A TEXT-BOOK 
OF 
PRACTICAL MEDICINE, 
WITH PARTICULAR REFERENCE TO 
PHYSIOLOGY AND PATHOLOGICAL ANATOMY. 
BY 
DR. FELIX YON 
PROFESSOR OF PATHOLOGY AND THERAPEUTICS, DIRECTOR OF THE MEDICAL CLINIC OF THE 
UNIVERSITY OF TUBINGEN. 
TRANSLATED FROM TILE EIGHTH GERMAN" EDITION", BY SPECIAL 
PERMISSION OF THE AUTHOR. 
BY 
GEORGE H. HUMPHREYS, M. D., 
LATE ONE OF THE PHYSICIANS TO THE BUREAU OF MEDICAL AND SURGICAL RELIEF AT 
BELLEYUE HOSPITAL FOR THE OUT-DOOR POOR, FELLOW OF THE NEW- 
YORK ACADEMY OF MEDICINE, ETC. 
AND 
CHARLES E. IIACKLEY, M. D., 
ONE OF THE PHYSICIANS TO THE NEW-YORK HOSPITAL, ONE OF TnE SURGEONS TO THE 
NEW-YORK EYE AND EAR INFIRMARY, FELLOW OF THE NEW- 
YORK ACADEMY OF MEDICINE, ETC. 
VOLUME I. 
REVISED EDITION. 
NEW YORK: 
D. APPLETON AND COMPANY, 
549 & 551 BROADWAY. 
1871. Entered, according to Act of Congress, in the year 1869, by 
D. APPLETON & CO., 
In the Clerk’s Office of the District Court of the United States for the 
Southern District of Mew York. The late PEOF. VON NIEMEYEK, M. D. 
From a recent Photograph. 
SPECIMEN OF ILLUSTRATIONS FROM TUE N. Y. MEDICAL JOURNAL. Descriptive Catalogue of Medical Works 
NEUMANN. 
Hand-Book of Skin Diseases. 
By Dr. ISIDOR NEUMANN, 
Lecturer on Skin Diseases in the Royal University of Vienna. 
Translated from advanced sheets of the second edition, furnished by the 
Author; with Notes, 
By LUCIUS D. BULKLEY, A. M., M. D., 
Surgeon to the New York Dispensary, Department of Venereal and Skin Diseases; Assist- 
ant to the Skin Clinic of the College of Physicians and Surgeons, New York; Mem- 
ber of the New York Dermatological Society, etc., etc. 
1 vol., 8vo. About 450 pages and 66 Woodcuts. Cloth, $4.00. 
SPECIMEN OP ILLUSTRATIONS. 
Section of skin from a bald head. 
Prof. Neumann ranks second only to Hebra, whose assistant he was for many years, 
and his work may be considered as a fair exponent of the German practice of Dermatolo- 
gy. The book is abundantly illustrated with plates of the histology and pathology of the 
skin. The translator has endeavored, by means of notes from French, English, and Ameri- 
can sources, to make the work valuable to the student as well as to the practitioner. 
“ It is a work which I shall heartily recommend to my class of students at the Univer- 
sity of Pennsylvania, and one which I feel sure will do much toward enlightening the pro- 
fession on this subject.”—Louis A. Duhring. 
“ I know it to be a good hook, and I am sure that it is well translated; and it is inter- 
esting to find it illustrated by references to the views of co-laborers in the same field.”— 
Erasmus Wilson. 
“ So complete as to render it a most useful book of reference.”—T. McCall Anderson. 
“There certainly is rio work extant which deals so thoroughly with the Pathological 
Anatomy of the Skin as does this hand-book.”—N. T. Medical Record. 
“ The original notes by Dr. Bulkley are very practical, and are an important adjunct to 
the text. . . . I anticipate for it a wide circulation.”—Silas Durkee, Boston. 
“I have already twice expressed my favorable opinion of the hook in print, and am 
glad that it is given to the public at last."—Tames C. White, Boston. r 
“More than two years ago we noticed Dr. Neumann’s admirable work in its original 
shape; and we are therefore absolved from the necessity of saying more than to repeat 
four strong recommendation of it to English readers.”—P?-actitimer. TRANSLATROS’ PREFACE TO THE REVISED EDITION. 
The translators are pleased to find that the medical public 
sustain their own opinion of the practical value of Prof. Nie- 
meyer’s Text-Book, and take pleasure in presenting the present 
edition, which is altered to correspond with the eighth and 
latest German edition. 
Two new articles on “ Relapsing Fever,” and “ Suette 
Miliaire,” and some extensive remarks on the employment of 
bromide of potassium in the treatment of epilepsy, hypodermic 
injections of corrosive sublimate in syphilis, and employment of 
the stomach-tube in dilatation of the stomach, etc., are the chief 
additions. 
The translators also take great pleasure in noticing the favor- 
able reception of this "work in England, showing the interest 
felt there as well as here in the ideas of the modern German 
school of medicine. PREFACE TO THE EIGHTH EDITION. 
The accompanying work, whose scope and contents are well 
known to the medical world, scarcely needs a preface. 
The task which I have undertaken is a twofold one: first, 
to give a picture of disease which should he as lifelike and 
faithful to nature as possible, instead of being a mere theoretical 
scheme; secondly, so to utilize the more recent advances of 
pathological anatomy, physiology, and physiological chemistry, 
as to furnish a clearer insight into the various processes of disease. 
The very favorable reception which my book has obtained, both 
from practitioners and students of medicine, proves that the 
undertaking was not only timely, but most urgently needed. 
A series of editions, renewed at very regular intervals, has 
enabled me to make my work constantly keep pace with the 
advance of modern medicine and her kindred studies. 
The eighth edition may truly be described as enlarged and 
improved. In many of the chapters important insertions have 
been made—chiefly upon the subject of therapeutics—and two 
entirely new chapters upon relapsing fever and the sweating- 
sickness have been added. 
(Signed) 
Felix vox JSTiemeyek. 
October 26, 1870 PEEFACE TO THE SEVENTH EDITION 
Is early ten years have elapsed since the first appearance of 
my text-hook. Meanwhile, clinical medicine owes a rich acces- 
sion of knowledge to investigations made, not only in her own 
province, hut in the provinces of physiology, pathological anat- 
omy, and physiological and pathological chemistry. Important 
questions have been settled; obscure points rendered clear; false 
theories corrected, and errors recognized. 
Although, in preparing previous editions, I have taken pains 
to keep my book well up to the existing state of science, to ren- 
der account of the most important advances made in the study 
of medicine and its kindred branches, yet the briefness of the 
time allowed for this purpose—owing to the rapidity with which 
editions have been renewed—and the conviction that the true 
value of many discoveries of supposed importance could be as- 
certained only by a longer probation, have hitherto deterred me 
from a full and thorough revision of the entire work. At last, 
ten years after its first appearance, the proper moment seems to 
have arrived. The somewhat longer respite now allowed me for 
my task, is due to the foresight of my publisher, who has made 
the previous edition of triple the usual size. 
In the present (seventh edition), but few portions of the work 
remain unaltered; and even those few have nearly all undergone 
revision on previous occasions. Most parts of it have received 
valuable emendations, and have been enriched by copious addi- 
tions. I have everywhere paid particular attention to the im- VIII 
PREFACE TO THE SEVENTH EDITION. 
portant results obtained in tlie domain of therapeutics by recent 
investigations, partly because I wish my book to maintain the 
honorable confidence which it has won for itself among practical 
physicians; partly because I regard the happy progress which 
therapeusis has made, as the most important acquisition of the 
last ten years. 
This progress I attribute mainly to the fact that, of late years, 
medical explorers have recognized the only path by which thera- 
peutic science can be advanced, and have followed it with bril- 
liant results. My outspoken assertions of ten years ago have 
come true. I then denounced the error of postponing all medi- 
cal treatment of disease, until our knowledge of the action of 
medicines, and our insight into pathological processes, should be 
so far advanced, that means of cure would be self-evident. I 
pronounced this ideal goal to be unattainable, and declared it 
idle to hope for a time wdien a medical prescription should be 
the simple resultant of a computation of known quantities. I 
lamented that physicians, instead of striving to promote the 
healing art by their own efforts, should seek aid from the insti- 
tutes of physiology and pathology, or from the laboratory of the 
chemist, obtaining now and then an ingenious suggestion, but 
never gaining an idea serviceable in the relief of an afflicted fel- 
low-creature. I further showed that experiments made with 
medicaments upon the lower animals, or upon healthy human 
beings, with all their scientific value, had as yet been of no direct 
service to our means of treating disease, and that a continuation 
of such experiments gave no prospect of such service. I finally 
declared, without reservation, that even the dazzling progress 
which pathology had made, had been of but little use to thera- 
peutics ; that, in spite of new discoveries, our present success at 
the bedside is scarcely more favorable than that of fifty years 
ago; nor in the future would pathological investigation promote 
therapeutic success, unless directed more in accordance with the 
requirements of general medicine, than has been done hitherto. 
Thus, after showing that therapeusis must expect no aid PREFACE TO TIIE SEVENTH EDITION. 
IX 
from other incomplete sciences, and that it must he conducted 
by itself as an independent and peculiar branch of knowl- 
edge; after showing, further, that the empirical method of 
investigation is the only rational and proper one for the 
study either of therapeutics, or of any other department of 
natural science, I pointed out more precisely what material 
we already possessed for the establishment of therapeusis as 
an independent empirical study; showed what still remained 
to be done, and how that which is still lacking is to be obtained. 
I then demonstrated that, before all else, empirical knowledge 
requires a profound and thorough acquaintance with facts, and 
that the more accurate the observation, so much the more cor- 
rect and trustworthy must the deduction be, and that observa- 
tions in therapeusis, if inaccurate or imperfect, are prolific of 
false conclusions and of erroneous proceedings, just as in other 
branches of natural science. I explained that, when ancient 
therapeutic laws, based sometimes upon the experience of cen- 
turies, have proved false, the error has been due to inexact and 
incomplete observation; that the general impression that a 
remedy has done good or harm, in this or that disease, is utterly 
worthless in a scientific point of view. I declared that empiri- 
cal matter, capable of affording trustworthy and useful rules for 
the treatment of disease, is only to be obtained by the most 
careful and intelligent investigation of the healing effects of 
medicaments; that no sure basis for therapeusis can be estab- 
lished until this shall occur; until clinical teachers and physicians, 
particularly those at the head of the science, familiar with all 
the accessories to diagnosis, shall comprehend that their main 
task is, most carefully (and, where possible, objectively) to ana- 
lyze the symptoms of a disease, prior to and subsequent to the 
administration of a supposed remedy; that such (no doubt very 
laborious) investigations have hitherto been totally neglected, 
because no one expected to obtain any results from such a method 
of study; but that these pessimist views evince an undervalua- 
tion of the brilliant progress of physical diagnosis, of physiol- X 
PREFACE TO TI1E SEVENTH EDITION. 
ogy, of pathological anatomy, and pathological chemistry, made 
in the last ten years. Although direct and immediate advantage 
to the art of healing is not to he expected of any of these 
branches of learning, yet every new discovery, in its way, tends 
to benefit that art, either by improving our knowledge of disease, 
or by assisting our comprehension of the modus operands of 
medicines. My conviction is, that from the present state of 
knowledge, from our deeper insight into the origin and relation 
of symptoms from the improved accessories, by means of which 
we are now enabled to follow the various phases and modifica- 
tions of disease, the; prospect of obtaining sure and authentic 
therapeutic facts, by dint of accurate comparison of results, is 
not only by no means unfavorable, but, judging from present 
experience, is positively certain. 
Seven years ago, I closed my inaugural address at Tubingen 
with the following words: “ The task is a laborious one; the 
“ difficulties are great; but the knowledge that this is the sole 
“path leading to the wished-for goal, the conviction that the 
“ smallest well-authenticated fact in therapeutics is of profound 
“ importance, will inspire the perseverance in research requisite 
“ to make tlierapeusis an exact science, a science which may take 
“equal rank with other branches of physical study.” I may 
now say that my anticipations have been well-nigh surpassed. 
A band of distinguished teachers have carried out these labori- 
ous researches with a thoroughness and perseverance which could 
not fail in its effect. The valuable labors, now under prosecu- 
tion, in the long-neglected field of treatment of disease, by 
means of which, already, the value of certain important articles, 
hitherto ill-appreciated, has been accurately determined, have re- 
ceived general recognition, and thus a final blow has been given 
to the dominion of a disheartening therapeutic nihilism. This 
success, as an example of which I will merely mention the dis- 
covery of the antipyretic action of quinia in typhus, pneumonia, 
etc., and the establishment of precise indications for the use of 
digitalis in disease of the heart, has caused the zeal for therapeu- PREFACE TO THE SEVENTH EDITION. 
XI 
tic experimentation to assume a direction destined to lead to 
great results. Rightly supposing that even the rude experience 
of the ignorant laity and their belief in the all-healing power 
of the “ cold-water cure ” and the “ bread cure ” have some foun- 
dation in fact, the effects both of hydropathic treatment and that 
of the continued limitation of the supply of water to the sys- 
tem have been subjected to rigid analysis. Such laudable abne- 
gation of sectarian pride has been richly rewarded. Among 
other results, we owe to it our more accurate knowledge of the 
effect produced by active abstraction of heat upon the tempera- 
ture of the body in acute febrile disease. This alone is a great 
achievement. By its means, a weapon, powerful for good in 
time of peril, is taken from the hands of the laity, where it has 
done much harm, and, under control of educated and experienced 
men, wdio know its capacity and how to regulate its effect, it has 
become the common property of science. It is a favorable sign 
that the warm recognition and support formerly enjoyed by the 
so-called “doctrine of Rademacher”—that wonderful offspring 
of a clear perception of the errors and failings of traditional 
therapeutic rules, and of blind submission to the obsolete teach- 
ings of Paracelsus—have become extinct; and still better, that 
the number of pure and devout homoeopaths, who, implicitly 
trusting in homoeopathic tenets and doses, make no use of the 
developments of therapeutic research, has grown small. 
May these words, and the contents of my book, aid clinical 
investigation in pursuing more and more the path by which 
alone its immediate and main object—the establishment of thera- 
peutic facts—is to be attained! 
In conclusion, I tender my cordial thanks to my numerous 
friends and patrons for their favor; especially to my honored 
friend and colleague Professor Seitz, of Giessen, for the good 
counsel with which he has assisted me in the preparation of mv 
new edition. (Signed) 
Felix yon Riemeyek. 
Tubingen, October, 1867 TABLE OF CONTEXTS OF VOL. I. 
DISEASES OF THE RESPIRATORY ORGANS. 
AFFECTIONS OF THE LARYNX. 
SECTION I. 
Chap. I.—Hyperemia and Catarrh of the Larynx, 1 
II.—Croup, Angina Membranacea, 15 
III. —Catarrhal Ulcers of the Larynx, 31 
IV. —Typhous and Variolous Ulcers of the Larynx, 33 
V.—Syphilitk>Diseases of the Larynx, 35 
VI.—Tubercular Ulceration of the Larynx, 38 
VII.—Growths in the Larynx, 43 
VIII.—(Edema Glottidis, . 45 
IX.—Laryngeal Perichondritis, 49 
Pi GH 
X.—Spasmus Glottidis, 51 
XI.—Paralysis of the Muscles of the Glottis, 54 
NERVOUS DISEASES OF THE LARYNX. 
SECTION II. 
Chap. I.—Hyperemia and Catarrh of the Air-passages, 59 
II.—Croupous Inflammation of the Trachea and Bronchi, .... 84 
III. —Spasm of the Bronchi, Bronchial Asthma, 86 
IV. —Spasm of the Bespiratory Muscles, 91 
V.—Whooping-cough, Tussis Convulsive, 92 
DISEASES OF THE TRACHEA AND BRONCHI. 
DISEASES OF THE PARENCHYMA OF THE LUNGS. 
SECTION III. 
Jhap. I.—Hypertrophy of the Lung, 104 
II.—Atrophy of the Lung, Emphysema Senile, 105 
III.—Emphysema of the Lung, 106 
IY.—Collapse of the Lung, 126 
Y.—Hyperemia, (Edema of the Lung, 130 
YI.—Bronchial Hemorrhage, 141 
VII.—Pulmonary Haemorrhage, 153 
VIII.—Apoplexy of the Lung, 161 
IX.—Croupous Pneumonia, 162 
X.—Catarrhal Pneumonia, 190 
XI.—Induration of the Lung, 195 
XII.—Gangrene of the Lung, 203 XIV 
TABLE OF CONTENTS OF VOL. I. 
TUBERCULOSIS OF THE LUNG. 
PAQK 
Chap. XIII.—Pulmonary Consumption, 208 
XIV.—Acute Miliary Tuberculosis, 247 
XV.—Cancer of the Lung, 251 
DISEASES OF TEE PLEURA. 
SECTION IV. 
Chap. I.—Inflammation of the Pleura, 253 
II.—Hydrothorax, 273 
III. —Pneumothorax, 276 
IV. —Tuberculosis of the Pleura, 283 
V.—Cancer of the Pleura, 284 
APPENDIX TO THE DISEASES OF THE RESPIRATORY ORGANS. 
DISEASES OF TEE NASAL CAVITIES. 
Chap. I.—Catarrh of the Nasal Mucous Membrane, 286 
II.—Bleeding at the Nose, Epistaxis 292 
DISEASES OF THE CIRCULATORY ORGANS. 
SECTION I. 
DISEASES OF TEE EEART. 
Chap. I.—Hypertrophy of the Heart, . 297 
II.—Dilatation of the Heart, 316 
III. —Atrophy of the Heart, 325 
IV. —Endocarditis, 328 
V.—Myocarditis, 340 
VALVULAR DISEASES OF THE HEAET. 
VI.—Insufficience of Semilunar Valve, 345 
VII.—Insufficience of Mitral Valve, 351 
VIII.—Insufficience of Semilunar Valve and Contraction of the Mouth of the 
Pulmonary Artery, 359 
IX.—Insufficience of the Tricuspid, 360 
X.—Degeneration of the Substance of the Heart, 361 
XI.—Bupture of the Heart, 364 
XII.—Fibrinous Deposits in the Heart, 365 
XIII. —Congenital Anomalies of the Heart, 366 
XIV. —Neuroses of the Heart, 370 
XV.—Basedow’s Disease, 374 
SECTION II. 
Chap. I.—Pericarditis, 379 
II.—Adhesion of the Heart and Pericardium, ...... 389 
III.—Hydropericardium, 391 
DISEASES OF TEE PERICARDIUM. TABLE OF CONTENTS OF VOL. I. 
XV 
Chap. IV.—Pneumopericardium, 393 
V.—Tuberculosis of the Pericardium, 395 
VI.—Cancer of the Pericardium, 395 
SECTION III. 
DISEASES OF THE GREAT VESSELS. 
Chap. I.—Inflammation of the Coats of the Aorta, 396 
II. —Aneurism of the Aorta, 400 
III. —Rupture of the Aorta, 409 
IV. —Stricture and Obliteration of the Aorta, 410 
V.—Diseases of the Pulmonary Artery, 411 
VI.—Diseases of the Great Venous Trunks, 412 
DISEASES OF THE OEGANS OF DIGESTION. 
SECTION I. 
Chap. I.—Catarrh of the Mouth, 414 
II. —Croupous Stomatitis, Aphthae, 420 
III. —Diphtheritic Stomatitis, Cancrum Oris, 422 
IV. —Excoriations and Ulcers of the Mouth, 424 
V.—Syphilitic Affections of the Mouth, 427 
VI.—Scorbutic Affections of the Mouth, 428 
VII.—Soor, Muguet, Thrush, . 430 
VIII.—Glossitis, 432 
IX.—Gangrenous Sore Mouth, 434 
X.—Parotitis, Mumps, ' . 436 
XI.—Salivation, Ptyalism, 441 
DISEASES OF TnE MOUTH. 
SECTION II. 
AFFECTIONS OF TnE PHARYNX. 
Chap. I.—Angina Catarrlialis, 445 
II.—Pharyngeal Croup, 451 
III. —Diphtheritic Inflammation of the Pharynx, 452 
IV. —Phlegmonous Inflammation of the Pharynx, 453 
V.—Syphilitic Affections of the Pharynx, 456 
VI.—Retropharyngeal Abscess, 458 
VII.—Angina Ludovici, 459 
AFFECTIONS OF THE (ESOPHAGUS. 
SECTION III. 
Chap. I.—Inflammation of the (Esophagus, 461 
II.—Strictures of the (Esophagus, . . 463 
III. —Dilatation of the (Esophagus, 466 
IV. —Morbid Growths of the (Esophagus, 467 
V.—Perforation and Rupture of the (Esophagus, 4:69 
VI.—Nervous Affections of the (Esophagus, 470 XVI 
TABLE OF CONTENTS OF VOL. I. 
SECTION IV. 
PAGE 
Chap. I.—Acute Gastric Catarrh, 472 
II.—Chronic Gastric Catarrh, 490 
III. —Croupous Inflammation, 503 
IV. —Gastritis Phlegmonosa, 503 
V.—Inflammations from Caustics and Poisons, 504 
VI.—Chronic Ulcer of the Stomach, 506 
VII.—Carcinoma of the Stomach, 516 
VIII.—Haemorrhage from the Stomach, 523 
. IX.—Spasm of the stomach, * 529 
X.—Dyspepsia, 533 
DISEASES OF THE STOMACH. 
SECTION V. 
AFFECTIONS OF THE INTESTINAL CANAL. 
Chap. I.—Catarrhal Inflammation, 542 
II.—Perforating Duodenal Ulcer, . 559 
III. —Contractions and Closures, 502 
IV. —Scrofu" ous and Tuberculous Diseases of the Intestines and Mesenteric 
Glands, 5T4 
V.—Carcinoma of the Intestines, 580 
VI.—Perityphlitis and Periproctitis, 583 
VII.—Haemorrhages and Vascular Dilatations, 585 
VIII.—Colic, Enteralgia, 593 
IX.—"Worms in the Intestines, 598 
X.—Gastric Fever, 606 
SECTION VI. 
DISEASES OF THE PERITONAEUM. 
Chap. I.—Peritonitis, 611 
II.—Ascites 622 
III.—Tuberculosis and Cancer, 627 
DISEASES OF THE LIVER AND BILE-DUCTS. 
SECTION I. 
Chap. I.—Ilypersemia of the Liver, 629 
II.—Suppurative Hepatitis, 637 
III. —Cirrhosis of the Liver, 642 
IV. —Syphilitic Hepatitis, 653 
V.—Inflammation of the Portal Vein, 655 
VI.—Fatty Liver, 657 
VII.—Lardaceous Liver, 662 
VIII.—Cancer of the Liver, 664 
IX.—Tuberculosis of the Liver, 668 
X. —Echinococci of the Liver, ......... 669 
XI. —Multilocular Hydatids, 673 
DISEASES OF THE LIVER. TABLE OF CONTENTS OF VOL. I. 
XVII 
PAGE 
Chap. XII.—Hepatogenous Icterus, 677 
XIII. —Hematogenous Icterus, 686 
XIV. —Acute Yellow xltrophy of the Liver, 689 
SECTION II. 
Chap. I.—Catarrh of the Gall-ducts, 694 
II.—Croupous and Diphtheritic Inflammation, 697 
III. —Obstruction and Closure of the Excretory Gall-ducts, etc., . . 698 
IV. —Gall-stones and their Consequences, 100 
DISEASES OF THE GALL-DUCTS. 
DISEASES OF TIIE SPLEEN. 
Chap. I.—Hypersemia of the Spleen, 707 
II.—Hypertrophy of the Spleen, 713 
III. —Lardaceous Spleen, 718 
IV. —Haemorrhagic Infarction of the Spleen, 719 
V.—Tuberculosis, Carcinoma, Hydatids, 722 
APPENDIX TO THE DISEASES OF THE SPLEEN. 
Chap. I.—Leuchsemia, Leucocythsemia, 723 
TI.—Melan®mia, 728 DISEASES OF THE RESPIRATORY ORGANS. 
SECTION I. 
AFFECTIONS OF TIIE LARYNX. 
CHAPTER I. 
HYPERCEMIA AXD CATARRH OF THE MUCOUS MEMBRANE OF THE 
LARYNX. 
Etiology.—Catarrh consists in engorgement of the blood-vessels of 
any mucous membrane, accompanied by abnormal secretion, swelling, 
succulence of its tissues, and copious generation of young cells. Catarrh 
may arise from a purely mechanical hypercemia of the mucous mem- 
brane ; gastric and intestinal catarrhs are not unfrequently the result of 
compression of the portal vein; bronchial catarrh, the consequence of 
embarrassed flow into a diseased heart from the bronchial and pulmonary 
veins. We are therefore fully wTarranted in treating of hyperaemia and 
catarrh of the larynx and bronchi in the same chapter, provided only 
that we do not, like the laity, limit the term to that class of inflamma- 
tions of the mucous membranes acquired by “ taking cold,” and to relieve 
which one wears flannel and drinks elder-blossom tea. 
Now we find that liability to catarrh varies greatly among persons 
exposed to the same exciting cause; and that in one this mucous surface, 
in another that, is always the favorite point of attack. Special predis- 
position, in some cases, seems to coexist with a thin epidermis and a 
strong tendency to perspire; for those who sweat readily are the more 
apt to be suddenly chilled by the rapid evaporation of their perspiration. 
Badly-nourished, cachectic persons too, who are less capable of resist- 
ing the action of hurtful agents, are, on the whole, more prone to ca- 
tarrh than full-blooded and robust individuals. In other instances 
there is no clew whatever to the cause of an intense predisposition to 
this affection. Effeminate habits seem to aggravate it. At all events, 
we see that country people, shepherds, and others, who live continu- 
ally exposed to changes of temperature and to stress of weather, are 
less frequently thus affected than persons of sedentary habits, and 
those who are but rarely subjected to such exposure. 2 
AFFECTIONS OF TIIE LARYNX. 
