patient dies from
exhaustion.

We cannot forbear to urge the importance of promptly and definitely
settling the diagnosis by exploratory aspiratory punctures. Properly
guarded, no evil can result, whereas a positive diagnosis enables us to
act promptly with effective mechanical means of relief. It is
undeniable that purulent effusions in the pleural cavity are very
serious in their results, and are followed by death unless Nature or
the surgeon evacuate them. Even when Nature does so, it is often
imperfectly done, and the termination may be death unless we assist her
to get entirely rid of the fluid.

PROGNOSIS.--Formerly the prognosis in every case was of extreme
gravity. The condition was looked upon as of necessity fatal. Surgeons
despaired of a successful result in operating. Now, thanks to thorough
drainage and Listerism, unless the case is an old chronic empyema, we
are hopeful of cure and a favorable prognosis may be given. We may look
for good results where the disease is early recognized and promptly
treated. J. G. Blake[123] cured 16 in a total of 19 cases. Since 1869
he cured 9 out of 10 cases. Homer[124] saved 26 out of 52. Feidler[125]
treated 112 patients, only 25 of whom died (all advanced tubercular
cases); 21 were restored to good health; 66 (tubercular) were cured so
far as return of effusion was concerned. Israel[126] had 10 recoveries
out of 11 cases. A. T. Cabot[127] reports 11 recoveries out of 14
cases. Of the fatal cases, 2 died of phthisis; the third had existed
four years.

[Footnote 123: _Med. and Surg. Rep. Boston City Hospital_, 2d Series.]

[Footnote 124: Quoted from _Med. Times_, Philada., Aug., 1883.]

[Footnote 125: _Ibid._]

[Footnote 126: Quoted from Dabney, _Amer. Journ. Med. Sciences_, Jan.,
1883.]

[Footnote 127: _Bos. Med.-Surg. Journ._, Aug. 16, 1883.]

{549} When purulent pleurisy follows fibro-serous effusions, and when
it occurs in vigorous children, the prognosis is more hopeful than when
it is preceded by scarlet fever or occurs in subjects debilitated by
diseases which have exhausted the recuperative forces of the body.
Empyema of tubercular origin has necessarily a grave prognosis. In
persons in advanced life the prognosis is very unfavorable. If hectic
fever or septicæmia occur, the prospects of cure are comparatively
slight. In cases of empyema necessitatis much depends upon the power of
resistance of the patient, and upon whether the matter is discharged
before it has produced caries of the ribs, sternum, or spine, or has
prostrated the vital powers. If these sequelæ have been produced, the
condition of the body is most unfavorable to the restoration of health.
If the pus in pyothorax has been discharged through the bronchi, though
it may give temporary relief, it is attended with great danger, and if
the discharge continues it will gradually wear out the patient's
strength.

TREATMENT.--The diagnosis being established, we at once realize the
great responsibility of treating a disease of such gravity. In many
other diseases of serious import we trust Nature to do her part toward
cure; here, as we have shown, we find her unable to come to our
assistance. One of the large serous cavities, connected as it is with
the lungs, is not only disabled, but contains a deleterious fluid which
cannot remain in a closed cavity without sooner or later affecting the
processes of nutrition. We can do little by medical treatment save to
sustain the organism by tonics and reparatory agents; we can give wine,
quinine, arseniate of soda, and cod-liver oil; we can administer a
sustaining diet and place the patient in the best hygienic and sanitary
condition. We cannot conscientiously hold out to the patient a prospect
of cure by medicines.

There is danger in resorting to the expectant plan of treatment. We
lose valuable time, and finally we shall be forced to resort to
surgical operations, which in fact constitute the modern treatment of
purulent pleurisy. By them only are we able to promote the primary
objects of our treatment, which are to get rid of the purulent matter
and to stop the suppurative inflammation. We thus endeavor to
obliterate the pleural cavity and promote the expansion of the lungs.

Surgical Treatment.--This has been the treatment which has been most
effectively used from the time of Hippocrates to modern times. There
has been, and still is, great diversity of opinion as to the best modes
of withdrawing the pus contained in the pleural cavity, but it is
settled that when the diagnosis is certain the fluid must be
removed--if not by spontaneous openings, by artificial means. We must
except to this rule cases of suppurative pleurisy of phthisical origin.
Bowditch years ago stated that in this class of cases it was advisable
not to make permanent openings into the chest. In these the suppuration
does not stop, and the operation appears to hasten the fatal issue of
the disease. Wilson Fox demonstrates from statistics that the mortality
in phthisical cases is increased by operations.

There is no room for discussion as to the indications, as in cases of
simple sero-fibrinous pleurisy. There is only one thing necessary to be
ascertained--the certainty of pus in the cavity. This is shown by the
pointing or by pus abstracted by exploratory puncture. The more
promptly we act, the greater the prospect of cure. As Powell[128]
emphatically says, "The prognosis is practically hopeless without
surgical help. We must adopt some surgical measures or take upon
ourselves responsibility for a large mortality." Bowditch, Trousseau,
Hamilton Roe, Anstie, Parker, Marshall, and Moutard-Martin all concur
as to the necessity of surgical interference. Clifford Allbutt[129]
says: "If pus or septic material be present in the body, we must not
{550} rest until it is removed. I therefore dislike and reprobate all
tampering with an empyema."

[Footnote 128: _Loc. cit._]

[Footnote 129: _Brit. Med. Journ._, Dec., 1877.]

We propose to mention, as briefly as we can in justice to the subject,
the several modes of operating, together with our conclusions and the
results obtained by us and by others of much larger experience.

Modes of Operating.--These are numerous, but they may be divided into
three classes: First, the simple immediate evacuation of the fluid by
subcutaneous thoracentesis with the ordinary trocar or with an
aspirator of some kind, without allowing the flow to be continuous:
this is the closed method; secondly, the open method--the operation by
incision with a bistoury, and the introduction of permanent canulæ or
of drainage-tubes of metal, of hard rubber, or of soft tubing; thirdly,
the more radical treatment by free incision (pleurotomy) with or
without washings or injections by the aid of syphons. With all these
modes of operating the strictest antiseptic precautions should be
taken.

Thoracentesis.--For this operation we have a choice between the
ordinary hydrocele trocar, the trocar protected by a soft valve at the
orifice (Reybard's instrument), Jules Guérin's or Wyman's aspirating
pumps, Dieulafoy's previous-vacuum aspirator with capillary needles,
and numerous modifications by others of Dieulafoy's, including
Potain's, and Reynard's modification of Potain's, or we can have
recourse to Potain's, Southey's, or Williams's syphon. If we select the
trocar (Reybard's), we prepare the instrument by cleansing it
thoroughly and Listerizing it. Reynard[130] recommends a hypodermic of
morphia previous to operation, to prevent the painful cough. The
simplest method is to pass the aspirator needle through the flame of a
spirit-lamp, and subsequently to plunge it in carbolic-acid solution.
We spray with a carbolized solution the point of puncture, which should
be at the sixth intercostal space, when possible, in the axillary line.
Powell prefers a lower opening, in the seventh or eighth intercostal
space and in the posterior axillary line. He wishes to completely empty
the pleural cavity of pus and promote the obliteration of the
abscess-sac by the descent of the lung as it re-expands, and by the
return of the heart to its normal position: these processes converge
toward the lower and postero-lateral position. We ordinarily prefer
local anæsthesia by sprays of ether or rhigoline or by cocaine
hypodermics to anæsthesia by inhalation. After drawing up the skin, so
as to be able to close the orifice by the flap after the operation, we
direct the trocar by the nail of the left index finger; we, with a
quick movement, insert the trocar to the extent of three or four
centimeters. By this quick insertion we do not run the risk of stopping
the canula with the thick membranes. We allow the fluid to flow out
slowly, but as completely as possible. In fibro-serous effusions we
only draw off sufficient to remove intra-thoracic pressure, to avert
the dangers caused by that pressure, and promote the process of
absorption. In suppurative pleurisy, while we aim at relief from
pressure, we wish to get rid of a fluid which is itself deleterious.
Consequently, our object is to prevent absorption and to ward off the
formation of fistulous outlets through the lungs or the parietes of the
chest. Therefore we endeavor to completely evacuate the pus, and, as
far as possible, to prevent its re-formation. While we desire to remove
all the fluid if we can, we must not run any risk by doing so. If the
cough annoys the patient, and the elasticity of the walls and the
pressure from the displaced organs do not continue to force out the
fluid, we had better stop the flow temporarily or renew the operation
next day. We must desist if the cough becomes very persistent. We
prefer Dieulafoy's aspirator or Potain's modification for the simple
evacuation of the fluid, unless we wish to wash out the pleura; then we
employ Potain's or Williams's (of Boston) syphon, because either can be
applied {551} with greater effect. It is best not to take needles of
too small a diameter, for the flocculi may easily choke them. We prefer
No. 2 (1 millimeter) or No. 3 (1 millimeter and a half). By using the
small-sized dome-trocar we avoid the possibility of injuring the lung.
Care must be taken in removing the canula to withdraw the aspiratory
force by turning the stopcock; otherwise we may draw the pus into the
texture of the walls and establish fistulous openings. In using the
common trocar fistulæ have frequently been made, causing a serious
complication.

[Footnote 130: _Brit. Med. Journal_, Sept., 1881.]

Thoracentesis thus performed has often cured empyemas, especially in
children. We find instances mentioned by Lacase, Duthiers, Dieulafoy,
Lebert, Hamilton Roe, and others. It has been demonstrated that the
operation is sometimes effective without resorting to injections and
washings of the pleural cavity. Bouchet[131] reports a case in a child
following typhoid fever, where he aspirated thirty-three times and
cured the patient; another case, a child four years of age, after two
operations; another child, seven years of age, after six aspirations.
Guérin[132] reported several cases. M. Fouson[133] reported 19 cases of
children treated by aspiration with success. The younger the child, the
greater are the chances of success. He advised complete emptying of the
cavity. Lewis Smith[134] prefers the use of an aspirator in operating
upon children. He does not think it necessary to remove all the pus
present. Cordet Gassicourt[135] reports cases of three infants, each of
whom was cured by one aspiration. C. Gerhardt of Würtzburg[136]
recommends in children complete evacuation of purulent fluid, through
incisions and washings, avoiding entrance of air. Adolph Bajincke of
Berlin[137] states that aspiration with antiseptic treatment is often
successful in children. He advises, if after two or three aspirations
the fever returns and the fluid increases, that free incisions be made,
with injections of salicylic acid (3 per cent.), with antiseptic
dressings. He recommends the removal of only a portion of the fluid. A.
Jacobi[138] mentioned having in a single year 3 cases of empyema in
young children, each of which required but a single aspiration; the
quantity of pus in 1 case amounted to 300 or 400 grammes. The
flexibility of the young ribs causes sufficient sinking in of the
thorax to promote recovery. F. Richardson[139] advises two aspirations
before incisions. R. W. Parker,[140] London, takes Richardson's view.
He strongly advocates antiseptic precautions and injections of quinine
(5 grs. to ounce j) and injection of filtered and carbolized air into
the pleural cavity. Austin Flint[141] advises that aspiration should be
used first, but if not successful, then incisions should be made at the
base of the thorax and a tent introduced to keep the orifice open.
Anstie[142] gives similar directions. According to Bowditch,[143]
"whenever the pus is pure there is no immediate call for thoracotomy,
for patients at times get well after simple aspirations. Youth and
recent uncomplicated disease favor this. Heretofore, after three
aspirations the author has resorted to thoracotomy." Dabney[144] says
that aspiration occasionally gives good results, even in adults. S. C.
Chew reported the case of an adult (twenty-five years of age) cured of
empyema by one aspiration of sixteen ounces, and also a case of a child
three years of age after three aspirations. Barnes[145] reports a case
of a patient nineteen years of age who recovered after four aspirations
of large quantities of pus. J. G. Blake[146] reports a case (boy ten
years of age) where one aspiration of ten ounces accomplished a cure.
He adds that in children repeated withdrawals of pus by aspiration are
justifiable, but in adults after {552} one unsuccessful operation he
advises permanent opening. Dupuytren[147] cured a case after
seventy-three aspirations. The author has had 3 cases perfectly cured
by aspiration: a child eleven months old, after three operations; a
child of five years, after five operations; a boy sixteen years of age,
after two operations.

[Footnote 131: _London Lancet_, 1860.]

[Footnote 132: _De la Thoracentèse par asp. dans la Pleu. Pur._, 1871.]

[Footnote 133: _Thèse de Paris_, 1877.]

[Footnote 134: _Diseases of Children_.]

[Footnote 135: _Soc. de Thér._, 26 April, 1882.]

[Footnote 136: _Trans. Int. Med. Con._, vol. iv.]

[Footnote 137: _Ibid._]

[Footnote 138: _Ibid._]

[Footnote 139: _Ibid._]

[Footnote 140: _Ibid._]

[Footnote 141: _Clinical Medicine_.]

[Footnote 142: _Reynolds's Sys._, vol. ii.]

[Footnote 143: Unpublished MSS.]

[Footnote 144: _Amer. Journ. Med. Sci._, Oct., 1882.]

[Footnote 145: _Brit. Med. Journal_, Dec., 1877.]

[Footnote 146: _Med. and Surgical Reports Boston City Hospital_, 2d
Ser., 1877.]

[Footnote 147: Altimont, _loc. cit._]

Such being the record, we are in duty bound to try simple aspirations
before making use of the more radical modes of treatment. The character
of the fluid as drawn off by the exploring-needle furnishes valuable
indications. Should it be found laudable and inodorous, we had better
aspirate once or twice before resorting to the free incision. It can do
no injury, and we thus enable the lung to expand, diminish the size of
the cavity, and prepare for the more radical operation. In children we
ought to try this mode repeatedly unless we have symptoms of emaciation
and hectic approaching; in adults only two or three times. The
operation is simple, painless, without danger, and occasionally
perfectly effective. If the fluid re-forms quickly--and it sometimes
does with astonishing rapidity--or there are evidences of depression
from fever, sweats, and diarrhoea, we must promptly have recourse to
one of the effective surgical methods producing free drainage. It is
undeniable that the treatment by thoracentesis is frequently
unsuccessful, notwithstanding repeated operations.

In sero-fibrinous effusions the close method is the most successful,
but in purulent effusion this is not ordinarily the case, and we are
forced to employ the open method to produce free, continuous
discharges, as the purulent fluid re-forms rapidly.

Open Methods.--Of these we have--(1) drainage through a single orifice
by the introduction of a permanent canula or soft india-rubber tube;
(2) drainage through two openings; (3) use of syphon; (4) pleurotomy;
(5) drainage by resection of ribs. Each of these modes has its
advocates. They have all been frequently used with varying results.
Each has its advantages and disadvantages.

The first point to be noted about these modes of operation is, that we
cannot prevent the introduction of a greater or less amount of air to
replace the fluid, and therefore it is of primary importance that we
should always render the air aseptic. The incision must be made after
thoroughly cleansing the point to be opened. The bistoury, the canula,
the dressings, the receptacles of the pus, the sponges, and everything
connected with the operation, should be purified to prevent the
possibility of the contamination of the pleural cavity and its
contents. At each subsequent dressing all these precautions should be
renewed. Antiseptic gauze of six or eight layers in thickness, with
finely-combed oakum or salicylated cotton, ought to be placed over and
around the orifice for an area of twelve inches. In this way what
little air enters after the operation may be rendered thoroughly
aseptic.

Lister[148] recommends that the coverings of gauze should be in eight
folds if the drainage be excessive--that these be charged with a
disinfectant composed of one part of carbolic acid to four parts of
resin and pure paraffin. The dressings, he directs, should be kept in
place by elastic bandages. This treatment stops suppuration promptly,
and converts the discharge into one of a serous nature. His views have
been amply confirmed. A. T. Cabot[149] recommends that the dressings be
covered with a piece of mackintosh large enough to project in every
direction. In his cases he found it acted as a valvular fold, forcing
the air and pus out and preventing air from entering.

[Footnote 148: "Lectures on Clin. Surgery, etc.," _London Lancet_,
Dec., 1879.]

[Footnote 149: _Loc. cit._]

Drainage by Canula through a Single Orifice.--The patient, having had
about three hours previously a good substantial meal of easily-digested
food, is placed in a semi-recumbent position, leaning over toward the
healthy side. {553} Before selecting the point of puncture, the side
ought to be first washed with soap and water, so as thoroughly to
remove all dirt and epithelium débris, and then bathed in a 1:20
solution of carbolic acid. As there is to be but one opening through
which the fluid is to pass, it is desirable to have it low down. The
eighth intercostal space, somewhat behind the posterior axillary line,
is ordinarily the best point for the puncture. Lower than that we may
encounter the diaphragm, and, as we must use a trocar of considerable
size, we may inflict serious injury. As we desire to completely empty
the pleural cavity, a higher point would not be as effective. After
having satisfied ourselves of the presence of fluid at the point
selected by the physical exploration, we ought always to insert, as a
crucial test, a new exploratory hypodermic needle which has been
rendered aseptic. Ordinarily, it is not necessary or expedient to
resort to etherization, unless in case of a child, for local anæsthesia
by cocaine hypodermically, by rhigoline or the ether spray, or by the
application of a small piece of ice covered with salt (as suggested by
Powell), will render the incision painless. It is needless to add that
a weakened heart, a sluggish capillary circulation causing a cyanotic
appearance, and marked dyspnoea contraindicate the employment of
etherization. We prefer cutting through the integument with a bistoury,
and then inserting the trocar, which must be pushed with a thrust
through to the pleura. All of the pus should be allowed to escape,
unless cough, oppression, or threatening syncope should be noticed, in
which case it is better to insert the tube and arrest the flow by a
cork. The outward flow should be rendered slow by covering the orifice
with the dressings and allowing the fluid to soak into them. The tube
should only be long enough to go well through the parietes into the
pleural sac; otherwise it acts as an irritant, and interferes with the
adhesion of the two pleural surfaces, which is necessary for the
obliteration of the pus-secreting cavity and the expansion of the lung.
The tube should be kept in position by a hard-rubber shield attachment,
with bandages previously soaked in disinfectants applied around the
body, and several layers of carbolized gauze. The firm canulæ, metallic
or hard rubber, straight or curved, as proposed by Woillez and
Dieulafoy, are now generally abandoned. These admit air either by the
sides of the opening or through their canals, and they sometimes
produce, at their extremities, local ulceration through the lung or
even through the diaphragm, and cause peritonitis. Their only advantage
consists in the facilities they offer for washing out the cavity. With
canulæ made of soft india-rubber there is no danger of injuring the
lung, etc. They are not painful to the patient, and they can be
protected by valvular strips of gold-beater's skin or some soft
substance at their orifices. Through these india-rubber tubes we can
inject all fluids and washes, except those containing iodine. It has
been proved by Dujardin-Beaumetz[150] that iodine hardens india-rubber,
renders it extremely brittle, and destroys its elasticity in a short
time, even after a contact of forty-eight hours. In a case of
Bucquoy's[151] the tube underwent such alterations that it could only
be extracted by a long and painful operation. If these tubes are in use
when iodized fluid is to be injected, they must be temporarily removed,
and a metallic one, with arrangements for a double current, substituted
during the process of washing. If the canulæ are to be kept in
permanently, they must be of large size, so as to allow free flow
outward of fluid.

[Footnote 150: Quoted by Dieulafoy, _Pneum. Asp._, English ed.]

[Footnote 151: _Ibid._]

After the operation the patient should always remain in bed in an easy,
comfortable position, with the orifice covered by the dressings. His
diet should be of an easily-digested and nutritious character. His
temperature, pulse, and the condition of his secretions should be
carefully watched. Ordinarily, it is not well to reopen the
discharge-tube for three days. The same antiseptic precautions should
be used then as at the operation, {554} and a fresh tube inserted. The
pus secreted ought, if the case be one of recent origin, to be small in
quantity and without odor. After a few days it is best to allow the
fluid to flow out on the dressings as it forms, which is done by
turning the patient well over on his side. An occasional cough assists
the discharge. Should the odor become putrid or gangrenous, or hectic
symptoms show that the secretion is profuse and has no free exit, it
becomes necessary at once to use washings and injections of simple warm
water or warm water feebly alcoholized--1:45 or 1:80--or feebly iodized
solutions. The greatest care should be taken with these washings that
very gentle force be employed. (See Pleurotomy.) This mode of operating
is most effective in recent cases, for it gives the best opportunity to
the lung to expand. It is the easiest to perform, and, subsequently,
the least troublesome. If it be found ineffective, an additional
orifice can be made and a fenestrated tube inserted, or the orifice can
be enlarged by a free incision. There have been many successful cases
of this mode of operating, but, as the author has sometimes found, it
is difficult to establish free drainage, which is most important for
the success of the treatment. The result of his experience has been
that, in chronic cases especially, the two-opening drainage or free
incision without tubes (pleurotomy) has finally to be employed. Powell
recommends, after removing intra-thoracic pressure by aspiration or
syphon, in a day or two to completely evacuate the fluid under the
antiseptic spray and insert a tube for a few days only; then to allow
the wound to heal, and await results, trusting nature to secrete a
fibro-serous fluid which can be easily absorbed.

Drainage by two openings, as first effectively employed by Chassaignac,
is made by the introduction, through a large covered canula, of a tube
of india-rubber, perforated with holes, drawn out at another orifice.
The tube has its two extremities on the outside, and one posterior, in
the eighth or ninth intercostal space, and the other in front, in the
seventh intercostal space, after the withdrawal of the canula. The
anterior orifice is first made, and a long curved probe with a bulb at
the end is passed through backward and downward until it strikes the
posterior lowest intercostal space. The operator cuts down on the
probe, which points outward. To this end the fenestrated drainage-tube
is securely fastened, and is then drawn out through the first orifice.
Both ends are retained out of their orifices, by a shield firmly fixed
on the tube, for at least an inch. The pus flows out little by little,
but continuously, through one or other orifice, according to the
position of the patient. This is the most effective method to prevent
accumulation. Unfortunately, false membranes and flocculi sometimes
stop up the orifices in its walls, the pus does not flow out as it is
formed, and there are all the evils of air and fluid mixed and retained
in the serous cavity. It is, however, generally admitted that by this
system of drainage a number of cases have been cured; but it is not
often employed as a primary operation, as we wish to avoid, if
possible, the irritation which may result from the presence of so much
tubing in the chest. Moreover, it is not the best operation if there is
any hope of the lung expanding again. In old chronic cases we cannot
hope for more than very limited expansion.

Gross[152] speaks of drainage-tubes as harsh and dangerous. Flint,
Sr.,[153] prefers free incisions, with introduction of tents, to
drainage-tubes. Dabney[154] considers continuous drainage in some form
vastly preferable in the majority of cases. Israel[155] had 10 cases
recover out of 11 treated by thorough and continuous drainage. Cheadle
believes that a large collection will certainly require a free opening
in the end, and the sooner the pus is let out the better.

[Footnote 152: _System of Surgery_, vol. ii.]

[Footnote 153: _Clin. Med._]

[Footnote 154: _Amer. Journ. Med. Sci._, Oct., 1882.]

[Footnote 155: Quoted by Dabney.]

Chassaignac's method of drainage will answer well unless, as frequently
{555} happens, the purulent pleurisies contain large fibrinous masses,
hydatid pouches, or pieces of sphacelous débris.

Syphons, as used in purulent pleurisies, have some very decided
advantages. Potain's ingenious instrument, based upon the syphon
principle, enables us alternately to empty the pleural cavity into a
basin of water, and, by reversing the instrument, to inject the water
into the pleural cavity, thus washing out as often as necessary and
with ease the purulent collection and cleansing the cavity. Potain's
syphon is composed of an india-rubber tube 30 centimeters in length, to
be introduced and remain in the pleural cavity. This tube is introduced
through the canula, after the withdrawal of the trocar, to the depth of
at least 20 centimeters, in order that its extremity should reach the
posterior wall, the tube having been previously filled with water. The
outer extremity is put into a basin containing water. The part of the
tube at the outside of the orifice is closed by a serre-fine just
beyond the shield, as is also the extremity in the water. Another tube
is connected with the chest portion. This can be used for introducing
water to wash out the pleura. The syphon of Potain has very decided
advantages over the metallic and hard-rubber drainage-tubes. It
prevents the introduction of air and enables us completely to empty the
cavity; it permits us to wash out the cavity as frequently as is
necessary without fatigue to the patient, without pain, and without
change of position, and thus prevents attacks of coughing. All this is
done slowly, and the flow can be arrested at any moment by means of the
stopcocks. Where repeated washings are required the patient himself can
perform them with ease. With the other modes the washings are practised
with difficulty. The improved syphon by F. H. Williams of Boston is
simple in construction, of small size, and inexpensive. Revilloid of
Geneva (1882) reports 10 cases thus treated, of which 6 were cured.
Bénard[156] reports 8 cases treated by syphon, of which 4 were cured.
Goodhart's[157] statistics are not favorable to the use of the syphon.
Of his 28 cases thus treated, 10 died; in only 6 did the syphon method
alone effect the cure. Powell[158] objects to the syphon method,
because by it the chest cannot be drained unless the lung expands
completely or air is freely allowed to enter the pleura. These
conditions are impossible in such cases with a single opening and a
single tube. Moutard-Martin, while speaking of the advantages of
Potain's syphon, admits that in chronic cases where there are pieces of
false membrane and flocculi floating in the fluid the tube may be
clogged up, just as occurs in the metallic tubes and the
drainage-tubes. The patient may thus die by retention of pus and by
putrid absorption, unless pleurotomy is employed. It must be borne in
mind that the syphon is a weak aspirating instrument. It ought to be 10
meters long to possess an aspirating force equal to that of a pneumatic
pump (water being taken as the standard), and its long arm should
measure from 7 to 8 meters, in order that its aspiratory force should
equal that of a good pneumatic aspirator. Thus we see how weak is the
aspirating power of a syphon which only measures the space which
separates the bed of the patient from the floor. The ordinary aspirator
can be easily changed into a syphon. The descending arm of the tube
must be emptied by a stroke of the piston; the current is then
established and the stream becomes continuous (Dieulafoy[159]).

[Footnote 156: _Thèse de Paris_, 1871.]

[Footnote 157: _Guy's Hospital Reports_, 1877.]

[Footnote 158: _Loc. cit._]

[Footnote 159: _Trea. Pneum. Aspiration_, Eng. trans., 1873.]

While all prominent modern authorities admit the value in some cases of
double metallic tubes, of those of hard rubber, of drainage-tubes, and
of syphons, with thorough and complete antiseptic treatment, yet
observation has taught us that there are many disadvantages and
uncertainties. The drainage-tube may give rise to considerable
irritation and prevent the closing of the sac--a very important aid to
the cure. If the flow is retarded, the {556} fluid may decompose.
Therefore it is well to remove the tube frequently, to wash, cleanse,
and renew it. The admission of air and stopping up of tubes, the feeble
force employed, the putrid pseudo-membranes, and sometimes sphacelous
débris, cause, in many instances, fatal results. It frequently happens
that at first, when trying the simple aspirations, we find a whitish
laudable pus which subsequently becomes thick and fetid. We use
drainage-tubes and Williams's syphon, with strict adhesions to
Listerism, and yet there may ensue continuous fever, emaciation,
sweats, drawn face, and general oedema. We resort to detergent washes,
with salicylate of sodium, of tincture of iodine, very diluted, yet the
patients get worse and the tubes become obstructed. There is not
sufficient free flow of the contents of the chest.

Pleurotomy.--We naturally shrink from freely opening the chest. It is
right to try the simpler methods--aspiration, tubes to remain in the
chest, drainage, use of syphons--but we are forced in many cases of
chronic empyema to use pleurotomy, the thoracotomy of Bowditch, the
operation of l'empyème of the ancients. It consists of a wide opening
into the thorax between two ribs, permitting the escape of the effused
liquids. If the orifice is large enough, we can remove from the cavity
of the pleura not only the pus, but the large fibrous masses,
gangrenous débris, hydatids, and putrefying material which produce
septicæmia and death. The literature of this subject shows that bad
results have ensued from this operation, and again and again it has
been abandoned, but now that we can, by means of large openings, freely
wash out the cavities, and can apply injections of antiseptic and
alterative medicines to the suppurating surfaces, many lives are saved.
Hippocrates' dogma as to the danger of free and rapid evacuation of pus
had often a dangerous influence in preventing a thorough emptying of
the sac. The object of this radical operation must be kept in view--to
evacuate the pus by a free current, to permit the discharge of plastic
products and organic débris, and to allow easy and frequent washings
with healing and purifying injections. By these means we arrest
suppuration, obliterate the sac, and allow the lung to expand. For this
purpose wide orifices should be boldly made. They should be made where
the chest bulges most, but not always at the most dependent portion.
Ordinarily, the eighth intercostal space, somewhat behind the posterior
axillary line, has been the one selected, because it has been supposed
that thereby the cavity could be most effectually drained. The author
has usually punctured higher, in the seventh intercostal space on the
left and in the sixth on the right side, for the fifth and sixth ribs
being more fixed, there is less danger of subsequent approximation. We
cannot always determine the exact position of the diaphragm. The lung
may be bound down by old adhesions to the diaphragm, and thus the
latter may be injured by too low an incision; we can, moreover, better
adapt the position of the patient to enable the matter to flow out from
a higher orifice. Cases have occurred where the liver has been
perforated on the right side by low punctures. In health the uppermost
point of the diaphragm may be as high as the fifth space on the left
side or the fourth space on the right. The cure does not depend upon
the exact position of the puncture, because we expect to insert a
mouth-tube to keep the orifice open, and probably resort to washings.
It is not by its weight only that we expect the fluid to escape;
incessant movements of the thorax assist in forcing the fluid through
the tubes. Marshall[160] urges the fifth space on the right side, and
as near the weak point of the chest under the nipple as possible. On
the left the pericardium must be carefully avoided. He advises that the
operation should never be lower than the sixth or seventh intercostal
interval. Douglass Powell prefers a lower puncture, in the seventh or
eighth space in the posterior {557} axillary line. In the punctures
lower down the tube as it ascends rubs upon the diaphragm and protracts
the healing, and the orifice closes too early. The emptying of the sac
and the washings can be thoroughly attended to higher in the chest. The
weak point selected by nature for empyema necessitatis ought always to
be examined to see if there be any thinning of the wall, for if that be
the case, the puncture should be made there. The incision should be
made on a plane somewhat below that of the aponeurotic and muscular
portions of the chest, to prevent the liquids from infiltrating into
the subcutaneous cellular tissue. If we ascertain first by exploratory
puncture that there is pus lower down, it is safe to operate at that
point. The exterior orifice should be wider and larger than the
interior, and not parallel with it, in order to avoid the gaseous
infiltration in the tissues by the respiratory movements. Care must be
taken that the bistoury should pass close to the upper border of the
inferior rib, to avoid the intercostal artery. In making the
incision--about 6 centimeters in length--should the artery be cut, it
can easily be remedied by torsion. We raise the skin, and thus make a
flap over the orifice. The bistoury should not be introduced with one
cut through the soft textures, as recommended by Woillez, but layer by
layer should be cut through. This secures avoiding the intercostal
artery, and gives a larger exterior than interior cut, thus preventing
danger of liquid infiltration. We can be guided by the index finger,
and feel the textures as we cut down upon them. Under a continuous
spray to thoroughly purify the air that may enter, a free opening
should be made large enough to allow the finger to be introduced. As
air enters the fluid contents escape through the orifice, protected by
antiseptic dressings of gauze, oakum, and salicylated cotton. At first
it is well to remove the dressings containing the pus twice daily;
later, once daily will be sufficient. The orifice must be kept patent
by a short, wide tube with a fine wire around it. We can thus, by
changing the position of the patient, get rid of the contents of the
chest cavity. If there should be fetidity, it is desirable to use
washes of warm water first, and afterward of feebly-alcoholized
water--a solution of salicylate of soda, chlorinated soda, or
permanganate of soda. Cabot[161] had most success in the use of sol.
chlorinated soda, one part to twelve or fifteen of water, for purposes
of injection. The average time that the tubes remained in, with his
cases, was only twenty-four days. His favorable results he imputed to
the mechanical action of the india-rubber covering over the antiseptic
dressings.

[Footnote 160: _Loc. cit._]

[Footnote 161: _Loc. cit._]

Resection of Ribs.--The ancient operation of resection of ribs, dating
back to Celsus, is strongly advocated by Pietavy, Thomas of Birmingham,
Lane, and other modern writers as affording the best means of
thoroughly evacuating the pleural cavity of its purulent contents and
of keeping up constant drainage. John Marshall[162] reports 4 cases
where he resected the ribs to make permanent openings. In all of these
cases the walls became gradually firm and new bone was formed. He
concluded that the removal of a portion of one rib was not sufficient,
but that a large space through four ribs is the proper size for the
opening, that the sixth rib is the essential one to deal with, and that
from one and a half to two inches of bone should be taken away. In one
case he performed a subcutaneous division of costal cartilage with a
view to weakening the thoracic walls and allowing them to fold in. A
number of cases are reported of resection of ribs, with varying
success, by Ewald,[163] Taylor, House,[164] and Thomas.[165]
Taylor[166] advises the removal of the periosteum to prevent the rapid
re-formation of bone. If after the puncture the rigidity of the ribs
seems to keep up the discharge, and the lung does not expand to meet
the rib, a resection of a considerable portion of two or three ribs may
be {558} made for relief. If, again, in the progress of the case the
adjoining ribs have fallen in and have approximated, and thus become a
source of pain in retaining a permanent drainage-tube, a portion of rib
may be resected. The principal object of resection of ribs is to favor
their falling in, for a sufficient orifice can thus be made between the
ribs for the discharge. The upper two-thirds of the breadth of a rib
may be trephined in order to give more room for exploration,
evacuation, ablution, and prolonged drainage. This is the operation of
Esthander,[167] who thus treated successfully 5 of his 6 cases operated
upon. Fenger of Chicago[168] operated in this manner on fourth, fifth,
and sixth ribs.

[Footnote 162: _London Lancet_, March, 1882.]

[Footnote 163: "Med. Soc. Berlin," _Lon. Med. Rec._, 1876.]

[Footnote 164: _London Med. Record_, Aug., 1876.]

[Footnote 165: _Trans. Clin. Soc._, vol. xiii.]

[Footnote 166: _Brit. Med. Journ._, Feb., 1881.]

[Footnote 167: "Resection du Côltes de Emp.," _Revue Mens. de Méd. et
Surg._, 1879, vol. B.]

[Footnote 168: _Med. News, Philada._, Sept., 1882.]

Jacobi[169] says that resections ought not to be practised upon
children. W. A. Lane,[170] from the observation of 5 cases of empyema
in children, strongly recommends that a portion of rib or ribs be
removed at first, and the cavity thoroughly drained from the beginning.
It assists, he argues, the cure by promoting the falling in of the
ribs, the expansion of the lungs, and the ascent of the diaphragm. In
children the difficulty in securing free drainage is that the spaces
between the ribs are small, and after the cavity is opened they become
much more contracted; soft tubes thus become compressed, and hard tubes
cause much local irritation. Resection of ribs enables the operator to
keep the orifice open and have perfect drainage. The opening should be
large enough to allow the introduction of the finger and of an
india-rubber tube of sufficient diameter to give free passage to the
contents of the chest, without the tube being displaced by movement of
the ribs. In only one of Lane's cases was trouble caused by rapid
increase of bone. He operated as low as the ninth intercostal space in
the axillary line, taking care always, by the hypodermic syringe, to
ascertain that there was pus at that point. He divided the periosteum
longitudinally, and removed with cutting forceps about three-quarters
of an inch of rib. After he had thoroughly cleared out the cavity he
introduced a short india-rubber tube, so that its inner end should not
project into the cavity. Wire sutures were passed deeply through the
intercostal tissues and tube, and, to render the position of the tube
more secure, soft pins were fixed through the wall of the tube, and
attached to them were pieces of elastic surrounding the chest.

[Footnote 169: _N.Y. Med. Record_, Jan., 1881.]

[Footnote 170: _Guy's Hospital Reports_, vol. xli., 1882.]

If necessary in order to have uninterrupted free drainage, children as
well as adults should have their ribs resected. The important point in
operating is to secure free exit to the fluid and purification of the
cavity by the necessary washings by the open method. Pleurotomy by
resection of ribs is almost universally acknowledged to be the most
effective treatment, for it promotes most rapidly the agglutination of
the pleural surfaces and the expansion of the lung.[171]

[Footnote 171: Lawson Tait strongly advocates this same method of
treatment in peritonitis. He has performed laparotomy successfully in
20 cases, using washings and drainage-tubes (_Bost. Med. and Surg.
Journal_, Aug. 16, 1883).]

Good drainage is the essential consideration after the operation. We
must prevent putrefaction or fetid decomposition in the pleural
contents. So long as pus is retained within the sac, it does not
putrefy, but putrefaction follows contact with the putrefactive
agencies which abound in ordinary air, as shown by Pasteur and Tyndal.
These are solid particles floating in the atmosphere. Although air must
be admitted, it should be rendered aseptic. The drainage-tube, which
should be just long enough to go thoroughly into the cavity, by itself
is in many cases insufficient. The upper part of the cavity may retain
on its surface pus and flocculi which may prove dangerous. By the
syphon we can fill the cavity slowly with medicated tepid water without
shock and {559} without risk of tearing away the neo-membranes.
Woillez[172] advises that pleurotomy should be promptly used whenever
pus is found. Béhier advocates the same treatment. E.
Moutard-Martin,[173] whose authority is high from his great experience
and conservatism, advises us always to commence the treatment with
thoracentesis by aspiration. He says, if the fever persists and the
general condition grows worse, he does not hesitate to resort to
pleurotomy. The author's more limited experience coincides with his. I.
Marshall[174] states as his opinion that purulent pleurisies require
the immediate or early adoption of the open method. In fibro-serous
pleurisy we wish to restore the physiological condition of the pleura,
whereas in purulent cases the object is to obliterate the sac by
adhesions throughout the surfaces, just as abscesses are cured. It is
necessary that the costal and pulmonary pleura and that of the
diaphragm should be brought closely in contact. This is produced
simultaneously by the dilatation of the lung and the diminution in
every way of the pleural cavity. The dilatation is produced by the
disappearance of the intra-pleural pressure and the pressure in the
opposite direction from the bronchial surfaces. This last depends upon
the condition of the lung and of the visceral pleura. If the lung has
been long compressed, it is almost carnified and reduced to a state of
foetal atelectasis. It rarely happens that the bands which bind the
lung down do not in time undergo granular fatty degeneration and
disappear. This enables the lung to expand, if not to its original
size, yet sufficiently to occupy the cavity, reduced in size by the
approach of the walls. The heart, which previous to the operation was
thrown more or less out of its normal position, comes back from the
empty side, and often passes the position that it normally occupied.
The lung follows the heart. The whole mediastinum finds itself altered
in its position and in its contents. The depressed diaphragm rises
promptly to its old position in the pleural cavity. The liver, spleen,
and the rib-wall undergo striking modifications. We do not expect the
lung to dilate to its full extent, as after aspirations in simple
pleurisies. The lung, indeed, is already impaired in its movement. We
admit air in order to secure treatment to these surfaces. When air is
admitted into the normal chest, the lung is retracted to about one-half
its size. In serous effusions we fear free admissions of air, because
it assists in compressing the lungs, and may contain germs which
promote suppuration. We must bear in mind that we may have double
pleurisy from the pus producing pleural necrosis at the point of
contact of the pleural sacs about the middle of the sternum opposite
the middle of the third rib. Elsewhere there is no such danger, for the
pleural surfaces remain a long distance from each other.

[Footnote 172: _Bul. Soc. Méd. des Hôp._, 26 April, 1872.]

[Footnote 173: _Pleurisie purulente_, 1872.]

[Footnote 174: _Loc. cit._]

Why should we postpone pleurotomy, with or without resection of ribs,
until we have used the drainage-tube, canula, etc.? The impression is
that this operation is attended with danger, whereas ordinarily, with
care, such is not the case. In pleurotomy there is not the same danger
of serious accidents as in thoracentesis, especially as performed by
canulas and trocars. Pleurotomy never causes acute oedema of the lung.
The forcible unfolding of the lung, with rush of blood to vessels that
have been almost emptied by compression, does not occur under these
circumstances. After the large openings of the chest the causes of the
forced expansion of the lung do not exist. The diminution of the
pressure on the mediastinum, the re-establishment of the thoracic
aspiration, and consequently the more free access of venous blood into
the right heart, favorably influence the general circulation. The pulse
increases in force, the cyanosis is dissipated, frequently within a few
hours, and the anasarca disappears in a few days.

Theory and observation show beyond a doubt that in all cases where
{560} there exists a decided intra-pleural tension pleurotomy of the
thorax modifies efficiently the circulatory and respiratory functions.
Instead of causing suffocation, it diminishes almost always, and that
instantly and remarkably, the dyspnoea. In 1868, Maisonneuve[175] made
the startling announcement, which he claimed was nevertheless rigidly
true, that of 100 patients who die after surgical operations, 95 are
poisoned by organic substances absorbed. He claimed that the liquids
exuded from the surface of wounds become corrupt when exposed to the
external air, and that subsequently they undergo morbific changes and
become formidable poisons. If, he said, we can prevent the dead liquids
from putrefying, the gravest operations could be performed without
danger. No one who studies the results of empyema in the past can
question that the greatest danger is from the blood-poisoning known as
septicæmia, caused by the absorption of the septic infection by the
lymphatics.[176] No matter what may be the nature of septicæmia, it is
sufficient that the vast surfaces of the pleura produce certain
prurient secretions, which, when absorbed and carried into the
circulation, cause hectic fever with its results. We claim that there
is less danger from putrid absorption when free incisions are made than
from those only large enough to introduce a drainage-tube. Rome[177]
collected 49 cases, but of these 10 contained fetid pus; 9 of the
number had been treated by one or many, even up to fifteen,
aspirations. He concludes that the surgical interventions, other than
pleurotomy, provoked in the purulent liquid of the pleura putrid
fermentations in one-fifth of the cases. The products of this
fermentation irritate actively the serous membrane, and cause an
abundant suppuration intractable in its nature, and there is imminent
danger of rapid exhaustion and hectic fever. One-third of Rome's cases
contained solid pieces which could not be removed in any other way than
by making free incisions. Although subserous cavities are not perfectly
analogous to phlegmonous abscesses, yet they closely resemble each
other. Histologically, the inflammatory process and its phases are the
same, but there is this difference--absorption of the deleterious
products is more active. Why allow a warm abscess to be transformed
into a cold abscess, which will open later spontaneously after having
caused grave disorders? We have seen how frequently large collections
of pus sooner or later open either through the lung or through the
chest-walls. If an opening has to be made, the more promptly the
better. In the first stage, especially in acute purulent pleurisy, the
slight neo-membranes and fibrinous deposits, barely solid, readily
undergo granular fatty degeneration, and are absorbed if relieved of
the pus. In this stage the two folds of the pleura are in their best
condition for becoming adherent to each other, and by obliteration of
the pleural cavity to end the disease. If acute empyema be treated
early and gently before the lung is compressed or injured, with free
opening and constant drainage, the patient being in a recumbent
position on face or side, the pleura needs no washings. The orifices
made spontaneously are frequently insufficient to completely empty and
to keep up the current of pus as it forms. In bronchial fistula, unless
the air is prevented from coming from the lung into the pleura by a
valvular opening, we have frequently to resort to pleurotomy. If in
empyema necessitatis the orifice partly closes or is not free enough,
we must not hesitate to enlarge it or make a counter-opening to enable
the matter to flow out. In tubercular pyo-pneumothorax, where the
purulent fluid has been the primary lesion and has perforated the lung,
the operation is not indicated. E. Moutard-Martin's treatise was
founded upon 17 subjects, 5 of whom died and 12 were cured. Of the 12
cured, 2 had bronchial fistula in pneumothorax without any sign of
tubercle; 5 had permanent fistulous openings and discharged {561}
occasionally a few drops of pus; 7 were cured without fistula.
Blake[178] reported 19 cases treated by permanent openings, with 15
"cured and much relieved." He operated by making incisions from one to
two inches long, parallel with the ribs, between the seventh and eighth
ribs, a little inside of the scapula. His practice was to keep the
orifice open. He used either a spiral wire covered with gutta-percha or
a gum-elastic catheter fastened to a shield and kept in position by
adhesive plasters. Martin Oxley[179] by pressing open the incision with
a pair of dressing forceps introduced a silver or india-rubber
tracheotomy-tube to keep the orifice open. He related several instances
where pieces of tubing fell into the cavity and remained there without
injury for months, and in one case as long as several years.
Dabney[180] urges with force the importance of our having a continuous
discharge of pus as far preferable to its daily removal, "not only
because it seems less liable to become fetid, but because, as the two
surfaces of the pleura have to come together and heal by granulations,
the retention of pus would delay this process by keeping the costal and
pulmonary surfaces apart." Thorough drainage by two orifices or a wide
incision kept open by two tubes is more effective than a simple
drainage-tube. Antiseptic precautions are essential to ensure success
at every stage of the operation.

[Footnote 175: _London Prac._, 1868.]

[Footnote 176: Ranney, _Annals of Anat. and Surgery_, 1881.]

[Footnote 177: _Thèse de Paris_, 1882.]

[Footnote 178: _Boston City Hospital Reports_, 2d series.]

[Footnote 179: _Liverpool Medico-Chirurg. Journal_, January, 1882;
_N.Y. Medical Abstract_.]

[Footnote 180: _American Journal Med. Sciences_, Oct., 1882.]

Value of Injections and Washings.--The object of injections is to
enable us thoroughly to wash out the cavity and to promote adhesions
between the pleural surfaces. The chief danger being from septicæmia,
it is of the greatest importance that the pus should not be allowed to
remain in the cavity longer than can be avoided. The body-temperature,
taken twice daily, is one of the best means of ascertaining the extent
of the re-formation of pus. Stagnant pus, mingled with air, will
undergo fermentation and cause putridity; hence the great value of
incessant drainage through unobstructed tubes. When the pus is free
from unpleasant odor and runs freely, it is not necessary to use
washings or injections of any kind, for the cavity will purify itself.
Washings and injections have sometimes been found very injurious and
irritating, and sudden deaths have been attributed to them. If flocculi
form, washings of tepid water with a very small percentage of alcohol
or of salicylic acid (1 per cent.), used without force for fear of
rupturing some of the recently-formed capillaries, are useful. When
modifying injections are used, the patient ought to lie on the opposite
side. In this way all the diseased parts are reached by the fluid. An
ordinary syringe should not be used, but a Thudicum bottle or a
fountain syringe: either of these can be raised sufficiently high to
allow a gentle flow into the cavity. If the discharge becomes fetid,
injections of solution of permanganate of potash (1 or 2 grains to
ounce j) or of tinct. of iodine (1:4) in water ought to be used. The
author has never seen any results of poisoning from the use of carbolic
acid, but he has always used a feeble solution, 2 or 3 per cent. Dabney
had symptoms of carbolic-acid poisoning in one of his cases where he
used a 2 per cent. solution, notwithstanding the fact that he had taken
every precaution to ensure its prompt return. A. T. Cabot[181] mentions
a case of carbolic poisoning in a boy four years of age produced by a
feeble solution of one part to thirty of water used only to cleanse the
instruments, tubes, and hand of the operator. Kuster's[182] experiments
show that anæmia and septic and pyæmic fevers predispose the system to
carbolic-acid poisoning. He recommends an 8 per cent. solution of
chloride of zinc. Chlorate of potassium drachm j to pint j has been
used with benefit. The medical journals contain so many reports of the
serious, and even fatal, results from absorption of carbolic acid when
thrown into abscesses {562} that we are compelled to abandon it in
favor of other injections. B. W. Richardson long since showed the great
value of iodine as a disinfectant. It not only corrects the fetor of
decomposed pus, but at the same time lessens the secretion from the
walls. The first injections should be weak, gr. 4 or 5 of iodine and
iodide of potassium to a pint of water. Liq. iodinii com., ounce ss to
ounce iv, ought not to be used until the surfaces have become
accustomed to the action of iodine. Injections of medicated fluid ought
not to be used unless they are absolutely necessary, because in some
instances they have produced fainting attacks and epileptiform seizures
with alarming convulsions. These results have followed injections of
different fluids--borax, carbolic acid, iodine, permanganate of
potassium, and even warm water. Similar phenomena have followed the
injection of the bladder, the uterus, and even from passing a catheter.
The shock may have been too sudden or the injection too forcible or the
fluid too cold. A. L. Mason[183] suggests that it is probably owing to
sudden irritation of the lymphatics through the great splanchnic nerve,
with anæmia of the brain. Paralysis of the limbs after convulsions
makes the theory of embolic origin probable. These accidents must not
make us underrate the great value of frequent washings with injections
when rendered necessary by the approach of putrid infection. The number
of these washings should depend upon the urgency of the symptoms, and
antiseptic injections should not be employed unless we find evidences
of fetor, because of one great objection: they do not favor the
expansion of the lung.

[Footnote 181: _Loc. cit._]

[Footnote 182: Quoted by Dabney, _loc. cit._]

[Footnote 183: _Boston City Hospital Reports_, 2d Series.]

Cases of long-standing compression of the lung could hardly result in
complete re-expansion, but the general health will be recovered and the
chest, contracted by approximation of the pleural surfaces from the
walls being pressed in or ribs resected, will cease to secrete pus. If
fever persists, with diarrhoea, sweats, emaciation, and fetid
suppuration, it shows that the washings are not sufficient in number.
They can be repeated as often as every three or four hours, to be
decreased in frequency as the patient improves. Under frequent washings
Feyrot[184] reports favorable results in almost hopeless cases. Time is
very precious when these symptoms of exhaustion or septicæmia set in,
as it is of the utmost importance that we should endeavor to prevent
promptly the absorption of the putrid products, the inevitable effects
of which are to produce, before long, fatty and amyloid degeneration of
the principal viscera. The most effective way of using detergent fluids
is by syphons through two tubes perforated at their extremities and
fastened with shields. A Thudicum douche-bottle or a fountain syringe
can easily be used by patients themselves as often as is required. The
orifice and the tubes should be protected by thorough and rigid
antisepticism. As the case improves the cavity gradually gets smaller,
the two pleuræ become adherent, and the quantity of fluid lessens until
only a small amount flows out. Every eight or ten days we carefully
draw out the tubes by degrees, until we have only a little canal
beneath the walls. We can thus let the orifice heal slowly, for the sac
is obliterated and the patient cured.

[Footnote 184: _Thèse de Paris_, 1876.]

In the hands of Boyer, Delpech, Dupuytren, and Sir Astley Cooper the
bistoury gave bad results, but as now used, with all modern appliances
and antiseptic precautions, it affords infinite relief and many cures.
We claim that by early pleurotomy, with Listerism scrupulously used at
every stage of the operation, and if necessary with detergent washings,
the mortality from this extremely grave disease can be very materially
lessened.


Double Pleurisy.

Pleurisy may occur on both sides at the same time. Double pleurisies
are secondary, not primary, and result from rheumatism, or still more
frequently, {563} according to Louis, from tuberculosis. In 150 cases
of pleurisy quoted by him, there were no bilateral cases which were not
produced by rheumatism, gangrene, or tuberculosis. A double pleurisy in
a previously healthy person creates a strong suspicion of tubercular
origin. There is generally an interval of some days before the attack
of one side is followed by that of the other. When effusion takes place
the dyspnoea is very great. Death is imminent unless the fluid is
withdrawn by aspiration. Maintenon[185] states that the inflammation
may be so intense and the fever so high as to destroy life before the
effusion is thrown out. The physical signs are the same as in
unilateral cases. The effusion is never so great on one side as on the
other. The progress of disease is rapid, and the result is almost
always fatal.

[Footnote 185: _Thèse de Paris_, 1873.]


Diaphragmatic Pleurisy.

The serous lining of the upper surface of the diaphragm may be involved
in an ordinary pleurisy, or inflammation may be limited to it without
involving either the pulmonary or the parietal membrane. In this latter
case we have modifications of the characteristic symptoms and physical
signs. Functional disturbances and special symptoms enable us to
diagnose it. There is a febrile movement with occasional delirium, and
some of the prominent symptoms, but without the physical signs to
indicate the exact locality. The pain is intense, and dyspnoea exists
even to the extent of orthopnoea and respiratory anguish, the
respiration jerky and convulsive. The pain comes on suddenly in one of
the hypochondriac regions, extending up to the attachments of the
diaphragm to the costal surfaces. The pain is intense, and increased by
full inspirations, by physical efforts, by vomiting, and even by the
eructations of wind. The position of the patient attracts attention: as
he sits with the trunk inclined forward, he has an anxious and
distressed expression of countenance, sometimes accompanied by nausea
and vomiting with singultus. Pressure elicits a characteristic
tenderness; if applied under the false ribs, it causes suffering. The
phrenic nerve is painful on pressure practised over the accessible
points of its course, between the two inferior bands of the
sterno-cleido-mastoid at the base of the neck. There are also painful
irradiations in the cervical plexus above the clavicle and in the
scapular region. Pressure over a circumscribed spot of the epigastric
region causes a sharp agony of pain. This point is at the intersection
of two lines--one, the external border of the sternum; the other, at
the osseous portion of the second rib. Guéneau de Mussey[186] has named
this the diaphragmatic bottom. This pain extends sometimes to the
vertebra and upward to the first intercostal space. Auscultation and
percussion at the base of the lung give us some results: impaired
expansion of the lung at the base and dulness on percussion; the
diaphragm is in a great degree immobile, owing partly to the pressure
upon it, and partly to a paresis from inflammation of its upper serous
covering (Stokes[187]). When the inflammation is on the right side, we
may find an icteroid tint, with vomiting, delirium, etc., with the
liver pushed below its normal position in the abdomen. The inflammation
of the pleural covering of the diaphragm may be caused by
sero-hepatitis extending through the diaphragm (Copeland[188]).

[Footnote 186: _Archiv. de Méd._, 1879, vol. ii.]

[Footnote 187: _Dis. of Chest_, 1837.]

[Footnote 188: _Dict. Med._, vol. iii., edited by Lee.]

If the effusion is confined to the space between the lung and
diaphragm, the diagnosis is obscure. There may indeed be cases where we
have but few of the symptoms already mentioned. If the fluid is not
confined to this portion, but flows into the pleural cavity, it gives
great relief, and the result is favorable. Diaphragmatic pleurisy may,
however, end in death, either by its discharge into the peritoneal
cavity or by constitutional disturbances.


{564} Interlobular and Mediastinal Pleurisies.

The effusion is sometimes confined by adhesions between two lobes. The
mediastinal variety is situated between the pleural boundary of the
mediastinum and the adjacent portion of the pulmonary serous membrane.
It is but rarely met with, and may be diagnosed by local symptoms. The
flatness on percussion in the interlobular variety is very
circumscribed. Both forms cause local pains, but in the mediastinal
variety the pain is very deep and perceptible at the middle of the
sternum, and is increased by the respiratory movements. In both
varieties there is more or less fever. If either variety exist on the
left side, the condition of the pericardium must be carefully examined,
as pericarditis may be confounded with it. These limited collections of
fluid may burst into a bronchus and be expectorated.


Multilocular Areolar Pleurisies.

Multilocular encysted collections of fluid in the pleural cavity are
due to the partitions made by pseudo-membranes which divide the pleura
into subcavities. These occur generally in subjects who have had
previously dry or adhesive pleurisies. They are more serious than
ordinary pleurisies. We meet with them in aspirating, when, after
draining off the fluid from the base of the pleural cavity, we find the
lung expanding, but above that point there is absence of respiratory
murmur and of other physical signs indicating the presence of fluid.
Reybard[189] divides multilocular pleurisy into three varieties, with
varying symptoms and physical signs, according to whether it exists at
the upper, middle, or lower portion, right or left side. Owing to the
thickness and distribution of neo-membranes, it is frequently difficult
to localize the points of collections of fluid. Aspiration is the most
accurate means of ascertaining the exact point and extension of the
effusion.

[Footnote 189: _Bullétin Acad. Méd._, 1879.]


Rheumatic Pleurisy.

HISTORY.--The recognition of the fact that we can have local
manifestations of rheumatism in the texture of the lung itself, of the
bronchi, and of the pleura is of comparatively recent date. There had
been indefinite, loose statements, or rather suggestions, in some of
the writers in the early part of the century, such as Chomel and
Andral, as to the possibility of rheumatism appearing in the pulmonary
textures; but we believe that the first definite description of the
disease was made by T. H. Buckler of Baltimore in 1865.[190] He claimed
that the white fibrous tissue of the bronchi could be the seat of
rheumatism, as well as similar textures about the joints. He
illustrated his views by cases observed and reported by himself. He
showed how, as a result, there were symptomatic engorgements, more or
less solid, of the pulmonary parenchyma or rheumatic pneumonia. In
1854, Black[191] found crystalline particles of uric acid and of urate
of soda deeply imbedded in the thin white fibrous tissue of bronchi.
Buckler showed the metastatic character of rheumatic inflammation in
the bronchi and lungs as elsewhere. Buckler's subsequent papers[192]
published in connection with this subject, show remarkable success in
treatment of fibro-bronchitis and rheumatic pneumonia based upon his
views of their pathology.

[Footnote 190: _Fibro-Bronchitis and Rheumatic Pneumonia_.]

[Footnote 191: _Edin. Med. Journal_, 1854.]

[Footnote 192: _Boston Med. Journal_, 1882, and _Amer. Med. Journal_,
Oct., 1882.]

SYMPTOMS.--We find rheumatic pleurisy coming on in the course of {565}
rheumatic fever with the characteristic mobility of the points of
inflammatory action. Laseque[193] gives the symptom with accurate
details--the acute pain in the side of the chest without cough or
expectoration. He describes the pain as differing from that of ordinary
pleurisy, in that the extent of pain is greater and not so limited, due
to the fact that the rheumatism invades the aponeurotic tissue which
forms the covering to the intercostal muscles. It persists longer and
is wider spread. The dyspnoea is caused by the inability to move the
respiratory muscles and by the disease invading the aponeurotic centre
of the diaphragm.

[Footnote 193: "Pleurésie rheumatismale," _Arch. Gén. de Méd._, 1873.]

The rapidity of the inflammation causes the sudden pain and the
accompanying effusion in even a few hours. In a well-defined case
recently seen by the writer in a lady forty-seven years of age the
rheumatism literally jumped from a large joint to the pleura, giving
rise to a severe pain, without cough or expectoration, with an increase
of 2° of temperature and 20 beats of pulse. There was a moderate
effusion. In forty-eight hours, under the influence of an initiatory
dose of quinine (20 grains), followed by free doses of salicylate of
sodium, the attack subsided and the friction sound at the base of the
lung disappeared. This case did not follow the rule mentioned by
Senx,[194] that the disease, upon leaving the pleura of one side,
appears in the same manner on the other. It sometimes goes to the
pericardium and endocardium from the pleura. Chomel[195] insisted upon
the frequent examination of the heart to ascertain whether this had
occurred.

[Footnote 194: _De la Pleurésie rheumatismale_, Paris, 1878.]

[Footnote 195: _Art. Pleurésie Dict._, in 30 vols., 1842.]

Rheumatism of the pleura does not always appear and disappear suddenly.
It sometimes is gradual in progress and slow in recovery. It usually
occurs when we have manifestations elsewhere, but the pleura may be the
point first attacked, as is more frequently the case in pericarditis.

DIAGNOSIS.--The diagnostic signs are hereditary or personal tendency to
the disease, the character of the local pain, the mobility of the
disease, violence of pain and its rapid disappearance, and the
existence of profuse sweats. Suppuration rarely occurs.

PROGNOSIS is in its nature serious, not from the intensity of the
disease, but from its being a visceral rheumatic affection. It is,
moreover, frequently double, and may recur often in the same subject.

TREATMENT is that of rheumatism elsewhere--salicylic acid and its
salts, alkalies with opiates. Thoracentesis is rarely indicated,
because mechanically the effusion does not seriously impede
respiration: if the pericardium be involved, it may be necessary in
order to relieve the pleura or the pericardium.


Hemorrhagic Pleurisy.

DEFINITION.--Pleurisy complicated by hemorrhage. Hemorrhagic pleurisy
is the union of an ordinarily slight hemorrhage in the pleura with
inflammation of that membrane (Laennec).

ETIOLOGY AND PATHOLOGY.--These must be studied together, because the
pathology of the disease explains its etiology. While hæmothorax
designates hemorrhage into the pleural cavity without inflammation,
hemorrhagic pleuritis involves necessarily the idea of inflammation
accompanied by effusion of blood, whether this occurs before, during,
or subsequently to the inflammation. We cannot assign the name
hemorrhagic pleurisy simply because there may be slight red coloration
of the effusion. Microscopic researches have shown that all effusions,
even the simplest, contain more or less white and red blood-corpuscles.
The presence of a certain number of the red discs no more justifies us
in calling the pleurisy hemorrhagic than the presence of {566} the
leucocytes would entitle us to call it purulent pleurisy.
Dieulafoy[196] states that there can be from 500 to 4000 red globules
to the cubic millimeter without producing any coloration. They must
reach 5000 before they will really attract attention. He says, however,
that when the number of red corpuscles reaches 2000 the effusion is
"histologically hemorrhagic," because the presence of blood is
analogous to the state of engorgement or congestion of the first stage
of pneumonia or other phlegmasia, and constitutes a particular phase of
pleurisy which must produce purulent matter. The name hemorrhagic
pleurisy ought to be used when the number of red blood-corpuscles is
sufficient to enable us, by the unaided vision, to detect the presence
of blood. We may, however, find a fluid in the pleural sac which is red
and yet does not contain blood-discs, but their coloring principle, the
dissolved hæmatin. Jaccoud[197] designates this condition
pseudo-hemorrhagic pleurisy. Vulpian and Charcot explain the slight
discoloration by the presence of hæmatin crystals, which, having been
imbedded in the false membranes, escape into the flow of the chest.
Nolais[198] included both of these discolored effusions among the
varieties of hemorrhagic pleurisies: "Hemorrhagic pleurisies include
all those of which the liquid borrows the red coloring matter of the
blood." Moutard-Martin (R.)[199] divides hemorrhagic pleurisy into
three varieties: simple, as produced in simple, acute, or subacute
pleurisy; tubercular; and cancerous. Trousseau[200] considered all
hemorrhagic pleurisies as caused by cancer. Beigel[201] states
positively that in cancerous pleurisy the effusion is limpid with a
yellowish tinge. Walshe[202] held the same views. Nolais,
Moutard-Martin (R.), and Fernet satisfactorily demonstrated that such
is not the case, but that the hemorrhagic effusion may be simple and
independent of any organic disease. It may be produced by acute
inflammations of the pleura as well as by cancer of the lung or pleura.
It may be connected with pleuro-pneumonia or miliary tubercle. It
comes, although more rarely, from fevers, such as measles, and from
certain dyscrasiæ due to renal, hepatic, or even splenic lesions. When
hemorrhagic pleurisy follows hæmothorax, the blood, after remaining
liquid at least one or two hours, initiates the inflammatory action
which has, according to Ch. Nélaton,[203] for its object the encystment
of the clot. Cornil and Ranvier[204] claim that the cyst is caused by
the retracted clot, and that after absorption of the serosity this cyst
may become organized. The presence of air causes fetidity of the blood
and purulent pleurisy.

[Footnote 196: _De la Thoracentèse par Aspiration dans la Pleurésie
aigue_.]

[Footnote 197: "De l'Humorisme ancien comparé à l'Humorisme moderne,"
_Thèse de Concours_, 1863; _Gazette Méd._, 1860, quoted by Nolais.]

[Footnote 198: _Thèse de Paris_.]

[Footnote 199: _Thèse de Paris_, 1878.]

[Footnote 200: _Clin. Méd._]

[Footnote 201: _Reynolds's Syst. of Med._, 1871.]

[Footnote 202: _Dis. of the Chest_.]

[Footnote 203: _Thèse de Paris_, 1880.]

[Footnote 204: _Path. Anatomy_.]

We may have hemorrhagic effusions occurring simultaneously with acute
pleurisy, with pulmonary congestions, pneumonias, and apoplexy of the
lung. They are caused by the violence of the inflammation with local
plethora, producing a sanguinary stasis--a mechanical result of intense
congestion. Moutard-Martin (R.) states that in these cases the red
globules come through the walls of the blood-vessels, as do the
leucocytes, by diapedesis. Jaccoud[205] admits that the blood-vessels
are altered by the inflammation, perhaps also by the derangement in the
vaso-motor innervation. The tissue of the pleura is penetrated by both
red and white blood-corpuscles, and the blood-vessels and lymphatics
are dilated, red corpuscles being found in lymphatics. By far the
greatest number of hemorrhagic pleurisies are secondary to pleural
inflammations, either resulting from acute causes or from cancerous or
tubercular disease, or from diseases causing a dyscrasia of the blood,
such as nephritic diseases, hepatic, cardiac, scorbutic affections, or
alcoholic excesses. The secondary result of these pleurisies is the
formation of neo-membranes, fibrous {567} in their nature, which
pathological anatomy shows contain, as they become organized, abundant
blood-vessels with thin and brittle walls. A slight exciting cause is
all that is necessary to produce their rupture. The primary cause is
the false membrane, and, in some cases, vascular granulations, which
have rapidly formed, perhaps in twenty-four hours--conditions eminently
favorable to the production of hemorrhage. In cancerous, tubercular,
and dyscrasial conditions of the blood, the blood-vessels are
especially weak and easily give way, owing to the defective nutritive
properties of the blood itself, just as, in typhoid fever, we have
nasal and intestinal hemorrhage, and in typhus, petechiæ. In 200 cases
collected by Moutard-Martin[206] there was found intra-pleural effusion
in three-eighths of the cases. Only one-third of that number were
hemorrhagic. In 42 cancers observed between 1872 and 1876, 35 were
without pleural effusion, 1 only was hemorrhagic. M. Moutard-Martin
reports 34 observations of hemorrhagic pleurisy produced by cancer, 19
by tubercle, and 31 following simple pleurisy. Of these last there were
7 cases of effusion complicated with a pneumonia, 3 with a cirrhosis, 6
with a cardiac affection: all except 12 of these cases had some
complication. Most of these (12) recovered, so he had not the autopsies
to verify his diagnosis. Rayer[207] cites 4 cases of bloody effusion in
the pleura occurring in the course of a nephritis. Poutin[208] reports
1 in renal sclerosis. M. Natalis-Guyon[209] reports an epidemic of
measles where many infants died of hemorrhagic pleurisy. Marguerite
cites 13 cases complicating pneumonia, granulations, chronic pleurisy,
small-pox, etc.

[Footnote 205: _Clin. Méd._]

[Footnote 206: _Loc. cit._]

[Footnote 207: _Traité des Mal. des Reins_.]

[Footnote 208: _Soc. Clin. de Paris_, 1879.]

[Footnote 209: _Soc. Méd. des Hôpitaux_.]

Rilliet and Barthez[210] say that it is common to find in infants
considerable discoloration of effused serum in variolic and other
organic poisons. It seems fair to conclude that hemorrhagic pleurisy
may occur in a large number of cases where the blood has undergone
alterations, but to produce it, it is necessary that the pleura should
have been rendered vulnerable by pre-existing causes, because it
ordinarily resists, better than many other membranes, the hemorrhagic
tendency. If we admit the existence of tubercular or cancerous
hemorrhagic pleurisies, we ought not to consider those as simple which
are produced under the influence of the other causes that we have
mentioned. The tubercular granulations are deposited either on the
pleural surface or in the parenchyma of the lung near the surface, the
most frequent locality being in the thickest parts of the organized
false membranes. The rupture of their blood-vessels causes the escape
of blood into the pleural cavity. The effusion, more or less
discolored, rarely exceeds a liter in quantity. Effused blood from
cancerous origin may either come from rupture of the vessels in the
growths themselves by ulceration, or from the neo-membranes in their
vicinity.

[Footnote 210: _Traité des Mal. des Enfants_, t. iii.]

The primitive seat of the cancer is rarely in the pleura, but most
frequently in the lung, the cancer being of secondary formation arising
primarily from ganglions of the mediastinum. Hemorrhagic pleurisy may
be caused by laceration of the newly-formed blood-vessels in the
neoplasms by aspiration or by the lung expanding too suddenly. We
conclude that hemorrhagic pleurisy is generally owing, directly or
indirectly, to vascular neo-membranes which are produced in simple, in
tubercular, and cancerous pleurisies.

SYMPTOMS.--The symptomatology of this form of pleurisy does not differ
materially from that of other varieties. We cannot attach much
importance to the initiatory symptoms nor to the march of the disease.
If the quantity of blood be great, we must expect general weakness,
pallor, and even fainting. We may have oedema of the walls, as in
purulent pleurisy, and exceptionally in serous pleurisy. Ordinarily,
however, hemorrhagic pleurisy is more extensive, and limited to the
inferior part of the chest, owing to the interference with the venous
circulation. If cancerous in its origin, we shall have dyspnoea {568}
and violent intercostal neuralgia from pressure of the tumor. When the
effusion is formed in the pleural sac, the physical signs already
enumerated indicate its presence. Some authors, especially Fernet,
Moutard-Martin, Alcoud, and Guéneau de Mussey, attach considerable
significance to Bacelli's whisper-pectoriloquy as showing that the
effusion is not serous in character. Nolais questions this view, and
says that this sound ought to be heard whenever there is blood, whereas
they state it is heard only at the base or summit of fluid. When
hemorrhagic pleurisy results from tuberculosis, it is never from the
ordinary ulceration form, but always from the acute miliary,
non-ulcerating variety. We must not, therefore, expect to be aided in
our diagnosis by the progress and symptoms of pulmonary phthisis. We
may, however, detect uncertain, indefinite symptoms which are hard to
interpret as indicative of tuberculosis. The effusion is rarely
excessive in this variety, whereas when resulting from cancer it is
often very abundant and is rapidly reproduced.

DIAGNOSIS.--We may suspect the presence of hemorrhagic effusions, but
only by exploratory punctures can we arrive at certainty of diagnosis.
We must bear in mind that we may withdraw with the aspirator-needle
some drops of blood at its insertion and at the close of the
exploration from the highly vascular neo-membranes or from the lung
itself. Having ascertained the nature of the fluid, the differential
diagnosis must be made as to the cause, simple, tuberculous, or
cancerous. We must study the manner of access of the disease, and
especially ascertain if its invasion was violent, with a quantity of
blood (d'emblée), or whether it came from the neo-membranes. In the
simple variety there are the ordinary acute or subacute symptoms of
pleurisy, without any preceding symptoms. In cases of tubercular origin
we have to aid us a small quantity of fluid effused and the insidious
character of symptoms. In cancerous cases we must expect to find traces
of hereditary or of personal taint which may have affected the general
health. We must look for cancer elsewhere, and examine carefully to see
if there be any tumor of the mediastinum or intra-thoracic pressure, or
any infiltration of the lymphatic glands, especially above the
clavicle. The fluid drawn in the exploration ought to be examined
microscopically, for we may detect evidences of cancer. Walshe[211]
cites a case where encephaloid débris was thus discovered. Other
authors also give similar cases.

[Footnote 211: _Diseases of the Chest_.]

PROGNOSIS.--This depends upon the nature of the disease producing it.
When caused by the newly-formed membranes connected with simple serous
pleurisy it is ordinarily not serious, for the mere presence of blood
in the pleura has no bad influence over the restoration of health. It
is more the intensity of inflammation, with the quantity of blood
effused, that indicates gravity of prognosis. Dieulafoy[212] considers
the prognosis as unfavorable in the hémorrhagie d'emblée form, drawing
the distinction between this and the histologically hemorrhagic. He
thinks that every purulent pleurisy was at first hemorrhagic, and the
presence of pus shows greater intensity of inflammation. Homolle[213]
also states that the pleurisies rich in red globules are ordinarily
very acute, and, in consequence of that fact, predisposed to purulence.
Purulency is not the sole cause of danger. We fear compression of the
lungs, and still more septicæmia. In the tubercular and cancerous forms
the prognosis must be very serious. When the hemorrhagic pleurisies
arise in the course of organic diseases of the heart, kidney, and
liver, they are of grave import.

[Footnote 212: _Loc. cit._]

[Footnote 213: _Rev. des Sci. Méd._, 1880.]

TREATMENT.--If the quantity is excessive, local applications and ergot
ought to be employed to arrest the flow. If the dyspnoea and oppression
are great, it is best to draw off at least some of the fluid. If the
quantity be not large enough to embarrass respiration, we must expect
nature to absorb {569} it, or by local inflammation to encyst it.
Lacaze[214] reports a case where a fistula was established, and the
case was cured. Dieulafoy gives another case where six punctures were
made, and no less than 6 liters, in all, were withdrawn. He injected
afterward a solution of 4 grammes of sulphate of zinc to 400 grammes of
water, and the patient was cured. In the first stage of the disease we
use palliatives--morphia hypodermically, bromides, and chloral--if
indicated. During febrile symptoms of acute cases we refrain from
withdrawal of fluid unless it is excessive. The question of
thoracentesis has been discussed in regard to simple pleurisies. The
same rules apply, a fortiori, when the nature of the fluid is
hemorrhagic. Ordinarily, the abundance of fluid, and the dyspnoea which
results therefrom, indicate the operation. We prefer not to draw off
the fluid completely--only enough to relieve the embarrassment of
respiration--because we destroy the equilibrium of pressure on one side
against the neo-membranes and the compressed lungs on the other.
Congestion of the lung may thus be produced with albuminoid
expectoration. Moutard-Martin (R.) coincides with Dieulafoy in limiting
the amount to be withdrawn to one liter. Of course the fluid is slowly
aspirated. After part of the fluid is withdrawn, what remains is
absorbed, remains stationary, or increases in quantity. We repeat the
operation, and slowly draw off greater quantities of fluid if it
returns; especially in cancerous cases, where the effusion is often
very large, the operation gives great relief. It is rarely large enough
in tubercular cases to justify thoracentesis.

[Footnote 214: _Thèse de Paris_, 1851.]


Tubercular Pleurisy.

Tubercular pleurisy may be acute or chronic. It may occur during the
course of ordinary tubercular disease of the lung, by extension of the
disease from the lung to its serous covering, or it may proceed from
tubercular deposit on the pleura independently of any previous disease
of the lung. Acute tubercular pleurisy may be dry and situated at the
summit of the chest, or may be what is called accidental pleurisy. Dry
pleurisy is almost constant in tuberculosis of the lung. Its existence
is, in itself, a powerful presumption of pulmonary phthisis, especially
when it is situated at the apex. In tuberculosis pleuritic inflammation
is lighted up by slight and scarcely appreciable causes. Its
commencement is insidious, with little or no pain or fever: indeed, it
is with subacute symptoms that the disease slowly advances. The first
intimation the patient has of the disease is the impairment of his
breathing-power by the presence of fluid. The fluid is not generally in
large quantities, and is serous or sero-fibrinous, and sometimes
sero-purulent. Latent pleurisy of the older writers was frequently
tuberculous in its origin. This form of tuberculosis may precede or
follow the deposit of tubercles in the lung-tissue. The tubercles may
be deposited to a slight extent in the tissue of the lung, and their
presence is shown by an irritating cough only when the pleurisy
approaches insidiously. The tubercular granulations over the visceral
pleura are extended to the parietal surface also, and notably to the
circumference of the fibrous leaflet of the diaphragm--an especial
point of elevation for the secondary products.

This disposition of tubercular lesions of the pleura is one of the most
striking examples of what is called infection from contiguity, and is a
powerful proof of the infective property of tubercular products which
from an initial nucleus is propagated from point to point. Acute
tuberculosis of the pleura is one of the most common manifestations of
acute phthisis. It more frequently causes acute than subacute pleurisy.
Chronic tuberculosis almost always produces purulent pleural effusions.
It is much {570} more common in infants than in adults, and is
sometimes met with in children from three to ten years of age (Barthez
et Rilliet[215]). Tubercles may be developed in the intra- or
extra-serous membrane. Among old people the tubercle sometimes appears
first in the recent false membranes produced by pleuritis (as
associated with caseous pneumonia, or genuine tuberculous processes in
the lungs), or in connection with tubercles of other organs
(Fraentzel[216]). The advance of this disease is habitually slow, or at
least not accelerated by the development of other tubercular diseases.
The diagnosis is often accompanied with great difficulties, for the
disease may be confounded with chronic or with purulent pleurisy,
especially if these are developed in a tuberculous subject. In both
cases we have hectic, night-sweats, emaciation, etc. Thoracentesis
alone can give definite results when the effusion is in considerable
quantity. When suppurative pleurisy supervenes in tuberculous subjects,
the prognosis is very grave. Should the pus be sufficient in quantity
to embarrass respiration, it can be drawn off cautiously by aspiration.
The open method of drainage and free incisions should not be used, for
experience has shown that they injure instead of benefiting the
patients.

[Footnote 215: _Mal. des Enfants_.]

[Footnote 216: _Ziemssen's Cyc._, vol. iv.]


Hydrothorax.

From [Greek: hydôr], water, and [Greek: thôrax], the chest.

DEFINITION.--Dropsy of the chest. The accumulated fluid in the pleural
cavity which resembles the serum of the blood is not the product of
inflammation, but is caused by mechanical obstruction to the
circulation or by blood-poisoning. Hydrothorax is never idiopathic, but
invariably secondary, resulting from disease, not of the pleura, but of
the circulatory system or of the blood itself.

HISTORY.--Before pathological anatomy had been accurately studied,
effusions resulting from inflammatory processes in the pleura were
confounded with simple hydrothorax, which is not a variety of pleurisy.
Royer[217] and Laennec[218] divided hydrothorax into idiopathic and
symptomatic; Darwell[219] adopted in a great measure their views. They
did not draw the distinction between the passive transudation of serum,
constituting the condition known as hydrothorax, and exudations
resulting from idiopathic pleurisy. Before physical modes of exploring
the chest were used there was great uncertainty in the diagnosis of
collections of fluid in the pleural cavity.

[Footnote 217: _Dict. de Méd._, 1832.]

[Footnote 218: _Dis. of Chest_, Forbes's edition.]

[Footnote 219: _Cyc. Pract. Med._]

ETIOLOGY.--Dropsical effusion in the thorax is produced by the same
causes which give rise to collections of watery fluid in other serous
cavities and in the connective tissue, constituting general anasarca.
Primary among the causes is obstruction of the venous circulation in
the walls of the chest or in the lungs. Mitral disease, especially
insufficiency with dilatation, deranges the normal circulation in the
lung and its serous coverings, producing hyperæmia, oedema of the lung,
and finally serous effusions into the pleural sac. General dropsy
results. According to Fernet,[220] in dropsies resulting from mitral
disease oedema of the lungs and hydrothorax always precede all other
oedemas. Fraentzel,[221] on the contrary, states that it does not occur
until there is no longer any room for the transuded fluid in the deeper
portions of the subcutaneous tissues. Other diseases of the heart
produce hydrothorax. Whenever there is abnormally high venous pressure,
which invariably follows dilatation of the right side after
compensatory hypertrophy has reached its limit, and the heart literally
yields to the backed current of blood, we must expect dropsical
results. Intra-thoracic tumors, aneurisms, emphysema, and sclerosis of
the {571} lung cause hydrothorax by pressing upon the venous trunks and
upon the thoracic duct without producing general dropsy. Chronic
diseases, such as cancerous disease, chronic malaria, etc., produce
great exhaustion and give rise to general hydræmia. Especially is this
the case in chronic disease of the kidneys, such as the several
varieties of nephritis and amyloid degeneration, where there has been a
loss of albumen for a long time and the blood-serum has been rendered
poorer in solid constituents. Hydrothorax is not a disease, but a
symptom resulting from a variety of causes which produce physical
exosmosis of the serum of the blood.

[Footnote 220: _Nouveau Dict. Méd._, vol. xxviii.]

[Footnote 221: _Ziemssen's Cyc._, Amer. trans., vol. iv.]

PATHOLOGICAL ANATOMY.--Hydrothorax being merely dropsy of the thoracic
cavity, there is no lesion of the pleura. There is a collection varying
from 100 grammes to many liters of fluid in the cavity. It differs from
the effusion in subacute pleurisy in its small quantity of fibrin, in
having far less of albuminoid material, and no white blood-corpuscles.
The water collects almost always in both sides of the chest, more on
the side on which the patient lies in bed. In the recumbent position
the fluid gravitates posteriorly more than the effusions of pleurisy.
In the upright position it will follow Ellis's curved line more
regularly than in effusions resulting from pleurisy, for there are no
adhesion-bands interfering with its doing so. The fluid is limpid, of a
light-yellow or citron color. Its composition resembles that of the
plasma of the blood, but it contains more water and less of the
constituent elements. Alex. James[222] found that the amount of mineral
matter was the same in dropsical fluids in all parts of the body, and
that the organic albuminoid substances were larger in quantity in the
pleura than in any other cavity. The amount of organic substances
varied directly in accordance to the degree of pressure on the
different capillary vessels. The anatomical changes in the pleura and
the subpleural connective tissue are similar to those found in other
collections of dropsical fluid. They are swollen and thickened by
maceration with water. They become opalescent and less firm of texture.
The lungs retract as the fluid increases in quantity. As the filtrates
collect in both pleural sacs, the lungs do not forcibly collapse. The
patient would sink at once were this the case. The arch-tension of the
diaphragm is but rarely overcome, and consequently we must not expect
to find the liver and spleen pushed down, especially when there is
fluid in the peritoneal cavity. The position of the heart, unless there
is a marked difference in the collections of the two sides, is but
little altered, the retractive force of both lungs being impaired.

[Footnote 222: _Med. Times and Gazette_, Jan., 1880.]

SYMPTOMS.--The general accumulation of watery fluid is not attended by
any pronounced symptom until it has reached the point of interfering
mechanically with the normal play of the lungs. At first dyspnoea is
only perceptible on increased physical exercise. When the quantity is
excessive, the individual suffers when perfectly quiet. The patient,
until the fluid is excessive, lies on his back as the most comfortable
position, but as the quantity increases he is often obliged to sit up
in bed.

The dyspnoea is ordinarily much more oppressive than in pleuritic
effusions, because both lungs are compressed. There is no rise of
temperature, no pain in the side, no tenderness on pressure, no
acceleration of the pulse, and but rarely any cough, as there is in
pleurisy. The dyspnoea often becomes very painful, and may even produce
orthopnoea, being accompanied by short and frequent acts of breathing.
Where there are very large amounts of fluid the mechanical interference
with the breathing is so great that cold sweats, cyanosis, and asphyxia
follow, the pulse becoming smaller and more feeble until the patient
dies.

The physical signs are, in general, the same as those of pleuritic
effusions, especially the subacute form, with some slight variation.
Inspection {572} and mensuration do not aid us as in pleurisy, for in
hydrothorax the accumulation of fluid is bilateral instead of
unilateral. The tension is not sufficient to dilate the walls of the
chest. Palpation shows absence of vocal resonance, but not invariably,
for we are unable to compare the two sides. We must remember that we
have oedema of the walls of the chest, which would partially prevent
the thoracic vibrations from being felt. Percussion flatness is not as
absolute as it is in pleurisy, unless the fluid is in excessive
quantity, for the tension of the fluid is feebler and the lung contains
more air. The lung is never completely compressed, as in pleurisy,
there being no fibrinous bands to constrict it. The percussion
vibrations, unless very lightly made, are communicated to the lung; and
so there is dulness instead of flatness. The absence of fibrinous bands
permits the fluid to change its position with the varying postures of
the patient. This rarely occurs in pleuritic effusions after the first
few days. Finally, Skodaic tympanic resonance at the apex is but seldom
met with in simple hydrothorax.

Auscultation.--The presence of fluid between the lung and parietes
prevents us from hearing the vesicular murmur. The distant bronchial
respiration is rarely heard in hydrothorax, as it is in pleurisy,
because the lungs are not completely deprived of air, and when present
is less intense. Ægophony is frequently heard over the upper limit of
the fluid, the whispering voice being transmitted through the fluid.
Owing to pulmonary oedema there are subcrepitant râles, but never
pleuritical friction sounds.

DIAGNOSIS.--Ordinarily, the diagnosis ought to be made without
difficulty. The only disease with which there can be any danger of
confounding it is subacute pleurisy. The principal points of
differential diagnosis have been enumerated above. In subacute pleurisy
(latent pleurisy) we have, in less intensity, the ordinary pleuritic
symptoms. The pleuritic friction murmur is present, and a fluid
containing the products of inflammation. Very exceptionally is subacute
pleurisy double, whereas hydrothorax is almost invariably so.

The history of the case enables us to arrive at an accurate diagnosis.
The withdrawal of a small quantity of fluid with a fine perforated
needle, and its chemical and microscopical examination, will complete
the diagnosis in doubtful cases.

Oedema of the lung can scarcely be confounded with hydrothorax. The
absence of the physical evidences of water in the cavity, and the
crackling sound heard in auscultation, are distinctive of oedema.

PROGNOSIS.--The prognosis is always serious, but it depends upon the
nature of the disease producing the dropsy. If this can be removed, the
collection of water may disappear. But, unfortunately, the circulatory
diseases which produce it are generally chronic and incurable. The
fluid can, by general treatment and mechanical means, be reduced, and
the life of the patient prolonged and made comparatively comfortable.
Sooner or later a large number of cases must succumb.

TREATMENT.--The treatment should first be directed to the primary
disease causing the dropsy. If heart disease be the promoting cause, we
must, by means of digitalis, endeavor to promote compensating
hypertrophy, and by arsenic and iron improve the quality of the blood.
If Bright's disease be the cause, the skimmed-milk diet, with iron and
manganese, must be given with remedies which lessen the hydræmic
condition of the blood. Digitalis, diuretics, jaborandi, and drastic
purgatives give decided results. Of all purgatives, elaterium in
decided doses (¼ grain), guarded by conium or hyoscyamus, causes most
relief by producing free watery stools. Mechanical means must be
resorted to without hesitation. It is best first to remove the fluid
from the lower extremities by the insertion of Southey's capillary
canula with caoutchouc tubing attached. Large quantities of water may
{573} thus be drawn off without local irritation, erysipelatous in its
nature, being produced. Thoracentesis by aspiration averts death very
often, and gives the greatest possible relief when the effusion is
large enough to produce dyspnoea. In a case under the author's care
life was prolonged many months and large quantities of fluid were
removed. Altogether, there were twenty-two operations and 1563½ ounces
of water removed. As often as every week one or other side had to be
emptied, the quantity removed each time varying from 49 ounces to 112
ounces. For two months previous to death filtrates collected in the
abdominal cavity also, and had to be frequently withdrawn.


Pneumothorax.

DEFINITION.--A collection of atmospheric air or of gas in the pleural
cavity. Pneumothorax ([Greek: pneuma] and [Greek: thôrax]).

In ancient times gaseous collections were frequently noticed in serous
cavities, especially on opening the chest for empyema and at
post-mortem examinations. The presence of air resulting from laceration
of the lungs by fractured ribs was known and designated as emphysema
thoracis. Air in the pleura was considered as an accidental
complication which occurred with empyema or as formed after death.
Morgagni and others mentioned the presence of gas as formed in the
pleural cavity. Itard[223] was the first to speak of it as a disease
and to name it pneumothorax. Owing to the imperfect knowledge of
pathology at that period, he attributed the production of the air to
the decay of the lung from chronic suppuration, and to the
decomposition of the long-retained pus. Laennec was the first to give
an accurate anatomical and clinical account of the disease.

[Footnote 223: _Thèse de Paris_, 1803.]

HISTORY.--Pure pneumothorax--that is, pneumothorax caused by the
presence of air alone in the pleura--is but rarely met with, except for
a short time, when it has been introduced from without by traumatic
injuries. The irritating effects of gas, unless it comes in small
quantities through the ribs from wounds in the chest-walls, are very
frequently followed in a short time by the production of a quantity of
serosity or of pus. If air is introduced into the pleural cavity from
perforation of the lung, there is also liquid matter from the lungs of
such a character as at once to provoke inflammatory action. Such a
condition is then denominated hydro-pneumothorax or pyo-pneumothorax.
The latter was, in fact, recognized by Hippocrates by the sign of
succussion, though not so designated.

ETIOLOGY.--Laennec divided pneumothorax into three distinct varieties:
1st, essential pneumothorax, resulting from the spontaneous formation
of gas in the pleural cavity; 2d, pneumothorax from putrid
decomposition of liquids effused into the pleura; 3d, pneumothorax by
perforation, due to rupture into the pleura or to an accidental opening
by which atmospheric air or gas from the lungs is introduced into the
pleural cavity. This division, having Laennec's high authority, was for
a long time generally received. It has now been established that the
pleuræ cannot secrete air.

Proust[224] collected 25 cases of so-called spontaneous pneumothorax,
and showed that they could all be otherwise satisfactorily explained.
In some cases errors of diagnosis had been made by mistaking tympanitic
sonority at the anterior-superior portion of the chest, or the
existence of the amphoric breathing found in pleurisy, for
pneumothorax. Some were cases of pneumonia in which tympanitic
percussion resonance deceived observers. Then, again, there was found,
among the cases cited, pneumothorax resulting from rupture of a
tubercular cavity or of a hydatid. In tubercular cases Proust found
that the orifices made were so small--no larger, as Gairdner of {574}
Edinburgh had stated, than a pin's point--that they could not be
detected, or that they had cicatrized before the post-mortem
examination, or perhaps closed by adhesive false membranes. Other
investigations by Ewald[225] and Jaccoud[226] have confirmed Proust's
views that essential pneumothorax does not occur. Researches in
pathological physiology disprove the possibility of a serous membrane
producing a secretion of gas or of its passing from the blood through
the capillary walls. We therefore conclude that pneumothorax from
secretion of air within the pleura is contrary to physiological facts
generally accepted, and is disproved by pathological investigations.

[Footnote 224: _Ibid._, 1862.]

[Footnote 225: Quoted by Fraentzel, _Ziemssen_, vol. iv.]

[Footnote 226: _Gaz. hébd._, 2^{ème} serie, 1864.]

The second variety in Laennec's division--namely, where the gas results
from decomposition of fluid in the pleural cavity--has been supported
by such high authorities as Hughes Bennett, Townsend, Wunderlich, and
Jaccoud. Yet it is difficult to understand how it could occur. The
contact of air appears to be necessary for the decomposition of serum
and pus in the pleural cavity. While shut up in a cavity coated with
neo-membrane, a fluid may certainly remain undecomposed for a long
time, and undergo decomposition as soon as taken out of the cavity.
Recent researches in regard to putrid fermentations appear to confirm
the view that the presence of air is absolutely necessary to produce
that effect.

We believe, therefore, that perforation, with rupture of the visceral
or parietal layer of the serous membrane, causing the introduction of
air into the pleural cavity, is the invariable cause of pneumothorax
and of hydro-pneumothorax. The causes of the rupture are in the lung,
in the pleura, or in the adjoining organs. They may be traumatic or
non-traumatic: the latter may be perfectly designated pathological
causes, because the pneumothorax is always secondary, following upon a
pre-existing pathological condition.

Traumatic pneumothorax may take place in consequence of an injury to
the thoracic walls, of an exterior injury, or of a penetrating wound.
The parts may be so bruised that pleural necrosis gives rise to sloughs
and resulting openings. Fracture of ribs may tear the lungs, and allow
air to enter the connective tissue and produce local emphysema. Violent
contusions, as in a case recently observed by the author, produce
laceration of the lung without the rib or costal pleura being injured.

Non-traumatic or Pathological Causes.--Laennec taught that pulmonary
tuberculosis was the most frequent cause of pneumothorax; and further
observation has demonstrated the correctness of this view. Walshe
states that such is the case in 90 per cent. of the cases of
perforation of the lung. In 131 observations reported by Saussier,[227]
81 were from pulmonary phthisis, principally from caseous pneumonia.
Fraentzel[228] says, from his own observation, that 90 out of 96 cases
of pneumothorax are produced by vomicæ on the surface of the lungs in
the course of caseous pneumonia. Grisolle states that nine-tenths of
the cases result from rupture of a lung-cavity. Fuller[229] reports 22
cases, in 18 of which the disease was produced by tubercular
ulceration. Chambers,[230] at St. George's Hospital, reports that 21
out of 23 were tubercular. Fernet[231] states that pneumothorax results
in nine-tenths of the cases from some of the forms of pulmonary
phthisis.

[Footnote 227: _Thèse de Paris_, 1841.]

[Footnote 228: _Ziem. Cyc._, vol. iv.]

[Footnote 229: _Dis. of the Chest_, p. 226.]

[Footnote 230: _Dec. Pathologicum_, cap. v. sec. v.]

[Footnote 231: _Nouveau Dict._, vol. xxviii.]

Ordinarily, pneumothorax is unilateral; only exceptionally is it met
with on both sides. In tubercular cases it is twice as common on the
left side as on the right (Condrin[232]). In the total of 146 cases
reported by Louis, Walshe, and Powell, 94 were on the left side;
whereas when it is consecutive to a pleuritic effusion it is almost
always on the right side--17 out of 18 (Saussier[233]).

[Footnote 232: _Thèse de Paris_, 1882.]

[Footnote 233: _Ibid._, 1841.]

{575} In tubercular cases perforation of the lung may occur at any
period of the disease; the most frequent time, however, is that of the
softening or while excavations are being formed, where adhesions have
not yet protected the two sides by binding them together with
neo-membranes. It may come from a small cavity. Andral met with cases
where only a few tubercles existed. Townsend reported a case where one
tubercle burst immediately under the pleura. The superior lobe of the
lung is where the perforation generally occurs, because it is there
that the tubercular lesion ordinarily commences and is most advanced
(Louis). It is least frequent in chronic fibroid phthisis and most
often met with in acute pneumonic phthisis. Douglass Powell[234]
reports cases where sinuses extended from cavities, and finally burst
into the pleura. Sometimes the rupture occurs at the base of the
superior lobe, about the third or fourth rib; it may happen, however,
at any point of the lung; it has even occurred at the base of the lung
lying on the diaphragm (Houghton[235]).

[Footnote 234: _Med. Times and Gaz._, Jan. and Feb., 1869.]

[Footnote 235: _Cyc. Pract. Med._, vol. iii.]

Saussier[236] shows by the following table the relative frequency of
the principal causes of pneumothorax in 131 cases:

  Pneumothorax with phthisis . . . . .  81
       "        "   empyema  . . . . .  29
       "        "   gangrene . . . . .   7
       "        "   pulmonary emphysema  5
       "        "   apoplexy . . . . .   3
       "        "   hepatic fistula  .   2
       "        "   hydatids . . . . .   1
       "        "   hæmothorax . . . .   1

[Footnote 236: _Thèse de Paris_, 1841.]

Empyema ranks second as a producing cause of pneumothorax. Ordinarily,
by direct necrosis of the parietal pleura, an orifice is made through
which the pus is evacuated through the bronchi, and air in inspiration
enters the pleural cavity by the bronchial fistula. Pyothorax is
converted into pyo-pneumothorax. The valvular opening may, however, be
closed by inspiration so that air cannot enter, or adhesions may limit
a portion of the pleura, and then we have a circumscribed pneumothorax.
Empyema, by producing ulceration of the thoracic walls and pointing
exteriorly (emphysema necessitatis), leaves fistulæ through which air
enters the pleural cavity.

Gangrene of the lung by sloughs allows air to penetrate. Bronchiectasic
cavities sometimes become the seat of putrefactive changes and
ulcerations through the lungs into the pleura. Infective emboli being
arrested in the smaller peripheral branches of pulmonary arteries, air
enters the cavity; it is thus that pneumothorax arises in various kinds
of surgical diseases when infective emboli pass into the circulation
(Fraentzel). Flint[237] reports a well-marked case of pneumothorax,
lasting less than one month, where there was every reason to suppose
that it had been caused by rupture from interstitial emphysema. W. T.
Gardner had previously reported a similar case. Saussier found
emphysema was a cause in only 5 out of 131 cases. Fraentzel speaks of
emphysema as rarely being a cause. Perforation of the oesophagus,
ulcerative, cancerous, or traumatic from the use of bougies, produces
pneumothorax. Suppurating bronchial glands--a case of which was met
with by the author--bursting into the cavity produce pneumothorax.
Hydatids of the lungs, abscesses of the abdomen, sometimes coming even
from the cæcum and from the liver, burst into the pleural cavity and
introduce air. Echinococcus cysts of the liver are occasionally emptied
into the pleural cavity.

[Footnote 237: _Practice of Medicine_, ed. 1881; _Series of Amer. Clin.
Lectures_, article "Pneumothorax," 1875.]

{576} Pneumothorax is more than four times as frequent in men as in
women. One-third of the whole number of cases occurs in persons between
the ages of twenty and thirty years; one-tenth between the ages of ten
and twenty; one-twelfth between thirty and forty (Saussier[238]).
Although pneumothorax has a number of exciting causes, yet they are all
comparatively rare except pulmonary tuberculosis and purulent pleurisy.

[Footnote 238: _Thèse de Paris_, 1841.]

PATHOLOGICAL ANATOMY.--In traumatic pneumothorax and simple cases, such
as from the bursting of emphysematous alveoli, the presence of air is
the only pathological product. If the pleura and adjoining organs are
not diseased, the rupture or tearing cicatrizes rapidly, and the air
disappears in a few days by absorption. If a quantity of air be
admitted, the pneumothorax may last for months; yet if the pleura is
healthy, the air itself will not produce local changes. If blood or
morbid products flow in with the air, then inflammatory changes occur,
and we have deleterious products effused. Demarquay and Leconte[239]
demonstrated the innocuousness of introducing air into healthy pleural
sacs of dogs, having injected it repeatedly into the same dogs without
any unpleasant result. These observers analyzed the air after it had
remained in the chest, and confirm Davy's[240] researches as to the
changes in its condition. The oxygen diminished gradually, and finally
disappeared, while carbonic acid replaced it to nearly the same amount.
This air from the pleura approximated in composition to the air of
expiration. When blood and bronchial secretions with pus are thrown
into the pleura, they promptly produce more serious results, especially
intense suppurative pleurisy. Duncan[241] found in a case of
pyo-pneumothorax a fetid gas to contain 26 parts of sulphuretted
hydrogen and carbonic acid and 74 parts of nitrogen. Secondarily,
lesions are produced--hydro-pneumothorax and pyo-pneumothorax. In other
cases, the pleura having been previously the seat of chronic disease
with purulent effusion, this latter undergoes fetid changes and
septicæmia results. Under these circumstances the pathological changes
are similar to those we have described as found in empyema. We find
like increase of tissue-formation, of pus, and of the development of
the gases, sulphuretted hydrogen and sulphydrate of ammonia, which give
rise to a horrible fetidity. The quantity of air varies very much, as
does the amount of fluid: there may be a small quantity of air and much
fluid, or the reverse.

[Footnote 239: _Gaz. Méd._, 1864.]

[Footnote 240: _Phil. Trans._, 1823.]

[Footnote 241: _Edin. Med. and Surg. Journal_, 1827.]

The opening into the pleural cavity may be direct or oblique: if
direct, it remains open; if oblique, it is generally more or less
valvular. The symptoms, prognosis, and treatment vary accordingly.
Through a patent orifice the air enters in inspiration, and goes out
with the expired air from the lungs. As it cannot accumulate, there can
be no positive air-pressure within the pleura. If, however, the orifice
be valvular, although the air enters it does not escape, for it presses
upon the valve and closes it. If the valvular fold be perfect, the air
soon becomes excessive in quantity, and exerts dangerous pressure upon
the lung and adjacent organs. By means of a trocar, attached by tubing
to a water-pressure gauge, Douglass Powell[242] ascertained post-mortem
the degree of intra-pleural pressure present in 16 cases of
pneumothorax. In 4 out of these cases the pressure was nil. In 12 there
was more or less intra-pleural pressure present, varying in degree from
1¾ to 7 inches of water.

[Footnote 242: _Medico-Chir. Trans._, 1876.]

Unless the lung be mechanically prevented, the entrance of air into the
pleural cavity at once produces a retraction of the lung, owing to its
elasticity. There is no compression of the lung unless the air is
increased in quantity by each inspiration, and, having no exit,
accumulates; then the lung may be forced against the spinal column and
the residual air actually {577} forced out of the alveoli. Powell[243]
questions whether the intra-thoracic pressure excited in pneumothorax
is ever equal to what is sometimes the case in pleurisy: the highest he
had ever met with in pneumothorax was 7 inches of water. Garland,[244]
in repeating Damoiseau's experiments in testing the effects of the
introduction of air into the pleural cavity, found that the air did not
penetrate between the lung and the lateral chest-walls until the lower
border of the lung had retracted upward the distance of several ribs.

[Footnote 243: _Loc. cit._]

[Footnote 244: _Loc. cit._]

One of the most pronounced effects constantly observed in pneumothorax
is the immediate displacement of the heart to a greater extent than in
pleurisy. Gaidy,[245] as far back as 1828, described displacement of
the heart as an important sign of pneumothorax. He related a case
where, at the moment of the perforation, the woman was conscious of the
heart's beat having been transferred to the right of the sternum.
Powell[246] out of 17 cases found the heart displaced in 16: in the
seventeenth the unruptured lung was so consolidated that it could not
collapse. In pneumothorax of the right side a careful examination is
sometimes required to detect the displacement of the heart. The apex
can be discovered at a considerable distance to the left of the nipple,
with the right ventricle drawn to the left edge of the sternum. It has
been generally believed that the cause of this displacement was the
intra-pleural pressure of the air, but this does not satisfactorily
explain it, for there can be no pressure until the elasticity of the
lung has been overcome. In 13 of Powell's cases there was great
displacement of the heart with different degrees of intra-pleural
pressure. In 3 cases there was great displacement of the heart with no
intra-pleural pressure. The same author[247] showed, experimentally,
that the elastic tension of one lung, when unopposed by that of the
other, was sufficient to draw aside the mediastinum, and with it the
heart. He thus demonstrated that these displacements are by no means
necessarily a sign of intra-pleural pressure, since they may occur to
the right of the sternum without there being any pressure. Clinically,
we know that the admission of air into the pleural cavity immediately
and constantly displaces the heart, unless the opposite lung be
consolidated or otherwise injured in its resiliency. This occurs even
when the patent orifice of the perforation prevents the accumulation of
any quantity of air. There is not enough air to produce direct
pressure, but there is enough to impair the elastic traction of the
lung, and thus to destroy the equilibrium of traction which keeps the
heart in its normal position. The healthy lung by its unimpaired
tractile force immediately draws over the heart. Skoda[248] maintains
that "air does not enter the pleural cavity simply at the cost of the
torn and retracted lung, but the sound lung also retracts to such a
degree as to move the mediastinum." Garland's experiments[249]
conclusively demonstrate that the air in pneumothorax is powerless to
exert an appreciable lateral displacing force until the lung has
completely collapsed; and this does not ordinarily occur. There can be,
he says, but one cause of constant and early displacement of the
heart--the elastic force of the opposing lung, which draws it over to
itself. He adds that "the explanation of the greater displacement of
the heart in pneumothorax is that the air, having practically no
weight, cannot exert upon the heart the negative pressure which an
effusion evidently would."

[Footnote 245: _Arch. Gén. de Méd._, tome xvii., 1828.]

[Footnote 246: _Medico-Chirurg. Trans._, vol. lix.]

[Footnote 247: _British Med. Journal_ and _Med. Times and Gazette_,
July, 1869.]

[Footnote 248: _Auscultation and Percussion_, Eng. trans.]

[Footnote 249: _Loc. cit._]

The fluid in hydro-pneumothorax is very rarely of a serous character.
Saussier found but 1 such example in 169 cases. It is almost always
purulent pneumothorax, and frequently it has a very offensive fetid
odor from putrid decomposition. Mixed with pus there are sometimes
found masses of {578} pseudo-membranes, débris of lung, and gangrenous
patches, as in purulent pleurisies. The fistulous orifice through which
the air has entered is not always easily found, being often hid away
among false membranes. It is small and tortuous, and can only be
discovered by placing the lung under water and blowing air through the
bronchial tubes. Sometimes the orifices close and the air becomes
encysted, interlobular, or diaphragmatic. There is sometimes only one
opening; again, there may be several. Nolais reports a case where there
were six openings. Orifices with lacerated edges are met with, varying
in length from one to ten or twelve centimeters. It must be borne in
mind that perforation can take place without producing pneumothorax.
Saussier found this occurred in 2 out of 74 cases, and in 8 out of 29
resulting from pleurisy. Fériol and Guéneau de Mussey give similar
cases.

SYMPTOMS.--The initiatory symptoms of pneumothorax vary according to
the cause which produces it. When the effusion of air into the pleural
cavity is from perforation of a diseased lung (most frequently
tuberculous, more rarely gangrenous or from an abscess), the first
symptom is a sudden agonizing pain in the side, accompanied with
dyspnoea amounting almost to suffocation. In rare instances, where
strong old adhesions limit the pneumothorax, there may be only slight
pain, without dyspnoea. The rush of a moderate quantity of air into the
cavity causes the lung to collapse; but should the amount of air be
excessive, it will render the symptoms of oppression most intense, for
it will compress the lung and heart and obstruct the capillary
circulation in the lung. Such must be the case, for there is no
aspiration of blood from the large veins, and no aëration of blood in
the lung. The patient often feels as if the chest were being torn away,
and the expression of his countenance betrays distress and alarm. If
the orifice be large and valvular, preventing the escape of the air,
the air accumulates rapidly and completely forces the air out of the
lungs, and death shortly follows, sometimes in a few hours. There is no
rise of temperature or fever. On the contrary, the temperature very
frequently falls one or two degrees below the normal in consequence of
the sudden collapse, the pulse from exhaustion being very frequent and
feeble, accompanied by cold sweats. The voice becomes exceedingly
feeble and whispering. In many cases the patient does not sink at once
from the shock of the perforation, but becomes less oppressed, although
he suffers considerably, being unable to lie flat in his bed.
Respiration is not only frequent (sometimes 60 per minute), but the
dyspnoea is oppressive and distressing to witness. Fever follows
invariably, and sometimes with great rapidity, caused by pleuritis.
When this occurs, the patient again suffers from dyspnoea as the
purulent fluid accumulates in the pleura and gradually dropsy comes on.
These cause dyspnoea and cyanosis. The position of the patient, leaning
forward, supporting his elbows on his knees, indicates his agony and
difficulty in breathing; the pain appears to go through and produce
local hyperæsthesia, and the patient dies from the empyema with hectic
and oedema of the lungs. The pleurisy excited may be simply serous in
its products, even when it is tuberculous in origin. Usually, however,
it is purulent, and we must then expect to find the grave symptoms we
have enumerated in speaking of empyema with hectic and septicæmia.

PHYSICAL SIGNS.--These are well distinguished and marked, and lead
easily to its diagnosis. Inspection shows the side to be immovable and
the dilatation permanent; the spaces between the ribs are obliterated
and the shoulder raised. There is no rhythmical expansion and
contraction of the walls of the chest, the diaphragm is not elevated,
and the liver and stomach are kept down. Air continues to enter the
cavity, until the quantity is so great that its tension is equal to the
atmospheric pressure. The contrast between this condition and that of
the healthy side is very great. In the former the breathing is labored,
with painful muscular contraction in the walls and whole side. {579}
Percussion over the chest gives a hyper-resonant sound, with a
graver-pitched tympanitic resonance. There is but little sense of
resistance to the finger, owing to the elasticity of the contained air.
When fluid is secreted in the second stage we have absolute flatness at
the base over a horizontal level, and tympanitic resonance above. The
pitch of this last sound varies according to the tension of the gas
contained in the chest and the correlative tension of the thoracic
walls. If this tension be feeble, the pitch is higher; if it be
extreme, the tone will be drum-like, muffled, acute, and the tympanitic
character will be less easily perceptible. It may happen that the pitch
will be so high that we may be misled and think there is flatness. It
is not true flatness, but a clean and high-pitched sound, very
different from the tympanitic sound usually found; it is sometimes
remarkably metallic in character. With auscultatory percussion, using a
solid pleximeter, we have the prolonged metallic resonance which
Trousseau appropriately named the bruit d'airain.

The area of hyper-resonance and flatness on percussion is changed with
the altered position of the patient. The fluid, obeying the law of
gravitation, takes its hydrostatic level, and when the patient's chest
is upright is horizontal. Hyper-resonance is often pronounced over the
sternum, and sometimes infringes upon the healthy side. When the
disease is on the left side it obliterates the normal dulness over the
cardiac area.

Palpation.--Thoracic vibrations of the voice are not felt over the
portion of the chest containing air, nor over that containing fluid.
This absence of vocal fremitus is very characteristic. The hand detects
that the heart has been displaced toward the sound side and that the
abdominal viscera are pushed down.

Auscultation.--The auscultatory phenomena vary according to the cause
of the pneumothorax and the size and direction of the orifice. In
tubercular cases, where perforation has produced a large, free opening,
as the air passes in and out of this large pleural cavity with firm
walls (the lung having collapsed perhaps to one-third or less of its
normal size), we have the physical conditions which give marked
amphoric and metallic respiratory sounds, with absence of respiratory
murmur. The amphoric breathing is of greatest intensity near the point
of perforation, which ordinarily is at the mammary or upper scapular
region, and is found in both inspiration and expiration. The cough and
the whispered voice give the characteristic metallic quality. There is
also metallic tinkling produced by droppings of fluid in the cavity, by
the shaking of the body, or by vocalization. Even when the orifice in
the lung is closed we may have amphoric echo, from sounds produced in
the bronchi, and passing through a cavity filled with air. The
intensity of these sounds varies in different cases. Sometimes they are
very loud; in other cases they are feeble and seem distant from the
ear. The fine metallic tinkling may be heard at one moment and
disappear at the next. These amphoric and metallic sounds, heard at
different points, are characteristic of pneumothorax with free
openings. When, however, the orifice from tubercular perforation is
small, oblique, or valvular, the respiratory murmur is inaudible,
except perhaps at the very apex of the lung, and we cannot perceive any
adventitious auscultatory phenomena beyond a faint, distant, hollow
sound.

There is, in both kinds of orifices, the well-known splashing
Hippocratian succussion sound on shaking the chest. The latter is
pathognomonic of hydro-pneumothorax, and is sometimes heard when no
other sign is present. The hands applied over the surface of the chest
feel the fluctuations of the fluid striking against the interior walls.
When pneumothorax follows purulent pleurisy we do not find immediately
the pronounced symptoms nor the physical phenomena heretofore described
as occurring when it is produced by rupture from the lung into the
pleural cavity. The condition {580} of the parts is very different. Pus
is present in considerable quantity in the cavity, and the ulceration
of the costal pleura and the soft walls of the chest allows the fluid
to flow outward and air to enter the cavity. Or there may be necrosis
of parietal pleura into a bronchus and consequent discharge of pus
through the mouth. The lung is already disabled. The violent pain in
the side and the dyspnoea are no longer found. Indeed, the exact time
of the rupture and commencement of the discharge is frequently unknown
to the patient himself. The symptoms of entrance of air into the
pleural cavity may not occur for some time. The patient who has had
empyema is made more uncomfortable; the discharge through the mouth is
offensive, and its quantity and its character call attention to the
chest, in which percussion shows the presence of air; auscultation
gives amphoric breathing, and succussion demonstrates the presence of
air and fluid in the pleural cavity. Very soon, however, the presence
of air produces putridity of the secretion, with loss of appetite,
fever, diarrhoea, and the other alarming symptoms of pyo-pneumothorax.
In some instances the pleura discharges its contents and heals over.
There is another variety of pneumothorax, which is ordinarily attended
with only temporary inconvenience, and which may soon disappear,
leaving the patient no worse than before the attack. This variety of
pyo-pneumothorax may be produced by the sudden rupture of emphysematous
vesicles, by coughing, or even without any unusual force in the
expiratory effort, the alveoli having become extremely thin and brittle
by degeneration of their walls. For the minute the pain is violent and
the dyspnoea great, but it soon subsides, and in a few days the gas may
be all absorbed, unless it is in large quantity. If the pleura is
healthy and the lung not otherwise diseased, the rupture may not cause
any inflammatory action, fever, or effusion. The rupture may heal over
entirely, or if some inflammatory effusion is produced it will probably
be rapidly absorbed. In exceptional cases pleurisy may be excited and
the case become prolonged. While the air remains in the pleura we have
the physical signs characteristic of pneumothorax--displaced heart, as
shown by palpation and auscultation, tympanitic percussion resonance,
amphoric breathing, and succussion.

DIAGNOSIS.--Ordinarily, there should be no difficulty in diagnosing
pneumothorax, no matter how it is produced. We have simply to consider
well the already-mentioned modes of the commencement of the disease,
and give due value to the characteristic physical signs, especially
displacement of the heart, hyper-resonance on percussion, absence of
vocal fremitus, amphoric respiration, succussion, and decided shifting
of flatness and resonance on change of position. When all these signs
are present, each being in itself almost characteristic, there can be
but little question. Obstruction of a large bronchus would be followed
by absence of health sounds and intense dyspnoea, but we should not
have the other physical signs of pneumothorax. Extensive emphysema
would produce some of the signs--exaggerated resonance on percussion
and enlargement of the side. Emphysema, however, is bilateral, and the
resonance over an emphysematous lung has not the same pronounced
tympanitic quality as in pneumothorax. The enlargement in emphysema is
more under the clavicle; the breathing not amphoric; the normal murmur,
although enfeebled, is never completely annulled; and the heart is not
displaced. Large superficial pulmonary cavities with firm but thin
walls give us several of the physical signs of localized pneumothorax,
such as amphoric respiration and metallic tinkling; but the succussion
sound is never heard over them. The tympanitic percussion is rarely so
pronounced in a cavity as in pneumothorax, and in the latter there is
never the cracked-jar sound. In phthisical cavities of large size there
probably would be depression instead of enlargement of the chest. The
situation will ordinarily enable us to make the differential diagnosis,
for localized pneumothorax is almost always low {581} down in the
thorax, and the pulmonary cavities but rarely below its middle third.
The progress of the case and clinical history would clear up the
diagnosis. If a circumscribed pneumothorax was present with phthisis,
the diagnosis might be difficult. Powell calls attention to the
similarity of some of the signs of acute congestion rapidly supervening
at the base of a comparatively sound lung to those of pneumothorax. But
in the former the resonance, although high-pitched, is not truly
tympanitic, and the heart is not displaced. There is no other disease
of the chest where we find in such close proximity the two extremes of
percussion sounds--flatness from the secondary effused fluid, and the
tympanitic resonance above. If delicate, slight percussion is used, the
line of demarcation can be clearly defined; if, however, the force of
the percussion stroke be even of moderate intensity, the flatness is
mingled with the tympanitic quality, as it is in percussing from the
left lobe of the liver to the stomach.

PROGNOSIS.--The prognosis is unfavorable and always uncertain. During
the first few days after the rupture of the pleura it is especially
bad, though it becomes less so as time goes by. There are cases where
the perforation and its results appear to prolong life. "If the
opposite lung be healthy, we may hope that arrest of the pulmonary
disease may convert the case into one of chronic empyema" (Powell).
But, unfortunately, the rupture often occurs when the patient is
emaciated and dying of chronic lung ulceration. Cases of
pyo-pneumothorax produced in advanced phthisis or by gangrene of the
lung are almost invariably fatal. The most unpromising cases at first
sometimes prove the least serious, and, again, those that appear at the
commencement slight, contrary to expectation, die. Much depends upon
the condition of the other lung and the position of the perforation. If
the other lung be healthy and the perforation low down, the chances of
recovery are better. The progress is most favorable in the cases where
the rupture occurs from emphysema. When from purulent pleurisy the
discharge passes through a bronchus, the orifice may heal and in due
time plastic material be thrown over it, and the air and fluid be left
in the pleura. Cases are reported where the orifice remains open and
pneumothorax lasts for a long time. Laennec reported one case where the
patient lived six years. Fuller[250] reports another where the orifice
was open at the end of eleven months, another nineteen months, and
another twenty-seven months. We have mentioned Demarquay and Marotte's
experiments of the innocuousness of air injected into the pleura. Air
is harmless, as they have shown, in the pleura, unless sulphuretted
hydrogen or sulphite of ammonia be developed. Fuller says the prognosis
is very unfavorable when the effusion is large, with great displacement
of the organs. Flint considers pneumothorax occurring as a complication
of phthisis as almost hopeless. It is important to ascertain promptly
the nature and direction of the opening, whether it be free or
valvular.

[Footnote 250: _Diseases of Chest._]

TREATMENT.--This is in a great measure palliative. Hypodermics of
morphia or opiates relieve the agony and lessen the shock caused by the
perforation. Alcoholic and diffusible stimulants may sustain the heart
in its struggle against the effects of dislocation and impaired
circulation. Care must be taken not to depress the powers of reaction
by too much morphia. Hot water in india-rubber bags applied to the
chest gives great relief. Alcoholic stimulants must be given to prevent
sinking from exhaustion. When the distension from air is excessive,
paracentesis gives marked relief, the lives of patients having been
prolonged for days by it. If the opening is valvular, to prevent the
air from accumulating in excessive quantity Reybard's protected
gold-beater's skin trocar may be used and kept in the chest. Otherwise
fine aspirators may be employed, which would seem to be harmless, and
the {582} operation be repeated whenever necessary. Larger points and
the trocar should never be used, as there is danger of making a
permanent fistulous orifice, as well as of injuring some blood-vessels
or the lung itself. After the excess of air has been removed by
aspiration the affected side should be strapped to control the
inspiratory movements on renewal of positive pressure. Anstie[251]
recommends drachm ss doses of ether every three or four hours.
Fernet[252] recommends inhalation of oxygen. If fluid should compress
the chest, some of it must be removed by aspiration, but care must be
exercised, for the presence of fluid is conservative in its effects.
Its pressure stops up the orifice and promotes its healing. If it
becomes fetid, pleurotomy, with detersive washes, ought to be resorted
to. Food should be frequently administered, with quinine and cod-liver
oil, and good hygienic surroundings prescribed.

[Footnote 251: _Reynolds's System of Medicine_, vol. iv.]

[Footnote 252: _Nouveau Dict. Méd._, vol. xxviii.]


Hæmothorax.

DEFINITION.--Accumulation of blood in the thoracic cavity unconnected
with inflammation of the pleuræ.

ETIOLOGY.--Hæmothorax may be caused by traumatic injuries, by the
bursting of an aneurism, from ulceration through the walls of the aorta
of the vena cava, or from the veins of the pleura. It may be caused by
laceration of the intercostal arteries in penetrating wounds. In very
rare cases a profuse bleeding takes place in caseous pneumonia or in
gangrene of the lungs, and bursts into the pleural cavity (Fraentzel).
Cancer of the lung or pleura may, by pressure, produce absorption and
destruction of the walls of the blood-vessels, and cause discharge of
their contents into the pleural cavity. Sir Thomas Watson[253] reports
a case where enormous hæmothorax caused enlargement of the left side,
pushing the heart to the right of the sternum from caries of two ribs
with ulceration through an intercostal artery. The blood never escapes
from the lung into the pleura when there is considerable pulmonary
apoplexy.

[Footnote 253: _Practice of Medicine_, vol. ii.]

PATHOLOGICAL ANATOMY.--Blood is found coagulated to a greater or less
degree in the pleural cavity, and the lesion producing the hæmothorax
can generally be found; the remains of blood may be found even after it
has been some time effused. If the hemorrhage does not prove fatal, it
may all be absorbed, or it may by its presence cause local inflammation
of the pleural membrane.

SYMPTOMS.--The symptoms are those of perforation into the chest--sudden
intense pain on the diseased side, with internal hemorrhage, great
pallor, feeble circulation, cold extremities, and syncope. Patients
often die in a few minutes. If the hemorrhage is moderate in quantity,
they revive and the circulation returns, but they complain of feelings
of suffocation and oppression. Slowly the general strength returns and
the patient recovers.

SEQUELÆ.--Most modern surgeons admit that serious hemorrhages into the
pleura come from the thoracic walls, or from the blood-vessels in the
neighborhood of the hilum, or from those which accompany the bronchial
diseases of the second or third order. Hæmothorax is always consecutive
to some primary lesion. Where it is caused by penetrating wounds or by
the bursting of blood-vessels in the lungs, air enters the cavity and
becomes mixed with the blood, producing a complication in the form of
hæmato-pneumothorax. This frequently gives rise to pyo-pneumothorax
with a collection of purulent and ichorous fluid.

DIAGNOSIS.--The previous history of the case, together with the
characteristic symptoms we have mentioned, enables us to diagnose
hæmothorax from {583} pneumothorax, which commences in a similar way.
The only other condition likely to be confounded with it is effusion in
pleurisy, the physical signs of which are somewhat the same. If the
blood remains uncoagulated we shall have absence of vesicular murmur,
with dulness on percussion, absence of fremitus, and no friction sound.
The introduction of a fine hypodermic needle enables us to be certain
of the nature of the fluid.

The PROGNOSIS is always serious. If the cause of the hemorrhage is the
bursting of an aneurism, death supervenes in a short time. Hæmothorax,
when caused by penetrating wounds, unless they produce hemorrhage, is
not necessarily serious. The blood may entirely disappear in a few
weeks. Entrance of air with the blood renders the prognosis more
serious. Secondary pleurisy is not ordinarily severe unless pus forms.

TREATMENT.--If time is allowed, every effort must be made by local and
general treatment to arrest the hemorrhage--ice-bags and hot-water bags
ought alternately to be applied to the chest and between the scapula;
the patient to be kept in the horizontal position and made to rest
quietly; ice taken by mouth; small doses of morphia and large doses of
ergotin must be given promptly hypodermically, as the stomach is in no
condition to absorb remedies readily. If the accumulation be excessive
and continues to embarrass the respiration very much, we recommend free
incisions to take out sufficient blood to relieve the pressure and
great dyspnoea. Unless danger is imminent, this is a hazardous
experiment, as letting in atmospheric air among blood-clots may
seriously complicate the condition. Should pleuritis or other
complications occur, they must be rationally treated.


Growths in the Pleural Cavity.

Some authors mention various tumors which are rarely met with in the
pleural cavity, and which are not peculiar to the serous membrane of
the pleura. Among them may be placed sarcomas, fibro-sarcomas, and
epithelioma. Their presence in other organs may assist in the
diagnosis. Other varieties exist more or less connected with chronic
pleurisies. Among these are fibromas, cartilaginous and osseous
formations. Rokitansky speaks of lipomas as deposited on the costal
pleura. The only varieties which we think it necessary to call
attention to are cancer and hydatids.

CANCER OF THE PLEURA.--Cancer of the pleura is not a very rare disease,
but ordinarily it is a secondary formation, coming from cancerous
disease of the mediastinum, of the lung, or of some abdominal organ.
Some authors doubt whether it is primary even in the lungs and
mediastinum. It certainly is not often met with as a primary disease of
those organs. Lebert[254] had only seen 6 observations, in 447 cases of
cancer, involving the mediastinum, the pleura, and the lungs.
Walshe[255] reported 29 cases of primitive cancer of the respiratory
organs; in 18 cases one lung was diseased with its pleura, and in 13
the right lung. Lépine[256] in 1869 communicated a very curious case of
primary cancer of the pleura in a child ten years of age. The right
pleural cavity was filled by a white scirrhous tumor. Darolles[257]
(1874) reported another example of primary cancer of the pleura, which
afterward spread to the lung. Andral, Vidal, and Lebert reported cases
where the tumors appeared to develop simultaneously in the pleura and
other organs. Primary cancer of the pleura may exceptionally occur, but
ordinarily the disease results from its extension step by step, or else
distant propagation, from lungs, breast, mediastinum, or the abdominal
organs. Most frequently the secondary {584} cancer appears more or less
independently of the primitive tumor, and is seen in the form of
disseminated points on the surface of one or both folds of the pleura.
This propagation of cancer is now generally admitted to be through the
intermediary of the lymphatic system; in fact, the lymphatics are
themselves attacked by the degeneration, and they are seen,
particularly on the surface of the pleura, in the form of white small
cords. Some modern pathologists consider that the serous cavities are
lymphatic cavities, which can, just as the vessels themselves, serve as
ways of generalizing the disease (Cornil and Ranvier, Charcot, Lépine,
and Virchow).

[Footnote 254: _Traité Prac. Mal. des Cancereuses_, Paris, 1851.]

[Footnote 255: _Nature and Treatment of Cancer_, London, 1846.]

[Footnote 256: _Bull. de la Soc. Anat._, 1869.]

[Footnote 257: Quoted by Fernet, _Nouveau Dict. Méd._, vol. xxviii.]

PATHOLOGICAL ANATOMY.--Primary cancer of the pleura is ordinarily
encephaloid and multiple. Extended infiltration is very rarely found.
Lebert reports one case in an infant of seven months. The multiple
masses are ordinarily soft and pulpy, varying in volume from the size
of a grain of millet-seed to that of a small nut. The aspect is
yellowish-white. The juice is rarely pressed out of them. Under the
microscope we see large cells and multiple cells with their nuclei. The
small granulations or the lenticular masses are flat, resembling drops
of wax. We may have solid bodies possessing all the characters of
scirrhous, encephaloid, and colloid, grayish, or gelatinous structure.
These cancerous productions are generally vascular, especially in the
encephaloid variety. Their rupture frequently produces hæmothorax and
hemorrhagic pleurisies. The bronchial glands, and finally the cervical
glands, often become involved.

SYMPTOMS.--The symptoms of pleural cancer, especially of the smaller
and secondary deposits, are often obscure and indefinite. They are not
sufficiently definite to attract attention during life. If the masses
are scirrhous and large, they press upon the lungs, impede respiration,
and give rise to dyspnoea. If the disease is propagated from the lungs
or breast, we may suspect cancer where we have a dull pain with some
cough. Pain, indeed, is constant, but not violent, unless the nodules
excite local inflammation. When scirrhous tumors press upon the
intercostal nerves, the pain is very persistent. External pressure over
the points gives rise to pain. The dyspnoea increases as the size of
the tumor increases. The expectoration is occasionally bloody. The
physical signs are sometimes characteristic--dulness on percussion,
absence of respiratory murmurs, friction sounds, no vocal fremitus.

DIAGNOSIS.--Generally very difficult. The progress of the disease is
ordinarily slow, and follows its development in other portions of the
body. Cancerous cachexia, degeneration of the glands above the
clavicle, hæmothorax, and hemorrhagic pleurisy, together with dry cough
and persistent intercostal neuralgia, are, when present, valuable aids
to diagnosis. Extensive caseous pneumonia and pleuritic effusions may
be confounded with cancer of the pleura. These tumors may not be at the
base, but in the middle of the thorax; dulness may not exist at the
base as is invariably the case in pleurisy. The position of the body
does not affect the limit of dulness in cancer.

The PROGNOSIS is always very serious, the disease being invariably
fatal. In Walshe's cases the duration of the disease was from three and
one-half months to twenty-seven months; average duration, thirteen and
one-fifth months. One-fourth of his cases occurred between the ages of
fifty and sixty years.

The TREATMENT is palliative--opium and other narcotics, and locally
chloroform and aconite for the intercostal pains. When effusion results
from cancerous inflammation the aspirator may be used to relieve the
great oppression caused by the quantity of fluid.


{585} Hydatids of the Pleura.

Trousseau[258] considered hydatids of the pleura a comparatively rare
disease. He believed that when found in the cavity it was frequently
caused by cysts of the lung which had fallen into the pleural cavity.
Vigla[259] mentions 3 cases. Davaine[260] met with 25 cases of
hydatids, only 1 of which he believed originated in the pleural cavity.
The acknowledged greater frequency of these hydatids in the right
inferior lobe of the lung, gives probability to Dolbeau's[261] view
that "they frequently proceed from cysts on the convex surface of the
liver." Hearn[262] reports 75 cases collected from various observers as
intra-thoracic, 15 of which were in the pleura, in the subserous
tissue, between the parietal pleura and thoracic wall.

[Footnote 258: _Clin. Med._, vol. i., Philada. ed.]

[Footnote 259: "Des Hydàtides intrathor.," _Arch. gén._, 1855.]

[Footnote 260: _Traité des Entozoaires, etc._, Paris, 1860.]

[Footnote 261: _Thèse de Paris_, 1856.]

[Footnote 262: _Thèse de Paris_, 1875.]

PATHOLOGICAL ANATOMY.--In the greater number of cases, as examined at
autopsies in Hearn's reports, the tumor was formed by a voluminous
pocket occupying a large part or the whole of the cavity of the pleura.
The walls of the envelope were formed of a transparent or slightly
opaline and whitish membrane composed of numerous thin layers,
containing on its interior surface the echinococci. In the interior of
the cyst there was a limpid hyaline liquid with living parasites.
Nothing different was noticed in cysts from those found elsewhere,
except the absence of the usual adventitious membrane--a fact
previously noticed by Davaine. When the cysts are very large they press
upon the lung and adjoining organs just as is the case with large
effusions in the pleural cavity. The heart, moreover, is pushed to one
side, out of its normal position; the lung is compressed and diaphragm
depressed.

SYMPTOMS.--The first appearance of cysts of the pleura causes but
little disturbance of the functions of the lung. It is scarcely
appreciable until it interferes with the play of the other organs. The
three prominent symptoms are the pain, the dyspnoea, and the cough. The
pain occupies the exact point where the tumor is situated, and radiates
from that point. Once developed, it persists with tenacity throughout
the duration of the disease. This persistence of the pain is indeed an
important characteristic of the disease, and is a sign of value in the
diagnosis between hydatids and pleuritic effusions. The dyspnoea
increases progressively with the volume of the tumor. The cough is not
heard as frequently as when the cysts occur in the lungs. It is dry,
and does not cause hæmoptysis.

DIAGNOSIS.--Physical signs must be marked to enable us to distinguish
fluid cysts of the pleura from cysts in the lung or effusions in the
pleural cavity. When the hydatid tumor has attained sufficient size to
cause pain and dyspnoea it generally presses outward the walls of the
chest after the lung has been compressed. It does not occupy the base
of the cavity, as the effusions do, and the dilatation has a globular
form. Trousseau[263] has given several examples in which this shape
determined the diagnosis. With this arching of the chest the immobility
of the chest is an important sign. Vocal fremitus is diminished or
totally abolished, and percussion elicits absolute flatness. These two
physical signs assist us in making the diagnosis between hydatids and
pleurisy. The auscultatory phenomena, from similar physical conditions,
closely resemble those of pleuritic effusions. It must be borne in mind
that sometimes hydatid cysts are complicated by pleuritic
inflammations, caused by their presence. The diagnosis is
unquestionably complicated by difficulties that are not removed unless
the cysts burst through a bronchial tube and discharge a transparent
and clear fluid in which the microscope shows the presence of
echinococci. Such hydatid expectoration is a pathognomonic {586} sign
of the existence of an intra-thoracic cyst. Hydatids of the liver may
press the diaphragm far up into the pleural cavity without bursting
through it. Trousseau maintained that without bursting they may make a
passage for themselves through the distended, attenuated fibres of the
muscular portion of the diaphragm, for the progress of these cysts is
necessarily slow. We must not hesitate to make an exploratory
aspiration to determine with certainty the nature of the fluid.

[Footnote 263: _Loc. cit._]

PROGNOSIS.--The prognosis is certainly very serious, but not so bad as
when cysts of the same nature are situated in the lungs. Their
spontaneous cure may be effected by bursting through a bronchus or even
through the walls of the chest. The patient may, however, die from
asphyxia during the discharge through the lungs. When not evacuated
they may produce death by compression of the lungs.

TREATMENT.--If the disease is recognized previous to its making an
opening through a bronchus, it can be treated safely and effectively by
aspiration. Bird[264] reports a number of cures by this operation in
Australia. Trousseau advises extreme caution, even in regard to
exploratory punctures, unless adhesions have taken place between the
tumor and the walls of the chest, for he fears the escape of fluid into
the cavity of the chest and consequent purulent pleurisy. It is well to
remember that this great practitioner was not aware of the
innocuousness of capillary punctures and aspiration. If the bronchus
has been perforated, we must hope for spontaneous cure. If empyema be
caused by the tumor pleurotomy must be used as recommended by
Moutard-Martin[265] and Vigla,[266] and constant washing of the pleuræ
must be used. This treatment gives us reasonable assurance of success.

[Footnote 264: Quoted by Hearn.]

[Footnote 265: _Purulent Pleurisy_.]

[Footnote 266: _Loc. cit._]


History of Thoracentesis.

Thoracentesis ([Greek: thôrax], chest, and [Greek: chentein], to
pierce) is the operation for the evacuation of collections of fluid,
serum, pus, or blood from the pleural cavity.

Among the ancients, dating back to the time of Hippocrates, it was
practised, and was known as the operatio empyematis. Hippocrates uses
the word [Greek: empyon], signifying, literally, an internal collection
of pus just above the cavity of the peritoneum, above the diaphragm.
Subsequently he speaks of empyema of blood, empyema of serum, empyema
of gas, but not of pus, applying the term to the operation, which he
employed principally for empyema necessitatis. Subsequently the name
empyema was used, as now, to designate a purulent collection in the
pleural cavity.

If we may credit the story which has descended from mythological times,
the operation for empyema had its origin in an accident. It is related
that a certain Phalereus, who was attacked with what was denominated an
ulcer on the lungs, was pronounced by all his physicians to have an
incurable disease. In his despair he exposed himself in battle so that
he might be slain; the enemy's weapon, however, pierced his side,
making an opening through which the pus escaped, and he recovered.[267]

[Footnote 267: Cicero, _De Naturâ Deorum_, lib. iii. cap. 28.]

It is certain that from the most remote periods the chest was opened
when collections of pus were formed. Galen states that the ancients
employed actual cautery for that purpose. He reports that Euryphon de
Cinde by this means saved the life of Cinesias, son of Evagoras.[268]
The details into which Hippocrates and his school entered in regard to
the operation show that it was frequently performed in their day. It is
very remarkable that many of the more important precautions in the
operation were observed by {587} Hippocrates. We find from the
_Aphorisms_ that the operation was considered the only means of
cure,[269] and that when these precautions were observed, and the fluid
was white and of good quality, the patients recovered.[270] The
principal precautions were not to delay the operation after the
existence of pus was recognized, and to draw off the liquid. He further
states that if the serous fluid in dropsy of the chest or pus in
empyema should be drawn off too rapidly the patient would die. So
impressed were the disciples of Hippocrates by this view that they
adopted the operation of perforating a rib instead of cutting through
the intercostal space, because they could with more ease stop up the
orifice and regulate the outward flow of the fluid. The later
Hippocratians preferred cutting instruments to actual cautery.
Hippocrates, if unable to discover the locality of the fluid in the
thorax by succussion, applied over the walls of the chest a linen
compress which he soaked in earth of Eretria and warm water, and
concluded that the collection existed at the points where the earth
commenced to dry!

[Footnote 268: _Comm. in Aphor. Hipp._, lib. vii.]

[Footnote 269: _Aphorisms_, lib. vii., Aph. 44.]

[Footnote 270: _Ibid._, lib. vi., Aph. 27.]

When these signs failed, he cut through the most prominent rib at the
base of the chest and toward the back. He made a large incision through
the rib, but only a small one the size of a thumb-nail through the
tissue beneath the rib. After allowing a small quantity of pus to
escape, he introduced a tent of undressed flax, with a piece of thread
attached to it. This he withdrew twice daily, to allow the pus to flow.
At the end of two days he permitted the remaining pus to be discharged,
and inserted a tent of linen. To prevent the lung, habituated to the
presence of fluid, from drying too rapidly he injected wine and oil
through a canula. When the excavated fluid was thin (serous?) he
replaced the tent by a tube of tin, and when it ceased to secrete fluid
he shortened each day the length of the tube, so that the cicatrization
of the wound extended from the inner end of the orifice.[271] The
genius of Hippocrates cannot but excite our admiration, as it did
Laennec's, who selected as the subject of his thesis "The Doctrines of
Hippocrates as applicable to the Practice of Medicine." Can it have
been Hippocrates's modes of physical explanation that suggested to
Laennec the idea that led to his great discovery of auscultation?

[Footnote 271: _De Morbis_, lib. i. p. 448.]

Hippocrates's operations were made by boring through the rib or with a
red-hot iron or a bistoury cutting through the intercostal space. Galen
(A.D. 150) had his pyulcon with which to draw out the fluid. Galen and
Roger of Parma bored through the sternum. Many of the ancient surgeons,
such as Eumphon of Cnidos, Paul of Ægina, Celsus, Solinger, divided the
soft parts by caustics and the knife after laying bare the pleura.
Blunt instruments were sometimes used, such as sounds. Celsus in his
latter years lost confidence in the operation, and it fell into
discredit among the Greeks and the Romans, by whom it seems to have
been nearly abandoned. In the Middle Ages the question was discussed
whether it was better to open the chest by steel or by fire in
traumatic pleurisies. Trousseau states that about the sixteenth century
the operation of trepanning the ribs was revived. About the same time
the detersive injections which had been recommended by Galen were again
advocated, especially by Fabrice d'Aquapendente. The operation was
unpopular among the greatest surgeons, and but seldom resorted to
except in extreme cases. Notwithstanding the servile obedience to
tradition in those days, some important points were advocated in regard
to the propriety of allowing the openings for empyema to remain
unclosed for an indefinite period. From the seventeenth to the
eighteenth century the operation of paracentesis was the topic of many
surgical treatises.

Early in the seventeenth century practitioners became less distrustful
of {588} puncturing the chest, and were led to believe in the
harmlessness of the operation (Trousseau). As a consequence of this
tendency, physicians began to study the question of puncturing the
chest in hydrothorax. In 1624, Gérome Goulée alleged that he succeeded
more frequently in hydrothorax than in abdominal paracentesis. Twenty
years later, Zacutus Lucitanus asserted that paracentesis was as
necessary in cases of serous effusion into the chest as incision in
empyema. In 1663, Robin and Duval recommended thoracentesis as the best
treatment for hydrothorax. Some time afterward this practice was put in
force by Willis. Lower also mentions a case, and subsequent authors
quoted these cases as an encouragement to the performance of
paracentesis of the chest for the removal of serous effusions. Jean de
Vigo brought out again the pyulcon. Druin about the year 1665 proposed
the use of the trocar as a substitute for the actual cautery in opening
the chest.

In 1658, Bontius for the first time took up in a precise manner the
subject of the introduction of air into the pleural cavity. He declared
there was no danger from it. Bartholin maintained the opposite opinion.
The indications for the operation were laid down, but they were
necessarily very imperfect. In proportion as attention was directed to
the question of the admission of air, the manner of operating was
modified. In 1669, Scultetus discussed thoracentesis in his work
_Armamentarium Chirurgicum_. He made use of a trocar, with a bladder at
the external orifice, principally to prevent the introduction of air,
as Reybard later used a piece of cat's intestine and a bladder of
gold-beater's skin. Scultetus used the sypho, a common syringe, for
injecting the chest, and also the [Greek: pyoulchon] ([Greek: pyon],
pus; [Greek: elchô], to draw out), or pyulcon, for drawing out matter,
as its name indicates. This was practically the syphon. Scultetus
describes the operation by incision with his gladeolo salicet longo,
and by puncture with the canula et acus, both figured in his plates; so
also his drainage-tubes, with directions for shortening them as the
cavity heals, and the long tubes, which probably acted by gravitation
after the manner of the syphon. Aspiration was made by the mouth, by
cups, and by syringes affixed to a canula or catheter.[272]

[Footnote 272: These facts were kindly furnished me by Morrill Wyman,
who carefully examined Scultetus' work (edition 1672) in the Harvard
Library.]

It is thus evident that more than two hundred years ago aspiration was
used to evacuate fluid from the pleural cavity. Trousseau says that "at
that period aspiration and suction were used for this purpose--timidly
pursued, in accordance with Scultetus' example; and that it became
afterward in vogue with the masters of surgical art."

Palfin preferred the trocar to incision for treatment of hydrothorax.
In 1707, Anel wrote a book on the art of sucking wounds without using
the mouth. Bourdelin (1742) rejected the trocar for fear of injuring
the lung. That Scultetus' practice was continued is evident from the
work of Laurence Heister (1742), who described puncture of the chest,
with drawings of exhausting syringes for the removal of pus or serum.

In 1765, one hundred years after Druin's use of the trocar, when
perforation by actual cautery was abandoned, Lurde timidly advocated it
on account of his fear of wounding the lung. He advised the operator to
close the canula with the finger at each inspiration, leaving it open
during expiration, so as to prevent the entrance of air. Chopart and
Desault opposed the use of the trocar as a coarse mode of operation,
involving the risk of wounding the intercostal artery and lung
(Trousseau). Van Swieten at the end of the last century questioned the
advisability of using the trocar. Later, in 1796, Benj. Bell,[273] in
cases of thoracentesis, used india-rubber bottles fitted to the opening
for the same purpose, first compressing them and then allowing them to
expand by their elasticity. He strongly recommended paracentesis {589}
of the pericardium when the amount was so excessive as to cause death.
He gives exact directions how and where to operate.

[Footnote 273: Vol. v.]

Isbrand de Diéonerbrock[274] plunged a bistoury between the fifth and
sixth ribs, and introduced into the wound a silver canula large enough
to fit the orifice, and stopped the canula with a tent which he
withdrew each day. Jean Scultetus[275] recommended several different
canulas, some of silver, some of gold. He also invented syringes,
straight and curved, to absorb the pus or make injections into the
chest. Scultetus operated in the sixth intercostal space; he raised a
piece of skin, so that it might lap over the orifice after the
operation. He used a tent until the eleventh day, when he inserted a
canula. After Scultetus, Lamzweerden[276] used suction, and contended
that it was very successful. Paul Barbette[277] considered
thoracentesis as indispensable in empyema and hydrothorax. He
maintained that it was less dangerous than the puncture for ascites. F.
Hoffmann at the commencement of the eighteenth century[278] gave his
full and complete approbation to the operation performed according to
the accepted rules. Dominique Anel[279] was an avowed partisan of the
suction of the effused fluids in the chest. He had seen soldiers very
successfully suck, with the mouth, wounds of the chest. He invented
different syringes and other machines to pump out the effused fluids,
some of which were very large, with canulæ whose orifices were very
wide and of different shapes.

[Footnote 274: _Medic. Morb. Pectoris Hist._, 2.]

[Footnote 275: _Armam. Chir._, Paris, vol. i. p. 20, quoted by
Sprengel.]

[Footnote 276: _Appendix ad Sculpt. Armen_, 1671, quoted by Sprengel.]

[Footnote 277: _Chirurgia_, lib. iii. cap. 2, Geneva, 1688, quoted by
Sprengel.]

[Footnote 278: _Medicina consultatoma_, vol. i., 1721.]

[Footnote 279: _L'art de Sucer les plaies sans se servir de la bouche
d'un Homme_, Amst., 1707.]

Laurence Heister[280] (1742) acknowledged that Anel's syringes were
valuable in pumping out the fluid from the middle or lower part of the
chest, but not when paracentesis was performed in the higher portions
between the second and third ribs. Heister gives[281] drawings of
exhausting syringes for the removal of pus or serum. C. G. Ludwig
published[282] a new apparatus invented by a surgeon named Bucer to
pump out the fluids contained in the chest. This machine was composed
of canulæ, to which was adapted a bowl to receive the liquid as it was
withdrawn. Ludwig claimed that the especial advantage of this
instrument was that it pumped all the fluid out at one time, without
the operator being annoyed by any disagreeable odor. Leber[283]
proposed a similar instrument which was easier of application. A. T.
Richter demonstrated the inutility of all these inventions; the blood,
he said, would be drawn out with the fluid and by coagula stop up the
canula. Valentin (1772) objected to the use of these pumps as applied
to chest fluids.

[Footnote 280: _Chirurgie_, Th. i. Buch. i. Kap. 10, p. 89.]

[Footnote 281: _Ibid._, p. 72.]

[Footnote 282: _Diss. de Vul. Pectoris_, Leip., 1768.]

[Footnote 283: Quoted by Sprengel, p. 60, vol. ix.]

In the latter part of the eighteenth century there were numerous
English and continental writers on the subject of paracentesis. Among
them were J. W. Belquer, Sharp Mohrenheim, Richter, Ponteau, Callisen,
Pierre Cooper, Allemoth, Zellar, and Audouard. Some of these preferred
the trocar to the bistoury. Some were in favor of prompt action, and
others objected to the operation unless there were threatening
symptoms. Valentin urged that the presence, on the surface of the
chest, of oedema and ecchymosed spots was a certain indication of fluid
effusion.

During the first twelve years of this century the operation seems to
have fallen into disuse. In 1808, Audouard objected to the Hippocratian
method, which had been practised for centuries, of drawing out small
quantities at a time, for fear that the sudden withdrawal of a large
quantity would produce a vacuum in the chest. He maintained, and
proved, that sudden and {590} complete evacuation had no such result.
In 1811, Corvisart[284] drew attention to thoracentesis. In 1812,
Larrey discussed its merits. Charles Bell[285] preferred the trocar to
the other methods in hydrothorax when he could be positive of the
presence of fluid, but he stated that he preferred first to introduce
the bistoury. He operated in the sixth intercostal space, but in
empyema he preferred to make the puncture higher up. Samuel Cooper[286]
recommended as small an orifice as possible for the evacuation of
serum, but larger and wider ones for pus and blood.

[Footnote 284: _Maladies du Coeur_, 1811.]

[Footnote 285: _System of Operative Surgery_, vol. ii. p. 194.]

[Footnote 286: _Dictionary of Surgery_, p. 749.]

In tracing the history of this important operation we have shown that
it has been performed from the time of Hippocrates, and that it has
been held in different degrees of estimation by the numerous authors
who have discussed it--that sometimes it has been popular, and again
regarded unfavorably.

Récamier operated, but unsuccessfully. Up to the period we have now
reached (1816) great difficulty of accurate diagnosis existed, and
crude notions of physiology prevailed. Errors of diagnosis as to the
character of the fluid when present, and still more as to its existence
in the chest, frequently led to unpleasant results. Laennec's genius so
completely cleared up the differential diagnosis of all diseases of the
chest, including pleurisy, that men grew less timid. Laennec[287]
himself was a strong advocate of the operation; he advised it in acute
pleurisy where dyspnoea, threatening life, supervened, and in chronic
cases where other remedies failed. He proposed to apply a piston
cupping-glass over the wound after the discharge of liquid, and to
produce a vacuum in the chest more or less quickly, continuously, and
completely according to effects.

[Footnote 287: _Traité d'Auscultation mediate_, 1818.]

As Bowditch[288] states, "We should be groping in the same dark way,
and perhaps getting into the chest by caustic pastes or by actual
cautery, had not Laennec discovered for us auscultation, with all its
admirable powers of diagnosis of thoracic affections."

[Footnote 288: Unpublished communication to the writer, 1882.]

In 1815, Blondel practised puncture of the chest with a bistoury.
Gendrin performed the same operation in acute pleurisy in 1831, but
with only bad results. Townsend[289] (1833) acknowledged that the
operation had fallen into disuse, as much from uncertainty of diagnosis
as from any experience of its general danger. He gives the results of
Thomas Davies's operations--8 out of 10 successful cases in empyema,
with 9 fatal cases in pneumothorax with effusion (probably tubercular),
and 3 fatal cases in hydrothorax. Davies used a grooved needle to
determine the presence of the liquid, its quality, and the thickness of
the walls. After the operation his practice was to inject a weak
solution of chloride of lime, which he found to have the effect of
diminishing the discharge and correcting its character. Crompton[290]
(1834) had 3 successful cases out of 10.

[Footnote 289: _Cyc. Prac. Med._, vol. ii. p. 43.]

[Footnote 290: _Ibid._, vol. iii. p. 400.]

Robert Law[291] pronounced paracentesis more successful in chronic than
in acute pleurisy. Townsend doubts whether the admission of air was
hurtful; he quotes Nysten and Spies's experiment, showing that air
introduced into healthy pleuræ was invariably absorbed in a few days.

[Footnote 291: _Ibid._, 1834.]

Townsend[292] and Law, as well as C. I. B. Williams,[293] speak of the
different kinds of syringes that have been proposed to draw off the
fluids.[294] Dupuytren proposed (1814) the introduction of a small
canula with a very flexible substance at its outward extremity, such as
the bladder of some domestic animal, which would allow fluid to escape,
and at the same time would oppose the entrance of air into the chest.
Becker (1834) published a work in which he investigated the nature of
the false membranes in pleurisy, and showed that the {591} access of
air did not produce unpleasant results. He reported 2 successful cases
out of 3 of operation.

[Footnote 292: _Ibid._]

[Footnote 293: _Library of Pract. Med._, 1841.]

[Footnote 294: Boyson, _Thèse de Paris_, 1814.]

R. Townsend[295] wrote an elaborate paper in 1833 on empyema, in which
he applied the principles of physical diagnosis. He cites numerous
cases of thoracentesis, and speaks of the operation as easy of
execution, productive of little pain to the patient, generally followed
by immediate relief, and as having been in numerous instances crowned
with complete success. Robert Law[296] (1834) speaks discouragingly of
the operation in consequence of the "unavoidable admission of air into
the inflamed cavity." He considered the operation of tapping the chest
more likely to be successful in chronic than in acute pleurisy.

[Footnote 295: _Cyclop. Prac. Med._, vol. ii., 1833, London.]

[Footnote 296: _Ibid._, vol. iii., 1834.]

In 1835, Faure[297] read his paper on thoracentesis before the Academy
of Medicine of Paris, which attracted a great deal of attention.
Contradictory opinions were given by prominent members as to the value
of the operation. The debate was prolonged, and no definite conclusion
was reached. Laennec, although he had recommended the operation in
excessive effusions and in chronic cases, was yet timid, and his advice
had not the overwhelming influence that it should have had. Becker of
Berlin in 1834 wrote his paper on chronic pleurisy, in which he also
laid down the principles of diagnosis by means of auscultation and
percussion. He detailed 5 cases which he had operated upon. To Thomas
Davies is due the credit of having in 1835 recommended the use of the
exploring-groove needle to ascertain the nature of the pleuritic
effusions, but Powell claims that Sir Benj. Brodie first suggested it.
Ringer first recommended the use of the hypodermic syringe for that
purpose. Stokes[298] insisted upon the evils attending paracentesis,
among which he mentions the converting of serous into purulent
effusions.

[Footnote 297: _Bullétin de l'Académie de Médecine_, 1838, tome i. p.
62.]

[Footnote 298: _Dis. of Chest_, Dublin.]

Watson's lectures on practice, delivered in 1836-37, show that while he
was much interested in the operation, the necessity of which he
discusses with his characteristic ability, yet his conservatism led him
to put prominently forward the dangers and evils connected with it.
According to these two prominent English practitioners, only imminent
peril to life justified the operation. Guérin[299] in 1841 applied his
subcutaneous method of operation to empyema. He drew fluids from the
chest by a suction-pump applied to a canula, using a curved trocar and
canula to prevent injury to the lung.[300]

[Footnote 299: _Essai sur la Méthode Sous-cutanée_, Paris, 1841.]

[Footnote 300: Drawings of the trocar and canula, with the aspirators,
are shown in Jacob and Bongeré, _Med. operatoire_.]

Reybard in 1837 took up Dupuytren's suggestion, and used gold-beater's
skin as a valvular means of excluding air at the mouth of the canula;
this is now known as Reybard's canula apparatus, and was the one used
and highly recommended by Trousseau. Stanski in 1839 invented an
apparatus for drawing off air from the chest, working on the principle
of aspiration. Bowditch states[301] that while in Paris from 1832 to
1835 he never saw a case of pleurisy in Louis's, Chomel's, Andral's, or
Trousseau's wards where thoracotomy was performed or even suggested.
Medical opinion was either indifferent or in actual opposition at that
time. H. I. Bowditch of Boston relates[302] that he saw 2 cases of
effusion in the pleural cavity in 1839, in which he proposed
thoracentesis, but the surgeons would not operate: both of these
patients died. He was convinced at the time that their lives might have
been saved. Schuh of Vienna published his work on the _Influence of
Auscultation and Percussion on Practical Surgery_, in which he boldly
maintained that paracentesis was a radical cure in cases of chronic
thoracic effusion, no matter how originating. This work had a great
influence in advancing {592} the popularity of the operation of
thoracentesis. Subsequently, Schuh and Skoda, both professors at
Vienna, published[303] a monograph on the treatment of pleurisies,
especially by surgical means, which, as Trousseau acknowledged, has
become a classical work in Germany, and occupies a distinguished place
in the history of paracentesis of the chest. They admitted that when
the effusion is not excessive in quantity, and there are no
complications, recovery generally takes place. When the effusion is
excessive even, it may in time disappear, but it may prove a matter of
months or years. They advised that the operation should be performed
when there was no marked improvement for three weeks. These authors
refuted the arguments urged against the operation, and gave details as
to the mode of operating. The Germans were the first to consider the
puncture as a means of radical cure in pleuritic effusions: Becker,
Schuh, and Skoda gave it a decided impulse. Hope's[304] paper
endeavored to prove that pleuritic effusions did not require surgical
interference, but would yield to general treatment.

[Footnote 301: Unpublished MS., 1883.]

[Footnote 302: _American Journal Med. Sciences_, April, 1852.]

[Footnote 303: _Medicinische Jahrbücher der K. K. Oesterreich Staates_,
1841.]

[Footnote 304: "Notes on the Treatment of Chronic Pleurisy," in
_Medico-Chir. Review_, London, 1841.]

Thus we see that up to 1841 these unsettled controversies over the
dangers and advantages of the operation were still going on. Fred.
Bird's results in 1843 proved the possibility of its successful
employment, doubted up to that time in England. Trousseau's attention
was strongly drawn to the necessity of the operation of thoracentesis
as early as 1832, when he attended a case at the Hôtel Dieu that died
from excessive pleuritic serous effusion. Louis, from the observation
of 150 cases of simple pleurisies that had recovered, had enunciated
the law that pleurisy is never the immediate cause of death. This fact,
together with Récamier's want of success, had so prejudiced the minds
of French practitioners against the operation that it was loudly
condemned in acute cases of effusion and in all cases of hydrothorax.
Having no fears of fatal termination in pleurisy, they saw naturally no
necessity for surgical interference. Trousseau states that it was not
until after he had witnessed three patients die from acute pleurisy
that he ventured to operate (Sept. 11, 1843). He did not summon a
consultation, for fear of being thwarted. It was so successful that he
was emboldened to operate without hesitation. After his third operation
he read his memoir to the Academy of Medicine in 1843. Trousseau in
these memoirs maintained the proposition which extensive observation
has now after forty years fully sustained, that dyspnoea and orthopnoea
may occur when the effusion is in moderate quantity, and that they may
be absent when the effusion is considerable, especially if it has
formed slowly. Furthermore, that the signs that constantly indicate the
gravity and imminent danger of effusions, and which consequently demand
the operation, are the displacement of the heart (whence results
syncope), displacement of the mediastinum, depression of the spleen and
of the liver, acceleration and feebleness of the pulse, and an anxious
countenance.

The next year (1844) Trousseau read another memoir on the same subject.
He used the trocar with Reybard's gold-beater's skin at the orifice.
While he was popularizing the operation and laying down the indications
which called for its performance, several English observers[305] were
turning their attention in the same direction. The paper by Hughes and
Cock[306] showed that they had been operating in Guy's Hospital for
four or five years, and with great success, using a simple trocar and
canula of the diameter of one-twelfth of an inch. They imputed their
success to the small size of the instrument used, which allowed the
fluid to flow slowly and never permitted air to enter the chest during
respiration. They gave a tabular account of 20 operations. Hamilton
Roe[307] at that time was operating successfully with the trocar. {593}
Roe's paper was replete with information and with practical
suggestions. He tabulated 39 cases where syncope (one great objection
which had been urged against the operation) did not occur even once. He
disproved another popular objection, that there was great danger of the
admission of air into the pleural sac. Owing to the size of his trocar,
a considerable quantity of air entered the pleura during his
operations, and in some of them so freely as to produce all the
physical signs of pneumothorax, but in none of them did it produce any
permanently evil effects. In one instance only was even temporary
inconvenience caused. When the fluid was ascertained by the
exploring-needle to be purulent, he advised the immediate performance
of the operation. In acute cases he recommended a delay of three weeks
as the time for testing nature's powers of absorbing the fluid. He
advised the closing of the orifice after operation. This author gave an
account of his 24 cases. He concluded by stating that the operation is
not more dangerous than any other which is performed upon the human
body, and that the evil consequences supposed to attend it are
imaginary rather than real, inasmuch as it was only fatal in 1 out of
24 cases, and does not produce even temporary inconvenience. Thompson
in the same year justly condemns the practice of leaving the canula in
the orifice--a proceeding he considers as capable of converting a
serous into a purulent fluid. In 1848,[308] at the request of H. I.
Bowditch of Boston, J. M. Warren operated by the usual method
recommended in the works on surgery. Partial relief was obtained, but
the amount of suffering undergone by the patient during the operation,
and the fact that an aperture was usually left open by this method,
decided Bowditch that he would never recommend it unless under very
urgent circumstances. Soon after this, Stone operated with the common
trocar and canula, by the advice, in consultation, of Bowditch. In
1849, Bowditch saw another death resulting from effusion where he had
advised the operation, but the consulting surgeon would not consent.

[Footnote 305: _London Medical Gazette_, 1847.]

[Footnote 306: _Guy's Hospital Reports_, vol. ii., 1844.]

[Footnote 307: _London Lancet_, 1844, copied into _Amer. Journal Med.
Sciences_, Oct., 1845.]

[Footnote 308: Bowditch, _Amer. Journal Med. Sciences_, April, 1852.]

To illustrate the opposition Bowditch found in the United States, he
quotes[309] a remark of W. W. Gerhard, the distinguished auscultator of
Philadelphia, "that he should be as willing to have a bullet shot
through his chest as to have paracentesis performed on one of his
patients."

[Footnote 309: Unpublished MS., 1882.]

About 1850,[310] Bowditch saw the paper published by Hughes and Cock,
and it determined him in future to try the trocar they had used or
something like it.[311] "Fortunately, a few weeks before (April 10,
1850) M. Wyman had a sudden and severe case with large effusion and
intense orthopnoea. Death was threatening, yet Wyman felt called upon
by public opinion, medical and lay, to summon a prominent practitioner
from Boston. They both agreed that the patient was in extreme danger,
and Wyman urged tapping with an exploring-trocar. It was decided to
postpone surgical interference until next day, when another meeting
would be held, the consulting physician returning to Boston to advise
with the ablest men of the faculty and render their decision the
following forenoon. That was done, and it was found that no prominent
practitioner in Boston would consent to the idea of tapping.
Nevertheless, the oppression was so severe, and death so imminent
unless the patient could be relieved by some means, that the country
physician agreed to Wyman's proposal that an exploring-trocar should be
introduced. The fluid flowed out imperfectly, but some relief and no
harm resulted" (Bowditch). Two days after this, Wyman operated again
with the exploring-trocar and a suction-pump. Wyman[312] demonstrated
to John Homans on the 23d of February, 1850, that the chest could be
safely punctured with his instrument and the serum evacuated in acute
pleurisy.

[Footnote 310: _Ibid._]

[Footnote 311: _Ibid._]

[Footnote 312: Private letter to author, 1883.]

Although suction, as we have shown, was used as far back, probably, as
Galen (second century), by Scultetus in 1662, and was in use in 1707,
as {594} shown in Anel's work, in 1742 in Laurence Heister's work, by
Ludwig and Lehren in 1768, again in 1796 (Benj. Bell), yet it had been
abandoned and lost sight of, with the exception of Laennec's suggestion
of its application in the form of a cupping-glass over the orifice of
puncture, until Guérin (1841) used it. The author followed Trousseau's
clinics in 1849 and 1850, and saw him repeatedly operate with Reybard's
canula guarded by gold-beater's skin, but never with Guérin's suction
apparatus. The French seemed to have lost sight of it until 1865, when
Guérin, at the French Academy, recalled attention to it, showing how he
aspirated liquids, instead of allowing them to flow outward after the
puncture. His apparatus consisted of a curved trocar, the end of which
was made tapering and sharp enough to puncture the thorax through the
skin and the muscles; of a pump, the piston of which was perfectly
adjusted to produce a vacuum; and of an adjuster at the extremity of
the pump, consisting of a stopcock which enabled the operator
alternately, without removing the instrument, to aspirate the fluid and
evacuate it into a basin. Wyman's pump, invented in 1850, was arranged
very much in the same way, only it contained valves which were opened
and closed by the movement of the barrel, to enable the operator to
suck out the fluid and then force it out of the pump. After the
operation the skin, being drawn over and closing the orifice, acted as
a valve which prevented at the same time the entrance of air and the
escape of fluid. Dieulafoy, in November, 1869, invented his aspirator,
which is based upon the same principles as those used by Guérin (1841)
and by Wyman and Bowditch (1850)--namely, pneumatic aspiration, which
the vacuum of the air-pump supplies. Guérin's instrument was large and
costly. Wyman's trocar was of a very small diameter, being only
one-twenty-fourth of an inch, and the canula but little larger. This
was attached, at first, directly to the aspirating syringe, afterward
by means of a flexible tube. With this apparatus Wyman demonstrated
that tissues could be safely punctured and cavities evacuated without
the admission of atmospheric air, that the wound, causing but a drop or
two of blood, was followed by no inflammation, and that no dressing was
required. The smallest trocar used previously to Wyman's was that of
Roe, which was one-twelfth of an inch in diameter. From 1850, Bowditch
appreciated the great value of Wyman's invention, as shown in one of
the first operations on a patient of his. He adopted and practised it.
His position as professor of diseases of the chest, and his great
reputation in that branch, gave him an extensive practice and brought
him many cases of pleurisy. He met with great opposition from the
surgeons and prominent practitioners of the country, but his results
were so favorable that he forced an unwilling and an unbelieving
profession to accept, as he expresses it, "the beautiful thought of
Wyman of thoracentesis or aspiration with a fine needle." "I considered
the operation so simple, and yet so effectual, and never harmful, that
I deemed it my duty to print cases illustrative of its value." Bowditch
had been for eight or ten years endeavoring to get some effective plan
of opening the chest without risk. He readily caught at Wyman's plan,
and he operated so frequently and successfully as to demonstrate its
value to the medical public both of this country and of Europe. As he
states,[313] it was, in fact, what he had been for years longing
for--viz. a simple and painless, or almost painless, operation for
removing fluids from the thorax--one that could be done without danger
and leave no open wound. Bowditch relates[314] that when he visited
Europe, nine years after his first publication of cases, he showed the
instrument in England, Scotland, France, and Germany, and that he met
with very indifferent recognition of its value. Only W. T. Gardner of
Edinburgh and Budd of London seemed to appreciate the plan. They had
instruments made after the American pattern. All others had no faith in
the operation. In Paris his old master, Louis, smiled {595}
incredulously at his enthusiasm for it and doubted its necessity. At
Vienna Skoda turned with apparent scorn and left the room as Bowditch
was demonstrating its employment. The Parisian authors, Woillez, Peter,
Moutard-Martin, Peyrot, and others, do not even mention Bowditch, but
give Trousseau alone the credit of popularizing thoracentesis.

[Footnote 313: Unpublished MSS., 1883.]

[Footnote 314: _Ibid._]

Trousseau's first publication was in 1843, and yet in 1859 there was no
general adoption of the operation, nor was there until 1869, when
Dieulafoy rediscovered Wyman's wonderful improvement of the application
of negative force to draw out fluids from the chest.

In estimating the value of the substitution of aspiration for the
trocar-and-canula method, we must bear in mind that with the latter
there was danger of the introduction of air into the thoracic cavity,
of the production of fistulous orifices, and the too rapid, and
therefore dangerous, evacuation of the fluid. Moreover, there are cases
where the trocar and canula is not effectual, although the quantity
effused be considerable--where, indeed, the fluid cannot flow out,
although the canula be pushed in actual contact with the fluid. The
explanation of this is now understood. The fluid is kept in the pleural
sac by a negative pressure of from 4 to 5 inches of water (Stone), 6
millimeters mercury (Donders), 5 millimeters mercury (M. Foster),
exercised by the lung in its elastic contraction, and by the passive
tension of the arched diaphragm. The fluid has no tendency to flow out,
and this suctional pulmonary force must be antagonized by an external
suctional force, that of aspiration, before the fluid can be withdrawn.

The invention can best be appreciated from the standpoint reached by
modern investigations of the physics of the living mechanism of the
chest. The principle of applying suctional force in pleurisy is in
imitation of nature's gentle methods in connection with respiration. We
have shown that most of the dangers connected with aspiration are
caused by not taking into consideration the adjustment of lung-tension
with thoracic resilience, and consequently of using too great negative
force and withdrawing the fluid too rapidly and in too great quantity.

Thoracentesis by aspiration, with greater or less force as may be
necessary, is now placed upon a scientific basis. We claim that this
modern method is an American invention--that Morrill Wyman was the
discoverer and H. I. Bowditch the utilizer of the discovery. As such
they may be regarded as benefactors of the human race.

It is extraordinary that Trousseau never alluded to Bowditch's
operations, and that Dieulafoy should never have heard of them.
Fraentzel acknowledges that Bowditch was the first to introduce
aspiration into practice. The Germans have been very slow in
appreciating its value. Fraentzel states that he did not use it until
1871, and that it was not until 1879 that it had in Germany any ardent
supporters. Bowditch[315] has now operated 387 times upon 246 patients
without any unpleasant result.[316] The distinctive points in
Dieulafoy's ingenious modification of the aspirator are that the
needles are very fine, even one-half of a millimeter in diameter; that
the barrel of the exhausting pump is of glass; that there is a
pre-existing vacuum; that we are not compelled to jar the side of the
patient by the process of pumping, and moreover by turning the cock we
produce at once a vacuum in the needle itself, and know with certainty
the moment the fluid is reached, and can see it flow through the glass
index in the tubing, even if it be in drops. We can judge of the nature
of the fluid, whether it be serum, pus, or blood. The minuteness of the
needle is a great cause of safety, because it allows the fluid to flow
so gradually that the lung has time to expand slowly. We can in an
instant arrest the flow of the fluid by turning the stopcock, and if
necessary by drawing out the needle. By giving the needle a downward
direction after it {596} enters the cavity, we prevent the point from
pricking the lung. So small an orifice is made that even if the needle
does touch the lung, there is no danger, for the orifice closes over at
once. As Dieulafoy claims, "the fineness of the needle guarantees the
harmlessness of the puncture." Castraux's concealed point (invented in
1873), and Fitch's (of Nova Scotia) protected canula (invented in
1873), are valuable additions to the aspirator-needle. These
dome-trocars, as they are called, prevent the possibility of injuring
the lung, for the sharp-pointed needle, after it has penetrated the
pleural cavity, is at once, by a slight movement, converted into a
blunt-pointed needle with an orifice near the end. With these very fine
needles the force is sufficient to draw up the thickest fluids. We are
compelled to admit that Dieulafoy's instrument is a great advance on
any other that has been invented. Its simplicity, its easy application,
its safety, have rendered paracentesis a harmless operation and one of
great value in serous effusions. While Guérin and Wyman may both claim
priority of invention, all must admit that Dieulafoy has improved upon
their ideas and given us a beautiful and effective instrument. There
have been proposed, since Dieulafoy showed his instrument in 1869, no
less than forty other aspirators, modifications in form or dimensions
of his apparatus. Of these, to us the most valuable is Potain's bottle
aspirator, with which aspiration can be so easily and effectually
employed. It is simple and cheap. An india-rubber cork accurately
fitting a strong bottle is perforated for two tubes each having a
stopcock. One of the tubes fits on the end at the exit in the basin,
and the other is adapted to an aspirating syringe.

[Footnote 315: _London Lancet_, vol. ii., 1879.]

[Footnote 316: Letter to author, 1883.]

One of the most important of the improvements to the aspirator-canula
is the addition--first suggested in 1858 by Charles Thompson,[317] and
afterward adopted by Potain, Powell, and Fraentzel--of a lateral tube
for the outflow connected with the main canula through which the trocar
passes. By this improvement, in case the canula is clogged up, the
trocar can be pushed down to remove the obstruction without danger.

[Footnote 317: _Med. Times and Gazette_, 1858.]

The principle of aspiration is now well established, and the
indications for its use are becoming more defined and more accurate.
New applications as a means of diagnosis, as well as of treatment,
daily render it more valuable.

To guard against the dangers shown by modern experience to be sometimes
attendant upon the operation of aspirating the pleura (see Dangers of
Thoracentesis), it is now generally admitted that the removal of the
contents of the chest should be slow and gradual; and that, ordinarily,
it is safest at one operation to remove only a portion of the effused
liquid. Our object should be to remove pressure and allow nature by
absorption to take away the remainder, for positive pressure is an
urgent indication for thoracentesis. It is therefore of primary
importance to properly estimate the quantity present, and thus to test
the intra-thoracic pressure. Great care and caution must be used,
because if we extract too much the operation may be followed by serious
results.[318] Large-sized canulæ should never be used, for fear of too
rapid withdrawal of fluid. It has been demonstrated that even with a
capillary perforated needle we can exercise more negative pressure than
is safe, especially toward the close of the operation, when there
supervenes a negative pressure exerted by the fluid remaining in the
pleural cavity. It is from these well-known facts that we recognize the
great value of Potain's ingenious addition to the aspirator of a
manometer of extreme simplicity, a kind of barometer or cuvette, which
is placed along the tube which withdraws the fluid. If we are not
satisfied with this new safety improvement of the aspirator, we may
adopt Douglass Powell's suggestion (_On Consumption, etc._) {597} of
fitting into the bottle a pressure-gauge, so as to know at any moment
what degree of aspiration is being used.

[Footnote 318: _Trans. de l'Assoc. pour l'Adv. des Sciences_, 6th
Session, 1877.]

The syphon method has been of late years very extensively used,
especially by Southey, W. H. Stone, and Garland, A. T. H. Waters,
Wilks, Oxley, and habitually by Douglass Powell. It is a feeble
aspirating force, which has very decided advantages. It is effective,
and acts slowly and uninterruptedly with a gentle and uniform negative
pressure. Its action allows the lung gradually to expand and the
displaced organs slowly to resume their normal position. It thus in
many cases furnishes us with a safe means of thoracentesis. (See
Surgical Treatment, in Pleurisy.)

{598}




{599}

DISEASES OF THE CIRCULATORY SYSTEM.


DISEASES OF THE SUBSTANCE OF THE HEART.

ENDOCARDITIS AND CARDIAC VALVULAR DISEASES.

CYANOSIS AND CONGENITAL ANOMALIES OF THE HEART AND GREAT VESSELS.

CARDIAC THROMBOSIS.

NEUROSES OF THE HEART.

DISEASES OF THE PERICARDIUM.

THE OPERATIVE TREATMENT OF PERICARDIAL EFFUSIONS.

DISEASES OF THE AORTA.

DISEASES OF THE CORONARY, PULMONARY, SUPERIOR MESENTERIC, INFERIOR
MESENTERIC, AND HEPATIC ARTERIES, AND OF THE COELIAC AXIS.

DISEASES OF THE VEINS.

THE CAISSON DISEASE.

DISEASES OF THE MEDIASTINUM.




DISEASES OF THE BLOOD, AND OF THE HÆMATOPOIETIC SYSTEM.


DISEASES OF THE BLOOD AND BLOOD-GLANDULAR SYSTEM.

DISEASES OF THE SPLEEN.

DISEASES OF THE THYROID GLAND.

SIMPLE LYMPHANGITIS.

{600}




{601}

DISEASES OF THE SUBSTANCE OF THE HEART.

BY WILLIAM OSLER, M.D.


Malpositions of the Heart.

We shall consider only such alterations as affect the whole organ;
faulty position of individual parts comes under the section upon
Malformations. It may, however, be mentioned that cases are known of
complete transposition of the chambers, the pulmonary artery and cavæ
being connected with the left, the aorta and pulmonary veins with the
right side, the valves being also transposed.[1]

[Footnote 1: Pazannuzzi, _London Med. Record_, 1877.]

Malpositions of the heart result either from errors of development, or,
more commonly, from changes in contiguous organs, usually the effect of
disease.

Of the congenital anomalies only a few are of practical interest. The
heart may be placed vertically in the chest, as in the foetus, the apex
beating at the lower end of the sternum; or, more rarely, the organ
lies transversely. Dextrocardia, the condition in which the heart is on
the right side of the body, is much more important, and is usually
associated with the transposition of the abdominal viscera--situs
inversus viscerum. In these cases the apex-beat is in the region of the
right nipple; a distinct area of dulness can be obtained to the right
of the sternum, in which situation the heart sounds are loudest; and,
lastly, there is pulmonary resonance in the place of normal cardiac
dulness. In the great majority of cases--70 out of 78[2]--the abdominal
organs are also transposed, the liver on the left side, the spleen on
the right; but in a few instances the heart alone has been misplaced,
and under such circumstances care is needed to diagnose the condition
from dislocation of the organ due to old-standing lung disease with
retraction.

[Footnote 2: Gruber, _Virchow's Archiv_, 1865.]

More serious congenital malpositions, but of less practical importance,
are the cases of ectopia cordis, which may exist in all grades, from
simple failure of closure in the sternum--fissura sterni--to the most
extreme condition, in which the naked heart lies outside the
chest-wall. Hodgen[3] and March[4] have each described remarkable
examples of the latter condition. In other instances the heart lies
free in the neighborhood of the neck, or it may be in a congenital
umbilical hernia.

[Footnote 3: _American Practitioner_, xviii. p. 107.]

[Footnote 4: _Trans. of the New York State Medical Society_, 1859.]

The malpositions with which we are more immediately concerned arise
from disease of the heart itself or its membranes, or from disease of
contiguous organs.

We judge of the situation of the heart by the site of the apex-beat, by
the position and extent of the area of dulness, and by the character of
the sounds. So constant in health is the position of the apex-beat in
the fifth intercostal {602} space that in our examination of the heart
we seek first to determine its existence as affording the most
important information of the normal situation of the organ. The area of
dulness is a much more variable guide, depending as it does so greatly
on the degree of distension of the lungs. When, as sometimes happens,
neither apex-beat nor area of dulness can be obtained, the position of
maximum intensity of the heart sounds becomes an important indication.

In regard to the effect of respiratory movements in the position of the
heart, with each inspiration it is drawn down slightly by the descent
of the diaphragm, and it is separated from the chest-wall by the
inflation and descent of the left lobe of the lung--in deep inspiration
to such a degree as to obliterate the area of dulness and to prevent
the systolic impulse from reaching the intercostal space.

The effect of gravity on the position of the heart is well illustrated
by the more forcible and extended beat when the chest is bent forward
or when the person is turned toward the left side--procedures
frequently resorted to when from any cause the apex-beat is obscure.

Of diseases of the heart itself, dilatation and hypertrophy are very
common causes of displacement, and in general enlargement the organ may
occupy a very considerable part of the left side of the chest, and the
apex-beat in the seventh or eighth space in the axillary line.
Hypertrophy of the left ventricle alone pushes out the apex-beat, while
enlargement of the right ventricle gives a stronger impulse toward the
left border of the sternum and a more marked pulsation below the
ensiform cartilage. Hypertrophy and dilatation of the auricles increase
the width of the cardiac dulness, and may cause marked pulsation in the
second and third spaces on either side of the sternum.

In pericardial effusion the heart is pressed backward and the apex
slightly raised.

To understand clearly the effects upon the position of the heart of
disease of contiguous organs, we must bear in mind their mutual
relations. Situated in the mediastinum between the lungs on either
side, it is subject to the elastic traction of these organs, which
counterbalance each other, but if from any cause the elastic tension of
one lung is suppressed, as in pneumothorax or in pleural effusions,
then the other lung may also collapse to a slight degree, and pull over
the mediastinum and with it the heart. The pericardium is firmly fixed
below to the diaphragm, chiefly to the central tendon, to a slight
extent also to the muscular substance, but the union with the diaphragm
is so intimate that there can be but little movement of the attached
portion. The mobility of the heart is measured by that of the
mediastinum and pericardium, and through these alone the displacing
forces act. The limits of dislocation are determined by the attachments
of the central tendon, of the inferior cava, and the great vessels at
the root. Within the pericardium the heart has a certain degree of
mobility, but this is confined, as regards pressure or traction
effects, to rotation upon its axes.

Of the malpositions due to changes in contiguous organs, the following
may be considered:

Changes in the Chest-wall.--The gradual incurvation of the ribs and
costal cartilages in some cases of rickets may alter the position of
the heart.

Curvature of the spine, particularly cases which narrow to a great
extent the upper outlet of the thorax, may produce very considerable
displacement of heart and great vessels. There may be areas of
extensive pulsation on either side of the sternum, and the condition
may simulate aneurism of the aorta, as in a case reported by
Bramwell.[5]

[Footnote 5: _Lancet_, 1878, i.]

In certain affections of the lungs the position of the heart is much
altered. {603} In emphysema, when extensive, the apex is directed more
to the right, and the organ is somewhat lower than normal, on account
of the depressed condition of the diaphragm. The heart may also occupy
a more transverse position. The area of cardiac dulness may be greatly
reduced by the distended left lung, and there is usually forcible
epigastric pulsation, due to the lower position of the organ and the
hypertrophy of the right ventricle which almost always accompanies
emphysema.

The most marked displacement is produced by fibroid induration of the
lung, with contraction--cirrhosis. As the process of condensation goes
on, the chest-wall is gradually flattened, and the mediastinum, with
the heart, drawn toward the affected side. When the left lung is
involved, the heart may be completely to the left of the median line,
and is usually drawn upward as well. There may in such cases be a very
wide area of impulse, as the heart occupies the position of the left
lung in front. In cirrhosis of the right lung the organ is drawn toward
the right side, and the area of visible impulse may be in the third and
fourth interspaces to the right of the sternum. In the process of slow
traction the heart revolves upon itself and the left chambers come
uppermost. In many cases of chronic phthisis, when the anterior margin
of the left lung is involved, the retraction from induration may leave
a large portion of the heart exposed and increase the area of visible
pulsation; sometimes, when there is much contraction of the upper lobe,
the organ is drawn up and to the left, and the apex-beat may be in the
fourth interspace.

The pressure of a pneumonic lung may depress the diaphragm and draw
down the heart.

Abnormal conditions of the pleuræ are frequent causes of cardiac
displacements. In pneumothorax there is collapse of the lung on the
affected side, and the elastic traction of the sound lung draws over
the mediastinum and heart. It is not that the heart is pushed over, as
so often stated, but the tension of the other lung, being unopposed,
pulls the mediastinum toward the sound side. Later, when, as usually
happens, effusion takes place, the pressure assists in the
displacement. In pleuritic effusion dislocation of the heart to one
side is almost constant if the amount of fluid is at all considerable.
Here pressure plays the most important part, and the heart is gradually
pushed over by the effusion; but the elastic tension of the lung on the
sound side is also concerned in the result. In right-sided effusion the
whole organ may be to the left of the median line, and from the
depression of the diaphragm it is usually lower in the chest, so that
the apex-beat may be in the sixth, rarely the seventh, interspace in
the axillary line. When the exudation is on the left side, the
dislocation is more marked, and there may be a cardiac impulse at the
right nipple or even beyond it. A common error is to regard the
pulsation as due to the apex, but it is invariably caused by some
portion of the right chambers, usually the ventricle. Even in the most
extensive effusion the apex is probably never pushed beyond the right
border of the sternum, and the relative position of apex and base is
not changed. This I have carefully noted in several autopsies.[6]

[Footnote 6: Fig. 76 of Sibson's article on "Displacements of the
Heart" in _Reynolds's System of Medicine_ gives an incorrect idea of
the position of the organ in these cases, as the apex is represented as
beating beneath the right nipple.]

In the gradual absorption of a pleuritic effusion, serous or purulent,
the heart may not only regain its normal position, but is in many
instances drawn toward the affected side by the contracting false
membranes.

Of conditions of the mediastinum producing displacement, two only need
be mentioned--aneurism and tumor. Very large aneurisms of the arch
usually press the heart downward, and its axis may be transverse; but
much depends on the direction of growth, and a slight lateral and
downward dislocation is most frequently met with. Tumors do not
necessarily {604} cause displacement, but when large there may be some
dislocation in the direction of the growth of the mass. Most extensive
masses of mediastinal cancer may occur without any disturbance of the
position of the heart.

Diseases of the abdominal viscera not uncommonly produce dislocation of
the heart, generally upward. Extensive peritoneal effusion, gaseous or
fluid, forces up the diaphragm, and with it the heart, which may assume
the transverse position, and the apex beat as high as the third
interspace. Gas much more readily than fluid rapidly lifts the
diaphragm and produces upward dislocation of the heart. Diaphragmatic
hernia of intestines or stomach may push the heart up or to one side.

Conditions of the liver not infrequently affect the position of the
heart. Abscess or hydatid cysts of the left lobe may push the organ up
and to the left. More rarely large hepatic tumors drag the diaphragm
down, and with it the heart. Very great splenic enlargement, as in
leukæmia, may push up the diaphragm and lift the heart.

Other abdominal growths, as large retro-peritoneal and ovarian tumors
or aneurism of the abdominal aorta, may occasionally produce the same
effect. Knowsley Thornton has given in Fothergill's work on the _Heart_
an excellent account of the upward displacement of the heart in ovarian
disease.

As a very rare circumstance, the heart is displaced by accidental
injury to the chest-walls. The case which Stokes relates of this kind
was probably, as he subsequently suggested, due rather to the effects
of the pleuritic effusion which followed the accident.

The dislocations of the heart when gradually induced rarely disturb to
any serious extent the functions of the organ.


Myocarditis.

Inflammation of the heart-muscle is rarely primary; usually it is
associated with endo- or pericarditis, strain,[7] embolic processes,
disease of the arteries, or the presence of certain
poisons--diphtheritic, rheumatic, etc.--in the blood.

[Footnote 7: Some French writers refer specially to the occurrence of
myocarditis from strain or prolonged muscular exercise--myocardite des
surmenes. Peter (_Maladies du Coeur_, Paris, 1883) gives two cases
(without autopsy), and quotes a case from Revilliod, whose work (_La
Fatigue_, Lausanne, 1880) I have not been able to consult.]

We may recognize three forms--acute suppurative, acute interstitial,
and chronic myocarditis. By many writers the parenchymatous
degeneration so frequent in fevers is regarded as an inflammation, but
it is the result of a process which we can scarcely term inflammatory.

Acute suppurative myocarditis is almost invariably associated with
pyæmia or with malignant endocarditis, and in most instances may be
regarded as embolic. In severe pyæmia from any cause foci of
suppuration are not infrequently met with in the walls of the
ventricles. There may be multiple abscesses or a single purulent
collection varying in size from a pea to a walnut. Numerous miliary
abscesses are not so often met with in ordinary pyæmia as in
endocarditis. If large, the abscess may burst into the heart or into
the pericardium and excite inflammation of this membrane; or, indeed,
without perforation, as I saw in one instance. The calcareous nodules
occasionally found in the muscle-substance have been regarded as healed
abscesses. Suppurative myocarditis is a frequent result of malignant
endocarditis, and we meet with it either in the form of miliary
abscesses, scattered in numbers through the substance, or as large
solitary abscesses at the bases of vegetative outgrowths or in
connection with excavating ulcers of the endocardium, valvular or
mural. The small embolic abscesses vary in size from {605} a pin's head
to a pea, and may occur in extraordinary numbers in the
muscle-substance of all the chambers. They present usually a central
grayish-white focus of suppuration surrounded by a zone of
deeply-congested and hemorrhagic tissue. Microscopically, there is a
central infiltration of leucocytes with destruction of the
muscle-fibres, and in every instance colonies of micrococci can be
readily discovered. These abscesses are identical in character with
those occurring in the kidneys, intestines, and brain. Sometimes at the
base of large endocardial outgrowths, particularly of the aortic
segments, abscesses are found extending deep into the muscle-substance,
and even perforating the wall. These occur most often in the left
ventricle, but occasionally in the right, as in a case of stenosis of
the pulmonary valves at the Montreal General Hospital, in which there
was an abscess cavity in the wall of the right ventricle the size of a
marble, situated at the base of some endocardial vegetations. The acute
ulcer of the heart is of the nature of a suppurative myocarditis,
having its starting-point, in the great majority of cases, in the
endocardium. It may perforate the wall of the ventricle, as in the
cases of Mackenzie[8] and Keating.[9] The blood-pressure in the
abscess-cavity may dilate the wall, and form what is known as acute
aneurism of the heart.

[Footnote 8: _Path. Soc. Trans. London_, xxxiii.]

[Footnote 9: _Trans. of the College of Physicians of Philadelphia_,
1879.]

Acute interstitial myocarditis occurs in connection with the infectious
fevers, and also with pericarditis, more rarely endocarditis. It is
characterized by the presence of numerous round cells in the
interfibrillar tissue, multiplication of the corpuscles, and
degeneration, granular or fatty, of the muscle-fibres. The coarse
appearances are--a relaxed state of the cardiac walls, pale or turbid
condition of substance, in extreme instances a sodden, soft friable
state, so that the muscle readily tears on pressure. In acute
pericarditis the superficial myocardium, for a line or two beneath the
membrane, frequently presents this condition in a typical manner; it
looks pale and turbid, contrasting strongly with the deeper parts, and
on examination presents infiltration of leucocytes, swelling of the
interstitial tissue, sometimes effusion of blood-corpuscles, and a
swollen, granular, or fatty state of the muscle-fibres. Although the
process may be intense, suppuration rarely occurs, whereas in
myocarditis supervening upon inflammation of the endocardium it is, as
we have seen, not uncommon. A similar diffuse interstitial process is
met with in many of the fevers. In rheumatism, typhus, scarlet fever,
small-pox, and diphtheria the myocardium may be found relaxed and soft,
the chambers dilated, the substance pale, easily torn, in some
instances extremely soft; and this condition has been variously
described as inflammatory or degenerative. While not denying that such
a state of the muscle-fibre may be brought about by the action of the
fever or the influence of some specific poison without any signs of
inflammatory action, yet in other instances changes have been found
which are evidently of the nature of a myocarditis. In these cases the
intermuscular connective tissue is swollen, infiltrated with round
cells and nuclei, the vessels are dilated, and often there are minute
extravasations and the muscle-fibres are granular and fatty, with
indistinct striæ and nuclei. As Leyden[10] has pointed out, this
condition probably affords an explanation of some of the cases of
sudden death in diphtheria. It may occur without the coarse or
microscopic appearance of degeneration of the muscle-fibres, and when
of any duration may produce areas of atrophy. Though usually diffuse,
it may be patchy and limited in distribution. Martin[11] has described
in cases of sudden death in diphtheria and typhoid fever an acute
endarteritis of the small branches of the coronary arteries, which
probably has a close relationship with this acute interstitial
myocarditis.

[Footnote 10: _Zeitschrift für klinische Medicin_, Bd. iv.]

[Footnote 11: _Revue de Médecine_, 1881.]

{606} The SYMPTOMS of acute myocarditis are those of cardiac weakness
and irritability, and it is the conditions under which these occur
which make us suspect involvement of the myocardium rather than any
special features pertaining to the disease. We may reasonably suspect
its presence in a case of rheumatism, puerperal fever, or other
specific fever when the patient complains of cardiac distress or actual
pain, with shortness of breath, and on examination we find a weakened
impulse, feeble, indistinct first sound, and a small, irregular pulse.
The area of heart-dulness is increased, and there may be a murmur due
to muscular incompetence. There is usually fever, but this is generally
due to the primary affection. The symptoms are those of a weak and
dilated heart, and are peculiar only in the mode of onset and the
circumstances under which they arise. A point of note observed by
Stokes is the weakening or disappearance of organic murmurs during an
attack of acute myocarditis. In acute pericarditis grave implication of
the myocardium may be suspected when the pulse gets small and rapid,
dyspnoea urgent, and the cardiac pain is increased. Such symptoms, in
the absence of copious effusion, would appear to indicate extension of
the inflammation to the heart-muscle. Even the occurrence of
suppuration has no distinctive symptoms, as it almost invariably occurs
as part of a pyæmic process, and the cardiac weakness which supervenes
may be regarded as an outcome of the septic or febrile condition. The
bursting of an abscess into the pericardium will excite violent
pericarditis. In the case of Kortüm, referred to by Friedrich,[12] an
abscess in the septum burst into the ventricle; the symptoms, which
developed suddenly during a lecture, were a sense of constriction in
the chest, dyspnoea, and lividity, and death occurred in six hours.

[Footnote 12: _Virchow's Handbuch_, Bd. v.: "Herzkrankheiten," S. 275.]

The DIAGNOSIS can rarely be made with certainty; at the best we can
suspect its presence under the conditions above mentioned.

The course of suppurative myocarditis is always unfavorable, but the
fatal termination of the case is usually dependent on concomitant
causes. The possibility of recovery in some instances of abscess of the
heart is suggested by the occurrence of caseous and cretaceous masses,
probably the remnants of collections of pus.

The chief danger in interstitial myocarditis is heart paralysis and
sudden death, as occur in diphtheria and occasionally in rheumatism.
From mild grades of the disease recovery may take place, and even when
general and severe it has often been some indiscretion which has
induced the collapse, as sudden sitting up in bed or getting out to
attend to the calls of nature. Possibly the slight intramuscular scars
and spots of atrophy furnish evidence of past acute myocarditis.

When suspected, the TREATMENT should consist of absolute rest, muscular
and mental, with careful feeding and stimulation. If a rheumatic case
upon the alkaline or salicylate treatment, the remedies should be
stopped. I saw sudden death from heart failure in a case of acute
rheumatism in which during four days the full alkaline treatment of
Fuller was followed, and in which, by mistake, a much larger quantity
of the bicarbonate of soda was given each day than had been intended.
Strychnia and small doses of quinine may be given. Shall digitalis be
employed in acute myocarditis? Upon this point authorities differ. If
we regard it as simply increasing the force of the muscular
contractions, we can understand the fear of straining a weakened heart;
but digitalis has important trophic influences, and, while it
stimulates the vigor of the contraction, improves the nutrition of the
heart-muscle and renders it better able to contract. After all, the
question amounts to the giving of digitalis in dilatation, and with a
weak first sound and feeble action the careful administration, in
conjunction with stimulants, will be found beneficial. Peter[13] speaks
highly of the application of a blister in the region of the heart.

[Footnote 13: _Loc. cit._]


{607} Chronic Myocarditis (Fibroid Heart).

A condition characterized by the substitution in areas of variable
extent of a fibrous connective tissue for the muscular substance. It is
an interstitial growth, comparable to the cirrhosis of other organs,
and the muscle-elements in the affected regions are wasted or entirely
destroyed. The process may occur in a mild grade throughout the organ,
but it is more common to find it distributed in certain parts which
seem specially prone to this form of degeneration.

The conditions under which it is most likely to occur are those which
we find in connection with arterio-sclerosis. It is an affection of
adult and advanced life, and is met with most frequently associated
with disease of the coronary arteries. In chronic valvular affections
it is very common, and may be part of the so-called cyanotic induration
or an extension from the thickened endocardium. Sometimes it seems a
part of a general arterio-capillary fibrosis. In a few cases there is
direct extension from the pericardium. Rheumatism is in this way
indirectly responsible; possibly some of the cases are directly
traceable to acute interstitial myocarditis occurring in this disease.
Chronic alcoholism, syphilis, and gout are prominent factors in the
etiology. Some of the most marked cases give no clue in the history or
habits of any conditions which we could reasonably connect with the
disease. Males are more often affected than females. The tendency to
arterio-sclerosis seems to run in some families. Mental anxiety is not
without influence, and when the disease is established seems very
liable to bring on the anginoid attacks. The situation and extent of
the fibrosis are very variable. The papillary muscles and the columnæ
carneæ of the left ventricle are most frequently affected, less often
the corresponding structures on the right side. The middle portion of
the muscular bundles and the apices of the papillæ are first involved.
In the latter the process may extend almost to their bases, but on
section it will be found that it is more advanced in the superficial
than the deep parts. This change is very common in cases of valvular
disease with hypertrophy, especially mitral stenosis, but it often
occurs in elderly persons who have had no special heart symptoms.

Beneath patches of pearly-white thickened endocardium local fibrosis
may occur, often seen at the upper part of the septum in left
ventricle, and in the dilated and thickened left auricle of mitral
stenosis, and occasionally in other parts. This is usually regarded as
an extension from a chronic endocarditis. More rarely the fibrosis
extends from a thickened pericardium, but cases are on record of the
conversion of the outer layers of the muscular fibres into a firm, hard
tissue. We frequently meet with scattered areas of fibrosis in septum
and ventricular walls without any implication of peri- or endocardium.
During foetal life an endo-myocarditis may occur in the conus of the
right ventricle, less frequently in the left, and produce very great
narrowing by the gradual contraction of the newly-formed tissue. But
the condition to which the term fibroid heart can be most properly
given is an extensive affection of the left ventricle, involving most
commonly the anterior wall near and at the apex and the lower part of
the septum. In these cases there may be marked bulging at the apex, and
on section the wall cuts with great resistance, and a dense fibrous
tissue of a grayish-white appearance occupies the position of the
myocardium. In extreme cases a large part of the septum and anterior
wall is in this state, and may present only traces of muscular tissue.
There is usually thinning, sometimes thickening, of the affected
portions, and the septum bulges toward the right ventricle. The
endocardium is opaque, often much thickened, and directly continuous
with the fibrous tissue. The columnæ carneæ may be narrow and
flattened, and the lacunæ {608} between them very small. The chamber is
usually dilated. The upper third of the septum and the base and
posterior wall of the ventricle in such cases present a marked contrast
to the affected parts, and may look natural, but more commonly are
hypertrophied. The other chambers may not show any special change or
there may be scattered areas of fibrosis. The thinning and dilatation
at the apex and septum are the conditions which precede and lead to the
formation of cardiac aneurism. The valves may be normal, but in many
cases there is sclerotic endocarditis and retraction. The histological
appearance varies much with the stage of the process. When early or
where advancing, the muscle-bundles are seen separated by round and
elongated cells. The process is usually more marked about groups of
fibres, which gradually become isolated by the increase of the growth,
and in this way one often sees streaks or patches of muscle-tissue
surrounded by the fibrous elements. The destruction of the muscle-cells
is apparently by pressure; they gradually waste and present the
condition of brown atrophy, the pigment of which remains and indicates
the position of the fibres. The intimate pathology of the process is of
great interest. Doubtless in some instances we may attribute the
fibrosis to an extension of an indurative process from the endo- or
pericardium, but the researches of Tautain,[14] Martin,[15] Huber
(Karl),[16] and others have thrown a new light on the subject, and it
seems probable that in most instances the fibroid degeneration is
associated with changes in the coronary arteries. The former describes
an endarteritis and a periarteritis of the small vessels, leading to
disturbance of nutrition and increase of the connective tissue
(sclérose dystrophique). Huber in a considerable number of cases has
traced the connection between the arterio-sclerosis, chiefly of the
smaller twigs, and the indurative process. The region supplied by the
obliterated arteriole is in the condition of an infarct and undergoes
an anæmic necrosis, and subsequently by a proliferating myocarditis is
transformed into a fibroid area. The condition is well described and
figured by Ziegler.[17] Why this obliterating endarteritis should be so
limited in the majority of cases to the vessels of the left ventricle
is not very clear. The parts most distant from the aorta seem most
liable to the process, as the apex and the tips of the papillæ; and it
is interesting in this connection to note that the left coronary artery
is more frequently diseased than the right.

