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Title: A System of Practical Medicine By American Authors, Vol. III - Diseases of the Respiratory, Circulatory, and Hæmatopoietic Systems
Author: Various
Language: English
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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