The fact, also, is inexplicable, that an agent which, in one subject, 
will almost always cause catarrh of the larynx, in another will, as inva- 
riably, give rise to coryza, catarrhal diarrhoea, or to a bronchial catarrh. 
Of one thing alone we may be sure—that, after repeated attacks, the 
laryngeal mucous membrane remains more vulnerable, becomes a weak 
place, as it were, and that trifling causes serve to excite fresh disease of 
the organ. 
The exciting causes are—first, local irritants which act upon the 
larynx. Among these are the breathing of very cold air; the inhalation 
of dust and acrid vapors; loud screaming too, and shouting, singing, and 
violent coughing. In the latter procedure the air is driven forcibly 
through the narrow chink of the glottis, causing severe friction upon its 
free edges, an injury quite as great as that occasioned by other agencies. 
If acrid liquids or hot water penetrate into the organ, the most intense 
form of laryngeal catarrh ensues. 
Secondly, chilling of the skin, particularly that of the neck and feet, 
will give rise to this disease. We are constantly seeing some one who, 
having left off his neckcloth or woollen stockings, suffers next day from 
laryngeal catarrh. Difficult as it may be to give a physiological expla- 
nation of the occurrence, a genetic connection between the two events 
is not to be denied. 
Thirdly, catarrh not unfrequently spreads from neighboring organs 
to the laryngeal mucous membranes. We often see it extend thus from 
the nose or bronchi without the supervention of any new irritant. The 
pharynx is sometimes the point of origin. This is especially the case in 
that form of the malady induced by the abuse of spirituous liquors, which 
have a direct action upon the pharyngeal mucous membrane. Indeed, 
we may often notice a hoarse, stridulous voice, or other sign of acute la- 
ryngeal catarrh, coming on in consequence of a debauch, although the 
person affected may not have shouted or sung much. Habitual topers 
almost always have catarrh of the pharynx, in which the laryngeal mu- 
cous membrane takes part. 
Fourthly, laryngeal catarrh is a common symptom of constitutional 
disease resulting from infection or contagion. Among the acute affec- 
tions, measles and exanthematic typhus; among the chronic, syphilitic 
disorders are the maladies especially prone thus to localize themselves 
upon the larynx. We still lack a thorough insight into the physiologi- 
cal connection between the blood-changes at the root of the disorders 
and the nutritive derangements visible upon the skin and mucous mem- 
branes in these complaints. 
Fifthly, those cases in which the disease forms a portion of a very 
extensive and severe catarrhal affection, the “ grippe,” or influenza. In 
its onset, in its extent, and in the severe constitutional disturbance HYPEILEMIA AND CATARRH. 
3 
which accompanies it, this epidemic bears great resemblance to the acute 
exanthemata. In influenza, catarrh must be regarded as a constitutional 
if not an infectious disorder. 
Sixthly and finally, morbid growths and ulcers, particularly tubercu- 
lous ulcers of the larynx, are accompanied by a catarrh. These symp- 
tomatic cases, which, like the liyperaemia about ulcers and carcinomata 
of the skin, are subject to exacerbations and remissions, form important 
exponents of certain conditions, and in particular account for the fluctu- 
ations in the symptoms of ulceration and malignant growths of the 
larynx. 
Anatomical Appearances.—In acute catarrh of the larynx, the 
mucous membrane of the cadaver does not always reveal a degree of 
redness and vascular engorgement such as the violence of the symptoms 
during life would lead us to expect, and such as could then be demon- 
strated by laryngoscopic observation. This is due to the richness of the 
laryngeal mucous membrane in elastic fibres, which, remaining extended 
by the blood contained in the vessels during life, after death contract, 
and expel the contents of the capillaries. However, in very violent 
catarrhs, apoplexies occur (ecchymoses) in the substance of the mucous 
membranes, which after death present either a mottled or a uniformly 
reddened aspect. 
On the surface of the mucous membrane the cylindrical-form ciliated 
epithelial cells, which constitute the most superficial layer of the stratified 
epithelium of the larynx, are wanting in places; but under the microscope 
we find in the slightly-turbid serum which adheres to the mucous mem- 
brane numerous transparent cells, for the most part uninuclear, and 
which are detached young epithelial cells of the deeper layers, or of the 
mucous follicles, and are called mucous corpuscles. The substance of 
the mucous membrane itself is swollen, moister, and flabby. The sub- 
mucous tissue may exceptionally be the seat of considerable serous infil- 
tration, a condition to be treated of by-and-by as oedema glottidis. 
In chronic laryngeal catarrh the mucous membrane appears more or 
less dark, dirty bluish-red, or brownish (from deposit of pigment in conse- 
quence of previous ecchymosis). The vessels are sometimes varicose and 
gorged with blood, the flabby mucous membrane having lost its elas- 
ticity. Its tissue is generally thickened, firmer, and hypertrophied. The 
surface appears, in many places, uneven and granulated, from the tume- 
faction and distension of innumerable mucous follicles which exist in the 
larynx. Sometimes it is covered by a scanty glairy mucus; sometimes 
with profuse yellow secretion. The young epithelial cells, upon the 
copious admixture of which the opacity and yellow color of this “ muco- 
purulent ” secretion depend, are indistinctly granulated, and their nuclei 
are often divided. They are quite analogous to the young cells found 4 
AFFECTIONS OF THE LARYNX. 
in abscesses. We now no longer call them mucous, but pus corpuscles, 
although it is not easy, in all cases, to distinguish between the two forms. 
The anatomical changes which the laryngeal mucous membrane 
undergoes can be better ascertained by means of the laryngoscope dur- 
ing life than by post-mortem dissection. We find that catarrh of the 
larynx does not always involve the whole surface of the organ, but is 
often confined to particular sections. Thus there may be catarrhs, lim- 
ited to the region of the epiglottis, the arytmno-epiglottidian fold, the 
arytenoid cartilage, the true or the false vocal chords. There is one very 
interesting form of circumscribed swelling of the membrane between the 
arytenoid cartilages and a little beyond, which Lewin has repeatedly 
ascertained to be a cause of the chronic hoarseness among officers who 
have been much in the habit of shouting the Avord of command. 
Apart from the catarrhal sores, and the polypous growths of which 
Ave are to treat in a separate chapter, chronic laryngeal catarrh, and 
chiefly that form of it Avhich accompanies syphilitic and tuberculous ul- 
cerations, sometimes leads to a thickening and induration of the sub-mu- 
cous tissues. Its metamorphosis into a braAvny fibrous mass, Avhich often 
greatly contracts the larynx, and renders the vocal chords stiff and im- 
movable, takes place in a manner quite analogous to that in which indu- 
ration of other organs arises, especially of the stomach. The process is a 
mere hypertrophy of the connective tissue, and has nothing in common 
Avith the so-called lardaceous or amyloid degeneration of other organs. 
Symptoms and Course.—Acute catarrh of the larynx rarely begins 
AA'ith shivering; indeed, in most cases, AA'hen it does not spread into the 
bronchi, catarrhal fever is also absent throughout the AAdiole course of 
the attack. The general condition is untroubled, and the symptoms of 
disease alone refer to the functional derangements of the suffering organ. 
The patients first oomplain of a feeling of titillation, or, in more 
severe cases, of a sensation of burning or soreness in the throat, Avhich 
is aggravated by speaking or coughing. Sensation in these parts ex- 
tends as far doAvn as the .bronchi of the second magnitude. If, therefore, 
the covering of the epiglottis, the arytenoid, or arytreno-epiglottic liga- 
ment be the seat of catarrh of some intensity, deglutition becomes painful. 
In addition to these symptoms, alteration of the voice furnishes a charac- 
teristic sign of disease of the larynx. The voice groAvs deeper, hoarse, 
cracked, and may finally become inaudible. The vocal sounds, as Ave all 
knoAV, originate entirely in the larynx, Avhich is formed like a reed-pipe, 
AA'ith membranous reeds. In the act of speech, the loAver Arocal chords 
approach one another so closely as to project into the organ as vibrating 
membranes. If thrown into vibration by the current of a strong expira- 
tion, a tone results whose elevTation or depth of pitch depends upon the 
degree of tension in which they are set. Noav, Ave have stated aboA’e 
that in catarrh of the larynx the mucous membrane SAvells up and HYPERiEMIA AND CATARRH. 
5 
becomes relaxed, and is covered by a secretion in more or less pro- 
fusion. If the vocal chords also become involved in this condition, 
the tension to which the laryngeal muscles can bring them is inadequate 
so to increase the frequence of their vibrations as to produce a tone of a 
pitch such as would result at the same tension in normal chords. Thus 
the voice is rendered deeper. From the irregular swelling, and from 
the presence of the mucus which covers the chords and makes then- 
surface uneven, the voice is hoarse and its tones are false (just as the 
note of a violin-string is altered when smeared with grease). At last 
the swelling and relaxation of the chords may so increase that the utmost 
tension to which the muscles can bring them is insufficient to allow of 
sonorous vibration. The voice then is noiseless or extinct. Extinction 
of the voice may also depend upon swelling of the false vocal chords, as 
the latter, when thus brought into contact with the true chords, render 
their free vibration impossible. Frequently the hoarse voice of the 
patient suddenly breaks into discord, or “ cracks.” This occurs when 
the tumid chords, bathed in mucus, momentarily touch one another, so 
as to produce vibratile nodes, a great increase in the frequence of vibra- 
tion, and consequent elevation of pitch in the tone. 
Besides the titillation, burning, and hoarseness, there is also violent 
cough. In the healthy larynx we see coughing-spells provoked as reflex 
phenomena upon exposure of the organ to any undue irritation—the 
intrusion of a foreign body, for instance. When the laryngeal mucous 
membrane has become the seat of catarrh, we find that analogous fits of 
coughing are excited by the most trifling and unobservable causes, and, 
to all appearance, spontaneously. Sometimes, in these paroxysms, so 
severe a spasm besets the muscles of the glottis that, in the inspiratory 
movement by which the fit commences, the air can pass but slowly 
through the contracted rima glottidis, and with a wheezing sound, while 
the expiratory effort consequent upon this long-drawn, sonorous inspira- 
tion, is only capable of effecting momentary openings of the constricted 
passage, thus producing the interrupted, rattling, short “ hacks ” of a 
cough. The effect of vigorous expiration through a narrow glottis, such 
as we make in blowing upon wind instruments or in straining, is to com- 
press the thorax, and thus to check the influx to it of blood from the 
veins, so that the jugulars distend and the face grows red, or even bluish. 
In other cases of long standing the tone of the cough likewise deepens, 
and grows harsh and hoarse from thickening and unevenness of the 
chords. Quite frequently, from some powerful expiratory effort, the 
thickened chords are made to bulge upward and are thrown into strong 
tension. The hoarse cough then changes into a “ bark,” or, upon mo- 
mentary contact of the chords, the sound of the cough is cracked. 
When catarrh is confined to the larynx, the expectoration is scanty. 6 
AFFECTIONS OF THE LARYNX 
At first it is either absolutely wanting, or else it is clear or glairy. Tliis 
mucous sputum, “ sputum crudum ” of the ancients, does not often con- 
tain detached ciliary epithelium. There is much more commonly a 
moderate admixture of young cells from the deeper layers of the epi- 
thelial covering, or of mucous corpuscles from the follicles. As the 
disease progresses and begins to abate, the expectoration becomes thicker 
and more rich in young cells, which rather resemble pus-cells. Tliis 
form of expectoration, the “ muco-purulent,” is the “ sputum coctum ” 
of the older physicians. 
As the submucous tissue is seldom much swelled or infiltrated, save 
in rare cases, dyspnoea in simple acute laryngeal catarrh of adults is of 
exceptional occurrence. In grown persons the glottis, especially the 
posterior part of it, the pars respiratoria of Longet, is a tolerably roomy 
triangular space, bounded by the base of the arytenoid cartilage, and 
does not become impervious to air by reason of swelling of its mucous 
membrane alone. Even among children it is rare for the dyspnoea of 
simple laryngeal catarrh to be continuous. Although in the latter the 
glottis is smaller, its entire space forming but a narrow chasm, yet the 
swollen chords are generally separated from one another by the free 
action of the posterior crico-arytenoid muscles, which act with every in- 
spiration, so that there is no hinderance to the entrance of air. A glance 
at the laryngoscope is enough to convince any one that the rima glottidis 
gapes during inspiration so widely that a moderate swelling of the mucous 
membrane cannot materially obstruct the passage of air or produce 
symptoms of dyspnoea. In certain well-authenticated cases of intense 
catarrhal laryngitis, however, there has been such serious swelling of the 
true chords, or of the false ones, which cannot be drawn asunder by 
muscular action, as to place the patient in danger of suffocation. 
Not at all rarely we see a child who has been coughing a little during 
the day, and been hoarse without feeling ill, wake up suddenly in the 
night with great oppression of breathing. The inspiration is troublesome 
and protracted; the terrified child throws himself about in bed, or springs 
up, clutches anxiously at the throat; the cough is hoarse and barking. 
These attacks, which are often confounded with croup, or called pseudo- 
croup, usually vanish completely after a few hours—often much sooner. 
It is to these that the warm milk, the hot sponge laid upon the throat, 
the judiciously-administered emetic owe their reputation as panaceas 
against croup, sure to cut it short if given in time. One might suppose 
that these accidents arose from an unusually aggravated but transient 
swelling of the mucous membrane, and from a narrowing of the glottis, 
which could not be compensated for by muscular action, just as in coryza 
we see sudden absolute closure of one or other of the nostrils; or we 
might think that a spasmodic closure of the glottis had allied itself to HYPEREMIA AND CATARRH. 
7 
the mucous irritation as a reflex symptom, such as we shall describe by- 
and-by as laryngismus stridulus. But there is another and more probable 
explanation. These attacks take place almost solely during sleep, pass 
off after the child has cried, coughed, and vomited awhile, to recur almost 
as soon as he falls asleep again. Hence it is likely that the dyspnoea is 
occasioned by a collection of tenacious secretion in the glottis, and per- 
haps also by a dryness of the rima glottidis, which tends, as it -were, to 
glue it up. At all events, this explanation likewise accounts for the 
action of the remedies alluded to above, and so justly prized. Attacks 
like these are often repeated for several successive nights, while during 
the day the children play about gayly, and, with exception of a slight 
cough, seem perfectly well. 
As regards the course, duration, and termination of laryngeal catarrh, 
the sputa cocta generally appear after a few days, when the sensitiveness 
of the larynx, the hoarseness, and the cough abate, the disease termi- 
nating by recovery at the end of about a week. In other cases the 
complaint lasts for several weeks. During the day the patient is some- 
what hoarse, but otherwise is well, save that in the mornings and evenings 
he is troubled by violent and protracted fits of coughing. The sputa 
remain crude, until at last, often upon some change of weather, the 
disease subsides. In other cases again, after repeated relapses, chronic 
laryngitis is the result. A fatal termination, uncomplicated by any other 
cause of death, is one of the greatest of rarities. 
Chronic Catarrh of the Larynx.—As, even in acute catarrh, the 
sensitn eness of the mucous membrane abates with the appearance of 
the sputa cocta, so in the chronic form we hardly ever find titillation, 
burning, or soreness in the larynx. Hypertrophy of the mucous mem- 
brane, however, and continued thickening of the vocal chords, as described 
in the last section, produce a permanent deepening of tone in the v oice, 
and render it harsh and hoarse. 
In the cases alluded to above, in which the mucous membrane of the 
posterior wall of the larynx close below the vocal chords is thickened 
and swollen, hoarseness proceeds from the intrusion of a fold of mem- 
brane between the posterior adjacent surfaces of the chords, whenever 
the voice is raised, so that the glottis cannot contract properly. This 
chronic hoarseness, the result of repeated acute attacks, is the chief and 
often the sole symptom of chronic laryngitis. A cracked voice usually 
accompanies long standing chronic hoarseness. From time to time, a 
slight aggravation or some acute irritation of the mucous membrane so 
thickens the vocal chords, as to render the voice quite inaudible. 
In many instances, besides the aphonia, there is also a periodical 
spasmodic cough, such as we have described as symptomatic of acute 
laryngeal catarrh, although the attack seems to proceed rather from an 8 
AFFECTIONS OF THE LARYNX. 
accumulation of secretion in tlie pouches of Morgani, and passes oil 
after the expectoration of a small quantity of peculiar lumpy yellowish 
mucus. Here too, for reasons already given, the cough may be harsh, 
hoarse, and grating, swelling into a bark. 
The addition of a whistling, stridulous inspiration and expiration, as 
it certainly does not proceed from mere swelling and hypertrophy of the 
mucous membrane, denotes the presence of a complication—either 
thickening and induration of the submucous tissue above described, or 
a morbid growth encroaching upon the cavity of the larynx, or else 
syphilitic laryngitis. 
It is only by means of the laryngoscope that we can determine 
positively with which of these three main forms of laryngo-stenosis we 
have to deal. On the other hand, the association of fever, emaciation, 
and night-sweats, with chronic laryngeal catarrh (catarrhal laryngeal 
phthisis being rare), should awaken our suspicion of latent disease of 
the lungs, and induce repeated physical exploration of the chest. 
The course of chronic laryngitis is usually tedious. It is only by 
most cautious and judicious treatment that a cure can be effected, and 
there is nearly always a strong tendency to relapse. 
Diagnosis.—Catarrh of the nose and that of the pharynx, which 
also produce alteration in the voice, are easily distinguishable from ca- 
tarrh of the larynx. In the former, the resonance of the contracted nasal 
and oral cavities, the “ timbre ” of the voice, is changed—the speech is 
nasal or guttural; in the latter, the tone itself is modified, the voice is 
deeper, cracked, and hoarse. 
Confusion with croup is more apt to occur. To anxious mothers, 
mere hoarseness and a barking cough furnish evidence enough of the 
presence of that dread disease, even although the child may be well 
enough otherwise. The addition of a nocturnal paroxysm of dyspnoea 
will often mislead the physician himself. Thus it is that we so often 
hear of children who have suffered eight, ten, or even more, attacks of 
croupous laryngitis. Croup is neither so frequent nor so innocent a 
disease as to admit of the likelihood of such frequent recoveries; In 
most of such cases there has been error of diagnosis. The points of 
distinction between the two diseases will be more fully given while 
treating of croupous laryngitis. For the present we call attention to 
one point only, upon which the laity lay greater stress than the profes- 
sion. Nasal catarrh is almost as surely symptomatic of the catarrhal 
form of laryngitis as is croupous pharyngitis of true laryngeal croup. 
The satisfaction of mothers at the “ running nose ” of their child is well 
founded—the rarity with which simple catarrh is complicated with 
graver disease having given rise to the old custom of salutation after 
sneezing. HYPEREMIA AXD CATARRH. 
9 
The distinctive points between chronic simple catarrh and ulcera- 
tion or growths in the larynx are to be discussed hereafter. 
Prognosis.—The prognosis both of acute and chronic laryngitis 
becomes apparent from the foregoing sketch of its symptoms. When 
uncomplicated, the disease is seldom fatal. The prognosis as to com- 
plete recovery is favorable in the acute disease, although a tendency to 
relapse remains; in chronic cases, it is more unfavorable. Induration of 
the submucous tissue is incapable of resolution. 
Treatment — Prophylaxis.—It is advisable, rather cautiously to 
habituate children to the causes of this disease than to enervate them 
by a systematic over-protection which tends to increase the liability to 
its attacks upon every trifling occasion. Do not shut up little children 
in the house, even though they have suffered from laryngitis; but keep 
them in the open air. 
In bad weather, let them be warmly clad; but their necks should 
never be overheated with thick woollen shawls, etc. A silk ribbon worn 
about the neck has the reputation of a sympathetic prophylactic. Wash- 
ing of the throat in cold water, and cold river and sea bathing, cannot 
be sufficiently commended. They form the best of prophylactics; but, 
in prescribing their use, the most definite and rigid rules must be laid 
down as to time, duration, and temperature. The more precisely we 
direct, so much more punctually do patients obey. 
Indication as to Cause.—If the cause of the catarrh be the direct 
action of some irritant upon the mucous membrane, the patient must be 
protected from its further influence. To guard the affected larynx from 
further irritation, let the patient be kept in a uniform temperature, regu- 
lated by the thermometer. Forbid all loud and continued talking or 
singing, and, above all, urge the patient to resist the inclination to 
cough. Even though not entirely successful in this, yet much may be 
gained by determination on his part. The assertion that he cannot help 
coughing should never deter you from persistently telling him not to 
couyh. In violent paroxysms, 'which, although consequent upon the 
catarrh, are active causes of its perpetuation, the common “ cough- 
drops ” and syrups containing antimony are useless. If the remedies 
mentioned above prove inadequate, we must resort to the narcotics. 
True, great caution in exhibiting these agents is demanded in treating 
children, but among adults they certainly have not been used with 
proper boldness and freedom. It is surely more reasonable, and in- 
dubitably more efficacious, to prescribe ten grains of Dover’s powder 
at night, or occasional small doses of morphia (morphias, gr. j; aqua 
laurocerasi, 3 ij; gtt. x every three hours) to a patient with severe 
laryngeal cough, than to plague him with liquorice, caramel, sulphuret 
of antimony, and the like. AFFECTIONS OF THE LARYNX. 
10 
When chilling of the skin, feet, or throat is the cause of catarrh, 
diaphoresis is indicated. The best and simplest of diaphoretics are hot 
elderbloom-tea, and warmth in bed, warm foot-baths, wrapping the 
throat in a woollen stocking, sinapisms repeated from time to time, or 
hot poultices, the chilling of which must be carefully prevented. En- 
velopment of the entire body in cloths wrung out in cold water, the 
use of brief cold foot-baths, the application of a cold, stimulating com- 
press to the throat, have a similar action to that of the above-mentioned 
procedures, and are to be regarded as local excitants, or cutaneous 
stimulants. The merits of such measures are overrated by the liydro- 
pathists. They are, nevertheless, quite useful in the hands of persons 
skilled in their employment, and who are generally enthusiastic in their 
favor. 
In cases where the catarrh has extended from the fauces into the 
larynx, the causal indications are for astringent gargles, and for pencilling 
the throat with a solution of nitrate of silver or alum. 
The indication, from the disease itself, in acute laryngeal catarrh, 
uncomplicated by oedema glottidis, never requires either local or general 
bloodletting, for, although the books give detailed direction for their 
use in most cases, it is quite sufficient to produce a determination to the 
skin, by means of cutaneous stimulants, and thus to reduce the mucous 
hyperaemia. In fact, the case usually does well without any treatment 
whatever, or even when mismanaged. Tincture of pimpinella, which 
has the reputation of a specific, may be tried, but is not much to be 
relied upon. For a drink, we may give seltzer-water, either pure or 
mixed with equal parts of hot milk. 
Quite empirically, it has been found that greasy materials are hurtful, 
while strongly salted ones act beneficially upon acute laryngeal catarrh. 
An unsoaked herring is a well-known popular remedy, and may, per- 
haps, set up a derivative action upon the mucous membrane quite as 
powerful as that produced by a sinapism upon the skin of the throat. 
For chronic laryngeal catarrh, Plummer’s pill (calomel, with sulphuret 
of antimony), combined with belladonna, or hyoscyamus, used to have 
the name of a specific. The latter ingredients might be of use in moder- 
ating the coughing fits. Whether they are more effectual than opiates 
may be doubted. The sulpliuret of antimony is superfluous; the calomel, 
in catarrhal inflammation, objectionable. Instead of the more moderate 
irritants, as sinapisms, and the like, in chronic laryngitis, we employ 
stronger derivatives. The commonest is croton-oil, either alone or 
with five parts of oil of turpentine, rubbed over the skin of the larynx 
for several successive days, until vesicles and pustules appear. Ac- 
cording to Tobolcl, the establishment of small blisters upon either side 
of the arytenoid cartilages is more efficacious and less severe. 
The use of the alkaline muriatic mineral waters (SHuerlinge, Halloid HYPERJEMlA and catarrh. 
11 
salts) has an unmistakable influence upon the course of many cases of 
chronic laryngeal catarrh, which, unfortunately, cannot as yet be distin- 
guished from cases in which it fails. For this mode of cure, it is best 
to send the patient to such places as Ems, Obersaltzbrunnen, or Gleichen- 
berg, and only when his means will not permit him to do otherwise, to 
allow him to use seltzer-water, or one of the so-called mineral waters as 
a cure, at home. We may let him drink the Ems or Kesselbrunnen 
water, or the Krahnchen of Ems, on the spot, as they have, respectively, 
a temperature of 117° F. and 90° F., without the addition of warm 
milk or warm whey. In order to warm them, it is better to mix the 
Obersaltzbrunnen, or the imported Ems-water, with equal parts of hot 
milk. That the far more customary addition of whey should have any 
real advantage over that of milk, is, at least, doubtful. The “ well-pre- 
pared whey,” at celebrated watering-places, furnished generally by a 
“ Swiss,” and, if possible, by an Appenzeller, in his national costume, so 
much lauded in the newspapers and bath-journals, and to which often 
more credit is given than to the springs themselves, is merely milk, 
minus cheese, and can hardly effect more than the milk from which the 
cheese has not been eliminated. It is only in the somewhat rare cases, 
in which milk is not well borne by the patient, while the whey is borne 
well or better, that I allow the latter to be added to the mineral water 
instead. 
Several hypotheses have been advanced as to the action of the alka- 
line-muriatic mineral waters. The fact that the ashes of the mucus are 
richer in salt (chloride of sodium) than the ashes of the blood, and that 
mucus becomes less tenacious upon the addition of salt, seems certainly 
to indicate that salt plays an important role in the formation of mucus, 
but it by no means justifies the conclusion that the use of salt effects a 
cure, or more rapid resolution of a catarrhal process. 