[Footnote 14: _Thèse de Paris_, 1878.]

[Footnote 15: _Revue de Medicine_, 1883.]

[Footnote 16: _Virchow's Archiv_, Bd. lxxxix.]

[Footnote 17: _Pathologische Anatomie_, Lief. ii., 1884.]

In the milder grades of fibrous myocarditis, when only the apices of
the papillæ and thin layers beneath the endocardium are involved, the
heart does not appear to be seriously affected; but when of any extent
the vigor and force of the contractions are impaired, and the ventricle
is unable to do the work of a healthy muscle. Compensatory hypertrophy
is not readily established, possibly on account of the arterial
sclerosis on which many of the cases seem to depend, although in rare
instances, as in a specimen referred to by Quain,[18] there may be very
great muscular hypertrophy. Dilatation of the left ventricle is much
more apt to follow, as the fibroid walls have not the resisting power
of muscular tissue, and the patients finally present a clinical picture
of heart failure. The gradual yielding of the fibroid region may result
in aneurism.

[Footnote 18: "Lumleian Lectures," _Lancet_, 1872, i.]

There are no characteristic symptoms to indicate the condition. The
fibroid heart is a weak heart, and it is scarcely possible to
distinguish it from fatty degeneration. A feeble, irregular, sometimes
slow, pulse, dyspnoea on exertion, and painful anginoid
attacks--symptoms which may have persisted for many years--are special
clinical features in many cases. In a patient I examined some years ago
for Palmer Howard of Montreal--a typical instance of the condition
under consideration--the first symptoms began eight years before death
with angina, and there were repeated attacks of cardiac asthma. {609} A
careful study of the case was made by Howard[19] extending over several
years, and weak heart, dyspnoea on exertion, and anginoid attacks were
the prominent symptoms.

[Footnote 19: "Fibroid Disease of the Heart," _Canada Med. and Surgical
Journal_, vol. viii., 1880.]

Several very careful studies of the disease have been made within the
past few years.[20] Among the symptoms the following may be specially
considered. The first place seems accorded by all to the cardiac
weakness, and in consequence the pulse is feeble. By some (Rühle)
irregularity is regarded as a special feature (delirium cordis), but
Ebstein refers to three cases in which the pulse was always regular.
Juhel-Renoy also speaks of it as frequent and regular. In many cases
the number of beats appears about normal; in others there is a great
increase; while in a third set the pulse may be very slow, sinking to
40 or 50 per minute. It is evident that in regard to regularity and
frequency of the pulse there are very great differences. In this
connection it is interesting to refer to the case of thrombosis of the
coronary artery reported by Hammer,[21] in which the pulse sank to 8
per minute.

[Footnote 20: Rühle, "Zur Diagnose der Myocarditis," _Deutsches Archiv
f. klin. Med._, Bd. xxii.; Ebstein, _Zeitschrift für klinische
Medicin_, Bd. vi.; Leyden, _Ibid._, Bd. viii.--a most important and
exhaustive article; Welch, in a paper read before the Medical Section
of the American Medical Association, Washington Meeting, 1884;
Juhel-Renoy, _Archives gén. de Médecine_, Juillet, 1883.]

[Footnote 21: _Wiener Med. Wochenschrift_, 1878, No. 5.]

Angina is a most important symptom; attacks may recur for years, and
death may take place in a paroxysm. Asthmatic attacks are very common:
a feeling of impending suffocation, and gasping for breath amounting in
some instances to urgent dyspnoea. Oedema of the lungs may occur in
these attacks. Fainting and pseudo-apoplectic attacks are frequent
symptoms. The physical signs are not very definite or constant. The
apex-beat may be displaced and weak, perhaps unrecognizable. With an
increase in the area of dulness this is a sign of dilatation. A
systolic murmur at the apex is not infrequent. There may be the bruit
de galop; gradual heart failure, with general dropsy, is the mode of
termination in a considerable number of cases.

The DIAGNOSIS can rarely be made with certainty. The combination of
weakened heart, atheromatous arteries, and angina attacks occurring in
a person above fifty years of age is certainly suggestive of the
existence of this condition; but, as will be seen, this group of
symptoms occurs also in fatty degeneration, although the anginoid
attacks are probably not so frequent.

In spite of the admirable clinical memoirs above referred to, we are
still in need of careful studies of an extensive series of cases,
whereby we can get information which will enable us to distinguish more
clearly than we can at present the diseases of the myocardium from one
another. In this respect our pathological knowledge is in advance of
our clinical.

The TREATMENT is largely that of cardiac dilatation and angina, which
will be elsewhere considered. The condition is a chronic one, and often
associated with hypertrophy, and many of the symptoms are dependent
upon failing compensation. Under such circumstances digitalis is
indicated, but when there are attacks of angina caution must be
exercised in its use.


The Degenerations of the Heart-Muscle.

Under this division we shall consider the following conditions, all of
which are characterized by an alteration in the quality and an
impairment of function in the affected tissue: 1. Anæmic necrosis; 2.
Parenchymatous degeneration; 3. Fatty changes, infiltration and
degeneration; 4. Brown atrophy; 5. Amyloid degeneration; 6. Hyaline
degeneration; and 7. Calcareous degeneration.

{610} 1. Anæmic necrosis is a condition which results in the
heart-muscle when a branch of the coronary artery is blocked either by
a thrombus or an embolus, or is obliterated by a progressive sclerosis.
The region supplied by the affected vessel is deprived of blood and
undergoes a process of infarction. In some instances the tissue is not
infiltrated with blood, as in an ordinary infarct, but has a pale
yellowish color and is very soft. When there is extravasation the color
is more reddish-brown. Histologically, the muscle-cells are found in a
state of granular degeneration, and on staining the nuclei do not take
the tint, and the whole tissue ultimately assumes the homogeneous
granular aspect of coagulation necrosis. There may be fatty
degeneration in the contiguous muscle-fibres, and finally, as with
infarcts in other organs, fibroid induration takes place. This process,
as before mentioned, plays an important part in the production of the
fibroid patches scattered through the myocardium. When fresh, the
softening of the affected region may be marked, and the name myomalacia
cordis which Ziegler[22] has suggested is so far suitable, but it seems
more appropriately applied to that condition of general softening of
the organ met with in severe fevers. This process most frequently
affects the left ventricle, and if extensive may lead to rupture.

[Footnote 22: _Loc. cit._]

The clinical aspects of this condition, as induced by sclerosis of the
coronary arteries, have been recently studied with great care by
Leyden.[23] In acute cases death occurs in a few hours with symptoms of
intense angina pectoris and heart failure. The subacute cases are
characterized by recurring anginoid attacks lasting from a few minutes
to half an hour. There may be attacks of asthma with heart weakness,
and signs of oedema of the lungs. The clinical picture is that of
angina pectoris, and the patient may have had similar attacks on
previous occasions.

[Footnote 23: _Zeitschrift f. klin. Med._, Bd. vii., 1884.]

2. Parenchymatous Degeneration.--The relation of inflammation of the
heart-substance to this degeneration is still somewhat indefinite. I
have under Myocarditis described an acute interstitial form
characterized by inter-fibrillar swelling with exudation and
proliferation of corpuscles, and often granular or fatty degeneration
of the muscle-cells. These changes may certainly be regarded as
inflammatory, and they are met with either in association with endo- or
pericarditis or in connection with specific fevers. Under the term
parenchymatous degeneration or cloudy swelling Virchow described[24] a
change of frequent occurrence in the heart-muscle and elsewhere, which
I think should be distinguished from myositis, although the two
processes may lead to alterations difficult to distinguish
macroscopically. It is characterized by a pale, turbid state of the
cardiac muscle, general, not limited, and a relaxed, soft, brittle
condition of the walls. The turbidity and softness are the special
features; there are no peri- or endocardial changes--simply the loss of
color and consistence. It is the softened heart of Laennec and of
Louis; and Stokes speaks of an instance in which "so great was the
softening of the organ that when the heart was grasped by the great
vessels and held with the apex pointing upward, it fell down over the
hand, covering it like the cap of a large mushroom."[25]
Microscopically, the fibres are indistinct, the protoplasm occupied by
fine granules which obscure the striæ, and sometimes the nuclei.
Proliferative changes rarely occur, although swelling and
multiplication of the nuclei and the interstitial cells have been
described. The granules may be extremely minute, or so large that they
are mistaken for fat. They are generally uniform in size, and are
scattered irregularly through the fibres. In extreme grades the entire
fibre may be occupied by them, and no trace of structure can be seen.
Dilute acids and alkalies dissolve the granules, but they resist the
action of ether, indicating their albuminous nature. This condition is
met with in the infectious diseases--typhoid, {611} typhus, small-pox,
pyæmia, remittent fever, etc.--particularly when the disease is
protracted and the temperature high. Apparently, we must regard it as
an expression of the effect of the poison upon the metabolism of the
fibres, inducing a separation of albuminous particles in a granular
form. That the high temperature alone does not produce it is
demonstrated by its absence in many other diseases in which this
condition prevails. The relation to fatty degeneration is not clear. It
would appear to precede the development of this change.

[Footnote 24: _Archiv_, vi.]

[Footnote 25: _Diseases of the Heart_, Am. ed., p. 373.]

The effect of this degeneration is virtually the same as that of
myocarditis, already described. It produces the weak heart of fever so
well described by Stokes,[26] with indistinct impulse, feeble or
imperceptible first sound, and progressive diminution of contractile
power. There is often a great reduction in the number of beats, which
may sink to 40 or 50 per minute. In severe cases of typhoid fever we
often have an opportunity of studying the progressive enfeeblement of
the heart with weakening or disappearance of the first sound.

[Footnote 26: _Loc. cit._, chap. vii.]

To Stokes we are indebted for the suggestion of the use of alcohol in
this condition, and the experience of the past forty years has fully
confirmed this practice of the Dublin school.

3. Fatty Heart.--Two conditions of the heart are recognized under this
heading--viz. fatty infiltration and fatty degeneration.

Fatty Infiltration.--Cor adiposum, Lipomatosis cordis, and Fatty
hypertrophy or overgrowth are synonyms found in the older and more
recent works.

A condition in which there is an excess of fat beneath the pericardium
and a growth of the same between the fibres of the myocardium. There is
normally a certain amount of fat in the cardiac groves, particularly
the auriculo-ventricular, and along the coronary arteries. An excess is
not infrequently met with in connection with general atrophy, whether
the result of disease or the natural decay of old age. Here it serves
as padding, and has no pathological significance. In very corpulent
persons there is always much subpericardial fat; it forms a part of the
general obesity, and in this state an excessive accumulation may lead
to a dangerous or even fatal impairment of the contractile power of the
heart. Obesity is the expression of a morbid tendency, generally
hereditary, to the deposition of fat in the connective tissues. A
sedentary life and the consumption of food rich in carbohydrates favor
this tendency, but we see it arise under conditions just the opposite
when the predisposition to polysarcia is marked. Males are more usually
affected than females, at least in Great Britain and Germany.

In the inspection of the bodies of very corpulent persons we find the
mediastinum occupied by masses of fat which may completely cover the
pericardium. The entire heart may be enveloped in a thick sheeting of
fat, through which not a trace of muscle-substance can be seen. Along
the groves, the regions of normal deposit, the layer may be an inch or
more in diameter. In some cases the muscle-substance beneath seems but
slightly involved; there may be superficial infiltration and
penetration of columns of fat between the bundles, but the thickness of
musculature is normal, and apart from the excessive deposition there is
not much amiss. In other instances the muscle-substance is seriously
affected; on section of the ventricular wall the fat is seen to
infiltrate the entire muscle, separating strands of fibres and reaching
almost to the endocardium. There may be places, indeed, in the thinner
parts of the ventricular walls in which there appears to be complete
substitution of the muscle by fat. Even the papillary bundles may
contain adipose tissue. The chambers are usually dilated and the entire
organ soft and relaxed. Microscopically, the fat-cells are everywhere
{612} seen infiltrating the muscle-tissue, separating the fibres and
inducing atrophy. In some cases, even when the condition is advanced,
the muscle-fibres appear normal, but in the majority fatty degeneration
is also present. Often in these cases the coronary vessels will be
found atheromatous.

The SYMPTOMS of fatty overgrowth will depend greatly on the degree of
infiltration, the state of the muscle-fibres--whether normal or
degenerated--and on the presence or absence of coronary atheroma. Many
very fat persons enjoy excellent health and have actively beating
hearts, which fail them only on severe exertion, when they get out of
wind and experience cardiac distress, perhaps palpitation. The pulse is
good and the heart sounds are clear. The signs of heart failure (which
may be due either to excessive infiltration or secondary degeneration
of the muscle, or both combined) in obese persons are generally very
marked--breathlessness on slight exertion, amounting oftentimes to
dyspnoea; attacks of asthma of a distressing nature coming on without
cause or after a full meal; cough, with or without bronchitis;
dizziness and pseudo-apoplectic attacks. Sudden death from syncope or
rupture of the heart is common. Dropsical symptoms and cyanosis may
supervene. The physical signs are those of heart weakness; impulse
imperceptible or very diffuse; area of dulness increased, but often
hard to delimit, with fat chest-walls and fatty mediastinum; sometimes
a soft systolic murmur at apex; radial pulse rapid, weak, and
irregular, in some instances very slow.

The DIAGNOSIS of the condition with such a series of symptoms in an
excessively stout person can offer but little difficulty.

The TREATMENT in the early stage should be directed to reducing the
general obesity, and such persons should be warned against taking too
violent exertion or subjecting the heart to unusual strain. Moderate
exercise, mental quietude, and careful dieting may do much toward
postponing heart failure, which, when established, calls for the
treatment which shall be described under Dilatation.

Fatty Degeneration.--An anomaly or disturbance of nutrition in which
minute particles of fat accumulate in the protoplasm of the
muscle-fibres, and impair the functional activity of the organ.

This is one of the most common of post-mortem conditions, and in mild
grades is met with in a great variety of diseases. The fat is a product
of the metabolism of the protoplasm of the muscle-fibres, and in a
normal state it (or its immediate antecedents) is oxidized; but when
either there is increased transformation or reduced oxidation the
products accumulate in the protoplasm, and are evident as minute
molecules or as distinct fine oil-droplets. The condition of cloudy
swelling or parenchymatous degeneration appears in many cases to
precede that of fatty degeneration, and sometimes the granules are of
such a size, so abundant, and resemble fat so closely that chemical
tests alone can distinguish between them.

A practical division of fatty degeneration is into--1, cases in which
the process has attacked a normal heart; and 2, cases in which we find
it associated with valvular disease and hypertrophic states of the
muscular walls.

In the first group we have _(a)_ The degeneration which accompanies the
failing nutrition of old age, of wasting diseases, and of cachectic
states. _(b)_ The fatty change in the heart-muscle so often a sequence
to, or coexisting with, the parenchymatous degeneration of fevers.
_(c)_ The extreme fatty degeneration so constantly associated with
profound anæmia. _(d)_ Certain poisons, particularly phosphorus;
arsenic, lead, and antimony also act in the same way. The slow
poisoning by alcohol is a very frequent cause of a gradually fatty
degeneration of the heart. And _(e)_ some local causes are important in
inducing this change in the previously normal organ. Pericarditis is
almost invariably associated with involvement of the superficial
myocardium, {613} either inflammatory or degenerative. Disease of the
coronary arteries is a frequent and important cause of fatty
metamorphosis. When due to the general conditions above mentioned, the
affection is widely distributed in the organ; when the result of
gradual narrowing of the vessels by atheroma, the distribution is in
the regions supplied by the affected vessels.

The second group comprises those cases in which the fatty degeneration
involves the muscle-substance in a condition of hypertrophy, and is an
important element in inducing the disturbance of compensation upon
which so many heart symptoms depend. Here the process may be more
local, affecting, for example, the left ventricle chiefly, as in the
hypertrophy from aortic valve disease or in association with contracted
kidneys, or the right ventricle in chronic lung affections and mitral
stenosis. More rarely we find the process confined chiefly to the
auricles, but there may be advanced changes of this nature in the
hypertrophied left auricle in mitral stenosis. The fatty degeneration
of an hypertrophied heart may be induced by any of the general causes
above referred to, but there are also special ones to which it is
liable. The chronic congestion which accompanies a dilated heart
affects the walls of the organ as well, and diminishes the vigor of the
coronary circulation. In emphysema and in mitral stenosis, and other
diseases which induce a dilated state of the right heart, fatty
degeneration, sometimes combined with fibroid change, is, as Jenner
pointed out,[27] very common. This state of the right chambers also
interferes with the proper oxygenation of the blood in the lungs, and
so acts in a double way. Degenerative changes in the coronary arteries
are specially prone to accompany valvular diseases, on which the
majority of cases of hypertrophy depend, and we have here one of the
most serious causes of fatty degeneration in this state. And, finally,
we see this change in some hypertrophied hearts without being able to
ascertain any exciting cause: a nutritive breakdown occurs, of which
the fatty degeneration is the expression. Possibly in such cases the
trophic nerve-influences may be at fault.

[Footnote 27: _Medico-Chirurgical Transactions_, xliii.]

Defective oxidation, in whatever way brought about, seems the common
factor in all forms of fatty degeneration. The process may be almost
confined to the heart or be more or less general in the solid viscera
and voluntary muscles. The diaphragm is sometimes much involved with
the heart, even when the other muscles show no signs of the change.
There certainly seems to be a special proneness to fatty degeneration
in the heart-muscle which may perhaps be associated with its incessant
activity. So great is the need of an abundant oxygen-supply that it
early feels any deficiency, and in consequence is the first muscle to
show nutritional changes.

Fatty degeneration is met with at all ages. I have seen it in the
hypertrophied right ventricle of a new-born infant, with stenosis of
the pulmonary artery. The cases dependent upon vascular changes are
most frequent after middle life. Males appear more frequently affected
than females. The form associated with anæmia is an exception to this
rule. Stout persons are not more liable to be affected than thin ones;
indeed, it is often, to use Paget's phrase, "a lean degeneration."
Sedentary habits, worry, grief, and other depressing emotions are
believed by some to have a predisposing influence. Persons with gouty
and arthritic tendencies are more prone to this change.

The anatomical condition is very characteristic even to the naked eye,
and the microscope may be required only in corroboration. It may be
local or general. In the former case the left ventricle is most
frequently affected, the right ventricle more rarely, and the auricles
very seldom. The amount of subpericardial fat may be slight. If the
process is advanced and in all the chambers, the heart looks large and
is flabby and relaxed. It is pale, of a light yellow-brown tint, buff
color, or, as it is sometimes expressed, a {614} faded-leaf color. The
consistence is greatly diminished, and the substance tears easily and
the finger can be readily thrust through the wall. Extreme grades are
met with in profound anæmia and in phosphorus-poisoning. The fatty
degeneration of coronary disease and of valvular affections is usually
more local, and the heart has often a brownish-yellow tint from the
coexistence of brown atrophy. In the left ventricle the papillary
columns and the layers of muscle just beneath the endocardium are most
affected, and in a curious streaked or patchy way--the tabby mottling
of some authors. A similar change may be seen in the right ventricle,
particularly in the hypertrophy from mitral disease. In the auricles
the right may show patches on the musculi pectinati, but on the left,
which is most often affected, the thick endocardium usually obscures
it. Chemically, it has been shown that in fatty degeneration the heart
may contain from 3 to 5 per cent. more fat than normal.

On microscopical examination of teased portions of the muscle the
fibres are broken and irregular, and there is much free fat, in form of
droplets, among them. The appearance of the fibres will vary with the
intensity of the process; in mild grades there are minute scattered
droplets in the protoplasm, not obscuring the nuclei or the striæ; but
in an advanced condition the fibres seem occupied completely with
minute globules, and no trace of structure can be seen. The patchy
distribution of the fatty degeneration in many cases, usually evident
to the naked eye, is corroborated by the microscope, and one may obtain
portions of the muscle with scarcely a normal fibre, while in a
contiguous bit the fibres are little if at all affected. In some
instances of general fatty degeneration in anæmia, and even in fevers,
as diphtheria, the process is so advanced that it is difficult to find
any normal-looking fibres. Brown atrophy is a frequent accompaniment of
fatty degeneration.

The effect of this change upon the heart is seen in a diminution of its
functional power; the contractile force is weakened and the organ
rendered incapable of doing its work efficiently. If the change occurs
in a previously normal heart, much will depend on the rapidity with
which it has supervened. Repeated hemorrhages or poisoning by
phosphorus will induce in a few days an extreme degree of weakness
rarely seen in the fatty degeneration of chronic anæmia--perhaps
equally extensive. As a consequence of the enfeebled action of the
heart, the arteries are not well filled during the systole, and there
is anæmia of the organs. The mural weakness readily permits of
dilatation, with imperfect emptying of the chambers and distension of
the venous system. In hypertrophy the failing compensation is
frequently due to the onset of fatty degeneration. During a sudden
strain or a more continued effort than usual there may be heart
failure, asystolism, or the walls may tear and sudden death occur from
rupture.

The SYMPTOMS of fatty degeneration of the heart are by no means
definite, being those of defective cardiac power. It is often met with
post-mortem when not expected, and on the other hand we may fail to
find it even when the symptoms seem to point very clearly to its
existence. In chronic anæmia, in chlorosis, in fevers and wasting
diseases the process may be extreme, without leading to any more marked
symptoms than feeble action of the heart, palpitation on exertion or
excitement, with signs of slight dilatation, and a soft mitral systolic
murmur from incompetency of the valves. In cases of idiopathic anæmia,
in which the fatty degeneration is perhaps more marked than in any
other condition except phosphorus-poisoning, the pulse is frequently
full, though soft, and regular so long as the patient is quiet. The
symptoms of fatty degeneration in cases of valvular disease with
hypertrophy are simply those of failing compensation, and we see the
same process in the non-valvular hypertrophy of chronic Bright's
disease. But, apart from these conditions, fatty degeneration occurs as
part of a process of general failure {615} of nutrition, premature or
senile. These form the cases of idiopathic fatty heart which seem so
constantly to be associated with atheromatous changes in the coronary
vessels. English writers have dealt specially with this form, which
certainly appears to be more prevalent in Great Britain than on this
continent or in Europe. In these cases there may be general obesity,
but as often the subjects are of spare habit, with full atheromatous
arteries, and other indications, perhaps, of early senility. They are
usually persons who have lived freely and taken stimulants in excess.
Among the symptoms believed to indicate fatty degeneration in these
cases are--weak, irregular action of the heart, with a small
intermittent pulse; cardiac pain, sometimes anginoid in character;
dyspnoea, particularly on exertion, as in ascending an incline; signs
of cerebral anæmia, indicated by vertigo or pseudo-apoplectic attacks
and loss of mental power; the presence of an arcus senilis; and, as a
final symptom, Cheyne-Stokes respiration.

Persistent irregularity in the action of the heart in a person with
atheromatous arteries, and dyspnoea on exertion, without signs of
valvular affection, are certainly suggestive of degeneration of the
muscle-fibres of the heart. In some instances there has been noted a
greatly diminished number of beats, 40 or 50 per minute, or even
slower. Irregular action of the heart may, however, persist for years
without indicating any serious mischief.[28] The yellow fatty arcus
senilis is believed by many physicians to indicate a weak fatty heart,
and it does occur in many persons of soft flabby habit of body with
degenerated arteries and evidences of premature decay; but by itself it
is of no value as a sign of vascular degeneration. It must not be
confounded with the opaque white calcareous arcus not uncommon in
elderly people, and met with occasionally in middle-aged persons. The
Cheyne-Stokes breathing so often referred to as specially associated
with fatty heart is, in my experience, a much more frequent concomitant
of uræmic states.

[Footnote 28: In the spring of 1882, I saw, for Geo. W. Campbell, a
gentleman aged eighty-two, a man of remarkable vigor, mental and
bodily. He had an extraordinarily irregular yet full pulse, with
atheromatous arteries--a condition which he assured me had been
constantly present for close upon forty years, and had been a source of
needless anxiety to many physicians, and for some years to himself.]

The physical signs of fatty degeneration of the heart are a weak
impulse, often diffuse, and if the patient is thin the area of dulness
may be found increased. In stout persons it is difficult to determine
dilatation on account of the fat inside and out. The sounds on
auscultation are generally weak, distant, and muffled, but in the fatty
degeneration of anæmia the first will often be found sharp and
distinct, though short and more like the second sound. A soft murmur,
systolic in character, is not infrequently heard at the apex, and
believed to be due to muscular incompetency.

The DIAGNOSIS is beset with difficulties, and in most cases we have to
be content with probabilities, except in the instances due to anæmia,
etc. Permanent weakness of impulse and the symptoms it entails, with
signs of degeneration of tissue as shown by atheromatous arteries, are
the most suggestive features, but even about them there are
uncertainties. My own errors and a contemplation of those of several
very eminent clinicians, taken in connection with the fact that some of
the most typical cases of fatty heart which come under my observation
have been instances of sudden death in persons pursuing their
avocations, have made me very cautious in the diagnosis of this
condition.

The PROGNOSIS depends entirely on the circumstances under which the
degeneration has developed. In the weak fatty heart of chlorosis and
anæmia, with a return to a normal blood-condition, the nutrition of the
heart is improved and its action strengthened. Doubtless many cases of
failing compensation are due to it, and a subsidence of the symptoms
under {616} rest, digitalis, and careful feeding may simply mean
improved nutrition of heart-muscle and disappearance of the fat which
clogs its action. Where due to atheromatous changes, no permanent
improvement can be expected; and in these cases, particularly if
combined with fatty infiltration, rupture or fatal syncope may occur.
In not a few of such cases the persons have not complained either to
their physicians or friends of cardiac distress. The case of the
celebrated Scotch divine, Chalmers, described by Begbie,[29] is an
illustration of advanced fatty heart with sudden death in a man of
extraordinary vigor of mind and body.

[Footnote 29: _Contrib. to Pract. Med._, 1862.]

The TREATMENT should be directed to the removal of the cause when
possible, as the anæmia, febrile condition, etc. In all cases rest,
quiet, and avoidance of excitement are to be rigidly enforced. Sudden
exertions may prove instantly fatal. In the cases where there is
hypertrophy with or without valvular disease, and the failing
compensation is due to this cause, digitalis acts well, and should be
combined with stimulants. In the senile and atheromatous cases great
care must be exercised: the bowels should be kept loose, and the
patient cautioned not to strain at stool or make any sudden exertion.
He should lead a very quiet, regular life, and exercise great
moderation in food, drink, and venery. Warm and Turkish baths are most
dangerous. Iron, arsenic, and nux vomica are remedies from which
benefit may be expected. Digitalis is, as a rule, contraindicated. We
must remember that, as Sir William Jenner has remarked, fatty
degeneration is sometimes a preservative lesion, and induces a due
proportion between the cardiac strength and the arterial resistance,
reducing the former when there is great atheroma and brittleness of the
vessels. The application of blisters is often of use in allaying the
pain, and nitrite of amyl should be given in the anginoid attacks.

4. Brown atrophy is a very common degenerative change in the
heart-muscle, particularly in the hypertrophied organ of valve
affections. In old people and in persons dead of wasting diseases it
seems invariably present. When advanced, the color of the muscle is
quite distinctive--a dark red-brown and the consistence may be greater
than normal. Microscopically, the fibres present a central accumulation
of brown pigment, generally arranged about the nuclei and extending up
and down the cells. The cement-substance between the cells is often
unusually distinct in these cases, and seems more fragile than in
healthy muscle. The composition of the pigment has not, so far as I
know, been determined, but it is doubtless, like that of the brown
induration of the lung and red atrophy of the liver, derived from the
hæmoglobin, and possibly, as in these latter conditions, is connected
with feeble venous circulation.

5. Amyloid degeneration of the heart is occasionally met with, but
rarely in so advanced a grade as to be recognizable macroscopically. It
occurs in the intermuscular connective tissue and in the blood-vessels,
not in the fibres, and occasionally may be extensive, as in a case
mentioned by Ziegler.[30]

[Footnote 30: _Pathologische anatomie_, 3te Aufl., Lief. i., §59.]

6. The hyaline degeneration of Zenker is sometimes seen in the
heart-muscle in cases of prolonged fever. The affected fibres are
swollen, homogeneous, translucent, and the striæ very faint or entirely
absent.

7. Calcareous degeneration may occur in the myocardium, involving the
fibres and forming a definite calcareous infiltration of the
protoplasm, as well figured and described by Coats.[31] It is a rare
condition, whereas extensive calcified plates in endo- and pericardium
are by no means uncommon.

[Footnote 31: _Pathology_, 1883.]


{617} Spontaneous Rupture of the Heart.

Laceration of the wall of the heart is usually associated with fatty
infiltration or degeneration, most frequently the latter. It is
doubtful if in any instance the healthy muscle has broken. Rare causes
are--acute softening, in consequence of embolism of a branch of a
coronary artery; abscess from pyæmia; or an acute ulcer of the
endocardium. Cysts simple or hydatid are mentioned, but the extreme
rarity of causes other than fatty changes may be inferred from the
statistics of Quain,[32] who states that of 100 cases of rupture
collected by him, fatty degeneration was noted (microscopically) in 77,
and in the others there was softening in all but 2, or no mention was
made of the condition of the wall.

[Footnote 32: _Loc. cit._]

Males are more frequently the subject of this accident than females,
and the great majority of cases occur in persons over sixty years of
age--two-thirds of the eases tabulated by Quain.[33]

[Footnote 33: _Loc. cit._]

The rent may occur in any of the chambers, but the most frequent site
is the left ventricle on the anterior wall, not far from the septum.
Statistics give, for 55 cases,[34] 43 in left ventricle, 7 in right
ventricle, and 3 in right auricle and 2 in the left auricle.

[Footnote 34: Elleaumé, _Essai sur les Ruptures du Coeur_, Paris,
1857.]

The break is generally a ragged, irregular rent in the course of the
fibres, and the trajét may be oblique and crossed by strands of muscle.
The internal orifice may be larger than the external; the opposite is
rarely the case. Two or more rents have been found. Usually the fissure
is not very long--from a quarter of an inch to an inch--but there are
cases of long rents extending from base to apex. Clots usually block
the orifices, and the pericardium also contains large coagula. Evidence
is sometimes found to indicate that the tear has occurred slowly, as
attempts at repair may be present.

The wall in the vicinity of the break has usually been found in a state
of degeneration, and we can readily understand how sudden and violent
contractions might strain a weak part and tear the substance. Perhaps
irregularity in the contractions may be an important factor, such as we
may suppose occurs when a wave of contraction reaches a patch of
advanced fatty change or softening from embolism.

The accident usually takes place during exertion or excitement. Many
cases are reported during straining at stool, others while lifting
weights, running, or during coitus. Cases are mentioned as occurring
during sleep or while at rest.

There may be no preliminary symptoms, and without warning the patient
falls, and with a few gasps or a cry is dead. This occurred in 71 of
the 100 cases collected by Quain. In other instances there is great
pain in the præcordial region, a sense of suffocation and anguish, with
vomiting, and life may be prolonged several hours. In one instance the
patient lived eleven days.[35] Probably in such cases there is a small
rent at first which gets blocked with clots, and only a small amount of
blood oozes into the pericardium with each systole. The symptoms may be
those of simple heart failure, as in a case I examined for Burland of
Montreal, in which the patient lived thirteen hours after the onset of
the symptoms, and was able, though with difficulty, to continue his
walk up a rather steep hill.[36] Death appears to occur from shock or
syncope, sometimes from compression of the heart by the extravasated
blood. In the case just mentioned the amount of blood in the
pericardium was {618} very much less than I have seen in cases of
rupture of an aneurism into this sac.

[Footnote 35: Barth, _Archiv. générales_, 1871.]

[Footnote 36: This was a case which illustrated well the latency of
many cases of fatty heart. The patient was an active merchant, aged
sixty, who had never complained of cardiac trouble, and had only a
short time before his death effected a reinsurance upon his life for a
large amount.]

In protracted cases the nausea and vomiting may for a short time lead
to the supposition that the case is one of severe indigestion, but, as
mentioned above, in the great majority of cases death occurs at once,
and in the others there can rarely be any question of diagnosis, and
still less of treatment.


Atrophy of the Heart.

DEFINITION.--A diminution in size and weight of the organ, due to
degeneration and atrophy of the muscular fibres.

The old writers applied the term phthisis of the heart to this
condition. The decrease is always in weight, and usually in size; it is
doubtful if there is an atrophic and dilated heart in which, with the
wasting, the size is maintained by the dilatation. In many of the
degenerations, particularly fatty and fibroid, there is local atrophy
of the muscle-fibres and yet the weight and size of the organ are not
changed.

The varieties which have been recognized correspond to those of
hypertrophy--viz. the simple, eccentric, and concentric forms, but the
two latter are probably only conditions of contraction or dilatation in
a wasted heart. The post-mortem contraction in the small left ventricle
of persons dead of chronic disease may be excessive; and here, as in
concentric hypertrophy, the examination must be made with care.

ETIOLOGY.--The atrophy is either congenital or acquired. The congenital
atrophy which is most frequently seen in women is in association with
defective development of the arterial system and the generative organs.
This is occasionally very marked in chlorosis, and is described and
figured by Virchow in his monograph on this subject.[37] But apart from
this general hypoplasia of the heart and vessels in women, we sometimes
in the post-mortem room find in a man, dead perhaps of an acute disease
and without any cardiac symptoms, a heart small out of all proportion
to the size and general nourishment of the body. Many of the older
writers mention this. Gowers refers to a case which Allan Burns
narrates, in which the heart of an adult was not larger than that of a
child of six or seven. Morgagni has a similar observation.

[Footnote 37: _Ueber die Chlorose_, Berlin, 1872.]

The great majority of the cases are secondary or acquired, and are met
with in the wasting diseases, as cancer, phthisis, prolonged
suppuration, and diabetes. The cardiac wasting is part of the general
marasmus which affects the whole body. In about half the cases of
phthisis the heart is small.[38] In cancer of the pylorus the most
extreme wasting has been found. Disease of the coronary arteries is an
occasional cause, but it most frequently produces local atrophy or
degeneration. Compression by pericardial effusion, fatty infiltration,
and pericardial adhesions are mentioned as rare causes.

[Footnote 38: Quain, _loc. cit._]

A rough guess at the proportional size of the heart may be made by
comparing it with the closed right fist of the person. Weighing gives
the most accurate test, and in each instance regard must be had to the
size of the body. In some instances the organ has weighed only two or
three ounces. The heart figured by Bramwell,[39] one of the smallest on
record, weighed only 2 ounces and 2 drachms. Quain[40] refers to one,
from a girl aged fourteen, which weighed only 1 ounce 14 drachms.

[Footnote 39: _Diseases of the Heart_, 1884.]

[Footnote 40: _Loc. cit._]

Usually, in secondary atrophy, the visceral pericardium is wrinkled and
the coronary arteries prominent and tortuous--two features of great
importance in determining atrophy and in distinguishing between the
acquired and {619} congenital forms. The pericardial fat is variable in
amount. Microscopically, brown atrophy is the most constant change;
fatty degeneration much less common. Senile atrophy may present very
similar appearances. The heart may be tough and firm from an increase
in the fibrous elements. The pericardial fluid I have often noticed to
be much increased.

There are no characteristic SYMPTOMS. The heart-muscle may be able to
fulfil the requirements of the wasted frame. A feeble impulse and
diminished area of dulness may be present, but in the marasmus of
middle-aged or elderly people emphysema of the anterior margin of the
lung may seriously interfere with a proper examination. The increased
pericardial effusion occurs toward the end. The heart sounds are feeble
and the pulse weak. Palpitation is frequent, and there may be the usual
signs of anæmia, dizziness, etc.

The condition may be suspected, but is rarely diagnosed during life.

The PROGNOSIS depends upon the disease to which the atrophy is
secondary, to the amelioration of which also the treatment must be
directed.


Hypertrophy of the Heart.

DEFINITION.--An increase in the size of the heart due to an increased
thickness, total or partial, of the muscular walls.

VARIETIES.--Two forms may be recognized--simple hypertrophy, in which
the cavity or cavities remain of the normal size; and eccentric
hypertrophy, in which with increased thickness of the walls there is
enlargement of the cavities. Dilated hypertrophy and hypertrophy with
dilatation are terms by which the latter form is most frequently
described.

By many writers a third variety, concentric hypertrophy, is recognized,
in which there is diminution in the size of the cavity with thickening
of the walls; but in these cases we have to deal with a post-mortem
change--rigor mortis; and if the organ is kept for twenty-four hours or
soaked in water, the so-called concentric hypertrophy will usually
disappear.

The increased size may affect the entire organ, general hypertrophy; or
only one side or one cavity, partial hypertrophy. The latter is the
most common. Of the single chambers the left ventricle is most
frequently involved, then the right. The auricles are rarely affected
alone, but the left is more often than the right.

ETIOLOGY.--Disturbed innervation and increased work are the two
principal causes of cardiac hypertrophy. We see hypertrophy from
deranged innervation (1) in Basedow's disease (exophthalmic goitre);
(2) in long-continued nervous palpitation from any cause, particularly
sexual excesses; (3) certain poisons and articles of diet appear to act
in this way, as tea, coffee, alcohol, and tobacco.

In all these cases there is simple over-action or increased functional
activity, which, if prolonged, certainly produces some degree of
hypertrophy. How this condition is brought about is not very clear. We
may suppose the increased frequency of contraction to result from
stimulation of the accelerator nerves, as seems probably the case in
exophthalmic goitre; from irritability of the cardiac ganglia
themselves, owing to the influence of such toxic agents as tea,
tobacco, etc.; or from defective vagus control. Long-continued neurotic
palpitation in reality causes hypertrophy by increasing the work of the
heart, for under perverted stimuli the ventricular contractions are
doubled in frequency--sometimes in force as well--while maintaining the
circulation in normal vessels offering no increased resistance to the
blood-flow.

There can be no doubt of the occurrence of actual hypertrophy as a
sequence of the irritable heart induced by sexual excesses and tobacco.
I had under observation on and off for several years a very emotional
and {620} hypochondriacal young man addicted to venery, whose left
ventricle became strongly developed and beat outside the nipple-line.
His entire thoughts became centred in his heart trouble, and he
travelled from one authority to another in this country and Europe
seeking advice.[41] The smoker's heart rarely leads to much
hypertrophy, but in young lads it may do so, and even induce more
serious disease, as indicated by the presence of murmurs and signs of
cardiac failure. The abuse of spirits as a cause of hypertrophy is not
very clearly established. Alcoholism appears to be a factor in the
production of atheroma. I have been struck by the fact that in four
typical instances of so-called idiopathic hypertrophy occurring in
powerfully-built workers there was a history of intemperance; and it is
quite possible that this may have combined with the muscular efforts in
inducing the heart disease; at any rate, it would prove an important
element in hastening the final breakdown when from any cause
hypertrophy had arisen.

[Footnote 41: After three or four years of most unnecessary worry in
the expectation of death from heart disease, this patient has quieted
into the belief that there is not anything seriously wrong with his
heart, and has now rarely any indications of trouble.]

The majority of cases of hypertrophy of the heart are due to mechanical
causes leading to increased resistance and increased work on the part
of the organ. Under these circumstances, as in other hollow viscera,
the muscle develops, gets thicker and firmer, and capable of
accomplishing the extra labor thrown upon it. Defects in the valvular
mechanism, obstruction, or incompetency, and increased resistance to
the blood-flow in the arteries, are the most important causes of
hypertrophy. The ultimate factor in all is heightened pressure within
the cardiac cavities due to one of two things--increased volume of
blood to be moved or difficulty in propelling the normal volume, caused
by obstruction to the flow either central or peripheral.

Pericardial adhesions may impede the action of the heart, and either
directly cause hypertrophy or induce dilatation and a consequent
hypertrophy.

The details regarding the etiology are best considered in a study of
hypertrophy as it affects the individual chambers.

Left Ventricle.--This chamber is much more frequently affected than any
other, and may be involved alone or as part of a general enlargement of
the organ. The more important causes are as follows:

(1) Aortic Stenosis.--To send the normal charge of blood through a
narrowed orifice the muscle must contract with increased force, and to
accomplish the work the walls increase in thickness. There may be
simple hypertrophy without dilatation of the chamber, but in the later
stages this inevitably supervenes.

(2) Aortic Regurgitation.--Curling and foreshortening of the aortic
cusps permits of a backward flow into the ventricle during its
diastole, with the production of dilatation and increased pressure, to
overcome which the walls thicken--eccentric hypertrophy. This is one of
the most common causes, and leads to enormous enlargement of the heart.

(3) Mitral Insufficiency.--In extreme grades of mitral stenosis the
left ventricle is usually small, but when the curtains are curled and
the patent auriculo-ventricular orifice large, there may be very great
hypertrophy. Free regurgitation is always accompanied by considerable
eccentric hypertrophy, due to the distension of the chamber by the
extra quantity of blood forced in at each auricular systole.

(4) Pericardial adhesions, particularly when in addition to union of
the layers the parietal membrane is firmly united to the pleura or to
the sternum, may cause hypertrophy of the left ventricle alone, but
more commonly of the whole heart.

(5) Abnormal Conditions of the Aorta.--_(a)_ Atheroma, with or without
dilatation of the arch, is a cause of hypertrophy, for the heart has to
{621} compensate for the loss of arterial elasticity, an important
factor in the onward movement of the blood during the diastole; and,
again, there is increased resistance in the wider tube. _(b)_ Great
narrowing, as in the congenital coarctation just beyond the ductus
arteriosus, which may produce colossal hypertrophy. Pressure upon the
large vessels in the thorax by tumors may act in the same way. _(c)_
Aneurism of the aorta is not often accompanied by hypertrophy unless
the valves are affected. Theoretically, it might be expected, as a
large saccular dilatation would certainly appear to be a cause of
increased resistance, but in uncomplicated cases the experience of most
observers appears to accord with that of Stokes,[42] who states that we
usually find a small heart. Occasionally, however, there is marked
hypertrophy even without valvular disease.

[Footnote 42: _Loc. cit._]

(6) Kidney disease, acute and chronic, is very frequently accompanied
with hypertrophy of the left ventricle. Indeed, simple hypertrophy is
more often met with in chronic Bright's disease than under any other
conditions. Increased blood-pressure in the smaller arteries throughout
the body is now very generally acknowledged to be the immediate cause.
But how this is brought about is a question not yet satisfactorily
determined.

We have to deal with two sets of cases. There is the cardiac
hypertrophy accompanying acute or subacute nephritis, particularly the
scarlatinal. Here there are no chronic arterial changes, and the
increased arterial tension appears to be due to contraction of the
smaller arteries under the influence of retained excreta, which may act
through the vaso-motor centre, as Ludwig observes, or possibly directly
upon the unstriped fibres of the tunica media of the arteries. Bright's
original explanation still holds good, I think, when he says that the
altered quality of the blood "so affects the minute and capillary
circulation as to render greater action necessary to send the blood
through the distant subdivisions of the vascular system."[43]

[Footnote 43: _Guy's Hospital Reports_, 1836.]

The hypertrophy of the left ventricle in connection with contracted
kidneys is more frequent and more marked. Traube suggested[44] that the
interference with the local circulation in the kidneys by the
obliteration of vessels increased the work of the heart and induced the
hypertrophy, but it is much more probable that the change is a
widespread one throughout the body. Gull and Sutton hold[45] that in
these cases there is a condition of arterio-capillary fibrosis in which
the small arteries are thickened and their calibre diminished, leading
in time to a more or less widespread sclerosis in various organs,
particularly the kidneys. As a result of this fibrosis, the movement of
blood in the smaller vessels is much impeded, the arterial tension
increased, and the work of the heart greatly augmented. On the other
hand, George Johnson[46] maintains that the muscular coat of the
arterioles becomes thickened under the influence of retained excreta,
and they are in a state of spasm which increases the tension and
heightens the blood-pressure in the left ventricle.

[Footnote 44: _Gesammelte Beiträge_, Bd. ii.]

[Footnote 45: _Medico-Chirurgical Transactions_, lv., 1872.]

[Footnote 46: _Ibid._, vol. xxxiii.]

The question can scarcely be considered settled as regards details, but
the general fact of increased peripheral resistance is well
established, and it is one of the most frequent causes of non-valvular
hypertrophy. It may be quite marked in persons without positive
evidence of renal disease as indicated by albumen or casts in the
urine, but in whom the condition of arterio-capillary fibrosis is
evident from the thickened state of the small arteries, the increased
tension, and the firm dislocated impulse of the heart.

(7) Prolonged muscular exertion has been much insisted upon as a cause
of cardiac hypertrophy by DaCosta, Myers, Albutt, Seitz,[47] and
others. {622} Soldiers, blacksmiths, miners, mountaineers, and men
whose occupations call for heavy and prolonged exercise occasionally
develop hypertrophy of the heart, which it seems reasonable to connect
with the over-use of the muscles. DaCosta's irritable heart in young
soldiers appears to represent the early stage of this condition. In 38
per cent. of the cases excessive marching was the cause. He was able to
confirm the existence of hypertrophy by autopsy. It is not uncommon to
meet with cases of pronounced heart disease, with symptoms of failing
compensation, dropsy, etc., in large, powerfully-built men who have
been engaged in laborious occupations, and who are admitted to hospital
with the clinical picture of chronic valvular disease. At the autopsy
one is surprised to find an hypertrophied and dilated heart without
valve lesion, perhaps no extensive arterial degeneration, and no kidney
disease. They are called cases of idiopathic hypertrophy, but I believe
that some of them, at any rate, are instances of a condition induced by
prolonged muscular effort. I have had an opportunity of studying
carefully four such cases, and I have seen autopsies in two other
instances. As I mentioned, alcoholism may be also a factor in these
cases, as most of them occur in hard drinkers.

[Footnote 47: _Die Ueberanstrengung des Herzens_, Berlin, 1875--a
collection of six monographs on the subject.]

How muscular effort acts in inducing hypertrophy has been much
discussed. It seems rational to suppose that prolonged action of the
heart at a rate more vigorous and rapid than normal would induce
enlargement of its muscle, just as constant exercise acts with others;
and possibly within limits this does take place. Albutt speaks of the
large red left ventricles in the Leeds iron-workers killed by accident
or cut off by acute disease. No doubt the thickness of the ventricle is
measured by the muscular needs of the system. Muscular contraction
affects the heart in two ways: first, the venous flow is accelerated,
more blood reaches the right heart, and is sent to the lungs, and more
reaches the left ventricle and the systemic arteries. The fuller
inspirations also favor flow to the heart. When the exercise is
excessive the right heart and the venous system become still more
distended, and the outflow from the peripheral arteries proportionately
retarded and the tension in them increased--particularly is this the
case in efforts requiring straining, as in lifting, etc.; and,
secondly, the effect of muscular contraction has been shown by Traube
to increase very greatly the pressure in the arteries. Gaskell,
however, states[48] that when a muscle contracts its own arterioles
dilate; but however that may be, the increased tension during muscular
contraction can be determined in the radial by the finger, and still
better by the sphygmograph, during steady contraction of the muscles of
the arm. In yet a third way the blood-pressure may be increased during
violent muscular efforts, particularly when the breath is held. The
vaso-motor centre is stimulated by the lack of oxygen, and in
consequence the blood-pressure rises in the peripheral arteries. At the
end of prolonged contests we sometimes see men get pale or the left
ventricle may become so embarrassed that they faint.

[Footnote 48: _Journal of Physiology_, iii.]

(8) That the heart becomes hypertrophied during pregnancy has been
specially insisted upon by French writers, Larcher[49] and others. Many
doubt the correctness of their deductions, but the weight of evidence
seems to point unmistakably to the existence of moderate increase in
the thickness of the walls of the left ventricle.[50] Cohnstein[51]
connects it with the hydræmic and chlorotic conditions of the blood, so
liable to develop during pregnancy.

[Footnote 49: _Archives générales_, 1859.]

[Footnote 50: McDonald, _Heart Disease during Pregnancy_, London,
1878.]

[Footnote 51: _Virchow's Archiv_, lxxvii.]

(9) Hypertrophy of the right heart in disease of the lungs or of the
valves is usually followed by more or less hypertrophy of the left
ventricle as well, caused by the increased work in consequence of
retarded outflow into the venous system.

{623} Right Ventricle.--Hypertrophy of this chamber is most frequently
met with in connection with disease of the left side of the heart; next
with various chronic affections of the lungs; and lastly with valvular
affections of the right side.

(1) Mitral lesions--incompetence or stenosis--are very common causes
which act by increasing the resistance in the pulmonary veins and
obstructing the free flow of blood in capillaries of the lung. To
compensate for this defect the walls of the right ventricle increase in
size, and the hypertrophy at first may be unattended with dilatation.

(2) Pulmonary Lesions.--The obliteration of any considerable number of
blood-vessels within the lungs by emphysema, cirrhosis, or phthisis
(sometimes), occasionally the compression of pleuritic exudation,
increases the blood-pressure in the pulmonary artery and rapidly leads
to hypertrophy of the right heart. Narrowing of the main branches of
the pulmonary artery by the growth of tumors or an aneurism of the
aorta occasionally produces the same effect.

(3) Valvular lesions on the right side are rare causes of hypertrophy
in the adult, but during foetal life, when endocarditis is more
prevalent in the pulmonary and tricuspid valve, stenosis or
insufficiency at these orifices leads to great enlargement of the
ventricle. Pulmonary stenosis is the most common lesion; incompetence
is not often met with. Lesions of the tricuspid valves in the adult are
almost always associated with mitral disease. When the dilated
hypertrophy of the right ventricle reaches a certain grade in cases of
mitral disease or pulmonary lesion, tricuspid incompetence develops.

(4) Among other causes which may be mentioned are pericardial
adhesions, which some think tend specially to the production of
right-sided hypertrophy and extensive pleuritic adhesions. Atheroma of
the pulmonary arteries is more often a consequence than a cause of
hypertrophy.

The auricles are usually dilated and hypertrophied; simple hypertrophy
is probably never seen. In the left auricle this condition develops in
lesions at the mitral orifice, particularly stenosis when it
compensates for the obstruction. In free mitral regurgitation the
hypertrophy is not so marked.

The right auricle hypertrophies when there is greatly increased
blood-pressure in the lesser circulation, whether due to mitral
stenosis or pulmonary lesions, and incompetency at the tricuspid
orifice. Stenosis of the auriculo-ventricular orifice is a less
frequent cause. The dilatation is always excessive.

MORBID ANATOMY.--In general hypertrophy the entire organ is increased
in size and weight; more commonly we find the condition limited to two
or three chambers or to one side. The estimation of slight grades of
enlargement is difficult, but where the increase is marked the process
is simple enough. The volume of the heart varies in different
individuals according to their age and size. The normal heart is about
the size of the closed fist, and, as Virchow suggests, a fair estimate
can be made by comparing the two together. By careful weighing we get
much more accurate information. The heart of an average-sized man
weighs about 9 oz., of a woman about 8 oz. In great hypertrophy the
organ may weigh three or four times the normal amount. A heart which
weighs over 12 oz. in a man, and over 10 oz. in a woman, may be
considered hypertrophied. Hearts weighing from 16 to 20 oz. are not
uncommonly met with. Weights above 25 oz. are rare. The heaviest hearts
on record are described by Beverley Robinson of New York,[52] 53 oz.;
Dulles of Philadelphia, 48 oz.; and there are several cases described
in the _Transactions_ of the London Pathological Society of the organ
weighing as much as 46 oz.

[Footnote 52: _New York Medical Record_, 1883.]

{624} Next to weighing, careful measurement of the thickness of the
walls is the best means of determining hypertrophy. When there is great
dilatation of a chamber the walls, though actually thick, may look
proportionately thin; and on the other hand, when rigor mortis is
present the cavity may be very small and the walls appear enormously
thick. In this case measurements should not be made until the heart has
been soaked in water and thoroughly relaxed. The normal thickness of
the left ventricle is about half an inch (12 or 13 millimeters), being
thicker toward the base. It is well to measure in two or three places,
not including the papillary muscles. A thickness of 10 lines or over
(20 to 25 mm.) indicates hypertrophy. It is rare to meet with the wall
thicker than 1 inch (25 mm.), even in very great hypertrophy. The right
ventricle is thinner than the left, and has an average diameter of from
2 to 3 lines (4 to 7 mm.). A thickness of from 6 to 9 lines (13 to 20
mm.) may be met with in great hypertrophy. It is very rare to see a
diameter of more than three-quarters of an inch, but cases are reported
of a thickness of over an inch. The left auricle has a normal thickness
of about a line and a half (3 mm.), which in considerable hypertrophy
may be nearly doubled. The wall of the right auricle is even thinner
than the left, rarely exceeding 1 line in diameter. In hypertrophy the
sinus does not present a marked increase in thickness, but the
appendix, particularly the musculi pectinati, may be greatly developed
and measure from 2 to 3 lines in diameter.

The shape of the heart is much affected by the degree of hypertrophy in
different cavities. Great enlargement of the ventricles broadens the
apex, and the conical shape is lost. In the enormous hypertrophy and
dilatation of aortic insufficiency the increased breadth and rotundity
of the apex becomes very marked. When the right ventricle is chiefly
affected, it occupies a large share of the apex, and the transverse
diameter of the organ is increased. When due to mitral stenosis the
contrast between the large broad right ventricle extending well to the
apex and the small left chamber is very striking.

When not degenerated the muscle-tissue of an hypertrophied heart is of
a deep-red color, firm, and usually cuts with slightly increased
resistance. The right ventricle often has a peculiarly hard, leathery
feel, which was noticed by Rokitansky. In simple hypertrophy of the
left ventricle the papillary muscles and columnæ carneæ may be
increased in size, but the former often appear flattened in great
eccentric enlargement. The trabeculæ are usually much more developed in
the right ventricle and in the appendix of the right auricle than in
the left chambers. Very often the tissue looks pale, and may be soft
from the occurrence of fatty degeneration.

The histological characters of the changes in hypertrophy have been
much studied, particularly with a view of determining the question of
numerical increase. Hepp[53] described an increase in the thickness;
but most recent observers regard the hypertrophy as due to numerical
increase, resulting from the development of new fibres, either by the
splitting of the old ones (Rindfleisch) or their growth from
interfibrillar nuclei.[54] Wilks and Moxon[55] and Gowers[56] find that
the fibres are not increased in size. Letulle[57] thinks that there is
a process of progressive hyper-nutrition of the fibres.

[Footnote 53: _Henle's Zeitschrift_, 1854.]

[Footnote 54: Zielonko, _Virchow's Archiv_, lxii.]

[Footnote 55: _Pathological Anatomy_, London, 1875.]

[Footnote 56: _Reynolds's System_.]

[Footnote 57: Quoted by Peter, _loc. cit._, p. 280.]

The toughness of the hypertrophied muscle is due to the increase in the
connective tissue, which is more marked as a rule in the right than the
left ventricle. Sometimes, indeed, it is not at all noticeable in the
latter, which may be soft and tears readily with the finger.

SYMPTOMS.--Hypertrophy is a conservative process, usually secondary to
some valvular or arterial lesion, and is not necessarily accompanied by
any {625} symptoms. So admirable is the adjusting power of the heart
that, for example, an advancing stenosis of aortic or mitral orifice
may be for years perfectly counterbalanced by a progressive
hypertrophy, and the subject of the affection be happily oblivious to
the existence of heart trouble. Particularly is this the case with
mitral stenosis and the consequent hypertrophy of the left auricle and
right ventricle. While leading quiet lives and not straining the heart
with violent exertion, such persons may not suffer in any way, or
perhaps only experience a little shortness of breath when going up
stairs. Indeed, the hypertrophy is in almost all instances an unmixed
good, and many of the symptoms which arise are to be attributed to its
failure, or, as we say, disturbance of compensation.

The left ventricle is most often involved, and the clinical features of
hypertrophy are best seen when it is affected. Inspection may reveal
decided bulging of the præcordia, producing in extreme instances marked
asymmetry of the chest. This is most frequent in persons under twenty
years of age, and it may occur without any pericardial adhesions, which
Shroetter[58] thinks are invariably associated with this condition. The
intercostal spaces may be widened, and the area of visible impulse is
much increased. On palpation the character and position of the
apex-beat give most important results. It is stronger, more forcible
and heaving, and may lift the chest-wall. With each systole the hand or
the ear applied over the heart may be visibly raised. A slow heaving
impulse is one of the best signs of simple hypertrophy; when there is
large dilated hypertrophy the forcible impulse is often more sudden and
abrupt. A second, weaker, impulse can sometimes be felt, due possibly
(as Gowers suggests) to a rebound from the aortic valves. The area of
impulse is greatly increased, and the beat may be felt in the sixth,
seventh, or eighth interspace from an inch to three inches outside the
nipple. The downward dislocation of the apex is an important sign in
hypertrophy of the left ventricle; simple outward displacement may be
due to enlargement of the right ventricle.

[Footnote 58: _Ziemssen's Encyclopædia_, vol. vi.]

In moderate grades of hypertrophy, as seen in chronic Bright's disease,
the apex-beat may be in the sixth interspace in the nipple-line or a
little outside it.

Percussion gives an area of increased dulness, due to the much larger
portion of the heart which comes in contact with the chest-wall. The
dulness in the parasternal line may begin at the third rib or in the
second interspace, and the transverse limits extend from half an inch
to two inches beyond the nipple-line, and an equal distance beyond the
middle line of the sternum. The dull region is more ovoid than in
health. When carefully delimited and measured, there may be in the
colossal hypertrophy of aortic valve disease an area of dulness from
seven to eight inches in transverse extent. In moderate grades a
transverse dulness of four inches is not uncommon.

On auscultation the heart sounds, when there is no valve disease, may
not present any special changes, but the first is often prolonged and
dull; but when there is dilatation as well, it may be very clear and
sharp. Reduplication is not uncommon, particularly in the hypertrophy
of renal disease. A peculiar clink--the tintement métallique of
Bouillaud--may sometimes be heard, with the impulse most frequently
just to the right of the apex-beat. The second sound is clear and loud,
sometimes ringing in character or reduplicated. When the hypertrophy
depends upon valvular lesions the sounds are of course much altered,
and replaced or accompanied by murmurs.

The pulse of simple hypertrophy not dependent on valvular lesions is
usually firm, full, and strong, of high tension, and regular. It may be
increased {626} in frequency, but often is normal. In eccentric
hypertrophy the pulse is full, but softer, and usually more rapid. So
long as the hypertrophy is maintained the pulse is regular; one of the
earliest signs of failure and dilatation is irregularity and
intermittence. The various modifications of the pulse in connection
with valve disease are considered elsewhere.

Among symptoms which patients complain of most frequently are
unpleasant sensations about the heart--a sense of fulness and
discomfort, rarely amounting to pain. This may be very noticeable when
recumbent and on the left side. Actual pain in simple hypertrophy is
rare, but in the irritable heart from tobacco and in neurasthenics with
slight enlargement it is often a very troublesome symptom. Palpitation
is not often complained of, nor do patients always have sensations from
the violent shocks of a greatly hypertrophied organ; others, again,
will have very uneasy feelings from a moderately exaggerated pulsation.
The general condition of health has much to do with this: we are not in
health conscious of our own heart's action, but one of the very first
indications of nervous exhaustion from excesses or over-study is the
consciousness of the heart's action, not necessarily accompanied by
palpitation. Flushings of the face, noises in the ear, flashes of
light, and headaches are not uncommon.

There are certain untoward effects of long-continued hypertrophy of the
left ventricle which must be mentioned, chief among which is the
production of atheromatous degeneration of the vessels. Particularly is
this the case when the hypertrophy results from increased peripheral
resistance. The heightened blood-pressure in the arteries (which is
expressed by the word strain) gradually induces an endarteritis and a
stiff, inelastic state of those vessels most exposed to it--viz. the
aorta and its primary divisions. In overcoming the peripheral
obstruction the hypertrophy "ruins the arteries as a sequential result"
(Fothergill). It is in this way that prolonged muscular exertion acts
injuriously, and leads to two common morbid conditions in athletes and
persons whose employment necessitates violent exercise of the
muscles--viz. aneurism and sclerosis of the aortic semi-lunar valves,
with incompetency. Syphilis certainly does not embrace the entire
etiology of aneurism, the occurrence of which in soldiers, strikers,
foundrymen, etc. can be traced to arterial strain. So also with the
sclerosis of the semi-lunar valves--just enough, perhaps, to produce
incompetency; how common it seems to be in strong, well-built men whose
excesses have been on the cinder-path or on the river! The increased
aortic tension, with the more forcible recoil and closure of the
semi-lunar valves, would seem to be factors in the production of this
condition. Aortic incompetency is the special danger of athletes, and
no inconsiderable number of the cases of this lesion occurring in men
without rheumatic or syphilitic history may be traced to over-use of
the muscles.

Another special danger is rupture of the blood-vessels, particularly of
the brain. In the condition of general arterial degeneration associated
with contracted kidneys and hypertrophied left heart apoplexy is
common; indeed, we may say that in the majority of cases of cerebral
hemorrhage there is sclerosis of the cerebral vessels, often with the
development of miliary aneurisms, and the rupture is directly induced
by the forcible action of the heart.

Hypertrophy of the right ventricle in the adult is rarely induced by
valvular disease on the right side, but is a result of increased
resistance in the pulmonary circulation, as in cirrhosis of the lung
and emphysema, or in stenosis of the mitral orifice. When the
compensation is perfect, and the hypertrophy fully maintains the
equilibrium of the circulation, there are no symptoms. Extra exertion,
as in ascending stairs or running, may induce shortness of breath, but
in many respects hypertrophy of {627} the right ventricle is the most
enduring and salutary form in the whole range of cardiac affections.
For long periods of years the effects of mitral stenosis may be
counterbalanced completely, and only sudden death by accident or an
acute disease reveals the existence of extensive unsuspected heart
disease. In the hypertrophy secondary to pulmonary disease,
particularly emphysema and cirrhosis, there may be sensations of
uneasiness in the cardiac region, with cough and shortness of breath;
but so long as the dilatation is moderate the symptoms are not marked.
With great dilatation and tricuspid regurgitation come the venous
engorgement, oedema, and pulmonary troubles. The increased pressure in
the lesser circulation not uncommonly leads to atheroma of the
pulmonary artery, and the full state of the capillaries leads
ultimately to a deposition of pigment and increase in the fibrous
elements in the lung--the brown induration. Pulmonary congestion and
apoplexy from thrombosis or embolism are more often associated with
dilatation. Hæmoptysis may result from rupture of vessels during sudden
exertion.

The physical signs of hypertrophy of the right ventricle are not so
marked as those of the left. Bulging of the lower part of the sternum
and left cartilages is occasionally met with. The apex-beat is forced
to the left, but is not so often displaced downward. The most marked
impulse may be in the epigastrium, in the angle between the ensiform
cartilage and the seventh rib or beneath the cartilages of the sixth
and seventh ribs. The pulsation is rarely the strong heave of
left-sided hypertrophy, and is apt to be diffuse, not punctuate,
particularly if there is much dilatation. In thin-walled chests there
may be pulsation in the third and fourth right interspaces. The area of
dulness is increased in the transverse direction, particularly toward
the right, where it may extend an inch or more beyond the border of the
sternum. On auscultation the first sound at the lower part of the
sternum is louder and fuller than normal, but the differences are not
very marked unless there is much dilatation, when it is clearer and
sharper. The second sound is accentuated in the pulmonary artery on
account of the increased tension, and there may be reduplication. The
pulse at the wrist is usually small. The jugular pulsation occurs when
there is tricuspid incompetence, which arises when the eccentric
hypertrophy reaches a certain grade.

Hypertrophy of the auricles is always associated with dilatation. It is
most common in the left chamber, which hypertrophies in mitral stenosis
and incompetency, and assists materially in restoring the balance of
the circulation and protects the lungs. There are no special physical
signs, and we usually can only infer its presence by the existence of
mitral stenosis and a presystolic murmur. Increased dulness may be
determined at the left of the sternum, and there may be a presystolic
wave in the second left interspace.

Hypertrophy and dilatation of the right auricle occur not infrequently,
and are almost invariably associated with a similar condition in the
right ventricle, and incompetency of the tricuspid. In emphysema,
cirrhosis of the lung, chronic bronchitis, and in mitral disease, it is
very common, much more so than the statement of some authors would lead
us to expect. In comparison with the left auricle the greater
development and hypertrophy of the appendix and its musculi pectinati
is very striking. The latter may be distributed over the anterior wall
of the sinus to a much greater extent than in health. There may be
increased dulness in the third and fourth interspaces, with pulsation
presystolic in rhythm. Usually there are signs of venous engorgement,
jugular pulsation, and other evidences of dilatation of the right
heart.

The DIAGNOSIS of cardiac hypertrophy does not usually present any
serious difficulties. Increase in size, more forcible contraction, with
displacement of {628} the apex-beat, and the character of the pulse,
are the most important signs. There are certain conditions which
require to be carefully distinguished. Neurotic palpitation, from
whatever cause, may be accompanied with forcible contraction, but it
has not the heaving impulse of genuine hypertrophy. Actual enlargement
of the organ may, however, result from prolonged over-action, as in
Basedow's disease, in the smoker's heart, and the irritable heart of
neurasthenics, but it is usually slight. Increased dulness in the
cardiac area may be due to a variety of causes, some of which may
simulate hypertrophy, as pericardial effusion, aneurism, mediastinal
growths, or displacement of the heart from pressure or the existence of
malformation of the chest; but with the exercise of ordinary care the
diagnosis can usually be made. There are two opposite conditions which
not infrequently give trouble. When the left lung is retracted from
pleurisy, phthisis, or cirrhosis, there is a large surface of the heart
exposed, and the pulsation may be extensive and forcible, and at first
sight resemble hypertrophy. There is usually in this condition some
dislocation upward and to the left. The history of pulmonary or
pleuritic disease, and the evident fixture of the lung on deep
inspiration, will usually suffice to prevent mistake. A similar
exposure of the heart occurs without any disease in very narrow-chested
persons with ill-developed lungs; and here, though the area of dulness
may be much increased, yet the normal position of the apex and the
absence of forcible heaving impulse, pulse signs, and of any obvious
cause of hypertrophy will afford satisfactory criteria for a diagnosis.
Just the reverse occurs in some cases in which a moderate cardiac
hypertrophy is masked by emphysema of the lungs or of their anterior
borders. The area of dulness may be normal, or even diminished, and the
pulsation diffuse and chiefly epigastric. The general condition, state
of the pulse, and character of the sounds would help in the diagnosis,
but it is sometimes a matter of no little difficulty.

The symptoms and physical signs above narrated sufficiently indicate
the points of difference between hypertrophy of the two sides of the
heart.

In all cases the greatest possible care should be exercised in
ascertaining the presence or absence of conditions likely to cause
hypertrophy.

The COURSE of a case of ordinary hypertrophy may be divided into three
stages: 1st. The period of development, which varies much with the
nature of the primary disease. Thus in rupture of an aortic cusp or in
sudden overstrain from exertion it may require months, or even years,
before the hypertrophy becomes fully developed. In these cases it may
never do so, and then death results. On the other hand, in sclerotic
affections of the valves with stenosis or incompetence the hypertrophy
develops pari passu with the lesion, and may continue to counterbalance
a progressive impairment of the valves. 2d. The period of full
compensation, the latent stage, during which the heart's vigor meets
all the requirements of the circulation. There may be no signs whatever
of heart weakness, but the hypertrophied muscle completely equalizes
the valvular or other defects. It may last an indefinite period of
years. In some cases this fortunate period is never fully attained, and
indications of incomplete compensation remind the individual that he
has a heart affection. 3d. The period of disturbed compensation, which
sooner or later awaits all victims of hypertrophy. It may come suddenly
during an extra exertion, and death follow from acute dilatation; or
more commonly it takes place slowly, and results from degeneration and
weakening of the heart-muscle, with consequent dilatation and all its
evils. There may be repeated failures before the end is reached,
represented clinically by attacks of cardiac dyspnoea and dropsy.

The breaking, as it is called, of a compensatory hypertrophy may be
induced by many causes. Among the most important is failure of general
or local (cardiac) nutrition. In many a chronic heart case readmitted
to {629} hospital, perhaps for the third or fourth time, with dyspnoea
and dropsy, exposure, poor food, and whiskey are responsible for the
failure. Gradual sclerosis of the coronary arteries leading to fatty or
fibroid changes is a fruitful source of disturbed compensation. It is
well known that during or after an acute illness, pneumonia, fever, or
a bronchial attack the first symptoms of heart disease may be
manifested. Mental emotions, severe grief, or fright have been known to
bring on symptoms of heart failure in hypertrophy. One of the most
frequent causes is sudden or prolonged muscular exertion, which may
disturb a compensation perfect for years, and induce death in a few
days.[59] The intimate pathology of broken compensation is not always
clear. It certainly does not always depend on degeneration of the
muscle-fibres, so far as microscopical examination can tell, and in
many cases we are forced to conclude that the ganglia are at fault and
the breakdown is nervous, not muscular.

[Footnote 59: Traube, _Gesammelte Beiträge_, Bd. iii.]

The PROGNOSIS depends entirely upon the nature of the cause which has
induced the hypertrophy. When remediable or removable, the heart may
return to its normal size, as after pregnancy, acute Bright's disease,
and some cases of hypertrophy from deranged innervation and muscular
exertion. When the cause is irremediable, as in chronic valve disease,
sclerosis of the arteries, or obliteration of pulmonary capillaries,
the case is quite different. Here the prognosis depends largely on the
capability of maintaining in its integrity a sufficient hypertrophy to
compensate for the obstruction: so long as this keeps up all is well;
the evils come with failure of the hypertrophy and increase of the
dilatation. Conditions of general and local nutrition are all-important
factors, and when these can be supported to the highest possible degree
the prognosis is favorable. Ill-health may be indicated at once by the
onset of cardiac symptoms, pointing to disturbed compensation. Much
depends on the seat of the original disease. Mitral stenosis carries
with it as good prognosis, quo ad longevity, as aortic stenosis,[60]
and the latter much better than aortic insufficiency. The nutrition of
the muscle of the heart demands a full and constant supply of blood,
but in aortic incompetency the rapid regurgitation does not permit of
the complete distension of the coronary vessels,[61] and the strain is
such that atheroma of these arteries is very apt to follow and still
further diminish the blood-supply. Hence the prognosis in aortic
insufficiency for enduring hypertrophy is bad. The hypertrophy which
accompanies general arterial degeneration, though compensating for
peripheral obstruction, carries with it certain dangers, as already
{630} indicated, in the liability to cause rupture. With care such
patients may survive for years, though exposed to risks other than
cardiac.

[Footnote 60: Brückes held that the coronary vessels were filled in
diastole alone, but there can be no question that blood also enters
during the systole. The sigmoid valves certainly do not in the majority
of cases cover the orifices of these arteries during this act.
Undoubtedly, however, the heart-vessels are more distended in diastole.
The pallor of the muscle in systole is a proof that the coronary
vessels are not well filled at this period.]

[Footnote 61: This is not the usual statement, but my
experience--limited, it is true--seems to point to the conclusion that
mitral stenosis may also exist for many years without exciting symptoms
of heart disease. It may, I think, be safely affirmed that a larger
number of persons with mitral valve disease live in blissful ignorance
of the existence of serious heart lesion than any other group of
cardiac cases. Particularly is this the case in women. Two points have
attracted my attention in this connection: the frequency with which we
find evidence of stenosis--as shown by the presystolic thrill and rough
murmur--in women complaining, perhaps, of shortness of breath on
exertion and slight cardiac distress--symptoms which are readily
relieved--and the discovery post-mortem of stenosis of the mitral
orifice in cases of sudden death by embolism or from some intercurrent
disease occurring in persons in whom heart disease had never been
suspected. The narrowing may be extreme--an orifice only 13 millimeters
in width in one case in which a woman was stricken with hemiplegia
while attending to her household duties. Such cases, and they are not
very uncommon, teach us how perfect compensation may be in this
lesion.]

The TREATMENT of hypertrophy consists largely of measures directed
toward its maintenance in a degree proportionate to the extra work
which the heart has to do. In organic disease the well-being of the
patient depends on this: we cannot remove the cause, but we can by
careful hygienic and dietetic regulations maintain the balance between
the defect and the compensation. The original lesion is usually beyond
control, and the special indications are to moderate certain dangers
associated with hypertrophy, and to promptly meet the earliest symptoms
of heart failure. The utmost moderation in food, drink, and exercise
must be enjoined. Quiet, regular habits are all important; excesses of
all kind quickly lead to impairment of the heart's action. In the
hypertrophy associated with arterial and renal disease a special danger
exists in the tendency to rupture of vessels. In these cases vigorous
heart-beat, with very high tension in the peripheral arteries,
indicates mischief which may be met by taking prompt measures for the
reduction of the high pressure. A brisk cathartic may avert an
apoplectic attack, and there are cases in which the old practice of
bleeding--formerly so much in vogue for hypertrophy--is justifiable.
Palpitation and shortness of breath are among the earliest signs of
failing compensation, and call for the treatment to be considered under
Dilatation. The condition of hypertrophy from organic disease is not
directly amenable to treatment; we cannot diminish the size of the
organ, but we can regulate its action by measures which control the
contractions when from any cause they become too forcible or irregular.
More particularly is this the case in hypertrophy due to disturbed
innervation. When vigorous, rest and the administration of cardiac
sedatives, such as aconite or veratrum viride, will generally suffice
to reduce the force of the contractions. The palpitation and irregular
action in cases of irritable heart from over-exertion, the abuse of
tobacco, or sexual excesses may subside with the removal of the cause.
The steadying action of small doses of digitalis is often well seen in
these cases.


Dilatation of the Heart.

DEFINITION.--An increase in the size of one or more of the chambers,
with or without thickening of the walls.

VARIETIES.--Two varieties may be recognized: (1) dilatation with
thickening, and (2) dilatation with thinning. Dilatation with
thickening is the most common, and corresponds with the dilated or
eccentric hypertrophy and the active dilatation of some writers. Those
cases of dilatation with walls of apparently normal thickness--simple
dilatation of authors--also belong to this category, for if the chamber
is distended, and yet the walls maintain their normal diameter, they
must of course be hypertrophied. The dilatation with thinning--passive
dilatation--is specially met with in the auricles, and is characterized
by increase in the size of the chamber and attenuation of the walls.

The diastole of the heart is partly an active, partly a passive act.
The cavities behave as would rubber balls, and their distension after
contraction is partly due to their elasticity. The heart is a
suction- as well as a force-pump. In the ventricles, for example, after
systole the active dilatation draws blood from the auricle--must do so,
in fact, in the very process of dilating--and then the auricular
systole completes the process, fully accomplishing the diastole.
Dilatation occurs during this period, and results from distension
beyond the limits of the contractile power of the wall. More blood is
contained in the cavity than the muscle of the wall can {631}
control--_i.e._ expel--but if the organ is healthy, hypertrophy ensues
and the chamber accommodates itself to the altered condition. It is the
heightened pressure during diastole which is dangerous; during systole
the pressure may be extreme, and yet no dilatation may ensue, as in
aortic stenosis, in which condition the size of the chamber may remain
normal, and yet the walls hypertrophy to meet the greatly-increased
resistance to the outflow of the blood during the systole. In the
auricles, however, the increased tension during contraction may be
accompanied with considerable dilatation, as in mitral stenosis.

ETIOLOGY.--There are two important causes in the production of
dilatation: increased pressure within the cavities, and impaired
resistance due to disease of the muscular substance of the heart. They
may act singly, but are often combined. Weakened walls may yield under
normal distending force, or normal walls may yield under a heightened
blood-pressure, or both factors may prevail.

1. Increased endocardiac pressure--which results, as before stated,
either from an augmented quantity of blood to be moved or an obstacle
to be overcome--is the most frequent cause of dilatation. It does not
necessarily cause it. Simple hypertrophy may be the result, as in the
early period of aortic stenosis and in the hypertrophy of the left
ventricle in Bright's disease.

Most of the important causes of increased endocardiac pressure have
already been considered under Hypertrophy, but we may refer to one or
two more particularly.

The size of the cardiac chambers is variable in conditions of health.
With slow action of the heart the dilatation during diastole must be
much more full and complete than with rapid action. Physiologically,
the limits of dilatation have been reached when the chamber cannot be
emptied during the systole. We find this as an acute, transient
condition in severe exertion--during, for example, the ascent of a
steep mountain. There may be great distension of the right heart, as
shown by the increased epigastric pulsation, and even increase in the
cardiac dulness. The safety-valve action of the tricuspid valves may
here come into play, and by permitting regurgitation into the auricle
relieve the lungs. Rest causes it to pass off, but if it has been
extreme, the heart may suffer a strain from which it may recover
slowly, or, indeed, the person may never again be able to undertake
severe exertion. In the process of training the getting wind, as it is
called, is largely a gradual increase in the capability of the heart,
particularly the right chambers. A degree of exertion can be safely
maintained in full training which would be quite impossible under other
circumstances, because by a gradual process of what we may call
physical education the heart has strengthened its reserve
force--widened enormously its limits of physiological work. Endurance
in prolonged contests is measured by the capabilities of the heart, and
its essence consists in being able to meet the continuous tendency to
overstep the limit of dilatation.

We have no definite information as to the nature of the change in the
heart which occurs in the process of training, but it must be in the
direction of increased vigor, muscular and nervous. The large hearts
often noted in athletes may be due, as already mentioned, to the
prolonged use of their muscles; but probably no one can become a great
runner or oarsman who has not naturally a large and capable heart.
Master McGrath, the celebrated greyhound, and Eclipse, the race-horse,
both famous for endurance rather than speed, had very large hearts.

Over-training and heart-strain are closely connected with this question
of excessive dilatation during severe muscular effort. Both mean the
same thing in many cases. A man, perhaps not in very good condition,
calls upon his heart for much extra work during a race or the ascent of
a very steep {632} mountain, and is seized with cardiac pain and a
feeling of distension in the epigastrium, and the rapid breathing
continues an unusual time, but the symptoms pass off after a night's
quiet. An attempt to repeat the exercise is followed by another attack,
or indeed an attack of cardiac dyspnoea may come on while he is at
rest.[62] For months such a man may be unfitted for severe exertion, or
may be permanently incapacitated. He has overstrained his heart and has
become broken-winded. We see the same thing sometimes in horses. What
exactly has taken place in these hearts we cannot say, but their
reserve force is lost, and with it the power of meeting the demands
exacted in maintaining the circulation during severe exertion.[63] The
heart-shock of Latham[64] includes cases of this nature--sudden cardiac
breakdown during exertion and not due to rupture of a valve. It seems
probable that some cases of sudden death in men and animals during
long-continued violent efforts, as in a race, are due to
over-distension and paralysis of the heart.

[Footnote 62: In _St. George's Hospital Reports_, 1872, Clifford Albutt
gives his own experience.]

[Footnote 63: H. C. Wood tells me he believes that wind in athletes is
in large part a question of vagus control, and that he has noticed in
races of dogs used in hunting and other violent exercise the vagi are
more sensitive and powerful than in sedentary breeds. He thinks that a
similar difference exists between tame and wild rabbits.]

[Footnote 64: _Diseases of the Heart_, New Sydenham Soc. ed.]

In the various forms of valvular disease we meet with numerous examples
of dilatation. In aortic incompetency during diastole blood enters the
left ventricle from the unguarded aorta and from the left auricle, and
the amount of blood at the termination of diastole subjects the walls
to an extreme degree of pressure, under which they inevitably yield: in
time they augment in thickness, and we have the typical eccentric
hypertrophy of this condition.

In mitral regurgitation a certain quantity of the blood which should
have been driven into the aorta is forced into the auricle from which
it came, dilating it; and then in the diastole of the ventricle a
larger amount is returned from the auricle, and with increased force,
by the hypertrophied walls of this chamber. In mitral stenosis the left
auricle is the seat of greatly-increased tension during systole, and
dilates as well as hypertrophies; the distension too may be enormous.
Dilatation of the right chamber is very common, and is produced by a
number of conditions, which were considered under Hypertrophy. All
circumstances which permanently increase the tension of the blood in
the pulmonary vessels will cause it--mitral stenosis, emphysema, etc.
The dilatation seems easily produced, but the accompanying hypertrophy
may hold it in check for years. We may here refer to the extreme
distension of the right chambers in pneumonia, particularly when the
consolidation is extensive. The passive dilatation may be very great
and the walls much thinned, and we see the same in states of asphyxia.
Valvular lesions of the right heart are not frequent causes of
dilatation. When the causes which bring about the dilatation act
suddenly, the degree of distension may be great, and there is much more
difficulty in the establishment of compensation, as in rupture of an
aortic cusp.

2. Impaired nutrition of the heart-walls from degeneration or
inflammation may lead to such a diminution of the resisting power that
dilatation readily occurs.

In fevers the loss of tone due to parenchymatous degeneration or
myocarditis may lead to a condition of acute dilatation which may prove
fatal. It is a well-recognized cause of death in scarlatinal
dropsy,[65] and may occur in rheumatic fever,[66] typhus, typhoid,
erysipelas, etc. The myocarditis accompanying acute endo- or
pericarditis may lead to dilatation, especially in the latter disease.
The cavities are usually large in fatty degeneration or {633}
infiltration from the relaxed and atonic state of the walls. In anæmia,
leukæmia, and chlorosis the dilatation of the chambers may be
considerable. In fibroid degeneration the wall generally yields where
the process is most advanced, as at the left apex. The impaired
nutrition in coronary disease may lead to dilatation. Under any of
these circumstances the walls may yield with normal blood-pressure, or
if increased tension is present the effect is the more readily
produced.

[Footnote 65: Goodhart, _Guy's Hospital Reports_, Series iii. vol.
xxiv.]

[Footnote 66: Samuel West, _Barth. Hospital Reports_, xiv.]

Pericardial adhesions are usually spoken of as a cause of dilatation,
acting by traction from without, and we generally find in a case of
extensive and firm union considerable hypertrophy and dilatation. In
this condition there is usually some impairment of the superficial
layer of muscle which may permit of over-distension.

MORBID ANATOMY.--Usually the condition exists in two or more chambers,
and is associated with hypertrophy, the appearances of which have
already been described. It is more common on the right side than on the
left. Perhaps the most general dilatation which we see is in cases of
aortic incompetency, in which all the cavities may be enormously
distended. In mitral stenosis the left auricle is often trebled in
capacity, and the right auricle and ventricle also are very capacious.
The former may contain eighteen to twenty ounces of blood. In many
chronic affections of the lungs the right chambers are chiefly
affected. Dilatation with thinning is often the result of an acute
process met with in the fevers. The walls may be very much thinner than
normal, almost membranous, and the dark color of the blood may show
through with distinctness. When the distension of one ventricle is very
great, there may be a distinct bulging of the septum toward the other
side. The shape of the organ is altered, and when the right chambers
are chiefly affected it is more globular in shape. Distension of the
left auricle may render it visible in the front of the heart, and the
appendix may be prominent. The right auricle when enormously enlarged,
as in some cases of pneumonia, in emphysema, and in leukæmia, may form
a large mass occupying a considerable space in the antero-lateral part
of the thorax. The walls in dilatation with thinning are flabby and
relaxed, and collapse at once when cut, but in dilatation with
hypertrophy they are firm, especially those of the right ventricle.

The auriculo-ventricular rings are often dilated, and there may be an
inch and a half, or even two inches, of increase in the circumference.
Thus, the tricuspid orifice, the circumference of which is about four
and a half inches, may admit freely a graduated heart-cone of over six
inches, and the mitral orifice, which is about three and a half inches
normally, may admit the cone to five and a half inches or even more.
Great dilatation is always accompanied with relative incompetence of
the valves, so that free regurgitation into the auricles is permitted.
The orifices of the cavæ and of the pulmonary veins may be greatly
dilated.

The muscle-substance varies much in appearance according to the
presence or absence of degenerations. The endocardium is often opaque,
particularly in the auricles. The microscopical examination may show
marked fatty or parenchymatous change, but in other instances of
dilatation and heart failure in eccentric hypertrophy there may be no
special alteration noticeable. I fully agree with Niemeyer's assertion,
"that it is not possible by means of the microscope to recognize all
the alterations of the muscular fibrillæ which diminish the functional
power of the heart."[67] We know too little as yet of the changes in
the ganglia of the heart in these conditions: as centres of control
they probably have more to do with cardiac atony and breakdown than we
generally admit. Degeneration of them has been noted by Putjakin[68]
and others.

[Footnote 67: _Textbook of Medicine_, vol. i., Am. ed.]

[Footnote 68: _Virchow's Archiv_, lxxiv.]

{634} SYMPTOMS AND PHYSICAL SIGNS.--Dilatation produces weakness of the
cardiac walls, diminishes the vigor of their contractions, and is thus
the very reverse of hypertrophy. So long as compensation is maintained
the enlargement of a cavity may be considerable: the limit is reached
when the hypertrophied walls can no longer in the systole expel all the
contents, part of which remain, so that at each diastole the chamber is
abnormally full. Thus in aortic incompetency blood enters the left
ventricle from the aorta as well as the auricle, dilatation ensues, and
also hypertrophy as a direct effect of the increased pressure and
increased amount of blood to move. But if from any cause the
hypertrophy weakens, and the ventricle during systole does not empty
itself completely, a still larger amount is in it at the end of each
diastole, and the dilatation becomes greater. The amount remaining
after systole is a cause of obstruction, preventing the blood entering
freely from the auricle. Incompetency of the auriculo-ventricular
valves follows with dilatation of the auricle and impeded blood-flow in
the pulmonary veins. Dilatation and hypertrophy of the right heart may
compensate for a time, but when this fails stasis occurs in the venous
system, with dropsy. The consideration of the symptoms of chronic
valvular lesions is largely that of dilatation and its effects. Acute
dilatation, such as we see in fevers or in sudden failure of an
hypertrophied heart, is accompanied by three chief symptoms--weak
usually rapid impulse, dyspnoea, and signs of obstructed venous
circulation. Cardiac pain may be present, but it is often absent.

The physical signs of dilatation are those of a weak and enlarged
organ. The impulse is diffuse, often undulatory, and is felt over a
wide area, and an apex-beat or a point of maximum intensity may not
exist. When it does it may be visible, and yet cannot be felt--an
observation of Walshe's which is very valuable. An extensive area of
impulse with a quick, weak maximum apex-beat may be present. When the
right heart is chiefly dilated the left may be pushed over so as to
occupy a much less extensive area in the front of the heart, and the
true apex-beat is not felt; but the chief impulse is just below or to
the right of the xiphoid cartilage, and there is a wavy pulsation in
the fourth, fifth, and sixth interspaces to the left of the sternum. In
extreme dilatation of the right auricle a pulsation can sometimes be
seen in the third right interspace close to the sternum, and with free
tricuspid regurgitation this may be systolic in character. Whether the
pulsation frequently seen in the second left interspace is ever due to
a dilated left auricle is not satisfactorily determined. I have
sometimes thought it was presystolic in rhythm, though it may be
distinctly systolic. Post-mortem, it is rare in the most extreme
distension to see the auricular appendix so far forward as to warrant
the belief that it could beat against the second interspace. The area
of dulness is increased, but an emphysematous lung or the full
distended organ in a state of brown induration may cover over the heart
and limit greatly the extent. The directions of increase were
considered when speaking of Hypertrophy with dilatation.

The first sound is shorter, sharper, and more valvular in character,
and more like the second. As the dilatation becomes excessive it gets
weaker. Reduplication is not common, but occasionally differences may
be heard in the joint sound over the right and left hearts. Murmurs
very frequently obscure the sounds; they are produced by incompetency
of the valves due to the great dilatation, or are associated with the
chronic valve disease on which the condition depends. The aortic second
sound is replaced by a murmur in aortic regurgitation; the pulmonary is
accentuated in mitral regurgitation and pulmonary congestion, but with
extreme dilatation it may be much weakened. The heart's action is
irregular and intermittent, and the pulse is small, weak, and quick.

The DIAGNOSIS is generally easy when the physical signs, the history,
and {635} the general condition are taken into account. In a case of
valvular disease with hypertrophy the onset of dyspnoea and venous
stasis with dropsy tell unmistakably of cardiac dilatation. Increased
præcordial dulness, with a weak, diffuse impulse, is not simulated by
many conditions, and one only, pericardial effusion, need be specially
mentioned. This may present very serious difficulties, and indeed a
dilated heart has been aspirated under the belief that effusion was
present. The points to be attended to are--the greater lateral dulness
in dilatation and the wavy impulse which may extend over a great part
of it; in effusion the dulness extends upward and is more pear-shaped,
the impulse is not so extensive, and may be tilted up an interspace or
may not be visible. The sounds in pericardial effusion are muffled and
distant over the dull region, but at its upper limit may be clear. The
absence of friction is an important negative sign. In some cases it is
extremely difficult to determine between the conditions, and I have
known a weak, feeble, irregular heart, with cyanosis, and oedema lead
to the diagnosis of dilatation when effusion was present.

The PROGNOSIS depends upon the cause of the dilatation. In anæmia and
fevers the temporary dilatation may undoubtedly pass away with the
improvement of health; but when the cause is not remediable the danger
must be measured by the presence or absence of compensation. In the
majority of the cases which we see the dilatation occurs in valve
disease, and no symptoms of importance arise so long as the
compensation is perfect. Failure of this, which may result from many
causes, as already mentioned, is always serious. It may be only
temporary, and with care the compensation can be re-established and the
symptoms pass away. We constantly see this in the eccentric hypertrophy
of the right heart from mitral disease; an attack of bronchitis
suffices to disturb the compensation, and with the relief of the
catarrhal trouble the dyspnoea and heart symptoms disappear.

The TREATMENT of dilatation is virtually that of chronic valvular
disease, and we shall only refer to general indications. With the
earliest symptoms of failure the work of the heart should be reduced to
a minimum by placing the patient at rest. This in itself may suffice
without any other measures. Time and again I have seen, particularly in
cases of aortic insufficiency, the dyspnoea relieved and the oedema of
the feet disappear and the compensation re-established by placing the
patient in bed, enjoining absolute quiet and carefully regulating the
diet. The importance of rest in the early stages of heart failure
cannot be too much insisted upon.[69] Quiet and careful dieting may
suffice for the milder attacks, but we have usually even in these to
resort to heart tonics. Digitalis is the most powerful remedy we
possess in restoring and maintaining compensation. Under its use the
irregular, feeble, and frequent contraction becomes regular and
stronger, and the embarrassed circulation is relieved. In hospital
practice the same chronic heart cases may return year after year with
attacks of cardiac failure, dyspnoea, dropsy, etc., and each time the
rest in bed and digitalis may suffice to restore compensation. A fourth
or fifth, even a sixth, attack may be safely weathered, and then the
final breakdown occurs when nothing avails to combat the dilatation. Of
substitutes for digitalis, caffeine and convallaria have been much used
of late. Caffeine in some cases acts more promptly, which is an
advantage, but its action is not so certain and not so enduring.
Convallaria is very variable {636} in its action; it has succeeded in
some instances in which digitalis has failed, and in others has been
quite without effect. In extreme cardiac failure with great dilatation,
lividity, orthopnoea, and feeble pulse, stimulants must be freely
given; ether may be employed hypodermically. In this condition of final
asystolism digitalis seems to have lost its influence. In the heart
failure of pneumonia I have found camphor a valuable adjuvant to the
diffusible stimulants. To improve the general nutrition, and with it
that of the heart-muscle, iron and arsenic are most valuable adjuvants,
especially in the dilatation of anæmia. The treatment of special
symptoms, dropsy, dyspnoea, etc., is considered under Valvular
Affections.

[Footnote 69: In Ortel's system (_Ziemssen's Handbuch der Allgemeine
Therapie_, Bd. iv.) of treating heart disease exercise, particularly
climbing, forms a very important part, but an analysis of his cases
shows that most of them were instances of fatty heart in obese persons.
It would scarcely be applicable to valvular disease. The severe
exercise, he thinks, stimulates the heart-muscle and helps in the
restoration of the hypertrophy. His other suggestion, the reduction of
the liquids ingested, seems much more reasonable, as in this way the
volume of blood to be circulated may be considerably reduced.]


Aneurism of the Heart.

This term is now restricted to local or partial dilatations of the wall
of one of the cardiac cavities. Formerly, dilatation of the heart or of
one of its chambers was spoken of as aneurism. This rare condition[70]
is most frequently associated with fibroid degeneration, but other
causes of local weakness of the walls, as ulcer, acute myocarditis, and
fatty degeneration, have been present in a few cases. An instance is on
record where the aneurism followed a stabbing wound of the chest.[71]
The left ventricle is usually involved; very few cases occur in the
other chambers. The condition may be acute or chronic.

[Footnote 70: In the index catalogue there are references to only 18
cases by American authors. In the museums of Philadelphia there are
only 5 specimens--3 in the museum of the College of Physicians; 1 each
in the University and Pennsylvania Hospital cabinets.]

[Footnote 71: Quoted by Legg, _Bradshawe Lecture on Cardiac Aneurisms_,
London, 1883.]

Acute aneurism is met with occasionally in ulcerative endocarditis,
more rarely as the result of local softening due to myocarditis or
plugging of a branch of a coronary artery. In severe endocarditis
perforation is, I think, more common than the production of aneurism.
In one case I saw a deep excavation at the upper part of the septum
produce a bulging the size of a marble in the wall of the left auricle,
and in another ulceration in one sinus of Valsalva had extended into
the septum, the upper part of which presented an aneurismal dilatation
which had ruptured into the left ventricle. Legg considers the
production of acute aneurism by the rupture of abscesses or cysts as
doubtful.

Chronic aneurism is almost confined to the left ventricle, and, as
Cruveilhier pointed out,[72] is the result of fibroid degeneration of
the muscle. In a few instances fatty degeneration appears to have been
the cause. The monographs of Thurnam,[73] Pelvet,[74] and Legg[75] give
the most complete account of the disease. They are more common in men
than in women, and the majority of the cases occur after middle life.

[Footnote 72: _Anatomie pathologique_, Paris, 1835-42.]

[Footnote 73: _Medico-Chirurgical Transactions_, vol. xxi., 1838.]

[Footnote 74: _Des Aneurysmes du Coeur_, Paris, 1867.]

[Footnote 75: _Loc. cit._]

The situation of the aneurism is most frequently at the apex--59 of 90
cases collected by Legg. They are usually rounded in shape, and may
vary in size from a marble to a cocoanut. The sac may be double, as in
a case described by Janeway,[76] or, as in a specimen in Guy's Hospital
Museum, the whole wall of the ventricle may be covered with aneurismal
bulgings. In the simplest form there is a rounded dilatation at the
apex, and the lower part of the septum is lined with thrombi. Often the
tumor is distinctly sacculated, and communicates with the ventricle by
a very small orifice. The pericardium is usually thickened, and
calcification may occur in the walls. Rupture seems rarely to occur--in
only 7 of the 90 cases collected by Legg. Of other {637} parts of the
ventricle, the septum and the undefended space at the highest part of
the septum just below the aortic ring are most often involved. This
latter situation is sometimes the seat of a congenital dilatation,
usually a small, thin, smooth sac without thrombi, which has no
pathological significance.

[Footnote 76: _N.Y. Med. Journ._, 1875, xxi.]

Cardiac aneurisms rarely produce any symptoms, and in the majority of
cases have been found accompanying other conditions which have proved
fatal. At the left apex the increase in dulness and area of pulsation
could scarcely be distinguished from hypertrophy unless associated with
marked bulging. They seldom perforate the chest-wall. Berthold (quoted
by Legg) has described one connected with the right auricle which
produced a pulsating tumor beneath the skin, the region of the second
and third ribs.


Adventitious Products in the Heart.

Tubercle.--In general tuberculosis and in tuberculous pericarditis
there may be nodules in the heart-substance, but, as a rule, this organ
is very rarely the seat of tubercle. Large caseous masses sometimes
occur, but unless associated with tubercle in other organs they are not
to be regarded as necessarily tuberculous. Miliary granulations have
been seen on the valves.

Cancer and sarcoma rarely are primary, and are not often met with as
secondary growths. Sometimes a mediastinal sarcoma penetrates along the
veins and involves the auricle, with or without great involvement of
the pericardium. The secondary tumors may be single or multiple. In a
case of cancer of the uterus I found a large mass in the wall of the
right ventricle, involving also the anterior segment of the tricuspid,
and partially blocking the orifice. The surface was eroded, and the
pulmonary arteries contained numerous cancerous emboli. In another
instance the heart was considerably enlarged by the presence of many
rounded masses of colloid cancer throughout the walls. In a remarkable
case of sudden death in a child I found the tricuspid orifice firmly
blocked with a sarcomatous mass which I thought at first had originated
in the heart, but dissection showed to have come from the renal vein,
which was filled with sarcoma extending from a large tumor of the
kidney. Melanotic cancer, fibromata, and myomata have occasionally been
seen, and a secondary epithelial growth has been described by Paget.

Syphilis of the heart is met with in the form of gummata or as a
specific arteritis leading to patches of fibroid induration. The
gummous growths form tumors of variable size, which usually occupy the
septum or the ventricles. Possibly many of the caseous and calcified
masses not infrequently met represent obsolete gummata. The syphilitic
myocarditis probably originates in an affection of the arteries, and
leads to patches of fibroid induration more or less extensive. Many
authors hold that syphilis plays a very important rôle in the
production of fibroid heart.

Cysts.--Simple cysts are rare in the heart. I have met with two
instances--one, the size of a marble, situated in the wall of the right
auricle near the septum, was filled with a brownish fluid; the other,
the size of a small walnut, occupied the base of the posterior segment
of the mitral, and was filled with a clear fluid. Blood-cysts
occasionally occur.

Parasites.--The Cysticercus cellulosæ, the larva of Tænia solium, and
the hydatid or echinococcus, the larva of Tænia echinococcus of the
dog, are sometimes found in the heart. The former, usually single, is
extremely rare; in the hog and calf the measles, as the cysts are
called, very often exist in the heart-muscle. In the recent paper by
Mosler[77] references are given to 13 cases of cysticerci in the heart.
The greatest number present was 19. The {638} hydatid is more common:
25 instances are mentioned in the statistics of Devaine and Cobbold,
and Mosler's more recent figures only give 29. They occur in the right
ventricle more frequently than in the left. Occasionally they attain a
larger size and compress the heart and push back the lungs. The cyst
may burst and the contents be discharged into the pulmonary artery or
aorta, as in a case given by Osterlen,[78] in which gangrene of the
right leg followed the plugging of the femoral by hydatid vesicles
discharged into the blood by the bursting of a cyst in the left
auricle.

[Footnote 77: _Zeitschrift für klinische Medicin_, Berlin, Bd. vi.,
1883.]

[Footnote 78: _Virchow's Archiv_, xlii.]




{639}

ENDOCARDITIS AND CARDIAC VALVULAR DISEASES.

BY ALFRED L. LOOMIS, M.D.


Endocarditis.

DEFINITION.--Endocarditis is an inflammation of the endocardium, and
may be either exudative, neoplastic, or ulcerative in character. While
its different varieties are closely connected in their etiology, they
are distinct in the extent, duration, character, and course of their
pathological changes. They cannot be classified as acute and chronic in
the ordinary acceptation of these terms, for they often so merge into
each other as to render it difficult, if not impossible, to determine
when they cease to be acute and become chronic; and some cases are at
no time acute. It has been claimed that an acute endocarditis becomes
chronic when its course is prolonged, but the advanced changes are only
a stage of the acute process.

So-called acute endocarditis is accompanied by a fibro-cellular
exudation into the substance of, and underneath, the endocardium,
causing elevations of its surface. The better term for this variety is
exudative endocarditis, it being borne in mind that the exudation does
not take place upon the free surface of the membrane, but into its
substance and underneath it. This form of endocarditis may be entirely
recovered from, or it may lead to interstitial changes in the
endocardial and myocardial tissue which will correspond to the changes
usually described as those of chronic endocarditis.

Interstitial endocarditis is a better term for these changes. The
disease may be the sequela of exudative endocarditis, or may be
interstitial from its commencement, for the valvular changes of
interstitial endocarditis are often found in those who never have had
either acute articular rheumatism or exudative endocarditis, but have
been the subjects of chronic rheumatism or gout.

Acute exudative endocarditis may, in certain cases, be stamped with an
ulcerative process, the result of septic infection, giving rise to
those pathological changes which have been described as acute
ulcerative endocarditis.

HISTORY.--The history of endocarditis is restricted to modern
pathology. It is not spoken of by the older medical writers. Before the
sixteenth century knowledge of the structure and functions of the heart
was imperfect and scanty, and its diseased conditions were altogether
unknown.

The history of the pathology of cardiac disease commenced with Harvey,
Lancisi, Vesalius, and Vieussens. They investigated not only the normal
structure of the heart and the mechanism of the circulation, but
accurately described a few of its valvular diseases.

There is little doubt but that Laennec, Senac, and Morgagni were quite
familiar with the valvular diseases of the heart, but Kreisig first
traced the relationship between valvular diseases and inflammation of
the lining membrane of the heart.

{640} The term endocarditis was first used by Bouillaud, who had the
advantage of Laennec's discovery of auscultation. Corrigan first
discovered the physical signs of aortic insufficiency. The most
important advance in the pathology of endocarditis is due to the
investigations of Virchow and Luschka, the former developing its
sequelæ or results, the latter its histological changes. Ulcerative
endocarditis is of modern date, and its literature scarcely extends
back twenty years. The labors of Kirk, Virchow, Charcot et Vulpian,
Moxon, Eberth, and Lancereaux are all connected with the etiology and
anatomical changes of ulcerative endocarditis.

The relationship of interstitial endocarditis to valvular diseases of
the heart and to cardiac murmurs is a subject which at present is
engaging the attention of many medical observers.

I shall describe endocarditis under three heads:
  1st, Exudative endocarditis;
  2d, Ulcerative endocarditis;
  3d, Interstitial endocarditis.

That the pathological changes which I shall describe may be readily
appreciated, I will briefly review the anatomical structure of the
endocardium.

The endocardium consists of connective tissue, with numerous elastic
fibrils, covered by and continuous with a layer of flattened cells.
Upon this lies the endothelial layer, which disappears in twenty-four
hours after death.

Luschka regards the endocardium as continuous with all the arterial
tissues, but the majority of histologists consider it a continuation of
the internal membrane. Some regard the endocardium and inner coat of
the arteries as analogous, since both are non-vascular and have an
endothelial covering upon a connective-tissue base. As endocarditis is,
for the most part, limited to the valves of the heart, a knowledge of
their anatomical arrangement is important.

A transverse section of a segment of an auriculo-ventricular valve
shows that upon the superior or auricular surface and upon the inferior
or ventricular surface there are flattened cells and endothelium, and
that next to each lies a fibro-elastic layer, the superior being the
thicker. These two layers are separated by connective tissue.

The layer of flat cells is thickest on the ventricular surface. The
fibro-elastic tissue is thickest at the base of the valve. The
semi-lunar valves have endocardium on one side and the tunica intima on
the other.

Although the endocardium has no vessels of its own, the capillaries
upon the cardiac walls are in contact with it. The arrangement in the
valves is different, as only a few vessels ramify between the layers of
the mitral valve, and none are found, normally, in the sigmoid valves.


Acute Exudative Endocarditis.

This variety of endocarditis is met with most frequently in connection
with acute articular rheumatism.

In adults it usually has its seat in the left heart; in intra-uterine
life it occurs in the right heart. The inflammation commences in, and
seldom extends beyond, the valves and the valvular orifices, but it may
involve the whole or any part of the ventricular or auricular portions
of the endocardium.

MORBID ANATOMY.--The endocardium becomes infiltrated with young cells,
the process beginning in the layer of flat cells. The new formative
cells are developed not only from the cells of the layer immediately
underneath the endocardium, but also from leucocytes. This hyperplasia,
this heaping up of embryo-plastic cells, is accompanied by softening of
the deeper {641} layers of the intercellular structure, and as the
softening goes on the intercellular substance is destroyed.

The endothelial elements also play an active part in the processes. The
masses of new cells push out the endocardium, and papillary elevations
are formed, filled with a fluid whose chemical properties resemble
those of mucin, since it coagulates into threads when acetic acid is
added. The cone-like vegetation is surrounded in the deeper layers of
the endocardium by a zone of proliferation which is never distinctly
limited, but which exhibits progressive hyperplasia from the periphery
toward the centre.

All these changes may have taken place in non-vascular tissue. Where
the capillaries are most numerous a punctuate or arborescent
vascularity is seen, and this is followed by opacity of the part which
is the seat of the inflammation. After death the endocardium and lining
membrane of the vessels are often stained; this staining is produced by
the coloring matter from the red corpuscles, and is the result of
post-mortem change.

There is no exudation upon the villous projections; the coagula found
upon them are a deposit of fibrin from the blood, the projections
acting as foreign bodies in the blood-current. The fibrinous deposits
occur chiefly on the surface which is opposed to the current of the
circulation, and sometimes they are distinctly conical; at others they
have the shape of a raspberry. They occupy the parts most exposed to
the friction of the blood, and are arranged on the borders of the
aortic valves at a little distance from their edges, the seat being
determined by the limit of the vascular network. The band of tissue
which passes from the attached border of the valve to the Arantian body
in the centre shows the inflammatory granulations most distinctly. They
consist of a cauliflower-like bulbous extremity, connected by a
constricted neck with a firm, hard base that is intimately blended with
the subjacent tissue. A thin hyaline layer covers each mass. At first
these granulations or vegetations are very small and numerous, so that
the membrane presents a granular appearance. Later, they become larger,
reaching oftentimes the size of a small pea.

Near the insertion of the tendons upon the auricular surface of the
mitral valve are found irregular wreaths of vegetations which enclose
the attachments of the chordæ tendineæ. Moxon has shown that the
friction of the vegetations or of fibrinous clots that gather upon the
vegetations may, by the irritation it produces, excite endocarditis at
points remote from the valves.

The tendon of the mitral valve may show the effects of endocarditis by
becoming soft and friable, and even rupturing, or the chordæ tendineæ
may adhere to one another. When such adhesions occur either with
agglutinations of the flaps to each other or to the heart-walls,
stenosis or regurgitation may result.

In connection with these changes new vessels are developed in the
substance of the mitral valve, or those that already exist become more
apparent. In the semilunar valves new vessels are formed or neighboring
capillaries send out prolongations into the parts destitute of vessels.
This, according to Charcot, is one way in which arborescent vascularity
occurs. These changes are most marked in those forms of exudative
endocarditis which run an acute course.

In some instances the hyperplasia is so extensive as to interfere with
nutrition, and may lead to fatty metamorphosis. A cavity is then formed
filled with granular fat-cells, discrete fat-globules, and
blood-pigment, whose endocardial covering ruptures, and the contents
are carried into remote capillaries to cause capillary embolism and
septicæmia. This has been called ulcerative endocarditis.


{642} Ulcerative Endocarditis.

Ulcerative endocarditis occurs in those diseases where there is great
vital depression. It is met with oftenest in pyæmia, puerperal fever,
scarlatina, and diphtheria. It has been called septic, diphtheritic,
and infectious endocarditis.[1]

[Footnote 1: Jaccoud, Klebs.]

MORBID ANATOMY.--Ulcers may form in endocarditis in either one of three
ways: 1st. The exudative process may be so rapid and extensive as to
cut off the nutrition of the endocardium covering the apices of the
papillary elevations, and ulcers result in non-septic inflammation. 2d.
Degeneration of the neoplastic tissue, due either to deficient
blood-supply or other causes of impaired nutrition, may so soften the
villi or efflorescences that their apices will be swept away by the
blood-current and ulcers thus be formed. Charcot especially insists
that the ulceration of these elevations is the consequence of granular
degeneration, and not of fatty metamorphosis, with which it is often
confounded. 3d. The exudative process may be purulent in character, and
form minute abscesses in the substance of the valves beneath the
endocardium, which, rupturing, leave comparatively deep ulcers. Acute
multiple abscesses in the aortic valves are of frequent occurrence in
ulcerative endocarditis.

The margins of the ulcers are irregular, but well defined; the edges
are swollen and thick, and their floor (the muscular substance of the
heart or the fibrous layer of the valve) is infiltrated with pus.

Where there is extensive loss of substance perforation of the valve may
occur. These perforations are sometimes closed or hidden by a fibrinous
exudation.

The soft and friable vegetations may be torn into long shreds by a
forcible blood-current, and subsequently may excite endocardial
inflammation where they come in contact with the walls of the
heart-cavity, or they may break off and form emboli. A fibrinous string
upon a flap of the aortic valve is not infrequently driven down and
back by a regurgitant current, so as to excite endocarditis in the
mitral valve.

Some observers state that micrococci and bacteria are found in
ulcerative endocarditis of a septic or diphtheritic origin, and they
have given to it the name of mycosis endocardii. It is probable that
these minute organisms are developed by the septic ulcerative process
rather than that they are the cause of such processes. They appear as
spheres, highly refractive, motionless, cohering in groups, without any
stroma. Acids, alkalies, ether, and chloroform have no effect on them,
so that they are not to be regarded as vegetable products.

The valvular ulcerations in this form of endocarditis give rise to the
most diverse lesions. Masses may be detached from the diseased cardiac
orifices, either from the fibrinous deposits on the valves or from
ulcerations of the valves themselves, and, having entered the
circulation, they will produce various symptoms in the organs and
tissues to which they are carried.

It is important to make a distinction between the results produced by
displacements into the blood-current of large masses and those arising
from the entrance of molecular fragments. It is also to be remembered
that the masses from the vegetations or ulcerated valves in ulcerative
endocarditis are often stamped with a septic element which leads to the
development of suppurative infarctions in different organs.

The size and site of the emboli are important, for they may be so large
as to obstruct vessels of large size.

The femoral and even the external iliac may suddenly become impervious
to the circulatory currents, on account of the presence of a large
embolus from the heart.

{643} When the arteries in the limbs are thus plugged, the result is
generally an ischæmia, terminating often in gangrene. Capillary
embolism may occur in a number of organs at the same instant, and give
rise to a variety of lesions. When the cutaneous capillaries are
obstructed ecchymotic spots are produced, followed by cellulitis. When
the cerebral vessels are obstructed softening may occur, which, if the
vessels are very small, may be developed without any evidence of
obstruction to the cerebral circulation. If the obstructed artery is of
large size, instantaneous hemiplegia and secondary softening will
result.

Capillary emboli may have their seat in the vessels of the spleen,
giving rise to infarctions and suppuration.

The kidneys may also undergo analogous changes. Rayer, without knowing
the origin of these changes, has given an excellent description of them
under the name of rheumatic nephritis.

In addition to the local lesions arising from these arterial or
capillary emboli, the septic phenomena are most important. When typhoid
symptoms, deep jaundice, and symptomatic intermittent fever are
associated with acute endocarditis, it establishes its ulcerative
character. In acute exudative as well as in ulcerative endocarditis,
when the inflammation progresses rapidly, the valves soften and become
less resistant than normal. As a result, they are stretched, bulged, or
torn by the stream of the circulating blood-current.

A rupture of the mitral valves will open into the auricular, and that
of the aortic into the ventricular, cavity. The reason for this is to
be found in the fact that when the valves are closed the blood-pressure
is exerted from the left ventricle toward the mitral valve, and from
the aorta toward the semilunar valves. If the blood penetrates a rent
in a flap of the valves, the endocardium is puffed out, and a valvular
aneurism is formed, and round or funnel-shaped aneurismal sacs may
project from the valves. The bottom of one of these sacs may be
perforated, and long, ragged, gray shreds, covered with fibrin, may be
found hanging in the ventricular cavity.

Microscopically, the torn shreds from a valvular aneurism, the result
of acute endocarditis, consist of nuclei and round cells imbedded in a
mass of granular matter. There is neither connective fibrilla nor
elastic tissue. When the ulceration is localized in the ventricle, the
pressure of the blood may bulge out the heart-wall, and thus give rise
to a so-called partial cardiac aneurism. By rupture of such aneurism
communication between the different heart-cavities may be established,
which will vary with the seat of the ulceration.

Acute exudative endocarditis may involve the muscular structure of the
heart. Such myocarditis (or carditis) may involve the deeper
structures, weaken them, and so alter their consistence that bulging
and the formation of a ventricular aneurism may result. Usually such
myocarditis is so slight that incomplete organization of the new
embryo-plastic cells occurs and the tissue undergoes fatty changes. The
results of all forms of acute endocarditis are best studied in
connection with the morbid changes of interstitial endocarditis, into
which they so often gradually merge.


Interstitial Endocarditis.

MORBID ANATOMY.--Interstitial (or chronic) endocarditis may be a
continuation of a process which commenced in an acute exudative
endocarditis, or it may be interstitial from its commencement, and be
so insidiously evolved as to escape notice. The anatomical changes may
sometimes be confined to the edges of the valves, at others to their
base, or they may involve the entire valves, which become thickened,
indurated, contracted, degenerated, and {644} adherent. It is more
closely allied to rheumatism, gout, and chronic interstitial changes in
other organs than either of the other varieties.

There is no part of the endocardium which is exempt from interstitial
inflammation. The favorite place for its development is the endocardium
of the valves and that at the apex of the left ventricle. The
thickening at first may be either translucent or opaque, and the valves
may become three or four times thicker than normal. In some instances,
although the valves are thickened and indurated, their functional
activity is not interfered with, and they offer no obstruction to the
blood-current.

White, thickened, opaque spots are often irregularly scattered over the
internal wall of the heart. The vegetations met with in interstitial
endocarditis differ from those of the acute exudative variety in that
they are less prominent and firmer. They rest upon an indurated base.
Their cartilaginous consistency is due to the fact that their cellular
elements are not round (as in acute exudative endocarditis), but
elongated and flattened, possessing an abundant intercellular
fibrillated tissue.

In and underneath the endocardium there is an increase of tissue, and
upon any prominence arising from the thickening of the endocardium
occur fibrin deposits. These fibrinous efflorescences assume a variety
of forms, and sometimes string out into the adjacent vessels and
cavities for half an inch or more. Their usual form is globular or
wart-like, and their seat is on the ventricular surface of the aortic
and upon the auricular surface of the mitral and tricuspid valves.

In interstitial endocarditis the cell-development is far less rapid and
abundant than in the acute exudative form, and this very slowness
accounts for the greater induration and thickening.

A microscopical examination of a cross-section of an indurated valve
shows a number of flat cells arranged in irregular layers, having
between them a fibrinous material which has in it here and there a few
elastic fibres. The new formations always originate in the layer of
flat cells. These changes are best marked in the fibrous zone at the
valvular orifices, upon the surfaces of the valves themselves, and in
the chordæ tendineæ. The new tissue, whether developed rapidly as in
acute exudative, or slowly as in interstitial endocarditis, becomes
fibroid and contracts, and this contraction is progressive.

As a consequence, the rigid valves, whose edges are round and hard, are
drawn toward their base, and thus are made to assume a puckered
appearance. A similar process in the chordæ tendineæ causes them to
become hypertrophied, rigid, and cartilaginous, while they are
diminished in length. In this way the valves are not only diminished in
depth, but not infrequently have their free edges approximated to the
cardiac walls, so that extensive valvular insufficiency is the result.
This, however, does not always happen, for a thickened cartilaginous
valve may have such abundant fibrinous or papillary excrescences upon
it that the onward current is obstructed and extensive stenosis
results.

As the thickening and rigidity of the flaps of a valve increase, their
mobility is diminished, and adhesions take place between their edges
which begin at their bases and progress toward their apices: so
thoroughly do they become adherent that in some cases all evidence of a
valvular outline is lost, and a fibrinous diaphragm is formed across
the valvular orifice having only a small slit at its centre, looking
and feeling like a buttonhole; hence the term buttonhole slit. The
mitral opening, which will usually admit the ends of three fingers, may
be so narrowed that the end of the little finger will scarcely pass
through it, and the aortic opening may become so diminished as not to
admit a small quill. These retractions and adhesions cause the mitral
valves, with their columns and cords, to assume the form of a
perforated cone.

{645} Long stringy masses of fibrin, when located on the aortic valve,
sometimes form adhesions with the aortic walls, and thus is induced a
sudden and extensive regurgitation.

Insufficiency and stenosis are often found at the same valvular orifice
as the result of the thickening, adhesion, and retraction.

Changes at the aortic orifice usually occur after middle life, and
induce more insufficiency, retraction, and adhesion than those which
are limited to the mitral valve. The mitral valves are the most
frequent seat of interstitial endocardial changes in early and adult
life. These lesions are analogous to those characteristic of
endarteritis deformans. The tendency of the lowly-organized tissue
which results from interstitial endocarditis is to undergo fatty and
calcareous changes.

The minute patches of fatty degeneration in the imperfectly organized
tissue underneath the endocardium sometimes form atheromatous masses
containing more or less granular débris. The endocardium over these
patches may be destroyed, or the patches may soften and ulcerate and
cause extensive destruction of the valves. Valvular aneurism may form
in the same manner as has been described in exudative endocarditis. The
formation of calcareous granules and plates is a very frequent
termination of interstitial endocarditis.

The aortic orifice is the most frequent seat of calcareous
degeneration. It is rarely associated with mitral stenosis. So
extensive may this process be that little beads of chalky material may
be seen studding the free edges of the valve and even extending into
the cardiac cavities.

When interstitial endocarditis has its seat in the endocardium of the
cardiac cavities, the endocardium will undergo changes similar to those
of the valves, and the muscular walls of the heart will be the seat of
interstitial myocarditis. As a result, the walls of the heart become
thinner and less resistant than normal, and depressions are formed on
its inner surface. The process is in reality a fibrous overgrowth,
which occurs in spots varying in size from half an inch to one inch in
diameter. When it extends through the entire heart-wall the columns and
cords may be so shortened as to cause valvular insufficiency.

If the cardiac walls yield so that a well-defined pouch is produced, a
condition results which is called aneurism of the heart. Cardiac
aneurism, thus induced, is usually seated at the apex of the left
ventricle; the aneurismal sac may vary in size from that of a marble to
that of a closed fist, and may communicate with the ventricle by a
funnel-shaped or ring-like aperture. The walls of the sac are solid and
rigid; the internal surface is smooth, but it may be anfractuous. In
the latter case clots adhere to its wall. Cardiac muscular fibres are
found here and there in the aneurismal walls. They are mostly, however,
made up of layers of flat cells, their flatness being the result of
pressure.

Aneurisms at the base and in the inter-ventricular septum may result
from the extension of a valvular aneurism.

ETIOLOGY.--In most instances endocarditis depends upon a constitutional
dyscrasia characterized by alterations in the vital, physical, or
chemical properties of the blood.

Acute exudative endocarditis rarely, if ever, occurs as a primary or
idiopathic affection. It seems to have a direct connection with those
diseases and dyscrasiæ in which the blood is altered either in the
relative proportions of its constituents or in its physiological
elements. So frequently is acute exudative endocarditis associated with
acute articular rheumatism that they have often been described as one
disease.

It is generally stated that acute endocarditis occurs in 50 per cent.
of those who suffer with acute articular rheumatism, but the statistics
of Bellevue {646} Hospital show that endocarditis complicates
rheumatism in only 33 per cent. of the cases. From these statistics it
is evident that a majority of the cases of acute rheumatism run their
course without endocardial complication.

The irritant action of the blood, the salts of which are changed or
which contains excrementitious products or a specific poison, is shown
most markedly upon the valvular surface of the endocardium; and it is
for this reason that the parts which are most exposed to friction of
the blood-current are those which first and most extensively exhibit
the pathological changes of endocarditis.

Charcot records a large number of observations in which endocarditis
developed in patients with chronic rheumatism and in which it never
assumed an acute form. It therefore seems evident that organic lesions
of the valves from endocarditis may occur in the course of chronic as
well as of acute rheumatism.

There is no disease in which a morbid blood-state exists in which
endocarditis may not occur. The essential fevers, the exanthemata,
diphtheria, septicæmia, pyæmia, and Bright's disease, are all
conditions in connection with which endocarditis is frequently
exhibited. It is met with occasionally in secondary syphilis.

Acute and chronic Bright's disease are often complicated by it. When an
individual who is already the subject of valvular disease of the heart
is attacked with acute rheumatism, the liability to endocarditis is
much increased.

Even when rheumatism and chorea are absent, endocarditis is liable to
occur when valvular disease exists. Some regard myocarditis,
pericarditis, pleurisy, and pneumonia as capable of exciting
endocarditis by the extension of the inflammatory process from the
surface of the heart; it is questionable if it ever results from such
extension. That it can be the result of traumatism is possible:
Bamberger records two cases of traumatic endocarditis. Wunderlich ranks
measles, next to rheumatism, as a cause of endocarditis.

In estimating the etiological importance that any disease bears in the
production of endocarditis, we must remember that not every blowing
sound or murmur is indicative of an inflamed endocardium. Bamberger and
Niemeyer think that the excited and irregular action of the heart in
children, by inducing irregular tension of the valves, may bring about
a blowing sound during the course of acute rheumatism.

Acute ulcerative endocarditis is met with in pyæmia, puerperal fever,
and endometritis, scarlatina, and diphtheria: it may occur as a
secondary affection to some inflammatory focus located in the
body--septic endocarditis.

Again, this form of endocarditis may appear without obvious
cause--spontaneously or in connection with some specific form of
inflammatory disease, as croupous pneumonia. Wilks calls it then
arterial pyæmia. Primary ulcerative endocarditis is a name recently and
perhaps more aptly given it.

Finally, ulcerative endocarditis may appear as a graft (recurrent
endocarditis) upon a valve the seat of interstitial endocarditis, and
have all the pathological appearances of the septic form, but none of
its clinical aspects.

The majority of cases of interstitial endocarditis are the sequelæ of
the exudative form. It is far more frequently associated with articular
rheumatism than with any other condition. In a certain proportion of
cases the process is interstitial from its onset, especially when it
occurs with gout, chronic rheumatism, in alcohol-drinkers, or in the
aged.

SYMPTOMS.--The subjective symptoms of acute exudative endocarditis are
more obscure than those of any other disease. They are not only few and
ill-defined, but they have no regular order of development. When the
muscular tissue of the heart is not involved the disease may run its
entire course without exhibiting a single subjective symptom.

{647} The urgent symptoms of acute rheumatism, the different phases
assumed by the dyscrasiæ and acute infectious diseases in which this
condition is liable to occur, so mask those of the endocardial
inflammation that they are often overlooked.

When the endocardial inflammation is extensive and the muscular tissue
of the heart is involved, the patient will complain of palpitation and
a sense of discomfort in the region of the heart; not infrequently
cardiac palpitation is accompanied by dyspnoea, and decubitus on the
left side is noticed. In a small percentage of cases the palpitation is
appreciable to the physician. The heart may beat with great force and
its action be tumultuous, and yet the pulse not be altered in
character.

The pulse, at first, is usually strong and forcible; later, it becomes
rapid, small, feeble, and irregular. In some cases it is very frequent
from the onset of the disease. As a rule, the force of the pulse will
not correspond to the cardiac activity; for, as the muscular fibres of
the heart become involved, its propelling power is diminished, and the
pulse is correspondingly feeble and compressible. It may be dicrotic.
The respirations are more or less accelerated, and sometimes labored,
and there may be paroxysmal dyspnoea. The face may be flushed and
covered with a profuse perspiration, or it may assume a dusky, pallid,
ashy-gray, or slightly cyanotic hue. In rare cases there may be
sleeplessness or nocturnal delirium of a typhoid type. If the muscular
tissue of the heart is extensively involved, nausea, vomiting,
giddiness, and syncope may be present.

When there is pain in the cardiac region, especially if it is augmented
by pressure, pericarditis is usually present, and slight pain or
tightness in the cardiac region is not an infrequent symptom, and is
quite common when endocarditis occurs in those who are the subjects of
chronic valvular disease.

The temperature in acute exudative endocarditis seldom exceeds 103° F.

When ulcerative endocarditis complicates septicæmia and a rupture of a
valve occurs, a typhoid state rapidly supervenes. The patient is forced
to assume the sitting position on account of the intensity of the
dyspnoea, cyanosis is sudden and extreme, and the symptoms of multiple
embolism make their appearance. The febrile symptoms are marked; the
temperature may reach 106-107° F.; the patient becomes jaundiced; and
there are frequent rigors, which, with the paroxysmal febrile attacks,
simulate the icteric form of malarial fever. The spleen becomes
enlarged and tender, the urine becomes scanty, dark-colored,
albuminous, and of high specific gravity, and in severe cases delirium
and coma occur.

Some cases of endocarditis putrida (as some German pathologists call
it) are attended with nausea, vomiting, and diarrhoea. The frequency
with which this form of endocarditis is associated with pneumonia
certainly suggests a blood-poison of great intensity. Although it is
rarely met with except in septic conditions, it may occur late in
severe forms of rheumatic and traumatic endocarditis or when there has
been pre-existing suppurative disease of the bones.

The symptoms which attend embolism from detachment of the fibrinous
efflorescences upon the valves are due to the arrest of such a plug in
an artery whose calibre is too small to admit of its passage. Beyond
the obstruction the circulation is arrested; hence results either an
infarction or necrosis of the part whose blood-supply is thus shut off.
The organ most liable to be the seat of such emboli is the spleen, and
after this the kidney and the brain. Hence the occurrence of hemiplegia
with aphasia or marked cerebral symptoms in the course of acute
endocarditis is indicative of cerebral embolism.

There are no positive subjective symptoms of interstitial endocarditis.
There may be palpitation and a sense of uneasiness, sometimes amounting
to {648} pain at the præcordial region, with irregularity in the action
of the heart, but all of these, when taken together, are not sufficient
for a diagnosis. This can be made only from changes in the heart-sounds
produced by changes in the valves and valvular orifices.

PHYSICAL SIGNS of exudative endocarditis.--Inspection.--Upon inspection
it will sometimes be noticed that the area of the cardiac impulse
exceeds the normal--that it is irregular and often tumultuous. As the
disease advances, the apex-beat and the impulse grow more indistinct,
but never to the same extent or so suddenly as in pericarditis. In
children the vessels of the neck exhibit venous stasis far more
frequently than in adults.

Palpation.--At the onset of an endocarditis the cardiac impulse is more
forceful than normal, and the heart-action is frequently irregular. In
some instances the heart thumps violently against the chest-walls. The
force of the cardiac impulse varies from day to day. The impulse is
stronger when pain is present over the præcordial space. If during the
entire course of the disease there is no decrease in the force of the
apex-beat, it may be inferred that there is no deficiency in the
muscular power of the heart. When acute endocarditis supervenes upon
long-standing valvular disease, there will be an alternate increase and
diminution in the area and force of the impulse. When the walls of the
heart become weakened by subsequent myocarditis, or when the
endocardial inflammation is itself very extensive, the force of the
apex-beat is diminished. An endocardial thrill is frequently present in
acute exudative endocarditis.

Percussion.--The area of cardiac dulness in endocarditis is normal,
unless changes at the valvular orifice retard the outflow of blood from
the lungs, and then the right-heart cavities become engorged and the
area of dulness will extend beyond the normal limits. But it is to be
remembered that the increase is always slight, except in those few
cases where the heart-cavities are both suddenly and extensively
distended with blood or masses of fibrin. Extensive myo- or endocardial
inflammation may so weaken the heart-walls that they will dilate, and
then percussion will reveal an enlargement in the area of cardiac
dulness.

Auscultation.--On auscultation a murmur or murmurs can be heard over
the various cardiac orifices. The fact that valvular disease may have
previously existed makes it important, at the first visit to a patient
who is suffering from acute articular rheumatism, chorea, Bright's
disease, etc., to carefully examine the heart. When cardiac hypertrophy
exists and valvular disease has pre-existed, it is difficult, if not
impossible, to recognize acute exudative endocarditis or to determine
the time of its advent if it exist. The most important and constant
sign of endocarditis is a systolic murmur, its greatest intensity being
over the apex; but this murmur, which is soft and blowing in character,
the so-called bellows murmur, may be either ventricular or valvular. In
all cases it is due to roughening or thickening of the endocardium. It
often changes its point of maximum intensity during the acute period of
the disease. It is developed at the onset of the disease, and when one
is on the lookout for endocarditis, this will be the first evidence of
its occurrence. And yet in some instances no murmur may be present
during the entire course of an endocarditis.

A mitral murmur alone occurs in about 50 per cent. of cases of
rheumatic endocarditis. It is usually developed early, and before it
becomes distinct it is preceded by prolongation of the first sound.
This is a transition sound between a normal heart-sound and a murmur.
It is a feeble, wavering sound, extending over the slight interval
which normally exists between the first and second sounds.

Other changes that are not murmurs, but which frequently precede them,
are loud, ringing normal sounds, muffled first sound, feeble first and
{649} intensified second sound, doubling of the first sound, roughness
of the first sound, and a humming over the right heart.

Complete absence of the heart-sounds is a rare but possible antecedent
of an endocardial murmur. A mitral murmur in acute endocarditis is
usually audible over a limited area. It is the exception to hear it
both in front and at the back. Very frequently it is heard most
distinctly over the stomach.

When the blood becomes dammed back into the lungs, there is an extra
strain upon the pulmonary semi-lunar valves, and then the second sound
will be accentuated over these valves on account of the sharp shock
which they sustain during diastole. With this accentuation of the
second sound over the pulmonary orifice, the first pulmonic sound may
be feeble or absent. A subdued or absent first sound shows tension of
the artery.

Reduplication of the second sound in a mitral endocarditis is probably
due to the difference in time occupied by the ventricles in emptying
themselves. A tricuspid murmur occurs in 50 per cent. of the cases of
acute mitral endocarditis--a pulmonic in about one-third of the cases.
They are superficial and scratchy in character, and indicate a relaxed
condition of the vessels and a thin condition of the blood. These
murmurs are never permanent. Mitral endocarditis is accompanied by
aortic murmurs in about 16 per cent. of cases. Acute mitral
endocarditis occurring with chorea is as apt to become interstitial as
when it is of rheumatic origin.

Aortic murmurs are usually soft and blowing, but they may be musical,
whistling, or twangy. In aortic endocarditis the second sound is
usually lost over the carotids. Incompetency of the aortic valves is
met with only in the interstitial form of endocarditis.

In about 12 per cent. of the cases of exudative endocarditis arising
from rheumatism a regurgitant murmur will be heard at the tricuspid
orifice, but such murmurs are not the result of endocarditis of the
right heart.

Tricuspid murmurs are present in 50 per cent. of all cases of recent
mitral murmurs, in about 40 per cent. of recent aortic murmurs, and in
about one-fourth of mitro-aortic murmurs. Such tricuspid murmurs are
due to an increase in the slight normal insufficiency existing at the
tricuspid orifice. They are of short duration, and are heard over the
body of the heart over the right ventricle. Sometimes they are
vibrating in character.

In children aortic endocarditis is rare; at this period obstruction at
and regurgitation through the mitral orifice commonly occur together.

The physical signs of interstitial endocarditis are such as are due to
those changes in the valves which will be considered under the head of
Cardiac Murmurs, and their Relations to Valvular Diseases.

DIFFERENTIAL DIAGNOSIS.--Acute exudative endocarditis may be mistaken
for pericarditis, and its murmur may be mistaken for the murmur
produced by aortitis and for those that develop during the course of
fevers.

The friction sounds of pericarditis are superficial in character, and
are limited to the præcordial space, while the murmurs of endocarditis
are distant, and each murmur will have its area of diffusion beyond the
præcordial space. A pericardial sound is distinctly a friction,
creaking, or rubbing sound; it has a to-and-fro character, while the
murmur of endocarditis is soft and blowing.

Endocardial murmurs accompany the heart-sounds, while pericardial
friction sounds are not always rhythmical with the heart-sounds.

The intensity of a pericardial friction is increased when the patient
bends forward at the end of a full inspiration or when the stethoscope
is pressed firmly over the præcordial region; and in the last-named
case it becomes distinctly grazing and rubbing in character. In
endocarditis these methods produce no difference in either the
intensity or the character of the murmur. There is an endocardial
thrill in endocarditis not present in pericarditis.

{650} As soon as effusion occurs in pericarditis the absence of pain,
the alteration in the character of the pulse, the great increase in
dulness, and the disappearance of the adventitious sounds will decide
the diagnosis.

Aortitis has most of the symptoms of endocarditis, but in addition the
pulse is more rapid, the respirations are more hurried, and pain which
shoots down the spine and is increased by motion is present in the
præcordial region. Not infrequently aortitis is accompanied by
cutaneous hyperæsthesia.

Acute inflammation of the aorta is exceedingly rare, and in the few
cases observed has been complicated by very grave diseases. Indeed,
Powell, Lebert, and Rindfleisch doubt its existence.

In the _Medico-Chirurgical Transactions_ (vol. xlvii. p. 129) Moore
gives a case where rigors, fever, intense and painful throbbing of the
aorta, and embolic infarction of distant organs occurred, with symptoms
so resembling those of endocarditis that few would venture to favor a
diagnosis of aortitis during life.

The functional cardiac murmurs which occur in fevers are usually heard
only at the base of the heart, while those of endocarditis are most
frequent and distinct at the apex. There are no symptoms of obstruction
present with febrile murmurs, while they are frequently present in
endocarditis.

It is often difficult to determine whether an endocardial murmur is of
old or recent origin: if during an attack of acute rheumatism an
endocardial murmur is developed under daily examination, it is a
certain index of acute exudative endocarditis. If a murmur exists at
the first examination which is systolic, soft, and blowing in
character, and not accompanied by the evidences of cardiac hypertrophy,
there is good reason to believe that it is produced by an acute
endocardial inflammation.

If, on the other hand, the murmur is rough in quality, diastolic, and
cardiac hypertrophy exists, it cannot be regarded as a sign of acute
endocarditis.

The rules for distinguishing murmurs due to interstitial endocarditis
from functional murmurs will be given under the head of Cardiac
Murmurs.

PROGNOSIS.--Exudative endocarditis is rarely a direct cause of death,
but it seldom results in complete recovery. Acute mitral endocarditis
terminates in permanent valvular disease in over 25 per cent. of the
cases. The elements that will render the prognosis immediately
unfavorable in any case are the symptoms of embolism or of metastasis.
Sudden splenic enlargement, with tenderness over its site, albuminuria
or hemiplegia, when accompanied by the physical signs of acute
insufficiency or perforation of a valve with cyanosis, dyspnoea, and
disturbance of the heart-rhythm, will render the prognosis exceedingly
unfavorable. All these symptoms are diagnostic of acute ulcerative
endocarditis, and therefore when the signs of endocarditis appear
during the course of pyæmia, diphtheria, or other septic condition, the
liability to these conditions must be considered.

When even exudative endocarditis is accompanied or followed by typhoid
symptoms its prognosis is unfavorable. In children bronchial
complications, catarrhal pneumonia, and intercurrent diarrhoea may lead
to a fatal issue. Death may result from acute insufficiency of the
heart or from complications.

The prognosis in interstitial endocarditis will depend upon the seat
and extent of the valvular lesions which it produces. It will be more
fully considered under the head of Valvular Diseases.

In cardiac aneurism death may result from rupture of the aneurismal
sac, from apoplexy, or from secondary diseases in other organs.

TREATMENT.--Acute exudative endocarditis is rarely, if ever,
idiopathic. It is so constantly associated with certain infectious
diseases, and especially with acute articular rheumatism, that its
treatment must be determined by the condition under which it occurs.

{651} In every case the patient must have absolute rest in bed in a
room whose temperature should never be below 70° or 75° F. The
præcordial region should be covered with flannel, and care exercised
not to expose the surface when physical examination of the heart is
made. Some authorities claim that an ice-bag applied to the præcordial
space during the active period of an acute endocarditis will arrest and
limit the inflammatory process. My own experience does not sustain the
results claimed for this plan of treatment.

In rheumatic endocarditis antirheumatic remedies are indicated, the
joints must be kept absolutely at rest, and such local treatment should
be resorted to as will relieve pain and give the greatest comfort to
the patient.

If the blood is kept alkaline, as indicated by the urine, the liability
to endocarditis is diminished.

To ensure rest small doses of opium are often required; but opium
cannot be administered as freely in endocarditis as in pericarditis.

During the whole course of acute endocarditis the strength of the
patient must be maintained by the judicious use of concentrated
nutriment, with some preparation of iron.

When endocarditis occurs with septic diseases and is attended by
typhoid symptoms, or when it assumes the ulcerative form, alcoholic
stimulants, quinine, and iron must be freely administered.

In endocarditis complicating Bright's disease the rapid elimination of
the urea must be established. The severe pain over the præcordial space
may be relieved in many subjects by the application of a few leeches to
the region.

Experience proved that the employment of mercury (internally) and blue
ointment (externally) to lessen the plasticity of the blood, and the
internal use of iodide of potassium (for the absorption of fibrinous
exudation), were harmful, before it was demonstrated that the theory on
which their use was based had no foundation.


Cardiac Murmurs, and their Relations to Valvular Diseases of the Heart.

DEFINITION.--A cardiac murmur is an adventitious or abnormal sound
produced within the heart or blood-vessels, either by obstruction to
the blood-current, an abnormal direction of the blood-current, or by a
change in the blood-constituents.

HISTORY.--The systematic study of cardiac murmurs and valvular diseases
dates from the discovery of auscultation by Laennec. Previous to his
discovery there are a few recorded cases where observers during the
seventeenth and eighteenth centuries described forms of valvular
diseases. One of the first to describe a valvular lesion of the heart
was Vieussens in 1716. At the close of the seventeenth century Willis
and Riverius published cases of valvular disease. In all these
instances it was the aortic valves that were diseased, and the
discovery of their condition was undoubtedly due to the peculiarity of
the radial pulse which is so marked and striking in aortic disease.

In Friedreich's article in Virchow's _Handbuch_, "Krankheiten des
Herzens," Meckel's essay of 1756 is given as the first paper on
endocardial disease.

John Hunter[2] in 1794 gives a lengthened account of a most interesting
case of aortic valvular disease. Senac[3] gives an account of disease
of the auriculo-ventricular valves; and Allan Burns, whose work was
published in 1809, describes aortic regurgitation and obstruction, and
supposes that "a reflux current can produce a hissing noise, something
like what is described as audible palpitation in some diseases of the
heart."[4]

[Footnote 2: _Treatise on the Blood_, etc.]

[Footnote 3: _Treatise on the Heart_, 1783.]

[Footnote 4: _Obs. on some of the most Frequent and Important Dis. of
the Heart_, Allan Burns, Edinburgh, 1809.]

{652} The subject of vegetations upon the valves was very fully
considered by Corvisart in 1806. Corvisart was the first to mention the
importance of what is now called the purring thrill. He stated that "it
probably came from a difficulty experienced by the blood in going
through an orifice disproportionate to the amount of fluid." Laennec
regarded murmurs or bruits as the result of spasmodic contraction of
the heart or arteries. Corrigan in 1829 defined murmurs as "the result
of the development of currents and the intrinsic collision of the
moving liquid."

In 1842, Gendrin gave cardiac murmurs as bruits de frottement
endocardiaques, and established the friction theory. He also called
attention to the fact that alteration in the constituents of the blood
will produce murmurs which are heard in arteries of medium calibre.

Bouillaud describes a murmur as an exaggeration of the normal bruit
caused by blood-friction against the segments of the heart, and he says
that according to the size or condition of the orifice the murmur will
be rasping, sawing, or blowing.

Chauveau states that bruit de souffle is produced by the vibration of a
nei e fluide, always formed when blood rushes through a part of the
circulatory system actually or relatively dilated.

This nei e fluide has its best development in anæmia, when it is termed
the bruit du diable, for the jugular veins do not collapse and the
volume of blood in anæmia is diminished. Chauveau's theory is
applicable to anæmic murmurs, but not to all cardiac murmurs.

Hope states that "valve murmurs are produced by collision of the
blood-particles against one another, or that either the liquid alone or
the liquids and solids conjointly may develop murmurs."

There are many who have advocated the tension theory--viz. that an
increase in tension and force can so exaggerate a normal sound as to
produce a murmur. This theory has no clinical foundation. Often,
however, valve-lesions may exist, and the blood-current be so weak, the
propulsive force so feeble, that no murmurs are audible.

Some observers are of the opinion that spasm of the papillary muscles
and chordæ tendineæ and weakening of these structures through fatty
degeneration can cause temporary murmurs.

The conditions that determine the character of a cardiac murmur, its
pitch, quality, and intensity, are subject to the same physical laws as
govern the formation and quality of sound elsewhere. They are the
rapidity and force of the moving body, the obstructions which it meets,
and the physical properties of the media of conveyance. The same
vibration that produces a murmur may produce an endocardial thrill,
called sometimes purring thrill.

Far more important, however, than loudness, pitch, or quality of a
murmur are its rhythm, its point of maximum intensity, and the area of
its diffusion, all of which can best be considered in connection with
the physical signs of each valvular lesion.

During a cardiac diastole the heart-cavities are all filling; just
before the commencement of the cardiac systole the blood is forced from
the lungs and the cavæ through the auricles into the ventricles, while
the mitral and tricuspid valves are pressed against the walls of the
ventricles, and no obstruction is offered to the blood-current. If, as
the result of disease, any obstruction exists at either one of the
auriculo-ventricular orifices, the blood as it passes through the
opening will impinge on such obstruction and cause a presystolic
murmur.

During a cardiac systole the filled ventricles contract; blood is
thrown through the semi-lunar openings, the flaps of whose valves are
pressed against the walls of the vessels, so that no obstruction is
offered to the outgoing {653} current. At the same instant the
auriculo-ventricular valves close their orifices, so that blood may not
be forced back into the auricles.

If, as a result of disease, the semi-lunar valves should obstruct the
outgoing current, or the mitral or tricuspid valves should not wholly
close the auriculo-ventricular orifices, then in the one case the
direct blood-current, as it passes over the obstruction at the
semi-lunar orifices, would produce a systolic murmur, and in the other
the backward current through the abnormal opening at the
auriculo-ventricular orifice would also produce a systolic murmur.

Again, if the lungs and the aortic system (when filled at the systole)
have, back of them, a semi-lunar valve that does not completely close
that end of the circuit, the blood will regurgitate into the ventricles
during the period of cardiac rest, so that semi-lunar incompetence will
cause a diastolic murmur.

ENDOCARDIAL MURMURS.

    Rhythm.        Situation.    Orifice.        Nature.
  Systolic    1      Basic,      Aortic,       Obstructive.
     "        2        "         Pulmonary,         "
     "        3      Apical,     Mitral,       Regurgitant.
     "        4        "         Tricuspid,         "
  Diastolic   1      Basic,      Aortic,            "
  Presystolic 1      Apical,     Mitral,       Obstructive.[5]

[Footnote 5: Pulmonary regurgitant murmur (diastolic) and tricuspid
obstructive murmur (presystolic) are so rarely met with that,
clinically, they may be disregarded.]

The following is the order of relative frequency of cardiac murmurs: 1.
Mitral regurgitation; 2. Aortic obstruction; 3. Aortic regurgitation;
4. Mitral obstruction; 5. Tricuspid regurgitation; 6. Tricuspid
obstruction; 7. Pulmonary obstruction; 8. Pulmonary regurgitation. The
most frequent combinations of murmurs are--1. Aortic obstruction and
regurgitation; 2. Mitral obstruction and regurgitation; 3. Mitral
obstruction and tricuspid regurgitation; 4. Aortic obstruction and
mitral regurgitation; 5. Double valvular disease at aortic and mitral
orifices (four murmurs).

It is often difficult, after having satisfied ourselves of its
existence, to determine the rhythm of an endocardial murmur. To resolve
this difficulty it is necessary to determine which is the first and
which the second sound of the heart.

The first sound of the heart is synchronous with the carotid pulse, the
radial pulse, and the apex-beat. It may be wholly replaced by a
systolic murmur, but the second sound is always heard following the
apex-beat, for the pulmonic and the aortic valves are never diseased at
the same time.

Having determined the existence of a murmur, its rhythm, pitch,
intensity, and quality, we next determine its point of maximum
intensity. These points of maximum intensity for murmurs at the four
valvular orifices of the heart may be briefly summarized as follows:
Murmurs arising at the mitral valve are loudest at the apex of the
heart or immediately above it; tricuspid murmurs are loudest over the
lower part of the sternum; pulmonary murmurs, in the second left
intercostal space close to the sternum; and aortic murmurs, in the
second right intercostal space at the edge of the sternum and over the
whole length of the body of that bone.

Valvular diseases which cause murmurs result either in a condition of
the valves that allows regurgitation, or one that obstructs the onward
blood-current. Valvular insufficiency arises when extensive retraction,
perforation, or partial detachment of the valves prevents them from
completely closing their respective orifices. And when the chordæ
tendineæ have been ruptured, or when calcareous degeneration has made
the valves or the parts in the immediate vicinity abnormally rigid, the
regurgitant current through the aperture thus left gives rise to a
regurgitant murmur.

{654} When the valves are thickened, retracted, adherent,
hypertrophied, or degenerated, so that their edges are prevented from
being accurately applied to the walls of the ventricles or vessels,
they obstruct the current of blood, and the impinging of the
blood-current against the obstruction gives rise to obstructive
murmurs. These conditions--stenosis and insufficiency--are often found
coexisting, but rarely in equal degree, one usually predominating
sufficiently over the other as to give a dominant character to the
murmur.

The lesions which produce these conditions may be temporary or
permanent--temporary when they occur during the course of acute
endocarditis, and permanent when they consist of a new growth either of
connective, fibroid, calcareous, or atheromatous tissue, which alters
the form of the valves and impairs their function. Acute and chronic
valvular disease may produce the same murmurs. The effect of the
valvular deformity depends entirely upon its seat.

In the study of the relations of valvular lesions to cardiac murmurs
physical signs are the important factors in their diagnosis, and it is
necessary always to bear in mind the normal physiological conditions
which constitute a complete cardiac pulsation.

The apex of the normal heart is felt between the fifth and sixth ribs
on the left side, about two inches below the nipple and one inch to its
sternal side. The base of the heart is on a level with the third costal
cartilages. The tricuspid valve lies behind the middle of the sternum,
on a line with the articulations of the cartilages of the fourth ribs
with the sternum. The mitral valve lies behind the cartilage of the
fourth left rib, near the edge of the sternum. The aortic valves lie
behind the sternum, a little below the junction of the cartilages of
the third ribs with the sternum, near its left edge. The pulmonary
valves lie behind the junction of the third left rib with the sternum.

Let it be remembered that the tricuspid orifice is the most
superficial, then the pulmonary, next the aortic, and, deepest of all,
the mitral orifice. Ranged from above downward, the pulmonary orifice
comes first, then the aortic, then the mitral, and lastly the
tricuspid.


Aortic Obstruction, or Stenosis.

Stenosis at the aortic orifice is a common cardiac lesion, and one that
is always accompanied by more or less hypertrophy of the left
ventricular walls.

MORBID ANATOMY.--In aortic obstruction the cardiac valves will be found
to present some or all of the changes which have been described as
taking place in the course of acute and interstitial endocarditis,
together with degenerative changes due to atheromatous, calcareous,
fibroid, fatty, or connective-tissue metamorphosis.

Sometimes the valves may be covered with thick, warty, irregular
excrescences that cause loud murmurs, and yet do not seriously
interfere with the outgoing blood-current. At other times stenosis of
the aortic orifice may be so extensive as to almost obliterate it. When
such is the case, the extent of the lesion will be measured much more
by the consequent hypertrophy and its effects on the systemic
circulation than by the loudness or harshness of the murmur which it
produces.

Very frequently the valves are so rigid that they cannot be pressed
back against the wall of the aorta, and these unyielding prominences
are greater obstacles to the outgoing current of blood than vegetations
on the surface of the valves.

In a few rare cases the outlet may be diminished by constriction of the
{655} aorta at the point of insertion of the valves. Adhesion of the
aortic valves begins at their bases and extends along their free edges
to their tips; sometimes they become fused together into a mass, so
that they project into the blood-stream in the form of a funnel
irregular in shape and studded with calcareous nodules. The line of
attachment of the valves to the aorta frequently becomes entirely
obliterated.

In some instances the contraction of the valves between their points of
attachment causes them to form a deep pocket or pouch, and their points
of attachment may be a quarter of an inch apart.

Obstructions at the aortic orifice are frequently accompanied by
atheromatous changes in the aorta, the result of chronic inflammation
of its tunics--arteritis deformans.

As a result of aortic stenosis the wall of the left ventricle becomes
hypertrophied. This change is a gradual one, and is called compensatory
hypertrophy: it is due to the increased force required to propel the
blood through the constricted orifice.

After a time insufficiency of the mitral valves is apt to occur, caused
either by the extension of endocardial inflammation from the aortic
valves or by the forcible pressure of blood upon the ventricular
surface of the valves.

A slight thickening or roughening of the aortic valves may cause slight
obstruction to the outgoing blood-current, which will interfere but
little with the emptying of the ventricular cavity, and which rarely
leads to hypertrophy of their walls.

ETIOLOGY.--Aortic obstruction is most frequently met with in early and
advanced life, the mean age being forty-seven years. It is not uncommon
in children; valvular lesions have been found in children under two
years of age. It may be induced where the aorta is defectively
developed, and some think that imperfect development of the trachea may
lead to imperfect expansion of the chest, and thus induce disease of
the aortic valve.[6]

[Footnote 6: Barlow in _Guy's Hospital Reports_, S. 1, vol. vi. p.
235.]

Its most frequent cause is acute exudative and interstitial rheumatic
endocarditis. The origin of nearly all valvular disease may be traced
back to an attack of rheumatic fever. Next to acute rheumatism, chorea
is its most frequent cause. Bright's disease and pyæmia may cause it,
and atheroma or arteritis deformans extending to the valves will give
rise to valvular lesions which cause obstruction.

Any of the conditions that cause acute exudative and interstitial
endocarditis may effect changes in the valves, and the tissue thus
developed, undergoing atheromatous, fatty, fibroid, calcareous, or
connective-tissue change, will cause obstruction.

Increased tension of the aorta may be the result of chronic spinal
deformity, and may be regarded as the indirect cause of aortic
stenosis.

The connection between cancer and cardiac valvular disease is to be
noticed, if not as cause and effect, at least as a remarkable and
noteworthy coincidence.

Women are far less subject to aortic obstruction after rheumatism than
men. In men the aortic valves are subject to more pressure and strain
than in women, and hence non-rheumatic disease of these valves is very
common, while in women it is very rare.

Aortic disease especially occurs in men whose occupations involve
repeated, sudden, and great muscular effort.

In old age the walls of the aorta are weakened, and when aortic disease
is met with in young subjects it must be regarded as the result of a
premature senile condition of the vessels. Allbutt says that in Leeds
quite young men have aortic valvular disease, and Peacock mentions
several cases where the {656} disease has occurred in young girls who
have been placed at service before they were fully developed.

Sometimes the valves are found to be studded with vegetations,
apparently of syphilitic origin. Corvisart and Virchow both admit the
possibility of such an origin for valvular disease of the heart, but no
unquestionable case has as yet been advanced in proof of it. It has
been claimed that this is the reason why soldiers so frequently suffer
from heart disease; but sailors are notoriously more subject to
syphilis than soldiers, and heart disease is rare among them.

The reason is evidently to be found in their mode of dress: sailors
wear loose clothes, soldiers have the tightest possible fitting
garments. More force is required to pump the blood through the
constricted vessels, hence arises more strain on the aorta and more
strain on the valves.

Single, sudden muscular efforts have in a limited number of cases
produced disease at the aortic orifice.

Aortic valvular disease more frequently than mitral is of non-rheumatic
origin; it is slower in its development, and is more commonly met with
in advanced life.

SYMPTOMS.--The subjective symptoms of obstruction at the aortic orifice
are not usually well marked. Extensive aortic stenosis is not
incompatible with a state of comparative good health. As the
obstruction to the outflow of blood from the ventricle increases,
compensatory ventricular hypertrophy enables the heart to fill the
arterial system and relieve the pulmonary pressure. As soon as the
ventricular hypertrophy no longer compensates for the obstruction, the
arteries are inadequately filled; the left auricle cannot empty itself
into the left ventricle, and hence the pulmonary vessels are abnormally
full, as is also the entire venous system. The scanty arterial supply
gives the pallor to the face which so frequently accompanies this
condition, and syncope is liable to occur as a result of partial
cerebral anæmia.

These are late effects, and in many cases do not make their appearance
until the mitral valve is secondarily involved. The pulse in aortic
stenosis is normal in frequency, diminished in volume and power,
usually regular in rhythm, though it may be intermittent, and is
compressible and jerky in character.

As a general rule, in aortic stenosis signs of arterial anæmia precede
evidences of venous engorgement. The obstruction to the exit of blood
is shown in the sphygmographic tracing by a slanting or oblique
up-stroke, as seen in the accompanying tracing, or, as Mahomed says,
"the influence of percussion is lost." Tracings of the pulse in aortic
stenosis sometimes show considerable separation between the percussion
and the tidal waves. In some rare instances the pulse is slowed. There
may be slight palpitation, and pain in the chest may sometimes occur in
paroxysms; but pain in the chest is far more common in regurgitation
than in obstruction. Aortic obstruction is more frequently connected
with cerebral embolism than any other valvular lesion.

[Illustration: FIG. 41. Aortic Obstruction (after Foster).]

The left middle cerebral artery is the most common seat of aortic
cardiac emboli. The left lower limb is more subject to embolism from
aortic valvular disease than the right. The splenic and renal vessels
are also the frequent seat of such emboli. Sometimes embolism is due to
small auricular or ventricular {657} clots that form behind the
obstruction. Such clots have occluded the aortic orifice and caused
sudden death.[7]

[Footnote 7: _Pathological Transactions_, vol. ix. p. 91.]

PHYSICAL SIGNS.--The physical signs of aortic obstruction are generally
distinctive and easily appreciated.

Inspection.--The visible area of the cardiac impulse is abnormally
increased. Very extensive increase in the area of impulse is frequently
accompanied by a lifting of the chest-wall over the heart.

Palpation.--The impulse is felt to be forcible, and is sometimes
accompanied by a heaving or lifting motion. The apex is displaced
toward the left and slightly downward. A sensation will sometimes be
imparted to the hand during systole similar to that produced on the
sense of hearing by the whizzing of a missile by the ear. This is often
nothing more than an intensified endocardial thrill. This systolic
frémissement radiates to the ensiform process of the sternum, being
most intense in the second right intercostal space.

Percussion.--The area of cardiac dulness will be increased in
proportion to the displacement of the apex-beat to the left. The
increase in dulness measures the amount of left ventricular
hypertrophy.

Auscultation.--Aortic stenosis produces a systolic murmur which more
frequently accompanies than replaces the first sound of the heart. The
maximum intensity of this murmur is usually at the second sterno-costal
articulation of the right side, but it may be heard with equal
intensity over the whole upper part of the sternum, and followed up the
aorta and along the carotids; again, it may be loudest at the xiphoid
cartilage, or it may be heard with greatest intensity at the junction
of the left third rib with the sternum. In most cases the first sound
is heard with the murmur, but the murmur may entirely replace or
obscure it. This murmur is usually loud and harsh in character, and is
loudest at the beginning of the systole. Harshness is one of its
distinguishing characteristics.

In pure aortic stenosis the aortic second sound may be inaudible, and
is always feeble, but the pulmonic second sound will always be audible.
The area of diffusion of this murmur follows the law that a murmur is
propagated in the direction of the blood-current. It is conveyed along
the aorta into the carotids, and one of its characteristics is that it
is heard in the great vessels of the neck. It may sometimes be heard in
the thoracic and abdominal aorta.

When an aortic obstructive murmur is heard at the apex its intensity is
diminished, and when heard behind it is most distinct at the left of
the third and fourth vertebræ near their spines, and frequently extends
downward along the spine in the course of the aorta, but with
diminished intensity. It is to be noted here that a systolic murmur,
audible at the base, and traceable along the ascending arch toward the
end of the right clavicle, is by no means limited to cases of aortic
stenosis, although aortic stenosis always produces a murmur with these
characteristics.

Arterial murmurs, synchronous with the cardiac systole, are far more
frequent than diastolic murmurs. When the mitral or tricuspid valves
are thickened or incompetent, or when the myocardium is the seat of
extensive fatty degeneration, the murmur of aortic obstruction will
entirely replace the first sound of the heart.

DIFFERENTIAL DIAGNOSIS.--Aortic obstruction may be mistaken for mitral
regurgitation, tricuspid regurgitation; an anæmic bruit, for the murmur
of a thoracic aneurism and for a murmur produced by a scabrous
condition of the ascending arch of the aorta.

1. Both mitral and tricuspid regurgitation, as well as aortic stenosis,
are recognized by a systolic murmur. The murmur of aortic obstruction
is heard with its maximum intensity at the second right sterno-costal
articulation, and {658} diminishes in intensity toward the apex. The
murmur of mitral regurgitation is heard with greatest intensity at the
apex-beat. The murmur of aortic obstruction is conveyed into the
vessels of the neck; that of mitral regurgitation to the left, in the
direction of the apex-beat, and is heard behind, between the fifth and
eighth dorsal vertebræ, at the left of the spine, with very nearly the
same intensity as at the apex. The pulse in aortic stenosis is hard,
firm, and wiry in character, but regular, while in mitral regurgitation
the pulse is irregular in rhythm as well as in force, is never
incompressible, and is easily increased in frequency. Gastric,
intestinal, renal, hepatic, and bronchial symptoms are present in
mitral regurgitation, while the subjective symptoms of aortic
obstruction are cerebral in character. The pulmonic second sound is
generally feeble in aortic stenosis, while in mitral regurgitation it
is intensified. The murmur of aortic stenosis is harsh; the murmur of
mitral regurgitation is soft, and frequently musical in character.

2. Tricuspid regurgitation is also accompanied by a systolic murmur.
But while the murmur of aortic stenosis has its maximum intensity at
the right second sterno-costal articulation, the murmur of tricuspid
regurgitation is very rarely heard above the third rib: this is an
important diagnostic sign. Tricuspid regurgitation is accompanied by
jugular pulsation, while the murmur of aortic obstruction is heard in
the arterial trunks of the neck. To distinguish between intrinsic
pulsation of the jugular vein and throbbing of the carotid arteries
press lightly on the vessel above the clavicle; this arrests pulsation
when due to tricuspid disease, while if due to aortic stenosis the
result is negative. Moreover, respiration influences jugular pulsation,
while it has no influence over carotid throbbing. The area of
transmission of tricuspid regurgitant murmurs is not more than two
inches from the point of their maximum intensity; whereas the aortic
obstructive murmurs are conveyed along the sternum into the vessels of
the neck. There is nothing peculiar or abnormal about the pulse of
tricuspid regurgitation, while the hard and wiry pulse of aortic
obstruction is quite characteristic.

3. An anæmic bruit may be mistaken for aortic stenosis, since the
rhythm and seat of the bruit are often identical with those of the
stenosis. Anæmia, however, produces a murmur that is heard loudest in
the carotids, and is accompanied by a venous hum, the bruit du diable,
which is continuous, and heard best on the right side of the neck. Thus
in anæmia there are three murmurs, arterial, cardiac, and venous. In
aortic disease the murmur has its maximum intensity at the second
sterno-costal articulation of the right side, and is not accompanied by
a venous hum. There is always more or less cardiac hypertrophy in
stenosis, and an increase in the force of the apex-beat, while anæmia
is attended by a feeble cardiac impulse. The murmur is soft and blowing
in anæmia and harsh and rasping in aortic obstruction. The pulse is
characteristic in aortic stenosis; in anæmia it may have a thrill, but
is never hard and wiry. Lastly, the subjective signs of anæmia will
render the diagnosis comparatively easy, especially when the hum in the
veins coexists.

Aortic disease usually occurs in those who have passed middle life as a
rule, and in men, while young females are the chief subjects of anæmic
murmurs.

4. Thoracic aneurism may produce murmurs resembling those of aortic
stenosis. The dilating impulse on palpation, the normal force of the
heart-beat, the single or double bruit, the pain,--all these symptoms
of thoracic aneurism are absent when aortic stenosis alone is present.
Moreover, the history of the case will greatly aid in the diagnosis;
and, lastly, aneurismal murmurs have their maximum intensity at the
seat of the tumor, and not at the base of the heart.

5. A murmur from a scabrous state of the arch of the aorta is
exceedingly {659} rare. It is located higher up than that of aortic
stenosis, is not transmitted into the cervical vessels, and has its
maximum intensity over the transverse portion of the arch.


Aortic Insufficiency, or Regurgitation.

Aortic insufficiency is an abnormal condition of the aortic valves
which prevents their complete closure and allows a backward current of
blood to flow from the aorta into the left ventricle during the
diastole. This lesion is rarely found unassociated with aortic
stenosis, and together they constitute one of the most important and
frequent valvular lesions. It is sometimes called aortic incompetence,
aortic inadequacy, and aortic reflux.

MORBID ANATOMY.--In a normal heart at diastole the aortic semi-lunar
valves are firmly closed, so as to completely fill the orifice between
the left ventricle and the aorta. In aortic insufficiency the valves
are prevented from performing their normal function, on account of the
following anatomical changes. As a result of interstitial endocarditis
the valves may have been thickened, puckered, and shortened, so that
they do not meet when brought into the plane of the orifice.

When the central portion of the segment is indurated, the whole valve
subsequently curls up, either toward the orifice or back against the
wall of the aorta, and in either case there is insufficiency of the
valves. In the first case there is insufficiency with great
obstruction; in the second, with but very slight obstruction.

These processes of thickening and shortening are usually the result of
the train of changes which attend and follow endocardial inflammation,
but they may also come as the result of an atheromatous process
extending from the aorta to the valves; and it may be mentioned here
that the atheromatous changes, by impairing the elasticity of the
aortic walls, become a source of imperfect coronary circulation, and
hence prepare the heart for that dilatation whose other causes will
subsequently be described.

Regurgitation may result not so much from shortening as from adhesion
of the valve-tips to the walls of the aorta. There may be depression of
the valves which comes from over-extension, and then extreme
insufficiency will be the result. When this pathological lesion occurs,
usually only one segment is involved. Complete retroversion of the
valves is a questionable lesion; still, it may occur. Again, one or
more segments may be more or less detached from their points of
insertion, or from the same causes a valvular aneurism or a diseased
valve may be torn or ruptured, and then perforation allows a free
opening for the regurgitant passage of the blood.

After extensive obstruction has existed for a long time little tunnels
may form by the side of the valves and permit a regurgitant current
from the aorta to the ventricle. The aortic valves are more liable to
laceration than any other valves. Not infrequently the ragged edge of a
lacerated or displaced aortic valve is found covered with fibrinous
efflorescences of larger or smaller size.

During a cardiac diastole, normally, the blood is passing from the
auricle into an empty ventricle; when, however, regurgitation has
persisted for a considerable time, there will be added to the primary
stream (which of itself is capable of filling the cavity of the
ventricle) a regurgitant stream from the aorta, and by this combination
of two streams the left ventricle becomes over-distended and
permanently dilated. This dilatation occurs all the more readily since
during the diastole the ventricular walls are relaxed and less capable
of resisting the increased blood-pressure. Thus, permanent dilatation
of the left ventricle occurs in a comparatively short time; and to
overcome {660} the dilatation and the obstruction to the cardiac
circulation the left ventricular walls hypertrophy. The hypertrophy
goes on increasing until it compensates for the dilatation; but before
this point is reached the ventricular cavity sometimes becomes very
much dilated and the left heart reaches an immense size.

This dilatation and hypertrophy may be so extensive that the organ
often weighs twenty or thirty ounces, a case being recorded where the
enormous weight of forty-eight ounces was reached.[8] The heart is then
frequently called the cor bovinum. In such cases the organ has a
peculiar pointed form, the right ventricle appearing like a mere
appendix. The left ventricle is thus capable of containing so much
blood, and such an abnormally large amount is thrown into the aorta at
each cardiac cycle, that the arterial system is largely over-filled.
Hence the arteries are elongated during their pulsations more than in
health, and often become distinctly flexuous with each cardiac
pulsation.

[Footnote 8: See Hilton Fagge, _Diseases of the Valves of the Heart_.]

The increase in the ventricular power and in the amount of blood
contained in the ventricles and thrown against the aortic walls leads
to endarteritis and subsequent atheromatous degeneration of the
arterial walls, and the arteries become so brittle that during
excitement they may suddenly rupture and cerebral apoplexy result;
aneurism is also liable to be developed under such conditions.

In the normal heart the aortic recoil is the force which propels the
blood into the coronary arteries. When the aortic valves are
insufficient, and furnish little or no resistance to the return
blood-current, the coronary blood-supply is consequently diminished.
When perfect compensation has existed for some time, it begins to fail,
and dilatation again commences at the expense of the walls of the
heart. This dilatation is aided, first, by the condition of the
coronary arteries above referred to, and, secondly, by the fact that
aortic recoil is now expended as much in driving a regurgitant current
into the ventricle as in forcing blood through the coronary vessels.

In some cases atrophy of the papillary muscles allows the mitral flaps
to swing back into the left auricle when increased pressure is exerted
upon them. When from any one of these causes mitral incompetence
becomes secondary to, and coexistent with, aortic insufficiency, all
the signs of impeded venous circulation will be present. These changes
will be considered under the head of Mitral Disease.

When over-distension of the left ventricle causes incomplete emptying
of the left auricle, a greater or less amount of passive hyperæmia of
the lungs may be present without mitral insufficiency.

ETIOLOGY.--The etiology of aortic insufficiency is similar to that of
aortic stenosis. Rheumatic endocarditis is undoubtedly its most
frequent cause, but it may also have its origin in sudden and violent
muscular effort, atheroma of the aorta, endarteritis, congenital
malformation, and enlargement of the aortic orifice. Congenital
malformation or congenital non-development is, according to Virchow, a
frequent cause in chlorotic females.

In many cases the atheroma that causes the incompetence is of gouty
origin, especially when gouty kidneys coexist or when alcoholismus is
associated with a gouty diathesis.

Sometimes aortic incompetence is the result of imperfect development of
the aortic valves. A rare case is recorded in the _Pathological
Transactions_ (vol. xvi. p. 77), where a young man fell from a height
upon his side and tore off an entire flap of the semi-lunar valve:
there was no external mark of injury, and the rupture was plainly due
to the transmission of rapid vibrations from the jarred surface.
Valvular inadequacy sometimes results from dilatation of the aorta at
its origin.

{661} There can be little doubt but that the interstitial inflammation
which gives rise to the valvular changes which allow aortic
regurgitation is often excited by the violence with which the aortic
valves are closed by the backward rush of blood on the aortic recoil
during prolonged and violent physical exertion.

Thus, although rheumatism plays a very important part in its
development, it is so far from being its sole cause that C. Hilton
Fagge says that in at least half the cases of this form of valvular
disease met with in London hospitals one fails to elicit a rheumatic
history.

SYMPTOMS.--Rational Signs.--So long as hypertrophy of the left
ventricle compensates for its dilatation, the individual will suffer
little or no inconvenience, even though the regurgitation is extensive.
When the regurgitant stream is a very small one there will also be
little or no disturbance of the general health.

But the compensation is only maintained for a short time. When the
equilibrium is lost the eccentric hypertrophy induces excessive
heart-action during mental excitement or violent muscular effort. The
action of the heart then becomes labored, and the patient becomes
anxious, nervous, and fretful. Sufferers from aortic regurgitation are
generally aware that exercise will augment all their uncomfortable
symptoms. Their respirations are accelerated by moderate exercise, and
are accompanied by cardiac palpitation. As the insufficiency increases
attacks of headache and vertigo become more and more prolonged and
severe; the patient complains of muscæ volitantes, dyspnoea, giddiness,
and is compelled to sleep with his head elevated. Palpitation is now a
constant symptom, and a visible carotid impulse is persistently
present.

A comparatively frequent symptom of aortic regurgitation is a
distinctly paroxysmal shooting or stabbing pain over the heart, in the
left shoulder, or extending down the left arm. Sometimes this pain is
accompanied by numbness and a peculiar whiteness of the skin along the
line of the pain. In other cases the pain passes from the middle of the
sternum to the right arm. This pain is increased by mental excitement
and muscular exertion, and sometimes by over-distension of the stomach.
In a few cases patients will complain of a sickening fluttering of the
heart.

When the nutrition of the hypertrophied ventricular walls becomes
markedly interfered with, or when insufficiency of the mitral valves
occurs, the veins of the systemic circulation become overloaded, as is
evidenced by cyanosis and dropsy; the dropsy appears first as oedema of
the feet, and gradually extends upward until a condition of general
anasarca is reached. The cyanosis is increased after slight exertion,
and is accompanied by dyspnoea, carotid pulsation, and puffiness of the
face.

In the advanced stages of the disease there is orthopnoea, sudden
starting in sleep, angina pectoris, and in some cases albuminuria and
enlargement and tenderness of the liver. Attacks of syncope at first
occur only after active muscular exercise, but later they occur
independently of it, and are extremely distressing. These patients are
in danger of death at any moment, either during a state of the utmost
calm or the most intense excitement; the danger is greater, however,
during exertion.

The pulse is the most characteristic subjective symptom of this form of
valvular lesion. It was first accurately described by Sir Dominick
Corrigan,[9] and it is frequently called Corrigan's pulse. He
especially said that the disease was indicated by visible pulsation of
the vessels of the head, neck, and upper extremities. On account of the
elongation of the arteries during their pulsation, and their becoming
distinctly flexuous, the pulse is frequently called the locomotive
pulse. It is large and distinct, rapidly projected against the finger,
and just as quickly the arterial tension sinks to its minimum and the
{662} impulse vanishes. It is sometimes accompanied by a vibrating jar,
on account of which it is called the water-hammer, jerking, splashing,
or collapsing pulse. Its characteristics are more apparent when the arm
is raised above the head. Although slightly infrequent, quick, and
jerking, it is always regular in rhythm; the radial impulse is felt a
little after the apex-beat. Thus the pulse-wave of aortic regurgitation
travels slowly along the arteries. This delay in the pulse is constant.

[Footnote 9: _Edin. Med. and Surq. Journ._, April, 1832.]

As soon as the systemic circulation is overloaded from insufficiency of
the heart or from secondary mitral insufficiency, the pulse becomes
feeble and irregular upon the slightest exertion, and may intermit, but
it is still of the same peculiar jerking character. The sphygmographic
tracings of this pulse show a high upstroke and absence of the dicrotic
wave.

[Illustration: FIG. 42. Aortic Regurgitation.]

[Illustration: FIG. 43. Aortic Obstruction and Regurgitation (from a
Patient in Bellevue Hospital).]

This vibrating pulse or pulse of unfilled arteries is usually possessed
of fulness of volume, but when obstruction coexists it may be small and
flickering unless the arteries are calcified or atheromatous. The pulse
of aortic insufficiency taken by the sphygmograph resembles strongly
the pouls des vieillards, but the senile pulse gives a rounded instead
of a pointed summit. Still, in old age the two tracings may be
indistinguishable.[10] The peculiar crochet or beak is noticeable in
graphic tracings of the pulse of aortic inadequacy.

[Footnote 10: Marey, _Phys. Méd. de Circ. du Sang_, Paris, 1863.]

Stokes has described, under the designation of steel-hammer pulse, a
peculiar and characteristic pulsation of the arteries which occurs in
cases of acute rheumatic arthritis supervening upon chronic inadequacy
of the aortic valves. The pulse is abrupt and energetic, as the rebound
of a smith's hammer from the anvil; it is exhibited, however, only in
the arteries adjacent to the affected joints.[11]

[Footnote 11: _Continued Fever_, 1874, p. 244.]

PHYSICAL SIGNS.--Inspection.--There is an increase in the area of the
apex-beat, which is plainly more forcible and is visible over a wider
area than in aortic obstruction. After compensation has ceased to
balance the forces in the heart the apex-beat becomes more and more
feeble and diffused. One of the most important points obtained by
inspection is pulsation of the carotids and the vessels of the upper
extremities. Becker and Quincke have observed pulsation of the retinal
vessels in cases of extensive aortic regurgitation.[12]

[Footnote 12: _London Ophth. Hosp. Rep._, Feb., 1873.]

Palpation.--On placing the hand over the præcordial region a heaving,
lifting impulse will be perceived, which is transmitted over a large
portion of the thoracic walls. The apex-beat is displaced downward and
toward the left, sometimes as far as the eighth rib and two and a half
inches to the left of the left nipple. Occasionally a continuous
diastolic thrill, equally intense during the whole of the diastole, is
felt over the sternum, most distinctly at the site of the aortic
valves. In some cases there is a slight pulsation in the scrobiculus
cordis.

{663} Percussion.--The area of percussion dulness corresponds to the
extent of the cardiac enlargement. Deep dulness is elicited below and
to the left of the normal area, and its outline has more of an oval
contour than in health. So soon as the cardiac dilatation exceeds the
hypertrophy, the area of dulness will extend horizontally rather than
vertically, and it may be carried slightly upward, the apex beating in
the axillary space. The area of dulness may extend six and a half
inches from right to left, and from the upper edge of the third rib to
the line of the liver dulness. The superficial area of dulness is
likewise increased horizontally and toward the left.

Auscultation.--Aortic regurgitation is characterized by a diastolic
murmur, which may take the place of, or immediately follow, the second
sound of the heart. It is very distinct at any point over the base of
the heart, but usually has its maximum intensity either at the sternal
end of the second right costal cartilage, in the second right
intercostal space, or at the sternal junction of the third rib on the
left side. It is transmitted over the sternum, and sometimes will be
loudest at the xiphoid cartilage, and is thence transmitted in the
direction of the apex. Its area of diffusion is greater than that of
any other cardiac murmur: it is not only conducted down the sternum to
the xiphoid cartilage and to the apex, but it may be heard at the sides
of the chest along the spinal column, and sometimes faintly in the
ascending and transverse portions of the arch, in the carotids, and in
rare instances as far as the radial arteries. The murmur of aortic
reflux is accompanying rather than substitutive, for the pulmonic
second sound is audible at the right base.

Foster[13] regards incompetency of the posterior segment of the valve
as producing a murmur which is conducted to the apex, whereas
inadequacy of either or both of the anterior segments is accompanied by
a murmur which is conducted to the ensiform cartilage. This point has a
practical bearing on account of the relationship of the anterior
segments of the valve to the coronary arteries. If the murmur indicates
a lesion of the posterior flap of the valve, the prognosis will be
better. When the second sound of the heart is distinct the murmur
immediately follows it. Many English writers call the murmur a
post-diastolic aortic murmur.

[Footnote 13: _Med. Times and Gaz._, 1873, vol. ii. p. 658 _et seq._]

Although having the greatest area of diffusion, aortic reflux has not
the loudest murmur; it is soft, blowing, sometimes rough, and
frequently musical. It is loudest at the beginning of diastole,
gradually decreasing in intensity, although it may preserve its
rushing, blowing character during all the diastole.

An aortic regurgitant murmur may temporarily disappear if a plug of
fibrin closes the orifice, or if the walls of the left ventricle are
the seat of extensive fatty degeneration, the aorta being rigid and
inelastic.[14] When aortic stenosis coexists there will be a double
murmur, audible over a very large space, having its maximum intensity
at the right edge of the sternum in the second interspace.

[Footnote 14: _Brit. Med. Journ._, 30th March, 1882.]

Systolic and diastolic murmurs, though sometimes separated by a
well-defined pause, may run into each other. If mitral regurgitation
occurs with aortic regurgitation, each murmur retains its own location
of maximum intensity. In rare instances, when two segments of the valve
are healthy, a clear aortic second sound is heard, which is preceded by
a faint reflux murmur. Such a murmur is said to be prediastolic in
rhythm. Aortic reflux murmurs are often very indistinct, and can only
be heard when the patient is in the recumbent posture. There is no
necessary connection between the amount of reflux and the loudness of
the murmur.

A diastolic murmur heard at or below the level of the aortic valves,
chiefly {664} audible in the line of the sternum, indicates
considerable aortic incompetence. If a diastolic murmur is inaudible in
the carotids, it is usually preceded by a systolic murmur, which has
its maximum intensity at the aortic valves or in the so-called aortic
area: such a murmur indicates comparatively trifling incompetence with
considerable obstruction, probably produced by calcified semi-lunar
valves.

If a diastolic murmur is distinctly audible in the carotid arteries, it
is invariably preceded by a loud systolic murmur in them, the systolic
portion of the murmur not being very plainly audible in the aortic nor
in any part of the cardiac area: this indicates very considerable
incompetence with comparatively trifling obstruction.

DIFFERENTIAL DIAGNOSIS.--The diagnosis of aortic regurgitation is
generally not difficult, as it rests almost exclusively upon the
existence or nonexistence of a diastolic murmur. It may, however, be
mistaken for aortic stenosis, for mitral obstruction, for pericarditis
localized over the aorta, for aneurism of the aorta, for aneurism of
the aorta immediately above the valves, patency of the ductus
arteriosus, for insufficiency of the pulmonic semi-lunar valves, and,
occasionally, for a rough and inelastic condition of the ascending
aorta.

1st. Mitral obstruction gives a presystolic murmur, while aortic reflux
produces a diastolic murmur. Mitral stenosis is accompanied by no
hypertrophy or dilatation of the left ventricle, whereas these
conditions are always present with aortic reflux. The quality of a
presystolic mitral murmur is harsh and rough, and it has a churning,
blubbering, or grinding character, while aortic reflux has a murmur of
low pitch and of a soft, blowing, or musical character. Mitral stenosis
is accompanied by a purring thrill which is absent in aortic
regurgitation. The murmur of mitral stenosis is the longest of all the
cardiac murmurs. The murmur of mitral stenosis is never heard behind,
whereas that of aortic regurgitation is often heard at the sides of the
chest and along the spinal column. Finally, mitral stenosis is attended
by well-marked pulmonary symptoms during active physical exertion,
which are rarely present in aortic insufficiency.

2d. A pericardial friction sound over the aorta has its maximum
intensity over the seat of its production, and is usually audible
during both the cardiac systole and diastole. In aortic regurgitation
the character of the pulse, the existence of hypertrophy and dilatation
of the left ventricle, and the carotid pulsation will establish the
diagnosis.

3d. An aneurism at the sinuses of Valsalva is diagnosticated by the
history of the case, the presence of the murmur over the pulmonary
artery, the evidences of arterial degeneration, the absence of left
ventricular dilatation and hypertrophy, and the peculiar jerking pulse.
An aneurismal murmur is circumscribed, has a booming quality, and is
usually systolic in rhythm and never transmitted to the apex of the
heart.

4th. Patency of the ductus arteriosus is a rare condition: in a case
where this was diagnosticated[15] the murmur was audible at the left of
the sternum, was not everywhere continuous with the second sound, was
only transmitted very feebly to the left, and had a wavy character,
sufficient of itself to distinguish it from an aortic regurgitant
murmur.

[Footnote 15: _Guy's Hosp. Rep._, Ser. 3, vol. xviii., 1872-73.]

5th. Insufficiency of the pulmonic semi-lunar valves is the rarest of
all valvular lesions: the murmur should be diastolic, having its
maximum intensity in the second intercostal space of the left side; it
should be transmitted only downward and toward the right apex; and
should not be attended by arterial pulsation, a jerking pulse, or by
left ventricular hypertrophy and dilatation.

6th. A diastolic murmur in the ascending arch, due to roughening,
rigidity, {665} and dilatation of the artery, is also rare, while the
condition which some say can produce it is very common.

Two cases are recorded in which the diagnosis rested upon the character
of the pulse, throbbing of the arteries, and the absence of hypertrophy
and dilatation of the left ventricle.[16]

[Footnote 16: Bellingham _Dis. of Heart_, 1857, p. 152; also _Trans.
Path. Society_, vol. iii., March, 1868, p. 3, article by Prof. Law.]


Mitral Stenosis.

Stenosis, or obstruction of the auriculo-ventricular opening of the
left heart, is due partially to constriction at the base of the mitral
valves, and partially to adhesions of the valve-tips or chordæ
tendineæ. It usually occurs as a consequence of rheumatic endocarditis,
rarely of atheromatous degeneration, and is most likely to occur in
endocarditis affecting young persons.

Mitral disease is present in one-half the cases of valvular diseases of
the heart. Usually, insufficiency and stenosis of the mitral orifice
occur together, and stenosis probably never occurs without some
insufficiency.

MORBID ANATOMY.--As a result of acute exudative or interstitial
endocarditis, the valves are rendered shorter and narrower, as well as
thicker and more cartilaginous, than normal. These rigid valvular
projections not only obstruct the flow of blood from the auricle to the
ventricle, but allow of its regurgitation from the ventricle into the
auricle. In mitral stenosis there is not only thickening and
contraction of the valves, but the valve-tips or the chordæ tendineæ
become adherent, and sometimes each papillary muscle gives rise to a
corrugated, cylindrical mass pierced with one or more slits, indicating
the chordæ of which it was originally made up. The wall of the valve,
especially toward its free edge, is greatly thickened, and these
thickened portions are so dense that they have a distinctly
cartilaginous feel. On the valvular flaps that have undergone this
sclerotic change calcareous masses are very frequently developed, and
are especially liable to form when a gouty diathesis exists.

When the chordæ tendineæ and papillary muscles have become adherent,
the edges of the valves are drawn down toward the apex of the heart;
and since the flaps are adherent for a greater or less distance upward
from their bases, the valve presents a funnel-shaped appearance with
its base looking toward the auricle and its apex toward the ventricle,
whose smaller opening, rarely circular, usually resembles a slit with
its axis in the line which unites the original segments of the valve.
This button-hole slit may scarcely admit the tip of the little finger,
while the normal mitral orifice permits the easy introduction of three
fingers.

Annular (ring-like) stenosis is far more common at the mitral than at
the aortic orifice. Hard, wart-like vegetations frequently develop on
the puckered and seamed flaps, which increase the already existing
obstruction. Sometimes the funnel-shaped appearance is wanting, and the
flaps are stretched horizontally across, with a small opening in the
centre, like a diaphragm: looked at it from the auricle, this slit is
often crescentic in shape.

In cases of long standing the vegetations may become calcified. If the
new tissue in the diseased valves undergoes fatty change and softens,
ulcerative processes are set up and the chordæ tendineæ may rupture. On
the floor of such ulcers calcareous masses and débris are frequently
found.

Hayden thinks that "all funnel-shaped mitral stenosis is the result of
primary acute inflammation and thickening of the valve-segments, with
cohesion of their adjacent edges." Out of 62 cases of mitral stenosis,
59 assumed the button-hole form, and 3 only the funnel-shape (Fagge and
Hayden).

{666} In rare instances the tendons will adhere to the wall of the
heart as well as become matted together. Adjacent to the valves the
endocardium will usually be found slightly thickened.

The following changes are developed in the heart and vessels as the
result of mitral stenosis: The left ventricle becomes smaller, and
sometimes its walls are thinner than normal. The aorta is also small
and thin-walled. An almost necessary result of mitral stenosis is
dilatation, with subsequent hypertrophy of the left auricle. Sometimes
the auricular cavity is enormously dilated--so much so that fifty years
ago Thurman described it as true aneurism of the left auricle.[17] Not
infrequently the left auricular walls are from one-eighth to one-fourth
of an inch in thickness. Its appendix is elongated, assuming a peculiar
curved form, the aperture between it and the auricle becoming wider
than normal. Moxon records a case of extensive mitral stenosis where
the appendix was two and three-quarter inches long.

[Footnote 17: _Med.-Chir. Trans._, vol. iii., Ser. 2, p. 244.]

As soon as the auricular hypertrophy ceases to be compensatory and
dilatation begins, the pulmonary circulation becomes obstructed,
causing increased tension in and distension of the pulmonary vessels.
The walls of the pulmonary vessels, especially those of the main trunk,
are thickened and hypertrophied; in rare cases they have been found
twice the thickness of those of the aorta.

Although mitral stenosis is a disease of youth, and atheroma one of old
age, yet it not infrequently happens that even before the age of
puberty atheromatous degeneration occurs in the pulmonary vessels,
especially in the small branches, as a result of the increased
blood-tension in the pulmonary system.[18]

[Footnote 18: _Trans. Path. Society_, vol. xvii. p. 90.]

The passive pulmonary hyperæmia which results from the obstructed
pulmonary circulation may lead to those changes which collectively
constitute brown induration of the lung. Another occasional occurrence,
directly due to extensive mitral stenosis, is nodular hemorrhagic
infarction. Hemorrhagic infarction of the lungs is in nearly every case
preceded by thrombosis of the right side of the heart.

In some instances the enormously dilated left auricle may, by pressing
on a bronchus, reduce its calibre one-half, and thus interfere with the
functional activity of the left lung. When the pulmonary hyperæmia is
extensive violent physical exertion or violent coughing may cause a
rupture of one of the larger pulmonary vessels, and true pulmonary
apoplexy result.

Bronchorrhoeal expectoration of large quantities of glairy mucus is a
very frequent result of the intense hyperæmia of the mucous membrane of
the bronchial tubes which sometimes occurs in mitral stenosis. The
secretion is increased with every increase in the passive hyperæmia.
The lungs are at all times so liable to congestion and oedema that any
sudden or violent exercise may lead to a rapidly fatal result. Again,
when the conditions enumerated have existed for some time, mitral
stenosis may lead to hypertrophy of the right heart. In some rare cases
the tricuspid orifice has become slightly insufficient.

ETIOLOGY.--Mitral disease is especially met with in the young, and in
the child it is almost invariably a stenosis. The average age is about
thirty-one; it is very rare to find it occurring after the fiftieth
year of life. It seems from statistics that it is nearly twice as
frequent in females as in males.

It is not infrequently of congenital origin. Acute rheumatic
endocarditis is its most frequent cause. The mitral valves are more
frequently affected in chorea than the aortic. In some few instances
stenosis results from extension of the inflammatory process from the
aortic semi-lunar valves, or prolonged aortic regurgitation and
stenosis may lead mechanically to mitral disease, but not to stenosis.
Niemeyer regards atheroma as an exceptional cause of mitral stenosis.
No other authority regards it as a possible cause.

{667} It is a question whether scarlatina or diphtheria tends to
produce in children a valvular endocarditis which is followed by mitral
stenosis. It seems plausible, since in many young children it is
certain that mitral stenosis has not resulted from either rheumatism or
chorea. Finally, with the exception of atheroma, all the causes
enumerated in the etiology of aortic stenosis may be the cause of
mitral stenosis.

SYMPTOMS.--Rational Signs.--The subjective cardiac symptoms of mitral
stenosis are few. There may be no such symptoms. Usually, after violent
exercise there is more or less cardiac palpitation, but this will cease
as soon as the auricle can relieve itself, which is readily
accomplished by the patient's assuming a recumbent position on the
right side with the head slightly elevated. This class of patients as a
rule are pale and anæmic. There is a sharp pain frequently felt in the
region of the apex, which is always suggestive of mitral stenosis. The
pulse is regular and normal in character so long as the auricular
hypertrophy compensates for the auricular dilatation.

When the ventricle is unable to receive and discharge its normal
quantity of blood with normal regularity, the pulse becomes small in
volume, feeble in force, rapid and irregular in rhythm. The
sphygmograph exhibits a tracing, frequently called the mitral pulse;
the sphygmograph tracing is the same as when the ventricle throws a
greatly diminished blood-current into the aorta (Fig. 44). This is
asystolism, and the pulse is a clear indication of the condition.

[Illustration: FIG. 44. Mitral Obstruction (from Patient in Bellevue
Hospital).]

Balfour differs from other authorities in the statement that among the
most remarkable subsidiary phenomena of mitral stenosis is irregularity
of cardiac rhythm, which, always present in a greater or less degree,
is sometimes a diagnostic phenomenon. The auricular systole commences
earlier than normal on account of its hypertrophy. This premature
contraction of the auricle, stimulating ventricular contraction, is
indicated by a second ventricular systole which is much less forcible
than the first.

The passive pulmonary hyperæmia attending the advanced stages of this
form of cardiac disease causes habitual dyspnoea, which is exaggerated
by physical exertion and is attended by a dry, hacking, teasing cough
which resembles the so-called nervous cough.

After violent or prolonged exertion there may be bronchorrhoea, a pint
of glairy, watery mucus often being expectorated in a few moments. Not
infrequently severe exercise induces attacks of profuse, watery,
blood-stained expectoration, indicative of pulmonary congestion and
oedema. Sometimes the exertion of walking rapidly against a strong wind
will induce such intense congestion and oedema of the lungs in one with
extensive mitral stenosis as to cause sudden death.

Hæmoptysis is not infrequent, small quantities of pure florid blood
being expectorated.

Orthopnoea is not a frequent symptom of mitral stenosis, for even in
extensive and long-standing cases the pulmonary congestion is not
constant, as the auricle is able ordinarily to empty itself, and only
becomes engorged during active physical exertion or great mental
excitement.

It should be mentioned here that the old idea, that "mitral stenosis
sometimes produces hypertrophy of the left ventricle," is fallacious.
In no instance can it be attributable to mitral stenosis.

{668} Physical Signs.--Inspection.--As the left ventricle does not
receive its normal quantity of blood, the cardiac impulse is feeble.
Sometimes it has a visible undulating movement.

Palpation.--On palpation, although the apex-beat is less forcible than
normal, a distinct purring thrill will be communicated to the hand:
this thrill is a constant attendant of mitral stenosis, and may be
regarded as its diagnostic sign. It should be remembered, however, that
a purring thrill does not always indicate mitral stenosis. It is most
distinct at the apex-beat, although it may be diffused over the whole
præcordial space. It either continues through the entire diastole or is
only present just before the systole. It is sometimes called a
presystolic thrill. It ceases with the apex-beat. The only conditions
besides mitral stenosis which will cause a purring thrill at the
cardiac apex are mitral regurgitation, with extensive dilatation of the
left ventricle, and left ventricular aneurism; in both instances the
thrill will not be presystolic, but systolic.

Percussion.--The increased size of the left auricle may cause an
increase in the area of cardiac dulness upward and to the left at the
inner part of the second left interspace. This increased area of
dulness will only be recognized on careful percussion during
expiration.

Auscultation.--Mitral stenosis is characterized by a loud churning,
grinding, or blubbering presystolic murmur; this murmur is of longer
duration than any other cardiac murmur, on account of the time required
for the blood to pass through the narrowed and obstructed orifice. It
ends with the commencement of the first sound and the apex-beat, being
synchronous with the purring thrill. The murmur is heard with its
maximum intensity a little above the apex-beat.

Cryan records a case where the murmur was absent, but the diagnosis of
mitral stenosis was made from the other symptoms. At the autopsy the
orifice would barely admit the tip of the little finger, and the
absence of the murmur was accounted for by the smallness of the
aperture.[19]

[Footnote 19: _Trans. Path. Society_, Dublin, Part 2, vol. iv., 1870.]

As a rule, mitral stenosis is accompanied by the loudest as well as the
longest cardiac murmur. The murmur is always louder when the patient is
erect than when in the recumbent posture. For a few days before death,
and at any time when there is great constitutional debility, the murmur
may be held in abeyance. A presystolic murmur is never present when
auriculo-ventricular narrowing does not exist. When this lesion does
exist it is never permanently, and very seldom temporarily, absent. A
prolonged murmur and a sharp first sound indicate a funnel-shaped
stenosis. A murmur immediately following the second sound, and running
through the apex-beat, indicates great contraction of the
orifice--diaphragmatic contraction. The murmur of mitral stenosis is
very rarely, if ever, conveyed to the left of the apex-beat, and it is
rarely heard more than two inches to the right of the apex. The second
sound of the heart is intensified over the pulmonary valves. When
mitral reflux and mitral obstruction coexist, the two murmurs run into
each other, constituting a single murmur that may be mistaken for a
systolic murmur. The harsh character of the presystolic element of the
murmur can always be recognized.

A mitral obstructive murmur is never soft or musical, but there is a
rare form of presystolic mitral which is so short as to resemble a
tone. A mitral stenotic murmur does not often merge into the first
sound of the heart, but is usually separated from it by a short
interval. Sometimes a stenotic murmur only becomes audible when the
patient sits up. In about one-third of all cases of stenosis of the
mitral orifice the second sound is reduplicated. It is best heard at
the apex and when the heart's action is slow. The reduplication may be
temporarily absent. Pulmonary congestion efficiently accounts for {669}
this reduplication. Geigel ascribes it to "non-coincidence in the
closure of the valves." Guttman regards it as originating at the
stenotic orifice itself. Balfour thinks that thrill and reduplication
of the second sound are sufficient to make a diagnosis in the absence
of murmur. Some regard the length of the pause between the murmur and
the first sound as a measure of the stenosis--the shorter the pause,
the greater the stenosis.

DIFFERENTIAL DIAGNOSIS.--The diagnosis of mitral stenosis is not
difficult; it mainly depends upon the existence of two physical
signs--the purring thrill and a loud, long, blubbering presystolic
murmur.

Mitral obstruction may be mistaken for the murmur of aortic
regurgitation (see page 657), for a pericardial friction located over
the apex, for a prolonged systolic murmur replacing the first sound at
the apex, and for a prediastolic basic murmur transmitted to the apex.

1. To diagnosticate between local pericarditis and mitral stenosis, the
same methods are employed and the same rules are to be observed as were
mentioned in the diagnosis between aortic reflux and local pericarditis
(p. 664).

2. A prolonged systolic apexial murmur, enduring as it does for the
period of the first sound, that of the short pause, and reaching the
second sound, is often accompanied by a muffled second sound readily
mistaken for the first. The diagnosis of this murmur rests upon its
soft and blowing character, the synchronism of the murmur with the
systolic impulse and carotid pulsation, and the fact that there is no
murmur with the second sound at the base.

[Illustration: FIG. 45. Mitral and Aortic Obstruction and Regurgitation
(from a Patient in Bellevue Hospital).]

A prediastolic murmur is distinguished from a mitral stenotic murmur by
its progressively diminishing intensity from the base to the apex, by
its being accompanied by hypertrophy of the left ventricle, and by a
jerking, irregular pulse. The preceding tracings explain themselves.


Mitral Regurgitation.

Regurgitation at the mitral orifice is due to a condition of the mitral
valves which allows the blood to flow back from the left ventricle into
the left auricle. The backward effects of mitral reflux are more varied
than those of any other valvular lesion.

It is a common form of valvular disease, and in the majority of cases
is the result of acute exudative or interstitial endocarditis.