In other quarters (Sprengler) the principal importance has been 
attributed to the amount of alkaline carbonates contained in these 
mineral waters, and, depending upon an observation of Virchow's, ac- 
cording to which very dilute solutions of alkalies are capable of exciting 
the ciliary movements in epithelium, they assert, in explanation of the 
beneficial action of the waters in question, that their use reestablishes 
the extinguished or repressed ciliary vibrations. Grave objections may 
be brought against this explanation of the action of the saline waters, 
which is not merely palliative, but in many cases absolutely curative, 
and we must be content with the empirical fact, that the springs of 
Ems, Obersaltzbrunnen, and Selters, have often alleviated or cured chronic 
laryngeal catarrh. The cold sulphur springs, too (such as those of 
Weilbach, in the dukedom of Nassau, of Eilsen, in the principality of 
Schaumburg-Lippe, of Langenbrlicken, in the grand-dukedom of Ba 12 
AFFECTIOXS OF THE LARYNX. 
den), which we usually make use of, like those of Obersaltzbrunnen, 
and Seltzer, mixed with warm milk, or whey; the sulphur springs, also, 
of the Pyrenees, above all the Eaux-bonnes, are, with good reason, in 
repute, in the treatment of chronic laryngitis. Our conjectures as to 
the modus operandi of these waters are as yet vague and untenable—a 
matter, however, far less to be regretted than the fact that we have no 
criterion whereby to predetermine the cases in which relief may be ex- 
pected, and those in which they do no good. 
In obstinate and inveterate cases of chronic laryngitis, local treat- 
ment deserves an extended trial. 
The attempt to blow medicated powders into the larynx is an ancient 
practice. For this purpose, a long quill, or a glass tube, eight or ten 
inches in length, and several lines in diameter, is employed. A few 
grains of the powder to be inhaled is laid within one end, the other end is 
introduced as far as possible into the mouth of the patient, who is then 
to close his lips, and to draw a deep inspiration, or else we may blow into 
the external end of the tube. If this procedure should excite violent 
inclination to cough, we may assume that a part of the medicament, at 
least, has reached its destination, although, no doubt, the greater part 
remains clinging to the velum-palati and pharynx. The medicines most 
frequently used in this practice by Trousseau are arg. nitrat. (gr. j—ij to 
sacc. alb. 3 j—ij), calomel (gr. x—xx to sacc. 3 j—ij), alumen. ( 3 ss—j 
to sacc. alb. 3 ij). At present, by aid of the laryngoscope, and of a curved 
tube, inserted as far as the entrance of the larynx, we can blow into it 
almost the whole of the powder. 
Another procedure, which acts with tolerable certainty, consists in 
expressing the contents of a small sponge, made fast to the end of a 
little rod of whalebone, and saturated with solution of arg. nit. (gr. xx to 
3 j) over the entrance of the larynx. The result of this mode of treat- 
ment is often both instantaneous and brilliant, and finds a striking 
analogue in the efficient use of solution of nitrate of silver in the treat- 
ment of catarrhal conjunctivitis. 
An adept in the use of the laryngoscope enjoys the great advantage 
of being able to assure himself by direct ocular observation of his suc- 
cess in passing the sponge behind the epiglottis. 
The most recent and generally-employed method of producing the 
direct action of medicaments upon the mucous membrane of the larynx 
consists in causing the patient to inhale them in solution reduced to the 
condition of a spray or mist. The apparatus hitherto employed for this 
purpose consequently bear the names of nephogene, pulverization, 
[nebulizer], inhalations apparatus. Of these there are two kinds. In 
one, the slender stream of liquid to be inhaled is driven forcibly against 
a small convex disk, and thus reduced to the condition of spray, as in the HYPEREMIA AND CATARRH. 
13 
machine of Sales- Giron and its modifications by Walderiburg, lew in, 
and Schintzler. In the second sort, small quantities of the liquid for 
inhalation are “ nebulized ” by the action of a jet of compressed air. 
The nephogene of Matthieu is thus formed, as well as the more simple 
and cheaper hydroconion of Bergson, which I formerly used at the 
clinique. By the happy ingenuity of Single the apparatus of Bergson 
has been so modified as to substitute steam for the current of compressed 
air, which nebulizes the medicament. This cheap instrument of Single, 
with its various modifications, consisting chiefly in the exchange of the 
fragile retort of the original for a small boiler of tinned brass, for the 
production of steam, has such advantages over all other inhalation ma- 
chines, as to have almost universally superseded them. At my clinique, 
instruments made on Single’s principle are the only ones in use. The 
controversy, as to whether the liquid inhaled actually penetrates into the 
air passages, has been decided. The fact is beyond all doubt. In 
recent catarrhs, with scanty and tough secretion, it is best to use a solu- 
tion of sal-ammoniac or of common salt for inhalation (gr. x—xx. to 
| j). In catarrh of longer standing, in which the secretion is more 
copious and muco-purulent, a solution of alum (gr. v—x : 3 j), tannin 
(gr. ij—x : § j), argent, nitrat. (gr. i—x : 3 j). During inhalation of 
the latter, in order to avoid staining the patient’s face, a mask must be 
used, or else an appliance such as accompanies the apparatus which we 
employ. I am unable to state, from my own experience, whether the 
inhalations of narcotic solutions (morphias acet. gr. -J — £ : 3 j), (tr. 
opii gr. ij—iv : 3 j), (ext. hyoscyami gr. ss—j : 3 j) are of any mate- 
rial service in allaying the impulse to cough. 
By exaggerated praise of the treatment by inhalation, a discovery 
of real value has not only been retarded but often brought into positive 
discredit in the estimation of thoughtful men, who have failed to ver- 
ify its great success in treatment of the various diseases of the air-pas- 
sages. However, “ in emptying the bath, one need not spill the baby.” 
The introduction of the inhalation apparatus does not mark a new era 
in therapeutics ; nevertheless, inveterate pharayngeal and laryngeal ca- 
tarrhs, which have resisted all modes of treatment, are now often cured, 
after persevering inhalation of a solution of alum or of nitrate of silver. 
For some very sensitive patients, however, the inhalation of astringents 
is contraindicated, since, in a few instances, haemoptysis has set in, 
either during the process or immediately after it. 
Spray-baths and inhalation-rooms have been established of late in 
many well-known watering-places, particularly at the “brine-baths” 
(Soolbtidern). The most simple baths of brine-spray are the prome- 
nades and galleries along the salt-works of Kreutznach, Koesen, Elmen, 
and Reichenhall. The atmosphere there is heavily charged with a weak 
solution of chloride of sodium. At Kreutznach and Reichenhall the 14 
AFFECTIONS OF THE LARYNX. 
brine is also nebulized in appropriate closets, after the method of Sales• 
Giron. In Rehme (Oeynhausen), a salt-spring, there is an excellent 
spray-bath. At Kreutznach, Reichenhall, and Ischl, besides the spray, 
the warm steam generated by the boiling brine is also inhaled. This 
contains less salt than the spray of the salt-works, and inhalation hall. 
Whether, and how, inhalation of the brine-spray acts as a remedy for 
laryngeal catarrh, is still a question. Many patients, especially those in 
the closets, complain of pain in the eyes, and contract a conjunctivitis by 
the same process, whereby they hope to be relieved of laryngeal or bron- 
chial disease, a fact which has many analogues, should further experience 
pronounce in favor of inhalation of brine in chronic laryngitis. In pro- 
posing the inhalation of brine in this disease, the fact that it contains 
iodine and bromine has also been borne in mind. The momentary relief, 
obtained by the patient during, and for a short time after, inhaling, is 
attributable simply to the liquefaction of the mucus in air-passages by 
the nebulized liquid, whereby, in the narrowest sense of the word, the 
cough is rendered “ looser.” At Ems the thermal gases, and at the sul- 
phur springs, the vapor of the richly sulphureted waters, have recently 
been similarly inhaled. With regard to the latter, it may be remem- 
bered that even Galen recommended an abode near Vesuvius to the 
“ phthisical,” that they might respire the moist sulphureted vapor as it 
rose. 
The diet for chronic catarrh of the larynx must be similar to that for 
the acute; salted articles, indeed, particularly the roe of a herring taken 
fasting, are in especially good repute. 
Besides allaying the cough, the symptomatic indication calls for a 
means of promptly relieving the nocturnal paroxysms of dyspnoea above 
described. To apply leeches to the throat, though often done, is useless. 
The repeated application of a sponge dipped in hot water to the throat, 
until the skin grows red, the exhibition of copious draughts of hot 
liquid, and, above all, the administration of an emetic, are often indicated 
and frequently are of surprising efficacy. As an emetic, ipecacuanha, 
or tartar emetic, is to be preferred in these cases to sulphate of copper, 
and should be given in efficient doses (best according to Hufeland, 
pulv. rad. ipec. Sj, ant. et pot. tart. gr. j, scillse. oxymel 3 iij, aqua 
3 j ss; shake well, a teaspoonful every ten minutes). 
Should the paroxysm recur, the emetic is to be repeated. It is a 
good rule not to let the child sleep too profoundly, but, from time to 
time, to waken it and let it drink. This will often cause it to expector- 
ate, and we thus prevent the accumulation and drying up of the secre- 
tions in the rima glottidis. CROUP, 
15 
CHAPTER II. 
CROUP.—ANGINA HEMBRANACEA.—LARYNGITIS CRUPOSA.—MEM- 
BRANOUS CROUP. 
Etiology.—Croupous inflammations are inflammatory disorders in 
which a fibrinous exudation which rapidly coagulates is thrown out 
upon the free surface of a mucous membrane, but which involves the 
epithelium only. If the croup-membrane thus formed be detached, the 
epithelium is quickly reproduced. No loss of substance occurs in the 
mucous membrane itself, and no scar remains. The diphtheritic process 
is also characterized by the production of a fibrinous rapidly-coagulable 
exudation, but differs from croup, the exudation forming, not merely 
upon the surface of the mucous membrane, but also within its sub- 
stance. The pressure upon the blood-vessels exerted by this interstitial 
exudation, as well as by the swollen elements of the tissue, results in 
sloughing of a portion of the inflamed mucous membrane, and in the 
formation of a so-called diphtheritic eschar, which, upon separating, oc- 
casions a loss of substance and consequent cicatrix. Of these two 
forms of inflammation (the essential duality of which has of late been 
much in dispute), it is almost exclusively the croupous form which ap- 
pears in the mucous membranes of the respiratory passages; and it is 
only in rare and solitary instances of secondary croup, when that malady 
forms part of some general acute infectious disorder, as measles, small- 
pox, typhus, scarlatina, or epidemic diphtheria, that a transition from 
croupous to diphtheritic inflammation is observable. Even here, too, 
though the pharynx may be the seat of a most exquisite diphtheria, it is 
far more common, and it is, in fact, the rule, for the laryngeal inflamma- 
tion to retain the characteristics of true croup. (See chap. “ Diphtheria.”) 
Croup is of far rarer occurrence upon other mucous membranes than 
upon those of the air-passages, and, during childhood, is almost ex- 
clusively a disease of the trachea and larynx, rarely affecting the 
alveoli of the kings. On the other hand, croupous pneumonia, a true 
croup of the air-cells, is one of the most common diseases of adults, in 
whom primary croup of the trachea and larynx scarcely ever occurs. 
Although peculiarly a disease of childhood, still the disposition to it 
is less during the period of suckling. After the second dentition, too, 
the disease is more rare; so that the period of greatest predisposition 
for croup lies between the second and the seventh year of life. Boys 
are more subject to it than girls; but it is an error to suppose that vig- 
orous, full-blooded, blooming children are especially liable. On the 
contrary, tender, delicate, ill-nourished offspring of tuberculous parent- 
age, with pale skin and conspicuous veins (an ominous sign even for the 16 
AFFECTIONS OF THE LARYNX. 
laity), children with a tendency to moist eruptions, to enlarged lymphat- 
ics, or to acute hydrocephalus, suffer from croup with equal or even 
greater frequence than those who are more robust. It is our daily 
experience that, in the great mortality which desolates certain families, 
a portion of the members die of croup, and another of hydrocephalus, 
while, in the survivors, pulmonary tuberculosis develops later in life (see 
“Pulm. Tuberculosis”). It would appear that the croup not unfre- 
quently begins very soon after the disappearance of a moist eruption on 
the head or face. 
The croup is more common in northerly, windy, damp places, bor- 
dering on the water, than in southerly, warmer, and more protected 
regions. Not unfrequently we observe its epidemic appearance. At 
such times many children are attacked even in one small place, and 
often several children of the same family in quick succession, and by 
the most intense and pernicious form of the disease. 
It is this epidemic croup of the larynx which seems most commonly 
to be combined with croup of the pharynx. In some croup-epidemics 
facts have been observed which make it somewhat probable that the 
disease may spread by contagion. It is questionable, however, whether 
there may not have been confusion with that liiglily-contagious malady, 
epidemic diphtheria, in these cases, as we shall hereafter demonstrate 
the fact that secondary croup of the larynx often accompanies diphtheria 
of the fauces. 
The exciting causes of croupous laryngitis are in most cases not to 
be explained. Sometimes the irritated condition of the mucous mem- 
branes, known as “ a cold,” occasions the disease. A sharp northerly 
or northeasterly wind stands in especially evil repute in this respect. 
We shall treat hereafter of the relation of secondary croup to the infec- 
tious diseases. 
Anatomical Appearances.—The affected mucous membrane shows 
a varying degree of reddening, partially through ecchymosis, and in 
part through injection. It has been maintained that the redness dimin- 
ishes when the exudation increases; nay, formerly the opinion pre- 
vailed, based upon the absence of inflammatory reddening in croup, 
that it constituted a peculiar form of inflammation wherein there was no 
hyperaemia. We have already shown that the pallor, after death, of the 
mucous membrane, which during life had been hyperasmic, is principally 
due to the abundance of elastic fibres in its tissues. 
The mucous membrane is deprived of its epithelium, and, together 
with the submucous tissue, is swollen and relaxed. Even the muscles 
of the larynx seem moist, pale, and softer. Very often too, but not 
always, the mucous membrane of the cadaver is still covered with exu- 
dation. The frequent absence of the croup-membrane, in the bodies of CROUP, 
17 
persons who have died with all the symptoms of croup, has given rise 
to an artificial division into true and false croup, and even to-day there 
are many physicians who maintain that, in the subjects in which, upon 
autopsy, no membrane has been found in the larynx, the cause of death 
has not been true croup. 
In croup, too, a fluid plasma first exudes, and it, of course, does not 
coagulate until after exudation. If ejected from the body, either in the 
coagulated or liquid form, on section we find the larynx to be free ; but 
we have to do with exactly the same disease as that in which a coagu- 
lated coating is found upon the mucous membrane. Croupous exuda- 
tion sometimes has the consistence of a thick cream ; sometimes it forms 
a compact, tough membrane; sometimes it entirely lines the interior 
surface of the larynx as a continuous sheet, and is prolonged into the 
trachea and even into the bronchi, forming tubular and ramifying clots ; 
sometimes it only presents isolated flakes and patches, which cling here 
and there to the mucous membrane. 
The softer and thinner pseudo-membranes may generally be de- 
tached from the mucous surface with ease; the tougher and more co- 
herent ones cling more firmly. Upon the external surface of this firm, 
strong substance, which is often more than a line in thickness, we fre- 
quently may notice numerous red streaks, and points of adherent blood, 
wrhich correspond to small bleeding spots of the mucous membrane 
upon whose areolar layer the exudation is situated. 
After persisting for a longer or shorter time, the pseudo-membranes 
gradually become loosened by a serous exudation which proceeds from 
the mucous surface, and are expelled either in the form of continuous 
tubes and sheets, or in small flakes and patches. 
Under favorable circumstances, the epithelium is soon reproduced, 
and the laryngeal mucous membrane returns to its normal condition. 
In other cases, a fresh membrane succeeds upon the fall of the first one, 
and thus the process may be many times repeated, until the disease ex- 
hausts itself, or until the patient succumbs. 
The membrane of croup consists microscopically of amorphous or 
finely-fibrillated fibrin, in which numerous young cells have been en- 
tangled during the process of its excretion. 
The frequent association of pharyngeal croup with croup of the 
larynx has a very important bearing, not only upon the diagnosis of the 
disease, but also upon the physiological elucidation of its symptoms. 
The French do not acknowledge any case as true croup, where this com- 
plication is absent; calling all others false croup. Since attention has 
been called to the subject in Germany, it has been found that the co- 
existence of both forms of the malady, although extremely frequent, is 
by no means constant 18 
AFFECTIONS OF THE LARYNX. 
Iii the bodies of croupous children we may almost always find intense 
hyperaemia of the lungs and bronchial mucous membrane, bronchial ca 
tarrh with copious secretion, oedema of the lungs, and not uncommonly 
croup of the bronchi, spots of pneumonia, atelectasis, with both vesicular 
and interstitial emphysema. It will be shown, hereafter, that such con- 
ditions are in a great measure the necessary consequences of laryngeal 
croup. 
Symptoms and Course.—In many instances prodromata give warn- 
ing of the attack. The child is cross and feverish; is hoarse, and coughs 
with suspicious tone. Such symptoms alone, however, may be of little 
moment, being quite as indicative of the approach of an insignificant 
laryngeal catarrh, as of the onset of one of the most fatal disorders of 
childhood. Even thus early, however, an observant physician may dis- 
tinguish between the two. In all cases examine the fauces forthwith, 
although the child do not complain of difficulty in swallowing. 
Should we find them swollen, and spotted here and there with small, 
firm, white patches, we have before us the signs of incipient croup, 
while the same symptom, accompanied by persistent sneezing, and by a 
profuse flow from the nose, is equally characteristic of laryngeal catarrh. 
A further diagnostic point is found in the predisposition of the individual. 
If a child habitually grows hoarse and coughs with a bark upon taking 
cold, but never exhibits other sign of croup; if his brothers and sisters 
show no tendency toward the disease, we may feel less concern for him, 
than for one who already has suffered an attack, or who has lost a 
brother or sister by this malady. These prodromata may precede the 
attack itself by one or two days. They are absent, however, in very 
many cases, the disease setting in suddenly and unexpectedly in all its 
terrors. Late in the evening, generally, or in the middle of the night, 
the child is roused from his sleep with a harsh, hoarse, inaudible voice, 
the deep, soft note of which breaks into shrill, piercing discord, as the 
swollen vocal chords, already frequently coated by exudation, come for an 
instant into contact. The cough, which was short and sharp in the 
beginning, soon becomes harsh, hoarse, and is no longer barking, except 
when, upon a violent expiratory effort, the air in its exit stretches the 
chords, and causes them to bulge. At last the cough loses all sound. 
We see the child cough and speak; we hear nothing. 
Besides these symptoms, which are, and indeed must be, entirely 
dentical with those of catarrh of the larynx, and which owe their origin 
to the thickening and relaxation of the vocal chords, from incipient 
palsy of the muscles, by which they are stretched, and to the exudation 
which coats them, there is dyspnoea, a persistent, perilous dyspnoea, char- 
acteristic of croup, and rarely seen in catarrh of the larynx, and only 
then as a transitory symptom. This dyspnoea, which proceeds from nar- CROLT. 
19 
rowing of tlie glottis, and the occurrence of which, where there is no 
false membrane, requires further explanation, is peculiar, and not easily 
confounded with any other form of impeded respiration. In the first 
place, it is tremendously laborious. The efforts made by the child, in 
order to draw breath, are very evident. Every muscle, which can aid 
in expanding the chest, is called into vehement action. He sits up, 
extends his spinal column, so as more effectually to dilate the thorax by 
upheaval of the ribs. In spite, however, of every effort, the air can pass 
but slowly through the contracted rima glottidis. The breathing is re- 
markably protracted and tedious, and hence, of course, much less fre- 
quent than in dyspnoea from other causes (pneumonia, for instance, 
where the muscles of respiration have no abnormal obstacle to over- 
come). It also gives rise to an exceedingly characteristic wheezing or 
sawing sound, which, if once heard, will always be recognized in future. 
During these laborious efforts at inspiration, the levatores aim nasi 
contract, dilating the nostrils (for, without this instinctive muscular ac- 
tion, the nostrils would tend to close, from the rapid rarefaction of the 
air within the nose). This “working of the nostrils,” however, is not 
peculiar to the dyspnoea of croup. 
Besides this, however, there is another and characteristic sign of 
croup, which is known even to the laity, and which depends upon the rare- 
faction of the air, within the thorax, when dilated during stricture of the 
glottis. We see, namely, that with every inspiration the epigastrium, 
instead of projecting, is strongly and deeply depressed. When the air 
within the chest becomes rarefied, the pressure upon the thoracic surface 
of the diaphragm becoming far lighter than that upon its abdominal 
surface, it yields, and is forcibly pushed upward, the xyphoid and costal 
cartilages being likewise drawn in by the inspiration. This, too, is 
easy of comprehension, if we only bear in mind the mechanism of normal 
respiration. If the air can enter the air-passages with freedom, the dia- 
phragm, upon contracting, causes its pars tenclinea to descend, but pro- 
duces no incurvation of the ribs; for their resisting power is far greater 
than that encountered by the diaphragm in the elasticity of the lung, or 
in the feeble pressure of the abdominal viscera. 
If, however, the tendinous centre be drawn up by the rarefaction of 
the air in the lungs, or if it be only fixed and hindered from moving 
downward, the inspiratory contractions of the muscles of the diaphragm 
must then, of necessity, cause the arch of the ribs to curve inward. 
The desire to draw breath, the efforts to do so, and the desperation 
which its fruitless exertions produce, are evinced in the entire being 
of the child. Now it begs to be taken out of bed into the arms of its 
nurse, and from its nurse to be put to bed again. The greatest terror 
is depicted in its manner; it beats about, throws itself hither and thither, 20 
AFFECTIONS OF THE LARYNX. 
clutches at its throat, pulls at its tongue, as if to remove the obstacle to 
its breathing. The face is distorted and bedewed with sweat. The 
look of a child sick of croup is, above all things, sad and piteous. 
The circumstance, that children often die of croup, who, during life, 
evinced signs of the greatest dyspnoea, but in whom, after death, neither 
pseudo-membrane nor considerable swelling, either of mucous membrane 
or of the submucous tissue, could be discovered, has given rise to the 
impression that, in these cases, spasmodic contraction of the laryngeal 
muscles has constricted the glottis. This view is contradictory to patho- 
logical and physiological fact. 
In all severe inflammation of mucous or serous membranes, we find 
not only the submucous, and subserous cellular tissues, but also the 
muscles covered by the inflamed membrane, infiltrated with serum, sod- 
den, and pale. Even a priori, it is not to be supposed that muscles in 
this. condition should be capable of a spasmodic contraction, and Jlo- 
Tdtansky declares his opinion, from a pathological point of view, that 
u the infiltrated, pale, relaxed muscular tissue, in croupous inflammation, 
is stricken with palsy.” That muscles in this condition really do lose 
their contractile power, is shown by the paralytic bulging of the inter- 
costal muscles in pleurisy, and in the loss of peristaltic action of the in- 
testine in peritonitis, or dysentery, from palsy of the intestinal muscles, 
covered by the inflamed mucous or serous membrane. These, and 
many other analogous observations, render it highly improbable that 
the laryngeal muscles should be spasmodically contracted, instead 
of palsied, where their mucous covering is inflamed. Section of the 
par-vagum nerve, in young animals (an operation originally practised 
for an entirely different purpose), furnishes absolute proof, that paralysis 
of the muscles of the larynx produces dyspnoea; nay, the dyspnoea 
arising in consequence of this experiment bears so strong a resemblance 
to croupous dyspnoea, is attended by such similar long-drawn whistling 
inspiratory efforts, and other signs, that the similarity of the two con- 
ditions must strike the most indifferent beholder. But the study of 
the anatomy of the larynx of a child makes it certain, that a forced 
effort at inspiration will contract or close the glottis, unless it be held 
open by muscular action. In childhood, we do not find that triangular 
space, bounded by the base of the arytenoid cartilage, stretching for- 
ward, and inward, to the processus vocales, known as the pars respira- 
toria of Longet. In children, the base of the arytenoid cartilage has no 
extension, the glottis forming a small cleft, running antero-posteriorly, 
and bounded by the membranous expansion of the vocal chords. These 
membranes lying obliquely opposed, one to the other, unless the glottis 
be held open by muscular action, the effect of an energetic inhalation 
must be to contract, and close the cleft, by rarefying the air within the 
trachea. CROUP. 
21 
In any juvenile larynx which we may cut out ci the body, the glottis 
is capable of being completely closed by the application of powerful 
suction to the trachea. As it is of the utmost importance, in the treat- 
ment of croup, for us to know whether false membranes occlude the 
glottis, or whether palsy of the laryngeal muscles, by oedematous infil- 
tration, be the main cause of the dyspnoea, we must carefully note 
whether inspiration and expiration are in equal degree obstructed, or 
whether inspiration alone be laborious, and expiration free. In the 
former, and most common case, false membranes clog the rima glottidis, 
impeding both exit and entrance of the air; in the latter, crippling of 
the muscles is the chief cause of the dyspnoea. Upon rarefaction of the 
air within the trachea during inspiration, the inflowing current, through 
the nose and mouth, forces the folds of the glottis together; but expira- 
tion follows freely, as the air, when expired, drives the vocal chords apart, 
without any need of muscular aid. Let us bear in mind, too, that the 
posterior crico-arytenoid muscles, which open the rima glottidis, are more 
easily paralzyed when the mucous membrane of the pharynx, which 
covers them, takes part in the inflammation. Thus, it is easily seen why 
those cases of croup, which the French alone admit to be true croup, 
cases in which croup-membrane can be seen upon the pharynx, must be 
by far the most dangerous. 
The wide gaping of the glottis during inspiration, when the laryn- 
geal muscles are acting normally, of which I have been able to convince 
myself as often as I have looked in the laryngoscope, has materially 
strengthened my conviction of the correctness of my theory, that palsy 
of the muscles of the glottis forms an important element in the dyspnoea 
of croup. 