MORBID ANATOMY.--The most common lesions which give rise to mitral
regurgitation are thickening, induration, and shortening of the mitral
valves. In rare instances it may occur independent of valvular disease
from displacement of one or more of the segments of the valve, the
result of changes in the papillary muscles, chordæ tendineæ, or the
ventricular walls. It may also occur in extreme anæmia, or from
relaxation of the papillary muscles and dilatation of the left
ventricle, without a corresponding elongation of the papillary muscles,
and from rupture of the chordæ tendineæ. In most instances, however,
the valves are shortened, thickened, and indurated.

In some instances lime salts and large masses of chalky matter are
found {670} imbedded in the indurated valves. In such cases the surface
and edges of the valves are so rough and jagged that more or less
obstruction accompanies the regurgitation.

All these changes, except calcification, may also occur in the chordæ
tendineæ and columnæ carneæ. The valves may also become adherent to the
walls of the ventricles, or as a result of the shrinking and shortening
of the chordæ tendineæ the valve-flaps may not pass back to the plane
of the orifice.

Again, the valves or the chordæ tendineæ may be ruptured, so that the
valves are pressed during the cardiac systole back into the auricle. If
the chordæ tendineæ which are inserted nearest the centre of the valve
become lengthened, that part of the flap will be bent upon itself,
having evidently yielded to the blood-pressure, and this allows of
regurgitation. Sometimes, when the valves appear perfectly healthy, by
the application of the water test they will be found to be
insufficient.

The first effect of mitral regurgitation is dilatation of the left
auricle, due to the pressure of the two blood-currents during its
diastole--one from the lungs, and the other from the left ventricle.
This dilatation leads to thickening and hypertrophy of the left
auricular walls. Following this, the pulmonary circulation is impeded,
the pulmonary vessels enlarge, and they may undergo degeneration as a
result of the continued regurgitant pressure.

Passive congestion of the lungs with brown or pigment induration is an
early pathological sequel of mitral regurgitation. The constant
interference with the return circulation from the lungs obstructs more
or less the outward current of blood to the lungs from the right
ventricle. As the obstruction is a gradual one, the right ventricle
becomes so hypertrophied as to overcome it. Consequently, the
hypertrophied right ventricle compensates at first for the mitral
regurgitation, and as long as the right ventricle is able to fully
overcome the abnormal pressure of the blood in the lungs from the
mitral regurgitation, so long the patients are comfortable. Sooner or
later, however, the compensatory hypertrophy of the right ventricle
ceases, and a secondary dilatation occurs which admits of no
compensation.

This final dilatation of the right ventricle is favored by the
myocardial degeneration, which occurs as a result of defective
nutrition of the heart-walls; when this condition is reached the veins
throughout the body are placed in a similar condition to those in the
lungs.

This general venous congestion is indicated by passive hyperæmia of the
abdominal viscera and by cyanosis of the surface during active physical
exercise.

The liver is the organ first affected, on account of its great
vascularity and from the fact that the hepatic veins do not collapse
readily and possess no valves. Thus the liver becomes enlarged and
stony (the nutmeg liver) as a result of the obstruction to the emptying
of the hepatic vein, and when there is coexistent obstruction of the
bile-ducts jaundice will be present.

This portal obstruction induces passive hyperæmia of the intestines and
stomach, enlargement of the spleen, and large and painful hemorrhoidal
tumors. The impediment to the return of blood from the brain causes
cerebral congestion; from the kidney, renal congestion; and, finally,
the obstruction to the systemic venous return leads to the accumulation
of fluid in the areolar tissue and in the cavities. This dropsy
generally begins in the feet and extends upward. In females the
obstruction in the vena cava inferior induces derangements of the
menstrual functions. Ascites, hydrothorax, hydro-pericardium, and
pulmonary oedema may subsequently develop.

In addition to these changes, the dilated and hypertrophied left
auricle throws an abnormal quantity of blood with abnormal force into
the left ventricle during its diastole, which leads to dilatation of
its cavity and necessitates a compensatory hypertrophy of the left
ventricular walls. This {671} hypertrophy of the left ventricle
increases the force of the reflux current, so that during excitement
and active physical exertion pulmonary congestion, oedema, and cerebral
apoplexy are liable to occur. In many cases of mitral regurgitation,
when the venous engorgement is excessive, general dropsy is favored by
the anæmia produced by the obstruction of the thoracic duct.

Friedreich maintains that the augmented tension in the venous system
causes an increased resistance in the systemic arteries, which leads to
left ventricular hypertrophy.

ETIOLOGY.--Mitral regurgitation may occur at any age; it is especially
liable to follow rheumatic endocarditis in the young.

Acute exudative and interstitial endocarditis of rheumatic origin is
the primary cause of most of the changes which lead to mitral
insufficiency. These changes cause the extensive retractions and
thickenings which are present in most cases.

It may occur in conditions of extreme anæmia or where there is
degeneration of the walls of the left ventricle.

It is not infrequently secondary to changes at the aortic orifice,
produced either by an extension of endocarditis from the aortic to the
mitral valves and their appendages, or by the secondary mitral
valvulitis excited by regurgitant blood-currents from the aorta.

Mitral insufficiency may also be the result of the enlargement of the
left auriculo-ventricular orifice which accompanies excessive
dilatation of the left ventricle.

Disease of the columnæ carneæ and chordæ tendineæ, when their
structures are so weakened as to allow the flaps of the valve to pass
back of the plane of the orifice, will also cause mitral insufficiency.

Ulcerative endocarditis may cause it, either by perforation and rupture
of the valves or by rupture of the chordæ tendineæ.

SYMPTOMS.--During the early stage of mitral insufficiency, when the
hypertrophy of the right ventricle compensates for the regurgitation,
there are no rational symptoms which would lead one to suspect its
existence; but when the right ventricle is unable to overcome the
obstruction to the pulmonary circulation caused by the regurgitant
blood-current, there will be more or less dyspnoea, accompanied by a
short, hacking cough, with an abundant expectoration of frothy serum.
Sometimes the watery expectoration is blood-stained.

Frequently, the blood-stained expectoration is accompanied by free
hæmoptysis, although it should be remembered that profuse hæmoptysis is
far more frequent with stenosis than with regurgitation at the mitral
orifice. But a cough and watery expectoration with occasional dark
blood-stains are usually present as an advanced symptom of mitral
regurgitation. Active physical exertion increases the dyspnoea and
causes cardiac palpitation.

In advanced cases the extremities, face, and lips become blue, the
result of the interference with the capillary circulation, and the
liver becomes enlarged and hardened--conditions easily recognized by
palpation and percussion.

The patient will complain of a sense of weight and fulness in the right
hypochondrium, and there will be anorexia, nausea, and a sense of
oppression in the epigastrium. Sometimes the hepatic circulation
becomes so obstructed that the biliary secretion is interfered with,
and jaundice will be added to the cyanotic discoloration, which gives
to the surface a peculiar greenish hue.

Following the hepatic derangement are frequent attacks of gastric and
intestinal catarrh and evidences of embarrassed renal circulation.

The urine is diminished in quantity, high-colored, and loaded with
lithates. Sometimes albumen and fibrinous or blood casts are found in
it.

{672} Headache, dizziness, vertigo, stupor, somnolence, and sometimes a
peculiar form of delirium of short duration, result from the passive
cerebral hyperæmia induced by obstruction in the superior vena cava.

A late symptom of mitral regurgitation is dropsy, which results both
from impaired general nutrition and the abnormal blood-pressure in the
venous system, both together causing an exudation of the watery portion
of the blood through the walls of the vessels. Dropsy, from mechanical
causes having their seat in the heart, first appears in the lower
extremities, the ankles becoming oedematous, and thence may extend over
the whole body. For this condition to be reached it may require several
years or only a few months, depending upon the general condition of the
patient and the amount of the reflux. With the general anasarca the
dyspnoea becomes extreme; the serous cavities of the body as well as
the lungs become oedematous; erythema may occur in the region of the
groins, the skin exhibiting a tendency to diffuse gangrene.

Late in the disease pulmonary hemorrhagic infarction may occur as a
result of metastasis, and this, in the vast majority of cases, lights
up a rapidly fatal pneumonia.

All these changes, however grave and urgent they may be, are gradual in
their development, so that the condition of the patient is not so
insufferable as its description would lead one to suppose.

The pulse of mitral regurgitation is at first in no respect
characteristic. It remains regular in force and rhythm, but later it
becomes somewhat diminished in force and volume, irregular in its
rhythm, and increased in frequency, but never jerking in character.
This tracing illustrates my meaning. While it remains full it is feeble
and always compressible. When the heart's action is excited, it has a
certain tremulousness: these last-named characteristics are to be
regarded more as the result of the failure of the left ventricle than
of changes in the valvular insufficiency. If a mitral regurgitant pulse
has any distinctive peculiarity, it is its diminution in volume.

[Illustration: FIG. 46. Mitral Regurgitation (from a Patient in
Bellevue Hospital).]

Coincident mitral or aortic stenosis may render the pulse regular even
in extensive mitral regurgitation.

[Illustration: FIG. 47. Mitral and Aortic Regurgitation (from a Patient
in Bellevue Hospital).]

Physical Signs.--Inspection.--The area of visible cardiac impulse
extends over an abnormal space, and is more or less distinct according
as the right ventricular hypertrophy is moderate or extensive.
Sometimes the thoracic wall is seen to rise and fall with each cardiac
cycle, and not infrequently the epigastrium exhibits slight pulsation
corresponding in rhythm with the heart-beats.

The epigastric pulsation is due to the right ventricular hypertrophy
always found with extensive mitral regurgitation.

Skoda, Bamberger, and Leyden record a few instances in which inspection
revealed a double impulse accompanying, with more or less regularity,
each cardiac systole. This double impulse only occurs in aggravated
cases of {673} mitral insufficiency, and arises from non-coincidence of
contraction of the two ventricles.

The jugular veins appear swollen, and this is always most conspicuous
when the patient is lying down.

Palpation.--The apex-beat is displaced to the left. When hypertrophy
predominates over dilatation, the apex-beat is felt lower than normal.
When the dilatation exceeds the hypertrophy, the apex-beat is carried
outward and often slightly upward. The impulse is diffused and more or
less forcible according as the right or left ventricular hypertrophy
predominates. This systolic frémissement is most noticeable when the
base of the heart lies close to the chest-wall from retraction of the
margin of the left lung.

Purring tremor, systolic in rhythm, felt most intensely at the apex and
becoming feebler the farther the hand is removed from that part, either
to the right or upward, is invariably due to mitral reflux.

Hayden says that it is exceptional to have a purring thrill with simple
mitral reflux. I have never found it except in those cases where left
ventricular dilatation greatly exceeded the hypertrophy.

Percussion.--Percussion reveals an increase in the area of cardiac
dulness, especially laterally; it extends both to the left and right of
the normal line, as well as downward. The area of superficial as well
as deep-seated dulness will be increased laterally and downward.

Auscultation.--Mitral insufficiency is attended by a systolic murmur
which either completely or partially replaces the first sound of the
heart. The quality of the murmur is variable, and not in itself as
distinctive as that of mitral stenosis. It is usually a soft and
blowing bellows murmur; sometimes, toward its end, the murmur will
assume a distinctly musical character.

While the first sound of the heart may be heard distinctly in the early
stages of mitral reflux, later the murmur in nearly all cases takes the
place of the heart-sounds. Hence many English writers rightly
denominate this murmur as post-systolic rather than systolic in its
nascent stages. It is heard with its maximum intensity at the
apex-beat. Its area of diffusion is to the left on a line corresponding
to the apex-beat. It is audible at or near the inferior angle of the
left scapula. It can be heard between the lower border of the fifth and
the upper border of the eighth vertebra, at the left of the spine, with
nearly the same intensity as at the apex. The murmur may be absent from
the latter situation until cardiac hypertrophy is developed.

The second sound of the heart over the pulmonary valves is accentuated,
while below the junction of the third rib with the sternum on the left
side both heart-sounds are feeble. Skoda first drew attention to
exaggeration of the second pulmonary arterial sound as a positive and
unerring indication of mitral regurgitation.

An intensified pulmonary second sound requires a strong right ventricle
and an intact tricuspid valve, and is not always present. In general
terms, the area of diffusion of a mitral regurgitant murmur is toward
the left of the apex-beat. Whatever may be its character, the murmur is
generally loudest at its commencement. A loud systolic murmur at the
apex, and not heard at the back, is probably not produced by mitral
reflux.

As at the aortic orifice, so at the mitral, stenosis and regurgitation
are apt to occur in the same individual, giving rise to a combined
presystolic and systolic murmur, which is a continuous murmur that
begins shortly after the second sound of the heart and often continues
until the second sound commences. The two sounds, although mingling to
form one murmur, can, in the majority of cases, be readily
distinguished from each other, for the point of maximum intensity and
the very limited area of diffusion of a presystolic murmur readily
distinguish it from a mitral systolic which is audible in the left
scapular region. It is important to recognize the existence of both
these {674} murmurs in estimating the prognosis in any case. Guttman
mentions a case where five distinct murmurs were combined and yet
clearly distinguishable.

DIFFERENTIAL DIAGNOSIS.--It is usually not difficult to recognize
mitral regurgitation. The seat and rhythm of the murmur and its area of
diffusion are sufficient to distinguish it from other cardiac murmurs.
The character of the pulse, the symptoms referable to the right heart,
and the pulmonary complications will also assist in its diagnosis.

It may, however, be mistaken for aortic obstruction, since both give
rise to a systolic murmur, for tricuspid regurgitation, for fibroid
disease of the heart, and for roughening of the ventricular surface of
the mitral valve or of the ventricular wall near the aortic orifice.

The diagnosis between mitral regurgitation and aortic stenosis has
already been given (see page 657).

Mitral and tricuspid insufficiency both produce a systolic murmur, but
a mitral regurgitant murmur has its maximum of intensity at the apex,
and is conveyed toward the left axillary and scapular regions, while
the maximum intensity of a tricuspid regurgitant murmur is to the right
of the base of the xiphoid cartilage, and it is transmitted upward and
to the right: the area of transmission establishes the diagnosis.

Pulmonary symptoms are prominent in mitral reflux, and absent in
tricuspid regurgitation. The pulmonary second sound is markedly
enfeebled in tricuspid regurgitation, and markedly intensified in
mitral regurgitation.

Fibroid disease of the heart may produce a systolic apex murmur, but it
is an exceedingly rare disease, a pathological curiosity.[20]

[Footnote 20: In the _Pathological Transactions_ (1874, vol. xxv. p.
64) Fagge records a few cases, and mentions that perhaps one positive
indication of fibroid disease of the heart, rather than of a valvular
lesion, may be found in its resisting treatment with greater
obstinacy.]

Roughening of the ventricular wall gives rise to a murmur which has its
maximum intensity at the base of the heart, and is transmitted along
the aortic arch and into the vessels which spring from it in the
thorax.

The vibration of an irregular chordæ tendineæ stretched across the
aortic orifice, its extremities being inserted into opposite walls of
the ventricle, may produce a systolic musical murmur, but the line of
its transmission will correspond to that of an aortic obstruction. A
systolic mitral murmur due to the sudden rupture of one or a number of
the valve-flaps, of the papillary muscles or tendons, is accompanied by
a loud systolic blowing murmur, which is immediately accompanied by all
the urgent symptoms of acute pulmonary congestion.


Pulmonary Obstruction.

On account of the infrequency of disease of the pulmonic valves very
little is known of the phenomena to which such diseases may give rise.
In fact, they are so rare that there is no written history of their
subjective symptoms; their diagnosis is only arrived at by exclusion,
and they cannot be recognized except by the physical signs which attend
them.

As has been already stated, endocarditis in the right heart is rare,
except in intra-uterine life, and the various conditions of the aorta,
atheroma, aortitis, etc., which I have mentioned in the etiology of
aortic valvular disease have no analogues in the pulmonary vessels.

Usually, valvular disease of the right heart is the sequela of lesions
in the left. It must be remembered, however, that the pulmonary artery
may become atheromatous. I have already shown (see p. 666) how certain
valvular diseases of the left heart may induce such a pathological
condition. But even under such conditions disease of the pulmonary
valves is rare. Balfour {675} believes that constriction of the
pulmonary artery may occur at various periods of intra-uterine life. As
a rule, the pulmonary valves are subject to no lesions except
congenital malformation.

MORBID ANATOMY.--Bertin records an instance of pulmonary obstruction
where the valves, distorted and adherent, formed a horizontal septum
across the orifice, it being barely one-fourth of an inch.

A rigid tricuspid valve has been found to be the cause of obstruction
at the pulmonary orifice, the pulmonary valves themselves being normal.
A few autopsies have revealed obstructions at the pulmonary artery,
caused not so much by valvular defect as by aneurisms, tumors of the
pericardium or of the anterior mediastinum, enlarged bronchial glands,
or pressure of a solidified lung.

The pulmonary artery may be occluded just beyond the valves by a
cancerous tumor, and there are examples where a phthisical process in
the left lung has induced it.

A murmur indicative of pulmonary obstruction may be produced by a
cardiac thrombosis.

I have placed these statements under the head of its morbid anatomy for
the reason that they cannot be appreciated and their pathological
significance realized during life.

Reasoning from analogy, obstruction at the pulmonary orifice ought to
be followed by compensatory hypertrophy of the right ventricle and
accompanied by tricuspid regurgitation and dilatation of the right
auricle.

Ormerod records 3 cases[21] where pulmonary obstruction was
diagnosticated during life, and where the post-mortem proved the
accuracy of the diagnosis: 2 of these cases occurred in men under
twenty-eight, and the other in a woman of twenty-one. In 2 of these
cases all the other cardiac valves were healthy. The pulmonic orifice
would barely admit the introduction of a goosequill. Warburton Bigbie
mentions a case (man æt. eighteen) where reflux and stenosis at the
pulmonary orifice coexisted. There were four valves, and these were
incompetent. All the other valves were normal.

[Footnote 21: _Edin. Med. and Surg. Journ._]

Congenital stenosis of the infundibulum of the right ventricle is the
probable result of foetal myocarditis or of syphilis.

I have never met but two pulmonic obstructive murmurs where subsequent
autopsies were obtained. In both cases it was found that the murmur had
been produced by mediastinal tumors pressing on the pulmonic artery so
as to diminish the calibre.

ETIOLOGY.--Pulmonary stenosis is rarely the result of endocarditis or
of degenerative changes in the pulmonary artery. Bertin states that
when abnormal communication between the two sides of the heart has
existed, the arterial blood has excited endocarditis in the right
heart.

Syphilis has been advanced as a possible cause of degenerations at the
pulmonic orifice.

SYMPTOMS.--The only rational symptoms that have been noted in the few
recorded cases of pulmonic disease admit of manifold explanations, and
no one is either constant or diagnostic. In some cases anæmia existed,
in others there were cardiac palpitation, dyspnoea, cyanosis, and
dropsy; but none of these belong exclusively to a pulmonic lesion nor
do they necessarily depend upon it.

Physical Signs.--Inspection, palpation, and percussion give negative
rather than positive results. In a few instances palpation may give a
systolic thrill confined to the second left intercostal articulation.
Such a frémissement results both from roughness and contraction of the
pulmonic orifice.

Auscultation.--A systolic murmur is heard with its maximum intensity
directly over the pulmonic valves; it is very superficial, and
consequently {676} very distinct, and it is limited in its diffusion.
It is never heard at the xiphoid cartilage nor along the course of the
aorta. If it has an area of diffusion, it is toward the left shoulder.
The murmur is loud and soft in character, sometimes bellows. It is not
audible in the vessels of the neck nor is it attended by arterial
pulsation.

When phthisical consolidation partially occludes the pulmonary artery,
a loud but soft systolic murmur is heard, which is sometimes
high-pitched and musical, and often entirely suspended during a full
inspiration. In some few instances there is a bruit de diable in the
jugular veins.

DIFFERENTIAL DIAGNOSIS.--It is possible to confound a pulmonic
obstructive murmur with a mitral regurgitation which is propagated
upward into the left auricular appendix. But the area of a mitral
regurgitant is also backward, and by this it could be distinguished
from a pulmonic obstruction. Besides, in mitral disease the pulse is
very different from the pulse of pulmonary stenosis.

Aortic stenosis can hardly be mistaken for pulmonary obstruction, for
the arterial pulsation, the peculiar pulse, and the transmission of the
murmur into the arteries of the neck will suffice to discriminate
between them.

An aneurism at the sinus of Valsalva may produce a systolic pulmonary
murmur by the pressure which it produces upon the pulmonary artery. It
would be impossible to distinguish it from a pulmonic stenosis.

The diagnosis of pulmonary obstruction is usually reached only by
exclusion.


Pulmonary Regurgitation.

This form of valvular lesion is exceedingly rare; indeed, many doubt
its occurrence. The lesion seldom occurs except as the result of injury
or congenital defect, and there are but few well-authenticated cases in
medical literature.[22]

[Footnote 22: _Path. Trans._, vol. xvi. p. 74.]

The statement[23] that the pulmonary valves exhibit a cribriform
condition nearly as often as the aortic is not sustained in this
country by the results of post-mortems. In one of the cases to which I
have referred (p. 675) as an example of pulmonary stenosis the valves
were likewise found insufficient. In Bigbie's case (referred to on p.
675), where there were four flaps to the valve (producing obstruction),
there was marked insufficiency coexisting.

[Footnote 23: _Dis. of the Heart_, Bellingham.]

The morbid anatomy, etiology, and rational symptoms do not require a
separate consideration. The anatomical appearances are the same as
those found in similar conditions of the aortic valves, and the
etiology and rational symptoms are the same as those of pulmonic
stenosis.

Physical Signs.--Theoretically, pulmonic regurgitation should be
accompanied by a diastolic murmur having its maximum intensity over the
pulmonic valves, and its area of diffusion should be downward and
toward the xiphoid cartilage. It should be soft and blowing in
character. This murmur is rarely heard alone: it is usually associated
with obstruction at the same orifice or with some murmur whose origin
is on the left side of the heart.

Niemeyer states that dyspnoea, hemorrhagic infarction, and consumption
of the lungs have followed insufficiency at the pulmonary orifice. No
other authority mentions any such symptoms, while the assignment of
valvular disease as a cause of phthisis is not based upon clinical
facts.

With a pulmonic regurgitant murmur there should be on palpation and
percussion physical evidences of hypertrophy and dilatation of the
right heart, the rationale of whose production would be identical with
that which was considered in aortic regurgitation. I have never heard a
regurgitant pulmonic murmur.

{677} DIFFERENTIAL DIAGNOSIS.--The murmur of pulmonary regurgitation
may be mistaken for that of aortic regurgitation. The points in
connection with their differentiation are fully discussed on p. 664.

The PROGNOSIS and TREATMENT are identical with those of the former
lesion.


Tricuspid Stenosis.

This valvular lesion is so rare that there are no established rules for
its diagnosis.

Its MORBID APPEARANCES and ETIOLOGY are the same as those of pulmonic
stenosis.

The SYMPTOMS of tricuspid stenosis would be those due to obstruction to
the entire venous circulation. The right auricle would be dilated, and
there would be visceral enlargements in the abdomen, cyanosis of the
face and extremities, scanty and albuminous urine, hemorrhoidal tumors,
headache, dizziness and vertigo due to passive cerebral hyperæmia, and
finally general anasarca. The few recorded cases were associated with
mitral stenosis with one exception, a case of Bertin's.[24]

[Footnote 24: _Traité des Maladies du Coeur_, Obs. 17.]

In a case exhibited by Quain the tricuspid flaps, thick and opaque,
were united for one-third of their extent. In the other cases the
valve-flaps formed a diaphragm whose central opening varied in size,
admitting only the point of one finger. In every condition of tricuspid
stenosis the heart was enlarged.

Tricuspid stenosis (as in pulmonic stenosis) may be the result of
pressure of tumors.

In all well-authenticated cases the chief symptoms seem to be extreme
lividity, palpitation, and dyspnoea.

Physical Signs.--Inspection reveals general cyanosis. The jugulars are
turgescent and exhibit presystolic pulsation. This pulsation is
sometimes the only inconvenience the patient suffers.

Palpation may discover a venous thrill at the base of the neck.

Percussion may show the right auricle to be greatly enlarged, and
cardiac dulness will be increased laterally and toward the right.

Auscultation.--Tricuspid stenosis should be attended by a presystolic
murmur whose maximum intensity would be at the lower portion of the
sternum just above the xiphoid cartilage. This murmur may be propagated
faintly toward the base, but never toward the apex of the heart. It is
sometimes accompanied by fremitus.

Hayden offers the following diagnostic point: The murmur of mitral
stenosis (without which tricuspid stenosis never occurs) is limited to
the apex region; a murmur of the same rhythm is produced at the sternum
by tricuspid stenosis, "and between these two localities there is a
point where no murmur can be heard."

It is unnecessary to consider its differential diagnosis.

The lesion would be diagnosticated (if at all) by exclusion, and
prognosis and treatment would depend on the gravity and sequelæ of the
accompanying condition--viz. Mitral Stenosis (q. v.), for the rule is,
that stenosis of the tricuspid never occurs unless there is extensive
mitral obstruction, and the latter condition is always the predominant
one.


Tricuspid Regurgitation.

Regurgitation at the tricuspid orifice is generally secondary to mitral
stenosis or regurgitation; primary disease of the tricuspid valves,
however, is not infrequent.

{678} MORBID ANATOMY.--The valvular lesions which lead to tricuspid
insufficiency are similar to those which produce mitral insufficiency.
The valves are thickened, shrunken, and opaque, the papillary muscles
are shortened, thickened, and the chordæ tendineæ undergo similar
changes and are sometimes adherent.

The valves or the chordæ tendineæ and columnæ carneæ may rupture; in
either case acute and extensive insufficiency results, as has been
stated. Acute endocarditis of the right heart is rare in adult life,
but when it occurs the tricuspid valves are its primary and principal
seat.

The reason for this is found in their anatomical structure and in the
tension to which they are subject in diseases of the mitral valves.
They are rarely the seat of rheumatic endocarditis or calcareous
degenerations.

Ulcerative endocarditis is seldom met with in the right heart. In a
case recorded by Charcot and Vulpian one of the tricuspid valves was
softened and perforated, presenting numerous vegetations. Scattered
abscesses in the lungs were found in this case.

Any infection through emboli from the tricuspid flaps will produce
secondary effects within the thoracic cavity. The first effect of
tricuspid regurgitation is dilatation of the right auricle; following
this there will be more or less hypertrophy of its walls. As soon as
the valves in the subclavian and jugular veins are no longer able to
resist the regurgitant current jugular pulsation follows. But before
this occurs the tributaries of the inferior cava and the organs to
which they are distributed will become greatly engorged, for they have
no valves to resist the regurgitant current, as are found in the veins
coming from the upper part of the body. The inferior cava and the
hepatic veins sometimes become enormously distended under these
circumstances, and the liver will show the peculiar section that has
gained for it the name of nutmeg liver.

Following the hepatic changes, the skin assumes a dingy yellow hue.
When this is combined with cyanosis it produces a peculiar greenish
tint which is only met with in heart disease. The spleen enlarges and
hardens; the mucous membrane of the stomach is congested, ecchymotic,
and often presents numerous hemorrhagic erosions. Intestinal catarrh is
subsequently developed, and the general venous congestion within the
abdominal cavity is exhibited by hemorrhoids and ascites. The kidneys
become congested and stony, and thrombi may form in the femoral vein
and induce subsequent pulmonary infarctions.

The stasis in the veins below the diaphragm is accompanied by
transudation of serum--first in the ankles, and thence the dropsy
progresses upward until the patient may finally reach a condition of
general anasarca. The obstruction to the general systemic circulation
which results may subject the left ventricle to so much extra labor
that it hypertrophies, and then we have the infrequent occurrence of
disease of the left heart following that of the right.

Since tricuspid reflux has mitral disease for its principal cause in
abnormal cases, the heart becomes greatly enlarged and a condition of
extreme cardiac dilatation and hypertrophy is reached.

ETIOLOGY.--As has been stated, the most frequent cause of tricuspid
regurgitation is mitral disease, either stenosis or regurgitation. Any
condition of the lungs which will produce hypertrophy and dilatation of
the right ventricle will lead to it; it is met with in extensive
pulmonary emphysema, in cirrhosis of the lung, and in extensive chronic
bronchitis. Balfour regards chronic bronchitis as its most frequent
cause after mitral stenosis.

It is possible for any valvular disease in the left heart, when of long
duration, to lead to tricuspid regurgitation. From all these causes the
rationale is {679} the same: the abnormal amount of blood in the right
ventricle presses with undue force against a valve, which physiologists
regard as normally slightly insufficient; the stress upon the
valve-flaps and the valvular attachments is such that endocardial
inflammation is excited at the part subject to the greatest strain, and
valvular insufficiency is the result.

It is possible for disease of the tricuspid valves to result from any
of the causes which have been enumerated on p. 666 as etiological
factors in valvular diseases.

SYMPTOMS.--Tricuspid regurgitation being in the majority of cases
secondary to some other valvular disease or some chronic pulmonary
affection, its symptoms during the early stages are vague and masked by
those of the primary disease. But as soon as the valves become so
insufficient that the venous return is markedly impeded, a train of
symptoms is developed which has its origin in the visceral derangements
already referred to.

In addition to these symptoms there may be, with extensive tricuspid
regurgitation, cardiac palpitation, cardiac dyspnoea, and marked
irregularity in the force and rhythm of the heart. The liver and spleen
are enlarged, the skin becomes dingy, and there is obstinate
constipation with hemorrhoids. The liver is likewise rendered very
liable under such circumstances to attacks of interstitial hepatitis.
Venous stasis is evinced by dyspepsia, nausea, vomiting, and
hæmatemesis. The secretion of the kidneys is scanty, dark-colored, of
high specific gravity, often containing albumen and casts.

Passive cerebral hyperæmia is marked by headache, dizziness, vertigo,
and muscæ volitantes, and there is a peculiar mental disturbance which
is not met with in any other form of heart disease.

Late in the disease, if the patient is placed in a horizontal position,
the face becomes turgid and blue, and if he remain long in the
recumbent position stupor and coma may supervene. Jugular and
epigastric pulsation are characteristic physical signs.

A very late symptom is dropsy, which begins at the ankles and extends
upward until there is general anasarca. It is a point to be noticed
that in the dropsy from tricuspid reflux the genital organs suffer
slightly if at all.

[Illustration: FIG. 48. Tricuspid Regurgitation (after Galabin): _a_,
_a_, anadicrotic wave synchronous with the auricular systole, and
caused by reflux into the large veins.]

Physical Signs.--Inspection.--In extensive tricuspid disease the area
of the cardiac impulse is increased more than in any other valvular
lesion. This area sometimes extends from the nipple to the xiphoid
cartilage, and it may reach as high as the second right intercostal
space. There is a visible impulse in the jugular veins, more apparent
in the right than in the left. Sometimes the veins in the face, arms,
and hands, or even the thyroid and mammary veins, are seen to pulsate.

Palpation.--The apex-beat is indistinct, except in cases where there is
marked hypertrophy of the left ventricle. Pulsation occurs in the
epigastrium, which may be due to reflux into the enlarged hepatic veins
or to the fact that the dilated and hypertrophied right ventricle so
presses on the liver that the impulse is conveyed through the diaphragm
with each cardiac pulsation. Guttman thinks epigastric pulsation is due
wholly to reflux into the veins of the liver, and not to right
ventricular pulsation.

{680} Early in the disease the impulse in the jugulars is confined to
the lower part of the vessels, particularly to the sinus. Beyond this
point the vein merely undulates. Later, a systolic pulsation is felt as
high up as the angle of the jaw, and may be accompanied by distinct
though feeble presystolic pulsation.

The liver may first simply undergo systolic depression, chiefly at the
left lobe; secondly, the whole liver may have an impulse coming from an
enormously dilated vena cava; and thirdly, the systolic pulsation of
the veins within the organ may give to it a palpable expanso-pulsatory
movement. The hepatic pulsation is rhythmical with the cardiac impulse.
In rare cases it precedes jugular pulsation. Sometimes pulsation is
felt in the femoral veins.

Sphygmographic tracings of the jugular pulse show it to be dicrotic.

Percussion shows an increase in the area of cardiac dulness to the
right and upward, sometimes as far as the second intercostal space.

Auscultation.--The murmur of tricuspid insufficiency is heard with, or
takes the place of, the first sound of the heart; it is superficial, of
low pitch, blowing, soft, and faint, and is heard with the greatest
intensity over the lower part of the sternum, at its left border,
between the fourth and sixth ribs. It is rarely audible above the third
rib or to the left of the apex-beat. This murmur is transmitted from
the region at the base of the xiphoid cartilage upward and to the right
from one to two inches. Sometimes it is heard only over a very limited
area, and then it may be overlooked.

DIFFERENTIAL DIAGNOSIS.--A tricuspid regurgitant murmur may be
confounded with that due to aortic obstruction, pulmonic obstruction,
and mitral regurgitation. A tricuspid regurgitant murmur is never
audible above the third rib; is not accompanied by an accentuation of
the second sound over the pulmonary artery, but by jugular and
epigastric pulsation; and is heard with maximum intensity near the base
of the ensiform cartilage. These points are sufficient to differentiate
it from an aortic or pulmonary obstructive murmur. The differential
diagnosis between it and a mitral regurgitant murmur has been given.

PROGNOSIS IN VALVULAR DISEASES OF THE HEART.--Any statements as to the
duration of life in valvular diseases of the heart, and their relative
frequency as a cause of death (especially of sudden death), must be
based upon personal observation, and necessarily will differ with
different observers.

In order to establish, if possible, a basis of comparison for the
different valvular lesions, I give a résumé which I have made of 81
cases, in all of which autopsies were made and the diagnosis of
valvular disease verified.[25]

[Footnote 25: _Med. Rec. N.Y._, April 1, 1870, p. 66 _et seq._]

In 14 cases of various valvular lesions, each of which was accompanied
by cardiac hypertrophy and dilatation, 50 per cent. of the deaths were
due directly to the valvular lesion. In 1 of these, where there was
stenosis at both auriculo-ventricular orifices, death was sudden.

In 15 cases of valvular disease, in which there was only cardiac
hypertrophy, there were 11 deaths from the heart lesion. In 5 of these
death occurred suddenly, and these 5 sudden deaths were all directly
due to the heart lesion.

In 6 cases of valvular disease accompanied by dilatation alone, 4
deaths resulted directly from the heart lesion, and 2 of these were
sudden.

In 15 cases where the aortic valves were involved (either calcified,
rigid, or atheromatous) the heart lesion was not the cause of death in
any case. Of these 15 cases, sudden death occurred but in 2; in 1 there
were firm and long-standing pericardial adhesions, and in the other
cerebral apoplexy.

In 12 cases of calcification of the mitral valve, no death occurred as
the direct result of the valvular lesion, and there were only 2 sudden
deaths, both from cerebral apoplexy.

{681} The aortic and mitral valves were diseased in 14 cases; in 2 of
these only did death result from the heart lesion, and the only three
sudden deaths in this class were from uræmia, apoplexy, and croupous
laryngitis.

The aortic and pulmonic valves were both diseased in 3 cases which died
suddenly, and in no instance was death due directly to the heart
lesions.

In 2 cases there was disease at the aortic, mitral, and tricuspid
orifices, and no sudden death.

Thus it will be seen that of these 81 cases, in 24 only was death due
directly to the heart lesion. There were only 8 sudden deaths due
directly to the heart lesion.

The results of personal, clinical, and pathological observation lead me
to the opinion that the loudness, harshness, and the area of diffusion
of any cardiac murmur have little to do with its prognosis.

I deduce from the above-mentioned cases that cardiac murmurs rarely
necessitate a bad prognosis unless hypertrophy and dilatation coexist;
but so soon as the signs of considerable dilatation and hypertrophy are
present a great variety of complications are liable to occur.

In 1870, I had a patient sixty years of age with extensive aortic
reflux, who had been under my observation eight years, during which
time he had three attacks of pneumonia. There were no appreciable signs
of cardiac dilatation in his case.

Walshe says: "The order of relative gravity, as estimated not only by
their ultimate lethal tendency, but by the amount of complicated
miseries they inflict, is--1, tricuspid regurgitation; 2, mitral
obstruction and regurgitation; 3, aortic regurgitation; 4, pulmonic
obstruction, 5, aortic obstruction."

The following are conditions which render the prognosis in each
valvular lesion more or less unfavorable:

In aortic stenosis the prognosis is less grave than in any other
valvular lesion. Life may be prolonged and good health enjoyed for many
years. Yet it must be remembered that extensive aortic stenosis rarely
exists without attendant regurgitation.

So long as the hypertrophy of the left ventricle compensates for the
obstruction, the prognosis is good; but when the hypertrophied walls
fail to overcome the obstruction, dilatation begins, and the
ventricular systole becomes feeble and intermitting, and the arterial
supply to the brain is so much diminished as to lead to cerebral
anæmia.

If after sudden exertion or violent muscular effort there is
interruption or great irregularity in the heart's action, sudden death
may occur from a complete arrest of the ventricular systole.

Evidences of excessive hypertrophy and dilatation, the occurrence of
syncope, signs of cerebral anæmia, attacks of vertigo, great muscular
prostration, continued and marked paleness of the face, and
irregularity of the pulse, render the prognosis exceedingly unfavorable
in aortic stenosis.

If the presence of vegetations can be determined, there is danger from
cerebral embolism.

When there are no evidences of alterations in the ventricular walls
after an aortic obstructive murmur has existed for some time, it may be
assumed that no vegetations exist on the valves, and that the murmur is
not due to extensive aortic stenosis, and consequently is not dangerous
to life.

When the mitral valves become involved, the combined lesions render the
prognosis unfavorable.

Death may result from cerebral complications, pulmonary oedema, or
cardiac degeneration.

Aortic insufficiency is a much graver form of valvular disease than
aortic stenosis. It is difficult to estimate the probable duration of
life in aortic {682} insufficiency, for it frequently gives rise to no
symptom that would lead to its diagnosis until it is far advanced.
Twenty-one days and five years are the extreme limits that have been
recorded. It must always be borne in mind in estimating the factors for
and against a good prognosis that in no other valvular lesion is sudden
death so liable to occur. Yet the record of the cases which I have
given (page 680) indicates that mitral stenosis is nearly, if not
quite, as frequently a cause of sudden death.

A diseased valve can never be restored to its normal functions, and the
shorter and more gushing the murmur the more extensive the
regurgitation. The effects of the regurgitation must be carefully
estimated before a prognosis can be given in any case. When one aortic
flap is puckered and shrunken, the other two may elongate and
compensate for the patency. But this occurs only in very young
subjects.

Aortic regurgitation is, however, more serious in the very young than
in adults. In children the valvular changes are less atrophic and more
inflammatory in character.

Where the disease is met with in middle life, in those who daily
undergo severe mental or bodily strain, the prognosis is unfavorable.
And when in such patients there are the evidences of arterial
degeneration or a tendency to it, the dangers are greatly increased,
for the hypertrophied ventricle drives out the blood from its dilated
cavity with greater than the normal force, and the vessels being
weakened there is great danger of their rupture; hence the frequent
occurrence of apoplexy and infarctions. In the very old I have seen
aortic incompetence last a long time and cause little inconvenience.

Again, the prognosis is bad when cyanosis and dropsy result from the
failure of a dilated and hypertrophied left ventricle to empty itself.
This weakness is the result of that interference with the coronary
circulation which brings about impaired nutrition, and therefore
degeneration of the heart-walls.

When mitral insufficiency is secondarily induced, then obstruction to
the systemic circulation leads to induration of the liver and kidneys,
which interferes with the performance of their functions and hastens
the fatal issue.

Sudden rupture of a valve or valvular disease that has developed very
rapidly is more dangerous than when the valvular insufficiency is
slowly developed. The flap or flaps involved can sometimes be
determined during life, and then the prognosis will be more or less
favorable according as the anterior or posterior are incompetent. In
all cases the prognosis depends more upon the condition of the
heart-walls and on the general nutrition than upon any other element.

When aortic regurgitation is complicated by aortic stenosis, mitral
regurgitation, or by the vascular and visceral conditions resulting
from the derangement of the circulation, the prognosis is exceedingly
unfavorable. Death may result from embolism, apoplexy, dropsy,
pulmonary oedema, from sudden cardiac insufficiency, or from visceral
complications. When the radial impulse is felt a little after the
apex-beat, it is always important to determine whether the action of
the heart remains regular under mental excitement or violent physical
exertion: if it does, the prognosis is far better than when it becomes
irregular.

Mitral stenosis admits of but slight compensation; if extensive, it is
always a grave disease. The prognosis in any case can be estimated by
the severity of the thoracic symptoms. When physical exertion greatly
exacerbates the thoracic symptoms, the prognosis is especially bad; for
during violent exercise such patients are not only liable to pulmonary
congestion and oedema, but to pulmonary infarctions and pulmonary
apoplexy with large extravasations.

Where mitral stenosis is extensive it ranks next to aortic
regurgitation in its danger of sudden death. The statistics furnished
by Bellevue Hospital show sudden death to occur as often in mitral
stenosis as in aortic reflux.

{683} Congenital mitral stenosis is not dangerous, and does not cause
much embarrassment, for it is invariably associated with hyperplasia of
the pulmonary arterial system. The later in life mitral stenosis
occurs, the more unfavorable the prognosis.

Mitral regurgitation uncomplicated by any other valvular lesion gives
rise to very little disturbance of the systemic or capillary
circulation. It is more often fully compensated for than any other
valvular lesion. The changes which lead to it are of slow growth and
their tendency is to remain stationary. Patients with a moderate
regurgitation at the mitral orifice suffer very little except during or
after violent physical exercise, and, were it not for the slight
dizziness which attends it, it would pass unnoticed. As long as the
compensatory hypertrophy of the right ventricle is sufficient to
overcome the obstruction to the pulmonary circulation, patients with
this form of heart disease may not suffer from dyspnoea even after
violent physical exercise. As regards the duration of life, the
prognosis in mitral regurgitation is good. When, however, mitral
stenosis and regurgitation coexist, the liability to sudden pulmonary
complications becomes so great that a very guarded prognosis must be
given; and it must be remembered that combined reflux and stenosis at
the mitral orifice is a frequent combination.

In very many instances it is unnecessary to tell a patient with mitral
reflux that he has an incurable heart disease, for with no other
valvular lesion the individual may live to advanced life. But when it
is combined with mitral stenosis it must be regarded as a very serious
form of valvular lesion. As soon as symptoms occur that show failure of
the right heart, the prognosis becomes unfavorable. Oedema of the
extremities or fluid in any of the serous cavities, cyanosis, dyspnoea,
and hæmoptysis, are indications of such failure.

Death may result from general anasarca, from serous effusions into the
pleuræ, peritoneum, or pericardium, from pulmonary oedema and
congestion, or from heart-insufficiency.

Extensive obstruction or regurgitation at the pulmonic orifice would
necessarily lead to serious results, but there are no reliable data
upon which the prognosis can be based.

The prognosis in tricuspid obstruction and regurgitation, when
associated with mitral disease, is very grave; but it is not as bad as
when it results from chronic bronchitis and pulmonary emphysema.

When in any case jugular and epigastric pulsation are marked, the
changes in the various organs of the body already referred to rapidly
ensue. Walshe says that "tricuspid regurgitation is the worst of all
valvular lesions." Patients with tricuspid reflux are in extreme danger
from intercurrent attacks of acute pulmonary hyperæmia.

Tricuspid disease, of all valvular lesions, leads most rapidly to
cyanosis and dropsy.

TREATMENT.--The treatment of aortic stenosis and of aortic
regurgitation may be summed up under three heads--viz. rest, diet, and
regimen.

Rest is most important; it must be mental as well as physical; the
appetite, emotions, and passions must be kept under perfect control:
these indications are best maintained by a sedentary country life.
Straining, especially when the hands are above the head, should be
carefully avoided.

The stomach also must have all the rest compatible with the most
perfect nutrition; it is frequently a difficult matter to combine both
indications, for it should be remembered that the more perfectly the
nutritive processes are maintained the longer will the cardiac muscle
resist degeneration. Sugar, sweet vegetables, and animal fat must be
sparingly indulged in. The food should consist of nitrogenous,
albuminoid material, and should be taken in quantities that do not
disturb the heart's action.

{684} In aortic incompetence patients in sleeping should assume, as
nearly as possible, a horizontal posture. By lying on their backs they
lower the height of the distending column of blood, and thus relieve
both the cardiac circulation and the tendency to pulmonary congestion.
Sometimes, when defective aortic pressure reacts injuriously on both
the gastric and hepatic secretions and limits both their supply and
their efficiency, moderate alcoholic stimulation may be cautiously
employed to tide over a weakly period. The bowels should be gently
moved once daily. That the cutaneous circulation may be active the body
should be warmly clothed. Any prolonged exposure of the surface to cold
is to be avoided. In winter the warm bath may be occasionally used, and
in summer the patient is frequently benefited by a warm sea-water bath.

Medicinal agents are not to be resorted to until the cardiac
hypertrophy fails to be compensatory. Then relief is demanded for the
failing heart-power. In aortic regurgitation with feeble heart-action
the tincture of digitalis and the tincture of the perchloride of iron
are to be given in ten-minim doses three times a day. The iron is
especially indicated whenever anæmia is evidenced. Digitalis is given
to produce a sedative action, and therefore should be given in very
small doses and regulated according to its effects on each patient. An
infusion of the English leaves is the preparation which is most
reliable, although the tincture, if fresh and well prepared, is equally
good. When rapid and immediate action is demanded, digitalis may be
given hypodermically. There is one guide to its use not unimportant to
remember: that is, as long as it causes an increase in the flow of the
urine it is safe to continue its use. When vertigo and syncope are
prominent symptoms quinine and strychnia may be given with the
digitalis. When the heart in aortic reflux acts with violence and
rapidity, and the arteries are in a state of high tension, aconite will
be found of service in quieting the heart's action. In aortic
incompetence small doses of arsenic seem to have a stimulating effect,
especially when given with digitalis and iron. Iron may disturb the
stomach, arsenic seldom if ever does. It is always a safe rule when
giving iron to administer at the same time a bitter vegetable infusion,
as quassia or columba.

When the hepatic and gastric vessels are engorged, three or four
leeches over the liver or epigastrium, followed by a warm fomentation,
will afford temporary relief.

At no time should a large quantity of fluid be taken into the stomach.
Symptoms of angina pectoris, with local pain and dyspnoea, are
evidences of aortitis. This demands the application of leeches over the
sternum and continued small doses of mercury.

The treatment of dyspnoea, dropsy, pulmonary oedema, and other late and
distressing symptoms will be considered in connection with mitral
disease. Sometimes the pain of aortic disease is so severe as to
require an anodyne for its relief: opium must not be given by the
mouth, but the sulphate or the hydrochlorate of morphine can be safely
given hypodermically. The severe angina-like pain of aortic
regurgitation can often be promptly relieved by the nitrate of amyl.

Barlowe and Fagge both advise senega and ammonia carbonate for the less
severe effects of aortic reflux. They advance no reason for the use of
these drugs, but their cases show that they have a markedly beneficial
effect. All authorities unite in regarding aortic insufficiency as less
amenable to treatment than other valvular lesions.

In all cases the idiosyncrasy of each patient should be carefully
considered.

No treatment can restore a diseased valve to its normal condition, or
prevent, for any considerable time, cardiac dilatation and hypertrophy
when the normal function of the valves is greatly interfered with.

{685} The first step in the treatment of a serious lesion at the mitral
valves is to make the patient clearly understand his exact condition,
that he may see the reasonableness of the advice given, for his
treatment for the most part must be carried on by himself. A patient
must be fully persuaded of its necessity before he will regulate his
habits and mode of life in accordance with the requirements of his
case. The rules as to nutrition are the same as those to be observed in
aortic stenosis and reflux. There should be a gentle and regular daily
evacuation from the bowels. Straining at stool must be avoided, and any
use of alcohol, strong tea, coffee, and tobacco is to be prohibited. If
in either form of mitral valvular disease the patient is anæmic, iron
should be given. This is given as a food to such patients, and is best
administered about half an hour after meal-time. Ten or twenty grains
of Vallette's mass may be given with benefit to anæmic patients two or
three times a day for a long period.

Patients with mitral reflux should avoid a prolonged use of the voice,
especially in speaking or singing. Small doses of quinine and
strychnine, alternating with the administration of iron, are often of
service. If there is anorexia, infusion of quassia or columba may be
given with the iron. The triple phosphates of iron, quinine, and
strychnine, or small doses of dilute sulphuric acid, will be found to
improve the condition of these patients when they show signs of extreme
debility.

In every case of mitral disease there comes a period when the pulmonary
hyperæmia shows that the compensation of the right heart has failed. An
adjustment of the heart to the circulation is now effected by the
judicious administration of digitalis. Digitalis should only be given
at those times when the heart-failure is imminent and there is marked
pulmonary congestion. Half an ounce of the infusion every two hours for
twenty-four or forty-eight hours is often required to overcome the
heart-failure. The time will come when digitalis ceases to have its
sustaining effect upon the heart-muscle; hence it should always be most
sparingly and carefully used, and the patient should never be allowed
to use it continually.

When the pulse is rapid, feeble, and irregular, more time is needed for
the flow of blood into the ventricle, and greater force and regularity
in the ejection of the blood from that ventricle are demanded.
Digitalis fulfils all these conditions: the pulse becomes regular,
beating about sixty per minute, full and forceful. The urine, before
scanty, now becomes abundant and normal. Pulmonary engorgement
diminishes, and commencing dropsy gradually but totally disappears.

Hayden advises ten minims of the spirits of chloroform and fifteen
minims each of the tincture of digitalis and the tincture of the
perchloride of iron in an ounce of water every three hours.

Whenever asystolism is present or suppression of urine is threatened,
digitalis should be given whether the other indications are present or
not. In most cases of mitral stenosis it is best to avoid the use of
digitalis as far as possible.

The dropsy which accompanies advanced mitral regurgitation may be
promptly relieved by compound jalap powder, combined with calomel in
sufficient quantity to produce prompt and free catharsis. In some cases
of cardiac dropsy, squill, juniper, brown cream of tartar, and copaiba
act as diuretics. This latter drug is best exhibited in the form of the
resin.

In mitral reflux a combination of digitalis and nitrous ether will
often be found to act as a diuretic. In all cases when a diuretic is
given in heart disease the loins should be cupped or warm poultices
applied and the bowels freely purged. In copious hæmoptysis in cardiac
disease ergotin may be given in full doses either by the mouth or
hypodermically.

The hæmoptysis which accompanies pulmonary apoplexy of heart disease
{686} sometimes temporarily relieves the dyspnoea. On this basis
Dickenson and Fagge and other English writers recommend venesection for
the relief of the pulmonary engorgement or heart-failure. Pain in the
præcordial region which accompanies valvular insufficiency may
sometimes be relieved by the application of leeches over the præcordial
space. Hyoscyamus, hydrochlorate of morphia, nitrate of amyl,
chloroform, and a belladonna plaster over the præcordial space have all
been employed for the same purpose.

It is to be remembered that such pain is the cry of the heart-muscle
for a higher degree of nutrition.

Bleeding in heart disease favors dropsy by thinning the blood and by
diminishing the heart-power. It should never be resorted to except in
great emergencies. Niemeyer advises arsenic and antimony in mitral
valvular disease, but does not say in what cases or for what reason
they are to be used. When in the late stages of mitral disease the free
use of digitalis fails to regulate the pulse and to relieve the
pulmonary engorgement, its prolonged administration does harm rather
than good; but in every case of mitral disease where the drug has not
been used it may be safely affirmed that its administration will give
prompt relief.

If it becomes necessary to use an anodyne or hypnotic at any period in
the course of mitral valvular disease, morphia hypodermically is to be
preferred to all others.

The rules in regard to hygiene, diet, and exercise which have been
given for the management of mitral disease are equally indicated in the
management of pulmonary obstruction or regurgitation. Beyond this their
treatment is purely symptomatic.

The treatment of tricuspid obstruction depends upon the gravity and
sequelæ of the accompanying disease--viz. mitral. Stenosis of the
tricuspid orifice never occurs until mitral obstruction is excessive,
and the latter condition is always the predominant one.

The same rules of hygiene and diet which have already been given for
mitral disease must be followed with the utmost care by those suffering
from tricuspid reflux. The patient must lead a life of perfect quiet,
and should live in a warm, equable climate. When occurring with mitral
disease digitalis should not be omitted; for although the drug, by
increasing the action of the heart, would seem to be injurious, yet it
promotes ventricular contraction, and thus tends to relieve the
tricuspid pressure. In tricuspid insufficiency with pulmonary emphysema
this drug should be very cautiously exhibited, and its use or omission
must depend upon the effects produced in each case. If the cerebral
symptoms are exaggerated, it must be discontinued. The indications for
the use of tonics, such as iron, quinine, strychnine, are the same and
follow the same demands as in mitral disease. When venous engorgement
demands prompt relief, drastic cathartics or the abstraction of a few
ounces of blood from the arm will temporarily diminish the high venous
tension. The treatment of the dropsy and the local oedema is the same
as for similar condition occurring in mitral disease. There are many
subsidiary remedies which will have to be employed for the relief of
gastric, hepatic, and intestinal symptoms, which are often the most
troublesome occurrences of this disease.




{687}

CYANOSIS AND CONGENITAL ANOMALIES OF THE HEART AND GREAT VESSELS.

BY MORRIS LONGSTRETH, M.D.


The questions involved in the subject of the congenital defects of the
heart and its great vessels and their causes are not easy of
settlement. In the first place, the seat, the extent, and the
consequences of the deficiency or defect are not regular or constant.
Secondly, the causes and the mode and date of their origin are involved
in great obscurity. Their classification either on a purely
topographical or on a purely etiological basis is almost impossible on
the one hand, because the changes are so irregular and varying, and, on
the other hand, because our knowledge of the primary cause or causes of
the alterations is quite defective. The views which at the present time
find most favor arrange the various malformations into classes
according to the period of development of the foetus at which the
arrest or change of tissue occurred--as it were, a chronological
classification. The ideas in respect to the pathology or the
pathological causes of malformed hearts have undergone great
changes--changing in some degree pari passu with the mode of
classification, and in great degree inducing and compelling such
changes.

In early times deformed hearts were looked upon as monsters,
curiosities, lusus naturæ. When a knowledge of foetal development and
circulation was acquired the deformed heart was compared with the
heart-formation in classes of a lower grade than mammals. Such were the
beliefs of comparative anatomy and physiology that it was held that the
human foetus was matured by stages from the forms found in the lowest
invertebrates through the various ascending scales of the animal
kingdom. This classification was, on the basis of comparative anatomy,
purely anatomical. The underlying thought of such pathological teaching
was that in the original ovum something was left out--an actual
deficiency of parts which, when developed in the natural manner, made
man different from the lower animals; or else, supposing these parts to
have been originally present, there was a defect of plasticity, causing
a failure of the proper adhesion of symmetrical portions. Excessive
development was looked upon as a surplus of parts in the ovum, and by
their growth certain of the openings of the heart were prematurely
closed. In this view of the pathological alterations no expression of
opinion was made how the excess or deficiency of structure was
occasioned: the malformation was merely a failure of the parts to rise
and pass through the various grades of development--a too rapid or a
too slow growth of one or more of the various parts of the foetal
heart. There was no reason assigned why the human ovum had in it
deficiencies or excesses of material, and thus came to resemble in one
of its parts the conditions found in lower animals.

About 1850, Dittrich of Erlangen, by his studies of inflammation of the
heart during intra-uterine life, quite diverted public opinion from the
older views of the subject. Peacock's earlier studies preceded this
work by a few {688} years, and a few years later came Meyer,[1] who
greatly extended the scope and influence of the inflammatory theory of
Dittrich. Ten years later commenced the clinical recognition of
congenital heart defects, and especially the anatomical changes in
congenital narrowing of the pulmonary artery, by Von Dusch and by
Mannkopff,[2] and by Stoelker.[3] Friedberg had, however, as early as
1844, published his studies of the stages of development of the
circulatory organs in the human embryo, and had in accordance therewith
divided the malformation of the heart into three groups, corresponding
to the three periods of the heart's growth. This was the classification
adopted quite independently by Peacock of London in his first
publication in 1857. It was not until after Dittrich's studies[4] and
Meyer's that any distinctive cause was assigned for the failure to
develop.

[Footnote 1: _Virch. Arch._, Bd. xii., 1857.]

[Footnote 2: _Ann. des Charité-Krankenh. zu Berl._, 1863.]

[Footnote 3: _Diss._, Bern, 1865.]

[Footnote 4: See Dorsch's (his student) dissertation, _Die
Herzmuskelentzundung als Ursache angeborner Herzcyanose_, Erlangen,
1855.]

Carl Heine,[5] and also Halbertsma, proposed a classification based on
the quantitative and qualitative differences. Under the first division
the former placed such changes as absence of the heart, deficiency of
individual parts, abnormal smallness, atresia, and fissures; and, in
the other direction, duplication of the heart as a whole or in its
individual parts, and abnormal largeness. The qualitative differences
were deviations of form, of position, and of the arrangement of the
great vessels.

[Footnote 5: _Angeborene Atresie d. Ostium arteriosum dextrum, Beitrag
z. Lehre v. d. angeborenen Herzanomalium_, Tübingen, 1861.]

Peacock's classification in his earlier edition (1858) was partly on
the basis of the time at which arrest of development occurs, and partly
on the degree of impediment to the circulation and the functions of the
heart. In his second edition he adheres to the same classes, with
slight modifications, thus: 1. Arrest of development early in foetal
life (fourth to sixth week; heart with two or three cavities; single or
imperfectly divided arterial trunk); 2. Arrests at a later period
(sixth to twelfth week; imperfect auricular or ventricular septa;
imperfect or misplaced vessels); 3. Those after the third foetal month
(closure and patency of foetal passages; irregularities of valves,
cavities, etc.).

Kussmaul (1865) published a very important work on malformations due to
defects of the pulmonary artery,[6] and these malformations he
considers under two general groups--viz. those having their origin
before the ventricular septum closes, and those occurring after this
period. His most valuable contribution to the subject is the importance
which attaches to the distinction between primary and secondary defects
or arrests of development--_i.e._ between an original alteration of
growth or morbid condition, and those which follow from it as a
necessary consequence. Of his classification, and of the importance of
pulmonary artery malformations, a further description will be given.

[Footnote 6: _Ueber angeborene Enge und Verschluss der
Lungenarterienbahn_, Freiburg, i. B.]

For study, one would wish to arrange the malformations in classes
convenient for clinical purposes. For example, separate them into
groups of the defects compatible with extra-uterine existence and those
incompatible with adult life. Unfortunately, this division is not
possible. We find many cases of defects involving originally the same
seat: in one the individual lives many years, in another the
obstruction immediately induces symptoms, and death soon comes. A
classification according to the seat of the disease alone, if it could
be made, would give the subject a simplicity equal to that of valvular
heart disease in the adult. Here, however, we find such variations in
the details of the alteration that if this principle of classification
alone is {689} employed the confusion becomes very great. It would
seem, therefore, that the principle first made use of by Kussmaul, of
classifying the defects by distinguishing the primary malformations
from their secondary effects, renders the subject the most simple, and
at the same time affords the advantage of more readily understanding
the mechanism of their production.

It will be useful to pass over seriatim, following the course of the
foetal circulation, the various valves, orifices, and foetal openings
to be able to comprehend which are most liable to defects or to see
which defects most frequently occur, and also to find which alterations
produce the greatest disturbance of the circulation.

1. The Foramen Ovale and Septum of the Auricles.--In markedly deformed
hearts the entire septum may be in greater or less degree wanting, as
seen in cases of the bilocular or trilocular organ. This defect is
comparatively rare, and the foetus has but a short extra-uterine life.
In other cases the septum is complete, but the foramen may be unusually
large, and remain unclosed wholly or in part; perforations may be
present, or the valve may merely fail to adhere. Of the latter cases,
the patent foramen is found in conjunction with defects at other parts,
while small sieve-like perforations or the mere non-adherence of the
membrane--both of very common occurrence--may be owing to a temporary
obstruction during the early hours of life or to any unknown cause, or
may possibly be due to a reopening of the foramen from an acquired
disturbance of the circulation. Opinions vary as to the mechanism of
the closure of the foramen. Some consider it a passive process due to
increased blood-pressure in the left auricle, coming from the entrance
of the current of aërated blood from the lungs; others speak of it as
an active process resulting from the excitation to contraction of the
muscular fibres in the membranous valve. Whatever may be the mechanism,
patency of the foramen ovale of undoubted foetal origin (excepting the
minute perforations and oblique slits) must be looked upon in nearly
every case as a secondary defect--secondary to an obstruction to the
outflow of blood from the ventricles through the great arterial trunks,
or it may be from the auricle itself through defect of the
auriculo-ventricular orifice. In a vastly preponderating number of
cases it results from pulmonary artery obstruction. The foramen may
close, however, in such a case if an outlet is provided by the aorta
through an open septum ventriculorum, or when this vessel arises from
both ventricles. Narrowing or closure of the right auriculo-ventricular
orifice, as a primary cause, can prevent the closure of the foramen
ovale; primary narrowing of the tricuspid orifice is very rare, single
or combined with other defects. In these cases the direction of the
blood is from the right auricle to the left. There are, however, cases
on record of patency of the foramen ovale in which the blood-current is
from the left to right side, the reverse of the foetal course. Here the
cause to be looked to is a congenital deficiency of the mitral orifice,
or a narrowing, closure, or malposition of the aorta.

2. The Right Auriculo-ventricular Orifice and Tricuspid Valve.--A
primary deficiency of this orifice and the valve guarding it very
rarely occurs as a primary defect and uncombined with malformation of
other parts of the pulmonary circulation. It does come in certain cases
in conjunction with great narrowing of the pulmonary orifice or artery,
but by no means commonly. If the pulmonary outlet is normal and in the
usual position, the right auriculo-ventricular orifice is never found
closed, although the leaflets have been seen defective, permitting
regurgitation. In certain other cases the orifice and valve, as well as
entire right ventricle, show a failure to develop, and all these parts
appear shrivelled. This condition is a secondary result, due to a great
deficiency of the pulmonary artery and narrowing of the pulmonary
conus. The malformation of the pulmonary artery in such cases results
from an unequal division of the truncus communis--the narrowing {690}
of the conus generally from endo-myocarditis. The aorta is unusually
large in diameter. The blood from the right auricle passes through the
foramen ovale to the left side of the heart; the ductus arteriosus
Botalli remains open, or in very rare cases the mixed venous blood
reaches the lung through collateral channels. In rare cases the blood,
in addition to the open foramen ovale, has a direct passage from the
right auricle into the left ventricle.

3. The Pulmonary Artery and the Right Conus Arteriosus.--This situation
presents by far the largest number of cases of congenital heart
malformation of primary occurrence. The defects at this part require
different interpretations according as they are found within the right
ventricle or in the pulmonary artery itself. So frequent are the
defects at these seats that Kussmaul bases his classification, for a
large proportion of cases, on the malformation of the pulmonary artery
track, and describes them as combined with defects secondarily
resulting in other parts.

The narrowing or closure may exist either at the limit between the
sinus and the conus of the right ventricle, the conus arteriosus may be
uniformly narrowed, or the defective development may involve the
orifice only or the whole length of the pulmonary artery. Many of these
defects, resulting in closure or narrowing, are due, as Rokitansky was
the first to show, to inflammatory changes. It is Kussmaul's great
merit to have pointed to the fact that a very large proportion of all
malformations owe their origin primarily to diseased conditions
originating at this seat. The varieties of these defects and their
secondary consequents will be described later.

4. Patency of the Septum Ventriculorum.--The degree of deficiency of
the septum varies greatly. The entire partition between the ventricles
may be wanting or exist in merely a rudimentary condition. Ordinarily,
there is found a triangular, rounded, or oval opening in the septum
close to the base of the heart, at the portion which in the normal
heart consists of only a membrane (pars membranacea). Besides this
usual opening, one, or even two, others may present themselves at other
points of the septum, thus forming multiple communications between the
cavities. In narrowing or closure of the pulmonary passage the septum
is more or less deflected toward the left ventricle to allow a freer
passage of blood from the right side of the heart through the open
septum into the aorta. In other cases the passage of blood may be from
the left ventricle into the right--the reverse of the usual direction.
The defects of the septum are usually of a secondary character,
dependent on primary malformation of other parts, and, as already said,
chiefly those of the pulmonary track. They are of congenital origin,
commencing early in foetal life, before the third month, when normally
the septum closes. Hence patency of this septum furnishes in many cases
a valuable means of determining the date of the primary defects with
which it is found combined. This malformation, however, does very
rarely stand as an isolated defect, and still more rarely it is
believed to have been acquired through an ulcerative destruction
(myocarditis) of a portion of the septum, either during foetal or
extra-uterine life; wasting or atrophy of the membranous part is
sometimes thought to have occurred. In these latter cases a
misdirection of the blood-current of a marked sort rarely occurs unless
the inflammatory or other changes affect the main arterial orifices.

5. The aortic and mitral orifices are very much less frequently found
narrowed or obstructed as the result of congenital primary defects than
the orifices and their valvular apparatus of the right heart; and, also
following the rule which obtains on the right side, the mitral is less
frequently affected than the aortic orifice.

6. Of the Malformations of the Great Vessels.--Such changes may come
alone, though usually they are combined with simultaneous or
consecutive defects in other parts of the central circulatory
apparatus. Of the sorts of {691} defects or malformation which these
two vessels suffer, there are two chief forms to be described: 1, such
as result from an unequal division of the vessels in their formation
from the truncus communis; 2, those which result in more or less
complete transposition of their origins. Of the transpositions we may
find two sorts: in one the vessels maintain nearly their normal
relative positions to each other, but each communicates with the
improper ventricle; in the other they are transposed relatively to each
other and also to the respective ventricles. In the first of these
classes, unequal division, one variety may be ascribed to a defective
or irregular development of the septum by which the vessels are formed
of unequal sizes; the other, originating later in foetal life--_i.e._
after the third month (for the septum between the vessels is completed
nearly simultaneously to the ventricular septum)--results from
inflammatory or other morbid change in or about the orifice and trunk
of one or other vessel, causing a narrowing or closure, the other
vessel showing compensatory enlargement. This form is not a true
unequal division of vessels. The apparent origin of one or both vessels
from the same ventricle in these cases is not a true example of
transposition of the vessel, but is due to a deviation of the septum
ventriculorum toward one side or the other from increased blood in the
ventricle from which the outflow is more or less completely obstructed.
True transpositions of the vessels, both relatively to each other as
well as to the ventricles, originate very early in foetal life, and
these as well as the unequally-divided vessels are primary defects, and
are usually accompanied by many secondary changes. Another malformation
occasionally found, involving the beginning portion of the great
vessels, is a failure of complete division: the septum truncus communis
remains rudimentary, and the blood of the aorta is free to mingle with
that in the pulmonary artery. This defect may be accompanied with a
rudimentary septum ventriculorum.

7. Ductus Arteriosus Botalli.--This foetal orifice varies greatly in
the conditions which are presented; sometimes it is entirely wanting,
in others patulous and even in a state of dilatation; in others, again,
a short portion is patent (this state is probably comparable to failure
to adhere seen in the valve of the foramen ovale or the sieve-like
opening in the fossa ovalis; unlike the valve of the foramen, the
ductus probably never reopens), or in yet others the ductus is closed
in some cases of malformation, and in others of very similar character
it remains open. It becomes difficult to explain the varied states of
the duct, so dissimilar are they to other defects of development
present. In none of the conditions which are presented can the
malformations be regarded as of a primary character. Our surprise at
certain of its conditions probably must depend on a failure to justly
appreciate the primary malformation present, or else on changes in the
heart and the circulation coming at a period subsequent to the date of
origin of the malformation of the duct itself. When the duct is open at
one end and closed at the other, the open part communicates usually
with the pulmonary artery, since the closing process commences normally
at the aortic extremity: the closure beginning at the pulmonic
extremity is occasionally seen in malformations of heart where the
blood-current has had a reverse direction through the duct.

The premature closure of the ductus arteriosus Botalli, which is spoken
of by some authors, seems to be a rather unfair designation to apply to
the condition. In most cases it is in reality an absence of the duct
dependent on the defective development of certain of the branchial
arches. In other cases the apparent premature closure is due to general
uniform narrowing, almost closure, of the pulmonary orifice and
vessels; in such cases the lungs are supplied by the enlarged bronchial
arteries or other collateral branches. The ductus arteriosus Botalli
remains patulous when the pulmonary artery is {692} narrowed or closed;
in these cases the blood from the right side of the heart to reach the
lungs must pass either through an opening in the septum ventriculorum
or through the patent foramen ovale. The duct is generally open in
cases of transposition of the main arteries, or even in cases of
obstruction of the aortic orifice, or of uniform narrowing of the
descending aorta or its main branches. Its usual length and its point
of origin from the pulmonary artery or its branches, as well as its
junction with the aorta, may vary. Two ducts have been found--one from
each pulmonary branch, one of them joining the aorta as usual, the
other seeking one of its branches. A distinct duct has been found
arising directly from the right ventricle. None of these defects are to
be considered as primary malformation, but as the secondary results
from alterations of the circulation occasioned by other malformations
of the heart or of its great vascular trunks.

       *       *       *       *       *

Fully bearing in mind the distinction which must be made between
primary and secondary defects, and the fact that congenital lesions of
the orifices and valves are mostly located on the right side of the
heart, let us look at various causes which are capable of producing
malformations. In many cases, from the condition of the parts, it is
possible to say positively that the alterations are dependent on an
inflammatory process commencing in the endo-myocardium at an early
period of foetal existence; this is true even after excluding cases in
which the inflammatory products present may fairly be considered to be
the result of defective development and not its cause. Inflammation
was, as has already been shown, long ago pointed out as the cause of
these obstructive malformations. Rokitansky (1844) was followed in his
views by many, who asserted, probably wrongly, that this condition was
the sole cause of the misdirection of development. It was considered
that while in very many cases the evidences of the inflammation
remained indubitable, in others, through a greater lapse of time, the
inflammatory products became less distinct or were wholly removed.
Thus, all defects of development may be traced as the results of some
obstruction of the pathways of the foetal blood, which, on the one
hand, effects the closure of certain vessels or orifices, or on the
other hand maintains patent others which normally should be
obliterated. It is much easier to trace these causes when they operate
during the later periods of development, after the heart and great
vessels have assumed the general shape they maintain, than those which
operate at the earlier periods of transition. It is plain to us that an
obstruction of the pulmonary artery or its branches coming before the
end of the third foetal month must, by preventing the flow of blood
through it from the right ventricle, maintain an opening of greater or
less size in the incomplete septum ventriculorum. It is much less
easy--or, in fact, impossible--to be positive about an obstruction or
other change which causes the transposition or an unequal division of
the great vessels, or which prevents entirely the development of either
septum. Nevertheless, we can believe that some obstruction of the
foetal circulation causes the former defect as well as the latter, if
we may judge of so dark a question by the analogies. In fact, what
would present itself as a trifling obstacle in the third or fourth
month of foetal life would in the sixth week be an impassable
obstruction.

It has been urged against the view that some inflammatory process is
the invariable cause of the obstacle, by those who support the
development theory, that, as the heart remains in a rudimentary
condition, the defects result from a want of formative or plastive
activity of the parts. It seems, however, as difficult to account for
the want of formative activity which prevents the development of the
septum or causes an unequal division of great arterial trunks as to
find the traces of an obstruction. Maternal impressions or shocks have
doubtless caused many headless {693} foetuses or otherwise misshapen
the product of conception during the early months of development. The
effect on the foetus from such shocks cannot of course be a direct
nervous impression, such as those seen producing local disturbances of
nutrition or of formative activity in the adult's own organism, but it
is due to disturbances of the placental circulation, by which the
blood-current is delayed in the foetal circuit. Such delay may result
in a temporary obstruction of the blood in certain foetal vessels. A
delay of the blood-current during a few hours in the early period of
development of the foetus, when formation is excessively rapid, may
result in changes which become permanent. The evidences of such
obstruction may fade completely. Osler[7] has recently urged that it is
difficult to suppose an endocarditis limited to the pulmonary valves in
an embryo not more than an inch in length, and whose heart could not be
above a few millimeters in size. But is it not possible to suppose an
endocardial inflammation which affects at the same time, for example,
the vascular orifices and the line of the rudimentary septum? The
septum may thus be prevented from further development, and the orifice
suffer malformation by subsequent contraction. The evidences of the
inflammation would greatly lessen as the size of the heart expanded.
Cannot inflammation, syphilis, or other communicable disease, from
which we know the foetus suffers, be substituted for the unknown "want
of formative activity"? In respect to the extent of surface involved in
the foetal heart in inflammatory or other morbid processes, can we not
suppose that the area exhibiting evidences of disease in the minute
heart would be as restricted as in the adult heart? In rheumatic
endocarditis of the adult the cause which leads to the inflammation is
a general one; the evidences we find of the morbid process, however,
are confined to very narrow limits. The reasons for this restriction
may be the same.

[Footnote 7: _Montreal Gen. Hos. Reps._, vol. ii.]

The simple narrowing of a blood-track where direct evidence is wanting
may be explained by the occurrence of a specific morbid process as
satisfactorily as by an appeal to lack or excess of formative power.
The real difficulty arises in the explanation of cases of transposition
of the great vessels. The problem is in every way a most difficult one
for solution under any supposition. If it were true that the formation
of the pulmonary artery and the aorta was from the start by separate
blood-channels, and these distinct vessels suffered a genuine
transplantation and became attached to the wrong ventricle, the aorta
to the right and the pulmonary to the left ventricle, then undoubtedly
we should be compelled to accept the developmental theory as usually
expressed. But it is not the case that these vessels are developed in
distinct trunks: their development results from the division of a
common trunk through an infolding of the walls or the gradual formation
of a septum proceeding contemporaneously with the septum of the
ventricles, the vessels at the same time making a half turn on their
axis. A delay in the formation of either septum may result in the
malapposition of the vessels to the ventricles. The septum which is
probably delayed in formation is the vascular septum, since it is
apparently the growth of this septum that applies the force which
results in the axis rotation of the vessels. Are we again to explain
the abortive formation of the vascular septum or any portion of the
branchial arches by the unknown want of formative power? The want of
formative power must have a cause; it does not come spontaneously. Are
not inflammatory endarteritis and syphilitic lesions of the
blood-channels probable causes of the contraction or obliteration of
portions of the branchial arches?

Another question, dark and obscure, requires a short comment. It is
commonly accepted, if an abnormal communication (speaking of small
openings) exists between the two ventricles, that the septum has been
prevented from {694} closing by the blood-current being diverted from
its usual course through narrowing of an arterial ostium, and compelled
to flow into one or the other ventricle. The patency or the closure of
the ventricular septum is held as a criterion of the date of origin of
the primary malformation. We know that certain ulcerations of the
endo-myocardium may result in forming openings between the two
ventricles, but is it not possible that a perforation may be made in
the ventricular septum after it has closed by a lesion originating at
an arterial ostium of the same character as one that prevented the
septum from closing? The muscular tissue of the heart from the third to
the sixth foetal month, and even later, is of very soft character. A
rapidly-coming closure, or even temporary obstruction, of one or the
other great arterial trunks would greatly increase the blood-pressure
within the corresponding ventricular cavity. The ventricular septum
would become stretched and thin, and might readily be perforated, so
delicate is the muscular tissue.

If such a possibility is consummated, it must alter the value which has
hitherto been placed on the opening in the ventricular septum as a
criterion of the date of origin of the primary lesions of the great
vessels which ordinarily are the cause of the patent condition of this
partition.

       *       *       *       *       *

It is to be seen from a review of the recorded cases of malformation of
the heart that defects of the arterial outlet of the right ventricle
are the primary cause of the largest number of cases. It is impossible
to state the proportion of these to those at other orifices or the
great vessels, so incomplete are the records and so unlike are the
opinions of the reporters. It is but natural that this the more active
ventricle of foetal life should exhibit more frequently defects of
development, since the left ventricle in adults suffers more commonly
in its valvular apparatus during its more active period.

The position at which the defects resulting in obstruction of the
blood-current through the pulmonary artery may occur have been
mentioned. The degree of the narrowing is of much importance--much more
than the seat of the obstruction; but of still greater consequence is
the date of origin of the defect of development, since on its
occurrence early or late in foetal life depend the condition of the
septum ventriculorum and the perfection of secondary compensatory
alterations which render the heart capable or incapable of a prolonged
extra-uterine life.

Narrowing or closure of the course of the blood passing through the
pulmonary artery may be divided into two classes: 1, those cases in
which the septum ventriculorum is imperfect to a greater or less
degree; and 2, those in which it is fully formed, the separation
between the ventricles being complete. The date of their origin
corresponds to different periods of the development of the foetus. The
earlier the obstruction comes in the normal outlet of the ventricle,
the more rudimentary is the ventricular septum. The size of the opening
of the septum depends on the degree of narrowing of the pulmonary
outlet as well as on the date of origin of the obstruction. If the
arteries are transposed in relation to the ventricles, and one of them
becomes obstructed, the effect on the septum is the same, although the
direction of the current through the opening is reversed. Kussmaul and
others have pointed to certain exceptions which may lead to errors. In
a congenital opening of the ventricular septum, isolated from other
defects, an endocarditis involving the pulmonary orifice may occur
subsequent to the time of the usual closure of the septum, or even
after birth. It would be difficult to distinguish such a case from one
of pulmonary narrowing occurring before the third foetal month. The
character of the inflammatory changes and the size of the pulmonary
artery beyond the point of narrowing would assist in marking the
distinction. It must be remembered, however, that the pulmonary artery
is {695} recorded as possessing a large size beyond the seat of
narrowing in cases of undoubted congenital origin.

The alteration in the form and size of the right ventricle varies
greatly according to the time at which the pulmonary obstruction
originates. The ventricle seems to maintain its size, and even to
become hypertrophied and dilated, when the pulmonary obstruction occurs
before the closure of the septum: if the pulmonary artery is
obliterated or exceedingly narrowed at a later period, the ventricle
shrivels, because no blood is able to pass, and gradually more and more
of the foetal current passes through the foramen ovale to the left
side; if, however, the pulmonary defect is but slight, the right
ventricle continues its function, becomes hypertrophied, and may
dilate. In pulmonary obstruction the right ventricle changes its form
somewhat in accordance with the seat of obstruction. Thus the primary
obstruction may be in the pulmonary artery or its branches; or in other
cases the malformation is found within the cavity of the right
ventricle. The last group is spoken of as conus stenosis.

The malformations of the conus of the right ventricle may present
themselves under three forms: they all act as constrictions, but alter
the shape of the ventricle very variously; their effect on the
circulation is practically the same, varying only with the closeness of
the constriction. If an inflammatory process occur at the seat of the
normal muscular constriction between the sinus and the conus, it may
result in fibrous thickening and contraction; thus the normal division
of the sinus from the conus becomes exaggerated and permanent. The
narrowed portion may continue to exhibit evidences of endocarditis, or
these may fade away, leaving a smooth surface. These narrowed parts
seem to be especially liable to inflammation at a subsequent period as
the bulk of the blood and the force of the circulation increase.
Peacock describes a condition of narrowing due to muscular hypertrophy
alone. It would seem in these cases that the hypertrophy was, in not a
few of the instances, an acquired condition, and not congenital.

These cases present a heart having, as it were, a double or subdivided
ventricle, comparable to that of the turtle. The condition has been
described by some writers as a supernumerary ventricle. The form and
size of the communication between the two portions of the ventricles
vary very greatly: in some of the cases due to inflammation the passage
merely admits of a large probe, and consists of a firm fibrous ring, or
there may be two or more such openings. In constriction by muscular
bands the opening is usually a large oval with smooth walls. In these
cases the size and the condition of the walls of the so-called
supernumerary ventricle present different appearances according to the
degree of constriction and the size of the pulmonary opening; it is
probable also that the condition of the ventricular septum influences
the consecutive alteration in the parts. When the constriction is close
and but little blood enters the conus, its walls are thin and flaccid,
while in cases of less marked narrowing, provided the pulmonary artery
remains nearly normal, the walls of the conus become hypertrophied, in
conjunction with a similar development of the other parts of the right
ventricle.

In other cases the entire conus may be uniformly narrowed: this change
is due almost invariably to inflammatory lesions, and in many instances
it is difficult to determine whether the condition is of foetal origin
or whether it arose during the early months of extra-uterine life or
even at a later period. Its occurrence in conjunction with other
malformations would point to its origination during the developmental
period. The conus may also present a constriction directly at or just
beneath the valvular orifice of the pulmonary artery. This condition is
almost invariably combined with some narrowing of the artery itself,
and there is so constantly present evidence of inflammation of recent
date that it is almost impossible to say whether the defect {696} is
not due to a myocarditis originating after the developmental period.
With this condition the entire conus usually presents more or less
shrinkage or collapse, becoming greater as the constriction at the
orifice is more marked. This collapse of the conus is to be looked upon
as secondary to the primary defect at the orifice.

Closure or narrowing of the pulmonary artery trunk may be traced to
many conditions acting at several different points of the course of the
blood. Nearly all these conditions are caused by inflammatory lesions
which result in contractions of the arterial walls. In fact, pulmonary
artery defects not dependent on inflammatory changes are very obscure
and difficult of explanation. In adult life we know of only two
conditions which lead to obliterations of vessels; first, inflammation
of the lining membrane (endarteritis); and second, stoppage of the
blood-current, usually through pressure directly applied to the
vascular trunk. The clots of blood which occupy the vessels form both
in advance and beyond the point of pressure; hence we can look for
obstruction, causing closure of the pulmonary artery, at either
extremity of the blood-course. Thus, we may think of a primary conus
obstruction which may secondarily have the effect of reducing the size
of the pulmonary artery, but it is never obliterated through this
means; nearly always some blood passes in this direction, and blood
also enters the pulmonary artery from the ductus arteriosus Botalli:
both conditions necessarily tend to keep the artery from complete
collapse; moreover, the artery, even in cases of very narrow conus, may
remain of its usual size. The same effect may be produced by narrowing
of the tricuspid orifice. This condition is a very rare one, and never
could lead to complete closure of the pulmonary artery unless this
orifice were entirely obliterated and the septum of the ventricles
remained closed. Peacock speaks of premature occlusion of the ductus
arteriosus Botalli as one of the causes of narrowing of the pulmonary
artery. The obliteration of this portion of the branchial arches, by
preventing the blood flowing in its usual course to the descending
aorta, he thinks results in narrowing the calibre of the pulmonary
artery. May not the condition be equally well interpreted in a
different manner? May not it be that the obstruction of the artery was
the cause of collapse of the ductus? One would think it possible, if an
obstruction arose in the ductus arteriosus Botalli, for the
blood-current in the pulmonary artery to maintain another branchial
arch patulous for its accommodation, or, failing this, to dilate the
pulmonary branches and thence return to the left side of the heart. In
rare cases the pulmonary artery has been found deficient in size when
the lungs are malformed, either by reduction in their size as a whole
or by the absence of one or more lobes. Such a cause has very little
opportunity of acting with much force on the pulmonary artery during
foetal life. This cause and all the others in this group are to be
looked upon as secondary in their effects.

In primary defects of the pulmonary artery trunk the vast majority
afford indubitable evidences of an original inflammatory causation;
others are due just as positively to a defective evolution of this
vessel from the common arterial trunk. Instances are on record of the
complete closure of the pulmonary artery and its conversion into a
ligamentous cord: these cases are very rare. In a somewhat larger
number a pretty uniform narrowing, sometimes to an extreme degree, and
often exhibiting thickened walls, is found. It is much more frequent to
see the obstruction of the artery, due to inflammatory changes, at its
valvular orifice.

Peacock describes the narrowing at the pulmonary orifice in many cases
to be due to disease of the pulmonary valves, whereby the number of
cusps are reduced in number, or to a membrane stretched across with
small openings in its central portion; or the obstruction may consist
of a duplicature of the lining of the vessels, or even to bands of
muscular fibres surrounding the {697} orifice. Two valves of unequal
size may be found at the orifice, giving evidence that the larger one
has been formed by the adhesion of two of the normal cusps; the
membranous obstruction is probably due to the union more or less
complete of the three cusps. The curtains thus formed protrude into the
course of the artery and form a deep circular sinus between the valves
and the walls of the vessel. The opening between these adherent valves
varies from a transverse slit to a tubular or barrel-shaped orifice--a
tube within a tube. These diseased valves are thickened, very firm,
fibrous, or even calcified. In other cases the obstruction consists of
abundant warty elevations, so numerous that they are equally effective
in preventing the passage of blood as the united valves. The size of
the opening is sometimes extremely reduced, measuring only five
millimeters in diameter. The pulmonary artery is most generally less in
size than normal, but never becomes reduced to the same extent as its
orifice, unless it has likewise suffered from inflammatory disease;
otherwise its walls remain thin, resembling the venæ cavæ.

In addition to disease within the calibre of the vessel, Meyer, who
strongly advocated the inflammatory cause for all these defects,
pointed to pericarditis, occurring at the origin of the pulmonary
artery and compressing the vessel, as a rare method of causation.

In a very large majority of the cases of pulmonary narrowing on record
the septum ventriculorum is found to be more or less defective. In
accordance with the usual principles, this defect of the septum, in
conjunction with narrowing of the pulmonary artery, is held to indicate
that the obstruction of the artery dates from a period of development
anterior to the closure of the septum. This view was advanced by Hunter
in 1783. But Peacock gives an account of many cases of pulmonary
narrowing, combined with open septum ventriculorum, in which the
obstruction was caused by adhesion of the pulmonary valves. It is,
however, a fact that the development of the valvular apparatus is not
effected until after the septum of the ventricles is completed. How,
then, can we suppose valves to adhere so as to obstruct the pulmonary
artery and prevent the closure of the septum when in reality the valves
themselves have not developed? Does it not seem possible that in some
rare cases the opening found in the septum ventriculorum is in reality
a reopening? Another case is on record of open septum ventriculorum and
narrowing of the pulmonary orifice in a child born of a mother who
suffered a prolonged fright during the fifth month of utero-gestation.
Strong mental impressions are accounted causes of malformation of the
foetus, and in this case the fright, if it was the origin of the
defective development of the septum, came more than two months too
late.

In cases of pulmonary narrowing with open septum the aorta communicates
freely with the right ventricle, or appears to arise from both
ventricles, or more rarely from the right cavity alone (the deficient
pulmonary artery remaining in its usual position). Many opinions have
been held as to which one of the three defects is primary. Hunter's
conclusion has most generally prevailed. The obstruction of the course
of the pulmonary artery is looked upon as the primary defect. From the
obstruction the right ventricle becomes distended, and the opening of
the septum is due to the blood-pressure, which prevents the final
closure. The blood-pressure also alters the direction of the septum and
pushes it farther to the right. Thus the septum comes to stand directly
under the aortic orifice, or by a further deviation to the left side
brings that orifice wholly within the right cavity. In these simple
cases the origin of the aorta from the right ventricle is not a real
but merely an apparent transposition or transplantation of this vessel;
the aorta has not been moved, but only the septum has been moved under
its orifice, and the right ventricle has consequently become more
extensive. In other cases the aorta {698} seems to move more toward the
right side, usually coming also more to the front, and in other cases
there is an actual transposition of these vessels. The method of this
transposition will be further described.

Meckel's original theory for open septum and narrowed pulmonary artery
was that the defect was primarily in the septum of the ventricles, due
to a want of formative energy, and the pulmonary artery closed itself,
as do other arteries, from want of use. Meyer showed that a defect of
the septum was incapable of causing narrowing of the pulmonary artery,
since the exit of blood is easier through the artery, from the form of
the right ventricle, than through the open septum; the passage of the
blood from right to left is opposed by the blood-mass in the left
cavity. Heine also thought the pulmonary-artery narrowing was a
secondary defect, but did not think the opening of the septum caused
the narrowing. He considered the primary malformation to be a deviation
of the septum to the left. The deviation of the partition before its
closure brought the aorta within the left cavity, and furnished a free
exit for the blood from this chamber shorter and more convenient than
through the pulmonary and the ductus arteriosus Botalli to the
descending aorta; the pulmonary artery collapsed for want of use,
similarly to other foetal blood-courses. Hence, Heine considered that
in all cases of open septum and apparent transposition of the aorta
which exhibited no evidences of inflammation as a conjectural cause of
narrowing or closure of the pulmonary artery the explanation was to be
found in a primary deviation of the septum ventriculorum.

The difficulty in Heine's theory lies in showing the mechanism of a
deviation of the septum without a primary obstruction of the flow of
blood through the pulmonary artery. The hypertrophy of the right
ventricle which Heine proposed as an explanation is almost certainly a
secondary effect of the obstruction, and therefore cannot be supposed
to originate a deviation of the septum; it is doubtful if hypertrophy
can be considered as a cause of increased blood-pressure within the
cavity of a ventricle under any circumstances, and certainly not as
exercising pressure in a direction to cause the supposed deviation of
the septum. An open septum without obstruction of the pulmonary
orifice, which rarely occurs, does not produce hypertrophy of the right
chamber.

The explanation of cases of open septum with obstruction of the
pulmonary artery seems entirely satisfactory by Hunter's theory, or by
what Kussmaul has named the engorgement theory. But when there is a
real transposition of the arteries, the pulmonary placed farther to the
left and behind and coming from the left cavity, the aorta in front and
to the right and arising from the right or pulmonary chamber, thus
changing their relative positions and their orifices exchanging
ventricles, the difficulty of explanation becomes great, and the cause
of the abnormal relations of the vessels cannot be traced to a simple
deviation of the septum ventriculorum.

For the explanation of these cases of complete transposition of the
vessels, as well as their transplantation relatively to the ventricles,
Rokitansky has traced respectively the development of the two arterial
trunks from the common trunk and of the septum ventriculorum. He
considers that the partitioning of the arterial trunks is the governing
factor in their formation, and that the ventricular septum is arranged
in conformity with the septum of arterial trunks. In tracing the
development of the circulatory apparatus in man there seems to be no
doubt that the heart develops exactly like that of other vertebrates.

The very first rudiment of the heart is a spindle-shaped thickening of
the intestinal fibrous layer of the fore part of the alimentary canal.
This spindle-shaped formation then becomes a hollow pouch, and
separates from the intestinal layer and lies free in the cardiac
cavity. The earliest condition {699} yet seen in the human being is
that from an embryo of about two weeks (Coste), in which the viscus
appeared as a simple tube in the shape of a letter S--the hollow
rounded pouch having slightly elongated and bent to this form, and
simultaneously turned spirally on an imaginary axis, so that the
posterior part of the tube rested on the dorsal surface of the anterior
part. The yelk-veins connect at its posterior part, while the arteries
form a continuation of its anterior extremity. The spiral turning and
curving increase, and simultaneously two shallow indentations appear in
the twisted pouch, transversely to its long axis, looking like kinks in
a flexible tube. These indentations mark the outline of the three
primitive portions of the central organ--viz. the first, with which the
veins communicate, represents the future auricles; the next, the
ventricles; the third portion, the common arterial trunk (aortic bulb
or truncus arteriosus communis). Early in development the first section
is the largest, but by the time the S is formed the middle or
ventricular portion exceeds in size the auricles and their appendages.
So far, the central organ remains a continuous tube, indented
transversely in its course at the points which mark its future
division; the blood moves through it as through a coiled tube, entering
by the veins and passing out by the aortic bulb to the vascular or
branchial arches; the venous entrance is posterior, the arterial exit
is anterior and is directed toward the future aortic arch. This is the
condition at the end of the second week. The future auricles and
ventricles now form a common cavity; the indentation between them,
called the auricular canal, represents the future auriculo-ventricular
orifice. The future fibrous ring forming this orifice is the first to
be developed of all the permanent structures of the heart; its
infolding to form the two auriculo-ventricular orifices comes early,
but at a later date than here spoken of. Its exact method of
development is not clearly described.

Between the second and fourth weeks is exhibited an indication of the
future most important step in development; this process does not really
step forth until the fourth week, although superficial traces of a
furrow antedate this time. This step is the division of three sections
of the tube into opposite halves, a right or venous, a left or arterial
half. This division results in the formation of the future septa
between the auricles and between the ventricles, and separates the
common arterial trunk (aortic bulb) into the future aorta and pulmonary
artery. This partition is spoken of as longitudinal; but it will be
seen, if the real lines of growth of the future auricular and
ventricular septa are carefully regarded, that the indentations which
mark their site are also transverse, as were the primitive ones for
division of the auricles from the ventricles. The proximal end of the
tube comes in contact with the distal portion by a further bending
movement, so that these two ends go to make the left half of the heart;
and the middle portion of tube, composed partly of auricle and partly
of ventricle, forms the right half of the heart. This secondary
indentation, commonly spoken of as longitudinal, is in reality
transverse, although, from the more markedly bent condition of the tube
which has come about, it does not advance in the same plane as the
primitive indentation of the tube. The mechanism of the division of the
aortic bulb will be described later.

This secondary indentation, which finally results in the formation of
the auricular and ventricular septa, appears earlier in the ventricular
cavity, about the fourth week, and later in the auricles, about the
eighth week. By about the twelfth week the process of formation for the
muscular partitions is completed; the septum ventriculorum normally is
gradually built up, and by this time has joined itself, at the base of
the heart, to the septum forming itself in the arterial bulb; thus the
right and left ventricles are finally separated. The septum in the
auricles is also finished in its muscular part, mostly built up from
the base and posteriorly toward the roof of the cavity, {700} leaving,
however, the foramen to be closed by the membrane some days after
birth.

The foetal heart from the fourth week onward becomes more and more
rounded in outline, and finally more or less rectangular. The auricular
appendages become conspicuous and overhang the ventricles. The future
left ventricle appears larger than the right, and the former projects
notably leftward and downward. The aortic bulb or common trunk appears
to arise wholly from the right ventricle, although the vessel
communicates with both cavities, since at this period the cavities are
undivided. The furrow which marks the line of the future septum
ventriculorum runs to the left of the root of the common trunk; and
until at least as late as the sixth week this trunk appears from the
exterior to be in connection only with the future right ventricle.

As early as the sixth week, possibly earlier, a distinct furrow is seen
on both sides of the common trunk running longitudinally from its root
at the ventricle to its first branch (branchial arch). This indentation
does not traverse directly to the ventricular furrow; in fact, at this
period the ventricular furrow is not conspicuous at the origin of the
trunk toward the base of the heart, the septum within not having risen
as yet to the base of the ventricles. During the formation of this
furrow the common trunk continues its slow partial rotation on its
axis; the rotation of the other parts of the cardiac tube has ceased;
the segments of the tube have come to a standstill--become, as it were,
fixed and adherent to each other, the proximal to the distal end, the
anterior surface to the posterior, through the previous bending of the
tube on itself.

Within the common trunk Rokitansky has described the changes, as seen
in cross-sections, which result in its division into a permanent aorta
and pulmonary artery, and also the adaptation of the septum arteriosus
trunci to the septum ventriculorum. He says that at an earlier period
than here described for the external furrow appearing, on the inner
surface of the truncus arteriosus communis (aortic bulb), to its left
side and somewhat posteriorly, above the starting-point of the anterior
limb of the septum ventriculorum, a little swelling appears, which
grows toward the right and slightly forward, so that the common trunk
is divided into an anterior rather left-hand, and a posterior right
portion, respectively the pulmonary artery and aorta. The growth does
not pass in a straight line through the lumen of the common trunk, but
so that the forming septum makes a concavity posteriorly toward the
aorta, and a convexity anteriorly toward the pulmonary; thus, on
cross-section the aorta has the outline of the gibbous moon--the
pulmonary, fitting into it, separated by the septum, of a new moon. The
septum ventriculorum, as seen starting at the base of the ventricles
from the fibrous ring of the auriculo-ventricular orifice (having
already been built upward from the future apex of the heart),
originates at a point on the posterior wall of the common ventricular
cavity in exact correspondence with the starting-point of the little
swelling on the inner surface of the common arterial trunk. The two
septa are thus formed in apposition. The septum ventriculorum, in
advancing forward to meet the other limb of the septum forming on the
opposite wall of the ventricular cavity, follows the septum trunci
arteriosus communis, surrounds the posterior vessel (the aorta) to its
front, then passes around it to its right; the pulmonary is on the
other side of the septum; the portion of the septum ventriculorum
between the orifices of the vessels is the pars membranacea of the
septum. The anterior portion of the septum ventriculorum forms one wall
of the arterial conus of the right ventricle. Thus it happens that by
the eighth week the common trunk is divided into aorta and pulmonary
artery; the structure of the septum ventriculorum is so far advanced
that these vascular trunks are connected with the proper ventricles,
but the {701} septum ventriculorum does not close completely until
about the twelfth week.

In explaining the occurrence of a transposition of the arterial trunks
in accordance with the facts of their normal development, Rokitansky
says, if the septum trunci, starting from the usual point of the little
swelling on the inner surface of the common trunk, turns abnormally
with its concavity forward (instead of backward as normally), and thus
passes through the trunk, there will be established an anterior left
aorta and a posterior right pulmonary, because the septum ventriculorum
in its growth conforms to the direction of the septum trunci. Thus,
another than the usual portion of the common trunk is partitioned off
and placed in communication with the respective ventricles. This
furnishes us with examples of transposition of the arterial trunks
relatively to each other, but not transposed in relation to the
ventricle into which they are implanted. The great majority of
specimens of this sort with which we are acquainted--and Rokitansky
knew no others--show an open septum. They are usually spoken of,
therefore, as instances of "both vessels arising from the same
ventricle (the right usually)," or of "aorta communicating with both
ventricles, the pulmonary artery normally placed." Rokitansky assigns
no reason for this deviation in the line of growth of the septum trunci
across the lumen of the common trunk; in fact, he never examined a
malformed heart during this stage of development. The deviation of the
septum trunci, the primitive factor in this malformation--since to it
the septum ventriculorum conforms its development--he accounts for by
chance (deviation of formative energy). It seems much more probable, as
it is always the pulmonary artery which must be reduced in size when
the concavity of the septum trunci presents anteriorly (the aorta
occupies the smaller area when the concavity of the septum is
posterior), that the deviation of the septum trunci is due to some one
of the many conditions (endo-myocarditis) which have already been
pointed out as the cause of pulmonary-artery narrowing or closure;
hence, another malformation of the heart can be thus traced to
pulmonary obstruction, the evident cause of so many other defects.

For examples of transposition of the vessels, both relatively to each
other and to the ventricles, with complete closure of the septum
ventriculorum, Rokitansky also gives a satisfactory explanation. It is
important to note the distinction between cases of closed and open
septum. Transposition of the vessels with open septum are, as already
shown, doubtful instances of transposition from one ventricle to the
other, although the vessels may be transposed in relation to each
other; furthermore, the mechanism which explains relative transposition
of the vessels does not explain the implantation of the vessels into
the improper ventricle. His explanation is that the starting-point of
the little swelling from which the septum trunci forms is shifted to a
point farther forward on the inner circumference of the common trunk,
and at the same time has its concavity anteriorly, and as in the
previous case decreasing also the area of the pulmonary artery; and
thus the aorta comes more forward and to the right, and the pulmonary
artery passes more to the left and backward. The septum ventriculorum,
in conforming itself to the abnormal starting-point and direction of
the septum trunci, must consequently pass across the common ventricular
cavity in such direction that the aorta comes in connection with the
pulmonary side of the heart, and the pulmonary artery with the systemic
heart. Consequently, Rokitansky traces both the relative and the actual
transposition of the arterial trunks to the deviation either of the
direction or of the starting-point of the septum trunci. The deviation
of the position of the little swelling on the inner surface of the
common trunk, which Rokitansky supposes, is probably not an actual
transference or misplacement of this point of formative energy, but in
reality a failure of the common trunk (aortic bulb) to continue its
axis-rotation, as it {702} normally does, after the other portions have
become fixed. This premature cessation of the rotation of the common
trunk would leave the starting-point of the septum trunci in a more
anterior position than normal, since the trunk rotates normally in a
direction to bring its left side, on which the starting-point of the
septum trunci is situated, more posteriorly. A pericardial inflammatory
adhesion, such as Meyer pointed out for certain cases of pulmonary
artery obstruction, would fix the common trunk, prevent its proper
rotation, and at the same time narrow the pulmonary orifice in certain
instances. In other cases, in which the pulmonary artery is found of
normal size, the septum trunci may be supposed to divide the vessel in
the usual direction (concavity posteriorly as normal), whilst the
septum trunci commenced to grow from an abnormal position, more
anteriorly and to the left than normal (through failure of rotation);
hence, as the septum ventriculorum conforms to its growth, the vessels
become connected with the improper ventricle; the pulmonary, however,
is not found permanently narrowed, and the septum ventriculorum is
completely closed. Here the cause is a failure of the common trunk to
rotate on its axis, probably from an external adhesion of its
periphery.


Malformations affecting primarily the Right Side of the Heart.

In classifying defects in the course of the pulmonary artery we come
to--

1. Closure or narrowing of the artery, with perfect ventricular septum.

Congenital obstruction of the pulmonary artery, with closed septum,
although more rare than with open septum, is nevertheless a frequent
defect. Unfortunately, it is very often impossible to distinguish with
certainty whether the stenosis is essentially congenital or is acquired
after birth. Complete closure is the least difficult to distinguish,
because this defect very soon causes death; the prognosis in a merely
narrowed orifice is much more favorable. The duration of life in
complete closure never extends beyond a full year, while in undoubted
congenital narrowing the age of sixty-five years has been attained.

From this atresia the most striking consequence is a reduction of size
of the right ventricle, increasing almost to closure. This result is so
common that Peacock thought it was the law that in atresia the right
ventricle reduced itself to closure, while in stenosis it dilated and
became hypertrophied. This is not the law, but only a rule of very
common occurrence. Instances of eccentric and concentric hypertrophy
are found among the records of these cases. Great reduction of the
right ventricle results probably only when the obstruction comes very
soon after the completion of the septum ventriculorum--thus at a time
when the ventricle is yet very small. The wasting of the right
ventricle can reach a very high degree, and when it becomes very great
the tricuspid orifice is also defective. The foramen ovale and the
ductus arteriosus Botalli are, in complete closure, usually found open.
The obstruction may come in the conus or at the valvular orifice, or
the artery is found converted into a cord.

In seven cases the duration of life varied from four days to nine
months.

When the stenosis does not reach a high grade, positive clinical signs
are often wanting for the determination of its existence, and the
difficulty becomes greater as the age of the person advances.

Clinically, we find congenital blueness with palpitation, dyspnoea,
together with the physical signs of pulmonary stenosis; these symptoms,
however, may make their first appearance only on the advent of some
acute disease. Sometimes they come in the first month or the first year
of life, or even much later. {703} If abundant congenital compensatory
changes are present, the symptoms may be postponed until further
compensatory alterations become impossible; or at the narrowed orifice
the development of a fresh endocarditis may determine the occurrence of
symptoms. The mere increase of the body and of the mass of the blood
may alter the relations of the circulation, and this disproportion may
show itself with suddenness. Febrile conditions may also suddenly
disorder the circulation.

The compensatory alterations which commonly are held to indicate a
congenital origin of stenosis of the pulmonary artery are patulousness
of the auricular septum and of the ductus arteriosus Botalli. When both
of these remain open there cannot be much doubt that the date of origin
is from the foetal state or in the first weeks of life. If only one of
the foetal passages remains open, the ductus gives a greater surety of
a foetal date than the foramen ovale. The closure of both foetal
passages does not exclude a congenital origin if the obstruction of the
pulmonary orifice is moderate. The patulousness of both foetal passages
indicates that the defect arose at least shortly after birth, because
these openings close within four or five weeks of this event. The
foramen ovale alone open indicates very little with certainty, as it is
so often found with one or more small openings without any probable
cause. Bézot found it partially unprotected in 44 cases out of 155;
Klob, 224 in 500; Wallmann, 130 in 300. Rokitansky has indicated that a
strong blood-pressure not unfrequently may press the fibrous valve of
the foramen strongly toward one auricle or the other, and thus lead to
its atrophy in part, forming larger or smaller openings of
communication between the two cavities. In doubtful cases of stenosis
of the pulmonary artery such small openings are not signs of much value
in determining the congenital origin of the stenosis. Unless there is a
marked defect in the septum atriorum, the congenital origin of the
pulmonary atresia or stenosis cannot be predicated on this ground.

Patency of the ductus arteriosus Botalli has been very rarely observed
as a primary malformation. A coincidence of this as primary defect with
post-natal stenosis of the pulmonary artery must necessarily be
extremely rare. In persistence of the ductus art. Botalli the current
passes from the aorta toward the pulmonary artery; the obstruction of
the pulmonary artery conditions a dilatation with hypertrophy of the
right ventricle. Reopening of the closed ductus is impossible.

The condition of the pulmonary valves as well as the diameter of the
pulmonary artery itself and its branches often afford valuable points
for the determination of the congenital origin of stenosis of this
orifice. The greater the narrowing, or the more extreme the thinning of
the wall, the earlier the coming of the obstruction.

Morgagni reported the first case of stenosis of the pulmonary
orifice--in fact, the first case of congenital malformation of the
heart--in a girl aged sixteen. He recognized the relationship of the
open foramen ovale and the dilatation of the right ventricle as
mechanical effects of the pulmonary stenosis.

2. Obstruction of the conus arteriosus dexter, with open ventricular
septum.

A. The separation of the conus in the form of a so-called supernumerary
third ventricle has been reported by Peacock in ten cases, and ten
others have been added by Kussmaul from various sources. The degree of
separation varies very greatly in individual cases: in some it is so
slight that the designation becomes doubtful, while in others it is so
great that the word stricture might with propriety be employed. In two
cases a goosequill-sized opening existed between the sinus of the right
ventricle and the conus; in others the communication between the two
was multiple. The size of the supernumerary ventricle varies greatly;
in one case of a girl of twelve years it would only contain a hazelnut.

{704} In most of the cases the partitioning probably commences by
hypertrophy of the muscular bands which are more or less marked in
normal hearts in this situation: to this, as the result of
endo-myocarditis, is added cicatricial contraction of the inflammatory
products, whereby the original partitioning becomes greatly increased.
The preponderating frequency of the seat of the stenosis directly at
the transition of the conus to the sinus increases the likelihood of
this explanation of its causation.

Alteration of the valves of the pulmonary artery, probably of foetal
inflammatory origin, is of very frequent occurrence with supernumerary
ventricle and conus stenosis; sometimes only two cusps are found,
though four cusps have been noted; they may be absent or be replaced by
a ring mass formed from their union. Normal valves have been observed
unaltered by inflammatory changes. The conus appears always to suffer
diminution, and the pulmonary artery is found more or less narrowed
according to the degree of obstruction. The sinus of the ventricle is
dilated and its walls hypertrophied. The aorta, mostly widened, springs
in all cases from both the ventricles, unless wholly from the right
one. The foramen ovale is generally more or less widely open, although
it has been found closed; the ductus art. Botalli is mostly closed. The
duration of life may be long; Kussmaul reports the oldest case at
thirty-eight years.

B. Of primary uniform narrowing or shrinkage of the right conus art.
dext. Kussmaul reports eight cases from various sources. The conus was
shortened, and formed a ring-shaped fissure, gradually reduced in size
toward the orifice of the pulmonary artery. The pulmonary valves were
variously changed, mostly by union of one or more of the cusps, though
sometimes remaining normal in shape, though very delicate. The
pulmonary artery was generally narrowed to about the width of the
calibre of the conus itself, unless further change came to it from its
special involvement by endarteritis.

In all cases the aorta arose from both ventricles. The right side of
heart was dilated, and the right ventricular wall hypertrophied. The
foramen ovale remained open. The ductus arteriosus Botalli has been
found absent or closed, and the collateral circulation effected by
anomalous communications, oftentimes duplicate or manifold; in most
cases the ductus remains open. The oldest patient in which this form of
heart has been found was twenty-five years.

C. Ring-formed narrowing of the conus, due to a muscular band. Peacock
reports this defect from a girl æt. nineteen, cyanotic from birth; the
constriction was situated at the bases of the valves, and was formed by
a muscular band covered by fibrous tissue, and the edges of the opening
were studded with warty vegetations. The pulmonary valves were two in
number, probably resulting from fusion of two of the cusps; were
thickened and opaque, but smooth. The index finger could be passed
between the valves. The artery was of small size, but much wider than
the constriction. The aorta was dilated, and arose from both ventricles
through a perforation of the septum ventriculorum. The foramen ovale
was closed. The ductus art. Botalli gave free passage to a crowquill.
The right side of heart showed dilatation and hypertrophy of both its
cavities, and the tricuspid valve was thickened and had vegetations on
its auricular aspect.

3. Simple stenosis and atresia of the pulmonary artery, with open
septum ventriculorum.

This class includes malformations, with stenosis or atresia of the
pulmonary artery, in which the defects occur before the completion of
the ventricular septum, as the result of engorgement already described,
but in which no other primary congenital defect exists; thus the
separation of the pulmonary artery from the truncus arteriosus communis
is completed; the auricles and ventricles are marked out by their
septa, though not completely divided; {705} the position of the aorta
in relation to the pulmonary artery is either normal or more to its
right; and there are no primary defects of any consequence in the other
orifices of the heart. The simple stenosis or atresia of the pulmonary
artery as thus defined is by far the most frequent malformation of the
heart. Kussmaul has found about 90 described; among these are 26 cases
of atresia.

As a rule, in partial obstruction the entire length of the artery, as
far as the bifurcation, shows narrowing, but the greatest narrowing
exists at the orifice of the pulmonary artery; only rarely are the
orifice and the tube equally narrowed. Exceptionally, the tube has been
found narrower just without the orifice, and later resumed its normal
circumference. The walls are very often thin, like those of veins, and
at times the vessel is shrunken. The valves are variously altered,
often to a greater or less degree united, thickened, and opaque.

In complete closure two different conditions are seen; in some the
artery itself to its bifurcation changes to a firm cord or thread; in
others the tube is more or less narrowed and the orifice alone is
closed.

As a rule, in stenosis and atresia of the pulmonary artery the conus is
only moderately narrowed and its walls hypertrophied, while the sinus
of the right ventricle is dilated and hypertrophied. The right auricle
is dilated and hypertrophied. The tricuspid leaflets are clouded and
thickened. The left ventricle is commonly small, and the wall not
thicker than the dilated right ventricle. Sometimes the aortic and
mitral valves suffer alterations of an inflammatory sort, probably of
foetal origin. The shape and position of the heart are changed, but the
size, as a whole, may not be much altered. The aorta may be widened,
often to double the normal size. As to the origin of the aorta, it is
often difficult to speak with certainty; its relative position to the
pulmonary artery and to the body and axis of the heart is, as a rule,
unchanged. Whether it is to be described as arising from one or both
ventricles, or from the right one alone, depends on the posture which
the septum ventriculorum assumes beneath its orifice. As a matter of
fact, this relationship makes little difference to the flow of blood
from the right ventricle, whose normal orifice is obstructed; provided
the septal opening is sufficient, the flow of blood is secured and the
hindrance to the circulation precluded. The opening in the septum
ventriculorum may be only at the membranous portion, or it may also
involve the adjacent muscular septum; the defect may be round or
triangular, with its apex above and with smooth margins.

The foramen ovale has been found open in 39 cases out of 53. Its
condition in this respect shows very great proportional variation in
the different collections of cases. The open or closed condition of the
foramen does not seem to depend on the degree of stenosis of the
pulmonary artery itself. It depends, probably, more on the freedom of
escape for the blood from both the ventricles through the
aorta--probably also on the condition of the ductus arteriosus Botalli.
The foramen ovale and ductus art. Bot. have been found closed much more
frequently in stenosis than in atresia of the pulmonary artery, and the
ductus is deficient or absent oftener in stenosis than in atresia. This
absence of the ductus occurs in 13 per cent. of the cases, and tends to
support Peacock's theory that narrowing of the pulmonary artery is the
consequence of the defective development of that branchial arch out of
which the ductus art. Botalli is formed.

It is of great interest to note the collateral circulation by which
blood reaches the lungs when the pulmonary artery is closed. When the
ductus arteriosus is open, the blood passes from the aorta into the
ductus and the branches of the pulmonary artery become branches from
it. When the ductus arteriosus is closed or very narrow, the bronchial
arteries become {706} the means of supply for the lungs, and through
them the blood passes to be aërated. Branches from the coronary
arteries have been found supplying a partial channel for the blood to
the lungs, as well as the oesophageal, pericardial, internal mammary,
and intercostal arteries.

The duration of life is often very considerable. Thirty-seven years
have been attained.

4. Combined Stenosis and Atresia of the Pulmonary Artery.--Under this
division are arranged other primary defects of the heart, which are
found combined with stenosis and atresia of the pulmonary artery. It is
very striking how frequently this artery is narrowed or closed in
defects of the heart which date from the early period of foetal life,
before the division of the truncus art. comm. and of the ventricles has
occurred. It is only very rarely that defects from this early period
show a normal width in this vessel; in the great majority it is
narrowed or closed. The aorta is rarely affected in this manner.
Changes in the aorta may come also, but a complete failure or great
narrowness of this circulation is so difficult to overcome by a
collateral circulation--more difficult than the pulmonary
circulation--that life must cease in the foetus, or at least the
conditions are incompatible with extra-uterine existence.

A. Combination with partial persistence of the truncus arteriosus
communis. The defects coming under this head show usually very great
deficiency of the organ and its great vessels, although the heart
itself in rare instances shows the proper arrangement of the cavities
and their valves. The persistence of the truncus art. comm. may be
complete or partial; the defect consists in the total absence or arrest
of growth of the septum of the truncus, which partitions it into two
portions. Normally, the two septa grow simultaneously and meet at the
base of the heart. In cases of persistence of the truncus art. comm.
the upper septum fails to develop. In incomplete division of the
truncus the pulmonary artery suffers more than the aorta, and the
former is always narrower than its fellow-vessel. This difference
varies greatly. The valves of the pulmonary artery often fail entirely,
and the ductus art. Botalli is many times absent.

B. Combination with cor biloculare.--Here we have a heart consisting of
two cavities--one auricle and one ventricle--where no partitioning has
taken effect. The defect results from the failure of the septum
ventriculorum to grow; and with this, as in the former division, comes
also a more or less complete failure of the septum trunci art. comm.

C. Combination with single ventricle and divided auricles (cor
triloculare biatriatum).--In the cases of single ventricle with more or
less complete division of the auricles the pulmonary artery generally
shows narrowing to a greater or less degree; it may still be pervious,
although its orifice is closed, or it may be throughout entirely
obliterated. The valves may be entirely wanting. The duration of life
is very short, though in a very few with effective compensatory changes
it may be prolonged very considerably.

D. Combination with divided ventricle and a single auricle (cor
triloculare biventriculare).--In strictness, this defect is nothing
more than an open foramen ovale with some deficiency of the pulmonary
artery; but, in reality, the heart is much more malformed. The whole
septum atriorum is wanting; the superior or descending vena cava is
doubled--one entering the left part of the common auricle, the other
opening more to the right. The ventricular septum shows a greater or
less defection, the pulmonary artery is narrowed, and the aorta arises
from both ventricles or wholly from the right one.

E. Combination with special anomalies in the position of both the great
arterial trunks.--Here come a variety of anomalies in the arrangement
of the aorta and the pulmonary artery in relation to their respective
ventricles and to themselves.

{707} _a_. In transposition of the great arteries, the aorta arising
from the right ventricle and the pulmonary artery from the left cavity,
either there comes a general transposition of all the viscera or the
heart alone is reversed. Very rarely in transposition of the vessels
the septum ventriculorum is closed, commonly open, and although the
size of the vessels may be normal, usually their relation and position
continue reversed throughout their course. In cases where the pulmonary
artery is narrowed the duration of life is short. _b_. The pulmonary
artery may arise from the left ventricle and the aorta from both
ventricles; or, _c_, the aorta may come wholly from the right
ventricle, and the pulmonary artery from both cavities; the latter
vessel may be narrowed or show its normal width or even be considerably
dilated. _d_. Both the great vessels may arise from the left ventricle,
very much dilated, with the aorta in front of the pulmonary artery and
the latter narrowed. _e_. The relation of the great arteries may be
found reversed--_i.e._ the aorta in front and the pulmonary artery
behind, and the aorta spring from both ventricles and the pulmonary
from the right alone.

F. Combination with primary defects of other valvular orifices of the
heart.

_a_. The tricuspid valve may be quite rudimentary, producing by the
regurgitation thus allowed, especially when combined with pulmonary
stenosis, great dilatation of the right auricle. When the pulmonary
artery is narrowed the septum ventriculorum remains open; the aorta
carries the blood, distributing it to the lungs by an open ductus
arteriosus Botalli or a collateral circulation. The collateral
circulation is less developed the greater the width of the pulmonary
artery. The foramen ovale may close in such a case, but when it remains
open the relief to the over-distended right auricle is very great.

_b_. Many cases of congenital stenosis and atresia of the right
auriculo-ventricular orifice are reported in which the condition of the
pulmonary artery is not described. In fact, it is a difficult matter to
determine if the auriculo-ventricular narrowing is a primary one. Its
defective size may be merely, as it were, a rudimentary condition, a
failure to enlarge through disuse. When the pulmonary orifice is closed
and the right ventricular cavity remains small, the tricuspid orifice
is naturally small in size. There are, however, undoubted cases of
tricuspid narrowing with or without stenosis of the pulmonary artery;
the defect consists in a primary contraction of the fibrous ring or in
the union by partial adhesions of the leaflets.


Malformations affecting primarily the Left Side of the Heart.

Primary defects of the systemic side of the heart are, for the reasons
already given, very much more rarely seen than those of the pulmonary
heart. In such cases the aortic conus and its orifice are found more
frequently affected than the mitral orifice; both of these orifices,
however, may be congenitally altered without foetal malformations at
other parts of the heart being present; such cases are on record,
though only sparsely scattered through the literature of cardiac
diseases. Dilg[8] has recently made an important addition to this
subject. He proposes a classification on a new basis for all forms of
cardiac malformation; to these classes he makes conform the
malformations of the left side of the heart. In the first class he
places all cases dependent on an inflammatory process occurring in the
foetal heart after its normal development is completed; in the second,
those cases of malformation in which the deviation from the normal
consists in defects of formation; in the third, those which present a
combination of endo-myocarditis with defective development.

[Footnote 8: _Virch. Arch._, Bd. xci., S. 193-259, 1883: "Ein Beitrag
zur Kenntniss seltener Herzanomalien in Anschluss an einem Fall von
angeborner linksseitiger Conusstenose."]

{708} Among the many cases of malformation of the heart which he
presents there are reports of 15 cases of stenosis of the conus, which
are to be divided into two categories, in accordance with his
classification. In the first group, in 7 cases the stenosis is due to
an inflammatory process, and is conditioned by the results of the
endo-myocarditis localized in the aortic conus. These cases must have
originated at a late period of foetal life, and they correspond closely
to the conditions arising in the adult organs from similar processes.
In all the specimens the mitral orifice was involved, and contributed a
share in the production of the conus stenosis; in all the cases the
aortic valves also had suffered inflammatory changes. Here Dilg also
speaks of a band-like hypertrophy of muscular fibres, marking the
outlines of the aortic conus, similar to the condition described by
Peacock in the right ventricle; in this condition there was no evidence
of endocarditis, and the condition may have been due to cadaveric
rigidity. The left ventricle presented varying conditions according to
the state of the aortic and mitral valves; in some cases there was
concentric hypertrophy, or, more strictly speaking, narrowing or
shrivelling of the cavity with hypertrophied walls; in others
dilatation existed. The other cavities of the heart were influenced by
the competency of the mitral orifice, but almost always showed
considerable hypertrophy and dilatation. The valvular apparatus of the
right heart was not free from evidences of old inflammation, but this
condition was not very marked. The ages of the reported cases reached
from thirty to seventy-five years.

In the second group there are eight cases in which the defective
condition of the aortic conus caused malformation of other parts of the
heart. Here the conus stenosis occurred at an early period of foetal
development, before the permanent structures of the heart were fully
formed. The conus stenosis is to be considered as primary, the other
defects as secondary. As we have already seen, the left side of the
heart is much less liable to deforming causes, and when such do occur
the secondary defects are less conspicuous. Thus, in only four of these
cases were there such malformations of other parts of the heart as
openings in the septa of the ventricles or auricles, patency of the
ductus arteriosus Botalli. The defects consist more usually in what
were formerly called excesses of development, such as the formation of
bands below the aortic orifice; or of deficiencies of development, such
as only two aortic valves. These conditions are very doubtfully due to
formative excesses or deficiencies, but rather to intense inflammatory
processes or other morbid conditions which have resulted in the
formation of excessive cicatrices or the removal of normal parts.

Another division of cases shows narrowing of the aortic trunk itself.
This condition is probably always a true defect of development; so far
as these cases, collected by Dilg, show, it is unquestionably so. In
narrowing or closure of the pulmonary artery trunk it is found that in
some instances this condition was dependent on an endarteritis
resulting in a partial occlusion of the lumen of the vessel; here,
however, the aortic trunk furnishes no evidences of such a process. It
must therefore be due to an unequal division of the truncus arteriosus
communis. The cause and the mechanism of this unequal division of the
common trunk, resulting in a reduction of the size of the aorta, are
probably similar to what Rokitansky indicated for the reduction in the
size of the pulmonary artery trunk.

In the specimens of aortic narrowing (no cases of complete closure are
reported) from this cause and mechanism the pulmonary artery has been
found unusually wide, but this condition of the pulmonary trunk is not
very conspicuous, and does not necessarily result from the narrowed
state of the aorta. The compensatory or secondary defect of open septum
ventriculorum, or even of the auricular septum, is, in these cases,
neither invariable nor necessary to a proper maintenance of the foetal
or adult circulation. In fact, {709} the open ventricular septum is
rare; the condition of the auricular septum is, in the reports, often
not stated. The left ventricular walls commonly show a preponderance of
hypertrophy over dilatation of this cavity, but in some cases the
distension of the cavity is marked.

       *       *       *       *       *

SYMPTOMS.--The most striking symptom which occurs in malformation of
the heart is the cyanosis, but the appearance of this peculiar symptom
may be postponed until some time, even a long period, after birth. In
the newly-born infant presenting a blue color the diagnosis rests
between the not infrequent temporary failure of respiration from many
causes and a defective development of the circulatory organs. In most
cases the doubt is promptly solved by the voluntary or artificial
efforts of breathing, whereby the cyanosis disappears. If the dark hue
persists after the respiratory movements have been developed, the
cyanosis may be found to depend either on cardiac malformation or an
imperfect expansion of the lungs (atelectasis). The distinction between
these two conditions can usually be made by a study of the respiratory
movements, by the state of the heart's action and of the pulse, aided
sometimes by an inspection of the outlines of the chest. In cardiac
malformation respiration seems to be well performed and full, though
often hurried or labored; in atelectasis this function is often found
characteristically altered by being short, high, and imperfect, with
imperfect distension; the ribs, instead of moving upward and outward,
fall toward the median line, and the chest fails to expand
transversely. In malformation the heart's action and the pulse are
rapid, and a murmur can often be heard. The thoracic outline may
deviate from the usual antero-posterior flattening by the sternum being
prominent in cases where the heart, instead of its usual position to
the left, is placed more centrally, as comes in certain defects of
development. Both of these conditions may be present, and then the
symptoms are mixed in character.

Cases of atelectasis, sufficiently marked to give rise to persistent
cyanosis, if not relieved too frequently show a pretty rapid increase
of color, becoming deeply livid, with convulsive movement, ending
shortly in death. The diagnosis in such cases between a cardiac
malformation and a non-expanded lung is almost impossible unless the
respiration shows characteristic features. It is probable that the
treatment proper for the latter would aggravate the condition of the
circulation in malformation. In a majority of cases a post-mortem
examination is necessary to determine whether the cyanosis is of
cardiac or of pulmonary origin. In the atelectatic condition, if death
comes within a few days of birth, the ductus arteriosus Botalli and the
foramen ovale may both be found open, especially the latter, their time
of normal closure not having arrived; in cases dying at a later period,
if the foetal openings are still found patulous, the open state must be
considered as dependent on the condition of the lung-tissue, since in
malformation of the heart the patulous state of these foetal openings
is, as has already been shown, rare as a primary defect, and, except in
connection with defects of development resulting in obstruction, which
operate at other points of the foetal circulation, is almost never
found. In other words, an open foramen or ductus is a secondary defect,
dependent, on the one hand, on a primary obstruction of the cardiac
ostia, or, on the other hand, it may be on a primary atelectasis or
malformation of the lungs.

If the child passes beyond the first weeks of life without exhibiting
cyanosis, the subsequent occurrence of the condition becomes almost a
pathognomonic symptom of cardiac or vascular malformation, unless it
can be shown that the coloration is dependent on some acute disease,
especially acquired valvular disease: in this connection collapse of
the lung (post-natal atelectasis), too, must be remembered.

{710} It is during the first week of life that cyanosis makes its
appearance in the great majority of cases of malformation of the heart,
in the proportion of more than two to one of the cases. The coloration,
once developed, may remain permanent and of equal intensity until
death, but as less than 8 per cent. of infants with malformation die
within the first week, and only 36 per cent. within the first year,
this symptom usually remits. It may wholly disappear, to return on very
slight provocation, such as excitement, or on exertion, on the advent
of acute disease, or without apparent cause. Probably about one-fourth
of those who die in infancy perish in paroxysms of dyspnoea, another
quarter of acute disease, and the remaining half of convulsions; and
toward death the cyanosis generally becomes very intense.

If the malformation is not of character or degree to develop cyanosis
early in life, the child grows and passes through the usual stage of
development, usually, however, feeble, poorly nourished, incapable of
common exertion, but often without any special phenomena to attract
attention, and the vice of formation is undetected unless by a special
examination. There are several other symptoms frequently present in
connection with malformation, but not of a pathognomonic character.
Dyspnoea, though rarely occurring without cyanosis, may attract
attention, and, if frequently brought on by active exercise, increases
in violence, to be later accompanied with the cyanosis originally
absent. Palpitation is not uncommon, especially in cases of great
hypertrophy with dilatation, in hearts struggling to overcome an
obstruction; in other cases it is absent or only occurs on exertion in
connection with dyspnoea and cyanosis. The degree of animal heat varies
greatly, judging by the various opinions expressed by writers. The
sensation of patients able to express their feeling is often that of
chilliness, and in some cases the surfaces of the body feel cold,
although the indications of the thermometer show no great variation
from the normal temperature. It is obvious that no very great variation
from this standard is compatible with the long duration of life,
although a depression may exist during or immediately after paroxysms
of dyspnoea or cyanosis. Cough is also frequent, but is probably always
due to some acquired pulmonary disease.

The physical signs offer increased facilities for the recognition of
defects of development. In the early reported cases there are of course
no records of these conditions, and there is therefore a lessened
number of instances from which to collate the physical signs. In the
early days of life it has been shown wherein the presence of a cardiac
murmur may lead to the distinction between malformation and
atelectasis. In later periods of life the physical signs cannot be
regarded as characteristic. There are no signs by which a malformation
can be distinguished accurately from an acquired cardiac disease, so
that without the clinical history and a grouping of symptoms the
diagnosis cannot be made from the physical examination.

Inspection and palpation of the chest often show the heart to be in an
unusual position, placed more centrally under the sternum. It must be
remembered that transposition of the heart to the right side is not
unfrequently unaccompanied with any malformation of its ostia giving
rise to symptoms; and this organ may be even more markedly displaced
without being malformed, although under both these conditions
irregularities of the principal trunks are usually found.

Percussion frequently shows enlargement of the area of cardiac dulness,
but, on the other hand, at the post-mortem examination the heart is
often found markedly defective without externally showing variation of
its size or shape, or of its position within the thorax; hence in such
cases no deviation from the normal will be revealed on percussion or
inspection of the chest. It is probable that cardiac murmurs are not
always to be detected in cases of even marked defects of development,
but when present it is recorded most {711} frequently that a single
murmur is heard over the base of the heart, blowing in character and
systolic in time. Such a sound is probably produced by the passage of
the blood through an abnormal opening between the ventricles or through
the foramen ovale. Other murmurs may also be present; if the arterial
ostia are defective from narrowing, roughness, or insufficiency of
their valvular apparatus, abnormal sounds of different characters,
diastolic or systolic in time, may be heard. Too few observations as
yet exist for a general diagnostic scheme to be formulated.
Auscultation of the intra-uterine heart may in the future become
sufficiently accurate to enable us to prognosticate a congenital
cardiac malformation or disease; there is one case on record in which a
correct diagnosis was made in this way.

The ends of the fingers and toes are frequently described as bulbous.
This rounding and retraction of the nails, frequently spoken of as
clubbing, does undoubtedly exist in many cases, but the condition
cannot be regarded as characteristic of malformation of the heart,
since it comes with even more frequency in tubercular disease of the
lungs, in chronic pleurisy, and in other chronic pulmonary maladies.

Lebert has recently insisted on the connection between stenosis of the
pulmonary artery and tuberculosis, not merely as a coincidence, but as
the cause of the development of the tubercles in the lungs. Many others
have spoken of this connection, and very many are the cases
recorded--perhaps nearly one-quarter of the whole number. In some cases
large or small single cheesy masses exist; in others cavities form, and
in rare cases a miliary tuberculosis exists, still more rarely
affecting other organs than the lungs. In view of the recent dogmas of
tuberculosis it is doubtful if many of these authors would at present
insist on the connection between malformation of the heart and
tuberculosis being other than a coincidence, since it is not apparent
why such patients are more likely to be invaded by a bacillus of
tuberculosis than other persons, and this organism is known to grow so
readily wherever the spores chance to fall.

       *       *       *       *       *

DURATION OF LIFE.--In connection with certain malformations some
indications have already been given in respect to the duration of life
in such defects. It is, however, apparent that the degree of the
obstruction to an orifice or vessel, and still more the completeness of
the secondary compensatory alterations, exert a greater influence than
the seat of the malformation on the continuance of life. The occasional
slight isolated malformations, such as open septa without obstruction
of the orifices, in themselves often entail no symptoms, and, unless
combined with acquired valvular disease, exercise no influence on the
duration of life; here, however, the prognosis merges entirely into the
acquired malady.

Of the other conditions of malformation, narrowing of the aorta and of
the aortic conus seems to be, on the whole, compatible with a longer
duration of life than any other condition, and these defects cause
death in the early days or months in fewer cases than similar
obstructions on the right side of the heart. This result apparently
comes from the fact that the left ventricle seems to possess unlimited
capacity for hypertrophy, and hence is able to overcome the
obstruction; when the aortic valves allow of regurgitation the
compensation fails and death comes sooner. When the main branches of
the aorta are defective or when the descending aorta is derived from
the pulmonary artery, the duration of life is much shortened.

In cases of pulmonary narrowing in general it may be stated that the
greater the obstruction the shorter the life. This rule is subject to
many exceptions; so frequent are the exceptions that the rule is almost
valueless for determining the life in any given case. Complete closure
of the pulmonary trunk has permitted of the continuance of life for
sixteen years, {712} and then ended from an intercurrent acute disease.
When the septa are maintained open--when, therefore, the communications
between the pulmonic and systemic sides of the heart are free--a
greater age is attained than when these openings have become closed.
This condition of the pulmonary artery in order to permit of a long
duration of life must be coincident with a considerable development of
the collateral circulation by which the blood freely enters the lungs
for aëration; otherwise the compensation fails very soon.

In transposition of the main trunk relatively to the ventricles, with
closure of the septum ventriculorum (very rare), life ends not many
weeks after birth; if the septa remain open, which is not common, life
may be prolonged for a year or two.


Cyanosis.

There are two views to be found, set in opposition to each other, to
account for the peculiar blue coloration of the skin and mucous
membranes in cases of malformation of the heart. The first explanation
attributes the phenomenon to a general congestion of the venous system,
due to the obstruction of the pulmonary artery. This view was proposed
by Morgagni in connection with his, the first described, case of
malformation of the heart. The other view considers that the
intermingling of venous and arterial blood through any channel, but
especially by means of abnormal openings in the septa, produces the
blue coloration. Numerous writers have defended each of these theories
of causation; from most of their observations darkness rather than
light has resulted through the attempt to defend one or the other
theory exclusively.

Gintrac defended the admixture theory for cyanosis, and his views
became so well known that a large majority of persons conformed their
belief to his teachings. This author distinguished four varieties of
blue coloration: first, that due to some malformation of the heart or
great vessels, by which the blood of the right side of the heart enters
the systemic arterial circulation; second, likewise due to intermixture
of the blood, but produced by conditions developed after birth through
the re-establishment of the passages of communication or other changes
in the circulation; third, where the coloration appears without direct
admixture of the blood, but from organic disease of the heart; fourth,
cases without malformation, from a suppression of the menses. Before
the time of Gintrac, cyanosis had a very indefinite signification, and
the condition was looked upon, and was classed by very many, as one of
the cachexiæ, and was often spoken of as a form of icterus. He,
however, held that the organic lesions of the heart and great vessels
were the necessary conditions of its production, and that the mixture
of the red and black blood, and the distribution of the mixed fluid by
means of the arteries to all parts of the body, determined its
essential character. He showed, too, that all communications between
the right and left heart were not followed by cyanosis; the explanation
of the absence of the blue color was that from the simultaneous
contraction of the auricles and ventricles of the two sides of the
heart an equilibrium was produced, and the blood did not deviate from
its normal course. This result followed only when the normal exits of
the blood were unobstructed. This supposition, as is apparent, is not
in accord with the facts. During the filling of the ventricles, before
the muscular contraction of the walls occurs, the blood has the
opportunity of freely mingling if the opening between the cavities is
sufficiently large: that the blood will not thus mingle when the
muscular contraction acts remains to be proved. Cases of open septum
ventriculorum, as an isolated defect, without obstruction of the great
vascular trunks (a rare condition), are not attended with cyanosis: the
absence of this symptom, as will be shown later, is readily to {713} be
explained on other grounds than those supposed by Gintrac. The normal
outlets of the blood are, however, almost always obstructed to a
greater or less degree; and here the explanation of the absence of the
cyanosis fails. In the delayed appearance of cyanosis Gintrac
considered the reason to be that the venous blood differed less from
the arterial in the young subject than in those of more advanced age,
because, on the one hand, the aëration was more active, and, on the
other hand, the deterioration of arterial blood was less marked. In
other cases he points to an increase of the obstruction, through
inflammatory changes, as the probable reason for the delayed appearance
of the blue color; in still other cases it was supposed to be due to a
disturbance of the equilibrium of the pulmonary and systemic
circulation from an increase in the blood-mass. In cases of unilocular
and bilocular hearts, of which the author speaks, his explanation
completely fails, for here the admixture of the blood within the heart
is very marked; yet such cases have been reported without cyanosis. He
further believed that openings in the ventricular septum, as well as
between the auricles, were effected after birth as the results of
acquired cardiac disease.

Gintrac, in speaking of the causes of cyanosis, says that the condition
shows no hereditary tendency; that the pregnancy during which the
defective infant is developed is without noticeable phenomena; and that
the confinement is normal. It is on some of these points that we are in
want of accurate information. It has been pointed out that many
congenital defects of the heart result from morbid processes affecting
the organ during its developmental stage. These lesions are the same in
kind as those which produce cardiac and vascular disease in the adult,
and are likewise of a sort capable of communication from the parent to
the foetus. Such diseases are found acting oftentimes temporarily in
the parent; and if they acted during pregnancy, or even if present only
at the time of conception, their results would rationally be expected
to be displayed in the foetus. Such diseases as rheumatism and
syphilis, which may be regarded as temporarily-acting maladies, would
come under this class, and doubtless many others might be added to the
list. The work of collecting the histories of pregnancies or the
condition of the parents at or before the time of conception would be
painfully tedious: such records do not exist at present, and they could
be made sufficiently full only in exceptional cases; but their value in
determining the causes which operate in the production of defective
development of the heart cannot be too highly estimated.

The conclusions stated by Moreton Stillé[9] seem to be the first which
justly cover the ground from a comparison of large numbers of cases of
malformation of the heart. The first conclusion by him is that cyanosis
may exist without admixture of the blood; by this was meant that no
abnormal communication between the right and left sides of the heart,
and no channels between the principal vascular trunks, are present. He
mentions five cases of cyanosis occurring in which no means of
admixture existed. The second conclusion is that there exists no
proportion between cyanosis and the degree in which the blood is mixed;
for this he cites four cases, some with the aorta arising from the
right ventricle, others of hearts with only two cavities and the common
trunk undivided, in which the cyanosis was only partial or transient.
The third conclusion, the converse of the first, and reinforcing the
preceding one, is that complete admixture of the blood may take place
without cyanosis. The fourth, that the variation in the extent, depth,
and duration of the discoloration is inexplicable by the doctrine of
the mixture of the blood.

[Footnote 9: "Inaug. Thesis." _Amer. Journ. Med. Sci._, N. S., vol.
viii., 1844.]

Having shown that commingling of arterial and venous blood cannot be
the cause in itself of cyanosis, Stillé proceeds to the study of the
other {714} theory--viz. that it is due to congestion of the general
venous system resulting from some obstruction in the right side of the
heart or in the pulmonary artery, impeding the passage of the blood
through the heart. These structural lesions must fulfil the three
following indications: 1st, that they shall be sufficient in degree to
account for the symptom; 2d, that they be present in every case of
cyanosis, or in their place some other cause acting on similar
principles; 3d, that they shall never exist without cyanosis or without
a satisfactory explanation of the exceptional occurrence. He holds that
contraction of the pulmonary artery is to be taken as the type of all
the lesions that may produce cyanosis, and that this type fulfils the
indications given above.

Most writers since Stillé have coincided with him, or have regarded
cyanosis as partly due to venous congestion and partly to commingling
of arterial and venous blood. Some writers, however, have pointed to
the abnormal communications between the right and left side of the
heart, and asked why, if admixture of the venous and arterial blood is
not the cause of cyanosis, should the admixture through such openings
be found in such a large proportion of cases. Such writers have failed
to distinguish between the primary and secondary defects of
development. They have failed to see that the pulmonary obstruction
which prevents the blood during extra-uterine life from passing to the
lungs for aëration, and consequently produced the cyanosis, prevented
the closure of the ventricular septum during intra-uterine life, or of
the auricular septum within a few days of birth. In reply to the above
question it may be pointed out, as Peacock has done, that such
communications between the two sides of the heart are all important for
the continuance of life, even for the shortest period, when the
pulmonary artery is occluded.

It is evident, as Peacock has shown, that if Stillé's first and third
conclusions are true, as the cases undoubtedly show, the theory of
intermixture of the blood does not account for the condition of
cyanosis. It is probable in many of these cases with abnormal openings
in the septa that the intermixture of the blood is but slight, since if
the pressure on the two sides of the heart is equal--and it may become
equal through the establishment of a collateral circulation, although
primarily it was unequal--no intermixture takes place through the
defective septa. Neither does the admixture theory account for cases of
intermittent or delayed cyanosis. Such cases can only be supposed to be
due to a varying propulsive power or to a subsequent increase of the
pulmonary obstruction. Neither does admixture account for localized
cyanosis; for example, in the face or in one extremity: this condition,
rare as it is, must be due to other causes. Peacock, while combating
the admixture theory, considers that Stillé's conclusions in favor of
the congestion theory as dependent on obstruction of the pulmonary
artery are too exclusive. He discusses also the relationship of
congenital cyanosis due to malformation, to cyanosis acquired through
pulmonary and cardiac disease as seen in the adult, and shows why the
latter condition is rarely ever as intense as the former, and also why
acquired obstruction of the pulmonary artery is not necessarily
productive of cyanosis. The reason of the difference he believes
consists in the compensatory hypertrophy of the right ventricle, with
perhaps a gradual diminution of the blood-mass, as seen in some cases.

On the whole, Peacock subscribes to the congestive theory, but thinks
that the intensity of the cyanosis is modified by the capacity of the
capillaries, by the period of development or duration of the
obstruction, by the natural coloration of the skin, and by the color of
the blood itself.

Under these two theories, and the arguments offered in support of them,
there seems to be no other explanation possible of the condition of
blueness, and yet the whole story of the mechanism of cyanosis does not
seem clear. Partly, this is due to the incomplete knowledge of the
physiology of the aëration of the blood which obtained during the most
active period of the {715} discussion of cyanosis and its causation.
Let us consider briefly the simplest case of cyanosis. Every child born
has in one sense a temporary malformation of the heart--an open foramen
ovale which does not close for several days after birth. Every child is
born partially cyanotic, owing to compression of the uterine sinuses or
pressure on the umbilical cord; it is completely cyanotic if there
occurs premature separation of the placenta. The cyanosis continues
until the child breathes. The cause of this cyanosis must be looked
for, not in the temporary malformation, but in the imperfect expansion
of the lungs. As soon as the respiratory function is assumed--as soon
as, in other words, the pulmonary-artery branches carry a full amount
of blood which becomes aërated in the lungs--the cyanosis ceases,
although the foramen ovale is not yet closed.

The closure of the foramen by a trapdoor valve is, as has already been
pointed out, not in accordance with the anatomical facts: turning the
newly-born infant on its right side does not favor, as it is commonly
supposed, the closure by gravity of a preformed swinging lid, which
when it has dropped down for ever partitions the right from the left
auricle. The right-sided position may favor the expansion of lungs or
in other ways promote the pulmonary circulation, but in itself it does
not tend to close the foramen. In fact, cyanosis does not here depend
on the defective development, but on want of aëration of the blood.

Again, looking to the skin or mucous membrane, what is the condition of
the blood and of the circulation which renders the parts of a blue
color, and in what do they differ from the normal? In the normal state
of the blood and circulation the capillaries of a given area are
filled, one half with arterial blood, and the other half with venous
blood; that is to say, the capillaries at the point of their origin
from the arterioles contain pure arterial blood: as the blood-current
proceeds outward the blood becomes progressively less and less red and
more and more blue or black; when the venous radicle is reached the
blood-current is of as dark a hue as it ever becomes. In general terms,
therefore, it may be said, taking the average, that in a given area
half the blood is venous, half arterial. Here, then, we see, with an
equal mixture of the red and blue blood, nothing resembling cyanosis.
It is evident, therefore, that to produce a cyanotic hue the blood must
be wholly venous; the intensity of the blueness will vary with the
amount of non-aërated blood present in the capillaries. But let us
suppose an equal admixture of right- and left-sided blood to take
place--for example, when the aorta arises from both ventricles, the
pulmonary artery obstructed. It cannot be supposed that the venous
blood would retain its dark hue. The contact of the two bloods within
the aorta on their way to the capillaries would result in arterializing
the venous blood at least one-half, so that when it arrives at the
capillary network the intensely blue color of a marked case of cyanosis
would have disappeared.

Besides this, there are other considerations to be taken into account
to show that neither of the two exclusive theories accounts for the
state of the blood and of the circulation in cyanosis. If the condition
of the cyanotic parts, due to acquired valvular heart disease or
various morbid states of the pulmonary tissue of an acute character be
compared with the same parts in cyanosis from malformation of the
heart, striking differences are discernible. If the simple condition of
cyanosis of the part due to localized pressure on the veins be
examined, the differences are even more perceptible. In the
malformation there is an admixture of blood; in the other condition
there is no opportunity for the intermingling of the currents. In the
latter the cyanotic area becomes swollen, and the intensity of the
color may become lessened through the oedematous condition; in the
former the skin of the cyanotic infant rarely if ever presents any
swelling; the veins of the part show little, {716} if any distension,
as is so frequent in the latter; cases of malformation in which
subsequent endocarditis with additional obstruction occurs may show
oedema and swelling similar to cases of acquired valvular disease. In
these cases of cyanosis the condition must be due to a want of aëration
of the blood, since it never appears until such alterations of the
pulmonary tissue and circulation are reached as to render it certain
that the blue coloration is due to a want of aëration of the blood.
Fulness of the veins and oedema may be present, but never general
cyanosis.

Another important consideration in the production of cyanosis does not
seem to have been fully appreciated. It is the fact that in all cases
of obstruction of the pulmonary artery the collateral circulation,
carried on by very varying channels, the bronchial arteries, the
oesophageals, the coronaries in some cases, the internal mammaries and
intercostal arteries in rare cases, or by the ductus arteriosus
Botalli, which alone must be always inadequate in marked narrowing of
the pulmonary trunk,--the collateral circulation must always remain
insufficient for carrying sufficient blood to the lungs for aëration.
Kussmaul was the first to call particular attention to this fact; and
it is to this condition of insufficient channels for the blood reaching
the lungs that certain cases of cyanosis must owe their causation.

Hence it must be that, in all the complex conditions found in cases of
cyanosis from defective development of the heart, a want of due
arterialization or aëration of the blood is at the foundation of the
state as seen in the cyanotic area. Whether it results in a given case
from excessive admixture of venous blood with the arterial when the
current reaches the capillaries, or from venous stasis due to central
obstruction, of which pulmonary-artery narrowing or closure is the
type, or whether from a failure of sufficient blood to reach the lung,
as where the collateral circulation remains imperfect, or as seen in
certain cases of defective development of the lungs, is most difficult
to ascertain. That sufficient consideration has not been given to the
third possible factor in the causation of cyanosis--viz. failure of the
blood to reach the lung, as distinguished from general venous
congestion alone--is evident. That intermingling of the blood from the
two sides of the heart must inevitably reduce the red color is
certain--that in very many cases the reduction in color does not cause
cyanosis can be readily understood from the consideration already
offered. The cases of free admixture in which cyanosis does occur may
coincide with a condition of very imperfect collateral circulation to
the lungs, and hence with a low aëration of blood of the left
ventricle, insufficient, therefore, to bring up the color of the blood
from the right side of the heart above the cyanotic point.

Whether non-aëration of the blood from failure to reach the lungs,
apart from general venous congestion, is a sufficient explanation of
the cyanosis in a large majority of cases or in the whole number, is
not apparent from the records of reported cases. Much more accurate
post-mortem accounts, made with a view to determine the question, than
at present exist will be required. In a number of well-reported cases
of defective pulmonary artery with a free admixture of blood the
pulmonary collateral circulation is found to be well developed, and no
cyanosis had appeared, or had been but trifling and inconstant. In
other cases of quite as marked pulmonary obstruction with but slight
commingling of the blood through abnormal apertures and but
slightly-developed collateral circulation, cyanosis has been found
intense and constant. In the two conditions the possibilities for
general venous congestion are about the same, though perhaps not equal,
while the striking difference, apart from the admixture of the
blood-current, consists in the conveniences for the aëration of the
blood.

The only variety of malformation of the heart in which intense and
constant cyanosis must inevitably be present is that very rare form of
{717} transposition of the great trunks, the aorta springing from the
right ventricle, the pulmonary artery from the left, with closure of
the septum ventriculorum; the pulmonary veins enter the left auricle
bearing red blood, and the venæ cavæ the right auricle with blue blood;
if the ventricular septum is closed, the aorta necessarily carries blue
blood to the systemic circulation, and the pulmonary artery is filled
with red, carrying it back to the lungs, whence the fluid has just
come. In such relation of the principal trunks, even if the ductus
arteriosus Botalli and the foramen ovale remain open, cyanosis is
necessarily present. The bulk of the blood in the aorta is blue: the
only points in which it comes in contact with red blood are, first, at
the foramen ovale: here the intermingling is not sufficient to bring it
above the cyanotic color; and, secondly, at the ductus arteriosus, and
here the tube is not favorably directed for a copious intermingling of
the two bloods, neither can it probably ever be sufficient in itself
for this purpose. Hence the aortic blood is almost wholly venous. If
these two foetal openings did not persist life could not continue
beyond a few hours, or even a few minutes, after birth. In such a case
the cyanosis does not depend on general venous congestion, and
specimens are reported of this sort in which the great vascular trunks
were without obstruction, life having been maintained for a few months;
adult existence is probably impossible. If, however, with such
transposition of the vessels to the improper ventricle, the septum
ventriculorum remains widely open, cyanosis may be absent or
inconstant, because, apparently, admixture of the blood and also
aëration are sufficiently free. But in cases of transposition of the
vessels, or even in the much more frequent specimens without
transposition, when the track to the lungs is defective either from
want of a collateral pulmonary circulation or directly from impervious
pulmonary artery, cyanosis becomes more intense and more constant or
comes in more frequent paroxysms, irrespective of the presence or
absence of evidences of general venous congestion.

It would seem to result from this grouping of facts, and looking at
them from a reverse bearing to Moreton Stillé's point of view, that
distal rather than proximal obstruction of the pulmonary artery, taken
as a type, was the cause of cyanosis. Admixture of arterial and venous
blood must reduce the redness of the arterial stream, just as certainly
as red paint mixed with black varnish will render the black less
intense: whether admixture alone ever produces a deep cyanotic hue of
the surfaces is probably more than doubtful; that admixture will
prevent constant cyanosis seems certain, when cases of complete
transposition of the vessels with open septum ventriculorum are
compared with those with closed septum, the other conditions remaining
the same. General venous congestion from pulmonary obstruction or other
causes outside the pulmonary tissue produces cyanosis, but of a sort
quite unlike the typical cyanotic condition of malformation of the
heart. It may therefore be doubted if the cyanosis seen in obstruction
of the pulmonary artery is due to general venous congestion; it may be
wholly produced by conditions on the other side of the
obstruction--viz. want of aëration of the blood, which must ever remain
the essential feature of cyanosis. This supposition allows of an easy
explanation of the difference between cases of apparently equal
obstruction of the artery, in some of which cyanosis is present and in
others absent; it also allows of the explanation of inconstant or
paroxysmal cyanosis where the obstruction, and consequently the venous
congestion, is uniform and permanent.




{718}

CARDIAC THROMBOSIS.

BY BEVERLEY ROBINSON, M.D.


DEFINITION.--In general, this name is given to every deposit of
coagulated blood or fibrin in one or more of the cardiac cavities. By
its derivation ([Greek: thrombôsis], coagulation, from [Greek:
thrombys], clot) it further implies the manner in which the coagulum is
formed and all the morbid alterations connected with it.

SYNONYMS.--Heart-clot. _Fr._ Thrombose cardiaque; _Ger._
Blutgerinnungen im herzen; _Lat._ Thrombosis cordis; _It._ Trombo;
_Sp._ Trumbo.

The definition offered is not wholly satisfactory, because, although it
is accurate as far as it goes, it is not complete. It does not
distinguish between concretions of different origin, etiology, mode of
formation, and age. No separation is made between fibrinous deposits
which increase from the beginning and layer by layer in the cavities of
the heart, and those transported there from a distance and forming a
nucleus for fresh deposits. To make the definition anything like
exhaustive would require many references to the general history of
THROMBOSIS AND EMBOLISM; we therefore direct our readers to that
article for what relates to the common facts of these morbid processes,
retaining for the present only those matters which relate specially to
the heart.

Heart-clots may be formed--1, during life, when the patient enjoys,
apparently, good health and strength; 2, toward the termination of
life, when the general forces are evidently depressed, or at the final
stage, when life ebbs low and the agony has appeared; 3, after death.
These clots have therefore been divided into cadaveric clots, those of
the agony, and ancient clots. To the clots of the agony exception is
properly taken, for the reason that agony is a term employed with a
somewhat badly-defined signification. At what period does it begin? Is
it not frequently of different length? Does it always exist? The
answers to these different questions render our objection proper, and
show that we had better employ the word terminal for coagula of the
second division.

Manifestly, the separate varieties of coagula have not an equal
importance. The clots which are post-mortem productions are only
interesting for their physical characters, which, fortunately, are well
marked, and enable us at once to distinguish them from the two other
varieties. The coagula in the first two divisions have an interest both
clinical and pathological.

The ancient clots are invariably accompanied with signs and symptoms
which should reveal their presence. As much might be affirmed for the
terminal clots in the majority of instances and when the patient is not
already in extremis. The pathological study of these varieties has
great value, and especially in so far as it will the better enable us
to distinguish the clots formed some time previous to death--be it of
shorter or longer duration--from those which are but the result of the
gradual stagnation of the blood-current in a weakened and wellnigh
powerless organ. Amongst the clots which are formed in the venous
system, some are transported, and pass {719} immediately through the
heart, to be arrested finally in some of the larger or smaller arterial
trunks, whilst others remain in situ in the heart, and are constantly
increased by successive additions or layers of new fibrin or cruor.

The nomenclature to be desired is one which would assign different
distinguishing names to each variety of coagulum, so that at once its
origin, mode of formation, and perhaps too its age, should be exactly
determined. The ancients employed the term polyp for deposits of every
description in the heart, but such use of the word was, generally
speaking, erroneous, since the true polyp is a very rare disease of the
cardiac cavities. Bartholetti and Pissini first made use of it, and
considered without doubt that the false polyps or fibrinous deposits in
the heart were of analogous nature with the true polypi which are found
so frequently in the uterus and nasal cavities. No doubt (as has been
inferred) the term polyp in regard to these formations came into
habitual use owing to lack of familiarity on the part of the older
writers with the varied aspects of clots, as well as their ignorance of
the distinct appearance offered by sections from them under lenses of
great power. This mistake, therefore, is to-day not to be wondered at,
if we duly consider how imperfect and unusual in olden times were
pathological researches. Heart-clot was, as will be seen in the
historical sketch which follows, the subject of numerous prolonged and
animated discussions. As a result of these latter, it was ultimately
believed that the great differences of appearance and formation which
exist between coagula depend in great measure upon their relative age,
and it is for this reason that the basis of distinction between their
varieties rests mainly upon the period of time previous to a death at
which they are formed. When we speak, however, of polypiform concretion
or deposit, we approximate nearer the truth and indicate in a measure
the local origin of a coagulum. Many others have employed the terms
post-mortem and ante-mortem as being the only suitable terms with which
to make a distinction between the coagula formed during active
existence and those which are revealed only with the scalpel in the
dead-house. In the consideration of this subject the symptoms shall be
fully described which indicate the presence of heart-clot found during
life, whilst in regard to clots formed in extremis or after death it is
desirable particularly to show the pathological characters which shall
definitely place them. For all that pertains to embolism of the heart
we shall refer the reader, except when it is essential to mention
certain details, to other articles in this work. Certain authors have
erroneously, it is believed, regarded this subject of heart-clot as one
of mere pathological interest, stating that the dead-house is the only
place to study its origin and many of its organic effects. This opinion
should be combated with vigor. Such a view is far too restricted, and
it is here believed that the clinical aspects of cardiac thrombosis are
worthy of attentive study, and that something better and further should
be attained than merely to watch the downward course of a patient thus
affected, and to bear in mind the pathological sequelæ of this disease.

HISTORICAL SKETCH.--The questions which have a present interest in
regard to heart-clot are very different from those which formerly
engaged medical attention. No longer are we uncertain as to the
formation of these coagula during life, nor doubtful as to the various
and important effects produced by their transport in different organs
through the arterial and venous vessels. Thanks especially to the
inaugural thesis of Legroux (1827), to those of Le Marchand and Ball
(1862), to that of Bucquoy (1863), but particularly to the experimental
researches of Virchow (1846-56) and to the observations of Senhouse
Kirkes[1] in regard to the formation and transport of emboli into the
cerebral vessels, these facts are all matters of ordinary information.
There is little doubt that Galen had noted the formation of {720}
intra-cardiac thrombi during life, and attributed to them interference
with circulation and respiration, and, at times, sudden death. With the
exception of Salius, mentioned by Morgagni as having remarked oedema
due to this cause, we reach the sixteenth century before again meeting
with any detailed mention of a similar pathological condition. Helidé
of Padua, according to some,[2] Benivenius, according to others,[3]
were the first authors to give full descriptions of cardiac polyps.
This, indeed, was the term affixed for a long period to fibrinous
concretions in the heart, beginning with Sebastian Pissini (Milan,
1654), who first employed it. The name took origin, without doubt, on
account of their resemblance to polyps of the nasal fossæ, and perhaps
to the animal thus named. It was particularly at this period that they
acquired their significance, and became the subject of animated
discussions between distinguished physicians of the last two centuries.
Some, exaggerating their importance, attributed to them the gravest and
most important symptoms, although a chronic affection of the heart or
lungs present at the time was frequently sufficient to explain them;
others, like Kerkring (1670) and Jos. Pasta[4] (1737), who contested
the possibility of the blood coagulating during life, and believed they
were invariably cadaveric formations, took from them even a
pathological interest. This latter extreme opposition to reality
originated very soon a mixed conviction, which was that held by Senac
and Morgagni. These distinguished observers recognized that
intra-cardiac thrombi formed both during life and after death, the
former being rarely encountered. The later, or anatomical school,
confirmed these views, but also added testimony to show that ancient
and terminal concretions were not phenomena of such unusual occurrence
as had been previously held. Testa (1810) and Kreyssig (1824) connected
fibrinous deposits with inflammation of the heart, and the last-named
writer described a disease which he named carditis polyposa. This view
and that of Laennec, which attributed globular vegetations to an
inflammatory cause, are in our day disproved. Amongst those authors who
rendered certain the formation of cardiac clots during life, we should
mention a few others whose names have a special importance in this
connection as having made a special study of diseases of the central
organ of circulation. These are Corvisart, Burns, Andral, and
Bouillaud. Since this period the field of research has become far less
limited, and investigations have been made in regard to similar
coagulations in the large vessels of the body.

[Footnote 1: _Med.-Chir. Trans._, 1844, pp. 281-325.]

[Footnote 2: _Dict. de Méd. pratique_, vol. viii. p. 558.]

[Footnote 3: _Ziemssen's Cyclopædia_, vol. vi. p. 292.]

[Footnote 4: Quoted by Grisolle, _Pathologie interne_, Paris, 1865, p.
464.]

In 1856 a new era was established in regard to these formations, and
especially with reference to their transport. Virchow at this period
showed conclusively, after long-continued and accurate clinical
observations and experimental researches, that a clot formed on the one
hand in one of the large veins might be carried to the pulmonary artery
and block up more or less completely the supply of blood to the lungs;
on the other, that a portion of a thrombus formed in the left
heart-cavity might become detached and plug completely one of the
arteries of some far-removed organ, as the spleen or kidney, and thus
give rise to those ultimate effects which we now understand under the
name of infarction. Thus was first established the new pathological
ideas which have become familiar with the words embolus and embolism.
True it is that Virchow was not the first writer who had described the
facts relating to the translation of portions of coagulum from one
region to another of the circulatory system, and its fixation in a
particular arterial branch. Already this subject had been clearly and
succinctly narrated by Van Swieten. A passage in which the causes and
mechanism of apoplexy are referred to gives lucid explanation of this
doctrine: "Whatever causes change the blood, lymph, and the matter
which supplies the spirits, so as they cannot pass freely through the
arteries of the brain, but are there impacted. Such are {721}
frequently--polypous concretions in the carotid and vertebral arteries,
whether first formed about the heart or within the cranium itself."[5]
These ideas of Van Swieten had not, however, produced any very
permanent impression, and were almost forgotten, when Legroux (1827)
promulgated his view in regard to the possibility of portions of
coagulum being carried from the heart into different portions of the
arterial system. He published, in fact, two most interesting cases of
gangrene of the hand and forearm in which the efficient cause of the
disease was found in an obliterating embolus of the brachial artery,
which was evidently similar in its nature to the thrombus found in the
heart of his patient. It is interesting to remark that Legroux's
inaugural thesis, in which these facts were brought to light, was only
the forerunner of some very complete articles on the subject of cardiac
and vascular concretions, in which he goes over much of the ground
which was covered in Germany by the work of Virchow. Legroux published
his ulterior researches in the _Gazette hébdomadaire_, Paris, 1856, pp.
716 _et seq._ In fact, under the head of correspondence we find in No.
20 of the journal of this year (pp. 349 and 350) an interesting letter
from Legroux to the editor, in which he claims for himself the priority
of publication (Van Swieten excepted) of the facts pertaining to
intra-cardiac thrombi and their effects due to transport of detached
fragments into a region more or less removed from their place of
development (p. 34). As this claim, according to my researches, appears
justified, a part at least of the credit awarded to Kirkes, Virchow,
and Schützenberger as discoverers and disseminators properly belongs to
Legroux.

[Footnote 5: G. Van Swieten, _Commentaries upon the Aphorisms of
Boerhaave_, Aph. mx., vol. iii. p. 159, ed. London, 1774.]

In spite, however, of these investigations, and those of Allibert
(1828), Louis (1837), Baron (1838), and Paget,[6] who showed how the
blood could coagulate in the heart and by transport block up the
pulmonary capillaries, we cannot dispute the glory to Virchow of having
in some sort created this study. Owing to his great sagacity, he was
able to seal his studies and experiments with the stamp of a
master-mind. The new words embolus and embolism introduced by him refer
to a process which was previously but badly understood, and which now
fix, as it were, a domain in modern pathology. The theory of Virchow
found many advocates--many who were opposed to it in the beginning. In
consequence of this it was the origin of numerous works undertaken in
this new direction. Amongst the most important are the communication of
Schützenberger,[7] the thesis of Lancereaux (1862), the great work of
Cohn (Berlin, 1862), the article of Weber in the treatise of Pitta and
Billroth--which contains recent theories about coagulation of the blood
and the transformation of clots--and the memoir of Polaillon upon
cardiac embolism (Paris, 1879).

[Footnote 6: _Med.-Chir. Trans._, 1844, pp. 162-188.]

[Footnote 7: _Gazette médicale de Strasbourg_, 1857.]

ETIOLOGY.--So soon as the blood is withdrawn from the influence of life
it no longer remains fluid, but rapidly coagulates. Thus it is we find
frequently after death coagula filling the cavities of the heart and
extending in long ribbon-like bands into the larger vessels, more
particularly in the veins. What occurs here is very similar to what we
notice in a bowl which receives the blood of a venesection. Here the
blood thickens rapidly, the clot forms, leaves the sides of the bowl,
assumes the appearance of jelly more or less colored owing to the
corpuscles enclosed in the meshes of fibrin, and is bathed in a
quantity of ambient serum. A similar change takes place in the heart:
the serum is imbibed by the tissues and the clot remains in its
cavities.

Coagulation of the blood is a very complex problem. Many theories seek
to explain it. On the one hand, it has been said the fibrin pre-exists
in the blood, and by the fact of the slowing of the circulation, the
reduction of the {722} temperature, etc. the fibrin separates from the
blood and coagulates. Again, it is admitted that the fibrin does not
exist formed in the blood, but that a fibrinogenous material is present
which is acted upon by the hæmoglobin or globulin contained in the red
globules, the leucocytes, and the corpuscles of connective tissue, and
sometimes is, sometimes is not, caused to precipitate as fibrin
(Virchow). The exact conditions which occasion the activity of the
globulin are unknown. The reaction which takes place has been said to
resemble that which takes place between amygdalin and emulsin when
prussic acid is formed, or between myrosin and myronic acid when the
volatile oil of mustard is produced. Further, it is stated, in
accordance with accurate chemical investigations, that the plasma of
the blood contains a substance called plasmin, which separates itself
into fibrin which coagulates and into fibrin which remains dissolved in
the blood (metalbumen, Robin). These fibrins are evidently of two
kinds. The plasmin divides itself under the influence of slowing of the
circulation, the action of acids, of foreign bodies, of oxygen in
excess, etc.; it remains intact in a fluid condition when the vascular
walls and globules are healthy, the blood circulating with normal
rapidity, and in presence of alkaline principles.[8] According to
Foster,[9] "Coagulation is the result of the interaction of two bodies,
paraglobulin and fibrinogen, brought about by the agency of a third
body, fibrin ferment." Schmidt concludes that when blood is shed a
number of white and intermediate corpuscles fall to pieces, by which
act a quantity of fibrin ferment and of paraglobulin is discharged into
the plasma. These meeting there with the already present fibrogen give
rise to fibrin, and coagulation results.

[Footnote 8: _Dict. de Méd. et de Chirurgie pratique_, vol. viii. p.
569.]

[Footnote 9: _A Textbook of Physiology_, p. 22, New York, 1880.]

As regards the formation of clots within the body, it is supposed that
injured or diseased spots or foreign bodies first attract, and then, as
it were, by irritation cause the death of, a certain number of
corpuscles.[10] The views of Schmidt of the fibrino-plastic function of
paraglobulin are not accepted by all investigators; and some authors
believe that the fibrinogen as well as the fibrin ferment arises from
the white corpuscles.[11]

[Footnote 10: _Pflüger's Archiv_, vi. (1872), p. 413; xi. (1875), pp.
291 and 515; xiii. (1876), pp. 93 and 146; quoted by Foster.]

[Footnote 11: Frédericq, L., _Recherches sur la Coagulation du Sang_,
Bruxelles, 1877, quoted by Foster.]

According to Bristowe,[12] the frequency of sanguineous concretions
does not depend upon sex, but is in a certain relation with age. He has
remarked, for example, that they are proportionately more often met
with at the extremes of life than toward middle age. This might be
explained satisfactorily, perhaps, on the supposition that at these
periods the circulation is at times very feeble, owing either to
congenital feebleness on the one hand or chronic organic affections on
the other. At all events, when we seek for the causes which have most
influence in determining the formation of cardiac concretions previous
to death, we find--I. the mechanical, or those which act specially in
slowing the current of blood through the heart. These causes may exist
within the heart or may be removed from it. II. The vital or
pathological. These causes are of somewhat difficult determination at
times, and pertain usually to affections in which there is notable
blood-change, in which the quantity of the fibrin has been augmented
absolutely or relatively, or to those of infectious type--viz.
diphtheria; or to those constitutional in nature--phthisis, cancer,
etc. III. The inflammation of the endocardium or endocarditis. This is
admitted by Andral, in a note upon the etiology of cardiac concretions
in the work of Laennec, as having special importance. Bouillaud also
attributed their formation in certain cases to the chemical action of
pus which was present in the economy.

[Footnote 12: _Pathol. Society's Trans._, vol. xiv. p. 71, quoted by
Bartholow.]

{723} I. Amongst the mechanical causes we should mention all organic
lesions of the heart, all obstacles in the pulmonary circulation, and
possibly, by analogy, certain badly-defined lesions of the
pneumogastric nerves. All the stenoses and dilatations of orifices, all
irregularities of the valves or heart-walls, all depressions or
roughened parts of the walls,[13] may determine the beginning of a
concretion. In the same way, a small mass of fibrin deposited on a
calcareous valve after transport from one of the veins of the limbs may
originate a voluminous heart-clot. Dilatation of the heart,
pericarditis, every cardiac change which weakens the contractile power,
is a predisposing cause of cardiac thrombosis. Every organic lesion of
the heart tending toward that final stage of asystolism so often
encountered, and which weakens so greatly cardiac contractility;
pouching of different portions of the cardiac wall, or aneurism;
pressure upon the right heart by a mediastinal tumor or a sacculated
aneurism of the arch of the aorta,[14]--all these have great power in
producing intra-cardiac thrombi. The mechanism of these different
lesions was familiar to Kreyssig, Laennec, and Hope. At the same time
it must be admitted that these changes in the heart are not of
themselves always sufficient to give rise to fibrinous deposits. We
encounter stenoses and regurgitations at orifices very frequently, and
concretions, on the other hand, are relatively rare. Moreover, we find
heart-clot at times when there is no cardiac alteration. We believe,
therefore, that the heart lesion is an aiding factor--that in the last
moments of life, when the force of the heart's contraction is weakened
and the conditions of the blood favor coagulation, they will act with
special power.

[Footnote 13: _Pathol. Society's Trans._, vol. xiv. p. 71, cases by J.
W. Ogle.]

[Footnote 14: Walshe, _Dis. of the Heart_, Lond., 1873.]

Among the mechanical causes which are removed or distant should be
mentioned all those which interfere with the pulmonary circulation.
Such are the effects left behind by pneumonia, pleuro-pneumonia, or the
compression of the blood-vessels by old congestion of the lungs. In
these cases, when the vis a tergo is impaired somewhat, and an obstacle
is placed in the pulmonary capillary circulation, even if cardiac
thrombosis does not directly result at first, we may have thrombi form
in the pulmonary veins. In the same way, the nervous affections which
are accompanied with slowing of the circulation tend to produce
coagulation of the blood. All lesions, as we have said, of the
pneumogastrics act in the same direction. In proof of this we should
cite the experiments of Meyer of Bonn, of Longet, and of Blondet, who
produced fibrinous concretions in the hearts of animals by tying or
cutting the pneumogastric nerves. At the same time, the heart-beats
became more rapid, wavering, unequal, and less energetic than in
ordinary physiological conditions. After all, however, all these
mechanical causes are but predisposing causes, for they do not always
produce cardiac concretions. Frequently, as we have said already, the
obstruction to the circulation may be present, and yet at the autopsy
no fibrinous deposit be found in the heart. In order that the
mechanical causes act efficiently to produce coagula, it is essential
that they be aided by the conditions of the blood which favor it.

All concretions do not form with the same rapidity nor are they of the
same size. At times their production is sudden, and but a few hours
elapse before the fatal termination is reached. Again, it is affirmed
that weeks, and even months, may pass before the concretion has reached
a volume sufficient to cause entire stoppage of the heart's
contractions. In the former category are found, of course, the softer,
least consistent coagula--usually, however, very voluminous; in the
latter are the smaller, more elastic, and resistant concretions, at
times even presenting a stratified structure[15] and {724} surrounded
habitually by a clot formed during the latter moments of life, and
having a large proportion of cruor in its composition. The heart
affected with fatty degeneration should, if we consider its weakened
power and deficient contractility, be a predisposing cause of
stagnation first, and finally of the formation of intra-cardiac
thrombi. As a matter of observation in the dead-house, however, such
hearts are not frequently accompanied with fibrinous deposits in their
cavities.

[Footnote 15: According to Legroux, roughening of the walls or valves
gives rise to stratified coagula of moderate size, or else to those
small clots which deposit on the surface or margin of the valves
(_Dict. Encycl. des Sci. méd._, article "Concrétions sanguines," Paris,
1876).]

All diseases which by their nature and duration produce great
exhaustion of the vital powers tend strongly to produce fibrinous
coagula in the heart. This is eminently true of those which at the same
time do not occasion a diminished plasticity of the blood. It is often
assumed that mere stasis in the blood-current through the heart is
essential to the formation of clots in its cavities, and to lend
support to this belief reference is made to the phenomena which take
place in bleeding. It is not true, however, that stasis is necessary to
coagulation, and the proof is afforded when we take a bundle of twigs
and by beating the blood forcibly produce the separation of the fibrin.
Besides a slowness of the circulation, there must be, once again, an
obstacle in the heart itself, and even then polypoid concretions are
not always formed.[16]

[Footnote 16: _Gaz. hébdomadaire_, Paris, 1856.]

II. The Vital or Pathological Causes.--In this class of conditions
leading to cardiac thrombosis are included all diseases in which
certain special changes have taken place in the blood itself. Among
these we should mention, first, certain sthenic inflammatory affections
in which the proportion of the plasmin (fibrin and metalbumen) is
notably elevated, and in which, on this account, there is a strong
tendency to the separation of fibrin from the blood and to the
formation of cardiac concretions. In fibrinous pneumonia and acute
rheumatism this is particularly true, and amongst the numerous
accidents we have to dread in the course of these diseases none strike
us with more dread than the possible production of intra-cardiac
thrombi. In fibrinous pneumonia this complication is so frequent that
Bouillaud has enunciated the following pathological law: "Fibrinous
concretions exist constantly in patients who succumb to a frank, acute
pleuro-pneumonia, well characterized, which has reached the second
stage."[17] According to Raynaud, this is without question a great
exaggeration, and results from the confusion this learned author
evidently made between terminal clots and those formed some time
previous to death. Nevertheless, there is here a proof of the great
frequency of coagula occasioned by this disease, and of the strong
tendency to their formation which the condition of the blood must
afford. What we have said of fibrinous pneumonia and acute articular
rheumatism is not true, singular to say, of lobular or
broncho-pneumonia. The lesions of this form of pneumonia are those of a
catarrhal inflammation of the lung, and the blood does not offer during
its course the remarkable tendency to coagulation that is shown in
fibrinous pneumonia. Usually, the heart-cavities and the vessels are
filled after death with a liquid of a black or violet-brown color, very
often sticky.[18] The fibrin in the heart-cavities in pneumonia is
fibrillar, and does not present those changes which indicate that it
has been deposited for a long while. Moreover, these coagula do not
present physical characters which show any considerable degree of age.
They are usually terminal coagula, or at least formed within a few days
of the fatal termination. Do globular vegetations occur in pneumonia?
At times they do, but they are at least very rare as compared with the
fibrinous conditions just referred to.

[Footnote 17: _Gazette méd._, 1843, vol. xi. p. 270, quoted by Armand,
_Thèse de Paris_, 1857, p. 41.]

[Footnote 18: Damaschino, _Thèse de Paris_.]

There are other general conditions in which there is a marked tendency
to {725} the formation of cardiac coagula. In the puerperal state,
according to Simpson, it is occasioned by the resorption of many new
elements which vitiate its composition and thus occasion this result.
In the poisoning following upon glanders or pyohæmia intra-cardiac
thrombi are often found. Lancereaux has found in this latter disease
fibrinous deposits in the right ventricle and pulmonary artery around
small masses composed of pus-cells. In the different cachectic states,
such as those caused by chronic Bright's disease,[19] advanced
phthisis, and cancer, although we have a diminution in the proportion
of red globules, there is present at the same time a relative increase
of fibrin; and the consequence is that concretions are often formed in
the heart. In fact, it is in these cachexiæ that we often encounter
those fibrinous cysts which will be described under the title of Morbid
Anatomy.

[Footnote 19: Here the retention of the excreta is an important factor
in the formation of cardiac thrombosis (Bristowe).]

Many well-known authors have declared that diphtheria was very powerful
in producing fibrinous concretions in the right heart some time
previous to death. Among those who have written specially on this
subject we would mention Winkler,[20] Richardson,[21] Meigs[22] and
Robinson.[23] According to the latter writer, elastic fibrinous clots
twisted in the valves and adherent to the cardiac walls are developed
frequently in children at a period quite removed from that of the
agony, and at a time when they are not as yet in a condition of extreme
weakness. Except in exceptional instances this influence of diphtheria
to produce cardiac coagula is doubted by Parrot.[24] He admits its
power, particularly when it is complicated with membranous croup, and
in these examples he believes the precocious formation of coagula is
determined probably by the asphyxic condition. Whilst denying the
influence of diphtheria, Parrot freely acknowledges that measles,
especially when complicated with broncho-pneumonia, tends to produce
cardiac concretions. The same tendency is recognized by Harley in the
early stage of scarlet fever where there is high pyrexia.[25]

[Footnote 20: _Die Bluthlumpen dann der Häutiger Bräune_, Wien, 1852.]

[Footnote 21: _Med. Times_, vol. i. p. 23, 1860.]

[Footnote 22: _Am. Journ. Med. Sci._, April, 1864.]

[Footnote 23: _De la Thrombose cardiaque dans la Diphthérie_, Paris,
1872.]

[Footnote 24: _Dict. Encycl. des Sci. méd._, vol. xviii. p. 484.]

[Footnote 25: _Medico-Chirurg. Trans._, vol. lv.]

Notwithstanding the diminished proportion of fibrin in typhoid fever,
and the impossibility of explaining, in many cases, any increase of the
plasticity by local inflammatory disorders, cardiac concretions have
been observed by Huss, Virchow, and Hardy.[26] Bucquoy also relates,
after Huxham, an epidemic which reigned at Plymouth in 1742 amongst
sailors who came from a long cruise, characterized by dyspnoea, cardiac
palpitations, and intermittences of the pulse. Many of those attacked
died, and at the autopsies made polypoid concretions of considerable
elasticity and adherent to the walls of the heart were found. Another
similar occurrence took place amongst the soldiers of the garrison of
Rocroy in 1746. Quite a number succumbed after having shown symptoms
similar to those of the sailors of Huxham. Cadaveric sections
discovered in the left ventricle several hard, consistent cardiac
thrombi.

[Footnote 26: Quoted by Bucquoy, _Des Concrétions sanguines_, Paris,
1863, p. 36.]

III. Endocarditis.--Whatever may be the opinion of different authors in
regard to the frequency of endocarditis when intra-cardiac thrombi are
present, it is certain that if it does exist the explanation of the
presence of these deposits is clear and ample. In endocarditis we have
both a local and mechanical cause and also a vital condition of
fibrinous deposits in the heart. As a mechanical cause we know that
often it is the cause of the stenoses of orifice which are present, and
that further, by its effect in producing roughening or fissuring of
surface, it offers a strongly predisposing cause of the {726} deposit
of fibrin. Ulcerative endocarditis acts still more efficiently in this
direction, owing to the fact that it produces its effects as much on
the surface of the valve, aortic and mitral, near the adherent portion
and in the neighborhood of the cardiac orifice, as between its layers.
The result is, that the surface is rough, unequal, presenting often
cauliflower excrescences, and showing sometimes, in the midst of a mass
of fibrin that has become deposited by degrees, portions of a softened,
partially-detached valve which was the nucleus of the outer layers of
fibrin. Further, endocarditis of both forms acts as a vital and
efficient cause of cardiac thrombosis, in that it belongs to the class
of inflammatory diseases which occasions an absolute increase in the
proportion of fibrin of the blood (from 25/1000, concrete fibrin 3, and
metalbumen 22, to 56/1000, concrete fibrin 17, metalbumen 36); and
also, more especially in ulcerous endocarditis, by the transport of
infectious materials into the blood, which still further tend to cause
coagulation.[27]

[Footnote 27: At times there is complete deprivation of epithelium over
a limited area, and in rare cases slight ulcerations of membrane. These
two conditions are efficient factors of the exudation of plastic
lymph.]

SYMPTOMATOLOGY.--According to Laennec,[28] it is equally erroneous to
attribute to cardiac thrombosis many symptoms which properly belong to
an organic lesion of the heart (notably hypertrophy) as it is to
believe that intra-cardiac thrombi never begin to form until the
terminal period of life. According to him, Haller, Vinckler, Staneari,
and Bonaroli[29] have observed obliterations of the internal jugular
vein and carotid artery by very firm concrete fibrin, and he himself
has seen a similar production in the inferior vena cava for the space
of four fingers' breadth. Although these concretions were evidently
formed during life, they occasioned no symptoms indicative of their
presence, nor were there any obstructions in the course of the
circulation which could explain their origin. Reasoning from these
facts and from the phenomena which occur in aneurismal tumors, it seems
highly probable that the blood should coagulate in the heart also
during life. Later writers frankly admitted that coagulations in the
veins caused partial dropsies, a usual instance of which is the white
swelled leg, or phlegmasia alba dolens, from obliteration of the
femoral vein.[30] This is not invariable, for I have seen, in patients
who have succumbed to diphtheria, both venæ cavæ obstructed by coagula,
without having observed during life either local or general oedema.[31]

[Footnote 28: _A Treatise on Diseases of the Chest_, p. 183, Philada.,
1823.]

[Footnote 29: Quoted by Morgagni, _Epist._ 64.]

[Footnote 30: Vide Bouillaud, _Archiv. gén. de, Méd._, t. ii. et v.,
quoted by Hope.]

[Footnote 31: _Thrombose cardiaque dans la Diphthérie_, Paris, 1872, p.
43.]

Scarcely any contemporary author doubts that cardiac thrombosis gives
rise to more or less well-defined symptoms. What these are we shall now
consider. Of course we are far less liable to-day, when the diagnosis
of organic cardiac disease is so accurate, to attribute to
intra-cardiac thrombi the signs, physical or rational, which properly
belong to them, and which ancient observers could not differentiate.
Nevertheless, there are complex cases in which one is at fault even in
regard to this problem.

The symptoms of cardiac thrombosis vary naturally with their size,
situation, and rapidity of formation. Certain authors have affirmed,
for example, that the concretions formed in an auricle cause a greater
amount of interference with the circulation than those elsewhere
situated. This they do partly by reason of their size and the less
contractile power possessed by the auricle, partly because from the
auricle prolongations are sent off which occlude the cardiac orifices.
When cardiac concretions form suddenly a few days previous to death,
they always aggravate all the symptoms of an obstructed
circulation.[32] If the case be one of pre-existing disease of the
heart, they soon obliterate the cardiac cavities and lead to a rapid
fatal {727} termination. According to Grisolle,[33] when the
concretions are small and form an obstacle neither to the play of the
valves nor to the cardiac circulation, they are not revealed by any
appreciable functional trouble. The opinion of Grisolle in regard to
small coagula is also shared by Legroux, especially when they are fixed
at a distance from a cardiac orifice or concealed in a sinus. When,
however, the thrombi are larger and interfere more or less with the
course of the blood, they occasion very marked symptoms.

[Footnote 32: Hope, _On the Heart_, p. 486, Philada., 1846.]

[Footnote 33: _Pathologie interne_, p. 467, Paris, 1865.]

Even before the days of auscultation there were certain rational signs
which were dwelt upon with much force as showing the presence of
cardiac concretions. Thus, Senac[34] writes that the patients thus
afflicted feel a weight or oppression in the præcordial region which
sometimes becomes extremely painful. Palpitations and irregularities of
the pulse were also noted as symptomatic of these productions. Laennec
believes that coagula of any size may be recognized; "when, in a
patient who till then had presented regular pulsations of the heart,
these suddenly became so anomalous, confused, and obscure that they can
no longer be analyzed, we may suspect the formation of a polypous
concretion."[35] He further adds that if the trouble takes place on one
side alone of the heart, the fact is almost certain. When the coagula
occupy the cavities of the right heart, the sounds of the left heart
may remain normal whilst those of the right side are more or less
distant and muffled (Legroux). Several authors, amongst whom we should
mention Legroux, Bouillaud, Barth, and Roger, have mentioned amongst
the physical characters which show the existence of intra-cardiac
thrombi the sudden development of a blowing murmur limited to the
præcordial region or propagated into the aorta. Sometimes this bruit
was soft, sometimes harsh and rough. These writers have also noticed,
in conjunction with grave general symptoms, the doubling of the first
sound of the heart, making occasionally a sort of galloping murmur. As
regards the recognition of concretions on one side alone, I acknowledge
that after auscultating carefully several cases in which the autopsy
showed coagula formed during life, I have been unable to note signs
sufficient to justify a differential diagnosis.

[Footnote 34: _Traité de la Structure du Coeur, de son Action et de ses
Maladies_, t. ii. p. 470 _et suix_, quoted by Bucquoy.]

[Footnote 35: _De l'Auscult._, t. ii. p. 597, quoted by Hope.]

The distinction appears to me difficult in like cases, for how explain
that a trouble so considerable, even though it exists on one side only,
should not influence the entire cardiac circulation? Moreover, it
should be emphasized that the phenomena dwelt upon do not always
manifest themselves when the cardiac contractions are perfectly normal.
The heart-beats may be increased in frequency and the rhythm be
changed. The passage, therefore, from a state of relative calm merely
to that of extreme agitation is appreciated less readily. This is
particularly true of the symptoms usually described as pertaining to
the presence of terminal coagula. For here, at a period approximating
the fatal termination, it is wellnigh impossible to determine
accurately special symptoms. For this reason it is not surprising how
authors have varied in their descriptions, and at best none of them are
completely full and satisfactory. I have myself many times sought to
recognize the blowing murmur given by Bouillaud as a physical sign of
cardiac concretions, but in not a single instance have I been able to
satisfy myself as to its existence. True it is that the cases I have
watched with greatest care were those of children affected with toxic
diphtheria, and it is possible, on account of the infrequency of
valvular diseases during childhood, that more than once there may have
been confusion between the signs afforded by newly-formed thrombi and
those which belonged exclusively to a pre-existing disease of the
endocardium.

Moreover, these murmurs have been heard and described by too many good
{728} observers (Walshe, Flint, Richardson) for any small negative
evidence to weigh against that which is very positive. Sometimes they
have been but the exaggeration of a bruit previously heard and which
characterized an organic affection of the heart. Sometimes the presence
of the thrombus has caused the diminution or complete disappearance of
the pre-existing structural murmur. Again, these murmurs are discovered
for the first time when the other signs indicate the existence of
intra-cardiac thrombi. When they are heard under these circumstances
they prove positively that the coagula have sent prolongations between
the cavities of the heart or into the great vessels, so as to prevent
the accurate coaptation of the valves or to obstruct the onward current
of the blood. In the first case a regurgitant murmur is occasioned,
tricuspid or mitral, which is heard at the apex; in the second case a
basic murmur is detected, which is pulmonary or aortic. Usually these
murmurs are systolic, although they may in rare conditions be
diastolic. The murmurs have been heard more frequently on the right
side of the heart, and have pointed by their location of greatest
intensity to the obstruction of the infundibulum and pulmonary orifice.
They are then basic or suprabasic, and carried upward toward the
infra-clavicular region on the left side. These murmurs are heard very
rarely on the left side--so infrequently, indeed, that Walshe cannot
affirm that he has ever observed clinically one in this region.
Theoretically, of course, such murmurs may be heard at any spot in the
præcordial region, and with the first or second sounds provided their
size and position in relation to orifices or valves could sufficiently
account for them. Whilst there can be little question that murmurs do
take place in the præcordial region wholly due to the presence of
heart-clot, it is probable that their frequency and diagnostic
importance is less than superficial consideration would cause one to
believe. Thus, Flint[36] states that "the presence of coagula may
occasion an endocardial murmur, but as a rule it is wanting, probably
in consequence of the enfeebled action of the heart." Richardson[37]
holds an analogous opinion, and writes: "There are sometimes abnormal
sounds, but it is difficult to distinguish these from murmurs the
results of valvular lesions." Walshe[38] is at variance with this view,
especially in regard to the thrombal de novo murmur, and has "heard
such a murmur when the examination post-mortem showed the fibrinous
coagulum as the only probable cause of it."

[Footnote 36: _Disease of the Heart_, Philada., 1870, p. 280.]

[Footnote 37: _The Coagulation of the Blood_, Lond., 1858, p. 428.]

[Footnote 38: _Op. cit._ (foot-note).]

Auscultation.--In the heart the single, constant sign that has been
observed consists in the modified tonality of the normal sounds. These
are rapid, irregular, muffled, obscured, and distant. There is notable
inequality also in the strength of successive beats, which is obviously
explained by the great difficulty the blood encounters in traversing
the heart. Now, as I have seen in frequent autopsies that the valvular
mechanism of the left heart is ordinarily free from any fibrinous
deposit, it is readily understood that it can produce the two sounds
normal as regards situation and time, but greatly modified in
transmission.

Percussion.--Percussion, except in particular cases which are rare, and
in which the cavities are much distended by their contents, will only
furnish us with negative signs. When the ventricles are swollen by
large coagula, the percussion dulness will be extended laterally. As
the right cavity is usually the seat of the deposit, it will be
particularly marked toward the right of the sternum. In those instances
where the area of præcordial dulness had been determined before the
formation of the fibrinous concretion this extension becomes a physical
sign of great value. It is to Piorry and the use of the plessimeter
that we owe whatever of exactness belongs in like cases to this method
of examination.

{729} Inspection and Palpation.--The cardiac impulse may be unaffected
by the presence of the thrombus, and if it has been regular in rhythm
previous to its formation it may still remain so. This condition is
infrequent, however, and usually the pulsations become irregular,
tumultuous, and rapid. The force of successive beats will also be
different. These signs can be determined by the sight and touch.

Pulse.--The characters of the pulse are variable. Sometimes it presents
manifest inequalities, occasional intermittences, and is extremely
frequent. It may be quite feeble in the beginning, and afterward gain
in strength. Sometimes, in spite of its weakness and depressibility, it
retains its regularity and its rhythm is unchanged. The coagulum
existing in the cardiac cavities, especially on the right side,
explains the variations of the pulse. Effectively, at each contraction
of the ventricle this chamber, containing a less quantity of liquid
blood, projects a smaller amount of venous blood to the lungs. Besides,
this quantity is insufficient to replace the volume of revivified blood
which leaves the lung with each inspiration. Soon the left cardiac
cavities contract with but small power upon an amount of blood below
the normal, and yet it is with this supply that the left heart must
satisfy the needs of all the organs. The arteries during life become
nearly empty, and it is to this condition, as well as to the lack of
synchronism between the action of the two sides of the heart, should be
attributed the signs we recognize in the characters of the pulse.[39]

[Footnote 39: Robinson, _loc. cit._]

In some instances of cardiac concretions the sonority of the chest
remains normal. In others it is obviously augmented, and even by
percussion very lightly performed a sound of raised pitch is produced.
According to Richardson, this acute emphysema is the direct result of
an insufficient blood-supply in the capillaries which surround the
pulmonary alveoli. Whilst such a condition may often be observed
amongst children, it is not unknown with adults. The affirmation,
therefore, of Walshe, that it can only be observed in young people, and
that in adults its place is supplied by considerable pulmonary
congestion, is not exact. Since Richardson first called attention to
the exaggerated sonority of the lungs in cases of heart-clot, other
observers have also referred to it. Lavirotte (1864) particularly has
insisted on it as a proof of fibrinous deposition in the right heart,
and has demonstrated with pathological specimens that it was occasioned
by the exsanguinated state of the lungs and their hyperdistension with
air.[40] On the other hand, Raynaud[41] states that when the left
cavities are the seat of the concretion there is considerable
stagnation in the lungs, and they show signs of great congestion.
Thoracic percussion becomes less resonant, and subcrepitant râles are
heard in an extended area. Sometimes, even, a moderate hæmoptysis takes
place. These signs of emphysema on one hand, of congestion on the
other, are not spoken of by the majority of writers on this subject;
yet when they are present they will serve to fix our diagnosis and
render it more certain. With respect to emphysema, especially amongst
children, we should mention its great frequency, and on this account
perhaps proper value has not been given to it when found at the autopsy
of a child whose death has been occasioned by cardiac thrombosis. When
the cardiac thrombus is present in the right side of the heart,
Legroux[42] has shown that there will be a more or less turgid
condition of the veins of the neck, and perhaps also of the right upper
limb. With this distension of the veins we shall remark, according to
him, a partial or general infiltration of the subcutaneous tissues.
Sometimes the oedematous condition is limited to the face and neck;
occasionally it extends below the diaphragm, especially on the right
side of the body. The extent of the oedema will depend upon the number
and size of the prolongations which are {730} given out by the main
coagulum. Occasionally these prolongations have been found not only
blocking up the pulmonary artery, but also filling one or both venæ
cavæ and branching out as far as the jugular and subclavian veins.

[Footnote 40: _Congrès Medico-Chirurgical_, Lyon, 1864.]

[Footnote 41: _Dict. de Méd. et de Chirurgie_, vol. viii. p. 573.]

[Footnote 42: _Gazette hébdomadaire_, 1856.]

In my own observations I have always found the veins of the neck
manifest, without in a single instance reaching any great size, and
never have I noticed the prominence of the eyes noted by Walshe. In
these cases cyanosis was limited, and was notable in a marked degree
only upon the lips, the cheeks, and in the upper extremities. The
general or local infiltration of tissue I have never remarked, although
closely looked for on several occasions. Some authors, indeed, have
described a bluish appearance of the entire surface of the body,
together with signs of general infiltration. The explanation given of
these phenomena is that there is a general obstruction of the capillary
circulation, and that the return of the venous blood to the cavities of
the heart is rendered almost impossible. In other words, we have here a
well-marked asphyxic condition. If this be true, it is only partially
so, and there must be great variation in different instances of
fibrinous deposition in the right heart. The rational symptom which was
for me one of great value in the diagnosis of these cases was that of
excessive pallor, not only of the face, but of the limbs and the entire
trunk. This pallor appeared constantly to increase until the last
moments of life.

Richardson indeed says the symptoms are those of syncope, not of
asphyxia. The different processes of life are arrested on account of a
simple absence of arterial blood, not owing to the presence of blood
unfitted to reconstitute the tissues. The tendency to fainting is
probably due, therefore, to the fact that the right ventricle being
more or less completely filled by a fibrinous coagulum, the blood is
prevented from passing through its cavity and entering the lungs. As a
result, there will be but a relatively small portion of blood which
becomes oxygenized after each right cardiac systole. When the clot
occupies the left ventricle and auricle, there will be a reflux of
blood into the pulmonary tissue, thus causing great congestion of this
structure. So intense will this congestion become that occasionally
hæmoptysis results and pulmonary apoplexy may be developed, due,
doubtless, to rupture of the capillary vessels. This condition occurs
before the right heart is much or at all obstructed by coagula. We can
appreciate that the physical signs must, if properly noted, show
manifestly in which cavity the clot is located. If it be in the right
heart, anæmia and emphysema of the lung should follow; hence
breathlessness and increased pulmonary resonance. If it be in the left
cardiac cavity, the lungs become engorged very rapidly, and we should
find dulness on percussion, moist râles, and perhaps an equal or even
greater amount of dyspnoea.

Difficulty of breathing appears to belong as well to the symptoms which
indicate cardiac thrombus on one side of the heart as to those which
characterize its presence upon the other. This symptom was first
accurately described by Hope, since his day by Richardson and
Meigs.[43] It has something special in its features which strikes one
particularly, but may deceive unless closely observed. It takes place
not because the movements of the thorax are interfered with, not
because the entrance of air into the lungs is prevented, for the
vesicular respiratory murmur is easily distinguished, but because the
amount of blood furnished by the pulmonary artery is diminished. The
anguish of the patient is sometimes terrible. The nares dilate, the
chest expands spasmodically with each inspiration, and the patient is
agitated, moans, and shows that extreme craving for air described by
Van Swieten in the summæ anxietates. Under these circumstances,
Hayden[44] states, the surface is cold, and often humid with
perspiration. Pain and great oppression {731} in the præcordial region
have occasionally been referred to, as in the patient of Beau, who
said, in placing his hand to his chest, "I have there a weight which
has suddenly formed and which stifles me." Often the anxiety is
extreme, and the painful sensations continue to increase steadily until
death occurs. In rare instances the suffering, when it has reached a
certain degree of intensity, may remain stationary, or even become
considerably less. If such a respite occur, it is only temporary,
however, and the anguish soon recommences. In milder cases sometimes,
and apparently after dissolution or disintegration of the clot, the
severe symptoms may by degrees disappear, and from this period the
patient makes a steady, uninterrupted march toward recovery. I have
only lately witnessed a similar example in a youth attacked with
typhoid fever, which had reached the third week. There are constant and
intense effort to breathe, extreme restlessness, and the patient will
throw himself from one side of the bed to the other, and scarcely
remain quiet for a few moments. These symptoms are usually more
developed when there is concomitant cardiac disease of organic nature,
and unless this be present may not be so pronounced as to concentrate
attention upon them.

[Footnote 43: _Am. Journ. Med. Sciences_, April, 1864.]

[Footnote 44: Cases 106, 107, and 111.]

The brain scarcely shows the effect of congestion when the patient
dozes for a few moments even in the midst of his great distress. These
times of repose are frequent, but very temporary. In a little while the
patient goes off in delirium or has a convulsion. Again, he relapses
into coma, in which state death may take place. In some instances there
has been obstinate vomiting during several days preceding a fatal
termination. It is possible that this symptom favored the rapid
development of the thrombus.