It is difficult to say whether any real pain in the larynx forms a 
symptom of croup. The clutching of the child at its throat may depend 
upon the desire to remove the impediment to its breathing, which it in- 
stinctively perceives. In the beginning of the disease, the expectora- 
tion, which is usually scanty, rarely contains masses of shreds, or of cohe- 
rent false membrane. The pulse, at first, is generally full, hard, and of 
moderately increased frequence; the face is flushed, and the tempera- 
ture of the body elevated. 
Croup, in a groat many cases, exhibits decided remissions in the 
morning, and through the course of the day, which might almost seem 
Intermissions. (Hence the homoeopathists promise that their medicines 
will not evince their wonderful effect until after a lapse of several hours.) 
Toward morning the respiration becomes more free. The voice returns. 
The cough is less frequent; it is hoarse, but not without sound. The 
fever abates; the general condition appears almost undisturbed; and 
only the thin piping, or the still suspicious tone of the cough, remains, 22 
AFFECTIONS OF THE LARYNX. 
to recall to mind the scene of terror of the previous night. But be- 
ware of building too great hopes upon these remissions. The coming 
night may bring with it a repetition of the same symptoms, and the 
greatest danger to the life of the child. The continuance of fever, even 
if only moderate, and, above all, the presence of pseudo-membrane in 
the pharynx, should excite the greatest solicitude. 
Sometimes the croup exhibits this rhythmical type throughout its en- 
tire duration, bad nights following upon tolerable days; in fatal cases, 
the remissions becoming more and more incomplete, and the nocturnal 
exacerbations growing more and more formidable. In other instances, 
which are far more dangerous, the symptoms of croup run a continuous 
course from the beginning. The remission expected in the morning 
fails to appear, and death may ensue in the course of two or three 
days. 
When, instead of abating, the malady tends to terminate unfavor- 
ably (an event but too common in croup), the scene changes. The 
flushed face of the child grows pallid, the lips lose their color, the eye, 
which hitherto has been gazing anxiously about it, assumes a drowsy 
expression. Quite frequently spontaneous vomiting sets in, while the 
emetics which we administer remain without effect, and the child grows 
insensible to sinapisms and other cutaneous stimulants. The respira- 
tion becomes diminished, and now the whistling sound of inspiration 
often ceases ; the child lies exhausted in a half-slumber; the symptoms 
of croup seem gone. It seems to have no more dyspnoea, until, upon 
awakening from sleep, or after coughing, it involuntarily attempts to 
draw a long breath. Then the glottis closes ; the child, once more in 
danger of suffocation, springs up, props itself up with its hands, looks 
desperately around it, anew makes violent efforts to drawT breath, and 
finally sinks back again exhausted, and falls into a state of semi-somno- 
lence. (In young animals in which the par vagum nerves have been 
cut, we observe precisely these phenomena. Respiration almost free as 
long as they breathe quickly; respiration impeded in the highest degree 
the moment they attempt to draw a deep breath—a condition easily un- 
derstood after the above explanation.) 
These changes in the child’s condition are a result of gradual blood- 
poisoning by carbonic acid, overcharge of the blood with this gas form- 
ing one of the main sources of danger from this disease. 
The above-described train of symptoms is by no means due to en- 
gorgement of the brain and its meninges (as has been generally assumed), 
nor is a child with croup ever cyanotic from impeded respiration alone, 
excepting when, in the act of coughing, the flow of blood within the 
jugulars is arrested by compression of the contents of the thorax. A 
child with croup cannot be otherwise than pale at this stage of the dis CKOUP. 
23 
order, and the pallor continues until, as palsy of the heart sets in, the 
contents of the arteries grow less and less, the veins fuller and fuller, 
and thus a livid tinge is imparted to the pallid lips. As the blood of 
the veins within the thorax is subjected to a pressure less than that upon 
the veins without, the tendency of the elastic lung being to contract, 
and thus to cause the vessels which border upon it to expand; as with 
each deep inspiratory effort the power of suction of the lung grows 
stronger (since the draught increases as the lung expands), this suction 
must reach its highest pitch of intensity; blood will be drawn with 
greatest power from the external veins into those within the thorax, 
when any one with constricted glottis rarefies the air within his lungs by 
trying to draw a long breath. Cyanosis and obstructed evacuation of 
the cerebral veins can never take place in this way. The process must 
always have an opposite effect. 
When inspiration and expiration meet with equal obstruction, the 
circulation is somewhat differently affected. As the glottis becomes so 
much occluded by false membrane, that very little air can enter into, or 
escape from, the lungs, inspiration and expiration can only be carried 
on by means of all the auxiliaries at command. Now, as we are able 
to expel our breath with greater force than we can inhale it, the influ- 
ence of the forced expiration over the discharge of blood from the 
thorax outweighs that of the forced inspiration, and then, indeed, cyano- 
sis takes place. 
Since the interchange of gases in the lungs depends principally 
upon the renewal of air contained in the air-vesicles, and as the blood 
does not give out carbonic acid, and absorb oxygen, unless the air 
within the vesicles contain less of carbonic acid and more of oxygen 
than the blood in the plexus of capillaries about it, the necessary conse- 
quence of the incomplete respiration in croup, and of the imperfect ren- 
ovation of the air in the vesicles is, that the carbonic acid which inces- 
santly forms in the blood cannot escape from it into the air of the vesicles 
which is already overcharged with it. The symptoms described are 
exactly the same as those produced by the inhalation of carbonic acid. 
In croup, the carbonic acid created within the body itself poisons the 
patient, while in the other case the poison is breathed with the 
atmosphere. 
In fatal cases, death almost always takes place with the symptoms 
described, through the gradual establishment of general paralysis, in 
consequence of carbonic-acid poisoning. In rare instances, the access 
of air to the lungs may be suddenly and absolutely cut off by the fall 
of a piece of loosened membrane before the glottis, and rapid death 
by suffocation may ensue. 
If the croup take a turn for the better, the improvement may take 24 
AFFECTIONS OF THE LARYNX. 
place gradually with occasional expectoration of quantities of tough 
sputum, containing a more or less profuse admixture of flakes of coagu- 
lum—the cough becoming easier, the voice louder, the symptoms of 
narcotism disappearing, as the embarrassment of respiration subsides. 
In other instances, however, which are far less numerous than is 
generally supposed, large masses of pseudo-membrane, and often tubular 
casts of the substance, are thrown out after violent coughing, retching, 
and vomiting, so that the breathing, till now extremely oppressed, sud- 
denly becomes much more free. The child is safe from immediate 
danger, if a reproduction of the exudation do not once more occlude 
the glottis, or a new exacerbation of the inflammation again produce 
oedema of the laryngeal muscles. 
After subsidence of the croupous process in the larynx, when its dura- 
tion has been somewhat protracted, many children perish from hyperaemia 
and oedema of the lungs, and of bronchial catarrh. The comparatively 
ill success of tracheotomy, after protracted croup, is entirely due to these 
complications, the frequence of which we can easily show to be a neces- 
sary result of the previous disease. When the thorax is expanded, and 
the alveoli are made to dilate without allowing the atmosphere to pene- 
trate into them, the air already contained in the bronchi and air vesicles 
must be expanded and rarefied. The bronchial mucous membrane and 
inner wall of the air-vesicles during croup are thus placed in a condition 
similar to that of a portion of external skin under a cupping-glass. 
Hyperaemia and increased secretion are the necessary result of the sus- 
pension or diminution of the pressure to which the capillaries are habitu- 
ally subjected. The circumstance recently urged by Bolin and Gerhardt 
in their two valuable works upon croup, that bronchial catarrh invariably 
and promptly associates itself with croupous laryngitis with constricted 
glottis, seems to me to argue in favor of the genetic connection of the 
two processes. With regard to the croupous pneumonia and bronchitis, 
however, which complicate laryngeal croup in many cases, it is quite 
otherwise. As I have stated in the opening words of this text-book, it 
is catarrhal inflammation only which arises in consequence of vascular 
engorgement of a mucous membrane.* I shall repeatedly recur to the 
impropriety of regarding other forms of inflammation as an exaggeration 
or a consequence of simple hyperaemia. “ That the danger from croupous 
laryngitis is considerably heightened by the addition to it of bronchial 
catarrh ” is perfectly admissible; that, however, in real croup, “ death 
always proceeds from bronchitis or bronclio-pneumonia ” (Bohn) is cer- 
tainly an exaggeration. The symptoms of the secondary croup which 
*1 have no objections to make against the opinions of authors who do not consider 
catarrh as an inflammation, but rather as derangement of secretion, characterized bj 
swelling and succulence. CROUP. 
25 
complicates measles, small-pox, scarlatina, epidemic diphtheria, and other 
infectious disorders, will be described hereafter when treating of the 
diseases themselves. 
Diagnosis.—We have already drawn attention to the points of 
resemblance between croup and laryngeal catarrh, and have also shown 
in what respects the two diseases differ. We have merely to add that 
the pharyngeal patches of croup membrane are of nearly as great diag- 
nostic value as the masses of membranous exudation discharged by 
coughing or vomiting; that dyspnoea is rare in laryngeal catarrh, and is 
never persistent, nor is there often much fever, while in croup, fever 
never fails. 
Prognosis.—Children who have passed their seventh year may 
survive attacks of croupous laryngitis of the utmost intensity, but during 
the earlier years of life croup is one of the most formidable of all dis- 
eases. We have already remarked that the dazzling reports of cures of 
which many practitioners boast are to be accepted with caution, most 
of them being based upon an error in diagnosis. 
The epidemic appearance of croup undoubtedly renders the bad 
prognosis of the disease still worse, and though it would be going too far 
to pronounce croupous laryngitis, complicated by croup of the pharynx, 
absolutely mortal, yet it is not to be denied that this complication renders 
our prognosis still more grave. 
Among the symptoms, the terror, the restlessness, the full pulse, the 
flushed face, the hoarseness or aphonia, are of far less prognostic impor- 
tance than the first indications of commencing blood poisoning. If the 
face grow pale, the lips colorless, the child drowsy, the sensorium be- 
numbed ; if an emetic remain without action; or if, on the other hand, 
vomiting spontaneously set in, we are rarely justified in expecting a 
favorable termination of the malady. 
Treatment.—Prophylaxis against croupous laryngitis requires the 
measures already recommended for protection against laryngeal catarrh. 
Never shut up a child permanently in its chamber because it has once 
had an attack of croup, nor accustom it to too much clothing. Mean- 
while, however, teach the mother not to let herself be deceived by bright 
sunshine alone, nor to send the child out without paying attention to the 
direction of the wind. When there is decided predisposition to croup, 
watch the weather-cock, and keep the child from exposure to a rude 
northerly or northeasterly wind. It is also advisable to keep the child 
within doors after sunset. Finally, cold washing of the throat and breast, 
provided that the skin be afterward carefully dried, is a capital prophy- 
lactic where there is predisposition to croup. 
As the real causes of croup are obscure, the causal indications cannot, 
in most instances, be met. Among the laity it is considered a settled 26 
AFFECTIONS OF THE LARYNX. 
fact, that the croup is the result of “ taking cold.” With true fanaticism, 
the moment that a child becomes hoarse, an incredible quantity of hot 
sweet milk (which is here preferred to elder-tea) is poured down his 
throat. Not until the child begins to sweat do they believe him safe, 
and the foe (often an imaginary one) driven from the field. The 
teachers of the hydropathic school claim similar results from envelopment 
of the body in wet cloths, by means of which, “ in a great number of 
cases, they attain the most brilliant success,” by thus restoring the re- 
pressed action of the skin. 
Granting, however, that many cases of croup arise from chilling of 
the surface, the disease is not so simple a one, the nutritive disorder of 
the mucous membrane is of far too grave a nature to admit of restora- 
tion by the mere production of diaphoresis. In catarrh it may be other- 
wise. Where hyperaemia alone has sufficed to swell the mucous 
membrane, active solicitation of the, blood to the surface may produce a 
depletion from the same and cure the complaint. 
As, however, it is almost impossible for the laity to distinguish be- 
tween the two maladies, and as even the physician is often obliged to 
reserve his decision when first called to see a child suffering from 
hoarseness, a barking cough, and sudden nocturnal dyspnoea, it is well, 
in such emergencies, while awaiting the doctor, to give the child hot 
drinks, to cover him warmly, and to apply a succession of hot, moist 
sponges to the throat. It has been stated that in many instances, espe- 
cially of epidemic croup, the inflammation seems to be propagated from 
the pharyngeal surface into the larynx. If, then, croupous patches be 
visible upon the fauces, the utmost energy is demanded on the part of 
the physician. He must not content himself with the application of a 
few leeches over the throat, as such practice is of very doubtful efficacy. 
Let him rather remove the false membrane from the tonsils, and 
thoroughly cauterize the affected part. This treatment is much more to 
be relied on, and (perhaps from the astringent action of the caustic) is 
one of the surest of antiphlogistics. 
With regard to the management of the disease itself, many phy- 
sicians, especially country ones, are in the habit of calling for leeches, 
and emetics, and of forthwith applying one or both articles, if the 
smallest trace of pseudo-membrane be discoverable. The leeches are 
to moderate the inflammation; the emetic to remove the exudation. 
Hardly any one has ever had the courage to treat croup expectantly, 
and to wait until special incidents in the disease shall call for special 
measures. It is chiefly to the homoeopaths that we owe the discovery, 
that even a child with the croup may get well without leeches or 
emetics. Leeches (of which we apply one or two upon the manubrium 
sterni, or throat of a child under a year old, increasing them in number CROUP 
27 
according to the age) are, moreover, of exceedingly doubtful assistance 
in croup. In far the greater number of instances they are directly 
hurtful. Their recommendation is, in great measure, supported upon the 
erroneous view that hypenemia and inflammation are identical, hence 
abstraction of blood will allay inflammation. A really inflammatory pro- 
cess is not interrupted by blood-letting, although it may moderate the 
collateral hyperaemia in the vicinity of the inflamed spot; however, if a 
stasis of the blood take place in the mucous membrane of the larynx, 
if its circulation be interrupted, the blood flows with greater force into 
the vessels of the neighboring tissues, and produces in them transuda 
tion, swelling, and oedema. 
We have shown that a part of the danger in croup proceeds from 
such swelling and infiltration; hence, when we have to deal with a vigor 
ous, blooming child (but only in such a case), we may apply a few 
leeches to the manubrium sterni. They must never be applied over the 
larynx, as at that point the bleeding is hard to stanch. In all cases 
we should apply the leeches ourselves, or employ an expert to do it, 
who can check haemorrhage. Among puny, badly-nourished children, 
leeches are contraindicated. It is most dangerous to exhaust the 
strength of a child, which he will require at a later stage of the disease 
to enable him to expectorate with vigor. Blood-letting has no power 
whatever to prevent the formation of the exudation. 
With regard to the employment of emetics, the revulsive action 
through which they are supposed to exert an influence upon croup is 
altogether problematic. Still less may we promise ourselves help from 
their diaphoretic effect. They are only indicated where obstructing 
croup-membranes play a part in producing the dyspnoea, and when 
the child's efforts at coughing are insufficient to expel them. We 
have stated, in describing the symptoms, that impeded expiration 
should cause us to infer that the glottis is becoming choked by false 
membrane. We, therefore, would lay great stress upon this symptom 
as an indication for emetics. As the formation of pseudo-membrane 
may take place at a very early period, an emetic, if indicated, may be 
given early in the disease. In treating croup, preference is given to 
sulphate of copper over tartar-emetic or ipecacuanha, and, as it seems to 
me, with reason. Beware, however, of giving this remedy in doses too 
small, for it may then act with uncertainty, and is much more apt to 
operate as a poison than when used in full doses. We prescribe ten 
or fifteen grains of sulphate of copper dissolved in two ounces of water, 
and let the child take a large teaspoonful of it every five minutes until 
vomiting sets in. The more complete the remission after the vomiting, 
the more the membrane thrown out, so much the more reason have we 
for repeating the emetic, should the peculiar dyspnoea above described 28 
AFFECTIONS OF THE LARYNX. 
rcurs, If there should be no remission, should no croup membrane be 
expelled, or if the expiratory act be free from impediment, the repe- 
tition of the emetic is contraindicated. This rule is often broken. How 
often do we see children incessantly dosed with different salts of copper, 
even when they have ceased to vomit, and they can do no more service! 
They lie bathed to the armpits in the bluish fluid which, mixed with 
curdled milk, flows from their bowels, and in vain turn away their head 
and push away the spoon containing the repulsive medicine which gives 
them so much griping and distress. 
The application of cold deserves a full trial, in the shape of cold 
compresses, quickly changed, laid upon the throat of the child, as soon 
as the signs of croupous laryngitis appear. In families where they are 
not afraid to use this treatment, we shall have a far more happy result 
than in houses in which the prejudice against it is not to be overcome. 
The employment of cold to the skin in inflammation of internal organs, 
as first recommended by ICiwisch in puerperal peritonitis, seems indeed 
to act as a direct antiphlogistic; and difficult as it may be to compre- 
hend what effect it can have upon an organ separated from it by skin 
and muscle, experience has here more right to respect than physiological 
abstract reasoning. (See treatment of pneumonia.) The fanaticism of 
the hydropatlis in this matter, who, while applying cold to an inflamed 
part, are loath to refrain froro other hydropathic measures, has done more 
harm than good. 
We have already recommended touching of the pharyngeal mucous 
membrane with nitrate of silver as a direct antiphlogistic, and now, 
after personal experience, cannot sufficiently urge the application of a 
solution of the lunar caustic to the inflamed mucous membrane of the 
larynx, as has been much practised in France, and but too little resorted 
to among ourselves. Bretonneau, with whom this local treatment of 
croup originated, uses a curved rod of whalebone, with a small sponge 
made fast to its lower end. This is dipped in a concentrated solution 
of nitrate of silver ( 3 ss to 3 ij). We press down the tongue of the 
child, and endeavor to reach the entrance of the glottis with the sponge. 
There the sponge is immediately compressed by the muscular contrac- 
tion which takes place, whereby certainly a portion of the liquid, if 
only a small one, arrives in the larynx. 
It is doubtful if calomel have indeed an antiphlogistic, or even a 
specific effect upon croup, although I cannot deny that very high 
authority is inclined to credit the beneficial effect of this agent in its 
treatment; nor that I myself make use of from a quarter to half a grain 
of calomel every two hours, in most cases of this disease, while my ex- 
perience leads me to shun the too customary employment of small 
doses of tartar-emetic and sulphate of copper (tart. stib. gr. i; aquas CROUP. 
29 
3 i—S. 3 i. 2 h.). (Cupri. sulp. gr. i; aqua?, 3 i; s. 3 i. 2 h.) Sulphuret 
of potassium (fii potas. sulp. 3ss.—2> j; aquae; syrup simplic. aa 3 i 
Tq, s. 3 i. every 2 hours), in spite of the warm eulogium of distinguished 
authorities, such as liilliet and Bcirthez, has never come much into use, 
and now is almost obsolete. The proposal of bicarbonate of soda in 
large doses is obviously based rather upon theoretical grounds than 
upon actual experience; hence deserves little reliance. The drug has 
been administered in the hope of loosening the false membrane, and 
preventing further coagulation of the exudation, or else of improving 
the state of the blood. 
Chlorate of potash, which is a favorite remedy in treatment of diph- 
theria of the fauces, and of the secondary croup of the larynx, which 
accompanies it, is also recommended in true primary croup, by those 
who make no distinction between the latter and the pseudo-membranous 
laryngitis of acute infectious disorders. I have no personal experience 
of the action of this article in treating primary laryngeal croup. 
When called to the bedside of a child, recently attacked, the physi- 
cian should not be misled by the idea that, without his immediate and 
active interference, the child must soon die. Leeches should never be 
applied, save under the exceptional conditions above stated, and the 
after-bleeding from the bites should be kept within bounds. It is bet- 
ter, in most cases, to confine one’s self to the use of cold, and do not 
hesitate to put on the first compresses with your own hand, until the 
parents perceive the relief which they afford. Besides this, if the 
bowels be confined, administer a clyster, so that the diaphragm may 
have free room to act. The best is a cold one, of three parts water, and 
one of vinegar. If the dyspnoea increase, if the respiration be impeded, 
give an active emetic, without suspending the cold applications. The 
emetic is to be repeated, under the conditions stated above; if, however, 
under this treatment, there be no remission, apply a solution of nitrate 
of silver, at intervals of several hours, to the entrance of the glottis. 
Do not forget, during the night, that, with the early morning hours, 
there often comes a remission, nor during the next day, that, in spite of 
the improvement, the coming night may again bring with it the greatest 
danger. However well the child may seem to be, it must not quit its 
bed. The temperature of the room must be kept uniform, and the air 
rendered moist by means of open vessels of water. Give half a grain 
of calomel every two hours; aud now change the compresses less often, 
and cover them with a woollen cloth. Continue meanwhile, but at longer 
intervals, to use the solution of nitrate of silver. The next night, if the 
croup grow worse, the same measures are required. 
Should this treatment remain without effect, should there be no 
improvement in the course of ten or twelve hours, do not lose time 30 
AFFECTIONS OF THE LARYNX. 
in giving Schwefelleber, or the “ liver of sulphur,” so long prized as a 
specific, carbonate of soda, chlorate of potash, or senega, or other ex- 
pectorant ; but proceed at once to tracheotomy. The earlier we under- 
take this, the more hope may we have that pulmonary bypersemia, 
oedema, and bronchial catarrh, will not injure our prognosis. However 
bad the results, it should never be neglected when other means have 
failed. Even death itself, after this operation, is far less painful, 
for even when the operation has been long delayed we rarely fail to 
obtain a transient but marked improvement; and often, indeed, there 
is a complete relief, upon which, however, slender hope should be based. 
Besides treating the dyspnoea upon the principles given above, we 
have also to relieve the paralytic symptoms due to blood-poisoning by 
carbonic acid. For this purpose, the powerful stimulus obtained by 
pouring cold water upon the child, while in a warm bath, is of great 
service. This is also a favorite remedy in treatment of asphyxia by 
charcoal vapor. Lose no time in making use of it, the moment the child 
begins to grow drowsy, the skin to cool, the sensorium to be benumbed, 
or as soon as emetics fail to act; for, at this period, their operation is often 
of the utmost importance. A few gallons of cold water, poured from 
a moderate height, over the head, nape, and back of the child, almost 
always cause it to revive for a while, and to cough vigorously. Thus, 
sometimes after the bath, masses of exudation are expelled. Other 
stimulants, such as camphor or musk, are much less effective, and ought 
not to be employed save when insuperable objections are opposed to the 
cold effusion. They should be given in large doses, immediately prior 
to the emetic. (!£. camphor gr. x. Ether acet. 3 iij. m. S. gtt. x— 
xv. every quarter of an hour. • moschi. gr. iv. Sacch. alb. 3 i. m. 
div. in. ch. vi. s., a powder, every hour or half hour.) 
The application of sinapisms to the calves of the legs and soles of 
feet, repeated bathing of the hands and forearms in water as hot as the 
child can bear, the use of “ flying blisters ” to the neck and chest, are 
recommended, partly to corroborate the action of the stimulants ad- 
ministered internally, and partly as a derivative from the larynx to the 
skin. Although we do not rate cutaneous irritants very high among 
the remedies against croup, yet, for want of better or more promising 
means, we make use of them where the disease is protracted, sometimes 
improving, and again growing worse; and where wre are dissatisfied 
with the effects of the treatment already described, and yet hesitate to 
proceed to tracheotomy. In order to accelerate the action of the flying 
blister, JBretonneau advises that the plaster be smeared with a solution 
of cantharidin in oil, and covered with blotting-paper before appli- 
cation. CATARRHAL ULCERS OF THE LARYNX. 
31 
CHAPTER III. 
CATARRHAL ULCERS OF THE LARYNX. 
Etiology.—When the cell-formation, which takes place upon the 
surface of the mucous membrane in acute and chronic catarrh, en- 
croaches upon the tissue of the mucous membrane itself, producing in 
it a solution of continuity, a superficial loss of substance occurs, con- 
stituting the simple catarrhal ulcer or catarrhal erosion. The pathogeny 
of this ulcer is easily understood, if we compare it with a very similai 
process upon the skin. Where a plaster of cantharides has raised the 
epidermis in a blister, the contents of the blister, in a few days, become 
turbid from admixture of young cells. These are formed upon the sur- 
face of the cutis, through the proliferation of the more deeply-situated 
epidermic cells. The substance of the cutis is intact. If, however, 
after opening the blister, we anoint the exposed cutaneous surface with 
an irritating salve, the cell-formation extends to the substance of the 
skin, causing its destruction, and forming a superficial sore completely 
analogous with the catarrhal ulcer of the mucous membrane. 
In other cases, the numerous mucous glands which exist in the larynx 
become the seat of a vast multiplication of cells. They enlarge consider- 
ably ; their covering is finally perforated, their contents are discharged, 
and, in place of the gland, there remains a round, crater-formed loss of 
substance—the second form of catarrhal ulceration, the follicular sore. 
Ulcers are rare in acute laryngeal catarrh. In the chronic form, how 
ever, especially in the follicular variety, affecting the fauces and larynx 
of preachers, singers, inveterate smokers, and immoderate drinkers of 
spirits, there is a decided tendency to ulceration. 
This is still greater in the chronic laryngeal catarrh which almost 
always accompanies pulmonary consumption, independently of tubercu- 
lous disease of the larynx. Finally, Turk has repeatedly noticed catar- 
rhal ulcers of the larynx, in the vicinity of which scarcely any trace of 
catarrhal disease could be discovered. 