The preceding signs and symptoms will sometimes declare themselves
suddenly in the midst of an inflammatory or cachectic affection, and
will then point directly to the presence of a cardiac thrombus of
considerable size which has rapidly formed, and which obstructs an
orifice or interferes with the normal play of the valves. Again, there
are all the physical evidences of an old organic affection of the
heart, or those of acute endocarditis or pericarditis, and rapidly all
the symptoms referable to the heart become greatly increased, whilst
orthopnoea, pallor, and coldness of the extremities take place. If a
careful examination of the chest reveals no intercurrent and pulmonary
nor superadded cardiac affection, we may then fairly assume the
existence of an intra-cardiac concretion. Nevertheless, we should
remember that in many of these cases there is a close resemblance of
the symptoms with those occasioned by a sudden rupture of one of the
chordæ tendineæ in the course of acute endocarditis (Walshe).

We should not lose sight of the fact that at times a clot will form in
the heart without giving rise to manifest symptoms unless the attention
be specially directed to its formation. This will be true in instances
where the coagulum forms slowly, is small, or occupies a place removed
from orifices or valves. In a cardiac sinus, for example, a coagulum of
inconsiderable size may remain fixed and latent for a long period. Such
is not the case, as we already have shown, when the coagulum fills in
part one or more of the cardiac cavities, is situated near an orifice,
is attached to the walls by a pedicle which allows it to float freely
in the ventricle, or is intertwined with the valves or chordæ tendineæ.
Under all these circumstances, they give rise to the signs and symptoms
we have dwelt upon above, and which ordinarily make known their
presence. Occasionally, however, there is such a combination of
symptomatic morbid phenomena relating to different organs that we are
at a loss to separate them accurately and to determine how this or that
symptom is occasioned. This statement is particularly true in regard to
the distinguishing symptoms which indicate the presence of terminal
coagula. At a period when the fatal termination is not far removed, and
when it is extremely difficult both to recognize and interpret special
{732} symptoms, it is readily understood why those pertaining directly
to cardiac thrombosis have not hitherto been fully and accurately
described.

COURSE, DURATION, AND TERMINATIONS.--Cardiac concretions may form more
or less rapidly, and in certain situations occasion death
instantaneously and surely. This is eminently true of large coagula
which fill up the infundibulum and pulmonary artery. Cases of this sort
have been mentioned by various authors. Amongst others, we would
specially direct attention to those instances in which sudden death has
taken place during the puerperal state after severe post-partum
hemorrhage. The patient has at times, in assuming an erect sitting
posture, been attacked with a syncopal attack resulting in a few
instances fatally.[45] In the same category we should include those
examples in which sudden death has followed severe surgical
operations.[46] Two cases of this termination, due to coagula in the
right heart, are reported by Robert Lawson.[47]

[Footnote 45: _Philada. Medical Examiner_, March, 1849, paper by
Charles D. Meigs; vide also Spiegelberg, _Lerbuch der Geburtshülfe_,
and Lusk, _The Science and Art of Midwifery_, p. 597.]

[Footnote 46: _Med. Times and Gazette_, vol. i., 1873, p. 58; also
_Pathol. Soc. Trans._, vol. xxvii. p. 70.]

[Footnote 47: _Med. Times and Gazette_, Feb. 8, 1873.]

In cardiac dilatation this mode of death is not infrequently seen. It
here seems to depend mainly upon stasis of blood caused by weakened
power of contractility in the right heart and "by impairment of
respiratory and nutritive attraction arising from feeble respiration
and arrested tissue-change" (Hayden). The post-mortem revelation has
afterward shown cardiac thrombosis to be the efficient cause of death.
In diphtheria[48] and pneumonia such examples are not infrequently
encountered. As Austin Flint[49] remarks, however, these coagula
present almost identical physical characters with those formed after
death, and consequently to fix precisely the moment of their production
will at best be but a matter for conjecture. According to Walshe, it
would be difficult to determine whether or not some of these almost
instantaneous deaths occurred as a coincidence or as an effect.
Besides, it is frequently impossible to determine the length of time
they have existed before completely obstructing the circulation through
the pulmonary artery into the lungs, and hence causing fatal syncopal
or asphyxic phenomena. Bristowe[50] goes so far even as to affirm in
the great majority of cases that cardiac concretions are unaccompanied
with appreciable symptoms. In this statement he includes coagula of
large size entirely filling one or more of the cardiac cavities, and
doubtless formed within a few hours of the final termination. To quote
his own words, "We ought to require very strong testimony indeed to
convince us in any case that concretions found in the heart at the time
of death have caused death, still more to convince us that those clots
which resemble in every point the clots which are the mere result of
dying have had this effect." How different does this sound from the
opinions of B. W. Richardson,[51] who attributes so many well-marked
symptoms to the formation of voluminous moulded clots in the heart!
And, indeed, is it not at variance with the views of a host of the best
medical observers? We believe Bristowe goes too far, and that cardiac
concretions are not infrequently the cause of very sudden death both in
acute and chronic diseases.

[Footnote 48: Robinson, _loc. cit._]

[Footnote 49: _Diseases of the Heart_, p. 276, Philada., 1870.]

[Footnote 50: _Reynolds's System of Medicine_, vol. v. p. 113.]

[Footnote 51: "Lectures" in the _British Medical Journal_, 1860.]

There are numerous instances in which the coagulum formed in the heart
is of smaller size, does not form so rapidly, and besides occupies a
position in which, as it does not interfere greatly with the function
of the heart, death does not of necessity immediately take place.
Little by little, however, the clot is added to, and before many days
have elapsed symptoms of gravest {733} import are pronounced. So usual
is it for the phenomena connected with the formation of a large cardiac
concretion to be accompanied by those which properly belong to another
serious affection which may likewise occasion rapid death (pneumonia,
endocarditis, typhoid fever, diphtheria, etc.) that we with the
greatest difficulty separate the symptoms, and can assign to the
intra-cardiac condition those doubtless occasioned by it.

The cases referred to above are not the only ones. Occasionally we meet
with cardiac concretions after death which have evidently existed for a
number of years, and sometimes without having ever revealed their
presence by notable interference with the circulation or in any way
affecting the habitual good health of the individual (Laennec[52]).
This is perhaps not to be wondered at when the coagulum is small and
situated near the apex of the heart, in one of the auricular
appendages, or in such a position as not to alter the play of the
cardiac valves or obstruct the orifices. But when we see a whole
cavity, as an auricle, forcibly distended by an old concretion which
fills its entire cavity, the absence of all symptoms during life
pointing to its existence occasions much surprise. Some of these large
coagula have nevertheless, by a sudden change in their position, caused
instantaneous death; others again, after giving rise to obscure
symptoms affecting both the pulmonary and cardiac circulation, have
likewise brought about a rapidly fatal termination.[53] Sometimes, in
consequence of the condensation or atrophy of the clot, the phenomena
which took place suddenly with great intensity and indicated its
presence became gradually modified, and we have known one remarkable
instance in a youth during the third week of an attack of typhoid fever
where the accidents thus occasioned completely disappeared, and the
patient left the hospital apparently cured.[54]

[Footnote 52: _Dict. Encycl. des Sci. méd._, article "Concrétions
sanguines."]

[Footnote 53: _Edin. Med. Journal_, April, 1868, v.--case by H.
Douglas.]

[Footnote 54: What occurred in this case I am of course unable to state
in a positive manner. All I know is, that the heart became suddenly
obstructed, followed by weak, irregular pulse and dusky countenance,
and that in twenty-four hours, under treatment with frequently-repeated
doses of digitalis and carbonate of ammonia, the accidents subsided.
Was there a solution and disintegration of an incompletely formed
heart-clot? It seems to me probable.]

COMPLICATIONS AND SEQUELÆ.--One, if not the gravest, complication which
can arise during the formation and duration of heart-clot is the
production of an embolus of the pulmonary artery, completely filling up
its cavity, arresting respiration, and causing sudden death by
asphyxia. More frequently smaller portions of heart-clot become
detached and are transported farther along by the blood-current.
Finally, they become arrested in vessels of smaller calibre. In these
they may remain for a short time, and then become dissolved and
resorbed, leaving the calibre of the vessel free after their
disappearance, or else they form permanent plugs and give rise to
inflammation, coagulation, or hemorrhage. According to the
investigations of Lefeuvre,[55] which are both clinical and
experimental, it would appear that the obstruction of the arterial
distribution to any given part is almost immediately followed by
engorgement of tissue and hyperæmia of the capillaries of the affected
region. Feltz[56] has further shown that this condition is brought
about by reflux from the veins and paralysis of the capillaries. It is
not infrequent, moreover, to find hemorrhage into the tissues as a
direct sequela of this changed condition of circulation.

[Footnote 55: _Brit. and Foreign Med.-Chir. Review_, Oct., 1871.]

[Footnote 56: _Traité clinique et expérimentale des Embolies
capillaires_, Strasburg, 1870.]

These are, in fact, the conditions described under the name of
infarctions. Small detached particles may be detached from the cardiac
clot, if it be found in the left cavity, and transported after a
similar manner by the blood-current of the aorta and its divisions
until finally arrested in the different {734} viscera of the economy
(spleen, kidney, liver) or in the arteries of the extremities.[57] In
these different situations they give rise, when finally arrested, to
results which differ considerably according to the structure of the
organs or tissues where they become impacted. In certain instances,
carefully studied by Senhouse Kirkes, the disintegrated and puriform
contents of old fibrinous coagula are carried throughout the vascular
system and determine marked typhoid phenomena. The patient is attacked
with irregular paroxysms of fever of intermittent type, diarrhoea,
vomiting, and extreme feebleness. Kirkes explains these symptoms partly
by the obstructions occasioned by small emboli, partly by a sort of
poisoning due to the transformation of the fibrin. The accidents thus
occasioned at times very closely resemble those which characterize
pyæmia.[58] The fluid contained in the interior of the old clots, which
give rise to these accidents by reason of their transformation, is
thick, grumous, and puriform. It is surrounded by a sort of
pseudo-cyst, and is composed mainly of altered fibrin and red and white
blood-corpuscles.[59]

[Footnote 57: _Gazette hébdomadaire_, 1856. Legroux reports a case of
acute rheumatism accompanied by endocarditis and followed by
concretions in the left cavities of the heart, and obliterations of the
arteries of the limbs by emboli without gangrene ensuing.]

[Footnote 58: _Dict. Encycl. des Sci. méd._, _loc. cit._]

[Footnote 59: _Pathol. Soc. Transact._, vol. xiv. p. 65, cases by J. W.
Ogle.]

Pulmonary apoplexy and hæmoptysis often take place in connection with
the presence of a fibrinous clot of the right heart. This connection,
however, is not absolute, and many cases of right cardiac coagulum have
been observed in which neither of these complications became manifest.
When there has been pre-existent valvular disease, especially of the
mitral, these sequelæ more surely follow than when there has not been
this organic disease. The connection between the pulmonary apoplexy and
the valvular affection is even more intimate than that of the
hæmoptysis, and the same statement is also true of its relationship
with cardiac thrombosis.

Upon this subject Hayden[60] writes as follows: "Pulmonary apoplexy
seeming to require it as a necessary antecedent condition, while
hæmoptysis, though generally associated with thrombosis in the last
moments of life, frequently does occur independently of it."

[Footnote 60: _Dis. of the Heart_, vol. i. p. 529.]

The doctrine of Ludwig, as supported by Niemeyer,[61] that the
pulmonary apoplexy is directly due to stasis and deposit in the
capillaries of blood-corpuscles, does not appear possible if we accord
faith to the researches of Waters,[62] who has shown an
intercommunication between the bronchial vessels and pulmonary veins;
and reasoning upon this basis we have a strong confirmation of
Virchow's theory of hemorrhagic infarction (Hayden) consequent upon
embolism.

[Footnote 61: _A Textbook of Practical Medicine_, 1869, vol. i. p.
156.]

[Footnote 62: _The Human Lung_, 1860, p. 201.]

PATHOLOGY AND MORBID ANATOMY.--In the great majority of cases clots
presenting different physical characters are found in one or more of
the cavities of the heart after death. According to the supposed time
of their formation, they have been very properly divided into--1,
cadaveric (post-mortem); 2, terminal (in actu mortis); 3, ancient
(ante-mortem). It is important at the very beginning of the
considerations which I shall make in regard to these formations to
determine, if possible, the physical characters of cadaveric and
terminal clots, so as to be able afterward to more clearly separate
from them the true cardiac concretions or those formed at a time more
or less removed from the period of death. Without much question, it is
owing to the indifference or neglect of later writers in making these
necessary distinctions that uncertainty has arisen in the minds of many
with respect of the age of many heart-clots. The cadaveric and terminal
clots would indeed have but slight pathological interest attached to
them were it not that occasionally during {735} life, in a spontaneous
manner, cardiac thrombosis suddenly takes place, and is always the
cause of symptoms of considerable gravity and which often occasion a
fatal termination.

I. Cadaveric Clots.--These present the characters of blood drawn from
the arm by venesection and which is allowed to coagulate in a vase. 1.
Sometimes they are large, soft, homogeneous, friable masses, distending
one or more of the cardiac cavities, and having an appearance very
similar to badly-cooked currant-jelly, and there is no apparent
separation of the fibrin and the globules. Such an aspect is found
particularly when the relative quantity of fibrin is below the normal
or the blood is deficient in plasticity. In alkaline poisoning and many
adynamic forms of disease this is notably the case.[63] It may likewise
occur in forms of death in which there has been considerable
obstruction to the circulation. 2. In a somewhat similar manner, when
the blood is removed from the influences which give it life and
stagnates, or is arrested within the heart, coagulation takes place and
the blood separates into two layers. The upper is fibrinous, and
resembles the buffy coat covering a clot after bloodletting; the under
layer is mainly cruoric, and encloses within its meshes by far the
larger proportion of the red globules. This latter mass always forms
the lowest stratum by relation with the position of the body after
death. Between these two layers, and from the fact of their smaller
density, we find more of the leucocytes. This formation of blood-clot
in distinct strata has been accomplished experimentally by Pasta,[64]
who poured some blood of an animal into the heart of an ox and allowed
it to deposit. The cruoric mass is always soft, and may be readily
washed from the fibrin by a stream of water. Frequently these clots
distend the cardiac cavities to such an extent that when they are
opened at the autopsy a portion will fall upon the table and the rest
is readily detached from them. The microscope shows the same condition
of globules and fibrin in these coagula as it does in those of a
venesection. According to Walshe, these cadaveric coagula are usually
voluminous, jelly-like masses of fibrin of a pale straw-color,
semi-transparent, and containing a quantity of serum in their meshes.
Never do they show the slightest signs of stratification, and are not
really adherent to the cardiac walls. Occasionally their prolongations
may be intertwined amongst the papillary muscles and fleshy columns.
According to Legroux, it appears difficult to understand how these
large masses of fibrin become separated from the blood and deposited in
the heart during life, and yet he is indisposed to regard them as a
strictly post-mortem production. They are for him simply the result of
the agony.[65] After death the serum is expelled from the clot in
larger or smaller quantity, and for a longer or shorter time according
to its own spontaneous retractility.

[Footnote 63: Magendie, "Lectures on the Blood," _Lancet_, 1839.]

[Footnote 64: _Dict. de Médecine_, t. viii. p. 560, Paris, 1868.]

[Footnote 65: _Gaz. hébdomadaire_, 1856.]

There are instances in which death has taken place very suddenly
(chloroform, lightning, blow on epigastrium), and the blood remains
liquid in the cardiac cavities and shows no tendency to coagulation
(Walshe). The intimate cause of this condition is difficult to state,
although the sudden shock to the nervous system is doubtless the main
explanation. Under these circumstances the lining membrane of the heart
is apt to become stained with the coloring matter of the blood.[66] At
times the ventricles of the heart contain no blood at the autopsy. This
is more frequently true of the left than of the right ventricle. Even
then the auricles are more or less full.

[Footnote 66: Bristowe, in _Reynolds's System of Medicine_, vol. v. p.
106.]

II. Terminal Clots.--These clots are found at a period more or less
removed from the time of death. It may be that they have been present
in the heart many days before the fatal termination is reached, or
indeed that the act of dying, when the whole organism is overcome by
the {736} numerous conditions which inevitably tend in this direction,
is mainly instrumental in their rapid production. Of course their
outward aspect as well as their intimate structure will vary greatly
with their age and with the disease which has been present. Never are
they formed entirely of cruor; frequently they are composed of a large
quantity of fibrin. Their coloration varies with the quantity of red
globules, leucocytes, and serum shut up in the meshes of the latter. In
the cruoric as well as the fibrinous clots time also works changes of
coloration. In the latter by the mere expression of the fibrin the
coagula become less shiny and take on a darker tint, and when deeply
colored by red globules they may go through many changes of tint from a
violet or red-brick color to a pink. Usually, however, these latter
changes require a much longer time to be effected than is properly
understood in the term terminal clot. The latter is white, with a
yellow or green tint, or again of a fleshy color with spots of deeper
hue upon their surface. These are nothing more than small masses of
blood, although to superficial inspection they may appear vascular. In
structure they may be homogeneous throughout, but this is extremely
rare, for in the same clot we habitually find different parts which are
evidently of different ages; and not only is this true, but what leads
more to confusion in regard to the precise age of a given clot is the
fact that a relatively old one is at times juxtaposed or intimately
annexed to a purely cadaveric one. To make the distinction of what
portion of clot has been formed some time, and what part in the agony,
is occasionally almost impossible. Owing to the manner of death or to
certain rapid chemical changes which may take place, the interior of
terminal clots is at times softened and filled with a puriform material
which is probably only softened fibrin.[67] These clots are more or
less firm and elastic. They adhere quite intimately by a number of
roots to the walls of the heart, and are twined around the chordæ
tendineæ, the musculi pectinati, and are closely attached after this
manner in the depressions between the columnæ carneæ. Sometimes they
send off long projections into the large vessels which proceed from the
base of the heart. These latter may be cylindrical in form and fill up
the vascular calibre, or appear like so many flattened and ribbon-like
strips. The elasticity of these clots is made especially evident when
we attempt to tear them away from the cavities in which they are
adherent. They come away in small pieces, and show a rough, irregular
surface where they have been torn asunder. Upon pressure the terminal
clots allow a smaller or larger amount of serum to exude from their
surface, according to their age and the site of their formation. If the
quantity be large, the clot is much reduced in size and changes
considerably its physical characters. It must be evident, therefore,
that if a clot be contained in the ventricle, and be submitted for any
notable length of time to active and forcible contractions, it cannot
contain any large amount of serum. In the auricles near the appendages
the clot does not bear any very strong outward pressure--not much more,
in fact, than it would in an aneurismal sac. Clots in this situation
may have existed, therefore, for quite a time before all or even a
great part of their serum has exuded (Legroux). Rarely, terminal clots
are somewhat stratified. The form of these clots is variable; usually
flat, they may also be globular, ovoid, or thick. As they pass through
the cardiac orifices they are narrowed. At a level with the sigmoid
valves the full margin of the cusps is marked upon their surface, and
discoid masses, formed usually almost exclusively of fibrin, fill the
cavities of the cusps and are moulded to their surface. To this
condition great importance has been attached as indicating the
formation of the coagula prior to death. In fact, Poullet[68] has
endeavored to prove irrecusably by experiments upon animals {737} that
in all cases where these masses were present the clot had been formed
quite a length of time during life. Raynaud,[69] although admitting the
ante-mortem foundation of these imprints, nevertheless holds that they
are produced in the act of dying. The author,[70] owing to the fact
that he has found more than once the amount of fibrin and globules
about equally proportioned in the deposits of the sigmoid sacs,
considers that they may be formed after death. In this opinion he is
upheld by Walshe, who goes even farther, and states that he has seen
coagula filling the right ventricle, the infundibulum, pulmonary
artery, and its branches, and tightly grasped by all these parts in
which this mark was apparent,[71] and yet the coagulum was certainly
formed post-mortem. This opinion was further sustained by more than one
case observed during life, and in which the final symptoms were not at
all those usually assigned to cardiac thrombosis. According to
Richardson,[72] the fact that the clot is grooved upon its surface or
contains a canicula through its interior is a positive proof of the
passage of the blood-current, and hence of its formation during life.

[Footnote 67: _Cycl. of Anatomy and Physiology_, p. 114, 1848.]

[Footnote 68: _Thèse de Montpellier_, 1866. In this sign Poullet also
endeavored to show a distinguishing feature between clots formed within
the heart and those transported from one of the large veins of the
extremities and arrested in the heart. Before Poullet, these sigmoid
prolongations had been mentioned by Gallard and studied by Chauveau of
Lyons and Gardner of Glasgow.]

[Footnote 69: _Dict. de Méd. et de Chirurgie_, vol. viii. pp. 562 and
565.]

[Footnote 70: _De la Thrombose cardiaque dans la Diphthérie_, Paris,
1872.]

[Footnote 71: V. (after Walshe) such a specimen, No. 3636 Univ. College
Museum, London.]

[Footnote 72: _On Fibrinous Deposits of the Heart_, 1860.]

Whilst attaching a certain amount of importance to the signs just
mentioned as indicating the age of a clot, Parrot[73] is disposed to
consider the color, consistence, intimate attachments, and histological
structure of far greater importance in determining their formation some
time prior to death. Usually speaking, the terminal coagula have gone
through no retrogressive changes as regards their primary elements. The
red globules are perhaps paler than normal, but the fibrillæ of fibrin
are still distinct and the leucocytes show well-defined nuclei and do
not contain any fat-granules. These coagula, both terminal and
cadaveric, are found more frequently in the right than the left side of
the heart (Bouillaud). For the terminal especially the right auricle is
a frequent location (Parrot). This does not coincide with the following
table, taken from Legroux, and which shows the relative frequency of
the products in the different cardiac cavities: In 48 cases concretions
were found "in all the cavities at the same time, 8 times; the right
cavities and the left ventricle, 2; the left cavities and the right
ventricle, 2; the two ventricles, 4; the two right cavities, 5; the two
left cavities, 3; the right auricle, 1; the right ventricle, 7; the
left auricle 8; the left ventricle, 8 = 48 times."

[Footnote 73: _Dict. Encyc. des Sci. méd._, Paris, 1876.]

III. Ancient Clots.--There are several varieties which differ
considerably in their outward conformation and appearances, and are
formed at a period more or less removed from the time of death: _(a)_
Stratified coagula, which are attached intimately to the cardiac walls,
and present frequently an aspect which has been confounded with that of
true vascularization. So intimate is their adherence at times that to
effect their separation the scalpel has to be used, and in the attempt
the endocardium is detached. This membrane is frequently affected at
the level of their attachments with an alteration of atheromatous
nature. The volume of these coagula differs considerably. According to
the old writers, they may have become large enough to fill the cavities
entirely of one side of the heart and weigh at least a pound.[74] This
is evidently an exaggeration, and coagula of this size could only be
formed after death. Still, very large clots, formed some time previous
to death, have been carefully described by Bouillaud.[75] These should
be considered very {738} exceptional cases, and according to
Raynaud[76] such masses would inevitably cause immediate death.
Notwithstanding this affirmation, an ancient clot so voluminous as to
fill an entire cavity has occasionally been found. Such an instance is
the one referred to by Parrot,[77] where the left auricle was found
distended by a stratified coagulum, whilst the other cavities were
relatively empty. Generally, the volume of these clots varies from that
of a walnut to that of a grain of millet. Sometimes they are flattened
out, cover a large surface, and extend from one cavity into another. It
is extremely infrequent to encounter a coagulum which fills more than
the one-third or one-half of the cavity which contains it. These
coagula have different shapes. They are ovoid, globular, sessile,
pedunculated. Their number is usually in inverse proportion with their
volume. When they have a certain mass and occupy the cardiac cavities
they are often unique.

[Footnote 74: Cited by Bucquoy, _Des Concrétions sanguines_, Paris,
1863, p. 62.]

[Footnote 75: _Traité des Maladies du Coeur_.]

[Footnote 76: _Dict. de Médecine et de Chirurgie_, vol. viii. p. 565.]

[Footnote 77: _Dict. Encyc. des Sci. méd._, 1 Série, vol. xviii. p.
481.]

_(b)_ Warty excrescences, which deposit generally upon the surfaces or
margins of the aortic or mitral valves, although they may be found
adherent to other portions of the endocardium. These warty growths or
vegetations are only so in appearance, for their real structure is
mainly that of fibrin. Rarely do we find them in the right heart. They
have a jagged mulberry or cauliflower aspect, and adhere to an
otherwise healthy endocardial lining or to points where an alteration
or fissure already exists. Sometimes they are in the form of rounded
pedunculated masses, as described by Laennec,[78] and have given rise
to no obvious symptoms during life. These deposits of fibrin should be
distinguished from morbid growths and exuded lymph. The latter may be
augmented in size by layers of fibrin, and may require close inspection
to clearly differentiate them. The two preceding varieties of clot are
often apparently due to some constitutional dyscrasia.

[Footnote 78: "Végétations globuleuses," _Traité d'Auscultation
médiate_, t. ii. p. 630.]

_(c)_ Globular concretions or fibrinous cysts, the latter term being
adopted on account of the well-known contents, which have a grumous or
purulent appearance[79] and are of fluid consistence. They are limited
by a cyst-wall, and are firmly attached to the walls of the heart
either by a single pedicle or by a series of roots intertwined with the
columnæ carneæ or musculi pectinati. Usually they occupy situations in
the cardiac cavities somewhat removed from the direct current of the
blood. The favorite situations for them are at the apex of the left
ventricle or in the appendix of the right auricle. According to
Rokitansky,[80] they almost invariably occupy the left ventricle, but
the observations of later writers show conclusively that this is an
error (Bristowe). Thus, Hayden states that in his belief the right
chambers are much more frequently the seat of thrombosis than the left
chambers. This difference is explained by the greater tendency to
stasis in the right heart, where also there is less considerable
muscular development. Of 44 fatal cases of valvular lesion, he cites 24
instances of cardiac thrombosis on the right side of the heart, and 12
instances on the left side. No case is reported by him in which the
coagulum existed solely on the left side.[81] They have been found
inserting upon the cardiac valves, and in this situation, owing to
their pedunculated formation and varying position, have sometimes
occasioned curious physical phenomena. A rare instance of this kind is
cited by Walshe,[82] where, the mitral valve being perforated, the
concretion caused at one time a systolic, at another a diastolic,
murmur. They vary in size from a pullet's egg to that of a hazelnut,
and exist singly in a cardiac cavity or are in considerable {739}
numbers. When we attempt to detach them from the cardiac parietes, we
frequently tear through some of their roots and leave small masses
behind. When quite numerous they are also small in size, and may then
be wholly lodged in the interspaces between the fleshy columns. Under
these circumstances they are usually continuous with one another and
extend their processes underneath the muscular bands, which are only
attached by their extremities to the walls of the heart.[83] These
clots have been found in the heart free of all attachments. In one such
instance reported by Pitres[84] they were very numerous and were
contained in all the cavities of the heart. This was a rare example.
Their surface is usually smooth and the cyst-wall occasionally very
thin. The cyst itself may be unilocular or divided into a number of
smaller intercommunicating cavities. Occasionally, through rupture of
the sac-wall, the contents have been emptied into the cardiac cavity
outside. The color of these globular or ovoid concretions is buff or
brick-red, and corresponds very nearly with the fluid contained in
their interior. The different coloration of the contents is due mainly
to the larger or smaller proportion of the coloring matter of the blood
mingled with them. Sometimes these ancient concretions are covered by
coagula of later formation, and it is only after close inspection that
we can determine their real character. The endocardium is usually
intact at their level, and rarely shows signs even of irritative
inflammation. Hence we conclude that in an analogous manner with
preceding forms of coagula they owe their existence to a constitutional
alteration of the blood. Whilst the rule is that on section these
globular concretions offer an interior consistence which is more or
less softened, yet occasionally we encounter one in which the structure
is homogeneous throughout, and presents very closely the appearance
everywhere revealed by its external aspect. The elements, under these
circumstances, of the sac-wall and the interior part of the concretion
are almost identical. Under the microscope these are recognized as
being mainly compound granular bodies, oil-globules, some imperfect
cells, or altered blood-corpuscles surrounded by a network of fibrin.
After a brief period, and in consequence of disintegration, the
contents of these cysts may resemble pus and show certain differences
in their constituents according to their appearance. "When white or
buff-colored they consist almost solely, if not solely, of molecular
matter, oil, and broken-down corpuscles, with which are frequently
mixed compound granular cells and colorless acicular crystals. When
presenting a brick-red or chocolate hue they exhibit, in addition to
the elements just mentioned, numerous blood-corpuscles more or less
altered, and consequently more or less indistinct, and occasionally
also ruby-colored, rhomboidal, hæmatoid crystals."[85]

[Footnote 79: _Pathol. Society's Trans._, vol. xiv. p. 65 _et seq._]

[Footnote 80: _Path. Anat._ (Syd. Soc. trans.), vol. iv. p. 217.]

[Footnote 81: _Dis. of the Heart and Aorta_, Part ii. p. 1020.]

[Footnote 82: _Dis. of the Heart_, 4th ed., p. 106 _(b)_.]

[Footnote 83: Bristowe, in _Reynolds's System of Medicine_, vol. v. p.
107.]

[Footnote 84: _Bull. Soc. anatomique_, Feb. 5, 1875.]

[Footnote 85: Bristowe, on "Softening Clots in the Heart," _Path.
Society's Trans._, vol. xiv.]

It is to the rupture of cysts of similar characters with those just
detailed that may be properly ascribed pyæmic symptoms occasioned by
the diffusion of their contents in the circulation.[86]

[Footnote 86: Ogle, _loc. cit._]

Coloration.--The color of ancient coagula varies from a dull white to
that of a grayish, slightly yellowish, or slate tint. These extremes of
color and all intermediary shades depend upon the age of the clot, the
manner of its formation, the larger or smaller number of red corpuscles
shut up in its fibrinous texture, and the chemical transformations it
has undergone. In order that the opinion at first formed of the age of
a clot by its coloration may be of some value, it is essential that
this ocular examination may be further aided by the results of
microscopic investigation. Occasionally, as already stated, the ancient
coagula are covered by clots of late formation, but these may
ordinarily be distinguished by even slight inspection.

{740} Consistence.--Usually the ancient coagula are firm, friable, and
without elasticity. They are then readily detached from their
insertions by traction, and always come away in small masses. On other
occasions they offer considerable cohesion, and preserve their form
when we attempt to tear through or break them. The degree of friability
is in proportion with the regressive alteration of their substance.
Sometimes the clinical history apparently indicates that a heart-clot
has remained soft during several years (Walshe). Coagula, however,
which have evidently been formed for a considerable period are
frequently fibrinous or cartilaginous in their structure, and a deposit
of calcareous material in their interior or upon their surface is
occasionally found.

Organization.--The question as to whether the coagula formed within the
cavities of the heart can become organized has been variously
determined. Amongst those authors who speak of the progressive
evolution of the clot, some admit the possibility, others absolutely
deny it. That these cardiac clots are frequently coherent, firm,
fibrous, or lamellated is no proof that they may become organized,
since the same features prevail in the old coagula contained in an
aneurismal sac. These latter, as we are aware, are readily separated
from the membranous walls which surround them, and never take on a
similar structure to theirs or give evidence of a new vascular
formation in their interior (Legroux). Cruveilhier, Monneret, and Robin
consider these coagula to be dead structures incapable of organization.
Those who believe in the possibility of the clot becoming organized
support their convictions by referring to certain rude resemblances
with organized tissues; yet even these (Hunter, Laennec, Bouillaud)
have never established their statements by any unquestioned examples.
Moreover, we should remember that formerly investigations were made in
a very imperfect manner. The instruments employed were insufficient and
poorly adapted to accurate research of this kind. Whenever the
organization of a clot was admitted, it was in connection with a
preceding inflammation of the endocardium, which itself occasioned a
plastic exudation. This exudation, becoming organized, was the means,
according to them, of introducing a new vascular formation into the
clot. According to the later researches of Virchow, Billroth, Feltz,
etc., there can be no doubt as to the vascularization at times of
ancient coagula contained in the vessels. In regard to cardiac coagula,
we should urge the facts of their greater size and different situation
as rendering their organization very improbable. Moreover, hitherto no
experimenter has injected any vascular twigs in a cardiac thrombus. To
sum up: whilst it appears possible that a cardiac clot may become
organized in view of what has been shown to take place in vessels,
still the facts thus far closely observed do not corroborate strongly
this opinion, and we cannot pronounce ourselves in an absolute manner
(Raynaud). Amongst the coagula least likely to become organized are the
very large ones and those connected with the heart-walls by a narrow
pedicle.

DIAGNOSIS.--From the preceding signs and symptoms can an accurate
diagnosis be established of the presence within the cardiac cavities of
fibrinous coagula? Evidently not if these formations be of small size
and be situated where they do not interfere notably with the
circulation. This is eminently true of those which are formed slowly in
the auricular appendix or at the apex of the ventricle. In order that
even a probable diagnosis of cardiac thrombosis should be made, it is
essential that the coagulum should occupy a certain space, that it
should be fixed near or at one of the orifices, or interfere in a
perceptible degree with the valvular play. Due consideration is always
to be had for etiological conditions when these can be wholly or in
part known. If, for example, there be present an acute or chronic
affection of the heart, and in a sudden manner, without apparent or
sufficient {741} cause, the symptoms and physical signs pointing to
greater disturbance of the function of this organ become developed, we
naturally suspect the formation of a cardiac coagulum. And this is
true, although the signs of this production are not dissimilar to those
indicating structural heart disease. Thus, the rapid development of
præcordial dyspnoea, of rapid, tumultuous action of the heart, of
feeble, depressible, irregular pulse, and of extreme pallor or lividity
of surface, combined with coldness of the extremities and extreme
anxiety, gasping for breath, and jactitation, indicate under like
circumstances the formation of heart-clot. This diagnosis is further
confirmed when upon listening to the respiration we find that the air
enters and goes out of the lungs freely, and that there is no evidence
in the lungs of any sudden obstruction or inflammatory condition. Of
course it is very important for the physician to be familiar with the
patient's previous condition and antecedents. If the accidents just
referred to become developed without these facts being known, it would
be far more difficult to make a diagnosis of cardiac clot than when the
accidents take place whilst the patient is being constantly watched and
when the physical state never varies without being observed and noted.
If there be a venous obstruction in one of the large veins of the
limbs, either at the time or prior to the formation of the cardiac
thrombus, the symptoms occasioned by it will give even more
significance to those which show heart trouble. The same information is
also afforded by sudden obstructions in different portions of the
arterial channels; and whenever these embolic transports take place
they show, with tolerable certainty, the pre-existence of an
intra-cardiac thrombus. As we can readily understand, it is far less
practicable to make the diagnosis of a clot which develops slowly, and
therefore gives rise to symptoms gradually, than of one which has
manifested itself more or less suddenly.

The physical signs of cardiac thrombosis as a complication of cardiac
disease are not necessarily very significative. This is true, first,
because there may not be an abnormal murmur owing to the weakness of
the cardiac contractions; second, because (even if it be present) the
murmur may be readily confounded with one already existing which is
occasioned by organic heart disease. Theoretically, the first sound of
the heart should be muffled by the presence of a coagulum of any
notable size which interferes with the play of the valves, but this
might be also occasioned by the presence of chronic cardiac valvulitis.
Still, if an abnormal murmur, harsh or soft in character, become
suddenly developed over the pulmonary or aortic orifice, where it was
known not to have previously existed, it is a physical sign which
points with much certainty to the presence of a heart-clot. Whenever
the signs and symptoms given above which show disturbance in the
heart's action occur in a similar sudden manner in the course of an
inflammatory or cachectic disease, such as pneumonia, cancer, or
phthisis, we should properly suspect the formation of an autochthonous
or embolic clot in the heart. These formations arise also, not
infrequently, as an instantaneous complication in the duration of acute
articular rheumatism, certain of the eruptive or acute
fevers[87]--_i.e._ measles, scarlatina, etc.--and the puerperal state,
as we have already pointed out in another portion of this article. In
pneumonia, as in the other affections just mentioned, if no fresh
inflammatory area either in the lungs or in another viscus can be
discovered which is sufficient to explain the occurrence of new
alarming symptoms of obstructed circulation, the difficulties of a
correct diagnosis are much less than if organic heart disease be
present. And this is particularly true because another solution of the
cause of the patient's condition is less available (Flint). Besides, if
it be sure that suddenly an endocardial murmur is developed where none
existed previously, this sign, {742} taken with the striking rational
and other symptoms referable to the heart, is one of great
corroborative value as regards diagnosis. Not only does cardiac
thrombosis occur under the circumstances mentioned already when we have
a certain right to expect it by reason of its relative frequency, but
occasionally it will become evident by its symptoms under conditions
where we have no right to look for its development. In these instances
it is only by a diagnosis of exclusion that we can discover the correct
interpretation of the phenomena presented. In the obstruction caused by
a heart-clot developed in the right cardiac cavities there is of course
stasis in the systemic venous circulation in consequence of the small
quantity of blood which can pass through the heart on its way to the
lungs. This condition, moreover, develops a peculiar dyspnoea which has
been very striking at times, and which has been particularly considered
by Richardson,[88] so as to differentiate it with an analogous but
dissimilar state which prevails when the obstruction exists in the
lungs or other portions of the respiratory tract. In the former case if
we listen carefully to the breathing the vesicular murmur is normal in
quality and pitch, although of exaggerated intensity, and the dyspnoea
is evidently due to the fact that the air lacks, so to speak, a
sufficient quantity of blood to arterialize it. Consequently, the
surface of the body is pale rather than cyanosed, and the heart-sounds
and pulse are feeble, tumultuous, or notably irregular. In the latter
case the lungs are congested or there is some other evident obstruction
of the larynx, trachea, or bronchial tubes which prevents the entrance
into the alveoli of a sufficient quantity of blood for the purposes of
hæmatosis. Hence a rapidly generalized cyanosis becomes developed, the
superficial veins are generally turgescent over the surface of the
body, and what with the irregular, feeble action of the heart, although
its normal sounds are distinctly defined, the violent convulsive
movements of the voluntary muscles, the abolition of the intelligence
of the patient toward the fatal termination, we have a sufficient
number of signs which point distinctly to an asphyxic state. Finally,
at the end of life in the former case it is the heart which first comes
to a stop, whereas in the latter the lungs are the organs which are
primarily arrested in their movements. These differential signs have
great practical importance. Unfortunately, there are instances in which
it is extremely difficult to assign in proper degree the symptoms
occasioned by the heart-clot on the one hand or obstructed respiration
on the other.

[Footnote 87: Keating, _Am. Journ. Med. Science_, Jan., 1885, p. 122,
v.--an able article, entitled "Heart-Clot as a Fatal Complication in
the Acute Fevers of Childhood."]

[Footnote 88: _Medical Times_, vol. i. p. 330, 1856.]

We have in another place pointed out this fact where at the same time
there was present a membranous deposit of diphtheritic membrane
blocking up the calibre of the larynx and a cardiac coagulum distending
the right cardiac cavities.[89] In like manner, there may be an
inflammatory complication in the lungs themselves--_i.e._
broncho-pneumonia--which by its sudden beginning and the rapid rise in
the number of the respirations and the pulse should awaken a suspicion
as to the cause of these symptoms. An error in regard to the modifying
influence of this accident would be possible were it not that
broncho-pneumonia, even of limited extent, reveals itself by
stethoscopic signs, and, moreover, would not explain all the phenomena
which arise. These are: the excessive pallor, the special kind of
anxiety, the weakness and inequality of the pulse, the muffled
heart-sounds, and the very rapid death. In exceptional instances, when
the lungs are merely affected with hyperæmia, the characteristic signs
of cardiac thrombosis are more readily recognized.

[Footnote 89: Robinson, _loc. cit._, p. 48.]

That form of uræmia known as the dyspnoeic or respiratory, which has
been well described by Fournier, is sometimes confounded with
heart-clot. Its commencement is often sudden. Soon labored respiratory
action is very marked, and approximates true orthopnoea, although there
is absence of {743} pulmonary lesion. From the cardiac disturbance it
can be differentiated by the pulse, the cardiac rhythm, bodily pallor,
and the usual evidences of kidney disease.

The distinguishing features between pulmonary embolism or thrombosis
and the deposit of fibrinous coagula in the heart are extremely
difficult to delineate. At times the cardiac coagula manifest their
existence quite as suddenly as does pulmonary embolism. Nothing,
moreover, prevents the formation[90] at a simultaneous moment of a
coagula in the veins as well as in the heart. The puerperal condition,
which is a predisposing cause of an excessive relative amount of
fibrin, is likewise an efficient cause of both these formations.
Besides, we should add, there is no reason why the fibrinous coagulum
of the heart in changing position should not throw off a plug which
will block up the pulmonary artery completely. To separate these
conditions or to make a diagnosis between them other than one based
upon probabilities is not possible.[91]

[Footnote 90: Ball, _Des Embolies pulmonaires_, Paris, 1862.]

[Footnote 91: Vernay, _Gaz. médicale de Lyon_, Nos. des 13 Mars et 22
Mars, 1868.]

We do not consider it essential in this place to go farther and make
known the signs by which we shall be able to distinguish cardiac
thrombosis from certain affections of the larynx, such as laryngitis
stridulosa, oedema glottidis, and membranous laryngitis, or indeed from
asthma or functional disturbance of the heart. It is easy, indeed, to
confound this affection with organic cardiac disease, but what we have
already said should enable us to make the distinction with facility. In
certain infectious diseases, and more particularly diphtheria, death by
cardiac paralysis has been described. In these instances there would
seem to be a real impairment, functional or organic, of the structure
of the pneumogastric nerves, which is accompanied by an irregular
action of the pharyngeal muscles, by vomiting,[92] extreme slowness of
the pulse,[93] a remittent form of syncopal attacks, and powerless
action of the heart. No such combined symptoms appear in our
description of cardiac thrombosis, and they are therefore sufficient,
in our opinion, to substantiate the opinion of a morbid entity which
can be satisfactorily explained by recognizing solely a lesion of
nerve.

[Footnote 92: Jenner, _Diphtheria, its Symptoms and Treatment_, London,
1861, p. 42 _et seq._]

[Footnote 93: Maingault, _Actes de la Société méd. des Hôpitaux_,
5^{ème} Fascicule, 1861, Obs. 40.]

In many examples of death by heart-clot the aspect of the patient is
very much that of one who dies in the period of a collapse from cholera
(Flint), the great difference between the two states consisting in the
fact that in the latter there is no notable degree of dyspnoea.

The diagnosis between coagulum of the right and left side of the heart
can be determined with some accuracy if strict attention be paid to the
effect of the presence of the clot on the normal cardiac murmurs. If,
for example, the clot is situated in the right ventricle, it is
probable that by interference with the tricuspid play it will render
the valvular sound occasioned by closure less distinct, and for this
reason the first sound of the heart will not be heard as well to the
right as to the left of the sternum. In a similar way, the diminution
of sound at the pulmonary orifice in the left second intercostal space
may be explained, for the extension of the concretion into the origin
of the pulmonary artery will almost certainly prevent the perfect
closure of its cusps (Richardson). In deposits of fibrin in the left
cavities of the heart we naturally distinguish less well the cardiac
sounds along the left border of the sternum than toward its right
margin. We also have congestion of the lungs, owing to the fact that a
smaller quantity of blood is able to pass through the partially-filled
left heart. To this is added a tumultuous, irregular action of the
heart and a feeble pulse. It is proper to add, however, that excepting
cases of chronic organic heart disease with dilatation or {744}
degeneration of the walls deposits of fibrin in the left heart are
relatively very infrequent.

In cases of acute endocarditis we have no means usually to distinguish
between the general symptoms of nervous shock and the physical signs
occasioned by cardiac thrombosis on the one hand, and rupture of a
valve or tendinous cord on the other. According to Walshe, this could
scarcely be otherwise, as clotting to a greater or less extent must
necessarily deposit around the spot where the tear takes place. In view
of a case reported by Hammer[94] of sudden cardiac failure in which the
symptoms prior to death pointed to possible intra-cardiac thrombosis,
and where at the autopsy thrombotic occlusion of one of the coronary
arteries was found, it is well to bear in mind the possibility of this
rare occurrence. The principal features of this case were the
suddenness of the collapse, pallor, slight dyspnoea, and extremely slow
pulse, ranging from 23 to 8 to the minute!

[Footnote 94: _Abstract of Med. Science_, 1878, p. 208; _Lond. Med.
Rec._, March 15th.]

PROGNOSIS.--The prognosis of fibrinous coagula in the cavities of the
heart is always extremely serious. The gravity of the situation is,
however, in some degree proportionate to their size, their situation,
and the rapidity of their formation. Thus, for example, those which are
spread out like a membrane over the interior surface of the heart, as
has been noted after endocarditis, are of less serious a nature than
those which are polypiform. As regards the polypiform concretions which
we encounter singly, which are small and formed slowly, they will be so
much more dangerous as the lobe held by the pedicle can become engaged
in the orifices of the heart or the vessels which take origin from
it.[95] Certain well-known observers, it is true, such as Bouillaud,
Barth, Roger, Racle, Meigs, and Armand, have stated their belief that
in rare instances these coagula may become dissolved and disappear.
Indeed, we ourselves have become convinced in more than one exceptional
case that the morbid phenomena manifested, both local and general, were
but the evident proofs of the beginning of fibrinous deposit in the
right ventricle of the heart, and yet we have seen these evidences
change their characters and finally disappear under proper treatment,
leaving the patients ultimately in as good health as they were previous
to their formation.[96]

[Footnote 95: Armand, _Des Concrétions fibrineuses polypiformes du
Coeur_, Paris, 1857, p. 49.]

[Footnote 96: We are more assured in regard to this possibility than we
were ten years ago (v. Thesis).]

Legroux does not believe cardiac concretions can be reabsorbed, and
with Cruveilhier he admits them to be dead formations. Nevertheless, he
admits that fibrinous cysts may entirely disappear by a process of
progressive liquefaction. Moreover, a case reported in his exhaustive
article which he observed makes him acknowledge that a fibrinous
coagulum may diminish, retract, atrophy, form adhesions with the
cardiac walls, and thus not interfere notably with the cardiac
functions.[97] The fact, however, that there may be no present
suffering does not shield such a patient surely from future accidents
of a serious nature brought on by his intra-cardiac condition. About
the diagnosis, however, of intra-cardiac thrombi, especially when a
perfect cure has been established, there always will remain an element
of justifiable doubt, and particularly in those conditions where an
underlying constitutional dyscrasia of grave import was present. This
latter state of itself often becomes either rapidly or eventually
mortal. Apart from the gravity of cardiac thrombosis in view of its
evidently pernicious influence upon the heart, it is likewise a very
serious affection on account of the possibility of its giving rise to
embolic transports into different viscera (brain, lungs, etc.), which
themselves may bring about a direct and speedy fatal termination. Even
when the embolic plugs do not occasion such considerable obstructions
{745} of important vascular channels as to cause rapid death, they may
fill up numerous capillaries of the economy with material of a kind
which shall be followed, sooner or later, by septic symptoms or those
of pyæmic poisoning.

[Footnote 97: _Gazette hébdomadaire_, 1856.]

TREATMENT.--According to certain well-known authors, all curative
treatment of heart-clot is useless (Bucquoy). Others, more sanguine,
repose confidence in the internal use of alkalies, even when a
fibrinous deposit in the cavities of the heart has commenced to form. A
third class of observers, whilst they doubt the efficacy of any
treatment under these circumstances in causing the disaggregation or
absorption of an intra-cardiac coagulum, nevertheless believe we can
limit the rapidity and size of its formation, and also retard the fatal
termination, by giving time sufficient for adhesions to form with the
cardiac walls. Richardson has proposed the administration of minim x
doses of liquor ammoniæ at short intervals in an ounce of water, in
order to dissolve existing coagula, and reports favorably upon its use.
Gerhardt[98] counts upon better results from the use of a saline spray
of bicarbonate of sodium of the strength of ½° to 1½°. This spray
should be frequently inhaled, and in this manner, he believes, the
heart is reached more directly and effectually. Successes are claimed
by the use of this method of treatment. According to Flint,[99] the
idea of giving any remedies with a view to dissolve solidified fibrin
is absurd, whereas as a preventive treatment it is legitimate in
circumstances where this state is likely to occur, and may even become
an important therapeutic object.

[Footnote 98: _Deutsches Archiv für klinische Medicin_, vol. v. p. 207,
summarized in the _Dublin Quarterly Journal of Medical Sciences_, May,
1869, p. 421, quoted by Walshe.]

[Footnote 99: _Diseases of the Heart_, p. 285.]

Alkaline remedies are said to have the power of holding the fibrin of
the blood in solution. If this be true, they are certainly indicated to
prevent coagulation. Moreover, if the fibrin in normal blood be held in
solution owing to the presence of ammonia, it must be evident that this
remedy is specially indicated in carrying out a secondary object of the
prophylactic treatment. Bartholow[100] still maintains, however, that
frequent small doses of ammonium carbonate afford the best chances of
relief even when the coagulum is already formed. The latter
distinguished author advises in cases which are most imminent
intravenous injections of ammonia. The proportions should be one part
of ammonia to three of water. The vein selected must be the jugular,
and special precautions taken to avoid the entrance of air or a foreign
body into the circulation. With attention to this formal indication
there is little or no danger from these injections, as has been many
times proven experimentally. Walshe[101] regards the use of carbonate
of ammonium, combined with bicarbonate of potassium, in five-grain
doses, repeated three times daily, as a mere prophylactic, but as the
best, after all, we possess, and recognizes from its use the only
practical outcome from the enormous sacrifices of canine life made by
Magendie in his experiments to illustrate his lectures on the blood. In
spite of the numerous attempts to fluidify the blood, these efforts
have always remained unsuccessful (Raynaud), and Legroux, who first
proposed it, in his later writings abandoned the alkaline treatment as
useless. The most he affirms that can be done is to combat with energy
cardiac inflammations.

[Footnote 100: _Practice of Medicine_, New York, 1880, p. 285.]

[Footnote 101: _Diseases of the Heart_, 4th ed., London, 1873.]

There is, however, a palliative medication which is indicated by the
presence of the obstacles to the circulation within the heart. The
general condition must be kept in view in carrying out treatment rather
than the local signs. A properly combined therapeutic method in which
the derivatives and counter-irritants play an important rôle offers, in
Legroux's estimation, the best solacing means to oppose to the
developed accidents. We must, however, maintain the patient in a quiet
attitude and administer drugs which {746} shall tranquillize pain and
diminish anxiety. The counsel to keep the patient absolutely at rest is
of primary importance in view of the sudden fatal accidents which have
frequently occurred either in getting into bed after descending from
it, or in sitting up and reaching for something the patient needs. The
patient should be placed in bed in a semi-recumbent position, properly
supported, and arrangements must be made so that all fatigue of eating
and drinking or attending to his excrementitial functions are provided
against. Of course we should treat a case of cardiac thrombosis
complicating a frank inflammatory condition, such as acute
endocarditis, certain forms of pleurisy or pneumonia, very differently
from a case in which the state is one of relative feebleness or
adynamia, as in the advanced stages of diphtheria, or after profuse
uterine hemorrhage during or after confinement. In the first category
of cases it may be in a few rare instances that local depletion of the
blood by means of leeches or venesection is still indicated, especially
if the patient be one of more than usual vigorous frame. In any example
of this sort it is obvious that the internal use of the alkalies, the
employment of revulsives (_i.e._ dry cups), and counter-irritants over
the chest (as previously mentioned), adjoined, perhaps, to the action
on the emunctories by diluent drinks, are the means which offer us the
best guarantee of success. But how shall we act with our second class
of cases? Certainly, we ought not for one moment, with our actual
physiological knowledge, to consider the propriety of taking blood from
a patient thus affected. May we use the alkaline treatment with
reasonable hopes of benefit in a curative way? Yes, if we employ
certain of the stimulating salts, like carbonate of ammonium, or even
this salt combined with moderate doses of bicarbonate of potassium. We
should remember, however, that these drugs are intended particularly to
combat the pathological condition of the blood which apparently
underlies the formation of fibrinous concretions in the heart.

Against the possible fatty degeneration of the cardiac muscular fibre,
or the functional or organic affection of the pneumogastrics, which
predispose to or accompany the production of cardiac coagula, we must
make use of digitalis in small, repeated doses, and nux vomica or some
other preparation containing strychnine. I have on more than one
occasion seen these agents do evident good,[102] and on this account am
encouraged to urge their exhibition. With Hertz, we are not disposed to
believe that digitalis, when given with a little precaution, and
especially in urgent cases, is contraindicated by the danger feared by
Gerhardt and Penzoldt, that it favors thrombosis of the right side of
the heart and gives rise to new emboli.[103]

[Footnote 102: _Loc. cit._, p. 68.]

[Footnote 103: _Ziemssen's Cyclopædia_, vol. v. p. 326.]

It is almost needless to add that under like circumstances we should
insist upon the frequent use of stimulants, like alcohol, chloroform,
and ether, in the form of brandy, whiskey, spiritus chloroformi, or
spiritus ætheris, or repeated doses of strong black coffee with one of
the preceding preparations added to it. In regard to the prophylactic
use of alkaline treatment continued during several days and in large or
frequently-repeated doses, we advise against it for the reasons, first,
that we do not know, in advance, the precise conditions in which
fibrinous intra-cardiac coagula will form; and second, because though
the alkalies have a well-known antiplastic action, they act as
depressants to the general economy when employed in the manner
mentioned, which is the sole method in which their internal use would
be of some practical advantage.

Whenever we have in diphtheria a case in which there is at the same
time obstruction of the glottis by a false membrane and clogging of the
heart by a fibrinous coagulum, we should abstain from performing
tracheotomy on account of its evident uselessness.[104]

[Footnote 104: _Medical Times_, vol. ii. p. 617.]




{747}

NEUROSES OF THE HEART.

FUNCTIONAL DISORDERS OF THE HEART'S ACTION; ANGINA PECTORIS;
EXOPHTHALMIC GOITRE.

BY AUSTIN FLINT, M.D.


The neuroses of the heart are those affections relating to this organ
which do not necessarily involve either inflammation or structural
lesion of any of its component parts. The larger proportion of these
affections may be grouped under the name functional disorders of the
heart's action. The affection called angina pectoris is characterized
by pain more or less intense. It is generally associated with
disordered action of the heart, and also with cardiac lesions. It may,
however, exist without either disordered action or lesion, and hence it
is with propriety included among the neuroses of the heart.
Exophthalmic goitre is invariably associated with disordered action of
the heart, but it has other very marked symptomatic traits which give
to it a distinctive character. The name of the affection refers to
these. The cardiac disorder is, however, the most constant, and,
pathologically, the most important, and therefore the affection may be
considered as one of the neuroses of the heart. In this article the
functional disorders of the heart's action, irrespective of angina
pectoris and exophthalmic goitre, will be first considered, and
afterward these two affections will receive separate consideration.


Functional Disorders of the Heart's Action.

The disorders of the heart's action which agree in respect of their
functional character present marked variations as regards the manner in
which the action is disordered. An account of these will be given under
the name Varieties, together with the symptomatology.

VARIETIES AND SYMPTOMATOLOGY.--The term palpitation denotes a violent
or tumultuous action of the heart. A type of this variety of disorder
is afforded when the heart is much excited by fear or some other
intense mental emotion. The fact that emotional excitement will produce
in some persons notable palpitation, and in others little or no
disturbance of the heart's action, illustrates differences inherent in
the organ itself as regards susceptibility to disorder. These innate
differences are exemplified in cases of disease. In certain persons the
heart readily takes on a morbid functional disorder from causes which
in other persons do not produce this effect. A peculiar susceptibility
to disorder is expressed by the term irritable heart, a term introduced
by DaCosta. Instead of the violence which characterizes palpitation,
there may be irregularity, with notable feebleness of the heart's
action. The patient often describes this variety of disorder as a
fluttering of the heart. The consciousness of the disorder is less
distinct than when the {748} disordered action is violent. With
irregularity are generally associated increased frequency of the
heart's action and præcordial distress. The degree of disorder as
respects either violence or feebleness and irregularity of action
differs in different cases within wide limits. Intermittence is another
variety of disorder. The intermission may extend over a period of one,
two, three, or more beats. It is sometimes preceded or followed by
increased frequency of action, and it sometimes occurs without any
other rhythmical disturbance. The patient is usually conscious of the
intermittence, and it is apt to occasion great alarm, especially before
the mind has become accustomed to it. The intermissions occur more or
less frequently in different cases and at different periods in the same
case. In the cases of palpitation in which the heart acts with violence
it is not probable that the power of the heart's action is increased.
The systolic ventricular movements are quick and have a spasmodic
violence, without actual increase of force. The first sound of the
heart over the apex under these circumstances is short and its quality
valvular. The valvular element of this sound is predominant and
intensified in consequence of the quickness of the systolic movements
and the small quantity of blood in the ventricles when the ventricular
systole takes place. Owing to the latter physical condition the range
of movement of the auriculo-ventricular valves is greater and the
valvular sound proportionately increased. The systolic movements of the
apex against the chest-wall sometimes give rise to a ringing or
metallic sound (cliquetis métallique).

A rare variety of functional disorder which has received but little
attention is notable infrequency of the heart's action. The revolutions
of the organ were reduced to sixteen per minute in a case reported by
Thornton.[1] In 1876, I reported 5 cases, the reduction in frequency
varying from 26 to 40 per minute.[2] In one of these cases there was
marked intermittency, and in another case the action of the heart was
irregular. With these exceptions the rhythm was regular. I have met
with a few additional instances since these cases were reported. In
this variety the disorder continues for several successive days, and it
may be for a much longer period. A persistent infrequency sometimes
remains as a sequel, recovery in other respects being complete. In one
of my reported cases the revolutions were 36 for several weeks after
recovery. In these instances the infrequency of the heart's action,
which is sometimes a congenital peculiarity, is acquired. Hewan has
reported his own case as an illustration of this fact. His normal
frequency had been 72, but after a period of intense study the
frequency gradually decreased, and finally remained at from 28 to 32
per minute.[3] This variety of disorder will claim distinct
consideration with reference to diagnosis and etiology. It may or may
not be accompanied by præcordial distress.

[Footnote 1: _Trans. Clinical Society of London_, vol. viii., 1875.]

[Footnote 2: _American Practitioner_, January, 1876.]

[Footnote 3: _London Med. Times and Gazette_, March, 1875.]

The more frequent varieties of disorder of the heart's action occur in
most instances in paroxysms. The paroxysms differ widely in duration as
well as in their intensity. They may last for an instant only or for
many continuous days. Exceptionally the duration is much longer. I have
known a persistent and very great increase of frequency of the heart's
action with irregularity, and such a degree of weakness that the pulse
could with difficulty be counted, to continue for several weeks,
leading to oedema of the lower limbs, prostration, and pallor, so that
the patient's appearance was that of one moribund. In this case before
the attack and after recovery there was no evidence of any other
affection than functional disorder of the heart, and to this the
patient had long been subject. In another case an extremely irregular
action of the heart continued unceasingly for more than two months,
there {749} being no signs of either an inflammatory or a structural
affection of the organ, and the functional disorder at length ceasing.
As a rule, an attack of functional disorder of the heart implies a
liability thereto; other attacks occur after variable intervals. This
fact involves a peculiar susceptibility, or, in other words, an
irritable heart.

The symptoms referable to the heart may be combined with those of
coexisting affections. Disturbances of digestion are frequently
associated. Paroxysms of disordered action of the heart are often
accompanied by gastric flatulence, and gaseous eructations afford
relief. Patients are apt to endeavor to eructate by voluntary efforts.
Other evidences of indigestion are not infrequent. The mind is much
disturbed, especially if previous paroxysms have not occurred. The
facial expression shows anxiety. The apprehension is of organic disease
of the heart and of sudden death. This apprehension is excited in a
marked degree by intermittence of the heart's action. It is often
extremely difficult to convince patients of the absence of immediate
danger. They require to be assured of this fact over and over again,
and whenever a paroxysm occurs. This statement applies even to medical
men who suffer from functional disorders of the heart's action. The
surface is usually cool or cold. It is sometimes bathed in
perspiration--a symptom probably due, in a great measure, to the
condition of mind. Exclusive of angina pectoris, paroxysms of
functional disorder are not attended by præcordial pain. The paroxysms
may cease either suddenly or after a gradual improvement. The cessation
is abrupt in the instances in which the paroxysms last but an instant
or but a few moments, and not infrequently when the paroxysms are of
much longer duration the normal rhythmical action is at once resumed.

The variety of disorder characterized by diminished frequency of the
heart's action is often associated with cerebral disturbance. In 2
cases cited in my paper there were severe epileptiform seizures,
together with frequent epileptoid attacks; in 2 cases there was mental
excitability amounting to delirium; and in 1 case there was great
mental and physical prostration with gastric irritability, the latter
due apparently to cerebral disturbance. In 1 case only there was no
evidence of disorder of the brain. Of 3 cases which have fallen under
observation since the publication of my paper, in 1 there was notable
mental disturbance, the mind remaining intact in the other 2 cases.

DIAGNOSIS.--Certain facts pertaining to functional disorders of the
heart's action in their ordinary paroxysmal forms render the diagnosis
probable. One of these is the occurrence in paroxysms, the action of
the heart being normal in the intervals. Another fact is the occurrence
of the paroxysms at night oftener than in the daytime. The ability of
the patient to take active exercise without exciting a paroxysm and
without discomfort is evidence that the paroxysmal affection is
functional. A diagnostic feature of a purely functional disorder is
great apprehension connected with the disordered action of the heart.
The patient is apt to feel that there is imminent danger of sudden
death. So strong is this apprehension that it is sometimes difficult to
overcome it by positive assertions of the absence of danger. On the
other hand, disordered action of the heart, when incident to structural
affections, occasions comparatively little mental disturbance; the
patient suffers chiefly or exclusively from the physical ailments. In a
purely functional affection the patient generally is vividly conscious
of the disordered action, whereas the action in structural affections
may be greatly disordered and the patient take no cognizance of it. The
existence of certain causes to be mentioned under the head of the
Etiology bears upon the diagnosis. The liability to functional
disorders, as evidenced by previous attacks, is also to be taken into
account. These facts, however, are not fully adequate for the exclusion
of {750} structural affections of the heart. Moreover, the persistence
in some cases of notable disorder for days, weeks, or even months,
would seem to render highly probable the existence of some structural
affection. The basis of a positive diagnosis is the exclusion, by the
absence of their physical signs, of inflammatory affections and lesions
of structure.

The physician who undertakes to diagnosticate functional disorders of
the heart by symptoms alone--that is, without physical
exploration--must often be in doubt, and if not prudently distrustful
of his ability as a diagnostician, he is liable to commit errors which
are sometimes extremely unfortunate. I was requested to see a young
woman who was represented as suffering from a disease of the heart from
which she might die at any moment. It was stated to me that her
situation was perfectly understood by herself and her family, and that
the object of my visit was simply to satisfy some of her friends. I
found her in a dark room, with every arrangement to prevent the least
mental excitement and physical exertion. Fearing that my questions and
the examination of the chest might occasion disturbance which would
prove fatal, it was proposed that one of her family be made the medium
of the former, and that the latter be dispensed with. This was of
course objected to on my part. My questions she answered in a feeble
whisper. The examination of the chest showed the absence of all
physical signs of disease. The affection was purely functional and
wholly devoid of danger. I could cite from cases which have come under
my observation not a few in which the error of imputing functional
disorders to organic lesions has occasioned the loss of years as
regards the duties and pleasures of life, together with the unhappiness
incident to living in daily expectation of sudden death. With a degree
of practical knowledge of auscultation and percussion sufficient to
recognize the signs of inflammatory and structural diseases, and
self-confidence sufficient to decide upon the absence of these signs,
there is but little liability to error in the diagnosis of functional
disorders.

If the apex-beat be in its normal situation, and the areas of the
superficial and deep cardiac regions be not extended, the heart is not
enlarged; and if there be no endocardial murmur it may be inferred that
the valves and orifices are normal. The exclusion of structural lesions
under these circumstances is almost positive. It is open only to the
exception that certain occult lesions may exist, such as fatty
degeneration and obstruction of the coronary arteries. Aside from the
infrequency of these, the history and symptoms may render their
existence extremely improbable. A hæmic murmur at the aortic or the
pulmonic orifices or at both orifices is not uncommon. That the murmur
is inorganic may generally be determined by other evidences of anæmia,
by an arterial murmur in the neck, and by the venous hum. With the
results of physical exploration as just stated, whatever may be the
form of disorder, whatever may be its intensity, whatever may be its
duration, and whatever may be the associated symptoms, it may be
declared to be purely functional.

The diagnosis is less simple and easy when functional disorders occur
in connection with structural lesions, but without any relation of
cause and effect. Lesions affecting the valves or orifices of the heart
often exist without giving rise to any appreciable disturbance. They
are either innocuous or their effects do not occasion any inconvenience
of which notice is taken. How often is it that an examination of the
chest reveals the signs of cardiac lesions which had not been suspected
by either the patient or the physician! How often are applicants for
life insurance astonished when told that they are not insurable on
account of the signs of a cardiac affection! Now these persons are
liable to functional disorders of the heart from the causes which
produce them in those with perfectly sound organs, the cardiac lesions
having no part in the etiology, but perhaps contributing to render the
disorders more {751} intense. The problem of diagnosis in these cases
is to determine that the functional disorders are not dependent on the
lesions. Were they thereon dependent they might denote grave disease,
but if not thus dependent they have little or no gravity. This
diagnostic problem is to be solved, in the first place, by attention to
the inquiry whether the lesions are in proportion to the disturbance of
the heart's action. Valvular lesions, if the heart be but little or not
at all enlarged, are either innocuous or occasion small inconvenience.
This fact will often suffice for the solution of the problem. Moreover,
the physical signs may show that the lesions involve neither valvular
insufficiency nor obstruction, or, at all events, not in a degree
adequate to account for the disturbed action; in the second place, the
symptoms are to be considered with reference to the inquiry whether
they belong to the clinical history of structural affections or of
functional disorders; and, in the third place, the existence of any of
the well-known causes of functional disorders is to be taken into
consideration. The error is not uncommon of attributing functional
disorders to coexisting lesions when the connection is one of mere
coincidence. This error may be as unfortunate as that of supposing that
functional disorders denote structural affections when the latter are
entirely wanting.

Certain considerations, aside from the exclusion of organic affections
of the heart, apply particularly to the diagnosis of that variety of
functional disorder characterized by infrequency of the heart's action.
It is to be ascertained that the infrequency is not a normal
peculiarity, either congenital or acquired. Napoleon the Great was a
well-known instance of normal infrequency, the number of beats being 40
per minute. As a rule, if an intelligent adult person has habitually a
notably infrequent pulse he becomes acquainted with the fact, and
therefore if he be ignorant of such a peculiarity it may be inferred
that it is not normal.

There is a curious form of functional disorder which would lead to the
error of inferring infrequency of the heart's action from the pulse.
The disorder is characterized by the regular alternation of a
ventricular systole giving rise to a radial pulse, with one too feeble
to be appreciated at the wrist. Assuming the number of ventricular
systoles to be 70 per minute, in such a case the radial pulse would be
35 per minute. I have met with several examples of this form of
disorder in which, as may be said, there is a regular irregularity of
the heart's action. The carotid pulse in these cases represents each
ventricular systole, and on auscultation of the heart's sounds there
will be found to be four sounds to each radial pulse. This form of
disorder is liable to lead to the error of supposing reduplication of
both the first and the second sound of the heart. It is hardly
necessary to add that in cases of obstructive and regurgitant lesions
with feebleness of the heart's action the diminished quantity of blood
expelled from the left ventricle, with some of its contractions, may be
too small to produce an appreciable radial pulse. The existence of
these cardiac lesions is easily ascertained by auscultation.

Infrequency of the heart's action is a well-known symptom in cases of
injury of the skull and in certain intra-cranial affections. Cerebral
hemorrhage, embolism, and thrombosis are easily excluded by the absence
of paralysis, but the exclusion of subacute or chronic meningitis is
not so easy. But infrequency of the heart's action, when a symptom of
the latter affection, is accompanied by cerebral symptoms denoting
compression of the brain--symptoms which are wanting when the
infrequency is the characteristic of a functional disorder of the
heart's action. Moreover, the absence of fever, of increased
sensibility to light and sounds, and of the symptoms embraced in the
clinical history of cerebral meningitis, will render the exclusion of
that affection positive. The heart's action is abnormally infrequent in
some cases {752} of cholæmia and of uræmia, but these affections are
easily excluded. Certain drugs--namely, aconite, digitalis, and
veratrum viride--diminish the frequency of the heart's action. These
drugs, given to a person in health, produce, in fact, a transient
effect which is equivalent to the functional disorder of the heart
thereby characterized.

PATHOLOGY AND ETIOLOGY.--The neuroses of the heart are functional
disorders involving the relations of this organ to the nervous system.
The functional disorders of the heart's action affect the frequency,
the rhythm, and the force of the cardiac movements. The pathology of
these disorders would be more fully understood were our knowledge of
the physiology of the heart's movements more complete. We know that
contractions of the heart continue when it is separated from all its
nervous connections and after removal from the body, especially in
cold-blooded animals. The rhythm, frequency, and force of its normal
movements are evidently dependent on influences derived through the
sympathetic and pneumogastric nerves. Experiments show that the
movements continue, but with increased frequency and with irregularity,
after division of the pneumogastrics; hence this nerve is regarded as
exercising an inhibitory and regulating influence over the action of
the heart. Disorders of the heart's action from causes which pertain to
the brain doubtless involve especially this nerve. Other causes act
through the relations with the different organs of the body by means of
the sympathetic system of nerves.

Impoverishment of the blood occasions disorder, probably by affecting
the nutrition of the heart. Toxical agents in the blood enter into the
pathology in certain cases.

The etiology of functional disorders of the heart's action involves, as
an important factor, a predisposition inherent either in the organ or
in its nervous connections. A peculiar susceptibility to the causes
which induce disorder is an idiosyncrasy. Causes which produce disorder
in those who have this idiosyncrasy are inoperative upon others. Some
persons are liable to functional disorders of this organ all their
lives, whereas some appear to be exempt from any liability thereto. In
this respect the cardiac muscular fibres are analogous to those of the
pulmonary bronchi. A peculiar susceptibility of the latter is requisite
for the capability of having bronchial asthma. The susceptibility of
the heart-muscle varies in different persons, and a reasonable
supposition is that in proportion to the degree of this susceptibility
will the causes of functional disorder be more readily and actively
operative.

Clinical observation furnishes evidence of various causes giving rise
to functional disorders of the heart. The more prominent
are--over-exertion of the faculties of the mind, prolonged mental
anxiety, the use of tobacco, tea and coffee taken in excess, too great
indulgence in venery, the unnatural abuse of the sexual system,
dyspeptic ailments, uricæmia, and anæmia. These causes are often
combined in individual cases. With reference to effective treatment,
inquiries should be directed in every case to facts relating to these
several causes.

Long-continued violent muscular exertions are supposed to lead to
functional disorders of the heart. DaCosta has described cases
occurring among soldiers during the late Civil War in which the cardiac
disorder seemed to him referable to severe marches. He applied the name
irritable heart to the condition in these cases.[4] It is probable that
mental excitement had more or less to do with the causation. Albutt,
Seitz, and other observers have attributed functional disorders to
over-straining of the heart by occupations which call for severe
exercise of the muscles.

[Footnote 4: _Medical Memoirs of the United States Sanitary
Commission_, 1867. See _Address before the Philadelphia Medical
Society_, by A. Stillé, 1883, p. 18. See also _Diseases of the Heart
among Soldiers_, by A. B. R. Myers, London, 1870.]

{753} Paroxysmal disorder of the heart belongs among the multifarious
symptoms referable to the nervous system in cases of hysteria. It is
among the toxical manifestations embraced in the clinical history of
gout, being referable, when it occurs in this pathological connection,
to uricæmia. It may have this causation in cases in which the ordinary
gouty manifestations do not occur.

In the variety of disorder characterized by infrequency of the heart's
action it may be assumed that the causative agency is exerted through
the pneumogastrics. The inhibitory function of this nerve is affected
in the same way as by the galvanic current in the experimental
observations on animals in illustration of this function. This view is
corroborated by the frequent association of this variety of disorder
with notable cerebral disturbance.

PROGNOSIS.--A purely functional disorder of the heart's action may be
said to be devoid of danger to life. This is a remarkable fact, taking
into view the importance of the organ, together with the degree and the
duration of disordered action in some cases. Of many thousand cases
which have come under my observation, I am not aware of having met with
a single instance in which death was fairly attributable to an
uncomplicated functional disorder. It is readily understood that
functional disorders superadded to, albeit not dependent upon, organic
affections of the heart may contribute to a fatal termination. But the
tolerance of functional disorders under these circumstances is often
very remarkable.

The assurance of the absence of all danger frequently lifts from the
minds of patients a heavy load of anxiety and apprehension. To be able
to give such an assurance is one of the delights of medical practice.
Patients often find it difficult to believe that the disorder from
which they suffer can take place while the heart is organically sound.
Many require very positive and repeated assurances in order to secure
their belief. The question is many times asked, "How is it possible
that I should suffer so much, and yet the heart be free from disease?"
Another question which is apt to be asked is, "How can you ascertain so
quickly that there is no disease?" In anticipation of the latter
question, in order to ensure the desirable moral effect, it is
sometimes good policy to prolong the examination, inasmuch as for the
exclusion of all the physical signs of organic disease a few moments
only are required. Another question, still, is, "Will not organic
disease be likely to be produced by the functional disorders?" The
physician is fully warranted in giving a negative answer. Exclusive of
the cases of exophthalmic goitre, functional disorders of the heart do
not involve liability to either inflammatory or structural affections.

Recurrences of functional disorders of the heart constitute the rule
rather than the exception. Their frequency will depend much on the
degree of the predisposition, but of course more or less on the causes
therewith associated. The mental anxiety and apprehensions which they
at first occasion after a time wear away, and they are at length
reckoned as belonging among those annoyances of life to which may be
applied the common expression, "What cannot be cured must be endured."

TREATMENT.--Prompt relief or palliation of suffering is often the
immediate object of treatment when cases first come under observation.
The medicinal remedies for this object are the ethereal or alcoholic
stimulants, the different antispasmodics, and opium. Chloric ether and
the compound spirit of ether (Hoffman's anodyne) often act efficiently.
An eligible prescription is the combination of one of these with an
equal part of the compound tincture of lavender, of which a
teaspoonful, properly diluted, may be given after short intervals.
Brandy, whiskey, or some other form of spirit in many cases will afford
prompt relief. It should be given not much diluted. These remedies
{754} are especially indicated in paroxysms of irregular or
intermittent and enfeebled action of the heart. They are less adapted
to cases in which the heart's action is violent. Of antispasmodics,
valerian, the valerianate of ammonia, camphor, and asafoetida are
appropriate. Some one of the preparations of opium is to be employed if
the disorder be not relieved by other remedies. Of the different forms
of opiate, codeia is the least objectionable, and perhaps as efficient
as any other. With a view to promptness of relief in certain cases of
severity, morphia may be administered hypodermically. Other palliative
measures are a sinapism to the præcordia, and, if the extremities be
cold, a mustard pediluvium. Of the efficacy of the ice-bag applied over
the heart, which is recommended by German writers, I cannot speak from
personal observation. The testimony in behalf of its usefulness is, to
say the least, sufficient for resorting to it without apprehension of
doing harm. In some cases of obstinate persistence of disorder the
opportunity is afforded for trying in succession the various remedies
which have been named. Digitalis is sometimes useful. Concomitant
disorders which may have originated or which tend to keep up the
disordered action of the heart are to be appropriately treated.
Flatulence and other ailments referable to indigestion and constipation
not infrequently are in this category. Paroxysms may be sometimes
arrested by certain mechanical means, such as pressure upon the
abdomen, holding the breath after a deep inspiration, and compression
of the vagus and sympathetic nerves in the neck.

In some cases of functional disorder there is a persistent increase of
the frequency of the heart's action without irregularity in rhythm. The
action of the heart in these cases is the same as in cases of
exophthalmic goitre, the enlargement of the thyroid body and the
prominence of the eyeballs which characterize the latter affection
being wanting. In these cases aconite in small doses is to be
recommended. From one minim to three minims of the tincture of the root
may be given, repeated after intervals of four or six hours and
continued indefinitely. In cases the opposite to the foregoing--namely,
those in which the disorder is characterized by infrequency of the
heart's action--a rational indication is to give remedies with a view
to excite the heart. In the cases which have come under my observation
alcoholics have had but little effect upon the heart, although
apparently useful as regards the nervous symptoms which are apt to
accompany this variety of cardiac disorder. As this disorder does not,
as a rule, occasion distress, the patient perhaps not being conscious
of any disturbances of the heart's action, and as the infrequency does
not appear to involve danger, the treatment may be directed to
fulfilling other symptomatic indications.

Positive assurances of the absence of danger have often a potential
influence in relieving paroxysms of functional disorder. The disorder
is not infrequently increased and kept up by mental apprehension, and
these assurances therefore do away with an active causative agency.
They are also useful in the way of preventing the recurrence of
paroxysms. It is evident that in order to exert this moral influence
the physician must be competent to decide that the disorder is purely
functional. He can so decide only if he have confidence in his ability
to exclude inflammatory and structural affections or to determine that
the disorder is not dependent on lesions which may coexist. If he have
not sufficient confidence in his opinion, he will naturally and
properly not give positive assurances, and a lack of positiveness will
be likely to lead the patient to infer that the disorder is not devoid
of danger. The good effect of certain measures of treatment is in part
attributable to a mental influence. This is legitimately a therapeutic
object here as in other affections.

The more important part of the treatment in the majority of the cases
of functional disorders of the heart's action is that which relates to
prevention. {755} The preventive treatment, in addition to the moral
influences already referred to, consists chiefly in removing as far as
practicable the causes of the disorder. The predisposition cannot be
removed, but the causes which are auxiliary thereto in producing
disorder are, to a greater or less extent, controllable.

Prolonged mental anxiety is often inseparable from the events of life.
"Therein the patient must minister unto himself" The voluntary exercise
of the mental faculties, however, can be restrained within
physiological limits. Tobacco can be abstained from, and, as a rule,
total abstinence is easier than moderate indulgence. Tea and coffee can
be used moderately if at all. Dyspeptic ailments are amenable to
appropriate dietetic and medicinal treatment. On no account should the
diet be reduced below the requirements for ample nutrition. Anæmia,
which exists in a large proportion of cases, especially in women, calls
for chalybeate tonics, to be continued persistently as long as the
blood remains impoverished. It is needless to add that in these cases
the causes of the anæmia are, if possible, to be removed, and that
chalybeates are to be supplemented by proper dietetic and regiminal
treatment. Sexual excess and abuses are to receive adequate attention.
There can be no question as to unnatural sexual excitation. But a
question often arises in individual cases concerning the physiological
limitations of natural indulgence. These limitations probably differ
widely in different persons. They are, however, always exceeded if the
indulgence exceed the instinctive demand--that is, if its increase be
made an object for voluntary efforts. Long-continued and violent
muscular exertions should be interdicted. Uricæmia or the gouty
diathesis claims appropriate remedies and hygienic regulations.

Several of the various causes just recapitulated are frequently
combined, so that the preventive treatment is by no means always
limited to the removal of a single cause. The treatment will prove
successful in proportion as the efforts to remove the causes are
effectual.


Angina Pectoris.

The name angina pectoris was introduced by Heberden in 1768 to
designate a group of symptoms which from that date has been regarded as
constituting an individual affection. The word angina, signifying
strangulation, has but little pertinency in this application of it, and
various other names have been proposed in its stead. For the most part
these are based on pathological views which are either erroneous or
hypothetical, and at the present time the name angina pectoris is
generally adopted in all countries.

The affection may be defined as a paroxysmal neuralgia, the pain of
which is seated within or near the præcordia, shooting thence in most
cases into the left shoulder, and extending downward to a greater or
less extent into the left upper extremity, the right upper extremity
being sometimes similarly affected. In some instances the pain extends
to the lower limbs; the paroxysms often accompanied by a feeling of
anguish and of impending death, the affection in the great majority of
cases being incident to organic disease of either the heart or the
aorta and involving liability to sudden death.

SYMPTOMATOLOGY.--The foregoing definition embraces the prominent traits
of a severe paroxysm. The pain may extend into situations other than
those mentioned--namely, in different directions throughout the chest,
into the neck, the jaws, and the temples, the abdomen, and the groin.
In describing the pain patients use such terms as constricting,
tearing, burning, etc. Perhaps in its most severe form there is no
disease attended with more intense suffering. It is related that the
description of the affection by Heberden led to a communication to him
from an unknown correspondent who gave an account of his own case, and
bequeathed to Heberden his body to be {756} examined after death. The
examination was made by John Hunter, who himself fell a victim to the
affection. An analogous instance occurred in my own experience. A
patient was led by the intensity of his sufferings to request that I
should make a post-mortem examination in his case, with the hope that
something might be thereby ascertained which would prove useful to
others. This request was complied with. Associated with the pain in
severe paroxysms is what has been called a breast-pang, giving rise to
a sensation as if death were at hand. A choking sensation, which is
implied in the name angina, is an occasional symptom, resembling the
globus hystericus. Respiration is not obstructed, but the patient may
voluntarily restrain the respiratory movements lest they increase the
suffering. Dyspnoea, if present, is thereby produced. During the
continuance of the paroxysm the patient refrains from movements of the
body or limbs, keeping a fixed position and grasping some firm support
in order better to remain motionless while the pain lasts. A sensation
of numbness in the affected limbs accompanies the pain. The circulation
is usually more or less disturbed. There is sometimes increased and
sometimes diminished frequency of the pulse. The action of the heart is
often intermittent and otherwise irregular. It may be strong, but
oftener it is weak. At the beginning the arterial tension has been
found to be increased, but later is diminished. The face is generally
pallid, but sometimes livid. The disturbances of the circulation are
often modified by coexisting organic disease of the heart, but
superadded are those of functional disorder incident to the paroxysm.
The countenance is haggard and anxious. The surface of the body is
cold, and may be bathed in perspiration. The mind remains unaffected.
The paroxysms usually commence suddenly, and, as a rule, so end.
Eructations of gas are apt to follow their cessation, together with a
free discharge of limpid urine. The duration of a paroxysm may be but a
few seconds; it is rarely longer than a few minutes. When it appears to
be protracted for a considerable period, there is generally a series of
attacks occurring in quick succession, instead of one continuous
paroxysm.

There is much variation in different cases as regards the severity of
the paroxysms, and the mildest offer a striking contrast to the
severest, the essential symptomatic characters of the affection,
however, being preserved. In mild paroxysms the pain is comparatively
slight, the anguish or heart-pang is less, and the heart's action may
be but little or not at all disturbed. Such paroxysms occasion
annoyance without great suffering. Different cases, and the same case
at different times, exemplify varying degrees of severity.

Recurrences of angina take place as a rule, to which there are but few
exceptions. The intervals between the paroxysms vary in different
cases, and often in the same case. Their recurrence is not governed by
any law of periodicity. Generally, they are at first infrequent, and
their frequency increases slowly. With increase in frequency their
severity is apt to be increased. At first, and for a certain length of
time, they are occasioned by some apparent exciting cause. A common
cause is the exertion of walking, especially against a current of wind.
Often for a considerable period patients are exempt whenever they are
at rest. Sooner or later, in most cases, attacks are produced by other
causes, such as a fit of anger or other mental emotion, and finally
without any appreciable existing cause. I have known attacks to be
caused by the act of swallowing solid food, so that eating became a
source of terror to the patient. They occur in some cases during sleep.
Occurring after intervals of a few moments, the affection in this
respect resembling certain cases of tic douloureux, it doubtless would
be difficult by any description to convey an adequate idea of the
lamentable condition of the patient.

On account of the wide range of the gradations as regards the degree of
severity or mildness, of the diversity of symptoms referable to the
different {757} forms of disease of the heart with which the affection
may be associated, and of the varied disorders which may be
accidentally connected, the clinical picture of angina is by no means
uniform. There is, however, no practical advantage in making formal
varieties of the affection. Eulenberg makes four different types, their
differential characters being based on the different nerves supposed to
be especially affected, as follows: 1st, excito-motor cardiac angina;
2d, regulator angina; 3d, excito-motor sympathetic angina; and 4th,
vasomotor angina. Assuming that there is ground for these pathological
distinctions (which, to say the least, admits of doubt), in a practical
point of view they involve difficulties not compensated for by
important bearings on diagnosis and treatment. One point of
distinction, however, has important bearings--namely, the existence of
angina with or without organic disease of the heart. It cannot be
doubted that in the vast majority of cases angina is incident to some
form of cardiac lesion. That it may exist without any appreciable
lesion is admitted. The propriety of recognizing it as a functional
disorder rests on the latter fact.[5] Practically, the coexistence of
organic disease of the heart or otherwise, and, if organic disease
exist, its nature and extent, are points which it is important to take
into account in the diagnosis with reference to prognosis and
treatment.

[Footnote 5: Of 71 cases analyzed by Gauthier, in 3 only was the
affection to be regarded as purely functional. Vide Eichhorst.]

DIAGNOSIS.--The diagnostic points in cases of angina are the præcordial
seat of the pain, its radiations thence into the shoulder and upper
extremity, generally of the left side, the character of the pain, the
accompanying anguish and sense of impending death, the coexisting
disorder of the heart (which occurs as the rule), and the voluntary
immobility of the body. These are positive criteria which, if marked,
render the diagnosis easy and certain. The diagnosis is further
substantiated by finding the signs of organic disease of the heart,
especially if there be lesions at the aortic orifice or within the
aorta. Well-marked angina is in itself strong presumptive evidence of
organic disease of the heart. Not infrequently the existence of the
latter is for the first time discovered by an examination suggested by
the occurrence of an attack of angina. The cases in which the diagnosis
involves difficulty are those in which certain of the above-mentioned
diagnostic points are either wanting or not well marked.

The affections which may be mistaken for angina are gastralgia and
intercostal neuralgia. In gastralgia the pain is seated below the
præcordia. It may radiate in different directions, but does not extend
to the upper extremities, and is not accompanied by irregularity of the
heart's action. The patient writhes and changes the position of the
body in the effort to obtain relief. There is not a sense of impending
death. The paroxysms are of much longer duration than those of angina.
These differential points should suffice for the discrimination.

An acute attack of intercostal neuralgia does not differ so widely from
angina, but the differential points are generally distinctive enough
for a positive diagnosis. The pain in intercostal neuralgia is not
seated in the præcordia. It does not shoot into the upper extremities;
it is increased by the act of inspiration; the peculiar anguish of
angina is wanting; the action of the heart is likely to be regular; and
the diagnosis is confirmed by finding tenderness over circumscribed
areas in the intercostal spaces anteriorly, laterally, and posteriorly.

Cardiac lesions in cases of angina are to be excluded by finding no
physical signs of their existence. But it is to be remembered that
angina is not infrequently associated with lesions not readily
recognized by signs--to wit, obstruction of the coronary arteries and
fatty degeneration of the heart. Persistent feebleness of the heart's
action and symptoms other than angina {758} incidental thereto render
it probable that one or the other or both of these lesions exist. It is
probable that these lesions have been overlooked in examinations after
death in some of the cases in which angina has been reported as not
connected with any organic affection of the heart.

PATHOLOGY AND ETIOLOGY.--The paroxysms of angina have the distinctive
traits of neuralgic affections as regards the character of the pain,
its extension in the course of sensory nerves, the occurrence of
intermissions, the absence of fever, the functions of digestion and
assimilation remaining often unaffected, and the attacks not always
being referable to any exciting cause. The association of the
affection, as a rule, with organic disease of the heart is evidence of
course of some pathological connection. What is this connection? A
difficulty in answering this question arises from the fact that the
affection is associated not with any one lesion, but with different
lesions. It may be associated with obstruction (usually from
calcification) of the coronary arteries, with insufficiency of the
aortic valves, with rigidity from calcareous degeneration of the aorta,
with aortic aneurism, and with fatty degeneration of the heart, these
different morbid changes existing either singly or more or less of them
in combination. The question then resolves itself into another--namely,
What is the pathological condition common to these different lesions
which stands in a special etiological relation to angina? It is a
logical conclusion that the affection must depend upon some condition
which is common to these lesions. The association with the lesions is
too frequent to be explained by mere coincidence. The etiological
relation involves evidently a condition which exists only in a small
proportion of the cases of these lesions. This statement is a logical
deduction from the great infrequency of angina and the frequency of
these varieties of organic disease of the heart. I submit, as the most
rational theory, that the pathological condition on which the angina
depends is ischæmia of the heart. This theory is supported by the
frequency of the instances in which in cases of angina the coronary
arteries are obstructed; by the fact that not very infrequently this is
the only lesion found after death (two instances having fallen under my
own observation within the past year); by the association with aortic
insufficiency and rigidity of the aorta, lesions which interfere
materially with the supply of blood to the heart if it be admitted that
the blood is driven into the coronary arteries, not during the
ventricular systole, but by the recoil of the arterial coats in the
ventricular diastole; and by the association with fatty degeneration of
the heart when, owing to the weakness of the heart's action, the supply
of blood to the muscular structure of the heart must be diminished.
That the sudden withdrawal of a supply of blood to a part may occasion
neuralgia is shown by the intense pain in the limb which directly
follows embolism of the femoral artery. Moreover, general anæmia, as is
well known, favors the recurrence of neuralgia in various situations.

The cardiac nerves in which the pain is seated are doubtless sensory
fibres of the pneumogastrics. Their anatomical connections with the
brachial plexus will explain the extension of pain to the left upper
extremities. To account for the pain in parts which have no direct
connection with the cardiac nerves, it may be assumed that in angina,
as in other neuralgic affections, a centripetal influence conveyed to
the nervous centres may occasion pain referable to different
situations. This explains the shifting of pains which is one of the
diagnostic traits of neuralgia. The explanation of the disturbed rhythm
of the heart's action so often coexisting with the neuralgic pain is
not more difficult than in cases of functional disorder disconnected
from angina. For what is to be said of the rationale the reader is
referred to that portion of this article which treats of Functional
Disorders of the Heart.

{759} Angina, as a purely functional affection--that is, not
symptomatic of any organic lesion of the heart, and not due to any
structural change in, nor mechanical pressure upon, nerves--is obscure
as regards its pathology and etiology, but not more so than many other
neuralgic affections. As already stated, cases in which it is thus
purely functional are few in number--fewer even than has been supposed,
because there is reason to believe that lesions have been overlooked.
Moreover, cases which have been reported render it probable that in
some instances in which the heart has been found free from appreciable
lesions nerves entering into the cardiac plexuses may be the seat of
structural changes or may be subject to pressure from a morbid growth.
But there are cases in which no lesions are discernible during life,
and in which the existence of lesions is disproved by complete
recovery. The affection under these circumstances must be regarded as
purely functional. There is no positive knowledge of the etiology in
these cases. The affection has been attributed to gout, to hysteria, to
the action of cold, to the use of tobacco, and to other causes. These
causes may have a certain amount of agency, but there is an unknown
intervening link in their etiological connection concerning which, in
the present state of our knowledge, it is useless to speculate.

Age and sex have an undoubted influence in the etiology. The affection
very rarely occurs under middle life, and it occurs in men much oftener
than in women.

PROGNOSIS.--As a very rare exception to the rule, a single paroxysm
only may occur, the patient living for many years without any
recurrence. Recurring paroxysms sometimes are separated by long
intervals--weeks, months, and years. In the majority of cases, however,
paroxysms recur with more and more frequency and with increasing
severity. Under these circumstances death may take place after a long
period of suffering.

The liability to sudden death is an important point in the prognosis.
This may occur in the first paroxysm. An instance has fallen under my
observation within a few months, there having been no signs previously
indicative of disease of the heart. Calcareous obstruction of the
coronary arteries was the lesion found after death. A person subject to
paroxysms of angina must be considered as in more or less danger of
sudden death with the recurrence of each paroxysm. The physician should
be sufficiently impressed with the importance of this fact. While it is
doubtful whether it be the physician's duty to apprise the patient of
the fact, the danger should always be communicated to some discreet
relative or friend. To do this is a duty which the physician owes to
himself as well as to the patient. If he omit it, he exposes himself to
censure should sudden death unexpectedly take place. The mildness of
the paroxysms which have already occurred does not afford a positive
security against the liability to a severe and fatal paroxysm. But it
is a hopeful consideration that paroxysms may recur more or less
frequently for an indefinite period without proving fatal. At this time
I am cognizant of three cases in which paroxysms have recurred
frequently for several years, the patients, with that exception, having
had fair health. Let not the physician, therefore, predict with
positiveness that a patient with angina will die sooner or later in a
paroxysm. The uncertainty is a ground of encouragement as well as for
apprehension.

The coexistence of organic disease of the heart and the nature of the
cardiac lesions have a very important bearing on the prognosis. The
danger is in proportion to the importance of these. Recovery is never
to be expected when the affection is associated with well-marked
cardiac lesions, and there is always great danger in the recurrence of
paroxysms when the associated lesions are in themselves dangerous.
Lesions which give rise to free aortic regurgitation and to fatty
degeneration of the heart involve more or less {760} danger of sudden
death, irrespective of angina. It is evidence of greatly increased
danger if paroxysm of angina be superadded.

During a paroxysm of angina the immediate danger is to be estimated by
the symptoms denoting disturbance of the heart's action. The danger is
great in proportion as the action of the heart is feeble, irregular, or
intermitting. Per contra, the danger is less in proportion as the
deviation from the normal force and rhythm is small. It may be said
that there is no danger so long as the heart's action remains
unaffected, but the disturbance may be slight or wanting at the outset
of a paroxysm and afterward become fatally great.

A favorable prognosis may be entertained when there are no signs of
cardiac lesion, and when there is little or no disturbance of the
heart's action during the paroxysms. Let it be borne in mind that such
cases are exceptional and extremely rare. Let it also be borne in mind
that lesions especially apt to be associated with fatal paroxysms may
be latent--namely, obstruction of the coronary arteries and fatty
degeneration. The latter fact renders it proper that a favorable
prognosis should always be formed with a reservation, while the fact
that recovery takes place in a few well-marked cases of angina renders
it improper to withhold encouragement whenever lesions are not
discoverable and the paroxysms are not accompanied by alarming symptoms
referable to the heart's action. The long tolerance of the affection in
some cases is not to be lost sight of with reference to the
encouragement which may be fairly derived therefrom.

The immediate cause of sudden death in a paroxysm is probably an arrest
of the heart's action in diastole, or such a degree of diminution of
the force of its action that the accumulation of blood within its
cavities induces paralysis from distension.

TREATMENT.--It is important that a paroxysm of angina be treated as
soon as possible, not alone with a view to the relief of pain, but to
remove immediate danger. If the physician be present, an opiate in a
form to act promptly should be given either by the mouth or
hypodermically; the latter mode is to be preferred. Laudanum or a
solution of a salt of morphia is the most eligible form if given by the
mouth. If the heart's action be weak and irregular, a diffusible
stimulant is indicated. If at once available, chloric ether, Hoffman's
anodyne, and the compound tincture of lavender act efficiently. If
these be not at hand, an alcoholic stimulant should be given, diluted
but little, and the doses repeated at short intervals until the
paroxysm ends and the disturbed action of the heart has ceased. The
duration of paroxysms is generally so short that a physician is rarely
present unless they recur after brief intervals. A patient, therefore,
subject to angina should be provided with remedies and instructions as
to their use at the instant a paroxysm occurs. The amyl nitrite, first
recommended in this affection by Brunton, is a remedy of signal benefit
in some cases. From two to five minims may be inhaled at the
commencement of the paroxysm. It is especially indicated when the
characters of the pulse denote arterial tension. Caution is to be
exercised in its use if there be notable weakness of the heart's
action. Sinapisms, stimulating embrocations, and fomentations applied
to the chest have a certain measure of utility, but they should not
take the place nor delay the use of remedies which are more efficient.

A still more important object of treatment than relief in the paroxysms
is their prevention. During the intervals this object claims assiduous
attention. First in importance is the avoidance of all exciting causes.
Bodily exercise is to be kept within the limits required in order to
incur no risk of a paroxysm being produced. The same precaution applies
to mental excitement. Unhappily, this is not as easy as the avoidance
of muscular exertion. John Hunter's saying, that his life was at the
mercy of any scoundrel who chose to {761} insult him, proved a
prediction. He fell dead on receiving an insult from one of his
colleagues at St. George's Hospital. Sexual intercourse I have known to
prove an exciting cause. Excesses in eating and drinking are in this
category. The diet, however, is not to be reduced below the full
requirements for nutrition, and wine or spirits, as conducive to
digestion, are in some cases serviceable. The use of tobacco is to be
interdicted.

Coexisting affections which have no special pathological connection
with the angina may act as auxiliary causes, and therefore claim
attention. Gout is to receive appropriate treatment. Anæmia especially
is to be removed. This condition strongly conduces to the development
and the continuance of neuralgic affections. Chalybeate remedies and
the dietetic treatment are called for if this condition coexist. It is
a rational indication to supply the heart with good blood if it be true
that angina depends on an ischæmic condition of this organ.

Associated cardiac lesions are to be treated according to symptomatic
indications, as in cases in which angina does not occur. Digitalis may
be used under the proper restrictions. I have known this remedy to
prove highly useful in preventing the recurrence of paroxysms. Nux
vomica is sometimes useful as a cardiac tonic.

Various drugs have had repute as empirical remedies. Of these may be
mentioned the preparations of zinc, arsenic, the nitrate of silver,
phosphorus, the bromine salts, the iodide of potassium, and quinine.
There is no proof that these remedies have any special therapeutical
effect in this affection, but that they are sometimes useful there is
abundant testimony. Trial should be made of them, with proper care in
their administration. Electricity in the form of the induced and of the
constant current has been advocated as not only serviceable, but as
effecting in some instances a permanent cure.[6] Beard and Rockwell
have found general faradization useful in a few cases.[7]

[Footnote 6: Vide Eulenburg in _Ziemssen's Cyclopædia_, vol. xlv. p.
54.]

[Footnote 7: Vide _Medical and Surgical Electricity_.]


Exophthalmic Goitre (Graves' Disease; Basedow's Disease).

This affection is characterized by three striking symptomatic
events--namely, persistent increase of the frequency of the heart's
action, enlargement of the thyroid body, and protuberance of the
eyeballs. The name exophthalmic goitre relates to the last two of these
three events. It is defective, inasmuch as it does not include the
increased frequency of the heart's action, which is the primary one of
the three events, and the only one which is never wanting. As an
individual affection it was first described by Graves in 1835, although
cases in which these events were associated had been previously
reported. Parry collected 7 cases in which the affection of the heart
was associated with thyroid enlargement, and in 1 of these cases
exophthalmia existed. An account of these cases was published in 1825.
The name Graves' disease, proposed by Trousseau, has been adopted by
French, English, and American writers. Basedow's disease is the name
given to the affection by German writers. The affection was described
by Basedow in 1840 under the name Glotz augenkrankheit.

There are cases in which one of the events in this symptomatic triad is
wanting, the cases in other respects corresponding to the affection.
The exophthalmia is the event oftenest wanting, the goitre, the
functional disorder of the heart, and the associated phenomena being
the same as if protuberance of the eyeballs coexisted. In some
instances the goitre alone is wanting. The name exophthalmic goitre is
not strictly applicable to these cases, but that the affection is
essentially the same as when the three events {762} are present cannot
be doubted. It is a chronic affection, being in the great majority of
cases of long duration. Exceptionally, it is developed suddenly and
disappears after a few days. In these cases the affection has been
distinguished as acute, but its claim to be so called rests exclusively
on the shortness of its duration.

SYMPTOMATOLOGY.--Of the three cardinal events, the increased frequency
of the heart's action is the first in the order of time. This precedes
the other events usually for several weeks or even months. The
frequency varies in different cases within wide limits--namely, from 90
or 100 to 150 beats, and even more, per minute. There is notable
variation at different times in the same case. Generally, the frequency
is greatly increased by exercise and mental emotions. In other words,
irritability of the heart is in most cases a marked feature. As a rule,
there are none of the disturbances of action, in other respects than
frequency, which are found in cases of functional disorder not
associated with exophthalmic goitre. The action may be intermittent or
in other respects irregular, but in most cases the rhythm is not
disturbed. The patient is conscious of the heart's action, and is
annoyed by it, especially under any excitement; but there is not that
distressing sense of the disorder which is felt in the paroxysms of
palpitation with irregularity of action considered in the first
division of this article. At the outset and for a considerable period
there are no signs of any organic disease of the heart, or if the
latter be present the association is accidental; the disordered action,
as far as it relates to the affection under consideration, is purely
functional. At a later period there may be enlargement of the heart as
a result of long-continued increased activity of function. From the
first cardiac murmurs are generally present at the base and over the
body of the heart. These are blood-murmurs due to coexisting anæmia.

Following the increased frequency of the heart's action, after a
variable period enlargement of the thyroid body occurs. The enlargement
may be rapid, but in most cases it takes place slowly, and ceases when
it has reached a moderate degree. Cases are exceptional in which the
degree of enlargement is such as to occasion any obstruction to
respiration. Almost invariably both lobes of the thyroid body are
enlarged, but the enlargement is generally not equal on the two sides,
and, as a rule, it is greater on the right side. The enlarged lobes are
soft at first, afterward becoming hard. The subcutaneous veins over
them are often distended. Pulsation of their arteries is apparent to
the hand and to the eye. A systolic arterial blowing murmur and a
continuous hum are heard when the thyroid region is auscultated. In
some instances the murmur is like that of an aneurismal varix. As a
rule, murmurs are heard over the carotid artery and the jugular vein. A
thrill or fremitus is often felt by the hand placed upon the thyroid
body. The thyroid enlargement is due at first chiefly to dilatation of
the arteries and veins. Hyperplasia of the fibroid tissue occurs
afterward, and then the enlarged gland becomes hard to the touch. The
size of the enlarged thyroid body is often found to vary considerably
at different times--a fact attributable to varying degrees of the
dilatation of the vessels and of the consequent hyperæmia.

A notable protuberance of the eyeballs has sometimes been observed to
take place suddenly, but, as a rule, it is at first slight and
increases slowly. The degree of protuberance varies considerably in
different cases. When marked, the patient has a remarkable staring
expression. Both eyeballs are alike protuberant with very rare
exceptions.[8] The pupils are unaffected and {763} vision is not
impaired. The protuberance is sometimes so great that the globes cannot
be covered by the eyelids. Under these circumstances inflammation of
the conjunctiva ensues, and perforation of the cornea has been known to
occur. The eyeballs can be pressed backward into the sockets without a
degree of force which occasions pain, but the protuberance returns
directly the pressure is discontinued. In most, but not in all, cases
the consensual movements of the upper eyelid and the globe, when the
latter is moved upward or downward, are impaired; that is, the
movements of the lids do not follow those of the globes. That this
symptom is not to be accounted for by the exophthalmia is shown by the
fact that it is not a symptom when the protuberance of the eyeball is
caused by an intra-orbital tumor. The symptom therefore has diagnostic
significance. The ophthalmoscope shows the veins of the retina to be
dilated and tortuous, with, in some instances, visible pulsation of the
retinal arteries. Anatomical conditions to which the exophthalmia is,
in a measure at least, referable, are enlargement of the intra-orbital
vessels by hyperæmia and an increased amount of post-ocular fat.
Paresis of the straight muscles, induced by stretching, is probably an
important factor when the protuberance is great. These muscles have in
some instances been found to have undergone fatty degeneration.

[Footnote 8: Allan McLane Hamilton, in his work on _Nervous Diseases_,
cites a case reported by Yeo, in which the exophthalmia effected only
the left eye, and the goitre was limited to the right thyroid body.
Cases of unilateral goitre with bilateral exophthalmia have been
observed.]

Anæmia is usually associated with the foregoing cardinal symptoms. It
is sometimes wanting. This was true of a case recently under my
observation. If anæmia does not exist, the blood-murmurs referable to
the heart and vascular system may be absent. If anæmia exist in a
marked degree, there are present certain symptomatic phenomena
referable thereto--namely, neuralgic pains in different situations,
want of physical and mental endurance, hysterical manifestations,
depression of spirits, etc. Mental irritability is apt to be a
prominent trait of the affection. This may in a great measure be
referred to sensitiveness occasioned by the exophthalmia. Owing to
this, patients often avoid observation as much as possible. They
naturally, women especially, are led to brood over the calamity of such
a singular and conspicuous deformity. Breathlessness on exercise is a
symptom more or less marked according to the increase in the frequency
of the heart's action and the impoverishment of the blood. The appetite
and digestion may or may not be impaired, and hence there may or may
not be emaciation. It cannot be said that the affection is accompanied
by fever, although in a certain proportion of cases the temperature of
the body is half a degree or a degree above the normal range. Reports
of cases embrace a considerable number of concurrent symptoms which are
occasionally present, such as cephalalgia, insomnia, vertigo,
amenorrhoea, neuralgia, unilateral sweating, etc. These have no special
connection with the affection, but are incident to associated
pathological conditions.

DIAGNOSIS.--The three phenomena which distinguish this affection are so
obvious as well as characteristic that a diagnosis cannot well be
avoided, after a description derived from books or lectures, when the
first case presents itself in practice. The wonder is that the
affection had not been clearly pointed out prior to the writings of
Graves and Parry. Any difficulty in diagnosis relates to cases in which
either the exophthalmia or the enlargement of the thyroid body is
wanting, or to the incipiency of the affection when its characteristics
are not fully developed. The bilateral protuberance of the eyeballs,
the absence of local symptoms other than those caused by the exposure
of the conjunctiva when the eyelids fail to cover the globes, the
mobility and normal size of the pupils, the want of the normal
consensus in the movements of the eyelids and the globes, and the
replacement of the latter by moderate pressure, are the diagnostic
points which distinguish the exophthalmia in this affection from that
incident to intra-orbital tumor. The moderate increase of the thyroid
body, its softness to the touch, its notable variations in volume at
{764} different times, its pulsation and the auscultatory murmurs which
it generally furnishes, are diagnostic points distinguishing the
enlargement in this affection from that of bronchocele. The persistent
frequency of the heart's action is not less marked when either of the
two phenomena just referred to is wanting than when both are present.
The degree of frequency varies, but more or less increase is a constant
symptom; and it is a symptom not likely to be present in either
exophthalmia or in goitre unassociated with Graves' disease.

Aside from the symptomatic triad, the clinical history offers in
different cases considerable diversity. The diverse inconstant symptoms
as they occur in other pathological conditions are without diagnostic
significance. A large proportion are incident to the anæmia so often
associated with the affection under consideration.

PATHOLOGY AND ETIOLOGY.--Inasmuch as the persistent frequency of the
heart's action is the first event in the order of time, the thyroid
enlargement and the protuberance of the eyeballs being epiphenomena, it
seemed a rational supposition that the latter events were dependent on
the cardiac disorder. This view was held by Graves and his colleague,
Stokes. A supposition much more rational is that the three events are
united by a common causation. Anæmia has been supposed to be the
causative condition. This supposition is disproved by the fact that
anæmia does not exist in all cases. Moreover, anæmia is a pathological
condition of frequent occurrence, whereas the affection under
consideration is extremely rare. It is, however, very probable that
anæmia may play an important auxiliary part in the causation, as it
does in all the neuroses. With the knowledge of the sympathetic and
vaso-motor nerves which has been acquired since the date of Graves'
discovery, the pathology seems clearly to involve these components of
the nervous system. This pathological view is perhaps generally held at
the present time. But to interpret all the phenomena satisfactorily by
reference to the known functions of these nerves is not easy.
Vaso-motor paresis will account for the dilatation of the vessels,
which is an important anatomical element in the enlargement of the
thyroid body and the exophthalmia. On the other hand, acceleration of
the heart's action is not an effect of paresis, but of excitation. To
account for this incongruity there have been different hypotheses,
which it does not fall within the scope of this article to discuss.
Some autopsies have shown anatomical changes in the cervical
sympathetic and its ganglia, but in others no morbid appearances have
been found. Whether the pathology involves peripheral nerves alone or a
central morbid condition in the spinal cord or the medulla oblongata is
an undecided question. For facts and arguments bearing on the different
points of inquiry relating to the pathological seat and character of
the affection the reader is referred to other works.[9] I will only add
that in view of the fact of the exophthalmia and the goitre being, in
the vast majority of cases, bilateral, it seems rational to suppose the
pathological nervous condition to be central rather than peripheral.
This is assuming that the three cardinal events involve a common
causative condition, and not that the exophthalmia and goitre are
dependent on the cardiac disorder. The termination in a certain
proportion of cases in recovery goes to show that the affection does
not necessarily involve structural lesions, and hence that it is
properly included among the neuroses. The constancy and prominence of
the disordered action of the heart render it proper to consider the
affection in connection with the neuroses of that organ.

[Footnote 9: For a résumé, vide article by Eulenburg in _Ziemssen's
Cyclopædia_, vol. xiv.]

In the etiology of Graves' disease sex and age have a decided
influence. In very much the larger proportion of cases the patients are
women. The proportion of 2 to 1, which is stated by some writers, is
not sufficiently large. Out of 20 or more cases which have fallen under
my observation, in 1 {765} only was the patient of the male sex. The
disease is extremely rare under puberty and after middle age. Between
these extremes of age there is no special predilection of the disease
for any particular period of life.

Of causes which are independent of sex and age we have no positive
knowledge. In particular cases the disease has been attributed to
traumatic causes, to fright or other kinds of mental excitement, to
sexual excess, etc. The evidence of a causative relation in these cases
is simply a post-hoc connection which obtains in but a single instance
or at most in a few instances. Etiological speculations, in the absence
of ascertained facts, are, to say the least, useless, and it is the
most politic as well as the fairest statement to say that in the
present state of our knowledge we have no adequate data for determining
the causation of the affection.

PROGNOSIS.--Graves' disease has no direct fatal tendency. It may not
interfere with fair health for a long period. It diminishes the ability
to tolerate other diseases, and in this way indirectly it threatens
life. If it supervene upon organic disease of the heart, the gravity of
the latter is thereby increased and its progress hastened. It induces,
as a result of long-persistent increased activity of the action of the
heart, enlargement of this organ. Sooner or later, if the disease
continue, dilatation predominates over hypertrophy of the heart, and
then occur the evils incidental to the inability of this organ to carry
on the circulation adequately. Want of breath on exercise, and at
length constant dyspnoea, become sources of suffering. Generally,
dropsy finally ensues, and thus, indirectly, the affection leads to a
fatal result. In most cases, however, death is caused by some
intercurrent malady before the effect upon the heart is sufficient to
occasion grave symptoms. Aside from the effect upon the heart, the
affection does not seem to involve an intrinsic tendency to any
particular complication.

The affection tends to long continuance. I have not met with an
instance of its rapid development and its disappearance after a brief
duration. Instances of complete recovery are rare; that is, the
exophthalmia and the goitre do not disappear entirely, and the action
of the heart does not become perfectly normal. A close approximation to
complete recovery is not very infrequent, and in some instances all
traces of the affection disappear.

The cases offering most in the way of a favorable prognosis are those
in which there is not great acceleration of the action of the heart,
this organ being free from organic disease, and those in which,
exclusive of the affection under consideration, there are no marked
unhealthful conditions. Impaired appetite, lack of digestive power,
defective nutrition, and persistent anæmia are unfavorable prognostics.
Any important antecedent disease affects of course the prognosis
unfavorably.

TREATMENT.--From what has been stated in relation to the etiology of
Graves' disease, it follows that there are no known special causative
indications in the treatment. It is, however, a rational consideration
that anything in the habits and surroundings of patients which is
prejudicial to health has perhaps some agency either in causing or in
maintaining the affection. It is therefore an important part of the
treatment to remove all causes of ill-health which can be ascertained.
The treatment, in this point of view, will embrace injunctions
respecting mental occupations and excitement, a proper proportion of
time devoted to out-of-door life, an adequate diet, avoidance of
dietetic excesses, moderation in the use of alcohol, the disuse of
tobacco, the regulation of sexual indulgence, etc. Without going
farther into details, the object, in general terms, is to place the
patient under the best attainable hygienic conditions.

Any disorders which coexist may possibly be involved, if not in the
causation, in the persistence of the affection. They claim, therefore,
appropriate treatment. Diminution of appetite and difficulties relating
to digestion are {766} to be treated by measures which must vary
according to the circumstances in each case, and which need not be here
considered. Uterine troubles are to be removed. These have been
supposed to stand in a special causative relation to the affection. The
anæmic condition which is so frequently associated (in addition to the
removal of its causes, if these be ascertained and if they be
removable) calls for the long-continued use of chalybeate preparations
in conjunction with dietetic and regiminal treatment. In a case under
my observation in which recovery took place the patient took two grains
of reduced iron three times daily for three years. It is generally
advisable to change from time to time the preparation of iron, partly
for the moral effect of giving a new remedy in order to secure
perseverance on the part of the patient, and in part because,
irrespective of this effect, changes seem to be of use. The prevalent
idea that iron is not well tolerated is to be overcome by assurances,
argument, and, if necessary, by stratagem. It is certain that in most,
if not all, instances this idea is a delusion. The anæmia in this
affection, as in other pathological connections, is only to be overcome
by the long-continued, uninterrupted employment of chalybeates
conjoined with the other measures of treatment. This should be clearly
stated to patients in order to forestall discouragement and neglect of
the treatment advised.

Hydropathic packing and the needle-bath have been highly recommended. A
patient of mine who has recovered apparently derived benefit from daily
sea-bathing. The propriety of these measures is to be determined by the
glow and feeling of invigoration to which they give rise if they be
useful. Should these effects not follow, daily sponging of the body
with cold or tepid water, to which may be added sea-salt or alcohol,
may be substituted. Mental diversion is an important hygienic measure.
The patient should be urged to conquer the feeling of mortification
which prevents social enjoyments and disposes to brooding over the
malady.

The enlargement of the thyroid body naturally suggests the employment
of iodine. This local affection, however, is very different from
bronchocele or goitre occurring independently of Graves' disease.
Experience shows that iodine employed either topically or for its
constitutional effect is useless if not injurious. Many years ago a
case was related to me by a non-medical friend in which thyroid
enlargement had been treated by the application of iodine. Remarkable
prominence of the eyes soon followed, which was attributed to the
iodine, and the physician fell under censure which, as I suspect, he
was not prepared to meet by an acquaintance with Graves' disease. If
the thyroid enlargement be sufficient to occasion tracheal obstruction
or give rise to great deformity, the injection into the gland of a
solution of ergotin may be resorted to. William Pepper has effected a
complete reduction of the thyroid enlargement by this measure, in
addition to ergot given internally. He employed a solution of
ninety-six grains of ergotin to an ounce of distilled water, of which
from six to ten minims were injected weekly by means of a needle
introduced from half an inch to an inch in depth.

For the relief of the exophthalmia, gentle compression upon the eyes by
a compress and bandage during sleep has been recommended. Aside from
this, the indications for local treatment relate to the inflammation
which is liable to be produced by insufficient covering of the eyeballs
by the eyelids and by the impaired consensual movements of the latter
with the former. The patient should, as far as practicable, abstain
from reading, writing, and other uses of the eyes which involve strain.

Insomnia and general nervous irritability may call for palliative
treatment. Opiates should if possible be withheld, owing to their
effect upon appetite and digestion, and also on account of the risk of
forming the opium habit. Other hypnotics and nervines are to be
preferred, but it is best to be {767} chary in the use of these. The
bromides are perhaps the least objectionable of the remedies given to
tranquillize the nervous system and promote sleep, but their prolonged
use is detrimental.

The most important part of the remedial treatment relates to the
accelerated action of the heart. Cardiac sedatives are rationally
indicated, and experience confirms their usefulness. All writers
recommend digitalis in order to diminish the frequency of the heart's
action. A difficulty pertaining to this drug is its liability to
disturb the stomach, and the consequent necessity for discontinuing its
use. It is proper to give it a fair trial. In my experience aconite has
proved more satisfactory. In a case already referred to two grains of
reduced iron and one minim of the tincture of aconite constituted the
medicinal treatment. These remedies, without any increase of dose, were
continued for three years. At the end of this period the patient was in
excellent health and had gained in weight forty pounds; slight
exophthalmia and goitre only remained. In another case the treatment
consisted exclusively of the tincture of aconite in doses gradually
increased to seven minims three times daily. Chalybeates were not given
in this case, because the patient was not anæmic. The remedy was
continued most of the time for two years. The recovery is complete
except that the heart is irritable and moderate prominence of the
eyeballs remains. The treatment has been discontinued in this case for
the past two years. Of veratrum and gelsemium as cardiac sedatives,
which have been recommended in this affection, I have no practical
knowledge. In paroxysms of unusual violence of the heart's action
German writers recommend the application of cold to the præcordia by
means of the ice-bag.

Galvanization of the sympathetic is strongly advocated by German
writers--namely, Eulenburg, Dusch, Guttmann, Von Chvostok, Meyer,
Leube--and in this country by Bartholow and others, as not only useful,
but sometimes effecting a cure. The following extract from a treatise
by Bartholow embraces rules for the employment of this therapeutic
agent: "Recent cases treated efficiently by galvanism are relieved
permanently or their course and progress much modified. During
exacerbations, which constitute a prominent feature of the clinical
history, the passage of a sufficient galvanic current through the
pneumogastric immediately lessens the cardiac excitement. In the
treatment for curative results a mild current is held to be most
efficient (Chvostok). An electrode--the anode--is placed in the angle
behind the jaw, and the cathode on the epigastrium, and a stabile
current is allowed to flow for three to five minutes. The cervical
spine should also be galvanized. It may be included in a circuit by
placing the anode over the vertebræ in turn whilst the cathode rests on
the epigastrium. Stabile may be varied by labile applications. The
faradic current may be used successfully. An instance of this kind has
come under my notice. The first published cases illustrating the
curative value of galvanism were those of Chvostok (1871), who followed
with a series of examples the next year, when Meyer also reported
several cases. In 1874, I read a paper before the medical section of
the American Medical Association advocating this plan of treatment, and
illustrated its advantages by the details of five cases. In 1878,
Vizioli, in a paper on electropathy, amongst others narrated several
cases of Basedow's disease cured. In making the claim for the curative
power for electricity the reader should understand that uncomplicated
cases only are referred to."[10] Rosenthal gives the following
directions: "The ascending stabile galvanic current, from one to ten
elements, is passed through the cervical sympathetic (the anode in the
mastoid fossa and the cathode upon the upper cervical ganglion) for
eight to ten minutes at a time. The current is also directed
transversely across the thyroid tumor, or an ascending current may
{768} be applied to the cervical and upper dorsal vertebræ."[11]
Guttmann states that temporary reduction of the frequency of the
heart's action is first produced, but by persisting in the electrical
treatment the reduction becomes permanent, together with progressive
improvement as regards the exophthalmia and the thyroid
enlargement.[12]

[Footnote 10: _Medical Electricity_, by Roberts Bartholow, M.D., LL.D.,
etc., Philadelphia, 1881.]

[Footnote 11: _Clinical Treatise on the Diseases of the Nervous
System_, by M. Rosenthal, translated by L. Putzel, M.D., New York,
1878.]

[Footnote 12: Vide article entitled "Basedowsche Krankheit," in
_Real-Encyclopedie_, Wien and Leipzig, 1880.]




{769}

DISEASES OF THE PERICARDIUM.

BY J. M. DACOSTA, M.D., LL.D.


Pericarditis.

The diseases of the pericardium, with a few exceptions, belong to the
inflammatory variety, and, as a rule, are the consequences or
accompaniments of other inflammatory diseases of the circulatory system
or of parts near the heart. The most common of the pericardial
affections is pericarditis, which may be simple or secondary, and acute
or chronic.

Pericarditis may occur upon either the visceral or the parietal layer
of the membrane, and may attack any portion or several or all parts at
the same time, being thus circumscribed or general. Usually, the whole
or a large part of the pericardium is affected. Pericarditis is further
characterized by effusions or exudations, which may be either fluid or
semi-solid, and in consequence of the varied character of these
exudations subdivisions are often made, such as the serous, fibrinous,
sero-fibrinous, purulent, sero-purulent, and hemorrhagic forms.
Pericarditis is generally marked by an effusion of fluid, the exception
being designated as dry pericarditis, in which serum or other thin
exuded material is almost or entirely absent.

Simple acute or idiopathic pericarditis is comparatively rare, and some
authorities doubt its existence, believing that the pericardial
inflammation is always secondary, plausibly supposing that the primary
affection has escaped detection. Bamberger and Hayden, for instance,
are of this opinion. I am, however, certain that I have met with
several instances of true acute idiopathic pericarditis. Cases of
so-called simple pericarditis are really often due to injury. It may
not be easy in many cases to determine the traumatic or other condition
in which the apparent simple acute pericarditis originated. The weight
of evidence is so much in favor of traumatism as a preceding and
efficient cause of simple acute pericarditis that a diligent search
should always be made for the same. But even these doubtful examples
are comparatively rare; and pericarditis is in the vast majority of
instances secondary, and not difficult to identify as such. By some,
traumatic pericarditis is classed with simple pericarditis as a
variety, although not idiopathic.

Inflammation of the pericardium is governed by all the laws which
control inflammatory processes elsewhere, being either acute, subacute,
or chronic. The subacute form probably exists frequently, but escapes
detection on account of the latency of the symptoms. The acute form is
the most readily recognized. If not relieved, it passes into the
chronic disease, which may be of long duration. The passage from one
kind to the other is so gradual as to make it almost impossible to
determine when one stops and the other begins, though it may be stated
that after an acute attack has continued for from two to three weeks
the chronic form is established. The chronic affection may begin,
however, insidiously, or develop out of the subacute variety.

CAUSES.--The causes of pericarditis are numerous, and range from simple
{770} cold and injuries to the thorax to those diseases of which it
becomes a companion, whether the seat be remote from, or in immediate
juxtaposition to, the pericardium. Simple cold as a cause of
pericarditis is, as has already been indicated, very much questioned.
Though a very rare, I believe it a possible, cause. Other causes of
simple pericarditis may be blows upon the breast, as with the fist;
crushing or compression, as in railway accidents; penetrating wounds,
as from gunshot or knife; and injury from foreign bodies in the
oesophagus, such as pins, false teeth, etc. Buist[1] records a case of
a man who swallowed a plate with artificial teeth attached. The plate,
becoming lodged in the oesophagus, finally penetrated the pericardium
posteriorly and produced fatal pericarditis. A similar case is recorded
by Flint.[2]

[Footnote 1: _Charlestown Medical Journal and Review_, Jan., 1858.]

[Footnote 2: _Diseases of the Heart_.]

By far the most common form of pericarditis may be termed secondary,
which, like simple pericarditis, may be divided into the acute and
chronic forms. It is termed secondary or consecutive, because it
follows as a result either of impoverishment of the system or a
pre-existing disease, constitutional or local. There are, however,
exceptions to this rule; for we meet with cases of secondary
pericarditis in which pericarditis preceded the onset of, and then
continued associated with, the other manifestations of the disease
which determined it. We see this sometimes in the history of acute
rheumatism.

The disease of the pericardium is often the result of contiguity, but
is much oftener determined by constitutional causes. Why the
pericardium should be the particular membrane selected to take on
inflammation as a complication to other affections has baffled the best
endeavors of the most careful inquirers to determine. The diseases
affecting the pericardium by continuity or contiguity of texture are
chiefly myocarditis, tubercle of the lung and mediastinal glands,
cancer of the same structures, pleurisy, pneumonia, and cancer of the
oesophagus. On fibroid disease of the heart pericarditis is a frequent
attendant.[3] The diseases affecting the pericardium by a special
election, and which are remote from the membrane, are, principally,
acute articular rheumatism, Bright's disease, inflammation and other
diseases of the liver, phlebitis, typhus, typhoid and eruptive fevers,
scurvy, and acute alcoholism. Without doubt, by far the most frequent
cause of pericarditis is acute articular rheumatism. Pericarditis does
not occur in chronic rheumatism, and it is doubtful whether it may be
occasioned by gout, notwithstanding the decided and weighty opinion of
Hayden that this is an efficient cause.

[Footnote 3: It was found in more than half the cases published by
Fagge in _Transactions of the Path. Soc. of London_, vol. xxv.]

Acute pericarditis resulting from acute articular rheumatism has some
peculiarities which it is well to bear in mind. It comes on early in
the disease. We also know of its great frequency as a result of
rheumatism, although the rheumatism be mild; for the intensity of the
rheumatic inflammation is no measure of the extent or severity of the
pericarditis. Nor does the number of joints involved nor their location
give any idea of the greater or lesser liability of the pericardium to
participate in the inflammatory action. Neither does the frequency of
the rheumatic attacks bear any direct relation to the pericardial
involvement; although experience has shown that the first attack
usually is the one most likely to be the cause of pericarditis, while
succeeding ones may or may not produce fresh seizures of pericarditis,
or an aggravation of the disease where it has remained as the result of
previous attacks of rheumatism.

Clinical literature is notably deficient in the reports of pericarditis
ending in recovery, while the recorded cases of death from the disease
as verified by autopsies are most numerous. Yet, although pericarditis
is a serious malady, it is not commonly fatal; and this is especially
true of the pericarditis of acute rheumatism. But it is a frequent
disorder. Sibson,[4] with large experience {771} and patient
observation, has collected and tabulated facts from many sources. In
that particular variety of pericarditis which is the accompaniment of
acute articular rheumatism he found that in 326 cases of acute
rheumatism admitted into St. Mary's Hospital, about one-fifth of the
cases (63) had pericarditis, which was accompanied in 54 cases by
endocarditis; and only in one-fourth of the whole number (79) was there
neither pericarditis nor endocarditis. One-third of the whole number of
cases (108) had endocarditis, and a fourth (76) had threatened
endocarditis, the signs being transient or imperfect. It is notable
that the majority of the cases, regardless of sex and occupation,
occurred prior to the twenty-fifth year of age; and what is equally
notable is that the severity both of the joint and the heart affections
was greatest at or before the same year. Of the 63 cases of
pericarditis in rheumatism, there were 35 males and 18 females; of
these, 11 males and 14 females were from sixteen to twenty years of
age, and the fatal cases were all under the twentieth year.

[Footnote 4: _Reynolds's System of Medicine_, vol. iv.]

Pericarditis happens most frequently between the first and second weeks
of acute rheumatism, although there are instances in which it occurs
later, and occasionally it follows a sudden subsidence of the disease.
It may be observed coincident with the onset of the rheumatic attack,
and even preceding it by several hours. Latham has pointed out how
acute pericarditis is more to be looked for when acute rheumatism is
shifting and inconstant in its seat than when it is fixed and abiding.

Having now looked at rheumatic pericarditis, we may examine the
pericarditis of some other disorders. In that class of affections known
as Bright's disease of the kidney the serous membranes are liable to
take on inflammatory action. A particular preference for the
pericardium seems to exist, and the affections are the cause of
pericarditis next in frequency to acute rheumatism. The tendency
varies, however, with the particular kind of disease of the kidney
which may be present. Pericarditis is common in the contracted kidney;
in amyloid degeneration it is rare.[5] Where uræmia happens, it is apt
to be developed. In warm climates it is less usual as an accompaniment
than it is in cold and damp. But whether this be the full explanation
of the varying frequency of pericarditis as an attendant upon Bright's
disease in different countries is doubtful. There is, however,
certainly, as we learn from the elaborate inquiry of Sibson, a varying
ratio. The complication is, he proves, more frequent in Germany than in
England, least frequent in France.

[Footnote 5: _Ziemssen's Cyclopædia_, vol. xv. p. 629.]

Let us now take into consideration other diseases which in their course
have strong, although less-marked, tendencies to involve the
pericardium. As a class, the eruptive fevers, especially scarlet fever,
may present a pericardial lesion. This is owing to the fact that the
serous membranes generally are liable to become inflamed in these
conditions; but another element in the production of acute pericarditis
may probably be found in the congestion of the kidneys which is apt to
occur. Pericarditis is not commonly present early in these diseases,
but rather in their later stages, when the body is enfeebled by the
specific poison and the skin is susceptible to the slightest variation
of temperature. It is then that the weakest and most vulnerable part
will be attacked, and the pericardium may prove to be the most
vulnerable part.

Other diseases which will cause pericarditis are those dependent upon
dyscrasia of the blood, as in the diatheses, injuries attended by
shock, and those conditions in which there is a great drain from the
system. Perhaps the diathesis most apt to induce pericardial
inflammation is the scorbutic, in which the impoverished and relaxed
state of the system frequently manifests itself by inflammatory lesions
of a low grade. In injuries or diseases {772} where there is excessive
suppuration the system is so weakened that a low form of pericarditis
is prone to develop itself. Diseases of the respiratory organs, as
phthisis, pneumonia, or pleurisy, also enteric inflammations, will
sometimes produce pericarditis. Indeed, any disease dependent upon or
attended by a greatly deteriorated condition of the blood may cause
pericarditis; for the health of the heart itself is determined by the
quality of the vital fluid from which it draws its own sustenance in
common with all other structures of the body, and any vitiated state of
the blood seems to make a special impression upon the heart itself, its
membranes as well as its structure.

MORBID ANATOMY.--In acute pericarditis the serous membrane first
becomes injected with blood, and the injection, starting at a single or
at several points, may become diffuse. If the engorged vessels do not
relieve themselves, infiltration of lymph into the transparent serous
layer follows, producing thickening and opacity as well as slight
roughness. Consequent upon this there is further congestion, the
membrane becomes red, with possibly here and there points of
inflammation of greater intensity than that surrounding the original
lesion; and at these places the vessels may give way and cause a
hemorrhage into the sac or there are little spots of ecchymosis in the
membrane. Usually there is a drying up or a partial suspension of the
serous secretion from the turgid membrane, but before long the
secretion generally recurs, and is even increased in quantity. Upon the
surface of the serous membrane patches of coagulable lymph, more or
less extended, are at the same time exuded. Under the microscope the
bundle of fibres of connective tissue of the membrane appear swollen
and broken up, and the proliferation starts which, as it progresses,
determines the new growth and the villosities. Portions of the exuded
lymph may be washed off and be found as shreds in the serum. The
appearance of the lymphous deposit, as just indicated, is not always
that of a plain smooth layer, but may be velvety and villous, like the
lining of the small intestine, or it may be more roughened, or it may
be honeycombed, as the interior of the stomach of the calf, or be in
ragged shreds of varying sizes, either single or in bunches. Again, it
may assume a lace-like texture, as of fibres coarsely woven together,
or it may appear as if the threads were attached at one end to the
pericardium and at the other floating free. All of these various forms
are largely due to the heart, which in its action presses and rubs the
lymph-covered surfaces together and keeps the softish exudation in
constant agitation. One layer of lymph may be superimposed upon another
until the deposit becomes very thick. It is this lymph which, existing
before fluid is effused to any extent, determines what clinicians
recognize as the dry or plastic stage of pericarditis.

Generally, however, there is effusion of considerable liquid,
occasioning what is termed the stage of effusion. The fluid poured out
is serous, alkaline, and albuminous, of a pale-yellow color, and
transparent, but it may be opaque and milky. It may have flocculi
floating in it, be stained any shade of color from red to brown by the
coloring matter of the blood or by exuded blood-corpuscles, and may
also contain pus. The quantity of fluid varies from a few ounces to
several pints, but the latter amount is rare. The fluid is usually
composed of the watery and saline elements of the blood, with a small
quantity of albumen and a trace of fibrin. If the amount of fluid be
small, the opposing surfaces of the pericardium come together, and the
lymphous layer, becoming more or less organized by the presence of
blood-vessels in it, makes attachments to the opposite wall; in this
manner adherent pericardium is produced. The adhesion may vary in
extent from the slightest filamentous attachment to complete
obliteration of the pericardial sac; and it may be readily peeled off,
or it may be so closely united as to become a part of the tissue upon
which it lies. As the disease progresses the serum and, in exceptional
cases, the fibrinous deposits may be entirely reabsorbed and leave
{773} but little evidence of the previous inflammation. The white
milky-looking spots often found in autopsies are regarded by many as
the remains of cured pericarditis, but they are more likely the result
of nutritive changes and consequent tissue-alteration. Fibrinous
deposits are not always entirely removed. In complete adhesion of the
pericardium they may be considerably reduced, but the sac never regains
its normal appearance, and when the adhesions are partial they remain
permanently.

The formation, density, and organization of the lymph depends largely
upon the cause of the pericarditis. The more acute the attack and the
greater the constitutional disturbance, the more likelihood there is of
rapid effusion of lymph and of its speedy organization, whether it form
adhesions or not. Where the fibrin is exuded under the influence of a
subacute or chronic disease, the formation will be slow, paler, less
highly organized, softer, and if adhesions form they will be less
strong.

The heart participates in the inflammation of the pericardium, and if
it be for any time subjected to the presence of the fluid effusion its
walls degenerate and a granular atrophy occurs. Besides this, in
extensive and firm adhesions there is likely to be primary hypertrophy
followed by dilatation, the walls being enfeebled by degeneration, and,
it may be, becoming thinner. At first, the effort to overcome the
pressure of the pericardial effusion produces the hypertrophy; then the
more or less complete binding down of the walls of the heart,
preventing complete systole and weakening their inherent elasticity,
and the pressure upon the coronary vessels, depriving the heart of the
blood necessary for its healthful existence, are the causes of the
degeneration and wasting of the walls and of the dilatation of the
cavities.

Pus in the pericardium, as a result of pericarditis, may appear very
early in the inflammatory attack, or it may occur after the effusion of
lymph and serum. It may happen but in small amounts smeared over the
surface of the membrane, or be profuse in quantity. Pus may also arise
from small abscesses in the tissue of the heart bursting through the
pericardium. It may be the result of injuries to the pericardium or to
the inflamed membrane, or it may originate in the migration and
proliferation of the leucocytes of the blood. The microscope in
doubtful cases gives us the best idea of their prevalence and quantity,
as well as of the amount of blood-corpuscles present. Where pus alone
exists it is yellow and creamy; but with an excess of serum or fibrin
it may be thinner or thicker in consistence, the entire heart being
bathed in the fluid.

The lesions of chronic pericarditis differ but little from the acute,
except as to their inception or the initial stage. The change from the
acute to the chronic form may occur in a very few days, or even in less
time, and an autopsy would not reveal anything to determine the fact.
Pericarditis in any form is apt to be associated with pleurisy, and
adhesions between the pericardium and adjacent pleura are common. In
some instances the distended sac is adherent to the back of the chest.
By its pressure on the lung and the oesophagus it may produce secondary
lesions in them as well as in the phrenic nerves.

SYMPTOMS.--The symptoms of pericarditis may be so slight as not to
attract attention. Where they are noticeable we find pain or a sense of
uneasiness or of pressure, with or without tenderness in the
pericardial region. The pain or uneasiness is not infrequently
accompanied by pain or tenderness in the epigastric region when
pressure is made upon it. This arises from the contiguity of the part
and the pressure of the diaphragm against the inflamed and tender
pericardium. The pain is sometimes preceded by a chill of varying
severity, and is followed by febrile symptoms of greater or less
intensity; but these may be so slight as to escape observation
altogether except by taking notice of the markings of the thermometer.

{774} Yet the thermometric record, although indicative of fever, has
nothing characteristic. It is, I think, more influenced by the
conditions under which pericarditis happens than by the pericardial
inflammation itself. Often the fever-curve is marked by decided
remissions, and as the result of the pericarditis alone does not attain
a high degree. In the aged, Charcot has pointed out that the
temperature of the body is lowered in some instances of acute
pericarditis. The setting in of pericarditis in acute rheumatism was
observed by Lorain to depress the thermometric marking, and Brouardel
has noted the same effect at the onset of pericarditis in typhoid
fever.[6]

[Footnote 6: Constantin Paul, _Maladies du Coeur_, Paris, 1883, p.
130.]

The action of the heart is increased in frequency and force, as
indicated by observing the impulse and the pulse at the wrist. There
may be present, in different degrees, difficulty of breathing or a
sense of suffocation; difficulty in swallowing; also cerebral
disturbance, as headache, dizziness, sleeplessness, mental depression,
fear of impending death. Besides these we may meet with hiccough and
nausea and vomiting. But any or all these symptoms may also occur in
myocarditis and in endocarditis, and are therefore not of themselves
diagnostic; they only serve as indicators of the direction in which to
seek the cause of disturbance. Some of the latter symptoms may be so
aggravated, particularly those manifested by the nervous system, that
attention is absolutely diverted from the seat of the disease. Indeed,
they are often very misleading; and I cannot even agree to Hayden's
statement[7] that with few exceptions the symptoms of pericarditis take
precedence of the physical signs, though they cannot be regarded as
sufficiently distinctive to warrant a positive diagnosis. Doubtless
these symptoms, however suggestive of pericarditis, may be found to
depend upon other causes. With so little, then, of a positive nature to
assist us in our search, we should be always at great loss were it not
for the physical signs.

[Footnote 7: _Diseases of the Heart and Aorta_.]

PHYSICAL SIGNS.--The chief of these are determined by inspection of the
chest, by palpation, by auscultation, and by percussion.

Inspection.--In inspection of the chest the age of the patient is to be
regarded in the interpretation of the appearances. In pericarditis with
effusion we are apt to find a change in the shape of the chest--a
bulging in the region of the heart, even though the effusion be
somewhat small in quantity. This change is more apparent when it occurs
in young persons, where the chest-walls are very elastic. In those
advanced in years, in whom the costal cartilages are more or less
ossified and the elasticity of the rib materially altered, or where the
chest-walls are bound down by pleuritic adhesions, the shape of the
chest may be materially altered and yet not be very apparent. The
intercostal distension is in any case a matter for investigation. The
chest shows a bulging in the pericardial region, slightly diminished by
a dorsal decubitus and but little influenced by the acts of
respiration.

Palpation.--This gives us an idea of the amount and outline of the
tenderness, which is often found to correspond with that of the
inflamed pericardium. It also enables us to determine to some extent
the limit of distension of the pericardium, the location of the heart,
and the shape of the sac. We also ascertain the impulse of the heart.
Now, at first this is somewhat increased, although it is apt to be
irregular. As effusion of liquid takes place, the heart is displaced
generally backward and upward, and the impulse becomes indistinct or
imperceptible. A slight wavy, irregular motion diffused over
considerable part of the cardiac region may take its place.

Percussion.--During the dry stage, unless a very considerable amount of
lymph be extravasated, the natural percussion dulness in the cardiac
region is not appreciably altered. When the pericardium becomes
distended with fluid the cardiac dulness increases markedly,
particularly in a transverse {775} manner; and as the pericardium is
conoidal in shape, but its position the reverse of that of the heart,
its base resting upon the diaphragm, with its distension a roughly
pyramidal outline of dulness is found, the apex being near the root of
the vessels, the base upon the diaphragm. A great deal of stress has
been laid on this shape of the percussion dulness--much more, I think,
than in point of fact is warranted, for it is not always to be
distinctly made out. Rotch[8] has called attention to the dulness being
early manifest in the fifth intercostal space of the right side, and in
all large effusions it is sure to extend across the sternum. It may,
when the sac is much distended, reach as high as the first rib, as low
as the seventh rib, and below the ensiform cartilage, and the line of
the lower dulness may become continuous with that of the displaced
liver. The dulness may extend on the left side backward almost to the
spinal column and across the sternum to the right nipple. The dulness
is somewhat influenced by position; changing from side to side alters
the line of the fluid.

[Footnote 8: _Boston Medical and Surgical Journal_, 1878, vol. xcix.]

Auscultation.--Pericarditis is not discoverable without the signs by
auscultation, and it is the interpretation of these signs which enables
us to distinguish the various stages. We must bear in mind that,
roughly speaking, there is first a stage of suspension of the serous
secretion, and consequent dryness of the pericardium; secondly,
effusion of lymph or fibrin; thirdly, effusion of serum or sero-pus.
Now, the question arises whether we can distinguish the first effect of
the inflammation on the serous membrane, which, indeed, may be
exceedingly short in duration, limited to a few hours. From the fact of
there being a suspension of secretion and absorption of that which has
been normally secreted, it becomes evident that, the parietal
pericardium coming into direct contact with the visceral layer, certain
sounds will be caused by the friction of the heart in its action. Can
we discern them? Great differences of opinion have been expressed with
reference to this; indeed, it has even been questioned whether sounds
would be or would not be produced. Stokes doubted the competency of
simple dryness of the pericardium to generate friction phenomena.
Collin, on the contrary, held that this is actually the condition of
the pericardium indicated by the new-leather sound. To this Walshe
makes assent. Hayden[9] says: "I have never met with a case which would
warrant me in asserting that a state of simple dryness and vascularity
of surface may give rise in the pericardium to veritable friction
sound. I do not, however, deny the possibility of an occurrence which,
theoretically, would seem not improbable. In every instance, without
exception, in which I have had the advantage of determining by
post-mortem examination of the body the condition of the serous surface
of the pericardium, where friction sound of indubitable pericardial
origin had existed during the patient's last illness, I have found
lymph in greater or less quantity effused upon the surface." My own
experience is entirely in accord with this. Theoretically, I grant the
possibility. Practically, I have never seen it; and in the suspected
cases lymph has always been found, with the single exception of a case
in which the friction sound had disappeared nearly a week before death,
which resulted from kidney lesion, and where it was reasonable to infer
that the lymph had been absorbed.

[Footnote 9: _Diseases of the Heart and Aorta_, Philada., 1875, vol. i.
p. 327.]

The friction sound, then, is the sign of exudation. Since it was
originally described by Stokes in 1833 it has been likened by different
observers to familiar objects, such as the crackling of parchment and
the new-leather sound. It is generally most evident at the base of the
heart, is considerably influenced by pressure, is more often double
than single, frequently resembles a double cardiac murmur, and
justifies the name of a to-and-fro sound given to it by Watson. The
friction sounds change from time to time according to {776} the
character, quantity, and stage of the exudation, ceasing altogether
when adhesions have taken place or fluid has been effused, to return
again as the fluid is absorbed, and to cease when recovery has taken
place. They exhibit an inspiratory rhythm very much intensified by full
inspiration. Although, as the place of election of the inflammation is
at the base of the heart, we are apt to find the friction there
earliest as well as longest, this is not invariable; for, as above
stated, the morbid process may begin anywhere in the continuity of the
pericardium.

Next to the friction sound, the most valuable signs in pericarditis are
derived from the muffling of the cardiac sounds. This is particularly
valuable in the stage of effusion, for prior, notwithstanding the
friction phenomena are somewhat obscure, they do not render the sounds
of the heart fainter to any material degree. The cardiac sounds become
less and less distinct as the fluid increases. The heart sounds cease
to be audible, just as is the case with the friction sound, from below
upward, beginning to be indistinct at the apex of the heart. Gradually
and lastly, the sounds of the aorta and pulmonary valves are lost, but
not entirely, unless there be a large amount of fluid pushing up the
pericardium at its attachment around the roots of the great vessels,
and the second sound at these valves is scarcely ever wholly gone.
Sudden effusions of large quantities of fluid are so rare that the
progressive extinction of the cardiac sounds becomes an important
element in diagnosis and prognosis. It has already been noted that the
friction sounds linger around the base of the heart; this may happen
with even considerable effusion. As regards the character of the fluid
influencing the distinctness of the cardiac sounds, I think it may in
general terms be stated that if the effusion be dense, sero-purulent,
or purulent, the sounds of the heart are, in proportion to the size of
the effusion, relatively more obscured than when this is thin.

DIAGNOSIS.--The diagnosis of pericarditis, as before remarked, cannot
be determined by any but physical signs, and even these signs may not
be sufficient for us to come at once to a positive conclusion: the
refinement of perception necessary to detect and properly interpret the
delicate changes which occur in some cases is still lacking to us. In
reviewing the general diagnosis of pericarditis we must bear certain
facts in mind. The acute malady has a very dissimilar origin. It
usually sets in with a fever, ordinarily not of high grade, which may
be preceded by a chill of differing intensity; the pulse is decidedly
accelerated and of varying regularity, not uncommonly strikingly
irregular; on the other hand, the nervous phenomena may be the most
prominent. Craigie[10] observed long ago in a case of pericardial
inflammation in a girl of fourteen that the only prominent symptom
besides the symptom of fever was constant tossing of the extremities
and person, jactitation similar to the motions of the dance of St.
Vitus. Roeser of Bartenstein observed the same symptom in a child of
nine years. There is at times early delirium, very frequently
considerable restlessness, with more or less of an anxious expression
of countenance. Quickened rather laborious breathing is often early
observed, and so is pain in the præcordial region directly under or
near the sternum, perhaps extending to the left shoulder, acute,
severe, and shooting, increased by pressure and motion, and, as
Peter[11] has pointed out, associated with pain in the phrenic nerve,
elicited by pressure between the two insertions of the sterno-mastoid
and also found on each side of the xiphoid appendix. But the pulse may
be regular, the breathing not perceptibly accelerated or laborious, and
even the important symptom, pain, may be wanting from the beginning to
the end of the disease. This occurs in the so-called latent cases.

[Footnote 10: _Elements of the Practice of Physic_, Edinburgh, 1837,
vol. ii. p. 151.]

[Footnote 11: _Clinique Médicale_.]

Since pericarditis is frequently attendant upon certain classes of
diseases, {777} as acute articular rheumatism, Bright's disease of the
kidneys, the eruptive fevers, it behooves the physician to be on the
alert and examine the heart, even though nothing point to its
involvement. Reminded of this fact, we must seek for those signs which
will enable us to diagnosticate early the cardiac disease. And in any
case the first sign of importance detected will be, in all probability,
the friction sound, generally, but not invariably, first heard at the
base, and prone to mask the natural sounds of the heart. At all events,
this is the case when the friction sound is localized at the apex of
the heart, as it occasionally is, before there is very marked
development of the lymph-deposit; it is then, too, that from its
softness the friction may be mistaken for a regurgitant mitral murmur.
The friction may at times be felt by applying the hand to the region of
the heart. This friction fremitus is, however, far from constant, and
can hardly be considered of much diagnostic value, notwithstanding the
high authority of Stokes, who looked upon it as distinguishing
pericarditis from valvular disease. Prior to the existence of the
friction sound we may suspect pericarditis by the sense of general
distress and the dropping of pulse-beats or the otherwise altered
cardiac rhythm. But the diagnosis is presumptive; the friction
phenomena make it positive. Until the quantity of fluid is sufficient
to separate the two walls of the sac the rubbing sound will be
apparent. The friction sound never disappears suddenly, and this
gradual disappearance points to the formation of fluid and may be
regarded as a truly diagnostic sign. The fluid, following the laws of
gravitation, seeks the most dependent portion of the sac, which it more
or less fully distends; in consequence, the disappearance of the
friction begins at the bottom of the sac and at the apex of the heart
and gradually extends upward to the base. Adhesions of the pericardium
will modify and may entirely prevent the formation of the friction
sounds. If the adhesions be local, and if no lymph-deposit be present
between them, there can be no friction; so also where the adhesion is
general the friction sound is destroyed. Where local adhesions and
portions of free surface more or less covered by the lymph exist, the
heart, being allowed sufficient motion, produces friction sounds which
may be found anywhere over its surface except at the points of
adhesion. From the character of these sounds the location and the
extent of the adhesions and of the cardiac movements may be determined,
for "the rhythm of the pericardial friction sound is as the natural
movement of the portion of the heart engaged and the mobility of the
opposed surfaces," says Hayden[12] very truly.

[Footnote 12: _Diseases of the Heart and Aorta_.]

In weighing the value of friction sounds in diagnosis, especially in
determining whether they are produced in the pericardium and not in the
adjacent pleura, we have the simple, though not infallible, method of
discrimination of letting the patient cease breathing for a moment and
then ausculting the heart: they persist if pericardial. This test will
fail, however, in case a portion of the pleura adjacent to the
pericardium also be covered with lymph: then the heart's motion,
transmitted through the pericardium, may produce pleuritic friction
even while the lung is at rest. In such a case if a friction fremitus
be felt it will pass beyond the cardiac area, while in pericarditis
without associated pleurisy it will not be likely to extend farther
than the normal limit of cardiac dulness. The pericardial friction
sound may be sometimes noticed more or less extensively over the whole
chest in children, and also in adults with hypertrophy of the heart,
but this is far from being usual. There may be a friction sound
produced by the action of the normal heart in an inflamed roughened
pleura. This is very difficult to distinguish except by the attending
symptoms. The sound is perceived near the apex of the heart. It is not
apt to occur with each beat of the heart, and may be absent in held
expiration.

{778} In the diagnosis of pericardial effusion, when at all extensive,
we have, in judging of the amount of fluid in the pericardium, to take
into account the increasing dyspnoea with a decided suffocative
tendency, the dizziness, the pallor or lividity of the countenance, the
swollen cervical veins, the bluish nails, the heart flutterings, the
weak, rapid, and irregular pulse, the drowsiness or tendency to mental
wandering. But the physical signs of the effusion above detailed are of
the greatest value, although they give us but little information as to
the character of the fluid. Even in large effusions the friction sound
may not disappear from the base. Indeed, Balfour[13] records as the
result of his observation that "however large may be the effusion,
basic friction, if it have once existed, is never effaced." It is
stated that when the amount of fluid does not entirely fill the
pericardium there may be a splashing sound, and the location of the
sound, as well as that of the percussion dulness, will be changed by
changing the position of the patient's body. I have never observed this
splashing sound. The extent of percussion dulness is no absolute sign
of the extent of effusion. The area of cardiac dulness may be
materially influenced by the following circumstances: the anterior
margins of the lungs which overlap the front of the heart may, from
emphysema, give rise to percussion resonance over the heart, even
though considerable effusion have taken place; the anterior margin of
the lungs, becoming solidified and having strong pleuritic attachments
to the pericardium and anterior chest-wall, may increase the dulness
over the heart and prevent the recognition of the effusion in the
pericardium; effusion in the pleural cavity of one or both sides may
produce similar results. Balfour[14] in fact mentions a case of his own
in which the pericardial dulness was merged in the pleuritic dulness,
and careful auscultation failed at any time to detect friction sound;
the coexistence of pericarditis was surmised, but could not be
detected. After death the pericardium was found to be distended with
reddish serum, and both its surfaces were coated with shaggy,
blood-stained lymph. Such cases are unusual, yet I have met with a
similar instance. Lastly, a growth in the anterior mediastinum may be
the means of masking or being mistaken for pericardial effusion by
changing the dulness in the cardiac region and altering the cardiac
sounds, or it may, by obstructing the circulation, cause effusion. When
an effusion of fluid takes place into a partially adherent pericardium,
the area of cardiac dulness may be irregular or restricted, or both,
the shape and size depending on the length and strength of the
adhesions.

[Footnote 13: _Diseases of the Heart_.]

[Footnote 14: _Ibid._]

Some of the results of large effusions show themselves on other organs.
The backward pressure of the fluid upon the bronchi, trachea, aorta,
and oesophagus interferes with their functions and actions. There may
be bronchial or blowing respiration heard over the lung, due to
compression of the parenchyma. The fluid around the heart prevents free
motion of the organ, although not to so great an extent as in adherent
pericardium; complete diastole does not occur; the auricles and
ventricles are not completely filled; the systemic and pulmonary
circulations become engorged, and pressure is exerted upon the coronary
arteries, thus disturbing the nutrition of the heart. The irregular
action of the heart occasions at times a vibration which is more or
less apparent to the touch. Percussion of the liver shows enlargement
of the viscus; this is due to the obstruction of the ascending vena
cava, which prevents a free emptying of its blood into the right
auricle, and consequently causes a backing up of the blood in the
gland. If the pericardial effusion press upon the anterior portion of
the chest, it may produce pain and aggravate all the other symptoms,
such as the pulmonary oppression, the dizziness, the hurried
respiration, the increase of pulse. Water, blood, or pus in the
pericardial sac gives rise to the same physical signs as serous
effusion, and {779} cannot be distinguished from it with any degree of
certainty, although a careful consideration of the general symptoms
presented may enable us to make a guess which can only be proved or
disproved by an autopsy.

Having endeavored to show the most prominent features characterizing
pericarditis in its various stages and bearing in a general way on its
diagnosis, we shall examine some of the special maladies which are
liable to be confounded with it. The diseases most likely to be
mistaken for the acute inflammatory stage of pericarditis are
inflammation of the pleura and of the endocardium. They are liable to
occur from the same causes, and may be--indeed, often are--concurrent.
Pleurisy gives rise to many of the symptoms of pericarditis. The chief
difference is in the physical signs, some of which, however, are alike
in kind, although different in locality; for in pericarditis they are
confined to the region of the heart: in pleurisy they are spread over
the whole side of the chest and are most perceptible at the back. This
is true of the dulness, and for the most part of the friction sound,
which when of pericardial origin is very rarely heard posteriorly. Then
stopping the act of breathing if the sound be pleural suspends it. At
times, however, as above described, we meet with cases in which a
friction sound discovered over the heart may in reality be produced in
the adjoining pleura. To confound the dulness on percussion caused by
liquid in the pericardium with that due to liquid in the pleura is,
from the different site of the liquid, not likely to happen unless the
effusion be extremely large; for ordinarily a pericarditis
uncomplicated with pleurisy or with pleuro-pneumonia does not change
the clear sound at the back of the chest nor enfeeble or abolish there
the breath sounds and the vocal fremitus. Besides, effusion into the
pleura, if it give rise to a flat sound anteriorly, does not occasion
the special præcordial bulging, and shows the sounds of the heart
unaltered unless the pericardium contain fluid also.

Acute pericarditis is likely to be confounded with acute endocarditis.
The chief difference consists in the physical signs--the friction
sounds and signs of effusion in pericarditis, the blowing sounds, the
slight alteration of percussion dulness in endocarditis, and the fact
that in this disease the abnormal murmurs are often transmitted beyond
the cardiac region and heard in the carotids and subclavian, and are
far less changeable in character and in pitch.

There are other affections with which pericarditis is likely to be
confounded, such as gastric irritation and acute inflammation of the
brain. When pericarditis resembles gastric disorder the thoracic
symptoms may be latent, but the disease produce the manifestations of
extreme gastric irritation or inflammation. There are nausea and
vomiting, and tenderness on pressure in the epigastric region, yet no
disease of the stomach may be present. An examination of the cardiac
region for the physical signs of pericarditis should be made in every
case of persistent vomiting or of hiccough.

Where the symptoms are chiefly cerebral, the cardiac disease may be
overlooked; indeed, in both endocarditis and pericarditis the insomnia
and the active delirium may throw all the other symptoms into the
shade. The violent disturbance of the brain may have its origin, in
part at least, in the contaminated state of the blood which occurs in
the affections, as rheumatism or Bright's disease, with which
pericarditis is often associated. But it is possible also that it may
be due to a coexisting endocarditis of which the products are washed
into the brain. In ulcerative endocarditis cerebral manifestations are
especially common, and there may be acute mania of the most violent
type, as in the case reported by Sioli.[15] Sibson in his exhaustive
analysis points out what I have known to happen in more than one
instance, that the desponding and taciturn--or, as he calls it,
sombre--delirium of pericarditis lasts from two to three weeks to as
many months. Indeed, it may terminate {780} in confirmed insanity. Any
form of nervous disturbance having its centre of disorder in the
cerebro-spinal axis and of any degree of intensity may be seen in cases
of pericarditis, whether produced as a consequence of rheumatism, of
albuminuria, or by other causes. The cases with marked nervous symptoms
are apt to present high temperature, 105° or more.

[Footnote 15: _Archiv für Psychiatrie_, Bd. x.]

The diagnosis of pericarditis from hypertrophy of the heart is made by
remembering that in pericarditis we find friction sound, præcordial
bulging, peculiar enlargement of percussion area, enfeebled impulse and
heart sounds, besides the presence of pain, of fever, of dyspnoea. In
hypertrophy the area of percussion dulness is enlarged, but the shape
is normal; the impulse and heart sounds are strong; no pain or fever,
no friction sounds exist. The chance of mistaking dilatation of the
heart for pericarditis is much greater. In the early stage of
pericarditis the area of percussion dulness is generally similar in
size and shape to the dulness in dilatation. But soon the difference
both in size and shape of the cardiac area becomes marked, the shape
being pyramidal or pyriform in pericardial effusion, while in
dilatation the increase is lateral and does not extend beyond the point
of impulse. There is no friction sound in dilatation; and if the first
sound be weakened, though it may be also sharp and short, the second
sound is everywhere distinct, unlike the muffling of the cardiac
sounds, except at the base, in pericardial effusion.

Tumor of the anterior mediastinum, whether solid or fluid, may become a
source of perplexity in determining the diagnosis of pericarditis; for
by the interposition of the morbid mass between the chest-wall and the
heart the cardiac dulness is increased and the heart sounds are
lessened in distinctness and perhaps in force; though if the tumor be
solid and very dense the sounds may be intensified. Pericarditis may
also be associated with a tumor, and a diagnosis under such
circumstances is attended with great difficulty. A tumor of the
anterior mediastinum is comparatively rare, and seems to be more
frequent in females than in males, although the statistics are meagre
and not conclusive. There may be displacement of the heart in any
direction as the result of pressure from the growth. Should this be
equable in front of the heart, the diagnosis becomes one of doubt, for
the same alteration of the shape of the chest may be present as in
pericarditis with effusion. If the tumor be malignant or scrofulous,
tumors of a similar character may be found in the neck, axilla, or
elsewhere, and aid us in arriving at a correct conclusion.

The differential diagnosis of pericarditis from inflammation of the
anterior mediastinum will cause at times no slight difficulty. However,
inflammation of the anterior mediastinum is infrequent. It may come on
without assignable cause or as the result of injuries. It may be
produced by extension of inflammation from adjacent parts, as in
pericarditis; it does not appear in association with, or as a
consequence of, other diseases, such as rheumatism, renal diseases,
scurvy, or the exanthemata, as is so largely the case with
pericarditis. The symptoms resemble those of pericarditis, and there is
likely to be chill, followed by fever, substernal pain and weight, pain
on pressure over the sternum, accelerated action of the heart.
Respiration is more or less difficult and painful, on account of the
movements of the cartilages and intercostal muscles. The disorder in
respiration becomes the more decided when the inflammation has extended
to the pleura; there is also pain on pressure in the epigastrium. The
physical signs of mediastinitis may be precisely similar to those of
pericarditis. The extension of the inflammation to the adjacent parts
produces the characteristics of uncomplicated inflammation of these
parts, and under such circumstances the distinction is far from being
easily made; the pleuritic and pericardial friction sounds which are
developed will naturally be ascribed to affections of the pleura and
pericardium alone. In accumulation of pus in the mediastinum no little
uncertainty {781} will exist in determining the difference between this
and pericardial effusion. The percussion dulness may extend beyond the
area of the heart, and take the form of the area in effusion into the
pericardial sac. It is true, however, that in purulent collections in
the mediastinum the shape of the percussion dulness is often more
elongated, extending upward to the sterno-clavicular articulation.
Should the accumulation be large, we meet with difficulty of
respiration and of deglutition from pressure, as in pericarditis with
effusion or in hydropericardium; and there may be elevation of the
sternum and intercostal bulging. Abscess of the mediastinum tends to
point at an intercostal space; it may also do so in the scrobiculus
cordis: the impulse of the heart is weakened or entirely lost and the
heart sounds are distant and obscured. There is apt to be hectic, with
headache, delirium, and syncope. In fact, there is no symptom of
pericarditis or of hydropericardium which may not also be found in
acute mediastinitis or in the accumulation of pus in the mediastinum.
Where the inflammation can be traced to an injury, as a blow upon the
sternum, or where there exists caries or necrosis of the sternum, the
diagnosis is greatly facilitated. The inflammatory symptoms, while of
all grades of intensity, are, as a rule, more intense in the forms of
mediastinitis than in any of the acute stages of pericarditis. In cases
of fibrinous mediastinitis associated with fibrinous or fibro-purulent
pericarditis, Kussmaul has called attention to the diagnostic value of
a pulse intermitting at regular intervals simultaneously with
inspiration, the pulsus paradoxicus.

PROGNOSIS.--The prognosis of pericarditis is exceedingly variable,
depending largely upon the primary cause, the intensity, the stage and
duration of the attack, the prior condition of the individual, and his
surroundings. The general prognosis is favorable to life: though some
of the older writers were disposed to look upon it as a highly
dangerous disease, it is clearly one from which recovery is frequent.
In many autopsies of individuals who have subsequently died of other
disease the evidences of cured pericarditis have been found. By cured
it is not wished to convey the idea that the pericardium was restored
to the condition it was in prior to the inflammatory attack, but that
the inflammation had ceased without injurious consequences. There may
be recurrent attacks, and they are frequently of a subacute character;
even when fibrinous deposit and attachments continue to exist, it often
happens that the movement and functions of the heart are not interfered
with. Unless the disease be exceedingly severe in the acute stage, the
prognosis is decidedly favorable. When the attack is very severe there
are strong reasons for believing that the structure of the heart is
also involved, and death ensues chiefly from the latter complication.

Should adhesions take place, the prognosis is unfavorable in proportion
to their extent, though to this rule there are decided exceptions. If
effusion rapidly develop, the prognosis becomes at once unfavorable,
death resulting in a short time from sudden pressure upon the heart and
its palsy. If, however, the effusion accumulate slowly, the parts
become tolerant, and a large amount of fluid may be thrown out without
fatal consequences. Where death occurs it usually comes on slowly, and
the immediate cause is from the pressure of the large effusion upon the
heart, preventing its free diastole. The lungs become engorged with
venous blood, and asphyxia of the heart ensues. There is apt to be
general dropsy in such cases, particularly oedema of the lower limbs
and accumulation of fluid in the serous cavities, as in the pleuræ, and
the patient becomes gradually exhausted. If effusion of serum be
accompanied by pus or by blood, or if there be pericarditis with pus or
blood alone, the prognosis is unfavorable. Balfour,[16] however, states
that recovery is not impossible in purulent pericarditis, "for the
elements of pus are more or less present in every pericarditis, and pus
may be only a transitional {782} stage, and may result in the breaking
down of cell-elements, the formation of a pathological cream, and its
complete absorption, and the perfect cure of the disease." The caseous
formation, or even the pathological cream, is rarely met with, and
cannot be detected prior to death. Burrows[17] records a case in which
there was a layer of concrete pus over a small space in a pericarditis
of seven days' duration. Pericarditis with large amount of membrane,
whether this be coated with pus or not, and even without liquid
effusion into the sac, is always of grave prognosis; so are cases with
high temperature, cases complicated with pneumonia, cases in which the
dyspnoea is of intensity disproportionate to the local symptoms, and in
which the pulse is not in unison with the impulse of the heart.

[Footnote 16: _Diseases of the Heart_, 1876, p. 299.]

[Footnote 17: _Disorders of the Cerebral Circulation_, London, 1846, p.
187.]

The pathological changes in pericarditis are such that it is quite
impossible to determine by the special signs or symptoms of the
affection between simple pericarditis and a pericarditis the result of
transmission from diseases in adjacent organs, as pleurisy or
pneumonia, or as a complication of rheumatism or Bright's disease,
except by the history and the general features of the case. Yet the
prognosis is vastly different. The prognosis of simple pericarditis
without carditis is good. Pericarditis in acute articular rheumatism is
generally favorable as to life, and is nearly as favorable as simple
pericarditis. Balfour[18] states that he has records of 1968 cases of
disease treated in the Royal Infirmary, 70 of which were cases of acute
rheumatism, with but 1 fatal case of rheumatic pericarditis. My general
experience of the favorable character of rheumatic pericarditis without
marked involvement of the deeper structures of the heart corresponds
with this. I except, however, the comparatively rare cases with high
temperature. A temperature of 105° is always grave. The prognosis of
pericarditis in Bright's disease is, speaking in general terms, as
unfavorable as that of the pericarditis of acute rheumatism is
favorable. The pericarditis of poisons, of pyæmia, or of scurvy is, as
a rule, a very serious malady. In the exanthemata recovery is the rule,
unless there be extensive pleurisy or pneumonia as a complication.

[Footnote 18: _Op. cit._, p. 288.]

In injuries, such as in rupture or puncture, the prognosis must depend
upon the extent and the character of the injury, the condition of the
patient, and whether or not the puncturing body has been removed from
the wound. Generally, these must be regarded as unfavorable cases,
although paracentesis of the pericardium is now accepted as a proper
operation and is attended with comparatively little risk. The cerebral
symptoms occurring in pericarditis can hardly in themselves be regarded
as unfavorable to life, but they are unfavorable when associated with
high temperature and when considered in connection with full recovery
of the mental powers. Relapses and recurrences of pericardial attacks
have strongly fatal tendencies. Age and sex contribute materially to
the prognosis. The very young and the aged are unpromising subjects;
and Sibson[19] has shown that while females are somewhat more liable
than males to acute articular rheumatism, males are more often attacked
with rheumatic pericarditis; also that endocarditis accompanies
pericarditis more frequently in males than in females, while simple
endocarditis is more frequent in the female than in the male. He also
shows that while pericarditis affects the two sexes below the age of
twenty-one in nearly equal proportions, after the twenty-fifth year
males are three times oftener subject to it than females. The disease
is greatly modified by occupation as well as by age. Thus, Sibson has
pointed out that female domestic servants under twenty-one years of age
are extremely prone to acute rheumatic pericarditis, endocarditis, and
carditis, as they are often unequal to labor and fatigue, and are
easily affected by draughts and by exposure to wet and cold.

[Footnote 19: _A System of Medicine_, by Reynolds.]

{783} The causes of death in pericarditis are various. Death may occur
in a few hours after the attack by the rapid effusion of a large
quantity of fluid, compressing and causing mechanical paralysis of the
heart; or it may happen from syncope due to the patient making sudden
exertion, as in getting out of bed, more especially if there be a large
amount of fluid in the pericardium; or, again, it may be owing to
paralysis of the heart from disturbance of the cardiac centres, or to
fatty degeneration of the cardiac walls largely induced by the
inflammatory condition. Again, a fatal termination may be caused by
pneumonia or extensive congestion of the lungs, or by a large quantity
of fluid in the pleura, having its origin really in the pressure
exerted on the veins and the other structures by the pericardial
effusion; or death may result from non-aëration of the blood and from
general exhaustion.

TREATMENT.--In the treatment of acute pericarditis the first thing to
insist upon is absolute rest--rest of body, rest of mind; all effort,
all fatiguing conversation, is to be avoided. The diet should be of an
easily-digested kind, nourishing, but given in small quantities at a
time, so as not to distend the stomach. Milk, eggs, animal broths, with
occasionally just enough solid food to gratify the wish of the patient,
constitute the best diet. Further, from the very outset the cause of
the malady should be clearly kept in view and the treatment directed in
accordance. As so many cases have their origin in rheumatism, an
antirheumatic treatment has usually to be carried out. But here let me
at once record the more than uselessness of the salicylates. They have
no influence when pericarditis has arisen, and if salicylic acid or its
compounds are being given, they should at once be stopped. The alkalies
have a far better action. Again, speaking in general terms, opium in
moderate doses, to keep the nervous system quiet and to moderate the
general discomfort, is of wide applicability and signal use; few are
the cases which its steady, judicious employment will not benefit.
Especially is this witnessed in the earlier stages and before marked
effusion occurs.

The treatment of acute pericarditis is much influenced by the stages of
the malady--whether it is seen in the stage with plastic exudation;
whether this exudation markedly persist and but little liquid effusion
takes place; whether the effusion is copious. Now, in the earlier
stages and before decided effusion bloodletting was at one time much in
vogue, but it has been by general consent abandoned, at least general
bloodletting has. Local bloodletting is still employed by some, and I
am sure I have known a few cups to the præcordial region or leeches
there applied relieve the pain and make the action of the heart more
regular. It is, I think, in robust subjects and in the early stages
decidedly to be recommended. Mercurials, like general bloodletting,
have fallen into disuse. Cases of pericarditis have been seen to
originate in those whose gums were touched by mercury, and it does not
prevent effusion. Certainly, in pericarditis with Bright's disease the
remedy must not be thought of; but under other circumstances, in
lingering cases with extensive plastic deposits, or in effusions that
remain uninfluenced, it is worth a trial.

The application of cold to the cardiac region, either in the shape of
cold compresses frequently changed or of a bladder of ice, is very much
lauded by some of the French and German physicians. Gendrin's method
consists in keeping a bladder of ice over the heart for from one to
three hours until the pulse and temperature come down to about a normal
condition. As these rise it is from time to time reapplied, although
for a shorter period; and it is thought to influence both the pain and
the inflammation. I have not seen the latter effects from it; and for
the pain it is less trustworthy than the more commonly employed
hot-water applications and poultices. Digitalis is in the earlier
stages an admirable remedy. Its use in small, frequently-repeated doses
will render the action of the heart more regular and reduce {784} its
frequency. Friedreich[20] and Bauer[21] both recommend its employment
in large doses, to be suspended when the pulse becomes slower or
irregular. Notwithstanding it might be thought particularly valuable in
marked effusions alike from its tonic action on the heart and its
diuretic powers, my clinical experience is against it under such
circumstances. It is far inferior to the free use of stimulants.

[Footnote 20: _Die Krankheiten des Herzen_.]

[Footnote 21: "Diseases of the Pericardium," _Ziemssen's Cyclop._]

When there is decided effusion diuretics are our main dependence, and
squills and tartrate or acetate of potassium are most employed. The
acetate of potassium is very serviceable--half an ounce or more in
twenty-four hours in broken doses. Nor need we wait for the occurrence
of the effusion to begin with this remedy. An occasional hydragogue
cathartic is also indicated where the strength of the patient permits;
but care must be enjoined not to let him rise to go to stool. In
lingering effusions iodide of potassium, not less than forty grains
daily, and repeated blisters are employed. The latter remedy may also
be used early in the case where the friction sound is extensive, and a
large blister then is better than a small one.

A state of things is at times met with in which the pulse is weak, the
extremities cool, the effusion large, the impulse of the heart very
faint, the heart evidently struggling. There is but one remedy for
this--the free use of stimulus, whiskey or brandy or wine, whichever is
best taken. Nor do cerebral symptoms contraindicate--on the contrary,
they more decidedly indicate--stimulants. Tonic doses of quinine and
hypodermics of brandy aid in this stage. Should the symptoms still
prove unyielding and the effusion large, the question of puncturing the
pericardium will arise; and as a means at least of gaining time the
operation is strongly indicated. Its manner of performance and its
general results have been carefully studied by John B. Roberts, and to
his remarks in this volume the reader is referred. We cannot be too
careful to be on the lookout for the pulmonary complications, pleurisy
or pneumonia, which are so apt to be found in acute pericarditis. They
require prompt treatment, but they ill bear depressants. They demand,
among other means, often quinine, and the greatest attention in
sustaining the action of the heart and in keeping the kidneys actively
at work. When the dyspnoea is very great, and there is considerable
pleural as well as pericardial effusion, it is best to tap the pleura.
I have several times given this advice in cases in which it was under
discussion to tap the pericardium, and after the relief afforded to the
lung the pericardial affection has yielded to remedies.


Chronic Pericarditis.

Chronic pericarditis, as such, requires but little consideration here,
since its main features have been discussed in this article under other
heads.

Chronic pericarditis is divided from the acute by a very shadowy line:
a few hours of the acute disease may terminate in the chronic form, as
in acute inflammatory affections elsewhere, or the malady may follow an
attack of acute pericarditis of several weeks' duration, or it may be
chronic from the beginning. In the first case the pericardium is the
organ primarily affected, generally from cold, or the lesion is
dependent upon some acute inflammatory disease adjacent or remote, as
carditis, pleurisy, mediastinitis, or upon rheumatism. In pericarditis
the result of the exanthemata, of Bright's disease, of scurvy, of
tuberculosis of the lungs or elsewhere, of profuse drainage from
abscesses or injuries--of, in fact, any wasting disease or fault in the
economy associated with malnutrition--the pericarditis may be subacute
at first, and is then apt to become chronic.

{785} The symptoms are slow of development, and are not usually rapidly
productive of discomfort. They are in the main the same as those of the
acute affection, although less decided, and the thermometer may mark a
normal degree or but little above the normal. The physical signs of
effusion of fluid, the presence of pus and blood or of adhesions, have
all been discussed under their proper heads. The prognosis is,
generally speaking, not as favorable as in the acute form; it depends
very much upon the cause, the duration of the case, and the character
of the fluid. In the treatment great attention must be paid to the
cause as well as to getting rid of the effusion and relieving any
direct oppression of the heart the result of the pressure of the fluid.
If this cannot be done by medical means, or if there be reason to
believe that the collection is purulent, paracentesis is indicated.
Adhesions are not, or are but very seldom, removed by any special
treatment directed to them. Indeed, it is by adhesions that most of the
cases of pericarditis with lymphous effusion get well. When adhesions
have disappeared after these attacks of inflammation, it has been
through the efforts of nature, and nothing is left but the milk spots
to testify to the previous condition of the membrane. But these, it
must be remembered, are also the result of altered nutrition in the
membrane, and do not in themselves bespeak a chronic pericarditis.


Adherent Pericardium.

Early in this article adhesions were mentioned as one of the results of
pericardial inflammation, and it was stated that the exudation may
appear in spots or extend over the visceral or parietal layers of the
pericardium or over both, and become organized tissue filled with
blood-vessels, gluing the walls together, and completely obliterating
the sac. Limited adhesions are much more common than those which are
extensive or complete. The intensity of the inflammation offers no
indication of the probability of the formation of adhesions. The
position of the body will materially assist in the adhesion of one
point in preference to another, more especially if the body should
retain a certain posture for any length of time; for the heart
naturally gravitates to the most dependent part, and these portions
coming into apposition will form attachments. If these are not too
large and firm they may become broken, their torn ends being absorbed
or remaining as pendent shreds or patches.

When the adhesions are long and flexible, the motion of the heart is
not interfered with; but when they are short, firm, and extensive, the
heart labors to perform its duties, without hope of relief. If the
adhesions do not contract, the heart retains its shape, and diastole is
easy; but in its systole the difficulty is marked, for besides the
effort to expel the blood there is restraint of motion, with great loss
of energy in drawing to itself the unyielding pericardium. If the
pericardium be adherent to the pleura and other surrounding parts, the
obstacle is increased and the sternum and costal cartilages are drawn
inward and the diaphragm upward. It is to this effort of the heart in
systole that the hypertrophy which is often found with pericardial
adhesions has been attributed; and in the main I believe this view to
be correct. But a number of distinguished observers have denied that
the pericardial adhesion is the cause, and think that the cardiac
hypertrophy is more probably accidental or dependent upon valvular
disease the result of endocarditis, or upon a condition of myocarditis
which, however slight, may coexist and lead to inflammatory deposit in
the walls, and consequent hypertrophy. It is not difficult to
understand how with altered walls dilatation, another consequence of
pericardial adhesion, may be caused. Adhesions to the more resisting
chest-wall and diaphragm prevent the approximation of {786} the cardiac
walls and also the complete closure of the valves. The weakened cardiac
walls begin to yield: this will be assisted by the traction of the
adhesions on the walls and by the persistent engorgement of the
cavities of the heart resulting from inability to empty themselves as
completely as when in the normal condition. Another element will be
that of shrinkage of the heart-walls, which comes on when the adhesions
become so firm and produce so much pressure by contraction that the
nutrition of the organ is materially interfered with. But the problem
is by no means an easy one to solve, and it seems to me that there is
more than one factor influencing it, and that in cases with predominant
dilatation the altered heart-walls play, most likely, the prominent
part.

Now, even as to the fact of hypertrophy occurring there is far from
unanimity. To cite, by way of illustration, the opinion of a few
observers. This condition has been asserted by Chevers[22] and by
Barlow[23] to be the usual and normal result of complete adhesion of
the pericardium to the heart and consequent obliteration of the sac.
Hope[24] very emphatically states: "I have never examined, after death,
a case of complete adhesion of the pericardium without finding
enlargement of the heart, generally hypertrophy with dilatation."
Stokes,[25] on the other hand, writes: "Without denying that generally
adhesion may induce hypertrophy and dilatation, experience leads me to
doubt that such an effect necessarily or even commonly follows the
condition indicated. I have often found the heart in a perfectly normal
condition with the exception of an obliterated pericardium." He adds:
"It has been stated to me by Smith that he has found general adhesion
of the pericardium coinciding with atrophy or with hypertrophy of the
heart in nearly equal frequency. In some of the cases of atrophy the
change was simple, consisting essentially in a diminished volume, with
perhaps a paler color of the heart, while in others a true fatty
degeneration had commenced." Bauer[26] records that "as a rule the
heart is found in a more or less marked condition of degeneration and
atrophy. The bundles of muscular fibres show evidences of fatty
degeneration, or even of hyalin and pigment degeneration, or the
appearances are those of an interstitial myocarditis, with its
results." To my mind, I repeat, the state of the muscular walls seems
of great importance, and it may explain the varying condition of
hypertrophy and dilatation found in association with the pericardial
adhesions in such a differing manner.

[Footnote 22: _Guy's Hospital Reports_, vol. vii. p. 421.]

[Footnote 23: "Gulstonian Lectures," _London Med. Gazette_, 1844, pp.
755, 756.]

[Footnote 24: _Diseases of the Heart_.]

[Footnote 25: _Diseases of the Heart and Aorta_.]

[Footnote 26: _Ziemssen's Cyclopædia_, vol. vi. p. 634.]

It is strongly held by some that hypertrophy is occasioned more by the
valvular disease that may coexist than it is by adherent pericardium.
Sibson[27] tells us that "when pericardial adhesions are associated
with valvular disease the heart is always enlarged. It was so in
twenty-five out of twenty-six cases, and in the remaining instance, a
case of mitral constriction, the heart was rather large." Undoubtedly,
this combination is not unusual, but there may be the most marked
hypertrophy with adherent pericardium without valve affections. I have
met with several such instances, and Blache[28] has recorded three of
striking character.

[Footnote 27: _A System of Medicine_, by Reynolds, London, 1877, vol.
iv. p. 440.]

[Footnote 28: _Maladies du Coeur chez les Enfants_, Thèse de Paris,
1869.]

Adherent pericardium may occur at any age. It has been found by Behier
as the result of chronic pericarditis in an infant of eleven
months.[29]

[Footnote 29: Constantin Paul, _Maladies du Coeur_, Paris, 1883.]

The SYMPTOMS of adherent pericardium are uncertain; the physical signs
are the only means we have of determining its existence, and even these
signs are far from invariable or well defined. In marked cases, on
inspection of the præcordial region, it will be noticed that there is
more or less complete {787} absence of the heart's impulse against the
chest-wall. This is due to the fixed or restrained condition of the
heart, particularly of its apex, and to the interposition of a layer of
plastic lymph, and possibly of some fluid. There is sometimes a
prominence of the costal cartilages over the heart, and the organ
itself may be abrupt and jogging in its motion. The intercostal spaces
to the left of the sternum are indented, and there is a drawing in of
the lower portion of the sternum and attached cartilages with each
systole of the heart, giving rise to a wavy movement in the
epigastrium.

The application of the hand over the heart detects the impulse, but
this is diminished in force and extends over a larger area than in
health. The pulse is usually accelerated and irregular in its rhythm.
When palpitation of the heart occurs--and this is far from a constant
sign--it is dependent upon pressure at the origin of the great vessels.
In some cases there is pulsation in the liver, also pulsation in the
epigastrium, and venous pulsation in the vessels of the neck. The
regularity of form of the chest in its rise and fall during the acts of
respiration will be interfered with if the adhesions be extensive.

The position of the heart is but little changed from the normal, though
of necessity the organ is more or less fixed in its position by the
adhesions. No matter what posture the patient may assume, the apex-beat
of the heart remains unchanged where bound by the adhesions; this is
especially the case if the adhesions have extended to the pleura. The
apex-beat may be entirely masked; but if it be in its normal site, a
depression of the intercostal space during the systole of the heart
occurs, caused by traction upon the intercostal muscle at that point.
If the pleura be implicated, greater expansion of the upper and outside
portion of the left side of the chest in inspiration takes place. In a
certain proportion of cases the position of the heart is more oblique
than normal.

On auscultation the sounds of the heart are found to be more distant
and muffled, though generally less so than in effusions of fluid into
the pericardium. They may be very faint; at least the first sound may
be, on account of the degeneration of the walls of the heart, and
murmurs may exist from attending valvular lesions. The sounds of the
heart may be reduplicated. Skoda and Friedreich laid great stress on
this. But reduplicated heart sounds are not pathognomonic of any
affection.

It has been stated that partial adhesions may exist in such form as not
to prevent the free surfaces of the pericardium from rubbing against
each other, and friction sounds will result, but as the adhesions
become general these sounds will disappear.

The cardiac percussion dulness is but slightly increased unless there
be also hypertrophy or dilatation. The area of cardiac dulness is
lessened during inspiration, because the anterior margins of the lungs
extend nearly to the middle line over the front of the heart. This is
so even in pericarditis with adhesions, unless the adherent pericardium
be attached to the front of the chest and the pleura be also adherent;
then the area of absolute dulness remains unchanged during the
respiratory acts.

The cardiac impulse will be found at times to be increased by the
traction of the adhesions in the pericardium and adjacent parts; at
others the impulse is diminished. A disproportion between the marked
beating of the body of the heart against the chest-walls and the feeble
impulse of the apex has a diagnostic significance--one much greater
than a double impulse. The point of cardiac impulse mostly remains
unchanged. A depression at and near that point, noticeable during the
systolic action of the heart, is among the more certain of the signs of
adherent pericardium. When the adhesions extend to the pleura, this
systolic dimpling is greater, and becomes often very marked; and it is
questionable whether it occurs to any extent without pleural adhesions
also existing. Often the apex-beat of the heart does not change {788}
with the change of position of the patient. The chest remains normal in
shape unless altered by extensive and strong adhesions to the adjacent
parts. Under such circumstances there is depression of the fifth and
sixth intercostal spaces, the epigastrium is sunken, and the sternum
and cartilages are flattened or drawn in; this becomes most apparent
during the systole of the heart. The inspiratory bulging is greatest on
the right side in consequence of the fixation of the diaphragm.

Hypertrophy or dilatation and valvular disease, if associated with
adherent pericardium, modify of necessity both the signs on percussion
and auscultation. The aortic and mitral valves are the ones
particularly affected. It is when these complications exist, rather
than merely from the pericardial adhesion, that we find more or less
dyspnoea or orthopnoea and a sense of faintness and dizziness, an
anxious expression of countenance, imperfect aëration of the blood,
lividity of the lips, dropsy, and difficulty of swallowing.

There is much uncertainty in the DIAGNOSIS of partially adherent
pericardium; for the friction sound may be present, the impulse normal,
the heart's action unrestrained, there may be no impeded respiration,
and the patient may present none of the physical signs of adhesions.
Indeed, under any circumstances the diagnosis of adherent pericardium
is not a very trustworthy one. More than one of the physical signs
mentioned must exist to warrant anything like a positive opinion, and
the disease may be latent.

William H. Webb[30] has recorded a case of complete obliteration of the
pericardial sac by inflammatory adhesions, associated with enormous
hypertrophy of the heart and valvular disease, in which there were no
symptoms nor physical signs to lead to a suspicion of the true state of
things.[31]

[Footnote 30: I take this opportunity of acknowledging the valuable aid
I have received from Dr. Webb in preparing this essay on affections of
the pericardium.]

[Footnote 31: _Philadelphia Medical Times_, vol. ii.]

The PROGNOSIS of adherent pericardium depends rather upon the secondary
consequences, upon the condition of the muscular walls, the
hypertrophy, the dilatation, the coexistence of valvular disease, than
upon the adherent pericardium itself. Yet there is a tendency to sudden
death caused by it. In 115 instances of sudden death, Aran has recorded
9 of complete pericardial adhesion.

The TREATMENT must be that of the consequences with careful attention
to the state of the muscular walls. Digitalis is indicated in cases
with dilatation and flabby walls. Early in the case repeated small
blisters and a course of iodide of potassium may be tried. But it is
doubtful whether any useful result will be accomplished.


Hæmopericardium.

Hæmopericardium, or blood or blood and serum in the pericardial cavity,
is rarely met with except as a result of rupture of the heart, injury
to the pericardium by perforation or crushing, aneurisms, and in
pericarditis occurring in diseases of a low type with degeneration of
the blood, as in scurvy and purpura hæmorrhagica.

In rupture of the heart the effusion of blood into the sac is rarely
rapid, and death is not immediate unless the rupture be large. Rapid
distension of the pericardium with blood speedily causes death by
embarrassing the action of the heart and by producing anæmia of the
brain. Thus the rupture of an aneurism into the pericardial sac is of
necessity quickly fatal. Penetrating wounds may be the cause of a
bloody accumulation in the pericardium and give rise to serious
symptoms. But the injury is not always fatal, since large vessels are
not likely to be cut; the {789} hemorrhage is slow, thus permitting the
pericardium to accommodate itself to the fluid; and if the amount of
blood be not very large, it may be ultimately absorbed. Crushing
injuries to the chest may produce effusion of blood into the
pericardium by lacerating small vessels, and may burst the coronary
arteries if they be diseased. The foregoing are traumatic causes; the
true hæmopericardium is due to the effusion of blood or blood and serum
in diseases of malnutrition and in dyscrasias which have special
tendencies toward the serous membrane, particularly to the pericardium.
This does not take note of the bloody effusions or of a certain amount
of blood in the serum which may occur in the course of acute
pericarditis; but rather of those diseases, such as scurvy, purpura,
and chronic alcoholism, in which the blood is broken down, the tissues
weakened, the degenerated vessels rupture or are no longer able to
contain their contents, and in which the blood or bloody serum
accumulates speedily in the pericardium, without or with but slight
previous inflammation.

The physical signs of hæmopericardium are the same as in other
effusions into the sac, with this difference--that in the traumatic
kind the area of cardiac dulness is rapidly increased, while at the
same time the fluid never reaches the bulk of other effusions, for
before this can happen death occurs. Friction phenomena are not
perceived. There are as symptoms dizziness and faintness, drowsiness,
difficulty of breathing, sense of præcordial oppression, weak pulse,
and, when myocarditis exists, pain in the heart. The prognosis
generally is unfavorable. Death, if not the direct result of the causes
producing hæmopericardium, is due to the hemorrhage or to failure of
the heart.

The TREATMENT consists in absolute rest, in giving readily-digested
food, and in supporting the action of the heart; for this purpose
stimulants may be required, unless something in the history of the case
forbid. Of course it will also be important to keep the emunctories,
especially the kidneys, freely at work, and to modify the condition of
the blood in the cases associated with dyscrasias. The mineral acids
and ergot are remedies to be borne in mind.


Hydropericardium.

Hydropericardium is the presence of serous fluid in the pericardium of
greater quantity than the normal, not dependent upon inflammation--a
pericardial dropsy. To constitute this it must be more than an ounce or
two; it must be sufficient to be recognizable during life.

The fluid in hydropericardium very rarely reaches the extreme quantity
effused in pericarditis. It is alkaline in its reaction and of a pale
straw color, or it may be of a deeper yellow and opaque, the color and
opacity depending upon the presence of hæmatin, biliary coloring
matter, and epithelium. It is chiefly water. According to the analysis
of Gorup-Besanez, there are of water, 95.51; albumen, 2.46; fibrin,
0.08; organic matter, 1.27; inorganic salts, 0.95.

Hydropericardium is apt to occur in conjunction with dropsies in other
parts, particularly with hydrothorax. It may be the result of local
stasis in the veins and lymphatics of the heart and pericardium or of
neighboring parts; or it is more usually the sequela, forming part of a
diffused dropsy, of certain general diseases, as of the exanthemata,
particularly scarlet fever; or is the accompaniment of Bright's disease
of the kidneys; or of obstructive diseases of the liver; or of
affections of the thoracic viscera which impede the circulation of
blood through the heart and lungs. The walls of the heart become soft
and flabby, and are consequently weakened; the circulation in the
coronary arteries and veins is sluggish.

It is almost invariably a chronic affection, coming on insidiously, and
its {790} existence may not be suspected until the disorder is well
advanced, when some symptom, suddenly developed, directs attention to
the heart.

After death the serous pericardium is found to be opaque, somewhat
thickened, and to have an anæmic appearance. The opacity is due either
to interstitial deposit or to the swelling of the epithelium.

The DIAGNOSIS of hydropericardium is surrounded by similar difficulties
to that of pericardial effusion. It presents the same physical signs as
this disease, except the friction at the base, and can only be
distinguished by the history of the case and the attending general
features.

The PROGNOSIS depends upon the extent of the dropsy and the cause
producing it; in point of fact, more upon the latter. The prognosis is
apt to be unfavorable when the disease is occasioned by any of the
exanthemata or by Bright's disease.

The TREATMENT is that of the disease occasioning it and of the dropsy
of which it forms part.


Pyopericardium.

Pus may accumulate in the pericardium as a result of pericarditis, and
this has been already described. Further, metastatic or pyæmic
abscesses occur occasionally in the tissue of the heart, and may be
sufficiently superficial to burst into the pericardium, provided the
patient survive the constitutional disturbance long enough. Morgagni
observed numerous small abscesses form in the pericardium in
consequence of inflammation. Abscesses in the lung and pleura may
rupture and discharge their contents into the pericardial sac, and the
communication may heal. Thus, Balfour[32] records a case of a boy aged
thirteen who had evidences of effusion into the pericardium.
Paracentesis of the pericardium was performed, and thirty ounces of pus
were drawn off. While there was no evidence of communication with an
abscess external to the pericardium, yet an abscess was found at the
base of the right lung which was partially adherent to the sac. A
communication which was closed up by the subsequent pericarditis was
believed to have existed. The quantity of pus does not often reach the
amount just mentioned. The fact is, a small quantity may be attended by
fatal consequence. There may be pus in the pericardium when death is
occasioned by diseases involving the general system, as in scurvy,
erysipelas, pyæmia.

[Footnote 32: _Diseases of the Heart_.]

The SYMPTOMS of pyopericardium are those of acute or chronic
pericarditis, with marked depression. The physical signs are the same.
Indeed, there is no certainty in the diagnosis. Where there is, the
operation of paracentesis is strongly indicated. Free incision of the
pericardium has been recently practised by Rosenstein and by Samuel
West[33] for purulent pericarditis.

[Footnote 33: _The Lancet_, Dec., 1883.]


Pneumopericardium.

Pneumopericardium, or accumulation of air in the pericardial sac, is a
very rare affection. Yet Laennec[34] has stated that in his opinion air
as well as fluid accumulates in the pericardium in all diseases just
prior to death. Pneumopericardium may be associated with fluid, and may
or may not be attended with inflammation of the pericardium. As the
pericardium is a closed sac, air does not readily gain entrance. But it
may do so through perforations of the walls by stabs or gunshot wounds,
or by openings communicating with the oesophagus, lung, or stomach. Air
is then drawn into {791} the sac during the contractions of the heart.
Cases are on record of perforation of the sac with a knife,[35] and
through the oesophagus by means of a sword swallowed by a juggler.[36]
Sometimes the perforations communicate with organs that contain gas, as
the stomach or intestine or the oesophagus. Graves has recorded a case
in connection with abscess of the liver. When the pericardial sac is
intact, the distending gas may arise from decomposing fluid in the
pericardium: it is supposed that it may even be secreted by the blood
of the coronary vessels. Pure air, such as we breathe, is never
developed in the sac.

[Footnote 34: _Traité de l'Auscultation mediate_, chap. xxiii.]

[Footnote 35: Flint, _Diseases of the Heart_.]

[Footnote 36: Walshe, _Diseases of the Heart_.]

The accumulation of air in the pericardium which is sometimes noticed
after death has been declared by many to be the result of the
death-struggle. But it most likely occurs shortly before life ceases.
In such cases the source of the air or gas must be the blood, for it is
well known that blood contains several gases which may leave the
corpuscles and fluid in which they are held mechanically.

The DIAGNOSIS of the condition under consideration is difficult, since
we must chiefly depend upon the signs elicited by percussion. The
general indications are a feeling of oppression in the præcordia, a
sense of suffocation, fluttering of the heart; these, however, would
only point to some functional disturbance. Percussion shows a
preternatural resonance over the heart, the area of cardiac dulness
being restricted and indistinct in proportion to the amount of air or
gas contained in the sac. Emphysema of the margins of the lungs which
overlap the front of the heart may give the same resonant sound, but it
is not likely that emphysema of the lungs would be confined to their
margins only.

Uncomplicated pneumopericardium is not frequently met with, for the
affection is usually associated with fluid accumulations, and with the
percussion resonance there will be other phenomena presently to be
noted. On auscultation the heart sounds have a ringing character.


Pneumo-hydropericardium.

This, too, is a disorder of great rarity, and may be considered one of
the curiosities of clinical experience. It is indeed an unsolved
problem whether pneumo-hydropericardium ever exists except as a result
of the ingress of air from without the body or from an adjacent organ
through an opening made into the pericardium. Nearly all the cases that
have been reported have upon careful investigation exhibited the
evidence of perforation either by mechanical means or by ulcerative
action.

The SYMPTOMS of the accumulation of gas or air in the pericardium
associated with fluid are largely, if not entirely, the same as in
pericarditis with effusion. There is the same sense of oppression in
the chest, irregular rapid action of the heart, pain in the præcordial
region, difficulty of breathing, and there may be febrile excitement.

These symptoms are thus not of much diagnostic value unless accompanied
by the physical signs indicative of the disease. They are præcordial
bulging, diminished cardiac impulse, and the sounds elicited by
percussion and auscultation which show the presence of air and fluid.
On percussion we have clear or tympanitic resonance in the cardiac
region, somewhat modified, especially at the lower parts, by the
dulness from the fluid, and very changeable with the altering postures
of the patient. On auscultation the signs are variable. Laennec placed
great reliance on fluctuation audible with the action of the heart and
on deep inspiration, the heart sounds being heard at a distance. We may
also find what has been called a splashing or a {792} churning splash,
or the sounds of the heart may be extremely ringing, and even metallic;
there may be a combination of sounds, as in the case recorded by
Stokes,[37] where "they were not the rasping sounds of indurated lymph
or the leather creak of Collin, nor those proceeding from pericarditis
with valvular murmurs, but a mixture of various attrition murmurs with
a large crepitating and gurgling sound, while to all these phenomena
was added a distinct metallic character." In the case recorded by John
F. Meigs[38] loud splashing or churning sounds were audible three or
four feet distant from the heart; while Reynier[39] directs particular
attention to an intermittent sound, at first metallic, and resembling a
water-wheel.

[Footnote 37: _Diseases of the Heart and Aorta_.]

[Footnote 38: _Amer. Journ. Med. Sci._, Jan., 1875.]