Special exciting causes render certain portions of the laryngeal 
mucous membrane particularly liable to catarrhal ulceration, namely, the 
posterior wall of the larynx, the aryepiglottic ligament, the anterior 
and posterior ends of the vocal chords and the epiglottis, at the point 
corresponding to the processus-vocalis of the arytenoid cartilage. The 
places first named are particularly rich in mucous glands, and the tissue 
of the mucous membrane is loose, as it here contains a lesser quantity 
of elastic fibre. At the latter-named spots the cause of ulceration 
seems to be mechanical. In all loud talking the vocal chords are forced 
toward one another, so that their edges almost touch. When their 32 
AFFECTIONS OF THE LARYNX. 
mucous integument is swollen by catarrh, a constant friction takes place 
during speaking, which results in excoriation and ulceration. (Leucin.) 
Anatomical Appearances.—In the beginning catarrhal erosions 
have either a rounded or an elongated shape, according to the arrange- 
ment of the elastic fibres; but they afterward coalesce, forming an ex- 
tensive loss of substance of irregular contour. The follicular ulcers, how- 
ever, retain their circular form, even when of long standing, and show 
less tendency to increase in width than in depth. They readily lead to 
disease of the cartilage, and, exceptionally, several of them run to- 
gether, and produce extensive destruction of the mucous membrane, 
the “ catarrhal consumption of the larynx.” 
The ulcers originating at the anterior and posterior ends of the vocal 
chords spread lengthways over the greater part of one, or still oftener 
of both chords. In many cases the loss of substance is so shallow that 
the chords appear as if they had been only superficially shaved off; in 
other cases the destruction is more considerable. Lewin describes ca- 
tarrhal ulcers upon the lower surface of the vocal chords, of which, during 
life, we can only make out the outer border, as a minute fold of mucous 
membrane, which seems to be inserted under the level of their upper 
membrane. 
In phthisical patients this author has so often found catarrhal ulcera- 
tion in that portion of the laryngeal mucous membrane where the vocal 
processes cover the arytenoid cartilages that he describes this laryngo- 
scopic appearance, which hardly ever is met with in persons with healthy 
lungs, as almost pathognomonic of pulmonary consumption. 
Symptoms and Course.—The general symptoms of a chronic laryn- 
geal catarrh are not materially modified when accompanied by ulceration. 
True, we may suspect the existence of an ulcer when a patient with a 
harsh, barking cough, of long standing, and chronic hoarseness, running 
from time to time into aphonia, complains of a sensation of burning, or 
soreness upon speaking or coughing; but these symptoms (although 
sometimes so distressing that the sufferer, in order to avoid pain, speaks 
without moving the vocal chords, that is to say, in a whisper) are often 
entirely absent, even when very extensive ulceration exists. The addi- 
tion of painful and difficult deglutition to the other symptoms renders the 
presence of an ulcer still more probable; and vrhen the epiglottis, the 
aryepiglottic ligament, or the arytenoid cartilage is involved, this 
symptom is rarely absent. But as painful deglutition also occurs in a 
severe case of simple catarrh at this point, no positive inference can be 
drawn from this symptom alone. Next to the objective signs of ulcera- 
tion, the admixture of small streaks of blood in the sputa furnishes the 
most reliable token of its existence. 
Among objective signs, the condition of the fauces and gullet is of TYPHOUS AND VARIOLOUS ULCERS OF THE LARYNX. 
33 
great diagnostic importance. Experience teaches that follicular ulcers 
of the larynx are often combined with follicular pharyngeal ulceration. 
If, then, in patient's with long-standing hoarseness and other symptoms 
of chronic laryngeal catarrh, we find a reddening of the mucous mem- 
brane of the soft palate, and see the posterior pharyngeal wall studded 
with small round, yellowish sores, it is to be presumed that the disease 
has also invaded the larynx. 
The majority of laryngeal ulcers may be brought into view by means 
of the laryngoscope, especially when situated upon the epiglottis, upon 
the arytenoid cartilages, on the aryepiglottic folds, and upon the true 
and false vocal chords. 
Treatment.—The treatment of catarrhal ulceration of the larynx is 
almost identical with that of the simple laryngeal catarrh; and, as in 
catarrh of other mucous membranes, we do not materially modify our 
treatment where ulceration supervenes upon simple inflammation. It 
cannot, however, be denied that the cure of catarrhal ulcers of the larynx 
takes place somewhat more rapidly when the medicaments are applied 
directly and solely to the sore itself, instead of over the whole mucous 
surface. Whoever has obtained sufficient laryngoscopic dexterity to 
enable him to touch the ulcers with lunar caustic in substance, or with a 
concentrated solution of nitrate of silver, will do well to adopt such 
local treatment, instead of that recommended in the last chapter, espe- 
cially instead of inhalation of alum or nitrate of silver in solution. While 
practising local treatment, however, whether by cautery or inhalation, 
the dietetic and other internal treatment already described is not to be 
neglected. The partiality to which specialists are so often prone is not 
only hurtful to the patient, but injures the credit of new therapeutic 
measures. When a chronic ulcer of the larynx, which has long resisted 
a regular course of caustic at the hands of a specialist, recovers under 
the use of Ems-water and careful nursing of the mucous membrane, 
perhaps after weeks of absolute enforced silence, it will generally be 
found that the patient had relied solely upon the local treatment for a 
cure, and had lived imprudently or absurdly. 
CHAPTER IV. 
TYPHOUS AND VARIOLOUS ULCERS OF THE LARYNX. 
Etiology.—From the teaching of PokitansJey, the belief has long 
prevailed that typhous ulceration of the larynx proceeded from “ me- 
dullary infiltration of the mucous glands of the larynx with subsequent 
sloughing,” and was therefore quite analogous to the intestinal ulcers 
of typhus, which are formed by the action of a similar morbid process 
upon the solitary glands and the glands of Peyer. 34 
AFFECTIONS OF THE LARYNX. 
This mode of origin, however, if it occur at all, is certainly not the 
sole, nor even the most frequent, source of typhous laryngeal ulceration. 
Rohitansky himself, in his last edition of his pathological anatomy, 
attributes typhous ulcer of the larynx to diphtheritic infiltration of the 
mucous membrane; and, indeed, it is entirely in harmony with this view 
of the matter that typhous ulcers appear upon the most dependent por- 
tions of the larynx, in which hyperaemia from gravitation is easily de- 
veloped, after long-standing disease; and, as is also the case in the lower 
parts of the lungs, and of the integument of the back and loins, at 
points most exposed to pressure or mechanical irritation. The most 
striking observation, however, is that of Muhle, according to whom, 
even in exanthematic typhus (a disease entirely foreign to abdominal 
typhus, which runs its course without medullary infiltration of the in- 
testinal glands), besides the products of catarrhal, croupous, and the 
diphtheritic processes, we find ulcers of the larynx exactly similar to 
those of abdominal typhus. 
While the infection of measles is followed by catarrhal, or, in rare 
cases, by croupous laryngitis, and while the poison of scarlatina does 
not localize itself in the larynx, excepting by propagation of diphtheritic 
inflammation from the fauces, the virus of small-pox, in a majority of cases, 
causes pustular inflammation of the mucous membranes of this organ. 
The variolous ulcer has its origin in the propagation of the exan- 
thema from the skin, and from the mucous membrane of the mouth and 
pharynx. We thus have to do with an eruption of small-pox in the 
larynx, which, however, as a rule, is complicated by a diffuse croupous 
inflammation—a secondary croup. 
Anatomical Appearances.—The typhous ulcer presents a loss of 
substance of the mucous membrane, bounded by relaxed discolored 
edges. Its most common seat is the posterior wall of the larynx above 
the transverse muscle, and on the lateral edges of the epiglottis. As a 
rule, it only has a circumference of a few lines. In some cases, however, 
it extends so as to involve the entire free edge of the epiglottis. In 
others it is more disposed to penetrate deeply, and thus may lead to 
laryngeal perichondritis, and to exposure and consequent necrosis of the 
cartilage. 
The variolous ulcer commences by the formation of a soft, flattened, 
non-umbilicated pustule, which soon bursts, forming a shallow, rounded 
sore, which readily heals. The croupous exudation which accompanies 
the small-pox eruption, and which, according to It tilde, is often found 
there ivhen the pustules are wanting, consists of a somewhat thin film, 
spreading over the swollen mucous membrane. The latter is at first 
somewhat reddened, but afterward grows paler. After the fall of the 
false membrane, which usually extends as far as the bifurcation of the SYPHILITIC DISEASE OF THE LARYNX. 
35 
trachea, the condition of the mucous membrane is normal, with the ex- 
ception of a few trifling abrasions. 
Symptoms and Course.—Owing to the position which it usually 
occupies, the typhous ulcer of the larynx does not cause alteration of the 
voice, unless there be a coexisting swelling, and relaxation of the vocal 
chords. Pain, or other sensation, is either slight or entirely absent. 
At all events, the sick, as they lie half slumbering, do not usually com- 
plain of it. Hence, we see that, during life, the typhous ulcer is not 
recognized, nay, cannot be recognized, and is often only discovered by 
accident upon the dissecting-table. Never neglect, therefore, in typhus 
subjects, to examine the larynx post mortem, even though during life 
no symptoms of disease of the larynx existed. In other cases the relax- 
ation and swelling of the vocal chords are so great, that the voice becomes 
rough and hoarse, and in cases where the stupor is not very great, there 
may even be violent fits of coughing, or of harsh, hoarse, inaudible 
“ hacks.” Although these symptoms are not so much signs of typhous 
ulcer of the larynx as of disease of the mucous membrane causing the 
ulcers, yet, from the fact of their appearance in the second or third 
week of the fever, we may diagnosticate the so-called laryngo-typhus 
from them. Although almost without importance of itself, this laryngeal- 
typhous ulcer may occasion danger from cedema glottidis and laryngeal 
perichondritis. 
Variolous ulcers necessarily give rise to symptoms identical with 
those of severe laryngeal catarrh. The two diseases would not be dis- 
tinguishable, did not the eruption upon the skin and the pustules in the 
mouth and throat furnish a distinct criterion. 
The secondary (variolous) croup, like the genuine, causes hoarseness 
and aphonia. The cough is generally moderate or entirely wanting. 
Either because the false membranes are not thick enough materially to 
occlude the passage of the glottis, or because oedema and palsy of the 
muscles of the glottis (to which we ascribe a part of the dyspnoea of 
croup) do not occur here, it is only on rare occasions that dyspnoea, like 
that of genuine primary croup, is met with in this form of laryngitis. 
Treatment.—Typhous and variolous ulcers usually heal, with subsi- 
dence of the primary disease, and need no particular treatment if uncom- 
plicated by oedema glottidis, or by perichondritis laryngea. 
SYPHILITIC DISEASE OF THE LARYNX. 
CHAPTER Y. 
Etiology.—Our knowledge of syphilitic disease of the larynx has 
been greatly extended and modified by means of laryngoscopy. Ger- 
hardt and Roth have shown that this class of disorders is much more 36 
AFFECTIONS OF THE LARYNX. 
common than had hitherto been supposed. By means of laryngoscopic 
examination, they have discovered laryngeal disease in a large number 
of syphilitic patients who evinced no outward signs of it, and have 
shown that, besides the grave and destructive disorders already known 
as tertiary syphilis, the so-called secondary forms—the catarrh, condylo- 
mata, and simple ulcer—also occur in the larynx with unexpected fre- 
quence. I prefer to base my description of this class of syphilitic affec- 
tions upon the work of these observers, who state that some of the 
patients dated their laryngeal affection from a “ cold; ” and hence think 
it probable that the localization of syphilis in this organ is, in some 
degree, determined by fortuitous catarrhal inflammation. 
Anatomical Appearances.—The anatomical lesions, arising from 
syphilitic laryngitis, are often merely those of catarrh, and are quite 
analogous with those of simple syphilitic angina. Although syphilitic 
laryngeal catarrh is not distinguishable from other laryngeal catarrhs by 
any palpable anatomical peculiarity, yet the time of its occurrence, after 
a primary syphilitic ulcer, its duration, its disappearance upon mercurial 
treatment, testify as to its specific nature, and to its dependence upon 
syphilitic infection. 
Condylomata and plaques muqueuse are much more frequently ob- 
served. They form flattened, reddish projections, and some of them 
show upon their surface the whitish thickening and loosening of the 
epithelium, which we see in the condylomata of the pharynx and 
mouth. The most common situation of condylomata is on the vocal 
chords, although they also occur at other points, particularly the pos- 
terior wall of the larynx, and on the arytenoid cartilages and on the 
aryepiglottic fold. 
Simple (secondary) syphilitic ulcers are, on the whole, rare. No 
ulcers, accompanying the condylomata in the larynx, existed in any of 
the cases reported by Gerhardt and Moth. These authors declare the 
diagnosis of this form of ulcer to be altogether uncertain, as both the 
yellow coating upon their base and the luxuriant condition of the 
neighboring parts are found in other forms of ulcers. Simple syphilitic 
ulcers occur in most varied positions in the larynx, upon the epiglottis, 
the true and false chords, or in the lower part of the organ. They are 
not always, nor even frequently, complicated with ulceration of the 
fauces. 
Finally, there are the well-known extensive and profound tertiary 
ulcers, which coexist with syphilitic lupus of the skin, and, like the lat- 
ter, are probably due to the breaking down of syphilitic tubercle. Such 
ulcers almost always begin upon the epiglottis, which they destroy, more 
or less completely, not unfrequently spreading thence throughout the 
entire larynx. As a rule, these ulcers have a dentated, ragged shape, SYPHILITIC DISEASE OF TnE LARYNX 
37 
and a smooth base, covered with a yellow coating. They show a ten- 
dency to cicatrize at the point first attacked, while the destruction ad- 
vances at other places. The very voluminous papillary and bulbous 
growths, which surround the sore, and its deeply-retracted scars, are 
especially characteristic. 
Symptoms ajtd Coup.se.—The simple catarrh and the condylomata of 
the larynx are among the earliest manifestations of constitutional syphilis 
which appear. If, then, a person, who, some months previously, has 
contracted a primary syphilitic ulcer, should begin to complain, without 
assignable exciting cause, of a feeling of tickling in the throat, should 
his voice become deep and hoarse, should he acquire a harsh, barking 
cough, and should these symptoms persist in spite of the most careful 
management, or should the hoarseness gradually increase to complete 
aphonia, we may suspect that the symptoms are not dependent upon a 
simple laryngeal catarrh, but upon syphilitic catarrh, or upon the devel- 
opment of condylomata in the larynx. Thus, it appears, from what we 
have stated in the previous chapters, about the origin of hoarseness, apho- 
nia, and harsh, barking cough, that both syphilitic and simple catarrhs, 
condylomata, as well as mucous accumulations upon the chords, are ca- 
pable of modifying the tone of the voice and of the cough, and of pre- 
venting the occurrence of sonorous vibrations of the vocal chords. 
The fact, therefore, that condylomata, so situated as not to disturb 
the vibrations of the chords, do not give rise to hoarseness, needs no 
further explanation. As, in almost all the cases reported by GerJiarclt 
and lloth, condylomata of the larynx have been accompanied by con- 
dylomata upon other parts, especially upon the mouth and throat, the 
existence of such growth should awaken our suspicions as to their pres- 
ence in the larynx, while their non-existence permits us to regard the 
case as probably one of simple catarrh. 
Simple (secondary) syphilitic ulceration seems to belong to a some- 
what later period, as its appearance does not coincide with that of sim- 
ple syphilitic ulceration of the fauces. Its presence should be suspected 
when, in an individual who, one or two years before, has had primary 
syphilis, and who has since had secondary symptoms, there arises a dis- 
ease of the larynx, which neither encroaches upon the cavity of the 
organ nor exhibits characteristics of other forms of laryngeal disease. 
Here, too, laryngoscopy affords the surest means of diagnosis. 
The extensive and profound (tertiary) ulcerations are the easiest to 
recognize. They form one of the later finks in the chain of syphilitic 
disorders, and almost exclusively attack patients who have for a series 
of years suffered first from one form of it, then from another, and have 
resorted to the various methods of treatment by mercury. The sufferers 
are here not simply hoarse and voiceless, with harsh cough, with pro- 38 
AFFECTIONS OF THE LARYNX. 
fuse and not unfrequently bloody expectoration, but these symptoms 
are always combined with a more or less intense dyspnoea. We mark 
the laborious, long-drawn breathing, so characteristic of stricture of the 
larynx, with its stridor audible even at a distance. This narrowing 
of the larynx may gradually become so extreme, from contraction of 
cicatrices and development of exuberant growths in their vicinity, that 
respiration becomes insufficient, and poisoning by carbonic acid sets in. 
In other cases, the dyspnoea suddenly rises to an alarming pitch from 
the occurrence of oedema of the glottis. The fact that the ulceration 
spreads gradually into the larynx from the root of the tongue and 
fauces, and there begins its ravages upon the epiglottis, makes it a duty 
carefully to examine the region of the larynx of all patients suffering 
from laryngeal stricture, and to press with the finger upon the epiglot- 
tis, in order to ascertain if it have suffered any loss of substance. In 
fact, the positive or negative result of this examination gives almost 
certain ground for diagnosis for or against the malady, although a closer 
insight as to the extent of the process is only to be obtained by means 
of laryngoscopic examination. 
In condylomata and simple catarrh the prognosis is good. It is not 
so good in the simple ulceration, from which sometimes the grave forms 
last described seem to develop. In the latter, the prognosis is a very 
unfavorable one. Most patients die, sooner or later, with symptoms of 
inci’easing marasmus, even although the respiration remain sufficient, or 
be made so by tracheotomy. However, in some cases, a partial improve- 
ment at least takes place. Tims, in one far-advanced instance, in which 
the relatives of the patient were confidently awaiting her speedy disso- 
lution, I have seen an almost complete recovery. In this patient, now 
a blooming female, there is nothing, save a slight stridor and a deficience 
in the soft palate, to recall to mind the once terrible malady under which 
for weeks she lay utterly emaciated, without voice, with racking cough, 
with profuse and often bloody sputum, and bereft of all hope of im- 
provement. 
Treatment.—For the treatment of syphilitic disease of the larynx, 
the same rules apply which are laid down for the general management 
of syphilis. In extreme contraction of the orifice, tracheotomy is indi- 
cated. 
CHAPTER VI. 
TUBERCULAR ULCERATION OF THE LARYNX. 
Etiology.—Prominent authors utterly deny the existence of a tu- 
berculous laryngeal consumption, and ascribe the ulcers so often found 
in the larynx of a consumptive to corrosion of the laryngeal mucous TUBERCULAR ULCERATION OF THE LARYNX. 
39 
membrane by contact with the acrid, sputa passing over it. ~Vir- 
choic, however, holds diametrically opposite views, and recommends 
the larynx as the very place in which to study true tuberculosis. 
He attributes the non-recognition of the tuberculous origin of 
these ulcers to the fact that the tubercles are superficial, and be- 
ing, therefore, very liable to accident from without, soon break down 
into shallow ulcers, and never become caseous nor form appreciable 
tumors. 
Tuberculous laryngeal consumption, though rarely arising as an in- 
dependent and primary malady, is one of the most common complica- 
tions of consumption of the lungs. Not only does it accompany the 
tuberculous form of pulmonary disease, but it is seen quite as often, 
if not oftener, in that form of consumption which we regard as the re- 
sult of inflammation (see chapter upon consumption). Since numerous 
experimenters have now succeeded in inducing an artificial generation 
of tubercle by inoculation, the frequent association of a tuberculous 
laryngitis with a pulmonary consumption of non-tuberculous origin 
will not appear extraordinary. Plentiful opportunity for such inocu- 
lation is afforded in the larynx of a phthisical patient; for the mucous 
membrane must suffer many small breaches of continuity through the 
strain of coughing, and these are constantly exposed to the contact of 
the passing caseous material. 
Anatomical Appearances.—The most frequent seat of laryngeal 
tuberculosis is that part of the mucous membrane which covers the 
transverse muscles of the larynx. The process, howTever, not uncom- 
monly begins at other spots, especially at the posterior wall of the 
epiglottis, and at the covering of the arytenoid cartilages. 
Small flattened elevations of a dull-gray hue are first observed at 
the spot just mentioned. They are situated upon a base which is 
either reddened and swollen, or else of a pale, flabby appearance. The 
early disintegration of these nodules results in small rounded cavities, 
bounded by hard, everted edges. The growth and decay of new nod- 
ules in the vicinity of those first formed, and the confluence of several 
ulcers, finally result in a loss of substance of irregular form. The mu- 
cous membrane in the vicinity of the ulcers shows various degrees 
of redness and swelling. 
Often, too, it is the seat of papillary growths with excessive 
formation of epithelium. Posteriorly the destruction often extends 
to the vocal chords, whose edges then seem corroded, and, as it were, 
worm-eaten by shallow sores. Sometimes penetrating more profound- 
ly, the posterior insertion of the chords is destroyed. Finally, the 
ulceration may involve the whole larynx, and spread to the root of the 
tongue and soft palate. 40 
AFFECTIONS OF THE LARYNX. 
In rare instances a tuberculous ulcer upon the posterior surface of 
the epiglottis perforates its entire thickness; in such cases, however, 
the contour of the organ is still preserved, thus forming a contrast 
with syphilitic ulcerations. 
Tuberculosis of the larynx is very often combined with ossification 
of its cartilages. If ulceration reach the cartilages, they become carious 
and necrosed, so that portions of ossified cartilages are often discharged. 
In rare instances, the ulceration has perforated the wall of the larynx, 
producing laryngeal fistulas and emphysema of the skin. 
Symptoms and Cottkse.—When hoarseness supervenes upon symp- 
toms of tuberculosis of the lungs of long standing, we may confidently 
infer the coexistence of tubercle of the larynx. (There are cases in 
which the hoarseness of tuberculous patients depends not upon an alter- 
ation of texture of the mucous membrane, but upon a paralysis of the 
muscles of the glottis. To this we shall recur hereafter.) Here, too, 
hoarseness, at least in most instances, is not the immediate result of a 
tuberculous ulcer, the latter, as we have seen, being, in the great ma- 
jority of cases, situated upon the posterior laryngeal wall, and upon 
the epiglottis. The hoarseness is occasioned by the relaxation and 
thickening of the vocal chords, and by the secretion which lies upon 
them. We can thus understand why the hoarseness comes and goes, 
while the ulcers are always growing and persistent. The mucous mem- 
brane of a diseased larynx is more vulnerable than that of a healthy 
one, and far slighter irritants suffice to produce in it a catarrhal 
affection. 
Nay, just as, without any assignable cause, the parts about every 
chronic ulcer of the skin become more sensitive, congested, and swollen 
at one time than at another, so, too, the laryngeal mucous membrane 
when the seat of ulceration seems always in a state of alternate swelling 
and detumescence. The nearer the destruction approaches to the vocal 
chords, so much the more persistent and obstinate does the hoarseness 
become. If, finalfy, the ulceration destroys their posterior attachment, 
it is no longer possible to tighten them, nor to throw them into sonorous 
vibration. The voice is totalfy extinguished; speech becomes whispering 
and inaudible. 
In other cases, in which the disease runs a more acute course, symp- 
toms of liyperaesthesia of the mucous membrane are more prominent. 
It is characterized by great irritability and violent reflex phenomena. 
The most distressing fits of coughing, brought on by the most insignifi- 
cant and often inappreciable causes, paroxysms of choking, which not 
unfrequently end in retching and vomiting, besides hoarseness or in- 
audible voice; all these very striking and painful symptoms forcing 
themselves so prominently into notice that the phenomena of tubercle TUBERCULAR ULCERATION OF THE LARYNX. 
41 
of the lung, if not very far advanced, are thrown into the background. 
The sufferer declares “ that he has nothing the matter with his chest,” 
ridicules the percussion and auscultation, and protests that the only evil 
with which he believes himself to be afflicted, or which he fears, is the 
“ consumption of the larynx.” 
It is rare for patients to complain of burning or smarting in the 
larynx, and usually, too, they are but slightly sensitive to pressure 
there, even though we push the organ back against the spine. The 
feeling of crepitation perceptible upon this manipulation is also felt in 
pressing upon this organ in a healthy person, and is of no diagnostic 
significance. The expectoration is useless as a means of diagnosis 
(unless, indeed, pieces of cartilage be ejected), since but a small portion 
of it springs from the larynx. The shortness of breath, the hectic fever, 
the night-sweats, the emaciation proceed equally from the coexisting 
tuberculosis of the lungs. In one case only of pulmonary tubercle, 
besides the symptoms just described, I have seen intense and gradually- 
increasing stricture of the larynx. The patient died in a few weeks, 
after having been materially relieved by tracheotomy. At the autopsy 
there were found in the larynx the thickening and induration of the 
submucous tissue (previously described as a cause of chronic stricture), 
together with tuberculous ulceration. 
Examination of the pharynx almost always shows that chronic catarrh 
exists there also. We find its blood-vessels varicose, and see small vesi- 
cles, phlyctaenas, or small, shallow, rounded erosions. The sufferer hawks 
a great deal; deglutition is difficult. At last it is often impossible for 
him to enjoy liquid food without choking himself, while solid food passes 
down more easily. In these cases the closure of the glottis is incom- 
plete. 
All of these symptoms, however, wrill not warrant a diagnosis of 
tubercle of the larynx unless we are able to show that the lungs, too, 
are affected. They are all capable of being produced by other kinds of 
laryngeal degeneration. It is well, therefore, in every chronic affection 
of this organ, at once to institute an accurate physical examination of 
the chest, and not to pronounce an opinion until we may have been able 
to avail ourselves of the revelations of percussion and auscultation. The 
subjective manifestations often fail us, being frequently obscured by 
those of the larynx. Hectic fever and emaciation are the only signs 
capable of rendering the diagnosis almost certain without the aid of 
physical investigation. By means of the laryngoscope we can easily 
bring the ulcers on the epiglottis and arytenoid cartilages into view. 
Of the posterior wall of the larynx above the transverse muscle, we, as 
a rule, can see at least the upper edge, in form of a fringe, with a few 
pointed jags of a dirty-whitish color (Turlc). 42 
AFFECTIONS OF THE LARYNX. 