[Footnote 39: _Arch. génér. de Méd._, Mai, 1880.]

In point of DIAGNOSIS we must be very careful not to confound the
resonance transmitted from a distended stomach to the cardiac region
with pneumo-hydropericardium. The rapid action of the heart and
shortness of breath due to the gastric distension may further mislead,
and the heart sounds may become sharply defined--the second more
ringing. I have several times been called upon for an opinion in cases
of the kind which were supposed to be pneumo-hydropericardium. Cavities
situated near the heart may also present transmitted cardiac sounds of
metallic timbre.[40]

[Footnote 40: Bauer, _Diseases of the Pericardium_.]

The PROGNOSIS is always very grave, yet cases of recovery have been
reported in instances of traumatic origin.

The TREATMENT is that of pericarditis, with great attention to
sustaining the action of the heart. This is chiefly effected by
stimulants. Opium for its quieting effect is also indicated. In cases
of marked cardiac pressure paracentesis has been recommended.


Cancer of the Pericardium.

Cancer of the pericardium is one of the rarest of all cancerous
affections, never occurring as a primary disease, but consequent on
cancer in some other part of the body, generally on cancer adjacent to
the heart. It may be the result of direct extension of cancer or of
secondary formations. In cancer of the pericardium the parietal layer
of the sac is the one always attacked. The extension of the disease
from the bronchi and mediastinal glands, from the lungs, pleura,
oesophagus, and stomach, is the common cause. Cancer will under certain
conditions produce lymphous exudation and adhesions and serous,
hemorrhagic, and even purulent effusions. When lymph is thrown out
friction sound exists and adhesions may follow. Serous effusion with
little or no inflammation is generally present in cancer of the
pericardium, and results from the obstruction in the vessels caused by
pressure or by direct extension of the disease to the vessels. If the
effusion be hemorrhagic, it can be attributed to the same cause. Pus is
generally the result of erosion of vessels and membrane.

The DIAGNOSIS of cancer of the pericardium is practically impossible,
for the physical signs are essentially the same as in pericarditis from
other causes, the darting, lancinating pain excepted; yet even the pain
may not be sufficiently typical to lead us to a correct conclusion.
Therefore, as a rule, the existence of the disease can only be
suspected, or regarded as very probable in consequence of the general
features of the malady.

The rarity of this affection is seen in the summary given in
_Ziemssen's Cyclopædia_. Köhler noted 6 cases of cancer of the
pericardium in 9118 autopsies; Günsburg found 1 case of cancer in 1700
autopsies; and Willigk, 7 cases in 477 autopsies of persons dying of
cancer.

Death, which is the result in all cases, is generally by exhaustion.
Other {793} diseases of a nature allied to cancer also attack or
involve the pericardium, such as lymphadenoma or lymphosarcoma in the
mediastinum; the pathology is practically the same as that of cancer,
and the general symptoms and the termination are alike.

Hydatids[41] give rise to growths which occasion a surmise of cancer;
so do those white calcified bodies formed in concentric layers known as
cardiliths. Neither has any diagnostic signs by which it can be
distinguished.

[Footnote 41: See Rokitansky's _Pathological Anatomy_, and Klob,
"Zeitschrift der K. K.," _Gesellschaft der Aertze zu Wien_, 1860.]


Tubercular Pericarditis.

Tubercular pericarditis is an exceedingly uncommon affection. Laennec
only met with 2 instances of it, Louis with but 1 case. It is never
primary, being always associated with tubercle in some other part of
the body. Among the earlier records we find the case of Baillie,[42]
who mentions "a case of two or three scrofulous tumors growing within
the cavity of the pericardium." The case had tubercles in the lungs,
and died with all the symptoms of phthisis, nothing indicating the
presence of tumors in the pericardium prior to death.

[Footnote 42: _Morbid Anatomy_, 5th ed., London, 1818, pp. 11, 17.]

Tubercle in the pericardium may remain latent or excite inflammation
which gives rise to the same physical signs and local phenomena as when
the pericarditis is of idiopathic origin. The tubercle is mostly found
beneath the serous layer of the pericardium, either cardiac or
parietal, and sometimes in the adhesions, and bears a close resemblance
to tubercular disease of the meninges, the peritoneum, and pleura. It
must be understood, however, that pericarditis may happen in a
tubercular person without being due to a deposit of tubercle in the
pericardium; and a deposit may occur in the adhesions in a case of
pericarditis in a tubercular person brought on by other causes than a
tubercular development in the pericardium, as the instances reported by
Burrows show.[43] Tubercular disease of the pericardium may be due, as
Weigert has proved, to infection by contiguity from the lymphatic
glands of the thorax. The pericardium may be free from tubercle, yet
the purulent fluid in it be filled with tubercle bacilli.[44]
Vaillard[45] declares the pericarditis to be dry in the majority of
cases. The disease generally happens under forty years of age, but in
Mickle's[46] case the patient died at the age of fifty-four.

[Footnote 43: _Med.-Chir. Trans._, vol. xxx. p. 77.]

[Footnote 44: Kast, _Virchow's Archiv_, June, 1884; see also _Medical
News_, Aug., 1884.]

[Footnote 45: _Journ. de Méd. de Bordeaux_, 1880, l. x.]

[Footnote 46: _London Lancet_, May 26, 1883.]

The differential DIAGNOSIS of tubercular pericarditis cannot be made,
as there is no positive physical sign distinguishing this form from any
other. If pericarditis either in its acute or advanced stage occur in a
tubercular person, and if there be neither rheumatism, Bright's
disease, nor pleuro-pneumonia, and if the person have not been
subjected to any injury in the præcordial region, the pericardial
affection may be presumed to be due to tubercle, but only an autopsy
would afford certain proof.

The PROGNOSIS is always unfavorable.

The TREATMENT is that of chronic pericarditis, sustaining the failing
nutrition as well as we can by cod-liver oil and other nutrients.




{794}

THE OPERATIVE TREATMENT OF PERICARDIAL EFFUSIONS.

BY JOHN B. ROBERTS, A.M., M.D.


The operative treatment of pericardial exudations and transudations has
received a new impetus within the last fifteen or twenty years from the
investigations of Trousseau,[1] Roberts,[2] Hindenlang,[3] Fiedler,[4]
West,[5] and others. Reference to the works of these writers will
furnish the reader with the history and statistics of such operations,
and with those details that I have not deemed necessary to incorporate
in the present article.

[Footnote 1: _Clinical Medicine_.]

[Footnote 2: _New York Med. Journ._, Dec., 1876, with analysis of 41
cases; also _Paracentesis of the Pericardium_, Philada., 1880; _Trans.
Am. Med. Ass'n_, 1880; and elsewhere.]

[Footnote 3: _Deutsches Archiv für klinische Medicin_, 1879.]

[Footnote 4: _Samml. klin. Vortr._, No. 215, Leipzig, 1882.]

[Footnote 5: _Medico-Chirurgical Transactions_, 1883.]

In all cases of bloody, serous, purulent, or aërial effusions into the
pericardium, that present dangerous symptoms of heart failure,
operative interference should be undertaken as soon as it is evident
that medication is not lessening the embarrassment of the central organ
of circulation. It is bad practice to delay the operation, which will
generally be aspiration, until exhaustion, pulmonary engorgement,
pericardial changes, and degeneration of the cardiac muscle render
permanent relief impossible. The tendency is to wait, instead of
affording immediate relief of the distressing symptoms by prompt resort
to pericardicentesis. Clinical experience has abundantly shown that
when the pericardial fluid is evacuated, dyspnoea, cyanosis,
irregularity of the pulse, and the other threatening symptoms are
lessened; and usually at once.

The time for aspiration depends less on the amount of fluid than would
at first be supposed, because the sudden effusion of a moderate amount
of serum will exert more pressure upon the heart than a much larger
quantity poured out in so gradual a manner as to allow the pericardium
to become stretched. Aspiration should therefore be performed in all
cases of pericardial effusion, in which dangerous symptoms of heart
embarrassment occur, as soon as medication fails, and without regard to
the supposed quantity of fluid. This should be the practice without
regard to any other visceral lesion that may be present as a
complication, except in the case of pleural effusion.

When pleural effusion of considerable amount coexists, the pleural sac
should be aspirated first, because of the difficulty of discriminating
between respiratory distress due to pulmonary pressure and that
resulting secondarily from interference with cardiac action, and
because the evacuation of the pleural effusion seems at times to lead
to absorption of the fluid in the {795} pericardium without resort to
operation. This rule applies to pleurisy of the right side as well as
of the left.

In dropsy of the pericardium from renal disease I admit that the
transudation is at times absorbed with great rapidity, and that
aspiration does not directly affect the primary disease; but still,
tapping should be done if the failure of circulation and respiration
seems to be dependent on the effusion. Pepper's case[6] of recovery
after pericardicentesis affords corroborative evidence of the propriety
of this advice. Before operation the urine was albuminous and contained
tube-casts, but these symptoms entirely disappeared in the course of a
few weeks.

[Footnote 6: _Medical News and Library_, Philada., March, 1878; and
_Am. Journ. Med. Sciences_, April, 1879.]

When the amelioration of symptoms following the operation is not
permanent because reaccumulation takes place, repetition of the
operative procedure is demanded. It is better, in my opinion, to vary
somewhat the point of puncture, lest the heart be wounded at the second
tapping because of adhesion of the parietal to the visceral pericardium
at the original point of puncture. Should repeated tapping be required
in serous effusions, I should at the time of the third operation inject
into the sac, after removing the serum, a solution containing tincture
of iodine, alcohol, or carbolic acid, with the purpose of modifying the
secreting surface and producing pericardial adhesion. Universal
pericardial adhesion has been found by examination subsequent to cure
by aspiration; and in a number of cases intra-pericardial injections
have been made without preventing, or apparently interfering with,
recovery.

The fluid injected ought probably to be concentrated, as the object to
be obtained is pericarditis of a grade that will furnish plastic
exudation instead of serum. Undiluted but liquefied carbolic acid, such
as is used in treating hydrocele of the vaginal tunic of the testicle,
would be the proper agent were it not for the possibility that its
contact with the heart-walls might induce dangerous cardiac spasm. The
strength of the fluid to be injected, as well as its utility, will have
to be determined by future observation. Aran used fifteen grammes of
tincture of iodine (French), one gramme of iodide of potassium, and
fifty grammes of distilled water, and his patient recovered. Malle
injected a solution of tincture of iodine "five times weaker than that
recommended for hydrocele operations," but suspended the operation
quickly because of the excessive pain in the cardiac region produced by
the injection. Violent inflammatory symptoms arose. The patient died of
diarrhoea before the exact result of the injection could be determined,
though the indications were that cure by pericardial adhesion was about
to take place. The autopsy seemed to confirm this belief.[7] It must be
remembered also that his operation was done by trephining the sternum,
which may have had something to do with the inflammatory reaction,
though the injection was not made until the sixteenth day after the
original operation.

[Footnote 7: _De la Paracentèse du Péricarde_, par Michel Labrousse,
Thèse No. 107, 1871, pp. 22, 27.]

When aspiration has shown the pericarditis to be purulent, a free
incision should be made, an antiseptic drainage-tube of good size
introduced, and the cavity washed out daily with antiseptic solutions
of carbolic acid (1 to 40) or corrosive sublimate (1 to 2000). In fact,
pericardial effusions should be managed exactly as pleural effusions by
tapping, injection, or drainage, according to the character of the
contents of the sac. I have advocated this course since 1876, and it
has been justified by the cases of Villeneuve, Jürgensen, Viry,
Rosenstein, West, Partzevsky,[8] and Savory. Although these operators
did not all practise free incision, yet the study of their cases shows
the absence from danger and the propriety of such incision. As far as I
{796} know, no cases of purulent pericarditis have recovered after
simple aspiration. The case of Rosenstein and that of West, however,
did recover after incision and drainage; and in that of Villeneuve,
which was originally serous, there remained a fistulous track
discharging pus for nearly six months, when spontaneous closure and
cure resulted. Gussenbauer has successfully treated pyopericardium
following acute osteo-myelitis at the shoulder by resection of five
ribs and washing out the sac with a thymol solution.[9]

[Footnote 8: See _Lond. Med. Rec._, Feb. 15, 1883.]

[Footnote 9: _Wien. med. Wochenschr._, Nov. 21, 1884, quoted in
_Medical News_, Philada., Jan. 17, 1885.]

Pericardial fistules, due to spontaneous or operative evacuation,
should be managed by dilatation, with compressed sponge, and irrigation
of the cavity with astringent or disinfectant solutions. Some supposed
pericardial fistules may be pleural fistules, or sinuses opening into
small pockets between the parietal and visceral layers of an adherent
pericardium, or entirely external to the pericardium in new tissue
occupying the mediastinum. Such sinuses should be laid open with the
scalpel, and compelled to granulate from the bottom. Sinuses dependent
upon diseased rib, sternum, or cartilage should be laid open, and the
necrotic or carious structure removed by burr or chisel.

Incision of the pericardium under antiseptic precautions may be useful,
and is justifiable as a diagnostic procedure in grave cases when doubt
exists between a large pericardial effusion and a dilated heart. The
wound will scarcely increase the danger if the pathological condition
be cardiac dilatation, and may save life if effusion be the cause of
the threatening symptoms. The case of Vigla upon which Roux operated
shows the value of such procedures.[10]

[Footnote 10: Trousseau's _Clinical Medicine_.]

Aspiration is the method to be employed at first in all instances of
pericardicentesis. Incision is to be reserved for the second step in
purulent pericarditis, for diagnostic purposes, and for the extraction
of foreign bodies, and similar operative designs. The best point for
aspiration is usually in the fifth interspace, just above the sixth
rib, and about five or six centimeters (2-2¼ inches) to the left of the
median line of the sternum. In a child it should be a little nearer the
sternum. The point advised is outside of the line of the internal
mammary artery, is in a wide portion of the intercostal space,
corresponds with the notch in the border of the left lung, is low
enough to preclude wounding the auricle, high enough to avoid the
diaphragm, and does not approach the point where a cartilaginous band
often joins the fifth and sixth costal cartilages. Both layers of the
pleura will probably be pierced by the aspirating-needle at this point,
but this is not an important complication, and can only be avoided with
anything like certainty by going close to the sternum, which is
objectionable on other grounds.

The aspiration may be performed by using the pump and the ordinary
needle or trocar which is furnished by instrument-makers in the
aspirator-case. In cases of emergency or for mere exploratory puncture
the common hypodermic syringe and needle will answer the purpose. The
puncturing instrument should be clean and anointed with carbolized oil,
and in all cases the vacuum-chamber should be attached to the needle or
trocar as soon as its point is buried beneath the skin, in order that a
flow of fluid may indicate the moment at which the pericardial sac is
entered. Abrasion of the heart, which may occur from contact with the
needle-point when the fluid is almost entirely evacuated, is not very
important, but should be avoided if possible by deflecting or partially
withdrawing the needle, or by using Roberts's improved pericardial
trocar or that suggested by Pepper. The instrument figured in my
monograph on _Paracentesis of the Pericardium_ was too large {797} for
use. The improved instrument here figured is no larger than a
moderate-size aspirating-needle. It consists of such a needle,
flattened at its upper extremity to give the surgeon a firm hold,
within which slides a canula. The distal end of the canula, made
flexible by a spiral, when thrust beyond the point of the needle curves
downward, and thus prevents the point of the puncturing instrument
injuring the heart when the sac is nearly emptied. During penetration
of the thoracic wall the canula is retracted, so that the flexible end
is contained within the needle, and the perforation at the end of the
canula allows the fluid to escape as soon as the sac itself is
punctured. The canula is then thrust forward until the sharp point of
the needle is guarded. This movement brings a lateral fenestra in the
canula opposite a similar opening in the needle, and thus provides a
second orifice for the escape of fluid in case the terminal one becomes
occluded. The external end of the canula has a square shoulder to
prevent rotation within the needle, and should be tight enough at that
point to preclude entrance of air. The canula finally terminates in a
ground end for attachment to the aspirator-tube. The needle--or outer
canula as it may be called--is marked on the surface to show the number
of centimeters concealed in the tissues. If the inner canula is
suspected to be clogged with shreds of lymph or with thick pus, it can
be withdrawn without disturbing the needle. The attachment may then be
made to the latter as if it were an ordinary aspirating-needle, or the
inner tube being cleaned may be reinserted. This is an important
element, gained by using a double aspirating-trocar; for plugging is
not uncommon in pericardicentesis done for chronic inflammation of the
sac.

[Illustration: FIG. 49. Roberts's Pericardial Aspirating Trocar.]

Beverley Robinson of New York has still further modified[11] my trocar.
His additions may have improved the instrument if they do not unduly
complicate it. Pepper, after operating upon his case, had made a
delicate double canula, the inner tube of which was furnished with a
fine needle-point. After introduction the inner tube was withdrawn
until its point was sheathed.[12]

[Footnote 11: _New York Med. Record_, March 29, 1884.]

[Footnote 12: _Medical News and Library_, Philada., March, 1878.]

It is said that at the meeting of the Italian Medical Association at
Pisa in 1878, Baccelli proposed a new method of puncture; but the
account given by Severi[13] in speaking of Baccelli's cases indicates
that his proposal referred not to a method of operating, but to a
method of selecting the point of puncture.

[Footnote 13: _Lo Sperimentale_, Aprile, 1881, p. 392.]

It must also be remembered that failure to obtain fluid when
pericardial effusion existed has occurred because the needle had been
passed through a costal cartilage, and was thus plugged by a disk of
cartilage. The manner in which the intercostal spaces are narrowed and
changed in direction by the curving upward of the anterior portion of
the ribs and by the curvature of the cartilages should be impressed
upon the operator.

If failure to obtain fluid occurs, and the diagnosis remains quite
certain from the symptoms, withdrawal of the needle and puncture in
another position should be done or an incision of an exploratory kind
made.

{798} In pericardicentesis care must be taken not to thrust the needle
or trocar into the heart. This may happen even in quite careful hands.
If the right ventricle is entered, venous blood will escape through the
canula; if the needle is buried in the cardiac muscle, no fluid or
blood can escape. The violent movements communicated to the needle will
usually indicate that the needle is either in contact with the heart or
thrust into its tissue. Of course such movements will occur from
cardiac contact when most of the fluid has been withdrawn; but are not
to be expected immediately after the introduction of the puncturing
instrument unless the fluid is very small in amount, the needle deeply
inserted, the pericardium adherent at the point of puncture, or the
diagnosis of fluid an error.

Puncture of the heart has occurred accidentally during pericardial
tapping without doing any harm, and has been suggested as a proper
surgical procedure in certain cardiac conditions. Still, it is an
accident to be avoided by the use of proper trocars and pumps, by the
selection of a proper site of operation, by the adaptation of the
suction power as soon as the point of the trocar or needle is buried
beneath the skin, and by other precautions that will suggest
themselves. In thick, oedematous, or fatty chest-walls no fluid will be
reached perhaps until a depth of four or five centimeters (about two
inches) has been attained by the point of the puncturing apparatus.

I must call attention to the fact that West[14] records a case of
pericardial tapping occurring at St. Bartholomew's Hospital in 1874
where a trocar and a canula were introduced through the fourth left
space near the edge of the sternum, and caused death in five minutes
from hemorrhage into the pericardium, due to tearing of the right
ventricle. The position chosen and the form of instrument may have had
to do with this unfortunate result, of which the details are not given.

[Footnote 14: _Med.-Chir. Trans._, 1883, pp. 259, 275.]

A few words on cardicentesis, or intentional heart-puncture, may here
be appropriate. It has been suggested as a means for rapid abstraction
of blood from the right heart in intense pulmonary and cardiac
engorgement, and for the abstraction of air after air-embolism has
occurred from wounds of the large venous trunks. It has been known for
years that aspiration and similar punctures of the heart are
comparatively harmless. Roger accidentally withdrew 200 grammes of
blood from the right ventricle of a boy of five years without doing
harm. Hulke seemed to benefit a case of pleuro-pneumonia by
accidentally aspirating the right heart. Cloquet, Bouchut, Steiner, and
Legros and Onimus have made similar observations on the absence of
danger from such wounds. Westbrook of Brooklyn, Corwin,[15] Dana,[16]
and apparently Janeway of New York, have performed intentional cardiac
aspiration in moribund patients without causing any noticeable harm.
The contributions of Westbrook,[17] Roberts,[18] and Leuf[19] on this
topic, as well as that of Senn[20] on air-embolism and its treatment,
will interest those who wish further information.

[Footnote 15: _N.Y. Med. Record_, March 10, 1883, p. 263.]

[Footnote 16: _Ibid._, Feb. 3, 1883, p. 140.]

[Footnote 17: _Ibid._, Dec. 23, 1882.]

[Footnote 18: _Philada. Med. News_, Jan. 13, 1883.]

[Footnote 19: _Amer. Journ. Med. Sci._, Jan., 1885, p. 79.]

[Footnote 20: _Trans. Amer. Surg. Ass._, 1885, and _Annals of Surgery_,
St. Louis, 1885.]

       *       *       *       *       *

The results of operations for pericardial aspiration or incision are
exceedingly good when the frequent postponement of the operation till
the patient is almost moribund is recollected. Elaborate statistical
tables would be out of place in this volume; and, besides, it seems
almost impossible to get a complete collection of the cases.
Hindenlang, West, and I have published {799} and analyzed long lists of
cases collected from various sources, and I have now references to
more, but this tabulation seems unnecessary, as the practical points to
be derived from their study are well proved by the previous work done.
In addition to the bibliographical notes already given, I add for the
use of inquirers in this field two recent monographs--one by a
German,[21] the other by a French writer.[22]

[Footnote 21: _Ueber Paracentese des Herzbeutels_, Gerhard Beck,
Würzb., 1882, p. 33 (Thesis).]

[Footnote 22: _Contribution à l'Étude de la Paracentèse du Péricarde_,
H. Ferraud, Bordeaux, 1883.]




{800}

DISEASES OF THE AORTA.

BY G. M. GARLAND, M.D.


Acute Aortitis.

The existence of inflammation of the membranes of the aorta was
mentioned by Galen and other early writers, but it was not until 1824
that a systematic treatise on this subject was published. Since that
time the subject has received more attention, but the results obtained
are unsatisfactory. There is grave doubt, according to many writers, as
to the existence of acute aortitis independent of other lesions,
although it is recognized that the aorta may participate in
inflammation of the neighboring organs. Even then, as Powell says, "the
aorta is very slow to share in such processes, and when it does so the
inflammation is very chronic and limited, giving rise to no special
symptoms." Peter treats the subject at length, and after enumerating
certain so-called symptoms of acute aortitis, confesses that these
symptoms are merely the ordinary phenomena of angina pectoris, and
these two affections cannot be distinguished from each other. It must
be concluded for the present, therefore, that acute aortitis is rare,
and that we know of no symptoms which are characteristic of it.


Atheroma of the Aorta.

Atheroma of the aorta is the result of chronic endarteritis, and is
always of slow development. The process may be limited to the intima or
it may extend to the middle and outer tunics. Beginning with a
thickening and softening of the wall, it finally develops plates of
calcareous deposit. These plates are most numerous in the region of the
aortic valves, and diminish in number as the artery proceeds from that
point. The descending portion of the aorta is relatively free from
these patches, but they reappear again near or at the bifurcation.

ETIOLOGY.--Atheroma is one of the ordinary products of old age, and is
therefore one expression of senility. Heredity probably exerts some
influence, and certain cachexias predispose to an early occurrence of
the process. Gout and syphilis render one especially prone to it. High
pressure and strain are also important factors. Continuous hard toil is
more productive of atheroma, according to Allbutt, than intermittent
work. The pre-albuminuric stage of Bright's disease, which is
characterized by high arterial pressure, is frequently productive of
atheroma.

SYMPTOMS.--When the inner coat alone is affected, there are no symptoms
of this disease. According as the degeneration extends deeper and
involves the middle and outer tunics, the aorta begins to dilate, and
the symptoms may vary from the slightest feelings of discomfort upon
exertion to the most violent attacks of palpitation and pain.

{801} Usually, at the beginning the symptoms are very obscure. A slight
dyspnoea on exertion, or palpitation, or dyspeptic troubles are the
chief complaint. The presence of these troubles in a man of fifty years
or over, whose heart and kidneys present nothing abnormal, and in whom
the smaller arteries of the extremities feel hard and calcareous, may
excite the suspicion of atheroma of the aorta. There are no distinctive
physical signs. Some writers speak of a short post-systolic murmur over
the aorta beyond the valves, which may be audible only when the heart
is acting strongly.

The aorta is almost invariably dilated, and Peter says that this
dilatation may be traced by percussion. According to him, the normal
aortic dull area measures from two to five centimeters transversely in
the male, and from two to four centimeters in the female. He says that
he has seen cases of atheroma where he was able to determine a dull
aortic area of eight centimeters in diameter. If the inflammation
extend from the aorta to the neighboring nerves, the patient may suffer
from the ordinary symptoms of angina pectoris.

TREATMENT.--This disease cannot be cured by drugs. The physician's task
is to regulate the habits of the patient, to remove so far as possible
all conditions which tend to aggravate and increase the trouble, and to
alleviate incidental symptoms of distress.


Thoracic Aneurism.

DEFINITION.--The origin of the term aneurism is buried in obscurity,
and the theories which have been advanced regarding it are not very
satisfactory. Montanus thought it was derived from _a_ privative, and
_neuron_, a nerve. Oetius declares it is from _aneurisma_, an
enlargement, from _eurumo_, I dilate. Coale thinks a ready origin is
offered in the words _aneu_, without, _rusmos_, a series, course, or
succession, from _ruo_, I flow.

Aneurism of the aorta is a local dilatation of that vessel. When all
the arterial tunics persist unruptured in the tumor, it is a true
aneurism. When one or more of the tunics are torn in the process of
expansion, it becomes a false aneurism. When all the tunics of the
artery rupture and the blood escapes into the neighboring cellular
tissue, it becomes a diffuse false aneurism. The internal and middle
coats of an artery may burst, and the blood escape into and coagulate
in the space between the middle and external tunics, and this is termed
a dissecting aneurism. In rare instances of this type of aneurism the
blood finds a second opening, and returns into the artery again, thus
forming a double tube for a short distance.

In former times great stress was laid upon the distinction of aneurism
according to the number and combination of persistent tunics, and we
read of the mixed internal and the mixed external type. These points
have less clinical importance, however, than a proper appreciation of
the size and shape of a tumor, because all aneurisms are false after
they exceed a certain size. When an aneurism involves the entire
periphery of the aorta, it may be cylindrical, fusiform, or globular in
shape, and receive names accordingly. When it is a mere bulging on one
side of the artery it is saccular in shape. Obviously, the opening into
the fusiform aneurism is quite or nearly the entire length of the
tumor, whereas in the false saccular type the orifice may be reduced to
a mere puncture of the arterial wall. The size of the orifice is a
matter of great importance, particularly in connection with the
question of operative interference, and therefore it will be referred
to later. The sacciform and fusiform aneurisms are often combined
together, or, in other words, it is quite common to find a lateral
bulging superimposed upon a local dilatation of the artery; but such
grouping is not necessary, as either form appears {802} without the
other. It is not uncommon also to find one bulbous aneurism
superimposed upon another, the dependent aneurism in this case being of
the false or diffuse type. The second aneurism often lies outside the
chest-wall, and it is connected with the mother aneurism by a narrow
opening or channel.

Varicose aneurism is a false aneurism formed by communication between
the aorta and the vena cava, the pulmonary artery, the right auricle,
or the right ventricle. It is almost without exception rapidly fatal
and not amenable to treatment.

Occasionally the aorta will present alternate bulgings upon one side
and the other, so that the vessel appears to wind in its course. This
condition is called cirsoid aneurism, but it has nothing in common with
external aneurism of the same name.

The size of an aneurism is variable, like its shape, but in general the
true aneurism rarely exceeds the size of an egg (Jaccoud). Beyond this
size one or more of the coats give way, and the aneurism becomes false,
in which condition it may grow as large as an adult's head if the
patient lives long enough to allow such development. Balfour refers to
two rare forms of aneurism--the intravalvular, which is situated within
the aortic valves and above the ventricle, and the intervalvular, which
is still more rare, and is situated between the valves themselves. The
symptoms of these aneurisms are merely those of valvular lesion, and
therefore present no differential points for diagnosis.

ETIOLOGY.--Local weakness of the aorta submitted to sudden strain is
unquestionably the most frequent cause of aneurism. It is rare to find
an aneurism in an otherwise healthy aorta, and some authors go so far
as to assert that aneurism never occurs without preceding degenerative
changes in the arterial wall. Naturally, strain is the physiological
burden of the aorta, and this strain tends sooner or later to
degeneration of the arterial tunics. Then, given a weakened spot, the
ordinary occurrences of every-day life are sufficient to precipitate
disaster. A sneeze, a cough, some sudden exertion of the body in
lifting or moving, have been the starting-points of aneurism. All
accumulated testimony indicates that sudden strain is more dangerous
than prolonged uniform strain, and therefore some occupations are more
productive of aneurism than others. Inasmuch as age, sex, occupation,
and personal habits influence the development and nutrition of the
aorta, it is obvious that they must exert an important influence upon
the occurrence of aneurism.

All records agree that aneurism is pre-eminently a casualty of middle
life, and a glance at the accompanying table, which I have prepared
from an analysis of 69 reported cases, shows that the disease is most
common between thirty and fifty years of age:

  From 20 to 30 years of age,  4 cases.
   "   30 "  40   "       "   21   "
   "   40 "  50   "       "   29   "
   "   50 "  60   "       "   14   "
   "   60 "  70   "       "    1 case.
  Youngest case, 20 years of age.
  Oldest     "   72   "       "

Crisp analyzed 551 cases, and reports 398 between the ages of thirty
and fifty.

Beneke has found in his records of arterial measurements that the
pulmonary artery greatly exceeds the aorta in circumference up to the
age of thirty. After that period the aorta begins to increase with
relatively greater rapidity, until in the forties it exceeds the
pulmonary artery in size, and it maintains its superiority from that
time forward. The aorta continues to increase in circumference
throughout life, but after the age of fifty this increase is considered
a senile dilatation rather than an actual growth. It is interesting to
{803} note that the era of greatest liability to aneurism coincides
with that of most rapid aortic development.

Sex furnishes a distinction in the frequency of aneurism. In 82 cases I
found that only a seventh were females; Crisp registers less than an
eighth. The radically different occupations and habits of women may
contribute somewhat to their relative immunity from aneurism, and their
physiological development also seems in their favor. Beneke states that
the blood-pressure during childhood is about the same for both sexes.
From puberty onward it is greater in the male. This is due to the fact
that after puberty the volume of the heart relative to the length of
the body is less in the female than in the male, and at the same time
the main arteries of the body relative to the length of the body are
only a trifle narrower in women than in men. The pulmonary artery,
indeed, is relatively a trifle wider in women than in men. It follows
from this that the blood-tension in both the large vessels emerging
from the heart is less in the female than in the male.

In general terms, it may be said that those people who are exposed to
heavy labor, as mechanics, laborers, soldiers, porters, cabmen, etc.,
are more liable to aneurism than those who are less exposed to such
straining efforts. Fixture of the chest during effort brings greater
strain upon the heart and aorta, and therefore men who wield heavy
hammers and sledges are especially liable to aortic disease.
Constriction of the neck or forcible extension of the same during
exertion is dangerous, because it thus happens that the arteries are
stretched in their long diameter at the same instant that the
blood-wave is expanding them laterally, and they are thereby subjected
to double strain. I knew of a trotting horse which was killed by this
very combination of strain upon the aorta. At the end of a trial of
speed the animal refused to stop; whereupon a groom sprang forward,
seized him by the bit, and threw his head strongly upward and backward.
His carotids and aorta were thus stretched to full length at the moment
when his heart was acting with great force. The horse dropped dead, and
the autopsy revealed a rupture of the aorta.

The frequency of aneurism among the soldiers of the English army was
long the subject of anxiety and thought to English surgeons. Finally,
some bright man recognized one cause in the dress of the soldiers. They
were obliged to wear a high stock, which constricted the neck and kept
it stretched, and their trappings were adjusted so as to keep the body
in a stiff and unnatural position. These objectionable details of the
dress have been removed, and it is now claimed that aneurism is much
less common in the army.

Syphilis and gout undoubtedly contribute to the formation of aneurism,
because they both dispose to degenerative processes in the arterial
tunics. Some writers, however, have laid too much stress upon syphilis.
It was claimed that this disease was the cause of the great frequency
of aneurism in the English army. Barwell, however, calls attention to
the fact that aneurism has been 13½ times more frequent per 1000 men in
the army than in the navy, and yet no one maintains that syphilis is
more common in the army than in the navy.

SYMPTOMS.--The diagnosis of aneurism of the aorta may be one of the
easiest problems of clinical medicine, or it may present difficulties
which defeat the most skilful diagnosticians. A large number of
aneurisms utter no sign of their existence, and are only revealed by
the manner of death or by an autopsy. Again, the so-called signs of
aneurism are so indefinite in character, and so associated with other
pathological conditions, that the greatest confusion often befogs their
interpretation. Mistakes therefore arise in two ways: either aneurism
is diagnosed as present when it is absent, or it is declared absent
when present. Robin reports the case of a vigorous young man upon whom
several of the most eminent clinicians of {804} Paris diagnosed
aneurism of the aorta, and yet a rest of a few days sufficed to remove
all symptoms of that disease. Three candidates for the diploma of the
Royal College of Physicians and Surgeons in England recently declared a
case of loculated pleurisy to be aneurism of the aorta, and B. W.
Richardson says he has "seen at least seven persons suffering severe
mental anxiety from the belief that they were fatally struck with
aneurism," and yet they were free of such disease. Balfour says: "There
is only one phenomenon positively characteristic of thoracic aneurism,
and that is the existence in some part of the thorax of a pulsating
tumor other than the heart, which beats isochronously with it, and at
least as forcibly, and which at each pulsation expands in every
direction." And yet simple dilatation of the aorta, combined with
mental excitement, will so increase the thoracic pulsations as to
simulate aneurism. It is necessary, therefore, that a patient during an
examination should be as quiet as possible, both in mind and body, and
if any doubt exist regarding the significance of the symptoms present,
the patient should be kept in bed for a few days in order to allay the
arterial excitement.

The phenomena produced by an aneurism are naturally divided into two
groups: 1. The direct symptoms, which are confined to the limits of the
tumor itself, and which are termed the physical signs. 2. The indirect
symptoms, which are due to the influence of the tumor upon neighboring
organs, and which present themselves often at remote points as signals
of distress within. This influence of the tumor upon its environment is
purely mechanical and due to pressure, and the resulting symptoms vary
according to the particular organ or function involved. These symptoms
are therefore classified as the physiological signs.

Pain is one of the earliest and most troublesome of the pressure
symptoms of aneurism. It is due to a stretching of the nerve-filaments
in the aortic wall and to the pressure of the tumor upon neighboring
organs, especially the vertebral column and sternum. When due to
nerve-stretching, the pain is neuralgic in character, and is not
necessarily confined to the chest. It may appear in the back, and is
intensified by coughing or sneezing. It may be rheumatic in type, and
affect the arm and shoulders for several months before other aneurismal
signs develop. In such cases the right arm and shoulder appear to be
most often affected. Sometimes the pain cannot be located, but is
referred indefinitely to the chest, or it may accompany acts of
deglutition. As a rule--and this point is important--this form of pain
from an aneurism exhibits wide variations of intensity and is usually
intermittent. Exercise, coughing and sneezing, mental excitement, or
anything which increases the activity of the circulation or raises the
blood-tension, increases the pain. It may resemble angina pectoris in
location and radiation, but it differs essentially otherwise. It is
more continuous, and is associated with less anxiety, which is such a
conspicuous element of angina.

When the pain is due to erosion of the vertebræ or sternum, it is more
steady and gnawing. It is still liable to violent exacerbations, and
excitement of all kinds increases it. Oftentimes the pain is so
excessive that the sufferer cannot lie down or obtain relief in any
position. This is especially the case with aneurism of the abdominal
aorta. Bennet reports the case of a patient who poisoned himself to be
free from the terrible pain, and deaths by exhaustion from pain and
distress are not uncommon.

Numerous other accidents besides pain arise from pressure upon the
neighboring veins. Balfour says that severe dyspnoea, vomiting, and
flatulency are frequently caused by pressure of an aneurism upon the
pneumogastric nerves, and that these symptoms may be relieved by gently
rubbing the tumor. Hiccough and paralysis of one-half the diaphragm are
caused by pressure upon the phrenic nerve. Occasionally destructive
inflammations of {805} the lung and pleura occur with aneurism, and
these have been attributed to pressure upon the pneumogastric nerves
and the pulmonary plexus. Palpitation of the heart is likewise often
produced in a similar manner. Sometimes the patient is conscious of a
pulsation in the tumor itself. Pressure upon the intercostal nerves
will produce herpes zoster, and cicatricial records of such attacks are
found upon patients with aneurism. Implication of the sympathetic
nerves produces modifications of the pupils according as the nerves are
merely irritated or paralyzed. In the first case the radial muscles of
the iris become permanently contracted and the pupil is dilated. In the
second case the radial muscle becomes paralyzed and the pupil is
contracted. Jaccoud says that this succession of changes is not rare,
and he has watched cases progress through both pupillary stages. The
nerves affected are those which emerge from the cilio-spinal region,
which extends, according to Budge and Waller, from the sixth cervical
to the sixth dorsal, or, according to Brown-Séquard, as low as the
tenth dorsal vertebra. From the anterior roots of this region
nerve-filaments pass through the cervical sympathetic to the iris. The
difference in the pupils is often so slight that it requires very
careful measurement to detect it. The application of atropia will
assist in the examination, because that drug has very incomplete
influence upon the affected pupil. The pupil is also much less
sensitive to light, but it contracts more strongly than the normal eyes
in its accommodation for near objects. Robertson cautions against
conclusions based upon mere casual observance of the eyes, because 1
person in every 14 has one pupil naturally smaller than the other.

Myosis is not pathognomonic of aneurism. It denotes merely some trouble
with the cilio-spinal nerves. The nature of that trouble must of course
be determined by the other associated symptoms of the case. The
contraction of the pupil is sometimes accompanied by paleness of the
corresponding side of the face and neck, while at other times the same
region may be swollen, oedematous, and perspiring. These symptoms are
due to local vascular changes from interference with, and
disorganization of, the vaso-motor nerves which govern these regions.
Remote local paralysis sometimes utters the first warning of aneurism,
and such cases are usually very striking. Paralysis of the recurrent
laryngeal is the most frequent of this group of signs. Urquhart reports
a case where for some months the chief symptom was a falling of the
head on the breast, as if it had been forcibly drawn down by the
sterno-cleido-mastoids. Another patient was supposed to have
rheumatism, but he soon became paralyzed on the right side and lost his
speech. He recovered somewhat, but died subsequently from bursting of
the tumor into a pulmonary cavity. Tufnell says if an amaurosis occur
suddenly look for valvular disease of the heart or for aneurism of the
aorta.

Dyspnoea.--The dyspnoea produced by an aneurism may vary from a slight
difficulty of breathing on exertion to the most marked orthopnoea. It
is produced by--_a_, direct pressure upon the trachea or bronchi; _b_,
pressure upon the recurrent laryngeal or the vagus. The two forms of
trouble are easily discriminated by physical examination. In cases of
pressure upon the respiratory tubes auscultation reveals very
characteristic signs. The constriction of the tube causes a peculiar
harsh sound, which, heard only in inspiration at first, becomes audible
later in expiration as well. If the pressure is upon the trachea, the
sounds will be heard equally in both lungs; whereas if only one
bronchus is involved, the sounds will be confined to the corresponding
side. If a bronchus be completely occluded by pressure, then the
peculiar breath-signs will disappear, and complete respiratory silence
reign instead. The dyspnoea of this origin is greatly relieved by
motion and by certain positions of the body. In capillary bronchitis,
pneumonia, asthma, etc. the patient sits with the head thrown back and
the shoulders raised, whereas a patient with tracheal compression finds
greater relief in leaning across the {806} back of a chair, with his
head resting upon his arms folded on a table, and the nights are passed
in this position. Again, the pressure dyspnoea is subject to sudden and
excessive variations. Any excitement which increases the cardiac
activity and the blood-tension will excite dyspnoea, whereas rest and
repose diminish it. This form of dyspnoea is likewise accompanied by
loud stridulous breathing, and by harshness and a metallic quality of
the voice. The stridor and dyspnoea bear no direct relation to the size
of the tumor, because a small tumor pressing upon the side of the
trachea, where the cartilaginous rings are thinner and less resistant,
will produce more discomfort than a larger tumor directly in front.
Where the compression of an air-tube is considerable, it usually
provokes inflammation of the mucous membrane, and the secretions
thereby engendered are liable to collect behind the obstruction and
increase the distress for breath. Cases are reported where, tracheotomy
having been performed, a catheter was pushed by the obstruction and the
backed-up secretion allowed to escape, to the great relief of the
sufferer. One case is recorded where the examining physician was able
to see by the aid of a laryngoscope an inward projection of the wall of
the trachea, which pulsated with each heart-beat.

The dyspnoea arising from pressure upon the recurrent laryngeal and
vagus may begin in two ways--either by a sudden paralysis of both vocal
cords, or by a preliminary spasm of the cords due to nerve-irritation.
When both cords are paralyzed, which is very rare, the voice is
entirely obliterated and the dyspnoea is intense and continuous. The
complete paralysis may be associated with choking at meals. When only
one cord is paralyzed, the breathing is not materially affected, though
the voice is altered in a characteristic manner.

If the compression of the nerves mentioned simply irritates them, then
the phenomenon of laryngeal spasm occurs. The voice becomes high,
squeaking, and false or whispering, with a muffled falsetto. Jaccoud
describes a condition where the nerves of the two sides are not
uniformly affected, and therefore the cords are not equally tense in
their spasm. The result of this difference of tension and vibration is
a peculiar commingling of high and low tones, which produces a very
discordant and unpleasant sound to the ear. Jaccoud terms this la voix
bitonale. The dyspnoea from spasm persists through both inspiration and
expiration, whereas with paralysis of the cords the inspiration is
alone or mainly affected. The cough in these cases is phenomenal in its
character, being very loud and metallic, often barking, and it is very
distressing to the patient and to all who hear it.

When a bronchus is compressed the percussion note on the corresponding
lung is higher in pitch and tympanitic. The inspiratory murmur is
ordinarily diminished, but bronchial breathing may (rarely) occur. The
coincidence of bronchial breathing with tympanitic resonance is an
eccentric combination of a very paradoxical character. The cough is
almost pathognomonic, with a loud barking, distressing metallic clang.
Such a cough is still more suggestive when combined with the high,
shrill, whistling vox anserina. The amount of expectoration is at first
small, consisting of glairy, frothy mucus. Later it becomes more
copious and muco-purulent, and may even be rusty and red. The presence
of bloody sputa with an aneurism is always grave, because it raises
suspicion of a so-called weeping aneurism which is approaching rupture.

Dysphagia.--This is a common symptom with aneurism, but it is not so
constant in appearance as it is with other mediastinal tumors. It
appears more often when the aneurism is situated upon the transverse
portion of the aorta. It is frequently painful, but always variable in
severity, and may disappear for long intervals at a time. Lying upon
the face usually relieves the difficulty, while it is aggravated by
reclining upon the back. Fluids are usually {807} swallowed more easily
than solids. Hayden says that a feeling of sharp pain in a particular
part of the gullet in swallowing when aneurism is present indicates
erosion of the mucous membrane and early perforation.

Pressure upon Veins.--Localized oedema and cyanosis are two common
symptoms of aneurism of the aorta. The sudden eruption, the limited
distribution, and the terrifying effect of these symptoms render them
especially interesting. They are due to pressure of the tumor upon the
veins near the heart, and particularly upon the superior vena cava.
Dujardin-Beaumetz says that, thanks to the vena azygos, compression of
the superior vena cava produces simply a varicosity of the neck and
upper part of trunk. Should the vena azygos be simultaneously blocked,
then the oedema and cyanosis will spread over the entire head, neck,
arms, shoulders, and upper trunk--_i.e._ over all parts drained by the
superior vena cava. Only two such cases have been reported, however.
One case was seen by Piorry and one by Dujardin-Beaumetz. In the latter
case the oedema and cyanosis of parts named above came on suddenly
without apparent cause. The face was swollen, blue, and covered with
red patches, and the eyes were injected. The ears were cold; the
abdomen and lower limbs retained their normal color. The contrast
between the upper and lower portions of the body under these conditions
is very striking.

Balfour says that "a thick oedematous collar covered with large veins
surrounding the root of the neck" is indicative of compression of the
superior vena cava.

Pressure upon the brachio-cephalic veins produces oedema and cyanosis
of the head and upper extremities; oedema of the glottis has occurred
under such conditions. Sudden swelling of one arm, unaccompanied by
inflammation, is suspicious of aneurismal compression of the
corresponding vein, especially if it comes on suddenly after exertion.
Compression of the descending vena cava or right auricle may give rise
to congestion and dropsy of the lower part of the body, but these are
later symptoms.

Pressure upon the thoracic duct is relatively rare. It may cause
emaciation, but loss of flesh with aneurism is more often due to
obstruction of the oesophagus or to dyspepsia and the exhaustion from
pain and sleeplessness.

Pressure upon Bones.--Pressure of a tumor on neighboring bones causes
absorption and dislocation of the same. The clavicles, sternum, and
ribs are rapidly eroded by the aneurism, and are pushed forward and
disarticulated. Pressure upon the spinal column causes absorption of
the vertebræ and of the cartilages, until oftentimes the cord is laid
bare and even subjected to direct pressure.

Inspection.--Inspecting a person suspected of aneurism, one should
examine the pupils, the color of the skin, the condition of the veins
of the head, neck, and arms, all movements of the neck and chest, and
especially the contour of the front part of the chest.

The conditions of the pupils, skin, and veins have all been described,
but the movements of the neck and chest require notice here. Any area
of pulsation apart from the normal apex-impulse should be critically
marked and examined. Fulness or beating in the episternal notch is
significant. Cheesman reports a case where a curious pulsation was
occasionally communicated to the larynx and the tongue by an aneurism
situated beneath the manubrium. Every now and then the thyroid
cartilage would rise and fall, and the tongue would pulsate backward
and forward with each beat of the aneurism.

Inspection of the larynx quickly determines the presence or absence of
paralysis of the cord, and may sometimes reveal pulsating tumors
pressing upon the trachea. While inspecting the shape of the chest it
is best to stand upon one side of the patient and look across the
surface of the thorax. In {808} this way slight deviations from the
symmetrical become most readily apparent. If any abnormal point seems
to pulsate, the fact can be rendered more obvious by pasting bits of
paper upon the suspected spot and around its immediate neighborhood.
Viewed thus in an oblique light, the relative movements of these pieces
may be easily discerned. If a tumor be present and the diagnosis
established, one should carefully note the color and condition of the
skin over the prominence. As the tumor develops pressure the skin
becomes tense and glossy. Then it turns red, and may be covered with
livid spots and even ecchymoses. In later stages a black dried scale of
flesh may be all that seems to restrain the heaving blood. Weeping of
blood may take place for some time before the final break.

Palpation.--Given a prominence of the chest-wall or a localized
pulsation in the abdomen, the next step is to examine the suspected
part with the hands. Any tumor lying across an artery will move forward
and backward with each pulsation of the artery, and conditions of this
kind have been repeatedly diagnosed as aneurism. An aneurismal tumor,
however, is distensile as well as pulsatile. Every tumor, therefore,
should be grasped as far as possible between the two hands, to
determine if it distends with each beat.

When one cannot reach the sides of the tumors in front, one can resort
to Stokes's plan. Place the flat of one hand upon the front of the
chest, and the other hand upon the back. By this means the expansile
character of the pulsation may sometimes be determined.

Many intra-thoracic aneurisms present a double impulse or two distinct
blows to the hand during the cardiac systole; and when these blows are
too faint to be felt, they may still be registered by the sphygmograph.
This double impulse is not characteristic of aneurism of the aorta,
because it may also be felt in aneurisms of the large branches of the
arch. Bellingham thought that the second blow was due to a reflex wave
from the aortic valves, and was therefore diastolic in rhythm. Jaccoud,
however, showed that it occurs even with great insufficiency of the
aortic valves, thus excluding reflex waves. François Frank also proved
that both blows were systolic in rhythm. He thinks they are due to the
fact that the blood enters the aneurism en deux temps. The blood,
rushing in at the beginning of the systole, gives a sudden distension
of the partially relaxed sac-walls, and thus causes the first impulse.
Then the bulk of the blood-waves, following more slowly on account of
greater resistance, produces a second elevation more or less
pronounced.

Balfour states that aneurismal pulsations are usually more forcible
than those of the heart, and that this point has not received the
attention which it merits. If the sac contains much fibrin the impulse
is feebler than that of the heart.

W. S. Oliver describes a new sign of aneurism and the method for
detecting it. Place the patient in the erect position and direct him to
close his mouth and elevate his chin to the fullest extent. Grasp the
cricoid cartilage between the fingers and the thumb, and push it gently
upward. If an aneurism of the arch of the aorta be present, its
pulsation will be plainly transmitted up the trachea to the hand. The
act of examining will also increase the laryngeal distress if such be
present.

The frémissement cataire, or thrill imparted to the hand by an
aneurism, has been frequently described. It is very characteristic when
felt, but Powers says it is not of frequent occurrence. He has felt it
in eight cases of aneurism, but four of them were complicated by
regurgitant disease of rheumatic origin, and all were probably of the
fusiform kind.

Pulse.--Partial or total obliteration of a large vessel, dilatation of
the aorta, compression of an artery by a tumor, may produce a radial
pulse {809} similar to that of aneurism. Moreover, we may find the
radials differing from each other in persons who are perfectly healthy.
It follows, therefore, that, taken by itself, the pulse does not
contribute very decisive evidence of an aneurism. When the diagnosis of
an aneurism is established or confirmed by other signs, then the added
evidence of the pulse does possess some value. The finger will often
detect the following characteristics of an aneurismal pulse:

1. Delay.--The pulse at the wrist is normally from 11/100 to 14/100 of
a second later than the cardiac impulse. With aneurism this interval
may be prolonged in one or both radials, and the additional delay may
amount to 4/100 of a second. This sign of delay is of most value when
the pulse in one wrist loiters behind its mate. The relative delay of
the impulse of the aneurism itself and of the carotid artery may give
useful information. If the beat of the tumor precedes that of the left
carotid, then the tumor is nearer the heart, whereas the aneurism is
evidently beyond the left carotid when the beat of the latter precedes.

2. Diminution in Volume.--The pulse in one radial may be much smaller
than in the other or altogether absent.

3. Diminution in Force.--The pulse of one side may convey a less sudden
and less forcible blow to the finger. This diminished suddenness of the
sensation imparted to the finger corresponds to the sloping up-stroke
of the sphygmographic tracing.

4. Thrill.--Under certain rare and not very clearly defined
circumstances the pulse imparts a sensation of thrill to the finger.
Mahomed says this probably occurs when the entrance to the aneurismal
sac is very narrow and the aneurism is directly in the course of the
vessel. It may also be occasionally produced by the rigidity of the
wall of the vessel or by a partially-dilated clot vibrating in the
blood-stream.

Under the enthusiastic and elaborate study of Mahomed the sphygmograph
has attained a certain degree of usefulness. Though difficult in its
application and limited in its results, yet many of the points
demonstrated by it are of sufficient importance to justify their
consideration. The sphygmographic tracing of the normal pulse is shown
in Fig. 50.

[Illustration: FIG. 50. AB. The Up-stroke. ABC. Percussion Wave. E.
Aortic Notch. D. Dicrotic Wave.]

Now, the points which distinguish an aneurismal tracing from the normal
are--1, a sloping up-stroke; 2, impairment or loss of the percussion
wave; 3, obliteration of the secondary waves; 4, diminished volume of
the curve; 5, vibratile waves; 6, a different blood-tension.

[Illustration: FIG. 51. Right and Left Radial Pulse in Aneurism of
Aorta.]

In comparing the curves shown in Fig. 51, taken from Powell's article
upon aneurism, it will be noticed that the up-stroke AB is more sloping
in the curve of the right wrist than in that of the left. The
percussion and dicrotic waves are entirely smoothed out into an almost
uniform wavy slope. As one writer has expressed it, an aneurism acts
like an air-chamber in an engine, and tends to break up the
intermittent pulse into a steady stream. The relative difference of the
blood-tension of two arteries is determined by the relative amount of
pressure required of the instrument to develop the tracing. This amount
of pressure is sometimes greater and sometimes less on the affected
side.

In comparing the tracings from the radials the following points are to
be noted: 1. Is there any difference in the percussion waves?--_i.e._
is the up-stroke more sloping or the apex less pointed in the one than
in the other? 2. Is the tidal wave equally high and sustained in both?
3. Is the dicrotic wave equally developed?

{810} If a difference exist in the tidal wave alone, it need not, and
probably will not, be due to aneurism. It is the loss of the percussion
wave and of the dicrotism which characterizes aneurism.

It must be conceded here that the use of the sphygmograph and the
interpretation of its tracings are beset by the greatest difficulties.
Mahomed, to whom I am chiefly indebted for these sphygmographic
details, declares that the use of the instrument requires great care
and skill, and it may easily lead to error. "No one should attempt to
use it who cannot readily obtain similar tracings from the two radials
of a healthy person." Great care in the application of the instrument
should be exerted, and we must guard against all causes of transient
excitement. It is well to let the patient see the instrument applied to
others before attempting it on him, in order that he may not fear it.
The patient must be placed in a comfortable position, with both arms
alike, and the points of application of the instrument must be alike on
the two sides. The amount of pressure on the two sides must be equal,
or the difference carefully noted. Moreover, one should never be
contented with one tracing, but a number on each wrist should be taken.
If, then, the two radials appear to differ, the precautions must be
redoubled, and the pulse tested again on another day. Inequalities of
the tracings may be produced by abnormal distribution of the radials,
and an old fracture or other injury of one arm may affect the flow of
blood in the arm.

Paralysis of the arm, by interfering with the vaso-motor nerves, and
thereby with the venous return of the blood, may alter the character of
the pulse. A tumor external to the artery, either intra-thoracic or
extra-thoracic, will produce aneurismal pulse and endarteritis, or
congenital contraction of the aorta may so block the artery as to
produce diminished pulse-waves. It may be said that the sphygmograph is
incapable of distinguishing between an endarteritis and an aneurism.

On the other hand, the instrument is very useful in distinguishing
between an aneurism and a tumor compressing an artery, because in the
latter case the up-stroke and percussion wave remain normal, whereas in
the former they are strongly modified, as described above. With
aneurism of the ascending aorta both radials must be similarly
affected, if at all, and in these cases the sphygmograph teaches very
little. If the right radial is alone or mainly affected, then the
aneurism involves the innominate and arch together. When an aneurism of
the innominate includes the aorta, then the whole sac forms virtually a
dilated aorta, and no difference in the radials will appear. Hence it
follows as a corollary: Given an innominate aneurism, if the radials
remain equal the aorta is certainly involved. When the left radial
pulse is alone affected, the aneurism lies beyond the brachio-cephalic
branch, and may or may not involve the left subclavian.

{811} The sphygmograph is of less avail in aneurisms of the descending
portion of the thoracic aorta or of the abdominal aorta. It may be of
service in affording information regarding the condition of the aorta
itself with reference to an operation, and it may also be of service in
determining the upper limits of an aneurism under the following
conditions: A case is reported which presented all the physical signs
of aneurism of the descending aorta, but the sphygmograph showed that
the left radial was affected, and thereby proved that the aneurism
extended as high as the left subclavian at least.

While the foregoing facts prove that the sphygmograph by itself affords
very inconclusive and untrustworthy evidence, yet when the presence of
a tumor and other physical signs prove the existence of an aneurism,
the written pulse-record will often be the guide to the accurate
placement of the tumor, and thereby will often furnish decisive
indications in the selection of the method of treatment.

Auscultation.--The typical aneurismal bruit is not an ordinary souffle,
but it is an accentuated booming sound of a very peculiar character.
Many writers describe it as a systolic jog or shock. Occasionally this
bruit de battement is double--_i.e._ one hears two shocks, so to speak,
just as one feels a double impulse. No satisfactory explanation for
this reduplication of murmur has yet been given. The aneurismal murmur
is almost invariably systolic. Balfour reports two cases of a diastolic
murmur heard with abdominal aneurism. One of these cases was observed
by himself and the other by Wickham Legg.

When this peculiar booming sound is heard over a circumscribed dull
patch, it is very distinctive of aneurism, but its absence possesses no
eliminative value. Many aneurismal tumors are absolutely quiet, and
some of them give only a soft murmur like an ordinary cardiac souffle.

Associated with the aneurismal sound one also hears the normal heart
sounds much intensified. This is peculiarly noticeable of the second
cardiac sound, which acquires a ringing, booming, accentuated character
when heard over an aneurism. Johnson thinks that this intensification
of the heart sounds is due to the sudden tension of the walls of the
sac. Balfour in referring to the same phenomenon considers it of
greatest diagnostic value, and thinks that proper emphasis is not
ordinarily given it.

A fundamental rule in the examination of a suspected case of aneurism
is to auscult over every inch of the thorax, front and back. Not only
the intrinsic signs of the tumor itself are important, but all
testimony from the neighboring organs must be collected and weighed.
The modification of the respiratory sounds have already been mentioned.
Stokes attaches great importance to this fact, that "over one lung,
more rarely over both, the breath sound has often communicated to it a
peculiar sonorous vibrating quality, probably by conduction from the
laryngeal stridor present."

Valvular complications of the heart are not necessarily associated with
aneurism. Cases are reported, however, where a tumor is situated so
near the aortic orifice as to interfere with its closure, and thus
induce the ordinary phenomena of aortic insufficiency.

Of course when valvular disease is coincident with aneurism the
customary signs will be added to those of the tumor, and must be
carefully distinguished.

Drummond of England has recently contributed a new sign of aneurism. It
is a familiar fact that after sudden exertion, and with the heart
acting violently, one can hear in the mouth during expiration a
well-marked whiff proceeding from the glottis. Under normal conditions
of the chest this whiff is only heard after exertion, and never during
perfect repose. Now, Drummond has noticed that this oral whiff, as he
terms it, occurs regularly in many cases of aneurism of the aorta. When
the sign is well marked the {812} whiff is audible in the trachea with
the mouth shut, but disappears on compressing the nostrils with the
fingers. The whiff may be double, synchronous with both the expansion
and contraction of the tumor. The sign does not exist in cases of
valvular lesions of the heart without aneurism. As indicated above,
this sign possesses a diagnostic value only when it is observed under
conditions of absolute bodily and cardiac composure. One should make a
patient lie quietly for a while before examining him for this sign.

Percussion.--Circumscribed dulness is always present when the tumor
reaches the chest-wall. Owing to the globular shape of the tumor, its
size is usually larger than the area of dulness would seem to indicate.
There is no abrupt line of demarcation, but the dulness shades off
gradually into the surrounding pulmonary resonance. The dull patch is
most frequently situated to the right of the sternum and on a level
with the second and third ribs. More rarely it may be found on the
sternum or to the left of the same. If the neighboring lungs are
solidified from any cause, the percussion signs of the aneurism will of
course be obscured.

Localization.--When the signs of aortic aneurism are all conclusive,
the next point in the diagnosis is to determine the probable seat and
extent of the tumor.

In a general way, it may be stated that the physical signs of an
aneurism of the ascending aorta are grouped about the upper two right
intercostal spaces. Tumor of the transverse portion presents itself at
the manubrium, and aneurism of the descending aorta may be detected in
the upper interscapular region to the left of the spinal column.
Balfour says that the aneurism is probably about the middle of the
transverse portion when the point of greatest pulsation is situated at
the middle of the manubrium or from that to the fourchette above, and
the veins of the root of the neck are congested.

An aneurism of the left extremity of the transverse portion usually
points below the left clavicle. There are many startling exceptions to
these rules. One case is reported where an aneurism of the ascending
aorta pointed at the left of the sternum and pressed upon the left
bronchus. Another case of aneurism of the descending aorta passed
behind the oesophagus and compressed the right bronchus. An innominate
aneurism occupies the episternal notch, and usually appears first along
the tracheal edge of the sterno-mastoid muscle. As it increases in size
it will extend across the episternal notch and push out the inner end
of the right clavicle. It may appear first under the end of the
clavicle, but then it is at the cardiac end of the vessel and involves
the aorta.

An innominate aneurism must be distinguished from a low carotid
aneurism. The latter usually appears between the sternal and clavicular
portion of the sterno-mastoid muscle, and its pulsations can be felt by
pushing the finger into this space when the muscle is relaxed. Cockle
said that he knew of no instance of a carotid aneurism distending the
episternal notch. Barwell also mentions the fact that the ear on the
affected side will gain color more slowly than its mate after pinching
when the aneurism is situated upon the carotid.

It is always serviceable, and often essential, to determine whether an
aneurism of the innominate also involves the aorta. If the tumor
appears first under the sterno-costal articulation, the aneurism
probably extends on to the aorta. Again, if the radials are both equal,
the tumor undoubtedly includes the aorta, for reasons already explained
in connection with the pulse-curves. If the right pulse alone is
affected, we can eliminate aortic complication. Barwell also states
that innominate aneurism involving the aorta presents the following
symptoms: The pulsation, dulness, and abnormally loud heart sounds are
on and to the right of the middle line. The various congestions {813}
are on the left side, and do not encroach upon the right side until
later. This venous symptom is especially marked on the left pectoral.

A subclavian aneurism may cause confusion when it occupies the first
third of the vessel. Such an aneurism, however, is an elongated oval in
shape, and is partly covered by the clavicle, and this bone will move
up and down in front of it with movements of the shoulders.

I have emphasized the unreliable character of the pulse as a diagnostic
sign of aneurism, but when other signs of this lesion are well marked
the pulse furnishes some evidence regarding the locality of the tumor.
The following summary of the pulse-signs serves as a useful guide,
therefore, in examining the pulse.

1. Both radials affected alike, the aneurism is limited to the
ascending aorta.

2. Right pulse more altered than the left, the aneurism involves both
the aorta and the innominate artery.

3. Right pulse alone affected, the left remaining normal, the aneurism
is confined to the innominate artery.

4. Left pulse not affected, the aneurism is situated beyond the
innominate.

5. Both pulses aneurismal. This occurs sometimes with aneurisms of the
arch which involve the large vessels.

Varicose aneurism can only be suspected by exclusion. Thurman
emphasizes one symptom which is significant when heard, but it is rare.
This sign is an intense superficial souffle, accompanied by a
frémissement cataire, and situated over the opening of the aneurism. It
is continuous in time, though louder during systole; and this element
of continuity serves to distinguish it from the ordinary bruits of
aortic aneurism or valvular lesions. When there is a varicose
communication between the aorta and the vena cava superior or the right
auricle, the souffle will be extended along the right border of the
sternum, with its maximum at the level of the second intercostal space.
If the aneurism opens into the pulmonary artery or the upper part of
the right ventricle, the souffle will be heard along the left border of
the sternum. When the signs are manifested as the result of some
excessive effort, and are accompanied by præcordial pain, Thurman
thinks them almost conclusive of varicose aneurism of the ascending
aorta. He adds a few other symptoms likely to be present, but less
characteristic of this particular lesion. These are anasarca, venous
congestion, dilatation of cutaneous veins, dyspnoea even to orthopnoea,
cough with sanguinolent sputa, a bounding pulse, and less frequently
general feebleness, with diminution of the animal heat. These signs
have a general significance, however, except when the vena cava
superior is involved, and there the venous congestion and oedema occupy
the upper half of the body. We have, however, previously seen such
phenomena limited to the upper part of the body, resulting from
pressure upon the vena cava.

T. Gallard has related a very interesting case of an arterio-venous
aneurism of the arch of the aorta communicating with the vena cava
superior. This case furnished all the ordinary signs of a tumor of the
mediastinum with compression of the vena cava superior. It emitted a
souffle which began with the first cardiac sound and persisted through
the short interval of silence and to the end of the second sound. This
souffle was especially pronounced at the base of the heart, and Gallard
diagnosed a communication with the vein above mentioned. The autopsy
revealed the accuracy of the diagnosis.

Hayden says that aneurisms opening into the heart, the pulmonary
artery, or the vena cava have, so far as he knows, without exception,
arisen from the ascending aorta. The simple projection of an aneurism
into one or more of the chambers of the heart is attended only by
symptoms of obstruction to the blood-current, and he knows of no
symptom characteristic of a communication between an aneurism and the
heart. When the sac opens into the {814} pulmonary artery there occur
sudden and most urgent dyspnoea and blood-expectoration, without spasm
or stridor. If aneurism of the ascending aorta has been primarily
determined, then the sudden eruption of such symptoms would be almost
pathognomonic of this accident.

DIFFERENTIAL DIAGNOSIS.--We have enumerated a large number of symptoms,
direct and indirect, which are grouped about aortic aneurism. It is an
unknown thing, however, for any one aneurism to present the entire
group in one tableau. A few only appear in a given case, and the
possible kaleidoscopic combinations of the whole number are almost
infinite. There are also numerous other conditions of the thoracic
organs which produce groups of phenomena closely resembling those of
aneurism, and requiring critical analysis.

An aneurism is a tumor, and the majority of its symptoms are simply
signs of a tumor. It is necessary, therefore, to determine whether the
tumor at hand is a solid growth or an expanded vessel. This is always
difficult when the tumor is beyond reach. It may be pulsatile from
lying upon the aorta. The following points, therefore, should be
carefully noted and tested:

1. A solid tumor may be pulsatile, but it is never distensile.

2. The shock of a solid tumor is not markedly stronger than that of the
heart (Balfour).

3. There is no accentuation of the second heart sound (Walshe), nor
bruit of a booming character (Hayden).

4. In the sphygmographic tracing of a tumor-pulse the up-stroke is
never sloping, and the percussion wave remains well marked.

5. Variations in the position and size of a tumor, and also in the
pressure phenomena, are important. An aneurism varies constantly in its
size and in its mural tension; hence all its signs vary
correspondingly; whereas with a solid tumor in the mediastinum the
phenomena are more constantly progressive. An aneurism which is visible
and palpable upon the external chest-walls will sometimes recede within
the thorax, whereas solid or cancerous tumors never act thus.

Abscess of a gland in the episternal notch may closely simulate
aneurism of the innominate. Mahomed and Golding-Bird report such a
case. The imitation was so close in this case as to balk a number of
very careful observers, and no absolute diagnosis was reached until the
sudden rapid increase of the growth and of acute superficial
inflammatory symptoms revealed the probability of pus. The abscess was
supposed to result from the pressure of a collar-button. A companion
case was reported by the same author where an actual aneurism of the
innominate presented such neutral signs that no diagnosis was reached
until the patient was etherized and an exploratory incision was made
down to the sac. It is well to remember that an aneurism may rise and
fall with deglutition and with coughing and straining when it is
adherent to the trachea. A case is reported of a very vascular sarcoma
attached to the manubrium sterni and projecting into the episternal
notch, which presented the double murmur, pulsation, and pressure
symptoms of an aneurism, and was diagnosed as such, the mistake being
discovered only at the autopsy. In such very obscure cases I know of no
reliable or distinctive signs on which a diagnosis may be established:
the only resort seems to be to await developments. In process of time
the appearance of cancerous growth in other parts of the body will
often throw light upon a thoracic tumor. Occasionally aneurism of the
aorta may simulate insufficiency of the aortic valves. Guttmann reports
a case which presented all the classical symptoms of aortic
regurgitation and none of aneurism. The autopsy revealed a large
aneurism of the ascending aorta and the aortic valves intact. The aorta
itself was notably dilated throughout, and it is probable that the
change in the arterial walls affected the proper systolic {815}
contraction of the aortic orifice, so that insufficiency resulted.
Chronic endarteritis of the aorta may produce aneurismal signs.
Dujardin-Beaumetz reports a case where there were contraction of the
left pupil, sudden reddening of the left side of the face, transient
aphonia, intermittent dyspnoea, suppression of the left radial pulse,
and a double souffle along the track of the aorta; and yet the autopsy
revealed simply endarteritis of the transverse portion of that vessel,
without the least dilatation. Many of the symptoms of this case could
be explained by the extension of the inflammation to the sympathetic
nerves.

Many aneurismal signs connected with the voice, eye, and vascular
supply of the heart may be produced by the implication of either vagus
in neighboring inflammation. Chronic empyema of the left side will
sometimes pulsate synchronously with the heart and simulate aneurism.
The following points are important:

1. Such pulsations occur only on the left side.

2. There is always a disproportion between the pulsations, which are
feeble, and the extent of dulness, which is large.

3. There is absence of expansile pulsations.

4. There is usually ample evidence of the presence of a pleuritic
effusion, displacement of the heart, etc.

5. Aneurism may be coexistent, however, and therefore it may sometimes
be advisable to make an exploratory capillary puncture before opening
the chest freely.

Berard reports a case of empyema which formed a tumor on the left side
of the sternum, which pulsated and looked like an aneurism. Finally,
the tumor burst and discharged pus.

DURATION.--The progress of aneurism of the aorta is very rapid, and in
the majority of cases the fatal termination is not delayed many months.
In 40 cases where the duration of the disease was well defined, I found
that 20 of them died within one year, 9 lived for two years, and 3
lingered five years. About 75 per cent., therefore, died within two
years.

TERMINATION.--Rupture of the sac is a frequent cause of death. In 106
cases analyzed by me, 39 terminated in this manner. The seat of the
rupture and the organs into which the blood escapes vary according to
the location of the sac.

Aneurisms of the ascending aorta burst most frequently into the
pericardium, right auricle, right ventricle, right pulmonary artery,
and rarely externally. Tumors of the transverse portion burst into the
trachea, left lung and left bronchi, left pleural cavity, oesophagus,
and externally. Those of the descending aorta empty into the
oesophagus, left pleural cavity, and spinal cord.

The most frequent point of rupture appears to be into the pericardium,
as 13 out of 39 ruptures emptied into that cavity. It will also be
noticed that the right side of the heart and the left pleura and lung
are the chosen seats of hemorrhage. I found no case of rupture into the
left side of the heart.

The bursting of an aneurism is not always an immediately fatal
accident. The so-called weeping aneurism may pour forth small amounts
of blood for weeks and months. Neligan reports a case of external
rupture near the second rib on the right side which discharged blood at
intervals for more than a year. At times the bleeding was with
difficulty arrested, and yet the aneurism finally solidified and the
patient left the hospital calling himself well. Another man with an
external aneurism thought it was a blood-boil, and squeezed it with his
chin to favor the flow until he fainted. The bleeding then ceased, and
never occurred again. He died one year later of typhoid fever. Such
cases, however, are very rare, and usually when an aneurism bursts
externally the death is sudden and tragic.

{816} Rupture of a sac into the pericardium or pleural cavity may not
prove fatal for several hours, and the patient will exhibit the
ordinary symptoms of internal hemorrhage. Rupture into the heart or
pulmonary artery causes great dyspnoea and distress, and death follows
rapidly.

Aneurism may cause death indirectly by starvation from pressure on the
oesophagus, or by suffocation from occlusion of the trachea. The pain
and distress occasioned by the tumor may cause death from exhaustion.
Pain at times is so great that the sufferers can neither lie down nor
stand, and, deprived of rest and food, they wear out. A few patients
die from intercurrent accidental diseases or complications, but it may
justly be said that the death of a patient with aneurism is usually
directly referable to the tumor itself.

TREATMENT.--Aneurisms of the aorta occasionally solidify by the
formation of a clot, and thus a spontaneous cure is established.
Unfortunately, however, such a result is a rare exception to the rule
of steady progress to death.

A number of methods of treatment have been advocated, and some of them
present here and there gleams of hope for some cases. The aim of all
these methods is to produce coagulation of the blood in the sac, either
by mechanical means or by the chemical action of drugs.

The introduction of fine wire has been attempted. A canula is plunged
into the aneurism, and then either short pieces of wire are dropped
into the sac or one long wire is pushed in. Murchison introduced
twenty-six yards of steel spring into an aneurism of the ascending
aorta. This method is attended with great danger, and has not been
successful, and is therefore abandoned at present.

The hypodermic injection of ergotin into the sac was also recommended
by Langenbeck, but it has not met with success.

Pressure upon the aorta can only be applied to cases of abdominal
aneurism, and here it has been successful. The pressure must be applied
under ether, and great care must be exercised not to injure the other
abdominal organs.

The starvation method was first advocated by Hippocrates, and was
espoused later by Valsalva. The idea of this treatment was to render
the blood more coagulable by making it less watery and richer in
fibrin. Valsalva commenced by bleeding a patient freely, and then
reduced his meat and drink until only half a pound of pudding was
allowed morning and evening. The bleedings were repeated at intervals
until the patient was too weak to lift his hand from the bed on which
he lay. The vital objection to this treatment is that starving renders
the blood less coagulable, though it may lower tension. Copland has
seen aneurisms previously quiet begin to grow and end fatally on the
starving and bleeding method.

A few years ago Valsalva's method was resurrected by Tufnell, but was
modified somewhat in detail. The bleeding was omitted and the starving
was less vigorous. Tufnell's three rules are--rest, restricted diet,
and medicine. The rest must be absolute repose in bed, and must
continue two months or ten weeks at least, without the patient sitting
once erect. By this means Tufnell reduces the frequency and force of
the heart-beats, and thereby lessens the number of distending blows
upon the interior of the aneurism. This is of course a very tedious
treatment, and many patients will be unwilling to submit to it. Others
who are unable to appreciate the gravity of their disease, and seek
merely relief from their subjective suffering, will refuse to continue
the treatment as soon as they obtain such relief. Hence the ingenuity
of the physician will often be taxed to the utmost in devising means
and measures for controlling refractory patients and lessening the
tedium as much as possible for all.

The room of confinement should be light, cheerful, and airy, and should
{817} command a view of outdoor life if possible. Tufnell urges the
choice of a south room, because the presence of sunlight is very
restful to the spirits, while absence of the same is depressing. The
bed should be made as comfortable as possible, and with mechanical
contrivances to obviate the necessity of raising the patient. It should
not be too narrow, and should be of a height most convenient for the
nurse attending. Tufnell recommends a large water-cushion, not over
full, under the hips. The sheets and protectives should be drawn taut
and pinned to the sides of the bed to prevent wrinkling. No movement
should be allowed the patient except to turn upon his side now and
then, and occasionally upon his face in case such movement relieves
dorsal pain. A urinal and bed-pan should be at hand, and a pleasant,
agreeable nurse who will be willing to read to, converse with, and
amuse the patient as desired.

The diet recommended by Tufnell is as follows: Breakfast: Two ounces of
white bread and butter; two ounces of cocoa or milk. Dinner: Three
ounces of boiled or broiled meat; three ounces of potatoes or bread;
four ounces of water or light claret. Supper: Two ounces of bread and
butter; two ounces of milk or tea. This makes an aggregate of ten
ounces of solid and eight ounces of fluid food in the twenty-four
hours, and no more. Thirst is liable to be present at first, especially
in the summer months; and this may be relieved by holding a pebble in
the mouth or by occasionally sucking a piece of ice. Tufnell thinks
that the diminished amount of fluids reduces the duty of the heart and
renders the blood thicker and more fitted for deposit. If the patients
are very intolerant and restless, it is better oftentimes to indulge
them in a little more liberal diet, but only enough to appease them and
keep them in control.

Medicinal Agents.--As rest is the great refrain of his method, Tufnell
recommends anodynes and soperfacients at night. For mere restlessness
he prescribes the following combination: Lactucarium, 20 grains;
extract of hyoscyamus, 10 grams--made into six pills, two to be taken
at bedtime. The bowels will naturally be constipated, owing to rest in
bed, and for this he recommends compound jalap powder. Too much
purgation should be avoided, as irritation of the bowels will hasten
the circulation. Obstinate constipation, however, must not be allowed,
or anything which can produce straining. The instant such a condition
manifests itself, enemata by tepid water should be administered.

The principal symptom to contend with is pain, and for this purpose
opiates should be used freely according to the exigencies of the case.
In one case it was found that smoking twenty grains of stramonium at
bedtime would produce a quiet night. This was discovered accidentally
by the patient, who began to smoke the stramonium under the false
impression that he was suffering from asthma.

Maclean recommends the use of eucalyptus globulus for the relief of the
distress due to irritation of the pneumogastric nerve.

Issues and blisters upon the back are not advisable, as they interfere
with the recumbent position. Relief to dorsal pain will often be
obtained by change of position, by turning upon the side or upon the
face. Sometimes the application of a heated flat-iron, with the
protection of brown paper, over the tender portion of the spine will
relieve the boring pain. Iron may be used in anæmic cases.

We have been explicit in giving the details of the Tufnell method for
two reasons. In the first place, the Tufnell method means to many
people simply putting a man to bed, but it also means keeping him there
for a prolonged interval of time; and this is a difficult task, and one
that requires great ingenuity and patience in its execution. In the
second place, when any method is attempted it should be carried out
conscientiously and literally in {818} every detail, and then the
results obtained can be legitimately scored to the credit or discredit
of the method. But it is neither fair nor honorable to pretend to
follow a method, and, neglecting important details, accredit the method
with the failures which follow. Tufnell claims to have cured many
cases, and he declares that absolute recumbency is the price paid. With
regard to the prospects in individual cases, he says that with a strong
pulse at the wrist and an excessively strong action of the heart, and a
healthy state of the cardiac valves and of the aorta in general, the
aneurism is difficult to cure. On the contrary, when the aorta in some
part of its course is dilated into a cavity, with its walls so plated
with atheroma as to be passively recipient of the blood, and not
capable of transmitting it with force, the cure is comparatively easy.
If this be true, it would appear that the Tufnell method is best
adapted to just these cases which are least amenable to the surgical
methods of treatment.

The use of iodide of potash for aortic aneurism was first advised by
Nélaton and Bouillaud in 1859, and this treatment has found its warmest
advocate in Balfour. The points in favor of this treatment are its
simplicity, the ease with which it can be carried out, and the frequent
happy results which have followed its employment. The drug may be given
with an infusion of cinchona in doses of 20 grains three times daily.
It almost invariably lessens the amount of pulsation in an aneurism,
and rapidly diminishes the subjective discomforts of the patient.

Balfour rejects entirely the starvation diet, and even bodily repose.
He allows his patients to keep about their ordinary employments while
under treatment. Kämmerer has shown that iodide of potash destroys the
albuminates in the blood, and therefore Balfour is inclined to feed
more freely than he formerly did. He avoids any unnecessary amount of
fluids in the food, but as the iodide of potash produces free diuresis,
this point does not require special attention. Balfour's theory is that
iodide of potash lowers the blood-tension of the artery, and also
brings about a thickening and contraction of the aneurismal sac. He
says: "Post-mortem examinations teach us that under the influence of
iodide of potassium coagula are only occasional and concomitant, and
that the essential relief is obtained by thickening and contraction of
the wall of the sac."

Barwell's Operation.--During the latter part of the last century a
French surgeon named Brasdor conceived the idea of placing a ligature
beyond an aneurism in cases where it is impossible to tie between the
tumor and the heart. A few years later Wardrop carried this idea one
step farther, and suggested tying the branches of an aneurismal artery
when the main vessel cannot be reached, and Cockle recommended tying
the left carotid for aneurism of the aorta. In this way the idea of
distal ligature for aortic aneurism was worked up. The operation was
attempted a number of times, but was not attended with great success at
first. Recently, Barwell of England has revived the operation and
elaborated its details, so that now it is attended by encouraging
success. Barwell says that one should try the milder measures first,
but when a case has resisted the effects of rest, diet, and medicine,
then it is time to consider the practicability of surgical
interference.

Barwell's operation consists in ligating the carotid and subclavian
arteries, and he performs it for aneurisms of the innominate and of the
aorta also. Contrary to the ordinary teaching that the inner coat of a
vessel must be ruptured in order to ensure the coagulation of the blood
after a ligature, Barwell declares that such a rupture of the inner
coat is a positive detriment to the operation, and more likely to lead
to secondary hemorrhage. He simply endeavors in his tying to bring the
inner surface of the artery into contact, and hold it thus; and in
order to accomplish this without cutting the arterial tunics, he
discards the round ligature in favor of a flat one. {819} Catgut is
unsafe, because it is liable to decompose, even in a preservative
fluid, and it is also too readily absorbable in a wound. After
considerable experimenting, Barwell has adopted the aorta of an ox as
the best material for a ligature. The aorta should be obtained
perfectly fresh from the butcher. Peel away the outer cellular coat,
and then with a pair of scissors cut the middle and inner coats
spirally round and round, taking care to keep the breadth equable. The
ribbon thus obtained is very elastic, and must be suspended with
weights (two to four pounds) attached to it. In this way, the ribbon
dries in about six hours into a horny or vellum-like substance. Any
irregularities of surface can be easily scraped off, and the cord
stored in antiseptic gauze. About fifteen or twenty minutes before it
is needed a piece of ribbon can be picked out and soaked in a 3 per
cent. solution of carbolic acid, when it will be ready for use. Care
should be taken not to bend these ribbons when in the dry state or
fibres in them will crack and render them fragile. In view of such
chances a piece should be soaked and tested by pulling. (For details
regarding the surgical work of this operation one should consult the
ordinary authorities upon surgery.)

The manner of the action of the distal ligature is not clear. Brasdor
and Wardrop supposed that it reduces the force and velocity of the
blood in the aneurism. But the tension and blood-momentum are still
transmitted to the sac. Holmes thinks that a clot forms on the proximal
side of the ligature and extends down the artery into the sac.

Bennet May, in a recent discussion of this operation, says that 35
cases of double distal ligature for aneurism at the root of the neck
have been recorded up to the present time. In 29 operations the two
vessels were tied simultaneously. In 6 cases the subclavian artery was
tied at varying intervals after the carotid. 23 of these cases died
outright or were hastened to a fatal termination by the operation. In 6
cases the progress of the disease was apparently not affected by the
operation. A practical cure is claimed for the remaining 6 cases. One
patient lived four and a half years, another three and a half years,
and the remainder are living from two years downward.

It is a noticeable fact that all the recoveries except one follow
operations performed since 1877, and the betterment in result is due to
improvements in the method of operating. Barwell acknowledges, however,
that "success in great measure depends upon a judicious selection of
cases, while want of judgment or insufficient care in examination will
most certainly bring a valuable operation into disrepute." He submits
the following conclusions from his own experience--

I. An aneurism commencing suddenly, especially if traceable to some
traumatism or over-exertion, is more likely to be benefited by
operation than one arising gradually and without assignable mechanical
cause.

II. Distinct sacculation is a most desirable condition; fusiform
dilatation of the innominate indicates almost certainly a similar
condition of the aorta and widespread arterial disease.

III. The absence of other aneurisms of the aorta should be determined
if possible.

IV. Absence of rasp-sound along the aorta or any other indication of
extensive atheroma should be verified.

V. Aortic incompetence (obstruction, regurgitation, or both), unless
very slight, is a decided objection, as is also mitral disease or
considerable hypertrophy of the heart.

VI. Patency of the vessels leading to the brain should be investigated
by making a few seconds' pressure on the carotids alternately and then
simultaneously.

VII. Absence of visceral disease must be ascertained.

Electrolysis.--Like all other methods of treating aneurism,
electrolysis has {820} had enthusiastic advocates and bitter opponents.
Cuisselli began employing it in 1846, and was able to report 4
successful cases in 1869. He says that success may be looked for when
one can diagnosticate that the aneurism is slightly developed, is
lateral, and communicates with the artery by a limited opening. The
heart and vessels otherwise must be in good condition. Balfour
recommends electrolysis as a dernier ressort in cases where an external
rupture is imminent. He says that four cells of a Bunsen's battery are
sufficient, as more than four cells cause pain and require the use of
chloroform. Balfour inserts both electrodes. Robin, however, strongly
insists that the use of both poles produces greater pain, is more
destructive to the neighboring tissues, and gives unsatisfactory
results in the aneurism. He advises one to place the negative electrode
upon the skin outside, and introduce the positive needle. This
invariably determines the formation of a coagulum which is more firm
and more resistant to the finger than the ordinary clot of stagnant
blood. This clot is always small, whatever the strength of the electric
current, but it forms a nucleus for further coagulation in the sac. The
negative pole should not be introduced into the sac, according to
Robin, because it forms only a soft diffluent clot which readily breaks
up and floats away. The negative pole also is much more destructive to
the surrounding tissues than the positive pole, and its withdrawal is
almost invariably followed by hemorrhage. The coagulation is more rapid
and more energetic when the needles are oxidizable, as iron or steel.

Robin lays down the following rules for operating: The patient should
lie comfortably in bed, with his shoulders elevated by pillows, and he
should be cautioned not to jump or move during the operation. Three or
four needles should be inserted about one centimeter and a half from
each other, and about thirty millimeters in depth. One will recognize
that the needles are well in the aneurism when they exhibit movements
synchronous with the sac itself. One of the needles is then attached to
the positive pole of the battery, while the negative pole is attached
to a sponge and pressed upon the outside of the chest. The galvanic
current is allowed to pass for ten or twenty minutes, when it is
gradually reduced to nothing. Then the positive pole is transferred to
the second needle, which is similarly treated, and so on until the
three or four needles have each been used in turn. After stopping the
current leave the needles quiet for some moments; then withdraw them
gently, so as not to disturb the clots, cover the punctures with
charpie in collodion, and apply ice or cold-water compresses if any
inflammation occurs. Sometimes morphine may be required on account of
pain, but the crises of pain, dyspnoea, and other painful phenomena of
the aneurism are calmed almost immediately.

The cure of an aneurism by electrolysis must not be expected from one
session. More often several sessions are required, but the repetitions
should be separated by four to five weeks, so that time may be allowed
to develop the full benefit of the preceding operation, and to heal any
secondary inflammation which may have been produced.

Acupuncture.--Constantine Paul conceived the idea of applying simple
acupuncture to aneurism. He treated one case as follows: Four needles
were introduced into the sac, and allowed to remain there fifteen
minutes. Little or no pain was experienced. In three days there was a
notable diminution of anxiety and dysphagia. A second introduction was
made four days later, which was followed by still greater improvement.
The patient felt so much better that he insisted on leaving the
hospital. Paul thinks that electrolysis and acupuncture produce an
endarteritis which thickens and strengthens the pouch-wall.


{821} Abdominal Aneurism.

This lesion is much more rare than aneurism of the thoracic aorta.
Among 551 cases of aortic aneurism accumulated by Crisp, only 59 were
abdominal. I find no one particular point of the abdominal aorta which
is especially liable to aneurism, but in general terms the upper part
is more often affected than the lower. Of 103 cases noted by Lebert,
only 3 occurred at or near the bifurcation. Abdominal aneurisms are
twelve times more frequent in men than in women, and they are more
common between the ages of twenty to forty than after that period.

They form adhesions with all the neighboring organs and tissues, and
thus develop a certain number of pressure symptoms. These symptoms,
however, are by no means so diversified or numerous as in the cases of
thoracic aneurism.

Abdominal aneurism is invariably false after it has attained cognizable
size, and it causes death in various ways. Oftentimes it kills from
exhaustion by reason of intense pain, which prevents sleeping or
eating. Again, by blocking up the arterial supply to neighboring
organs, as in the lower aorta itself, it will cause secondary diseases
which produce death. The most common termination, however, is by
rupture. The sac may rupture into the peritoneum, retro-peritoneal
tissue, bowels, bladder, pleural cavity, vena cava, or into the spinal
column. Lebert says he has never found a case of external rupture
through the skin, but Bramwell reports a case of rupture into the
retro-peritoneal tissues and subsequent escape of blood through a
bedsore.

SYMPTOMS.--In a large majority of cases pain in the back is the first
symptom which heralds abdominal aneurism. This pain may precede the
appearance of a tumor for weeks and months. At first the pain is
usually due to a stretching of the nerve-plexus which surrounds the
dilating vessels, and hence it is of a neuralgic character. It is
intensely severe and shooting. Beginning in the lumbar region, it
shoots down into the hips and knees, or through the abdomen to the
epigastric and umbilical region. It is usually more or less continuous,
but subject to great exacerbations. Motion, change from reclining to
upright posture, acts of coughing and sneezing, increase it. One
peculiarity of this pain is that it is increased by eating and
drinking. This is explained by the fact that the taking of food and
drink increases the amount of blood and thereby stretches still more
the sensitive wall of the aneurism. The pain often obliges patients to
keep in bed, and even there the relief is very slight, so that death
may result from the exhaustion of sleepless days and nights.

When the aneurism encroaches upon the vertebræ there is added a
gnawing, grinding pain which is constant, and is relieved but little by
change of posture. Pressure upon the stomach and bowels and upon the
nerve-plexuses which supply these organs produces dyspepsia, vomiting,
constipation, and a tendency to accumulation of gas in the bowels. This
interference with the nutrition of the body invariably causes marked
cachexia, so that a patient who has suffered some time from abdominal
aneurism will look as if he were affected with cancer.

Pressure upon the renal vessels causes atrophy of the kidneys and
hemorrhagic impactions. Patients may die with uræmic symptoms, such as
convulsions, dropsy, and stertor.

Pressure on the bladder causes painful micturition, which is a not
uncommon symptom of this complaint. Pressure upon the aorta itself
below the seat of the tumor will produce symptoms of obliteration of
that artery, and will be treated of under that head. Rupture of an
abdominal aneurism into the vena cava produces orthopnoea, pallor, and
dropsy. Smith reports such {822} a case in which gangrene of the right
leg followed a puncture to relieve the dropsical tension.

Physical Signs.--The aneurismal tumor often appears suddenly after a
preceding interval of pain or after some sudden strain. It may show
itself in the epigastrium, iliac regions, or about the umbilicus. It
presents the classical symptoms of expansile pulsation and souffle. But
these are often wanting. Every case should be auscultated both front
and back, because the murmurs are sometimes more audible behind than in
front. François Frank calls attention to the fact that manual pressure
upon an abdominal aneurism will produce an increase of tension in the
vessels of the lower extremities. This rise of tension is caused by the
forcing of the blood in the aneurism out into the lower vessels.

If the pressure be now suddenly removed, the general pulse will almost
entirely disappear for one to two pulsations. This is due to the
aspiration of the elastic wall of the tumor, which goes back to its
original size. The reverse of these phenomena is true in case the tumor
is solid and lies across the artery.

Scheele of Dantzig draws attention to a new diagnostic sign, which he
considers pathognomonic. This is a suddenly-heightened pressure in the
region of the aneurism when both femorals are compressed. This test is
not without danger, however, as Sandsby found in one case which he
compressed for ten to fifteen seconds. There was a momentary
retardation, and then increase of impulse in the tumor, with an
increased loudness of the systolic murmur. Directly after, the patient
complained of a sharp attack of pain which continued during the day,
and that night death followed from rupture of the tumor.

DIFFERENTIAL DIAGNOSIS.--A few diseases of the chest and abdomen may
simulate this affection, and require to be eliminated in the diagnosis.
A gravitating empyema may present symptoms of abdominal aneurism. The
distinguishing points are the signs of an effusion in the left chest,
the reducibility of the tumor by pressure, and the absence of a thrill
or bruit.

A case is reported of a vast aneurism of the thoracic aorta which grew
downward until it pointed in the right iliac fossa. It was considered
an abscess with pulsations from the iliac arteries. It would seem as if
the only safeguards against mistake in such cases were great skill in
examining the whole breadth and depth of every doubtful case and a
knowledge of the fact that eccentric developments may occur. Aneurism
of the abdominal aorta may be simulated by excessive pulsation of that
vessel. This condition appears usually in nervous, weak people, and is
often the occasion of great alarm. It occurs frequently in anæmia, and
may follow hæmatemesis from gastric ulcer, and thus lead to a fear of a
ruptured aneurism.

The diagnosis is easy if the abdominal wall is thin enough, so that the
aorta can be reached and felt. If the abdomen is distended by gas, the
diagnosis may be more difficult. Duckworth reports a case where it was
necessary to give ether and entirely relax the muscles of the abdomen
before a satisfactory examination could be made.

Finally, in examining the abdominal aorta by auscultation, one should
be careful about any murmur which may be heard. It may be due simply to
pressure of the stethoscope upon the vessel. Constriction at a low
point of the oesophagus, which causes an accumulation of food above and
a dilatation of the tube, may closely resemble aneurism. Hayden refers
to a case which exhibited dysphagia, epigastric pulsation with
tenderness and percussion dulness, pain in the back and shoulder, and a
tearing or raking sensation at the epigastrium on attempting to
swallow.

No opinion regarding an abdominal aneurism should be formed until it is
certain that the bowels are not loaded with fecal accumulations.
Evacuation {823} of the bowels, therefore, is a proper preliminary to
an examination for abdominal aneurism. The condition of the bladder and
uterus must also be carefully noted, and the bladder should be emptied.

TREATMENT.--Excellent results have been obtained by the Tufnell method.
Compression of the aorta above the tumor has been recommended, and has
been followed by good results. One case is reported in which the
tourniquet was applied four inches above the umbilicus on three
occasions, the patient being under an anæsthetic. The first session
lasted half an hour, the second three-quarters of an hour, and the
third for one and a half hours. The tumor was as large as a
cricket-ball, and it became solid in forty-eight hours after the last
application. Three weeks later there was no evidence of an aneurism to
be found. Another case is reported of one compression of five hours,
and another of ten and a half hours. One case in England required
fifty-two hours of pressure under chloroform.

These results encourage one to persevere in repeated sessions in case
of failure at first. But a word of caution must be given to avoid
injury to the abdominal organs during pressure.


Rupture of the Aorta.

Although very frequent in connection with aneurism, rupture of the
aorta is otherwise relatively rare. It almost never happens in a normal
aorta, but a few cases are reported where the arterial wall is
described as merely thin. Usually the rupture occurs at a spot weakened
by atheromatous disease, and is produced by sudden strains, falls, or
blows upon the chest, or by rapid exercise of the arms. Congenital
narrowing of any part of the aorta will produce so much strain behind
the obstruction as to cause rupture. Fernand reports such a case in a
boy fifteen years old. The ascending and transverse portions were
dilated, and the inner surface was covered with small red vascular
plaques. The remainder of the aorta was contracted to the size of the
iliac vessels.

Men and women are both liable to rupture, but the former more than the
latter. One would suppose that women during the terrible strain of
childbirth would be especially liable to such an accident, but I have
found only one such case reported. This woman, thirty-eight years of
age, died suddenly during the first stage of labor, and a living child
was extracted five minutes later by forceps. The rupture was seated one
and a half centimeters above the aortic valves, and reached nearly
round the entire circumference of the artery. Heinricius reports the
case,[1] and says that he has been unable to find any similar case
recorded. I have found one case of rupture of the aorta during the
sixth month of pregnancy, but not associated with any sign of labor.

[Footnote 1: _Cent. f. Gynäkol_, No. 1, 1883.]

The majority of the ruptures occur in the immediate neighborhood of the
valves or within two inches of the same. It is a very rare thing to
find a rupture of the transverse or descending portion of the arch. One
case is reported of a girl twelve years of age who was trampled upon by
a pony and never rallied. The descending aorta was found ruptured, and
the tear was apparently produced by the nipping of the vessel between
the vertebral column and the heads of three left ribs, which projected
forward and could be protruded still farther by pressure upon the
sternum.

When the inner coat of the aorta ruptures and the blood escapes, it
immediately forms a pocket between the arterial tissues, and then one
of two things may occur: the escaped blood may coagulate solid, and so
fill up the opening and prevent further leakage. This occasionally
happens; more often, {824} however, the escaped blood pushes along,
dissecting apart the tissues of the artery, and advancing until it
finds some point of escape. Sometimes the blood bursts back into the
aorta and rejoins the main current. In such cases the separation of the
tissues continues transversely until the entire circumference of the
aorta is included, and then the vessel forms a double tube. When the
blood does not re-enter the aorta, it may push ahead until it reaches
the iliac arteries, which is not at all uncommon. While advancing in
this direction the blood also dissects backward toward the heart, and
finally bursts into the pericardium. Almost invariably in these cases
the pericardium is found more or less full, and the pressure of a large
amount of blood in the pericardium upon the heart no doubt contributes
largely to the fatal result by obstructing the action of that organ.

There may be two pints of blood in the pericardium. Death by rupture is
by no means instantaneous. As a rule, the victims continue to live
several hours, and even days, after the initial accident.

If the escaped blood coagulates and plugs, several months may elapse
before death, as in a case examined by myself. A washwoman while
shaking out a heavy piece of wet cloth in November was suddenly seized
with severe pain in the chest. This pain continued with other
distressing symptoms which disabled her for work, but she did not die
until the latter part of the following January. The autopsy revealed a
rupture, plugged by a clot, two inches above the aortic valves.

Rupture is usually announced by sharp pain coming on during exertion.
There may also be a sense of choking, but this is not invariable.

Generally, the head is clear, and there is no paralysis, but
occasionally the patient will swoon and appear collapsed. This of
course depends upon the size of the rent and the freedom of the escape
of blood. The heart is excited and rapid. The pain is located in the
front of the chest or in the epigastrium, and the victims are a prey to
great anxiety. Excessive trembling and inability to restrain muscular
movements have been noticed. Profuse sweating, together with vomiting
and evacuations of the bowels, may occur. Often the only record is,
"Obscure symptoms, referable to the heart." There are no
characteristics or pathognomonic symptoms of rupture of the aorta.
Death is the invariable result, sooner or later, and no treatment has
yet been devised to remedy the evil.


Perforation of the Aorta.

This accident causes death very rapidly, but not always instantly.
Instances are reported where patients, after the piercing of all the
arterial coats, have lived from one hour to three days. A case is
reported of a boy sixteen years old who swallowed a needle. It passed
through the wall of the oesophagus into the descending aorta, where it
remained impacted. Blood poured out into the connective tissue and
acted as a plug. Food escaped from the oesophagus, and putrefaction,
hemorrhage, and death occurred in ten days.


Occlusion of the Aorta.

Occlusion of the aorta is produced by the formation of a clot. Such
clot may occur in any part of the aorta. It may extend out from the
heart or from the ductus Botalli. Such localization of the clot,
however, is comparatively rare, and the most common seat of occlusion
is in the abdominal aorta. The clot is usually associated with an
aneurism, but it may sometimes be occasioned by an atheromatous patch.
The attack is always abrupt and {825} unheralded by any prodromata. The
effect of the clot is to cut off the blood-supply to all organs below
the obstruction and disturb the nutrition and function of the same.

SYMPTOMS.--The attack is sudden, and begins with a shooting pain in the
abdomen or sometimes under the sternum. Almost immediately the patient
loses power over his legs and falls completely paraplegic. At the same
time there is an intense desire to stool, which rapidly increases to
involuntary evacuations. This lesion may be accompanied by intense pain
at the anus. The abdomen may be very tender to pressure. The head is
always clear, and the inability to stand is not associated with
giddiness. There is no anxiety of the face, and often no sign of
distress there.

In a few moments the legs become cold and numb, and patients complain
of a sense of deadness in them. The reflexes are entirely abolished. If
the renal arteries are occluded the urine is suppressed at first, but
reappears as soon as collateral circulation is established through the
capsule. The urine rapidly becomes albuminous and foul smelling from
the cystitis which develops. In the course of forty-eight hours bullæ
appear upon the legs and thighs, bedsores appear over the sacrum;
violent cystitis and inflammation of the rectum follow. Some patients
live long enough for gangrene of the lower extremities to form.

Great thirst is present, and vomiting with hiccough may aggravate the
suffering. The bodily temperature rises above 100° F., while the
temperature of the legs falls. It may reach 94° F. There is usually no
pulsation perceptible in the abdomen or legs, except in rare cases,
when the occlusion is incomplete.

DURATION.--Death results from exhaustion, and occurs in a few days. Two
weeks is a long time for life to continue under such circumstances. One
case is reported, however, where the occlusion was evidently imperfect
and the man survived seven months. Collateral circulation was
developed, and the epigastric was mentioned as very much enlarged.

TREATMENT.--The treatment is wholly symptomatic. Pack the extremities
for warmth and protect from bedsores if possible.


Stenosis of the Aorta.

PATHOLOGY.--In 1789 attention was first called to a peculiar
constriction of the thoracic aorta at the insertion of the ductus
arteriosus Botalli. Careful search for this lesion since that date has
discovered a series of cases, so that in 1878, Kriegk was able to
report 55 instances of it. This constriction is a definite, locally
circumscribed lesion, always limited to the same region, and is
entirely independent of all other affections of the aorta, although it
may itself be the cause of atheroma and aneurism. Beyond the locality
specified stenosis of the aorta is an extremely rare affection, except
as the result of outside pressure or of local arteritis. Kriegk says he
found only two cases of stenosis of other parts of the aorta, although
he searched through forty years of medical literature. A few instances
of complete obliteration of the aorta have been recorded, and some
instances of universal narrowing of the aorta from congenital
obstruction in the heart are given.

The constriction at the ductus Botalli is a congenital lesion, and
consists of a sinking in of the superior wall of the aorta just at the
insertion of the ductus arteriosus or a little above or a little below
the same. This sinking may extend to and involve the origin of the left
subclavian artery, but this is not usual. The lower wall of the aorta
rarely exhibits any depression.

The ascending and transverse portions of the aorta, together with the
main branches, become very much enlarged. As the aorta approaches the
{826} constriction, its dilatation does not terminate abruptly, but the
vessel tapers down to the stenosed section in a funnel shape. Beyond
the stricture the descending aorta may recover its normal size or may
remain smaller than natural.

In many cases the aorta, barring the stenosis, is perfectly healthy,
but the increased pressure behind the obstruction tends to develop
atheroma, aneurism, hypertrophy of the heart, and rupture.

Naturally, the lower part of the body must be deprived of a portion of
its quota of blood except for the compensatory circulation which
develops. This collateral supply may be so complete that the person
affected is unconscious of any circulatory deficiency, and may live an
active life to old age. An Austrian officer born with this lesion was
able to serve in all the campaigns from 1790 to 1815, and then died one
day sitting at a card-table. Another man lived ninety-two years with
his aorta constricted. The collateral communication between the upper
and lower segments of the aorta is established by means of the deep
arteries of the neck, the transversus colli, the dorsalis scapulæ, the
subscapularis, the intercostals, and the lumbar arteries. The internal
mammary also communicates directly with the epigastric artery. These
vessels become enormously dilated, so that the superior intercostal,
for instance, may equal the femoral in size.

[Illustration: FIG. 52. A, Appearance of Aortic Arch in Early Foetal
Life.--B, Stenosis of the Aorta.]

ETIOLOGY.--The lesion is a congenital one, and results from a defective
development of the aorta. In early foetal life the descending aorta is
a continuation of the ductus Botalli, and the aortic arch looks like an
independent communicating vessel. (See fig. 52, A.) As the arch
develops, however, it gradually forms a more direct union with the
descending portion, until finally the longitudinal axes of the two
parts form one uniform curve and the ductus Botalli becomes a side
branch. At birth there is physiologically a slight nicking of the upper
wall of the aorta at the point where the two sections are joined, and
the stricture we are studying seems to be merely an exaggeration of
this physiological mark. Just how the depression becomes established is
not clear and the explanations given are not satisfactory.

SYMPTOMS.--Indications of this lesion are usually very obscure or
absent, and it is only discovered at the autopsy. Severe headache is
sometimes complained of, and dyspnoea, cough, hæmoptysis, and vertigo
may occur if the stenosis is excessive.

Physical Signs.--One of the most marked signs is the conspicuous
beating of the dilated arteries around the shoulders and ribs. These
arteries may be seen and felt. If the patient is very fleshy, however,
they may be {827} concealed. There is usually a marked contrast between
the arteries of the upper and lower extremities. The former are full
and strong, while the latter are weak and barely perceptible. In many
cases it is almost impossible to feel any pulse in the abdominal aorta
or in the crural arteries. A loud murmur is also described as occurring
over the aorta. This murmur is post-systolic, and does not correspond
to any of the ordinary aortic murmurs.

DIAGNOSIS.--This lesion has rarely been suspected, much less diagnosed,
during life, but a better knowledge of its peculiarities may lead to
more frequent recognition of it hereafter. When the collateral
circulation is fully established, stenosis of the aorta could hardly be
mistaken for anything else. The resulting excessive dilatation of the
great vessels at the root of the neck may simulate aneurism, and it
should be borne in mind that aneurism is liable to follow stenosis.

PROGNOSIS.--The death of most of the victims of stenosis of the aorta
is directly referable to the lesion itself, although the existence of
the trouble is compatible with long life and active occupation. The
duration of life and the amount of suffering caused by stenosis both
depend upon the amount of obstruction in the aorta and the efficiency
of the collateral circulation.

In 49 cases death occurred in the following manner:

  Rupture of the aorta    10 times.
  Rupture of the heart     3   "
  Sudden pulmonary oedema  4   "
  Cardiac failure          8   "
  Apoplexy                 4   "
  Pneumonia                8   "
  Capillary bronchitis     4   "
  Paralysis                2   "
  Pleurisy                 1 time.
  No cause assigned        5 times.
                          --
                          49 times.

TREATMENT.--Obviously, no treatment for the lesion itself is possible.
If recognized, the existence of the sufferer may be prolonged by
adopting moderation in all things as the maxim of his life. Subjective
symptoms of discomfort must be combated on general principles as they
arise.




{828}

DISEASES OF THE CORONARY, PULMONARY, SUPERIOR MESENTERIC, INFERIOR
MESENTERIC, AND HEPATIC ARTERIES, AND OF THE COELIAC AXIS.

BY E. G. CUTLER, M.D.


DISEASES OF THE CORONARY ARTERY.


Chronic Endarteritis (Arterio-sclerosis; Atheroma).

This is the most important inflammatory disease of the coronary artery
which has been observed. It resembles chronic endarteritis elsewhere,
and frequently accompanies the same affection of the aorta, though it
may occur alone. The disease may be general, affecting both coronary
arteries equally, or one may be more involved than the other, or the
disease may be confined to one vessel or to even a small branch.

ETIOLOGY.--Chronic endarteritis of the coronary arteries is especially
a disease of middle and advanced life. It occurs most frequently in the
male sex. The coronary artery stands fifth in the order of frequency in
which the vessels are attacked. The disease is attributed to the misuse
of alcoholic drinks, syphilis, chronic lead-poisoning, gout, and
chronic kidney disease, by encouraging an early senescence of the
tissues, and hence favoring the occurrence of the arterial change.

SYMPTOMS.--There are no symptoms which are peculiar to the disease,
those which exist being due to the consecutive changes in the substance
of the heart. We may divide cases for convenience of description into
those with an acute course and rapid death; those pursuing a subacute
course; and, finally, those having a chronic one. In the first
instance, sudden death either occurs in a person apparently in perfect
health after the manner of a syncope, as in one getting out of bed or
standing on the street, while straining at stool, or under sudden
emotional excitement. Death may not follow on the instant, but occurs
in the course of a longer or shorter time. The attack begins with
pressure in the cardiac region, anxiety, restlessness, streaming pain.
The complaints and anxiety increase; the breath becomes short and
troublesome, the pulse small, frequent, and intermittent; finally,
collapse occurs, with oedema of the lung. Death takes place with either
a clear mind or slight delirium. Such a fatal ending may cover a day or
two or only a few hours. Almost always careful subsequent inquiry
elicits the fact that for some time past respiratory or cardiac
difficulties have existed, which appeared and disappeared and were not
regarded as serious or suspicious. Sudden death may also occur in cases
of protracted chronic heart disease following arterio-sclerosis, with
an old history of the symptoms of angina pectoris, under the appearance
of a fainting fit or of a severe attack of angina or oedema of the lung
lasting several days. In such a case rupture of the heart may be found,
with bloody infiltration of the cardiac {829} muscle and effusion of
blood into the pericardium. In other cases there may be small
hemorrhages, often with pronounced infarct formation and softening. In
still other cases neither hemorrhage nor infarction is found, but fatty
degeneration of the muscle or beginning softening. The sclerosis in
such cases is usually very distinct, and affects the trunk and anterior
descending branches of the left coronary artery. Sometimes it is hard
to find the diseased spot, as it may be circumscribed or on a side
branch. In the last-mentioned cases, where sudden death occurs in a
chronic process, no post-mortem signs of acute disease are usually
found. A chronic fibroid process, with atrophy, exists, which has run a
tolerably latent course and leads to death under the appearance of
sudden cardiac weakness.

PATHOLOGY.--There are two stages of chronic endarteritis: 1. The stage
of simple thickening of the intima; 2. The stage of ulceration and the
accompanying further changes.

At first, the normal smooth, shining inner surface of the intima is
interrupted here and there or in long stretches by flat rounded
elevations, which gradually merge into the healthy surrounding tissues,
and are characterized by a paler, more transparent character, and at
the same time softer but elastic consistence. The surface of these
thickenings, which are frequently located at the point where branches
are given off, is either perfectly smooth or slightly wrinkled. Besides
these translucent spots there are similar ones which are opaque,
whitish or yellowish in color, and have a somewhat rougher surface.
Lastly, there are very pronounced thickenings with a yellow color. In
the slighter degrees these spots occur singly. In the more pronounced
cases they may take up the greater part of the surface; the wall of the
vessel is thickened, the inner surface is uneven, and the vessel itself
more or less dilated. In the beginning the intima retains its shining
surface: after the disease has lasted a long time this is changed, and
the second stage appears. Roughnesses, erosions, and ulcerations
appear, or more commonly calcification of the wall. This latter appears
at first as little thin layers, and finally in large shield-like plates
of lime salts, which may occupy the whole circumference of the artery
and change it into a stiff, bony tube. It is found where ulceration has
occurred, and often without the appearance of the latter. Together with
the rigidity of the wall there occurs a slight tortuousness of the
vessel. At first the superficial layers of the intima are soft; next
they become more sclerosed, and their tissue denser and finally
striated; or disintegration, commencing deep in, may reach as far as
the surface and lead to an atheromatous ulcer. A more or less abundant
deposit of lime salts follows in the sclerosed layers of the intima,
leading to the formation of homogeneous plates as hard as bone.

The result of the process at first is diminution of the calibre of the
vessel, next diminution of the elasticity and contractility of the
artery: it loses its resistance and suffers dilatation in consequence
of the blood-pressure, and may attain aneurism. Or if calcification
occurs early the diminution of the lumen remains, or perhaps even
increases, and may reach an almost complete occlusion of the vessel.

The effects on the heart which follow this form of disease of the
coronary artery, though described in another place, had best be
enumerated here: 1. The flow of blood not being sufficiently interfered
with to cause disease, the heart may remain unchanged. 2. Hemorrhagic
infarction may result, accompanied by simple fatty degeneration or
softening, which is the most frequent cause of rupture of the heart. 3.
Fibrous degeneration or myocarditis may occur, leading perhaps to
aneurism of the heart. 4. There may be a combination of these two--a
greater or less marked fibrous degeneration, to which a fresh
hemorrhagic softening is added.

DIAGNOSIS.--There are no pathognomonic symptoms of this disease, and
{830} it is doubtful if a diagnosis can be arrived at. When the
conditions spoken of under Etiology pertain, and certain of the
symptoms mentioned in connection with the disease are present, a
suspicion of chronic endarteritis of the coronary artery may be
entertained with some degree of probability.

PROGNOSIS.--This must necessarily be unfavorable where the suspicion of
the disease is entertained.

TREATMENT.--Little is to be expected in the way of treatment beyond
mere palliation. In the rapid cases death occurs so soon that the
medical attendant barely has time to reach the patient. In those cases
which last longer the treatment must bear special reference to the
symptoms. Pain and spasm may be allayed by opiates or by the inhalation
of some anæsthetic cautiously administered, as ether or nitrate of
amyl, or by the cautious use of nitro-glycerin and the application of
counter-irritants, as mustard, over the cardiac region. Digitalis is to
be used with the greatest caution, if at all, as its action may be
positively harmful. The same is true of the bromides.


Obliterating Endarteritis.

Besides the preceding, another form of endarteritis has been met with
in the coronary artery--namely, the obliterating endarteritis, more
especially found in cases of syphilis and occurring in the smallest
branches. It is characterized by a gradually increasing thickening of
the intima through the formation of a connective tissue rich in cells,
and which leads to a narrowing, or even complete closure, of the lumen
of the artery. This thickening may involve one side of the artery or
its whole circumference. The inner surface of the intima on microscopic
examination is found to be covered by a layer of intact endothelium
where occlusion is not complete. There is deposit of neither fat nor
lime salts in the thickened intima. The outer coats of the artery show
little change.

The disease is accompanied by indurating myocarditis. Its symptoms are
those seen in this disease--namely, weakened cardiac activity, cardiac
dilatation and irregularity, possibly cardiac murmurs, an accentuated
pulmonary second sound, a pulse of moderate frequency, weak and
non-rhythmical, dyspnoea, cough.

DIAGNOSIS.--Impossible.

TREATMENT.--Purely symptomatic.


Aneurism.

Aneurism of the coronary artery is of rare occurrence. There is no
place of election for the disease, all parts and each artery being
alike liable to be affected.

ETIOLOGY.--The most common cause of the affection is chronic
endarteritis, where, through disease of the intima, the resistance to
the blood-pressure is diminished. Embolism is another though far less
frequent cause of the disease, several such cases having been reported;
and other highly suggestive cases are on record in which embolism of
the artery had occurred, with the production of considerable dilatation
for a short distance above the obstruction.

PATHOLOGY.--This does not differ from aneurism in other vessels. The
number may be from one to many, usually not more than two or three. The
size is generally that of a pea, often it is smaller, and sometimes it
is as large as a large nut. The termination is usually rupture with
fatal hemorrhage, and in far the majority of cases this occurs into the
pericardium.

{831} SYMPTOMS.--In most all of the cases I have found recorded there
were no symptoms till rupture of the sac occurred, giving rise to death
from hemorrhage. Then those symptoms which might be expected
occurred--namely, great præcordial pain, dyspnoea, suffocation,
tumultuous heart, irregular and intermittent pulse, and sudden death.

DIAGNOSIS, PROGNOSIS, and TREATMENT need not be considered, as the
disease is not recognizable.


Occlusion of the Coronary Artery.

Occlusion, more or less complete, of one or both of the orifices of the
coronary artery has been met with in connection with chronic
endarteritis of the root of the aorta. The accompanying sclerosis may
draw the orifices up like the strings of a purse, or a calcific plate
may extend from one side, or perhaps, detached, may lie simply applied
to the orifice. In rare cases the chief disease may be in the artery
itself, one of the main trunks or a branch being affected.

The PATHOLOGY is the same as that already described under Endarteritis,
stenosis being an early consequence of the process, and persisting, or
even increasing, to the last.

The SYMPTOMS observed in such cases are neither peculiar nor
diagnostic. They consist of those depending on the concurrent
affections, as of the cardiac valves, muscular tissue, or aortic
arterio-sclerosis. Prominent among them are dyspnoea, palpitation,
sudden cardiac distress, painful pressure in the region of the heart,
great anxiety; at last pallor of the skin, feeble cardiac impulse,
indistinctness of the cardiac sounds, the right ventricle continuing to
contract forcibly till the end. There is oedema of the lungs at last,
and on post-mortem examination fatty degeneration of the heart-walls is
found as a secondary consequence of the occlusion.


Embolism and Thrombosis.

Although these conditions are rarely found, yet a sufficient number of
cases is already on record to enable us to form a tolerably good idea
of the symptoms which accompany them. These latter in embolism
remarkably resemble those observed in the lower animals on ligation of
the coronary arteries. In the animals experimented on a rapid
enfeeblement of the heart's action ensued. The phenomena occurred in
the following order: First, there was retardation of the rhythmical
cardiac contractions, the left ventricle being primarily affected. At
first, the right ventricle beat faster, and then gradually became slow.
The beats became slower and slower till they ceased, the left ventricle
ceasing to contract a little before the right. The second result was a
gradual loss of power of the cardiac contraction. The third result was
the gradual distension of the left auricle when the left coronary
artery was compressed. The auricle swelled up more and more, became
bright red, and the rhythmical contractions changed to oscillatory
movements, which ultimately ceased entirely. The right ventricle and
auricle continued to contract powerfully, and the left ventricle
feebly.


EMBOLISM.

ETIOLOGY.--Rheumatism with its attendant complications--that is,
disease of the valves, and especially of the aortic valve, atheroma of
the coronary artery and possibly cardiac or other thrombosis--forms the
chief cause of {832} embolism, a small fragment of tissue being borne
away by the current of blood.

SYMPTOMS.--These are acute paralysis of the heart's movements, pain,
feeling of impending annihilation, retained consciousness, and regular
respiration. Nausea and vomiting have been observed. The lips are
livid, extremities cold and covered with a clammy sweat. In one case
there was inability to lie down. No pulse could be felt in any of the
accessible arteries, and neither apex-beat nor heart-sounds could be
detected. The ear applied to the cardiac region could hear only a kind
of cardiac tremor, which was very like the sound of a vibrating steel
plate. There was no loss of consciousness. The respiration was regular
and rhythmical, not exceeding eighteen or twenty in the minute. The
patient died twenty hours after the first symptoms.

DIAGNOSIS.--Although a positive diagnosis is impossible, the negative
pulmonary physical signs, the regular and rhythmic character of the
respiration, and the enfeeblement of the heart's action may lead to a
very strong suspicion of embolism of the coronary artery.

PATHOLOGY.--A small coagulum may stop up the main branch, usually the
left anterior, of one artery, or both arteries may be occluded by a
larger coagulum. In one instance an atheromatous softened patch
ruptured into the anterior portion of the left coronary artery, and
filled up the lumen with a soft putty-like mass (the sculptor
Thorwaldsen). A fatal issue is likely to occur in a very short time, as
the anastomosis cannot be sufficient for the sudden demand.

PROGNOSIS and TREATMENT need hardly be considered, as the affection is
necessarily fatal in cases which can be made out.


THROMBOSIS.

The same causes which give rise to thrombosis elsewhere are operative
in this case. They are chiefly arterio-sclerosis and rheumatism.

SYMPTOMS.--There have been observed slight tightness in the cardiac
region, lasting a few days, or a sense of oppression or constraint at
the back of the sternum. The pulse has been quickened, but is usually
very much slowed and very feeble; it has been observed as low as eight
beats in the minute. There is a sense of great lassitude and feebleness
of all the limbs. The respiration is normal in rhythm and frequency.
Auscultation reveals nothing but ordinary respiration till near a fatal
issue, when moist râles indicative of oedema of the lungs are heard.
Percussion gives at all times a normal resonance. There is no dyspnoea.
The heart-tones are clear, though weak, if occlusion is not complete or
anastomosis is perfect. (West was able to inject the arterial system of
the heart completely from one coronary artery, the other having been
tied.) If there is complete obstruction, we may expect to hear a
fremitus such as is produced by muscular spasm instead of normal
heart-sounds (observed in two cases). The skin of the body and face is
cool, pallid, and covered with sweat. The visible mucous membranes are
anæmic and pale. The mind is clear.

DIAGNOSIS.--The cardiac feebleness and progressive slowness, together
with the absence of symptoms connected with the lungs, might lead one
to suspect the presence of thrombus.

PROGNOSIS.--If a large branch of the artery is affected a fatal
termination is probable. If, on the other hand, the affection occurs in
a small branch, there is reason to believe that the circulation is
sometimes re-established through anastomosis.

TREATMENT must be purely symptomatic.


{833} Rupture of the Coronary Artery.

This may occur independent of aneurism. There are no premonitory
symptoms in some cases, death taking place suddenly. In other cases
vague and irregular symptoms lead the patient to understand that he is
not in perfect health. The symptoms of the disease are not
characteristic. Those which have been recorded are a difficulty of
breathing, a sense of constriction across the chest, or a pain and
feeling of anxiety in the præcordia; a frequent, feeble, and perhaps
very irregular pulse; epigastric pain and tenderness. The extremities
are cold. The mind remains clear. The physical signs are increased area
of flatness in the cardiac region, due to the escape of blood into the
pericardium, and scarcely audible cardiac sounds. The symptoms may
extend over a period varying from a few moments to several days.
Usually, some of the changes indicative of arterio-sclerosis are found
in the artery.


DISEASES OF THE PULMONARY ARTERY.

Acute inflammation of the coats of the pulmonary artery has only been
found associated with the pyæmic process as circumscribed abscesses of
the wall.


Chronic Endarteritis (Atheroma; Arterio-sclerosis).

Endarteritis of the pulmonary artery, though quite rare, is
occasionally met with in persons the subject of rheumatism, gout,
syphilis, or alcoholism. It is seen only when the pressure is
abnormally increased in the pulmonary vessels, especially in diseases
of the mitral valve. It is usually accompanied by a more pronounced
disease of the aorta, but is occasionally seen alone. The extent of
disease is hardly ever so great as that found in the other large
vessels, and at most amounts to the presence of prominent hard yellow
or gray patches in the intima, with perhaps ulcerated surfaces, and
rarely containing a deposit of lime salts. Complete rigidity has been
observed extending far into the lung. The wall of the vessel may be
irregularly dilated and its elasticity diminished. Usually, the disease
is in a much milder form, presenting perhaps a small amount of fatty
degeneration of the intima, and is not infrequently associated with
mitral stenosis or insufficiency (notably the former), pulmonary
fibrosis or emphysema, with accompanying hypertrophy of the right
ventricle. No symptoms have thus far been found to be distinctly
referable to atheroma of this artery.


Dilatation and Aneurism.

Dilatation of the pulmonary artery from primary disease of its walls is
of so rare occurrence that it may be merely mentioned. It depends on
chronic endarteritis, just spoken of. Where, on the other hand, there
is great pressure in the pulmonary circulation, as in marked mitral
stenosis, or insufficiency, collapse, or emphysema of the lung, with
great hypertrophy of the right ventricle, general dilatation of the
pulmonary artery may take place. The artery has been found to be six
and a half inches in circumference in a case of emphysema, the normal
average being three and a half inches; the semilunar valves were
insufficient, and the walls of the artery very much diminished in
thickness. From this as a maximum all degrees of dilatation have {834}
been recorded, with sometimes thickening and degeneration of the coats,
at others thinning with or without degeneration.

A systolic murmur has been observed over the artery when the dilatation
was considerable. The second pulmonary sound is usually strengthened
(unless the elasticity of the pulmonary artery is very much diminished
or the blood-pressure lowered in the right ventricle by changes of its
walls, or the pulsation is very quick and irregular). A circumscribed
dulness on percussion has been found in a few cases at the left edge of
the sternum, when the position of the heart was normal, between the
second and third cartilages. Sometimes there is a double impulse, a
systolic thrill, or more often a systolic pulsation, felt in this
position without any perceptible dulness, the edge of the lung being
retracted and the dilated artery taking its place. It is to be borne in
mind, however, that this sign (impulse, thrill, or pulsation) may be
present without any dilatation of the pulmonary artery or hypertrophy
of the ventricle, when inflammatory contraction of the lung has
occurred or the respiration is superficial, as may happen in phthisical
subjects, women, feeble and anæmic individuals, pregnant women,
convalescents, and persons afflicted with acute rheumatism. In such
persons the pulmonary second sound frequently seems to be unusually
loud when compared with the aortic second sound, without any evidence
of hypertrophy of the right ventricle being present. The determination
of the position of the lung establishes the diagnosis in such cases. On
the other hand, a lung dilated by emphysema may interpose and
completely cover the heart and pulmonary artery, which, though dilated,
may thus be masked.

Aneurism of the trunk or primary branches of the pulmonary artery, on
the other hand, is an exceedingly rare disease. But few cases are on
record. Aneurisms may be spindle-shaped or sacculated, of moderate
size, and are usually situated on the trunk. Lividity of the face,
dyspnoea, cough, dysphagia, headache, pain in the chest and
epigastrium, are the principal symptoms; and a systolic pulsation
(sometimes also diastolic) between the second and third left ribs near
the sternum, more or less prominence here, a superficial rough systolic
murmur propagated to the left and upward, a purring thrill, and
flatness on percussion in the same region and a little above it, are
the principal physical signs which have been recorded.

But the physical signs and symptoms above enumerated are not all
present in each case, nor are they when present distinctive of
pulmonary aneurism. Dysphagia is mentioned in but a single case,
dyspnoea is not constant, and cyanosis was at times absent. Also, the
physical signs were not constant. Even if all were present they might
be produced, as has been the case, by aneurism of the left wall of the
aorta, infiltrated lung-tissue, or by a solid tumor lying over the
vessels. The locality of the cardiac hypertrophy and dilatation aids in
establishing the diagnosis. If it is on the left side of the heart,
aneurism of the aorta is indicated; if it is on the right side,
pulmonary aneurism. These aneurisms tend to rupture into the
pericardium sooner or later.

Dissecting aneurism of the pulmonary artery has been observed once. It
was of small extent.[1]

[Footnote 1: _Bul. de la Soc. Anat. de Paris_, 1881, pp. 589-591.]


Stenosis of the Trunk or Main Branches of the Pulmonary Artery.

Narrowing of the trunk or of one of the main branches of the pulmonary
artery is of very rare occurrence. It may follow compression by an
aneurism of the ascending or transverse portion of the aorta,
compression by tumors in {835} the mediastinum, as from new growths or
enlarged glands; it may be caused by cicatricial contraction following
mediastinitis, inflammation of a portion of lung or of the bronchial
glands, or it may follow disease of the coats of the artery
(endarteritis).

The phenomena produced by stenosis of the trunk of the pulmonary artery
are similar to those found in stenosis at the orifice, which are
treated of in another place. They are anæmia of both lungs, accompanied
by persistent dyspnoea with occasional exacerbations (the patient
assumes a horizontal position either habitually or during the
paroxysm--a fact of true diagnostic importance [Chevers], as in all
other forms of disease of the heart and great vessels the patient
breathes easier when the shoulders are raised. But in this the dyspnoea
results from insufficiency of the supply of blood to the lungs and
system generally, and hence the recumbent posture affords relief by
removing the impediment of gravity, and thus promotes the supply of
blood to the brain), congestion, dilatation and hypertrophy of the
right side of the heart, cardiac palpitation, and finally general
venous congestion. Hypertrophy of the right ventricle is shown by
increase in the transverse measurement of the cardiac area of flatness
and increase in the force of the cardiac impulse. The artery up to the
point of constriction is dilated; the second sound is abnormally loud
and accentuated. Pulsation may be felt and a systolic murmur heard in
the second left intercostal space (observed in the right once),
propagated upward to the neck at the left of the sternum, or heard in
the interscapular space close to the spinal column.

PROGNOSIS is unfavorable.

There is nothing to be gained by treatment.


Rupture of the Pulmonary Artery.

Violent effort and great excitement have been followed by rupture of
the trunk or a main branch of the pulmonary artery. In the majority of
cases the coats were degenerated, though this was not always the case
(Chevers). Death is often instantaneous, but sometimes is delayed some
hours. In one case observed by Ollivier the duration was twenty-seven
hours.


Thrombosis and Embolism.

The pulmonary artery, from its position, is especially prone to become
plugged, either by substances coming from other parts of the body or by
coagula originating in the vessel itself. Pieces of disintegrated
coagula from the systemic veins, the contents of echinococcus cysts
ruptured into the venous current, fragments of new growths, are carried
to the heart and pass into the pulmonary artery, or large thrombi may
be detached from their position in a vein and lodge in the trunk or
main branches of the pulmonary artery.

Primary thrombosis of the pulmonary artery is very uncommon. In certain
septic conditions, in parturient women, in typhoid fever, and in
extreme anæmia thrombosis of the pulmonary artery may occur. It
commences perhaps in the right ventricle or at the pulmonary valves,
though it is also seen farther up.

SYMPTOMS.--The severity of the symptoms depends on the completeness of
the obstruction. There is dyspnoea, more or less marked according to
the size of the thrombus or embolus, pain in the præcordia, great
distress, anxiety, faintness, sense of suffocation, tightness in the
chest, palpitation, lividity and extreme pallor, cold sweats, an almost
imperceptible pulse, great restlessness, {836} and occasionally
convulsions. The mind remains clear. The symptoms develop gradually or
rapidly--in the former case depending on the slow increase of a small
thrombus--and remissions are often seen; in the latter case depending
on the sudden lodgment of an embolus of large size. Sometimes the
symptoms are extremely marked, and death takes place in a few minutes.
The appearances are not those of asphyxia, and death is usually
attributed to want of arterial blood-supply to the brain and medulla
oblongata, and not to suffocation or paralysis of the heart.

Percussion shows a normally resonant chest. Auscultation gives normal
breath sounds with free inspiration and expiration. There is very
likely a basic systolic murmur conducted along the course of the
pulmonary artery, but this is not constant. The cardiac second sound
and impulse are increased. At the post-mortem examination the heart is
found in diastole, the left cavities and pulmonary veins empty, the
right cavities filled with blood, and the cardiac veins strongly
distended.

DIAGNOSIS.--The diagnosis is often uncertain. When not developing with
extreme rapidity the symptoms are very similar to those caused by
stenosis of the pulmonary artery, and in the suddenly fatal cases they
are almost identical with rupture of the heart or rupture of a thoracic
aneurism, or even angina pectoris. The history of an antecedent
thrombus or of a disease of the heart which is likely to be accompanied
by thrombus, together with the absence of physical signs, render a
diagnosis many times probable.

PROGNOSIS.--To be regarded as of the gravest character.

TREATMENT.--In the rapid cases death occurs before anything can be
attempted. In the less severe cases absolute rest must be enjoined, and
free stimulation with brandy, ammonia, and ether attempted. It might be
worth while to place the patient with the head lower than the body, to
favor the flow of blood to the brain.


DISEASES OF THE SUPERIOR MESENTERIC ARTERY.


Aneurism.

Aneurism of both the superior and the inferior mesenteric arteries
occurs. The former is the more frequent, though still a rare disease.

The symptoms are pain in the epigastric and lumbar regions, a globular
pulsating tumor in the median line, the pulsation being accompanied by
a bellows murmur. The tumor has been seen in at least one instance to
be so large as to press on the renal arteries. Rupture is apt to take
place with the signs of internal hemorrhage. The cause of the disease
is the same as of aneurism elsewhere. Embolism is said to be a not
infrequent precedent. The aneurism is seldom larger than a hen's egg,
and is usually globular.

A positive DIAGNOSIS of the locality of the aneurism is not possible.

The TREATMENT must follow individual indications. Compression has been
successful in a few instances.


Embolism.

Several cases where the superior mesenteric artery was found at autopsy
to be completely occluded by coagulated fibrin were mentioned by
Tiedemann in a work published in 1843. Virchow first described the
characteristic {837} post-mortem appearances which follow this lesion
in his _Gesammelte Abhandlungen_, and since then records of cases have
been numerous.

CLINICAL HISTORY.--In by far the majority of cases there is an evident
source for an embolus. Pain in the abdomen is the first symptom, and
usually remains one of the most prominent throughout. At first it may
be a dull aching just below the borders of the ribs, but soon there is
superadded paroxysmal pain resembling colic, and which may at times
even be relieved by pressure. The occurrence of this colic in cases
where embolism might happen ought to put the physician on his guard for
other symptoms; for, though insufficient in itself to establish a
diagnosis of embolism, the presence of a colic resisting treatment in
the course of cardiac disease justifies the suspicion that this may be
the case. The pain is usually located near or above the umbilicus.

Intestinal hemorrhage occurs in nearly every case; death may take place
before any change in color of the stools is observed or any blood
appears at the anus, but on post-mortem examination blood is found in
the intestine. The cause of this hemorrhage is the infarction of the
intestine analogous to that which takes place in other organs supplied
by end arteries, the superior mesenteric having been proved
experimentally to be functionally such an artery, owing to its great
length, the extent of tissue supplied by it, and the comparative
smallness of the vessels with which it anastomoses on the borders of
its territory. The collateral circulation is thus so long in being
established that ample time is allowed for those disturbances of
nutrition in the walls of the vessel which render them permeable and
allow the blood to escape. In view of the hemorrhage certain other
symptoms are readily accounted for, as, for example, pallor of the face
and surface of the body, the considerable and rapid fall of the
temperature, syncope, hæmatemesis, diarrhoea, and melæna. These two
latter symptoms are important though inconstant. There is reason to
believe that the first effect of the embolism is to paralyze the bowel
and prevent peristaltic action. Diarrhoea is of frequent occurrence,
and may be profuse, the stools remaining of their natural color; or
fresh blood may be passed at first from the rectum, followed by the
continuous passage of tar-like masses; or the stools may be of pulpy
consistence, mixed with blood, or consisting of tarry blood. Lastly,
profuse hemorrhage may take place in which the stools resemble
tar-water. The character of the blood does not give any kind of clue to
the locality of the lesion.

Vomiting is a frequent symptom, and may consist of altered blood of
variable consistency. A fall in temperature can often be determined by
the thermometer, especially after severe hemorrhage. Not rarely the
temperature is normal or may be even increased, especially if secondary
inflammation has set in.

Tension and tympanitic swelling of the abdomen may occur or fluid may
be detected late in the case, these being evidence of peritonitis.

PATHOLOGY.--Before proceeding to consider the pathological changes
occurring in embolism, a few words on the blood-supply of the intestine
might perhaps render what follows clearer. The superior mesenteric
artery supplies the whole of the small intestine except the first part
of the duodenum; it also supplies the cæcum and the ascending and
transverse colon. The inferior mesenteric supplies the descending and
sigmoid flexure of the colon and the greater part of the rectum. The
anastomoses are as follows: The pancreatico-duodenalis, a very small
artery and a branch of the hepatic, anastomoses with the first branch
of the superior mesenteric, also a very small artery and given off
under cover of the pancreas. The middle colic artery anastomoses with a
branch of the inferior mesenteric. Both these arteries are given off
from the main trunks of the arteries.

The experiments of Litten in 1875 show that the superior mesenteric
artery, {838} though not so anatomically, is functionally a terminal
artery, the anastomosis not being developed with sufficient rapidity in
case of extensive embolism to ensure the integrity of the circulation.

1. The result of sudden total closure by embolism of the trunk of this
artery, therefore, is precisely like that of ligature of this artery in
animals, and is first to produce sudden abdominal pain, attacks of
colic, vomiting, uncontrollable intestinal hemorrhage, death. The
intestine from the lower transverse portion of the duodenum to the
middle of the transverse colon is found to be suffused, brown-red,
blackish, or grayish. All the layers are swollen; innumerable capillary
extravasations of small and great extent are seen, with venous
hyperæmia and oedematous infiltration. In other words, there occurs
necrosis with oedema and hemorrhage in all those portions of the
intestines which are supplied by this artery.

2. Closure of large branches by embolism gives rise to infarction of
the portion of intestine concerned, followed by death. The symptoms
differ only in intensity, if at all, from the preceding. A case has
been seen where there was every reason to believe that embolism had
occurred, and yet the patient recovered. (The patient, suffering from
acute rheumatism complicated with peri- and endocarditis, suddenly
developed profuse intestinal hemorrhage of tar-like color, which was
repeated twice. Colic pains, tympanites, depression of the temperature
of the body, followed. At the same time symptoms of embolism of various
other arteries were present. Recovery took place after eight weeks.)
This result of course depended on the subsequent perfection of the
collateral circulation.

3. Closure of the smallest branches may produce the same kind of
symptoms as the above, though less in degree. Limited portions of
intestine have been found to be in a gangrenous condition from embolism
of very minute branches, more especially when the embolus extended well
into the artery. In place of gangrene of the intestine ulcers of the
mucous membrane have been seen independent of typhoid fever or
tuberculosis. Considerable stenosis has followed such ulcers.

The affected portion of intestine in embolism is found to contain a
variable amount of blood mixed with the other contents of the gut.
Peritonitis, dry and limited or general and accompanied by effusion, is
the rule. The mesenteric glands are found enlarged and succulent, with
perhaps here and there necrosed spots. Thrombosis of the corresponding
veins is not uncommon. Large collections of blood under the peritoneum
and in the mesentery have been observed. The color of the mucous
membrane has been slaty, and a diphtheritic appearance has been
observed.

DIAGNOSIS.--The following are the most important points in forming a
diagnosis: 1. A source exists from which an embolus might be derived.
2. Profuse and even exhaustive intestinal hemorrhage sets in, which can
neither be explained by primary disease of the intestinal walls nor by
hindrance to the portal circulation. 3. There is a rapid and
considerable fall of the temperature. 4. Pain in the abdomen comes on,
which may resemble colic and be very severe. 5. Finally, tension and
tympanitic swelling of the abdomen occur, and there may be fluid in the
abdominal cavity. 6. Evidence of embolism of other arteries may have
been obtained before the symptoms of embolism of the superior
mesenteric artery come on, or such evidence may appear at the same time
as the latter. 7. Palpation may reveal the presence of collections of
blood between the folds of the mesentery.

PROGNOSIS.--The prognosis in embolism of the superior mesenteric
artery, though not absolutely bad, is exceedingly grave. It must be
borne in mind that the symptoms of occlusion of one of the large
branches are similar to those where the main stem is involved, while
the probabilities of recovery in the former are much greater, as
already explained, from the shorter extent of {839} the anastomosis.
There is evidence that recovery from the immediate effects of embolism
may take place even where subsequent ulceration has been so great as to
cause complete closure of the intestine through cicatrization. (A case
is related by Parenski where the patient was operated on for stricture
of the bowel, and only at the autopsy was it discovered that the
stricture was due to cicatrization from ulceration caused by embolism
of one of the branches of the superior mesenteric.) There are at least
three cases of recovery on record where occlusion of the main stem was
supposed to have taken place; but inasmuch as the situation of the
embolus cannot be determined with certainty if the patient recovers,
these cases are open to the suspicion that one or more of the larger
branches only were occluded. The profuseness of the hemorrhage, though
it may imperil the life of the patient from exhaustion, bears no
constant relation to the gravity of the case. Copious and repeated
hemorrhages per anum took place in cases of recovery, while in other
fatal cases this symptom was entirely absent. Extreme fetor of the
stools must be regarded as of evil omen, as it may be the evidence that
gangrene of the bowel has taken place.

TREATMENT.--One of the first symptoms calling for relief is the colic,
which is best met by morphia given subcutaneously or by suppository.
For the hemorrhage ergot by the mouth and alum enemata have proved
serviceable, or the application of ice to the abdomen. The lowering of
the heart's action by sedatives is to be avoided when we remember that
their use would lower the blood-pressure, and thus tend to retard the
establishment of the collateral circulation.


Thrombosis.

The symptoms of thrombosis have not been determined apart from
embolism, and it is doubtful if the affection proves fatal unless the
extent of artery involved is very considerable or the formation of the
thrombus is very rapid, for the anastomosis is gradually made
compensatory. In either of the latter cases the symptoms are identical
with embolism, and the pathological appearances are the same. With
regard to treatment, general indications must be pursued.


Endarteritis.

This disease is met with, but it is usually slight and unaccompanied by
symptoms.


DISEASES OF THE INFERIOR MESENTERIC ARTERY.


Aneurism.

Aneurism of this artery has been seen after death. The diagnosis could
not be made, in all probability, during life. Pain might be a prominent
symptom, though not necessarily, as many of the aneurisms of the
abdomen are unattended by any symptoms. Rupture is not unlikely as a
termination.


Embolism.

Embolism has been observed. Sudden pain in the abdomen comes on,
followed by vomiting and diarrhoea. The patient looks miserably; the
{840} belly is drawn in and painful on pressure almost exclusively in
the left iliac region. Severe spontaneous colic-like pains continue,
with occasional vomiting and diarrhoea. At first the stools are
feculent and pap-like; then they begin to smell bad, and even stink.
Red blood is passed. Soon there is a mixture of blood and slimy masses.
Finally, the stools are slimy, blackish, almost tar-like, and have a
terrible odor, and are passed with griping and tenesmus. Occasional
vomiting still continues. The pulse becomes smaller and more frequent,
and gradually irregular and intermittent. Soon collapse and death
follow.

The predisposing and exciting causes are the same as in embolism of the
superior mesenteric artery.

The duration is usually short, lasting from a few hours to three or
four days. The termination is ordinarily fatal, though doubtless cases
of recovery have occurred, as stated under Embolism of the Superior
Mesenteric Artery, the size and position of the embolus not precluding
the possibility of the establishment of collateral circulation.

Complications are varying degrees of peritonitis, evinced by
tympanites, pain, and tenderness, either localized or diffused, and
later by the occurrence of effusion. Sequelæ, when the disease is not
immediately or rapidly fatal, are ulceration of the colon with
subsequent cicatrization and contraction.

PATHOLOGY.--The mucous membrane of the descending colon, sigmoid
flexure, and rectum is somewhat swollen, strongly reddened, and
contains ecchymoses and extensive suffusions of blood; or the color may
be blackish or slaty and the surface sloughy.

DIAGNOSIS.--The diagnosis can only be made by exclusion. The same
points are to be carefully verified as in embolism of the superior
mesenteric artery, only the pain and symptoms are in a different place,
and the secondary peritonitis also begins on the left.

PROGNOSIS.--The prognosis is very grave, but recovery may take place,
contractions or constrictions being left behind.

TREATMENT.--The treatment combines perfect rest, the exhibition of
wine, opium, vegetable astringents, and the subcutaneous injection of
morphia.


ANEURISM OF THE HEPATIC ARTERY.

The tumor varies in size from a hazelnut to a child's head, and is
egg-shaped. Pain in the epigastrium and right hypochondrium or upper
abdominal region is a characteristic symptom. At first the pain is not
severe, and is occasional, recurring after a pause of several months'
duration; later it becomes very severe and lasting. The abdomen is not
tender to the touch or on pressure during the remissions from the
attacks of pain, but after rupture of the aneurism, whether temporary
or lasting, it is very severe. The abdomen is sometimes distended, at
others not. The tumor, owing to its position, cannot be felt, nor can
pulsation be detected, as the wall of the aneurism consists of
connective tissue and blood-clot, and the stream of blood coming from a
small artery is slow. In but a single case has increase in size of the
spleen and liver been observed. The functions of the stomach and
intestines remain normal in spite of the pain. The locality of aneurism
of the hepatic artery is such as to readily cause temporary or lasting
icterus--a phenomenon which occurs in perhaps two-thirds of the cases.
Rupture, with the ordinary signs of internal hemorrhage, seems to be
the usual termination. Inflammatory processes or fever does not follow
hemorrhage into the abdomen. {841} If perforation occurs into the
gall-bladder, a gall-duct, or the intestine, the hemorrhage may appear
to be moderate. In such instances repeated discharges of blood may
occur from the intestine, or at the same time may be thrown off from
the stomach.

There is no means of determining how long aneurism of the hepatic
artery may exist without giving any kind of sign of its presence.
Judging from analogy, it is very probable that a considerable time may
elapse before the disease is observed. Since pain in the abdomen is the
first pathological indication, and rupture the last, we may measure the
probable duration of the disease by these phenomena and also by the
clinical course. This was not over ten days in two cases, and in three
cases it was three to four months. Since aneurisms of the hepatic
artery, even when they have reached their greatest dimensions, are not
palpable, the pains which appear with them have in themselves no
diagnostic worth. The same is true of the icterus which appears sooner
or later. It is only after rupture has occurred that all the chances
are so placed that a comprehensive estimate of them may be made and a
diagnosis arrived at by exclusion. The fact that the function of the
stomach remains unchanged in spite of rupture (hemorrhage), and the
totally unchanged character of the blood-clots vomited, enable us to
locate the situation of the hemorrhage as outside the stomach. If at
the same time there is an alternate relation between the occurrence and
disappearance of the icterus and the hemorrhage, the inference is
admissible that the latter is located in the immediate vicinity of the
gall-ducts. Other peculiarities of the blood-clots passed at stool are
perhaps the imprints of the valvulæ conniventes of the jejunum.

The DIAGNOSIS of aneurism of the hepatic artery is usually impossible.

Aneurisms of the splenic, renal, and other abdominal arteries are
recorded, but not in sufficient numbers to warrant a detailed
description of them.


DISEASES OF THE COELIAC AXIS.


Aneurism.

Aneurism of the coeliac axis, when the tumor is large, is accompanied
by very much the same symptoms as aneurism of the abdominal aorta. The
disease is rather uncommon.

ETIOLOGY.--Syphilis, rheumatism, and advanced age play important parts
in the etiology of this disease as predisposing causes of arterial
degeneration. Many persons affected have been immoderate
spirit-drinkers, which of itself does not directly tend to the disease,
but does so indirectly, in that it encourages an early senescence of
the tissues. In the same way any debilitating conditions may act as
predisposing causes. Chronic endarteritis is most frequently found at
the seat of the aneurism. Secondary or exciting causes are
peculiarities of occupation, as those which are laborious and require
much physical exertion and entail exposure to inclemencies of the
weather.

SYMPTOMS.--Pulsation is usually the first symptom observed. It is felt
in the epigastrium about two and a half inches below the ensiform
cartilage, or even higher, and a little to the left of the median line;
or it may be midway between the ensiform cartilage and the umbilicus,
on the left. It is not unfrequently of a distensile character, and is
unaffected by changes in the position of the patient. It is not
synchronous with the cardiac systole, but follows in rapid succession
to, and terminates with, the ventricular {842} diastole. A tumor,
usually globular, is felt in the region of the pulsation. It is of
variable size, from that of a hen's egg to a cricket-ball, or in case
of false aneurism even much larger. The tumor is slightly tender; it
moves with the diaphragm, and sometimes when it presses upon the
pancreas ptyalism has been observed, which in one instance was
increased by external pressure on the aneurism with the hands.

Another constant symptom is pain in the left side, extending from well
up in the chest to the region of the hip, or located in the lower part
of the chest alone, or perhaps in the epigastrium. This pain is either
constant or excited by exertion, and paroxysmal in character.

Flatness on percussion over the tumor of varying extent is observed in
many cases, and a systolic bruit, perhaps of a whistling character, is
heard.

The usual termination of aneurism of the coeliac axis is rupture with
internal hemorrhage. The symptoms of this accident do not differ from
those of the same occurrence in abdominal and thoracic aneurism, and
are likewise usually fatal.

PATHOLOGY.--Strain doubtless forms an important factor in the
production of this aneurism in an artery previously weakened by disease
of its coats. The tumor is frequently a false aneurism, and has for
walls connective tissue and the neighboring organs. When it is of large
size, on account of its position it sometimes presses upon the pancreas
or vertebræ, and produces absorption with consecutive symptoms. In the
former case ptyalism has been observed, which perhaps may have been due
to reflex action through the coeliac plexus and pneumogastric nerve,
the reflex centre being the medulla oblongata with the facial origin.
The wall of the aneurism is usually thin, and in some cases it has
given way, leading to the formation of so-called false aneurism. Not
infrequently the wall is atheromatous. The size of the aneurism varies
greatly, though it is never larger than the two fists.

DIAGNOSIS.--This aneurism is apt to be confounded with aortic aneurism,
and can only at times be distinguished from it by its locality and
small size.

PROGNOSIS.--This must be grave if a diagnosis is made, for the ultimate
result is usually rupture and hemorrhage.

TREATMENT.--The general principles recommended in treating abdominal
aneurism should be followed out. It is but rarely the case that
compression is admissible, and then the distal pressure is to be used.
Rest and diet form the most reliable means of treatment at our command.




{843}

DISEASES OF THE VEINS.

BY ANDREW H. SMITH, M.D.


The principal affections to which the veins are liable are the
following: Inflammation (phlebitis), acute and chronic; Dilatation;
Narrowing or obliteration; Degeneration; Concretions.


Inflammation.

Idiopathic phlebitis occurs for the most part under one of three
conditions: First, as a simple primary inflammation of the tissues
composing the walls of the vessel; second, as a participation in an
inflamed or diseased condition of surrounding structures; third, as the
result of the absorption of poisonous material into the blood.

Like any other structure of the body, the veins are liable to
inflammation as a purely local affection. It is nevertheless true that,
in the acute form, this inflammation is most likely to occur in
connection with certain conditions of the system which seem to act as
predisposing causes, although the connection between them and the local
phlebitis is not apparent. Thus it occurs (perhaps associated with more
or less of lymphangitis) in the puerperal state, in phthisis, in heart
disease, and in other conditions of general depression. I have met with
it, for example, during recovery from pneumonia after typhoid fever and
after suffocative laryngitis. Under these circumstances it constitutes
the chief element in the affection known as phlegmasia dolens. Now,
none of the above conditions implies, so far as is known, any source of
irritation to the venous structures, much less to a limited portion of
the venous system; and the only explanation of their association with
phlebitis seems to be in the assumption that these conditions favor
coagulation of the blood, and that, in these cases, the formation of a
clot precedes the local inflammatory process. The location of this clot
is probably determined by anatomical conditions.

In other cases, however, the process evidently begins in the wall of
the vessel, and the formation of the thrombus is secondary. Any change
which interferes with the smoothness of the inner coat, whether by loss
of endothelium or by producing inequalities of the surface, will very
certainly determine the deposition of fibrin and the formation of a
coagulum. The glossy smoothness of the intima seems to require the most
perfect nutrition of the subjacent tissues for its maintenance, and its
loss produces an immediate slowing and ultimate stoppage of the
blood-current. This is admirably shown by the experiments of
Nicasse,[1] which demonstrate that simply denuding a portion of a vein,
and thus cutting off its vascular and nervous supply, induces almost
immediately the formation of a thrombus coextensive with the denuded
portion.

[Footnote 1: _Des Plaies et de la Ligature des Veinse_, Thèse, Paris,
1872.]

{844} Inflammation affecting the inner coat of a vein and extending
along its surface, as in the case of a serous membrane, probably never
occurs. The picture of phlebitis formerly drawn, and which embraced the
exudation of false membrane or the formation of pus upon the inner
surface of a vein, the pus in the latter case floating off with the
blood and constituting pyæmia, the formation of a clot being a later
and unimportant event, has little or no resemblance to what actually
occurs.

The observations upon which these assumptions were based were
erroneous, as shown by Virchow, in that the staining of the intima by
absorption of coloring matter from the blood was mistaken for
inflammatory redness, and changes in the clot itself were confounded
with exudation and suppuration. Indeed, when we reflect that the intima
is not vascular, we should scarcely expect from it anything analogous
to serous inflammation. The only acute process to which it appears
liable is an erosion or crumbling away under the same conditions which
determine, in the middle or outer coats, increased vascularity,
exudation, and the formation of pus.

Thus, from some general condition favoring the coagulation of the blood
we may have a thrombus formed, followed by secondary inflammation of
the wall of the vessel, or, without such general condition, we may have
inflammatory changes, commencing in the outer or middle coat and
causing the secondary formation of a thrombus. In either case the clot
shuts off the affected portion of the vein from the general
circulation. Changes take place in the clot which are more properly
considered under the head of thrombosis, and by which it is ultimately
removed. Exudation takes place into and between the tunics which form
the venous wall, the latter becoming thickened and comparatively rigid,
so that when the vein is cut across its lumen remains open like that of
an artery.

Sometimes pus is formed between the different coats, constituting small
mural abscesses; sometimes the intima crumbles away and exposes the
middle coat, which suppurates on its inner surface, and the pus mingles
with the débris of the clot. In this way a larger abscess is formed,
bounded by the wall of the vein and by a partly-organized coagulum on
either side. These coagula sometimes break down, and fragments from
them, infected by the pus and its contained micrococci, are swept on in
the current of the blood until they find a lodgment, where the process
begins anew, and whence it may be propagated in like manner to other
and more distant parts.[2] It is only to the condition above described
that the term suppurative phlebitis can properly be applied.

[Footnote 2: Ziegler, _Path. Anatomie_, Jena, 1881, p. 429.]

But, instead of a suppurative process taking place, the endothelium may
be thrown off and replaced by minute vegetations of the character of
granulation-tissue, which, penetrating into and blending with the clot,
may temporarily or permanently occlude the vein, and the contraction
which follows may ultimately leave only a fibrous cord to represent the
vessel.[3]

[Footnote 3: Leroux, _Gaz. méd. de Paris_, 28 Juin, 1879.]

This process is designated adhesive phlebitis, and is one of frequent
occurrence and very important in its results. It takes place in
connection with suppurative phlebitis, and by closing the vessel on
either side of the suppurating portion serves to prevent the pus from
mingling with the general circulation.[4] By its action the largest
veins, including the venæ cavæ, are occluded, and extensive and
important changes in the circulation are brought about.

[Footnote 4: While this is true of a pus-cavity forming within a vein,
an abscess originating outside of a vein or between the layers of the
venous wall may open into the vessel at a point not protected by a
clot, and the pus mingling with the blood will constitute veritable
pyæmia.]

The second condition under which phlebitis occurs is that in which a
vein, {845} coursing through an inflamed or diseased structure, becomes
itself inflamed. This takes place most frequently in phlegmonous
erysipelas and in diffused inflammation of the cellular tissue, but it
may be the result of any inflammation in the neighborhood of a vein.
Under these circumstances the external layer of the venous wall is
first affected, and the others subsequently. Only a portion of the
circumference of the vessel may be involved, and the wall may bulge
inward considerably without necessitating the formation of a thrombus
(Virchow). But if the nutrition of the walls is seriously impaired, the
intima becomes roughened by the loss of its endothelium, the
blood-current is slowed by the increased friction thus caused, and, the
uneven surface favoring at the same time the adhesion of fibrin, a clot
is formed, and the course thereafter is the same as when the vessel is
primarily affected.

Suppuration may also take place between the vein and its sheath, and
extend for a considerable distance along the vessel. The walls
participate secondarily, and the vein becomes occluded as before
described.

In the third class of cases, those depending upon toxic infection, the
inflammation is caused by the irritation of some poisonous material
circulating in the blood. The phlebitis is therefore secondary, and is
to a great degree overshadowed by the general condition which
accompanies it. Aside from instances in which there is a direct
inoculation of a poisonous material--as, for example, the venom of a
serpent--the conditions merge into those which come under the
designations pyæmia and septicæmia--diseases which were formerly
confounded with phlebitis, but which are now recognized as distinct
from, though often coexisting with, it.

If in acute phlebitis the inflammation does not result in the formation
of pus, the vein may recover its normal condition, or the walls may
remain thickened and the lumen contracted, but still pervious, or it
may be entirely occluded. Suppuration, however, always results in
complete and permanent closure of the vein.

The symptoms of acute phlebitis are chiefly such as indicate
obstruction of the vein. When a large vein, situated in one of the
extremities, is the seat of the affection, there are usually severe
pain of a tensive character and decided tenderness on pressure. The
limb swells, sometimes to a very considerable extent, and becomes stiff
and unwieldy. If a superficial vein, such as the long saphena, is
affected, there will be subcutaneous oedema and pitting; but when the
vessel lies beneath a firm, tense fascia, this will limit the swelling,
and the limb will be hard and brawny, while the tension will greatly
aggravate the pain.

When the vein is sufficiently near the surface it may be felt at the
affected part as a hard cord, usually more or less knotted. The skin
over it may be discolored, presenting a red or somewhat coppery hue and
a streaked or mottled appearance, or the pressure from the effused
serum may empty the capillaries of blood and render the skin pale and
shining.

The temperature of the limb may be elevated, normal, or subnormal. In
the outset, under the influence of the inflammation, there is usually
increased heat, but as the tension from the oedema interferes more and
more with the circulation, the temperature falls, and the limb may
become colder than its fellow.

Inflammation of a limited portion of a vein may not be attended by any
notable symptoms, the collateral circulation being quickly established,
and the effects of the obstruction thus obviated, while, at the same
time, the local symptoms are masked by the morbid conditions in the
surrounding tissues which give rise to the phlebitis.

The constitutional symptoms accompanying phlebitis are those of
inflammatory fever, the grade of which will depend upon the extent and
severity of the inflammation. When a considerable length of vein is
involved, as {846} may be the case in the form of phlebitis already
referred to, which progresses along the sheath of the vessel, the
irritation of the general system may be great, especially if pus is
formed, when hectic or even typhoid symptoms are not uncommon.

The differential diagnosis of phlebitis in its local appearances
requires only its distinction from lymphangitis. The latter disease is
more abrupt in its invasion, depends almost always upon some wound or
injury with which the local symptoms are directly connected, is more
diffuse, affecting a network of vessels rather than a single one, and
is invariably accompanied by engorgement of the lymphatic glands to
which the affected vessels lead, as, in the case of the extremities,
the axillary or inguinal glands.

In complicated cases the occurrence of phlebitis may not be marked by
any distinctive symptoms. It may be suspected if, in the course of
erysipelas, diffuse cellulitis, etc. in the neighborhood of an
important vein there is a somewhat sudden increase of pain and
swelling, and if an enlargement of the tributary cutaneous veins is
soon observed.

The treatment of phlebitis consists in complete rest, in the use of
such constitutional means as may be necessary to allay the irritation
of the system, and locally in the application of leeches and warm
fomentations. If, on the other hand, the local temperature is very
high, the use of ice may be indicated.

Nonat, in cases of commencing phlebitis from venesection, tried the use
of flying blisters over the part affected. Obtaining good results, he
extended the treatment to phlebitis following typhoid fever, etc., and
the morbid phenomena were at once arrested.[5]

[Footnote 5: _Gaz. des Hôp._, No. 86 (_Med. Times and Gaz._, Aug. 7,
1858).]

Much disturbance of the parts, either in examining them or in the use
of frictions, etc., is to be avoided, as there are not a few instances
on record in which portions of thrombi have been detached in this way,
and, floating off in the current of the blood, have resulted in
pulmonary and even cardiac embolism, the latter causing immediate
death.[6] The tendency to oedema will be lessened by placing the
affected part in a position that will favor the return of the blood by
the collateral circulation.

[Footnote 6: _Lyon Médicale_, June 18, 1876 (_N.Y. Med. Rec._, Sept. 2,
1876).]

As an internal remedy the calcium sulphide is worthy of trial.[7] The
administration of ammonia is thought to lessen the tendency to the
formation of coagula and to promote their absorption if already formed.
Abscesses occurring in superficial localities should be promptly
opened, antiseptic precautions being observed. The strength of the
patient should be maintained by every possible means, the danger of an
extension of the mischief being proportioned to the lowering of the
vital forces.

[Footnote 7: "Report of N.Y. Therapeutical Society," _N.Y. Med.
Journ._, June, 1882.]

As already stated, acute phlebitis plays a very important part in the
affection known as phlegmasia alba dolens or white leg. Indeed, many
writers consider that it is the only essential factor in the affection.
This view is strongly insisted upon by Hervieux, but the researches of
Mackenzie,[8] Simpson,[9] Barker,[10] and others have shown that
something more than phlebitis is embraced in the disease. Tilbury Fox
claims that there is an association of lymphangitis with the phlebitis.
At all events, whatever may be the exact pathology of the affection, it
appears to be certain that an abnormal condition of the blood, favoring
the formation of coagula in the veins, is an essential prerequisite.

[Footnote 8: _Pathol. and Treat. of Phleg. Dolens_, London, 1862; _Med.
Times and Gazette_, Aug. 22, 1866.]

[Footnote 9: _Med. Times and Gazette_, Jan. 14 and 18, 1859.]

[Footnote 10: _The Puerperal Diseases_, New York, 1876.]

Phlegmasia dolens occurs chiefly in the puerperal state, and affects
chiefly {847} the lower extremities; but it may affect males and
non-puerperal females, and may be seated in the arms as well as the
legs. Outside of the puerperal state it is met with in conditions of
depressed vitality, as during convalescence from acute disease, and in
those suffering from phthisis, cancer, and other cachexiæ. When one of
these conditions is present a degree of venous obstruction--from
pressure, for example--which would ordinarily cause merely a slight
amount of oedema may result in an adhesive or even suppurative
phlebitis, and the associated phenomena which form the disease in
question.[11]

[Footnote 11: Murchison, _Med. Times and Gaz._, May 23, 1863, reports
the case of a man recovering from typhus in whom phlegmasia dolens
resulted from the pressure of a diverticulum from the bladder upon the
right iliac vein.]

The preponderance of cases, however, occurring from the second to the
fourth week after delivery indicates a special condition present at
that time tending to produce the disease. Some cases, doubtless, are
due to the cause suggested by Lee--viz. the formation of clots in the
uterine veins, and the growing out of these thrombi through the
hypogastric and into the iliac and femoral veins. But that this is not
the only or the usual cause is proved by numerous autopsies in which no
evidence of thrombosis has been found in the uterine veins. Still, the
puerperal period is very generally one of vital depression, in which
hyperinosis and inopexia are presumably present. To this is added
another source of irritation, in the loading of the blood with the
material absorbed from the uterus in the rapid reduction of its bulk
which is taking place.

It is not improbable also that small amounts of decomposing blood, and
even clots, may be retained in the uterine sinuses, and ultimately be
forced suddenly on into the venous circulation by the pressure
resulting from the shrinking of the tissues by which they are
surrounded. This would explain the suddenness with which symptoms of
toxæmia or embolism often occur.

The principal difference between phlegmasia dolens and simple
obstructive crural phlebitis is in the degree rather than the character
of the symptoms.

When, in a healthy animal, phlebitis of the crural vein is set up
artificially, causing complete obstruction, there is but little pain,
and only a comparatively slight effusion into the cellular tissue, and
the limb pits readily. In phlegmasia dolens, on the other hand, the
pain may be very severe and the oedema very great, and the limb is
stiff, hard, tense, and shining, and pits only with firm and continued
pressure (Barker). Moreover, crural phlebitis may occur and prove fatal
without causing phlegmasia dolens.

These facts have perhaps been allowed undue weight in the argument for
non-identity. It would seem that we have only to admit a depraved
condition of the blood favoring thrombosis and secondary phlebitis, and
disposing to more abundant effusion of a more plastic character as the
result of the obstruction, and all the distinctive phenomena of
phlegmasia dolens are covered. The experiment has never been tried of
producing phlebitis artificially in a subject, with the blood-condition
predisposing to white leg, in order to determine whether this condition
would follow; but clinically it has more than once been demonstrated
that in such a subject phlegmasia dolens may result from simple
pressure upon the iliac vein.

The fact, too, that the disease occurs three times in four on the left
side, where the iliac vein is pressed upon by the rectum and by the
iliac artery, is not to be forgotten in this connection. If
lymphangitis were a necessary factor in the disease, pressure upon the
vein would not have such a marked causative influence.

The symptoms of phlegmasia dolens may be gathered from the preceding
remarks, together with the description of the symptoms of acute
phlebitis. {848} It is to be noted, however, in addition, that the
majority of cases are ushered in by one or more chills, and that the
progress of the case is usually marked by a tendency to profuse
perspirations. In the puerperal woman lactation is generally very much
interfered with or entirely suspended. "The lochial discharges seem, in
very many cases, to be very little influenced by the onset and progress
of this disease, but in others they have been observed to become very
fetid and offensive" (Barker).

The tendency of this affection is to terminate by resolution. The
hardness diminishes before the size of the leg becomes less, and with
this diminution of tension the muscles regain their power. Gradually
the oedema subsides, and the knotted cords which indicated the course
of the affected veins disappear. If all goes well, the limb is restored
in the course of three or four weeks apparently to its normal
condition. Yet even in these cases the affected vein probably remains
entirely obliterated, the circulation being carried on by the
subsidiary vessels.

But in many cases the recovery is only partial, and for months or years
the limb remains larger than its fellow, the superficial veins are
enlarged, and the skin congested and of a dusky hue. Long standing or
walking causes increased oedema, and there is a disposition to eczema
and ulceration above the ankle.

What was said in regard to the treatment of phlebitis is applicable to
that of phlegmasia dolens. As the tension subsides the application of a
roller bandage will hasten the return of the limb to its normal size.
But care must be taken that it is not tight enough to still further
impede the already obstructed circulation. At a later period the
support of an elastic stocking may be required. Constipation is to be
avoided, especially in those cases in which the left lower extremity is
affected, as the pressure of the loaded rectum interferes with the
return circulation.

Chronic phlebitis is usually the sequel of an acute attack or else is
developed in a vein already varicose. The coats of the vessel become
thickened and hardened by interlamellar development of nucleated
fibrous tissue, so that the walls become more or less rigid. This
thickening may be partly at the expense of the lumen of the vein, thus
reducing its calibre, or it may be entirely excentric. The vasa vasorum
are sometimes developed in chronically-inflamed veins to a remarkable
extent. Quincke states that they may attain the size of cuticular
veins.[12]

[Footnote 12: _Ziemssen's Cyclopædia_, art. "Dis. of the Veins."]

Except in the case of superficial veins, in which the vessel may be
felt as a hard cord, the affection cannot be recognized during life. It
may be assumed to exist when the symptoms of acute phlebitis continue
in a less degree, or when tenderness, without other active symptoms, is
found along the course of a vein. Under these circumstances there are
apt to be acute attacks of pain and swelling from the operation of
slight causes, the attacks subsiding, but the chronic condition
remaining through the intervals.

The treatment looks to the avoidance or removal of the causes which
tend to produce acute exacerbations. Rest is of the first importance.
In chronic inflammation of a superficial vein the local use of iodine
or of the ointment of iodide of lead will be of service. A succession
of flying blisters along the course of the vein may be employed with
advantage. When there is chronic enlargement of the limb the persistent
administration of potassium iodide may be useful in promoting the
absorption of effused material. After the subsidence of all
inflammatory action massage may be resorted to.


{849} Dilatation of the Veins.

This condition results either from undue pressure of the blood within
the veins or from impaired resistance of their walls. The former
condition is found in certain forms of heart disease affecting the
right chambers; on the distal side of an obstruction in a vein; when
collateral veins are required to carry on the circulation, the natural
channel being narrowed or obliterated; and in the veins of a limb when
the position is such, a great portion of the time, that the blood is
forced to mount against gravity.

The second condition, that of diminished resistance of the walls, is
found in enfeebled constitutions and in the degeneracy of tissue
incident to advancing age. A familiar example is furnished by the
enlargement of the veins on the back of the hand in old persons.

Excessive dilatation of the veins which go to make up the superior cava
often results from insufficiency of the tricuspid valve. When this
insufficiency exists a proportionate part of the systolic energy is
expended in driving the blood back into the systemic venous
circulation, and the superior cava, from the nearer correspondence of
the axis of its opening with the axis of the auriculo-ventricular
opening, receives the larger share. Hence with every contraction of the
ventricle a direct distending force is exerted upon this vessel and its
branches which they are not fitted anatomically to resist. In such
cases the distended veins may reach an enormous size, and are seen to
pulsate synchronously with the arteries. The distension is greatest in
the neck, but affects also the veins of the chest and of the upper
extremities.

Whenever a vein is obstructed, either by some process taking place
within it or by pressure from without, the distal portion is more or
less dilated. Examples of this are seen in the closure of veins from
phlebitis and by the pressure of abdominal tumors or the gravid uterus.

Under like conditions the tributary veins also, being forced to carry
more than the normal amount of blood, become enlarged. This we see
constantly in the dilated veins of the abdomen when the internal
vessels are pressed upon by large dropsical effusions.

The term caput Medusæ is applied to a collection of enlarged veins
radiating from a common centre or arranged in the form of a corona.
Such collections often occur on a small scale above the ankles, but
under some conditions they assume vast proportions. When there is
obstruction of the inferior cava a great mat or pad of dilated,
convoluted veins may form on the abdomen or thighs. Some of these veins
may be as large as the little finger.

In the erect posture the veins of the lower extremities are subject to
a distending force proportioned to the height of the column of blood
which they have to sustain. For short periods at a time the resistance
of the walls is ordinarily sufficient to bear this pressure without
yielding, but in persons whose occupation requires them to stand a
considerable portion of each day, and especially in those past middle
life, there is a gradual giving way, which results in increasing not
only the diameter but the length of the vein.

The dilatation takes place irregularly, being greater at one point than
at another, and in one place affecting the entire circumference of the
vessel, while in another it produces a bulging on one side or even a
pouch or diverticulum. Especially just above the valves in the veins of
the lower extremities, where the diameter is naturally a little
greater, the larger area gives rise to greater pressure, and more
marked dilatation results. Their breadth remaining the same, the valves
are no longer able to reach across the vein, and the circulation is
deprived of the aid which it is their office to give. Instead of the
column of blood being divided into a number of portions, each resting
upon the valve beneath it, there is now a continuous column which
exerts its full static pressure. Dilatation is thenceforth doubly
rapid, and at the same {850} time the vein is stretched longitudinally
and becomes tortuous, thus adding another impediment to the
circulation. The nutrient vessels ramifying in the venous walls are
pressed upon, and the nutrition of the several tunica is impaired. From
this arises fatty or calcareous degeneration. Under these combined
influences the walls often become so thinned that rupture takes place.
But it is rare that the blood is effused into the tissues surrounding
the vein, for the overlying integument or mucous membrane, atrophied
from the pressure of the vein beneath, usually gives way at the same
time, affording a means of escape. Even bone is not capable of
resisting the continuous pressure of an enlarged vein, but may be
absorbed in the same way as in the case of arterial aneurism
(Bristowe).

Sometimes the dilated vein becomes thicker instead of thinner by
addition to the outer tunic; probably the result of a slow inflammatory
process, to which, as already stated, varicose veins are peculiarly
liable.

The slow circulation, especially in pouched and tortuous veins, favors
the formation of coagula which frequently close up the vein entirely,
thus bringing about a spontaneous cure. Independently of this, there is
a disposition to recovery when the cause is removed, and the vessel
may, under favorable circumstances, regain its normal condition. If,
however, the valves have atrophied, as they are apt to do after their
efficiency has ceased, entire recovery is impossible.

Oedema is apt to occur in connection with dilated veins if the
impediment to the circulation is considerable. Chronic ulcers of the
legs, accompanied by eczema, are a very common result of a varicose
condition of the superficial veins of the lower limbs; and a permanent
cure can seldom be effected unless the varicose condition is first
removed.

Dilatation of the hemorrhoidal veins is an important factor in
hemorrhoids. But it is far from constituting the disease, as was
formerly supposed, the tumors being largely made up of dilated
capillaries and hypertrophied connective tissue. Indeed, in some of the
worst forms of piles it is not possible to find any evidence of
varicose veins in the extruded mass.

In most cases, however, these varices are present, and may be
distinguished as smooth blue or purple nodules. When a hypodermic
needle is thrust into one of these, the point is felt to be in a free
cavity, which immediately becomes filled with a solid coagulum when a
few drops of a weak solution of carbolic acid are injected--an
operation which usually effects a cure.

Obstruction of the portal circulation predisposes to hemorrhoids; hence
they are a frequent attendant upon diseases of the liver. The habitual
presence of fecal accumulations in the rectum, pressing upon the veins,
operates directly to impede the return circulation, while the straining
at stool which accompanies this condition greatly aggravates the
difficulty.

The TREATMENT of external varicose veins belongs properly to the
province of surgery. When the dilatation can be traced to changes
occurring in any of the internal organs, treatment should be directed
to removing the cause or mitigating its effects. A constipated habit
should be corrected and the hepatic circulation be promoted.

The presence of ascites will call for the use of diuretics or
purgatives or of the aspirator. In cases having a cardiac origin much
good may often be accomplished, for a time, by the judicious use of
digitalis.

In all cases advantage is to be taken of position to aid the
circulation as far as possible.

In the case of superficial veins the application of moderate and
evenly-distributed pressure is of much service.


{851} Narrowing of a Vein.

This condition may occur as the result of inflammation which has
stopped short of occlusion.

Under the name of hypovenosity has been described a condition of the
saphenous system in which there is a deficiency in the number and size
of the veins. The outlines of the limb (bone, muscle, etc.) are
effaced, the skin is dusky, the limb brawny, and there are no veins
visible. The motion of the limb is painful and difficult. There is
degeneration of the superficial veins, collateral dilatation of the
deep veins, and ultimately atrophy of the muscles.

Exercise, frictions, and hot applications are to be employed. Rest and
bandaging as a mode of treatment aggravate the disease.[13] The
affection is of rare occurrence.

[Footnote 13: J. Gay, _Lancet_, Nov., 1871.]


Occlusion of Veins.

Venous occlusion results very frequently from adhesive phlebitis. It is
also brought about by the presence of cancerous or other tumors. The
complete arrest of the current of blood through a vein rarely produces
the serious results which may occur from a like obstruction of an
artery. The aggregate diameter of the venous system is much greater
than that of the arterial, and the venous walls are much thinner and
more distensible. Hence an adequate collateral circulation is more
readily established. In a healthy individual and in a healthy condition
of the part simple occlusion of a vein produces only a moderate oedema
of the tissues on the distal side of the obstruction. In unhealthy
conditions, however, as already pointed out in discussing phlegmasia
dolens, very serious results may follow.

Occlusion of either the superior or the inferior vena cava is of not
very rare occurrence. It may be the result of pressure from a cancerous
or other growth,[14] which is the most frequent cause, or in the case
of the inferior cava it may be brought about by a thrombus gradually
extending upward in one of the iliac veins until it reaches the
bifurcation, when a thrombus in the other iliac is occasioned by the
partial obstruction of its entrance into the cava. These united thrombi
then extend upward into the cava, producing complete occlusion. This is
an occasional event in phlegmasia dolens.

[Footnote 14: Watson describes a case arising from pressure from
hydatids of the liver.]

Occlusion of the superior cava is less frequent than that of the
ascending. It is nearly always the result of pressure from an
intra-thoracic tumor, and its symptoms are more or less masked by those
directly referable to the growth. There are, however, great dilatation
of the veins and oedema of the tissues of the head and neck and of the
upper part of the thorax. These symptoms in a case in which there are
physical signs of a substernal growth would afford a strong presumption
of obstruction of the cava.[15]

[Footnote 15: Stocks, _Med. Times and Gaz._, April 22, 1876; Williams,
_Tr. Dublin Path. Soc'y_, July, 1878.]

The glandulæ concatenatæ of the neck are apt to be enlarged from the
chronic engorgement. Watson mentions a case in which this added so much
to the volume of the neck as to give a superficial resemblance to
goitre.

Occlusion of the inferior vena cava produces, if life is continued, an
immense dilatation of the veins of the abdomen and of the thighs. By
compressing the abdominal veins it can be seen that the blood-current
is reversed, flowing upward through vessels anastomosing with the
intercostal and internal mammary veins. Internally, the circulation is
carried on chiefly by the azygos, which may become as large as the
normal cava.

{852} There is usually, but not always,[16] an extreme degree of
ascites, together with anasarca of the lower half of the body. After a
time, however, as the tributary circulation becomes established, the
effusion will be reabsorbed.

[Footnote 16: _Le Progrès Médical_, May 26, 1877; _Med. Record_, July
28, 1877.]

If the obstruction involves the portal vein, the ascites will be still
more marked. In this case there is also enlargement of the spleen. When
the cava is occluded above the point at which it receives the renal
veins, congestion of the kidneys results, which in time produces
interstitial change. Yet even here the establishment of the collateral
circulation may be sufficiently prompt to avert the danger.

Anomalies of the cava are occasionally observed. Osler has reported a
case in which the inferior cava was represented only by a fibrous cord.
The condition was probably congenital.[17] Greenfield mentions a case
in which the descending cava was absent, both brachio-cephalic trunks
passing into the heart by the coronary sinus.[18]

[Footnote 17: _Journal of Anatomy and Physiology_, April, 1879.]

[Footnote 18: _Med. Times and Gazette_, April 22, 1876.]

If the cause of the occlusion of either cava be not such as of itself
to destroy life, the patient may get on with some degree of comfort for
many years. The establishment of the collateral circulation sometimes
keeps pace with the increasing obstruction, so that little or no
ascites or oedema occurs.[19]

[Footnote 19: Turpin, "Obliteration Inf. Vena Cava," _N. O. Med. and
Surg. Journal_, 1881, p. 575.]

The TREATMENT of obstruction of either of the venæ cavæ can, as a rule,
be only palliative. In the great majority of cases the cause is
entirely beyond our reach. All violent muscular exertion, making an
excessive demand upon the circulation, should be avoided. While the
blood should not be impoverished, as that would favor dropsical
effusions, the patient, on the other hand, should not be allowed to
become plethoric through the influence of his enforced sedentary
habits. The diet should therefore be light and digestible, and
over-feeding should be carefully avoided. The occasional use of saline
purgatives may be required. Dropsical accumulations may call for the
administration of diuretics or drastic cathartics, and perhaps for
tapping.

Occlusion of the vena portæ, by obstructing the return of the blood
from the intestines, gives rise to rapid and abundant effusion into the
abdominal cavity. As the gastric vein cannot empty itself, there is
congestion of the stomach, often ending in hemorrhage, the blood being
both vomited and passed by stool. The spleen also is enlarged by
passive engorgement, its vein depending upon the portal for an outlet.
This assemblage of symptoms renders the diagnosis almost positive.[20]
There is no enlargement of the liver unless the hepatic vein is also
involved.

[Footnote 20: An interesting case is reported by A. A. Smith in the
_N.Y. Med. Journal_, January, 1880.]

Paget maintains that the occlusion of the principal vein of a limb may
result in an increased growth of some of the tissues, especially of the
muscles.


Degenerations.

Fatty degeneration is rarely observed in the veins, but it occasionally
occurs in those which have long been subjected to excessive strain,
which by compressing the nutrient vessels affects the nutrition of the
walls.

Calcification is less rare. It results in the formation of plates or
rings which closely resemble bone in their structure. Such plates may
not unfrequently be felt in old superficial varicose veins. Sometimes
these formations project as spines into the lumen of the vessel, and,
coagula forming about them, a thrombus is the result.[21]

[Footnote 21: See preceding reference.]

{853} Cancer of the veins is rare as a primary affection, but it is not
uncommon when the vessel traverses a cancerous mass. The morbid process
readily penetrates the thin wall of the vessel, and cancerous nodules
form on the inside and become the starting-point of thrombi which are
soon permeated and supplanted by the heterologous growth. This is
sometimes moulded to the shape of the vein, and fills it for some
distance in the form of a cylindrical plug. Fragments may be swept away
in the blood-current and give rise to secondary cancer at the point of
arrest in the liver or lungs. Virchow has described a case of primary
sarcoma of the inferior cava.

The existence of syphilitic lesions in the veins has not been
satisfactorily demonstrated. It is positively denied by some
authorities, while certain appearances found in the veins, especially
of new-born children, are attributed by other writers to syphilitic
inheritance.


Phlebolithes.

Vein-stones are roundish, oval, or cylindrical bodies found in the
veins or in pouches connected with the veins, or sometimes in the
connective tissue adjacent to a vein. Their size varies from that of a
hempseed to that of a nutmeg. Externally they are white, but when
divided they are found of a yellowish color at the centre. There is
generally a central cavity, around which are disposed concentric laminæ
such as are observed in vesical calculi. Chemically, these bodies are
composed of an animal substance in which are deposited phosphate and
carbonate of lime, and sometimes magnesia. The inner part is hard and
brittle, the outer softer and more earthy.

Usually, phlebolithes are found loose in the vein, but if large they
may be firmly impacted in the vessel, causing complete obstruction.
Sometimes the outer portion is of a gelatinous texture, from which a
delicate mesh extends to the wall of the vein and becomes incorporated
with it.

Frequently these concretions occupy sacs or diverticula connected with
the vein. Occasionally these sacs become detached from the vessel and
are absorbed and removed, and the stone, then entirely outside of the
vein, becomes enveloped in a fibrous cyst formed from the surrounding
connective tissue.

Some doubt exists as to the manner in which these concretions are
formed, but the probability is that a small clot first forms in the
vessel, and that around this, as a nucleus, successive layers are
deposited from the plasma of the blood. These layers then undergo
chalky transformation by the deposit within them of salts of lime and
magnesia. These formations seem to be conditioned by a slow current in
a dilated vein. Hence they are most frequently found in the enlarged
pelvic veins of old people, and especially about the neck of the
bladder in those suffering from prostatic enlargement. They are also
found in the varicose veins of the extremities.

Except in superficial situations they are usually not recognized during
life. They seldom produce discomfort, and therefore rarely call for
treatment. When accessible they may be excised if requisite, the vein
being secured above and below if not already permanently occluded.[22]

[Footnote 22: Rokitansky, _Path. Anat._, Philadelphia, 1858.]




{854}

THE CAISSON DISEASE.[1]

BY ANDREW H. SMITH, M.D.

[Footnote 1: This article is mostly drawn from a report by the writer
on _The Effects of High Atmospheric Pressure, including the Caisson
Disease_, published in 1873 by the New York and Brooklyn Bridge
Company.]


Persons exposed for a considerable time to a greatly increased
atmospheric pressure are liable, after the pressure is removed, to
certain morbid effects which comprise what is known as the caisson
disease. It is observed principally in those employed in submarine
operations by the aid of compressed air, and who labor for hours
together in what is termed by engineers a caisson. The pressure varies
with the depth at which the work is carried on, and reaches sometimes
fifty or more pounds to the square inch. The disease rarely if ever
occurs when the pressure is less than fifteen pounds, and its severity
is, other things being equal, in direct ratio to the increase in the
density of the atmosphere.

SYMPTOMS.--These are, in the order of their frequency, intense
neuralgic pain in one or more of the extremities, and sometimes in the
trunk; epigastric pain; nausea and vomiting; more or less complete
paralysis, which may be local or general; headache; vertigo; and coma.

The pain, which is often very severe, is usually paroxysmal,
exacerbations and remissions occurring at short intervals. It may come
on suddenly in its full severity, or it may be slight at first and
rapidly increase until it becomes absolutely intolerable, "as if the
flesh were being torn from the bones." The pain begins most frequently
in the knees, extending rapidly to the legs and thighs, but the upper
extremities may be first attacked. Sometimes the most severe pain is
felt in the spine, and especially in the lumbar region. There is
usually some tenderness with the pain, and a stiffness of the muscles
of the affected limbs.

Epigastric pain occurs in a considerable proportion of the cases. It is
often very severe, and if not relieved by treatment is liable to be
followed by nausea and vomiting. The vomiting is usually limited to the
ejection of the contents of the stomach, but it may persist, sometimes
even after the pain has ceased. Vomiting accompanied by giddiness may
occur without epigastric pain, and is then probably of cerebral origin.
Paralysis, to a greater or less degree, occurs with considerable
frequency, the percentage of cases increasing in proportion to the
pressure of the atmosphere to which the patients have been exposed and
the duration of the exposure. It affects most frequently the lower half
of the body, but it may include the trunk or one or both arms. In rare
cases an arm alone is affected.

The paralysis is of sensation as well as motion. It comes on soon after
the invasion of the pains, but affords no relief from them. Thus, while
pinching or pricking occasions no pain, the part may still be the seat
of exquisite suffering. Paralysis may, however, occur in cases in which
the pain is very slight or entirely absent. The paralysis varies in
degree from a transient {855} weakness of the limbs and slightly
impaired sensation to complete loss of motion and sensation in the
affected part. Even the minor degrees generally affect the bladder.

Symptoms of a transient character are often observed depending upon
changes in the brain. They consist of headache, dizziness, double
vision, incoherence of speech, and sometimes syncope. They usually pass
off in a few hours. In fatal cases, however, coma is the usual
forerunner of death.

The duration of the caisson disease is from three or four hours to six
or eight days. When paralysis occurs it may continue for weeks, or it
may pass off within twelve hours. The cases marked only by neuralgic
pains do not generally last more than six to twelve hours, though some
continue five or six days. Death occurs only in cases which are severe
from the first and show symptoms of cerebral or spinal effusion.

MORBID ANATOMY.--The constant lesion in fatal cases of caisson disease
is congestion of the brain or spinal cord. This congestion may be
pretty evenly distributed or it may vary in intensity in different
localities. This is especially true as regards the cord. It affects
both the meninges and the substance of the brain or cord. In most cases
there is more or less of serous effusion into the arachnoid. The
tissues of the scalp and those surrounding the spinal column are
sometimes engorged.

When sufficient time elapses before death the brain may be softened in
spots. This is probably due to the occlusion of vessels by coagula
formed during the primary congestion.

Congestions also occur in other localities, and especially in the solid
abdominal viscera. The liver and spleen have been found engorged in
nearly every case. Jaminet has found clots of blood in the kidneys.[2]
The mucous membrane of the stomach, intestines, and bladder is often
injected and marked with patches of ecchymosis. The lungs in cases of
true caisson disease, though occasionally found in a state resembling
red hepatization, seldom present any other change than simple
hypostatic congestion.

[Footnote 2: _Physical Effects of Compressed Air_, p. 20.]

PATHOLOGY.--It is probable that the pathology of this disease is not
entirely uniform in all cases. Doubtless the chief element in it is the
congestions already described, and especially of the brain and spinal
cord. The mechanism, therefore, of these congestions becomes a subject
of paramount importance.

It was suggested by François[3] that the morbid phenomena might be due
to the liberation in the vessels of air which had been absorbed by the
blood while under pressure, but which was set free again when the
pressure was removed. This theory has been reasserted by Paul Bert,[4]
with this difference: that he claims that bubbles of nitrogen instead
of air are the cause of the interruption of the circulation. These
bubbles he has discovered after death in the vessels of the brain and
cord. But he states that when the pressure does not exceed five
atmospheres three minutes allowed for the restoration of the normal
pressure will be found to prevent the formation of these globules of
nitrogen. Now, we find the caisson disease occurring when the pressure
does not exceed two atmospheres and when six to eight minutes are
allowed for locking out.[5] It would seem that under these conditions
the gas should escape through the lungs as rapidly as it is disengaged
from the blood. Moreover, we find that the attack often comes on
several minutes or even hours after leaving the caisson. During this
time any free nitrogen in the blood should be constantly becoming less
by diffusion through the {856} pulmonary membrane, and if enough were
not present at first to cause obstruction, such an effect could
scarcely take place at a later period.[6]

[Footnote 3: _Annales d'Hygien publique et de Méd. legale_, t. xiv.,
1860.]

[Footnote 4: _Comptes Rendus_, August, 1872, and February and March,
1873.]

[Footnote 5: _I.e._ passing from the caisson into the open air through
the lock, or antechamber, where the pressure is gradually reduced.]

[Footnote 6: In a private letter to the writer, T. Lauder Brunton
suggests that a bubble of air might pass from a larger vessel, which it
had only partially obstructed, into a smaller branch, which would be
entirely occluded by it, or that additional nitrogen might be
disengaged when the pressure was lessened by relaxation of vascular
tension.]

It is also very difficult to reconcile with Bert's theory the fact of
the comparative immunity from danger which results from repeated
exposures to the effects of compressed air. If the action were that of
purely physical causes, habit could make no difference. The obstruction
of the vessels, as described by Bert, is a condition of which the
system could never become tolerant by frequency of repetition.

In the writer's view, the explanation is to be found in the changed
conditions of the circulation, which result first from the increased
pressure upon the surface, and then from the sudden removal of the
pressure. While the subject is in the caisson the blood is driven from
the peripheral vessels toward the interior of the body, where the
pressure is less than at the surface.[7] It is also forced from the
more compressible tissues into the solid and resisting organs, such as
the liver and kidneys; and lastly, it flows toward bony cavities, for
the reason that their walls resist the effect of direct pressure, and
equilibrium of pressure can be restored within them only by an afflux
of blood. Thus the distribution of the blood is everywhere changed, and
the size of the vessels is no longer determined by the muscular action
of their walls, but by the amount of blood forced into them, the vital
action which should regulate the circulation being entirely overpowered
and set at naught by an overwhelming physical force operating from
without. The vessels become merely passive tubes, distended in some
places where they are protected from pressure, and compressed in others
where the tissues about them are compressible. By this transfer of
blood from one part to another the equilibrium of pressure is restored
and the circulation goes on, though without any regard to the
physiological demands of the different organs. There is no stasis
anywhere so long as pressure and counter-pressure are equal, thus
allowing fair play for the action of the heart.

[Footnote 7: This is shown by the marked pallor of the skin and the
shrunken and wrinkled appearance of the hands.]

If, now, the external pressure is suddenly removed, what will be the
result? Vessels which have been compressed and almost emptied of blood
will now offer new channels through which the blood can rush, and
vessels overcrowded with blood, with their walls paralyzed by
over-distension, will have the current within them slowed almost or
quite to the point of stopping. The vessels of the brain and spinal
cord, being within bony walls, where the direct pressure of the
condensed air could not affect them, will be found the most distended
and the most helpless to relieve themselves. They will get little aid
from the vis a tergo of the circulation, for the blood will find easier
courses by other ways, vascular tension being almost nil and the
vaso-motor system out of use.

The longer the sojourn in the caisson has been, the more entirely
passive the vessels will have become, and the longer will be the time
they will require to resume their normal condition. At some points the
circulation will be greatly slowed or entirely interrupted, and
nerve-elements lying beyond and deprived of their blood-supply will
express their want by pain or paralysis. Areas of stasis once formed
will be likely to extend, and may thus affect nerve-elements which at
first escaped. This would explain those cases in which the attack is
deferred until some time after leaving the caisson.

It is readily conceivable that in persons beginning work when the
pressure is slight and continuing day by day, as the pressure slowly
increases the {857} vessels should acquire the power of adaptation to
the variations in the amount of their contents, since this is only an
extension of the physiological principle which we see exemplified in
all organs having an intermittent function.

The influence of the trophic system of nerves also, as the connecting
link between central nerve-lesions and peripheral vascular
disturbances, must not be forgotten in this connection. Suspension of
function in trophic cells, either in the cerebral cortex or in the
anterior horns of the cord, could easily be brought about by the action
of the mechanical causes already described, and would result in areas
of vaso-motor paralysis and consequent congestion at the termination of
the corresponding nerve-fibres. The proneness of the large joints, and
especially the knees, to be attacked is suggestive, in view of the like
circumstance in chronic degeneration of the cord.

CAUSES.--The one essential cause without which the disease can never be
developed is transition to the normal atmospheric pressure after a
prolonged sojourn in a highly-condensed atmosphere. Hence we have to
consider two elements, pressure and time, the danger in these cases
being as the degree of pressure to which the person has been exposed
multiplied by the duration of the exposure.

But inasmuch as a prolonged sojourn in the caisson does not in every
case produce the disease (many of the men employed escaping it
entirely), it follows that there must be concurrent causes which
determine its development.

The first of these is a special predisposition. This is occasionally
strongly marked, some persons being affected by a short exposure to a
low pressure from which there would generally be experienced no
inconvenience whatever.

Perhaps the most frequent exciting cause of the caisson disease is too
rapid locking out. Indeed, it is altogether probable that if sufficient
time were allowed for passing through the lock the disease would never
occur. But what is sufficient time for one is too short for another;
and all that can be done is to fix upon a duration for the process
which shall be proportioned to the pressure, and as great as is
consistent with the circumstances, and then to see that the rule is
rigidly observed. At least five minutes should always be allowed for
each additional atmosphere of pressure.

Newness to the Work.--Unquestionably, the liability to the caisson
disease is greatest in those exposed for the first time to the
influence of the compressed air. New hands are very apt indeed to
suffer more or less during the first week. Those least affected are
such as begin work when the pressure is comparatively slight, and
continue without intermission as the pressure increases. It seems that
the system after a time becomes adapted to the changed conditions, and
is protected in a measure from their effects. Nevertheless, some
serious cases occur among old hands, especially when for any reason
their stay in the caisson is prolonged beyond the usual time, thus
showing that their immunity is merely relative. A sudden increase of
pressure also, even though very slight, is certain to develop new
cases, men thoroughly inured to the work often being affected under
such circumstances.

Fulness of Habit.--During the progress of the work on the East River
Bridge in 1872 the writer, who had medical charge of the men, observed
that among those taken sick there was a very marked preponderance of
men of heavy build and with a tendency to corpulency. Of 39 men of this
build, only 3 escaped illness, while of 53 lank and spare men 25
escaped. Of the 39 stout men, 8 were more or less paralyzed; of the 53
slender men, only 2 were paralyzed. The deaths, 3 in number, were all
of heavy men.

These figures show unmistakably that a tendency to fulness of habit
renders work in a compressed atmosphere much more hazardous. Persons of
this build have more fluids in the body, the distribution of which is
changed by the pressure in the manner before stated, and it is
therefore not surprising {858} that the effect upon them should be
greater than upon lean and sinewy persons, whose bodies contain a
minimum of fluid.

Severe Exertion immediately after Leaving the Caisson.--As at the
moment of going out of the compressed air the system undergoes a
violent reaction, it is manifestly unfitted to bear in addition a
severe tax upon the muscular strength. Hence the ascent of a long
flight of stairs immediately after leaving the air-lock is as wrong in
theory as it has proved bad in practice. Triger, whose apparatus at
Chalonnes was so arranged that the ascent of the ladder took place in
the compressed air, the lock being placed at the top instead of the
bottom of the shaft, found that the men ascended a distance of seventy
feet without becoming in the least out of breath--making the ascent, in
fact, more easily than if it had been in the open air.[8]

[Footnote 8: _Comptes Rendus_, t. xiii., 1841.]

The Abuse of Alcohol.--Several writers have remarked that habitual
drinkers are more likely to be affected than those who used spirits
moderately or not at all. It is stated by the director of the work at
Douchy[9] that the attacks from which the men suffered were "almost
always coincident with some excess committed in the interval of the
shifts." It is easy to perceive that, as the disease is characterized
by cerebral congestion, the abuse of alcohol, which has a tendency to
produce the same result, would act as a predisposing cause.

[Footnote 9: _Annales d'Hyg. pub. et de Méd. legale_, 1854.]

Entering the Caisson Fasting.--Jaminet insists very strongly upon the
influence of this cause, and cites instances to prove his position.
Several cases corroborative of his views occurred under the observation
of the writer. One of the rules for the men working in the New York
caisson prohibited entering the compressed air without having taken
food, and in addition to this each new hand was especially cautioned as
to the danger of disregarding this precaution, and the foremen were
directed to use every effort to secure its observance. Yet,
notwithstanding all this, a number of very severe attacks were found to
be coincident with, if not dependent upon, violations of this rule. In
these cases epigastric pain and retching were prominent symptoms.

TREATMENT.--The treatment of this disease will depend upon the severity
of the case and the presence or absence of gastric symptoms or of
paralysis. If we have to deal with the neuralgic pains only, the chief
reliance must be upon anodynes administered with a liberal hand.
Fortunately, the pain, though very severe while it lasts, is in most
cases of short duration, the attack passing off usually in a few hours.
It is therefore quite practicable to keep the patient under the
influence of morphine during the whole time, and thus enable him to
escape entirely all extreme suffering. But large doses will be
required, the intense pain inducing a remarkable tolerance of the drug.
Half a grain may be given at the outset, and a quarter of a grain every
half hour afterward until relief is obtained. When employed
hypodermically somewhat smaller doses may be used.

In some instances the very best results are obtained from hypodermic
injections of atropine at the seat of pain, but in other cases they
fail to procure relief, and, upon the whole, atropine is inferior to
morphine.