The praises of specific remedies in cases of pretended cure of tubercle 
of the larynx are founded chiefly upon error of diagnosis. On the other 
hand, a number, although a small one, of actual cures of this malady 
can be authenticated beyond doubt. Death takes place, in most cases, 
from exhaustion, or with the symptoms of consumption, which we shall 
treat upon more fully in discussion of the subject of tubercle of the 
lungs. In some very rare cases, oedema glottidis is suddenly set up, 
under which the patient rapidly succumbs. 
Treatment.—In the treatment of laryngeal tuberculosis, we are not 
in condition to meet either the indication as to cause or the indication 
from the disease. The symptomatic indications are, first of all, to combat 
the burdensome cough and attacks of choking, which not unfrequently 
rob the sufferer of his rest. The treatment in the main must be the 
same as that recommended for chronic laryngeal catarrh, small as the 
result to be looked for may be. The Obersaltzbriinnen and the Emser 
Krahnchen waters, mixed w ith equal parts of hot milk, and drunk fasting 
in the morning, seem, in some degree, to moderate the cough. Do not 
make any objection to the roe of a herring, to be swallowed fasting, 
nor to the hope which the patient attaches to this prescription. If the 
pharynx be reddened; if its blood-vessels be varicose; if phlycteenae and 
ulcers be visible in it, swab it with a concentrated solution of nitrate of 
silver, and let the patient gargle assiduously with alum. In this way 
we can best guard against the too frequent “ hawking,” which is in 
itself a source of annoying cough. The insufflation of lunar caustic, 
the squeezing of a sponge saturated with a solution of nitrate of silver 
over the entrance to the glottis, by moderating the cough, sometimes 
have a palliative effect, if repeatedly applied; and, in the few rare in- 
stances in which also pulmonary phthisis recedes, this treatment may 
even have a radical effect. Here, too, we must concede a certain prefer- 
ence to the direct and exclusive application of nitrate of silver in solu- 
tion, or substance, to the surface of the ulcer itself, when accomplished 
by skilful and practised hands. 
The most important medicaments in the treatment of tubercle of the 
larynx are the narcotics. Little as they contribute to the healiug of the 
ulcers, their palliative action upon the burdensome symptoms of the dis- 
ease is indispensable. It has been customary to prefer the use of hy- 
oscyamus and belladonna to that of opium; nevertheless the preparations 
of the former remedies are seldom as uniform, and their effects, conse- 
quently, Seldom are as trustworthy as those of opium. 
As a matter of course, the patient whose larynx suffers from ex- 
cessive irritability from tuberculous ulceration must remain in a uni- 
formly heated and, if possible, in a somewhat moist atmosphere. We 
forbid him all loud speaking; nay, in especially bad cases, compel abso- GROWTHS IX THE LARYNX. 
43 
lute silence of weeks’ duration. When we reflect that, with every act 
of speech, the vocal chords are subjected to friction from the air which 
is driven past them, this direction must seem as rational as in practice 
it will be found to be serviceable. 
CIIAPTER YII. 
GROWTHS IX THE LAEYXX. 
The growths most commonly found in the larynx are fibrous tu- 
mors. They attain the size of a hemp-seed or bean ; and, when attached 
by a peduncle, they are called fibrous polypi. They consist of vascu- 
lar connective tissue, whose texture may be dry and dense, or succu- 
lent and open, and is covered by layers of tesselated epithelium. 
Papillomata, which are likewise common and usually multiple, are 
white transparent growths, either nodular, tufted, or of a mulberry 
form, and proceed from the upper strata of the mucous surface. Of 
the carcinomata, epithelial cancer is more common than medullary. 
The latter appears as a cauliflower growth, prone to ulceration and 
haemorrhage. Cysts are more rare; occurring as little bladders of the 
size of a pin’s head or perhaps a pea, without peduncles. They con- 
sist of mucous follicles whose mouths are occluded, and whose con- 
tents have become a serous or colloid liquid. Very rarely lipomata 
and myxomata are observed in the shape of globular or peduncu- 
lated vegetations. Fibrous tumors, lipomata, and carcinomata, do 
not generally spring from the mucous membrane itself, but rather 
from the sub-mucous tissue. Among the great number of cases of 
laryngeal tumor which Middeldorpf (1854) and Lewin (1802) have 
collected, twenty-two had their seat upon the epiglottis, nine on 
the aryepiglottic ligament, twenty-one on the ventriculus Morgani; 
thirty-two on the true, five on the false vocal chords; three on the 
arytenoid cartilages ; eight on the anterior wall of the larynx; while 
in only two instances were pathological growths observed upon its 
hinder wall, the most frequent seat of ulceration. Lewin seeks to ex- 
plain this circumstance by the fact that the latter point is subjected to 
alternate folding and extension during the motions of the glottis. 
Such a position would therefore be the more prone to ulceration, while 
commencing growths would soon break down; so that, instead of 
tumors, ulcers would form. It is a fact that tumors of the larynx, 
and particularly polypi, which used to pass for pathological rarities, 
have lately been observed and described in tolerably large numbers. 
From the care with which autopsies are conducted at present, it is hard- 
ly to be supposed that hitherto most polypi of the larynx have been 44 
AFFECTIONS OF THE LARYNX. 
overlooked in the cadaver. On the other hand, the numerous observa- 
tions of polypous growths of the larynx come, in great part, from such 
trustworthy investigators, that we cannot believe that insignificant 
growths or folds of mucous membrane can have been mistaken for and 
reported as polypi. Until the introduction of the laryngoscope, a 
positive diagnosis was impossible, save in rare instances. It is true, that 
sometimes we could surmise, with a certain degree of confidence, that a 
tumor was growing in the larynx, when the symptoms of laryngeal 
stricture began to supervene on those of laryngeal catarrh, and the 
dyspnoea underwent fluctuations as the varying engorgement or deple- 
tion of the growth made it vary in size. The probability became 
greater, when, in the course of the disease, repeated attacks of suffo- 
cation took place, which we could only attribute to contraction or 
closure of the glottis caused by the sudden change of position of the 
tumor’ However, even the periodical return of such choking-fits, 
which used to be considered pathognomonic of growths within the 
larynx, by no means made the diagnosis sure. Certainty was possible 
in those cases only in which the growth protruded, so as to become 
accessible to palpation or to inspection, or where the patients coughed 
up fragments of the tumor. 
To-day, the recognition of a tumor in the larynx presents no diffi- 
culties ; but the majority of the polypi and excrescences so easily and 
certainly detected by laryngoscopy have not produced the symptoms 
hitherto described as pathognomonic. Most of the patients had suffered 
merely from hoarseness, aphonia, or troublesome cough, and many of 
them had in vain been sent to Obersaltzbriinnen, Ems, or even to Cairo 
or Algiers, there to recover from their supposed laryngeal catarrh or 
Consumption. It is just this class of cases which shows what high time 
it is that a greater number of physicians should pay more attention to 
the laryngoscope, so as not to leave this very important art, so 
essential for the diagnosis of disease of the larynx, and which is not so 
very difficult to learn, in the hands of a few specialists. With the aid 
of the excellent books of Czermalc, TilrJc, Bruns, Leicin, Malbertsma, 
and by dint of assiduous practice, the necessary skill may be acquired to 
enable us, in doubtful cases, to make use of laryngoscopy, to effectually 
confirm our diagnosis. It is not necessary to examine all patients who 
are suffering from an acute laryngeal catarrh; and, as the procedure is 
always a fatiguing one, it would be cruel to subject patients to it wTho 
have advanced pulmonary phthisis, with hoarseness and aphonia, and 
who, in their desolate condition, so often turn to the specialists. If, 
however, hoarseness, a harsh cough, and other symptoms which we had 
supposed dependent upon a simple catarrh, persist in spite of sedulous 
treatment, even though no signs of laryngeal stricture may exist, we (EDEMA GLOTTIDIS. 
45 
ought never to neglect to ascertain positively, by means of the laryn- 
goscope, whether a tumor be not the source of the affection. 
In others of the newly-observed cases, however, besides the signs 
of chronic laryngitis, the other symptoms formerly regarded as pathog- 
nomonic were actually present, so that it would have been possible to 
decide as to the existence of these tumors in the larynx, even before the 
introduction of laryngoscopy. There was that long-drawn, laborious, 
stridulous respiration, characteristic of stricture of the larynx, particu- 
larly when, after any bodily exertion—mounting stairs, rapid running, and 
the like—the dyspnoea had increased, and the inspiratory movements be- 
come more energetic and frequent. Gzermah and Leicin have called 
to our attention, that in tumors above the glottis it is frequently inspira- 
tion alone which is impeded, while if the growth be below the glottis 
expiration may be embarrassed. 
It finally remains to be told that contrary instances have been met 
with, which not only evinced no signs of laryngeal stricture, but in 
which there was neither harsh cough nor hoarseness. 
The sole complaint of these patients was, of an ill-defined feeling of 
distress in the throat, or the sensation as if an accumulation of mucus 
were sticking in the larynx. 
The great variety in the symptoms of laryngeal tumors is easily 
comprehensible, after what we have taught in the first chapter, about 
the physiology of the voice. It is only in the cases in which the tumor 
hinders the approximation of the vocal chords, or interferes with their vi- 
bration, that they, of necessity, occasion hoarseness or aphonia. On the 
other hand, all tumors which do not implicate the functions of the vocal 
chords cannot possibly give rise to such symptoms. Thus it depends 
entirely upon the seat of a growth, and upon its size, as to whether it 
cause the symptoms of laryngeal stricture or not. The treatment of 
growths of the larynx comes under the domain of surgery. 
Since the year 1861, when my colleague Bruns, with the aid of the 
laryngoscope, and without incision, first extirpated a laryngeal polypus 
from the throat of his brother, the operation, which forms one of the 
most brilliant advances of modern surgery, has been performed repeat- 
edly, both by Bruns and by other surgeons familiar with the use of the 
laryngoscope. 
CHAPTER YIII. 
(EDEMA GLOTTIDIS. 
Etiology.—During inflammation of a part where the skin is attached 
to the subjacent region by loose areolar tissue, effusion into the latter 
often takes place with extraordinary rapidity. 46 
AFFECTIONS OF THE LARYNX. 
Let us recall to mind the oedema about th® eye during inflamed 
wounds of that neighborhood, the post-horn-like swelling of the penis 
when oedema besets a chancre of the fraenulum. This oedema, called by 
Virchow collateral oedema, is the result of increased lateral pressure, 
occurring in the capillaries in the region about a focus of inflammation, 
through the capillary stasis at the inflamed point. The more yielding 
the tissue is, so much the more does the serum transude. 
The mucous membrane of the larynx, at most points, is attached to 
its cartilages and muscles by a close connective tissue. Upon the epi- 
glottis alone, especially at its root, above all, over the bands which stretch 
from the epiglottis to the arytenoid cartilages (therefore above the ary- 
epiglottic ligament), and in lesser degree from these downward, to the 
superior vocal chords, there is a loose submucous tissue particularly 
prone to cedematous swelling. 
The exciting causes which usually produce the sudden serous transu- 
dation into the submucous tissue, known as oedema glottidis, are some- 
times acute morbid processes in the larynx, rarely acute catarrh, more 
frequently the pustulous laryngitis of small-pox, and sometimes chronic 
diseases, as syphilitic and tuberculous ulceration. Laryngeal perichon- 
dritis often gives rise to sudden oedema glottidis, just as an oedema of 
the prepuce suddenly associates itself to a long-standing chancre. 
Finally, in rare cases, a violent angina, an extensive inflammation 
of the submucous tissue of the throat, or even facial erysipelas, may 
occasion danger to life, from the supervention of this affection. In all 
these instances we have to do with collateral oedema, and but very few 
cases can be added to these, in which oedema glottidis is a partial mani- 
festation of a general dropsy and accompanying Bright’s disease, etc. 
The above-named diseases (with the exception of variola) are more com- 
mon in adults than in children, and thus it happens that oedema glottidis 
is observed almost exclusively among grown persons. 
Anatomical Appearances.—The serous infiltration which takes 
place at the points above described is often so great, that the swollen 
epiglottis projects above the roots of the tongue; and out from its base 
two great loose pendulous rolls reach backward to the arytenoid carti- 
lages and to the pharynx. They may attain almost the size of a pigeon’s 
egg, and lie so close together, that the entrance of air to the glottis be- 
comes extremely difficult, or even impossible. In rare instances, and, as 
it would seem, only when one half merely of the larynx is diseased, a 
single puffy swelling is to be found, which projects inward, and more or 
less contracts the entrance to the glottis. These swellings are some- 
times pale in color, sometimes more or less reddened. If cut into, there 
flows from* the distended meshes of the connective tissue, at times, a 
clear, serous liquid; at others a turbid, yellowish matter; the swellings (EDEMA GLOTTIDIS. 
47 
collapse, and now the mucous membrane appears to be wrinkled and 
thrown into folds. A similar evacuation and collapse of the swelling’, 
with folding of the mucous membrane, sometimes occur post mortem, 
when there has been no scarification, and the post-mortem appearances 
correspond but in small degree with the anatomical changes which, a 
few hours before death, we have had under our finger. In the upper 
section of the larynx, in which, as we saw, the submucous tissue is 
lighter and closer knit, the swelling is less visible. We find the mu- 
cous membrane itself covered with flakes, or plastic layers, the laryngeal 
muscles pale, discolored, and sodden. 
Symptoms and Course.—(Edema giottidis commences with the 
usual symptoms of an acute or chronic laryngeal ulcer. There is a 
rapidly-increasing hoarseness, which soon passes over into aphonia, and 
a harsh, barking cough (symptoms which prove that the vocal chords, 
too, are swelled, or that the infiltrated laryngeal muscles are not in con- 
dition to render the chords tense). But, simultaneously with these 
symptoms, there arises the most frightful dyspnoea. As soon as the air 
in the trachea becomes rarefied, the swellings described above settle 
themselves over the upper aperture of the larynx, and the laborious, 
long-drawn, whistling respiration can bring but little air into the lungs. 
This inspiration, audible at a distance, and only practicable with body 
bent forward, arms planted, and by cooperation of all the auxiliary 
muscles of respiration, is followed by an expiratory movement, which is 
almost free, although sometimes noisy; for the exit of the air drives 
asunder the obstructing swellings just as the inspiration sucks them to- 
gether. JPitha describes the inspiration as “protracted, forced, sharp, 
resonant, whizzing, and hissing; the expiration as short, easy, inaudible, 
scarcely perceptible.” 
The symptoms of oedema giottidis, then, are very similar to those 
which we have described as belonging to croup, a similarity which, after 
a physiological explanation of the symptoms, is seen to be a natural con- 
sequence. Nevertheless, we shall seldom mistake the two diseases, 
when we bear in mind that croup occurs almost exclusively during 
childhood—oedema giottidis almost as exclusively among adults; that 
croup almost always attacks individuals previously in good health, 
oedema giottidis scarcely any, save such as have already suffered from 
acute or chronic disease of the larynx. Moreover, the distinction be- 
tween the two diseases is facilitated by the great disproportion between 
inspiration and expiration in oedema giottidis, which, in croup, is neither 
so pronounced nor of so long duration. Finally we may, in many 
cases, succeed in seeing the swollen epiglottis as a# reddened, pear- 
shaped tumor behind the root of the tongue, and in almost every 
instance, if we introduce the finger with sufficient boldness, we may 
manage to feel the two swellings. 48 
AFFECTIONS OF THE LARYNX. 
The dyspnoea, which, in severe cases, increases from minute to min- 
ute, is usually associated with a feeling of a foreign body or other im- 
pediment in the throat. “ Here it lodges,” “ here’—in the throat ”— 
“ tighter and tighter.” “ It is strangling me.” “ I can’t stand it! ” 
“ I’m choking ! ” these are the words which, according to the classical 
picture of JPitha, the frightfully-terrified sufferers gasp out with tremu- 
lous haste and gesture. Fear and desperation are depicted in their entire 
being; they dash themselves about, they spring up, groan and sob— 
until gradually the countenance grows livid and lead-colored, the ex- 
tremities cool, the pulse small and irregular, the sensoriiun benumbed. 
Then the patient falls into a stupor, rattlings in the chest begin to be 
heard, and death sets in with the symptoms of oedema of the lungs. 
These final manifestations, also, are the same which we studied in croup, 
and depend not upon impeded evacuation of the cerebral veins, but 
upon poisoning of the blood with carbonic acid (see above). 
Treatment.—Blood-letting, leeches in large numbers to the throat, 
blisters to the nape of the neck, emetics, drastic cathartics, hot foot- 
baths, are the customary prescriptions which are usually applied, ptlfr 
mtle, as soon as this frightful malady has declared itself. We cannot 
allay oedema of the prepuce by such measures, and they generally are 
applied in vain in oedema glottidis. Only when the danger is not 
urgent may we diminish the mass of blood by efficient blood-letting, 
and by giving half a drop of croton-oil hourly, in order to decrease the 
volume of the blood in the vessels, through copious transudation of serum 
into the intestine. Experience teaches that, after great haemorrhage, and 
after inspissation of the blood, through profuse loss of its water, the ves- 
sels greedily take up liquid from the organs, and that, during cholera, 
even large pathological effusions have thus been absorbed. There is, 
therefore, some theoretical support for such treatment, although little suc- 
cess can be ascribed to it in practice. As but little air passes the larynx, 
in spite of the most forcible inspiratory efforts, that which the bronchi 
already contains becomes rarified, and, just as in the skin upon which a 
cupping-glass has been applied, so upon the mucous membrane intense 
hyperremia arises, usually accompanied by increased secretion. The 
dyspnoea is greatly augmented by this collection of bronchial secretion, 
so that loud moist rales become audible. In cases like this, but only in 
such cases, an emetic is indicated, and is often productive of the best re- 
sults. It is sometimes necessary to repeat it. 
Local treatment is of far more value. The effect of slowly swallow- 
ing small bits of ice is sometimes of remarkable benefit. Under this treat- 
ment I once wihiessed the recovery of one of my colleagues, in whom 
suffocation seemed so imminent that we hardly dared to defer traclieot- 
omv. The insufflation of pulverized nitrate of silver, or its application in LARYNGEAL PERICHONDRITIS. 
49 
solution, is of questionable service. When the ice fails, we should en- 
deavor to effect scarification of the swelling, either by means of the 
finger-nail or with a bistouri, guarded with adhesive plaster almost to the 
point. If we should be unsuccessful, or should the scarification be with- 
out effect, or should the symptoms of carbonic-acid poisoning arise, the 
pulse growing small and irregular, and the senses benumbed, we must 
proceed forthwith to tracheotomy and insert a canula until the danger is 
past. In cases like this, the operation, as a whole, is more successful 
than in crcup, and fife has been preserved for months in cases where 
oedema glottidis has occurred in tuberculosis of the larynx. 
CHAPTER IX. 
LARYXGEAL PERICHONDRITIS. 
Etiology.—The perichondrium or fibrous tissue immediately in corn 
tact with the cartilages is tolerably firm and resisting in texture, so that 
it long withstands any ulcerative process which advances from the mucous 
membranes. When finally perforated, the cartilage is laid bare, and its 
connection with its nutrient vessels is suspended. The portion thus de- 
nuded, and deprived of nourishment, sloughs off, and is discharged. 
We have already stated that these necrosed bits of cartilage generally 
show traces of ossification, which is one of the early effects of ulcera- 
tion of the mucous membranes of the larynx. 
By perichondritis laryngea, however, we do not generally mean in- 
flammation and ulceration of portions of the perichondrium, penetrating 
from without inward, but refer rather to an affection in which an ex- 
udation forms between the cartilage and the perichondrium, and by 
which the latter, from its density and impenetrability, undergoes very 
extensive separation. Necrosis of the cartilage is the natural result of 
so great a detachment from its nutrient vessels. 
Its exciting causes are sometimes ulceration of the laryngeal mucous 
membrane above mentioned, in which, however, the perichondrium, in- 
stead of suffering penetration from without, becomes the seat of suppu- 
rative inflammation, which causes an effusion between perichondrium 
and cartilage. 
In other cases the malady arises independently, or at least, without 
previous inflammation of the mucous membrane, and chiefly in persons 
with constitutions broken down by syphilis, mercury, or by the infection 
of typhus, septichaemia, and the like; and sometimes even in subjects 
who apparently are robust. Of course, in the latter instance, “ catching 
cold ” is assigned as the cause; the inflammation is called a rheumatic 
inflammation, and the destruction of the larynx which follows is called 
a rheumatic laryngeal phthisis. 50 
AFFECTIONS OF THE LARYNX. 
Anatomical Appearances.—The point of preference of this dis- 
order is the perichondrium of the cricoid cartilage; but from this point 
it spreads rapidly to the coverings of the other cartilages. At first 
there is only a small abscess between the latter and its sheath. Very 
soon, however, the cartilages are floating in a sack of pus, formed by 
the perichondrium. They become rough, degenerate, discolored, after- 
ward thinned and softened, and then, not unfrequently, fall to pieces, 
fragment by fragment. At last, the pus bursts through the perichon- 
drium, and runs into the submucous tissue of the larynx. At times, 
too, the mucous membrane is perforated; pus and fragments of carti- 
lage fall into the larynx and are coughed up; or else the pus forces its 
way to the external surface. Abscesses and sinuses of the neck are 
thus formed, and the pus and fragments of cartilage are discharged ex- 
ternally or into the pharynx. In rare instances recovery has taken 
place, the lost cartilage being replaced by dense fibrous tissue. 
Symptoms and Course.—As a rule, the symptoms of a disease are 
not rendered easier of comprehension by any arbitrary and artificial 
classification according to stages, but rather the reverse. When, how- 
ever, as in perichondritis laryngea, very distinct phases form natural 
divisions in its course, the study by stages is both commendable and 
practical. 
In its first stage the symptoms are obscure, but, as in all inflamma- 
tion of dense unyielding structures, the disease is attended by greater 
pain than occurs in other affections of the larynx; and, as the inflamma- 
tion generally begins at an insignificant point, the painful region is also 
quite limited in extent. One might readily be led to suppose that a for- 
eign body were lodged in the larynx; the more so, as the pain is com- 
bined with an irrepressible cough. 
In the second stage, hoarseness, aphonia, harsh cough, and character- 
istic symptoms of intense dyspnoea and laryngeal stricture set in, arising 
either gradually, as the perichondrium becomes more and more dis- 
tended by the increasing volume of pus, and is pushed further into the 
cavity of the larynx, or suddenly, by its perforation and by effusion of 
the matter below it, into the submucous tissue. Many patients perish in 
this stage. 
In some cases a third stage is added. The pus which has accumu- 
lated under the perichondrium, or the submucous tissue, bursts through 
its confines. The symptoms of laryngeal stricture disappear. I have 
seen a young girl in the most frightful danger of suffocation relieved 
on the instant, and rendered completely convalescent, after expectora- 
ting quantities of pus, and with it the entire left arytenoid cartilage, in 
a state of maceration. 
But, even in such cases, after a time, the patients usually perish in a SPASM OF THE MUSCLES OF THE GLOTTIS, ETC. 
51 
state of marasmus, in consequence of the continuance of the malady, 
the suppuration, and the fever by which it is attended. 
Treatment.—The treatment of laryngeal perichondritis can, of 
course, be only a treatment of symptoms, seeing that the disease is not 
generally recognizable until after the effusion has formed in the sub- 
mucous tissue. There then remains nothing to do except to perform 
tracheotomy, and this operation and the opening of any abscesses about 
the neck are about the only measures at our disposal, and even they are 
merely palliative. 
NEUROSES.—NERVOUS AFFECTIONS' OF THE LARYNX. 
Deranged sensibility of the larynx, excessively exalted excitability 
of its sensory fibres (hyperaesthesia), and their abnormally diminished 
sensibility (anaesthesia) are never observed as independent diseases. 
We may count certain cases of globus hystericus and of spasmodic 
cough, in hysterical persons, to the first of these forms. True, persons 
suffering from the latter complaint do not complain of abnormal sensi- 
bility in the larynx, but the coughing-fits to which they are subject are 
to be regarded as reflex phenomena, independent of the morbid condi- 
tion of the sensory nerve-fibres, whose excitability is increased. The 
neuroses of the motor function in the larynx are divisible into hyperci- 
nesis and acinesis / into spasm and palsy. We shall treat of each in 
the following chapters. 
CHAPTER X. 
SPASM OF THE MUSCLES OF THE GLOTTIS—SPASMUS GLOTTIDIS—ASTHMA 
LARYNGEUM—ASTHMA ACUTUM MILLABI—ASTHMA THYMICUM—LA- 
RYNGISMUS STRIDULUS. 
Etiology.—This disease depends upon a morbid excitement of. the 
nerves, by means of which contraction of the muscles of the glottis is 
effected. By uniform shortening of all the muscles at once, the vocal 
chords become tightly stretched, and the glottis is closed. The term 
laryngeal asthma, or laryngismus stridulus, however, is not to be applied 
to the occurrence of such reflex symptoms during any inflammatory dis- 
order of the laryngeal mucous membrane. It seems rather to be an 
independent affection of the par vagum, or of its recurrent branch, due 
either to pressure along some part of the course of one of these nerves 
or to centric irrigation at the root of the vagus; or else we may be com- 
pelled to regard its exalted sensibility as a reflex phenomenon arising 
from excitement of some other nervous trunk. In most cases the 
pathogeny of this disease is obscure. 52 
AFFECTIONS OF THE LARYNX. 
Spasm of the glottis occurs almost exclusively during' childhood, and 
especially in the first year of life. It is most frequent during the period 
of the first dentition. Romberg considers congenital predisposition to 
exist beyond doubt, as in many families almost all the children in suc- 
cession are affected by the disease. In great cities, and among children 
brought up by the bottle, it seems to be more common than in the 
country and among children who receive the breast. Among adults, 
none but hysterical persons suffer from spasm of the glottis, and these 
only exceptionally. There have been solitary cases noted in which hys- 
teria has produced death by protracted spasmodic closure of the glottis, 
but I have seldom seen instances in which such spasm had attained even 
a dangerous degree of intensity in hysterical persons. 