Jaminet, regarding the affection as wholly the result of exhaustion,
relies entirely upon stimulants and concentrated nourishment, ignoring
the aid of anodynes altogether. It is difficult to see the reason for
this, even admitting to the fullest extent his theory of the disease,
for nothing can be more exhausting than the intolerable pain which
characterizes this affection, and nothing could act more promptly as a
restorative than an efficient anodyne.

Starting from the theory already given as to the mode in which the
disease is produced, the writer was led to the idea that benefit would
be derived from {859} the use of an agent that would induce contraction
of the capillaries, and thus correct the want of tone which was
considered to lie at the foundation of the difficulty. For this purpose
ergot was employed, with the belief that it would be useful, first, by
contracting the vessels of the brain and spinal cord and relieving
their congested state; and, secondly, by restoring tone to the
superficial vessels, and thus imparting vigor to the circulation.

An extended trial warrants him in saying that the results justified the
theory. In his hands, though not always successful, ergot was certainly
very useful in a considerable number of cases. He has seen very severe
pain completely relieved within half an hour after the administration
of a drachm of the fluid extract. In other instances unsteadiness of
the limbs, which seemed about to usher in paralysis, yielded promptly
to one or two doses. A teaspoonful of the fluid extract may be given,
and the dose repeated in half or three-quarters of an hour, unless the
pain is relieved.

Frictions, with or without stimulating liniments, are very generally
resorted to, and seem sometimes to give momentary relief, but it
appears to be rather by occupying the attention of the patient than by
any action occasioned in the part. In some instances, when the pain is
confined to a particular locality, having the part immersed in hot
water will afford temporary relief. But the use of the general hot bath
is not advised, as it is unsafe to increase the already existing
relaxation of the vessels. In several of Jaminet's cases paralysis came
on while in the hot bath. In two of the writer's cases cold was applied
to the spine, with apparent benefit in each.

Epigastric pain is almost always relieved at once by the use of an
alcoholic stimulant with ginger, as employed by Jaminet.

Vomiting is best treated with sinapisms to the epigastrium and
swallowing small bits of ice.

When paralysis occurs it is to be treated on general principles. Cups
or leeches, with douches and frictions to the spine, may be useful;
and, if the case be protracted, the use of strychnine may be called
for. Electricity may be of service in preserving the nutrition of the
muscles. The bladder will almost certainly be involved, requiring the
constant use of the catheter.

The cerebral symptoms which occasionally occur are, with the exception
of coma, so transient in their nature as to call for no special
treatment. Coma, when it takes place, is to be managed according to the
circumstances of the case, as when proceeding from other causes. If
accompanied by a full, strong pulse, venesection may be expedient.

There remains to be considered a plan of treatment originally suggested
by Pol, and carried out to some extent by Foley--viz. returning the
patient at once into the compressed air. Foley says, as the result of
his experience, "A true specific is returning to the caisson, through
which means all such accidents (pains, vertigo, etc.) speedily
disappear. It is to be resorted to unhesitatingly in all threatening
cases, and the pressure should be admitted rapidly." But the means of
access to the caisson are usually such that it would be difficult to
remove a patient into it, even if he could be comfortably cared for
while there or if his presence would not interfere with the work. It
would therefore be desirable to have facilities for employing
compressed air at some point above ground which would be easily
accessible.

Of course the secondary effects which arise in protracted cases would
not be capable of direct relief by simply reproducing the physical
conditions existing in the caisson. The most that might be hoped for in
such cases would be that the pressure might result in giving a new
impulse to the circulation in the congested part, and thus favor
resolution.

Reasoning from his view of the pathology of the disease, Bert has
proposed the inhalation of oxygen in order to displace the free
nitrogen from the blood by diffusion. Experiments upon animals
demonstrated that the sounds {860} produced in the heart by the
presence of free nitrogen speedily disappeared when the animal was made
to inhale oxygen, the nitrogen diffusing into this gas much more
readily than into common air. But, though immediate death was averted
by this expedient, paralysis nevertheless occurred, and the post-mortem
examination showed the presence of bubbles of nitrogen in the vessels
of the cord.




{861}

DISEASES OF THE MEDIASTINUM.

BY EDWARD T. BRUEN, M.D.


Inflammation of the Mediastinum.

SYNONYMS.--Mediastinitis. _Fr._ Médiastinite; _Ger._ Mediastinitis.

Lesions caused by inflammatory processes in the mediastinum may,
theoretically, occur in the duplicatures of the pleura, separating the
pleural from the mediastinal cavity. This condition may terminate in
resolution or in effusion of plastic lymph, as in a case reported by
Wildemann, in which the anterior mediastinum was filled with layers of
solid exudation, the pericardium inflamed, and its cavity distended by
six ounces of pus. The effusion appeared to have been occasioned by
long-continued pressure on the sternal region. The process is
practically unrecognizable during life, or at least possesses no
described clinical features.


Abscess of the Mediastinal Space.

Galen has alluded to trephining of the sternum for caries or necrosis
inducing the formation of pus; and Petit[1] has furnished many
instances of mediastinal abscess from the warfare of preceding
centuries.

[Footnote 1: _Traité des Maladies chirurgicales_, tome i. p. 143.]

ETIOLOGY.--I. Predisposing Influences.--Mediastinal abscess is very
rare, at least of such dimensions as to simulate tumor. The condition
is sometimes idiopathic, possibly due to sudden exposure to cold,[2] or
is associated with the rheumatic diathesis, but in these cases some
forgotten injury may have been received.

[Footnote 2: Gunther, _Oesterreich Zeitschrift f. Prak. Heilk._, 1859;
Gross, _System Surgery_.]

Symptomatic or secondary purulent collections may occur in connection
with operations upon the neck, as tracheotomy, also from softening
gummata or glanders, or they may be due to a constitutional cause, the
so-called metastatic inflammation of the mediastinal connective tissue
in the course of pyæmia.

Scrofulous suppuration of the lymphatic glands may result in secondary
abscess.[3]

[Footnote 3: Bristowe, _Path. Soc. Trans._, London, vol. ix. p. 46.]

II. Exciting Causes.--The mediastinum has been penetrated by balls and
sabres, and in one case the shaft of a carriage passed through the
anterior space, yet without damage to the contained viscera. Gunshot
fracture of the sternum, recorded in the history of the Civil War in
America, seems to have been very rarely followed by suppuration, even
though the tissues have been exposed to such a degree as to render the
arch of the aorta distinctly visible.

The anterior mediastinum may be threatened with inflammation, which may
sometimes terminate in abscess, as in cases of caries, necrosis, or
fracture of the sternum.

{862} Warner[4] reports a case in a boy aged thirteen in which two
weeks after fracture of the sternal bone a separation of the edges of
the fracture was observed, the interval being occupied by a tumor of
considerable size, which contracted and dilated with as much regularity
as the heart. It receded on palpation, and on removal of the pressure
the tumor immediately resumed its former size. It subsequently
ruptured, discharged the contents of an abscess, and the patient
recovered.

[Footnote 4: _Amer. Journ. Med. Sci._, Apr., 1873.]

Goodhart[5] records a case of acute mediastinal abscess resulting
apparently from injury produced by the sticking of a piece of meat in
the oesophagus. A case illustrating the possibilities of direct injury
to this region by a blow or fall has been recorded by Bennett. In a
middle-aged lady, previously in good health, an abscess slowly formed
and presented a prominence over the upper part of the sternum. Two
months before the lady had fallen in going up stairs, and struck the
sternum against the stone edge of the stairs. These examples have been
selected because they seem to cover the possibilities of directly
determining causes.

[Footnote 5: _Path. Trans._, London, vol. xxvii.]

SYMPTOMS.--There are three separate groupings under which the symptoms
may be classified: _(a)_ The latent symptoms, which include chiefly
manifestations of intra-thoracic irritation or pressure; _(b)_ the
fulminating phenomena; _(c)_ the physical signs.

As a rule, mediastinal abscess is accompanied from first to last by
deep-seated and gradually increasing pain and tenderness on pressure
over the sternum; but it may be a sense of constriction and oppression
with boring or throbbing sensations. Sometimes there is merely a sense
of uneasiness about the chest, with pains of a rheumatic or neuralgic
character in the shoulders or neck, brought about by irritation of the
intercostal and humeral nerves. The general health may be impaired, and
irritation of the pneumogastrics may be manifested by dyspepsia,
nausea, vertigo, syncope, headache, dyspnoea, and inability to lie
down. Laryngeal irritation is shown by cough, or spasm, with dryness of
the throat; a frothy mucus may be expectorated, with occasional rigors,
sweatings, and irregular febrile movement. When abscess follows severe
injuries, such as fracture or wounds, distinct evidences of phlegmon
appear, possibly within a week, accompanied by intermittent fever with
rigors, and a sense of weight and oppression in the front of the chest,
with pain in coughing and drinking, or breathlessness, "as if one had
been running" (Petit).

The pressure symptoms of mediastinal abscess are never so grave as in
other forms of mediastinal tumor, since the diffluent contents of an
abscess occasion less compression of the mediastinal viscera, or when
the intra-thoracic tension is excessive it seeks a channel by which the
pus is evacuated. The pressure symptoms are least marked when the
abscess is located in the anterior mediastinum.

There may be, on inspection, a distinct prominence over the upper part
of the sternum, with or without redness or oedema. Palpation may enable
one to recognize fluctuation on the borders of the sternum with
tenderness. The tumor may pulsate, but the pulsation never acquires the
expansile character of aneurism. Dulness on percussion may be marked,
and, according to Daudé, the dulness under the sternum may undergo a
change by alteration of the position of the patient. The heart sounds
may be heard distantly and indistinctly. The respiratory murmur may be
whistling over the region of the trachea, and in the chest a few moist
râles may indicate venous congestion, with exudation into the bronchial
passages; otherwise the condition of the lungs will probably be normal.
The entire series of pressure symptoms common to intra-thoracic growths
may be present, especially if the {863} posterior mediastinum is
invaded, and may correspond with those of mediastinal tumors in
general.

DURATION AND PROGNOSIS.--The causal relations of abscess in the
mediastinum are so various that it is only possible to decide the
question of duration after weighing the possibilities of treatment. The
persistence of the abscess is also decidedly governed by the
thoroughness of the drainage after opening has been affected.

The PROGNOSIS depends upon the etiology and the fulfilment of the
indications for treatment by drainage. Pressure on the heart and the
great vessels which proceed from its base, the descending aorta,
oesophagus, the pneumogastrics, and the internal thoracic circulation,
must be considered as complications adverse to a favorable prognosis
unless speedy relief is possible. Prominent pressure symptoms indicate
an implication of the intra-thoracic glandular system.

COMPLICATIONS, TERMINATION.--The abscess may open into any of the
internal viscera--the trachea, bronchi, or oesophagus. A favorable case
terminating by rupture into the latter passage is reported by Bennett.
At first a teaspoonful of bright fluid blood was coughed up, and the
day following from two to three ounces of purulent matter followed. The
discharge of pus continued five weeks, the sternal swelling subsiding
pari passu.

The pleura and pericardium have both been recorded as points of outlet.
The pus can even sink down into the inguinal or lumbar region.
Spontaneous external opening is said to occur most frequently on a
level with the second rib to the left of the sternum.

DIAGNOSIS.--The differential diagnosis between abscess and other
mediastinal growths will be considered in the section on Mediastinal
Tumors.

TREATMENT.--The exploratory puncture is to be recommended if a
fluctuating tumor appear presenting the general symptoms of abscess.
Rest, local sedative applications, and the relief of pain are positive
indications. Petit, Agnew, and others have applied the trephine to the
sternum in search of pus, with a satisfactory result. It is, however,
generally conceded that it is better to wait until pointing occurs, as
the area of the sternum is so limited that in all probability matter
forming behind it would speedily make its way to the surface in an
intercostal space at one of the margins of the bone. If the abscess be
deeper or due to scrofulous or syphilitic caries of the sternum, the
matter which forms may escape into the neck or through perforations of
the bone. The latter may be congenitally present or due to disease.
Caries, necrosis, or fracture of the bone may make trephining
obligatory, or the same indication may prevail if a dependent flow of
pus sufficient to drain the cavity is not otherwise obtainable.[6]

[Footnote 6: Chassaignac, _Traité de la Suppuration_, tome ii. p. 330.]

A similar line of treatment would be indicated if there was no tendency
to external pointing, and evacuation into the viscera seemed
threatened.

Excision of the whole or part of the sternum for abscess, cancer, or
other causes seems to have been fairly successful. Heyfelder[7] had
collected, in 1863, 18 established cases, in which there were 17
recoveries and 1 death.

[Footnote 7: _Traité des Resections_, traduit de l'Allemand avec
Additions et Notes, par le Docteur Boekels, Strasburg et Paris, 1863.]

Adhesions usually prevent a double pneumothorax, even when the sternum
and ribs have been resected. Unilateral pneumothorax is not necessarily
fatal.


Mediastinal Tumors.

ANATOMY.--The mediastinum is the space which the two pleural sacs leave
between them in the antero-posterior plane of the chest, and which
{864} contains all the thoracic viscera except the lungs. It is
subdivided into three parts--the anterior, middle, and posterior
mediastinum. A superior mediastinum has also been described. The space
between the pleural sacs occupied by the heart enclosed in the
pericardium, the vena cava superior, the ascending aorta, the pulmonary
arteries and veins, the phrenic nerves with their accompanying
arteries, and the bifurcation of the trachea and roots of the lungs
with some bronchial glands, takes the name of the middle mediastinum.

The anterior mediastinum is narrow in the middle, where the edges of
the lungs nearly meet, wider above, where the lungs diverge, and widest
of all below, for the same reason. It is very shallow from before
backward, and it is limited posteriorly by the anterior layer of the
pericardium, in front by the sternum, with the fifth, sixth, and a
small portion of the seventh costal cartilages, and by the triangularis
sterni muscle. The region is occupied simply by connective tissue, save
in its upper part, where lies, when it still persists, the shrivelled
remnants of the thymus body. It also contains a few lymphatic glands
and the left internal mammary artery and vein.

The superior mediastinum is bounded by a plane passing through the
lower part of the body of the dorsal vertebra behind and the junction
of the manubrium and the gladiolus in front. Its upper limit
corresponds to the superior aperture of the thorax. The contents of
this space are the transverse portion of the arch of the aorta and its
three large branches, the trachea and oesophagus, the thoracic duct,
the innominate veins, upper part of the superior vena cava, left
recurrent laryngeal nerve, phrenic, pneumogastric, and cardiac nerves,
with lymphatic glands and remains of the thymus body.

The posterior mediastinum is triangular in shape, placed in front of
the lower border of the fourth dorsal vertebra downward, and bounded
anteriorly by the pericardium and roots of the lungs. The lateral
boundaries are formed by the pleuræ. The space contains the descending
thoracic aorta: in front of the aorta the oesophagus with the
pneumogastric nerves, the left in front, the right behind. On the right
of the aorta is the vena azygos major; between this vein and the aorta
is the thoracic duct; superiorly is the trachea; inferiorly are the
splanchnic nerves and the posterior mediastinal lymphatic glands.

DEFINITION.--There are three principal forms of morbid growths in the
mediastina--sarcoma, lymphoma or lymphadenoma, and carcinoma.
Hyperplasia of the mediastinal glands also may arise, intertwined with
various diseases, such as phthisis (especially the form known as
pneumonic), pertussis, aneurism, rachitis, and syphilis. Enlargement of
the lymphatic glands may occur in connection with the scrofulous
diathesis, or similar enlargement associated with primary subacute or
chronic bronchitis and the varieties of catarrhal fever and influenza.

Allusion in this place will only be made to the rare instances in which
uncomplicated enlargement of the thoracic glands occurs in the
mediastinal spaces. Aneurism, abscess, and pericardial effusions will
be referred to only in so far as they affect differential diagnosis.

Mediastinal tumors, however, include certain forms which have the
interest of pathological curiosities rather than possessing a clinical
importance. Cysts in this region are rare, mostly of embryonic origin
(dermoid), and contain epithelial structure, such as hair, sebaceous
and sweat-glands, teeth, and occasionally bone, cartilage, and other
tissues. These cysts often develop rapidly and may attain great size.
Lipomata[8] occur as the result of an undue increase of the mediastinal
fat, and are associated with accumulation of the same in the
pericardium and in the system at large. Such tumors are rare and of
very gradual development. Kronlein[9] has described a congenital lipoma
of the {865} anterior mediastinum in a child aged one year, which found
its way through an intercostal space and then rapidly increased in
size. Fibromata, osteomata, and enchondroma are also possible
mediastinal and pulmonary tumors, but are seldom met with. Exostoses
may form upon the internal surface, and gummata upon the anterior and
posterior surfaces of the sternum.

[Footnote 8: Reigel, _Virchow's Arch._, vol. xlix.]

[Footnote 9: Langenbeck, _Klinic_, p. 157.]

PATHOLOGY AND MORBID ANATOMY.--Pulmonary processes associated with
bronchial catarrh frequently lead to enlargement of the bronchial
glands, because, owing to the impervious character of the basement
membrane of the bronchial passages, the mucous and epithelial portion
of the exudation is expectorated, and that portion of the exudate which
occurs from the bronchial blood-vessels is absorbed and carried by
means of the pulmonary lymphatics to the bronchial glands. Tubercular
deposits frequently occur in the glands of the posterior, and much less
frequently in those of the anterior, mediastinum.

Independently of the above conditions, caseating bronchial glands have
been found as complications of scarlatina with nephritis or tubercular
meningitis. An interesting case of this condition has been reported as
following an abscess in the glands at the root of the neck as a sequel
to measles nine months before.[10] Riegel also mentions an instance in
which some of the mediastinal glands were enlarged to the size of hen's
eggs. The trachea was compressed at the point of bifurcation, so that
its calibre was reduced to one-third its natural size. This case was
free from other glandular enlargements. Coupland has described a case
in a boy four years of age, in whom the cervical glands were enlarged
and idiopathic hyperplasia of the bronchial glands was suspected.
Autopsy: On raising the sternum a collection of indurated glands was
found in the anterior mediastinum, and over the root of the right lung
one of these glands had broken down into a cheesy mass. A chain of
enlarged lymphatics accompanied the right bronchus. The largest caseous
mass had ulcerated through the trachea just above the origin of the
right bronchus by an aperture measuring half an inch along the axis of
the tube, while for half an inch above its lumen was compressed. In
this case the right lung was solidified and contained cheesy matter,
with a cavity at the apex. The father of the child had also suffered
from increase in the glandular tissues.

[Footnote 10: See _Path. Soc. London_, 1884.]

The historical literature of intra-thoracic morbid growths has been
exhaustively reviewed in a monograph by Cockle, but until within the
last fifteen years little attempt was made to separate mediastinal
tumors into definite groups.

Our present knowledge on this subject was first shaped by Virchow,[11]
since which period numerous cases have been recorded.

[Footnote 11: _Virchow's Archiv_, Bd. xciii. Heft 3.]

Sarcoma of the Mediastinum.--Primary sarcomatous growths are relatively
uncommon. In 7566 cadavers examined at the Marine Hospital at Kronstadt
there were found 158 malignant tumors, 127 being carcinomatous, the
other 31 being sarcomatous. In 24 cases reported by Kahnlich, 13
occurred in the anterior mediastinal region, and a similar location was
found in a case reported by the writer,[12] also in one instance
reported by West.[13]

[Footnote 12: _Philada. Med. News_, March 15, 1884.]

[Footnote 13: _Path. Soc. London_, 1883.]

The anterior mediastinal space is a favorite location for the origin of
the purely sarcomatous form of tumor. Sarcoma may arise from a
persistent thymus (as in cases reported by Gee, Church, and Powell),
from the parietal or visceral layers of the pericardium or pleura, from
the periosteum of the sternum, or from the mediastinal connective
tissue.[14]

[Footnote 14: Kahnlich, _loc. cit._, describes 13 as originating in the
connective tissue of the anterior mediastinum, 5 in the periosteum of
the sternum, and 1 in the pericardial substance.]

{866} [Illustration: FIG. 53. 1, tumor; 2, aorta; 3, right ventricle of
heart.]

In a disease of this rare nature we can best formulate an idea of the
character of the growths by the recital of a few typical cases. In an
autopsy made by the writer, on removing the sternum and cartilages they
were found to be adherent on the right side to a mass which occupied
the anterior mediastinum (see Fig. 53). The growth was seven inches
long, measuring from the sternal notch, and terminated in a somewhat
diffused thickening of the visceral pleura, which covered the anterior
margin of the upper and middle lobe of the right lung. The growth was
two and a half inches broad. It overlaid the aorta, pulmonary artery,
and the vessels of the neck. The calibre of the trachea was slightly
diminished. The glands of the neck were unaffected on either side. The
posterior mediastinal glands were very slightly enlarged along the
sides of the trachea and upper bronchi. Laterally, at the lower portion
of the growth, the pulmonary pleura was thickened at the line of
contact with the tumor, but the lungs were free from any traces of
disease. The new formation was of fibrous consistence, of a gray-white
color, and through its centre a softened tissue was found. Microscopic
examination showed the growth to be composed of medium-sized lymphoid
cells mixed with spindle-shaped cells, and imbedded in a homogeneous
stroma or a stroma which consisted of reticulated fibres and wavy
fibrous tissue. Other portions of the body were normal.

In West's case the tumor also occupied the anterior mediastinum,
extending toward the second left intercostal space. The mass was about
the size of a boy's head, soft, cellular, and adherent to the upper
lobe of the left lung; it also rose into the episternal notch and left
supra-clavicular fossa. The brachial plexus and vessels of the left
side, subclavian and carotid arteries, the jugular and innominate
veins, were imbedded in the tumor. The left bronchus and a portion of
the trachea were flattened. The left phrenic and left pneumogastric
nerves passed through the mass, and on dissection were found much
thickened as they ran through the tumor. The tenth nerve measured {867}
three times its normal diameter, and was pushed out of its course
nearly an inch from the carotid. The recurrent laryngeal was also
thickened; the right pneumogastric and phrenic nerves were not
involved. The heart lay beneath the tumor; nodules of the new growth
were found upon the anterior surface of the heart and along the vessels
issuing from it. No secondary deposit was found in the lungs except at
the margin of the left upper lobe, into which the tumor spread
directly. The spleen, liver, kidneys, and lumbar glands were normal.

Microscopic examination determined the growth to be a round-celled
sarcoma, the thickening of the nerves being due to infiltration by
similar small-celled growth.

In primary sarcoma of the mediastinum--and the same is true of
lymphadenoma--the invasion of the various intra-thoracic organs is
chiefly by continuity or direct spreading of the growth. The lymphatics
of the neck are very rarely implicated in this form of malignant
disease; and while in lympho-sarcoma the glands may be involved, they
are not so frequently as in cancerous processes. Sarcomata of the
mediastinum with implication of the lungs and pleura are more
frequently secondary processes; indeed, the lungs would seem never to
be the seat of primary sarcoma. The pleural tissues, however, may be
primarily involved. Lepine, Birch-Hirschfeld, Böhme, Eppinger, Schultz,
Greenish, and others have reported cases in which the growths were
abundantly distributed in the pleural tissues as primary formations.
The point of origin is believed to be either directly from the ordinary
connective-tissue cells or from the endothelium of the lymphatics.

Secondary sarcomata may form in the mediastinum or in the lungs within
a month or so long as a year after the removal of tumors from other
parts of the body, probably by metastasis prior to the removal. In some
of these cases the seat of original growth and the neighboring glands
may be entirely healthy.

In a typical case of multiple osteoid sarcoma of the lung reported by
West fleshy vegetations were found on the visceral pleura: upon the
parietal pleura, over the seventh rib, two inches from the spine and
growing from it, was a lobular spongy mass as large as an orange, but
perfectly disconnected with the parts beneath. The right lung was
irregular in shape, owing to the presence of masses of new growth in
its different parts. The middle lobe seemed almost completely converted
into the new growth. Between the lower lobe and the diaphragm, but
attached to the lung, was a mass the size of a cricket-ball, covered
with a dark, laminated, but easily separated coagulum. The tumor
occupied the upper lobe of the left lung, forming an irregular oval
mass six by four and a half inches. It was white in color, and adherent
to its upper border was compressed lung-tissue. There were also four or
five independent nodules situated near the surface, and of a white
color. The lower lobe contained one medium-sized growth and four or
five small ones. The bronchial glands were not involved. The tumors
appeared soft and spongy, but on incision they were found so hard that
a knife could scarcely divide them.

Frequently, the lungs are found infiltrated with sarcomatous nodules of
a soft consistency, varying in size from a walnut to an orange. To sum
up: primary sarcomata may be the round- or spindle-celled variety; but
myeloid sarcomata also occur, chiefly as secondary growths. (See Fig.
54.)

[Illustration: FIG. 54. From photograph of a case of Professor Osler's,
showing secondary myeloid sarcoma of mediastinum--appearing six months
after removal of myeloid sarcoma of radius. The tumor figured in the
plate occupied the front of the thorax lying beneath the sternum and
the cartilages and ribs of the left side, pushing back and completely
covering the pericardium. It was loosely adherent to the ribs and
sternum, and appeared to grow from the pulmonary pleura, to which it
was attached in a large part of its extent, and only had penetrated the
lung at one spot on the anterior border of upper lobe. Right lung
contained secondary masses, chiefly in the pleura.]

Lympho-sarcoma of the Mediastinum.--Lympho-sarcoma, lymphoma, or
lymphadenoma is the form of malignant process which probably includes
the majority of cases of primary mediastinal growth. It is sometimes,
however, a part of a more general disease, affecting more or less the
whole glandular system.

{868} Murchison[15] classified the first case of this disease involving
the intestines, liver, mesentery, and heart. The same observer the
following year described a case in which the glands of the neck,
mediastinum, axillæ, and spleen were involved. Wunderlich has recorded
a case of malignant mediastinal disease which commenced in the glands
of the neck; but the cervical glands may be enormously enlarged without
implication of the bronchial.

[Footnote 15: _Path. Soc. Trans._, London, vols. xx. and xxi., together
with a summary of the literature of the subject.]

The general disease dates back to the time of Hodgkin, Bright, and
Wilkes, and was then known as anæmia lymphatica. It has been
specifically described by Virchow,[16] Cornil, and Ranvier as
independent of leukæmia, and was designated lymphadénie. It was noticed
by Trousseau under the title of adénie, and Ogle and numerous clinical
observers since have also recorded cases.

[Footnote 16: _Die Krankhaften Geschwülste_, Band ii. p. 376.]

As a mediastinal growth the characteristics of lympho-sarcoma can be
made more vivid by the reproduction of one of the first cases recorded
of this disease. On removing the sternum and cartilages they were found
adherent to a mass occupying the anterior mediastinum. The morbid
growth reached backward to the trachea, surrounding it with a thickness
posteriorly of a quarter of an inch; it extended downward to the
bifurcation of the trachea, and, involving the superior prolongation of
the pericardium, invaded and greatly thickened the parietal part of
that membrane, covering the heart at {869} its upper half. The diseased
structure reached upward to the root of the neck, involving the
anterior mediastinal glands, and surrounded the trachea by a thin layer
as high as the thyroid cartilage. Some of the glands on each side of
the neck were affected as high as the angle of the jaw. Laterally, the
morbid growth extended on each side to the line of junction of the
cartilages with their ribs, displacing the anterior margin of the lung.
The pulmonary pleura was involved and thickened at the line of contact,
and the right lung at the upper part of its anterior margin was invaded
from the pleura by white, fibrous-looking branched bands. At the lower
part of the anterior lobe the lung was also invaded from the
pericardium. Some of the glands at the root of the lung were involved
by extension, but they were not generally affected, nor was the lung
invaded except to the limited extent above mentioned. The heart and
pericardium were free from disease.[17]

[Footnote 17: Powell, _Path. Trans._, vol. xxi., London.]

The malignant growths of the mediastinal region implicate the
surrounding structures so rapidly that it is, as a rule, quite
impossible to determine, even after death, the starting-point of the
disease; and while lymphadenoma can originate in the same tissues as
the other forms of sarcoma already alluded to, yet it in most cases
probably originates in the lymphatics of the anterior or posterior
mediastinum.

In reference to the location of this form of morbid growth, we find, on
consulting a series of cases reported by Fenwick, Eve, Payne, Peacock,
Powell, Murchison, Bennett, Dickinson, that the region for principal
development seems to be the anterior mediastinal space, although in
several instances the posterior mediastinal region was also involved.

The characteristics of the growth of lymphadenoma are the involvement
by continuity of all adjacent tissues, thus affording a contrast to
secondary sarcomata. The glands of the neck are sometimes invaded, but
are unaffected in a considerable proportion of cases. The lungs may be
involved slowly, the growth following the lymphatic paths along the
bronchial or vascular sheaths. The malignancy of lympho-sarcoma is
unquestionable, but as a local growth it is less so than when the
process is general; it is less malignant than cancer or certain forms
of sarcoma.

Carcinoma of the Mediastinum.--Primary carcinoma of the mediastinum, as
separated from the foregoing groups, is relatively rare; even as a
secondary growth the same is true, unless it directly penetrates the
chest-wall from a cancerous breast. The cancerous growths present a
special peculiarity in the fact that they incorporate all the tissues
with which they come in contact, and are followed by contraction.
Carcinoma often originates in the lymph-tissue at the root of the lung,
and may form a mass which may involve the bronchial glands, lower part
of the trachea, the right and left bronchi, and surround the aorta and
oesophagus. Scirrhous cancer frequently originates in the tissues at
the root of the lung surrounding the bronchi and vessels, compressing
them, and extending by branching rays through the lung-substance toward
the periphery, following the course of the large bronchi, the lymph or
arterial vessels. Carcinomatous formation may also originate in the
follicles of the mucous glands of the bronchial tubes, and the mucous
membrane of the same is frequently ulcerated by extension of the morbid
process. The mucous membrane of the bronchi may be covered with
villous-like formations springing from the surrounding growth.[18]
Obstruction of the bronchial lumen by carcinomatous growth may prevent
the expectoration of the bronchial secretions, and dilatation of the
bronchial tubes may be consecutive. These dilated tubes may become
filled with pus from associated bronchitis or forms of catarrhal
pneumonia.

[Footnote 18: See cases by Bennett and Williams, _Lond. Path. Trans._,
vols. xix. and xxiv.; also Burrows, _Med.-Chir. Trans._, vol. xxvii.]

{870} The special pathological characteristics of cancerous growths are
that they exist most frequently in the posterior mediastinum, and
therefore exert special pressure on the respiratory passages. Again,
they are subject to contraction, by which the various pulmonary
structures are fused together. Hard, nodulated, cervical glands usually
appear in the supra-clavicular spaces, affording special contrast in
this respect with the pure sarcomata. Since, in general, the same
tissues may be affected as in lympho-sarcoma or other processes
affecting the bronchial glands, a positive diagnosis can usually only
be made by a microscopic study of the growth. Only one lung is usually
implicated, while the sarcomata spread by extension in all directions
and may involve both lungs.

The effect upon the lungs of mediastinal pressure on the bronchial
tubes may be very serious. Collapse of the bronchial tubes and oedema
of the lungs may ensue, or subacute catarrhal inflammation with
consolidation--a process which has been described by Fuchs as a form of
pneumonia under the title of apneumatosis. The affected tissues not
uncommonly break down by necrotic disintegration, which may lead to the
formation of cavities sometimes erroneously described as resulting from
softening of cancerous nodules.

Pleural effusions are prominent in the clinical history of malignant
intra-thoracic disease, and especially in mediastinal processes. These
effusions are consequent on pressure on the intra-thoracic circulation,
or may be traceable to inflammation, either developed by irritation of
the contiguous morbid process or extension of the same upon the serous
membrane. Purulent pleural collections have been noted in certain
cases, and they may be hemorrhagic. In 31 cases in which the character
of the effusion was mentioned, 6 only were tinged with blood. This
characteristic is therefore simply of relative importance. Pericardial
effusion is also possible from causes similar to those operating upon
the pleural tissues. Pressure may occasion dilatation or thrombosis in
the vena cava. The vessels of the neck suffer, either directly from
pressure inducing dilatation, or by being converted into rigid tubes,
allowing of no adaptation to the amount of blood passing through them.
There may be corresponding collateral swelling of the azygos or
hemi-azygos veins, and at the same time collateral circulation is
established between the jugular and the subclavian on the one side and
the azygos and hemi-azygos on the other through the superior
intercostal veins. The external thoracic veins may, in some cases,
become enlarged, and infrequently compression of the inferior cava may
occasion effusion into the abdominal cavity and cause oedema of the
lower extremities. Morbid growths have occasionally invaded the spinal
canal and excited sufficient pressure to occasion paralysis.[19]

[Footnote 19: Bennett, _loc. cit._]

There are certain forms of mediastinal and pulmonary tumors very seldom
met with; for example, fibromata and osteomata,[20] the latter
sometimes occurring as an exostoses springing from the posterior
surface of the sternum. Dermoid cysts of this region, as in the lungs,
are also most unique. Mohr records the case of a woman æt. twenty-eight
who had spat up hair since her sixteenth year. In the left lung was
found a cyst which communicated with the bronchus. Inside of it was
found several rounded knobs, here and there pedunculated, varying in
size from a nut to a hen's egg, consisting of fibrous tissue provided
with sebaceous and sweat-glands, and from which sprang numerous long
hairs. The remaining contents consisted of fat and balls of hair.
Teeth, bone, and cartilage can sometimes be recognized in these
cysts.[21]

[Footnote 20: _Die Krankhaften Geschwülste_, ii. p. 102; Förster, _loc.
cit._, p. 105; Wagner, _Arch. für Physiol. Heilk._, 1859, p. 411;
Luschka, _Virchow's Arch._, Bd. x. p. 500; Förster, _Ibid._, Bd. xiii.
p. 105; Didardier, _L'Union méd._, 1867, No. 83.]

[Footnote 21: _Nederland Weekblat. vor Geneesk._, 1851, p. 44.]

{871} Enchondroma may occur in the mediastinum or lungs; it is rare as
a primary process, but is more often found as secondary to
enchondromata of the bones.[22]

[Footnote 22: Lebert, _Physiol. Pathol._, ii. p. 213; also, Förster,
_Virchow's Arch._, xiii. p. 106.]

ETIOLOGY.--Predisposing and Exciting Causes.--The etiology of morbid
growths in the mediastinum, as elsewhere, is subject to debate and
conjecture. The most practical query relates to location--viz. that
sarcomatous growths originate in the anterior mediastinum, and
carcinoma more frequently in the posterior.

The trade of shoemaker was followed by several subjects of sarcoma
observed by the writer. These men were accustomed to press the last
against the sternum. With a pure family history free from taint of
malignant disease the etiology of sarcomata may be more readily linked
with some cause of irritation than is the etiology of cancerous tumors.
This irritation may be a blow or other direct injury or some local
irritation, as antecedent inflammatory process in the lungs, bronchial
mucous membrane, or pleura. Intemperance, insufficient food, and
over-exercise have been noticed in rare instances as antecedents. In
reference to lympho-sarcoma, preceding causal irritation may have
existed, but in two-thirds of the cases the etiology is obscure.
Hereditary transmission has not been distinctly proven in regard to any
of the forms of sarcomata. The etiology of cancerous tumors is still
more vague, though possibly the previously-named conditions may have
preceded the growth. Louis, speaking generally upon intra-thoracic
cancer, places it fourth in the scale of comparative frequency of
organs affected--viz. uterus, stomach, liver, and lungs. The history of
the removal of a morbid growth may attest the secondary character of
some growths apparently primary.

In the question of age and sex the autopsies at Kronstadt already
referred to show that in 158 malignant growths 127 were carcinomatous;
81 occurred in men of an average age of fifty-three, and 46 in women of
an average age of fifty-six. So we may conclude that carcinomatous
growths occur after the middle period of life. In 31 cases of
sarcomatous tumors, 20 occurred in men of an average age of
thirty-eight, and 11 in women of an average age of forty-eight. Powell
gives 24.8 as the mean age for the occurrence of mediastinal growths in
general. As a rule, a mediastinal tumor recognized at a relatively
early period of life, before the thirtieth year, is most likely to be
one of the forms of sarcomata. Sarcomatous tumors, however, sometimes
occur in the aged; for example, in a woman æt. seventy-six
(Laboriou[23]) and in a woman over sixty reported by Wilson.[24] The
question of liability through sex is somewhat uncertain, but while
these growths may occur in either, a slight preponderance exists in
favor of the male sex, especially if the growth be a lympho-sarcoma.

[Footnote 23: _Virchow's Arch._, _loc. cit._]

[Footnote 24: _Trans. Path. Soc. Philada._, Jan., 1884.]

SYMPTOMS.--In studying the semeiotic characteristics of mediastinal
growths an accurate history of the case is a prerequisite of paramount
importance to a correct understanding of the essential features of the
malady. It should be borne in mind that no single fact determined by
the methods of physical diagnosis has special pathological
significance, but simply indicates certain definite physical conditions
in the region under examination. The purely objective physical signs
are so closely intertwined with the general symptoms of morbid process
that any study is partial which does not recognize this combination.
Both physical signs and general symptoms must be in turn considered in
connection with a thoughtful analysis of the processes of morbid
anatomy, because symptomatology is the study of the expression of
pathological changes. The general nutrition of patients suffering from
primary sarcoma or lympho-sarcoma is often good in the early stages of
the disease unless the oesophagus is pressed upon or implicated, and at
the last {872} patients may even die in a well-nourished condition.
Indeed, the special import of the peculiar respiratory disturbance with
pain seems set at naught by the appearance of fair health. In some
cases of sarcoma or lympho-sarcoma, however, emaciation is progressive,
though slower than in cancerous growths.

When cancer itself is primary, the ordinary characteristic train of
disturbances of nutrition, with cachexia, follows, and then emaciation
is rapid and decided. The loss of nutrition with anæmia is more marked
in secondary sarcoma, and in cases of secondary cancer cachexia is the
rule.

In reviewing the clinical history attention is specially directed to
the development of the mediastinal growth by the gradual increment of
subjective sensations of shortness of breath, with a sense of
discomfort or tightness in the chest, with or without radiating pains.
The respiratory phenomena present great diversity, yet the neurotic
character of the dyspnoea is characteristic. Rest or change of posture
may remove all oppression, or on the least exertion dyspnoea may be at
once manifested. With limited physical signs there may be great
distress of breathing or orthopnoea, while in many cases with
unquestioned evidence of tumor there may be only a little quickening of
respiration. As a rule, tumors of the anterior mediastinum are less
characterized by dyspnoea than those involving the posterior space. The
dyspnoea depends upon the size and seat of the tumor, and increases day
by day with its growth; but in certain cases the tumor is so placed
that pressure on the trachea, bronchus, or direct pneumogastric
irritation may induce severe paroxysmal attacks of dyspnoea, with
laryngeal symptoms resembling the condition so common in aneurismal
tumors. Pressure symptoms, traceable to irritation of the
pneumogastrics, are, however, as a rule, less marked than in aneurism.
Pressure on the trachea without implication of the laryngeal nerves can
occasion many of the symptoms usually assigned to the latter cause.[25]
Even when the tenth nerves have been surrounded or involved by the
growth, special symptoms may be absent, although in other cases serious
phenomena follow, such as vomiting or other gastric disturbance, or
even inability to swallow; sometimes palpitation, angina, irregular
action, or tendency to faintness may follow implication of the cardiac
plexus.

[Footnote 25: Bristow, _St. Thomas's Hosp. Rep._, vol. lxxi.:
"Influence of Pressure on Trachea without Implication of the Recurrent
Laryngeal Nerves."]

The symptom of pain is usually far less than in cases of aneurism,
since it is only in rare instances that the chest-walls become eroded
by the outward pressure of the tumor, as so frequently occurs in
aneurism. Moreover, the growth more readily adapts itself to the
contour of the chest, and tends to envelop rather than compress organs
or nerves. From the time that pressure commences, either on the
trachea, bronchi, or intra-thoracic nerves, cough is more or less
constant. It may, however, be due to pulmonary changes occasioned by
the pressure or actual involvement of the lung by the growth. Cough is
an earlier symptom when the growth is situated in the posterior
mediastinum than when it is located anteriorly. It is usually laryngeal
and ringing in timbre, and may occur paroxysmally, as in pertussis. It
is ineffectual, dry, or attended with only scanty mucous or frothy
expectoration. The sputa may be tinged with blood, or profuse
hæmoptysis is a possible symptom. A microscopic examination of the
sputa in a case of intra-thoracic tumor is always important, because
portions of the morbid growth may be found, or by perforation of the
trachea or oesophagus the pus from a mediastinal abscess may be mixed
with the sputa. Mediastinal tumors are not, as a rule, characterized by
febrile symptoms. Inflammatory complications of the lungs or pleura may
account for the exceptional thermometric variations. Cases have been
reported by Bennett and Church in which there was persistent elevation
of temperature, with daily fluctuations and rapidity of pulse and
respiration. In one instance of lympho-sarcoma the paroxysms of fever
corresponded with the periods of {873} growth in the enlarged glands,
but in this case the lymphatics of the general system were also
implicated. From the fact that the growths are strictly mesial,
dysphagia is a far more common and persistent symptom than in aneurism,
especially in growths of the posterior mediastinum. When the growth is
situated in the anterior mediastinum the dysphagia is less frequent;
but it must be borne in mind that prolongations of the tumor may
occasion lateral oesophageal pressure, or narrowing of the lumen of the
oesophagus can occur from pressure upon the trachea by the growth.
Exceptionally, dysphagia may be due to implication of the oesophagus in
the new growth. (See Cancer of the Lung.) Neural influences may
increase the dysphagia, in which case it is doubtless a reflex
phenomenon and is associated with hiccough or vomiting. The passage of
a bougie can be readily effected in such cases.

In reference to the foregoing pressure symptoms one fact deserves
recognition--viz. that in aneurismal tumors the pressure symptoms are
subject to variations in intensity due to changes in the
intra-aneurismal tension, while in morbid growths in the mediastinum
the pressure symptoms exhibit a progressive tendency, advance upon the
same lines, and are more constant than in aneurism. With this principle
in mind, the additional pressure symptoms in doubtful cases of
mediastinal growth must all be considered; for instance, in some
histories recorded by Rossbach the pupils could be dilated by firm
pressure on the tumor above the clavicle. The pulses in the brachials
or radials may be unequal, and variations of rhythm, volume, and rate
may be noted as evidences of pressure, which may occasion thrombosis by
retarding the circulation in the innominate, subclavian, or azygos
vein. The blood may reach the heart by the collateral circulation
elsewhere described or by the dilated mammary superior and inferior
epigastrics and the inferior vena cava. Pressure may therefore give
rise to cyanosis, oedema of the upper or lower portions of the body,
with enlargement of the superficial veins, or dropsy may be traceable
to hydræmia.

PHYSICAL SIGNS.--When mediastinal tumors are of small size, physical
signs may afford no help in making a diagnosis, and they will always
vary according to the location of the growth.

Inspection may reveal venous repletion of the veins of the face and
neck, with distension of the superficial veins of the chest; the latter
symptom is more frequently obvious than in aneurism. In the case of
sarcoma represented by Fig. 53 the foreign growth was so limited to the
mesial line as not to involve the vessels or create pressure symptoms
upon them. If the anterior mediastinum is implicated, there may be
circumscribed alterations in the contour of the chest. Prominence of
the upper piece of the sternum and of the sternal attachment of one or
more ribs may be recognized. The sternum itself may appear thickened
upon palpation of the notch. One side of the chest may be larger than
the other above the nipple-line; the affected side, however, may be
smaller, since vicarious respiratory function may create distension.
The usual changes in the contour of the chest-walls will indicate
pleural effusions. (See Cancer of the Lungs.) Since tumors of the
anterior mediastinum overlie the aorta, transmitted pulsation may be
detected in rare instances; this pulsation can be differentiated from
aneurismal vibrations by the absence of the sense of expansile
pulsation characteristic of dilated aorta or aneurism, but it sometimes
closely resembles that yielded by an aneurismal sac thickly lined by
coagulum.

Lympho-sarcoma and cancer are often accompanied by painless, movable
glandular enlargements, recognizable by palpation in the
supra-clavicular spaces; but the absence of the glandular implication
in sarcomata is conspicuous; swelling occasionally manifests itself in
the suprasternal notch. Tumors of the posterior mediastinum must attain
considerable size before {874} they can be recognizable by the
foregoing methods. Growths in the latter space are those especially
liable to complication by pleural effusion in one or both sides.
Mediastinal growths may occasion collapse of the lung, or cirrhotic
processes or pleural adhesions may diminish the circumferential
measurements of the chest. The heart may be displaced backward,
downward, to the left or to the right side; and since in aneurism,
uncombined with valvular disease, little cardiac displacement occurs,
this sign is of importance. Rarely, as in Cotton's case in Brompton
Hospital, the heart may be fixed in situ by the extension of the growth
on both sides of it.

Percussion.--It has been observed that a very small tumor may, from its
particular site, at a very early stage give rise to symptoms both of
pressure and disordered innervation of great severity, whilst another
may attain considerable magnitude before the patient experiences any
distress or any decided evidence of pressure is manifested. It is
equally true that percussion and auscultation may be most valuable, or,
on the other hand, indefinite. The degree of dulness occasioned by a
morbid growth in the anterior mediastinum is dependent on its size,
large growths yielding flatness; but when the tumors are small the
osteal resonance of the sternum is simply hardened. Respiratory
percussion is available if the growth lies anteriorly. The full, clear
resonance of full-held inspiration contrasts with the increased dulness
developed when the lungs are stripped from the mediastinal space by
forced expiration. The boundaries of the growth on either side of the
sternum may be defined by percussion, and it is possible that the
greater part of one side may be occupied by the new formation. The
adjacent tissues are involved by direct invasion, or indirectly by
extension along the bronchus from behind forward, thus involving the
middle tier of the lung. Mediastinal tumors therefore in their mode of
growth yield a contrast with pleural effusions, because the latter
usually advance steadily from below upward. When the growth is located
in the posterior mediastinum, percussion should be practised after the
manner recommended by Mussey to facilitate recognition of enlarged
bronchial glands. (See Pulmonary Syphilis.) The apices, humeral,
scapular, basic, or marginal regions often yield a tympanitic type of
resonance, since they are often in a condition of vesicular emphysema.
The pericardial sac may be distended with effusion or implicated in the
growth, and an area of pyramidal dulness with the base above may be
recognizable.

Auscultation.--In growths situated anteriorly, in the mesial line, one
of the most forcible lessons may be impressed by the distance and
obscurity of the second sounds of the heart over the aortic and
pulmonary artery, cartilages, or the upper piece of the sternum. The
cardiac sounds may be transmitted downward, and can be heard distinctly
in some abnormal position. Even a murmur can occur due to compression
of the aorta, or pericardial friction. The respiratory murmur will
probably seem feeble and distant over one or both apices, and whistling
near the trachea.

If the posterior mediastinal space be involved, the respiratory murmur
may represent some type of bronchial breathing, or if the lumen of the
trachea or one of the bronchi be decidedly lessened, the respiratory
murmur may be whistling, feeble, or suppressed over the affected side.
Over the other bronchus the respiratory murmur may be more high-pitched
than in health, and slightly exaggerated. The rhythm is often jerky and
paroxysmal; the paroxysms are more or less constant, but are liable at
times to increase. Auscultation should be especially practised over the
roots of the lungs or in the neighborhood of the second dorsal
vertebra. Frequently it can be demonstrated, both by auscultation and
percussion, that there is diminished air-supply to one or other of the
lungs, while the respiratory murmur is not sufficiently changed for
classification. The respiration may acquire a stridulous or sibilant
character, most marked on expiration, but {875} less often than in
aneurism, because there is a greater tendency to occlusion of the
bronchi. It should always be remembered that the lung undergoes very
various and opposite changes as the result of pressure on the bronchi,
interrupting the entrance and egress of air from the lobules, and the
physical signs of emphysema, infarction, congestion, or consolidation
may exist in one or the other side. The ordinary methods of physical
examination indicate the existence of pleural effusions, but large
growths extending from the mediastinum or originating in the lung may
so closely simulate such effusions that a positive diagnosis can be
arrived at only by paracentesis.

When tumors exist in the form of very small nodules as diffused
sarcomata, no changes in the character of the respiration may be noted.
Friction râles and pleuro-pericardial frictions may be heard in some
cases. Distension of the bronchial tubes from pressure may occasion the
dilatation of the distal bronchial passages and pulmonary lobules with
retained muco-purulent secretions. The cross-sections of the bronchi
have been described as multiple abscesses. Areas of collapse or slow
inflammation with softening of the secondary inflammatory product can
follow. The bronchial pressure may prevent the sufficient transit of
air through the bronchi to create râles, or moist râles indicative of
tracheo-bronchitis or oedema may abound.

The study of the vocal resonance and fremitus presents nothing novel,
but corresponds with the generally-understood principles.

DURATION.--It is very difficult to determine accurately the duration of
malignant diseases of the mediastinum, since for a long time the
patient may be quite free from any local subjective symptom, even
though a growth may have attained to a considerable size. Moreover,
intra-thoracic malignant disease, especially in the non-cancerous
varieties and if the digestive tract be normal, may be unattended by
any of those symptoms commonly associated with malignant process, such
as a peculiar tint of skin, progressive and great emaciation, or the
aspect of suffering. Sarcomatous tumors usually grow rapidly, as in a
case related by Jaccoud, in which death occurred within eight days
after admission to the hospital. Prior to this time the patient had
suffered from no objective symptoms whatever, although when admitted
there was physical evidence of a large growth extending from the
clavicle to the nipple.[26] West records a fatal case at two and a half
months; Horstman, one in which the disease originated on the right of
the sternum, as evidenced by a very small area of dulness; the entire
right side of the thorax was invaded within five weeks.[27] Berevidge
reports a case of sudden death from hæmoptysis in a man aged sixty-four
years, who up to that time had appeared healthy, and only a few days
before had complained of a slight cough and a feeling of oppression in
the chest. At the autopsy two cancerous masses the size of a hazelnut
were found, one of which overlaid a bronchus which was ulcerated to a
considerable extent. The bronchi were filled with blood. Virchow
mentions a case the duration of which was only two months. Walsh,
speaking of malignant growths in general, assigns three and a half
months as the minimum duration of these cases.

[Footnote 26: _Leçon de Clin. méd._, p. 636, Paris, 1867.]

[Footnote 27: _Trans. Path. Soc. London_, 1883.]

Undoubtedly, the duration will depend on the freedom from pressure upon
the oesophagus, or from interference with digestion due to
pneumogastric irritation, or from malignant processes in the stomach or
intestines. Pain, and consequent loss of sleep, will also accelerate
the termination of any case. Lebert assumes an average duration of
thirteen months, and Walsh states the maximum duration in
intra-thoracic malignant processes at twenty-seven months. The soft
secondary malignant sarcomata or carcinomata grow more quickly, and
have a relatively shorter course, than the harder forms of the same
species. Lymphadenoma may persist a long time, and appear for a while
to be stationary and unattended by any serious impairment of the
general {876} health, but the cases are exceptional. The persistence of
fibrous, fatty, or cystic tumors depends chiefly on the mechanical
inconvenience occasioned by them. All forms of malignant intra-thoracic
disease, however, are steadily progressive to a fatal termination.
Death commonly arises from the gradual increase in seriousness of the
pressure symptoms. Inability to lie down, harassing cough, want of
sleep, all tend to induce fatigue which may prove fatal. Deficient
aëration of the blood may occasion stupor, or sudden simultaneous
pleural and pericardial effusion or general pulmonary oedema may
terminate the scene. In exceptional instances death has resulted from
laryngeal spasm or from acute hypertrophy of the thyroid gland with
tracheal occlusion. In a remarkable case reported by Bennett paroxysmal
dyspnoea had been the only symptom of intra-thoracic disease for a few
months, when suddenly a severe seizure occurred which persisted
uninterruptedly for three days, till weakness and exhaustion terminated
in death by asphyxia. In this case the thyroid gland was found enlarged
to the size of a double fist, but the enlargement was mainly below the
sternum and along the sides of the trachea, which was literally
surrounded by the greatly-enlarged and firm lateral lobes of the
thyroid, so as to be completely flattened laterally. The structure of
the thyroid appeared healthy, but very firm, and the enlargement was
due solely to hypertrophy, and not to cystic or other disease, nor was
there any exophthalmos.[28] Death is possible from sudden asthmatic
attack, or, more rarely of all, by hæmoptysis.

[Footnote 28: See "Cancerous and Other Intra-thoracic Growths,"
Bennett, _The Lumleian Lect._, 1872, p. 169.]

PROGNOSIS.--The prognosis is invariably unfavorable, and must continue
so unless the more recent attempts for removal of primary growths in
the anterior thoracic regions yield grounds for a more hopeful outlook.
We may also hope that some remedy may influence or control the
development of lymphoma. Considerable relief may be obtained by rest,
suitable feeding, careful regulation of the digestive system, and such
hygienic measures as may seem most available.

DIAGNOSIS.--From Aneurism.--When we consider that in the diagnosis of
aneurism of the aorta every sign and symptom has in turn been found
fallacious in the ever-varying conditions under which aneurisms appear,
and that one is forced to say that aneurism has no pathognomonic signs
or symptoms, the difficulties in the way of the diagnosis of
intra-thoracic morbid growths may be recognized. Moreover, the
diversity in the peculiarities of each case, the multifarious character
of the pressure symptoms and physical signs, and the absence of a
precise order of phenomena peculiar to tumors in this situation, may
render a positive diagnosis in the early stages very difficult.

Aneurism in the absence of unequivocal signs of its existence may be
excluded on the following grounds: the absence of conditions which
predispose to disease of the coats of the arteries--_i.e._ syphilis,
alcoholism, Bright's disease, rheumatism, laborious avocations, violent
exercise. Aneurism may occur at any age, but it is rare before the age
of thirty years, and most prevalent between the ages of forty and fifty
years. Aneurism is also less frequent in the female sex. The distal
pressure symptoms of aneurism are more variable than in other morbid
growths of the mediastinum, and especially dysphagia is less constant.
Great emaciation without intense pain is adverse to the diagnosis of
aneurism, while severe pain with occasional exacerbations is favorable
to this diagnosis. However, instances of morbid growths are recorded in
which intercosto-humeral neuralgia was an initial symptom.

"An extensive area of dulness must in aneurism mean a large sac, and
with such a large tumor we should almost invariably get marked
expansive pulsation. Again, aneurismal sacs, before they produce
extensive dulness in {877} any portion of the parietes of the chest,
point, as it were, in some particular direction, becoming distinctly
prominent and producing an eccentric motion around them in consequence
of the thoracic parietes being absorbed or yielding at the point of
greatest pressure" (Graves). Hæmoptysis may occur not only from
aneurismal leakage, but from the effects of pressure of morbid growths
upon a bronchus or the invasion of the same by the malignant process.
Blood-spitting cannot therefore be regarded as an important
differential symptom. Unless valvular disease be associated with
aneurism, the displacement of the heart is less frequent in aneurism
than in morbid growths.

From Abscess.--The etiological relation in this process is traumatic,
or mediastinal abscess occurs in connection with caries or fracture or
after an operation in the neighborhood of the throat or neck, or of
suppurative disease elsewhere in the thorax, as abscess of the lung or
empyema. The pain in cases of abscess is deep-seated, constant, slowly
increasing, rather than the paroxysmal pain of aneurism or solid tumor.
The febrile movement may afford decided aid in the diagnosis, but it is
also true that high temperature may mark the progress of
lymphadenomata, as in Bennett and Sutton's case, in which from Jan.
11th to Feb. 28th the thermometrical wave vibrated between 103.5°
maximum, with a pulse of 148 per minute, to 100.5° minimum, with a
pulse of 108. In this remarkable case sweating was also a prominent
feature; and a somewhat similar example has been recorded by Murchison.
In corresponding circumstances the existence of secondary processes in
the lungs or elsewhere, with enlarged glands in the neck, may prevent
error. In mediastinal abscess there will probably be a tendency to
point, with the appearance of a fluctuating, circumscribed, superficial
tumor at the sternal border or adjacent to this bone. There may also be
tenderness on pressure associated with the pain, and an oedematous
condition of the tissues of that portion of the sternal region covering
the tumor, although this symptom sometimes attends malignant new
formations. Pulsation may accompany abscess, but will be of the
transmitted variety. In suspicious cases the sternal bone can be
drilled and an exploratory needle introduced into the tumor.

The general diagnosis of mediastinal tumor can be more easily made upon
the basis of regional invasion. But in any suspicious case an elaborate
and thorough clinical history is an essential prerequisite. In
proportion as one completes the natural history of a case of obscure
intra-thoracic disease the more likely one is to approach by exclusion
a correct interpretation of the existing physical signs and symptoms.

Growths in the Anterior Mediastinum.--Tumors located in the anterior
mediastinal space overlie the heart and aorta, and consequently the
heart-sounds, especially the second, may be indistinct or muffled; or
the second sounds may be audible in some new situation, owing to
displacement of the heart. The sternal region may be distinctly
prominent or bulged, and at the notch the bone may appear thickened.
The resonance in the interscapular regions remains unimpaired, but over
the sternum percussion should yield a very dull sound if the growth be
large, but when a comparatively small tumor exists the sternal
resonance will be hardened and high-pitched. An additional explanation
of this modification exists in instances where the growth is not
adherent to the sternum and the bone is arched over the tumor.

The respiration may be whistling or stridulous if the stethoscope is
placed over the trachea, and over one or other apex anteriorly the
respiratory murmur may be feeble or blowing, in proportion to the
volume of air which is permitted to enter the chest. Posteriorly, the
respiratory murmur may be unaffected at first, although as the growth
advances evidence of pressure on the bronchial tubes may be detected
over the interscapular region. The superficial veins of the chest may
be enlarged, especially those below the level of the upper segment of
the sternum. Dysphagia is usually slight in {878} proportion to the
other pressure symptoms or entirely absent. It may be simply a symptom
of irritation of the intra-thoracic nerves or due to enlargement of the
glands of the mediastinum.

Mediastinal growths usually develop in the middle line; they spread in
all directions, especially laterally, but avoid at first the roots of
the lungs. Pressure is rather exercised upon the parts in the mesial
line. They reach a large size and grow with great rapidity, producing
symptoms rather as a consequence of their size than by virtue of
contractile properties.

From Pericarditis.--A possible pericarditis may be mistaken for a tumor
of the anterior mediastinum. The diagnosis of pericarditis must be
sustained by evidence showing the dependence of this process upon
rheumatism, syphilis, nephritis, or propagated inflammation. The
distension of the pericardial sac due to pericarditis exhibits a
definite outline. The dulness of a tumor is irregular, with a tier of
dulness upon a higher level than in effusion. The absence of various
pressure signs is marked in pericarditis, while disturbance of the
heart's rhythm is more frequent. Kussmaul states that there are two
signs characteristic of chronic pericardial inflammation with
thickening and adhesion--viz.: a "complete or almost complete failure
of the radial pulse during inspiration, and simultaneously visible
swelling of the great veins of the neck, instead of the collapse that
usually takes place during this portion of the expiratory act. Adhesion
of the great vessels to the sternum, either directly or through the
medium of the pericardium, is supposed to account for these phenomena."

Febrile movement is usually present in pericarditis, and, while a
possible temporary feature in new growths, is not persistent unless
complicated by inflammation in the pulmonary tissues. Finally, the
progress of the case will often decide the question.

Growths in the Posterior Mediastinum.--In growths located in the
posterior mediastinum one or the other bronchus is one of the earliest
structures implicated by the pressure, because in these cases the chief
mass of tumor is found at the root of the lung. Secondary lesions in
the lungs directly traceable to pressure are frequent, but unilateral,
although secondary cancer from malignant lesions elsewhere than in the
lungs may be bilateral. Pressure symptoms as a class occur early, are
grave, constant, and progressive. Percussion according to directions of
Guéneau de Mussy may be made available. Abolition or great impairment
of breath and voice sounds over one or other posterior aspect of the
chest is the rule, since these tumors are prone to contraction.
Sometimes the respiratory murmur is whistling or blowing if the
bronchial pressure is less decided. Progressive emaciation and cachexia
are commonly present, not only from the inherent tendencies of the
disease, but also depending upon the disturbance of the functions of
many important organs which have been encroached upon by the tumor. The
exclusion of a malignant disease of the oesophagus is very difficult.
The passage of a bougie might determine the seat of obstruction, and
thus assist in the diagnosis, but great caution must be observed lest
penetration of the softened tissues occur. (See Cancer of Oesophagus.)

From Pleural Effusion.--The greatest difficulty may be experienced in
deciding between uncomplicated pleurisy and effusion complicated by
morbid growth.

Aside from the history of the case and state of nutrition, paracentesis
may aid the diagnosis, since, if the fluid is turbid, highly
albuminous, with a large proportion of coagulable fibrin, it is an
evidence of inflammatory origin; but if it is clear, limpid, and on
standing gives but a delicate veil of pseudo-fibrin, it indicates a
passive or mechanical cause. Hemorrhagic exudation is only of relative
importance. The recognition of pleural friction râles over parts flat
on percussion will be an evidence of tumor. Hæmoptysis in this {879}
association would negative the idea of simple effusion. The presence of
signs of pressure on central parts is indicative of tumor (Walsh), but
Powell has recorded an instance of simple pleural effusion accompanied
by husky voice and laryngeal cough; and also an instance in which, from
a similar cause, there was increased size, tortuosity, and throbbing of
the radial and brachial arteries on the affected side without oedema of
the limb, yet probably attributable to obstruction of the return
circulation.

Enlarged glands in the neck, or enlarged veins with evidence of
thrombosis of the descending vena cava, would indicate tumor. Dulness
from a tumor itself might resemble sacculated effusion, yet there might
be retraction in place of distension of the chest, and particularly
characteristic dulness in the mediastinal region as compared with the
circumferential regions, or peripheral patches of resonance may be
suggestive and lead to critical revision of the symptoms.

From Chronic Pneumonia.--Mediastinal growth invading the lung from its
root has been mistaken for chronic pneumonia. Walsh lays stress on the
following signs as distinguishing tumor: 1. A tendency to increase
instead of diminution of bulk of the affected side. 2. Implication of
the mediastinum, with dyspnoea out of proportion to the extent of
consolidation. 3. Different characters of respiration in the two
diseases. To these may be added pressure symptoms in general in cases
of tumor, with displacement of the heart toward the side unaffected by
the pulmonary process. Hæmoptysis is very often a concomitant of
bronchial pressure, but occurs so frequently in basic pneumonia,
especially in the syphilitic, that it is devoid of importance except
from the standpoint of relative investigation. With reference to
symptoms of bronchial irritation without assignable cause, we should
always do well to remember the observation of Stokes, that they may be
characteristic of disseminated morbid process.

Differentiation of Malignant Growths.--The younger the patient the more
probable the existence of lymphoma or sarcoma. The majority of primary
tumors of the mediastinum are lymphomatous, and when the growths
originate in the anterior space they are almost certainly
lympho-sarcoma or sarcoma. Widespread enlargement of the lymphatic
glands, with or without enlargement of the spleen, indicates a
lymphadenoma.

Finally, primary lympho-sarcoma or sarcoma tends to spread by extension
of the process by continuity of structure, although secondary forms of
the process present lesions distributed through the lungs.

The evidence in favor of sarcoma may be drawn from exclusion of the
other forms of morbid process, from the rapidity of the growth, and
from the history of previous operative interference for the removal of
foreign growth, especially if the previous disease were sarcomatous.

Carcinomata may be suspected in cases in which there has been an
hereditary predisposition to carcinomatous disease or the previous or
concomitant existence of cancerous disease in the mammæ or elsewhere,
particularly if the period of life is relatively advanced. The
development of the tumor may be more slow than other forms of growth,
and is associated with tendency to progressive emaciation in the
absence of evidences of direct pressure on the oesophagus and the
existence of cachexia. Carcinomatous disease is more commonly
coincident with the presence of hard, nodular, immovable masses in the
neck.

Cystic tumors present signs of fluctuation. Syphilitic gummata must be
diagnosticated by exclusion and the existence of the syphilitic
history. The possibility of substernal thickening due to syphilis, with
reflex disturbances, particularly oesophageal spasm, must be borne in
mind.

Those rare forms of disease due to hyperplasia or caseous deposit in
the thoracic glands, independent of pulmonary disease, must be
recognized by {880} exclusion. The fact must be remembered that with
great enlargement of glands in the neck and elsewhere the bronchial
glands may remain constantly unaffected.

TREATMENT.--From the inaccessible location of these growths but little
assistance can be rendered by surgery. The progress of this branch of
science has of recent years included resection or excision of the
sternum or some of the ribs for the removal of growths involving the
mediastinum or pleura. Küster[29] has successfully made partial
resections of the sternum for the removal of mediastinal tumors, and
the entire bone has been excised by König[30] in a case of sarcoma. The
pericardial and both pleural cavities were opened in the course of the
dissection; the wound became gangrenous, and the heart was afterward
surrounded with pus: notwithstanding this, the wound slowly healed and
the patient ultimately recovered. In cases treated by this method
pleural adhesions usually prevent double pneumothorax; portions of the
ribs have been resected with the sternum, and have been succeeded by
unilateral pneumothorax, and recovery has ensued. (See Fig. 55.)

[Footnote 29: _Berliner klinische Wochenschrift_, No. 20, 1883, pp.
127, 136, 274.]

[Footnote 30: _Centralblatt f. Chir._, No. 42, 1882.]

[Illustration: FIG. 55. From a case of Kolaczek's, in which the
resection of the third to the sixth ribs, with a portion of the
sternum, was practised for the removal of an enchondroma. Diagram
exhibits the aperture in the thoracic wall which permitted the exposure
of the pericardium. Pneumothorax occurred, but patient recovered
(_Deutsches Archiv für klinische Medicin_, Bd. xxx. 1882).]

Paracentesis must sometimes be practised to relieve accumulation of
fluid in the pleural sacs in instances in which dyspnoea is serious,
and life may be prolonged by repeatedly practising this operation.
Reflex laryngeal irritation, or paroxysmal dyspnoea with stridulous
breathing, requires the use of inhalations or atomization of
antispasmodics, and among the most useful of these are ether and
chloroform. This group of neural symptoms can sometimes be markedly
palliated by hypodermic use of morphia with atropia. But too often the
symptoms are caused by actual pressure, and not by nerve-irritation,
and this mode of treatment is futile, and therefore these measures
should be employed with caution.

{881} Sleeplessness, cough, bronchial or other pulmonary complications,
must be managed upon general principles. The local pains may be met by
local treatment, such as mustard sinapisms or soothing lotions; even
blisters may secure temporary relief. The digestive system should be
carefully studied, and assimilable and appropriate food should be
selected. In lymphadenoma combinations of iodine with arsenic, as in
Donovan's solution, may be tried, but, unfortunately, the utmost aid
from present resources consists in a palliative and expectant policy.




{882}

DISEASES OF THE BLOOD AND BLOOD-GLANDULAR SYSTEM.

BY WILLIAM OSLER, M.D.


INTRODUCTION.

The blood is a fluid tissue composed of cells floating in an albuminous
plasma, and it differs from other tissues not less in the arrangement
of its elements than in the activity of the changes which go on in it.
It is the mart into which is poured from the alimentary canal the
commodities needed in nutrition, and the elements of the body select
from it the various materials which they require, giving in exchange
those chemical combinations which result from the metabolism of the
tissues. In spite of ceaseless changes, a uniformity of composition is
one of the most striking features of the blood in health. This is
maintained, as regards the constituents of the plasma, by the activity
of the organs which regulate income and expenditure--the alimentary
canal and liver on the one hand, and the kidneys, lungs, and skin on
the other; while histological uniformity is maintained by the adenoid
or cytogenous tissue throughout the body, the function of which is to
replace the wornout blood-corpuscles.

The corpuscles form rather less than one-half by weight of the blood.
The plasma contains about 90 per cent. of water, which holds in
solution proteids in the form of serum, albumen, and the fibrin-forming
factors; sugar in traces; creatin, hypoxanthin, and urea; various fatty
bodies in small amount; salts, chiefly sodium; and gases. The
corpuscles (red) consist of hæmoglobin (90 per cent.), proteid bodies,
and traces of lecithin and cholesterin.

So far as we know at present of the function of these two portions of
the blood, the plasma ministers to the general nutrition of the
tissues, while the corpuscles (red) are chiefly concerned with
respiratory processes, acting as the carriers of oxygen and carbonic
oxide.

We shall first give a brief account of the histological characters of
the blood, and of the relation of the groups of adenoid or cytogenous
tissue to the corpuscles.

Two forms of corpuscles are usually described, but we can recognize
four varieties of blood-corpuscles in the body: (1) red, (2) white, (3)
nucleated red, and (4) the hæmatoblasts (Hayem), or blood-plates of
Bizzozero.

(1) Red Corpuscles.--In each cubic millimeter of plasma there are about
5,000,000 red cells. The percentage may vary within health limits from
90 to 110. The corpuscles are circular, non-nucleated, biconcave disks,
homogeneous, to ordinary inspection structureless, and consist of a
colorless stroma which is possibly reticulated, and a red coloring
matter, the hæmoglobin. In {883} health they are tolerably uniform in
size, about 7.9 µ[1] in diameter, or in English measurement 1/3200 of
an inch (Gulliver). Even in normal blood there may be slight variations
in size between 6.5 µ and 8.5 µ, the average, according to Hayem, being
7.5 µ.

[Footnote 1: µ is used to signify a micro-millimeter or 1/1000 part of
a millimeter.]

(2) Colorless or white corpuscles, nucleated masses of protoplasm, with
an average diameter of 10 µ, or about 1/2500 of an inch. The majority
have a finely granular protoplasm, but in a few the granules are coarse
and do not completely fill the clear protoplasm. The ultimate structure
is reticular (Heitzman). Erhlich[2] has shown by their varying reaction
to eosin that there are chemical differences among the colorless cells
quite unrecognizable by other means. In healthy blood they display
active amoeboid changes at ordinary temperatures. Their protoplasm does
not, as is commonly stated, rapidly disintegrate, but if kept at a
medium temperature retains its vitality, as shown by movements, for
hours. The number per cubic millimeter is from 8 to 15 millions, and
the ratio to the red is variously computed as 1 to 300 or 1 to 500.

[Footnote 2: _Frerichs find Leyden's Archiv_, Bd. i.]

(3) Nucleated red corpuscles, which occur in the blood of the foetus
and the infant, gradually diminishing until at the third or fourth year
they disappear. In the adult they do not occur in the blood in health,
but are normal constituents of the red marrow of the short bones. They
measure from 1/1500 to 1/2000 of an inch, and are of somewhat variable
intensity of color, often quite as deep as the ordinary red forms.
There may be two or even three nuclei, not colored, grouped together,
often eccentric, and in some instances protruding from the cell.

(4) The hæmatoblasts of Hayem, the blood-plates of Bizzozero, the
elementary or intermediate corpuscles, are small discoid colorless
corpuscles about 3 µ in diameter, and are normal constituents of
healthy blood. When the blood is withdrawn, they aggregate together
into irregular clumps or masses, which have long been known as
Schultze's granule-masses. It can be readily demonstrated in new-born
rats or kittens, in which these masses abound, that the corpuscles
composing them are isolated in the vessels, and only run together when
the blood is drawn. The statement is commonly made that the
granule-masses of Schultze result from the disintegration of the white
corpuscle (of the red, Erhlich), but half an hour's study of the
question in a new-born rat will convince any competent histologist that
we have here to do with a separate blood-element.[3] It appears to have
important relations with the production of fibrin.

[Footnote 3: Consult _Proceedings Royal Society_, 1874; _Centralblatt
f. d. Med. Wissenschaften_; _Medical News_, 1882, 2; Bizzozero,
_Virchow's Archiv_, Bd. xi.; Hayem, _Recherches sur l'Anatomie normal
et pathologique du Sang_, Paris, 1878.]

Of the origin and life-history of the red corpuscles during
post-embryonic life we have still much to learn. They are stated to
develop--

(1) From colorless corpuscles, the lymph-cells or leucocytes. In the
lymph-glands, the Malpighian bodies of the spleen, in the thymus, or
the adenoid tissue of the tonsil, of the lymph-elements in the
intestines and other regions, colorless cells are constantly being
manufactured, and the general belief has been since Hewson's time that
the red corpuscles develop in some way or other from these leucocytes.
How or where has not yet been settled. It does not apparently go on in
the blood, or we should surely catch, in the many observations and with
the excellent powers now in use, a glimpse of the birth of one of them.
Some observers (Johnstone[4]) maintain that they develop from the
granular protoplasm of the adenoid reticulum by a process of budding.
This may be so, but we should expect to find the lymph in the efferent
{884} vessels and of the thoracic duct much more rich in red cells than
is usually the case, and in specimens of healthy glands we should find
young-looking elements such as he describes.

[Footnote 4: _Seguin's Archiv_, vol. vi.]

(2) From the nucleated red corpuscles. In the embryo this undoubtedly
takes place, and as the weeks of development proceed, the ordinary red
forms gradually predominate. In the child the red nucleated cells
disappear early, and are then found only in the red marrow. So far as
my observations go,[5] they apparently originate from colorless
marrow-cells, which gradually become more homogeneous, and hæmoglobin
develops in the protoplasm. The nucleus degenerates and disappears,
when the cell has the appearance of an ordinary red disk. Rindfleisch
thinks that the nucleus of the nucleated red is extruded in the
development. It is possible that from these nucleated red corpuscles
cells may originate in another way--viz. by budding. This I have seen
and sketched in the marrow-cells,[6] and Malassez has studied the same
process.[7] The gemmæ are small, and sprout from the protoplasm, not
the nuclei, and when they break off they resemble the microcytes which
occur so abundantly in certain anæmic states. Bizzozero[8] holds that
these nucleated red corpuscles are independent elements which do not
develop from the colorless marrow-cells. They multiply by fission, and
develop into the ordinary red forms with the disappearance of the
nuclei. Several recent investigations support this view.[9]

[Footnote 5: _Centralblatt f. d. Med. Wissensch._, 1878.]

[Footnote 6: _Trans. Am. Ass. Ad. Science_, 1882.]

[Footnote 7: _Archives de Physiologie_, 1882.]

[Footnote 8: _Centralblatt f. d. Med. Wissenschaften_, Bd. xix.]

[Footnote 9: _Fortschritte der Medicin_, 1885, No. 1.]

(3) Hayem believes that the red corpuscles develop from the small
hæmatoblasts, but, so far as I know, his observations have never been
confirmed. He states that in normal blood they occur in the proportion
of about 1 to 20 red. In all states of blood reparation they increase
greatly. He describes a hæmatoblastic crisis as occurring after
hemorrhage, fevers, etc., when the number of these elements rapidly
augments, and is succeeded by the addition of many small pale-red
corpuscles, which he looks upon as intermediate between the
hæmatoblasts and the ordinary red forms.

The colorless corpuscles are regarded as the direct offspring of the
cells of the follicular cords in the lymph-glands and adenoid tissue,
but whether by process of division of existing leucocytes or by
sprouting from the endothelial places, or from the protoplasm in the
fibres of the reticulum, remains to be settled.

The nucleated red corpuscles are in the healthy adult confined to red
marrow, in which they probably develop from colorless cells, and may be
regarded, as Neumann originally suggested, as transitional or
intermediate forms between white and red cells. In anæmic states they
may occur in the spleen and in the lymph-glands.

Of the origin of the hæmatoblasts or blood-plates we know absolutely
nothing. They occur most abundantly under two most opposite
conditions--in the young growing animal just entering upon life, and in
the diseased, cachectic, wornout animal just preparing to abandon it.

Our knowledge of the relation of the cytogenetic organs to
blood-formation may be thus briefly stated: The spleen certainly takes
part in the development of colorless corpuscles, but its participation
in red blood-formation is more doubtful. The nucleated red or embryonal
forms do not occur, at least in any numbers, in health, though some
observers have noted that after a repeated bleeding the organ was
swollen and contained many such cells, as if it was the seat of an
active development. Though the opinion prevails widely that the spleen
is one of the important organs in the formation of red corpuscles, the
evidence for this belief is of an exceedingly scanty nature.

The lymphatic glands and the adenoid tissue in other regions are the
seats {885} of constant production of colorless corpuscles, but of
their relation to the red corpuscles there is the same lack of
information as in the spleen. I do not know of any corroboration of the
observation of Johnstone above mentioned, and in any case the number of
red cells in the efferent vessels of a lymph-gland is so small--and
indeed in the thoracic duct itself--that we cannot believe they are
produced as red corpuscles in large numbers within the lymphatic
system.

The red bone-marrow, as pointed out by Neumann[10] and Bizzozero,[11]
appears to be the seat of blood-formation, and in the adult body is the
only region in which the embryonic or nucleated red cells are found. It
is a tissue similar in many respects to the spleen, and, though
confined to the short and flat bones, the total amount in the body is
very considerable. In the young it also fills the long bones. The
evidence of the development of red corpuscles in the marrow rests upon
the constant presence of nucleated cells infiltrated with hæmoglobin,
and of their fission. Forms undergoing the process of karyokinesis can
be seen without difficulty. In excessive hemorrhage, natural or
induced, it appears to undergo an active proliferation, and in the long
bones a red marrow may replace the fatty tissue.

[Footnote 10: _Centralblatt f. d. Med. Wissenschaften_, 1868.]

[Footnote 11: _Ibid._, 1868.]

The liver is doubtless the seat of blood-destruction, for the
bile-pigments and leucocytes with red corpuscles in their interior have
been found in its tissue. Nicolaides[12] has shown that in the blood of
the hepatic vein there may be a reduction of from one million to one
million and a half of red corpuscles per c.m. In the embryo Neumann[13]
has shown that it may be the seat of the production of corpuscles, but
there is no satisfactory evidence that in the adult this ever takes
place.

[Footnote 12: _Archives de Physiologie_, 1882.]

[Footnote 13: _Archiv der Heilkunde_, xv.]

The remarkable rapidity with which, after a profuse bleeding, the
normal proportion of red corpuscles is reached shows with what activity
the development may proceed, and how favorable the conditions must be
for their production. After the loss of a large quantity of blood the
manufacture of new corpuscles may proceed at the rate of 30,000,
40,000, or even 50,000 a day.

What becomes of the red corpuscles? Here, again, is a question not
satisfactorily settled. We do not know the average length of life of
corpuscles. They are supposed to be short-lived--three weeks, according
to Quincke. The need for their dissolution is assumed to provide
pigment for the various secretions and tissues, and we occasionally see
a few cells in the blood with a pallor which may be regarded as an
indication of senility.

Positive evidence, however, of their destruction is afforded by the
occurrence of the so-called corpuscles containing red corpuscles, which
occur normally in red marrow and in the spleen, and under some
circumstances in the lymphatic glands and liver. The red cells undergo
gradual transformation into a yellow granular, and finally black,
pigment. In normal spleen and marrow the numbers found are very
variable; in fevers and cachectic states they may be in extraordinary
numbers. Quincke and his pupil Peters[14] have studied with great care
this process of transformation of the red corpuscles and accumulation
of the pigment in the cells of the marrow, spleen, liver, and
lymph-glands, to which the term siderosis is applied. These
pigment-granules are in the form of an iron albuminate, and are used in
the development of new corpuscles. Thus, after repeated bleedings in
animals, they may disappear completely in the restoration of the blood,
while in animals into whose vessels blood has been transfused or
injected subcutaneously the iron-containing cells in the various organs
are very numerous, and even the cortical cells of the kidney contain
numerous granules.

[Footnote 14: _Deutsches Archiv f. klin. Med._, Bds. xxv., xxvii.,
xxxii., xxxiii.]

The amount of hæmoglobin in 100 grammes of healthy blood is {886} 13.45
grm. (Preyer). Malassez estimated the quantity in a cubic millimeter of
blood at between 0.125 and 0.134 milligramme, and, taking the
corpuscular richness at from 4,000,000 to 4,600,000, he has estimated
approximately the amount of hæmoglobin in each corpuscle.


PLETHORA.

General and persistent polyæmia or plethora has scarcely a place in
recent pathology. Formerly it was thought that either from
over-production or lowered expenditure the total amount of blood
accumulated and filled the blood-vessels to an abnormal extent. The
amount of blood undergoes, within limits, constant daily alterations,
and after a full meal the vessels are in a state of plethora compared
with their condition at the end of a ten hours' fast. If a
plethysmograph could be devised to record graphically the variations in
the total quantity of blood, each ingestion of food or drink into the
vessels would be followed by a rise, and each interval by a gradual
decline. So long as the organs of secretion and excretion are active
the quantitative and qualitative condition of the blood is maintained
at a tolerably uniform standard in each individual. At different
periods of life the relation of blood-weight to body-weight varies. In
the new-born the blood amounts to one-eighteenth part by weight of the
body, while in the adult the average is from one-twelfth to
one-fourteenth; so that in the infant there is a condition of
comparative plethora. There are no reliable observations on the
proportion of blood- to body-weight at respective ages, but there
appears to be a reduction in old age. In women it is stated that just
before each menstrual period there is a state of polyæmia.[15]

[Footnote 15: Mary Putnam Jacobi, _The Question of Rest for Women_, New
York.]

Worm-Müller[16] and Cohnheim[17] have made some very interesting
experiments on this question of plethora. By transfusion in dogs a
state of artificial plethora is readily established, and the animals
stand the injection of as much as 10 or 12 per cent. of the body-weight
of blood, above which quantity a fatal result ensues. After an
injection of 20 or 30 per cent. of the total amount of blood, the
superfluous plasma and corpuscles are got rid of in a few days, while
with a larger injection of 60 to 80 per cent. it takes two or three
weeks before the normal state is again reached. The albuminous and
nitrogenous materials are largely got rid of by the urine, which
increases rapidly in quantity and also in the amount of urea. The
excess of corpuscles gradually disappears, and the hæmoglobin becomes
deposited, as Quincke has shown, in the form of small granules in the
cells of the liver, spleen, and bone-marrow.

[Footnote 16: _Transfusion and Plethora_, Christiania, 1875.]

[Footnote 17: _Allgemeine Pathologie_, 2te Auflage.]

In a similar way, it is reasonable to think that the body is quite
capable of disposing of surplus albuminous materials in over-fed, lazy
individuals with active digestion, whose red faces, full vessels, and
bounding pulses give the impression of a distended circulatory system,
and whom we term plethoric. Their appearance is the result rather of
blood-distribution than of actual increase in the total volume, and
there is no evidence that under any circumstances a rich and abundant
diet without much exercise can permanently increase the amount of
blood. It was formerly held that the healing of an old sore or the
cessation of an accustomed discharge or loss of blood, by diminishing
expenditure while the blood-making power was maintained, could induce
plethora if no local disorder was excited "before the vessels {887} in
general reached a state of plethoric tension." Of such a condition, and
of the plethora apocoptica that was thought to occur after the
amputation of a limb, we do not hear much now, and the prevalent
opinion of pathologists is expressed by Cohnheim, when he says "that,
except as a transitory state, polyæmia does not occur under any
circumstances." What, then, is the meaning of the full-blooded,
rubicund condition which we see in some men, not necessarily large
feeders, but often with vigorous active constitutions and perfect types
of health? The appearance of plethora is caused chiefly by the
distension of the superficial vessels; the circulation of the skin is
remarkably active, particularly in the face, and it is probable that we
have here to deal with local peculiarities of the vessels or of their
innervation, and not with any general augmentation of the total
blood-mass. It may be, however, that in such persons there is a
plethora of certain of the constituents of the blood--viz. the red
corpuscles--and there may be a state of polycythæmia rubra, as it has
been called, in which the percentage of red cells is increased. In
several such cases I have found, as has been previously noted, the
number of red corpuscles considerably over the average. A relative
increase in the number of red corpuscles also occurs in those sudden
and excessive losses of fluid, as in cholera, in which the blood may
become thick and sticky from the great reduction in the plasma,
particularly of the water and salts--anhydræmia--or in cases in which
the income of fluid is greatly restricted. Henry (F. P.) has recorded a
case[18] of stenosis of the cardia, in which, with great emaciation,
the corpuscles per c.m. were 5,525,000.

[Footnote 18: _Archives of Medicine_, New York, vol. vii.]

The condition known as hydræmic plethora develops whenever there is a
great reduction in the number of corpuscles, as after a hemorrhage, or
when the blood has been impoverished by long-standing suppuration,
albuminuria, or in the growth of large tumors. So also when the
secretion of urine is diminished, as in some cases of Bright's disease,
and at the same time charged with albumen, the blood may become very
watery; but in these states there is not an absolute increase in the
entire blood, but only a relative excess of the water. Occasionally,
this great excess can be noticed in the blood-drop as it comes from the
finger-tip; the corpuscles do not fill the entire drop, and
consequently leave irregular areas unoccupied by the red disks.


ANÆMIA.

A reduction in the amount of the blood or of its corpuscles occurs
under a great variety of circumstances. Broadly speaking, we can
recognize two great clinical and pathological groups of cases: I. Those
induced by causes acting upon the blood itself; and, II. Those induced
by disturbance in the functions of the blood-making organs.

I. Of causes acting directly upon the blood, we shall consider--

1st. Hemorrhage, traumatic or spontaneous. A high grade of anæmia may
be quickly produced by loss of a large quantity of blood, and the
reduction is in all the constituents; there is a true oligæmia. If the
amount lost be excessive, death results from the diminution in the
total volume of blood and general lowering of the arterial pressure. If
the hemorrhage is sudden and profuse, as from a large vessel, the loss
of four or five pounds of blood, or even less, may be sufficient to
induce fatal syncope. In hemorrhage into the pleura or peritoneum from
rupture of aneurisms, etc., it is rare to meet with more than three or
four pounds of clot and serum; seven and a half {888} pounds is the
largest amount I know of shed into one of the cavities (pleura) by
rupture of an aneurism. When the bleeding extends over several days,
the amount lost may be very much greater. In cases of hæmophilia
extraordinary accounts are given of the amount collected in the course
of a few days. In a case of hæmoptysis a patient lost over ten pounds
by measurement in one week, and then recovered from the immediate
effects. After the most severe hemorrhages the reduction in the number
of red corpuscles is not nearly so great as in forms of idiopathic
anæmia. Thus in the case just mentioned at the termination of the week
of bleeding there were 1,390,000 red corpuscles to the cubic
millimeter. In any single bleeding a fatal result follows the loss of
one-third or one-half of the total blood-volume. The process of
regeneration of the blood goes on with astonishing rapidity, and in
some bleeders a week or ten days will suffice to re-establish the
normal amount. The restitution begins even during a hemorrhage by the
absorption of lymph from the tissues under the lowered pressure in the
vessels. The dryness and stickiness of the serous membranes after death
from a profuse hemorrhage is usually very marked. The water and saline
constituents of the blood are readily restored by absorption from the
gastro-intestinal tract. The albuminous elements are also quickly
renewed, but it may take weeks or months before the number of
corpuscles reaches the normal standard. Indeed, this condition of
oligocythæmia, as it is called, may persist, grow worse, and ultimately
prove fatal. The microscopical characters of the blood after severe
hemorrhage are not much changed, except as regards the white
corpuscles, which are relatively increased, and the fibrin network,
which is much less marked than in health. The white corpuscles may be
very slightly reduced in number per cubic millimeter--a fact to be
accounted for either by a relatively diminished loss during the
bleeding, owing to their adhesiveness and wall-loving properties, or to
a quick restitution from the lymph which is poured into the
blood-stream. It has been observed both in dogs and men by Lyon[19]
that after a severe hemorrhage the number of red per cubic millimeter
diminished for several days after the bleeding had been checked. How
and where does the regeneration of red corpuscles take place after a
severe hemorrhage? One would think that under these circumstances, if
any, we should be able to get information which might be of service in
determining the problem of blood-development; but, in spite of the
numerous experiments on the subject, we are still far from a knowledge
of full details. The observations of Neumann,[20] Litten and Orth,[21]
Bizzozero,[22] Lepine,[23] and others appear to prove conclusively that
the bone-marrow plays an important part in the formation of the new red
disks, becoming lymphoid, losing its fat, and the nucleated red cells
increase enormously. The same process has been observed in many cases
in man. In a case of profuse metrorrhagia with profound anæmia
Neumann[24] found the marrow in all the bones of a rich raspberry red,
full of the nucleated forms, which were also very abundant in the
blood, and more in the vena azygos than in the aorta. The evidence in
favor of the active participation of the spleen is not so conclusive.
Neumann[25] concludes that the spleen takes no share in the process,
and holds that the nucleated red cells found in it are probably derived
from the bone-marrow. Bizzozero, on the other hand, has found the
spleen swollen and showing signs of lively blood-formation. He states
that after removal of the spleen the restitution of the red corpuscles
takes place much more slowly. Pouchet, on the contrary, says the
regeneration goes on just as rapidly without the spleen. {889} Of the
action of the lymph-glands there is even less evidence. They have been
found swollen, but in traumatic anæmia I do not know of any
observations on their swelling and conversion into a red spleen-like
tissue, such as have been found in some cases of idiopathic anæmia.

[Footnote 19: Of Norwich, Conn.: _Virchow's Archiv_, lxxxiv.]

[Footnote 20: _Archiv der Heilkunde_, Bd. x.; _Frerichs and Leyden's
Archiv_, Bd. iii.]

[Footnote 21: _Berliner klin. Wochenschrift_, 1877, li.]

[Footnote 22: _Centralblatt f. d. Med. Wissenschaften_, 1879, xvi.]

[Footnote 23: _Revue Mensuelle de Méd. et de Chirurg._, 1877.]

[Footnote 24: _Loc. cit._]

[Footnote 25: _Loc. cit._]

The microcytes which occur in numbers in blood in some cases of
traumatic anæmia have been regarded as young developmental forms, but
there is a great diversity of opinion as to their real nature, and
their connection with productive blood-processes is somewhat doubtful.

Cohnheim suggests[26] that after a profuse hemorrhage the rapid
consumption of red corpuscles may be reduced, in which case we need not
suppose such an active development; but the fact noted by Lyon[27] and
others of the increased reduction after a bleeding is against the view.
In any case, if Quincke is right in assuming that the average life of a
red corpuscle is only three or four weeks, what is the restitution of a
couple of millions of corpuscles per cubic millimeter in comparison
with the monthly renovation of the entire mass?

[Footnote 26: _Loc. cit._]

[Footnote 27: _Loc. cit._]

In the regeneration of the blood the development of the hæmoglobin does
not keep pace with that of the corpuscles, so that they may, even when
normal in amount, have a lowered hæmoglobin percentage, indicated under
the microscope by a paleness in the cells.

2d. There is a large group of cases in which the anæmia is induced by a
long-continued drain on the albuminous material of the blood--pus in a
chronic suppuration, albumen in Bright's disease, prolonged lactation,
etc. Rapidly-growing tumors act in the same way.

3d. The anæmia of inanition, brought about by defective food-supply or
by conditions of the digestive organs which interfere with the proper
reception and preparation of nourishment, as cancer of the gullet,
chronic dyspepsia, etc. The reduction in the blood-mass may be extreme,
but the plasma suffers proportionately more than the corpuscles, which
even in the extreme wasting of cancer of the oesophagus may not be
reduced more than one-half or three-fourths.

4th. Toxic anæmia, induced by the action of certain poisons in the
blood, such as lead, mercury, and arsenic among inorganic substances,
and the virus of syphilis and malaria among organic poisons. They act
by increasing the rate of consumption of the red corpuscles, and the
reduction may be considerable. The gradual impoverishment of the blood
in pyrexia may be in part due to the toxic action of the
fever-producing agent on the blood itself; but in this there is
probably also disturbance of function in the blood-making organs.

The last three groups comprise what are known as secondary anæmias, and
the condition of the blood is characterized by an increase in the water
and diminution in the albuminous elements; the fibrin is often
increased, and the network which separates, as seen under the
microscope, is unusually dense; the white corpuscles are not much
increased; there is rarely microcytosis or poikilocytosis; the
reduction in the number of red corpuscles is not so great; hemorrhages
do not often occur; when fever is present it is due to the disease or
some complication, and is not the pyrexia of anæmia; and, lastly, they
are more or less amenable to the action of iron and other remedies.

II. A consideration of the anæmias induced by disturbance in the
blood-making organs themselves presents difficulties proportionate to
our ignorance of the details of hæmatogenesis. We may regard, as above
stated, the spleen, the general lymphatic tissue, and the marrow as the
sites of production of corpuscles which are passed into the circulation
fully formed. Certain of these organs--the spleen and marrow
particularly--are also concerned with blood-destruction as well as
blood-elaboration; but there is evidence to show[28] that {890} they,
to use an ordinary simile, consume their own smoke, using the waste
products for the purpose of further manufacture. Looking now upon the
hæmatogenetic tissues as a single organ scattered through the body, let
us consider what general disturbances of function it may suffer
comparable to those met with in other structures. We can evidently
suppose the physiological activity to be diminished or increased, and
we should expect to find corresponding to these changes equivalent
alterations in the character of the blood. Unfortunately, our knowledge
of the normal processes as they go on in these tissues is so scanty
that it amounts to a discussion upon the disturbances of a function
itself imperfectly understood.

[Footnote 28: Quincke, quoted above.]

With diminished functional activity in an organ we commonly meet with
reduction in volume, the one depending on the other: now, the only
instance in the blood-making organs in which a decrease in size and
diminished functional activity go together is in the senile atrophy in
which the spleen becomes small, the marrow more fatty, and the
lymph-glands sclerotic, and in consequence the blood also is reduced in
amount; but this is only a part of the general failure of nutrition in
old age. Pathologically, there is no such well-recognized condition of
uniform atrophy of spleen, lymph-gland, and bone-marrow, with a
corresponding general reduction in the elements of the blood. Certain
cases of idiopathic anæmia come close to it, in which these parts are
wasted, but there are other differences which make the two conditions
scarcely comparable. In fact, as we shall see, diminished activity in
blood-making is usually associated with an increase in what we call
hæmatogenetic tissues. Of increased functional activity in these parts
we know very little, apart from the changes met with in cases of
traumatic anæmia, in which the hyperplasia of the spleen and
bone-marrow may be regarded as intimately connected with the rapid
development of red corpuscles.

One fact is evident: that a progressive increase in the cytogenic
tissues, local or general, is associated with disturbance in the
process of blood-formation, and sooner or later induces anæmia. Thus,
progressive enlargement of the spleen or of the lymph-glands or marked
hyperplasia of the marrow, either singly or combined, is invariably
accompanied with alteration in the characters of the blood. Even in
those rare instances in which the lymphoid elements of the tonsils and
fauces or of the gastro-intestinal canal are chiefly involved the same
change may take place.

The nature of the process in the organs is of a hyperplastic character.
In the spleen the pulp at first increases and the Malpighian bodies
enlarge, but ultimately there is such a development of the fibrous
reticulum that the consistence is greatly augmented and the organ
becomes indurated. Histologically, there is very little distinction to
be made between forms of chronic enlargement of this organ. In the
lymph-glands there is increase in the cells; the tissue becomes more
succulent, and is in a state of hyperplasia which may terminate in a
great development of the fibrous elements, with induration. So also
with the bone-marrow: in the short and flat bones, where in the adult a
reddish or slightly fatty tissue exists, the fat disappears entirely,
and the long bones, normally filled with yellow marrow, become occupied
with a red-gray or greenish-gray cytogenous tissue not unlike
spleen-pulp, and in many instances more consistent than the red marrow
of early life.

A reduction in the number of red corpuscles is the chief and most
constant change in the blood; anæmia seems to be the invariable result,
whether the spleen, marrow, or lymph-glands are affected singly or
together, and is the central feature in the entire group of cases. This
diminution in the red cells may or may not be accompanied by an
increase in the white corpuscles, which in some cases may be so
striking as to be regarded as the special blood-change, and is, as a
rule, permanent, though it may be a variable or even a transitory
state.

{891} The general and histological differences between forms of
hypertrophy of these blood-making organs are exceedingly slight, and in
their clinical features they present a large number of symptoms in
common; indeed, we may say that all the important symptoms are present,
whether the spleen is affected alone or with the lymph-glands and
bone-marrow, or whether these parts are independently involved, and
whether there is simple reduction in the red or with it an increase in
the white corpuscles. Such common features are--the progressive anæmia
with its group of circulatory symptoms; the irregular febrile reaction,
essential fever of anæmia; the absence of marked emaciation; the
tendency to effusions of serum; the progressive debility; the
occurrence of hemorrhages; gastric and intestinal disturbances; and
resistance to treatment.

The affections characterized pathologically and clinically by so many
similar features are known and recognized as distinct diseases under
the names leukæmia, Hodgkin's disease or pseudo-leukæmia, splenic
anæmia, and idiopathic anæmia (some cases); and we shall now consider
these a little more closely.

First, of the hyperplasias of the cytogenic tissues associated with
simple anæmia. The various groups, spleen, lymph-glands, and marrow,
may be involved singly or together; usually one is first affected, and
the others, if at all, subsequently. Progressive enlargement of the
spleen induces sooner or later anæmia, the anæmia splenica of
Griesinger. These cases are by no means rare: certain of them represent
the final stage of a malarial intoxication, but there are others in
which the enlargement seems causeless. There may also be hyperplasia of
the bone-marrow, less often of the lymph-glands. The anæmia may be
profound, and the clinical picture is that mentioned above. Two cases
of it under my care died of hæmatemesis. The diagnosis of this
affection from splenic leukæmia rests solely on the microscopical
examination of the blood. It is also classed as the splenic form of
Hodgkin's disease or pseudo-leukæmia.

Primary enlargement of the lymph-glands with anæmia constitutes
Hodgkin's disease or pseudo-leukæmia, in which there may be general
hyperplasia of the lymphatic elements throughout the body, with nodular
growths of adenoid tissue in other organs. The spleen and marrow are
not often affected. Here, too, the diagnosis from lymphatic leukæmia
rests with the microscope.

Is there a form of anæmia dependent upon hyperplasia of the
bone-marrow--an anæmia medullaris? In 1875, Pepper and Tyson[29] found
affection of the marrow in idiopathic anæmia, and Pepper suggested that
this might be the starting-point of the disease, which could thus be
regarded as a medullary form of pseudo-leukæmia. Cohnheim in 1876[30]
described the same condition, and I had an opportunity of examining
several cases.[31] Granting that the marrow is a tissue which shares in
the blood-making functions, it seemed reasonable to suppose that a
general hyperplasia of its elements might disturb the processes of
hæmatosis and produce anæmia, just as in hyperplasia of the spleen and
lymph-glands. Two facts soon came to light which seem opposed to this
explanation of the pathology of idiopathic anæmia. A hyperplasia of the
marrow was found in cases of chronic disease with wasting, and cases of
idiopathic anæmia were described in which the marrow was normal. The
numerous observations of the past five or six years have not brought us
nearer to a solution of the problem. The observations of Neumann,[32]
and those of Litten and Orth,[33] on the changes in the marrow in
chronic diseases have been abundantly confirmed, and a red lymphoid
marrow may be met with in various cachectic states. This, too, I have
frequently seen, {892} yet it is in my experience rare to find such
marked, rich hyperplasia of the marrow, such an entire absence of fat,
as in some cases of idiopathic anæmia. In 9 autopsies in typical cases
at Montreal, not parturition cases, the marrow of the long bones was
lymphoid and red in 6; in 1 it was not examined; in 1, which I did not
see, the marrow was stated to be normal; and in 1, an old woman over
sixty years of age, the marrow of the short bones was rich in lymphoid
cells and nucleated red corpuscles, and the long bones contained a
grayish gelatinoid--atrophic--marrow. It does not appear possible with
our present knowledge to arrive at a satisfactory conclusion on this
question. Some regard the marrow-change as the consequence, others as
the cause, of the anæmia. Both Cohnheim[34] and Pye-Smith[35] regard
those cases of idiopathic anæmia in which the marrow-changes are
pronounced as cases of anæmia medullaris.

[Footnote 29: _American Journal Med. Sciences_, 1875, ii.]

[Footnote 30: _Virchow's Archiv_, Bd. lxviii.]

[Footnote 31: _Centralblatt f. d. Med. Wissenschaften_, 1877, Nos. 15
and 28; 1878, No. 26.]

[Footnote 32: _Berl. klin. Wochenschrift_, 1877, xlvii.]

[Footnote 33: _Ibid._, 1877, li.]

[Footnote 34: _Loc. cit._, Bd. i. S. 467.]

[Footnote 35: _Loc cit._]

Next of the parallel series of hyperplasias of the blood-forming organs
with anæmia, plus an increase of the colorless corpuscles--leukæmia.
Here, too, we have the three forms--splenic, lymphatic, and medullary.

The splenic leukæmia is the most common, and in its general features is
identical with splenic anæmia, the excess of white corpuscles being the
only distinguishing feature. It is almost invariably associated with
changes in the marrow.

The lymphatic leukæmia may arise in connection with hyperplasia of the
lymph-glands or of the adenoid elements in the alimentary
tract--tonsils and Peyer's glands. It is much less common than
lymphatic anæmia or Hodgkin's disease, and there are not many
uncomplicated cases on record. Apparently, a very limited bunch of
glands--cervical--may induce the change in the blood.[36] Medullary
changes are almost invariably associated with a great increase of
colorless corpuscles in the blood, and a myelogenous form of leukæmia
is now, owing chiefly to the investigations of Neumann, well
established. Indeed, he would regard the change in this tissue as the
primary and important, and those in the lymph-glands and spleen as
secondary.

[Footnote 36: Gowers, _Reynolds's System of Medicine_, art.
"Leucocythæmia."]

The hyperplasia, either lymphadenoid in character or pyoid, may result
in the expansion and softening of the bones, with the production of
irregular tumor-like masses.

We have, then, the following group of anæmias induced by a primary
disturbance of function in the blood-making organs:

  PRIMARY OR | Leucocytic     | Splenic,   |
  CYTOGENIC  |                | Lymphatic, | Leukæmia.
  ANÆMIA.    |                | Medullary, |
             |
             | Non-leucocytic | Splenic, Anæmia splenica.
                              | Lymphatic, Hodgkin's disease.
                              | Medullary, Idiopathic anæmia
                                                       (certain cases).

There remain for consideration the relation of the tissue-change to the
anæmia and the nature of the leucocytosis; but until the chief facts in
the development of the corpuscles are thoroughly known we cannot expect
a satisfactory solution of these problems.

The anæmia may be explained on the view of diminished production
(anæmatosis) or increased consumption of the red corpuscles
(hæmophthisis). We know nothing of the intimate processes connected
with lessened production, but as anæmia so constantly accompanies the
hyperplasia, we assume they are intimately connected with each other,
and the diminution in the number of corpuscles in some way the result
of disturbed functional activity in the blood-making organs. An
increased consumption of corpuscles in anæmia is {893} indicated by the
presence in large numbers of cells containing red blood-corpuscles in
the spleen and marrow, and occasionally in the lymph-glands; by the
increased amount of iron which has been found in the liver; and in some
cases by the deep color of the muscles and an intensification of the
color of the urine. Either a failing production with normal rate of
consumption, or a normal output with heightened destruction, would
produce anæmia. Possibly, in some instances, both factors may prevail.
Quincke's interesting observations[37] may enable us to determine the
cases in which one or other has been dominant. Where there is great
destruction we shall expect to find the granules of iron albuminate in
the spleen, bone marrow, and liver-cells, possibly in the cells of the
cortex of the kidneys, and the iron reaction should be present.

[Footnote 37: _Loc. cit._]

The relation of the hyperplasia of the cytogenic tissues to the
increase in the colorless corpuscles is even more obscure. A prime
difficulty is the circumstance that apparently identical tissue-changes
may be associated with either a leucocytic or non-leucocytic anæmia.
The splenic hyperplasia of leukæmia and of anæmia splenica are
histologically identical. The excess of white corpuscles may be due
either to over-production or to failure in their transformation into
red. That they develop in the hyperplastic spleen, marrow, and
lymph-glands is not to be doubted, and it seems reasonable to attribute
the excess to the hyperplasia. Their variable size, as spleen or
lymph-glands are chiefly affected, was early observed by Virchow, and
when the marrow is involved there may be many large leucocytes similar
to the larger marrow-cells. Virchow's original explanation, that the
excess of colorless cells was due to a failure in their transformation
into red corpuscles, rests upon the presumption that such a
transformation is the normal process--a view not fully established. If
this is the case, we should expect to find some relation between the
increase of the white and the decrease in the red, but this is not
always constant; as a general rule, with a diminution of the white
there is an increase in the red, but the red and the white cells may
increase or diminish in numbers simultaneously, or, again, the
leucocytes may be greatly reduced while the red corpuscles remain about
stationary. Griesinger,[38] Biesiadecki,[39] and others regard the
increase in leucocytes as a primary blood-change. Several recent French
writers support this view, as Renant,[40] who believes that the unequal
size of the leucocytes indicates their division in the blood, and
Variot.[41] One of the most interesting features in connection with an
increase in the colorless cells is that it may be only transitory, and
a case which clinically and pathologically may present the features of
idiopathic anæmia to-day may to-morrow present the characters of
leukæmia; a case of splenic anæmia may become one of splenic leukæmia,
or vice versâ. Thus, in Litten's oft-quoted case--about which there can
be no doubt[42]--of acute anæmia of three weeks' duration, an enormous
increase of colorless corpuscles took place, and finally a ratio of one
white to four red was reached. Quite as interesting is the case of
Fleischer and Penzoldt,[43] in which for eight months the patient
presented the ordinary symptoms of anæmia lymphatica or Hodgkin's
disease, and then, before death, the blood became intensely leukæmic,
the ratio 1:9. Still more so as the case of Goodhart's,[44] in which,
with an enlarged spleen and lymphoid growths in liver and kidneys,
there were variations in the number of corpuscles every few days--at
one time great excess of white, at another no increase whatever. Again,
a case may early come under observation as one of leukæmia, with a
ratio of 1:20 or 1:30, and in the course of a few months, with
persistence or even aggravation of {894} the general symptoms, the
normal ratio of white to red may be reached. This was the history in
one of the Montreal cases.[45]

[Footnote 38: _Virch. Archiv_, Bd. v.]

[Footnote 39: _Wien. Med. Jahrbuch._, 1876.]

[Footnote 40: _Archives de Physiologie_, 1881.]

[Footnote 41: _Thèse de Paris_, 1882.]

[Footnote 42: _Berl. klin. Wochenschrift_, 1877.]

[Footnote 43: _Deutsches Archiv f. klin. Medicin_, Bd. xxvi.]

[Footnote 44: _Clin. Society's Transactions_, London, 1877.]

[Footnote 45: Howard, _Montreal General Hospital Reports_, vol. i. p.
39.]

It seems questionable whether such a variable feature as increase in
the colorless corpuscles should be permitted to separate diseases which
have all essential characters in common. We shall probably, however,
continue for a long time to speak of these conditions as separate and
distinct, but it is evident that as time goes on, and our knowledge of
the diseases and of blood-development increases, the identity of many
of them will be acknowledged, and we shall find that here, as so often
the case in natural history, the multiplication of species has been the
result of imperfect information, and that as points of resemblance in
essential characters and development are studied minor differences
disappear.

With reference to the general tissue-changes in anæmia there are two
points of interest: The metabolism of the proteids is increased, as
shown by the increased excretion of urea, and owing to defective
exudation the decomposition of the fats is lessened; hence the
retention of fat, or even increase, in anæmic persons. The influence of
repeated small bleedings in hastening the fattening of cattle has been
known since the time of Aristotle, and horse-dealers still affirm that
there is nothing like bloodletting to put an animal into good
condition.


CHLOROSIS

is a special form of anæmia distinguished by certain etiological and
anatomical peculiarities. In the first place, it is a disease of the
female sex; cases in the male are of extreme rarity. In the majority of
instances it is associated with disturbed menstrual function or with
the evolution of the reproductive organs at the period of puberty.
Occasionally it occurs in pregnant women and in children. It is a
common disease among the ill-fed, overworked young girls in large towns
who are confined all day in close, badly-lighted rooms or who have to
do much stair-climbing. Girls of the better classes are by no means
exempt; indeed, some writers speak of it as specially prone to affect
the higher ranks of life. Lack of proper exercise, good food, and fresh
air, the mental stimulation of unhealthy literature, and masturbation,
are important factors. Emotional and nervous symptoms may be
prominent--so much so that the disease is regarded by some as a
neurosis.

The anatomical peculiarities relate to the blood and circulatory
system. There is anæmia, but the impoverishment is less in the number
than in the corpuscular richness in hæmoglobin. This fact, first
pointed out by Duncan,[46] has been abundantly confirmed. Thus, for
example, in one case, with a globular richness of 85 per cent., the
hæmoglobin was only 52 per cent., and in another, with 92 per cent. of
red, the hæmoglobin percentage was as low as 64. The numerous
investigations of the past few years[47] have, among other points,
fully established this as perhaps one of the most striking features in
chlorosis. The color-value of the individual corpuscle is very much
reduced. Of 22 observations of Hayem, the average number of red
corpuscles was {895} 3,740,000, and the hæmoglobin reduced to about 50
per cent. In Laache's 13 cases the average percentage of corpuscles was
72, and of hæmoglobin 45. This author has pointed out that in certain
cases with all the clinical symptoms of chlorosis well marked there may
be very slight reduction in the corpuscles or hæmoglobin; and such he
terms pseudo-chlorosis. The red corpuscles in chlorosis vary much in
size. Very large forms--giant red cells--are common, and microcytes are
sometimes to be seen; but there is not the extreme irregularity in size
and outline of the blood in idiopathic anæmia. The presence of a large
number of young, imperfectly-formed corpuscles, especially as regards
the hæmoglobin, is the distinguishing feature of chlorotic blood. Hayem
and Willcocks both regard the average corpuscular diameter to be lower
than normal, though many large forms occur. The color of the red
corpuscles is noticeably pale, and the marked deficiency in hæmoglobin
can be observed in individual corpuscles as well as in the
blood-mixture prepared for counting. Quinquaud found the serum normal
in quality, but the solids were slightly reduced in amount. Hunt[48]
has shown that there are peculiar inter-menstrual oscillations in the
blood in chlorotics. There is usually a fall in numbers just before the
flow, but the individual value remains good; subsequently the number
rises, but the color-value is not maintained (Willcocks). Virchow[49]
pointed out that in many cases of chlorosis there was a defective
development of the circulatory system, either congenital or resulting
in failure of the normal rate of growth; the parts remained infantile.
The heart and arteries were small, the walls of the latter thin, and
the calibre of the aorta narrowed. In some instances there was found a
compensatory hypertrophy of the heart. Defective development of the
uterus and ovaries has also been noted, but these changes on the part
of the circulatory and generative organs are not constant features in
chlorosis.

[Footnote 46: _Sitzungsbericht d. Kais. Akad. d. Wissenschaften zu
Wien_, 1867.]

[Footnote 47: Leichtenstern, _Hæmoglobingehalt des Blutes_, Leipzig,
1878; Hayem, _Recherches sur l'Anatomie, etc. du Sang_, 1878; Malassez,
_Archives de Physiologie_, 1877; Moriez, _La Chlorose_, Paris, 1880;
Laache, _Die Anämie_, Christiania, 1883; Willcocks, _Practitioner_,
1883.]

[Footnote 48: _Lancet_, ii., 1880.]

[Footnote 49: _Ueber die Chlorose_, etc., Berlin, 1872.]

The SYMPTOMS of chlorosis are those of anæmia of moderate grade. As in
idiopathic anæmia, the subcutaneous fat is in full, or even extra,
amount. The complexion is most peculiar, neither the blanched aspect of
hemorrhage nor the muddy pallor of grave anæmia; but there is a curious
yellow-green tinge in marked cases which has given the name to the
disease ([Greek: chlôros]), and also its popular designation, the green
sickness. Breathlessness, palpitation, and tendency to fainting are due
to the anæmia. Digestive troubles are also common, and the appetite is
often depraved. There are venous and cardiac murmurs. The menstrual
functions are almost always deranged, and there may be hysterical and
nervous manifestations. Relapses are not uncommon. The intimate
pathology of the disease is unknown. In its insidious onset, sometimes
causeless, and in certain features of the blood-state, it resembles
pernicious anæmia, but it differs from it in many essential
particulars. The association with menstrual disorders, the hypoplasia
of the circulatory and generative organs in some cases, the favorable
course and response to suitable treatment, as well as the sex and
period of life, are features peculiar to chlorosis. Then, again, the
anæmia is not so intense, and the relation of the hæmoglobin is just
the reverse; in chlorosis the individual corpuscles are deficient in
hæmoglobin, while in idiopathic anæmia the reverse appears to be the
case.

Some regard the blood circulatory and uterine condition as the
expression of a congenital defect leading to the formation of a
diathesis--and in certain cases this may be so--but some of the most
marked cases I have seen have been in girls of healthy families, who
after a healthy childhood developed chlorosis at puberty, from which,
under suitable treatment, they recovered to become robust and vigorous
women. The almost specific action of iron suggests failure of the
digestion or assimilation of the minute traces of this substance which
are contained in our ordinary foods, and from which {896} the iron of
the corpuscles must be derived. Zander[50] holds that it is largely due
to a defect in the hydrochloric acid of the gastric juice, by which the
iron-holding compounds are dissolved, and claims that in chlorosis the
administration of this remedy after eating fulfils every indication and
enables the iron in the foods to be converted into an absorbable
compound.

[Footnote 50: _Virchow's Archiv_, lxxxiv.]

The condition of the blood-making organs themselves throw no light on
the PATHOLOGY of the disease.

The TREATMENT of chlorosis requires special mention. Iron may be
regarded as a specific when given in sufficient doses. I have found
Blaud's formula, as given in Niemeyer's textbook (ferri sulph. potass.
carb. et tart. aa ounce ss; tragacanth q. s. Make ninety-six pills. Two
or three pills to be taken three times a day), the most satisfactory
method of administering the drug. Under their use I have repeatedly
seen the number of the red corpuscles per cubic millimeter double in a
fortnight; and it is one of the most interesting therapeutic phenomena
to watch with the hæmacytometer the progressive development and
increase of red corpuscles under the influence of fifteen or twenty
grains of iron daily. Other forms may be used--reduced iron, dialyzed,
the lactate, the tinct. of the perchloride--and it does not really make
much difference which form is employed so long as enough is
administered. Dilute hydrochloric acids or the vegetable acids may be
given, and special attention should be devoted to dietetic and hygienic
regulations.


MELANÆMIA

is a condition characterized by an accumulation of granular pigment in
the blood and various organs, particularly the spleen, liver, marrow,
and brain. It is almost invariably associated with prolonged malarial
infection, and the pigment results from the transformation of the
hæmoglobin of the corpuscles, many of which undergo destruction as a
direct consequence of the influence of marsh miasm. Very exceptionally,
however, the dark particles are extraneous, and result from the passage
of carbon-granules into the circulation in cases of intense
anthracosis. Soyka[51] met with a case of this kind in which the coal
particles were distributed throughout the spleen, liver, and kidneys.
In blood the pigment occurs either free in the form of fine granules or
in cloud-like collections of various sizes and shapes, often surrounded
by a hyaline margin, or it occurs enclosed in cells. The free pigment,
not often met with, is either molecular or in the form of irregular
particles which may equal a red corpuscle in size. Aggregations of the
granules are not uncommon, forming various-sized masses which may be
imbedded in a hyaline substance. More commonly the pigment is contained
in cells, ordinary leucocytes or large flattened--endothelial--cells
derived from the spleen or liver. The color varies from yellowish-brown
to a deep black. Except during periods of intense malarial infection
and in the most severe and chronic cases melanæmia is rarely observed.
In most ordinary cases of intermittent one may seek in vain for the
pigment-granules, and I have examined many chronic cases with
well-marked ague-cake with negative results. In other instances the
pigment is found during or after a paroxysm; and this is the period
when an examination of the blood should be made. The greatest care and
cleanliness should be exercised in obtaining the blood-drop; and it
should be remembered that in some of the glass slips used for
microscopic purposes {897} irregular brownish flakes may occur which I
have known to be mistaken for pigment.

[Footnote 51: Quoted by Hindenlang, _Virchow's Archiv_, lxxix.]

The melanæmia is but the expression of extensive destruction of
corpuscles and accumulation of pigment in the spleen, liver, and
bone-marrow; and these organs in cases of fatal intermittent or
remittent fevers may present important changes. In the spleen, which is
usually enlarged and indurated, the pigment is chiefly in the vicinity
of the arteries and veins, the tissues about which may be absolutely
black, and in both stroma and pulp innumerable cells are found filled
with blood-corpuscles and blood-pigment in all stages of transformation
to melanin. The color of the organ may be of a deep reddish-brown, or
in very chronic states gray or even a dark olive. In the liver the dark
granules are chiefly at the periphery of the lobules, fixed within the
connective-tissue elements and leucocytes, not in the liver-cells
themselves. It may be abundant about the portal branches, staining the
connective tissue of Glisson's sheath, and it is also met with in the
vicinity of the hepatic veins. When much affected the liver may have a
deep bronze tint. As Arnstein has shown,[52] the bone-marrow may
present similar changes and have a grayish-brown color. There may be
deep pigmentation of peritoneum and omentum. The deposition of the
granules in and about the vessels of the cortex cerebri may give a
slate-gray color to the brain, or even a graphite tint in very severe
cases. The capillaries have been found occluded with cells filled with
the pigment-granules. The kidneys--particularly the Malpighian
tufts--the mucous surfaces, and the skin may also be the seat of
pigmentary deposition. These coarse changes in the organs in chronic
malaria were known to the older writers, and in Bright's _Medical
Observations_ a beautiful representation is given of the condition of
the brain. To American physicians, with their extensive experience of
malarial fevers, these changes were well known, and Stewardson of the
Pennsylvania Hospital gave an admirable description of them in
1841;[53] and from the same institution in 1868 came another important
contribution to the subject by Meigs, Pepper, and Rhoads.[54]
Meckel[55] and Virchow[56] gave the first satisfactory explanation of
the discoloration, showing that it was due to pigment, which might also
be free in the blood. Frerichs in his well-known work on the liver gave
an exhaustive account of the coarse and microscopical appearances.

[Footnote 52: _Virchow's Archiv_, lxi.]

[Footnote 53: _Am. Journal Medical Sciences_.]

[Footnote 54: "On the Morphological Changes of the Blood in Malarial
Fever," _Penn. Hospital Reports_, 1868.]

[Footnote 55: _Deutsche Klinik_, 1850.]

[Footnote 56: _Virchow's Archiv_, Bd. i.]

There is still some difference of opinion as to the mode of origin of
the pigment. Most writers hold that it results from the destruction of
the red corpuscles in the spleen and liver, and from these situations
the pigment gets into the blood; but more recently Arnstein[57] and
Kelsch[58] have urged the view that the melanæmia is the primary
process, the destruction of corpuscles going on in the blood itself,
and the particles and coloring material taken up by the leucocytes are
transformed into melanin, and then the cells collect in the spleen,
liver, and bone-marrow, producing the condition of melanosis. It is
probable that the older view is the true one, and we may regard the
process as an exaggeration or intensification, under the stimulus of
the malarial poison, of the normal process of blood-destruction which
goes on in the spleen and bone-marrow, and under some circumstances in
the liver and lymph-glands. We can often trace in the cells of these
organs the stages of transformation from red corpuscles to
melanin-granules, just as can be done in the tissues in the
neighborhood of an extravasation, where also the process is chiefly
intracellular (Langhans). On the other hand, in those very states in
which the red corpuscles are destroyed in the blood and the hæmoglobin
set free, we do {898} not find melanæmia. It happens occasionally in
fevers that we meet with colorless cells in the blood containing red
blood-corpuscles, which in time would be transformed into pigment, but,
so far as we know, such a condition has not been observed in the blood
in malaria. The connection between the fever paroxysm and the
appearance of the pigment in the blood depends, most likely, on changes
in the volume of the organs under the influence of the fever, whereby
cells containing the pigment are dislodged and get into the
circulation. This explains, too, their rapid appearance in some cases
with the onset of a paroxysm. No doubt, as Virchow originally taught
and as well shown in Gussenbauer's[59] observations, the pigment may
result from the diffusion of the coloring matter and gradual
precipitation of it in the granular form within the protoplasm of
colorless cells; but of the occurrence of such a process in the
circulating blood in malaria we have no satisfactory evidence, and we
incline to the belief that the melanosis of the organs is the primary
condition, while the melanæmia is secondary and inconstant.

[Footnote 57: _Loc. cit._, and _ibid._, lxxi.]

[Footnote 58: _Archiv de Physiologie_, 1875.]

[Footnote 59: _Virchow's Archiv_, lxiii.]

Occasionally, in cases of extensive melano-sarcoma, pigment-granules
may be found in the blood in large numbers, and even appear in the
urine and be deposited in the organs and skin. In a few instances also
free pigment has been observed in the blood in Addison's disease.


PROGRESSIVE PERNICIOUS ANÆMIA.

DEFINITION.--Extreme and progressive anæmia developing without evident
or apparently adequate cause.

SYNONYMS.--Idiopathic anæmia (Addison); Essential anæmia (Lebert);
Anæmatosis (Pepper).

HISTORY.--During the first two or three decades of this century cases
of severe and fatal anæmia were noted by Andral and others, but the
credit of having given the first accurate series of cases belongs to
Walter Channing of Harvard, who in the _New England Quarterly Journal
of Medicine_ for 1842 published a paper entitled "Notes on Anhæmia,
particularly in connection with the Puerperal State and with Functional
Disease of the Uterus, with Cases."[60] Any one who reads this
communication will be convinced that Channing's description,
particularly of the seven cases occurring in the puerperal state, is
that of the disease to which Gusserow and Biermer have more recently
directed attention.

[Footnote 60: My attention was accidentally called to Channing's
observations in the Periscope of Hall's _British-American Journal_ for
1845. Since then Musser, in the _Med. News_, Oct. 7, 1882, has given a
valuable abstract of the paper.]

In Addison's monograph on the suprarenal capsules (1855) there is a
brief but clear account of the disease, which he speaks of as follows:
"For a long period I had from time to time met with a very remarkable
form of general anæmia occurring without any discoverable cause
whatever--cases in which there had been no previous loss of blood, no
exhausting diarrhoea, no chlorosis, no purpura, no renal, splenic,
miasmatic, glandular, strumous, or malignant disease. Accordingly, in
speaking of this form of anæmia in clinical lectures, I, perhaps with
little propriety, applied to it the term idiopathic, to distinguish it
from cases in which there existed more or less evidence of some of the
usual causes or concomitants of the anæmic state." As early as 1843
this acute observer had spoken in his clinics of this condition.[61]

[Footnote 61: McKenzie, S., _Lancet_, 1879, ii.]

{899} The physicians at Guy's appear to have been well acquainted with
the disease, and in 1857 Wilks described cases under the heading
"Idiopathic Fatty Degeneration." To the labors of Zurich professors we
are indebted for much of our knowledge. That versatile clinicist
Lebert, then at Zurich, published in 1853 cases of puerperal chlorosis,
and we owe to him the excellent designation of essential as applied to
these cases of anæmia (1858). It was in 1871-72 that the communications
of Gusserow[62] and Biermer[63] aroused a very general interest in the
disease. Gusserow's cases, like some of Channing's, were in connection
with pregnancy. Biermer, thinking he was dealing with a previously
unknown affection, gave it the name of progressive pernicious anæmia.
In the past ten years the literature of this form of anæmia has
enormously increased. In Germany, in addition to the articles in the
encyclopædias (Ziemssen's, Eulenberg's) and innumerable contributions
and dissertations, two important monographs have appeared by Müller
(Zurich, 1877) and Eichorst (Leipzig, 1878). In France, Hayem, Lepine,
and others have published important observations. In England, the Guy's
Hospital physicians, Taylor and Pye-Smith, in the _Hospital Reports_
(1878-83) have fully established Addison's claim to having given a
clear account of the disease. Important contributions have been made by
Stephen Mackenzie, Coupland, Bramwell, Bradbury, and others. In this
country Pepper in 1875 brought the disease to the notice of the
profession and suggested the name anæmatosis. Howard (R. P.) of
Montreal at the Centennial Medical Congress (1876) gave a full account
of the affection, the existence of which he had long recognized and
taught. Musser[64] has reviewed the American literature, and has given
a tabular synopsis of 39 cases which have been recorded in this
country.

[Footnote 62: _Archiv f. Gynäkologie_, ii.]

[Footnote 63: _Correspondenzblatt für Schweizerische Artze_, 1872.]

[Footnote 64: _Proceedings of Philadelphia County Med. Society_, 1885.]

ETIOLOGY.--The disease is widely distributed, and there are no special
geographical influences. In Germany and certain of the Swiss
cantons--Zurich particularly--the cases seem to occur more frequently
than in England or America. In this country it can scarcely be called
one of the rare diseases, although up to January, 1885, Musser[65]
could collect only 39 cases. During ten years in Canada I saw 16 cases,
most of them with colleagues at Montreal.

[Footnote 65: _Loc. cit._]

That bad hygienic conditions have much to do with the induction of the
disease is shown by the records of Zurich and Berne, where the cases
have been very numerous among the lower classes, who are hard worked,
ill fed, and poorly housed. Possibly here other unknown causes may be
at work, as the conditions which prevail in the Zurich canton are not
unknown in other countries. In Ireland, where the peasants have poor
food and wretched houses, the disease does not appear to be common. In
the Montreal cases the subjects were chiefly of the upper or of the
higher mechanic classes.

The age most subject to the disease is the adult period; cases are rare
under twenty and over fifty. In Pye-Smith's table of 103 selected cases
there were only 6 under fifteen years of age; 4 between fifteen and
twenty; 29 between the twenty-first and thirtieth years; 26 cases
between the thirty-first and fortieth years; 21 between the forty-first
and fiftieth years; 13 between the fifty-first and sixtieth; and only 4
above sixty. The youngest case I have seen was in a girl of twenty, and
oldest in a woman over sixty. The youngest case on record was at the
fifth year.[66]

[Footnote 66: Quoted in _Am. Journ. Med. Sci._, Jan., 1885.]

Sex.--If we exclude all cases in women directly connected with the
puerperal state, primary idiopathic anæmia is more frequent in men than
in women. Of the 16 Montreal cases, 4 were dependent upon parturition,
and of the remainder, 9 were in men and only 3 in women. But most of
the {900} collected figures include the parturition cases, and the
women are in excess; thus, of 93 cases from the Swiss clinics at Zurich
and Berne, 67 were females. Eichorst's figures are 65 women and 30 men.
Of 110 cases collected by Coupland, 56 were men and 54 women. In
Pye-Smith's careful tabulation of 103 selected cases, 48 were men and
59 women.

As observed by Channing, Lebert, and Gusserow, pregnancy and
parturition are important factors in the production of a grave form of
anæmia. In the majority of cases the symptoms develop post-partum,
often, but not necessarily, in consequence of loss of blood during
delivery. Obstinate vomiting during pregnancy and prolonged lactation
may bring about the same condition. Of 29 cases of this sort in
Eichorst's table, in 19 the symptoms developed during pregnancy and in
10 after delivery.

Gastric and intestinal disturbance, dyspepsia, vomiting, and diarrhoea
have occurred in a number of cases prior to the development of the
anæmia.

In some instances loss of blood, chronic discharges, ulcers, or other
sources of drain have been present.

In not a few cases there has been mental worry, grief, or fright. This
has been specially noted by Wilks and Howard, and more recently by
Curtin.[67] It does not seem probable that malaria has any predisposing
influence.

[Footnote 67: "Nervous Shock as a Cause of Pernicious Anæmia," _Med.
Times_, Philada., April 4, 1885.]

It is by no means always the ailing or delicate who are attacked; many
of the cases have occurred in men previously strong and robust.

After excluding all these factors, which prevail in a considerable
proportion, there still remain cases without, as Addison says, any
discoverable cause whatever--cases to which in our present knowledge we
may apply the term idiopathic. These may be primary, and the others, in
which some one or other of the above-mentioned causes appears to have
prevailed, secondary anæmias, the latter to be distinguished from a
host of other sequential anæmias only by the fact of a progressive and
pernicious course.

Of 91 observations collected by Eichorst, in 24 cases the disease
appeared to have come on spontaneously, and 67 as the result of various
causes: pregnancy and parturition, 29; digestive troubles, 24; loss of
blood, etc., 7; bad hygienic conditions, 7.

SYMPTOMS.--The classical description of Addison must ever be quoted in
this connection: "It makes its approach in so slow and insidious a
manner that the patient can hardly fix a date to the earliest feeling
of that languor which is shortly to become so extreme. The countenance
gets pale, the whites of the eyes become pearly, the general frame
flabby rather than wasted, the pulse perhaps large, but remarkably soft
and compressible, and occasionally with a slight jerk, especially under
the slightest excitement. There is an increasing indisposition to
exertion, with an uncomfortable feeling of faintness or breathlessness
in attempting it; the heart is readily made to palpitate; the whole
surface of the body presents a blanched, smooth, and waxy appearance;
the lips, gums, and tongue seem bloodless; the flabbiness of the solids
increases; the appetite fails; extreme languor and faintness supervene;
breathlessness and palpitations are produced by the most trifling
exertion or emotion; some slight oedema is probably perceived about the
ankles; the debility becomes extreme--the patient can no longer rise
from his bed; the mind occasionally wanders; he falls into a prostrate
and half-torpid state, and at length expires: nevertheless, to the very
last, and after a sickness of several months' duration, the bulkiness
of the general frame and the amount of obesity often present a most
striking contrast to the failure and exhaustion observable in every
other respect."[68]

[Footnote 68: Monograph on _Disease of Suprarenal Capsules_, p. 3.]

The mode of onset is variable: in many cases there are etiological
{901} conditions, such as pregnancy, loss of blood, etc., which for
weeks or months precede, and perhaps determine, the development of the
anæmia. There may have been mental worry or shock, and after a
prolonged period of ill-health the anæmic symptoms become marked.
Failure of strength, lassitude and disinclination for exertion, with
shortness of breath and palpitation and an increasing pallor,
accompanied by headache, giddiness, and dyspepsia, are the symptoms for
which the patient seeks advice.

The condition of the skin is remarkable in pronounced cases: the color
is rarely a deep white or ashen, as in the pallor of fear or fainting
or the bloodlessness from hemorrhage, but there is a peculiar lemon
tint, a light straw-yellow or grayish-yellow color, which may be
mistaken for a mild icterus. This is one of the most characteristic
features of the disease.

The subcutaneous fat does not waste; on the contrary, the fatty
panniculus may increase, and, as Addison remarked, there may be a
bulkiness of the frame. Actual emaciation is very uncommon.

Slight oedema is present in the feet, particularly toward the close,
and it may extend up the legs, but rarely reaches a high grade.
Occasionally it may appear in the face and hands.

Cutaneous hemorrhages in the form of small petechiæ are liable to
appear on the legs and arms, not often on the trunk.

The sweat secretion is not affected, but in several instances, as in
other chronic affections where death is protracted, a cadaverous odor
has been perceived from the skin or breath.

The blood, as expressed, often with difficulty, from the finger-tip,
has not the rich color of health, but is pale, like a light claret. The
corpuscles usually fill the drop, and we do not see, as in certain
cachectic states, an extreme degree of hydræmia in which the red
corpuscles do not entirely occupy the plasma. It is sometimes difficult
to get a drop of blood from the finger-tip, and to do so the arm should
hang by the side and may be squeezed from the shoulder downward to
press the blood into the hand. The microscopical characters of the
blood are as follows:

(1) The red cells present a great variation in size, and there can
usually be seen _(a)_ large giant forms, the megalocytes measuring 8,
11, or even 15 mm.: these are not often very numerous, and may show
irregular foldings at the edges; _(b)_ medium-sized disks, such as are
usually found in the blood: these always predominate; _(c)_ small round
cells, microcytes, 6, 4, or even 2 mm. in diameter, and of a deep
color. They are rarely absent in typical cases, though varying in
number at different periods. The color of the large and medium-sized
corpuscles may be much less intense than normal.

(2) In addition to the variation in size, the corpuscles show a
remarkable irregularity in form--an irregularity which, so far as my
observation goes, is never met with to the same extent in other
conditions. They may be elongated and rod-like, scarcely recognizable
as blood-disks. Balloon and kidney shapes are common. One end of a
corpuscle may retain its shape, while the other is extended as a
pointed or blunt process. The normal concavity may be lost on one side
and deepened on the other. Many of the large forms are longer than
broad, often quite ovoid, and with sinuous margins. The microcytes are
either globular or present a pit-like depression on one surface. To
this condition of irregularity of the corpuscles in size and form
Quincke has given the name poikilocytosis ([Greek: poikilos], variously
shaped). It possibly depends on an altered state of the serum; I have
failed to produce it with dilution. The corpuscles in the blood of
idiopathic anæmia do not form such well-defined rouleaux as in health.

(3) The colorless corpuscles may be relatively increased, but are
usually diminished to some extent. They present no very special changes
in form or stricture. Larger forms may occasionally occur, but I have
not noted their {902} presence, specially the cases in which the marrow
was found red and lymphoid after death. In two cases the majority of
the corpuscles at several observations were smaller than normal. The
amoeboid movements are active.

(4) In only two instances, in the cases I have examined, were nucleated
red corpuscles present, and these very scanty. They have been noted by
several observers. Ehrlich states[69] that they are present in all
cases.

[Footnote 69: _Berl. klin. Wochenschrift_, 1880.]

(5) Schultze's granule masses, composed of the hæmatoblasts or
blood-plates, are either absent or very scanty. In some cases not a
trace of them could be found, and in others they are less abundant than
in health. In this respect the blood offers a marked contrast to that
of various cachectic states, and also to leukemia, in which the masses
are sometimes very numerous. Leube,[70] however, has recorded a case in
which they were abundant.

[Footnote 70: _Ibid._, 1879.]

(6) The fibrinous network between the corpuscles is thin and
indistinct. The Cercomonas globulus and Cercomonas navicala, described
by Klebs[71] as occurring in pernicious anæmia, are possibly peculiar
to Prague.

[Footnote 71: _Real Encyklopädie_, art. "Flagellata."]

The reduction in the number of the red corpuscles is the special
feature of the disease, the diminution reaching far below that met with
after the most severe hemorrhage. Instead of a corpuscular richness of
5,000,000 per cubic millimeter, the number may be reduced to
one-quarter, or even one-tenth. In the more extreme anæmia from
hemorrhage, in cancer or in phthisis, the reduction rarely reaches as
low as 1,500,000, while this figure is common in pernicious anæmia, and
in advanced cases may sink below 1,000,000, or even to 500,000. This
latter figure is exceptional. In only 2 cases have I counted the number
so low as this. In a case of Quincke's the red were reduced to 143,000
per c.m., and, strange to say, the man recovered. Great variations may
occur from month to month in the course of the disease. An increase in
the number is not always associated with an improvement in the
patient's condition.

The hæmoglobin is also greatly reduced, but not in proportion to the
reduction in the red corpuscles. The relative coloration of the
corpuscles is increased, and this seems as marked a feature in
pernicious anæmia as the relative reduction is in chlorosis.[72] Owing
to the fact that the hæmoglobin value of individual corpuscles is
increased, the anæmia is never quite so intense as the number of
corpuscles would appear to indicate.

[Footnote 72: Laache, _Die Anämie_, Christiania, 1883; _Deutsche
Medicin Wochenschrift_, 1884, No. 43.]

The circulatory system presents many symptoms of importance. When the
patient is recumbent and at rest, the heart's action is quiet, but on
exertion or excitement the action becomes rapid, and there are
palpitation, fluttering, and sometimes painful sensations in the
cardiac region. Stairs are particularly trying to these patients. There
may be slight enlargement of the heart, indicated by an increased area
of visible pulsation, and an impulse in the third or fourth left
intercostal space, near the sternum, is frequently seen. The hæmic or
functional murmurs are usually present, variable in intensity and site,
most often heard at the base and in both aortic and pulmonary areas,
but also at the apex. Indeed, their variability is often puzzling;
sometimes it would seem that there might be a murmur at each orifice,
at another limited only to one; and for the bruit to be present at one
examination and absent at the next is not uncommon. In several of
Eichorst's cases there was a variable diastolic murmur at apex or base.

The larger arteries pulsate visibly--so much so that at times it
suggests the water-hammer pulsation of aortic insufficiency. The
carotid pulsation may be most evident, and still more so in the
abdominal aorta, the throbbing of which may be very distressing to the
patient. A systolic arterial murmur may be heard in all the arteries.
The pulse is soft, compressible, usually {903} rapid (80 to 100 or
over), depending a good deal on the position and state of excitement.
One is sometimes surprised in these cases to find a full and at the
same time very soft pulse. It may be dicrotic.

The venous hum is well marked, and is rarely absent except after
prolonged rest in bed, when both cardiac and venous murmurs may
disappear, to return at once on making the patient stand up. Channing,
in the paper already referred to, speaks of the thin, scanty state of
the blood, and yet notes the prominent appearance of the veins beneath
the skin, particularly about the hands and wrists.

Hemorrhages occur very frequently. Epistaxis is most common, and may
have preceded for years the onset of the grave anæmia. It may recur
repeatedly and be a source of constant drain, or ultimately be the
cause of death. From other mucous surfaces bleeding is not so common. I
have seen one case in which there were for months repeated small
hemorrhages from the bowels, and bleeding from the gums has been
observed in several cases. The petechiæ on the skin have already been
referred to. Retinal hemorrhages, as first noticed by Biermer, are very
common. They are numerous and small, scattered around the disk. They
are not peculiar to any special form, but are liable to occur in severe
anæmia from any cause.

Respiratory symptoms are not prominent: a short cough may be present,
but the only special feature is the shortness of breath, which is often
early and troublesome, and depends on the condition of the blood, not
of the lungs. There may be a very distressing and persistent sense of
insufficient aëration (Pepper). Toward the close hydrothorax may
develop.

The gastro-intestinal system is in the majority of cases more or less
deranged. Dyspepsia may precede for years the anæmia, and may persist
throughout the illness. There is loss of appetite, amounting sometimes
to a positive repulsion toward all forms of nutriment. Nausea and
vomiting are rarely absent throughout the illness, and there are some
cases in which the gastric symptoms are so marked as to suggest a
primary stomach lesion as the atrophy to which Fenwick[73] has called
attention, or even arouse a suspicion of cancer.

[Footnote 73: _Lancet_, 1877, ii.]

Diarrhoea is also a frequent symptom, and in some cases hastens the
fatal result. There may be melæna, and in Müller's monograph a case is
given in which leucin and tyrosin were found in the stools.

The urine is pale, acid, and of low specific gravity. Occasionally it
becomes darker in color. The urea may be diminished, but it has been
found increased in some cases by Quincke, Eichorst, and Laache. The
uric acid is more commonly increased, and the phosphoric acid. The
percentage of iron has been found larger than normal. Albumen is rarely
found. Peptones, leucin, and tyrosin may be present (Laache). Blood
does not often occur.

Fever is not a constant symptom; some cases run their course without
any elevation, but there is usually slight febrile reaction of an
irregular, remittent type, an evening elevation of two or three
degrees, and a morning remission to the normal standard. There may be a
week or ten days of fever, and then a long spell without any. Toward
the close there is commonly an elevation, occasionally depression, of
temperature, as in one case reported by Müller in which it sank to
24.8° C.

COURSE.--In the majority of cases the disease runs a steadily downward
course, well indicated by the terms progressive and pernicious. In
almost every case periods of temporary improvement occur. Recovery is
possible, and Pye-Smith[74] gives a summary of 20 undoubted cases which
got well. The lactation and parturition cases stand a better chance of
recovery than others. {904} The average course of the affection is from
six to twelve months; there are rapid cases in which a fatal
termination may be reached in a few months, and there are others which
drag on for two, or even three, years, periods of improvement
alternating with relapses. Death is usually by asthenia. It may be
hastened by hemorrhage from the nose or bowels or by persistent
vomiting or diarrhoea.

[Footnote 74: _Guy's Hospital Reports_, 1883.]

MORBID ANATOMY.--The body is not often emaciated; usually, indeed, the
panniculus adiposus is well developed. The peculiar lemon tint of the
skin is present in the majority of cases, and there may be petechiæ.
The voluntary muscles may appear normal, but are often of an intense
flesh color, more like horse muscle. In six cases the words "rich red
color" and "remarkably deep red color" occur in my notes. In other
instances they are pale. When the cavities are opened the general
pallor of all the organs is most striking. The serous surfaces are
smooth and glistening, and occasionally present ecchymoses. The amount
of fluid may be increased. The mucous membranes are pale; minute
hemorrhages are not uncommon.

The heart is in many cases large and flabby, in others normal, and in a
few undersized. The pericardial fluid may be in excess, and the
subpericardial fat is often increased. The flaccid relaxed state of the
walls is very noticeable, and on opening the chambers the amount of
blood is always very slight. In one case I could only obtain two
drachms from the right heart, and between three and four from the left.
There may be small clots entangled with the chordæ tendineæ of the
valves. The muscle-substance is pale, of a faded-leaf, light-yellow
color, and beneath the endocardium, particularly of the left side and
of the papillæ, there are flaky spots (tabby mottling) of fatty
degeneration. The peculiarities of general fatty degeneration of the
heart are nowhere better seen than in these cases. The valves and
orifices are usually normal. The intima of the aorta may show fatty
changes. The smaller arteries and veins contain most of the blood.

The lungs are crepitant, pale, with a slight bloody oedema at the
bases. The fluid expressed has often a yellowish tinge. Exudation into
the pleural cavities is common. The air-passages do not offer any
special changes.

The liver is of normal size, pale and generally fatty, not invariably;
in none of Eichorst's cases was this a marked feature. Quincke and
others have found the amount of iron increased.

The mucous membrane of the gastro-intestinal tract is pale, covered
with a thin mucus, and may present ecchymoses. Post-mortem solution of
the gastric mucosa is common, and I have seen oedema of it. Fatty
degeneration of the cells of the peptic tubules is common, and they may
be in an atrophic state, as well described by Fenwick.[75] Ecchymoses
of the small and large bowel are common; ulceration is rare. In a few
instances the lymphatic elements of the mucosa have been found swollen.
Extensive atrophy of the mucosa has been found associated with
degeneration of the nerve-elements, but these changes, as shown by the
observations of Nothnagel[76] and Schleimpflug,[77] are not uncommon in
many other conditions.[78]

[Footnote 75: _Loc. cit._]

[Footnote 76: _Beiträge zur Phy. u. Path. des Darms_, Berlin, 1884.]

[Footnote 77: _Zeitsch. f. klin. Med._, ix., 1885.]

[Footnote 78: Sasaki, _Virchow's Archiv_, 96.]

The blood vascular organs have naturally received special attention.
The spleen offers, as a rule, no important changes; the size is
variable, rarely enlarged, occasionally reduced in size, but for the
most part normal. The smallest I have seen was in one of Howard's
cases, in which the organ weighed only one ounce and five drachms. In
the 51 autopsies noted in Howard's paper the spleen was stated to be
normal in 36 and enlarged in 13. Ten ounces is the heaviest I have
seen. The spleen-tissue is moderately firm, of a light brown-red color.
I have never noticed either the extreme softening of an acute splenic
swelling or the hardness of chronic induration. {905} The histological
characters present nothing special. Cells containing red corpuscles
occur, but not in such numbers as in cases of acute splenic swelling
from fever. I have seen the nucleated red corpuscles in several
instances.

The lymph-glands are, as a rule, normal in size and appearance. In
three instances I found them decidedly smaller than normal, and in two
they had a rich deep-red color, and on section looked more like
spleen-tissue than lymph-gland. Weigert has noted the same
appearance.[79] In one of the cases there were nucleated red corpuscles
in the glands, as has been observed by Rindfleisch in a case of
rickets,[80] and more recently in tuberculosis.[81]

[Footnote 79: _Virchow's Archiv_, Bd. lxxix.]

[Footnote 80: _Archiv f. Mikros. anatomie_, Bd. xxiii.]

[Footnote 81: _Med. News_, xiv. No. 23.]

The fatty tissue of the long bones is in many instances replaced by a
red marrow resembling that of the short bones of the adult and the
entire osseous system of the infant. This was first noticed by Pepper
in 1875,[82] and has since been frequently observed. The color is
usually of a reddish-purple when fresh, becoming a bright red on
exposure. Sometimes there is a grayish-red appearance. It may not be
universally distributed in the long bones, and the change would appear
to proceed from the trunk toward the periphery--a direction the reverse
to that in which the red marrow of the child becomes fatty. In many
cases the marrow has been found normal; in others, the change known as
gelatinoid has been observed. In five Montreal cases I found the marrow
of the long bones lymphoid, in one gelatinoid, and in two the long
bones could not be examined. It must be borne in mind that the short
and flat bones of the adult contain a red lymphoid marrow mixed with a
variable amount of fat, in which nucleated red corpuscles can always be
found.

[Footnote 82: _American Journal of Medical Sciences_, lxx.]

The brain and cord present an intensely anæmic appearance; the
membranes are relaxed and oedematous, and petechiæ may exist. The
convolutions are often wasted, and the amount of cerebro-spinal fluid
increased. No important changes have been found in the substance.

The ganglia of the sympathetic system have been examined by Queckett in
one of Addison's cases and found fatty. Wilks and others have found
them normal. Brigidi[83] has described an increase in the interstitial
tissue and pigmentation of the cells. In two instances I found nothing
abnormal. Sasaki[84] has described marked degenerative changes in
Auerbach's and Meissner's plexuses in two cases of pernicious anæmia.

[Footnote 83: _London Med. Record_, 1878.]

[Footnote 84: _Loc. cit._]

The kidneys are usually pale and without special change beyond the
fatty degeneration. Quincke has found the amount of iron increased. The
suprarenals have in several instances been found very small. The sexual
organs show no constant changes.

PATHOLOGY.--Under the general subject of Anæmia the pathology has been
discussed at sufficient length. After excluding pregnancy, parturition,
lactation, and inanition cases, as partaking more of the characters of
secondary anæmia, we can recognize three groups of cases: First, those
in which the bone-marrow has been found extensively affected--cases of
anæmia medullaris; second, cases in which a primary atrophic change in
the mucous membrane of the stomach appears to have been the
starting-point of the trouble; and, third, cases in which after death
no special changes have been found sufficient to explain the anæmia. To
the latter the term idiopathic is applicable, and possibly they may be
instances of hæmophthisis due to increased destruction of the
corpuscles from causes unknown at present.

DIAGNOSIS.--A case in which anæmia comes on without obvious cause and
without enlargement of the spleen, and progressively increases in spite
of remedies, diet, change of air, etc., may be regarded as one of an
idiopathic or essential character. If the case goes on to a fatal
termination, the designation of pernicious is appropriate. I would
place some reliance on the {906} microscopical examination of the
blood, and would consider the presence of microcytes with great
irregularity in the ordinary red corpuscles strong confirmatory
evidence. The absence of wasting, the peculiar lemon tint of the skin,
the occurrence of epistaxis and retinal hemorrhages, would render a
diagnosis certain.

In that class of cases so well described by Fenwick,[85] Nothnagel,[86]
and Nolen,[87] in which there has been an interstitial inflammation of
the gastric mucosa and atrophy of the glands, the question has not yet
been decided how far this condition is to be considered causal, and how
far a part of the general disturbance of nutrition. The clinical
picture may be identical with that of idiopathic anæmia, and in some of
the cases the gastric symptoms have been so marked that the relation of
the atrophy and the anæmia has evidently been that of cause and effect.
And yet in these cases there does not appear to be the pronounced
emaciation of inanition anæmia. In other instances the diarrhoea and
chronic intestinal trouble may, with or without gastric participation,
bring about a similar condition.

[Footnote 85: _Loc. cit._]

[Footnote 86: _Deutsches Archiv f. klin. Med._, xxiv.]

[Footnote 87: _Centralblatt f. d. Med. Wissenschaft._, xx.]

Profound anæmia may arise during or after pregnancy, and a considerable
proportion of the cases on record have been in this connection.

From ordinary cases of Hodgkin's disease, anæmia lymphatica, there
could be no difficulty in making a diagnosis if the superficial glands
were enlarged. In splenic anæmia, if the enlargement was not great,
there might for a time be uncertainty, which the progressive increase
of the organ would remove. Neither in anæmia splenica nor lymphatica
are we so likely to meet with the microcytes or irregular corpuscles.

Chlorosis occurs chiefly in young girls, and is amenable to treatment.

From the various cachexias--malarial, syphilitic, metallic--the history
will commonly afford grounds for a diagnosis, and in these states, as
in latent cancer, the wasting is apt to be more pronounced than in
essential anæmia. Cases of gastric cancer are occasionally met with
which simulate closely pernicious anæmia, and the diagnosis may be
doubtful for months.[88]

[Footnote 88: Richard Neale, _Practitioner_, 1883.]

The enteritis and hemorrhages caused by the presence of Anchylostoma
duodenale in the intestines may produce an aggravated form of anæmia
resembling closely the form under consideration. It prevails among the
workers in mines and tunnels, hence the name miner's anæmia or
anchylostomiasis. The diarrhoea and the detection of the ova or worms
in the discharges would afford grounds for a diagnosis.[89]

[Footnote 89: _Trans. of the International Med. Congress_, London,
1881, vol. i. 437.]

The PROGNOSIS is unfavorable, particularly in those cases which have
arisen without any cause or previous ill-health. In the cases arising
from defective food, etc.--inanition anæmias--pregnancy, or lactation,
the outlook is less grave. Of the 64 Zurich cases in Müller's
monograph, 7 recovered, and of Quincke's 31 cases, 11 recovered.
Pye-Smith gives a table of 20 recorded cases of recovery.[90] Great
improvement may occur, or even recovery for a period of several years,
after which the disease may recur and prove fatal. This was the history
in a case under the care of Wilkins at the General Hospital, Montreal.

[Footnote 90: _Loc. cit._]

TREATMENT.--The designation pernicious applied by Biermer indicates the
hopeless character of the disease in perhaps a majority of the cases;
of late the records happily show a considerable percentage of
recoveries. Thus, Pye-Smith has collected 20 cases in which
convalescence was established after severe and profound anæmia,
belonging undoubtedly to the class here considered. The intractable
nature of a case and the resistance to ordinary treatment are points
which may first suggest to the practitioner the fact that he is dealing
with a something more than simple anæmia.

{907} Hygienic and dietetic regulations are of the first importance.
Cases appear to have got well with change of air and a better diet
after resisting all ordinary means. In other instances no benefit
whatever has been derived from residence at the sea or in the
mountains. As a rule, the cases are best treated at home. The greatest
care must be exercised in the regulation of the diet, which should be
light and nutritious. So long as the digestion keeps tolerably active
there is hope: anorexia, vomiting, and other dyspeptic symptoms are
among the most troublesome and serious features. The bitter tonics,
hydrochloric acid, and pepsin may be administered. But the stomach may
fail absolutely and reject even the smallest amount of liquid food, and
rectal alimentation must be employed. The gastric symptoms have been
specially marked in cases in which there has been found post-mortem
atrophy of the peptic glands. In certain of these cases the problem of
feeding will tax to the uttermost the resources of the physician.
Rectal injections of blood (fresh or dried), as recommended by A. H.
Smith, I have found beneficial in several cases. Intestinal
symptoms--diarrhoea, flatulence, and in some cases melæna--call for
treatment.

Of medicines, arsenic is the most important, and in the form of
Fowler's solution should be employed in small and increasing doses. We
are indebted to Bramwell[91] for pointing out the great value of this
medicine, and in certain cases it acts almost as a specific. In 8 of
the 20 cases of recovery noted by Pye-Smith the improvement seemed due
to the arsenic. Padley[92] has collected in the literature 48 cases
treated without arsenic, of which 42 were fatal, while of 22 cases
treated by arsenic 16 recovered, 2 improved, and only 4 proved fatal.
The testimony of recent observers is very strongly in favor of this
drug as the most efficacious we possess in this grave disease. The use
should be continued long after the convalescence is apparently
established; indeed, it should be given at intervals for many months
after recovery, as there are dangers of relapse. There are cases which
are not benefited by arsenic, even when well borne. Finlay[93] has
recently reported a case which was cured by iron after the failure of
arsenic.

[Footnote 91: _Edinburgh Med. Journal_, 1877.]

[Footnote 92: _Lancet_, 1883, ii.]

[Footnote 93: _Lancet_, 1885, i.]

Iron, as a rule, seems quite useless in the majority of these cases. I
have frequently seen the percentage of red corpuscles gradually sink
under its administration, and then rise in a remarkable way when the
arsenic was employed. This is in curious contrast to the effect of this
drug in the various secondary anæmias and chlorosis in which it is
rightly regarded as a specific. The cases which are benefited may have
a different etiology, and where the arsenic does not succeed some form
of iron should be given, as Finlay's case, just mentioned, shows that
there are instances where it cures after the failure of the arsenic.

Broadbent advises the use of manganese when the anæmia is associated
with uterine or menstrual trouble. Phosphorus has been extensively
employed, and occasionally with benefit.

When all remedies have been tried in vain the question of transfusion
of blood arises. As a substitute for the intravenous transfusion the
blood has been injected into the peritoneum: this has been practised in
Italy with success.[94] The subcutaneous injection has also been used,
and lately the inhalation of a spray of blood has been recommended.[95]
In four or five instances intravenous injection has succeeded, but in
the majority of cases it has proved useless. Von Ott's[96] interesting
researches show that the injected blood-corpuscles and albuminous
materials always undergo destruction in the blood, and a 6/10 per cent.
solution of common salt seems to answer just as well, and is much more
available and less dangerous.

[Footnote 94: _Practitioner_, vol. xxxi.; Ponfick, _Berl. klin.
Wochenschrift_, 1879.]

[Footnote 95: _Med. News_, 1885, i.]

[Footnote 96: _Virchow's Archiv_, Bd. xciii.]

{908} The injection of milk, as first practised in cholera by my
preceptors, Bovell and Hodder[97] of Toronto, has also been employed in
anæmia (Pepper, Wulfberg).

[Footnote 97: _Canadian Journal of Science_, 1854.]


LEUKÆMIA.

DEFINITION.--A disease characterized by a great and persistent increase
of the colorless corpuscles of the blood, associated with enlargement
of the spleen, lymphatic elements, and bone-marrow.

SYNONYM.--Leucocythemia (Bennett).

HISTORY.--Our knowledge of this affection dates from the description of
two cases by Craigie and Bennett in the October number of the
_Edinburgh Medical Journal_ for 1845. The altered state of the blood
was thought to be due to the presence of pus--a suppuration of the
blood. In the November number of Froriep's _Notizen_ for 1845, Virchow
described a case in which the proportion between the red and white
corpuscles seemed reversed, and the blood had in consequence a
grayish-white appearance. He attributed the condition to an increase in
the colorless corpuscles. A case of Rokitansky's is referred to in this
article. In 1846, Fuller described a case before the Medico-Chirurgical
Society of London, in which the increase in the colorless corpuscles
was noted during life and after death.

In the August and September numbers of _Medicinische Zeitung des
Vereins für Heilkunde_ (1846) Virchow reviewed these four cases, and
insisted upon the fact that the colorless cells in the blood were not
pus, and vindicated a place in pathology for the white blood-corpuscle.
In the January number (1847) of the same journal he gives further cases
of white blood which he had collected in the literature--cases of
Bichat (1801), Velpeau (1827), Caventon (1828), Andral (1839), Barth
(1834),[98] and several others--and discussed the conditions under
which the colorless elements might increase and the relation of the
spleen to the white cells. In the same year (1847), in the first volume
of his _Archiv_, Virchow proposed the name leukæmia. Vogel in 1849
diagnosed a case during life.[99]

[Footnote 98: Donne (_Cours de Microscope_, 1844), who examined Barth's
case, seems to have been the first to recognize that the colorless
cells were blood- and not pus-corpuscles. See note by Gowers in
_Lancet_, i., 1878.]

[Footnote 99: _Virchow's Archiv_, Bd. iii.]

Bennett in 1851 collected additional cases, and gave the name of
leucocythemia to the disease, and in 1852 published a monograph
entitled _Leucocythemia; or, White-celled Blood, in Relation to the
Physiology and Pathology of the Lymph-gland System_. He claimed
priority in the discovery of the condition, and for several years a
lively paper war raged between the Edinburgh and the Berlin professors.

At this distance of time and place we can, now that the clouds of
controversy have blown away, see the truth. Bennett certainly described
cases before Virchow, but only in a manner similar to that in which
Bichat, Velpeau, and others had previously done, and he distinctly
stated his belief that the grayish-white color of the blood was due to
pus. Virchow from the first grasped the idea that the altered state of
the blood was due to an increase in the colorless cells, and he first
suggested the relation between their increase and the condition of the
spleen and lymph-glands, and he first gave a satisfactory name to the
disease; so that, while acknowledging the great and valuable services
of Bennett, we must, perforce, recognize the greater merit {909} of
Virchow, and recognize his priority in the scientific description of
the disease and in giving to it a suitable name. The further
investigations of Virchow enabled a splenic and a lymphatic form to be
recognized, and many years later Neumann[100] described the myelogenous
variety.

[Footnote 100: _Archiv der Heilkunde_, Bd. xi.]

FORMS OF THE DISEASE.--According as the pathological changes are
located in the spleen, lymph-glands, or marrow we speak of splenic,
lymphatic, and medullary or myelogenous forms; but it is very
exceptional for pure unmixed varieties to occur. More commonly, the
spleen and marrow, or these with the lymph-glands, are involved. The
disease may begin and make great progress in one of these regions, or
be confined to it for months, before appearing elsewhere. The spleen is
most often affected, and with it the marrow. According to many recent
writers, the myelogenous form is the most general, and certainly the
marrow is rarely found unchanged. The unmixed lymphatic variety is not
of frequent occurrence. An intestinal form, characterized by swelling
of the solitary and agminated lymph-glands and the general adenoid
tissue of the bowel, has been described by Behier.[101] In a few
instances the tonsillar and pharyngeal lymph-elements have been early,
perhaps primarily affected, and Kaposi has recently recorded a
case[102] under the name lymphoderma perniciosa, in which the lymphatic
elements of the skin were first involved.

[Footnote 101: _L'Union médicale_, 1869.]

[Footnote 102: _Wiener Med. Jahrbücher_, 1885.]

ETIOLOGY.--We know scarcely anything of the causes of the disease, but
it is usual to take into account certain factors which may possibly
influence its production, such as climate and country, age, sex, etc.

Climate and Country.--The disease appears to be more common in
temperate regions; not many instances are reported from the tropics. It
does not appear to be often met with in India. It is, I think, more
common in Europe than in this country. The determination of its
prevalence is rendered difficult by the fact that many cases reported
simply as enlarged spleen, without any examination of the blood, have
possibly been leukæmia. It does not seem to be more common in the
southern part of this continent.

Age.--No age appears exempt. Cases are recorded in infants of eight or
ten weeks and in men of sixty-nine and seventy years of age. The
youngest case I have seen was in a suckling of eight months. The
majority of cases occur at the middle period of life, from thirty to
forty. After the fiftieth year the cases diminish very much in number.

Sex.--Males are more prone to the affection than females, in the
proportion of at least 2 to 1. Of 11 cases which I saw in Montreal,
only 3 were in females; of 200 cases collected in the literature, 135
were in males and 65 in females (Birch-Hirschfeld[103]).

[Footnote 103: _Lehrbuch der Path. Anatomie_, 2te Auf., 1883.]

Social and sanitary conditions do not appear to have much influence,
though the lower and middle classes furnish the majority of the cases.
Mental worry and depression are specially mentioned as predisposing
causes in some cases.

Previous Disease.--In women it has frequently been noticed that
disturbance in the menstrual and sexual functions has preceded the
onset of the disease. The climacteric period has the greatest number of
cases, and in a few instances the disease had developed during
pregnancy.

The hemorrhagic diathesis has been noted in many cases, and the patient
may have been the subject of slight hemorrhages for years. In one case
of Howard's[104] the lad had been subject to nose-bleeding as a child,
and his mother and one sister had been much troubled in the same way.

[Footnote 104: _Montreal Gen. Hosp. Reports_, vol. i., 1880.]

Malaria.--On account of the frequency of chronic splenic tumor in
malarial infection, inquiries are always carefully made in any
suspected case as to the occurrence of intermittent fever. An intimate
connection is believed by {910} certain writers to exist between the
affections, and a few cases seem to have followed directly upon chronic
malaria. In Mosler's statistics of 112 cases there were only 4 in which
the sequence was well marked.[105] In Gowers' 150 cases there was a
history of malaria in 30.[106] In the Montreal cases there was an
account of malaria in 3 certainly--possibly in a fourth. In the reports
of 33 American cases there were only 6 with a history of malarial
attacks within twelve years from the date of the onset of leukæmia.
Guiteras of Key West (now of Charleston, S.C.) states that it is a rare
affection in the South. Schmidt of New Orleans writes me that it is not
uncommon in Louisiana, but there are very few cases reported in
Southern journals.

[Footnote 105: _Die Leukæmie_, Berlin, 1872.]

[Footnote 106: _Reynolds's System_, art. "Leucocythæmia."]

Syphilis appears to have been in a few cases closely connected with the
onset of the disease.

Injury.--Many patients give an account of a blow or strain in lifting.
In 3 cases which I have seen the patients laid great stress on this.
One had received a kick in the side from a horse, and the two others
had strained themselves in lifting. De Chapelle[107] has dealt
specially with this feature in the etiology of the disease.

[Footnote 107: _De la Leukémie dans ses Rapports avec la Traumatisme_,
Paris, 1881.]

Previously-existing splenic enlargement does not seem, as we might
expect, to predispose to leukæmia. It is rare for a case of simple
chronic hyperplasia of the spleen--from malaria, for instance--to
terminate in leukæmia.

The disease occurs in the lower animals, and cases have been described
in horses, dogs, oxen, cats, swine, dogs, and mice. The majority of
cases have been in dogs.[108] A study of the comparative pathology of
the disease has not thrown any light on the etiology.

[Footnote 108: Siedamgrotzky, _Ueber die Leukæmie bei den Hausthieren_,
Leipzig, 1878; Bollinger, _Virchow's Archiv_, lix.; _London Med.
Record_, vol. ii., 1874.]

SYMPTOMS.--A division of the disease into two or three stages has been
made by some writers, but as no special regularity is observed in the
sequence of events, we need only recognize a period of development, in
which the disease gradually becomes established, and a final period of
cachexia, when there are symptoms of profound blood-change and the
viscera are involved.

The mode of onset is insidious. In the majority of cases there is
failure in health and strength, and the patient seeks advice for
progressive enlargement of the abdomen with dragging pain in the side,
or for the shortness of breath, the enlarged lymph-glands, the pallor,
or the various symptoms of anæmia, as headache, palpitation, and
dizziness. Bleeding at the nose is common. Vomiting and diarrhoea may
be early symptoms, and in a few cases oedema of the face and feet has
been noted early in the disease. Occasionally the first symptoms to
attract the attention of friends or physician are of a serious
nature--a sudden hemorrhage, for example. In one of Howard's cases the
lad had played lacrosse two days before the onset of the fatal
hæmatemesis, and in another case, a girl, there was early and fatal
hemorrhage from the stomach before the condition of splenic enlargement
was suspected.

Digestive System.--Gastric symptoms are rarely absent in the form of
oppression after eating, nausea, and vomiting; the latter may be an
early and troublesome feature. The appetite is variable, and when the
spleen is greatly enlarged the mechanical pressure is apt to cause
uneasy feelings after eating.

Diarrhoea is common, and may come on very early in the disease (Case
I.[109]), and it is a frequent cause of death. The stools are usually
thin and catarrhal, not often dysenteric, but melæna occurs in many
cases. The diarrhoea may be due to a dysenteric process in the colon
(Case II.), and tenesmus may {911} be present. It has not been noted
that the diarrhoea is more frequent when the lymph-glands of the
intestines are involved.

[Footnote 109: These figures refer to Montreal cases, some of which I
saw with my colleague, Palmer Howard, others with John Bell,
Lachapelle, and G. T. Ross.]

The liver shows no alterations in the early stage, but as the disease
advances it is almost invariably enlarged. Jaundice is not often
present, but there may be recurrent attacks (Case II.), due either to
catarrh of the ducts or to pressure of glands in the hilus. Ascites is
a variable feature; a slight degree is not uncommon as part of a
general dropsy dependent upon the blood-condition, but in some cases it
is a prominent symptom and calls for frequent tappings (Case IX.). In
some cases it is due to pressure of leukæmic growths in the branches of
the portal vein or the liver, or of enlarged glands upon the trunk at
the hilus. The ascites is not always hepatic; like the hæmatemesis and
melæna, it may be of splenic origin and occur without any disturbance
in the portal vein or liver. Leukæmic peritonitis has been met
with.[110]

[Footnote 110: Willcocks, _Proceedings of Conn. Med. Soc._, 1874.]

Nervous System.--Headache, dizziness, and attacks of fainting are
common, and due chiefly to the anæmia. In some cases the headache is
severe and persistent. The intelligence is well preserved; only toward
the close is there rambling delirium. Mental disturbance may occur, and
in one case the patient committed suicide. Some writers speak of
special sadness and moroseness. This I have never noticed; on the
contrary, in most of the cases I have seen the patients seemed
specially tranquil and resigned. Coma may come on suddenly from
cerebral hemorrhage (Case X.).

Sleep is not usually disturbed; some patients doze incessantly.

Special Senses.--Weak vision is often complained of, due to the anæmia,
sometimes to the leukæmic retinitis. Blindness rarely supervenes, even
when the retinal changes are extensive. Marked intolerance of light may
be present.

The condition of the retina is variable. There may be simply turbidity
and swelling of the retina, with large and tortuous veins, or more
commonly with the opacity there are hemorrhages, such as occur in
profound anæmia from any cause. A peculiarity, however, of the
extravasations in some cases of leukæmic retinitis is the appearance
produced by the aggregation of colorless corpuscles, often in the
centre of the hemorrhage, so that there is a yellow or white nucleus
and a zone of red. The collections of colorless corpuscles may indeed
have the characters of small leukæmic growths. In one case (XI.)
throughout the retinæ were numerous small raised opaque white bodies
one to two millimeters in diameter, some of them surrounded by rings of
extravasation. There was no swelling of the disk.

Deafness has been frequently observed, and may appear early. It was
specially noted in the cases of Edes,[111] Morrill,[112] Seguin,[113]
and Pepper,[114] and DaCosta.[115] No satisfactory explanation has been
given, and the suggestion that it is due to hemorrhage has not, so far
as I know, been confirmed by autopsy. Noises in the ears may be very
troublesome, and even be so bad as to disturb hearing and necessitate
the writing of questions (Case XI.).

[Footnote 111: _Boston Med. and Surg. Journal_, 1871.]

[Footnote 112: _Loc. cit._]

[Footnote 113: _Archives of Scientific and Practical Medicine_, New
York, 1873.]

[Footnote 114: _Med. and Surg. Reporter_, 1883, 48.]

[Footnote 115: _Ibid._, 1874.]

Blood-vascular System.--In a well-marked case the blood-drop squeezed
from the finger-tip is more or less turbid, of a reddish-brown or in
extreme cases chocolate-brown color.

The blood should be examined in a thin layer, and for this purpose it
is better to take a small than a large drop. A rough estimation of the
proportion of white corpuscles can be much better obtained when a
uniform thin layer is beneath the top cover. The red corpuscles, as a
rule, present no striking changes, no special alterations in size or
shape. Microcytes are {912} occasionally seen, and now and then larger
forms, but the extreme variations of pernicious anæmia are rarely met
with. They are reduced in number, but not often to a great extent. A
reduction below 2,000,000 to the cubic millimeter has been exceptional
in cases which I have examined. In only one did the number sink to
1,500,000 per c.m. Laache[116] has noted a case in which, with
enlargement of the spleen and a ratio of white to red of 1:17, the
number of red corpuscles was little if at all reduced.

[Footnote 116: _Die Anämie_, Christiania, 1883.]

The colorless corpuscles are enormously increased. Instead of eight to
ten millions per c.m., as in normal blood, they may reach 500,000 per
c.m. or even 700,000 per c.m. The ratio of white to red cells may be
1:20, 1:10, 1:4, or they may even equal or exceed the red. Without a
proper apparatus (Gowers, Malassez, or Zeiss) an accurate estimate is
impossible, and it is chiefly upon the rough-and-ready method that the
statements are made of the white exceeding the red in numbers. It is
very seldom indeed that this is the case, and even in extreme leukæmia
the ratio does not often reach 1:3 or 1:2. In none of my observations
did the ratio rise to 1:1; the highest was 1:2. Cases are on record in
which the white have exceeded the red: Sörensen's,[117] where the red
per c.m. were 470,000 and the white 680,000, and in an interesting
observation of Fleischer and Penzoldt,[118] as a mean of 57 accurate
counts, the ratio of white to red was 115:100. The corpuscles have the
natural grayish-white appearance of leucocytes, but differ in certain
points from normal white blood-cells. The variations in size are
greater: in normal blood only a few may be seen less than 1/2800 or
1/3000 of an inch, but in leukæmia on a single slide there may be
colorless cells with the extreme measurements of 1/2000 and 1/3500. In
ordinary cases we meet with--(1) cells of the average size, about
1/2800 of an inch in diameter, like normal corpuscles, with two or
three nuclei and fine granular protoplasm; (2) smaller forms, 1/3000 of
an inch and under, with single nuclei, resembling rather lymph-cells,
and they were believed by Virchow to indicate special involvement of
the lymph-glands, but they are present in all forms, though possibly
more prevalent in the lymphatic variety; (3) large forms, 1/2000 to
1/1500 of an inch, with bold nuclei and bearing a close resemblance to
the marrow-cells. They are not always present, and are believed to
originate in the marrow.

[Footnote 117: _Virchow-Hirsch's Jahresber._, 1874.]

[Footnote 118: _Deutsches Archiv f. klin. Med._, Bd. xxvi.]

Cafavy states[119] that the colorless corpuscles of leukæmia do not
display active amoeboid changes, indicating thereby a diseased and
enfeebled condition of protoplasm. I find a note made in Sanderson's
laboratory in 1873 on the very sluggish and imperfect movements of the
colorless corpuscles in a case of leukæmia in University College
Hospital. In Case V. the note on one day is, "Active amoeboid changes,"
and in two other cases since Cafavy's paper I have seen the
protoplasmic movements tolerably active, but not in all equally.
Possibly the leucocytes from the marrow do not move so freely as the
others; normal marrow-cells have very feeble amoeboid powers.
Ehrlich[120] has observed that the number of leucocytes in leukæmic
blood which contain granules reacting with eosin is very great, whereas
in normal blood very few occur.

[Footnote 119: _Lancet_, ii., 1880.]

[Footnote 120: _Zeitschrift f. klin. Med._, Bd. i.]

Nucleated red blood-corpuscles, such as occur in the blood of the
foetus and in the red marrow of the adult, have been found in leukæmic
blood by Klebs, Mosler, and others. I have observed them in four cases.
They are scanty, usually isolated, rarely more than one or two in a
field; often, indeed, many fields must be searched before finding one.
On two occasions (Case IX.) they might be called numerous--three or
four in each field of the No. 9 immersion lens.

Schultze's granule-masses, the aggregations of the discoid
hæmatoblasts, are {913} present in variable numbers, sometimes very
numerous. I have examined slides in which they were absent. A curious
mistake was made by a writer in the _Lancet_ (1878, ii.) when he
described these as a hitherto unnoticed feature of the blood in
leukæmia.

The fibrin network which separates between the corpuscles is usually
very thick and dense.

Peculiar crystals, elongated octahedra or spindles, of variable size
and bright-white appearance, separate very commonly on a slide of
leukæmic blood, particularly if kept surrounded with oil or paraffin
for twenty-four hours. They are known as Charcot's crystals, and are
identical with those which occur in the bone-marrow, in semen, and in
sputum in some cases of bronchitic asthma. White of Boston described
them well in 1859,[121] and believed they were produced by the
separation of a neutral principle which he named leukosin. I can
confirm Zenker's observation,[122] that they form sometimes in the
colorless cells.

[Footnote 121: _Boston Medical and Surg. Journal_.]

[Footnote 122: _Deutsches Archiv f. klin. Med._, xviii.]

Leukæmic differs from ordinary blood, and from that of other anæmic or
cachectic states, by the readiness with which the hæmoglobin
crystallizes. Often if a slide is kept and prevented from evaporating
by a rim of paraffin, beautiful plates of hæmoglobin will crystallize.

The pulse is always quickened--80 to 100, and in the final stages
110-130--usually soft and compressible, and not always small in volume.
The heart's action is readily excited. A systolic murmur is not
infrequent at the apex; basic hæmic murmurs are not so often heard as
in anæmia, but a venous hum in the neck is generally present. The
apex-beat of the heart may be pushed up an interspace by the enlarged
spleen. Oedema of the ankles and feet from the feeble circulation is
constantly met with, particularly toward the close, and there may be
general anasarca. Effusion into the pleural cavities is not common.

Hemorrhages are among the most constant features of the disease, and
may occur at any time, early or late, in the course. The tendency to
bleeding is greater in this than in any of the allied affections.
Epistaxis is the most frequent form, and may precede the development of
the disease for months or years. Hæmatemesis may carry off a patient
early (Case II.), or even before the nature of the trouble is suspected
(Case VI.). Hemorrhage from the bowel is common. Hæmoptysis and
hæmaturia are rare. Bleeding from the gums may be present (Cases V. and
VII.). In women there may be profuse menstruation. Petechiæ on the skin
are frequent; occasionally there are large extravasations beneath the
skin or between the muscles. Hemorrhage into the brain may prove
quickly fatal (Case X.), and the extravasations into the retinæ may
impair vision.

The respiratory system offers few special symptoms. The shortness of
breath on exertion is due in great part to the anæmia, and
progressively increases with the advance of the disease. The free
action of the diaphragm is hampered by the enlarged spleen. There may
be cough from bronchitis, and toward the end signs of oedema at the
bases of the lungs. Pneumonia is not uncommon as a final complication.

The temperature in the early stages presents very slight variations,
but when the disease is advanced there is always fever of the remittent
or of the continuous type. There is usually a morning remission, and an
evening exacerbation which reaches 101° or 103°. Periods of pyrexia may
alternate with prolonged intervals of freedom from fever. In some cases
the febrile movement is very slight throughout the entire course.

Genito-urinary System.--The urine is usually normal in amount, pale,
strongly acid, and its specific gravity above the normal. Considerable
variations occur in individual cases. Sediments of lithates are very
common. {914} The urea presents no constant changes; sometimes it is
increased, at others diminished, the quantity depending probably on the
food and the presence or absence of fever. The quantity of uric acid
excreted seems always to be increased, due either to a lessening of the
oxidation processes in consequence of the reduced number of red
corpuscles, or, as Salkowski suggests, it stands in relation to the
existing splenic tumor; but observers have not found the amount
proportionately increased in other forms of splenic enlargement, and
the cause of the constant increase is still doubtful. Hypoxanthine,
lactic, formic, acetic, and hippuric acids have been found, but their
presence is neither constant nor apparently of special import. Albumen
may be present. Sugar is rare. Hæmaturia, as before observed, very
seldom occurs. Cystitis may arise and be troublesome (Case XI.).

A curious symptom in connection with the generative system is priapism,
of which a number of cases have been recorded. Edes[123] narrates the
case of a boy of fifteen in whom obstinate priapism was the first
symptom. Longuet[124] reports a case of six weeks' duration.
Saltzer[125] mentions five cases, in one of which the condition
persisted for seven weeks, and Peabody[126] gives a case in which it
lasted six weeks. It is not definitely settled whether the priapism is
due to thrombosis in the corpora cavernosa or to irritation of the
nervi errigentes.

[Footnote 123: _Boston Med. and Surg. Journ._, 1871.]

[Footnote 124: _Progrès méd._, 1875.]

[Footnote 125: _Berliner klin. Wochenschrift_, 1879.]

[Footnote 126: _New York Med. Journ._, 1880, xxi.]

In women there are the usual menstrual irregularities consequent upon a
grave constitutional disease. Occasionally the flow is excessive; more
commonly it is interrupted altogether.

Blood-glandular System.--Slow increase in the volume of the spleen,
causing a sense of weight in the left hypochondrium, is an early
symptom in many cases. Patients do not usually come under observation
until the enlargement is established and the organ can be felt below
the costal border. Pain and tenderness over the organ are very common,
though sometimes it is painless throughout. Palpation often elicits a
creaking fremitus due to the rubbing together of the adhesions. The
gradual enlargement causes an evident increase of girth in the lower
thoracic and upper abdominal zones, and marked prominence of the left
hypochondrium. The tumor extends to the right and downward, and may
occupy a large portion of the abdomen, extending even to the pelvis.
When there is no ascites the edge can be easily felt with the anterior
notch or notches. The pressure of a large spleen causes distress after
a full meal, and by its mechanical effect may even compress the bowels
and produce fatal obstruction.[127] The effect upon the heart and
respiration has already been noticed. The adhesions may interfere with
the depression of the organ during a deep inspiration. The size varies
in an inexplicable way, considering the indurated fibroid nature of the
enlargement. It may be perceptibly larger after a meal.[128] A
hemorrhage or free diarrhoea may reduce the size very much, as in
Morrill's case.[129] A murmur may occasionally be heard, and an
enlarged spleen has been known to pulsate.[130]

[Footnote 127: Collins, _Brit. Med. Journ._, 1882, i.]

[Footnote 128: Johnson, _Lancet_, 1870, Jan.]

[Footnote 129: _Bost. Med. Journ._, 1877.]

[Footnote 130: Gerhardt, _Zeitschrift f. klin. Medicin_, Berlin, Bd.
iv.]

Lymphatic Glands.--In the great majority of cases the lymph-glands are
but slightly if at all involved. Even when they are affected it is rare
to see such large bunches as in Hodgkin's disease. When they are
growing there may be pain and tenderness, and if large they may be a
source of inconvenience, but severe pressure symptoms are not often
witnessed. Enlargement of the glands in the superficial groups is
readily detected, but the deep-seated collections in the mesentery and
retro-peritoneum can rarely be palpated unless of considerable size.
Mediastinal lymph-tumors in leukæmia are exceptional. In none of the
cases I have seen were the lymph-glands {915} greatly enlarged. It is
stated that in children the lymphatic variety is more common than in
adults.

There may be tenderness over the bones, and in rare instances swelling,
but unless the tenderness is marked and accompanied by some local
expansion or softening, we cannot determine positively the existence of
the myelogenous variety. The sternum, ribs, and flat bones are most
often affected, and there may be great irregularity and deformities, as
in a case I saw with Riess of Berlin. It is well to bear in mind that
in perhaps the majority of persons there is a tender spot upon the
sternum which may cause marked wincing when touched firmly. No reliance
should be placed upon tenderness without swelling or softening. Such
tenderness may exist, and post-mortem the marrow be found normal;[131]
and, on the other hand, there may be extensive changes in the
bone-marrow without any tenderness (Litten).

[Footnote 131: _Deutsches Archiv f. klin. Med._, xxvi.]

MORBID ANATOMY.--There may be extreme wasting. Dropsy of the feet is
common, and ascites may be present.

A noteworthy feature is the full amount of blood in the heart and
blood-vessels, usually in the form of large coagula. In one case (XI.)
the weight of clots alone in the heart-chambers, not including what
came from the veins, was 620 grammes. The portal, cerebral, pulmonary,
and subcutaneous vessels were also greatly distended with clots. The
portal vein just above the union of the branches measured eleven
centimeters in circumference.

The blood is usually clotted in the heart and vessels, and the
aggregation of the colorless corpuscles densely infiltrating the
fibrinous clots and the serum gives a pus-like appearance, so that it
has not infrequently happened, as in Virchow's memorable case, that the
observer on opening the right auricle believed for the moment that he
had cut into an abscess. The leukæmic clots often have a peculiar
greenish color, and resemble somewhat the fat of the turtle. Similar
coagula may fill the veins of the brain and abdominal viscera. The
tendency of the white corpuscles to aggregate together, and the
subsidence of the red to the lower part of the heart-chambers and
vessels, may give an appearance of more intense leukæmia than actually
exists. The reaction of the blood is usually acid. The chemical
constitution has been carefully studied, but with no very satisfactory
results. Hypoxanthine, lactic acid, leucin, tyrosin, a mucin-like body,
and a gelatinous substance have been described, but none of them may be
regarded as characteristic of the disease. The octahedral crystals are
thought by some to be tyrosin,[132] but Schreiner[133] says they
consist of the phosphate of an organic base, the composition of which
is not yet settled.

[Footnote 132: Huber, _Archiv der Heilkunde_, Bd. xviii.]

[Footnote 133: _Liebig's Annalen_, cxciv.]

The specific gravity of the blood is lowered, 1036 to 1049. The water
is increased. The fibrin in many observations has also been found
increased; 4.8 per 1000 was the average of ten observations by Bennett.
The albumen and the salts have not often been estimated. The former is
stated to be diminished. The fatty bodies have been found in excess of
the normal quantities.

The heart is often pushed up by the large spleen; the pericardium, more
rarely the endocardium, may present ecchymoses, and the fluid may be in
excess. In a few instances leukæmic growths have been met with. The
chambers are usually distended, the walls soft, and a moderate grade of
fatty change is very common. No special alteration has been met with in
the blood-vessels. I have seen extensive fatty degeneration of the
intima and small arteries.

In the great majority of cases the spleen is increased in size, but the
shape is retained. It is usually of a deep violet-red color, and strong
adhesions may unite it to the abdominal wall, diaphragm, or stomach.
The capsule {916} may be greatly thickened, forming a firm
fibro-cartilaginous investment. The vessels are enlarged, particularly
the veins at the hilus. The weight may vary from two to eighteen
pounds. The largest on record is given by Langley Browne[134]--18½
pounds. Six or seven pounds is an average weight. The length may vary
from seven to twenty inches, and the breadth eight to twelve. The organ
is in a condition of chronic hyperplasia--hard, firm, cuts with
resistance, and displays a uniform reddish-brown surface on which the
trabeculæ are more or less prominent. There may be hemorrhages or
infarcts, and it is not uncommon to see regions of yellow or
rusty-brown staining, indicating where an extravasation had occurred.
As a rule, no trace of the Malpighian bodies can be seen.
Grayish-white, circumscribed lymphoid tumors may occur throughout the
organ, contrasting strongly with the reddish-brown matrix. The process
of gradual enlargement is a simple hyperplasia. In the early stage, not
often seen, there is swelling of the pulp, increase in the
cell-elements, without the firmness and induration of the
fully-developed leukæmic organ. Rupture may occur at this period from
the intense hyperæmia. The Malpighian bodies are enlarged and prominent
by their grayish-white color. A gradual and progressive induration
results from the increase in the adenoid network and the fibrous
trabeculæ. A section shows the enormous development of the fibrous
elements. The cells may be scanty, only two or three in meshes, or,
indeed, the reticulum may be so close that only a single cell is
enclosed. As a rule, the hyperplasia extends over the whole organ, and
the Malpighian bodies become involved and lose their distinctness. In
only one of the cases which I have examined were they at all prominent.
Leukæmic new growths in the spleen are rare.

[Footnote 134: _Lancet_, 1877, ii.]

Uncomplicated cases of the lymphatic form are very uncommon: usually
they enlarge with the spleen, and in the majority of instances the
hypertrophy is not extensive, scarcely ever reaching the high grade
seen in Hodgkin's disease. The groups of cervical, axillary,
mesenteric, and inguinal are most frequently affected; the bronchial
and mediastinal but rarely. The bunches of glands are not usually
larger than walnuts, moderately soft, isolated, movable; large matted
groups do not often occur. They may vary a good deal in size during the
course of the disease, often diminishing notably before death. In
chronic cases they may become very indurated. The leukæmic
lymphadenitis is a simple hyperplasia, and the soft glands may look, on
section, of a normal gray color or may have a deep gray-red appearance.
Hemorrhages may occur, and twice I have seen the enlarged glands deeply
hyperæmic. Histologically, the appearance is very like a normal gland,
only the lymph-spaces are more closely packed. In the harder glands the
fibrous reticulum is much increased, the capsule thickened, and the
section more grayish in color. Caseation or suppuration rarely occurs,
and invasion of contiguous parts is most exceptional.

The tonsils and the lymph-follicles of the tongue, pharynx, and mouth
have been found much enlarged.

The bone-marrow is usually the seat of important changes, which in some
cases appear early and persist as very prominent features of the
disease. The most constant alteration is a uniform substitution of a
grayish-red or gray-green puriform-looking tissue for the normal red
and fatty marrow of the long and short bones. The entire medulla may
resemble the consistent matter which forms the core of an abscess, and
the term pyoid applied to this condition by German authors well
expresses the general characters. More rarely the marrow has a
reddish-brown hue. The difference depends largely on the number of
colorless corpuscles, which in the pyoid form are enormously increased,
and there are but few red cells. Ponfick has met with dark-red, dense
hemorrhagic infarctions in leukæmic marrow. The condition of the {917}
bones is variable; usually, the compact and cancellated tissues appear
normal, but the hard shell may be much thinned and expanded, the
cancellæ widened, and the whole substance rendered spongy. In marked
cases there may be localized swellings which are tender, and even
yield, on firm pressure. The sternum and ribs are most frequently
affected in this way. There are instances in which the bone-marrow has
not been involved, and in one case there was osteo-sclerosis.[135]
Histologically, the chief change is hyperplasia of the colorless
marrow-cells, which in the pyoid variety compose the chief part of the
tissue. They vary much in size and appearance. Three forms can usually
be recognized: large granular cells with distinct nuclei; medium-sized
cells, like colorless blood-corpuscles; and smaller forms, like
lymph-cells, with large nuclei and a narrow zone of investing
protoplasm. The red corpuscles and microcytes are in variable numbers.
In one case the latter were very abundant. Nucleated red corpuscles are
very constant elements. Corpuscles containing red blood-corpuscles are
not so numerous as in ordinary red marrow, nor, as a rule, are the
myeloplaques abundant. Charcot's crystals are always to be found--if
not at first, when the marrow is quite fresh, certainly later, when
decomposition has begun.

[Footnote 135: Heuck, _Virchow's Archiv_, lxxviii.]

The thymus is rarely affected, and even in children is not often
swollen. A few cases of enlargement have been recorded.

The thyroid is even less frequently involved.

In one case the suprarenal capsules were large and swollen,[136] and in
addition to the leukæmia there was bronzed skin. Hemorrhage, caseous
degeneration, and in one instance rupture,[137] have been noted.

[Footnote 136: Barclay, _Lancet_, 1863, i.]

[Footnote 137: Fleischer and Penzoldt, _loc. cit._]

In the digestive system the stomach rarely presents any changes other
than catarrhal. Even when death has occurred from hæmatemesis the
mucous membrane may be pale, without erosion, hemorrhage, or ulceration
(Cases II. and VI.). In a few instances lymphatic growths have been
described. In many cases the intestines have been the seat of leukæmic
tumors which have originated in the solitary and agminated glands of
Peyer. Occasionally the lymphoid infiltration is diffuse in the mucosa
and not confined to the follicles. Ulceration may occur in the patches,
and in a few cases the bowel lesions have been so pronounced that the
term intestinal leukæmia seemed justifiable.[138] The cæcum and colon
may also present these new growths, and in a few cases dysenteric
processes have been observed (Case II.). The peritoneum has been found
covered with small lymphoid growths. In Willcocks' case of lymphatic
leukæmia[139] there were growths on the surface of the stomach and
gastro-splenic omentum. Blood may be found in the cavity from rupture
of the spleen. Ascitic fluid is common. Fibroid thickening, induration,
and adhesions are very often met with, particularly in the neighborhood
of the spleen.

[Footnote 138: Behier, _loc. cit._]

[Footnote 139: _Loc. cit._]

The liver is very commonly enlarged, pale, smooth, and retains the
normal shape. It may be greatly increased in size, as in case of
Walshe's, where it weighed 13½ pounds. The substance is usually firm,
of a grayish-brown color, or even marbled. Two chief changes have been
met with--a diffuse leukæmic infiltration and numerous small leukæmic
tumors. The infiltration may be very slight, and not noticeable with
the naked eye, or it may be in the form of irregular scattered areas of
a yellowish-white appearance, not distinctly isolated, but merging into
the hepatic tissue. When moderate, a section shows the columns of
liver-cells to be separated by wide spaces occupied by leucocytes,
which are partly within and partly outside of the capillaries. The
accumulation of these elements produces atrophy of the liver-cells, and
their aggregation and increase in certain regions produce the
grayish-white areas, in the midst of which traces of liver-tissue may
be found. {918} The defined leukæmic growths are small, not often
attaining a large size, and may resemble tubercles. They are usually
situated in the interlobular tissue, and consist of lymphoid cells in a
well-defined reticulum, and they possibly have a different origin from
the diffuse infiltrations.

Fatty degeneration of the liver-cells is a very common change.

The respiratory system is not often the seat of important lesions.
Lymphoid growths have been found in the mucous membrane of the trachea
and bronchi, and occasionally in the lungs, in which situation they may
closely resemble tubercles, but differ from them in not tending to
caseate or soften. Oedema of the bases of the lung is almost always
found. Many patients are carried off by a low pneumonia. The greenish
leukæmic clots projecting from the cut ends of the vessels may give a
very curious appearance to the section of the lung. The pleural
surfaces may be the seat of lymphoid growths.

The kidneys are usually pale, often enlarged, and show signs of
parenchymatous swelling. The capillaries, like those of the liver, may
be distended with leucocytes, and leukæmic tumors may occur, generally
situated in the cortex and ranging in size from a pea to a cherry. In
none of the cases I have examined were there any special changes in
these organs beyond slight enlargement and filling of the capillaries
with leucocytes.

The generative organs are usually normal. No changes have been found to
account for the persistent priapism met with in certain cases.

The meninges of the brain, the veins, and sinuses, are often filled
with grayish clots. Occasionally meningitis has been found, with
exudation of lymph. The small vessels of the brain may be plugged with
leucocytes, forming thrombi, from which softening results. Cerebral
hemorrhage may prove rapidly fatal. In Case X. of the Montreal series
the patient died suddenly, and without any premonition, with a huge
apoplexy of the ventricles and posterior part of the hemispheres.

Leukæmic growths in the skin have been described.

The leukæmic tumors demand further consideration. They are not common.
In 10 of the 11 Montreal cases careful post-mortem examinations were
made, and in not one were there definite new growths. In Case I. there
was diffuse leukæmic infiltration of the liver, the histological
characters of which were carefully studied. In the 157 cases collected
by Gowers[140] there were only 13 instances of leukæmic nodules in the
liver, and 10 in the kidneys. They are still more uncommon in the
lungs. In the spleen--unlike this organ in Hodgkin's disease--they are
very rarely seen. The nodules consist of leucocytes in a meshwork of
delicate reticular tissue. Their mode of origin has been much
discussed. There can be no doubt, I think, that they are new growths of
lymphoid tissue of local origin. Possibly they start from accumulations
of colorless corpuscles which pass out of the capillaries. In the
infiltration of the liver one sees diffuse collections which resemble
new growths, but which have evidently resulted from the aggregation in
and outside of the capillaries of enormous numbers of leucocytes, which
cause the atrophy of the cells of the organ. Doubtless, they multiply
in loco by a process of fission, and these aggregations may themselves
be foci for the origin and development of colorless cells which pass
into the blood-current and augment the number.[141] Quite recently
Bizzozero has studied the development of these leukæmic new growths,
and has shown clearly that the cells which compose them are in process
of active fission.

[Footnote 140: _Loc. cit._]

[Footnote 141: "On the Histology of Leucocythæmia," _Canada Medical and
Surgical Journal_, 1876.]

The COURSE OF THE DISEASE is slow and chronic, a matter of months and
years. There are exceptional instances in which the disease has proved
fatal in a few weeks; this occurs sometimes in children,[142] but acute
leukæmia is {919} very rare. In a table of 63 cases collected by
Gowers, in which the date of the first symptoms was fixed with
tolerable accuracy, the duration was less than one year in 13 cases;
from one to two years in 16; from two to three years in 19; from three
to four years in 9; from 4 to 5 years in 3; and five years and upward
in 3 cases. The course is rarely uniform, but periods of improvement
occur in which the fever subsides, the painful sensations in the
abdomen diminish, the appetite improves, and the spleen reduces in
volume. Such intervals, corresponding to the administration of certain
drugs, are apt to lead to therapeutic errors. A patient may sometimes
get about for months, and even attend to a light business, with an
enormous spleen and a ratio of white to red corpuscles of 1 to 6 (Case
VIII.). Hemorrhages, high fever, profuse diarrhoea, and the occurrence
of dropsy shorten the course. Toward the close there is great muscular
debility, and usually a wandering delirium.

[Footnote 142: Golitzinsky, _Jahrb. f. Kinderheilkunde_, 1860-61.]

In the majority of cases death is by asthenia--a gradually progressive
weakness and ultimate failure of the heart. Diarrhoea and hemorrhage
hasten the fatal result. A profuse hemorrhage may cut off a patient
early or after the disease is well established. Cerebral hemorrhage was
noticed in 6 of 60 cases in which Gowers was able to ascertain
accurately the cause of death. A few are carried off by pleurisy or
pneumonia or peritonitis after tapping.

Pyæmia and rupture of the spleen are mentioned as causes of death in
some cases.

The DIAGNOSIS of leukæmia rests upon the determination of a great and
persistent increase in the colorless elements of the blood. Cases of
Hodgkin's disease and of splenic anæmia, almost identical in general
features, can only be distinguished by an examination of the blood. I
should say that in any case we can speak of the blood as leukæmia when
the ratio of white to red cells falls below 1 to 50. Some writers hold
that to determine leukæmia the ratio should be at least 1 to 20, but
when the study of the variations in the proportion of the corpuscles in
any case extends over weeks or months, we not uncommonly find that the
ratio, which, at one observation may be 1 to 8, or 1 to 10, a week
later may be 1 to 60 or 80, or even 150. Indeed, the state of the blood
is a variable factor, and too close attention to it has diverted our
minds from the broad features which this disease has in common with
others. For practical clinical purposes we have to distinguish ordinary
lieno-lymphatic leukæmia from--(1st) chronic malarial infection with
splenic hypertrophy; (2d) from cases of non-malarial splenic
enlargements with anæmia; (3d) from general lymphadenoma or Hodgkin's
disease. The history in malarial cachexia, the absence of lymphatic
enlargement, and the blood-condition will usually be sufficient for
purposes of a diagnosis. Great increase in the white blood-corpuscles
is not often seen in the chronic splenic tumor of malaria; indeed they
may be much diminished in number. Toward the end in very chronic cases
the clinical picture may be very similar: the large abdomen, possibly
ascites, dropsy of the feet, and irregular fever may resemble closely
splenic leukæmia, and the absence of an increase in the colorless
corpuscles may be the only marked difference. From anæmia splenica
there is still greater difficulty, and I have seen instances in which
the absence of an excess of the colorless corpuscles in the blood
formed the sole criterion: the hemorrhages, the dropsy of feet and
abdomen, retinal extravasations, the general cachexia, and the fever
were identical with those of leukæmia. Still greater may be the
difficulty of separating certain cases of lymphatic leukæmia from
general lymphadenoma or Hodgkin's disease; but in the latter affection
the glandular enlargement is usually greater and altogether a more
prominent feature, and the spleen is not so often increased in size.
There may, however, be a considerable increase in the number of the
white corpuscles, 1 to 150 or 1 to 100 red, and cases do occur which
appear intermediate {920} or transitional in character, and upon which
judgment must be reserved until the progress of the case decides the
question.

Pure cases of myelogenous leukæmia are almost unknown; if the osseous
symptoms are not marked the course is very like that of pernicious
anæmia. Indeed, there are two interesting cases on record in which the
progressive anæmia seemed to pass into leukæmia. In Litten's case[143]
the patient presented the symptoms of profound anæmia, and five days
before death the blood became markedly leukæmic. There was no
enlargement of spleen or lymph-glands, but the bone-marrow was
intensely leukæmic--_i.e._ of the pyoid form. In the case reported by
Leube and Fleischer[144] the patient, aged thirty, four months after
her confinement became anæmic and the left leg was swollen. Though at
first only anæmic, subsequently the ratio of white to red corpuscles
rose to 1 in 10. Gangrene of the leg supervened, necessitating
amputation, from the effects of which she died. There was no affection
of spleen or lymph-glands, but the marrow was of the red lymphoid
variety. A gastric ulcer was also present. This was no doubt a case of
post-partum anæmia aggravated by the presence of ulcer of the stomach,
and the great interest of the case lies in the transition of the anæmia
into leukæmia.

[Footnote 143: _Berliner klin. Wochenschrift_, 1877.]

[Footnote 144: _Virchow's Archiv_, lxxxiii.]

There are certain general conditions, accompanied by an increase in the
colorless corpuscles, which must be distinguished from leukæmia. In
suppuration there may be marked leucocytosis; so also in cancer and
protracted cachectic states, as phthisis. In cases with large cancerous
masses about the stomach and omentum, or where, as occasionally happens
in chronic phthisis, there is a greatly enlarged amyloid spleen, if the
white blood-corpuscles are much increased, care may be necessary to
escape a mistake in diagnosis. In diphtheria the colorless elements may
be much increased. Bouchat says that in some instances there may be an
acute leukæmia.[145] In puerperal fever also the condition of
leucocytosis is not uncommon.

[Footnote 145: _Gazette des Hôpitaux_, 1877.]

The PROGNOSIS is in the highest degree unfavorable, and in those cases,
few, indeed, in number, in which there were symptoms like leukæmia and
which disappeared under treatment, the doubt remains whether they were
true examples of the disease. When once established, the spleen and
glands enlarged, the hemorrhages and dropsies present, and the blood
condition marked, death is the only termination to be expected.
Specially unfavorable signs are a tendency to hemorrhage, persistent
diarrhoea, early dropsy, rapid increase in the splenic tumor, great
excess of colorless corpuscles, and high fever. Temporary improvement
may occur for weeks or even months, and the white blood-corpuscles
reduce in number, but such breaks are usually transient.

TREATMENT.--If, as some writers hold, chronic malarial poisoning is an
important factor in the induction of leukæmia, we should take special
pains with patients so affected, and endeavor by the use of quinine and
arsenic to free the system and reduce the volume of the spleen. There
certainly may be danger of the development of leukæmia in any case of
chronic splenic tumor, though my own experience has been that in these
cases the production of anæmia of high grade, without increase in the
white blood-corpuscles, is more common. It is a mistake to suppose that
anæmia always accompanies chronic splenic enlargement: it may persist
for years with a percentage of red corpuscles little if at all below
normal, but grave anæmia or leukæmia are probabilities to be dreaded.

In an early stage, when the spleen is moderately enlarged, the
lymph-glands scarcely swollen, and the leucocytosis not intense, there
is a hope that by the persistent use of quinine, iron, and arsenic a
cure may be effected; but when the disease is fully established and the
leukæmia marked, a recovery {921} is rarely if ever witnessed, and the
treatment is largely palliative and symptomatic. To reduce the volume
of the spleen various remedies are recommended, and so long as the
organ is only moderately enlarged and hardened some of them may be
beneficial. Quinine should be given a full and prolonged trial, as
undoubtedly under its use the organ may reduce in size. As anæmia is
almost always present, iron may be administered at the same time. That
the quinine has any special influence over the production of the white
corpuscles, as some think, I have not been able to satisfy myself. To
be of use, it must be employed early and in large doses. Ergotin
internally and by injection into the spleen has been recommended. I
have not seen any permanent benefit from its use. Local measures, such
as inunction of biniodide of mercury ointment over the spleen, the
interrupted voltaic current, the application of cold, either ice or the
cold douche, may be employed. Moderate reduction in the volume may be
effected by these means--most effectually by the electricity and
mercurial inunction.

Arsenic should always be given a trial, and pushed for several months
in increasing doses. Several cases are reported in which the
improvement lasted for many months. Direct injections into the spleen
are also of service. Phosphorus, from which much was expected after the
favorable reports of Broadbent and Wilson Fox, has not proved of much
value. There are very curious remissions in the course of the disease
which render therapeutical deductions somewhat fallacious. I have seen
the most marked improvement occur without any special treatment:
ascites and dyspnoea disappear, the white corpuscles decrease in
number, and the patient from a bed-ridden, wretched condition get up,
attend to light duties, and walk half a mile to hospital (Case IX.). In
Case VIII. there were also during eighteen months remarkable
variations, depending more on the state of the gastro-intestinal canal
than the blood condition.

Transfusion has proved useless. Leukæmic blood to the amount of several
ounces has been withdrawn and other healthy blood substituted.

Excision of the spleen has been frequently practised in leukæmia.
Collier[146] gives a résumé of 16 cases, and concludes that it is a
useless and unjustifiable operation, as all of them proved fatal. A
successful case, however, is reported from Italy. If performed early,
there is a possibility of success, but when the organ is enormously
enlarged and the blood intensely leukæmic, the conditions are most
unfavorable.

[Footnote 146: _Lancet_, 1882, i.]

Gastric symptoms and diarrhoea call for careful treatment, as the
comfort of the patient depends largely on the condition of the primæ
viæ. Hemorrhage is frequent, and is a dangerous symptom, particularly
when it depends upon engorgement of the portal system, and calls for
appropriate remedies. Purgatives are to be employed with caution. The
dragging pain in the left hypochondrium, and the sense of weight and
distension after eating, are very distressing, and the splenic pain may
require sedatives. Inhalations of oxygen relieve the dyspnoea and have
been found to check the progress of the disease.


HODGKIN'S DISEASE.

DEFINITION.--A disease characterized by progressive hyperplasia of the
lymph-glands, sometimes also of the spleen, with anæmia and the
development of secondary lymphatic growths in various parts of the
body.

SYNONYMS.--Pseudo-leukæmia; General lymphadenoma; Malignant {922}
lymphoma (Billroth); Lympho-sarcoma (Virchow); Adénie (Trousseau);
Desmoid carcinoma (Wagner); Anæmia lymphatica (Wilks); Lymphatic
cachexia (Mursick); Adenoid disease (Southey).

HISTORY.--Morgagni and other writers mention cases of enlargement of
the lymph-glands proving fatal, but Hodgkin of Guy's Hospital first
called special attention to the subject in a paper before the
Medico-chirurgical Society of London,[147] entitled "On Some Morbid
Appearances of the Absorbent Glands and Spleen." Some of the cases then
described were undoubtedly examples of scrofulous glands, but four at
least were instances of the disease which now bears his name; and at
the meeting of the London Pathological Society in 1878, when a
discussion on lymphatic disease took place, Wilks exhibited the
original specimens collected by Hodgkin. Other cases were recorded in
England by several observers, and in 1856, Wilks[148] reported several
examples of enlarged lymph-glands with growths in the spleen associated
with anæmia, but without any leukæmia; and again in 1865 this observer
published additional cases,[149] and gave the name of Hodgkin's disease
to the affection characterized by enlargement of the lymph-glands,
growths in the spleen and other organs, and anæmia. The cases and
discussions contained in the _Transactions_ of the Pathological Society
of London and Gowers' exhaustive article in _Reynolds's System of
Medicine_ embrace the most valuable of the English contributions. In
Germany, Virchow described the cases under the term lympho-sarcoma, and
in his work on tumors gave a full account of the histology. Billroth
gave the term malignant lymphoma to these growths to distinguish them
from local non-infective lympho-sarcomas. Cohnheim and Wunderlich used
the term pseudo-leukæmia to express the distinction between these cases
and leukæmic enlargements.

[Footnote 147: _Transactions_, vol. xvii., 1832.]

[Footnote 148: _Guy's Hospital Reports_, 3d Series, vol. ii.]

[Footnote 149: _Ibid._, vol. ix.]

In France, Trousseau described it under the term adénie, and Ranvier
used the term lymph-adénie. In America many cases have been described,
and one of the first and fullest analyses of recorded observations is
by J. H. Hutchinson in the _Transactions_ of the College of Physicians
of Philadelphia, Series 3, vol. i.

ETIOLOGY.--No satisfactory etiological relations have been determined
in the disease.

Age has an important predisposing influence. The majority of the cases
are young persons. In Gowers' table of 100 cases, 30 were under twenty
years, 34 between twenty and forty, and 36 above forty. Most of the
cases I have seen have been in young adults.

Sex has a still more marked influence; at least three-fourths of all
cases are in males, the proportion being considerably higher than in
leukæmia--75 per cent. in Gowers' tables, and 40 out of 58 in
Hutchinson's tables.[150]

[Footnote 150: _Loc. cit._]

Heredity has in a few instances been adduced as a possible cause, but
not, I think, on very reliable grounds. In two cases (II. and
III.[151]) the patients were each a twin. It might be supposed that
members of tuberculous families, or those who had suffered from
scrofulous enlargements when young, would be more liable to the
disease, but the cases in which such connection can be traced are very
few in number.

[Footnote 151: These figures refer to cases of which I have notes.]

Antecedent syphilis has been noted in a few instances.

Exposure, intemperance, bad food, etc. are possible predisposing
causes.

Local irritation, which so often produces lymphatic swellings, appears
to stand occasionally in causal connection with the development of
general lymphadenoma. Trousseau lays particular stress upon this, and
gives instances in which chronic irritation of the skin, otorrhoea,
chronic nasal or pharyngeal catarrh, irritation of a decayed tooth,
gave rise to local gland swelling which preceded the general
development of the disease. But this {923} is a comparatively rare
affection, and think of the hundreds of instances met with of local
lymphatic irritation!

SYMPTOMS.--Enlargement of the lymphatic glands in the neck, axillæ, or
groins is the earliest symptom noticeable in the great majority of
cases. This may be quite painless at first, and the patient seeks
advice on account of the disfigurement or the inconvenience felt in
adjusting the collar. Occasionally the anæmic and constitutional
symptoms first attract attention. When the trouble begins in the deeper
groups--bronchial, mesenteric, or retro-peritoneal--pressure effects
are the first complaint, and there may be great obscurity and
uncertainty about the nature of the case. Thus, the first symptom may
be dyspnoea, with pain in the chest, or pain in the abdomen with
swelling of the legs and shooting pains in the course of the nerves; or
in rare cases symptoms of a totally different nature may be among the
first to attract attention. Thus in J. H. Hutchinson's case there was
paraplegia from pressure of a secondary growth, and the same was
observed in a case which I dissected at the Montreal General Hospital
(Case VI.). But such are very exceptional, and in the great majority
swelling of the superficial glands is the earliest phenomenon. In rare
instances the tonsils and pharyngeal adenoid tissue have been first
affected.

Hemorrhage is not an early symptom. Epistaxis has been noted, but not
with the frequency with which it occurs in leukæmia.

With the progressive enlargement of the glands the patient becomes
anæmic, and finally cachexia is developed.

The Lymphatic System.--In an early stage it is difficult or impossible
to distinguish the affection from syphilitic or scrofulous adenitis.
The gradual increase in the size and the involvement of other groups,
and the oncoming anæmia, will alone in certain cases render a decision
possible. In the cervical group, in which the trouble usually begins,
the chain of glands on one side becomes enlarged--perhaps only those
just above the clavicle, or in some instances the posterior ones are
also affected. They are isolated, movable, and not, as a rule, tender.
Months, or even years (three years, Case VII.), may elapse before the
enlargement becomes general or affects the other side. With their
increase in size and number the separation between the glands, at first
evident, disappears, and they form distinct groups or bunches. Thus the
submaxillary set, those of the anterior triangle, and those of the
posterior may form irregular aggregations of various sizes. Ultimately,
huge tumors may develop which obliterate the neck, extending upon the
shoulders and over the clavicles and sternum. When these grow inward,
toward the trachea, great dyspnoea may be produced, and the pressure
may be so extreme that tracheotomy must be performed.

The skin becomes involved, and ulcerates. Usually it is freely movable
over the masses. The pharynx and oesophagus may be compressed, and
occasionally the carotids. The submaxillary tumors may limit the
movement of the jaws.

Next to the cervical, the axillary glands are most frequently involved.
If small, no inconvenience is felt, but when large bunches occur there
is great pain in moving the arms, and pressure upon the brachial or
axillary veins may cause swelling of the limbs. The tumors may pass far
out, almost to the nipple.

The inguinal glands are not so often involved. In only one of the ten
cases which I have seen were they affected, but they may form large and
even pendulous tumors, as well shown in the cases of Surgeon-Major
Porter.[152]

[Footnote 152: Figured in _Path. Soc. Trans._, xxix.]

Of the internal glands, those of the thoracic cavity are most often
attacked. The chain in the posterior mediastinum may be involved and
surround the aorta or compress the gullet; or they may pass up the
trachea to the {924} neck, and involve the thyroid (Case V.). When the
bronchial group is enlarged there are signs of pressure on the tubes,
dyspnoeal attacks, and serious implication of the lung (Case VI.) In
the mediastinum there may be large masses covering the aorta, extending
over the pericardium, and producing bulging of the sternum and ribs,
perhaps pulsation, and ultimately erosion of the bones and outward
projection of the tumors (Cases II. and III.). There may be
considerable pressure upon the veins and obstruction to the flow in the
superior cava and jugulars.

In the abdomen the mesenteric glands are often affected, and if the
belly-walls are thin can be readily felt. The continuous chain of
retro-peritoneal glands may be greatly enlarged, and extend from the
diaphragm into the pelvis, surrounding the aorta, cava, and nerves.
When the patient is thin there may be no difficulty in detecting these,
but when there is an enormously thick panniculus the diagnosis may be
impossible, as in Case I., in which intense lumbar and sacral pain and
swelling of the legs were the only symptoms. The matting of organs in
the pelvis caused by these growths may be a source of great difficulty
in the diagnosis, as in a case in which I saw an eminent and careful
surgeon open the abdomen to extirpate a uterus for fibroids, and found
general lympho-sarcoma of the retro-peritoneal and pelvic glands.

It is probably in connection with affection of the abdominal glands
that the bronzing of the skin occurs which is mentioned in a few
instances. It was well marked in Case IV. of my series.

The glands present great variations in the rate of growth and there may
be fluctuations from month to month. They may diminish rapidly, and
almost disappear from a region to develop again in a few weeks. The
enlargements may diminish very much before death.

The spleen does not present the almost constant enlargement of
leukæmia, and in the majority of cases cannot be felt below the ribs.
Moderate hyperplasia is common, but I have never seen the large splenic
tumor. In some instances it has been found extending into the umbilical
region, and if there are secondary lymphoid growths the surface may be
very irregular.

The thyroid may be enlarged; it was so in Cases II. and IV., and in
Case V. the growth in the glands of the neck involved the right lobe.

The thymus has also been found affected; indeed, the disease may,
according to Virchow, sometimes begin in the gland.

Blood and Circulation.--The blood presents the characters of anæmia,
and as a rule the more advanced the glandular trouble the greater the
impoverishment. The red corpuscles are reduced in numbers one-half or
even three-fourths, but never, in my experience, to the extent in
pernicious anæmia. The lowest number per cubic millimeter which I have
counted was in Case II., when on one occasion the numbers sank to
2,100,000 per c.m. There may be most advanced disease without great
anæmia. In one case (IV.) with enormous enlargement of the cervical and
axillary gland there were 4,250,000 to the c.m., and during his three
weeks' stay in the hospital the numbers were never much reduced. So
also in Case III. there was not profound anæmia to within two months of
the patient's death.

The red corpuscles are usually uniform in size. I have never seen
extreme poikilocytosis, though occasionally the microcytes have been
numerous. The colorless corpuscles are not greatly increased, although
there may be moderate leucocytosis, as in Case IV., in which the ratio
of white to red kept about 1:150. A condition of actual leukæmia may be
induced. The corpuscles may be smaller than usual, and present the
characters of the blood in lymphatic leukæmia. I have not met with
nucleated red corpuscles in any of the cases which I have examined.

The granule-masses of Schultze are in variable numbers.

{925} Cardiac weakness and palpitation are common, due chiefly to the
anæmia. The mediastinal growths in some cases cause great embarrassment
from pressure. Fatty heart-muscle is an almost constant sequence of the
anæmia. The pulse is quickened--80-110, or, if much fever, 120-130.
Hæmic murmurs may be heard at the base of the heart, and the venous hum
at the root of the neck is often very distinct. Pressure of the tumors
upon the nerves may influence the heart's action, and in one case in
which sudden death took place it may have been due to interference with
the innervation of the heart by pressure on the nerve-trunks.

Respiratory System.--Shortness of breath from the anæmia is common,
particularly on exertion. When the tracheal and bronchial glands are
affected urgent attacks of dyspnoea may occur and suffocation be
induced. Pressure on the pneumogastric or recurrent laryngeal may cause
hoarseness or aphonia. The gland-tumors may invade the lung, or there
may be secondary growths. These are not usually large enough to induce
symptoms. The shortness of breath may be caused by pleuritic effusion,
which may be an early symptom and the one for which the patient is sent
to hospital (Case X.). It is due to pressure on the azygos and
intercostal veins.

Fever is observed in nearly all cases; even in the early stages slight
elevation of temperature may be noted. When the disease is firmly
established the fever is a marked feature. It may be of an irregular
hectic type, with morning remissions--this is, I think, the most
common--or it may be continuous, with an evening exacerbation. More
rarely there are ague-like paroxysms, with rigor, hot and sweating
stage (Case I.), and during these the fever may rise to 104° and glands
may become more swollen. The range is never very great, rarely
exceeding 103°.

Digestive System.--Difficulty in swallowing may result from the
enlargement of the lymph-follicles at the base of the lungs and of the
tonsils and pharyngeal adenoid tissue. This may be so great as to
necessitate feeding with a tube. There may be early gastric trouble
when the mesenteric and abdominal glands are first affected--dyspepsia,
nausea, and vomiting. Secondary tumors of the stomach are not common.
The loss of appetite and feeble digestion, prominent symptoms in so
many cases, are largely due to the anæmia.

Diarrhoea is not met with so frequently as in leukæmia; it may come on
toward the close and carry off the patient. New growths in the
intestine may produce severe attacks and sometimes hemorrhage.
Obstinate constipation may be the result of pressure.

The liver is rarely enlarged, and there are not often hepatic symptoms.
The new growths do not produce irregularity in the enlargement.
Pressure of enlarged glands at the hilus may cause jaundice and
ascites.

Genito-urinary System.--The urine is usually clear and presents no
striking changes. Reaction acid; albumen may be present. The testicles
may be the seat of secondary growths.

Nervous System.--Headache, giddiness, and noises in the ear are common,
and are dependent upon the anæmic state. Southey[153] has noticed
delirium and coma in some cases.

[Footnote 153: _Barth. Hospital Reports_, vol. ix.]

Special Senses.--Deafness is not uncommon, caused by pressure of the
large glands in the neck or by the growth of adenoid tissue about the
pharynx, closing the Eustachian tube. Inequality of the pupils has been
noted, from pressure of a gland on the sympathetic. Retinal hemorrhages
are uncommon.

Skin.--There may be definite secondary lymphatic tumors apart from
direct infiltration by continuity.[154] Bronzing may occur (Case IV.).
Papular rashes may be very troublesome. Subcutaneous oedema of feet and
eyelids may occur when the anæmia is very profound.

[Footnote 154: Greenfield, _Path. Soc._, xxvii.]

{926} MORBID ANATOMY.--The Lymph-glands.--Virchow made the division
into the hard and soft varieties, the difference depending on the
proportion between the cells and the adenoid reticulum. Where the cells
predominate the growth is soft--may be semi-fluctuating--but when the
stroma is much hypertrophied the glands are hard, firm, and feel like
organs in a state of chronic induration. The great majority of the
cases are of the soft variety. When first affected the glands may be
hard, and as the development proceeds become less consistent; but there
are cases in which they maintain their firmness and solidity
throughout.

When examined in the early stage the individual glands are more or less
isolated, perhaps not larger than almonds or walnuts, adherent by their
capsules, but readily separated and movable. Even when death has been
caused, some groups may generally be found in this state, as it is rare
for all to be equally developed. When advanced, the glands fuse
together, distinction is lost between them, and the bunch may form a
large tumor the size of an orange or even a cocoanut. When of moderate
size the section may show normal-looking gland-substance, and the
distinction between cortical and medullary portions may be well
preserved. When much enlarged the section has usually a grayish-white
appearance, smooth, and of variable consistence, either firm and dry or
soft and juicy. The vascularity is not often marked, and extravasation
and areas of congestion are not seen so frequently as in some
actively-growing neoplasms of the lymph-glands.

The capsules are thinned, and may disappear in the fusion of contiguous
glands, traces being seen on the section as strands of connective
tissue. About large groups the capsular tissues may be much condensed,
forming a very firm investment. The growth may perforate the capsule
and invade contiguous parts--muscle, skin, or the solid organs.

The chief changes which the tumors may undergo are fibroid induration,
suppuration, and caseation. The gradual increase of the stroma may give
a high degree of density, and the gland on section may present a
smooth, glistening appearance. Suppuration is most frequently seen when
the growth reaches the skin; it may point and an abscess discharge. In
the deep glands the formation of pus is not often met with. Caseation
is extremely rare. Hemorrhages may take place from rupture of the
thin-walled vessels.

The chief characters of the lesions in the different groups have been
dealt with in the section on Symptoms. The superficial glands are most
often attacked, and the cervical or axillary may form huge masses
before there are any signs of internal trouble. The superficial and
deep cervical groups may be uniformly affected, the muscles lifted and
wasted, and vessels and trachea surrounded by a solid mass. Sometimes
all distinction between the tissues is lost, and the carotids run in
the midst of the new growth, which may extend far out beneath the
trapezius and down into the chest or over the clavicle on to the
outside. When the neck is not primarily affected the groups are more
isolated, and can be traced as chains of enlarged glands along the
trachea and the carotids continuous with those of the axillæ and
mediastinum.

The axillary group is next involved in the order of frequency, and the
masses when large grow out under the pectorals and back beneath the
scapulæ and high into the fossa, compressing the axillary vessels and
causing great swelling of the arm. In Case VII. the growth infiltrated
the neighboring muscles and eroded the humerus and neck of the scapula,
perforated the blade, and exuded on its outer surface. Though an
enormous mass, the vessels were not infiltrated, and only moderately
compressed. The inguinal glands when very large may obstruct the
femoral artery and vein, and seriously interfere with the circulation
in the legs.

{927} Of the internal groups, those of the thorax are most often
affected, and we may have the chain in the posterior mediastinum along
the aorta and the sides of the trachea and gullet, and along them pass
into the neck (Case V.), or the bronchial group may be primarily
attacked, with the formation of a great bunch at the fork and numerous
small masses along each bronchus at the root of the lung, which may be
extensively involved (Case VI.); or those of the anterior mediastinum
beneath the sternum may be affected, with the production of large
masses extending over the pericardium and passing even to the
diaphragm. In these cases bulging of the sternum and ribs, with erosion
and perforation, may occur. In Case II. the sternum was completely
destroyed to a level with the fourth rib. The heart may be pushed aside
and the aorta and its branches completely surrounded by growths (Cases
II. and VI.). It is remarkable in these cases that great vessels do not
suffer more from compression. When the abdominal glands are involved,
the retro-peritoneal are most frequently enlarged, and form a
continuous chain from the diaphragm to the internal rings on either
side of the aorta and its branches, extending into the pelvis. Pressure
effects are not common, but they may compress the ureter, causing
hydronephrosis, the sacral and lumbar nerves, the iliac veins, and, as
in the case I mentioned, may adhere to the broad ligaments and uterus
in such a way as to deceive the most skilled gynæcologist. The
mesenteric glands may present slight enlargement, but in my experience
they are but little affected, even when the retro-peritoneal are of
large size. When the glands at the portal fissure are involved they may
compress the vein and duct. Phelps of Chateaugay, N.Y., sent me a
specimen in which the glands of this region formed two huge masses the
size of cocoanuts, and, so far as I could ascertain, they were primary
lympho-adenomatous growths. The possibility of ovarian disease had been
discussed by several consultants.

The chief change is an increase of the cells with or without thickening
of the reticulum. The cells correspond to ordinary lymph-corpuscles;
some may be a little larger, with darker granules and more pronounced
nuclei. Giant cells are frequently met with, more often in the small
glands. I have not seen them in the large soft tumors. In the early
stage there may be simple hyperplasia and the relations of the
lymph-paths are maintained, but when the glands are much developed the
normal arrangement is disturbed and they cannot be injected. The
reticulum varies much; in the very soft form it is expanded and can
scarcely be found; the substance may be semi-diffluent. The firmer the
structure the more evident is it, and in the hard forms the network of
fibres in whose meshes the cells are enclosed can be distinctly seen
and by pencilling very clearly brought out. It is not merely a
thickening of pre-existing fibres, but probably there is a new
development of adenoid tissue. In some cases of advanced fibroid change
very few cells can be seen. The vessels passing to the glands are
sometimes dilated.

Spleen.--In about 75 per cent. this organ is hypertrophied or presents
lymphoid growths (Gowers). The enlargement is not often great, rarely
approximating the colossal size of the leukæmic organ. It is due to
either simple hyperplasia or to the presence of the new growths,
sometimes to both. In the 75 cases of enlarged spleen new growths
occurred in 56 (Gowers). Of the 38 cases in Hutchinson's table, 27
presented the splenic tumors. These are grayish-white bodies, ranging
in size from a small pea to a walnut or larger, scattered irregularly
through the substance, usually rounded in outline, but in some
instances irregularly shaped. They contrast by color strongly with the
red spleen-pulp. The numbers may vary from one or two to many dozens,
the spleen-substance being a mere remnant between them. These masses
often resemble the lymph-glands in appearance and consistence. {928}
They are not encapsulated, but in immediate contact with the
spleen-tissue. They originate from the Malpighian corpuscles, and may
be regarded as the enlarged and developed lymph-elements in the spleen.
The larger ones probably arise from the fusion of several small ones.
When uniform in size and scattered throughout the organ, they may
resemble coarse tubercles, but the absence of any caseation may serve
to distinguish them. Their histological characters are those of the
glands, lymph-corpuscles in a fibrous reticulum; the consistence
depends on the preponderating element.

Amyloid degeneration was found by Gowers in two cases in the growths.

The thymus has been found involved in the mediastinal growths, and is
occasionally affected primarily. The thyroid may be attacked by the
cervical tumors.

The suprarenals may contain secondary growths. In Case VII. both were
extensively involved.

The medulla of the long bones has been found converted into red
lymphoid marrow, and in a few instances into the pyoid variety met with
in leukæmia. It has been found normal in other cases.

Digestive System.--In the mouth and pharynx the lymphatic elements are
very commonly affected when the cervical glands are enlarged, sometimes
independently. The tonsils may form large masses, and with the
follicles at the root of the tongue and at the pharynx produce great
obstruction. Sloughing may occur. In the gullet and stomach secondary
tumors have occasionally been seen. In Case VII. there was a flat
elevated mass at the cardia beginning to ulcerate.

The small intestines may be extensively involved; the glands of Peyer
enlarged and even ulcerated. In Case VII. there were over twenty ulcers
in the jejunum and ileum, ranging in size from a split pea to a bean,
edges elevated and indurated and the bases sloughing. The large
intestines may be secondarily affected, the intertubular adenoid tissue
be greatly developed and compress the crypts of Lieberkühn, and lead to
thickening of the mucosa.

The liver is often enlarged, and presents scattered lymphoid tumors,
rarely larger than a pea, of a white or yellow-white color, and may be
readily mistaken for tubercles. They are most common beneath the
capsule and in the interlobular tissue. A diffuse interacinous growth
may also occur. Cirrhosis has been observed in the vicinity of the
growths, and fatty degeneration.

The pancreas may be the seat of secondary masses.

Genito-urinary System.--The kidneys are very often the seat of new
growths, usually small and of a character similar to those in the
spleen and liver. When the disease is very rapid the tumors may be
large and very vascular. The texture of the kidney is usually soft, and
parenchymatous change is common. The testicles may also be the seat of
adenoid growths; this was the case in one of Hodgkin's patients.

The Respiratory System.--Growths in the trachea are rare. The lungs are
frequently affected, either by the direct invasion at the root from the
bronchial glands (Case V.), or by numerous scattered nodules through
the substance. They develop about the bronchi, and may reach the size
of marbles. Intense bronchitis, oedema, and congestion may be secondary
changes induced by pressure on the bronchi or trachea.

The serous membranes occasionally present lymphoid growths. Pleural
effusion is not uncommon.

The heart presents no very constant changes. When the anæmia is
profound it may be very fatty. It may be compressed by mediastinal
growths, and has been found much atrophied. Lymphoid growths may occur
in it.

The Nervous System.--The brain itself is rarely affected, but growths
have been found in the dura mater. In Case VI. a secondary mass
compressed the spinal cord, as in Hutchinson's case, producing
paraplegia.

{929} The skin may be the seat of adenoid growths, as in Greenfield's
case.[155] The growing tumors may involve it (Case IV.), and ulceration
may occur.

[Footnote 155: _Loc. cit._]

COURSE, DURATION, AND TERMINATION.--Trousseau and other French writers
have divided the disease into different stages--the latent and period
of early development, the period of generalization, and the cachectic
state; but the course of the disease is very variable, and depends much
upon the position of the glandular enlargements, the rapidity of
development of secondary growths, and also the constitutional
peculiarities of the patient. Early and rapid growth in the mediastinal
groups may produce pressure effects, and cause death before any marked
anæmia--much less cachexia or the development of secondary masses in
important organs, as the cord, may prove quickly fatal. In some cases
the glandular enlargement rapidly spreads, and group after group is
involved in the space of a few months; in others there may be
hyperplasia of a single set, as the cervical on one side, for months,
or even years, before the glands on the other side or in other regions
become involved. The most acute cases may run a course in three or four
months, the most chronic in as many years. Periods of quiescence are
not uncommon, and the tumors may not only cease to grow, but actually
diminish, or even disappear in a region, and this without any special
treatment.

The mode of death is commonly by asthenia; cachexia is gradually
developed, the anæmia becomes more profound, and finally, with local or
even general dropsy, the end comes from heart failure. Very frequently
the patient is cut off before grave constitutional disturbance is
established, particularly by asphyxia from the pressure of enlarged
glands on the trachea and bronchi or occlusion of the pharynx.
Hemorrhage and diarrhoea, such common symptoms in leukæmia, are rarely
seen. Coma has been the cause of death in a few cases. Oedema of the
lungs, pneumonia, extensive pleuritic effusions, may hasten, and in
some instances cause, the fatal result.

The DIAGNOSIS is in most cases easy; in others time alone will decide
the true nature of the glandular enlargement. Of the chronic forms of
adenitis which are liable to be confounded, the scrofulous is the most
common. The points to be attended to in the diagnosis are--the age;
scrofulous glands affecting chiefly the young and individuals
presenting other signs of the so-called scrofulous habit, or there may
be a well-marked family history of phthisis. In the question of age,
however, it is to be remembered that there is a condition known as
adult or senile scrofula, in which there may be general enlargement of
the glands. Of all groups the cervical are most frequently involved in
scrofula, and the submaxillary set more often than those of the
anterior and posterior triangles, while in Hodgkin's disease the latter
are usually affected first. The enlargement in scrofula is rapid at
first, and may last for years in a group without extending; the bunches
are often, even when small, welded together, and, most important of
all, they tend to suppurate--a feature scarcely ever seen in true
lymphadenosis. Size is an uncertain criterion. I have seen masses of
scrofulous glands in the neck as large as two fists and without
suppuration. A single large bunch in the neck, particularly if
submaxillary, persisting for over a year or eighteen months without
involvement, however slight, of the glands in the same or the opposite
side or in the axillæ, is almost certainly not malignant lymphoma. On
the other hand, a group of slowly-enlarging glands in the anterior
cervical triangle, with gradual affection of those of the opposite side
of the axillæ, particularly if in a person between twenty and thirty
and becoming anæmic, would render the suspicion of Hodgkin's disease
strongly probable.

In connection with this it may be mentioned that occasionally in acute
{930} phthisis there may be great swelling of the glands, from a growth
of miliary tubercles in them. A case of the kind was admitted into my
wards in the General Hospital, Montreal: a man aged twenty-four, with
great swelling of the cervical glands in both sides, tonsillitis, and
sloughing pharyngitis, irregular fever, and diarrhoea, and for a time
the case was believed to be one of Hodgkin's disease.

PATHOLOGY.--Local benign lymphomata occur, identical in histological
characters with the tumors of Hodgkin's disease, and differing only in
the absence of any tendency to extend in the neighborhood or to
generalize. They are not uncommon about the neck, may grow slowly, and
last for years.

The lymphatic growths of leukæmia are not in any essential particular
different from those of Hodgkin's disease, and the diagnosis rests upon
the examination of the blood. There are, however, certain broad
differences when any considerable number of cases of the two diseases
are compared. Thus the lymphatic element in leukæmia is less
pronounced, the splenic and medullary forms predominate; in Hodgkin's
disease exactly the reverse prevails. It is rare in leukæmia for the
internal glands to be much involved, and patients do not often die from
the pressure effects of the tumors. The hemorrhages so common in
leukæmia, and the diarrhoea, are rare symptoms. The bone-marrow is more
generally affected, and, lastly, the tendency to generalize seems
greater in the growths of Hodgkin's disease.

From other forms of malignant growths in the lymph-glands there may be
difficulty in the diagnosis, and even a microscopical examination may
not serve to make the distinction.

Thus there is a true lympho-sarcoma, a small-celled growth of the
lymph-glands, which must be distinguished, though it is hard in some
cases, from the general lymphadenoma. The distinctions laid down by
some writers, such as a special tendency to attack contiguous parts,
and a more general distribution of the metastatic growths, will not
hold, as we have seen that cases of lymphadenosis or Hodgkin's disease
may attack neighboring structures, and the secondary tumors, though
preferably in lymphatic textures, may occur in every organ. In the
retro-peritoneum, for example, true lympho-sarcoma is not uncommon,
forming large tumors which may press forward the viscera and produce a
very prominent mass in the abdomen. They are not uncommon in children,
and with renal sarcomas make up three-fourths of the abdominal growths
of early life. But they may occur in adults and attain large size,
involving adjacent organs, such as the kidneys, or, as in a case I saw
a short time since, grow into the colon and cause death by gradual
hemorrhage. These are local growths as regards the lymphatic system,
not involving distant glands, and not often, indeed, producing
metastasis.

We may recognize in the lymphatic glands--1st, the local benign growth
which seems nothing more than hypertrophy, lymphadenoma, and which may
persist for years; 2d, a local malignant growth, lympho-sarcoma, which
invades contiguous structures and may be followed by metastasis, but
there is not general involvement of the lymphatic tissues; and 3d,
there is a generalized lymphoma involving groups of glands in
succession, and the adenoid tissue throughout the body, usually
accompanied by anæmia alone, in which case we term it Hodgkin's
disease--sometimes by an excess of colorless corpuscles as well, when
we call the affection lymphatic leukæmia.

PROGNOSIS.--When established sufficiently to make a sure diagnosis, the
prognosis is in the great majority of cases bad; true examples of the
disease rarely if ever recover. A hopeful prognosis may be given in
those cases in which only a few glands are involved, and where there is
any suspicion of a scrofulous habit or where the enlargement has
persisted for years without {931} extending. The presence of profound
anæmia, the existence of swelling in distant groups and in internal
glands, are grave indications. High, irregular fever, rapid growth, and
the development of cachexia are symptoms of the full establishment of
the disease. The physician must not be deceived by intervals of
improvement, with perhaps subsidence of the glandular swelling in
places. Such breaks in the onward progress are not uncommon.

TREATMENT.--When small and localized, the question of the removal of
the glands may be raised. If they persist after appropriate remedies,
and if there is not grave anæmia, and other groups and the spleen are
not affected, excision should certainly be performed. Circumscribed
lymphadenoma, particularly of the neck, may exist for years before the
glands in other regions become involved; and in such cases removal
affords the best guarantee that the disease will not extend.

Local applications are of doubtful benefit. I have never seen any
permanent improvement follow the persistent use of iodine, biniodide of
mercury ointment, or friction with oil. Galvano-puncture has not been
successful, and the same may be said of the various substances injected
into the glands--iodine, arsenic, chromic acid, etc.

Internally, iodine and iodide of potassium have been extensively used,
but without much benefit. Quinine, iron, and cod-liver oil are useful
as tonics, but have no influence on the size of the tumors. Arsenic is
the only medicine which has seemed to me of positive value, and under
its use I have seen the gland-tumors decrease greatly in size. It
should be given in increasing doses until some of the unpleasant
effects of the drug are manifested, when a return should be made to a
small dose, and again gradually increase. When well borne, large doses,
20 or 25 minims, of the liquor arsenicalis should be taken three times
a day for many weeks. In two cases with moderate enlargement of the
cervical and axillary glands the progress of the disease seemed
arrested, and the glands certainly became smaller and softer. In the
history of these cases the patients will often speak of changes in the
volume of the gland quite uninfluenced by any treatment; and these
fluctuations must be taken into account in estimating the value of a
drug; but, making due allowance for this, the beneficial effects of the
arsenic are unquestionable when given early in large doses and the
administration kept up for months. Many recent writers have borne
testimony to this, among them Karewski,[156] who reports three
recoveries.

[Footnote 156: _Berl. klin. Wochenschrift_, 1884, 17 and 18.]

Phosphorus has been of service in the hands of Gowers and Broadbent,
and when arsenic is not well borne it should be tried.

Change of air and scene has benefited some cases. The patient's
strength must be supported by every possible means; fortunately,
gastro-intestinal disturbance is not so marked as in leukæmia, and even
with most extensive and progressive enlargement of many groups of
glands the appetite may be good and the digestion excellent.

When the glands of the neck compress the trachea, or when the lymphoid
elements of the tonsils and pharynx obstruct the orifice of the
glottis, tracheotomy may be necessary.


HÆMOPHILIA.

DEFINITION.--An hereditary or congenital fault of constitution,
characterized by a tendency to bleeding, spontaneous or traumatic, and
often associated with swelling of the joints.

{932} SYNONYMS.--Hæmatophilia; Hereditary hæmorrhage; Hæmorrhagic
diathesis; Idiosyncrasia hæmorrhagica. _Ger._ Bluterkrankheit,
Blutsucht; _Fr._ Hémophilie. The term bleeder is applied to a patient.

CLASSIFICATION.--In this article the congenital or hereditary disease
will alone be considered, to the exclusion of cases of transient
hemorrhagic diathesis, the hemorrhages of scurvy, fevers, anæmia,
purpura simplex, and purpura hæmorrhagica.

HISTORY.--So far as is known, the classical writers make no mention of
the disease, though in the _Pharsalia_ of Lucan there is a passage,
quoted by Legg,[157] which well describes the hemorrhagic diathesis.
The first positive reference is in the writings of Alzaharvi, a
physician of Cordova who died in 1107 A.D. A doubtful case is mentioned
by Benedictus in 1539, who relates the history of a barber who bled to
death from slight wounds of the nose caused by clipping the hairs.
Hochstetter described a case in 1674 to which Virchow has called
attention.[158] Legg[159] found a well-recorded case by Banyer in the
_Philosophical Transactions_ (1743). Fordyce in 1784 described a
Northamptonshire family the members of which suffered from
hemorrhages.[160] With brief references to the disease by two German
writers in 1793 and 1798, these scanty materials comprise the facts
known at the beginning of this century.

[Footnote 157: _Hæmophilia_, London, 1872.]

[Footnote 158: _Virchow's Archiv_, Bd. xxviii.]

[Footnote 159: _Loc. cit._]

[Footnote 160: _Fragmenta Chirurgica et Medica_, London, 1784.]

To American physicians belongs the credit of the full recognition and
description of the disease and the discovery of its remarkable
hereditary nature.

Otto[161] gave an account of a New England family members of which had
been bleeders for several generations. He also referred to a Maryland
family observed by Rush. Otto appears to have been the first to note
the immunity of females in bleeder families, and their tendency to
transmit the disposition. In the _Philadelphia Medical Museum_, vol.
i., 1805, a letter of E. H. Smith is published, written in 1794, in
which he gives an account of a boy affected with the disease. Hay[162]
reported the Appleton-Swain families of Reading--one of the most
remarkable histories ever published of the disease. In 1817 the Buel
Brothers described the Collins family,[163] and Coates[164] a family in
Delaware county, Pa. Hughes[165] and Gould[166] also described notable
examples. Holton, Harris, and Dunn have studied other American bleeder
families, and a brief record of the local literature of the subject
will be found at the end of this article.

[Footnote 161: _Medical Repository_, New York, 1803, vol. vi.]

[Footnote 162: _New England Medical Journal_, 1813, vol. ii.]

[Footnote 163: _Transactions of the Medical and Physical Society of New
York_, 1817.]

[Footnote 164: _North American Medical and Surgical Journal_, Philada.,
vol. vi., 1828.]

[Footnote 165: _Transylvania Journal_, 1831, vol. iv., and _American
Journal Med. Sciences_, 1833, vol. xxi.]

[Footnote 166: _Boston Medical and Surgical Journal_, 1857.]

In Germany, Nasse (1820), Rieken (1829), Schönlein, Canstatt,
Wachsmuth, Lange, Virchow, and others added greatly to our knowledge of
the disease. Grandidier published a monograph in 1855, a new edition of
which in 1877[167] contains a most exhaustive account of the disease
and a statistical résumé of all cases to date. In England the disease
has not attracted much attention. Legg published an important monograph
in 1872, and many papers of value are scattered through the
_Transactions_ and journals.

[Footnote 167: _Die Hämophilie_, Leipzig, Zweite Auflage, 1877.]

In France the articles in the encyclopedias and a few theses--of which
Gavoy's (1861) and Simon's (1874) are the most important--comprise the
chief literature.

ETIOLOGY.--The disposition is, in the majority of cases, hereditary,
but there may be a spontaneous origin, the disease appearing in the
child of a family in which no previous cases had occurred. Nothing is
known of the {933} conditions under which the disease may thus arise in
a healthy stock. Many of such cases die early, but others live and may
become the starting-points of new bleeder families. In the history of
sixty families Grandidier[168] found statements of this mode of origin
of the affection.

[Footnote 168: _Op. cit._, p. 136.]

The two most interesting features in the etiology relate to sex and
heredity. The disease is much more common in males than females, the
proportion being variously estimated at 11 to 1, or even 13 to 1. In 64
bleeder families, in 5 were sons and daughters alike affected; in 27
all the sons were bleeders; and in 6 of these there were no daughters.

There is no disease with so marked a tendency to transmission, and it
may appear in four or five generations in succession. In the
Appleton-Swain family of Reading, Mass., there have been cases since
the early part of the last century, and F. F. Brown of that town writes
me that cases still occur in the descendants.[169] Legg gives a chart
of the Clitherow family, in which it has existed for the past two
hundred years.[170]

[Footnote 169: The last case Brown has been able to ascertain was in a
lad, Warren Coburn, aged seventeen, who died about twelve years ago.
His mother's brother was a bleeder, and died of hemorrhage from a
slight scalp wound after having been brought to death's door on three
or four other occasions by trivial wounds. Mrs. Coburn was a daughter
of Daniel Hart, whose wife was a Norton. Her mother was a Bacheller and
a granddaughter of Oliver Appleton's daughter. This lad is an instance
of the transmission of the disposition to the seventh generation within
a period of two hundred years. Brown further states that there do not
appear to be in the vicinity of Reading any Appleton or Swain families
in which bleeders exist. As the tendency is chiefly transmitted through
the female members of a family, who lose the patronymic by marriage, it
is often difficult to trace the relationship. I think if we had fuller
genealogical details we should find that several of the bleeder
families now thought to be distinct belonged to the same stock.]

[Footnote 170: _St. Barth. Hospital Reports_, 1881.]

                            YEATON.
                               |
      +----------+-------------+---------+---------+----------+
      |          |             |         |         |          |
Son, bleeder. Daughter.     Daughter. Daughter. Daughter.  Daughter.
                 |             |         |         |          |
                 |             |         |         |          |
      +----------+-----+       |         |         |          |
      |                |       |         |         |          |
Son, bleeder. Three daughters. |         |         |          |
    |                          |         |         |          |
Son, bleeder.                  |         |         |          |
                               |         |         |          |
      +------------+-----------+         |         |          |
      |            |           |         |         |          |
Son, bleeder.   Daughter;   Daughter.    |         |          |
         children not bleeders.          |         |          |
                                         |         |          |
      +-----------+-----------------+----+         |          |
      |           |                 |              |          |
Son, bleeder.  Daughter.         Daughter.         |          |
                  |                 |              |          |
            Son, bleeder.     +-----+-----+        |          |
                              |           |        |          |
                        One son   Four daughters.  |          |
                     bled to death.                |          |
                                                   |          |
      +-----------+----------+----------+----------+          |
      |           |          |          |                     |
Son, bleeder.  Daughter.  Daughter.  Daughter.                |
                   |         |          |                     |
              Twin boys,  Son, not   Son, not                 |
              bleeders.   a bleeder. a bleeder.               |
                                                              |
                              +--------------+-----------+----+
                              |              |           |
                        Son, bleeder.  Son, bleeder.  Daughter.

In the celebrated bleeder families of Tenna, Switzerland, five
generations have been affected. The modes of transmission are as
follows: (1) Father {934} to son, grandson, etc. This is rare, but
instances are on record. (2) Father not a bleeder, but of bleeder
stock, transmits the tendency to son--very uncommon. (3) Father to
daughter, granddaughter, etc.--not common. The daughters of a bleeder
are usually free, though their brothers may be affected. (4) Mother a
bleeder, transmits to sons and daughters. (5) Mother not a bleeder, but
daughter of one, transmits to her sons, the daughters remaining free,
but their sons affected. This is the most common mode of inheritance.
Atavism by transmission through the female line is almost the rule, and
the daughters of a bleeder, though healthy and free from any tendency,
are almost certain to transmit the disposition to their male offspring.
The 657 cases analyzed by Grandidier occurred in two hundred families.
The chief facts of heredity are well illustrated by the preceding chart
of the Yeaton family, given by Gould in the _Boston Medical and
Surgical Journal_, 1857.

The Anglo-Germanic nations appear especially prone to the disease. Of
194 families in Grandidier's table, 154 were of the Teutonic stock.
Records of the disease among the Latin races are rare. Jews are
probably not more liable than other people, but the rite of
circumcision gives an unusual opportunity for its manifestation at an
early age.

The age at which the bleeding tendency first appears was determined by
Grandidier in 113 cases as follows: in 63 during the first year; in 17
during the second, and up to the end of the second year in 93. It is
rare for the first manifestation to occur after the twelfth year, and
there was only one case in which the first bleeding appeared after the
fifteenth year.

The constitution and temperament of bleeders, about which the older
writers had much to say, probably present no peculiar characteristics.
Some persons claim to be able to recognize bleeders even before they
have manifested any tendency to hemorrhage. They are usually fresh,
healthy-looking persons, with fine, soft skins, through which the
superficial veins may show with more than usual distinctness. A
division of cases into erethetic and atonic forms has been made by
Wachsmuth and Grandidier. The mental activity of bleeders has been
noted to be above the average, due, doubtless, to the fact that the
liability to bleed from slight blows and cuts has made sedentary and
studious habits preferred to out-of-door employments and amusements.

Families in all conditions of life are affected. Much interest was
excited in the disease in England from the fact that the late Prince
Leopold was a sufferer.

Climate appears to have an influence in determining attacks. Cold,
damp, changeable weather is favorable, while a residence in a warm,
equable climate diminishes the tendency in a very marked manner. Some
patients have an extraordinary susceptibility to changes in the
weather.

All observers have noted the great fertility of bleeder families. Those
first born seem less liable to bleed than subsequent ones.

SYMPTOMS.--The existence of the defect of constitution may not be
suspected until an uncontrollable hemorrhage follows some trivial
injury or operation, or a spontaneous bleeding may occur and present
great or insuperable difficulties in its arrest. The symptoms usually
occur in the first years of life, and in the great majority of cases,
as mentioned above, the first bleeding occurs before the fifth year.
The symptoms may be grouped under three divisions (Legg, Grandidier):
external bleedings, spontaneous and traumatic; interstitial bleedings,
petechiæ, and ecchymoses; and the joint affections. Legg recognizes
three grades of the disease. The first and most severe is characterized
by bleedings of every kind, external and internal, and by troublesome
joint affections: this form is most often seen in men. The second grade
is less severe; there are spontaneous hemorrhages from the mucous
surfaces, but no traumatic bleeding or ecchymoses and no joint {935}
troubles: this form is most often seen in women. The third and lowest
degree is when there is a tendency simply to ecchymoses; no dangerous
bleedings occur: this form is often seen in members of bleeder
families, and if in women the menstruation may be early and profuse.

External Bleedings.--The spontaneous bleedings may occur from the skin,
the mucous, and in rare instances the serous, membranes. There are
frequently preliminary symptoms--prodromata--such as flushing, fulness
of the head, and throbbing of the arteries--signs of so-called
plethora; often there is irritability of temper, but sometimes, in
children, extra cheerfulness has been observed. The localities affected
and the frequency are shown by the following analysis of 334 cases by
Grandidier: Epistaxis, 169 times; from the mouth, 43; stomach, 15;
bowels, 36; urethra, 16; lungs, 17; cerebral hemorrhage, 2; skin of
head, 4; tongue and finger-tips, 4 each; tear-papilla, 3; eyelids, 2;
external ear, 5; female generative organs, 10; ulcer of skin, 2; navel
(long healed), 2. An odd situation for spontaneous bleeding is
mentioned by Townsend,[171] in which a child bled to death from the
scrotum. In many cases these spontaneous hemorrhages prove fatal--most
frequently the epistaxis. The traumatic bleeding may result from blows,
cuts, scratches, etc., and the blood may be effused into the tissues or
discharged externally. Fatal hemorrhages have occurred from the
following wounds: blow on head, 11 times; slight scratches on skin or
abrasion of dermis; laceration of the frænum of the lip, slight cut
(two lines deep) in a duel wound; bite of the tongue (7 cases); fall on
the mouth; blow on the nose; blow of a stone on the finger; cut in
paring the nail; fall on the head with meningeal hemorrhage (2 cases,
brothers); and rupture of the hymen on the wedding-night.

[Footnote 171: _Boston Med. and Surg. Journal_, lv.]

After operations, trivial and severe, many fatal cases have occurred,
and the statistics of the same author give the following: cutting of
the frænum linguæ, 1; leeching, 5; venesection, 4; blister, 2;
extraction of tooth, 12; circumcision, 8; cutting umbilical cord, 4;
vaccination, 2; fistula, stone, ligation of carotid, of radial, of
ulnar, of femoral arteries, amputation of arm and of thigh, 1 each;
phimosis, 2. Leeching, extraction of teeth, and circumcision are most
dangerous operations in bleeders.

The bleeding is always a capillary oozing, and the vessels are not
seen. It may last for hours, or even many days and weeks, and the
amount of blood lost may be enormous. Epistaxis may be fatal in
twenty-four hours. In Coates' case a medical student lost half a gallon
of blood in twenty-four hours, and in the ten days which the bleeding
continued it was estimated that he lost about three gallons.

The healing of a wound in a bleeder may take place rapidly, either with
or without suppuration. When the hemorrhage is large or prolonged,
severe anæmia follows, from which, as a rule, the patients recover with
remarkable rapidity.

The interstitial hemorrhages--petechiæ, ecchymoses, hæmatoma--may be
spontaneous or the result of injuries. The petechiæ occur most
frequently in the skin, particularly of parts distant from the
heart--the legs and arms, less often the face. On the mucous and serous
surfaces they are less common. They resemble ordinary purpuric spots,
and crops may come out with symptoms of swelling and pain in the
joints. Large extravasations--hæmatoma--are most frequently of
traumatic origin and may follow the slightest blow, as in a case of Sir
Wm. Jenner's, in which from the fall of a rubber ball on the thigh an
enormous extravasation took place between the knee and trochanter.[172]
They are blue, black, or reddish-black at first, and in their
absorption go through the various changes in color which we notice in a
bruise. These blood-tumors may occasionally arise spontaneously.

[Footnote 172: Legg, etc., p. 68.]

The arthritic affections in hæmophilia are very remarkable, and so
{936} common as to form prominent features in the disease. There may be
simple pain in and about the joints, or swelling with redness and signs
of intense inflammation. The attacks may come on suddenly with fever,
resembling closely acute rheumatism. The large joints are usually
affected, the knees most often, then the elbows, ankles, and shoulders.
There may be repeated attacks, and at last great crippling and
deformity. The small joints are rarely affected. In cold, damp weather
the attacks are most common; occasionally they follow traumatism. In
addition to the joint troubles, bleeders suffer much with irregular
pains in the limbs, particularly during change of weather, or these
pains with arthritis may usher in an attack of hemorrhage.

Many other irregular symptoms are described in the monographs, some of
which have no intimate relation with the disease. The anæmia has, of
course, all the features of the traumatic form. Digestive troubles,
after the bleeding, are common, and are due to the anæmia. The Buel
Brothers[173] mention that in two of their cases the patients showed a
marked inclination to eat sand and earth. Children with the hemorrhagic
tendency pass through the ordinary diseases of infancy like others.
Whooping cough is very liable to cause epistaxis. Rheumatism and
scrofula are said to be common in bleeder families.

[Footnote 173: _Op. cit._]

The blood in bleeder cases is, as a rule, normal, so far as our present
means of investigation enable us to decide. When a hemorrhage has
continued for some time, it is thin and watery, but at the beginning of
the bleeding the blood is usually rich in corpuscles and fibrin and
coagulates firmly. The salts have been found increased in quantity. No
change has been noted in the corpuscles, the number of which is stated
by several observers to be increased. Prior to a hemorrhage there may
be, according to some writers, a state of plethora or increase in the
total quantity of blood, and the tolerance of the loss, so much greater
in bleeders than in ordinary persons, is adduced in support of this
view.

MORBID ANATOMY.--Not many changes other than those of profound anæmia
have been found in the bodies of bleeders. An unusual thinness of the
walls of the vessels, first noted by Bladgen in 1817,[174] has been met
with in a number of cases; in a few instances hypertrophy of the heart;
in others a rounded foetal shape of the organ. Within the past few
years careful microscopical examination has been made of the tissues
and blood-vessels of bleeders. Kidd[175] found degeneration of the
muscle-fibres of the middle coat of the arteries, and the endothelium
of the small arteries, veins, and capillaries was swollen,
proliferated, and some of the small veins were blocked with the
products. Legg[176] reports a case in which Klein made a most careful
examination with negative results, and he stated that of six such
examinations which had heretofore been made, in only one case (Kidd's)
were important changes found. At the same meeting of the London
Pathological Society, Theodore Ackland also reported a case with
negative results as regards histological changes.

[Footnote 174: _Medico-Chirur. Transactions_.]

[Footnote 175: _Medico-Chirurgical Society's Transactions_, vol. lxi.]

[Footnote 176: _Lancet_, Oct. 27, 1884.]

The joint changes have been studied in a number of cases. Hemorrhage
has been found in and about the capsule, and the acute swelling may be
due largely to it, as was shown in Hutchinson's case,[177] in which he
aspirated the joint. When it lasts any time, there is great staining of
the cartilages and discoloration. There may be inflammation of the
synovial fringes and erosion and destruction of the articular surfaces
(Legg).

[Footnote 177: _Trans. State Med. Soc. N.Y._, 1877.]

The PATHOLOGY of the disease is unknown. No doubt two circumstances
combine in hæmophilia--congenital fragibility of the vessels and a
defect in coagulability of the blood--but whereon these depend we are
as yet entirely ignorant. There is no evidence of the nature of the
anatomical changes in {937} the vessels which permits of their ready
laceration, and none on the nature of the alteration of the blood which
prevents the normal thrombus formation in a wound; and in the absence
of information on these points theories must necessarily be
unsatisfactory, and their discussion, in a work of this practical
nature, profitless.

The DIAGNOSIS presents no difficulty in members of a bleeder family, in
whom slight joint trouble and petechiæ are as much manifestations of
the disease as the more severe hemorrhages. In a large majority of
cases the tendency becomes manifest at an early date. The spontaneous
umbilical hemorrhages of infants are, as a rule, to be excluded, being
dependent upon, or associated with, jaundice or syphilis or a mycosis
(Weigert[178]). The hemorrhagic diathesis may develop in children or
members of a healthy family and prove fatal, and the question in such
cases always comes up, Are they instances of hæmophilia? There seems to
be a desire to limit this term to cases of an hereditary nature only;
but when a child shows a marked tendency to multiple hemorrhages,
spontaneous or traumatic, which tendency persists and is not merely
transitory, and particularly if there are joint troubles, I think that
under these circumstances we have a genuine case of hæmophilia; and
such a child, if he--it is more likely to be a male--survives and
marries, may be the founder of a bleeder family. These are the
congenital in contradistinction to the hereditary cases. In the
histories of the bleeder families we frequently come back to the origin
in a person born of a healthy stock in which there have been no
hemorrhagic tendencies. On the other hand, single severe uncontrollable
hemorrhages in children or adults are not to be ranked as hæmophilia
unless there have been other features pointing to the existence of the
diathesis. The literature abounds in cases of this kind, many of which
are described as hæmophilia. In doubtful cases it is very difficult to
decide, as in a case of Forscheimer brought before the Academy of
Medicine of Cincinnati.[179] In the review of American literature we
have excluded all cases in which the hereditary or congenital
characters were not well marked.

[Footnote 178: _Cohnheim's Pathologie_, i. 382.]

[Footnote 179: _Cincinnati Lancet and Clinic_, 1884.]

It may be useful to put down here for the guidance of the practitioner
the varieties of bleeding commonly met with, and which must not be
confounded with hæmophilia:

(1) The umbilical hemorrhages of infants, due to jaundice or to
syphilis hæmorrhagica neonatorum, etc.

(2) Purpura simplex, seen often in debilitated, rarely in healthy,
children, usually confined to the legs, and in some cases I have seen
it associated with rheumatic pains or swellings in the knees and
ankles.

(3) Peliosis rheumatica, an affection which in the large interstitial
hemorrhages and the joint swellings touches hæmophilia in a curious
way. It too may show itself in several members of the same family.

(4) Purpura hæmorrhagica, Morbus maculosus Werlhöfii, a grave disease,
characterized by extensive cutaneous ecchymoses, mucous hemorrhages,
but not dependent on any local disease, or, so far as is known, on any
specific poison. The bleedings in scurvy may be mentioned here, but
there could be little difficulty in determining their nature.

(5) Infective purpura, due to the action of some specific
poison--small-pox, measles, scarlet fever, cerebro-spinal fever, etc.
The hemorrhages may be cutaneous and trivial, or may be in the most
aggravated form of interstitial and mucous bleedings, as seen, for
example, in black small-pox.

(6) Toxic purpura, as in snake-bites and many poisons, such as
phosphorus.

(7) Simple hemorrhagic diathesis, under which may be included those
cases in which, without any hereditary disposition or previous
hemorrhagic history, there is a tendency to uncontrollable hemorrhage
from a slight wound.

{938} (8) Hæmatidrosis, bloody sweats, which occur usually in
hysterical or epileptic females, and are in rare instances accompanied
with mucous hemorrhages.

In considering the PROGNOSIS it is well to remember that the patients
rarely die in the first bleeding. The younger the individual the worse
is the outlook. As above stated, the attacks are most frequent under
five years of age, and of 152 boys the subject of the disease, 81 died
before the termination of the seventh year (Grandidier). Legg, however,
states that it is rarely fatal in the first year. The longer a bleeder
lives, the greater the chance of his outlasting the tendency; but that
it may persist to the end of a long life, and then prove fatal, is
shown by the case of old Oliver Appleton, the first recorded American
bleeder, who died at an advanced age of hemorrhage from a bedsore and
from the urethra. A bleeder may have years of existence, in which the
tendency seems lessened or even absent. The prognosis is always worse
in a boy than in a girl. In the latter menstruation is sometimes early
and excessive, but, happily, in the female members of hæmophilic
families neither this function nor the act of parturition bring with
them special dangers.

TREATMENT.--The prophylaxis is all-important. The members of a bleeder
family, particularly the boys, must be guarded from injury as much as
possible, and operations of all kinds must be avoided, except when life
itself is in jeopardy. The extraction of a tooth should be absolutely
prohibited. Occupations must be sought which will give the least
possible risk of injury. Daughters of bleeder families should not be
permitted to marry, as it is through them that the tendency is chiefly
propagated, and, even if not bleeders themselves, some of their male
children are certain to be affected. The question of the marriage of
male bleeders is more difficult to decide, but in any case where the
tendency is marked it should be prohibited.

When an injury or wound has occurred, absolute rest, cleansing the
wound, and compression should first be tried. If in a favorable
locality pressure on the artery may be employed, failing in this, the
various styptics may be used. In epistaxis, ice, tannin, and gallic
acid may be tried before plugging.

Internally, ergot seems to have been of use in several cases. Otto[180]
speaks of the value of sulphate of soda in purgative doses. The
perchloride of iron, 30-40 minim doses, every two hours, is advised by
Legg, with a purge of sulphate of soda if there is no bleeding from the
bowels. Venesection has been resorted to in several instances.
Transfusion has been employed, but without benefit. The diet should be
light and supporting. After the attacks the patients should take iron
and cod-liver oil until the health seems restored. When possible, a
residence in the South during the winter is advisable, as most cases
are aggravated by the cold weather, and in any case care must be taken
to protect patients against cold and wet.

[Footnote 180: _Loc. cit._]

The joint troubles must be treated on general principles.


AMERICAN LITERATURE OF HÆMOPHILIA.

Buel: _Transact. of the Med.-Physic. Society of New York_, vol. i.,
1817; 1 F., 4 cases.

Coates: _North Am. Med. and Surgical Journal_, Philada., 1828, vi. p.
37; 1 F., 5 cases.

Dunn: _Am. Journal Med. Sciences_, 1883, vol. lxxxv. p. 68; 4 F.

Felt: _History of Ipswich_, 1834--Appleton family referred to.

Gould: _Boston Med. and Surgical Journal_, 1857, p. 500; 1 F., 11
cases.

Harris: _Philada. Med. Times_, 1872; 2 F., 7 cases.

Hay: _New England Journal of Med. and Surgery_, 1813, vol. ii. p. 221;
1 F., 15 or 16 cases (accurate number rather difficult to make out).

{939} Holton: _Am. Journal of Med. Sciences_, April, 1874; 1 F., 7
cases.

Hughes: _Transylvania Med. Journal_, 1831, vol. iv. p. 518, and _Am.
Journal Med. Sciences_, 1833, vol. xxi. p. 543; 1 F., many cases.

Hutchinson: _Trans. State Med. Society of New York_, 1877, p. 208.

Otto: _Medical Repository_, 1803, vol. vi.; 3 F., 8 cases.

Pepper: _Philada. Med. Times_, 1881, vol. xii. p. 109; 1
case--Lancaster county family described by Dunn.

Sewell: _Med. Chronicle_, Montreal, 1857, vol. iv.; 2 F., 4 or 5 cases.

Smith: _Philadelphia Medical Museum_, 1801, vol. i. p. 284.

Traneus: _St. Louis Med. and Surgical Journal_, 1870, p. 535; 1 F., 4
cases.

Townsend: _Boston Med. and Surgical Journal_, vol. lv. p. 447; 1 F., 3
cases.


ADDISON'S DISEASE.

DEFINITION.--A constitutional affection characterized by asthenia
without emaciation, a depressed circulation, gastric irritability, and
usually pigmentation of the skin. In the majority of cases it is
associated with a fibro-caseous degeneration of the suprarenal
capsules, and in many there are changes in the abdominal sympathetic
system.

SYNONYMS.--Morbus Addisonii; Bronzed-skin disease. _Fr._ Maladie
d'Addison, Maladie bronzée; _Ger._ Addisonische Krankheit.

HISTORY.--In the _Halle Hospital Reports_ for 1823 Schötte describes a
case, and one is also given by Bright in vol. ii. of his _Medical
Reports_, 1831. A few other instances are also on record before 1855,
when Addison published his monograph _On the Constitutional and Local
Effects of Disease of the Suprarenal Capsules_, from which we may date
our knowledge of the affection. Following close upon the work of
Addison numerous observations were made in England, where the disease
appears to be more common than elsewhere. Wilks of Guy's Hospital,[181]
and Greenhow of the Middlesex Hospital, may be mentioned among those
who in England have specially studied the disease, and the latter
published an important monograph in 1875.[182] In France, besides
numerous minor contributions, the exhaustive articles in the
encyclopædias have been the most important publications. In Germany the
monograph of Averbeck (1869) and the abstracts of Meissner in
_Schmidt's Jahrbücher_ may be specially mentioned. Virchow, Griesinger,
Oppolzer, Bamberger, and others have made valuable contributions.
Recently Burger[183] has published a small monograph. In other European
centres contributions have been made, among which may be mentioned that
of Schmidt of Amsterdam, who brought forward cases in support of the
view that the disease was an affection of the sympathetic ganglion. In
America the first cases were reported by Ranking[184] and Taylor.[185]

[Footnote 181: In numerous communications in _Guy's Hospital Reports_
and _Trans. Path. Society_.]

[Footnote 182: "On Addison's Disease," _Croonian Lectures_.]

[Footnote 183: _Die Nebeunieren und der Morbus Addison_, Berlin, 1883.]

[Footnote 184: _Am. Journ. Med. Sci._, 1856.]

[Footnote 185: _New York Med. Journal_, 1856.]

ETIOLOGY.--The causation of the disease is unknown. Cases are more
frequent in hospital than in private practice. Males are more often
attacked than females; the proportion in Jaccoud's table[186] is 79 to
48, and in Greenhow's[187] analysis of 183 good cases, 119 were males
and 64 females. Under ten and over fifty years of age the disease is
very uncommon; the majority of the cases occur between the twentieth
and the fortieth year. Greenhow {940} has called attention to the fact
that in a number of instances the disease appears to have followed an
injury, such as a blow upon the abdomen or back, and in several cases
caries of the spine has preceded the attack. He refers also to the
greater frequency of the disease in the laboring classes and those
exposed to injury from over-exertion. The disease does not seem to be
more prevalent among members of phthisical families, although the
morbid process in the glands has been regarded as of a tuberculous
nature, and it is common for other tuberculous lesions to occur in the
course of the disease.

[Footnote 186: _Dictionnaire de Médecine_.]

[Footnote 187: _Op. cit._]

The disease is rare in America--apparently much more so than in
England.

SYMPTOMS.--In the words of Addison, the leading and characteristic
symptoms are: "Anæmia, general languor and debility, remarkable
feebleness of the heart's action, irritability of the stomach, and a
peculiar change of color in the skin occurring in connection with a
diseased condition of the suprarenal capsules."

Although, perhaps, not the most essential, the symptoms pertaining to
the skin are in the majority of cases the most prominent, and have
given rise to the names bronzed skin, melasma suprarenale, etc. which
have been applied to the disease. A gradual increase in the pigment of
the rete mucosum, either patchy or diffuse, causes a gradual
discoloration, which may ultimately reach such a degree that a
previously blonde individual may have the aspect of a Malay or a
mulatto. The grades of coloration may range from a light yellow to a
deep brown, or even black. In some instances there is a greenish-brown
tinge, to which the term bronzed is peculiarly applicable. In typical
cases it is diffuse over the whole surface, but as a rule deeper on
exposed parts, face, neck, and hands, and also in those regions where
the normal pigmentation is most intense, nipples, scrotum, and penis,
or in the vicinity of cicatrices or regions of chronic irritation. It
is usually first noticed on the face, either diffuse or in spots, and
the extension may be rapid or gradual, in many instances not reaching a
high grade and not becoming universal. It may be absent, and is not to
be regarded--as was formerly the case--as an essential feature of the
disease. Patches of leucoderma may occur in connection with the
pigmentation, as beautifully delineated in Pl. xi. of Addison's
monograph. The pigmentation is not confined to the skin, but may extend
to the mucous surfaces--mouth, conjunctivæ, vagina. In the mouth the
patches may be as dark as in the dog; they are usually scattered, often
on the margins of the lips and on the edges and under surface of the
tongue and on the cheeks. The conjunctivæ are less often affected. The
vagina may be very deeply pigmented. An intensification of the
choroidal pigment has been observed. In some cases a patchy
pigmentation of the serous membranes has been found, and is figured in
one of Addison's original plates, and pigmentation of the nails, hair,
and teeth may also occur. A variation has been observed in the
intensity of the coloration with the general health of the patient. The
discoloration rarely precedes the general symptoms, but more usually
follows the asthenia.

Some observers have noted a peculiar odor of the breath and from the
skin, particularly during the last few days of life.

Anæmia of a moderate degree may exist, but it is not, as often stated,
a constant symptom. Greenhow states that "there is no real anæmia, the
blood being often rich in red corpuscles, even in excess, and there is
no increase in the white." No special alterations in the appearance of
the corpuscles have been noted. In some instances free pigment has been
found.[188] In a case recently at the hospital of the University of
Pennsylvania, Hughes found the number of red corpuscles over five
millions per cubic millimeter, and there were free pigment-granules in
the blood.

[Footnote 188: Corput, _Gazette hébdomadaire_, 1863.]

Hemorrhages are rare; extravasations into the retinæ have not, so far
as I {941} can ascertain, been observed, nor are there often the other
common features of anæmia.

The pulse is frequent and small, the heart's action weak--sounds clear;
a venous murmur may sometimes be heard. In some cases there appears to
be a special enfeeblement of the heart and a liability to fainting
attacks, and without any warning a fatal syncope may occur. Cold feet
and hands result from the weak circulation, and may be a most annoying
symptom.

Symptoms in connection with the respiratory system are not common.
There may be dyspnoea, and the complication of phthisis may give rise
to all the features of that disease. There may, however, be extensive
lung trouble with but few symptoms. The temperature is rarely elevated,
more often it is subnormal.

Gastric disturbances are very common--anorexia, nausea,
vomiting--particularly toward the close, but they may be early and
prominent features, persisting in spite of all remedies and proving the
most formidable symptoms of the malady. They appear to be of nervous
origin, and not referable to changes in the organ itself. It is
doubtful if the case reported by Gilliam,[189] in which there was
degeneration of the gastric mucosa, was Addison's disease. The state of
the bowels is variable; constipation is more frequent than the normal
condition. Diarrhoea is common, and may come on suddenly without
obvious cause, and is a not infrequent cause of death.

[Footnote 189: _Phil. Med. and Surg. Reporter_, xxiv.]

The urine is usually pale, free from albumen, not often increased in
amount. It is interesting to note, in connection with the involvement
of the abdominal sympathetic, that in a few cases there has been
polyuria. The nitrogenous elements may be greatly reduced, the urea to
13-20 grammes daily, and the amount of indican may be increased as much
as 64-75 milligrammes in 1000 c.c. (Samuel). In one case Thudichum
found the urinary pigments greatly reduced in amount, the uromelanin
not amounting to more than one-twelfth the normal quantity. A recent
observation of Nothnagel is of interest.[190] In a patient aged twenty,
who had the typical symptoms of the disease for two years, death took
place by coma and the condition of acetonuria was determined.

[Footnote 190: _Zeitschrift für klin. Med._, Bd. ix.]

The symptoms connected with the nervous system are the most prominent
in the disease, and are more constant than the anæmia or the bronzing.
The most marked is a depression and enfeeblement of the nervous forces,
a profound asthenia out of all proportion to the general condition. The
patients complain of a lack of energy, mental and bodily; the least
exertion is an effort, and there is a feeling of tire and weariness
with which the facial expression is quite in keeping. The fainting
fits, giddiness, noises in the ears, may also be due to faulty
innervation, as they occur in cases in which the anæmia is by no means
advanced. Headache, lumbar and abdominal pains are frequent, and in a
considerable proportion of cases there is tenderness on pressure in the
lumbar region. With the advance of the disease the prostration becomes
more marked, the patient remains in the recumbent posture, the voice
gets weak and small, the intelligence dulled, and occasionally there is
delirium. Head symptoms may suddenly supervene, and death by coma or
convulsions cut short the progress even early in the disease
(Pye-Smith). In Jaccoud's series convulsions were noted in 19 cases.

The disease may be said to be invariably fatal, but the course presents
many variations. The majority of cases die within eighteen months of
the first onset of the symptoms. B. Fenwick, in an analysis of 30
recent cases,[191] calls attention to the fact that when bronzing does
not occur the course is more rapid. Thus the average duration of the
non-bronzed cases was only 4.8 months, while for bronzed ones it was
23.6 months. There are acute cases {942} in which, with great weakness,
vomiting, and diarrhoea, the fatal end may occur in a few weeks. Some
of these rapid cases resemble typhus. Syncopal attacks, coma, or
convulsions cut short not a few cases. In a few instances it is much
prolonged--six years (Niemeyer) or even ten years (Greenhow). Whether
recovery ever takes place is doubtful. Finney[192] has reported an
apparently genuine case which got well. Some French observers (Potain)
think that recovery takes place more often than is supposed. Sir Wm.
Gull mentioned a case of recovery.[193] Periods of improvement lasting
many months may occur.

[Footnote 191: _Path. Soc. Trans._, vol. xxxiii., London.]

[Footnote 192: _Dublin Med. Journ._, April, 1882.]

[Footnote 193: _Int. Med. Congress_ (London) _Transactions_, vol. ii.]

MORBID ANATOMY.--The panniculus adiposus and subperitoneal fat may be
in normal quantity. There is rarely great emaciation, nor are the
organs blanched and bloodless. The most constant lesion is in the
suprarenal organs, which present a caseo-fibrous change, more rarely
simple atrophy or other alterations. So frequent is the caseo-fibrous
condition that some writers (Wilks) hold that it is the specific lesion
of the disease. The organs are enlarged--may weigh several ounces each.
The capsules are thickened, and may present caseous or even calcareous
masses. The normal shape of the gland is lost, and it forms an
irregular nodular mass closely adherent to contiguous parts--liver,
kidney, and cava on the right side, kidney, spleen, and often pancreas,
on the left. There is usually a good deal of fibrous thickening and
matting in the vicinity, and the adhesions to adjacent structures may
be very strong. The peritoneum often shows patches of fibroid
induration. On section the diseased organ cuts with great resistance,
and to the touch has an almost cartilaginous hardness. The exposed
surface shows caseous masses of a yellow or grayish-white color,
varying in size from a pea to a walnut, imbedded in a grayish
semi-translucent fibrous tissue, pale when first cut, becoming reddish
on exposure. These caseous masses may undergo softening or
calcification, and pockets of pus are not uncommon. Definite small
miliary granulations are not often seen, though nodular grayish-yellow
bodies the size of small peas may occur. The strands of fibrous tissue
which separate and enclose the caseous masses have often a very
peculiar translucent, infiltrated appearance. When the cheesy lumps are
small, the amount of this tissue is considerable and gives a remarkable
character to the section. Wilks has described a case in which this
tissue made up the entire mass. The substance of the gland is usually
destroyed. The vessels and nerves can be traced to the organs where
they become imbedded in the fibrous tissue.

Histologically, the soft translucent tissue consists chiefly of
spindle-shaped fibre-cells, and in firmer older parts of ordinary
fibrous stroma. In the immediate neighborhood of the cheesy masses
there are round corpuscles--about the size of or a little larger than
white blood-cells--imbedded in a fine reticulum of fibres. Giant-cells
are sometimes found, but they have not been common elements in the
specimens which I have examined. The caseous substance consists of
granular débris in which the remains of cells and fibres can be seen.
In coarse and microscopical features the lesion resembles closely local
tubercular affections. The extension is by a small-celled growth, which
gradually invades the adjacent parts, extending peripherally as the
central portions caseate. Distinct miliary granulations are not often
met with. The relation of this local growth to tuberculosis is a very
interesting question. It is usually regarded as a scrofulous or
tuberculous process, to which in its general features it quite
conforms. I have been interested in ascertaining whether the bacillus
tuberculosis existed or not in the local lesion. In Cohnheim's
laboratory Karl Hüber kindly gave me an opportunity of examining the
adrenals in two cases, in only one of which were the {943} bacilli
evident. Since then I have re-examined the fibro-caseous tissue in
Ross's case,[194] which was a most typical one, the suprarenals alone
involved, and in the recent case reported by Pepper,[195] and in
neither have I been able to demonstrate bacilli. Future examinations
must decide whether the local affection is inflammatory or whether it
belongs to the infective granulomata.

[Footnote 194: _Can. Med. Assoc. Trans._, vol. i., 1877.]

[Footnote 195: _Phila. Med. Times_, 1885.]

That other alterations may occur in cases of Addison's disease appears
well established, though some still regard the caseo-fibrous change
essential and specific. Atrophy of one or both glands has been
frequently seen. Jaccoud gives 7 cases in his tables. Good recent cases
have been described by W. B. Hadden,[196] Hebb,[197] and Goodhart.[198]
The atrophy is due to a chronic interstitial process similar to
cirrhosis of the liver. Hadden[199] states that the lesion is identical
with that in the thyroid gland in myxoedema.

[Footnote 196: _British Medical Journal_, 1885.]

[Footnote 197: _Lancet_, 1883, i.]

[Footnote 198: _Path. Soc. Trans._, 1882.]

[Footnote 199: _Loc. cit._]

Absence of one or both the capsules has been noted by Legg, Spender,
Borland[200] and Hubbard.[201]

[Footnote 200: _Boston Med. and Surg. Journal_, 1867.]

[Footnote 201: _Proceedings of Conn. Med. Society_, 1868-71.]

Cancer of the adrenals, by no means uncommon as a secondary process,
rarely produces any special symptoms; but there are cases which are
difficult to exclude from the category of Addison's disease. Jaccoud
gives several, and in the case of Edes, often quoted,[202] the asthenia
and discoloration may have been due to the capsular affection, but
there was also extensive peritoneal cancer.

[Footnote 202: _Boston Med. and Surg. Journal_, 1878.]

By far the most constant morbid change after that in the adrenals is a
more or less widely distributed tuberculosis, particularly of the
lungs. A very considerable proportion of the cases are complicated with
chronic phthisis. Regarding the disease of the suprarenals as primary,
the general tuberculous affection may be secondary; and it is just in
these organs, as Weigert has shown, that the veins are apt to be
perforated by tubercles and systemic infection induced. The
retro-peritoneal and mesenteric lymph-glands may also be tuberculous.
Ulcers of the ileum may occur, and swelling of Peyer's glands and the
solitary elements in the bowels is very common. In Ross's case there
were numerous lymphoid infiltrations of the mucosa of the stomach,
chiefly about the pylorus and cardia. The changes in the skin are
confined to an increase of the pigment in the cells of the rete
mucosum, most pronounced in the deeper layers and in the deeper parts
in the connective-tissue cells of the papillæ and subcutaneous tissues.
The condition is not to be distinguished from a deeply-pigmented
scrotum or from the dark skin of the negro. The pigment resembles the
ordinary coloring matter of the skin, but is possibly different from it
in containing no iron.[203] Nothnagel has made[204] an exceedingly
interesting study of the pigmentation in Addison's disease, and
concludes that it is identical in distribution with that in the skin of
the dark races; that it does not originate in the cells of the rete
mucosum, but is elaborated in deeper cells, about the vessels of the
cornium, and transported by them to the more superficial layers--a mode
which recent observations seem to show is the normal one; and, lastly,
that it is a process induced through the nervous system in some way as
yet unknown.

[Footnote 203: Arnold, _Virchow's Archiv_, xxxv.]

[Footnote 204: _Loc. cit._, Bd. ix.]

The spleen has been found enlarged. The thymus gland may also persist
or be much larger than normal. In Ross's case it weighed six ounces.
The heart and blood-vessels do not present any constant changes: the
heart has been found small in some cases. Venous engorgement of the
abdominal viscera has been noted in a few cases, but it is not a common
feature. It was not present in two typical cases which I have examined.

{944} In the nervous system the condition of the abdominal sympathetic
has received special attention, and in a number of cases definite
changes have been met with, chiefly of a sclerotic or chronic nature
and intimately associated with the fibroid induration about the
capsules. The nerve-cells of the semilunar ganglia are described as
degenerated, deeply pigmented, and often present a new growth of
connective tissue about and between the cells. There are at least
thirty or more cases in which such alterations have been found. In some
instances the medulla of the nerves passing from the ganglia has been
found wasted and the fibres in a state of fatty degeneration. In some
cases these parts have been found normal (Foa,[205] Huber,[206]
Hebb,[207] and Hadden[208]). In a most typical case under Ross at the
Montreal General Hospital, I could find no differences in the cells and
nerves, comparing them with those of a woman dead on the same day of
heart disease. More recently, I have examined a case for Pepper in
which the right semilunar ganglion was imbedded in the sclerotic tissue
of the right adrenal; the nerve-cells were undergoing atrophy from
compression; and there were fatty changes and degenerations in the
nerves connected with this ganglion. The left was uninvolved, and the
cells and fibres appeared normal.

[Footnote 205: _Virchow-Hirsch_, 1879.]

[Footnote 206: _Virchow's Archiv_, 86.]

[Footnote 207: _Lancet_, 1883, i.]

[Footnote 208: _Loc. cit._]

Jacquet has described pigmentary changes in the ganglia of the cord as
well as in those of the abdomen, and Guermonprez[209] alterations in
the brain similar to those of senile dementia. At the Congress in 1881
at London, Semmola of Naples showed a figure illustrative of
degeneration of the ganglia of the abdomen, and also an infiltration of
leucocytes in the neighborhood of the central canal of the cord, from a
case of Addison's disease without affection of the adrenals.

[Footnote 209: Quoted by Burger, _loc. cit._]

PATHOLOGY.--The suprarenal organs are usually grouped with the
blood-vascular organs. From the number of nerve-fibres--sympathetic,
pneumogastric, and even phrenic--passing to the medullary part, and
from the presence of cells resembling nerve-corpuscles, Leydig and
others have thought that this portion belonged to the nervous system.
We know absolutely nothing of their functions. They do not appear to be
essential to life, but may be removed, crushed, or destroyed with
impunity, though the operation is not without danger from their close
proximity to important structures. They are sometimes congenitally
absent. They are proportionately larger during foetal life, but they do
not appear to atrophy as age advances; indeed, it would appear from the
observation of Mattei (Jaccoud) that they augment in volume with
increasing years. Their chemistry has attracted much attention. Vulpian
has described a material which gives a green, blue, or black color with
perchloride of iron, and with oxidizing substances a rose-red; and the
same observer found also hippuric and taurocholic acids. Leucin,
margarin, myeline (Segilsohn), and a special coloring matter (Arnold),
have been described. Henle has pointed out that the central part in the
horse became of a rich brown with bichromate of potash from the
reduction of the brown oxide of chromium. MacMunn's[210] observations
on the spectroscopic appearance of the pigment of the suprarenals point
to these glands as in some way concerned with the transformation of the
effete coloring matters of the body.

[Footnote 210: Paper read before the Physiological Society of London,
_Journal of Am. Med. Assoc._, 1885, March 21.]

An immense number of experiments have been made with a view of
ascertaining the function of these bodies, and extirpations, crushings,
etc. have been made--among others by Brown-Séquard,[211]
Gratiolet,[212] Phillipeaux,[213] Harley,[214] Nothnagel,[215] the
general result of which appears to be that they are not {945} important
organs and that they have no influence in the production of pigment.
Recently, Tizzoni[216] has stated--as Brown-Séquard had done--that
pigmentation followed extirpation in the rabbit; but there is a large
amount of negative evidence by most careful observers; as, for example,
Nothnagel, who found no changes in 153 animals in which he had
destroyed the suprarenals.

[Footnote 211: _Archives générale_, 1858.]

[Footnote 212: _Ibid._, 1856, ii.]

[Footnote 213: _Ibid._, 1858.]

[Footnote 214: _Med.-Chir. Review_, vol. xxi.]

[Footnote 215: _Zeitsch. f. klin. Med._, Bd. i., 1879.]

[Footnote 216: _Lancet_, 1884, ii.]

Various attempts have been made to explain the phenomena of the
disease, to two or three of which we shall refer:

1st. That the disease is directly dependent upon destruction of the
capsules and consequent abnegation of their functions. This was the
view of Addison, and it appeared to be supported by the experiments of
Brown-Séquard (performed shortly after the publication of Addison's
memoir), who held that after extirpation of the glands pigment
accumulated in the blood; which he explained on the supposition that
their function was the disposal of a material in the blood readily
converted into pigment. Subsequent experiments appear to have
demonstrated conclusively that, like the spleen, the adrenals are not
necessary to life, and that no important changes occur after their
removal, or even after the induction of caseous and fibroid induration
(Nothnagel). A much stronger argument against this view is found in the
fact that cases have been reported in which the capsules presented
little or no change.[217] Taylor[218] held that the pigmentation was
induced by destruction of the cortical part of the organs, and the
general nervous phenomena by involvement of the central part, which has
such close relation with the nerve-structures. This view has again been
advanced by B. Fenwick.[219]

[Footnote 217: Care must be exercised in the examination of apparently
normal capsules. There may be extensive small-celled infiltration and
destruction of the gland-elements without either reduction or increase
in size.]

[Footnote 218: _Loc. cit._]

[Footnote 219: _Path. Soc. Trans._, xxxiii., 1882.]

2d. That it is an affection of the abdominal sympathetic system,
induced, most commonly, by capsular disease, but also by other chronic
affections which implicate the solar plexus and its ganglia. Addison
hinted at this explanation, and had the ganglia examined in one of his
cases, but Schmidt of Amsterdam (1859) was the first to point out the
possible connection and to record a case. Many corroborative
observations have since been made, and this view has the support of the
leading authorities. The changes which have been met with are very
varied--fibroid thickening of the sheaths with atrophy of the
nerve-tubes, fatty degeneration and wasting, excessive pigmentation of
the cells, myxomatous degeneration of the stroma of the semilunar
ganglia, and in a few instances there have been changes in the spinal
cord. The chronic caseo-fibrous process in the capsules seems specially
prone to involve contiguous tissues, and the close proximity of the
semilunar ganglia renders them more liable to be attacked by the
sclerotic process than in other affections in the vicinity, such as
aneurism or tumors. According to this view, the symptoms of Addison's
disease are to be regarded as the expression of a severe nutrition
disturbance caused by a morbid state of the sympathetic ganglia, or, as
Semmola puts it, the entire affection, beginning with disturbance of
digestion and running its course with asthenia, low temperature, and
marked debility in the oxidation and nutritive processes, is a
pathological demonstration of the physiological functions of the
sympathetic ganglia. The pigmentation may have its origin in changes in
the trophic nerves, and the pronounced debility is the outcome of the
disturbed chemical activity in the tissue-elements. It is, in short, a
disease of the nervous system of organic life. Greenhow, who is a
strong advocate for this view, also thinks that the circulatory,
respiratory, and digestive symptoms may in part be due to implication
of the pneumogastrics, the peripheral branches of which are frequently
{946} involved in the thickened tissues about the capsules. The feeble
action of the heart, small pulse, the nausea, vomiting, and the gasping
respiration, may arise reflexly from irritation of these branches.

There are about thirty cases on record in which changes have been found
in the sympathetic system. Riesel[220] compares the symptoms of
Addison's disease with those which follow extirpation of the semilunar
ganglia in animals. There is a paralysis of the vaso-motor nerves of
the abdominal viscera, induced either by degeneration of the ganglia or
reflexly by irritation, and consequently the blood accumulates in these
parts, and there is a corresponding spanæmia of other organs, which
explains the weak circulation, anæmia and the heart symptoms, fainting,
and loss of energy. Recently this theory has been advocated by F. P.
Henry.[221]

[Footnote 220: _Deutsches Archiv f. klin. Med._, Bd. vii.]

[Footnote 221: _Philada. Med. Times_, 1885, No. 452.]

The occasional occurrence of pigmentation of the skin in abdominal
tuberculosis, retro-peritoneal tumors, cancer of pancreas, and in
uterine irritation lends support to this view.

The weak points of this view are--the doubtful nature of the changes in
the ganglia and the nerves in many cases. Mere increase of the normal
pigment, slight fatty degeneration or swelling, so often recorded,
should not be regarded as important, for they occur under a variety of
conditions. Of positive swelling and redness of the ganglia, fibroid
atrophy with destruction of nerve-cells and degeneration of the
nerve-fibres, there can be no doubt, but about less marked alterations
opinions will differ whether they are truly morbid or not. The fact
that in certain well-observed cases the ganglia and nerves were found
normal is hard to reconcile with a theory that the disease is an
affection of the abdominal sympathetic. Burger states[222] that there
are nine cases in which changes could not be found, and there are the
recent cases of Huber,[223] Hebb,[224] Foa,[225] and Hadden.[226]

[Footnote 222: _Loc. cit._]

[Footnote 223: _Virchow's Archiv_, Bd. lxxxviii.]

[Footnote 224: _Lancet_, 1883.]

[Footnote 225: _Virchow-Hirsch_, 1879.]

[Footnote 226: _Brit. Med. Journ._, 1885, i.]

Hale White's recent observations,[227] as well as those of
Saundby,[228] on the histological changes in the sympathetic clearly
show that many of the changes which have been described in cases of
Addison's disease are common in other affections, and have probably no
direct association with the characteristic symptoms of the malady.

[Footnote 227: _Ibid._]

[Footnote 228: _Ibid._, 1883, i.]

Then, again, the absence of the characteristic symptoms of Addison's
disease in so many cases in which the matting and implication of the
nerves seems quite as great as in capsular disease. In aneurism of the
abdominal aorta in the neighborhood of the coeliac axis the tissues in
the vicinity may be indurated and cicatricial, the semilunar ganglia
compressed, and the nerve-fibres atrophied, without bronzing and
without the constitutional symptoms. Cases, too, of retro-peritoneal
cancer rarely induce pigmentation, though in some instances--as in a
case of Paget's (Geo.),[229] in which there was extensive lymphadenosis
with involvement of the abdominal sympathetic--the bronzing may be
intense. Induration about the pancreas and stomach in cancer has
induced the same change, and recently Jürgens has recorded a case of
aneurism[230] of the abdominal aorta with symptoms of Addison's disease
and degeneration of the sympathetic nerves.

[Footnote 229: _Lancet_, 1879, i.]

[Footnote 230: _Berliner klin. Woch._, March, 1885.]

3d. That the essence of the disease is to be sought in some injurious
agent--a poison introduced from without or possibly arising within the
body as a result of faulty metabolism. There is not the slightest
evidence for the existence of any such specific poison, which Averbeck,
in his monograph, brings forward to account for the anæmia and the
local disease in the capsules.

A more plausible theory, one closely related to the first one
mentioned, is {947} that the blood is gradually poisoned by the
retention of some material the destruction or alteration of which it is
the function of the adrenals to effect. The disease is in this view
analogous to chronic uræmia.

The relation of affections of the thyroid gland to myxoedema and
cretinism, and the experimental production of these conditions by the
removal of the thyroid, have widened our view of the importance of the
ductless glands. It is interesting to note the analogy between
myxoedema and Addison's disease. In both there are distinct
histological changes in the tissues--in one an increase in the mucin,
in the other an increase in the pigment--and in both marked nervous
phenomena: mental dulness, a progressive dementia in myxoedema, a
profound asthenia in Addison's disease. We regarded the thyroid as
unimportant to life until the experience of surgeons and extirpation in
monkeys by Horsley demonstrated that abolition of its function was
followed by a serious train of symptoms; and perhaps the experimental
removal of the suprarenals in monkeys--so much more closely allied to
man than the animals hitherto experimented upon--may demonstrate that
these little bodies are also not without their influence upon health.

Although the view of disturbed innervation consequent upon involvement
of the abdominal sympathetic meets the case, theoretically, better than
any other, and is at present widely held, yet there are signs of a
return to the old view of Addison, which has been so consistently
advocated by Wilks.[231] The data are not yet forthcoming for a final
decision of the question, but it is possible that future investigations
may establish the truth of Addison's view, that suspension of the
function of the glands is the essential factor in the causation of the
disease. That the sympathetic may be normal in genuine cases, and again
that all the symptoms of the disease may occur without affection of the
adrenals, are, however, facts difficult to harmonize with either
theory.

[Footnote 231: Discussions at Pathological Society of London, session
1884-85.]

DIAGNOSIS.--It is of the first importance to remember that an increase
in the pigment of the skin is by no means confined to Addison's
disease, and, on the other hand, that the constitutional symptoms may
be present without a trace of bronzing; and in their absence a positive
diagnosis cannot be made. The conditions which give rise to a deepening
of the color of the skin are--(1) Abdominal growths, tubercle, cancer,
lymphoma. The patches of pigmentation in such cases are usually
scattered, most often about the face and forehead. Occasionally the
pigmentation may be deep and extensive, as in one case I saw of
abdominal tuberculosis believed to be Addison's disease. Guéneau de
Mussey[232] has called special attention to the frequency of this
complication in chronic tuberculous peritonitis. Pigmentation may also
be on the mucous surfaces in these cases. (2) Pregnancy, in which the
discoloration is usually limited to the face, the so-called masque des
femmes enceinte, and which, it is to be remembered, does not always
disappear with the pregnancy. Chronic uterine disease, especially
fibro-myoma, is a very common cause of patchy melasma. (3) Hepatic
disease, which may induce definite pigmentation as well as the
yellow-brown color of jaundice. Overworked persons of constipated habit
and sluggish livers may present a patchy staining about the face and
forehead. (4) The vagabond's discoloration, caused by the irritation of
lice and dirt, may reach a high grade, and has been mistaken in several
instances for the pigmentation of Addison's disease. (5) In rare
instances there may be deep discoloration of the skin in connection
with melanotic cancer--so deep and general that it has been confounded
with melasma suprarenale. Wagner,[233] Wickham Legg,[234] and
Falls[235] have {948} described remarkable cases of the kind. The
occurrence of melano-sarcoma of the choroid or skin should render the
diagnosis in these cases easy enough, but if deep seated a difficulty
might readily occur.

[Footnote 232: _Étude sur la Pigmentation de la Face dans la
Tuberculose abdominaire_, Paris, 1879.]

[Footnote 233: _Archiv der Heilkunde_, Bd. v.]

[Footnote 234: _Path. Soc. Trans._, London, vol. xxxv., 1884.]

[Footnote 235: _Philada. Med. Times_, 1883.]

It must be borne in mind that there are cases without bronzing, in
which the profound asthenia and gastric symptoms are the prominent
features, and, as mentioned above, these cases seem to run a very acute
course. Indeed, they have been mistaken for typhus.

TREATMENT.--As cure is out of the question, the treatment is
symptomatic and directed to the avoidance of certain perils associated
with the disease. We have no means of checking the progress of the
capsular affection. Pepper advises counter-irritation, and in the early
stages the cautery may be used. Rest of mind and body must be enjoined,
and the dangers of exertion and exhaustion set before the patient. Even
in the early stage fatal syncope may occur.[236] The sense of weakness
and tire at times becomes greatly aggravated, and may deepen into
attacks of the most profound asthenia, during which the patient should
be strictly confined to bed. It is in these paroxysms that special
dangers occur. General tonic measures must be employed for the support
of the strength. When there is anæmia, iron may be given, and Greenhow
speaks of the good effects of the citrate or perchloride given with
glycerin. Arsenic, strychnia, phosphorus, have been found useful in
individual cases. Galvanism has been used, but without much benefit.
The paroxysms of profound asthenia call for stimulants--wine, brandy,
and ammonia. The gastro-intestinal symptoms require the most careful
treatment. Bismuth, hydrocyanic acid, creasote, soda-water, ice, and
champagne will be found useful in allaying the vomiting and
irritability of stomach, but in some cases these symptoms prove most
intractable. Purgative medicines must be given with very great caution
on account of the liability to profuse diarrhoea and serious collapse.
The constipation, which may be obstinate, is best treated by mild
enemata. The greatest care should be exercised in the diet, which
should be plain and easily digested. Though the vomiting is not
directly dependent upon the state of the stomach, yet indigestible food
and irregularities in eating may induce the gastric attacks. When there
is much irritability of the stomach the patients seem to do best on a
strict milk diet.

[Footnote 236: Quite recently an active professional man consulted me
for bronzing of the face and hands, and he had had one fainting spell.
With the concurrence of Pepper he was advised to give up business for a
year and live quietly abroad. His general condition was so good and the
pigmentation so limited that there seemed just a possibility that it
was not Addison's disease. He went home and prepared to follow out our
advice, but a second sudden attack of syncope proved fatal.]


{949} OTHER DISEASES OF SUPRARENAL BODIES.

ANOMALIES.--There may be four glands, two on each side. More commonly,
there are small supplementary organs--glandulæ succenturiatæ--situated
in the neighborhood, seldom reaching the size of a pea. Grawitz has
recently shown that many of the small adenomas of the kidney are in
reality minute portions of suprarenal tissue which have become included
in the course of the development of these organs. Fusion of the two
glands has been observed (Klebs). They may be absent.[237]

[Footnote 237: Defect of adrenals is very rare. There are not a few
observations in which it is stated that the right gland was absent.
Now, if the examination is not made with care, and particularly if the
liver is removed first, the right gland may be taken away with it
closely lodged in the fossa suprarenalis, and so escape observation.
Time and again have I directed the attention of the student making the
autopsy to the right adrenal on the under surface of the liver.]

It is curious how liable the suprarenals are to anomalies in position
or form in connection with defective development of the brain and cord.
In anencephalous monsters the glands may be absent or very small.[238]
In one instance I found them normal in size, but they were below, not
above, the kidneys.

[Footnote 238: Lomer, _Virchow's Archiv_, Bd. xc.; Weigert, _ibid._,
Bd. c.]

ATROPHY.--Extreme wasting may be met with as an accidental
circumstance: there may be only a trace of gland-tissue left. Several
such specimens have been found in association with Addison's disease.
There may be an interstitial growth of fibrous tissue, cirrhosis, with
shrinking of the organ. More often the glands are larger and harder in
connection with the cyanotic induration of heart disease. It is stated
by some writers that the adrenals of the negro are larger than those of
the European races--a statement which I have not been able to confirm
in several observations.

APOPLEXY.--In the new-born and young children congestion is not
infrequent. Hemorrhage into the central medullary substance is by no
means uncommon, either on one side or bilateral. The amount may be
considerable, and the glands greatly distended, forming large tumors.

INFLAMMATION.--Suppuration is rare except in connection with the
caseo-fibrous change already described as specially associated with
Addison's disease. Abscesses in the vicinity, as from caries of the
spine, may involve one or both capsules.

DEGENERATIONS.--Fatty changes are very common, particularly in the
cortical layer, which then has a light-yellow color, instead of the
normal dark gray-red. Yellow oil-drops appear to be normal constituents
of the cells of the cortex.

Amyloid degeneration may occur, but only in connection with similar
changes in other organs. The glands are enlarged, very firm, and the
medullary part translucent. The iodine reaction shows it to be limited
to the fibrous septa and blood-vessels.

The brown pigment of the intermediate zone, zona reticularis, may be
greatly increased. Normally in man, the amount is very variable, and
the deeper color may be due to congestion of the blood-vessels.

CYSTS with serous or hemorrhagic contents are occasionally found,
chiefly in the cortical part. They may be multiple. Hydatid cysts have
been met with.

TUMORS are not very uncommon. Cancer may attack them primarily, but
more often they are involved in secondary growths after carcinoma of
stomach or other organs. They are not infrequently affected in cancer
of the kidneys {950} by direct extension of the growth. Sarcomas are
also not uncommon, and may form large masses the size of the foetal
head. They may be melanotic.

These varied pathological conditions are not usually associated with
any special or distinctive symptoms, and in the great majority of cases
have been unsuspected during life. The organs may be totally destroyed
without inducing any of the phenomena of Addison's disease. In a few
cases, however, bronzing of the skin has been met with.




{951}

DISEASES OF THE SPLEEN.

BY I. E. ATKINSON, M.D.


Morbid processes affecting the spleen have been and remain involved in
great obscurity. Older writers, who were accustomed to reach their
conclusions in great measure through the observation of symptoms alone,
were obliged in the absence of anything like correct knowledge of
anatomy, physiology, and pathology to supply from the imagination most
of their theories of disease. Untrammelled by the bonds of accurate
investigation and ignorant of pathological anatomy, they found no
difficulty in ascribing to various parts and organs peculiar groups of
symptoms, both physical and moral; and for a number of these the spleen
was held responsible. We now know that many of the symptoms thus
supposed to indicate splenic disease depend upon alterations in other
parts of the body, and may be observed in persons possessing perfectly
healthy spleens. But while we have learned that symptoms formerly
supposed to depend upon splenic disorder may, in reality, have nothing
to do with this organ, we still remain ignorant of many of the real
symptoms of splenic disease, as well as of many of the morbid
conditions that induce them. Such knowledge as we have, however, is
based upon comparisons of symptomatology with dead-house revelations
and the experience of the laboratory, and, while as yet imperfect,
cannot fail to increase under modern methods of research.

In order to begin the study of diseases of the spleen in an intelligent
manner it is manifestly necessary to have some settled ideas regarding
its anatomy and physiology. No apology is needed, therefore, for the
brief anatomical and physiological descriptions that follow.

The spleen is the largest of the ductless glands, and is situated in
the left hypochondriac region. It is of a dark slate or bluish-gray
color, and often of wrinkled appearance. It is of soft, friable
structure. It rests between the stomach, diaphragm, and left kidney,
and in form resembles a flattened oval. It extends from the level of
the eleventh rib, beginning one or two centimeters distant from the
vertebral column, downward and forward to a position about four
centimeters from the point of the eleventh rib (Lushka). It is
separated from the ninth, tenth, and eleventh ribs by the diaphragm. It
presents two surfaces--one external and convex, facing the diaphragm;
the other internal and concave, applied to the cardiac end of the
stomach. The hilum divides the internal portion into two parts by a
deep fissure, which marks the line of attachment of the gastro-splenic
omentum. The larger and anterior part is bound to the fundus of the
stomach by delicate areolar tissue, and the posterior and smaller
portion to the left pillar of the diaphragm and the left suprarenal
capsule. The upper portion is connected with the diaphragm by
peritoneum forming a suspensory ligament. The bottom of the hilum is
perforated by a number of openings for the transmission of
blood-vessels, nerves, and lymphatics. The anterior border of the organ
is notched and thinner than the posterior border. The pointed lower end
touches the splenic flexure of the transverse colon and rests upon the
costo-colic ligament. {952} The spleen varies in size and weight within
wide limits. Its average weight in adults is 250 grams, its length from
11 to 13 centimeters, and its thickness from 4 to 6 centimeters (Orth).
Its volume is from 150 to 180 cubic centimeters. According to Gray, the
proportionate weight of this organ to that of the whole body varies
from 1:320 to 1:400, gradually diminishing until old age, when the
proportion becomes as 1:700.

In the vicinity of the spleen are often found a number of small bodies
similar to it in structure. These are known as accessory spleens, and
are usually situated in the gastro-splenic or in the greater omentum.
The attachments of the viscus are not very close, and much variation in
size and position is possible.

Except at the hilum the peritoneum forms everywhere one of the
coverings of the spleen. Its peculiar sheath or capsule is composed of
fibro-elastic tissue of a whitish color, prolongations of which extend
into the substance of the organ and form the trabeculæ that constitute
its supporting framework and sheaths for blood-vessels and nerves. A
close meshwork is thus created in which are contained the splenic
vessels and pulp. This fibrous coat and these trabeculæ contain
involuntary muscular fibres. These, with the elastic fibres, provide
for the changes in size that the organ undergoes. When incised, the
normal spleen presents a reddish-brown color, and its substance may be
readily broken down with the finger into a pulp. This pulp consists of
a mass of branched intercommunicating connective-tissue corpuscles of
different sizes, within the substance of which remains of red
blood-corpuscles may often be detected. The interstices of these cells
are filled with blood. The very large splenic artery enters the spleen
by numerous branches, ramifying within the trabecular sheaths and
terminating in pencils of minute size.

The external coats of the smaller arteries are converted into lymphoid
tissue, which, suddenly expanding here and there, forms the bodies
known as the Malpighian follicles, which are supplied with capillary
vessels, and which may often be distinguished by the naked eye as
points of whitish color, sometimes attaining the size of pinheads.
These small arteries end in capillaries, which, according to Müller,
gradually lose their cylindrical character and emerge into a system of
connective-tissue corpuscles, inosculating with the corpuscles of the
splenic pulp in such a manner that the blood passes into the
pulp-tissue freely, and is gradually brought to the veins by the
transition of this tissue into that of the blood-vascular system. The
splenic lymphatics originate in the arterial sheaths and in the
trabeculæ. In the former case they accompany the blood-vessels; in the
latter, they communicate with a superficial network in the corpuscle.
All join at the hilum and enter the neighboring lymphatic glands. The
splenic nerves are from the right and left semi-lunar ganglions and
right pneumogastric nerve. They accompany the branches of the splenic
artery, and have been traced deeply into the tissue of the organ.

It is perfectly established that under normal conditions the volume of
the spleen may vary considerably, and especially during the act of
digestion, and that this does not occur through simple engorgement of
the vessels. The very important experiments of Roy show that, in cats
and dogs at least, the splenic circulation does not depend upon the
ordinary blood-pressure, but is carried on "chiefly, if not
exclusively, by a rhythmic contraction of the muscles contained in the
capsule and trabeculæ of the organ."[1] This rhythmic contraction and
expansion Roy observed to occur with great regularity at the rate of
about sixty contractions an hour, with extremes of rapidity of rhythm
of forty-six seconds for the most rapid and two minutes three seconds
for the slowest. He also observed that stimulation of the central end
{953} of a cut sensory nerve, or of the medulla oblongata, or of the
peripheral ends of both splanchnics and both vagi, causes a rapid
contraction of the spleen. Unsatisfactory as is our knowledge of
splenic physiology and of its exact relations to the maintenance of
life (for that the spleen is not the seat of a peculiar and exclusive
function has been demonstrated by the survival of individuals after
extirpation of the organ), at present certain theories of its nature
find pretty general acceptance. Thus, it is considered that in the
lymphoid tissue of the blood-vessels and Malpighian corpuscles
leucocytes are produced--that the cells of the splenic pulp appear to
take red blood-corpuscles into their interior, where their
disintegration takes place. There are not sufficient grounds for
believing that in the spleen red blood-corpuscles are formed. Recent
observations of Tizzoni, Crédé, and Zesas have led them to the
conclusion that they are made in the spleen; but Bizzozero and others
deny that this occurs except after serious hemorrhage.

[Footnote 1: _Journal of Physiology_, vol. iii., 3 and 4, p. 203.]

It is impossible to detect by palpation any part of a healthy spleen.
Its area may be approximately defined by percussion alone, though even
by this method it is not always easy to determine its position and
size. Loomis advises that the patient be placed upon his right side in
order to facilitate the examination. The anterior border of the spleen
is then "readily determined by the tympanitic resonance of the stomach
and intestines. Inferiorly, where the organ comes into contact with the
kidney, it is difficult, and often impossible, to determine its
boundary. Its superior border corresponds to the line which marks the
change from flatness to pulmonary resonance." The vagueness of these
directions is necessitated by the difficulties of the subject, the
splenic outlines being liable to frequent variations. Schuster and
Mosler give excellent reasons for prosecuting the investigation with
the patient in the right semi-supine position.


Acute Congestion of the Spleen.

Except within the physiological limits already referred to, acute
congestion of the spleen never occurs as a primary process. Under
pathological conditions it is known to take place under a great variety
of circumstances, principally, however, in connection with those states
of the system in which disease is supposed to depend upon some specific
principle or germ. To a minor extent it is probable that splenic
congestion accompanies nearly all febrile conditions, and from the
border-lands of health to that highest and most intense degree of
hyperæmia by which the organ acquires a volume and prominence that have
caused it to be designated as acute splenic tumor, all gradations may
be observed, though in many instances these may be so slight as to be
incapable of recognition clinically, and are only brought to our
knowledge through necroscopic examination. The congestion becomes most
marked in the course of the acute specific fevers. In typhus and
typhoid fevers, in small-pox, scarlatina, diphtheria, in epidemic
cerebro-spinal meningitis, in acute tuberculosis, in erysipelas,
puerperal fever, in conditions of blood-poisoning and in malarial
fevers, more especially those of more severe type, it reaches its
highest development. According to Friedreich, a form of pneumonia
(differing from ordinary croupous pneumonia in its serpiginous course),
acute coryza, and acute pharyngitis and tonsillitis are accompanied by
enlargement of the spleen in consequence of the septic nature of these
disorders. During the fever of secondary syphilis a splenic enlargement
purely hyperæmic in character may sometimes be detected. Similar
conditions are occasionally observed in a number of other affections.
This tendency of the spleen to active congestion is to be accounted for
by its peculiar anatomical structure, whereby unusual facilities for
hyperæmia are {954} afforded, more especially in the infective fevers,
in the course of which the organic germs which are supposed to
constitute their essential principles collect in the pulp, and by their
accumulation and multiplication serve to excite a more or less intense
determination of blood to the part, the organisms themselves being
taken up by the leucocytes and connective-tissue corpuscles composing
the pulp. We can thus account for the multitudes of these organisms to
be found in the splenic pulp after various infective disorders, as in
relapsing fever as observed by Ponfick, in pyæmia by Birch-Hirschfeld,
and in splenic fever of animals by various observers. The less intense
degrees of congestion occurring during the various specific fevers and
in many simple febrile disturbances are usually so slight as not to
attract attention. When the hyperæmia has been unduly prolonged, as
more especially occurs as a result of chronic malarial poisoning,
leucocythæmia, pseudo-leucocythæmia, or Hodgkin's disease, there is a
well-pronounced tendency toward permanent structural changes and the
development of hypertrophy.

SYMPTOMATOLOGY.--Milder degrees of congestion do not, generally, reveal
their existence by symptoms, and those of more pronounced character
give for the most part signs that are vague and nearly obscured by the
more prominent features of the pathological processes that occasion or
accompany the splenic changes. It may happen that acute splenic tumor
of considerable size may be quite painless. It has been objected,
indeed, that when pain accompanies splenic enlargements it is not
attributable to any sensibility of the spleen itself, but to the
participation of the investing peritoneum in the morbid action or to
the dragging of the enlarged organ upon the parts with which it is
connected (Mosler). Patients, however, will often complain of a dull,
aching pain and a sensation of weight in the left hypochondrium.
Occasionally, this pain may be severe and lancinating or may extend to
the shoulder. Headache and various digestive disorders--anorexia,
vomiting, flatulence, and diarrhoea--may prove distressing
accompaniments. Other symptoms, such as melæna, voracious appetite,
vertigo, extreme anæmia with its various concomitants, etc., belong
rather to conditions of protracted congestion where new formation and
true hypertrophy have been developed.

It is evident that it will often be extremely difficult, and sometimes
even impossible, to determine the extent to which symptoms are
occasioned by the splenic congestion or by the general affection to
which it owes its origin. Mosler declares that he is nearly always able
to detect during the cold stage of intermittent fever a peculiar murmur
over the splenic region and upward and downward in the abdominal
region, which he attributes to the contraction of the splenic artery.
This murmur he has not been able to perceive in chronic splenic
tumors.[2]

[Footnote 2: _Ziemssen's Cyclop._, vol. viii. p. 468.]

The normal splenic area can only be defined by percussion, and
congestion to a not insignificant extent may occur without revealing
itself by other symptoms than increase of the extent of percussion
dulness. When the organ projects beyond the margin of the ribs and can
be felt by the fingers of the examiner, it is enlarged, unless the
patient is the subject of displaced or of wandering spleen. But whether
the enlargement be due to hyperæmia simply or to hypertrophy can only
be determined by a consideration of all the concomitant circumstances.
Unless under the influence of chronic irritation or as a result of
mechanical hyperæmia, congestions of the spleen are commonly of sudden
development and of transitory duration. In ordinary inflammations, such
as pleurisy, etc., the degree of congestion is so slight as to be
unnoticeable; but as an epiphenomenon of the various specific fevers
the enlargement occurs rapidly and acquires a prominent interest in
many cases. Acute splenic tumor, for example, is almost of constant
occurrence during the course of typhoid fever, and, according to
Friedreich, its presence may {955} be ascertained some days before the
specific symptoms of the disease have declared themselves. A similar
early development has been claimed for it in diphtheria and other
affections. The congested spleen of typhoid fever and of relapsing
fever, however, differs from that of most other acute disorders in
returning to its normal dimensions much more slowly; and it is
important to remember that until the splenic tumor has disappeared
there is reason to believe the danger of relapse still imminent. In
most cases the enlargement disappears pari passu with the disorder that
occasioned it. In malarial fevers and in septic diseases the splenic
tumor may acquire excessive dimensions. Acute splenic tumor, however,
never attains the dimensions often encountered in chronic congestion
and hypertrophy.

PATHOLOGY AND PATHOLOGICAL ANATOMY.--Simple splenic congestion presents
at first no anatomical features differing from purely physiological
hyperæmia. There is simply more blood in the dilated vessels and
vascular spaces, and consequently in the viscus, than is usual. Very
soon, however, there is hyperplasia of the cells of the pulp.
Enlargement, tension of the capsule, and diminished consistency of the
spleen appear. The color will depend upon the condition of the capsule,
being most dark and blue when this is thinnest. In high grades of
congestion the parenchyma upon section will be found distended and
semi-diffluent, and after acute malarial fever (pernicious remittent
fever), the organ may resemble a bag of half-liquid pulp. Softening in
varying degree may be found after acute congestion from whatever cause.
In the congestions due to some infective processes at least additional
factors are introduced, although as yet definite knowledge of their
exact pathogenetic influence has not been attained. The observations
connecting minute organisms with the origin of these affections have
been so elaborate, so carefully and conscientiously reported, extend
over such wide and varied fields, that it is difficult to refuse to
place reliance in them. It seems that in a number of affections the
presence of these microscopic organisms is constant and essential, and
that the splenic congestion that accompanies them is a direct result of
their presence in the spleen itself. The micro-organisms will be found
infesting the cells of the pulp, and, so far as we have definite
knowledge, they show peculiar characteristics according to the
particular infectious disease to which the patient succumbed. While the
conditions in acute splenic tumor are identical with those of
inflammation, and in the affections properly designated as septic,
should the life of the patient have been sufficiently prolonged, may be
found to have led to the formation of embolic centres with hemorrhagic
infarctions and abscess, in infectious diseases not septic they do not
prove equal to the production of suppuration. Where the action is
acute, resolution will speedily follow the subsidence of the febrile
process. But in prolonged hyperæmia new formation will be developed,
and the enormous collection of leucocytes will give a reddish-gray
color to the organ. This change will also be sometimes observed in the
spleens of those in whom the infectious diseases have run a more
protracted course.

DIAGNOSIS.--Acute splenic tumor, if at all pronounced, may usually be
diagnosticated without much difficulty. The development of an
enlargement in the splenic region, with pain and tenderness to
pressure, during the course of any acute febrile disease will nearly
always indicate splenic hyperæmia. It may sometimes be difficult to
determine whether the tumor may not have existed prior to the invasion
of the present malady. In such cases one must have recourse to the
previous history of the patient, or, failing in this, must observe the
behavior of the tumor upon the subsidence of the general affection.

PROGNOSIS.--The prognosis of acute congestion and acute splenic tumor
will depend rather upon the exciting cause. When of simple origin it is
of but insignificant importance. Even in specific fevers the spleen
will in most {956} instances return to its normal volume upon the
establishment of convalescence. Rupture of the spleen has been known to
occur in congestion from severe malarial fever, but this is a most rare
accident in the absence of traumatic influences. The congestion may
become chronic, and frequently does become so, in cases where the
stimulus continues to exert an influence upon the spleen, as is done in
chronic malarial poisoning.

TREATMENT.--The transitory hyperæmia of a brief malarial attack or of
any ordinary febrile seizure will disappear with its exciting cause,
and will require no special treatment. For the acute congestions of
most specific fevers but little is to be done except through attention
to the general condition: it is only when pain and discomfort in the
splenic region are sufficient to attract the attention of the patient
that measures for the relief of the congestion will be necessary. In
that most common exciting cause of it, malarial fever, patients will
often complain bitterly of the pain in the left hypochondrium for some
time after the febrile attack has been overcome. In such cases it may
be pretty safely concluded that the poisonous influence of the malaria
has not been entirely overcome, and the proper employment of quinine
and other derivatives of Peruvian bark, and bitter tonics, will
undoubtedly prove most serviceable. In very many cases benefit may be
derived from local applications. Experiment has clearly shown that the
stimulation of the splenic nerves is capable of effecting a notable
reduction in the bulk of the organ. Clinical experience gives similar
proofs, and cold effusions, evaporating lotions, etc. will sometimes
secure prompt unloading of the spleen; indeed, Mosler considers that
there is danger in treating the acute splenic tumor of typhus fever of
inducing unfavorable changes by the too sudden reduction of its bulk by
local applications. The use of stimulating applications to the splenic
region will also prove beneficial in many cases. Among the most
valuable of these will be found the tincture of iodine.


Chronic Congestion and Enlargement of the Spleen.

Within narrow limits there may be simple increase in the size of the
spleen from hyperæmia, without alteration of the relations between its
structural parts. The common results, however, of hyperæmia of long
standing are overgrowth of the elements of the reticulum, with new
formation of connective tissue and hyperplasia of the pulp-tissue. This
condition of chronic enlargement or hypertrophy of the spleen may
develop as a result of chronic active hyperæmia or through passive or
mechanical engorgement of the portal system. Chronic active hyperæmia
of the spleen is in much the greater number of instances caused by
chronic malarial poisoning. It also occurs as a cause or a result of
leucocythæmia and of pseudo-leucocythæmia or Hodgkin's disease, and is
always associated with more or less true hypertrophy of the structural
elements of the organ. Enlargement from the above-mentioned causes
constitutes the vast majority of those abnormalities generally
designated as chronic splenic tumor. In persons living in malarious
countries, and subjected for prolonged periods to the intoxicating
influence, the peculiar splenic enlargement tends to become chronic.
After the earlier attacks the spleen returns more or less promptly to
its normal dimensions. Usually it is only after repeated attacks of
intermittent or remittent fevers, and often only after exposure to the
malarious influence for years, that the splenic tumor becomes
established as a permanent disorder and assumes the characteristics
that have secured for it the popular denomination ague-cake. Persons
living in the localities referred to may develop this enlargement
without ever having had unequivocal attacks of malarial fever. They
will betray, however, the effects of the poisoning by malarial
neuralgias and {957} neuroses or by a well-marked periodicity in the
course of simple maladies, or they will exhibit its effects by the
peculiar facies and by general paludal cachexia. Under these conditions
the splenic enlargement sometimes attains enormous proportions.

Splenic enlargement of considerable extent may result from mechanical
hyperæmia of the portal circulation from cirrhosis of the liver. It is,
however, certainly not a necessary consequence of cirrhosis, since this
may exist to a pronounced degree and yet the spleen remain normal--a
condition that is probably favored by extensive distribution of
muscular and elastic fibres to the viscus, that enable it to a great
extent to regulate its own circulation. On the other hand, the spleen
may be atrophied by a fibrotic contraction of its trabeculæ, the result
of long-standing hyperplasia. Chronic engorgement and enlargement of
the spleen may also result from mechanical obstruction to the systemic
venous circulation, especially that due to insufficiency of the mitral
valve, whereby obstruction to the portal circulation arises
secondarily. (The ulcerative endocarditis of septic origin is
associated with splenic congestion, which is, however, always of the
acute active variety, and complicated for the most part with embolic
abscess and hemorrhagic infarction.)

SYMPTOMATOLOGY.--Long-continued or frequently-recurring attacks of
splenic hyperæmia, occurring under the stimulus of chronic malarial
poisoning or of leucocythæmia or pseudo-leucocythæmia, will ultimately
induce those structural changes that result in new formation.
Enlargements from the two latter diseases will be more appropriately
considered elsewhere. After repeated attacks of remittent or
intermittent fever or other forms of malarial intoxication the symptoms
of acute will gradually merge into those of chronic congestion. They
will usually prevail to a more intense degree. The dragging weight of
the tumor will excite pain, and may render rest upon the right side too
uncomfortable to be indulged in. Hemorrhage from the stomach and bowels
may occur, and at times will be excessive. The patient may be reduced
to an extreme degree by the profuse and repeated losses of blood. In
the intervals of the malarial attacks the temperature will be
unelevated, and the pulse may be slow and irregular, though oftener
feeble and rapid. All the symptoms will be, however, commingled with
those from other causes. Those of malarial cachexia will sometimes be
very pronounced. The pale, sallow complexion, the pallid lips, the
extreme anæmia and generally unhealthy aspect, and the general symptoms
accompanying such states, the history of miasmatic fevers, of
characteristic neuralgias, etc., will generally be present. Oedema may
be observed, but will usually be hydræmic in origin. Anomalous symptoms
due to the systemic condition will be often developed when the
enlargement arises from other than malarial causes.

Under the influence of the latter cause the spleen may acquire many
times its normal dimensions, and may easily be felt below the border of
the ribs, where its irregularly curving and notched border will serve
to identify it. The tumor sometimes becomes so large that it reveals
its presence by causing a bulging and asymmetry appreciable by the
patient. Here, however, congestion will have been supplanted by
hypertrophy. The tumor may vary greatly in size. It may fill the left
part of the abdominal cavity, reaching to the pubes and distending the
belly-wall with its dense enlargement, dull upon percussion, and
perhaps moving within narrow limits under the hand of the examiner.
This tumor may attain a size and weight many times greater than the
normal. Hypertrophy once established, it may remain more or less
pronounced for years, directly occasioning unimportant symptoms. It is
difficult to determine the exact influence exerted by these tumors upon
the duration of life.

PATHOLOGICAL ANATOMY.--In simple hypertrophy there is both hyperplasia
of the pulp and of the trabecular connective tissue. The spleen is
{958} enlarged, sometimes to an extreme degree, equalling fifteen or
sixteen times its normal weight.[3] Such enlargement is not observed in
any other form of splenic disorder, excepting in some rare cases of
leucocythæmia and tumor. Its density is also increased. The capsule is
thickened, and adhesions to the surrounding parts may be quite
intimate. The color of the surface is darker than normal. Upon section
the structure appears dense, smooth, of a dark color (from deposit of
pigment), and showing to the naked eye great increase of the trabecular
tissue. The pigmentation more especially observed in malarial
intoxication occurs in the intervascular cords of the pulp
(Rindfleisch), where it can be seen as black, flaky masses of hæmatin
(the origin of melanæmia). According to Friedreich,[4] there may be a
circumscribed splenic hypertrophy, consisting of little points of
granulation imbedded in the pulp. In ordinary diffuse hypertrophy all
the elements are involved, though the trabeculæ show the greatest
increase and encroach more or less upon the pulp. The Malpighian
corpuscles may show little or no enlargement. The processes are
indistinguishable from those of chronic inflammation. In hypertrophy
from obstructed portal circulation the organ will be dark red and very
full of blood. It sometimes happens that obstructive hypertrophy
terminates in fibrotic contraction, when the connective tissue will be
found to have almost completely crowded out the pulp.

[Footnote 3: Hertz, _Ziemssen's Cyc._, vol. ii.]

[Footnote 4: _Virchow's Archiv_, xxiii., 1865; _Ziemssen's Cyc._,
viii., Mosler.]

DIAGNOSIS.--Decided enlargement will usually be recognized with but
little difficulty. A tumor in the left hypochondrium, occupying and
transgressing the normal splenic boundaries, will probably be of
splenic origin. Occasionally enlargement may be simulated by a spleen
of normal size displaced downward by intra-thoracic growths or
effusions or by that remarkable abnormality known as wandering spleen.
The course of the primary affection in the one case, and the free
movability of the organ in the other, will suffice generally to guard
against error. Rarely, the tumor may be due to cancer of the stomach,
enlargement of the left kidney or of the left lobe of the liver,
omental tumors, fecal accumulations in the colon, or ovarian tumors.
The concomitant symptoms will suffice to distinguish cancer of the
cardiac end of the stomach. Percussion will reveal the presence of
subjacent gases, and palpation will detect the greater hardness of the
gastric tumor. Enlargement of the left kidney may be due to cancer,
abscess, or other causes, and may simulate splenic hypertrophy. The
renal tumor may be traced farther backward, and will not present the
characteristic outline of the spleen. The clinical history and symptoms
will here, again, prevent error. Omental tumor is usually separated
from the splenic region by an area of resonance. Enlarged liver may be
traced toward the right side of the body, becoming more noticeable as
the spleen is receded from. Fecal accumulation may closely resemble
splenic tumor, as it does other abdominal enlargements. The doughy
consistency of enlarged spleen may be like that of the fecal mass, but
one may often permanently alter the shape of the latter by the pressure
of the fingers, and in any case doubt may be dispelled by the use of
purgatives. Ovarian tumors may be traced into the pelvis, as may also,
for the most part, fibro-cystic and fibroid tumors of the uterus and
its appendages.

On the other hand, recognition of splenic tumors may be prevented by
gaseous distension of the stomach and bowels, by abdominal dropsy,
diffuse or encysted, by fecal distension of the colon, and may, indeed,
be impossible until these conditions have been remedied. Enlargement of
the spleen from simple hyperplasia must also be distinguished from
other forms of splenic enlargement--from splenitis, from lardaceous
degeneration, from tumors, from leukæmia and pseudo-leukæmia, from
syphilitic and tuberculous {959} spleen, etc. In such cases the
diagnosis will rather depend upon concomitant symptoms than upon the
physical characters of the enlarged organ. Percussion and palpation
will not seldom enable one to determine the presence of tumor (cancer),
hydatids, etc. Pressure will often serve to elicit expressions of great
tenderness in splenitis; enlargements with fluid contents will be
revealed by fluctuation. In the greater number of cases where the
enlargement is evident, but is without distinguishing characteristics,
the general condition of the patient and the history of his illness
will disclose its true nature. Lardaceous degeneration will have been
anteceded by prolonged suppuration, by tubercle, by scrofula, or by
syphilis, and will generally be associated with the same processes in
other parts. Syphilitic disease may be indicated by the history of the
patient, though in this case, of course, lardaceous degeneration could
only with difficulty be excluded. Tubercle, rarely giving rise to an
appreciable tumor, can only be conjecturally diagnosticated from the
history and general condition of the patient. The condition of the
blood and of the lymphatic system in leukæmia and pseudo-leukæmia will
suffice to determine the nature of the splenic enlargement. The
ague-cake of chronic malarial poisoning is usually accompanied by a
degree of cachexia, as is shown in the earthy pallor of the complexion.
This is often sufficient to enable one to discriminate between several
forms of enlargement, for it differs from the intense pallor of
leukæmia by its sallow hue, and is not at all like the hue of the
complexion in lardaceous disease. The cancerous cachexia, it is true,
may closely resemble it, but here the history and symptoms assist in
avoiding mistakes.

PROGNOSIS.--When the hyperplastic processes have amounted to true
connective-tissue formation, a complete return to normal conditions
will not occur after the removal of the stimulus. The permanence of the
enlargement will be proportionate to the extent of organization of the
hyperplastic elements. In ague-cake some reduction in size will follow
the exhaustion of the malarial influence, though the spleen probably
never ceases to be appreciable as a distinct enlargement. At the same
time, the enlarged organ may not, of itself, exert any specially
unfavorable effect upon its bearer. Not a few persons will live for
years with it, and eventually die from other causes. It may be assumed,
however, that the presence of ague-cake is indicative of profound
malarial cachexia, by which the powers of life are much less resistant
to unfavorable influences. It may be said, in a general way, that the
larger the spleen the less favorable is the prognosis. It should be
remembered that a considerable proportion of persons suffering from
leucocythæmia have also suffered from chronic malarial poisoning, and
that the enlarged spleen of this affection may possibly have begun its
morbid course under the influence of malaria.

TREATMENT.--In passive congestion relief is often secured through the
use of remedies that diminish portal engorgement or enable the heart to
find compensation for a damaged mitral valve--conditions in which the
splenic disorder is really an unimportant concomitant. In the
enlargement that has for its cause chronic malarial intoxication
cinchona and its alkaloids are preferable to all other remedies, not
only in arresting the new growth otherwise progressive under the
stimulus of the poison, but by neutralizing the latter and facilitating
the absorption of the hyperplastic elements that have not already
become converted into more highly-developed tissue. To effect these
objects the agents must be given in fair doses (twenty grains of
sulphate of quinia daily) until the malarial cachexia shall have been
overcome--until the bulk of the enlarged spleen shall have been reduced
to the smallest possible proportions. To bring about the desired result
the treatment may have to be continued during several months,
occasionally suspended upon the supervention of symptoms of cinchonism.
A drug of deserved repute {960} (probably through its anti-malarial
influence) is arsenic. This should be given for protracted periods.
Many remedies possessing anti-malarial properties have also been
recommended and employed in these conditions. Eucalyptus and eucalyptol
have recently been used with promising results, though the sanguine
expectations of some will hardly be realized. Iron, preferably as a
sulphate or as the tincture of the chloride, is invaluable in
correcting the profound anæmia always present in these cases, though
its influence in reducing the splenic bulk immediately is, at best,
doubtful. Remedies competent to reduce hepatic and portal engorgement
will often prove beneficial. Salines and vegetable cathartics may more
especially be employed, but the use of mercurials, except for
occasional administration, is almost universally condemned as
productive of evil consequences.

Local Treatment.--The systematic application of cold by effusion or by
ice-bags will at times undoubtedly reduce the size of an enlarged
spleen. Alleviation will often be afforded by solutions of nitric acid
to the splenic region, and counter-irritants are of occasional service,
either by means of the tincture of iodine persistently employed or by
blistering fluids or plasters. These, however, should be used with
great caution in debilitated subjects, as gangrene has been known to
follow their application. Mosler thinks that the practice of injecting
tincture of iodine, carbolic acid, etc. into the substance of the
spleen is sufficiently promising to justify further experiment. The
continuous electric current and electrolysis have also been recently
recommended as of advantage in reducing the splenic bulk. In cases of
excessive enlargement, where accompanying or consequent cachexia
threatens to end in death, extirpation of the spleen has been advised
and practised. While the removal of the leucocythæmic spleen is so
constantly followed by death that the operation cannot be considered
justifiable, it seems that the spleen enlarged from other causes may
sometimes be removed with safety. In the _Lancet_ of Feb. 11, 1882,
Herbert Collier tabulates all (until then) known cases of removal of
the spleen for disease, 29 in number: 16 of these operations were upon
leukæmic subjects, and had a fatal termination; 8 of the remaining
cases recovered. Crédé[5] concludes from an analysis of 30 cases of
extirpation of splenic tumor that the adult spleen may be removed
without detriment; that its removal causes temporary derangement of the
blood-making function; and that this is compensated for by activity of
the thyroid body and red marrow of the bones. As bearing further upon
the question of the practicability of splenectomy, should surgical art
succeed in reducing the dangers immediately dependent upon the
operation, are the highly interesting experiments of Tizzoni[6] and
Griffini,[7] wherein extirpation of the spleen in dogs was followed by
reproduction of true splenic tissue.

[Footnote 5: _Centralbl. f. d. med. Wissensch._, June 23, 1883.]

[Footnote 6: _Arch. Ital. de Biologie_, 1883, iii. 2, and i. 1.]

[Footnote 7: _Ibid._, 1883, iii. 2.]

In chronic congestion and enlargement of the spleen from malarial
poisoning the removal of the patient to a non-malarious locality will
always materially assist in the recovery of health.


Hemorrhagic Infarction of the Spleen.

The investigations of Virchow, and more recently of Cohnheim, into the
pathogenesis and pathology of hemorrhagic infarction have afforded an
easily intelligible explanation of the causes of the frequency of this
morbid process in the spleen. A moment's reference to the anatomy of
the splenic blood-vessels will show that the conditions most favorable
to the production of hemorrhagic infarction in the presence of an
exciting cause are here afforded. Instead of terminating in a capillary
network with free and abundant {961} anastomoses, the splenic arteries
end in fine pencils, opening, not into capillaries leading to venous
radicles, but into vascular spaces in which traces of both afferent and
efferent blood-vessels gradually become effaced. These arterioles have
no other vascular communications than with the small arteries, the
terminal extremities of which they are. This arrangement may be very
perfectly demonstrated in injected spleens where the material has been
imperfectly driven through the vascular system of the organ, so that
wedge-shaped areas of successful injection become sharply defined. This
distribution of the blood-vessels renders the area supplied by each
almost completely dependent upon it for efficient nutrition, and almost
certain to become structurally altered if its lumen should become in
any manner obstructed. To this arrangement of the arteries and
arterioles upon one side is added, upon the other, a valveless
condition of the splenic veins, whereby regurgitation may readily
occur. We have here, therefore, evidently conditions most favorable to
the development of hemorrhagic infarction.

The process through which hemorrhagic infarction occurs has been
definitely observed by Cohnheim. The area of the distribution of the
obstructed artery or arteriole, receiving no blood-supply from
anastomosing branches, undergoes disintegration. The walls of the
blood-vessels as far as the nearest communicating branch participate in
the process of disorganization. After a while a backward movement of
the blood-current begins in the nearest still pervious vessels, and is
continued into the obstructed vessels, through whose disintegrating
walls the blood escapes and the hemorrhagic infarction is established.
The future course of the infarct depends almost entirely upon the
nature of the causes that brought it about.

In the spleen, as in other organs, the causes of hemorrhagic infarction
may be widely different, though an essential condition of each is that
it be competent to produce plugging of the blood-vessel. The most
important cause is probably ulcerative endocarditis, in the course of
which minute fragments of the endocardium or of the vegetations that
have formed upon it, especially of the neighborhood of the valves, in
consequence of inflammation, constitute the emboli. The plugs largely
consist of fibrinous matter enveloping colonies of micrococci, or they
may be derived from detached portions of thrombi, or from solid
particles that may have in any way gained access to the circulatory
current, as from endarteritis, from atheroma, primary emboli in the
pulmonary circulation, etc.

Hemorrhagic infarction has also been described by Ponfick[8] as
occurring in relapsing fever and originating in the veins, and not to
be referred to any of the already-mentioned causes. It is thrombotic in
origin, and due to some peculiarities of the morbid processes of the
affection.

[Footnote 8: _Virchow's Archiv_, Bd. lx.; Mosler, _Ziemssen's Cyclop._,
viii. p. 443.]

SYMPTOMATOLOGY.--Hemorrhagic infarction of the spleen, as such, reveals
its presence by no signs during life. Its importance depends almost
entirely upon the nature of its exciting cause. When this is of simple
origin there is hardly ever any deleterious influence exerted upon the
health of the individual. That hemorrhagic infarction was present in
any given case can only be ascertained by the evidences of it
discoverable after death. Rarely by its presence localized inflammation
and abscess may be excited. Far different, however, is the result where
the embolic material has been derived from an ulcerative endocarditis
or other septic centre. In this event the infarction serves surely as
the starting-point for metastatic abscess.

PATHOLOGICAL ANATOMY.--Hemorrhagic infarctions of the spleen may vary
in number from one to many, and in size from that of a large shot to a
bulk nearly equal to that of the spleen itself. They are usually
situated at the surface of the organ in a wedge-shaped distribution,
the base looking toward the capsule and causing a slight projection,
the apex pointing toward {962} the deeper portions. Infarctions,
however, may also occasionally occur in the central parts of the
spleen. A definite wedge-shape may be destroyed by the coalescence of
several neighboring infarcts.

The appearance and density of the infarction will depend very much upon
its age. When recent it is of a dark-red color, of firm consistency,
and of homogeneous aspect, and is surrounded by a zone of hyperæmia. As
it grows older the dark color gradually fades to a paler hue, in
consequence of the absorption of the color-elements of the hemorrhage,
and a yellowish shade appears, from fatty degeneration of the cellular
constituents. With the fading in color the infarction decreases in
size; contractions and scar-formations are developed, later to become
converted into bands of dense fibrous tissue. Occasionally complete
fatty metamorphosis of the cellular elements may ensue and caseation of
the infarct take place. The caseous mass may soften and form a cavity,
or may ultimately undergo calcareous degeneration. Not very
infrequently one may detect at necroscopic examinations of spleens
these calcareous nodules, equal to shot or peas in size, witnesses of
the bygone metamorphoses of which we are speaking. When, instead of
being of simple origin, the infarct is the result of septic changes,
the course is different. Coincident with or immediately preceding the
hemorrhagic infarction inflammatory symptoms will develop around the
embolic masses (consisting principally of fibrinous material
imprisoning multitudes of micrococci), and metastatic abscess rapidly
becomes established. Pus will then be commingled with the softening
mass, and the microscope will reveal the swarming organisms. In the
latter event the changes of the hemorrhagic infarction are much more
rapid than in simple infarction, when they may be very protracted.


Splenitis.

Although it is impossible to separate acute splenic tumor and chronic
splenic enlargement from the processes of inflammation, for practical
purposes it is convenient to consider as splenitis only those morbid
conditions in which the tendency is toward suppuration. Simple
idiopathic splenitis is undoubtedly very rare, and, although formerly
its symptoms were described with great detail, most recent writers are
content to acknowledge an almost complete ignorance of them. Indeed,
splenic abscess is often detected after death when it had not even been
suspected during life.

Diffuse Splenic Abscess.--In the rare cases of idiopathic splenic
inflammation the exciting cause will commonly have been a fall or blow
or other violence by which the spleen has been injured, or it may have
followed chronic malarial poisoning or an extension of inflammation
from the capsule or neighboring parts.

SYMPTOMATOLOGY.--The rarity of this affection makes accurate
description of its symptoms almost impossible. Mosler has never seen
it. The descriptions of it are based, at best, upon observation of but
few cases. Its onset may be sudden; more commonly it is insidious, the
patient complaining of weight and dull pain in the left hypochondrium,
irradiating to the left shoulder. The presence of pain depends upon the
participation of the capsule in the process. Cough and dyspnoea may be
present, and febrile phenomena are constantly to be observed. Vomiting,
want of appetite, furred tongue, etc. will be noticeable. After a time
a tumor will be detected that will, at first, almost certainly show no
sign of fluctuation. Coincidently with the development of the tumor a
small degree of ascites and of anasarca of the lower extremities may
appear.

Up to this point the presence of abscess may only be conjectured, and
indeed throughout its entire course it usually escapes positive
identification. {963} Fluctuation may, however, be detected, and from
its location and concomitant symptoms may reasonably be ascribed to a
splenic abscess. The fluctuating tumor has been known to fill the whole
abdominal cavity from epigastrium to pubes. Grisolle reports such a
case where the tumor presented the appearance of ascites. In this form
of splenic abscess the progress is generally insidious. Under symptoms
of hectic fever, wasting, etc. the physical signs of splenic
enlargement are gradually manifested until the presence of fluid may be
determined. After months of suffering the patient will expire from
exhaustion or from the consequences of rupture of the abscess into the
abdominal or pleural cavity or into the lungs, lighting up
rapidly-fatal inflammation; or, discharging into the bowel or stomach
or through the abdominal wall, the abscess may temporarily improve and
allow a short prolongation of a wretched life. In the event, however,
of an escape of pus from the body, as through the abdominal wall,
bowel, etc., recovery is possible in a very small proportion of cases.
Wardell has seen such a case discharging through the abdominal
parietes. Zweifel has met a similar condition. Nasse has known of
recovery after the pus had been expectorated, and Webb, after discharge
into the intestine. Occasionally, splenic abscess may become
encapsulated and undergo caseous metamorphosis, when it may become
inactive, ultimately cicatrize, or become calcareous.

PATHOLOGICAL ANATOMY.--In abscess of the spleen, when of small size, a
non-metastatic origin may be recognized by the absence of micrococci
from its purulent contents and of concomitant signs of blood-poisoning.
When not spontaneously arrested, these abscesses attain a size not
equalled by metastatic splenic abscess. The splenic substance will then
be reduced to a semi-fluid or fluid mass of reddish pus enclosed within
a pyogenic membrane. In extreme cases all traces of true splenic pulp
and trabeculæ will be obliterated; but when the inflammatory action is
less intense the trabeculæ will extend in all directions through the
abscess cavity. The capsule, thickened and indurated, will have formed
adhesions or will have entirely disappeared before the advancing wall
of the abscess.


Embolic Abscess.

It has been shown that hemorrhagic infarction in the spleen is the
result of an embolic obstruction of the splenic blood-vessels. If the
embolus be simply a detached portion of an aseptic clot or fibrinous
vegetation or of atheromatous degeneration, the subsequent changes will
be those characteristic of the involution of hemorrhagic infarction.
Under exceptional circumstances and from not understood causes
inflammation and abscess may follow. These, however, are to be reckoned
among the rare results of simple hemorrhagic infarction of the spleen.
Altogether more frequently the embolus is derived from the ulcerative
endocarditis of septic origin or from other septic centre, and consists
of congeries of micro-organisms, themselves the infecting agents or the
vehicles of the poison that lights up the characteristic morbid
processes. A colony of these micro-organisms, lodged in and occluding
splenic arteries, by the irritation of their presence and by their
multiplication excite the inflammatory processes that accompany and
follow the hemorrhagic infarction. Embolic splenic abscess is, then,
nearly constantly a secondary result of conditions of blood-poisoning,
and as such can only play a subservient part in the train of
pathological events in which all parts reached by the blood-supply may
be engaged. The vascular distribution in the spleen is such as to
afford exceptionally favorable opportunities for the development of
metastatic abscesses, and in a large proportion of spleens of those who
have died from blood-poisoning they will be detected. They are rarely
{964} present without the appearance of similar changes in other
organs, and there is, therefore, but little difficulty in attributing
them to their true cause.

SYMPTOMATOLOGY.--Unless inflammation of the splenic capsule be excited,
these abscesses give rise to no pain, neither do they (except rarely)
produce discoverable splenic enlargement as distinct from the general
splenic enlargement always present in septic fever. Their course is
usually brief, in consequence of the usually acute course of the
disease that occasions them. When, in chronic pyæmia, splenic embolic
abscess may develop more slowly, exceptionally palpable fluctuating
tumor becomes manifest.

Fever, with all the accompanying phenomena of blood-poisoning, is
present in these cases, and commonly masks any splenic alteration that
might otherwise become apparent. Embolic abscess should always be
suspected in blood-poisoning, though in most cases its detection could
have but little influence in determining treatment.

PATHOLOGICAL ANATOMY.--Embolic abscess may develop from a hemorrhagic
infarction, in which case the necrotic central mass is surrounded by a
zone of inflammation which rapidly converts the whole area into a
broken-down, reddish, purulent, semi-fluid matter. If the abscess
supervene without the occurrence of hemorrhagic infarction, its
situation is still nearly always peripheral, the wedge-shaped embolic
area pointing toward the centre. It varies in size from that of a
pinhead to that of a pea and larger. It consists of a necrotic centre
composed of pus-cells and detritus, a surrounding mass of exudation,
and a circumscribing border of hyperæmia. Microscopic examination will
usually reveal swarms of micrococci. In the progress of the abscess the
whole mass becomes converted into a grumous brownish fluid. The
peritoneum rarely participates in the activity of the inflammation, but
may form deposits of lymph over the seats of the abscesses.

Mosler[9] summarizes Ponfick's description of a peculiar splenic
inflammatory process resulting from relapsing fever. It differs from
ordinary embolic abscess in being limited to the splenic venous system.
It may equal two-thirds of the entire spleen in bulk. It resembles in
appearance embolic abscess, but the arteries remain pervious. These
abscesses may heal or may enlarge and peritonitis may be excited. The
possibility of their originating in a venous thrombosis is entertained
by Ponfick. A peculiar inflammatory condition of the follicular tissue
of the spleen has also been described by Ponfick as a result of
relapsing fever.

[Footnote 9: _Ziemssen's Cyclop._, vol. iii.]

DIAGNOSIS.--The diagnosis of splenic abscess presents very often great
difficulties, and is frequently quite impossible. In ordinary embolic
abscess a diagnosis cannot be made with certainty. The existence of
pyæmia with enlargement and pain would make it probable that splenic
abscess had formed. In the larger abscesses of malarial, traumatic, or
unknown origin the detection of a fluctuating tumor in the region of
the spleen will suggest its true cause, but examination of the contents
will alone clear up the diagnosis between the real disease and hydatid
tumors, nephritic and perinephritic accumulations of fluids, etc. Even
where the contents of the cavity are purulent, it will often be
impossible to decide upon their splenic origin unless in the event of
portions of the splenic tissue escaping at the orifice of the abscess.
In cases of constant and increasing pain and tenderness in the splenic
region, with enlargement, associated with general failure of health,
splenic abscess may be suspected, and an exploratory puncture with the
aspirating-needle may not only be justifiable, but imperatively called
for. In all cases it must be remembered that splenic abscess of this
character is a most rare disease.

PROGNOSIS.--Splenic abscess usually terminates fatally. The
life-destroying influence, however, is not exerted through the spleen
itself, for this may {965} be converted into a simple bag of semi-fluid
contents, with complete destruction of all its tissue, and yet danger
is to be apprehended only from the effects of suppuration or of rupture
into the closed cavities or from peritonitis, etc. Of itself, embolic
abscess rarely excites alarming symptoms, because, being usually of
septic origin, the stress of the general condition is thrown more upon
the whole body, or upon a number of its parts, of which the spleen is
not the most important.

TREATMENT.--Treatment should be directed more toward prophylaxis than
toward cure. In those congestions and hyperplasias that may result in
abscess the remedies indicated for these conditions should be actively
employed. The application of ice to the splenic region, of
counter-irritants, the use of local bloodletting, the unloading of the
intestinal circulation by saline purgatives, the proper employment of
quinine, etc. in chronic malarial poisoning, seasonably adapted, may
prevent the formation of abscess. In the event of fluctuation declaring
itself, evacuation under antiseptic precautions should be practised;
ordinarily, the most effective general treatment is that directed
against the primary disease.


Perisplenitis.

Inflammation of the splenic capsule is a more common affection than
clinical observation would lead one to suppose. It consists of a more
or less localized splenic peritonitis, and its lesions are often found
at the necropsy when its existence had not been suspected during life.

ETIOLOGY.--Its commonest cause is the extension of inflammation from
neighboring parts. Chronic ulcer of the stomach may be the origin of
chronic perisplenitis, leading to the formation of dense inflammatory
deposits. Persons who have long suffered from miasmatic poisoning
frequently develop strong adhesions between the spleen and diaphragm.
And from the same cause the spleen may become closely adherent to the
neighboring viscera. Chronic enteritis, perinephritic inflammation, and
the like may excite it. It has been shown that the pain in splenic
affections is nearly always due to the capsulitis present; and it is
probable that much pain in the splenic region, stitches in the side,
etc. are really the results of this inflammation. It can only be
conjectured that in given cases one has to do with perisplenitis.
Almost all that is known about it comes from the dead-house.

PATHOLOGICAL ANATOMY.--The simplest post-mortem signs of bygone
perisplenitis are the unusually dense fibrous adhesions between the
spleen and surrounding parts. These may vary within wide limits.
Exceptionally, the spleen will be found intimately adherent to
surrounding parts throughout, and can only be separated from them by
tearing it away. Under these circumstances, mostly in chronic malarial
subjects, the capsule will be uniformly much thickened and sac-like.
The splenic tissue may be reduced to a tarry, semi-fluid pulp that
oozes through the lacerated walls. Sometimes the capsule of the spleen
will show localized thickenings of dense cartilage-like consistency,
usually on the convex surface. According to Wilks and Moxon (p. 487),
"section shows them to be laminated parallel to the surface, and the
microscope reveals a fibrinous structure, the fibres being arranged in
dense areolated lamellæ." The same authors consider these to be among
the most decisive evidences of chronic alcoholism. They may become
calcified (Orth). It is not unlikely that they may often be the effects
of syphilis. They undoubtedly often occur in syphilitic subjects. The
interest attaching to them is entirely a pathological one, as the
affection is never detected during life, and as they probably exert no
influence whatever upon the duration of life or even upon the
well-being of their bearer.


{966} Lardaceous Spleen.

The spleen is more liable to lardaceous or amyloid disease than any
other organ of the body. And, although in the further course of the
degeneration other organs and tissues inevitably become implicated
(unless the patient die of some intercurrent affection), the spleen may
in the earlier stages be alone involved. In 58 cases of lardaceous
disease compiled from the records of the London Hospital, the spleen
was the only organ in which the degeneration was detected in 28 cases,
while it remained unaffected in only 10 cases.[10]

[Footnote 10: Turner, _Transactions Patholog. Soc. Lond._, vol. xxx.]

The tendency of lardaceous disease toward generalization shows that it
is under systemic and not local influence, though whether this
influence is exerted in depositing preformed albuminoid material in the
affected parts (infiltration), or in bringing about a special
alteration in situ (degeneration), is even yet not definitely decided.
Upon the one hand, the infiltration theory is upheld by Rindfleisch,
Billroth, and others, while Fehr, Kyber, Cohnheim, and others consider
it to be a result of tissue-metamorphosis. Cohnheim concludes that the
infiltration theory could only be accepted upon the presumption that
the lardaceous material is not a soluble but a corpuscular substance,
or that it is only deposited in consequence of some acquired
predisposition of the part. He regards the process as a local
degeneration due to general causes in which the lardaceous material is
derived from the pre-existing albumen of the tissues. According to
Virchow and Kyber, there is brought to the tissue whose nutrition is
somehow lowered a substance, between which and a malarial substance
formed in loco an intimate combination occurs, the result being
lardaceous material (Ziegler).

This form of degeneration involves the spleen in one or both of two
ways. It may appear as scattered points throughout the splenic
substance, corresponding to the Malpighian bodies and presenting a
resemblance to grains of boiled sago, or in a diffused manner,
constituting true lardaceous spleen, in which the entire organ appears
to be involved.

ETIOLOGY.--As in lardaceous disease of other parts, by far the most
common causes of its development in the spleen are prolonged
suppuration, especially of bone, the suppurative processes of phthisis
pulmonalis and of scrofulosis. The next most frequent causative
influence is syphilis, whether accompanied by prolonged suppuration or
by the cachexia so often observed in this disorder. Chronic malarial
poisoning, chronic diarrhoea, chronic alcoholism, and occasionally the
less-rapidly fatal malignant new growths, may induce the degeneration.
Exceptionally, it has been observed where no other general disturbance
of nutrition had existed. The various causes of lardaceous degeneration
have in common one feature, chronicity, though Mosler quotes from
Cohnheim instances where lardaceous spleen was discovered in one case
five months after joint injuries had been received, and in another four
months after a compound fracture of the right leg.

SYMPTOMATOLOGY.--Lardaceous disease of the spleen is usually associated
with similar disease of other organs--the liver, kidneys, stomach,
intestines, heart, etc.--and its symptoms are so frequently accompanied
by those of the affection that has given origin to it that it must
always be difficult to distinguish them as attributable to the
condition of the spleen itself. Profound anæmia with an appearance of
cachexia is always present in advanced cases. Milder cases may reveal
themselves by no signs. The symptoms arising from other parts
implicated in the degeneration may completely mask those depending upon
the spleen. When the stomach is involved, vomiting and hæmatemesis even
to a fatal termination may occur, or uncontrollable diarrhoea from
intestinal changes may supervene. Splenic enlargement is not {967}
unusually accompanied by enlargement of the liver. Ascites, however, is
always a rare accompaniment.

Rarely, the spleen attains enormous size, and may then occasion
sensations of weight and tension, and occasionally acute pain from
implication of the capsule in inflammatory action. When the organ can
be felt through the abdominal walls it will generally be hardened,
painless, and with its boundaries much thicker and rounder than normal.

PATHOLOGICAL ANATOMY.--As has been already remarked, lardaceous disease
of the spleen is observed in two forms. In both the spleen is enlarged
and hardened. Its structure presents a tough, waxy consistence, and the
organ has entirely lost its friability. In sago spleen, light-brown or
grayish waxy bodies are scattered throughout the splenic structure. The
pulp may remain quite healthy, or it may also be involved. These
sago-like bodies correspond to the enlarged and lardaceous Malpighian
corpuscles, and stand out with some prominence from the general
surface. They may vary in size from that of a pinhead to that of a
small pea. The color of the spleen may shade from a pale fawn color to
a reddish-brown. In many cases where the parenchyma is involved there
will be exhibited scattered areas of semi-transparent, wax-like
material.

In the diffusely lardaceous spleen the organ is enlarged throughout,
pitting to pressure, and upon section presenting a waxy,
semi-translucent appearance, usually of a reddish-gray, but sometimes
of a deep-red, color. Instead of a pulpy, easily broken-down condition
of the splenic parenchyma, there will be found a dense tissue that can
be cut into tough, glistening slices. Minor degrees of the change
cannot be readily detected by the unaided eye, and even in advanced
cases the judgment will often be at fault. Under these, and in fact
under all circumstances a correct conclusion as to the nature of a
given change can only be reached after the employment of reagents that
exert peculiar influences over the lardaceous material. The action of
iodine upon this material is quite characteristic. If a watery solution
of iodine with iodide of potassium be applied to the cut surface of the
suspected organ, the normal portions will be stained a yellowish color,
while those parts that have undergone lardaceous degeneration will
assume a rich mahogany red or brown, which will become violet or purple
upon addition of sulphuric acid. This latter reaction is not constant,
and may usually be omitted. Cornil has recently proposed as a test a
solution of methyl-aniline-violet, which possesses the property of
staining lardaceous matter red, while ordinary tissues will be stained
a deep, bright blue. This reaction possesses the advantage of being
permanent and very delicate, and on that account preferable for
microscopic examination of specimens. According to Cohnheim, this
reagent enables one to distinguish commencing lardaceous change.

In lardaceous disease of the Malpighian corpuscles the alteration will
be found to begin in the arterial twig to which the corpuscle is
attached, soon extending to the entire tissue of the corpuscle, which
it causes to enlarge considerably. When the splenic pulp is attacked it
is said to be the vessels of the pulp that are first involved. It is
held by most pathologists (Virchow, Kyber, etc.) that the change is
chiefly seated in the muscular coat of the small arteries, but that the
intima is also very frequently affected, and that occasionally all the
coats are involved. Thence the degeneration spreads to the cells and
nuclei of the splenic tissue. Later investigations, however, seem to
make it probable that the lardaceous degeneration is mostly limited to
the connective-tissue trabeculæ and walls of the venous sinuses; that
the pulp-cells are for the most part not implicated, but that they
disappear in consequence of the pressure of the ever-increasing
lardaceous material and the consequent anæmia (Cohnheim, Ziegler).

DIAGNOSIS.--This will depend more upon the history and concomitant
{968} symptoms and general condition of the patient than upon any
positive evidence to be gained by special reference to the spleen. In a
patient predisposed to lardaceous degeneration by any of the influences
enumerated above the presumption in favor of splenic lardaceous disease
is strong if, in addition to splenic enlargement, there is evidence of
hypertrophy of the liver and albuminuria, indications of the
participation of other organs in the process, and an anæmic and
cachectic appearance of the individual always observed in advanced
degrees of the degeneration.

PROGNOSIS.--The prognosis is almost always unfavorable, not so much on
account of the splenic condition as from the general depreciation of
the powers of life. The disorder being progressive, the tendency is
toward death by complications resulting from degenerations of other
organs. And yet it seems quite probable that mild grades of lardaceous
degeneration may be entirely recovered from occasionally; but this will
be almost invariably in cases where the spleen alone is implicated. At
all events, when not advanced it may be long held in abeyance. The
duration of the disease generally is indefinite and may cover a space
of years.

TREATMENT.--The treatment of lardaceous degeneration of the spleen will
consist rather in combating its exciting causes than in efforts
directed toward the condition of the spleen itself. It may, however, be
possible to effect some good by resorting to remedies supposed to be
useful in subduing ordinary splenic enlargement.


Echinococcus of the Spleen.

Echinococci invade the human body in the United States far less
frequently than in many other countries, where the canine race occupies
much closer relations with man (as in Iceland). The echinococci are the
larval forms of Tænia echinococcus, a tape-worm of minute size
inhabiting the intestinal tract of the genus Canis, more especially
that of the dog. The ova of the tæniæ are voided in countless numbers
in the feces of their hosts. Still unhatched or in an embryonic form,
they are thence conveyed through the medium of water or otherwise to
the stomach of man, whence the embryos (scolices) escape into the
tissues and develop into ordinary hydatid cysts. Rare as is this
affection in the human body, it is relatively extremely uncommon as
implicating the spleen, and recorded instances of its occurrence are
not numerous. Hydatids of the spleen may coexist with those of other
parts, and in occasional instances are said to be secondary to these.
They are commonly encountered about the middle period of life, and
appear to affect the sexes in equal proportions.

In cases of multiple hydatid cysts in different parts of the body it
has been asserted, upon the one hand, that a single older cyst serves
as the parent cyst, germs from which become transplanted in other
localities through the blood. This view receives some support from the
fact that one cyst, usually seated in the liver, is commonly much
larger than the others. An objection to its universal acceptance,
however, as pointed out by Budd, is that it is very difficult to
imagine that a germ from a larger cyst can travel through the portal
vein, against the current, toward the spleen, mesentery, etc., to form
a secondary cyst. On the other hand, it seems likely that an individual
exposed to infection by the echinococcus would be liable to ingest many
scolices at one time or on repeated occasions, and that the differences
in development depend upon varying degrees of assimilative power on the
part of the parasite and of the conditions of its environment.

SYMPTOMATOLOGY.--Whether echinococcus of the spleen will betray
symptoms of its presence depends upon varied circumstances. Small
cysts, {969} certainly, may occasion no signs, subjective or objective.
Cysts may even attain very large dimensions without exciting discomfort
to their bearer, and may consequently escape detection. Pain may
precede the appearance of a tumor, but will be irregular and
paroxysmal, increasing in severity with the growth of the cyst. The
most constant annoyance, however, is that occasioned by the size and
weight of the enlargement. The patient may detect its presence
accidentally, or his attention may first be directed to it by his
medical attendant. He may give a history of its growth during a number
of years without its having occasioned more than passing uneasiness.

The tumor may exceptionally attain a large size, nearly filling the
left side of the abdominal cavity. It may encroach upon the area of the
thoracic cavity. Upon examination, the tumor, when of sufficient size,
will be rounded, not resembling the appearance of a simply enlarged
spleen. Fluctuation will be detected, and occasionally the peculiar
hydatid thrill, upon the diagnostic importance of which great stress
has been placed. This, however, is a very inconstant sign, and in the
majority of cases is not to be discovered. Frerichs only found it where
the sac was not tense and contained other vesicles. A peritoneal
friction sound may sometimes be detected by the ear placed over the
region of the tumor. These cysts differ from other fluctuating tumors
in being of very slow growth, remaining almost without change for
years, and in exciting no constitutional reaction, unless, as is quite
possible, inflammation of the sac is developed, when rigors, hectic,
and other symptoms indicative of suppurative inflammation will be
observed. Pressure of the tumor upon the stomach may excite anorexia,
vomiting, epigastric uneasiness, and gastric catarrh. If the pressure
is exerted upon the portal vein or vena cava, dropsy may result; if
upon the bowel, constipation may be produced.

It is possible for the development of the cyst to be arrested through
the death of the echinococcus. This may occur if it is of small size.
Its walls may then become calcareous, and the mass will cease to exert
any injurious influence upon the host. In other cases, as a result of
inflammation, rupture will take place, and the contents of the cyst,
with the characteristic formations, will escape into the peritoneal,
pericardial, or pleural cavities, or into the alimentary tract, the
urinary passages, or even into the vena cava; or they may be discharged
through the body-wall. In any of these events a fatal termination is
almost inevitable. Rupture may also occur in an unaltered cyst from any
sudden or excessive violence. Death will usually speedily ensue from
collapse or as a result of inflammation of the peritoneum. Finally,
complete recovery will sometimes be secured through treatment.

DIAGNOSIS.--Echinococcus of the spleen presents no characteristic
symptoms. When the tumor is small and escapes observation, or when the
fluid nature of its contents cannot be recognized, its existence cannot
be determined. In larger tumors the hydatid thrill will, when present,
assist the observer, and the presence of fluctuation will of course
serve to exclude all solid enlargements of the spleen from
consideration. Abscess will differ in its shorter course, its rapid
increase in size, and its inflammatory symptoms, the general condition
contrasting with the excellent condition of health usually observed in
simple hydatid tumor. The diagnosis will become greatly obscured in the
event of inflammation of the cyst. Certainty can only be attained
through an exploratory puncture and examination of the contents of the
cysts. These will consist of a clear, non-albuminous fluid, rich in
sodium chloride, and revealing the echinococcus scolices and hooks and
membranous shreds when examined under the microscope. Doubt may arise
where inflammatory changes have made the fluid albuminous and where the
scolices and hooklets have been destroyed or do not accompany the
escaped fluid.

{970} MORBID ANATOMY.--The spleen may be almost destroyed by the
hydatid cysts, which, usually single, may exist in large numbers.
According to Wardell,[11] "they are seldom found in the pulp, usually
in the gastro-splenic epiploon or in the cysts constituted of the
serous investment." The cysts consist of a thick fibrous investment and
an inner parenchymatous layer, from which the little heads develop in
tiny vesicles. Compound systems, one enclosed within the other, are
thus formed, varying from the size of a pea to that of a marble, and
even very much larger. The cysts may undergo atheromatous or calcareous
degeneration. In these cases the echinococci are destroyed, and the
mass becomes encapsulated in a calcareous envelope and remains
quiescent. The microscope will reveal the remains of the echinococci,
even after long periods. Where rupture has taken place the rent in the
cyst will have allowed characteristic matters to escape into the
communicating parts, where they may be detected.

[Footnote 11: _Reynolds's System of Medicine_, vol. v.]

The PROGNOSIS of echinococcus of the spleen is always serious, usually
most unfavorable. The best results are observed in those cases where,
the cyst being small, spontaneous arrest of development has occurred.
Puncture of the cyst and partial evacuation of its contents, when
practicable, increase what would otherwise be almost hopeless chances
of ultimate recovery in cysts of moderate and large size.

TREATMENT.--The only treatment that promises good results is the
evacuation of the cyst fluid. Murchison recommends the removal of the
fluid with a very small trocar, whereby the admission of air into the
cavity is avoided. The withdrawal of the fluid is sufficient to destroy
the life of the parasite, and in favorable cases to secure the
degenerative changes of which mention has been made. The adoption of
antiseptic precautions will undoubtedly increase the chances of
recovery. Unfortunately, a certain number of cases will run into
suppuration, when all the dangers of suppurating cavities have to be
encountered, and must be treated in the usual way. Various injections
into the cyst-cavity have been recommended, but they do not seem to
afford better results than simple evacuation. These will probably most
successfully be employed in cases where the cyst has formed
inflammatory adhesions to the skin, which may be effected through the
external application of caustic agents capable of exciting inflammatory
changes in the deeper parts (Vienna paste, etc.). Injections may be
then made through incisions carried into the cyst, without danger of
exposing the peritoneal cavity. Internal medication, except for general
purposes, has no efficacy in the treatment of these tumors.


Syphilis of the Spleen.

The spleen is not very frequently affected by syphilis. Nevertheless,
this viscus may become the seat of syphilitic disorder during either
its early or late phases. It has even been asserted by Weil that the
spleen may become enlarged in the interval between the appearance of
the primary sore and the first cutaneous eruption. Whatever changes the
spleen may undergo during the course of early syphilis are essentially
of the simple congestive type, and are comparable to the acute splenic
enlargements of the ordinary specific fevers; certainly, no essentially
syphilitic changes can be detected at this stage. In fact, throughout
the whole secondary period the splenic derangement is of the nature of
simple hyperplasia. In the later stages of syphilis there is a more
permanent enlargement of the spleen, due to a chronic interstitial
inflammation that should be distinguished from that very much more
common result of old syphilis, lardaceous degeneration. The
histological characteristics of these enlargements are not known to
differ essentially from the simple chronic enlargements of the spleen
already considered.

{971} It is only toward the end of the secondary period, and during
tertiary syphilis and in inherited syphilis, that products essentially
syphilitic can be recognized. Gummy infiltrations and tumors of the
spleen have been observed by a few writers--not, however, clinically,
but for the most part in the dead-house. These tumors are found
scattered throughout the substance of the organ, but most commonly near
its surface. They vary in number within not very wide limits, and in
size from that of a pinhead to that of a pea or larger. They may be
sharply circumscribed (but not encapsulated) or more diffused. The
portions of the spleen affected become changed by the syphilitic
material into grayish-red, homogeneous masses in recent cases. At a
later stage they are "gray or grayish-yellow, homogeneous, somewhat
dry, tough, almost cheesy."[12] The spleen under these circumstances
is, as a whole, somewhat enlarged.[13] Gummy tumors of the spleen may
be confounded with tubercle and old hemorrhagic infarction.

[Footnote 12: Wagner, Mosler, _Ziemssen's Cyclop._, vol. viii. p. 485,
Am. ed.]

[Footnote 13: Gold, _Viertelj. f. Derm. und Syph._, 1880, p. 463.]

There is a form of circumscribed enlargement from new growth that is
sometimes observed in the spleens of syphilitics, and which is probably
of syphilitic origin, producing changes similar to certain forms
already described as a variety of perisplenitis. It is situated at the
surface of the spleen, and consists of hard whitish or pale-yellow
plates but slightly elevated above the normal level, but of
considerable superficial extent. When incised, these plates remind one
of cartilage.

Splenic enlargements are common in the subjects of inherited syphilis.
According to Cornil, infants syphilitic by inheritance have very
frequently enlarged spleens, the capsule being inflamed and thickened
and the splenic tissue abnormally hard. The organ may thus become
sufficiently enlarged to be detected by palpation. Sée considers that
enlargement of the spleen is present in one-fourth of all cases of
inherited syphilis, and Haslund reports splenic enlargement in 58 of
154 necropsies of such infants.

The clinical signs of syphilitic spleen are almost beyond recognition,
if indeed they can be said to exist. Circumstances of growth, etc. may
excite the suspicion that a given splenic tumor may be syphilitic.
Jullien, it is true, describes symptoms of splenic syphilis, but his
views do not seem to be well founded.

TREATMENT.--In recent enlargements therapeutics may effect much in
reducing the tumor, and the facility with which its reduction is
effected will afford a valuable indication of the success of treatment.
Gummy tumors are probably within the reach of antisyphilitic treatment,
and it is not unlikely that some of the shrunken, indurated areas often
detected post-mortem, and usually ascribed to infarctions, are in
reality due to the cicatricial remnants of old gummata. Chronic diffuse
splenic enlargements of syphilitic origin are but little influenced by
treatment.


Rupture of the Spleen.

The peculiar texture of the spleen renders it especially liable to
rupture--more so than any of the other abdominal viscera. By far the
most common cause of splenic rupture is external violence from blows,
kicks, falls, squeezing force, and wounds incised or punctured. It may
be the direct result of the injury, or the rent may be made by the
penetration of broken ribs or of foreign bodies. The rupture may even
occur spontaneously from causes located within the organ itself. It has
been previously observed that in the enlargement accompanying the acute
infectious fevers, malarial fever, etc., while the distension of the
capsule renders the spleen tense and elastic, {972} section through its
substance will often reveal a semi-diffluent condition, the exact
nature of which is not well understood, but which undoubtedly
originates in excessive vascularity. This occurs especially in malarial
fever and typhus. Rupture may here take place spontaneously, or, as is
commonly the case, a very slight degree of violence is sufficient to
produce it: a wrench, the effort to preserve a disturbed equilibrium,
an otherwise insignificant blow, may determine the lesion. Pregnancy
and the puerperal state may be the predisposing causes to the accident,
and vomiting has been known to produce it. It has also been known to
follow the softening and breaking down of a hemorrhagic infarction or
the rupture of varices and aneurism. The normal spleen is only with the
greatest rarity subjected to a degree of violence sufficient to rupture
it, while in countries where enlargement of the spleen is of common
occurrence, as from malaria, the accident occurs more frequently.

SYMPTOMATOLOGY AND COURSE.--When the rupture is of traumatic origin
there may be no marks of external violence: the symptoms usually are
those that follow sudden and great losses of blood, faintness, pallor
following intense pain in the splenic region, frequency and weakness of
pulse, sighing, coldness of the extremities, and the rapidly developing
signs of profound prostration. A fatal termination usually quickly
follows the rupture. Where the hemorrhage is not immediately great the
patient may not succumb at once, but may live for hours, even
days--nay, may even recover, as has occurred in the experience of some
observers. Wilks and Moxon saw a case of splenic laceration where five
ounces of laminated clot in process of absorption were found lying upon
the spleen, death having occurred eighteen days after the accident in
consequence of abscess of the brain. In cases where rupture has taken
place, perhaps from very slight violence, in a spleen enlarged and
softened from disease, the above-mentioned symptoms may have been
preceded by pain and a sense of weariness in the splenic region, and by
distinguishable enlargement of the organ.

PATHOLOGICAL ANATOMY.--Except in injuries caused by the penetration of
foreign bodies or fractured ribs the rupture will usually be linear,
and either straight, curved, angular, or stellate. If the rupture have
occurred spontaneously it will probably be single, but in the event of
its following violence it will most often have resulted at several
places. In cases of traumatic splenic rupture in persons suffering from
chronic malarial poisoning, Konaraloff[14] invariably found the rents
in the lower portion of the organ, the greater ones on the outer
surface, the smaller ones mostly on the inner surface near the hilum.
They were widely gaping and deep. In ruptures consequent upon disease
alone or slight violence to a diseased organ the spleen will usually be
found enlarged, sometimes to three or four times its normal volume,
with its substance softened and of a cherry-red color. In such cases
signs of bruising or injury to the integument will not usually be
discoverable. Splenic hemorrhage has been known to occur from the
rupture of varices and aneurism, in which case characteristic
appearances have been found after death. After death from rupture of
the spleen the abdominal cavity will be more or less filled with blood,
dark and coagulated. Though the contrary has been held, it is doubtful
if multiple rupture of the spleen can be regarded as certainly
indicative of a traumatic origin.

[Footnote 14: _Lond. Med. Rec._, No. 97, 1883, p. 259.]


Tubercle of the Spleen.

Tubercle not unfrequently attacks the spleen, but only as secondary to
general tuberculosis. Wilks and Moxon indeed think the larger nodules
of tubercle may be primary, but there seems to be no evidence in
support {973} of this opinion. As a symptom of general tuberculosis,
splenic enlargement from congestion, simply and quite without any
specific deposit, is observed as a form of acute splenic tumor. It is
at the later stages of general tuberculosis that distinct deposits of
tubercle are formed in the spleen, and these are consequently almost
always crude. They are generally scattered throughout the pulp, and,
according to Billroth, they but rarely affect the Malpighian
corpuscles. They are of very small size, and may be present in great
numbers; their color is grayish and they are translucent, and only the
largest show the yellow tinge of commencing fatty degeneration.
According to Orth, they are not always easily distinguishable from the
Malpighian bodies. Occasionally, and especially in scrofulous children,
larger nodules are formed by the confluence of several tubercles that
may equal a pea in size and present numerous yellow points of
caseation.

It is usually impossible to diagnosticate the existence of splenic
tubercle during life. After death the general splenic tissue will be
darkened from hyperæmia and the tubercles surrounded by a vascular
halo. When incised the tubercles will stand out from the tissue in
which they are imbedded, unlike the Malpighian bodies, and when exposed
to a stream of water the latter will disappear, while the tubercles
will remain unaffected.


Tumors of the Spleen.

The spleen is very rarely invaded by new growths other than those
already mentioned, and then almost exclusively either from direct
extension from other parts or by metastasis. In pseudo-leukæmia or
Hodgkin's disease the spleen is usually enlarged by a hyperplastic
process quite like that of leukæmia. In that variety of this disease
that has been called lympho-sarcoma, in which the spleen is invaded
subsequently to the implication of the lymphatic glands, especially
those of the cervical region, the Malpighian follicles may become
enlarged, and even attain the size of walnuts. They contain
spindle-cells and connective tissue. The trabeculæ likewise participate
in the enlargement. Apart from the hyperplastic follicles thus
occurring and also seen in leukæmia, small-pox, scarlatina, etc.,
lymphoma has been observed by Virchow, Weichselbaum, and others. The
tumors consist of bright grayish-red or reddish, not sharply defined,
nodules projecting from the dark-red mass of the spleen. Primary
sarcoma is said to have been observed in the spleen, but malignant
tumors of this organ are usually secondary growths, and even thus
occurring are exceedingly rare. They are soft and very rapidly-growing
sarcomata and carcinomata. As a rule, they depend upon malignant
disease of the liver or abdominal glands through metastasis or by
extension of growth. They sometimes grow with almost incredible
rapidity. The symptoms are very obscure, and the presence of the
malignant infiltration cannot be detected unless hard nodulated masses
are formed, which become perceptible through the abdominal wall, as in
hepatic cancer. The prognosis is always bad, and depends generally upon
the existence of splenic cancer only in so far as this indicates the
dissemination of the primary affection and becomes the forerunner of
the cancerous cachexia. Fibroma and angioma have also been encountered
in the spleen: they are both exceedingly rare. The latter has been
known as a pulsating tumor (Langhans).




{974}

DISEASES OF THE THYROID GLAND.

BY D. HAYES AGNEW, M.D., LL.D.


The thyroid body occupies a very important position in the neck, being
closely related to the larynx, the trachea, the carotid blood-vessels,
the pneumogastric, sympathetic, and recurrent laryngeal nerves. These
relations render quite intelligible the phenomena which are so
frequently present when the gland becomes the subject of disease. It is
richly supplied with blood-vessels from the external carotids and the
subclavian arteries.

Notwithstanding the obscurity which enshrouds the physiological
function of the gland, there are good reasons for supposing that its
office in the animal economy is not an unimportant one: indeed, its
presence, not in the vertebrata alone, but also in birds, reptiles, and
fishes, tends to strengthen this conclusion. The experiments of Zesas
appear to show that the thyroid body plays an important rôle in
regulating the supply of blood to the brain, and also of supplementing
the work of the spleen. The place, therefore, of the gland in the body
as an appendage to the vascular system appears to be well chosen.

Congenital absence of the thyroid body is uncommon, though it has been
noted by a few writers. Curtin[1] met with one case in which the gland
was replaced by a mass of fat. Possibly in this instance the fat was
the result of a morbid change in the thyroid, and not an evidence of
the latter having never been present. Beach[2] furnishes another case
where on dissection no trace of the gland could be found. Hyrtl speaks
of the isthmus being frequently absent--a fact observed by other
anatomists.

[Footnote 1: _Lancet_, 1850, vol. ii. p. 25.]

[Footnote 2: _Medical Times and Gazette_, May 30, 1884, p. 603.]


Goitre.

Various names have been employed by different writers to designate
enlargements of the thyroid body. Among these may be named bronchocele,
tracheocele, thyrophraxia, Derbyshire neck, struma, and goitre. Among
English-speaking people the disease is generally spoken of as goitre or
Derbyshire neck.

Hypertrophy of the gland may be either general or partial; when
general--that is to say, involving the entire body--the term
symmetrical or bilateral is employed to designate the enlargement; when
confined to a single lobe, it is said to be asymmetrical or unilateral.
Not unfrequently limited portions or small areas of one lobe only are
affected, causing irregularities or nodosities which may be readily
detected by the eye or the touch.

SYMPTOMS.--The earliest evidence of bilateral goitre is the appearance
of an unusual fulness and breadth of the lower part of the neck or that
part between the sternum and the larynx. This fulness extends laterally
under the sterno-cleido-mastoid muscles, partially effacing the
suprasternal fossa, {975} and is entirely unattended by pain, heat,
redness, or other sign of inflammation. When the disease is unilateral,
the swelling is seen to extend from the side of the trachea and larynx
outward under the sterno-cleido muscle. The tumor, in consequence of
its attachment to the trachea, follows the movements of the latter, and
hence will be seen to rise and fall during the act of swallowing or of
deglutition.

The progress of the enlargement varies greatly in different cases.
After its first appearance it may remain quiescent for years, scarcely
causing any change in the appearance of the neck which could be deemed
a deformity; in other instances the growth will be progressive,
attaining to the size of a goose egg, when it may again remain
stationary. It is not common in the United States to meet with those
excessive hypertrophies of the thyroid so common in Switzerland, where
the gland extends up behind the ears, outward to the margins of the
trapezii muscles, and hangs down in front of the sternum a large
pendulous mass and imparting a most hideous appearance to the patient.

Pressure Symptoms and the Attendant Phenomena.--It is very remarkable
to what a degree hypertrophy of the thyroid may reach without giving
rise to any marked functional disturbances. This is due, no doubt, to
the character of the enlargement, the cystic and vascular causing less
inconvenience than the fibrous or more solid varieties. The pressure
symptoms which may ensue are--first, difficulty of respiration. This is
likely to follow when the central portion of the gland enlarges in
common with the lateral masses, thereby causing pressure directly upon
the trachea. This pressure may result in softening, and even complete
absorption, of one or more of the rings of the trachea. An irritative
cough may appear in the course of the hypertrophy, which is to be
referred to the encroachment by the gland on the pneumogastric nerve.
Hoarseness and a peculiar croaking voice are also sometimes witnessed,
indicating the contact of the tumor with one or both recurrent
laryngeal nerves.

Redness of the skin and elevation of temperature on one side of the
neck are occasionally present, and sometimes accompanied by dilatation
of the pupil of the eye corresponding to the affected side. These
symptoms result from pressure upon the sympathetic nerve, and may exist
in either unilateral or bilateral goitre. When associated with the
latter form of the disease, the sides of the tumor will be found
asymmetrical.

GEOGRAPHICAL DISTRIBUTION.--Goitre is met with in all parts of the
world. There are, however, localities in which it prevails to a
remarkable extent, assuming, indeed, the importance of an epidemic
disease. In some portions of Switzerland, as in Savoy and in the Tyrol,
there are villages in which scarcely a single inhabitant escapes. The
disease is very common in Piedmont and in all deep valleys of the Alps,
the Pyrenees, the Apennines, and about the foot-hills of the
Cordilleras. In the valley of the Maurienne, Larrey states, nearly all
the residents were subjects of goitre. According to the government
reports in Piedmont and Savoy, there are 22,371 persons afflicted with
bronchocele. There is a notable prevalence of the disease at
Schlettstadt on the Rhine. In France the districts where the largest
number of cases of goitre is observed are St. Aubin and Rosieux. These
places, with others less noteworthy in the same country, it is
estimated, furnish not less than 500,000 cases of the disease. In the
government of Irkoutsh, which is drained by the sources of the Lena and
its tributaries, there were in 1870, according to Hachine, as many as
3400 persons laboring under goitre. Among the inhabitants of Siberia
antecedent to the conquest by Russia the disease was scarcely known.
Its prevalence after this event was attributed to the habit adopted by
the Russians of living in heated and uncleanly rooms, altogether unlike
the Siberians, who spend most of their time in the open air. {976}
Humboldt speaks of goitre being so common in Honda and Moussa, towns
contiguous to the Magdalena River, that very few of their inhabitants
escaped the disease.

In England the counties of Derbyshire, Surrey, Nottingham, and Norfolk
furnish a large number of cases. In this country New Hampshire,
Connecticut, Vermont, and New York are the States which supply the most
examples of goitre. In Lower Canada goitre is also quite common.

In Switzerland the disease is frequently associated with mental
imbecility (cretinism), though it is not at all established that
between the two there exists any necessary connection, as cretinism is
often met with in persons free from goitre, and the latter in those
whose intellectual powers are unimpaired. Indeed, it has been observed
by Burns, that in some countries where goitre is very prevalent
cretinism is exceptionally rare; nevertheless, the observations of
Lemon and the experiments of Horsley are of a character to leave the
relation between the two still an open question.

CAUSES.--The causes of goitre are quite obscure. The disease is in some
way associated with countries the topographical features of which
consist in high mountains and deep valleys. In illustration of this
fact we have only to cite the great prevalence of the disease in
Switzerland, in the central mountainous parts of Asia, on the Himalayas
and the Andes, as also in the mountains of Brazil. In Europe it may be
said that goitre is much more common in the south and south-west
countries than in the north and north-west. Sea-coasts are generally
exempt from the disease. Bardeleben during the many years in which he
acted as chief of the surgical clinic at Greifswald saw only two cases
of goitre.

The use of glacier- or snow-water has been charged with the production
of this evil, containing as it does large quantities of carbonic acid
and other matters not generally found in pure potable water. In
opposition to this view we are able to present the testimony of Captain
Gerard that in those portions of the Himalayas where the inhabitants
for a number of months in each year drink snow-water goitre is really
less frequently observed than among those who live at the foot-hills of
the same region. This coincides with what Lebert states, that if water
from the regions of ice and snow constitutes a cause of goitre, then we
should expect to find the disease increasing more and more as the
glaciers are approached, when, really, just the reverse is the case,
the subjects of such enlargements being seen in greater numbers at the
bottom of valleys than in the more elevated regions. The Polar
expeditions of Lenstake and Kolleweg, undertaken in the years 1868 and
1870, also contradict the supposed connection between goitre and
ice-water, as not a case of the disease was reported, notwithstanding
the men drank nothing else; and in Sumatra, where snow is never seen,
goitre is quite common. Nor is there any satisfactory evidence that
lime- or magnesia-water, also charged with exerting a determining
influence in the causation of goitre, has anything to do with its
existence. The testimony of Humboldt as to the rareness of the
affection at Mariquita, where the water is strongly impregnated with
lime salts, and my own observation that throughout the Pequea and
Conestoga valleys, both limestone districts, goitre seldom occurs, are
inimical to such a theory. From St. Maurice to Martiny in Wallis,
Lebert speaks of goitre being very common, notwithstanding the absence
of lime formation.

That water, however, does become the medium for certain materials
which, taken into the system, produce enlargements of the thyroid, is
unquestionably true. In corroboration of this statement we have two
notable facts recorded by Frank, who says that at Rheims, where goitre
was very common, quite one-half of the tumors disappeared after the
source of the old water-supply was abandoned and the town supplied by a
branch from the river Verle. {977} And again at Stenseifen, near
Schmideberg, where goitre prevailed as an endemic, the disease
disappeared on the closing of a fountain which furnished water to the
inhabitants of the place.

Atmospheric causes have also been invoked in order to shed light on the
production of goitre. Thus it is said that the common occurrence of the
latter in very deep valleys, so overshadowed by the dense foliage of
timber as to prevent a proper interchange or circulation of air, is
favorable to this theory; yet as against this view we have the
statement of Humboldt, who says that on the plateaus of Bogota, which
are swept by constant currents of air and are quite sterile in
vegetation, goitre is common.

That local or geological conditions do exist which are directly
concerned in the development of endemic goitre cannot be gainsaid, and
these of so active a nature that persons coming from remote districts
into such goitrous centres and entirely free from all enlargements of
the gland, are liable to suffer in common with the native born. Not
only so, but, as has been observed by Virchow, even domestic animals in
such localities become subjects of the disease.

The very careful study of this subject by Labour of Newcastle, England,
furnishes strong evidence that water passing through calcareous soils
alone had little if anything to do with goitre, but when such soils
were impregnated with ferruginous and earthy salts the geological
conditions were present for developing the disease.

Enlargement of the thyroid body is occasionally seen as one of the late
manifestations of syphilis, usually bilateral and attaining in some
instances a great size.

Gestation is another and not an uncommon cause of goitre, the tumor
appearing in the last months of pregnancy or immediately after
parturition. Three cases clearly traceable to the above cause are under
the writer's care while penning this article. It is in such cases that
the tumors sometimes grow with frightful rapidity. Roberts reports
three cases in primiparæ, all of which ran an acute course and
terminated fatally by asphyxia.

In Graves' or Basedow's disease goitre forms one of the elements in the
morbid circle, and when thus associated may be regarded as a neurosis.

VARIETIES.--Goitre appears under different forms, and not unfrequently
one variety is transformed into another. The following classification,
resting on a pathological basis, will be adopted, namely--Follicular;
Gelatinous; Cystic; Fibrous; Vascular.

In follicular goitre there is a proliferation, both in the
cell-elements of the follicles and in the connective tissue
constituting their walls. This general hyperplasia of the normal
histological components of the gland constitutes a tumor which, for a
time at least, remains quite soft and compressible, even communicating
to the touch the sensation of fluctuation. The tendency, however, of
the growth is not to remain long in this condition, but to become more
firm and even hard to the feel.

The fibrous is often a transformation from the follicular goitre, an
advanced stage in the life-history of the latter. There occurs a new
formation of interstitial connective tissue, which by its accumulation
and encroachment upon the follicles lessens, and finally obliterates,
them to a degree which converts the gland into a fibroma. It is rare,
however, to find this metamorphosis general. Generally the change is
limited to portions of the thyroid, and accordingly the tumor in this
variety of the disease is found hard, knotty, and incompressible at
different points corresponding to the sclerosed portions. The
vascularity of the fibrous variety is quite insignificant in those
portions of the gland which have been the subject of this morbid
change, though in other parts there is a liberal supply of
blood-vessels.

Vascular goitre may also be a transformation from the follicular
variety, in {978} which, with an increased hyperplasia of the
follicular elements of the gland, there is a new formation of
blood-vessels taking the place of the connective tissue present in the
fibrous form of goitre. When the arterial element predominates, the
vessels will be found to be very much dilated and anastamosing freely.
These goitres are compressible, have a soft, spongy feel, sometimes
pulsate, and on auscultation disclose a distinct bruit, hence the term
aneurismal goitre often applied to such. In other instances the venous
element predominates, when the swelling will, as in the arterial
variety, be compressible and communicate to the ear a well-marked
blowing sound or murmur. As the superficial veins, in common with the
deep ones, are enlarged and tortuous, the surface of the tumor will
often exhibit at different points a bluish appearance. In two
instances, and in females of a highly-wrought nervous temperament, I
have known the vascular goitre to enlarge in a few minutes to wellnigh
twice its usual size, threatening the patient with suffocation for the
time, and almost as quickly subside after a free emesis.

In gelatinoid goitre the follicles of the gland are distended so as to
form large cavities filled with a gelatinoid- or colloid-looking
substance, the product of the enclosed cells. As the distension of the
follicles progresses the vascularity of the gland becomes notably less,
the vessels being obliterated by the pressure. This tumor may attain a
very great size, is much firmer than the vascular goitre, and to the
touch has a doughy feel.

Cystic goitre is rarely such in the beginning of its history, being
often an advanced stage of the follicular variety. In the transition
the compartments of the latter undergo enlargement, their normal
cell-contents being replaced by an albuminoid transudation from the
vessels of the follicles. This process continuing, the interfollicular
connective tissue disappears--a mechanical result caused by pressure.
Still later, and from this cause, the walls of the adjoining follicles
suffer a similar fate, and as these melt away larger cavities are
formed, until at length the whole interior of the gland is converted
into a number of loculi, and in some rare instances into one great sac.
The gelatinoid or colloid goitre may undergo a similar transformation,
and much in the same way. The fluid contents of cystic goitre vary in
their physical properties as also in their chemical constitution.
Generally the substance contained in the cysts is rich in albumen, has
a ropy appearance resembling somewhat the white of an egg, and to the
feel is viscous or unctuous, similar to that of the synovial secretion.
Sometimes it is dark, resembling coffee-grounds--a condition due to the
decomposition of extravasated blood derived from ruptured blood-vessels
belonging to the gland. Crystals of cholesterin are also present,
formed by fatty degeneration of the cells of the follicles, and mingled
with a variable amount of sodium chloride. The cystic goitre is soft
and fluctuating, and often grows to a large size.

       *       *       *       *       *

The blood-vessels of goitre are not exempt from pathological changes,
but frequently become the subjects of atheromatous and amyloid changes.


Carcinoma and Sarcoma of the Thyroid Gland.

Malignant growths of the thyroid body are comparatively rare, and when
present are accompanied by symptoms sufficiently significant to
differentiate them from those which are benign. In both carcinoma and
sarcoma the increase of the tumor is rapid; the surface veins become
very distinct, and the enlargement is general, affecting the entire
gland. In addition to the above phenomena, the evil effect resulting
from pressure is sooner realized and more pronounced than in goitre,
and in a short time the generalization of the disease becomes apparent
in the loss of flesh and strength. Should {979} the tumor be a
carcinoma, there will likely follow the infection of those lymph-glands
in nearest relation to the neoplasm.

EVIL EFFECTS OF GOITRE.--In this country, though goitre may grow to a
large size, it is not common for patients to suffer any inconvenience
other than that which results from the unsightly appearance of the
tumor; hence life is not seriously imperilled by the disease.
Occasionally, however, there are exceptional instances in which
unpleasant and even troublesome symptoms are developed. Among these may
be mentioned alteration of voice or a slight aphonia in consequence of
pressure by the tumor on the recurrent laryngeal nerve. An irritating
cough may also exist, and when no evidence of pulmonary trouble is
present it must be referred to pressure upon the pneumogastric nerve.
Dyspnoea when present results usually from pressure upon the trachea.
It has been observed that when this pressure is long continued,
particularly in cases of vascular goitre, some of the rings of the
trachea gradually disappear, leaving only a membranous tube, which may
collapse and cause the sudden death of the patient.

Hiccough and diaphragmatic spasms have also occurred when the
enlargement of the gland extended laterally, in consequence of pressure
on the phrenic nerve. In addition to the above phenomena there is often
experienced in goitre severe neuralgic pains on the side of the neck,
in the ear, and over the back of the head, and indeed in the course of
any of the branches of the cervical plexus of nerves.

Occasionally I have seen a red blush of the integument on the side of
the neck, answering to the largest portion of tumor, accompanied by
increased heat, doubtless from the growth encroaching on the
sympathetic nerve.

TREATMENT.--The treatment of goitre may be divided into constitutional
and local. Too often the management of the disease is conducted in an
empirical manner, every variety being subjected to the same routine of
remedies. No greater mistake can be made. To attain any satisfactory
success it is absolutely necessary that a correct diagnosis of the
composition of the tumor shall be known. In follicular and in fibrous
goitre much may be anticipated from constitutional and local measures.
Those remedies which possess the property of inducing retrograde
changes of structure and their subsequent absorption are the ones to be
selected for administration, and among these iodine and its
combinations rank highest. The compound solution of iodine, the iodide
of potash, and the iodide of iron, all have their therapeutical
adaptiveness. The earlier treatment is commenced the more hopeful will
be the prognosis. If the patient is in all other respects in good
health, and especially is somewhat fleshy or given to obesity, the
compound solution of iodine should of preference be selected. At first
the dose should be small, in order to test the tolerance of the
stomach, not exceeding five or six drops three times a day, taken in
some sweetened water, orange syrup, or curaçoa, and always about one
hour after meals. Every two or three days the dose may be increased one
or two drops until eighteen or twenty are taken, beyond which it is not
desirable to go. It is in these forms of goitre that the burned sponge
(spongia usta) was at one time very generally used as an internal
remedy, half a drachm to a drachm being taken twice or thrice daily. As
the virtue of the article was due to the iodine it contained, it must
necessarily be inferior to the solution of the same substance.

In addition to the constitutional treatment the local use of alterative
ointments will be indicated, the best of these being iodoform, iodide
of lead, and iodide of mercury. Iodoform will be found most efficient
employed in the following formula:

  Rx. Iodoform,       drachm iss;
      Benzoated lard, ounce j.

This ointment is to be rubbed into the goitre for fifteen or twenty
minutes {980} morning and evening, after which a piece of lint smeared
with the same should be laid over the tumor, covered with oiled silk,
and retained in position by a strip of muslin. If the officinal
iodide-of-lead ointment be used, it will be desirable to lessen its
strength by the addition of a little simple cerate, as it is liable to
cause severe irritation of the skin when thoroughly applied, thus
neutralizing in a great measure the value of the application. Whatever
unguent is selected, the application will be best made before an open
fire.

There are several natural waters which can at the same time with the
other treatment be taken with advantage, their efficiency being due to
the iodine which they contain. The most valuable of these are
Adelheid's Quelle and Wildegger. A glass of either can be drank morning
and evening. If after two or three months' continuous treatment under
the plan described no impression is made on the disease, or in the
event of the iodine acting unpleasantly by causing symptoms of iodism,
the iodide of potash should be substituted, administering three times a
day from five to twenty grains of the salt dissolved in water and
syrup, and well diluted.

Boinet has proposed the mixture of iodine with the food as a very
satisfactory mode of introducing the drug into the system; and I
suppose that it was on the strength of this suggestion that Michaud,
with a view to protect the garrison of Étiennes against the prevailing
goitre, ordered iodine to be baked in the soldiers' bread. In cases of
goitre associated with a pale, anæmic state of the system it will often
be found necessary to alternate, for a time, the remedies already
directed with iodide of iron and cod-liver oil.

In follicular and fibrous goitres which prove rebellious to the plan of
treatment detailed a resort may be had to injections. From eight to
twenty drops of the tincture of iodine should be introduced deep into
the substance of the gland by the hypodermic syringe. This procedure
can be repeated every three or four days, selecting at each operation a
different section of the gland, at the same time carefully watching the
effect produced. Any marked elevation of temperature, local or general,
accompanied by pain or stiffness of the neck, is the signal for
suspending temporarily this form of medication. The favorable signs
following injections are the shrinking and increasing hardness of the
tumor; and so long as these processes continue progressive no
repetition of injections will be necessary.

Electrolysis constitutes another therapeutic resource, applicable not
only to the treatment of follicular and fibrous, but also to the
vascular, goitre. This agent has been favorably employed by Chvostek of
Vienna, and to some extent in this country by Baird and others. The
current used by Chvostek was one from a Siemens battery of thirteen
elements and strong enough to cause a moderate degree of burning. The
time consumed at each sitting is not to exceed five minutes, during
which the points of application must be frequently changed.