Anatomical Appearances.—Enlargement of the thymus gland, 
which Kopp regarded as the organic cause of spasm of the glottis, in 
many instances does not exist. This is also the case with the soft occipuf 
of JEJlsdsser (a rachitic phenomenon). Enlargement and degeneration of 
the glands of the throat and bronchi, the occurrence of hypertrophy, of 
hyperaemia, or of exudative processes in the brain, are in part accidental, 
and in part (as we have said regarding the pathogeny) are matters not al- 
ways found post mortem after asthma laryngeum. At all events, we must 
find the larynx apparently sound if the autopsy is to bear out the diagnosis. 
Symptoms and Course.—The course of the disease, like that of most 
neuroses, is an interrupted one, marked by paroxysms and intervals of ex- 
emption. A sudden violent interruption of the respiration, which may 
last for several minutes, is pathognomonic of the seizure. By-and-by the 
air again begins to penetrate into or out from the glottis, which at first is 
completely closed, and still remains contracted. In addition to this, the 
attack is accompanied by the often-mentioned prolonged whistling, in- 
spiratory noise, the fear, the restlessness, the livid countenance, the 
strenuous contraction of the inspiratory muscles, and the position up- 
right, or bent forward. After a few minutes, as soon as the child has 
forgotten his fright, he is completely restored. There is no cough in 
laryngeal asthma, as the laryngeal mucous membrane and the vocal 
chords are healthy; nor, as the vocal chords are neither relaxed nor 
thickened, is there any hoarseness. If, therefore, we only hold fast to 
the idea that laryngeal asthma is a nervous affection of the par vagum, it 
becomes easy to avoid all confusion of it with croup, or with those noc- 
turnal attacks of dyspnoea which accompany catarrh of the larynx. 
In many instances the spasm does not confine itself to the motor 
fibres of the vagus alone. Sometimes spasmodic contractions of the 
Sngers and toes, or of the hands and feet, accompany the attack, or 
cramps of these parts alternate with spasm of the glottis. Occasionally 
even general convulsions occur, in which the sufferer may perish. SPASMS OF THE MUSCLES OF THE GLOTTIS, ETC. 
53 
The paroxysms thus described take place at varying intervals; a 
week or more may pass without their repetition. In bad cases the fits 
multiply, and follow one another more closely, and it is these cases that 
are most apt to be accompanied by general convulsions. There always 
remains a great tendency to relapse, which is still to be feared, even 
though a child have remained for months without a paroxysm. Finally, 
instances have no doubt been observed in which laryngeal asthma has 
shown itself but once, never again to recur. In rare instances a par- 
oxysm terminates in suffocation, the closure of the glottis, and conse- 
quent privation of oxygen, outlasting the endurance of the organism. 
The pallid face assumes a deathly hue, the muscles are relaxed, the child 
sinks back and expires. 
Treatment.—The indication as to cause cannot be met, as the 
causes of spasm of the glottis are obscure. However, we should en- 
deavor most carefully to allay all disorders of digestion and nutrition in 
children who show a tendency to this malady, before we proceed to the 
employment of specifics of doubtful efficacy. This is what is meant 
when we prescribe calomel, rhubarb, and other remedies in spasm of the 
glottis. Children fed by hand should be placed to the breast when they 
show signs of the disease. In older children, examine the milk, and 
cause the nourishment in use at* the time of the attack to be changed, 
and so forth. 
In hysterical glottic spasm, the causal indication first of all demands 
treatment of the main disease. Meantime the hysterical symptoms, like 
all other hysterical manifestations, are to be combated by psychical 
measures. I have cured both glottic cramp and glottic palsy by means 
of local faradization of the laryngeal muscles, the treatment undoubtedly 
acting solely by the psychological effect which it produced. 
The indicatio morbi in this obscure and incomprehensible affection 
is equally difficult of fulfilment. Romberg recommends and lauds the 
effects of the aqua foetida anti-hysterica which he orders for children in 
their first year, mixed with equal parts of simple syrup, a small spoonful 
four to six times a day. If, in spite of the assafoetida, the seizures recur, 
we may give musk instead, a medicine almost universally prized as a 
specific. (Moschi gr. iij.—iv., gum. mimos. 3 S3., syr. simpl., aqua 
foeniculi, aa 3 j, liq. ammon. succin. 3 j. tq. s. a teaspoonful every 
two hours.) 
During the fit it is impossible to give the patient medicine, as he is 
unable to swallow. We should instruct the parents to take the child up 
as soon as the paroxysm begins, to fan it in fresh air, to rub its back, 
and to administer a clyster of camomile or valerian tea. It is well to 
have a mustard plaster in readiness, and to lay it upon the precordium 
when the fit occurs. If the injections of camomile or valerian fail, it is 54 
AFFECTIONS OF TIIE LARYNX. 
advisable to substitute a clyster of assafoetida. (Assafoetid. 3 ss—i, 
vitell. ov. no. j. tt[ f. emulsio. c. infus. valerian 3 ss— § iv. S. for two 
clysters.) 
PARALYSIS OF THE ML'SCLES OF THE GLOTTIS.—DYSPHONIA (APHONIA 
paralytica). 
CHAPTER XI. 
It is not improbable that, in many cases of supposed spasm of the 
glottic muscles, instead of spasm, there has been palsy. According to 
Morriberg, the signs of palsy of the recurrent laryngeal branch of the par 
vagum consist in fits of oppression, amounting almost to suffocation, in 
noisy, hissing respiration, and whispering, hoarse voice, and, above all, in 
dyspnoea, aggravated by every vigorous inspiratory act, symptoms easily 
accounted for, at least in children. In treating of the dyspnoea of croup, 
we have alluded to the strong resemblance between it and that produced 
in young animals by dividing the par vagum or its recurrent branch ; and 
we then gave so full an account of the physiology of this fact that we 
may now refer the reader to what has already been said. Turning from 
this rare and insufficiently-studied form of paralysis of the glottis, let us 
now briefly direct our attention to that form of loss of power of its 
muscles in which the respiration proceeds undisturbed, while the defec- 
tive innervation of the muscles of the larynx modifies the vibrations of 
the vocal chords, or renders the occurrence of sonorous vibrations im- 
possible. We are accustomed to call these cases “nervous,” or, better, 
paralytic dysphonia, or aphonia, or phonetic paralysis. 
Etiology.—The fact of the existence of a paralytic aphonia was no 
doubtful matter, even before the introduction of laryngoscopy. In- 
stances in which loss of voice constituted the sole symptom of laryngeal 
disease, which had arisen suddenly, and afterward as suddenly had sub- 
sided, scarcely admitted of any other interpretation than this. But it 
has only been by means of the laryngoscope that we have obtained 
more accurate knowledge of the important part which the motor dis- 
orders of the laryngeal muscles play as the proximate causes of hoarse- 
ness and aphonia. 
In most cases in which laryngoscopy has discovered imperfection, or 
total inaction of one or of several muscles of the larynx, the palsy was 
one of the symptoms of acute or chronic catarrh, or other laryngeal affec- 
tion. This form of paralysis is very closely related to the subparalytic 
condition wduch we at times observe in the corresponding parts of the 
bronchi, stomach, intestines, and, above all, of the urinary bladder when 
in a state of chronic catarrh. Indeed, there is hardly any doubt but 
that the muscles, or their finer nervous fibrillce, participate in the nutritive PAKALYSIS OF THE MUSCLES OF THE GLOTTIS. 
55 
disorder of the mucous membrane. In other instances the paralysis 
manifestly depends upon disturbances of nutrition in the course of the 
par vagum or its ascending branch. To this category belong the inter- 
esting cases of phonic palsy resulting from pressure and tension of the 
recurrent branch of the par vagum by aortic aneurism, carcinomata, 
enlarged or degenerated bronchial glands, pleuritic thickenings about 
the apices of tuberculous lungs, etc. Certain observations render it 
quite probable that “ a cold ” may produce nutritive disorder in the 
vagus or the recurrent, whereby its irritability is destroyed, so that the 
muscles which it supplies become paralyzed. Hereafter we shall learn 
that rheumatic palsy of the facial, a cutaneous nerve much exposed to 
the influence of cold, is one of the most common instances of this form 
of paralysis. It is doubtful whether palsy of the glottis arising from 
metallic poisoning, especially lead-poisoning, ought to be regarded as of 
peripheral or centric origin. This holds true also in the cases of the 
paralytic aphonia which often remains after typhus and diphtheria, and 
in the still more enigmatical malarial palsies. 
It is very rare for a phonic palsy of the glottic muscles to have a 
centric origin—that is, for it to arise from an affection of the brain, or 
of the cervical portion of the spinal cord. The majority of cases of 
serious disease of the brain, in which the sufferers lose the power of 
speech, are not taken into consideration here, as in them palsy of the 
glottic muscles can neither be proved, nor is it even probable—the few 
shambling and awkward words which this kind of patient is still able to 
utter being usually pronounced in a loud, unaltered voice. 
Next in frequence to the forms just treated of comes hysterical 
aphonia. I have met with this affection with comparative frequence, 
both in males and females. We cannot properly include hysteric palsy 
either in the centric or peripheral forms of the disease, in the ordinary 
meaning of the term. I prefer to follow the example of Romberg, who 
calls certain forms of spasm “ psychical spasm,” and to designate hys- 
teric palsy as “ psychical palsy.” In this affection the excitability of 
the peripheral nerves is manifestly retained, and its dependence upon 
nutritive derangement in the motor centres is in the highest degree im- 
probable. On the other hand, psychological influences have so marked 
an effect upon the appearance and disappearance of hysterical palsy, 
and especially of hysterical aphonia, that we may almost with certainty 
ascribe its origin to that portion of the brain concerned in the function 
of the higher psychical acts. 
Anatomical Appearances.—The anatomical alterations which give 
nse to phonic palsy of the glottis are but rarely susceptible of demon- 
stration in the cadaver, excepting in cases where the paralysis is depend- 
ent upon structural change in the larynx, or in which the nervous 56 
AFFECTIONS OF THE LARYNX. 
trunks are compressed by tumors, pleuritic induration, and the like. 
T uric and Gerhardt have shown that, in cases of long-standing palsy, 
the laryngeal muscles, like other muscles, undergo atrophy and fatty 
degeneration. 
Symptoms and Course.—We are not well enough acquainted with 
the physiological action of the muscles of the glottis, and, moreover, 
our knowledge as to how far lack of power in one can be compensated 
for by additional exertion on the part of others, is insufficient to enable us 
to say with confidence what modification of the voice will naturally fol- 
low palsy of any individual muscle, or group of muscles. Pathological 
observations of pure paralysis of the glottis, independent of relaxation 
of the mucous membrane, are not numerous enough as yet to admit of a 
clear, comprehensive view of the relations of its partial paralysis to any 
particular derangement of plionation. Meanwhile, through the labors 
of Tilrlc and Lewin, and, above all, through that of Gerhardt, the path 
is already beaten out, and some ground has been gained. Consistently 
with the purpose of this volume, I must confine myself to calling atten- 
tion to a few, merely, of the most important of the facts set forth in 
these detailed works. 
As palsy of the muscles of the glottis generally prevents the normal 
tension, and approach to one another of the vocal chords, hoarseness 
and aphonia are the most common symptoms of this affection, but in 
the majority of cases the approximation and tension of the vocal chords 
in straining, coughing, and swallowing are not impeded. This form Turk 
calls “ phonic palsy of the glottis-closers,” in contradistinction to the 
rarer “ general palsy of the glottis-closers,” in which the performance 
of the acts just alluded to is also embarrassed by the non-closui'e of the 
glottis. But hoarseness and aphonia are not the only forms of dysphonia 
in the disease in question, since the palsy does not always affect the 
glottis-closers. Cases occur, not only as a result of catarrh, but also of 
compression or irritation of the recurrent, in which the muscles of one 
half of the larynx become paralyzed, the other half remaining unaffected, 
and in these cases it sometimes happens that a permanent falsetto voice 
is the result, a circumstance which is to be explained by the supposition 
that the sound vocal chord vibrates in normal manner, while the edge 
of the palsied chord remaining near the median line, but subjected to 
little or no tension, cannot be thrown into vibration. Palsy confined to 
the thyro-arytenoid muscles, by which merely the shortening and tension 
of the vocal chords are embarrassed, according to Gerhardt, results not 
only in the production of too deep a tone, but also in incapacity to pro- 
duce a tone other than this deep one; hence a true monotony of the 
voice. These brief hints may serve as incentives to study of the works 
mentioned, and induce new investigation of this interesting subject. PARALYSIS OF THE MUSCLES OF THE GLOTTIS. 
57 
The diagnosis of palsy of the glottis is of course only possible by 
means of the laryngoscope. In palsy of the glottis-closers, laryngoscopic 
observation reveals that, during attempted phonation, the rima glottidis 
remains open, and the chords do not tremble as they should do. In 
palsy of one side of the glottis, the point of the arytenoid cartilage 
stands out in a remarkable manner, reaching to the median line, or even 
overstepping it toward the other side. The inner edge of the palsied 
chord comes almost to the middle line. Upon drawing breath, or upon 
an attempt to speak or cough, there is little or no motion in the aryte- 
noid cartilage and the vocal chord of the affected side. In palsy of the 
thyro-arytenoid muscle, according to Gerhardt, the glottis vocalis forms 
a somewhat wide ellipse when the patient attempts to speak. 
Treatment.—In treatment of palsy of the glottis, it is important 
above all things to meet the causal indication. "When the palsy has 
arisen in the course of a catarrhal attack, energetic local treatment of 
the main affection, particularly by use of solution of nitrate of silver, 
promises the best results. In paralysis attributable to derangements in 
the course of the nervous trunks, a treatment of the cause is in many 
instances impracticable; in others, the reabsorption of a strumous deposit, 
the resolution of an enlarged lymphatic, judicious management of metal- 
lic poisoning, perhaps the administration of quinine, by allaying the 
cause, cure the palsy. In centric paralysis, therapeutics are always 
powerless. On the other hand, in hysterical cases, a systematic and 
cautious management of the primary complaint most frequently has a 
permanent effect. 
We can seldom meet the indications of the disease it3elf, as most of 
them proceed from irreparable nutritive disturbance of centric or peri- 
pheral nerves. An exception is made in this respect by the somewhat 
small class of cases in which the normal irritability of peripheral nerves 
has suffered from too long-continued rest, or in which it has been im- 
perfectly reestablished, after removal of the original cause of the palsy. 
In methodical excitement of the nerves by the induced electric current, 
■we possess a most efficacious remedy. The indication for the employ- 
ment of localized faradization having grown more precise, the curative 
power originally ascribed to it, -which upon its introduction into prac- 
tice was estimated to be a panacea against all forms of palsy, has, 
within the past few years, grown much more limited, exactly as was 
predicted by Ziemssen, who distinguished himself at the time of its in- 
troduction. 
It is therefore a most remarkable circumstance that localized faradi- 
zation should seem to have a curative action, beyond all comparison 
greater in palsy of the glottis than in all other forms of paralysis. In 
the few years which have passed since we have learned to diagnosticate 58 
AFFECTIONS OF THE LARYNX. 
glottic palsies with certainty, an astonishingly great number of cures 
have been brought about by the application of the induced current. 
(Althaus alone has cured eleven out of thirteen cases.) In certain in- 
stances the sufferers were made well of their aphonia at the first sitting. 
In the majority of cases an improvement, at least, was apparent at the 
first application, and the treatment remained without effect in but a 
comparatively small number of those upon whom it was employed. 
Had these cures been performed upon cases of mere hysteric aphonia, 
they would be easy of explanation, since, according to my previous ex- 
perience, I have often enough seen hysteric aphony made to vanish by 
means of psychical emotions of a lighter kind than that which the ap- 
plication of the electrodes to the throat produces; but these cures were 
performed in a great variety of forms of glottic palsy. From my great 
reliance in the trustworthiness of the witnesses, I do not feel the slightest 
doubt as to the facts; but I hope that further observation will furnish 
an explanation to this very remarkable phenomenon. 
In order to stimulate the laryngeus superior, according to Gerhardt, 
we select the point of the throat corresponding to the superior horn of 
the thyroid cartilage; to excite the recurrent, we choose the point cor- 
responding to the thyroid cartilage itself. To faradize the recurrent, it 
is best to apply one electrode at the spot above named, and the other 
over the manubrium sterni. SECTION II. 
DISEASES OF THE TRACHEA AND BRONCHI. 
CHAPTER I. 
HYPEREMIA AND CATARRH OF THE AIR-PASSAGES AND BRONCHIAL 
MUCOUS MEMBRANE. 
Etiology.—We have already stated that every considerable hyper* 
femia gives rise to a series of nutritive and functional disorders, known 
as catarrh; and that, if catarrh be included among the inflammatory 
affections, the terms hyperasmia and inflammation must be regarded as 
synonymous, although the words are not generally considered identical 
in meaning. 
Predisposition to catarrh of the bronchial mucous membrane is as 
variable as is predisposition to catarrh of the larynx, developing either 
readily, or with difficulty, from the same causes, according to individ- 
ual peculiarity. “ An increased susceptibility of the skin to change of 
temperature,” or an “augmented vulnerability of the mucous mem- 
branes,” is simply an hypothetical assumption to which we have recourse, 
where no other explanation is at hand, to account for the excessive 
liability in certain persons to suffer from catarrh of the bronchi upon 
slight exposure. Experience, however, permits us to bring forward 
certain particular conditions as predisposing causes. In the first place, 
in childhood, and especially during the period of dentition, there is a 
strong tendency to catarrh of the mucous membrane in general and of 
the bronchi in particular. We daily hear it said that children have 
“a tooth-cough,” and hear intestinal catarrh of this period called a 
“ tooth-diarrhoea.” 
In middle age this predisposition diminishes; in old age, again, it is 
more marked, senile chronic catarrh becoming a most frequent com- 
plaint, and furnishing a large contingent to the hospitals and infirmaries. 
Secondly: badly-fed, flabby individuals show unmistakable general pre- DISEASES OF TIIE TRACHEA AND BRONCHI. 
60 
disposition to catarrh, and, when exposed to the action of even trifling 
irritants, are much more liable to bronchial catarrh than well-nourished 
persons of firmer fibre. This predisposition depends, probably, upon 
increased susceptibility, or feebler capacity for withstanding noxious 
influences ; or it may be attributed to the poor nutritive condition and 
weak resisting power of the walls of the capillaries, and yielding nature 
of the tissues through which they run. An augmented tendency to hy- 
percemia and to increased transudation would result from such a con- 
dition. The disposition to catarrh in general, and hence to bronchial 
catarrh, seen in scrofula and rickets, should also be placed under this 
heading. Thirdly: those who have often suffered from bronchial ca- 
tarrh showT a proneness to the disease; chronic disease of the paren- 
chyma of the lungs augments this inclination, if it does not give rise 
to the disease itself. The old saying, “ Tibi irritatio ibi affluxus,” 
still holds good; although the afflux is only produced by dilatation of 
the vessels leading to the point of irritation, or by defective resisting 
power of the vascular walls, and must not be supposed to be due to 
attraction. Lastly: the liability to this affection is less among those 
who inure themselves to exposure. 
The exciting causes of bronchial catarrh, which act more or less 
readily, according to the tendency of the individual, are as follows: 
First: it may proceed from an impeded evacuation of the bronchial veins. 
For the bronchial arteries which spring from the aorta, or intercostal 
arteries, transmit only a portion of their blood into the bronchial veins, 
whence it proceeds by the vena azygos into the vena cava. Another 
portion of the blood of the small bronchial veins flow’s within the sub- 
stance of the lung into the pulmonary veins; hence, both in contrac- 
tion of the mitral valve, impeding the outflow from the left auricle, 
and in cases of insufficience of the mitral, with systolic regurgitation 
from ventricle to auricle, and consequent impeded outflow to the con- 
tents of the left auricle and pulmonary vein, the immediate effect will 
be, hyperremia of the lungs (that is, capillary engorgement of the al- 
veoli) ; yet, if the cardiac lesion be severe, bronchial catarrh not only 
is one of the most constant but one of the most and in- 
evitable symptoms which arise. To understand this condition, we 
must keep in mind that a part of the blood of the bronchial mucous 
membrane flows into the left side of the heart instead of the right. 
The fact that chronic affections of the pulmonary substance are com- 
plicated with bronchial catarrh is ascribable to the above-mentioned ar- 
rangement of the vessels; for if the circulation of the lung-tissue be de- 
ranged, then the task of the smaller bronchial veins in returning blood 
to the pulmonary veins will be increased, so that engorgement arises in 
the corresponding bronchi, which becomes all the more intense if any of 
the bronchial veins be compressed by inflammatory foci or by growths. ACUTE BRONCHIAL CATARRH. 
61 
Secondly. If the current of the blood in the great branches of the 
aorta encounter an obstacle, and more especially if the aortic stream 
itself be impeded below the point of origin of the bronchial arteries, the 
pressure of the blood is augmented in the other arteries which are not 
compressed or otherwise constricted, and hypermmia ensues throughout 
the range of their capillary system. As an instance of this process 
(which Virchow aptly terms “ collateral fluxion ”) we find sometimes 
that, in consequence of compression of the abdominal aorta by liquid in 
the peritoneum, or by accumulations of excrement or gas in the intes- 
tines, augmented pressure from within takes place in the bronchial and 
carotid arteries, resulting in “ congestion of the brain or lungs.” So in 
the cold stage of intermitting fever the circulation encounters a mate- 
rial obstruction (throughout the periphery of the body), from the cutis 
anserina, and the spasmodic contraction of the peripheral arteries. Per- 
haps this is the reason of thehypersemia, and catarrh of the bronchial mu- 
cous membrane, which often complicate intermitting fever, and of the 
cough which, in certain patients, is very distressing during the attack. 
Thirdly. Irritants which act directly upon the mucous membrane, 
such as dust, vapors, too cold or too hot air, occasion in it hyperaemia 
and catarrh. Those who follow certain trades, as bakers, millers, and, 
above all, stone-cutters, suffer constantly from this disorder. 
Fourthly stands chilling of the external skin, and the action upon 
it of a sudden change of temperature. As we have observed, we can- 
not satisfactorily account for the phenomenon, almost daily observed, 
of a person suffering from bronchial catarrh after seating himself in a 
draught of air while perspiring freely. The process cannot be ascribed 
to collateral fluxion, since a mere change of temperature or exposure to a 
current of air, or to a degree of cold by no means severe, suffices to bring 
on the attack. In bleak, damp localities, particularly on the sea-side, 
such exciting causes are so numerous that bronchial catarrh is endemic. 
Fifthly. It forms a symptom of typhoid fever, measles, and small- 
pox. Here it must be looked upon as the result of a morbid state of 
the blood, which has absorbed some deleterious material, with the nature 
of which we are unacquainted. However, although we cannot explain 
what we see upon physiological principles, there is something analogous 
to it in the symptoms of poisoning, which we can produce at will by 
the exhibition of an inorganic material (iodide of potassium) in large 
doses. As is well known, a very violent bronchial catarrh, often 
accompanied by an exanthema of the skin, not unfrequently arises 
during the employment of this agent, no other irritant having come 
into operation meantime either upon skin or mucous membrane. 
Sixthly. Under the operation of unknown atmospheric or telluric 
influences, from time to time, epidemics arise, in which very extensive 
catarrh occurs, with unusually severe constitutional disturbance. It is 62 
DISEASES OF TIIE TRACHEA AND BRONCHI. 
doubtful if an infection like that of the acute exanthemata be the cause 
of this complaint, to which it bears a certain similarity. Such an epi- 
demic, the “grippe,” or influenza, appeared in the year 1732, and, 
travelling through Europe, from east to west, attacked at least one half 
of its population. The disease was a dangerous one, especially for chil- 
dren and for old persons, partly from the intensity of the fever, partly 
through extension of the local affection into the pulmonary alveoli, and 
partly from participation of the intestinal mucous membrane in the com- 
plaint, and from other complications. Since that time there have been 
repeated epidemics of influenza, particularly in 1800 and 1835. With 
this repeated reappearance of the malady, the vicious custom has gradu- 
ally crept into use, both among physicians and people, of calling all the 
non-epidemic bronchial catarrhs influenza, when associated with violent 
general disturbance, and showing unusual obstinacy, or when the intes- 
tinal canal takes part in the disorder, using the term gastric influenza 
(gastrische Grippe). This bad custom has, in one respect, its advan- 
tage. No one suffering from a mere catarrhal fever is willing to consider 
himself seriously ill, or to keep his bed. For an attack of “influenza,” 
however, he is content to lay up for a week or ten days. 
Finally, we must observe that, in very many cases, the exciting 
causes of catarrh are unknown, unless we accept the explanation with 
which people usually content themselves, that “ they must have taken 
cold somewhere.” 
Anatomical Appearances.—In the cadaver, acute catarrh of the 
trachea and bronchi leaves a redness, sometimes diffuse, sometimes 
mottled, the one being due to injection, the other to ecchymosis. The 
mucous membrane has a clouded look, is opaque, relaxed, and tears 
easily. This condition arises from infiltration occasioned by the aug- 
mented pressure of the blood within the capillaries. Owing to this 
oedema of the mucous membrane in which the submucous tissue partici- 
pates, the calibre of the bronchi is reduced. The younger the subject, 
the smaller the calibre of the tubes, so much the more readily does 
tumefaction of the mucous membrane impede or prevent access of air 
into them, especially into those of the third and fourth magnitude. This 
is an important fact in symptomatology, particularly as regards the con- 
trast between the symptoms of bronchitis in childhood and that in adults, 
and in the difference of the danger from the disease at the two periods. 