In vascular goitre, iodine, either internally or locally, effects
little good. Ergot is to be preferred. From ten to twenty drops of the
fluid extract should be given internally three times a day, with
injections of the same amount and used in the same general manner as
has been directed for the iodine.

Recently I have been using injections of carbolic acid in vascular
goitre, and thus far with the most promising results. Four or five
drops of a solution of the crystals of the acid dissolved in glycerin,
using no more of the latter than will be barely sufficient to liquefy
the crystals, should be deposited by means of the hypodermic syringe
deep into different portions of the gland at intervals of four or five
days. On the withdrawal of the instrument the puncture can be covered
with a strip of rubber adhesive plaster. The acid when thus employed
causes the tumor to shrink and become hard.

{981} Gelatinous and cystic goitres are quite intractable to
constitutional remedies. They require to be attacked locally. Bonnet
has tried caustic potash and chloride of zinc. The applications were
made over the front wall of the tumor, and in some instances to the
inner surface of the sac. The results were not of a kind to make the
method a popular one. Iodine and alcohol have also been thrown into the
parenchyma of the gland, and with a like unsatisfactory effect. Setons
have had numerous trials. The method is an old one, having been used by
Celsus, and revived from time to time by Quadi of Naples, Hutchinson,
Kennedy, and Stanton. The object in using the seton is to develop in
the tumor a destructive inflammation and suppuration. Any one who has
witnessed a case of acute suppuration in the thyroid gland will not be
anxious to repeat the experience. The purulent products are profuse,
highly offensive, and tax severely the powers of the general system;
and to these disadvantages may be added the risks of sloughing,
hemorrhage, and septic poisoning.

The treatment which promises most in gelatinous and cystic goitre is
either that practised by Gosselin or that by Morrell Mackenzie of
London. The plan of Gosselin is to make a very small incision in the
skin over the front of the tumor, in order to lessen the resistance to
the introduction of a small trocar and canula, through the latter of
which, after evacuating the cyst and washing it out with tepid water,
he injects the tincture of iodine (fluidrachm j). This injection is
allowed to remain about five minutes. Should its discharge be followed
by a flow of blood, a second and even a third injection is made before
withdrawing the canula. This operation does not materially differ from
that practised by V. Dumreicher, except that this practitioner emptied
the cyst with an aspirator previous to washing out the sac and
injecting the iodine. The method of Mackenzie, however, has succeeded
so well in practice that it is to be preferred both for efficiency and
safety. In this plan perchloride of iron is substituted for iodine. One
part of the iron is mixed with four parts of water, and after partially
emptying the cyst with a trocar and canula at its most dependent part
the fluid (fluidrachm j-fluidrachm ij) is thrown into the sac by a
syringe. The canula is now plugged with a stopper that the injection
may be retained. After three days the stopper is removed and the
contents of the sac are allowed to flow out. In case the discharge
proves to be bloody or serous, the injection is repeated; if, on the
contrary, it exhibits signs of pus the iron solution is withheld, but
the canula is permitted to remain, that free drainage may be maintained
until the goitre has been destroyed by suppuration. During the presence
of the instrument the affected part of the neck is covered by a
flaxseed-meal poultice.

In gelatinous goitre, when the tumor is multilocular, after tapping and
before injecting, I introduce through the canula a plunger, and by
pushing it in different directions through the interior of the tumor
break up the separating walls of the cysts, and thus open a way for the
better diffusion of the injecting material. The plan of Mackenzie,
destroying as it does the tumor by a slow chronic form of suppuration,
and at the same time draining away the pus as it forms, greatly lessens
the risk which might otherwise arise from diffused suppuration,
bleeding, or sloughing. At the Copenhagen Congress, Mackenzie stated
that he had by the method described treated 193 cases of goitre with
only 2 fatal cases, the latter being those of a fibro-cystic form.

In making a comparison between the relative safety of perchloride of
iron and of iodine as injections in goitre, the great superiority of
the former over the latter is well brought out in the cases collected
and analyzed by Schwalbe, 106 in number, for the cure of which iodine
was used, death following in 5 cases and diffused suppuration in 22
cases.

When all measures fail to control the growth of a goitre, and the life
of the patient is jeopardized from the effects of pressure, the case
ceases to be {982} a medical one and must be relegated to the domain of
surgery. Fortunately, the necessity for operation rarely occurs. It may
be remarked, in closing this article, that the excision of the gland
has been followed in several instances by evils greater than those for
which the operation was performed. The experiments of Zesas and Horsley
on lower animals, and the observations of Kocher after the removal of
the thyroid in man, place the question of extirpation of goitre among
the unsettled problems of surgery.




{983}

SIMPLE LYMPHANGITIS.

BY SAMUEL C. BUSEY, M.D.


ANATOMY AND PHYSIOLOGY.--The pathological relations of the absorbent
system are important, because of their direct connection with the
morbid processes and structural changes taking place in a variety of
diseases; therefore, before discussing the subject of lymphangitis, a
brief reference to the anatomy and physiology of the lymphatic system
is necessary.

The lymphatic system consists of large and capillary vessels,
interstitial spaces or juice-tracks, lacteals, follicles, and glands.
The serous cavities are also considered lymph-chambers, and the loose
cellular tissue is a vast chambered lymphatic sac communicating with
lymphatic vessels. The larger vessels are divided into two classes--the
superficial, which in the subcutaneous tissue accompany the veins,
while in the solid viscera they lie under the capsule, and in the
tubular viscera under the serous membrane; and the deep-seated vessels,
which accompany the deep-seated blood-vessels, ramify through the
interior of the organ in the solid viscera, and emerge at the hilus;
while in the tubular viscera they lie in the submucosa, and by free
anastomosis form plexuses. There is no communication between these two
sets of vessels, except in the solid viscera and in the glands which
may be common to both sets. Between the vessels of each set there is,
however, a free anastomosis, by which large-meshed plexuses are formed.
In consequence of these peculiar arrangements each set may be
separately diseased, and inflammation may spread rapidly from vessel to
vessel of the same set.

The lymph-capillaries are arranged in networks which lie in the meshes
of the plexuses of the blood-capillaries, from which they are separated
by intervening tissue-elements. Their walls consist of a single layer
of endothelium resting upon elastic tissue. In their continuity they
are sinuous, and are provided with an incomplete valvular arrangement.

The large vessels have three coats, not unlike the coats of the veins,
and are provided with numerous valves. These valves are the more
abundant in the superficial vessels, and the intervals between them
grow gradually less as they approach the glands.

The whole lymph vascular system terminates either in the right or left
thoracic duct.

The origin of the lymphatics has not been definitely settled. It has
been demonstrated that lymph circulates in the connective-tissue
interstices, and it seems to have been established that these spaces
are lymph reservoirs, discharging through lymph-capillaries. It is
admitted that the capillaries commence either in closely-meshed
networks or lacunar spaces. Plexuses of lymphatic capillaries,
corresponding with the distribution of the blood-capillaries, lie under
the endothelium of the serous membranes, and are in open communication
with the serous cavities through the stomata. The stomata vera are
either the openings of lymph-channels communicating directly with
lymph-capillaries, or discontinuities between the cells of the surface,
leading {984} into superficial lymph-sinuses. The pseudo-stomata are
the interstitial or intercellular cement substance, and represent the
communication of the lymph canalicular system with the free surface of
serous membranes.

Lymph-follicles consist of a reticulum of connective tissue, the meshes
of which are crowded with cells, thus forming patches in the submucous
or subserous tissue. Around these patches there is a plexus of
lymph-capillaries.

Lymphatic glands are round or oval bodies situated in the course of the
lymphatic and lacteal vessels. They are composed of follicular tissue,
trabeculæ, and lymph-tracts, all enclosed in a capsule. No doubt exists
in regard to a channel of communication between the afferent and
efferent vessels through a complex system of lymph-paths which
communicate more freely with the afferent than with the efferent
vessels. They are very vascular.

Every lymphatic vessel passes through one or more glands before
reaching the trunks. Before penetrating the peripheric fascia of a
gland these vessels divide into a number of smaller ones, which are
distributed upon the surface of the cortical portion, and empty
directly into the superficial lymph-sinuses. A number of vessels emerge
from each gland, but they are less numerous and larger than the
afferent vessels. The lymph is poured through the afferent vessels into
the lymph-spaces of the cortical alveoli, and thence into the channels
of the medullary substance, from which it escapes, enriched in
corpuscular elements, into the efferent tubes. The current of fluid
passing through such a complex structure must necessarily be retarded.
This relation of the glands to the lymph-current is, moreover,
especially interesting in its pathological significance. Whatever
enters the lymph may, if small enough, pass through the glands and be
swept along with the current, but the structure of the gland is, in a
mechanical sense, a filtering apparatus, interrupting the free current
of the fluid and retaining the coarser particles. The lymph in passing
through the glands derives constituents not previously possessed, but,
nevertheless, the retention of elements which for a time might arrest
the dissemination of hurtful material may eventually convert the gland
into a new source of infection. This fact is illustrated in the history
of malignant growths.

Perhaps the most interesting consideration connected with this relation
of the lymph-glands to the fluid passing through them is presented by
the anatomical arrangement of the chyle-vessels and the mesenteric
glands. The lacteals, commencing as the central efferent vessels of the
intestinal villi, pass between the folds of the mesentery, through
several tiers of mesenteric glands, and, uniting into one or more
trunks, terminate in the receptaculum chyli. During digestion these
vessels are full of chyle, and during the intervals of digestion they
convey lymph.

The lymphatic system may be considered an appendage of the blood
vascular system. By the blood the tissues are supplied with nutriment
and oxygen. By both the blood and lymph the surplus and waste are
conveyed away. The current of the lymph is in a reverse direction to
that of the blood-supply. The lymphatic vascular system receives
through its rootlets, which are distributed through the tissues, the
surplus transudation from the arterial capillaries, the products of
tissue-waste and transformation, and the chyle, and empties its
contents into the great venous trunks near their termini. It therefore
performs the double function of absorption from without and absorption
from within. In other words, it introduces into the blood the material
from both the food and the air which is required for the sustenance and
repair of the tissues, and conveys away the unassimilated surplus,
waste, and effete material.

The forces concerned in the locomotion of the lymph are numerous.
Recklinghausen believes the movement of the lymph to be mainly due to
the difference between the arterial and venous blood-pressure. The
greater this {985} difference the more rapid its current. The lymph
canalicular system is not in vascular continuity with the
blood-capillaries, and consequently the force of blood-pressure can
only be communicated to the column of lymph by the passage of the
plasmatic fluid into the lymphatic system by peripheral transudation
and endosmosis. These are favored by the single homogeneous walls of
the lymphatic plexuses and the enormous absorbing surface. These forces
are essentially vis a tergo, for the difference between the arterial
and venous blood-pressure is the excess of the former over the latter.
To these must be added other factors, not less important or necessary,
derived from the contractility of the walls of the lymphatic vessels,
from the compression of the surrounding and contiguous parts, from the
movements of respiration, and from the absorption of chyle. Besides
these, the slowness of the movement of the lymph as compared with the
rapidity of the arterial and venous blood-currents; the varying amount
of pressure in the lymph vascular system, and the absence of distension
in a normal condition; the entrance of the lymphatic trunks into the
veins near the confluence of large branches, where the venous
blood-pressure is almost inappreciable and the current is most rapid;
the marked effect of active muscular movement in accelerating the flow
of lymph; and the contractility of the vascular walls,--are all
conditions which cannot be omitted from a consideration of the forces
concerned in the locomotion of the lymph.

The supply of valves is very abundant, and they are always more
numerous where pressure from surrounding and contiguous parts is most
effective, though not infrequently most irregular in its operation, and
consequently where isolation of small sections of the column of the
fluid is most needed. The valves prevent regurgitation only so far as
the superimposed column of fluid is insufficient to impair their
integrity, or where there is no solution of the continuity of the
vascular walls, and distension is within the limits of ordinary and
normal extensibility. In cases of lymphangiectasis it is not usually
necessary to look beyond the nearest neighboring and connected gland
for the cause of such distension. Nature has increased the number of
valves in the afferent vessels as they approach the glands, as well to
modify and direct the flow as to prevent regurgitation; but if from any
cause the passage of the lymph through the glands is obstructed or
prevented, dilatation of the afferent vessels will ensue as a
consequence. Valvular insufficiency and dilatation may exist in
opposite relations to each other, either as cause or effect. The
dilatation of a vessel may result from thinning or loss of
contractility of its walls, caused by increased resistance to the
onward movement of the fluid, and by the lesser extensibility of the
intima than of the adventitia.

Lymphatic varices usually have their beginning in the vessels and
extend to the plexuses, but the plexuses may be alone affected.
Varicosities always extend backward from the point where the flow of
the contained lymph is arrested, and may result from a repletion of
each proximal intervalvular section with valvular incompetency.

The propulsive power of the heart diminishes with increased distance,
due to increased friction and increasing resistance from flexures,
bendings, and anastomoses, but chiefly from the increased carrying
capacity of the vascular subdivisions. Hence, as the current of the
lymph is in reverse relation to the capacity of the vessels, flowing,
as does the venous blood, from subdivisions into trunks of diminished
aggregate capacity, the velocity of the current of the lymph should be
faster in the trunkal vessels than in the subdivisions. Such is the
fact, though farther removed from the left heart and peripheral
plasmatic circulation; and yet it is much slower in the thoracic duct
than the blood-current in the venæ cavæ, which are not supplied with
valves. The movement of the venous blood is in a measure due to cardiac
and arterial contraction, but that force is least where the current is
most rapid--in the {986} venæ cavæ. The increased rapidity of the
venous blood-current as it approaches the heart must, therefore, be
derived from some other source; and it is equally manifest that the
velocity of the venous blood in the terminal trunks is transmitted to
the column of lymph and chyle flowing from the thoracic duct into the
blood-channels.

The foregoing reference to the anatomy and physiology of the absorbent
system shows very conclusively the importance of its pathological
relations. It is certainly concerned in the morbid processes of a
variety of diseases. But not less important is the fact that it is the
main channel for the diffusion of infections throughout the body.
Disease may be conveyed by the lymph from a single focus to many and
distant parts, whilst the intervening channel of communication may
remain free from injury. Along the course of the current every gland
may become an additional focus, intensifying the infectiveness of the
noxious material and increasing the area of its diffusion. This is
alike true of poisons introduced from without and of those originating
in the system.

SYNONYM.--Angioleucitis.

DEFINITION.--Lymphangitis may be either simple or septic. As a rule,
the disease is localized, but may, especially when induced by some
septic poison, be widely diffused, implicating extensive areas of
lymphatic tissue and extending to contiguous structures.

Simple lymphangitis may be either reticular or tubular. In the former
the fine capillary network or plexus is involved; in the latter the
trunkal vessels are inflamed. Very frequently both forms exist at the
same time.

ETIOLOGY.--Simple lymphangitis may be either idiopathic or traumatic.
It is, however, rarely spontaneous. External irritation, such as solar
rays, pressure, and friction, may set up a superficial inflammation,
though usually there is some form of injury--a wound, scratch, sprain,
contusion, abrasion, prick, or sting of an insect. The graver forms are
caused by neighboring inflammation, suppuration, and ulceration. The
products of these morbid changes are absorbed and conveyed along the
vessels. The inflammation may be continuous along the course of the
vessel, or separated from the origin of the morbid product by an area
of intervening healthy tissue. Absorption of the secretions and
parenchymatous fluids of inflamed parts is an active and frequent
agency in the causation of lymphangitis. It may also be caused by
contiguous inflamed tissue and by obstruction of the current of the
lymph. Lymph-thrombosis, from whatever cause produced, may excite
inflammation at the locality of formation, which is usually in the
immediate vicinity of a valve, or the thrombi may disintegrate or
undergo puriform liquefaction, and thus extend and diffuse the
inflammation.

Slight pricks, scratches, and abrasions, which in themselves are so
trifling as not to attract attention, may admit irritating substances
from without. This is a frequent cause among medical men, whose hands
and fingers are constantly exposed to irritating and ichorous
discharges.

Localized lymphangitis is frequently set up by specific kinds of
irritation. The adenitis and periglandular inflammations in cases of
scarlet fever and diphtheria are familiar illustrations. The indurated
glands in syphilis and suppurating buboes in chancroid exhibit the
different effects of the virus of these forms of disease. The
lymphatics of the solid viscera are often inflamed when the organ is
the seat of disease. Pelvic cellulitis, if not in itself a
lymphangitis, may be the starting-point of a severe and extensive
inflammation of the absorbents, occasionally involving both the
superficial and deep-seated vessels along one or both thighs.

Age and constitution are recognized factors. Lymphangitis is more
frequent in the young, and is much more easily excited in the strumous
and persons in a low state of health. Unhygienic conditions predispose
to its development.

{987} Lymphangitis may also find its cause in excessive exercise of
function, paralysis of vessels, mechanical obstruction to the
lymph-stream, lodgment of particles of cancerous or tuberculous matter
in the vessels, compression from cicatrices, indurated connective
tissue, tumors, diseased glands, stasis in large veins, and regurgitant
heart affections.

SYMPTOMATOLOGY.--Reticular lymphangitis is characterized by
rapidly-increasing localized redness, attended with a burning,
throbbing pain, and usually quickly implicates the skin and its
capillaries. Oedema to a greater or less extent may soon ensue, which,
when present, increases the pain. Fever may or may not be present,
depending in some measure upon the extent, intensity, and cause of the
inflammation and upon individual peculiarities. Erythema usually
represents a reticular lymphangitis with hyperæmia of the skin and its
capillaries, and erythema nodosum is the same associated with lymphatic
oedema. Any trivial injury may induce this form of inflammation, such
as a prick or the sting of an insect, which in extent, duration, and
intensity will vary with the cause, nature of the poison introduced,
location, and susceptibility of the sufferer.

Tubular lymphangitis is usually a much more serious form of the
disease. When the vessels of the superficial set are involved, wavy or
straight irregularly reddened lines are seen along the course of the
vessels, extending from the point of beginning to a single gland or
ganglion, which is usually tender and enlarged. These lines feel like
hard, knotted cords. The inflammation may be limited by the first tier
of glands, or it may extend to one or more distant ganglia. From the
inflamed gland the disease may be conveyed along the connecting
branches of the deeper set of vessels, and both sets may become
involved. The inflammation may also extend through the intervening
tissues from the superficial to the deeper-seated vessels. When both
sets are involved, the disease assumes a graver form and the symptoms
are aggravated. The pain becomes more acute, and the swelling is
greatly increased and more diffused. Fever may or may not be present,
and is usually moderate when the inflammation is confined to the
superficial vessels, but when the deeper set is implicated it often
commences with a rigor and is usually considerable. When the deeper set
is alone affected the red wavy, knotted lines cannot be seen, but may,
unless the oedema is great, be felt. The parts are swelled, indurated,
and stiffened, due in the acute stage to increased saturation of the
tissues, and in the chronic stage to hypertrophy of the connective
tissue. When the oedema is great the covering integument presents a
glossy, shining appearance.

PATHOLOGY AND MORBID ANATOMY.--In lymphangitis the adventitia of the
vessels and surrounding connective tissue are chiefly affected. The
external coat is thickened, injected, and infiltrated with cells. The
intima becomes opaque and is stripped of its endothelium. The lymph
coagulates in the interior of inflamed vessels and blocks up the
channel. These thrombi may become organized and permanently obliterate
the lumen of the vessel, or they may liquefy or suppurate. Their
products may enter the circulation and cause septicæmia or pyæmia. In a
few instances the clots have undergone calcareous degeneration. In some
instances coagula are found independently of any disease of the coats
of the vessels. In such cases the coagulation has been caused by the
entrance of some foreign material into the lymph-stream. The thickening
and relaxation of the coats of the vessels lead to dilatation, and
consequently to slowing of the current and stasis of lymph. From this
may result the serious consequences of an extensive lymphangiectasia,
which may involve either or both the superficial and deeper vessels of
a large area or an entire extremity. In such cases enormous development
of the adipose tissue usually takes place, not infrequently associated
with rupture of the dilated radicals and exhaustive periodic discharges
of lymph. In most of the {988} cases of lymphangiectasia and
lymphorrhagia the fluid, which either accumulates in the affected area
or is discharged through the ruptured orifices, presents the physical
characteristics and appearance of chyle, due to the quantity of fat it
contains. In some cases the fluid at first discharged is serous, and
gradually changes, as the flow continues, to a chylous or milk-like
fluid. In these cases there is also a tendency to frequently-recurring
attacks of an erysipelatous or elephantoid inflammation. This
predisposition is traceable to the structural changes produced by the
previous inflammation, traumatism, or thrombosis. Inflammation and
lymph-thrombosis are the pathological processes which usually cause
circumscribed narrowing or complete occlusion of lymph-channels; and
within the area from which the narrowed or occluded vessels originate
there is lymph-stasis, dilatation of trunkal vessels, and oedema of the
tissues. Lymphangitis may also cause adhesion of the internal surfaces
of the vessel, fibroid transformation or calcification of their coats,
and suppuration.

The alterations which take place in the lymph consist chiefly of an
increased proportion of fibrin, the addition of numerous cell-elements,
not unlike endothelial cells, white and occasionally red
blood-corpuscles, lymphoid cells, granular matter, and a varying
quantity of albumen and fat, which in a measure must owe their presence
to pathological processes affecting the intima and to transformation of
the inflammatory products.

All forms of inflammation of the lymphatic vessels exhibit a tendency
to extend to the connective tissue. Cellulitis is almost a constant
accompaniment of lymphangitis. In other cases the inflammation and
consequent thrombosis and obstruction of the lymph-stream produce
oedema and saturation of the tissues. Hyperplasia and sclerosis of the
connective tissue follow.

Adenitis is characterized by swelling, congestion, and hardness. If
resolution takes place, as is usual in all forms of simple
lymphangitis, the gland or ganglion will be restored to its normal
condition, though not infrequently some enlargement and firmness will
remain for a considerable time, which favor recurrences from very
trivial causes. It often happens, however, that structural changes
occur. Exudation and suppuration may take place. Suppuration begins in
the centre, and sooner or later the whole gland-structure is converted
into a pus-cavity. Buboes are usually associated with periglandular
abscesses. In fact, the latter are very frequently present when the
glands do not suppurate, but have assumed a condition of chronic or
subacute inflammation, which subsides very slowly and is subject to
recurring acute exacerbations from some continuous or repeated
irritation. Glands may be devastated or rendered wholly or partially
impermeable, thus forming permanent and irremediable obstacles to the
lymph-stream. Inflamed and swollen glands are not necessarily
impermeable, but the flow of the lymph through them is undoubtedly
impeded. The subacute or chronically inflamed glands may become
adherent to and imbedded in a mass of indurated connective tissue, and
may finally undergo calcareous or caseous degeneration.

Lymphangitis sometimes extends by contiguity of tissue to the synovial
membrane of joints, most frequently the knee-joint. So likewise may
synovitis and other joint affections set up a lymphangitis. In either
case the tendency to suppuration is imminent.

DIAGNOSIS.--The diagnosis of the forms of simple lymphangitis is very
easy. The red, wavy, corded, and irregularly-knotted lines following
the course of lymphatic vessels readily distinguish it from phlebitis.
These lines lead to a gland, which soon also becomes tender and
swollen. Oedema soon takes place. An inflamed lymphatic vessel is much
smaller and more tender to the touch than an inflamed vein, and usually
lies between the injured locality and an inflamed gland. Fever is more
constantly present and higher than in phlebitis.

{989} Reticular lymphangitis is usually a circumscribed inflammation,
with more or less oedema, located in the region of a lymphatic network.
It invades the integumental structures. It is not necessary to
distinguish it from an erythema, for the latter can scarcely ever be
present without implication of the lymphatic radicles. Tubular
lymphangitis and lymphangiectasia, which are so frequently associated
conditions and attended with oedema, present objective appearances very
similar to those present in oedema from phlebectasis. Phlebectasis is
excluded by the absence of pain, of dilatation of the superficial vein,
and of changed color, and of a single hard cord along the course of the
varicose vein; by the non-appearance of oedema in the neighborhood of
the ankle and on the dorsum of the foot during the earlier stages of
the disease, and its gradual extension upward. The infiltration in
phlebectasis results from increased transudation in consequence of
increased blood-pressure in the venous radicles, and their dilatation,
or from interrupted venous circulation. The accumulated fluid is
consequently watery, poor in solid constituents, and the resulting
swelling presents all the characteristics of ordinary oedema.
Absorption may be normal or perhaps increased, and with rest of the
limb the intumescence will probably diminish or disappear. In
consequence of the poverty of the transuded fluid the changes in
nutrition are very slow, and the enlargement partakes more of the
nature of an anasarca than of an hypertrophy; and, finally,
phlebectasis is usually connected with some constitutional affection or
distant local disease, and attacks the most distal parts, where the
circulation is least supported by the muscles. Lymphangiectasis is most
often found in circumscribed localities where the networks of
lymph-capillaries are most numerously distributed. The swelling is more
diffused, and is not in the form of single hard cords. It is more
resistant, and the color of the surface is unchanged. It usually
extends downward, and is not so much influenced by continued rest and
posture. The accumulated fluid results from diminished absorption or
interrupted lymph-circulation, and consists of the normal pre-existing
parenchymatous fluids, the nutritive juices continually conveyed
thither, and the fluids consumed by the functions of the parts
saturated with organic débris. It is, however, more abundantly supplied
with organic elements from both progressive and retrogressive
metamorphosis. It also contains more albumen and fibrinous substances
than the accumulated fluid in phlebectasis and ordinary oedema. The
swelling or enlargement is formed of more consistent, coagulable, and
partly organizable material, possesses greater consistence, and is
nearly compact to the touch, which increases as the fluid undergoes the
changes due to its retention in the parts. The development is peculiar,
and not altogether unlike phlegmasia. The pus-formations which
sometimes ensue partake of the nature of cold abscesses, and are
located in the connective tissue. The pus-formations in phlebectasis
usually begin in the venous thrombi within the dilated and enlarged
veins, are associated with acute symptoms, and result, usually, in
purulent absorption.

In view of later anatomical and pathological researches, it must be
admitted that phlegmasia dolens is occasionally a lymphangitis, having
its origin in inflammation of the vessels or areolar tissue. Some
pathologists have advanced the theory that, as seen in lying-in women,
it is a parametritis commencing in the cellular tissue in the immediate
vicinity of the womb and extending to remoter parts. The writer saw
recently, in consultation with J. Taber Johnson, a case of puerperal
pelvic cellulitis associated with a firm, resistant, diffuse, painful,
and tender swelling involving the inner aspect of both thighs, and
extending from the groin on each side downward below the middle third
of the thigh. The pelvic inflammation appeared first in the left iliac
fossa, and was associated with the swelling before described on the
thigh. This subsided, and was immediately followed by a similar
condition {990} in the right iliac fossa, accompanied by a precisely
similar intumescence on the right thigh. At no time could any enlarged,
hard, or corded veins be discovered. The swellings presented the usual
objective and tactile characteristics of those inflammatory affections
so frequently supervening within areas abundantly supplied with lymph
networks, in communication with the original lymphangitis and
lymph-thrombosis. In this case the swellings were located in a region
specially rich in lymph capillary networks. With the subsidence of the
pelvic cellulitis the thigh intumescence on either side gradually
disappeared.

Tubular lymphangitis is readily distinguished from erysipelas by the
presence of the knotted and corded lymphatic vessels. Reticular
lymphangitis is characterized by fine, closely-arranged red lines
limited to a circumscribed area, and is usually associated with and
starts from some injury. In erysipelas the redness is uniform. It does
not follow the course of the lymphatic vessels, nor extend from a wound
in the direction of and to a gland or ganglion of glands. The fever is
usually higher and of longer duration. The inflamed surface is marked
by the appearance of blebs.

PROGNOSIS.--Simple lymphangitis is usually unattended with danger
unless complicated with suppurating arthritis. The disease, as a rule,
runs a rapid course to recovery. It is more favorable the nearer the
inflammation lies to the surface.

TREATMENT.--The treatment is both constitutional and local. The first
indication is to remove the cause. The wound should be cleansed and
disinfected. For this purpose solutions of carbolic or acetic acid may
be employed, or it may be cauterized with caustic potash or chloride of
zinc. The fever should be controlled by the employment of antipyretics.
One or more full doses of the sulphate or hydrochlorate of quinia,
administered at shorter or longer intervals according to the quantity
given at each dose and the intensity of the fever, may be sufficient.
Antipyrin is a very valuable remedy. It will reduce the fever more
speedily and decidedly than the salts of quinia. If the fever is
reduced and kept under control by the judicious administration of this
remedy in moderate doses, the tendency of the inflammation to extend is
very greatly diminished, and may be arrested. Its antipyretic effect
is, however, less durable than that of the salts of quinia, but is
unattended with the cerebral disturbances usually associated with the
employment of quinia salts. The bowels should be kept solvent by the
use of saline cathartics. The diet should be restricted during the
pyrexial stage. After the acute stage has passed, tonics and improved
diet may become necessary; especially will this be the case in those
previously debilitated. In healthy, robust subjects it is not probable,
under proper and prompt treatment, that the disease will continue long
enough to endanger convalescence by serious exhaustion. When needed,
iron, cod-liver oil, and the salts of quinia may be resorted to. But,
after all, a good appetite and a sufficient supply of nutritious and
easily-digested foods constitute the best and most available tonics.
Rest of the affected part is very important, and the posture should be
such as to remove pressure and relieve tension.

In the beginning of the acute stage cold applications may be employed,
but, as a rule, the local treatment should be confined to the assiduous
application of hot soothing and emollient fomentations, to which opium
or belladonna may be added. By these means the tension of the swollen
and inflamed parts, and consequently the pain, are assuaged. It is
rarely necessary to employ internally any anodyne to relieve the pain;
but in occasional cases, occurring in persons keenly susceptible to
pain, an opiate or some less powerful anodyne may be administered. Some
advise the local abstraction of blood by leeching, but it is admissible
only when the pain is very acute and confined to a limited and defined
area. After the subsidence {991} of the fever and acute inflammatory
stage the remaining oedema and indurations may be treated with the
local application of the tincture of iodine, inunction with mercurial
ointment, bandaging, massage, and rest.

For the oedematous condition, which is sometimes very persistent,
pressure is the most available and potential remedy. This should be
secured by systematic bandaging either with a flannel or an elastic
bandage. In such cases passive movement and massage or kneading of the
part constitute an important and valuable auxiliary to pressure.

To allay itching, which is sometimes almost intolerable even after the
acute inflammation has subsided, the part may be painted with a
solution of nitrate of silver or collodion. If these fail, an alcoholic
solution of benzoic acid, twenty grains to the ounce, may be employed.

If suppuration takes place, the abscess should be promptly and
effectually incised. It should be thoroughly evacuated and dressed
antiseptically. When this occurs a more or less tonic and supporting
treatment is necessary. Iron, cod-liver oil, quinia, and stimulants may
be, according to circumstances, administered. The devastating effects
of suppurating cavities should be controlled by the liberal use of the
appropriate remedies to arrest exhaustion and to rebuild waste.

In occasional instances the initial stage, consentaneous with the
receipt of the injury, such as the sting of an insect, is marked by
violent shock and threatening collapse. The writer has witnessed two
such cases occurring in robust, healthy men stung by honey-bees on the
forearm, where great exhaustion and alarming collapse, with violent
retching, profuse diarrhoea, and agonizing pain, were accompanied by
rapidly-developed inflammation and swelling at the locality of the
puncture. In such cases the free administration of alcoholic stimulants
seems imperatively demanded.

The general plan of treatment of acute simple lymphangitis is
antiphlogistic, by the employment of remedies to reduce inflammation
and promote resolution. The danger of suppuration should not be
overlooked or underestimated. A single suppurating focus may widely
diffuse disease and impair the entire organism. A single and apparently
trivial inflammation of lymphatic tissue may be the initial stage of a
fatal pyæmia or septicæmia.

{992}




{993}

INDEX TO VOLUME III.


A.

Abdominal aneurism, 821
  viscera, lesions, in catarrhal pneumonia, 358

Abscess, diffuse splenic, 962
  embolic, of spleen, 963
  of the lung, 296
  of the mediastinal space, 861
  termination of croupous pneumonia in, 311, 332

Abscesses, seat and nature, in suppurative endocarditis, 604

Accidents during tracheotomy, 156

Acephalocysts, expectoration of, in pulmonary hydatids, 469

Aconite, locally, in chronic laryngitis, 127
  use, in exophthalmic goitre, 767

Acupuncture, use, in thoracic aneurism, 820

Acute general diseases, resemblance of croupous pneumonia to, 317
  miliary tuberculosis, 472

ADDISON'S DISEASE, 939
  Definition, synonyms, and history, 939
  Diagnosis, 947
  Duration, 941
  Etiology, 939
  Morbid anatomy, 942
    Nervous system, lesions, 944
    Spleen, lesions, 943
    Suprarenal capsules, lesions, 942, 943
  Pathology, 944
    Theories regarding origin, 945-947
  Symptoms, 940
    Anæmia and hemorrhages, 940
    Bronzing of skin, seat and characters, 940
    Dyspnoea, 941
    Gastro-intestinal disorders, 941
    Nervous symptoms, 941
    Pain, characters and seat, 941
    Pulse in, 941
    Urine, condition, 941
  Treatment, 948

Adductors of vocal cords, paralysis of, 81

Adenitis, in lymphangitis, 988

Adherent pericardium, 785

Adhesions, pericardial, seat and characters, 785

Adults, grave form of catarrhal pneumonia in, 360

Adventitious products of the heart, 637

Ægophony, significance, in pleurisy, 510

Aërial fistula, following tracheotomy, 163

After-treatment of tracheotomy, 159

Agaricus, use, in pulmonary phthisis, 438

Age, influence on aortic obstruction, 655
    on causation of acute catarrhal laryngitis, 93
      of acute miliary tuberculosis, 478
      of angina pectoris, 759
      of aortic regurgitation, 655
      of asthma, 190
      of bronchitis, 157
      of cardiac thrombosis, 722
      of catarrhal pneumonia, 353
      of croupous pneumonia, 314
      of exophthalmic goitre, 764
      of fatty degeneration of the heart, 613
      of fibroid phthisis, 441
      of fibro-serous pleurisy, 492
      of gangrene of lung, 301
      of hæmoptysis, 275
      of hay asthma, 212
      of Hodgkin's disease, 922
      of laryngismus stridulus, 70
      of leukæmia, 909
      of mediastinal tumors, 871
      of mitral regurgitation, 671
      of mitral stenosis, 666
      of pernicious anæmia, 899
      of phthisis, 396
      of pneumothorax, 576
      of pseudo-membranous laryngitis, 101
      of purulent pleurisy, 540
      of simple lymphangitis, 986
      of thoracic aneurism, 802

Air, compressed, use, in bronchial asthma, 208
  moist, use, in acute catarrhal laryngitis, 97
  rarefied, exhalation into, in emphysema, 246

Albuminoid expectoration following thoracentesis, 535

Alcohol, abuse, influence on causation of chronic laryngitis, 121
        of the caisson disease, 858
  influence on causation of fatty cardiac degeneration, 612
  use, in acute miliary tuberculosis, 481
    in bronchial asthma, 205
    in catarrhal pneumonia, 370
    in croupous pneumonia, 348, 349, 351
    in endocarditis, 651
    in gangrene of the lung, 305
    in parenchymatous degeneration of the heart-muscle, 611
    in pseudo-membranous laryngitis, 108
    in pulmonary phthisis, 435

Alcoholism, influence on causation of chronic myocarditis, 607
      of pleurisy, 493
      of croupous pneumonia, 314

Alkalies, use, in pseudo-membranous laryngitis, 105
    in rheumatic pericarditis, 783
    in prevention and treatment of pulmonary embolism, 389, 390

Alkaline sprays, use, in chronic laryngitis, 125, 127

Allen's nasal forceps, 54

Altitude, influence on causation of hæmoptysis, 277, 278

Alum, use, in laryngismus stridulus, 73

Ammonium, carbonate, use, in cardiac thrombosis, 745
      in croupous pneumonia, 349
      in prevention of pulmonary embolism, 389
    and chloride of, use, in catarrhal pneumonia, 370, 371
  chloride, use, in chronic laryngitis, 124, 125

Amphoric respiration in pulmonary phthisis, 417

Amyl nitrite, use, in angina pectoris, 760
    in bronchial asthma, 204
    in chronic endarteritis of the coronary artery, 830
    in fatty cardiac degeneration, 616

Amyloid degeneration of heart-muscle, 616
    of suprarenal bodies, 949

ANÆMIA, 887
  Albumen, continuous loss of, influence on causation, 887
  Blood, changes in, 890, 891
  Bone, spleen, lymph-glands, enlargement of, and relation to
        production of blood-corpuscles, 888-894
  Hemorrhage, influence on causation, 887
  Inanition, influence on causation, 889
  Toxic causes of, 889

Anæmia in Addison's disease, 940
  in exophthalmic goitre, 763
  in pulmonary phthisis, 406

ANÆMIA, PROGRESSIVE PERNICIOUS, 898
  Course, 903
  Definition and history, 898
  Diagnosis, 905
  Etiology, 899
    Age and sex, influence on causation, 899
    Hygiene, bad, influence on causation, 899
    Loss of blood, chronic discharges, etc., 900
    Mental worry and anxiety, 900
    Pregnancy and parturition, 900
  Morbid anatomy, 904
    Bones, changes in, 905
    Lymph-glands, changes in, 905
    Spleen, changes in, 905
  Pathology, 905
  Prognosis, 906
  Symptoms, 900
    Blood and blood-corpuscles, changes in, 901
    Gastro-intestinal disorders, 903
    Hæmic heart-murmurs, 902
    Hemorrhages in, 901-903
    Oedema in, 901
    Onset, mode of, 900
    Skin, changes and color of, 901
    Temperature, 903
    Urine, changes in, 903
  Treatment, 906
    Arsenic, use, 907
    Diet in, 907
    Iron, use, 907
    Milk, injection of, 908
    Transfusion of blood, 907

Anæmic necrosis of heart-muscle, 610

Anæsthesia of larynx, 65

Anæsthetics, use, in laryngismus stridulus, 73

Anatomy of tracheal region, 146, 147

ANEURISM, ABDOMINAL, 821
  Diagnosis, 822
  Symptoms, 821
  Treatment, 822
    Compression of aorta, good results of, 822

Aneurism, diagnosis of, from mediastinal tumors, 876

ANEURISM, THORACIC, 801
  Definition, 801
  Diagnosis, 814
    From abscess, 814
    From tumors, 814
  Duration, 815
  Etiology, 802
    Age and sex, influence on causation, 802, 803
    Occupation, influence on causation, 803
    Syphilis and gout, influence on causation, 803
  Morbid anatomy, 801, 802
  Symptoms, 803
    Auscultation in, 811
    Bone, signs of pressure upon, 807
    Bruit, characters, 811
    Cyanosis and oedema, 807
    Dysphagia in, 806
    Dyspnoea in, 805
    Frémissement cataire, frequency, 808
    Inspection, 807
    Localization of tumors, 812
    Myosis in, 805
    Of varicose form, 813
    Oral whiff of Drummond, significance, 812
    Pain, characters, 804
    Palpation in, 808
    Percussion in, 812
    Physical signs in, 807
    Pressure signs, 804-807
    Pulse, peculiarities of, 808-810
    Thrill in pulse, 809
    Veins, signs of pressure upon, 807
    Voice, modifications of, 806
  Terminations, 815
  Treatment, 816-820
    Acupuncture, use, 820
    Barwell's operation of ligation, 818, 819
    Ergotin, hypodermic use, 816
    Electrolysis, method of applying, 819, 820
    Opiates, use, 817
    Potassium iodide, 818
    Pressure, use, 816
    Starvation method, 816
    Tufnell's method of rest and diet, 816, 817
    Wire, introduction of, into sac, 816

Aneurism of the coeliac axis, 841
  of the coronary artery, 830
  of the heart, 636
  of the hepatic artery, 840
  of the interior mesenteric artery, 839
  of the superior mesenteric artery, 836
  of the pulmonary artery, 833

Aneurismal form of hæmoptysis, 284

Angina, in anæmic necrosis of heart-muscle, 610

ANGINA PECTORIS, 755
  Death, cause of, 760
  Definition, 755
  Diagnosis, 757
  Etiology, 758
  Morbid anatomy, 758
  Prognosis, 759
  Symptoms, 755-757
  Treatment, 760
    Amyl nitrite, use, 760
    Chalybeates, use, 760
    Digitalis and nux vomica, 761
    Opium and morphia, use, 760
    Preventive, 760
    Stimulants, 760

Angina pectoris in aortic regurgitation, 661

Anginoid attacks in chronic myocarditis, 608, 609

Anomalies, congenital, of heart and great vessels, 687
  of blood-vessels of tracheal region, 147
  of suprarenal bodies, 949

Ante-mortem heart-clots, character, 737

Anthracosis, appearance of lungs in, 458

Antimony, use, in bronchitis, 179, 180
    in croupous pneumonia, 347

Antipyrin, use, in acute miliary tuberculosis, 480, 481
    in simple lymphangitis, 990

Antiseptics, use, in croupous pneumonia, 352

Antispasmodics, use, in functional heart disease, 754
    in laryngeal oedema, 116
    in laryngismus stridulus, 73
    in spasm of the glottis, 74

Anxiety, in cardiac thrombosis, 731

Aorta, atheroma of, 800
  disease of, influence on causation of hypertrophy of the heart, 620
  diseases of, 800
  occlusion of, 824, 825
  perforation of, 824
  rupture of, 823
  stenosis of, 825

Aortic arch, localization of aneurism of, 812
  conus, defects of, in cyanosis, 708
  obstruction, 654
  regurgitation, 659
  stenosis and regurgitation, treatment, 683
  trunk, narrowing, in cyanosis, 708
  and mitral orifices, defects of, in cardiac malformations, 690

Aortitis, acute, 800

Apex-beat, in dilatation of the heart, 634
  in hypertrophy of the heart, 625, 627
  normal position of, 654
  significance of position of, in diagnosis of functional heart
        disease, 750

Apex of lung, tendency to tuberculous deposit in, 408

Aphonia, in paralysis of adductors of vocal cords, 82
  in pulmonary phthisis, 403

Apomorphia, use, in catarrhal pneumonia, 371
  in acute catarrhal laryngitis, 97, 98

Apoplexy of suprarenal bodies, 949
  pulmonary, 293

Appetite, impaired, in pulmonary phthisis, 406

Arch of aorta, localization of aneurisms of, 812

Arsenic, use, in acute miliary tuberculosis, 482
    in Addison's disease, 948
    in atrophic nasal catarrh, 49
    in bronchial asthma, 207
    in carcinoma of larynx, 131
    in chronic congestion and enlargement of the spleen, 959
    in chronic laryngitis, 125
    in dilatation of the heart, 636
    in Hodgkin's disease, 931
    in leukæmia, 921
    in pernicious anæmia, 907
    in pulmonary phthisis, 436

Arterio-sclerosis of the coronary artery, 828
  of the pulmonary artery, 833

Artery, coronary, diseases of, 828
  hepatic, aneurism of, 840
  pulmonary, diseases of, 833
  inferior mesenteric, diseases of, 834
  superior mesenteric, diseases of, 836

Arytenoideus, paralysis of, 84

Aspiration in pericardial effusion, 776, 780
  of the pleura, dangers of, 596
      history, etc., 593-596

Aspirators in thoracentesis, varieties, 530, 532

Asthenic pneumonia, treatment, 351

ASTHMA, BRONCHIAL, 184
  Definition, 184
  Diagnosis, 198
    From dyspnoea of bronchitis and cardiac disease, 198
        of laryngeal affections, 199
    From embolism of pulmonary artery, 200
    From emphysema, 198
    From spasm of diaphragm, 199
  Duration, 189
  Etiology, 190
    Age and sex, influence on causation, 190
    Cold and damp, influence on causation, 192
    Enlarged bronchial glands, 191
    Heredity, influence on causation, 190
    Pollen of plants, vapors, gases, etc., 192
    Uterine, nasal, and stomachic irritation, 193
  History, 184
  Morbid anatomy, 197
  Pathology, 193-197
  Prognosis, 200
  Sequelæ, 189
  Synonyms, 184
  Symptoms and course, 185
    of intervals, 184
      paroxysms, description, frequency, and time of onset, 185-187
      heart-circulation, state of, during, 188
      physical signs of, 187, 188
    Physiognomy of asthmatics, 186, 190
  Treatment, 201
    Hygienic and dietetic, 206
    Locality, change of, 206
    Of intervals, 206
    Of paroxysms, 201
    Use of arsenic, 207
      of belladonna and stramonium, 203
      of chloroform, 202
      of cigarettes, medicated, 203, 207
      of compressed air, 208
      of electricity, 205
      of emetics, 204
      of lobelia and tobacco, 204
      of morphia and chloral hydrate, 201, 202
      of nitrite of amyl, 204
      of nitro-glycerin, 208
      of potassium bromide, 204
          iodide, 207
          nitrate, 203
      of stimulants, 205

Asthma complicating emphysema, 239
  hay, 210

Astringents, use, in chronic laryngitis, 125, 126
    in laryngeal oedema, 116

Atelectasis, influence on causation of bronchial dilatation, 228

Atelectasis. See _Lung, Collapse of_.

Atheroma of the aorta, 800
  of the coronary artery, 828
  of the pulmonary artery, 833

Atmospheric causes of goitre, 977

Atomizer, use, in hyper- and paræsthesia of the larynx, 64

Atresia of the pulmonary artery, 702

Atropia, use, in profuse expectoration of bronchiectasis, 231
    in pulmonary phthisis, 438
    in the caisson disease, 858

Atrophic form of chronic nasal catarrh, 47
  lobar emphysema, 248

Atrophy of suprarenal bodies, 949
  of the heart, 618

Auricles of the heart, hypertrophy of, 627

Auriculo-ventricular orifice and tricuspid valve, defects of, 689
    rings, condition, in cardiac dilatation, 633

Auscultation during paroxysm of asthma, 187
  of mediastinal tumors, 874
  in bronchial dilatation, 229
  in bronchitis, 170-174
  in cardiac malformation, 710, 711
      thrombosis, 728
      valvular disease, 657, 663, 668, 673, 675, 677, 680
  in catarrhal pneumonia, 359, 360, 362, 363
  in collapse of the lung, 253
  in croupous pneumonia, 335, 337, 338
  in emphysema, 238
  in endocarditis, 648
  in fibro-serous pleurisy, 507-510
  in hydrothorax, 572
  in mediastinal abscess, 862
  in pericarditis, 775
  in pneumothorax, 579
  in pulmonary phthisis, 412-418
  in purulent pleurisy, 543, 544
  in pyo-pneumothorax, 545
  in thoracic aneurism, 811

Auscultatory percussion in fibro-serous pleurisy, 503

Auto-laryngoscopy, 29

Axillary glands, enlargement of, in Hodgkin's disease, 926


B.

Bacelli's sign of pleurisy, 510, 517, 543

Bacillus tuberculosis, relation of, to acute miliary tuberculosis, 477
      to hæmoptysis, 279, 280
      to pulmonary phthisis, 398

Balfour's treatment of aneurism, 818

Balsams, use, in chronic bronchitis, 182

Bandage, use, in phlegmasia dolens and lymphangitis, 848, 991

Barrel-shaped chest of emphysema, 237

Barwell's operation for cure of thoracic aneurism, 818

Basedow's disease. See _Exophthalmic Goitre_.

Baths, cold, use, in bronchial asthma, 206
      in croupous pneumonia, 349
  hot, use, in laryngismus stridulus, 73

Belladonna, use, in pulmonary phthisis, 438
  and stramonium, use, in bronchial asthma, 203

Bellocq's canula, use, in epistaxis, 52

Benign form of pulmonary embolism, symptoms, 382
  growths of the larynx, 128
  tumors of the trachea, 140

Benzoin, use, in chronic laryngitis, 124, 126

Bilious pneumonia, 334

Binaural stethoscope, use, in auscultation, 412

Black sputa of pitmen, 455, 459

Blaud's pills, use, in chlorosis, 896

Bleeder families, 933

Bleeding in heart disease, question of, 686

Bleedings, seat and amount, in hæmophilia, 935

Blisters, use, in acute myocarditis, 606
    in capillary bronchitis, 180
    in chronic phlebitis, 848
    in pericardial effusion, 784
    in pleurisy, 521
    in thoracic aneurism, 817

Blood changes in, in croupous pneumonia, 313
    in hæmoptysis, 287
    in Hodgkin's disease, 924
    in leukæmia, 911, 915
    in pernicious anæmia, 901
  condition of, in chlorosis, 894
    in hæmophilia, 936
  diseases of the, 882

Blood-corpuscles, changes in, in pernicious anæmia, 901
  relation of spleen, lymph-gland, and bone-marrow to production, 890,
        891

Blood-glandular system, diseases of, 882

Bloodletting, local and general, in pulmonary congestion and oedema,
        263, 264

Blood-vessels, pulmonary, changes in, in emphysema, 243
  relation of, to miliary tubercles, 474, 475

Bone-marrow, hyperplasia of, in anæmia, 892
  influence on blood-formation, 885
  lesions, in leukæmia, 916
    in pernicious anæmia, 905

Bones, pressure upon, in thoracic aneurism, 807

Bowditch's connection with history of thoracentesis, 591-595

Brain, lesions, in croupous pneumonia, 313
    in pernicious anæmia, 905
  and membranes, lesions, in catarrhal pneumonia, 358
      in leukæmia, 918

Breath, fetid, in chronic pharyngitis, 122

Breathing, in collapse of lung, 252

Bright's disease, complicating phthisis, 407
    influence on causation of pericarditis, 771
        of congestion and oedema of the lungs, 259

Bromides, use, in exophthalmic goitre, 767

Bronchi, diseases of, 164

Bronchial asthma, 184
  breathing, in pleurisy, 508
  catarrh, complicating emphysema, 247
    influence on causation of collapse of lung, 251
  glands, enlargement of, in croupous pneumonia, 313
    lesions, in bronchitis, 175, 176
      in catarrhal pneumonia, 357
      in pneumonokoniosis, 457
  lesions of syphilis of the lungs, 451
  respiration in croupous pneumonia, 337

BRONCHIAL TUBES, DILATATION OF (Bronchiectasis), 227
  Definition, history, and etiology, 227
  Diagnosis and prognosis, 230
  Morbid anatomy, 230
  Symptoms, 228
  Treatment, 230

BRONCHITIS, 164
  Definition, 164
  Diagnosis, 176
    From phthisis, 177
    From pneumonia, 176
    Of chronic form, from emphysema, 177
  Etiology, 164
    Age and sex, influence on causation, 165
    Cold and damp, season, etc., 166-168
    Exciting causes, 168
    Predisposing causes, 165
  History, 164
  Morbid anatomy, 175
  Mortality, 165, 177
  Prognosis, 177
  Synonyms, 164
  Symptoms--acute form, 169
    Capillary form, 171
      Cough, characters, 171
      Dyspnoea in, 171
      Physical signs of, 171
    Chronic form, 174
      Cough and expectoration, characters of, 174
    Mechanical form, 170
    Pseudo-membranous form, 173
    Rheumatic form, 172
  Treatment, 178
    Of acute and capillary forms, 178-180
      Antimony, use, 180
      Counter-irritation, 178
      Emetics, 180
      Expectorants, 179
      Quinia, use, 179
      Venesection, 178
    Of chronic form, 181
      Alteratives, 182
      Change of climate, 183
      Compressed air, 183
      Diet, 181
      Inhalations, 182
      Iron, use, 182
    Of pseudo-membranous form, 180
    Of rheumatic form, 180

Bronchitis and pneumonia, influence on causation of phthisis, 394
  complicating emphysema, 239
    tracheotomy, 162
  of acute infectious diseases, influence on causation of catarrhal
        pneumonia, 354

Broncho-vesicular respiration, characters and significance of, 412

Brown atrophy of heart-muscle, 616
  induration of lungs, 256

Bruit, in thoracic aneurism, 811


C.

Caffeine, use, in dilatation of the heart, 635

CAISSON DISEASE, 854
  Definition, 854
  Duration, 855
  Etiology, 857
  Morbid anatomy, 855
  Pathology, 855
  Symptoms, 854
    Headache, vertigo, and coma, 855
    Nausea and vomiting, 854
    Pain, seat and characters, 854
    Paralyses, 854, 855
  Treatment, 858
    Atropia, use, 858
    Compressed air, 859
    Ergot, use, 859
    Morphia, use, 858
    Of paralysis, 859

Calcareous degeneration of the heart-muscle, 616

Calcification of the vein, 852

Calcium sulphide, use, in acute phlebitis, 846

Canulas, tracheotomy, 151, 152

Cancer of adrenals in Addison's disease, 943
  of the heart, 639
  of the lungs, 460
  of the pericardium, 792
  of the pleura, 583
  of the veins, 853

Capillary bronchitis, 171
  emboli of lungs, effects, 385
  vessels, relation to miliary tubercles, 475

Caput Medusæ, 849

Carbolic acid, danger of, in injections into pleural cavity, 561
    use, in abscess of lung, 300
      in gangrene of lung, 305
    injections, in goitre, 980
    and iodine, injections, in pericardial effusions, 795

Carcinoma of the larynx, 128
  of the mediastinum, seat and characters, 869
  of the nasal passages, 55
  of the thyroid gland, 978
  of the trachea, 141

Cardiac action, irregular, in fatty degeneration of the heart, 615
  disease influence on causation of chronic splenic enlargement, 957
  hæmoptysis, symptoms, 285
  hypertrophy, relation to adherent pericardium, 786
  murmurs, relation to valvular disease, 651
  sedatives, use, in hypertrophy of the heart, 630

CARDIAC THROMBOSIS, 718
  Complications and sequelæ, 733
  Definition, 718
  Diagnosis, 740
    From dyspnoeic uræmia, 742
      laryngeal affections, 743
      nervous shock of acute endocarditis, 744
      pulmonary embolism, 743
  Duration and terminations, 732
  Etiology, 721
    Age and sex, influence on causation, 722
    Mechanical causes, 723
    Vital or pathological causes, 724
    Endocarditis, influence on causation, 725
  History, 719
  Morbid anatomy and pathology, 734
    Of ancient clots, 737
      cadaveric and terminal clots, 735
    Physical characters of clots, 735-740
  Prognosis, 744
  Synonyms, 718
  Symptoms, 726
    Blowing murmur of Bouillaud, significance, 730
    Dyspnoea, 730
    Mental condition, 731
    Pain, 730
    Physical signs, 727
    Physiognomy in, 730
    Pulse, characters, 729
    Syncope, 730
  Treatment, 745
    Alkalies, as solvents, use, 745
    Ammonium carbonate and liquid ammonia, use, 745
    Counter-irritation, 746
    Digitalis and nux vomica, use, 746
    Intravenous injections of ammonia, 745
    Rest, value, 746
    Sodium bicarbonate, use, 745
    Stimulants, use, 746

Cardicentesis, 798

Caseated morbid products, influence on causation of pulmonary phthisis,
        400

Caseous pneumonia following pleurisy, 514
  pus, influence on causation of acute miliary tuberculosis, 473

Casts of bronchi, in pseudo-membranous bronchitis, 176

Catarrh, chronic nasal, 42

Catarrhal pneumonia in children, symptoms, 359
    relation of, to collapse of lung, 354, 355
  tendency, influence on causation of hæmoptysis, 275

Catheterization of larynx in true croup, 107

Cavernous form of hæmoptysis, 284

Cavities, diagnosis of, in pulmonary phthisis, 416
  tubercular, injection of, 439, 440

Cell-walls, changes in, as a cause of emphysema, 334

Cerebral anæmia, in aortic obstruction, 656
  disturbance in functional heart-disease, 749
  hyperæmia in tricuspid regurgitation, 649

Cerebral symptoms in cardiac thrombosis, 731
    of croupous pneumonia, 329
    of pericarditis, 774

Chest, alterations of, in pleuritic effusions, 497, 498
  changes in, in emphysema, 236, 237

Cheyne-Stokes breathing in fatty degeneration of the heart, 615

Children, catarrhal pneumonia in, 359

Chills in croupous pneumonia, 320
  in pleurisy, 494
  in purulent pleurisy, 542

Chloral hydrate, use, in bronchial asthma, 202
      in catarrhal pneumonia, 372

Chlorides, diminution of, in croupous pneumonia, 330

Chloroform, use, in bronchial asthma, 202

Chlorosis, 894
  Definition and etiology, 894
  Morbid anatomy, 894
  Symptoms, 895
  Treatment, 896

Chondritis of the larynx, 117

Chorea of the larynx, 76

Chronic bronchitis, 174
    influence on causation of bronchiectasis, 228
  congestion and enlargement of the spleen, 956
  endarteritis of the coronary artery, 828
    of the pulmonary artery, 833
  interstitial pneumonia, 391, 440
  lobular emphysema, 233
  myocarditis, 607
  pericarditis, 784
  phlebitis, 848
  purulent pleurisy, symptoms, 342

Cigarettes, medicated, use, in bronchial asthma, 203, 207

Circumscribed pleurisies, 545

Cirrhosis of the liver, influence on causation of splenic enlargement,
        957
  of lung, displacement of heart by, 603

Classification of hay asthma, 221
  of pleurisy, 454
  of pneumonokoniosis, 454
  of pulmonary embolism, 373

Climate, change of, in acute laryngitis, 96
    in chronic bronchitis, 183
  influence on frequency of hæmoptysis, 277

Climatic treatment of pulmonary phthisis, 427

Clothing, proper, for phthisical patients, 433, 434

Clots, ancient or ante-mortem, of heart, characters, 737
  cadaveric, in cardiac thrombosis, 735
  terminal, in cardiac thrombosis, 735

Clubbing of fingers in cyanosis and cardiac malformations, 711

Cocaine, use, in chronic laryngitis, 127
    in coryza, 42
    in epiglottic ulceration, 112
    in hyper- and paræsthesia of the larynx, 65
    in morbid growths of the larynx, 131

Codeia, use, in bronchitis, 180, 182
    in cough of miliary tuberculosis, 480

Cod-liver oil, use, in acute miliary tuberculosis, 482
      in atrophic nasal catarrh, 49
      in chronic bronchitis, 182
      in chronic laryngitis, 125
      in pulmonary phthisis, 434
      in purulent pleurisy, 549
      in ulceration of trachea, 139
      in vesicular emphysema, 245

Coeliac axis, aneurism of, 841
    diseases of, 841

Coffee, use, in bronchial asthma, 205
  black, use, in cardiac thrombosis, 746

Colchicum, use, in rheumatic bronchitis, 181

Cold applications in epistaxis, 51
  influence on causation of congestion and oedema of the lungs, 258
      of pericarditis, 770
      of perichondritis and chondritis of larynx, 117
  use, in catarrhal pneumonia, 371
    in pericarditis, 783
    in reduction of temperature in croupous pneumonia, 349
    in simple lymphangitis, 990
  and damp, influence on causation of asthma, 192
        of bronchitis, 166
        of croupous pneumonia, 315
        of fibro-serous pleurisy, 491
  and moisture, influence on causation of acute catarrhal laryngitis,
          93

Collapse of lung, 250

Color of ante-mortem heart-clots, 739

Columnæ carneæ, lesions, in chronic myocarditis, 607

Communicability of pulmonary phthisis, 396

Complications after tracheotomy, 161
  of acute coryza, 41
  of cancer of the lungs, 464
  of cardiac thrombosis, 733
  of catarrhal pneumonia, 364
  of emphysema, 239
  of fibro-serous pleurisy, 512
  of mediastinal abscess, 864
  of pulmonary phthisis, 400

Compressed air, use, in bronchial asthma, 208
      in chronic bronchitis, 183
      in emphysema, 245

Compression in treatment of abdominal aneurism, 823

Congenital anomalies of the heart and great vessels, 687
  malpositions of the heart, 601

Congestion, acute, of spleen, 953
  and enlargement of the spleen, chronic, 956
  and oedema of the lungs, 258

Congestive form of hæmoptysis, 283

Contagiousness of acute miliary tuberculosis, 472
  of pseudo-membranous laryngitis, 102
  of pulmonary phthisis, 396-400

Conus arteriosus dexter, obstruction with open ventricular septum in
        cyanosis, 703

Convallaria, use, in dilatation of the heart, 635

Convulsions, in croupous pneumonia, 329
  in pseudo-membranous laryngitis, 102

CORONARY ARTERY, DISEASES OF, 828
  Chronic Endarteritis (Arterio-sclerosis; Atheroma), 828
    Diagnosis and prognosis, 829, 830
    Etiology and symptoms, 828
    Pathology, 829
    Treatment, 830
  Aneurism of, 830
  Embolism of, 831
  Embolism and thrombosis of, 831
  Obliterating endarteritis of, 830
  Occlusion of, 831
  Rupture of, 833
  Thrombosis of, 832

Corpuscles of the blood, changes in, in Hodgkin's disease, 924
      in leukæmia, 912
      in pernicious anæmia, 901

Coryza, acute, 41

Cough in acute catarrhal laryngitis, 94
  in asthma, 188
  in bronchial dilatation, 228
  in capillary bronchitis, 171
  in cardiac malformations and cyanosis, 710
  in catarrhal pneumonia, 358-361, 363
  in chronic bronchitis, 174
    pharyngitis, 122
  in croupous pneumonia, 322
  in emphysema, 236
  in fibro-serous pleurisy, 495
  in hydatids of pleura, 585
  in laryngismus stridulus, 71
  in mitral regurgitation, 671
    stenosis, 667
  in morbid growths of the trachea, 140
  in pseudo-membranous laryngitis, 102
  in pulmonary congestion in oedema, 260
    phthisis, 400
      treatment, 436
  in purulent pleurisy, 542
  in thoracic aneurism, 806
  nervous, 71

Counter-irritation in acute bronchitis, 178
  in atelectasis, 255
  in cardiac thrombosis, 745, 746
  in catarrhal pneumonia, 369
  in croupous pneumonia, 347
  in pericarditis, 783

Course of anæsthesia of the larynx, 67
  of cardiac thrombosis, 732
  of fibro-serous pleurisy, 510
  of hyperæsthesia of the larynx, 163
  of hypertrophy of the heart, 621
  of laryngismus stridulus, 71
  of leukæmia, 818
  of pernicious anæmia, 903
  of pulmonary congestion and oedema, 261

Crepitant râle of croupous pneumonia, 335

Crico-arytenoid muscles, hysterical paralysis of, 83

Cricotomy, 148, 156

Critical phenomena in croupous pneumonia, 331

Croup, false. See _Laryngismus Stridulus_.

Croupous pneumonia, 307

Cubebs, use, in chronic laryngitis, 124

Cyanosis, admixture theory of origin, 712
  congestive theory of origin, 714
  in cardiac malformation, 709
  in fibroid phthisis, 442
  in fibro-serous pleurisy, 496
  in mitral regurgitation, 671
  and congenital anomalies of the heart and great vessels, 687

Cysts, fibrinous, in cardiac thrombosis, 738
  hydatid, of lungs, number and seat, 467
  of suprarenal bodies, 949
  of the heart, 637

Cystic goitre, 978


D.

Dangers of thoracentesis, 534

Death, cause of, in angina pectoris, 760
    in croupous pneumonia, 345
    in leukæmia, 919
    in pericarditis, 783
    in pulmonary embolism, 380, 381
    in thoracentesis, 536, 537
    in valvular heart disease, 681
  mode of, in cardiac thrombosis, 732
    in Hodgkin's disease, 929

Decubitus in fibro-serous pleurisy, 495

Definition of acute miliary tuberculosis, 472
  of Addison's disease, 939
  of angina pectoris, 755
  of anæsthesia of larynx, 65
  of bronchitis, 164
  of bronchial asthma, 184
    dilatation, 227
  of brown induration of lungs, 256
  of cancer of the lung, 460
  of cardiac thrombosis, 718
  of catarrhal pneumonia, 353
  of chronic laryngitis, 121
    nasal catarrh, 42
  of collapse of the lung, 250
  of congestion and oedema of lungs, 258
  of croupous pneumonia, 307
  of dilatation of the heart, 630
  of endocarditis, 639
  of emphysema, 232
  of epistaxis, 50
  of gangrene of the lung, 301
  of hæmophilia, 931
  of hæmoptysis, 266
  of hæmothorax, 582
  of hay asthma, 210
  of Hodgkin's disease, 921
  of hydrothorax, 570
  of hyperæsthesia of the larynx, 62
  of hypertrophy of the heart, 619
  of laryngeal oedema, 112
  of leukæmia, 908
  of lymphangitis, 986
  of mediastinal tumors, 864
  of morbid growths of larynx, 128
      of trachea, 139
  of pericarditis, 169
  of perichondritis and chondritis of the larynx, 117
  of pernicious anæmia, 898
  of pleurisy, 483
  of pneumonokoniosis, 454
  of pneumothorax, 573
  of pulmonary abscess, 296
    embolism, 373
    hydatids, 466
    phthisis, 391
  of purulent pleurisy, 539
  of simple tracheitis, 133
  of spasm of the glottis in adults, 74
  of stenosis of trachea, 142
  of syphilis of the lung, 447
  of the caisson disease, 854
  of thoracic aneurism, 801

Deflected septum in chronic nasal catarrh, 44

Degenerations of heart-muscle, 609-616
  of the suprarenal bodies, 949
  of the veins, 852

Dermoid cysts of the mediastinum, 870

Delirium in croupous pneumonia, 329

Dentition, influence on causation of laryngismus stridulus, 70

Depressing influences, influence on causation of croupous pneumonia,
        315

Diagnosis of abdominal aneurism, 823
  of abscess of the lung, 299
  of acute and chronic bronchitis, 176
  of acute catarrhal laryngitis, 95
  of acute congestion of spleen, 955
  of acute miliary tuberculosis, 480
  of acute myocarditis, 606
  of acute phlebitis, 846
  of Addison's disease, 947
  of adherent pericardium, 788
  of anæsthesia of larynx, 66
  of aneurism of the coeliac axis, 842
  of angina pectoris, 757
  of aortic obstruction, 657
    regurgitation, 664
  of asthma, 198
  of atrophic emphysema, 249
  of bronchial dilatation, 230
  of cancer of the lung, 464
    of the pleura, 584
  of cardiac thrombosis, 740-744
  of catarrhal pneumonia, 365
  of chronic congestion and enlargement of the spleen, 958
    endarteritis of the coronary artery, 829
    laryngitis, 124
    myocarditis, 609
  of collapse of the lung, 254
  of coryza, 41
  of croupous pneumonia, 339
  of cyanosis, 709
  of dilatation of the heart, 634
  of echinococcus of the spleen, 969
  of embolic splenic abscess, 964
  of embolism of the coronary artery, 832
    of the superior mesenteric artery, 838
  of endocarditis, 650
  of epiglottic affections, 109-112
  of exophthalmic goitre, 763
  of fatty cardiac degeneration, 615
    infiltration of the heart, 612
  of fibroid phthisis, 443
  of functional heart disease, 749-752
  of gangrene of the lung, 304
  of hæmophilia, 937
  of hæmoptysis, 289
  of hæmothorax, 582
  of hay asthma, 221
  of hemorrhagic pleurisy, 568
  of Hodgkin's disease, 929
  of hydatids of the pleura, 585
  of hydrothorax, 572
  of hyperæsthesia and paræsthesia of the larynx, 64
  of hypertrophic lobar emphysema, 243
  of hypertrophy of the heart, 627
  of interlobular emphysema, 249
  of lardaceous spleen, 967
  of laryngeal oedema, 115
  of laryngismus stridulus, 72
  of leukæmia, 919
  of mediastinal abscess, 863
    tumors, 876
  of mitral regurgitation, 674
    stenosis, 669
  of morbid growths of the larynx, 130
    of the trachea, 141
  of paralysis of adductors of vocal cords, 83, 85
    of tensors of vocal cords, 85, 86
  of pseudo-membranous laryngitis, 103
  of pericardial effusion, 778
  of pericarditis, 776
  of pernicious anæmia, 905
  of pleurisy, 514
  of pneumonokoniosis, 459
  of pneumothorax, 580
  of pulmonary apoplexy, 294
    congestion and oedema, 262
    embolism, 387
    hydatids, 469
    phthisis, 410
    regurgitation, 677
    stenosis, 676
  of purulent pleurisy, 543
  of simple lymphangitis, 988
    tracheitis, 134
  of spasm of the glottis in adults, 75
  of stenosis of the aorta, 827
    of the trachea, 142
  of syphilis of the lungs, 453
  of thoracic aneurism, 815
  of thrombosis of the coronary artery, 832
  of tricuspid stenosis, 677

Diaphoretics, use, in laryngeal oedema, 116
    in pulmonary abscess, 264

Diaphragm, displacement of, in pleurisy, 497, 498, 507

Diaphragmatic pleurisy, 563

Diarrhoea in Hodgkin's disease, 925
  in leukæmia, 910
  in pernicious anæmia, 903
  in pulmonary phthisis, 406
    treatment, 439

Diathesis, the tubercular, 477

Diet after tracheotomy, 161
  in acute miliary tuberculosis, 481
  in Addison's disease, 948
  in bronchial asthma, 206
  in cardiac valvular disease, 683, 685
  in catarrhal pneumonia, 369, 370
  in croupous pneumonia, 348
  in collapse of the lung, 256
  in endocarditis, 651
  in fatty degeneration of the heart, 616
  in hay asthma, 224
  in pericarditis, 783
  in pernicious anæmia, 907
  in pseudo-membranous laryngitis, 108
  in simple lymphangitis, 990
  restricted, in thoracic aneurism, 817

Dietetic treatment of pulmonary phthisis, 431

Digestive disorders in functional heart disease, 749
    influence on causation of pernicious anæmia, 900

Digitalis, use, in acute myocarditis, 606
    in angina pectoris, 761
    in aortic disease, 684
    in chronic endarteritis of the coronary artery, 830
    in croupous pneumonia, 349
    in dilatation of the heart, 635
    in exophthalmic goitre, 767
    in fatty degeneration of the heart, 616
    in functional disease of the heart, 754
    in hypertrophy of the heart, 630
    in mitral disease, 685
    in pericarditis, 783
    in pulmonary congestion and oedema, 263
    in vesicular emphysema, 247, 248

Dilatation of the pulmonary artery, 833
  of the bronchial tubes, 227
  of the heart, 630
  of the trachea, 143
  of the veins, 849

Diphtheria, influence on causation of anæsthesia of the larynx, 66
      paralysis of the larynx, 80
  of the trachea, 136

Displacement of adjacent organs in pleurisy, 504
  of the heart in pneumothorax, 577

Displacements of the heart, 601-604

Disseminated form of catarrhal pneumonia, lesions, 357

Diverticular dilatation of trachea, 143

Double pleurisy, 562
  pneumonia, prognosis, 343

Drainage of pleural cavity, methods of, 552-562

Dropsy in aortic regurgitation, 661
  in mitral regurgitation, 672
  of emphysema, treatment, 247
  time of appearance in tricuspid regurgitation, 679

Drummond's oral whiff in aneurism, 812

Ductus arteriosus Botalli, defects of, in cardiac malformation, 691

Duration of anæsthesia of the larynx, 67
  of asthma, 189
  of cancer of the lungs, 463
  of cardiac thrombosis, 732
  of catarrhal pneumonia, 368
  of fibro-serous pleurisy, 511
  of Hodgkin's disease, 929
  of laryngismus stridulus, 71
  of life in cardiac malformations and cyanosis, 711
  of mediastinal abscess, 863
    tumors, 875
  of pulmonary phthisis, 424
  of stenosis of the aorta, 825
  of the caisson disease, 855
  of thoracic aneurism, 815

Durham's tracheotomy canula, 151

Dysphagia in chronic pharyngitis, 122
  in hysterical affections of the glottis, 83
  in inflammation of the epiglottis, 110
  in laryngeal oedema, 114
  in mediastinal tumors, 872, 873
  in morbid growths of larynx, 129
  in perichondritis and chondritis of the larynx, 118
  in thoracic aneurism, 806

Dysphonia in morbid growths of larynx, 129
  in perichondritis and chondritis of the larynx, 118
  in pulmonary phthisis, 408

Dyspnoea in acute catarrhal laryngitis, 94
  in Addison's disease, 941
  in angina pectoris, 756
  in aortic regurgitation, 661
  in cardiac thrombosis, 730
  in catarrhal pneumonia, 359, 360, 363
  in chronic pharyngitis, 122
  in croupous pneumonia, 321
  in cyanosis and cardiac malformation, 710
  in dilatation of trachea, 144
  in fatty infiltration of the heart, 612
  in fibro-serous pleurisy, 493, 495
  in Hodgkin's disease, 925
  in hydatids of pleura, 585
  in hydrothorax, 571
  in hypertrophy of the heart, 626
  in laryngeal oedema, 114
  in leukæmia, 913
  in mediastinal tumors, 872
  in mitral regurgitation, 671
    stenosis, 667
  in morbid growths of the larynx, 129
  in paralysis of abductors of vocal cords, 88
  in pernicious anæmia, 903
  in pneumothorax, 578
  in pulmonary embolism, 379-381
  in stenosis of the trachea, 143
  in thoracic aneurism, 805


E.

Echinococcus of the spleen, 968

Effects of cardiac hypertrophy, 626
  of pulmonary embolism, 383

Effusions, characters, in purulent pleurisy, 540, 541
  of fibro-serous pleurisy, 487-491
  of pericarditis, 772

Elaterium, use, in hydrothorax, 572

Electric illuminator, use, in laryngoscopy, 24

Electricity, use, in anæsthesia of the larynx, 68
    in angina pectoris, 761
    in bronchial asthma, 205
    in paralysis of the larynx, 90

Electrolysis, use, in goitre, 980
    in thoracic aneurism, 819

Embolic abscess of the spleen, 963

Embolism and thrombosis of coronary artery, 831
    of pulmonary artery, 835
  complicating cardiac thrombosis, 733
  from aortic obstruction, 656
  influence on causation of gangrene of the lung, 302
  of inferior mesenteric artery, 839
  of pulmonary artery distinguished from asthma, 200
  of superior mesenteric artery, 836
  relation to acute myocarditis, 604
  symptoms of, in endocarditis, 647

Emetics, use, in acute catarrhal laryngitis, 97
    in catarrhal pneumonia, 371
    in collapse of the lung, 255
    in pulmonary congestion, 263
    in pseudo-membranous laryngitis, 106

EMPHYSEMA, 232
  Definition and history, 232
  Varieties, 232
    _Interlobular or Extra-vesicular Emphysema_, 249
    _Vesicular Emphysema_, 232
      Acute lobular form, 232
        Symptoms and treatment, 233
      Atrophic lobar form, 248
        Symptoms and treatment, 248, 249
      Chronic lobular form, 233
      Hypertrophic lobar form, 233
        Complications, 239
        Diagnosis, 243
        Duration, 242
        Etiology, 234
          Changes in alveolar wall, influence on causation, 234
          Expiratory and inspiratory theories of causation, 235, 236
          Heredity, influence on causation, 234
        Morbid anatomy, 242
        Prognosis, 244
        Symptoms, 236
          Cough and dyspnoea, 236
          Chest, shape of, 237
          Physical signs, 236-238
          Respiration, peculiarities of, 238
        Treatment, 245
          Cod-liver oil, use, 245
          Compressed air, use, 245, 246
          Digitalis, use, 247
          Expectorants, use, 246
          Expiration into expired air, 246
          Iron, use, 245
          Potassium, iodide, 246
          Quinia hydrobromate, hypodermatically, 247
          Strychnia, use, 245

Emphysema after tracheotomy, 162
  distinguished from asthma, 198
  following asthma, 189

Empyema, pulsating, 596
    See _Pleurisy, Purulent_.

Enchondroma of the mediastinum, 871

Encysted pleurisies, 545, 546

Endarteritis, obliterating, of the coronary artery, 830
  of the pulmonary artery, 833
  of the superior mesenteric artery, 839

ENDOCARDITIS, 639
  Definition, 639
  Diagnosis, 649
    From aortitis, 650
    From pericarditis, 649
  Etiology, 645
    Acute and chronic Bright's disease, 646
    Acute rheumatism, 645, 646
    Pyæmia, puerperal fever, the specific fevers, etc., 646
  History, 639
  Morbid anatomy, 640-645
    Of acute exudative form, 640
    Of interstitial form, 643
    Of ulcerative form, 642
  Prognosis, 650
  Symptoms, 646
    Dyspnoea, 647
    Mitral murmurs, frequency and characters of, 648
    Of exudative form, 647
    Of interstitial form, 647
    Of ulcerative form, 647
    Pain in, 647
    Physical signs, 648, 649
    Physiognomy, 647
    Pulse, characters, 647
    Tricuspid and aortic murmurs, characters, 649
  Treatment, 650
    Iron, use, 651
    Opium, use, 651
    Rest, value, 651
    Stimulants, use, 651

Endocarditis, influence on causation of cardiac thrombosis, 725
  ulcerative, influence on causation of splenic infarction, 961

Engorgement stage of croupous pneumonia, 308

Enlargement of the spleen, chronic, 951, 956
    in lardaceous disease, 967
    in syphilis, 971

Epigastric pulsation in mitral disease, 672
  in tricuspid disease, 679

Epiglottis, erosion of, 110
    treatment, 111
  inflammation of, 109, 110
  ulceration of, 111
    symptoms and treatment, 112

Epistaxis, 50-52
  in croupous pneumonia, 331

Ergot, use, in epistaxis, 51
    in embolism of superior mesenteric artery, 839
    in hæmophilia, 938
    in hæmoptysis, 291
    in morbid growths of larynx, 131

Ergotin, use, in aneurism, 816
    in exophthalmic goitre, 766
    in hæmoptysis of heart disease, 685
    in hæmothorax, 583
    in pulmonary phthisis, 437

Erosion of epiglottis, 110

Eruptive fevers, influence on causation of pericarditis, 771
      of pleurisy, 493

Erysipelas of the trachea, 136

Ether, use, in pneumothorax, 582

Etiology of acute catarrhal laryngitis, 93
    miliary tuberculosis, 473
    splenic congestion, 953
  of Addison's disease, 939
  of anæsthesia of the larynx, 65
  of aneurism of the coeliac axis, 841
    of the coronary artery, 830
    thoracic, 802, 803
  of aortic obstruction, 655
    regurgitation, 660
  of asthma, 190
  of atheroma of the aorta, 800
  of atrophic lobar emphysema, 252
  of bronchial dilatation, 227
  of bronchitis, 164
  of brown induration of the lungs, 256
  of cancer of the lungs, 460
  of cardiac malformation, 694
      thrombosis, 721
  of catarrhal pneumonia, 353
  of chronic congestion and enlargement of spleen, 956
      endarteritis of the coronary artery, 828
      laryngitis, 121
  of collapse of the lung, 250
  of congestion and oedema of the lungs, 258
  of croupous pneumonia, 324
  of dilatation of the heart, 631
    of the veins, 849
  of embolism of the coronary artery, 831
  of emphysema, 234
  of endocarditis, 645
  of epistaxis, 50
  of exophthalmic goitre, 764
  of fatty degeneration of the heart, 612
  of fibroid phthisis, 440
  of fibro-serous pleurisy, 491
  of functional heart disease, 752
  of gangrene of the lung, 301
  of goitre, 976
  of hæmophilia, 932
  of hæmoptysis, 272
  of hæmothorax, 582
  of hay asthma, 212
  of hemorrhagic pleurisy, 565
  of Hodgkin's disease, 922
  of hydrothorax, 570
  of hyperæsthesia of the larynx, 62
  of hypertrophy of the heart, 619
  of hysterical affections of the glottis, 83
  of lardaceous spleen, 966
  of laryngeal oedema, 113
  of laryngismus stridulus, 70
  of leukæmia, 909
  of lymphangitis, 986
  of mediastinal abscess, 861
    tumors, 871
  of mitral regurgitation, 671
    stenosis, 666
  of morbid growths of the larynx, 127
      of the trachea, 139
  of paræsthesia of the larynx, 63
  of paralysis of abductors of vocal cords, 87
    of adductors of vocal cords, 81
    of constrictors of larynx, 80
    of tensors of vocal cords, 85, 86
    of the whole larynx, 79
  of pericarditis, 769
  of perichondritis and chondritis of larynx, 117
  of perisplenitis, 965
  of pernicious anæmia, 899
  of pneumonokoniosis, 454
  of pneumothorax, 573
  of pseudo-membranous laryngitis, 101
  of pulmonary abscess, 296
    apoplexy, 293
    embolism, 374
    hydatids, 466
    phthisis, 394
    stenosis, 675
  of purulent pleurisy, 539
  of spasm of the glottis in adults, 74
  of stenosis of the aorta, 826
    of the trachea, 142
  of syphilis of the lung, 447
  of the caisson disease, 857
  of tricuspid regurgitation, 678

Eucalyptol, use, in bronchial dilatation, 231

Evil effects of goitre, 979

Exciting causes of asthma, 191
    of bronchitis, 168
    of gangrene of the lung, 302
    of hay asthma, 214

Excision of the spleen, 960
  of the sternum in mediastinal abscess, 863
  of the thyroid gland, 981

Exercise, importance, in pulmonary phthisis, 432, 433
  in chronic bronchitis, 183

EXOPHTHALMIC GOITRE (Graves' Disease; Basedow's Disease), 761
  Definition, 761
  Diagnosis, 763
  Etiology, 764
  Morbid anatomy, 764
  Prognosis, 765
  Symptoms, 762
    Dyspnoea, 763
    Digestive disorders, 763
    Eyeball, protuberance of, 762
    Increased heart-action, 762
    Thyroid body, enlargement of, 762
  Treatment, 765
    Aconite, use, 766
    Digitalis, use, 767
    Ergot, hypodermically, 766
    Ice-bag to præcordiæ, 767
    Iron, use, 766, 767
    Iodine, use, 766
    Hydropathic packing and the needle-bath, 766
    Galvanization, 767
    Of exophthalmia, 766
    Opiates, use, 766

Expectorants, use, in bronchitis, 179
    in simple tracheitis, 135
    in pulmonary phthisis, 436

Expectoration, albuminoid, following thoracentesis, 535
  characters in, in acute catarrhal laryngitis, 79
    in asthma, 188
    in bronchial dilatation, 228
    in capillary bronchitis, 171
    in catarrhal pneumonia, 359-361
    in croupous pneumonia, 322
    in chronic bronchitis, 174
    in fibroid phthisis, 441

Expectorations, characters in fibro-serous pleurisy, 496
    in gangrene of the lung, 303
    in pulmonary congestion and oedema, 260
    in pulmonary phthisis, 401
    in simple tracheitis, 133, 134
  of acephalocysts in pulmonary hydatids, 469

Expiratory movement in asthmatic paroxysm, 186
  theory of origin of emphysema, 235

Exploratory puncture in mediastinal abscess, 863
    value, in diagnosis of pleurisy, 518
        of purulent pleurisy, 543, 548

Extra-pulmonary hæmoptysis, 285

Exudations of fibro-serous pleurisy, characters, 486

Exudative endocarditis, acute, 640

Eyeball, protuberance of, in exophthalmic goitre, 640


F.

Faintings in Addison's disease, 941

False membranes of true croup, nature, 100
    seat and character, in purulent pleurisy, 541

Fatality of Addison's disease, 941

Fatty degeneration of the heart, 612
    of the veins, 852
  infiltration of the heart, 611

Fevers, influence on causation of dilatation of the heart, 632

Fibroid heart, 607
  phthisis, influence on causation of bronchial dilatation, 228

Fibroma of nasal passages, 55

Fibromata of trachea, frequency, 140

Fibro-serous pleurisy, 484

Fibrous goitre, 977

Fistula, aërial, following tracheotomy, 163
  in phthisical persons, treatment of, 439

Fistulæ, pleuro-bronchial, seat and characters in purulent pleurisy,
        542

Fistules, pericardial, 796

Flatness, level of, pleuritic effusions, 487, 491, 500

Fluctuation in pulmonary hydatids, 468

Flush of pneumonia, 328

Follicular goitre, 977
  and fibrous goitre, treatment, 979, 980

Fomentations, use, in phlebitis, 846

Fragility of pulmonary vessels as a cause of hæmoptysis, 275

Frémissement in pulmonary hydatids, 468
  cataire in thoracic aneurism, 808

Friction sounds in fibro-serous pleurisy, 507-509
    in pericarditis, 775, 777

Functional heart disorders, 747


G.

Gallic acid, use, in epistaxis, 51
    in hæmoptysis, 291

Gangrene of the lung, 301
    influence on causation of pneumothorax, 575
    complicating catarrhal pneumonia, 364
  termination of croupous pneumonia in, 332

Gastric pneumonia, 334

Gastro-intestinal canal, lesions, in catarrhal pneumonia, 358
    in croupous pneumonia, 313
    in Hodgkin's disease, 928
    in leukæmia, 917
    in pernicious anæmia, 904
  disorders in abdominal aneurism, 821
    in Addison's disease, 941
    in catarrhal pneumonia, 360, 362
    in croupous pneumonia, 330
    in endocarditis putrida, 647
    in functional heart disease, 749
    in Hodgkin's disease, 925
    in leukæmia, 910
    in mitral regurgitation, 671
    in pernicious anæmia, 903
    in pulmonary phthisis, 406
    in tricuspid regurgitation, 679

Galvanism, use, in Addison's disease, 948

Galvanization, use, in exophthalmic goitre, 767

Galvano-cautery knife, use, in tracheotomy, 150
  snare, use, for removing nasal growths, 56
  use, for removal of nasal hypertrophies in hay asthma, 224
  in chronic nasal catarrh, 44, 45, 47, 48, 50
  in epistaxis, 51

Gelatinous goitre, 978
    treatment, 981

General diseases, influence on causation of phthisis, 396

Geographical distribution of goitre, 975
    of hay asthma, 218

Gestation, influence on causation of goitre, 977

Giddiness in Addison's disease, 941

Glacier- and ice-water, influence on causation of goitre, 976

Glands, bronchial lesions of, in bronchitis, 175

Glottis, hysterical affections of, 83
  spasm of, in adults, 74, 75

GOITRE, 974
  Definition, 974
  Etiology, 976
    Atmospheric causes, 977
    Gestation and syphilis, influence on causation, 977
    Glacier- and ice-water, influence on causation, 976
  Geographical distribution, 975
  Symptoms, 974
  Treatment, 979
    Electrolysis, use, 980
    Ergot, use, 980
    Excision of gland, 982
    Injections, use, 989, 981
    Iodides of lead and mercury, locally, 980
    Iodine, use, 979-981
    Iodoform, use, 979
        local, 979
    Natural mineral waters, use, 980
    Of follicular and fibrous form, 979
    Of gelatinoid or cystic form, 981
    Of vascular form, 980
    Syrup of iodide of iron, 979-981
    Tincture of iron, injections, 981
  Varieties, 977

Goitre, exophthalmic, 761

Gold, chloride of, use, in epiglottic erosion and ulceration, 111, 112

Gout, influence on causation of aortic regurgitation, 660
    of thoracic aneurism, 803

Granulations, exuberant, complicating tracheotomy, 162

Grave form of pulmonary embolism, 380

Graves' disease. See _Exophthalmic Goitre_.

Great vessels, malformations of, 690

Gray hepatization stage of croupous pneumonia, lesions, 310

Gummy tumors of the spleen, 971

Gummata of the lung, 449, 450


H.

Hæmatemesis, distinguished from hæmoptysis, 289

Hæmopericardium, 788, 789

HÆMOPHILIA, 931
  Classification, synonyms, and history, 932
  Definition, 931
  Diagnosis, 937
  Etiology, 932
    Age and sex, influence on causation, 933
    Heredity, causation, 932
  Morbid anatomy, 936
  Pathology, 936
  Prognosis, 938
  Symptoms, 934-936
    Blood in, 936
    External bleedings, seat, 935
    Interstitial bleedings, seat and characters, 935
    Joints, affections of, 935, 936
  Treatment, 938
    Diet, 938
    Ergot and iron, use, 938
    Prophylaxis, 938

HÆMOPTYSIS, 266
  Definition, 266
  Diagnosis, 289
    From hæmatemesis, 289
  Etiology, 272
    Age, influence on causation, 275
    Bacillus tuberculosis, relation of, to, 279, 280
    Catarrhal predisposition, influence on causation, 275
    Exciting causes, 278
    Fragility of blood-vessels, influence on causation, 275
    Heredity, influence on causation, 272-275
    Injury, influence on causation, 279
    Pregnancy, influence on causation, 278
    Sex, influence on causation, 276
    Season, climate, etc., influence on causation, 277, 278
  History, 266-272
  Mortality, 290
  Pathology and morbid anatomy, 286
    Aneurisms of pulmonary artery, appearance of, 287
    Heart, changes in, 288
    Of cardiac hæmoptysis, 288
    Of pulmonary infarction, 288
    Seat of, and changes in hemorrhages, 288
  Prognosis, 290
  Synonyms, 266
  Symptoms, 281
    Frequency of attacks, 284
    Of aortic aneurism discharging into air-passages, 285
    Of cavernous form, 284
    Of extra-pulmonary form, 285
    Of hemorrhagic infarction and cardiac form, 285, 286
    Of simple, congestive, and ulcerative forms, 283, 284
    Physical signs, 282
  Treatment, 291, 292
    Absolute quiet, necessity of, 291
    Astringent inhalations, 291
    Ergot and turpentine, use, 291
    Gallic acid, use, 291
    Ice, use, 291
    Ipecacuanha, use, 292
    Opium, use, 291, 292
    Quinia for fever following, 292

Hæmoptysis in hypertrophy of the heart, 627
  in pulmonary phthisis, 401
  influence on causation of pulmonary phthisis, 395

HÆMOTHORAX, 582
  Etiology and pathology, 582
  Symptoms, 582
  Treatment, 583

HAY ASTHMA, 210
  Classification, 221
  Definition, 210
  Diagnosis, 221
  Etiology, 212
    Age, sex, and heredity, influence on causation, 212, 213
    Certain plants and grasses, 215, 216
    Dust and animal parasites, 216
    Exciting causes, 214
    Heat and dryness, 214, 215
    Occupation and temperament, 213, 214
    Pollen theory of origin, 216-218
    Predisposing causes, 212
  Geographical distribution, 218
  History, 210
  Prognosis, 222
  Symptoms and course, 218-221
  Treatment, 222
    Diet, 224
    Climate, change of, 224
    Galvanism, 224
    Nasal hypertrophies, removal of, 224, 225
    Nasal injections, use, 224
    Quinia, use, 224

Headache and vertigo in mitral regurgitation, 672
  in acute congestion of spleen, 954
  in croupous pneumonia, 329
  in Hodgkin's disease, 925
  in leukæmia, 911

Head-reflector, use in laryngoscopy, 22

Heart and circulation, effect of asthmatic paroxysm upon, 188

HEART AND GREAT VESSELS, MALFORMATIONS OF, 687
  Diagnosis, 709
  Duration of life in, 709
  Etiology, 692
    Defects of arterial outlet of right ventricle, the most frequent
        primary cause, 694
    Narrowing of pulmonary artery and patency of septum ventriculorum,
        theories of origin of, 697-702
    Development of foetal heart, relation to course, 698, 700
    Malformation affecting primarily left side, 707-709
    Narrowing of aortic trunk, 708
    Stenosis of the conus, 708
    Affecting primarily the right side, 702-706
    Of conus arteriosus dexter, with open ventricular septum, 703
    Of pulmonary artery, combined stenosis, and atresia of, 706
    Of pulmonary artery, closure of, with perfect ventricular septum,
        702
    Of pulmonary artery, stenosis of, with open ventricular septum, 706
  Symptoms, 709
    Clubbing of fingers and toes, 711
    Cyanosis, 709
    Dyspnoea and cough, 710
    Physical signs, 710
    Temperature in, 710

Heart and lung, disease, influence on causation of pulmonary embolism,
        375
  aneurism of, 636
  atrophy of, 618
  cancer of, 637
  changes in, in emphysema, 240
  clot, as a cause of death in croupous pneumonia, 343
  condition of, in hæmoptysis, 288
  cysts of, 637

HEART, DILATATION OF, 630
  Definition, 630
  Diagnosis, 634
  Etiology, 631
  Morbid anatomy, 633
  Prognosis, 635
  Symptoms, 634
  Treatment, 635
    Caffeine, use, 635
    Convallaria, use, 635
    Digitalis, use, 635
    Rest, value of, 635

Heart disease, death from, following thoracentesis, 536
    displacements of heart from, 602
    influence on causation of congestion of the lungs, 258
    influence on causation of hydrothorax, 570
  diseases of the substance of, 601

HEART, DISPLACEMENTS OF, 602
    From abdominal disease, 604
    From changes in chest-wall, 602
    From cirrhosis of lung, 603
    From disease of pleura, 498, 504, 603
    From heart disease, 602
    From mediastinal tumors, 603
    From pericardial effusions, 602
    In pneumothorax, 577

HEART, FATTY DEGENERATION OF, 612
  Diagnosis and prognosis, 615
  Etiology, 612
    Age and sex, influence on causation, 613
    Cardiac hypertrophy, influence on causation, 613
    Mineral and alcoholic poisoning, 612
  Morbid anatomy, 613, 614
  Symptoms, 614
    Physical signs, 615
    Pulse in, 615
  Treatment, 616
    Amyl nitrite, use, 616
    Digitalis, use, 616
    Iron and vegetable tonics, 616

HEART, FATTY INFILTRATION OF, 611
  Diagnosis, 612
  Etiology, 611
  Symptoms and treatment, 612

HEART, FUNCTIONAL DISORDERS OF, 747
  Diagnosis, 749
  Etiology, 750
  Morbid anatomy, 752
  Prognosis, 753
  Symptoms, 748
    Cerebral disturbances, 749
    Digestive disturbances, 749
    Infrequency of intermittence of heart's action, 748
    Palpitation, 747
    Paroxysms, characters, and frequency of, 748
  Treatment, 753
    Aconite, use, 754
    Alcohol, use, 755
    Antispasmodics, use, 753, 754
    Digitalis, use, 754
    Opium and morphia, use, 754
    Preventive, 754
    Tonics, chalybeate, use, 754

HEART, HYPERTROPHY OF, 619
  Definition, 619
  Diagnosis, 627
  Etiology, 619
    Disturbed innervation, influence on causation, 619
    Kidney disease, 621
    Mechanical causes, 620
  Morbid anatomy, 624
  Prognosis, 629
  Symptoms, 624
    Dyspnoea, 626, 627
    Physical signs, 625-627
    Pulse, characters, 625, 627
    Sensation, uneasy cardiac, 626, 627
  Treatment, 630
    Digitalis, use, 630
    Sedatives, use, 630
  Varieties, 619

Heart, lesions of, in Hodgkin's disease, 928
    in interstitial endocarditis, 644, 645
    in pernicious anæmia, 904
  malpositions of, 601
  murmur, cause of, in pleurisy, 510
  muscle, amyloid degeneration of, 616
    anæmic necrosis of, 610
    brown atrophy of, 616
    calcareous degeneration of, 616
    degenerations of, 609-616
    hyaline degeneration of, 616
    parenchymatous degenerations of, 610
  neuroses of, 747
  normal positions of, 601, 602
  palpitation of. See _Heart, Functional Disorders of._
  parasites of, 637
  rupture of, spontaneous, 617

Heart's action, increase of, in exophthalmic goitre, 762
    mechanism of, 652

Heart, sarcoma of, 637
  sounds, in adherent pericardium, 788
    in pericarditis, 776
  syphilis of, 637
  tubercle of, 637

HEART, VALVULAR DISEASES OF, AND CARDIAC MURMURS, 651
    Definition, 651
    History, 651
    Murmurs, 654
  _Aortic Obstruction or Stenosis_, 654
    Diagnosis, 657
    Etiology, 655
    Morbid anatomy, 654
    Symptoms, 656
      Cerebral anæmia, 656
      Cerebral and other embolisms, 656
      Murmurs, characters, 657
      Physical signs, 657
      Pulse, characters, 657
  _Aortic Regurgitation or Insufficiency_, 659
    Diagnosis, 664
    Etiology, 659
    Morbid anatomy, 659
    Symptoms, 659
      Carotid pulsation, 661, 662
      Pain, characters, 661
      Physical signs, 662
      Pulse, characters, 661
  _Mitral Regurgitation_, 669
    Diagnosis, 674
    Etiology, 671
    Morbid anatomy, 669
    Symptoms, 671
      Cough and expectoration, 671
      Cyanosis and physiognomy, 671
      Digestive disorders, 671
      Dropsy, occurrence of, 672
      Headache, vertigo, etc., 672
      Murmurs, seat and characters, 673
      Physical signs, 672
      Pulse, characters, 672
  _Mitral Stenosis_, 665
    Diagnosis, 669
    Etiology, 666
    Morbid anatomy, 665
    Symptoms, 667
      Hæmoptysis, 667
      Murmurs, characters, 668
      Pain, 667
      Physical signs, 668
      Pulmonary congestion, cough, etc., 667
      Pulse, characters, 667
      Purring thrill, significance, 668
  _Pulmonary Obstruction_, 674
    Diagnosis, 676
    Etiology, 675
    Morbid anatomy, 675
    Symptoms and physical signs, 675
  _Pulmonary Regurgitation_, 676
    Physical signs, 677
  _Tricuspid Regurgitation_, 677
    Diagnosis, 680
    Etiology, 678
    Morbid anatomy, 678
    Symptoms, 679
      Cerebral hyperæmia, 679
      Jugular and epigastric pulsation, 679
      Physical signs, 679
  Prognosis in valvular heart disease, 680-683
  Treatment, 683
    Arsenic, use, 684, 685
    Calomel and jalap, use, 685
    Diet in, 683-686
    Digitalis, use, 684, 685
    Ergotin, 685, 686
    Hygienic, 683, 684, 686
    Iron, use, 684, 685
    Nitrate of amyl, use, 684, 686
    Of aortic disease, 683, 684
    Of dropsy, 684, 685
    Of hæmoptysis, 685
    Of mitral disease, 685
    Of tricuspid disease, 686
    Opium and morphia, use, 684, 686
    Quinia and strychnia, use, 684, 685
    Rest, value, 683
    Squill, juniper and cream of tartar, use, 685

Heat and dryness, influence on causation of hay asthma, 214
  use, in laryngismus stridulus, 73

Hemorrhage and congestion in pulmonary embolism, 384
  during and after tracheotomy, 158, 162
  in croupous pneumonia, 331
  influence on causation of anæmia, 887
  intestinal, in embolism of the superior mesenteric artery, 837
  seat, in hæmoptysis, 287

Hemorrhages in Addison's disease, 940
  in leukæmia, 913
  in pernicious anæmia, 903
  in pulmonary phthisis, 401, 402
  interstitial, of hæmophilia, 935
  seat and amount, in hæmophilia, 935

Hemorrhagic infarction of spleen, 960
  pleurisy, 565

Hemorrhoids from obstruction of portal vein, 850

Hepatic artery, aneurism of, 840

Hepatization of croupous pneumonia, lesions, 309

Heredity, influence on causation of acute catarrhal laryngitis, 93
      of asthma, 190
      of emphysema, 234
      of epistaxis, 50
      of hæmophilia, 934
      of hæmoptysis, 272-275
      of hay asthma, 212
      of Hodgkin's disease, 922
      of pulmonary phthisis, 395
    on prognosis of phthisis, 423

Hernia of trachea, 143

Herpetic eruptions of croupous pneumonia, 328

Hiccough in goitre, 979

History of Addison's disease, 939
  of bronchial asthma, 184
      dilatation, 227
  of bronchitis, 164
  of brown induration of the lungs, 256
  of cardiac murmurs, 651
      thrombosis, 719
  of collapse of the lung, 252
  of congestion and oedema of the lungs, 258
  of croupous pneumonia, 307
  of cyanosis and cardiac malformations, 687
  of emphysema, 232
  of endocarditis, 639
  of gangrene of the lung, 301
  of hæmophilia, 932
  of hæmoptysis, 266
  of hay asthma, 210
  of Hodgkin's disease, 922
  of hydrothorax, 570
  of the laryngoscope, 19
  of leukæmia, 908
  of pernicious anæmia, 898
  of pleurisy, 483
  of pneumonokoniosis, 454
  of pneumothorax, 573
  of pulmonary abscess, 296
      embolism, 373
      hydatids, 466
      phthisis, 392, 394
  of purulent pleurisy, 539
  of the rhinoscope, 21
  of syphilis of the lung, 447

Hoarseness in acute laryngitis, 94

HODGKIN'S DISEASE, 921
  Course, duration, and termination, 929
  Definition and synonyms, 921
  Diagnosis, 929
  Etiology, 922
  Morbid anatomy, 926
    Lymph-glands, lesions, 926, 927
    Spleen, lesions, 927
  Pathology and prognosis, 930
  Symptoms, 923
    Blood and circulation, changes in, 924
    Digestive disorders, 925
    Genito-urinary system, changes in, 925
    Hæmic murmurs in, 925
    Lymphatic glands, enlargement of, seat and characters, 923
    Skin, changes in, 925
    Special senses, modifications of, 925
    Spleen, enlargement of, 925
    Respiratory system, disorders, 925
  Treatment, 931
    Arsenic, use, 931
    Local, 931
    Iodine and potassium iodide, use, 931
    Phosphorus, use, 931
    Quinia, iron, and cod-liver oil, use, 931

Hoffmann's anodyne, use, in functional heart disease, 753

Hyaline degeneration of heart-muscle, 616

Hydatids of the pleura, 585
  pulmonary, 466

Hydropathic packing in exophthalmic goitre, 766

Hydropericardium, 789, 790

HYDROTHORAX, 570
  Diagnosis and prognosis, 572
  Definition, etiology, and history, 570
  Pathological anatomy and symptoms, 571
  Treatment, 572

Hygienic treatment of croupous pneumonia, 347
    of pernicious anæmia, 907
    of pleurisy, 519
    of valvular heart disease, 683-685

Hyoscyamia, use, in catarrhal pneumonia, 372

Hyoscyamus, use, in acute catarrhal laryngitis, 98

Hyperæsthesia of larynx, 62

Hyperplasia of cytogenic tissues, relation to increase of white
        blood-corpuscles, 893
  of spleen, lymph-glands, and bone-marrow, influence on causation of
        anæmia, 890, 891

Hypertrophic lobar emphysema, 233
  nasal catarrh, 44

Hypertrophy of auricles of the heart, 627
  of erectile tissue in chronic nasal catarrh, 44
  of the heart, 619

Hypophosphites, use, in acute miliary tuberculosis, 481
    in emphysema, 245
    in phthisis, 435

Hypostatic pneumonia. See _Lungs, Congestion and Oedema of_.

Hysteria, influence on causation of paræsthesia of the larynx, 64

Hysterical affections of the glottis, 83


I.

Ice, use, in acute catarrhal laryngitis, 97
    in laryngeal oedema, 117
    in pericarditis, 783
    in pseudo-membranous laryngitis, 104

Iceland, frequency of hydatid disease in, 466

Idiosyncrasy, influence on causation of cardiac functional disease, 752

Image, the laryngeal, 30
  the rhinoscopic, 39

Impulse, cardiac, in adherent pericardium, 787
    in aortic obstruction, 657
        regurgitation, 662
    in mitral regurgitation, 672
        stenosis, 668
    in pericarditis, 774
    in tricuspid regurgitation, 679
  in dilatation of the heart, 634
  in hypertrophy of the heart, 625, 627

Inanition, influence on causation of anæmia, 889

Incipient phthisis, diagnosis of, 411

Indications for paracentesis of the pericardium, 794
  for thoracentesis, 521
  for tracheotomy, 145

Infarction, hemorrhagic, of lungs, symptoms, 286
    of spleen, 960
  pulmonary, lesions of, 288
  in pulmonary embolism, characters and seat, 384

Infectious fevers, influence on causation of acute interstitial
        myocarditis, 605

Inferior mesenteric artery, diseases of, 839
  tracheotomy, 148, 155

Inflammation of the epiglottis, 109
  of the mediastinum, 861
  of suprarenal capsules, 949
  of the veins, 843

Inflammatory theory of origin of cardiac malformations, 692

Inflation of lung in atelectasis, 253, 254

Infrequency of heart's action in functional disease, 748

Inhalations, astringent, in hæmoptysis, 291
  in chronic bronchitis, 182
  in fibroid phthisis, 444
  in pseudo-membranous laryngitis, 106
  in simple tracheitis, 135
  in ulcer of trachea, 139

Injections, use, in chronic enlargement of the spleen, 960
  in echinococcus of the spleen, 970
  in goitre, 980, 981
  into pericardial sac, 795
  into pleural cavity in purulent pleurisy, 551, 553, 562
  of arsenic into spleen in leukæmia, 921
  of tubercular cavities, 439, 440

Injury, influence on causation of hæmoptysis, 279
      of paralysis of the larynx, 79

Innervation, disturbed, influence on causation of hypertrophy of the
        heart, 619

Innominate aneurism, localization of, 812

Inoculability of tuberculous disease, 397

Inspection in bronchitis, 163
  in cardiac malformations, 710
      thrombosis, 729
      valvular disease, 657, 662, 668, 672, 675, 677, 679
  in catarrhal pneumonia, 360, 361
  in croupous pneumonia, 335, 336, 338
  in endocarditis, 648
  in fibro-serous pleurisy, 497, 498
  in hypertrophy of the heart, 625, 627
  in mediastinal abscess, 862
      tumors, 874
  in pericarditis, 774
  in pneumothorax, 578
  in thoracic aneurism, 807

Inspiratory and expiratory theories of origin of emphysema, 235

Instruments necessary in tracheotomy, 149

Insufficiency, aortic, 659

Insufflator, use, in chronic laryngitis, 126

Intercostal spaces, bulging of, in pleuritic effusion, 497, 498, 507

Interlobular emphysema, 249
  pleurisy, 564

Intermittence of heart's action, 748

Intermittent pneumonia, 334

Interstitial endocarditis, 643
  myocarditis, acute, 605
  pneumonia, chronic, 391, 440

Iodine, locally, in acute congestion of the spleen, 956
    in chronic congestion and enlargement of the spleen, 960
        inflammation of the epiglottis, 110
        laryngitis, 126
    in exophthalmic goitre, 766
    in pulmonary phthisis, 435
  injection of, in goitre, 980, 981
  internal use, in goitre, 979, 980
  test for lardaceous spleen, 968
  use, in Hodgkin's disease, 931

Iodoform, use, in chronic epiglottic inflammation, 110
    in chronic laryngitis, 125

Ipecacuanha, use, in acute catarrhal laryngitis, 98
    in bronchitis, 180
    in hæmoptysis, 292
    in laryngismus stridulus, 73

Iron, perchloride, injection of, in goitre, 981
  pernitrate, use, in epiglottic ulceration, 112
  syrup of the iodide of, use, in goitre, 979
  use, in Addison's disease, 948
    in anæsthesia of the larynx, 68
    in angina pectoris, 761
    in chlorosis, 896
    in chronic congestion of the spleen, 960
    in dilatation of the heart, 636
    in endocarditis, 651
    in exophthalmic goitre, 766, 767
    in fatty degeneration of the heart, 616
    in functional heart disease, 755
    in hæmophilia, 938
    in paralysis of the larynx, 91
    in passive pulmonary congestion, 263, 264
    in pernicious anæmia, 907
    in pulmonary phthisis, 436
    in valvular heart disease, 684, 685
    in vesicular emphysema, 245

Irregular cardiac action in fatty degeneration, 615

Irritable heart, 747

Irritants, influence on causation of pseudo-membranous croup, 101
  to pulmonary tissue, influence on causation of phthisis, 394

Ischæmia of the heart, influence on causation of angina pectoris, 758

Itching of skin and mucous membranes in hay asthma, 220, 221


J.

Jaborandi, local use, in chronic laryngitis, 125
  use, in fibro-serous pleurisy, 520, 521
    in laryngeal oedema, 116

Jacquemet on causes of death in pulmonary embolism, 381

Jarvis' snare for removal of nasal polypi, 54

Jaundice in mitral regurgitation, 671

Joint affections of hæmophilia, 935

Joints, lesions of, in hæmophilia, 936

Jugular pulsation in tricuspid regurgitation, 679


K.

Kidney disease, influence on causation of cardiac hypertrophy, 621
      of pleurisy, 493
      of pulmonary embolism, 375

Kidneys, lesions, in Hodgkin's disease, 928
    in leukæmia, 918
    in pernicious anæmia, 905
  state of, in pseudo-membranous laryngitis, 102


L.

Lactic acid, use, in pseudo-membranous laryngitis, 106

Lardaceous spleen, 966

Laryngeal image, the, 30-33

Laryngectomy in morbid growths of the larynx, 131

LARYNGITIS, ACUTE CATARRHAL (False Croup), 92
  Diagnosis, 95
    From diphtheritic laryngitis, 95
    From membranous croup, 95
    From tubercular laryngitis, 95
  Duration, 94
  Etiology, 93
  Pathology, 92
  Prognosis, 96
  Symptoms, 93
  Treatment, 96
    Alkalies in, 97
    Apomorphia in, 97, 98
    Baths, cold and sea, in, 96
    Emetics in, 98
    Ice in, 97
    Inhalations in, 97
    Narcotics in, 98
    Of oedema of glottis in, 98
    Potassium chlorate in, 91
      iodide in, 97
    Silver nitrate in, 97, 99

LARYNGITIS, CHRONIC, 121
  Definition, etiology, and synonyms, 121
  Diagnosis, 123
  Morbid anatomy, 122
  Prognosis, 124
  Symptoms, 121
  Treatment, 124
    Ammonium chloride, use, 124
    Anodynes, 127
    Arsenic and cod-liver oil, use, 125
    Cocaine, use, 127
    Cubebs, use, 124
    Inhalations, use, 126
    Insufflations, use, 126
    Iodoform, use, 125
    Respirators, use, 126
    Tar, use, 125, 126
    Tracheotomy in, 127

Laryngitis, chronic tubercular, 123
    syphilitic, 123
  complicating pulmonary phthisis, 403

LARYNGITIS, PSEUDO-MEMBRANOUS, 100
  Complications, 103
    Contagiousness, 101
  Diagnosis, 103
    From catarrhal laryngitis, 104
    From general oedema of glottis, 104
  Etiology, 101
  Mortality, 103
  Pathology, 100
  Prognosis, 103
  Symptoms, 101
  Treatment, 104
    Alkalies in, 105
    Diet in, 107
    Emetics in, 106
    Ice in, 104
    Inhalations in, 106
    Lactic acid in, 106
    Massage of larynx, 107
    Mercury in, 104
    Pilocarpine in, 106
    Quinia in, 105, 108
    Stimulants in, 108
    Strychnia in, 108
    Tracheotomy in, 107

Laryngoscope, description of, 21
  history of, 19

Laryngoscopy and rhinoscopy, 19

LARYNGOSCOPY, ART OF, 25-29
  description of the laryngeal image, 30-33
  methods of illumination in, 23-25
  obstacles to, 28, 29
  position of observer, 26
  position of patient in, 26
  use of electric illuminator, 24
  use of head-reflector in, 22

Laryngotomy, in morbid growths of the larynx, 31

Larynx, anæsthesia of, 65
    treatment, 67

LARYNX, CHOREA OF, 76
    Symptoms, 76
    Treatment, 77
  Diseases of, 109
  Disorders of motion of, 68
  Exalted action of, 69
  Hyperæsthesia of, 62
    Treatment, 64
  Lepra of, 132
  Lupus of, 132
  Muscles of, 59
  Nerves of, 60

LARYNX, MORBID GROWTHS OF, 127
  Definition and etiology, 127
  Morbid anatomy, 128
  Prognosis and diagnosis, 130
  Symptoms, 129
  Treatment, 131
    Cocaine, use, 131
    Laryngectomy, 131
    Laryngotomy in, 131

Larynx, muscles of, 59
  nerves of, 60
  neuroses of, 59

LARYNX, OEDEMA OF, 112
  Definition and synonyms, 112
  Diagnosis and morbid anatomy, 115
  Prognosis, 116
  Symptoms, 113
  Treatment, 116
    Antispasmodics, use, 116
    Astringents, use, 116
    Diaphoretics, use, 116
    Jaborandi, use, 116
    Ice, use, 117
    Morphia, use, 116
    Purgatives, use, 116
    Scarification, 116
    Tracheotomy, 117

LARYNX, PARÆSTHESIA OF, 63
  Symptoms and treatment, 64
  Paresis and paralysis of muscles of, 78
  Paralysis of constrictors of, 80
  Perversions of sensations of, 61

LARYNX, PERICHONDRITIS AND CHONDRITIS OF, 117
  Definition and etiology, 117
  Diagnosis and prognosis, 120
  Morbid anatomy and symptoms, 118
  Treatment, 121

LARYNX, SPASM OF, IN CHILDREN (Laryngismus Stridulus), 70
  Course and duration, 71
  Diagnosis, 72
    From true croup, 72
    From simple laryngitis, 72
  Etiology, 70
  Pathology, 71
  Prognosis, 72
  Symptoms, 70
    Voice in, 71
  Treatment, 73
    Alum in, 73
    Anæsthetics, 73
    Antispasmodics in, 73
    Baths, hot, in, 73
    Emetics in, 73
    Ipecacuanha, 73
    Potassium bromide in, 73

Latent pneumonia, 334, 342

Laxatives, use, in pleuritic effusions, 520

Leeches, in acute bronchitis, 178

Left ventricles, hypertrophy of, 625

Lepra of the larynx, 132

Lesions of cancer of the lung, 460, 461
  of chronic congestion of the spleen, 958
  of croupous pneumonia in children, 312
  of fibro-serous pleurisy, 485
  of lungs in pneumonokoniosis, 457, 458
      in pulmonary phthisis, 408, 410
  of nervous system, in Addison's disease, 944
  of pulmonary hydatids, 467
  Seat in syphilis of the lung, 450

LEUKÆMIA, 908
  Course, 918
  Definition, synonym, and history, 908
  Diagnosis, 919
  Etiology, 909
    Age and sex, influence on causation, 909
    Climate, influence on causation, 909
    Malarial and previous disease, causation, 909
    Syphilis, influence on causation, 910
  Morbid anatomy, 915
    Blood, and heart-changes in, 915
    Bone-marrow, changes in, 916
    Lymphatic glands, changes in, 916
    Leukæmic growths, characters of, 918
    Spleen, changes in, 915
  Prognosis, 920
  Symptoms, 910
    Blood-corpuscles, changes in, 911, 912
    Digestive disorders, 910
    Genito-urinary disorders, 913
    Hemorrhages, seat and characters, 913
    Lymphatic glands and spleen, enlargement of, 914
    Nervous symptoms, 911
    Pulse, characters, 913
    Respiratory symptoms, 913
    Special senses, modification of, 911
  Treatment, 920
    Arsenic, use, 921
    Ergot, use, 921
    Excision of spleen, 921
    Iron, use, 921
    Quinia, use, 921
    Transfusion, 921

Ligation of carotid and subclavian arteries in thoracic aneurism, 818

Lime, use, in pseudo-membranous laryngitis, 105

Liver, changes in, in tricuspid regurgitation, 678, 679
  displacement of, in pleurisy, 497, 507
  enlargement of, in leukæmia, 911
  influence on destruction of the blood, 885
  lesions, in catarrhal pneumonia, 358
    in Hodgkin's disease, 928
    in leukæmia, 918
    in mitral regurgitation, 670

Lobelia, use, in bronchial asthma, 204

Local treatment of chronic congestion and enlargement of the spleen,
        960
    of chronic laryngitis, 125
    of epiglottic inflammation, 109, 110
        ulceration, 112
    of laryngeal oedema, 116
    of simple lymphangitis, 990
    of ulceration of trachea, 139

Locality, change of, in bronchial asthma, 206
  choice of, in treatment of hay asthma, 223

Localization of thoracic aneurisms, 812

LUNG, ABSCESS OF, 296
  Definition, history, etiology, and synonyms, 296
  Diagnosis, 299
  Pathology and morbid anatomy, 298
  Prognosis, 300
  Symptoms and course, 297
  Treatment, 300

LUNGS, CANCER OF, 460
  Definition, 460
  Diagnosis, 464
  Duration, 463
  Etiology and morbid anatomy, 460
  Prognosis, 465
  Symptoms, 461

LUNG, COLLAPSE OF (Atelectasis), 250
  Definition and history, 250
  Diagnosis, 254
  Etiology, 250
    Age, influence on causation, 251
    Bronchial catarrh, relation of, to, 250, 251
    Mechanism of production, 251
    Thoracic effusions, influence on production of, 252
  Morbid anatomy, 253
  Prognosis, 255
  Symptoms, 252
  Treatment, 255
    Diet in, 256
    Emetics, question of use, 255
    Expectorants, use, 255
    Of congenital form, 255

LUNGS, CONGESTION AND OEDEMA OF (Hypostatic Pneumonia), 258
  Course and termination, 261
  Definition, 258
  Diagnosis, 262
  Etiology, 258
  History, 258
  Morbid anatomy, 261
  Prognosis, 262
  Symptoms, 260
  Treatment, 263
    Of passive form, 263
    Of pulmonary oedema, 264
    Use of bloodletting, general and local, 263, 264
      of diaphoretics, 264
      of digitalis, 263
      of emetics, 263
      of iron in chronic form, 263, 264
      of stimulants, 263
      of quinia hydrobromate, hypodermatically, 264

Lung, displacement of, in pleurisy, 506

LUNG, GANGRENE OF, 301
  Course and duration, 305
  Definition, synonyms, and etiology, 301
  Diagnosis and prognosis, 304
  Pathology and morbid anatomy, 303, 304
  Symptoms, 302
  Treatment, 305

Lungs, appearance of, in congestion, 262
  brown induration of, 256
  changes in, in hæmoptysis, 287
  condition of, in pneumothorax, 576
  early lesions of, in pulmonary phthisis, 408-410
  lesions of, in croupous pneumonia, 308-313
    in Hodgkin's disease, 928
    in leukæmia, 918
    in pernicious anæmia, 904
    in pneumonokoniosis, 457
  syphilitic disease of, 447

Lung-tissue, gross and microscopic appearance of, in catarrhal
        pneumonia, 356, 357

Lupus of the larynx, 132

Lymph, mechanism of circulation of, 984, 985

LYMPHANGITIS, SIMPLE, 983
  Definition, 986
  Diagnosis, 988
  Etiology, 986
    Age, influence on causation, 986
    Specific irritation, 986
    Traumatism, influence on causation, 986
  Pathology and morbid anatomy, 987
  Prognosis, 990
  Symptoms, 987
    Oedema, 987
    Of tubercular form, 987
    Pain, characters, 987
    Temperature, 987
  Treatment, 990
    Antipyrine, use, 990
    Bandage, use, 991
    Cold, locally, 990
    Diet in, 990
    Fomentations, use, 990
    Iron, arsenic, and cod-liver oil, 990, 991
    Local, 990
    Quinia, use, 990
    Rest, 990
    Silver nitrate, locally, 990

Lymphatic glands, changes in, in leukæmia, 914, 916
    enlargement of, in Hodgkin's disease, 923, 926
    influence on blood-formation, 884
    lesions, in pernicious anæmia, 905
    relation to production of blood-corpuscles, 890
    swelling of, in perichondritis of larynx, 118

Lymph-spaces, seat of miliary tuberculosis in, 475

Lymph-vessels, lesions, in lymphangitis, 987

Lympho-sarcoma of the mediastinum, 867


M.

Mackenzie's method of injecting goitre, 981

Malaria, influence on causation of acute splenic enlargement, 954
      of lardaceous spleen, 966
      of leukæmia, 909

Malformations of left side of heart, 707
  of right side of heart, 702

Malignant tumors of trachea, 141

Malign growths of larynx, 128

Malpositions of the heart, 601

Marriage of bleeders, 938
  of phthisical persons, 439

Marrow of bone, lesions, in leukæmia, 916

Massage of larynx in true croup, 107

Measles, influence on causation of acute miliary tuberculosis, 473

Mechanical bronchitis, 170
  causes of cardiac thrombosis, 723
    of collapse of the lung, 251

Median tracheotomy, 148, 155

Mediastinal pleurisy, 564

MEDIASTINUM, DISEASES OF, 861
  _Abscess of the Mediastinal Space_, 861
    Complications and terminations, 863
    Diagnosis and prognosis, 863
    Etiology, 861
    Symptoms, 862
    Treatment, 863
  _Inflammation of the Mediastinum_, 861
  _Tumors of the Mediastinum_, 863
    Anatomy of the mediastinal space, 863
    Definition, 863
    Diagnosis, 876
      From abscess, 877
      From aneurism, 876
      From chronic pneumonia, 879
      From pericarditis, 878
      From pleurisy, 878
      Of anterior growths, 877
      Of posterior growths, 878
    Differentiation of malignant growths, 879
    Duration, 875
    Etiology, 871
    Pathology and morbid anatomy, 865-871
      Carcinoma, characters, seat, and method of growth, 869
      Lympho-sarcoma, characters, seat, and method of growth, 867
      Sarcoma, characters, seat, and method of growth, 865-867
    Prognosis, 876
    Symptoms, 871
      Cyanosis and oedema, 873
      Dyspnoea, peculiarities of, 872
      Pain, characters and seat, 872
      Physical signs, 873
      Pressure symptoms, 872, 873
    Treatment, 880
      Donovan's solution, use, 881
      Morphia, use, 880
      Paracentesis, 880
      Resection of sternum, 880

MELANÆMIA, 896
  Definition and etiology, 896
  Morbid anatomy, 897
    Pigment, mode of origin, 897, 898

Membrane of pseudo-membranous laryngitis, nature, 100
      seat, 101

Membranous exudation, nature of, in pseudo-membranous bronchitis, 176

Menstrual disorders in chlorosis, 894, 895

Menstruation in fibro-serous pleurisy, 497, 498

Mental emotion, influence in evoking paroxysms of angina pectoris, 456

Mercury, use, in pseudo-membranous laryngitis, 104

MESENTERIC ARTERY, INFERIOR, DISEASES OF, 839
  Aneurism, 839
  Embolism, 839, 840

MESENTERIC ARTERY, SUPERIOR, DISEASES OF, 836-839
  Aneurism, 836
  Embolism, 836-839
  Endarteritis, 839
  Thrombosis, 839

Metallic tinkling in pneumothorax, 579

Meteorological conditions as a cause of bronchitis, 168

Miliary tubercles, physical characters of, 474
  tuberculosis, acute, 472

Mineral and coal-dust, influence on causation of pneumonokoniosis, 455
  poisoning, influence on causation of asthma, 191
      of fatty degeneration of the heart, 612

Mitral disease, influence on causation of hydrothorax, 570
    Prognosis, 682, 683
    Treatment, 685, 686
  Regurgitation, 669
  Stenosis, 665
  Valve, disease of, influence on causation of brown induration of the
        lung, 256

Morbid anatomy of acute congestion of the spleen, 955
        exudative endocarditis, 640
        myocarditis, 604, 605
    of Addison's disease, 942
    of aortic obstruction, 654
        regurgitation, 659
    of asthma, 197
    of bronchial dilatation, 230
    of bronchitis, 175
    of brown induration of the lungs, 256
    of cancer of the lungs, 460
        of the pleura, 582
    of cardiac thrombosis, 734
    of catarrhal pneumonia, 354
    of chronic myocarditis, 607
        congestion of the spleen, 957
        pharyngitis, 122
    of croupous pneumonia, 308
    of dilatation of the heart, 633
    of fatty cardiac degeneration, 613
    of fibroid phthisis, 440
    of fibro-serous pleurisy, 484
    of gangrene of the lung, 304
    of hæmophilia, 936
    of hæmoptysis, 286
    of hæmothorax, 582
    of hemorrhagic infarction of spleen, 961
    of Hodgkin's disease, 926
    of hydatids of pleura, 585
    of hydrothorax, 571
    of hypertrophy of the heart, 623
    of interstitial endocarditis, 644
    of lardaceous spleen, 967
    of laryngeal oedema, 115
    of leukæmia, 915
    of mediastinal tumors, 865
    of mitral regurgitation, 670
        stenosis, 665
    of morbid growths of larynx, 128
    of pericarditis, 772
    of perichondritis and chondritis of the larynx, 118
    of pernicious anæmia, 904
    of phthisis, 408
    of pneumonokoniosis, 456
    of pneumothorax, 576
    of pulmonary abscess, 298
        congestion and oedema, 261
        emboli, 382
        hydatids, 467
        stenosis, 675
    of purulent pleurisy, 540
    of rupture of the spleen, 972
    of simple lymphangitis, 987
        tracheitis, 134
    of splenitis, 963
    of syphilis of the lung, 450
    of the caisson disease, 855
    of tricuspid regurgitation, 678
    of ulcerative endocarditis, 642
    of vesicular emphysema, 242

Morbid growths of the larynx, 127
    of nasal passages, 52
    of trachea, 139

Morphia, use, in bronchial asthma, 201
    in chronic laryngitis, 127
    in epiglottic ulceration, 112
    in fibro-serous pleurisy, 520
    in hæmothorax, 581
    in hyper- and paræsthesia of the larynx, 64
    in the caisson disease, 858
    in ulceration of the trachea, 139
    in valvular heart disease, 684, 686

Mortality of acute and chronic bronchitis, 177
  of catarrhal pneumonia, 368
  of croupous pneumonia, 342
  of hæmoptysis, 290
  of laryngismus stridulus, 72
  of pseudo-membranous laryngitis, 103
  of stenosis of the aorta, 827
  of valvular heart disease, 680

Murmurs, blowing, in cardiac thrombosis, 727
  cardiac, relation to valvular disease, 651
  characters, in aneurism of the pulmonary artery, 834
    in aortic obstruction, 657
        regurgitation, 663
    in mitral regurgitation, 668
        stenosis, 673
    in pulmonary stenosis and regurgitation, 675, 676
    in tricuspid disease, 677, 680
    and seat, in endocarditis, 648, 649
  disappearance of, in acute myocarditis, 606
  hæmic, in pernicious anæmia, 902
  over splenic region, in splenic congestion, 954
  significance, in abdominal aneurism, 822

Mucous membrane, bronchial swelling of, as a cause of asthma, 197

Multilocular areolar pleurisies, 564

Muscular exertion, influence on causation of aortic disease, 656, 660
    influence on causation of hypertrophy of the heart, 622
    prolonged, influence on causation of functional heart disease, 752

Muscle-substance, condition in dilatation of the heart, 633

Muscles of larynx, 59

MYOCARDITIS, 604
  Etiology and morbid anatomy, 604, 605
  Diagnosis, 606
  Interstitial form, 605
  Suppurative form, 605
  Symptoms and treatment, 606

MYOCARDITIS, CHRONIC (Fibroid Heart), 607
  Diagnosis, 607
  Morbid anatomy and etiology, 607, 608
  Symptoms and treatment, 608

Myosis, in thoracic aneurism, significance, 805

Myxoma of nasal passages, 53


N.

Narrowing of a vein, 851

Nasal catarrh, acute, 41

NASAL CATARRH, CHRONIC, 42
  Atrophic form, 47
    Prognosis, 48
    Symptoms, 47
    Treatment, 48
      Arsenic and cod-liver oil in, 49
      Galvano-cautery in, 48
      Phosphates in, 49
  From defective nasal respiration, 43-46
      Deflected septum, 44
      Hypertrophy of erectile tissue, 44
      Osseous obstruction, 44
    Treatment, 44-46
      Galvano-cautery, 44-46
      Iodine, use, 45
  From necrosis of nasal bones, 49, 50
    Inflammatory form, without hypertrophy, 46
      Prognosis, 47
      Treatment, 47
        Electricity, 47
        Silver nitrate, 47

Nasal cavities, anatomy of, 33, 35
  diseases, table of, grouped by symptoms, 50
  hypertrophies, removal of, in hay asthma, 225
  injections in hay asthma, 224
  mucous membrane, hypertrophy of, influence on causation of asthma,
        193
  passages, diseases of, 41
    fibroma of, 55
    morbid growths of, 52
    myxoma of, 53
    polypi of, 53
      treatment, 54
    sarcoma and carcinoma of, 55

Nausea and vomiting in acute congestion of spleen, 954
    in Addison's disease, 941
    in croupous pneumonia, 330
    in pernicious anæmia, 903
    in splenitis, 962

Needle-bath, in exophthalmic goitre, 766

Nervous cough, 77
  lesions, of Addison's disease, 944
    of Hodgkin's disease, 928
    of leukæmia, 918
    of pernicious anæmia, 905
  symptoms of Addison's disease, 941
    of Hodgkin's disease, 925
    of leukæmia, 911
    of pulmonary phthisis, 407

Neuralgia in hyperæsthesia of the larynx, 63

Neuroses of the larynx, 59
  of the heart, 747

Night-sweats, of pulmonary phthisis, 405
        treatment, 438

Nitro-glycerin, use, in bronchial asthma, 208

Nutrition, bad, influence on causation of catarrhal pneumonia, 354
  impaired, of heart-walls, influence on dilatation of the heart, 632

Nux vomica, use, in angina pectoris, 761


O.

Occlusion of the aorta, 824
  of the coronary artery, 831
  of veins, 851

Occupation, influence on causation of hay asthma, 213
      of mediastinal tumors, 871
      of pneumonokoniosis, 455, 456
      of pulmonary phthisis, 396
      of thoracic aneurism, 803
  in-door, influence on causation of bronchitis, 165

Oedema, from dilatation of veins, 850
  in pernicious anæmia, 901
  of glottis, 94, 103
  of the lungs, 258
  of thoracic walls, in purulent pleurisy, 542, 543

Onset of acute catarrhal laryngitis, 93, 94
  of laryngismus stridulus, 70
  of leukæmia, 910
  of pseudo-membranous laryngitis, 102

Operations, various, in tracheotomy, 48

Operative treatment of pericardial effusions, 794

Opiates, use, in exophthalmic goitre, 766

Opium, use, in acute catarrhal laryngitis, 98
    in croupous pneumonia, 348
    in hæmoptysis, 291, 292
    in pericarditis, 783
    in pulmonary phthisis, 436, 437, 439
    in valvular heart disease, 684, 685
  and morphia, use, in angina pectoris, 760

Organization of heart-clots, 740

Orthopnoea, in mitral stenosis, 667

Osseous obstruction, as a cause of chronic nasal catarrh, 44

Over-training and heart-strain, influence on causation of cardiac
        dilatation, 631

Oxidation, defective, in fatty degeneration of the heart, 613

Oxygen, inhalations in true croup, 107

Ozæna, 47


P.

Pack, cold, use in croupous pneumonia, 349

Pain, characters, in croupous pneumonia, 322
    in lymphangitis, 987
    in mediastinal abscess, 862
    in pulmonary phthisis, 402
  in acute and chronic congestion and enlargement of the spleen, 954,
        957
  in acute phlebitis, 845
  in aneurism of the coeliac axis, 842
  in aortic obstruction, 656
      regurgitation, 661
  in caisson disease, 854
  in cancer of the pleura, 584
  in cardiac thrombosis, 731
  in chronic endarteritis of the coronary artery, 828
  in endocarditis, 647
  in hydatids of the pleura, 581
  in hyperæsthesia of the larynx, 62
  in morbid growths of the larynx, 129
  in pericarditis, 773, 774
  in perichondritis and chondritis of the larynx, 118
  in splenitis, 962
  in stenosis of the trachea, 142
  in ulceration of the trachea, 139
  seat and characters, in angina pectoris, 756
      in diaphragmatic pleurisy, 563
      in fibro-serous pleurisy, 493
      in mediastinal tumor, 872
      in thoracic aneurism, 804
  seat, in abdominal aneurism, 821

Palpation in cardiac malformations, 710
  in cardiac thrombosis, 729
  in cardiac valvular disease, 657, 662, 668, 673, 675, 677, 679
  in croupous pneumonia, 335, 336, 338
  in endocarditis, 648
  in fibro-serous pleurisy, 503, 504
  in pericarditis, 774
  in pneumothorax, 579
  in thoracic aneurism, 808

Palpitation in cardiac valvular disease, 656, 661, 667, 671, 675, 679
  in hypertrophy of the heart, 626
  of the heart, 747

Papilloma of larynx, 128, 130

Papillomata of trachea, frequency, 140

Paracentesis in endocardial effusions, 784, 794
  in pulmonary hydatids, 470

Paræsthesia of larynx, 63

Paralysis in caisson disease, 854
  of adductors and abductors of vocal cords, 81, 84, 86
  of arm in thoracic aneurism, 810
  of constrictors of larynx, 80
  of muscles of larynx, 78
  of posterior crico-arytenoids, 86
  of tensors of vocal cords, 85, 86
  of the whole larynx, 79

Parasites, influence on causation of hay asthma, 216
  of the heart, 637

Parenchymatous degeneration of heart-muscle, 610

Paroxysms, frequency of, in angina pectoris, 756
    in functional heart disease, 748
  of asthma, description and frequency of, 185-187

Patency of septum ventriculorum, 690

Pathology of acute catarrhal laryngitis, 92
      phlebitis, 843-845
      congestion of spleen, 955
  of Addison's disease, 944
  of anæsthesia of larynx, 67
  of aneurism of the coeliac axis, 842
  of angina pectoris, 758
  of asthma, 193
  of bronchial asthma, 193
  of bronchitis, 175
  of caisson disease, 855
  of cancer of the lungs, 460
  of cardiac thrombosis, 734
  of catarrhal pneumonia, 354
  of chronic endarteritis of the coronary artery, 829
      pharyngitis, 122
  of collapse of lung, 253
  of embolism of the coronary artery, 832
      of the superior mesenteric artery, 837
  of exophthalmic goitre, 764
  of fibroid phthisis, 440
  of functional heart disease, 752
  of gangrene of lung, 303
  of hæmophilia, 936
  of hæmoptysis, 286
  of hemorrhagic pleurisy, 565
  of Hodgkin's disease, 930
  of hysterical affections of glottis, 84
  of laryngismus stridulus, 71
  of mediastinal tumors, 865
  of morbid growths of trachea, 140
  of perichondritis and chondritis of larynx, 118
  of pernicious anæmia, 905
  of phlegmasia dolens, 847
  of pneumonokoniosis, 456
  of pseudo-membranous laryngitis, 100
  of pulmonary abscess, 298
      congestion and oedema, 261
      emboli, 382
      phthisis, 408
  of simple lymphangitis, 987
      tracheitis, 134
  of spasm of the glottis in the adult, 75
  of stenosis of the aorta, 825
      of the trachea, 143
  of syphilis of the lung, 448
  of vesicular emphysema, 242

Pectoriloquie aphonique in pleurisy, significance, 510, 517

Percussion during paroxysm of asthma, 187
  in bronchial dilatation, 228, 229
  in cardiac malformation and cyanosis, 710
      thrombosis, 728
      valvular disease, 657, 663, 668, 673, 675, 677, 680
  in catarrhal pneumonia, 359-363
  in collapse of lung, 253
  in croupous pneumonia, 335, 337, 338
  in emphysema, 237
  in endocarditis, 648
  in fibro-serous pleurisy, 499-503
  in hydrothorax, 572
  in hypertrophy of the heart, 625, 627
  in mediastinal abscess, 862
      tumors, 874
  in pericarditis, 774
  in pneumothorax, 579
  in pulmonary congestion and oedema, 260
      phthisis, 411, 413, 415-418
  in purulent pleurisy, 543, 544
  in pyo-pneumothorax, 544
  in thoracic aneurism, 812

Perforation in purulent pleurisy, 542-547
  of the aorta, 824
  of lung, in thoracentesis, 538

Pericardial effusions, displacements of heart, from, 602

PERICARDIAL EFFUSIONS, OPERATIVE TREATMENT OF, 794
  Aspiration, method of, 796, 797
  Free incisions and drainage, 795
  Indications for, 794, 795
  Injections into pericardium, 795
  Puncture of heart, results of, 798
  Results, 798
  Site of puncture, 796

PERICARDITIS, 769
  Definition, 769
  Diagnosis, 779
    From cardiac hypertrophy, 780
    From cerebral affections, 779
    From mediastinal tumors and inflammation, 780
    From pleurisy and endocarditis, 779
  Etiology, 769
    Bright's disease, influence on causation, 771
    Cold, influence on causation, 770
    Eruptive fevers, influence on causation, 771
    Rheumatism, acute, influence on causation, 770
    Traumatism, influence on causation, 769, 770
    Secondary causes, 770, 771
  Frequency, 770, 771
  Morbid anatomy, 772, 773
  Prognosis, 781
  Symptoms, 773
    Auscultation, 775
    Cerebral symptoms, 774
    Friction sounds, characters, 775
    Pain, 773
    Percussion and palpation, 774
    Physical signs of, 774
    Pulse and temperature in, 774
  Treatment, 783
    Blisters, use, 784
    Cold, locally, 783
    Counter-irritation, 783
    Diet in, 783
    Digitalis, use, 783
    Of effusion, 784
    Paracentesis, 784
    Potassium, bitartrate and acetate, use, 784
      iodide, 784
    Quinia, use, 784
    Stimulants, 784

Pericarditis, chronic, 784
  tubercular, 793

PERICARDIUM, ADHERENT, 785
  Adhesions, seat and character, 786
  Impulse in, 787
  Prognosis, diagnosis, and treatment, 788

Pericardium, cancer of, 792, 793
  diseases of, 769

Perichondritis of larynx, 117

Perisplenitis, 965

Peritonitis complicating pulmonary phthisis, 406

Pernicious anæmia, progressive, 898

Phlebitis, 843

Phlebolithes, 853

Phlegmasia alba dolens. See _Veins, Diseases of_.

Phosphates, use, in atrophic nasal catarrh, 49

Phosphorus, use, in Hodgkin's disease, 931
    in leukæmia, 921
    in pulmonary phthisis, 435

PHTHISIS, FIBROID, CHRONIC INTERSTITIAL PNEUMONIA, CIRRHOSIS OF LUNG,
        440
  Course and duration, 441
  Diagnosis, 443
  Etiology, 440
  Symptoms, 441
    Cough and expectoration, characters, 441
    Cyanosis in, 442
    Physical signs, 442
    Sputa, characters, 441
    Treatment, 444

Phthisis, incipient, diagnosis, 411, 413

PHTHISIS, PULMONARY, 391
  Definition, 391
  Diagnosis, 410
    Auscultation in, 412, 416, 417
    Bacilli, significance of presence in sputa, 413
    Broncho-vesicular respirations, characters, 412
    Dry cough, significance of, 411
    Inspection in, 417
    Of cavities, 416, 417
    Of incipient form, 411
    Of intercurrent pneumonia in, 418
    Percussion in, 411, 415, 416
    Stethoscope, necessity of use in, 412
    Vesiculo-tympanitic resonance, characters, 415
    Whispered voice, transmission of, 413-417
  Etiology, 394
    Age, occupation, and sex, 396
    Bacillus tuberculosis, relation of, 392, 398
    Bronchitis, relation of, to, 394
    Communicability of, 396-398
    General diseases, influence on causation, 396
    Hæmoptysis, influence on causation, 395
    Heredity and constitutional predisposition, influence on causation,
        395
    Season, humidity of soil, etc., influence on causation, 396
  History, 392
  Morbid anatomy and pathology, 408
  Prevention, 444
  Prognosis, 419
  Symptoms and complications, 400
    Anæmia in, 405, 406
    Cough, characters, 400
    Dysphonia, aphonia, and laryngitis, 403
    Genito-urinary disorders, 408
    Hæmoptysis, frequency and significance, 401, 402
    Heart, and circulatory disorders in, 405
    Intercurrent pneumonia, occurrence of, 403, 404
    Nervous symptoms, 407
    Night-sweats in, 404
    Pain in, 402
    Peritonitis, occurrence of, 406, 407
    Pleurisy and pneumothorax in, 404
    Respiration in, 403
    Sputa, characters, 401
    Temperature in, 404, 405
    Vomiting, diarrhoea, and digestive disorders, 406
  Synonyms, 391
  Treatment, 425
    Agaricus, use, in night-sweats, 438
    Alcohol, use, 435
    Arsenic, use, 436
    Belladonna and zinc oxide, use, 438
    Climatic, 427-430
    Cod-liver oil, use and value, 434
    Cold use, 437
    Dietetic, 431
    Ergotin, use, 437
    Injection of cavities, 439
    Iodine, use, 435
    Iron, use, 436
    Marriage of consumptives, question of, 439
    Of cough, 436
    Of diarrhoea, 438
    Of night-sweats, 438
    Of pyrexia, 437
    Out-of-door life, necessity of, 432
    Picrotoxin, use, 438
    Quinia, use, 438
    Sea-voyages, value, 433
    Sanitaria, value, 430
    Use of opium, 436, 439

Physical signs during paroxysm of asthma, 187
    in emphysema, 236, 237
    in fatty degeneration of the heart, 615
    in mitral regurgitation, 671
    in pulmonary congestion and oedema, 260, 261
        regurgitation, 697
    in purulent pleurisy, 543
    of abdominal aneurism, 822
    of acute bronchitis, 169
    of acute miliary tuberculosis, 480
    of adherent pericardium, 787
    of aortic obstruction, 657
    of aortic regurgitation, 662
    of atrophic lobar emphysema, 248
    of cancer of the lungs, 462, 463
        of pleura, 584
    of capillary bronchitis, 171
    of cardiac malformations, 710
    of cardiac thrombosis, 728, 741
    of cardiac valvular disease, 668
    of catarrhal pneumonia, 359-363
    of collapse of lung, 252, 253
    of croupous pneumonia, 334, 335
        in children, 335, 338
    of diaphragmatic pleurisy, 563
    of dilatation of the heart, 634
    of endocarditis, 648
    of fibroid phthisis, 442
    of fibro-serous pleurisy, 496
    of hæmopericardium, 789
    of hæmoptysis, 282
    of hydrothorax, 572
    of hypertrophy of the heart, 625
    of mediastinal tumors, 873
    of pericarditis, 774
    of pneumothorax, 578
    of pulmonary abscess complicating croupous pneumonia, 339
    of pulmonary hydatids, 468
        phthisis, 411
    of pulmonary stenosis, 675
    of senile pneumonia, 336, 338, 339
    of stenosis of the aorta, 826
    of syphilis of the lung, 452
    of thoracic aneurism, 807
    of thrombosis and embolism of the pulmonary artery, 836
        of the coronary artery, 832
    of tricuspid stenosis, 677

Physiognomy in angina pectoris, 756
  in asthma, 186, 190
  in croupous pneumonia, 328
  in endocarditis, 647
  in laryngismus stridulus, 71
  in pulmonary embolism, 379-381

Picrotoxin, use, in pulmonary phthisis, 438

Pigment, seat and treatment of, in melanæmia, 896, 897

Pigmentation of Addison's disease, 940
  of lungs in pneumonokoniosis, 451, 458

Pilocarpine in laryngeal oedema, 116
  use, in pleuritic effusions, 521
    in pseudo-membranous laryngitis, 106
    in pulmonary oedema, 264

Pimpinella saxafraga, use, in acute catarrhal laryngitis, 99

Plants and grasses, certain, influence on production of hay asthma, 215

Plethora, 886

Pleura, cancer of, 583
  diseases of, 483
    displacement of heart from, 603
  hydatids of, 585
  lesions of, in croupous pneumonia, 313

Pleural cavity, morbid growths of, 583
  effusions, frequency, in cancer of the lungs, 461
    influence on causation of collapse of lung, 251
    occurrence in course of mediastinal tumors, 870

Pleurisies, circumscribed, 545
  encysted, 545, 546
  multilocular areolar, 564

PLEURISY, 483
  Complications, 512
  Course, 510
  Definition, 483
  Diagnosis, 514
    From abscess of liver, 516
      Atelectasis, 517
      Hydrothorax, 515
      Intercostal neuralgia, pleurodynia, etc., 516
      Pneumonia, 514, 515
      Tumors and cysts, 516
    Of nature of effusion, 517
  Duration, 511, 512
  Etiology, 491
    Age and sex, influence on causation, 492
    Atmospheric changes, influence on causation, 491
    Of primary form, 491
    Of secondary form, 491
    Pulmonary affections, acute and chronic, influence on causation,
        492
    Rheumatism, gout, and nephritic affections, 493
    Syphilis, influence on causation, 493
    Traumatism, influence on causation, 492
  Pathological anatomy, 484
    Effused fluid, chemical characters of, 486
      distribution of, 487
    Exudation, seat, nature, and appearance of, 485, 486
    Level of line of flatness assumed by effusion, 488, 489
  Prognosis, 518
  Sequelæ, 483
  Symptoms, 493
    Bronchial breathing, significance of, 508
    Chills, frequency, 494
    Cough, characters of, 495
    Cyanosis, 496
    Displacement of organs in, 504, 507
    Expectoration, characters, 496
    Friction sounds, seat and characters, 507, 509
    Heart murmur in, 510
    Mensuration, necessity of frequent, 497, 498
    Pain, seat and characters, 493
    Physical signs in, 496
    Pneumo-pericardial friction sounds, 509
    Pulse, characters, 494
    Respiration in, 494
    Skodaic resonance, seat and characters, 501
    Temperature, 494
    Voice sounds in, 510
    Whispered voice, significance of, 510, 517
  Synonyms, 483
  Terminations, 512
  Treatment, 519
    Alkalies, use, 520
    Blisters, use, 520, 521
    Counter-irritants, use, 520, 521
    Effusion, removal of, 520
    Iron, use, 520, 521
    Jaborandi and pilocarpine, 520, 521
    Laxatives and purgatives, 520, 521
    Opium and morphia, use, 520
    Potassium iodide, use, 520
    Quinia, use, 520
    Rest, 519
    Strapping of chest in, 520
    Thoracentesis, 521
      Albuminous expectoration following, 535
      Contraindications, 530
      Death from, causes, 536, 537
      During febrile stage, question of, 525
      Indications for, 521
      Mode of operating, 530, 534
      Secondary pneumonia and tuberculosis following, 536

Pleurisy, complicating pulmonary phthisis, 404
  diaphragmatic, 563
  double, 562

PLEURISY, HEMORRHAGIC, 564
  Diagnosis, 568
  Etiology and pathology, 565, 567
  Prognosis, 568
  Symptoms, 567
  Treatment, 568

Pleurisy, interlobular and mediastinal, 564

PLEURISY, PURULENT, 539
  Definition, 539
  Diagnosis, 543
    Exploratory puncture, value, 543
    From tubercular cavities and dilated bronchi, 545
    Of perforation, 543, 544
  Etiology, 539
    Age and sex, influence on causation, 540
    Eruptive fevers, influence on causation, 540
    Puerperal condition, the, influence on causation, 540
    Rheumatism, gout, and nephritic diseases, 540
    Traumatism, influence on causation, 540
  History, 539
  Pathological anatomy, 540
  Prognosis, 548
  Symptoms, 542
    Physical signs, 543
  Synonyms, 539
  Terminations, 547
  Treatment, 549
    Alteratives, use, 549
    By free drainage, 552-556
    Injections and washing of cavity, value of, 561, 562
    Modes of operating, 550
    Pleurotomy, 555
    Resection of ribs, 556
    Surgical, 549
    Thoracentesis, 550-552

Pleurisy, rheumatic, 564, 565
  tubercular, 569

Pleuro-bronchial fistulæ, signs of occurrence of, in purulent pleurisy,
        543

Pleurotomy, 556, 557

Pneumonia, acute lobar, complicating pulmonary phthisis, 403

PNEUMONIA, CATARRHAL, 353
  Complications and sequelæ, 364
  Definition, 353
  Diagnosis, 365
    From acute miliary tuberculosis, 367
    From collapse of lung, 366
    From croupous pneumonia, 366
  Duration, 368
  Etiology, 353
    Age, influence on causation, 353
    Infectious diseases complicated with bronchitis, influence on
        causation, 354
  Mortality, 368
  Pathology and morbid anatomy, 354
    Bronchi, lesions, 356
    Bronchial glands, lesions, 357
    Lung-tissue, gross and microscopic appearance of, 356
    Relation to collapse of lung, 355
  Prognosis, 368
  Symptoms, 358
    Cardiac failure in, 363
    Cough, 360, 361
    Death, cause of, 362
    Gastro-intestinal, 360
    In children, 358
    Nervous, 362
    Of grave forms, in adults, 360
    Physical signs, 358, 360, 362
    Pulse and respiration, characters, 360, 361
    Sputa, 360, 361
    Temperature, 358, 360, 361
  Synonyms, 353
  Terminations, 368
  Treatment, 368
    Alteratives, use, 372
    Ammonia preparations, use, 370, 371
    Apomorphia, use, 371
    Chloral hydrate, use, in nervous symptoms, 372
    Climate, change of, 372
    Counter-irritation, use, 369
    Diet in, 369, 370
    Emetics, use, 371
    Hyoscyamia, hypodermatically, use, 372
    Of gastro-intestinal disorders, 370
    Of nervous symptoms, 372
    Opium, use, 372
    Quinia, use, 370, 371
    Strychnia, use, 371

Pneumonia, chronic interstitial, 391, 440
  complicating pleurisy, 512

PNEUMONIA, CROUPOUS, 307
  Definition, 307
  Differential diagnosis, 339
    From capillary bronchitis, 340
    From catarrhal pneumonia, 340
    From hypostatic congestion, 340
    From meningitis, 342
    From pleurisy, 340
    From pulmonary apoplexy, 341
      congestion and oedema, 339
    From typhoid fever, 342
  Etiology, 314
    Age and sex, influence on causation, 314
    Cold, damp, season, etc., influence on causation, 314
    Depressing influences, influence on causation, 315
    Klebs on specific germ of, 319
    Nature of, 315-318
    Resemblance to acute general diseases, 317, 318
  History, 307
  Morbid anatomy, 308
    Changes in abdominal viscera, 313
      in bronchial glands, 313
      in heart and blood, 313
      in lung, 308-313
      in pleura, 313
  Prognosis, 342-345
    Cause of death, 345
    Mortality, 342, 343
  Symptoms, 319
    Alimentary tract, state of, 330
    Cerebral, 329, 330
    Chills, characters, in, 318
    Cough, characters, in, 322
    Critical phenomena, 331
    Dyspnoea, characters, 321, 322
    Expectoration, characters, 322
    Herpetic eruptions, occurrence, 328, 329
    Indicating danger, 331
    Objective, 334-339
    Of abscess and gangrene, 332
    Of bilious and gastric form, 334
    Of latent form, 334
    Of purulent infiltration, 332
    Pain, characters, 322
    Physical signs, 334-339
    Physiognomy, 328
    Pulse, characters, 326, 328
    Respiration, characters, 321
    Sputum, characters, 322
    Subjective, 319-334
    Surface of body, state of, 328
    Temperature in, 324
    Urine, condition, 330
  Synonyms, 307
  Treatment, 345-352
    Alcoholic stimulants, use, 348
    Antiseptics, use, 352
    Carbonate of ammonium, digitalis, musk, camphor, etc., use, 349
    Cardiac depressants, danger, 346
    Cold, use, 349
    Counter-irritation, questionable utility of, 347
    Diet in, 347, 348
    Expectorants, use, 347
    Of convalescence, 351
    Of delirium, 351
    Of senile variety, 351
    Opium, use, 348
    Quinia, use, 350
    Reduction of temperature in, 349
    Rest in, value, 347
    Venesection, harmfulness, 346

Pneumonia, hypostatic, 258

Pneumo-hydropericardium, 791

Pneumo-hydrothorax complicating phthisis, 404

PNEUMONOKONIOSIS, 454
  Definition, etiology, and history, 454
  Diagnosis and prognosis, 459
  Pathology and morbid anatomy, 456-459
  Symptoms and treatment, 459

Pneumo-pericardial friction sound, 509

Pneumo-pericardium, 790

PNEUMOTHORAX, 573
  Definition, 573
  Diagnosis, 580
  Etiology, 573
    Age and sex, influence on causation, 576
    Traumatic causes, 574
  History, 573
  Pathological anatomy, 576
    Air, quantity, 576
    Heart, displacement, 577
    Opening, shape and seat, 576
  Prognosis, 581
  Symptoms, 578
    Pain, seat and characters, 578
    Physical signs, 578-580
    Respiration, characters, 578
  Treatment, 581, 582
    Diet, 582
    Opium and morphia, use, 581
    Paracentesis, 581
  Stimulants, 581

Pollen of plants, influence on causation of asthma, 192
  theory of origin of hay asthma, 216

Polypus, nasal, 53, 54

Post-mortem heart-clots, 735

Potain's syphon, use, in purulent pleurisy, 555

Potassium acetate, use, in pericarditis, 784
  bicarbonate, use, in cardiac thrombosis, 745, 746
  chlorate, use, as an injection in pseudo-membranous laryngitis, 105
      in purulent pleurisy, 562
  bromide, use, in bronchial asthma, 204
      in bronchitis, 179
      in chronic inflammation of epiglottis, 110
      in hyper- and paræsthesia of larynx, 64
      in laryngismus stridulus, 73
      in pulmonary hydatids, 470
  iodide, use, in acute catarrhal laryngitis, 97, 99
      in acute tracheitis, 136
      in bronchial asthma, 207
      in chronic bronchitis, 182
      in chronic phlebitis, 848
      in paralysis of the larynx, 91
      in pericardial effusions, 784
      in pleurisy, 520
      in pseudo-membranous laryngitis, 105
      in pulmonary hydatids, 470
      in thoracic aneurism, 818
      in vesicular emphysema, 246, 247
  nitrate, use, in bronchial asthma, 203

Predisposing causes of asthma, 190
    of bronchitis, 165
    of gangrene of the lung, 301
    of hay asthma, 212

Pregnancy, influence on causation of hæmoptysis, 278
      of pernicious anæmia, 900
      of pulmonary phthisis, 396

Pressure symptoms in aneurism of the pulmonary artery, 834
    of abdominal aneurism, 821
    of goitre, 975
    of mediastinal abscess, 862
        tumors, 872, 873
    of thoracic aneurism, 804-807
  upon aorta, for relief of thoracic aneurism, 816

Prevention of angina pectoris, 760
  of phthisis, 444-446
  of pulmonary embolism, 388

Preventive treatment of functional heart disease, 755

Priapism in leukæmia, 914

Prognosis in lardaceous spleen, 968
  in pseudo-membranous laryngitis, 103
  in simple tracheitis, 135
  in valvular heart disease, 680
  of acute catarrhal laryngitis, 96
      congestion of the spleen, 955
  of adherent pericardium, 788
  of anæsthesia of the larynx, 67
  of angina pectoris, 760
  of asthma, 200
  of atelectasis, 255
  of atrophic emphysema, 249
  of bronchial dilatation, 230
  of bronchitis, 177
  of cancer of the lung, 465
      of the pleura, 584
  of cardiac thrombosis, 744
  of catarrhal pneumonia, 368
  of chronic congestion and enlargement of the spleen, 959
  of chronic laryngitis, 124
      nasal catarrh from defective respiration, 46
  of croupous pneumonia, 342
  of dilatation of the heart, 635
  of embolic splenic abscess, 964
  of embolism of the superior mesenteric artery, 838
  of endocarditis, 650
  of epiglottic ulceration, 112
  of exophthalmic goitre, 765
  of fatty degeneration of the heart, 616
  of fibro-serous pleurisy, 518
  of functional heart disease, 753
  of gangrene of the lung, 303
  of hæmoptysis, 290
  of hæmothorax, 583
  of hay asthma, 222
  of hemorrhagic pleurisy, 568
  of Hodgkin's disease, 930
  of hydatids of the pleura, 586
  of hydrothorax, 572
  of hyper- and paræsthesia of the larynx, 64
  of hypertrophy of the heart, 629
  of laryngeal oedema, 116
  of laryngismus stridulus, 72
  of leukæmia, 920
  of mediastinal tumors, 876
  of morbid growths of larynx, 130
      of trachea, 141
  of pericarditis, 781
  of pernicious anæmia, 906
  of phthisis, 419
  of pneumonokoniosis, 459
  of pneumothorax, 581
  of pulmonary abscess, 300
      congestion and oedema, 262
      embolism, 388
      hydatids, 470
  of purulent pleurisy, 548
  of simple lymphangitis, 990
  of stenosis of the aorta, 827
      of the trachea, 143
  of syphilis of the lungs, 453
  of ulceration of the trachea, 139
  of vesicular emphysema, 244

Progressive pernicious anæmia, 898

Prophylaxis of acute catarrhal laryngitis, 96
  of hæmophilia, 938
  of phthisis, 444-446

Prune-juice expectoration, significance in pneumonia, 319, 344

Pseudo-membranous bronchitis, 173
  laryngitis, 100

Puerperal state, influence on causation of phlegmasia dolens, 846
        of pulmonary embolism, 377
        of purulent pleurisy, 540

Pulmonary apoplexy, 293
    Definition and history, 293
    Diagnosis, etiology, and symptoms, 294
    Prognosis and treatment, 295
    and hæmoptysis, complicating cardiac thrombosis, 734
  artery, closure of, with perfect ventricular septum, in cyanosis, 702
    combined stenosis and atresia of, in cyanosis, 706

PULMONARY ARTERY, DISEASES OF, 833
  Chronic endarteritis (atheroma; arterio-sclerosis), 833
  Dilatation and aneurism, 833
  Rupture of pulmonary artery, 835
  Stenosis of trunk or main branches, 834
  Thrombosis and embolism, 835, 836

Pulmonary artery and right conus arteriosus, defects of, 690
    and vessels, anatomy of, relation to hæmoptysis, 269-272
  disease, influence on causation of cardiac hypertrophy, 622, 623
    influence on tricuspid regurgitation, 678

PULMONARY EMBOLISM, 373
  Classification, 373
  Death, cause of, 380, 381
  Definition, 373
  Diagnosis, 387
  Etiology, 374
    Diseases of thoracic, abdominal, and pelvic viscera, influence on
        causation, 375
    Puerperal state, influence on causation, 377
    Source of emboli, 374, 375
    Surgical affections as a cause, 377
  History, 373
  Pathology and morbid anatomy, 382
    Effects of emboli, 383
    Infarctions, mechanism of production, 384, 385
    Specific and septic emboli, effects, 386
  Prevention of, 388, 389
  Prognosis, 388
  Symptoms, 378
    Dyspnoea, characters of, 379-381
      Of benign form, 382
      Of grave form, 380
      Of sudden form, 379
    Physical signs, 381
    Physiognomy in, 379-381
    Sputa sanguinolent, in benign form, 382
  Treatment, 388
    Carbonate of ammonium and bicarbonate of sodium, use as solvents,
        389
    Counter-irritation and venesection, use, 390
    Purgatives, use, 390
    Surgical measures, 389

PULMONARY HYDATIDS, 466
  Definition, etiology, and synonyms, 466
  Diagnosis, 469
  History, 466
  Morbid anatomy, 467
  Prognosis, 470
  Symptoms, 468
  Treatment, 470
    Anthelmintics, use, 470
    Of old suppurating cysts, 471
    Paracentesis in, 470
    Potassium bromide and iodide, 470
    Surgical measures, 471

Pulmonary hyperæmia in mitral stenosis, 666, 667
  infarction, lesions of, 288
  orifice, narrowing or closure of, as a cause of cardiac malformation,
        694
  phthisis, 391
  regurgitation, 676
  stenosis, 674
  vein, anatomy of, 270

Pulsating empyema, 546

Pulsation in abdominal aneurism, 822
  jugular and epigastric, in tricuspid regurgitation, 679
  seat of, in aneurism of the cardiac axis, 841

Pulse, characters, in chronic myocarditis, 608, 609
    in endocarditis, 647
    in fatty degeneration of the heart, 615
    in leukæmia, 913
    in pericarditis, 774
    in thoracic aneurism, 808
  in acute miliary tuberculosis, 479


Q.

Quinia, use, in acute congestion of spleen, 956
    in acute miliary tuberculosis, 480, 482
    in anæsthesia of the larynx, 68
    in bronchitis, 79, 181, 182
    in catarrhal pneumonia, 370, 371
    in chronic congestion and enlargement of the spleen, 959
    in croupous pneumonia, 350
    in endocarditis, 651
    in fever following hæmoptysis, 292
    in gangrene of the lungs, 305
    in hay asthma, 224
    in Hodgkin's disease, 931
    in hyper- and paræsthesia of larynx, 65
    in laryngismus stridulus, 73
    in leukæmia, 921
    in pericarditis, 784
    in pseudo-membranous laryngitis, 105, 108
    in pulmonary phthisis, 438
    in purulent pleurisy, 549
    in simple lymphangitis, 990, 991
        tracheitis, 135
    in valvular heart disease, 685
  hydrobromate of, hypodermic use, in pulmonary congestion and oedema,
        264


R.

Ragweed, influence on causation of asthma, 215, 216

Râle crepitant of croupous pneumonia, 335
  redux of croupous pneumonia, 338

Recovery from pulmonary phthisis, 420-423

Recurrence of pulmonary phthisis, 424

Redness of skin, one-sided, in goitre, 975

Reduplication of second sound in mitral stenosis, 668

Reflex causes of laryngismus stridulus, 70
  symptoms of nasal polypus, 53

Regiminal treatment of pulmonary phthisis, 432

Regurgitation, aortic, 659
  mitral, 669
  pulmonary, 676
  tricuspid, 677

Relapse in croupous pneumonia, frequency, 326

Remissions, frequency, in acute catarrhal laryngitis, 94

Remittence of pulse in croupous pneumonia, 328

Remittent pneumonia, 334

Resection of ribs in purulent pleurisy, 557-562

Resolution stage of croupous pneumonia lesions, 310

Resonance, subclavicular, in pleurisy, 501-503

Respiration, characters, in catarrhal pneumonia, 359-363
    in chronic bronchitis, 171
    in collapse of lung, 252
    in croupous pneumonia, 321
  in fibro-serous pleurisy, 495, 497
  in morbid growths of trachea, 140
  in pneumothorax, 578
  in pseudo-membranous laryngitis, 102
  in pulmonary phthisis, 403

Respirator, use, in chronic laryngitis, 126

Respiratory power, defective, relation of, to catarrhal pneumonia, 356
  sounds in emphysema, 238
    in purulent pleurisy, 543

Rest, absolute, necessity of, in croupous pneumonia, 347
  in treatment of thoracic aneurism, 817
  necessity, in endocarditis, 651
  value, in cardiac hypertrophy, 630
    in acute and chronic phlebitis, 846, 848
    in dilatation of the heart, 636
  and quiet, necessity of, in hæmoptysis, 291
    value, in cardiac thrombosis, 745, 746

Retention-cysts of trachea, 141

Reticular lymphangitis, symptoms, 987

Retina, condition of, in leukæmia, 911

Reybard's trocar, use, in pneumothorax, 581

Rheumatic bronchitis, 172
  pleurisy, 564, 565

Rheumatism, acute, influence on causation of endocarditis, 645
    as a cause of pericarditis, 770
  influence on causation of paralysis of vocal cords, 82
      of valvular heart disease, 655, 661, 666, 671
  and gout, influence on causation of pleurisy, 493
      of purulent pleurisy, 540

Rhinoscope, history of, 21

Rhythm of endocardial murmurs, method of determining, 653

Ribs, resection of, in purulent pleurisy, 557

Rickets, influence on causation of laryngismus stridulus, 70

Right ventricle, physical signs of hypertrophy of, 627

Rigors in croupous pneumonia, 320

Rupture of splenic abscess, 963
  of the aorta, 823
  of the coronary artery, 833
  of the heart, spontaneous, 617
  of the pulmonary artery, 835
  of the spleen, 971
  of thoracic aneurism, 815


S.

Sacculated form of bronchial dilatation, 230

Salicylate of sodium, use, in rheumatic bronchitis, 181

Sanitaria for phthisical patients, 430

Sarcoma of larynx, 128-130
  of nasal passages, 55
  of thyroid gland, 978
  of the heart, 637
  of the mediastinum, frequency and history, 865-867

Scarification in laryngeal oedema, 116

Schrötter's tubes, use, in perichondritis and chondritis of larynx, 121
  dilators, in laryngeal oedema, 117

Schultze's granule-masses, absence of, in blood of pernicious anæmia,
        902
    in blood of Hodgkin's disease, 924
    increase of, in leukæmia, 912

Season, influence on causation of bronchitis, 168
      of croupous pneumonia, 315, 316
      of hæmoptysis, 277

Seat of collapse, in atelectasis, 253
  of lesions, in croupous pneumonia, 312
  of nasal polypus, 53
  of oedema of the lungs, 260
  of pulmonary emboli, 383
  of rupture of the aorta, 823
  of tracheal ulcers, 138

Sea-voyages, benefit upon course of pulmonary phthisis, 433
  value, for relief of hay asthma, 222

Secondary nature of pericarditis, 770
  pleurisies, etiology, 492

Secretion, alterations of, in chronic pharyngitis, 122

Semi-lunar ganglion, lesions, in Addison's disease, 944

Senegæ, use, in bronchitis, 179

Senile pneumonia, treatment, 351

Sensation of larynx-perversion, 61

Sensations, peculiar cardiac, in hypertrophy of the heart, 626

Septum, deflected, as a cause of chronic nasal catarrh, 44
  of auricles, defects of, cardiac malformations, 689
    and foramen ovale malformations, 689
  ventriculorum, patency of, in cardiac malformations, 690
    theories regarding patency, 699

Sequelæ of asthma, 189
  of cardiac thrombosis, 733
  of catarrhal pneumonia, 364
  of emphysema, 239
  of fibro-serous pleurisy, 512
  of hæmothorax, 582

Sex, influence on causation of angina pectoris, 759
      of aortic obstruction, 655
      of asthma, 190
      of cardiac thrombosis, 722
      of chronic myocarditis, 607
      of chronic pharyngitis, 121
      of croupous pneumonia, 314
      of exophthalmic goitre, 764
      of fatty degeneration of the heart, 613
      of fibro-serous pleurisy, 492
      of gangrene of lung, 302
      of hæmophilia, 933
      of hæmoptysis, 276
      of hay asthma, 212
      of Hodgkin's disease, 922
      of laryngeal oedema, 113
      of laryngismus stridulus, 70
      of leukæmia, 909
      of mediastinal tumors, 871
      of perichondritis and chondritis of larynx, 118
      of pernicious anæmia, 899
      of pneumothorax, 576
      of pseudo-membranous laryngitis, 101
      of thoracic aneurism, 803

Sexual excess, influence on causation of exophthalmic goitre, 765
        of functional heart disease, 752
        of hypertrophy of the heart, 619
    avoidance of, in functional heart disease, 755

Shape of heart in hypertrophy, 624

Shoemakers, frequency of mediastinal tumors in, 871

Shrinkage of lung in pulmonary phthisis, 417

Silver nitrate, spray, use, in acute catarrhal laryngitis, 97, 99
    use, in chronic inflammation of epiglottis, 110
      in chronic laryngitis, 125, 126
      in epiglottic ulceration, 112
      in erosion of epiglottis, 111
      in inflammatory non-hypertrophic form of chronic nasal catarrh,
          47
      in laryngeal oedema, 116
      in simple tracheitis, 135

Simple lymphangitis, 983

Skin, color, in chlorosis, 895
    in pernicious anæmia, 901
  discoloration of, in Addison's disease, 940
  state of, in croupous pneumonia, 328
  tumors of, in Hodgkin's disease, 925

Skodaic resonance on percussion in pleurisy, 501-503

Sodium bicarbonate and borate, use, in chronic laryngitis, 125
  sulphate, use, in Addison's disease, 938

Soil, humidity of, influence on causation of phthisis, 396

Souffle in abdominal aneurism, 822

Southey's capillary tubes, use, in hydrothorax, 572

Spasm of diaphragm, distinguished from asthma, 199
  of glottis in adults, 74
  of larynx in children, 70
  theory of origin of asthma, 193, 194

Special senses, modifications of, in Hodgkin's disease, 925
      in leukæmia, 911

Specific and septic emboli of the lungs, 386
  fevers, influence on causation of acute splenic congestion, 953
  germ of croupous pneumonia, 319

Sphygmograph, value, in diagnosis of thoracic aneurism, 809

Splashing sound in pneumothorax, 580

Spleen, changes in, in tricuspid regurgitation, 678, 679

SPLEEN, DISEASES OF, 952
  _Acute Congestion of_, 953
    Diagnosis, 955
    Etiology, 953
    Pathology and morbid anatomy, 955
    Prognosis, 955
    Symptoms, 954
    Treatment, 956
  _Chronic Congestion and Enlargement of_, 956
    Diagnosis, 958
    Etiology, 956
      Malaria, influence of, 956
    Pathological anatomy, 957
    Prognosis, 959
    Symptoms, 957
    Treatment, 959
      Arsenic, use, 960
      Extirpation, results of, 960
      Ice, locally, 960
      Iodine, use, 960
      Iron, use, 960
      Local, 960
      Quinia, use, 960
  _Echinococcus of_, 968
    Diagnosis, 969
    Morbid anatomy, 970
    Prognosis, 970
    Symptoms, 968
      Size and characters of the tumor, 969
    Treatment, 970
  _Embolic Abscess of_, 963
    Diagnosis and prognosis, 964
    Etiology, 963
      Micro-organism, influence of, 963
    Prognosis, symptoms, and treatment, 964
  _Hemorrhagic Infarction_, 960
    Etiology, 961
    Pathological anatomy, 961
      Infarcts, seat and characters, 961, 962
    Symptoms, 961
  _Lardaceous Spleen_, 966
    Diagnosis, 967
    Etiology, 966
    Pathological anatomy, 967
    Prognosis, symptoms, and treatment, 966, 968
  _Perisplenitis_, 965
    Etiology, 965
    Pathological anatomy, 965
  _Rupture_, 971
    Pathological anatomy, 972
    Symptoms and course, 972
  _Splenitis_, 962
    Pathological anatomy, 963
    Symptoms, 962
  _Syphilis of_, 970
  _Tubercle of_, 972
  _Tumors of_, 973

Spleen, displacement of, in pleurisy, 497, 507
  enlargement of, in Hodgkin's disease, 924
    in leukæmia, 914
  influence of, in production of blood-corpuscles, 889
    on blood-formation, 884
  lesions, in Addison's disease, 943
    in Hodgkin's disease, 927
    in leukæmia, 916
    in melanæmia, 897

Splenic abscess, diffuse, 962
  enlargement in syphilis, 971

Splenitis, 962

Spot, pneumonic, 328

Spray-producers, proper, in chronic laryngitis, 125, 126

Sputa, characters, in catarrhal pneumonia, 359-361
    in pneumonokoniosis, 455, 459
    in pulmonary phthisis, 401
  in fibroid phthisis, 441
  sanguinolent, in pulmonary embolism, 382

Sputum of croupous pneumonia, 322

Starvation method of treatment of thoracic aneurism, 816

Steam, inhalations, in chronic pharyngitis, 126

Stenosis, aortic, 654
  mitral, 665
  of trachea, 142
  of the trunk and main branches of the pulmonary artery, 834
  pulmonary, 674
  tricuspid, 677

Stillé, Moreton, on causation of cyanosis, 713

Stitch in the side in pleurisy, 493

Stimulants in catarrhal pneumonia, 371
  use, in abscess of lung, 300
    in Addison's disease, 948
    in angina pectoris, 760
    in cardiac thrombosis, 746
    in collapse of the lung, 256
    in croupous pneumonia, 348
    in functional heart disease, 753
    in pulmonary phthisis, 435
    in pseudo-membranous laryngitis, 108
    in simple lymphangitis, 991
    in thrombosis and embolism of the pulmonary artery, 836

Stomach, disease of, influence on causation of pulmonary embolism, 375
    displacement of, 507

Stomachic asthma, 193

Strain, influence on causation of thoracic aneurism, 802

Strapping of chest in pleurisy, 520

Stricture of trachea, 142

Strychnia, use, in acute myocarditis, 606
    in Addison's disease, 948
    in anæsthesia of larynx, 68
    in paralysis of larynx, 91
    in pseudo-membranous laryngitis, 108
    in respiratory failure of catarrhal pneumonia, 371
    in valvular heart disease, 685
    in vesicular emphysema, 216

Subclavian aneurism, localization of, 813

Subjective symptoms of croupous pneumonia, 319

Succussion sound in pneumothorax, 579

Sudden or fatal form of pulmonary embolism, symptoms, 379

Suffocation, sense of, in laryngeal oedema, 114

Sulphur, use, in pulmonary phthisis, 436

Sulphuretted hydrogen, use, in bronchial asthma, 209

Sulphuric acid, use, in epistaxis, 51

Superior tracheotomy, 148, 153

Suppurating hydatid cysts, treatment, 471

Suppuration, influence on causation of lardaceous spleen, 966
  of veins, 844, 845

Suppurative myocarditis, acute, 604

Suprarenal bodies, anomalies, 949
    atrophy of, 949
    changes in, in Addison's disease, 942
    cysts of, 949
    degenerations of, 949
    inflammation of, 949
    tumors of, 949

Surgical affections, influence on causation of pulmonary embolism, 376
  measures in pulmonary embolism, 390
  treatment of paralysis of vocal cords, 89
    of purulent pleurisy, 549

Sympathetic ganglia, lesions, in pernicious anæmia, 905
  system, relation of Addison's disease to, 945

Symptoms and course of asthma, 185
    of bronchial asthma, 185
  and treatment of atheroma of the aorta, 800
    of hydropericardium, 789, 790
    of pneumo-hydropericardium, 791
    of pyopericardium, 790
  of abdominal aneurism, 821
  of acute catarrhal laryngitis, 93
      congestion of the spleen, 954
      coryza, 41
      miliary tuberculosis, 478
      myocarditis, 606
      phlebitis, 845
  of Addison's disease, 940
  of adherent pericardium, 786
  of anæsthesia of larynx, 66
  of aneurism of the coeliac axis, 841
      of the coronary artery, 831
      of the inferior mesenteric artery, 839
      of the superior mesenteric artery, 836
  of angina pectoris, 755-757
  of aortic obstruction, 656
      regurgitation, 661
  of atheroma of aorta, 800
  of atrophic form of chronic nasal catarrh, 47
      lobar emphysema, 248
  of bronchial dilatation, 228
  of brown induration of lungs, 257
  of the caisson disease, 854
  of cancer of the lungs, 461, 462
  of cancer of pleura, 584
  of cardiac malformations, 709
      thrombosis, 726
  of catarrhal pneumonia, 358
  of chlorosis, 895
  of chorea of larynx, 76
  of chronic bronchitis, 174
      congestion of spleen, 957
      endarteritis of the coronary artery, 828
      inflammation of epiglottis, 110
      laryngitis, 121
      myocarditis, 608
      nasal catarrh due to necrosis, 49
        from osseous and membranous obstruction, 44
  of collapse of lung, 252
  of croupous pneumonia, 319
  of dilatation of the heart, 634
      of trachea, 144
  of echinococcus of spleen, 968
  of embolic abscess of spleen, 964
  of embolism of the coronary artery, 832
      of the superior mesenteric artery, 837
  of endocarditis, 646-649
  of epiglottic ulceration, 112
  of exophthalmic goitre, 762
  of fatty degeneration of the heart, 614
      infiltration of the heart, 612
  of fibroid phthisis, 441
  of fibro-serous pleurisy, 493
  of functional heart disease, 747-749
  of gangrene of lung, 302
  of goitre, 914
  of hæmophilia, 934
  of hæmoptysis, 281
  of hæmothorax, 582
  of hay asthma, 218
  of hemorrhagic infarction of spleen, 961
      pleurisy, 567
  of Hodgkin's disease, 923
  of hydatids of pleura, 585
  of hydrothorax, 571
  of hyperæsthesia of larynx, 62
  of hypertrophy of the heart, 624
  of hysterical affections of glottis, 83
  of inflammation of epiglottis, 109
  of inflammatory non-hypertrophic form of nasal catarrh, 47
  of lardaceous spleen, 966
  of laryngeal oedema, 113
  of laryngismus stridulus, 70
  of leukæmia, 910
  of mediastinal abscess, 862
      tumors, 822
  of mitral regurgitation, 671
      stenosis, 667
  of morbid growths of larynx, 130
        of trachea, 140
  of nasal polypus, 53
  of occlusion of the coronary artery, 831
      of the aorta, 825
  of paræsthesia of larynx, 64
  of paralysis of abductors of vocal cords, 87, 88
      of adductors of vocal cords, 82
      of central adductors of vocal cords, 85
      of constrictors of larynx, 80
      of external tensors of vocal cords, 86
      of tensors of vocal cords, 85
      of the whole larynx, 79
  of pericarditis, 773
  of perichondritis and chondritis of the larynx, 118
  of pernicious anæmia, 900
  of phlegmasia dolens, 847
  of pneumonokoniosis, 458
  of pneumothorax, 578
  of pseudo-membranous laryngitis, 101
  of pulmonary abscess, 297
      apoplexy, 294
      congestion and oedema, 260
      embolism, 378
      hydatids, 468
      phthisis, 400
      stenosis, 675
  of purulent pleurisy, 542
  of rheumatic pleurisy, 565
  of rupture of the aorta, 824
      of the heart, 617
      of the spleen, 972
  of sarcoma, carcinoma, and fibroma of nasal passages, 55
  of simple lymphangitis, 987
      tracheitis, 133
  of spasm of the glottis in adults, 74
  of splenitis, 962
  of stenosis of the aorta, 826
      of the pulmonary artery, 835
      of trachea, 142
  of syphilis of the lung, 451
  of termination of pneumonia in abscess, 332
  of thoracic aneurism, 803
  of thrombosis and embolism of the coronary artery, 832
      of the pulmonary artery, 836
  of tricuspid regurgitation, 679
      stenosis, 677
  of ulceration of trachea, 139
  of vesicular emphysema, 233, 236

Syncope and suffocation in pulmonary embolism, 379-381
  in cardiac thrombosis, 730

Synonyms of Addison's disease, 939
  of bronchial asthma, 184
  of bronchial dilatation, 227
  of bronchitis, 164
  of cancer of the lungs, 460
  of cardiac thrombosis, 718
  of catarrhal pneumonia, 353
  of chronic laryngitis, 121
  of croupous pneumonia, 307
  of gangrene of lung, 301
  of goitre, 974
  of hæmophilia, 932
  of hæmoptysis, 266
  of hay asthma, 210
  of Hodgkin's disease, 921
  of laryngeal oedema, 112
  of leukæmia, 908
  of lymphangitis, 986
  of perichondritis and chondritis of the larynx, 117
  of pernicious anæmia, 898
  of pleurisy, 483
  of pneumonokoniosis, 454
  of pulmonary abscess, 296
      embolism, 393
      hydatids, 466
      phthisis, 391
  of purulent pleurisy, 539
  of simple tracheitis, 133

Syphilis, influence on causation of abductors of vocal cords, 87
      of aneurism of the coeliac axis, 841
      of chronic myocarditis, 607
      of goitre, 977
      of lardaceous spleen, 966
      of leukæmia, 910
      of paralysis of adductors of vocal cords, 82
      of pleurisy, 493
      of thoracic aneurism, 803
  of the heart, 637

SYPHILIS OF THE LUNG, 447
  Definition, history, and etiology, 447
  Diagnosis and prognosis, 453
  Morbid anatomy, 451
  Pathology, 448
  Symptoms, 451
  Treatment, 453

Syphilis of the spleen, 970

Syphilitic and chronic laryngitis, 123
  disease of the lung, 447

Syphon process of draining pleural cavity, 555, 556
  use of, in thoracentesis, 530, 531


T.

Tannic acid, use, in chronic laryngitis, 126

Tapping in gangrene of the lung, 305, 306

Tar, use, in chronic laryngitis, 124

Taste and smell, loss of, from nasal polypus, 53

Temperament, influence on causation of hay asthma, 214

Temperature, changes of, influence on causation of bronchitis, 168
  diurnal variations, significance of, in diagnosis of catarrhal
        pneumonia, 365
  in acute catarrhal laryngitis, 94
  in acute miliary tuberculosis, 478
  in cancer of the lung, 462
  in capillary bronchitis, 171
  in catarrhal pneumonia, 358, 360, 361, 363
  in croupous pneumonia, 324-326
  in endocarditis, 647
  in fibro-serous pleurisy, 494
  in Hodgkin's disease, 925
  in leukæmia, 913
  in pernicious anæmia, 903
  in pseudo-membranous laryngitis, 102
  in pulmonary phthisis, 404
  in purulent pleurisy, 542
  of pericarditis, 774
  of the limb in acute phlebitis, 845

Termination of cardiac thrombosis, 732
  of fibro-serous pleurisy, 512
  of Hodgkin's disease, 929
  of pulmonary hydatids, 468
  of purulent pleurisy, 547
  of thoracic aneurism, 815

Theories regarding causation of cyanosis, 712
    origin of Addison's disease, 945
      of the caisson disease, 856

Thirst in croupous pneumonia, 330

Thoracentesis, albuminoid expectoration following, 536
  danger of, and objections to, 534
  death from, cause, 536-538
  duration of proper time to wait for absorption, 528
  during febrile stage of pleurisy, 526
  heart affections following, 536, 537
  history of, 586
  in fibro-serous pleurisy, 521
  in hemorrhagic pleurisy, 569
  in hydrothorax, 573
  in pleurisy, indications for, 521
      mode of operating, 530
  in purulent pleurisy, 550
  perforation of lung in, 538
  point of puncture, 532-534

Thoracic aneurism, 801

Thorax, shape of, in emphysema, 236, 237

Thrill, in thoracic aneurism, 808, 809
  purring, in mitral stenosis, 668, 669

Thrombosis and embolism of the pulmonary artery, 835, 836
  of the coronary artery, 832
  of the superior mesenteric artery, 839

Thyro-cricotomy, 148-154

Thyroid body, enlargement of, in exophthalmic goitre, 762
  gland, carcinoma and sarcoma of, 978
    diseases of, 974

Tinnitus aurium, from nasal polypus, 53

Tobacco, abuse of, influence of, on causation of chronic laryngitis,
        121
  avoidance of, in functional heart disease, 755
  influence on causation of hypertrophy of the heart, 619
      of functional heart disease, 752
  use, in bronchial asthma, 204

Tongue-spatula, proper mode of using, 109

Tongue, state of, in catarrhal pneumonia, 360
    in croupous pneumonia, 330

Tonics, use, in paralysis of larynx, 91

Toxic causes of anæmia, 889

Trachea, dilatation of, 143, 144
  diseases of, 133
  hernia and fistule, 143

TRACHEA, MORBID GROWTHS OF, 139
  Diagnosis and prognosis, 141
  Etiology, 139
  Pathology and symptoms, 140
  Treatment, 141

Trachea, stenosis of, 142, 143

TRACHEA, ULCERATION OF, 136
  Prognosis, 139
  Seat, 138
  Symptoms and treatment, 139

Tracheaectasy, 143

Tracheitis, complicated, 136

TRACHEITIS, SIMPLE, 133
  Diagnosis and prognosis, 134
  Morbid anatomy, 134
  Symptoms, 133
  Treatment, 135

Tracheocele, 144

Tracheoscopy, 134

TRACHEOTOMY, 145
  Accidents during, 156
  After-treatment, 159
  Complications arising after, 161
  Cricotomy, 156
  Indications for, 145
  Inferior tracheotomy, 155
  Median tracheotomy, 155
  Methods of operating, 155, 156
  Superior tracheotomy, 153
  Thyro-cricotomy, 154
    tube, choice, 150
      removal, 161

Tracheotomy in chronic laryngitis, 128
  in laryngeal oedema, 117
  in paralysis of abductors of vocal cords, 88
  in paralysis of larynx, 89
  in pseudo-membranous laryngitis, 107
  in spasm of the larynx, 75

Transfusion in pernicious anæmia, 907

Transposition of great arteries in cyanosis, 707

Traube's semi-lunar space, tympanitic sound in, in pleurisy, 503

Traumatism, influence on causation of fibro-serous pleurisy, 492
      of leukæmia, 910
      of lymphangitis, 986
      of mediastinal abscess, 861
      of pericarditis, 770
      of purulent pleurisy, 540

Treatment of abdominal aneurism, 823
  of acute catarrhal laryngitis, 96
      congestion of spleen, 955
      miliary tuberculosis, 480
      myocarditis, 606
      phlebitis, 846
  of Addison's disease, 948
  of adherent pericardium, 788
  of anæsthesia of larynx, 67
  of aneurism of the coeliac axis, 842
  of angina pectoris, 760
  of asthma, 201
  of atheroma of aorta, 801
  of atrophic emphysema, 249
  of atrophic form of nasal catarrh, 48
  of bronchial dilatation, 230
  of bronchitis, 170
  of caisson disease, 858
  of cancer of the lungs, 465
  of cancer of pleura, 584
  of carcinoma and sarcoma of nasal passages, 56
  of cardiac thrombosis, 745
      valvular disease, 683
  of catarrhal pneumonia, 369
  of chlorosis, 896
  of chorea of the larynx, 77
  of chronic congestion and enlargement of spleen, 959
      endarteritis of the coronary artery, 830
      inflammation of epiglottis, 110
      laryngitis, 124
      myocarditis, 609
      nasal catarrh due to necrosis, 50
          from osseous and membranous obstruction, 44
      phlebitis, 848
  of collapse of the lung, 255
  of coryza, 42
  of croupous pneumonia, 345
  of deflected nasal septum, 46
  of dilatation of the heart, 635
      of the veins, 850
      of trachea, 144
  of echinococcus of the spleen, 970
  of embolic splenic abscess, 965
  of embolism of the superior mesenteric artery, 839
  of endocarditis, 650
  of epiglottic ulceration, 112
  of epistaxis, 51
  of erosions of epiglottis, 111
  of exophthalmic goitre, 765
  of fatty degeneration of the heart, 616
  of fatty infiltration of the heart, 612
  of fibroid phthisis, 444
  of fibroma of nasal passages, 56
  of functional heart disease, 753
  of gangrene of lung, 305
  of goitre, 979
  of hay asthma, 222
  of hæmopericardium, 789
  of hæmophilia, 938
  of hæmoptysis, 291
  of hæmothorax, 583
  of hemorrhagic pleurisy, 568
  of Hodgkin's disease, 931
  of hydatids of pleura, 586
  of hydrothorax, 572
  of hyper- and paræsthesia of larynx, 64
  of hypertrophy of the heart, 630
  of inflammation of the epiglottis, 109
  of inflammatory non-hypertrophic form of nasal catarrh, 47
  of lardaceous spleen, 967
  of laryngeal oedema, 116
  of laryngismus stridulus, 71
  of leukæmia, 920
  of mediastinal abscess, 863
      tumors, 880
  of morbid growths of larynx, 131
        of trachea, 141
  of nasal polypus, 54
  of nervous cough, 77
  of paralysis of larynx, 88
  of pericarditis, 783, 784
  of perichondritis and chondritis of the larynx, 121
  of pleurisy, 519
  of pneumonokoniosis, 459
  of pneumothorax, 581
  of progressive pernicious anæmia, 906
  of pseudo-membranous laryngitis, 104
  of pulmonary abscess, 300
      apoplexy, 295
      congestion and oedema, 263
      embolism, 388
      hydatids, 470
      phthisis, 425
  of purulent pleurisy, 549
  of rheumatic bronchitis, 181
      pleurisy, 565
  of simple lymphangitis, 990
      tracheitis, 135
  of spasm of the glottis in the adult, 74
  of stenosis of the aorta, 825, 827
      of trachea, 143
  of syphilis of the lung, 453
      of the spleen, 971
  of thoracic aneurism, 816
  of thrombosis and embolism of the pulmonary artery, 836
  of ulceration of trachea, 139
  of vesicular emphysema, 245
  operative, of pericardial effusions, 794

Tricuspid disease, prognosis, 683
    treatment, 686
  regurgitation, 678
  stenosis, 677
  valve, defects of, in cardiac malformations, 689

Tube, tracheotomy, choice of a proper, 150
  management of, after tracheotomy, 160

Tubercle, influence on causation of purulent pleurisy, 540
  of the heart, 637
  of the spleen, 972

Tubercles, histology, mode of formation, etc., 474-476
  miliary, formation, 475, 476
    physical characters, 474

Tubercular diathesis, 476, 477
  laryngitis, diagnosis, 95
  pericarditis, 793
  phthisis, following pleurisy, frequency, 513
  pleurisy, 569
  process, nature, 375

TUBERCULOSIS, ACUTE MILIARY, 472
  Contagiousness of, 472
  Definition, 472
  Etiology, pathology, etc., 472-478
    Age, influence of, 478
    Bacillus tuberculosis, relation to, 473
    Bad air, hygiene, etc., influence of, 473
    Catarrho-pneumonia, relation to, 476
  Symptoms and course, 478
    Of partial or local form, 479
    Physical signs, 479
    Temperature, 478
  Treatment, 480
    Antipyrine, use, 481
    Codeia, use, 482
    Cod-liver oil and hypophosphites, 482
    Diet in, 481
    Quinia, use, 480
    Stimulants, 481

Tuberculosis complicating and following catarrhal pneumonia, 364
  in Addison's disease, 943
  relation of, to stenosis of pulmonary artery, 711
      to chronic laryngitis, 123

Tubular lymphangitis, symptoms, 987

Tufnell's method of treating aneurism, 816

Tumor, aneurismal, of abdomen, characters, 822
  characters of, in echinococcus of spleen, 969
  presence of, in dilatation of trachea, 144
  splenic, size in congestion of spleen, 954

Tumors, leukæmic, frequency, characters, etc., 918
  of mediastinum diagnosed from pericarditis, 780
  of suprarenal bodies, 949
  of the spleen, 973

Turpentine, inhalations in acute catarrhal laryngitis, 97
  use, in bronchial dilatation, 231
    in hæmoptysis, 291
    in pseudo-membranous laryngitis, 106
    in pulmonary hydatids, 470

Tympanitic resonance in pneumothorax, 571

Typhoid pneumonia, 333


U.

Ulcer of the heart, 605

Ulceration of trachea, 136
    following tracheotomy, 162

Ulcerations of epiglottis, 111
  of septum as a cause of epistaxis, 51

Ulcerative endocarditis, 642
  form of hæmoptysis, 283

Urine and ovarian irritation, as a cause of asthma, 193
  changes in, in Hodgkin's disease, 925
    in leukæmia, 913
  condition in pernicious anæmia, 903
  in Addison's disease, 941
  in tricuspid regurgitation, 679
  state of, in capillary bronchitis, 171
    in catarrhal pneumonia, 360
    in mitral regurgitation, 671
    in pneumonia, 330

Uterus, disease of, influence on causation of pulmonary embolism, 375


V.

Valves, changes in, in aortic obstruction, 654, 655
        regurgitation, 659
    in mitral regurgitation, 670
        stenosis, 665
  condition, in tricuspid regurgitation, 678
  lesions of, in acute exudative endocarditis, 641
    in interstitial endocarditis, 643
    in tricuspid stenosis, 675
    in ulcerative endocarditis, 642

Valvular disease, influence on causation of dilatation of the heart,
          632
        of hypertrophy of the heart, 620, 623

Varicose aneurism, 802
    signs of, 813
  veins, 849

Varieties of dilatation of the heart, 630
  of goitre, 977
  of hypertrophy of the heart, 619

Variola, acute tracheitis in, 136

Vascular goitre, 977
    treatment, 980
  supply of lung, relation to hæmoptysis, 269

Vegetations in ulcerative endocarditis, 642

Vein-stones, 853

VEINS, DISEASES OF, 843
  _Degenerations of_, 852
  _Dilatation_, 849
    Treatment, 850
      Pressure, 850
  _Inflammation_, 843
    Diagnosis, 846
    Pathology and morbid anatomy, 843-845
      Formation of a clot preceding inflammation, 843, 844
      Suppuration of vein, seat and character, 844, 845
    Symptoms, 845
      General, 845, 846
      Local, 845
    Treatment, 846
      Blisters, use, 846
      Calcium sulphide, use, 846
      Fomentations, 846
      Ice, use, 846
      Rest and position, necessity of, 846
    Phlebitis, chronic, 848
    Phlegmasia dolens, 846
    Puerperal state, influence on causation, 847
    Symptoms and treatment, 847, 848
  _Narrowing of a Vein_, 851
  _Occlusion of Veins_, 851
    Treatment, 852
  _Phlebolithes_, 853

Veins of neck, turgidity of, in cardiac thrombosis, 730
  pressure upon, in thoracic aneurism, 807

Venesection, harmfulness of, in croupous pneumonia, 346
  in acute bronchitis, 178
  in pulmonary embolism, 390

Venous hum in pernicious anæmia, 903

Ventricle, right, alteration in form in cardiac malformation, 695

Vesicular emphysema, 232

Vessels, great, congenital anomalies of, and cyanosis, 687

Viscera, lesions, in pseudo-membranous laryngitis, 101

Vision, distortion of, in croupous pneumonia, 329

Vital or pathological causes of cardiac thrombosis, 724

Vitality, depressed, influence on causation of croupous pneumonia, 314,
        315

VOCAL CORDS, PARALYSIS OF ADDUCTORS OF, 81
  Abductors, 86
  Central adductors, 84
  External tensors, 86
  Tensors, 85
  Treatment, 88
    Electricity in, 90
    Surgical, in, 90
    Tonics in, 91
    Tracheotomy in, 89

Vocal resonance in pulmonary phthisis, 413, 417

Voice, alteration of, in chronic laryngitis, 122
    in dilatation of trachea, 144
    in goitre, 975
    in morbid growths of the larynx, 129
  improper use, influence on causation of hyperæsthesia of the larynx,
        62
  in epiglottic ulceration, 112
  in hysterical affections of glottis, 83
  in laryngismus stridulus, 71
  in morbid growths of trachea, 140
  in paralysis of adductors of vocal cords, 82
      of tensors of vocal cords, 85, 86
      of whole larynx, 80
  over-use of, influence on causation of chronic laryngitis, 121
  sounds in fibro-serous pleurisy, 510
  transmission of, in purulent pleurisy, 543, 545

Vomiting in the caisson disease, 854
  in diaphragmatic pleurisy, 563
  in embolism of the superior mesenteric artery, 837
  in endocarditis, 647
  in pulmonary phthisis, 406


W.

Waldenburg's apparatus for emphysema, 246

Wasting of pleural cavity in purulent pleurisy, 551, 553-562

Water, influence on causation of goitre, 976

Whispered voice, importance in diagnosis of pulmonary phthisis, 413,
        417
    transmission of, and significance in pleurisy, 510, 512

White corpuscles of the blood, increase of, in leukæmia, 912
  leg, 846

Whooping cough, influence on causation of acute miliary tuberculosis,
        473

Wildegger water, use, in goitre, 980

Wire, fine, introduction into sac for relief of aneurism, 816

Worms, influence on causation of laryngismus stridulus, 70

Wounds, etc., influence on causation of pulmonary embolism, 376


Y.

Yeo's respirator, use, in chronic laryngitis, 126


Z.

Zinc sulphate, use, in chronic laryngitis, 126




END OF VOLUME III.






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