At first the mucous membrane is dry, or covered with a scanty, 
tenacious, transparent secretion, containing but few young cells, and a 
very few mature detached cells of ciliated epithelium. Somewhat later 
an active development of cells usually takes place upon the surface, the 
product of which, when mingled with the secretion, now more copiously 
and freely poured out, imparts to it a turbid, yellowish appearance. ACUTE BRONCHIAL CATARRH. 
63 
Upon opening the thorax, if the finer bronchi be obstructed or 
occluded by mucus, the lungs evince little or no disposition to collapse. 
Indeed, if the contraction or obstruction have attained a very consid- 
erable degree, the lungs bulge forcibly out of the opened thorax, so as 
almost to convey the impression that the chest was too small. And, in 
point of fact, the cavity of the thorax has not sufficed to accommodate 
the lungs without compression of the air contained in them. The in- 
spiratory expansion of the chest has ceased with death, but the lungs 
have not been able to diminish in a corresponding manner, because the 
obstructed bronchi have not allowed the air to escape from the alveoli. 
This appearance has nothing in common with emphysema, with which 
it is frequently confounded. 
Chronic bronchial catarrh usually presents to view a more intense 
brownish or dirty reddening of the mucous membrane. Its vessels are 
diluted, its tissue puffed and uneven, but, at the same time, more 
coherent and less easily torn. The mucous membrane itself is hyper- 
trophied, and the fibrous longitudinal bands and muscular layer beneath 
the mucous membrane are still more so. As, simultaneously with this 
thickening, the elasticity of the mucous membrane and of the fibrous 
coat is lost, and as the swollen, sodden bronchial muscles are, in a 
great measure, deprived of their power of contraction, a diffuse dilata- 
tion of the bronchi, consequent upon relaxation of the bronchial wall, 
associates itself, in many cases, to chronic bronchial catarrh. This diffuse 
bronchial dilatation may become so considerable that, upon section, even 
small bronchi gape widely, exhibiting a larger calibre than the branches 
from which they spring. 
Saccular bronchial dilatation, which is usually connected with im- 
portant changes of structure in its surrounding pulmonary parenchyma, 
is again to be considered while treating of diseases of the lung, as is also 
emphysema, one of the common sequelae of chronic bronchial catarrh. 
In many cases of this disease there lies upon the mucous membrane 
a profuse layer of yellowish puriform secretion, containing great num- 
bers of young granulated cells, with divided nuclei, while in others it is 
sparingly coated by a tenacious, glairy, semi-transparent substance. The 
latter form, in which the swelling of the mucous and submucous tissues 
is often very great, is called dry catarrh (catarrh sec). In the former 
the copious secretion often completely fills the smaller bronchi, while in 
the larger it is frequently mixed with air, and is frothy. 
The diffuse and follicular catarrhal ulceration wdiich we have described 
as occurring in the mucous membrane of the larynx seldom appears 
upon that of the bronchi. Heinhard, however, claims constantly to 
have noticed it in the finest bronchi, when surrounded by tubercular de- 
generation of the lung substance, and believes, that the disintegration of 64 
DISEASES OF THE TRACHEA AND BRONCHI. 
the tuberculous pulmonary tissue proceeds from this ulceration as soon 
as the wall of the bronchus has been destroyed, a view which we fully 
share with him as regards infiltrated tuberculosis (or cheesy pneumonia). 
I. Acute Catarrh of the Trachea and Larger Bronchi. 
Symptoms and Course.—Acute catarrh of the trachea and greater 
bronchi is often combined with catarrh of the larynx, nasal mucous 
membrane, that of the frontal sinus, and of the conjunctiva. More 
rarely it spreads into the smaller bronchi. The greater its extent, so 
much the more frequently does it begin with shivering, and, in sensitive 
persons, perhaps even with a chill. This chilliness, however, is rarely 
confined to a single rigor, and this is an important point of distinction 
between the onset of a catarrhal and of an inflammatory fever. It often 
happens that throughout the whole attack, with every slight alteration 
of temperature, or upon changing the linen, and especially if the patient 
be laid in a fresh bed, shivering-fits continue to recur. During the in- 
tervals the patient experiences a sensation of burning heat, without any 
indication from the thermometer of an actual increase of temperature. 
Added to this, there come distressing frontal headache, pulsation of the 
temporal arteries, soreness of the limbs, sensation of pain in the joints, 
increased upon pressure, constituting “ catarrhal rheumatic fever.” 
Should the appetite fail, too, and the tongue become coated, we even 
hear “ gastro-catarrhal-rlieumatic fever ” spoken of. It is very indicative 
of catarrhal fever that the intense feeling of weakness does not bear any 
proportion to the trifling elevation of temperature and frequence of the 
pulse, which seldom exceeds the number of eighty to a hundred beats 
per minute. In children, and irritable subjects, delirium sometimes is 
added to these symptoms, and in very rare instances, and in exceedingly 
sensitive children, convulsions may take place. The mother, and even 
the physician, may be temporarily alarmed by these manifestations, until 
a profuse flow from the nose, or repeated sneezing, allays the dread of a 
commencing disease of the brain. In such a case the doctor, who, the 
day before, with a long face, has been applying leeches to the head, 
may find his position embarrassing, now that the harmlessness of the 
case has become obvious, even to the bystanders. 
Catarrh of the trachea and larger bronchi is not always attended by 
fever, often running its course from beginning to end without it. In 
most cases of severity it is accompanied by perverted sensations along 
the course of the air-passages and under the sternum. Hence the sensa- 
tion of tickling after inhaling acrid vapor, and the feeling of soreness 
and burning in the chest. Not uncommonly, the integument of the 
sternum is unduly sensitive, and the cause of this phenomenon is sup- 
posed to be an excitement transmitted to the skin through central HYPERJEMIA AND CATARRH. 
65 
ganglia from the sensory nerves of the bronchial mucous membrane. 
The cough is not quite so distressing as that of catarrh of the laryngeal 
mucous membrane,* which is more fully provided with sensory nerves. 
It never has a hoarse tone except when the larynx participates in the 
disease. At first the sputa are scanty, or entirely wanting; afterward 
the expectoration becomes more copious; and, as the secretion only pro- 
ceeds from the larger bronchi, a few efforts suffice to cough it up. The 
patients say that the “ cough is loose.” In the beginning the sputa are 
transparent and viscid; at a later period they are turbid and yellowish. 
There is, of course, no real dyspnoea in catarrh of the trachea and 
larger bronchi; or, at most, there is but a slight oppression, and the pa- 
tients say that “ their chest is stuffed up.” A swelling even of consid- 
able magnitude, with the most profuse secretion, is incapable of ma- 
terially and injuriously diminishing the large calibre of these channels. 
Percussion of the chest shows no change of sound during catarrh of 
the larger bronchi. The vibrations of the thorax, and its capacity for 
air, remain normal. Auscultation, too, often gives negative results— 
that is, we hear everywhere the whispering sound which the inflowing 
air creates at the points of division of the finer bronchi, and in the air- 
vesicles, and which we call vesicular respiration. All thought of the 
graver catarrh of the minuter bronchi may be excluded, and catarrh of 
the larger tubes is to be diagnosticated when we hear vesicular breath- 
ing alone in the chest of a person suffering from cough and expecto- 
ration. When the mucous membrane of the greater bronchi is much 
swollen at one circumscribed point, the air, passing through it as through 
a reed pipe, produces a buzzing, humming sound (the sonorous rhon- 
ehus), audible to the ear applied to the thorax, not only over the point 
of origin, but beyond, and often with perceptible vibration of the tho- 
racic walls. If an accumulation of mucus forms within the bronchi, 
the air sets the liquid in motion, or bursts through it, so that bubbles 
are formed and broken, causing rattling noises, which, as the bubbles 
are larger here than they can be in the finer tubes, we call large moist 
rales, to distinguish them from the rales in the lesser bronchi. 
Catarrh of the trachea and greater bronchi, wdiich we often hear 
called a “ slight cough ” by the laity, as a rule runs its course favorably, 
and with tolerable rapidity. The fever disappears, when there has been 
any ; the cough, particularly in the mornings, brings up sputa cocta, 
nowadays called muco-purulent homogeneous sputum, and finally sub- 
sides, the perverted sensation of the chest having previously vanished. 
* Nothnagel has proved, by experimenting upon animals, that irritation of the 
tracheal and bronchial mucous membrane causes coughing ; and has found that at the 
bifurcation of the trachea in particular coughing-fits may be excited as promptly and 
of as severe a character as those originating in the larynx. Other regions evince a 
lesser susceptibility. 66 
DISEASES OF THE TRACHEA AXD BRONCHI. 
A. As it occurs in the Adult.—When extensive, the disease often 
exhibits the signs of sympathy and reaction of the general system 
against local, disorder, already described as catarrhal fever. 
The minuter bronchial tubes have no sensibility; hence, when the 
catarrh is confined to these alone, there is none of that feeling of itch- 
ing, nor soreness, felt in catarrh of the larger bronchi. The occurrence 
of acute pain, at any time throughout the attack, shows the existence of 
a complication. After a while, however, pain is felt at the points of in- 
sertion of the muscles upon the chest and epigastric region. This pro- 
ceeds from overstraining of the abdominal muscles, by whose spasmodic, 
jerking contractions the act of coughing is effected. This pain, which 
is observable elsewhere when muscles have been overstrained, is aggra- 
vated by any movement of the muscular fibres, but especially so upon 
coughing, and, during the fit, the sick man sits up instinctively, so as to 
relax the abdominal muscles. The cough is of far more violent charac- 
ter than that previously described, coming on in long paroxysms. It is 
not “ loose,” that is, the air, driven from the pulmonary vesicles by the 
spasmodic contractions of the chest, has difficulty in clearing the lesser 
bronchi of the secretion. Here, too, at first, the sputum is usually 
scanty; but it gradually changes, as described above, becoming more 
copious. As the sputum from the smaller tubes is unmixed with air, it 
is specifically heavier than water, and sinks in it; but, owing to its 
tenacity, it retains the shape of the tube from which it came, and by its 
adhesiveness it clings to the frothy, lighter secretion from the larger 
bronchi, which is mixed with air and floats. Thus the expectoration of 
acute bronchial catarrh of the smaller air-passages, when cast into water, 
forms a frothy layer upon the surface, with fine filaments hanging 
from it. 
Extensive catarrh of the lesser bronchi is always accompanied by 
more or less dyspnoea. In adults, however, this rarely amounts to more 
than a somewhat laborious, or impeded respiration. Air enough can 
always reach the air-vesicles, and terror and sensation of suffocation are 
scarcely ever observed. Indeed, it is the mild and insignificant distress 
caused by this disease in adults, and the great danger and totally differ- 
ent symptoms to which it gives rise during childhood, which obliges us 
to describe the two forms separately. It is true that, even in adults, 
catarrh of the finer bronchi is sometimes accompanied by severe period- 
ical dyspnoea; but this very periodicity indicates the existence of a 
nervous complication, which is causing spasm in the muscles of the 
smaller bronchi. The sound, upon percussion, is not altered in this 
form of bronchial catarrh, any more than in catarrh of the larger 
bronchi. Instead, however, of the sonorous rhonclii, sibilant rhonchi, 
II. Acute Catarrh of the Smaller Bronchi. ACUTE BRONCHIAL CATARRH. 
67 
whistling, wheezing sounds are heard in the narrower tubes from par- 
tial thickening of the mucous membrane. When secretion becomes 
more free, rattling sounds, or redes, are produced, and, as large bubbles 
cannot form in the small tubes, the subcrepitant rales are heard. In 
adults, catarrh of the finer bronchi also usually subsides in from eight to 
fourteen days. The fever ceases, the cough, the expectoration, and the 
slight dyspnoea disappear. In other cases chronic catarrh remains, but 
the disease rarely is dangerous. 
If catarrh of the finer bronchi develop in an old man, or a younger 
person in very debilitated condition, and if it be accompanied by violent 
fever, the latter assumes an adynamic character, and symptoms attend it 
which indicate the assumption of a “ nervous condition ” (a very com- 
mon term among the people). The sensorium becomes involved. De- 
lirium or coma sets in; we notice the ominous dryness of the tongue, a 
symptom upon which we lay great stress, both for diagnosis and prog- 
nosis. The pulse is small, irregular, and very frequent; the skin, pre- 
viously dry, flows with sweat; rattling noises arise in the chest (which 
may be coarse or fine, according as they occur in the greater or smaller 
bronchi), but which do not cease after coughing. At last the sound of 
still larger bubbles, tracheal rales, can be heard even at a distance. 
This gurgling (kochen) in the chest, which has also been called the 
“ death-rattle,” and during which the patient usually lies unconscious, 
indicates the approaching end. The older physicians applied the term 
“pneumonia notha” to attacks occurring in marasmic subjects, and 
which, originating usually in chronic disease, rapidly progressed to a 
fatal termination. Here the patient, in a few days, succumbs to a sim- 
ple bronchial catarrh; and it is not the pernicious nature of the malady, 
but the peculiar condition of the patient, which leads to the danger. 
In old or enfeebled persons there is no disease, especially no inflamma- 
tory one, which may not threaten life. Fever, with its constant symp- 
tom of elevated temperature, the immediate cause of which is augment- 
ed combustion, or greatly accelerated consumption of tissue, rapidly 
consumes the scanty remnant of vital force which yet exists in these 
cases. There is nothing specific in any of these symptoms. They are 
repeated in exactly the same manner, wherever a febrile disorder is con- 
suming the organism, and the physician does w'ell in promising to the 
non-professional in these cases “that he can save the patient if ‘ nervous ’ 
(typhoid) symptoms do not arise.” For hours and days before the end 
the function of the brain is disturbed, its nutrition being vitiated by 
overcharge of the blood with excrementitial products. The tongue be- 
comes dry, the elevated temperature of the body causing an increased 
evaporation from the surface. 
In almost all acute diseases, the pulse, toward the end, becomes 68 
DISEASES OF TIIE TRACHEA AND BRONCHI. 
small, irregular, and scarcely to be counted. In nearly all, too, the 
muscles of the skin are paralyzed, the skin becomes relaxed, and covered 
by profuse perspiration—the death-sweat. The bronchi, too, are pro- 
vided with muscular fibre; the discharge of the secretion, which fills 
them, depends materially upon their contraction. If, too, these muscles 
are palsied with the others, the secretion accumulates. CEdema of the 
lung supervenes (see oedema of the lung), the palsied bronchi (not the 
palsied lung, as is often said) having lost all power to expel their con- 
tents, and thus finally the symptoms of suffocative effusion arise, which 
we have depicted above. 
A chronic bronchial catarrh, which, as shown above, of itself relaxes 
the muscular element of the bronchi, must, of course, aggravate the peril 
in pneumonia notha, which is nothing more than a febrile bronchial 
catarrh in a marasmic subject. 
B. Acute Gatari'h of the Smaller Bronchi in Children.—While 
bronchial catarrh of adults is a mild complaint, devoid of danger, and 
only perilous to old people on account of the accompanying fever, it is 
one of the most pernicious of diseases of childhood from causes purely 
physical. Let us first consider that intense form of catarrh to which a 
great number of children fall victims, especially during the period of den- 
tition, and which may be called capillary bronchitis provided that this 
expression shall not be understood to mean a process differing essen- 
tially from catarrh, which is the basis of all the forms of disease hitherto 
described. 
Sometimes the disease commences with the symptoms of a catarrh 
of the greater bronchi, apparently slight and free of danger; but, the 
further it descends into the smaller and finer canals, so much the more 
hinderance is there set up against the entrance of air into the air-vesicles. 
It is not limited in this case to that slight feeling of indisposition which 
adults experience in this disorder, but the feeling of oppression arises, 
and that nameless dread which always accompanies imperfect oxygena- 
tion and repressed liberation of carbonic acid. The same restlessness, 
the same violent efforts at inspiration, the same desperation which we 
have described in croup, are presented by a child, the tips of whose 
bronchi are contracted or closed by bronchial catarrh. As soon as we 
enter the chamber, and while still far from the bed, we hear the whis- 
tling, wheezing noise which the air produces as it is driven through 
the constricted canals. It accompanies both inspiration and expiration, 
and is easily distinguished from the whistling of croup; as we dis- 
tinctly hear that, it does not proceed from one narrowed tube, but from 
many. If we husband the strength of the child and do not beset it 
with blood-letting and emetics, its strenuous exertion may often long 
remain adequate to the task of inhaling a proper supply of air to the CAPILLARY BROXCHITIS. 
69 
air-vesicles. As the glottis is closed, the contents of the thorax com- 
pressed, the outflow of the jugulars restrained in this as in every other 
cough, the countenance becomes red, and even bluish, during the cough- 
ing-fits, which are exceedingly violent and distressing, seldom bringing 
up any secretion, and which, even then, is not ejected, but is swallowed 
by the child. Excepting during the paroxysms of cough, the color of 
the face remains normal. But, as the disease goes on (often through 
fault of the physician), if the child, either from exhaustion of its strength 
and inability to make further and adequate muscular effort, can no 
longer draw a sufficient supply of fresh air through the obstructed 
bronchi into the air-vesicles, or else because the obstruction has so in- 
creased that many of the tubes have become totally impervious to air, 
the picture changes. The previously full pulse now becomes small, the 
hot skin cool, the reddened countenance pale, the terror turns into 
stupor, and the well-known manifestations of carbonic-acid poisoning 
arise. 
The first threatening of danger is not difficult to recognize, if we 
pay attention to the following points: As long as the epigastrium and 
the hypochondria remain prominent, air enough reaches the vesicles. 
If, however, instead of this, we see, at each inspiration, that the jugular 
and epigastric regions sink in, and that the lower ribs are drawn inward, 
we may feel sure that the air in the vesicles is being rarefied upon 
inspiration (as no new air can reach it), and that the respiratory function 
is being imperfectly performed. A symptom of imperfect inspiration 
of quite as much importance, and hitherto too little appreciated, or else 
falsely interpreted, is the prominence of the supra and infra clavicular 
regions, and the enfeeblement of the respiratory movement in tliis por- 
tion of the thorax. It often attracts the attention of the mother sooner 
than that of the physician, that a child, during its illness, has “ got too 
high a breast.” We must avoid confounding the permanent inspiratory 
expansion of the air-vesicles, to which this appearance is due, with vesic- 
ular emphysema. In tliis case the vesicles remain permanently in a 
state of expansion, such as they would attain normally at the height of 
inspiration. In emphysema they are abnormally distended, and it is 
curious that two such different conditions should hitherto have been so 
often confounded with one another. The manner in which the perma- 
nent inspiratory expansion of the vesicles takes place seems difficult of 
explanation upon a mere superficial glance at the mechanism of respi- 
ration. We are tempted to assume that the obstruction in the finer 
bronchi, which could be overcome by the action of the inspiratory 
muscles, should be still more readily conquered by forced expiration; 
since, as daily experience teaches, we are able to expel our breath with 
greater force than is required to draw it in, or, as the physiologists ex* 70 
DISEASES OP THE TRACHEA AND BEOXCni. 
press it, the pressure of expiration is greater than the inspiratory pres- 
sure. But, if we keep in view the action of forced expiration, and the 
condition of the lung in intense and extensive bronchitis, the matter 
assumes a different aspect. In forced expiration we press the dia- 
phragm upward by energetic contraction of the abdominal muscles, and 
thus exert a considerable pressure upon the lungs. This pressure acts 
as well upon the air-vesicles as upon the contracted bronchial tubes. 
The former cannot be cleared by the pressure, as this very pressure 
closes their outlets. Even when removed from the body, we are unable 
to diminish the volume of such a lung by squeezing it. I have been led 
to this simple explanation, by frequent observation that, in this class of 
patients every expiration is forcibly effected by means of the muscles of 
the abdomen, the sibilant rhonchus alone being audible at the time. 
If we lay the ear upon the thorax, we hear nothing but that disseminated 
sibilant rhonchus. Air enters in too small quantity, and, above all, too 
slowly to give rise to the whispering friction-sound which we call 
vesicular murmur. Where it exists it is overborne by the whistling 
sounds. Afterward we hear the wide-spread fine rattle, of minute bub- 
bles (subcrepitant rales). 
C. Bronchial Catarrh of the JYeto-horn.—New-born children very 
often contract catarrh of the respiratoiy passages, principally from inef- 
ficient protection against chilling during washing and bathing, etc. 
The symptoms of it have hardly any resemblance to those of the 
disease described above, although the malady is exactly the same. 
The complaint is almost always mistaken by unphysiological phy- 
sicians, and regarded as an “ organic affection of the heart, in conse- 
quence of which the child is fortunate in dying so soon.” In such 
cases children have sneezed a few times, have perhaps coughed a little, 
otherwise appear well, and often inclined to sleep. The parents rejoice 
over their quiet, contented babe; they do not notice that it only 
breathes superficially. The physician is not called in, or, if he comes, 
he finds no occasion to take account of the breathing; but a great 
change comes over the child, usually with suddenness. The face be- 
comes pale, or, together with the whole body, changes to an ashy hue ; 
the nose grows peaked, the eyes dull, the arms and legs hang down 
inertly. The temperature of the surface is lowered, and unequal; an 
acute cyanosis is diagnosticated, an unhappy conception, wherein ex- 
treme vascular engorgement is confounded with the condition which 
imparts the bluish hue to the lips of the dying, and which is really 
owing to the beginning of that contraction of the arteries and discharge 
of their contents into the capillaries and veins which we always find 
post mortem. 
The explanation of these symptoms is easy. As long as only BRONCHIAL CATARRH OF NEW-BORN CHILDREN. 
71 
“ snuffles ” and catarrh of the larger bronchi exist, the illness is indeed 
trifling. By-and-by the catarrh spreads to the finer bronchial tubes. 
These, very small by nature, are easily closed. The as yet undeveloped 
child is unable to make powerful efforts to overcome the obstruction. 
There is no rhonchus sibilans, which otherwise would occur, to afford a 
diagnostic mark. Nor does the child cough as often as an older one 
would do, for a portion only of a cough is involuntary; the other 
part is voluntarily made in order to remove impediments to respiration. 
Experience has not yet taught the child this art, and so the symptoms 
of carbonic-acid poisoning both suddenly and unexpectedly as 
soon as the minuter bronchial tubes become involved in the catarrh. 
In the bodies of such children, we often find the air-vesicles collapsed, 
to which the obstructed bronchi led. (Atelektasis, see disease of the 
lung, Chap. II.) The described symptoms, however, are just as capable 
of occurring without collapse of the lung, and the latter, as well as 
carbonic-acid poisoning, is a consequence of bronchial catarrh. 
If we can succeed in making the baby cry or vomit, and thus bring- 
ing about energetic respiratory movements, fresh air once more enters 
the lung. The carbonic-acid poisoning vanishes, the symptoms of palsy 
cease, and as the heart now contracts again "with vigor, blood anew 
streams from the veins into the arteries, and into the empty heart 
Circulation is reestablished, and with it normal color and warmth return 
to the skin. 
The attacks are very apt to recur. It may not be possible a second 
time to render the air-passages pervious, and the children may perish in 
a subsequent seizure. If the autopsy be conducted without care, or 
science, the cause of death often remains concealed, unless accompanied 
by extensive atelektasis; since an accurate examination of the bronchi 
is not attempted, the more ordinary symptoms of bronchitis not having 
been observed during life. 
III. Chronic Bronchial Catarrh. 
The symptoms which we have ascribed as belonging to acute bron- 
chial catarrh are only slightly modified in chronic catarrhal bronchitis, 
an extensively prevalent disease. The seat of the affection is not usu- 
ally confined to solitary portions of the bronchial mucous membrane, as 
in the acute form, but the anatomical changes given above reach from 
the trachea, in greater or less degree of development, into the ramifica- 
tions. 
The disease almost always develops from a frequently relapsing and 
protracted catarrh, which has habitually recurred every spring and fall. 
At first, during the summer, the patients remain exempt, until, finally, 
the symptoms become perennial, although somewhat moderated in in- 72 
DISEASES OF THE TRACHEA AND BRONCHI. 
tensity. The most violent distress arises from that form of the disease 
in which a gray tenacious secretion lies upon the mucous membrane, 
which is particularly swollen in such cases, while chronic bronchia 
catarrh, with more copious and more liquid yellow secretion, occasions 
comparatively slight trouble. In the former variety (catarrh sec of 
Laennec), it is the protracted and tormenting cougliing-spells (due to 
the toughness of the secretion, and its situation in the smaller bronchial 
tubes) which are the chief source of suffering to the patient. During 
these paroxysms of coughing, the interruption to the current of the 
jugulars causes them to swell greatly, the countenance becomes dark- 
red and bluish, the eyes weep, the nose drips, k{the head seems as if 
about to split,” and is spasmodically grasped by the patient with both 
hands. Not unfrequently the veins, distended by constant coughing-fits, 
remain varicose, even where there is no emphysema, and thick blue ves- 
sels show themselves on the cheek and alas nasi. An attack of cough- 
ing, of great violence, frequently terminates in retching or vomiting, 
the contents of the stomach being pressed out by the contracted ab- 
dominal muscles. 
Permanent dyspnoea is much more common in this disease than in 
acute catarrh, since in this the mucous membrane is more thickened and 
swollen, and thus offers greater impediment to the entrance of air. 
When, as often happens, an acute attack of bronchial irritation sets in 
upon a chronic catarrh, the dyspnoea becomes much aggravated, the 
affection receives the name of humid asthma. After a short walk in a 
cold, dry atmosphere, which seems particularly hurtful to such invalids, 
they often remain for weeks in the most miserable condition, obliged 
constantly to sit upright, and to pass even the entire night in an arm- 
chair, in order to aid the expansion of the chest as much as possible. 
In consequence of the dyspnoea and of the continuous and im- 
moderate exertion of the inspiratory muscles induced by it, the latter 
become hypertrophied. This hypertrophy is most marked in the sterno- 
cleido-mastoid muscles and in the scaleni, which stand out upon the 
neck like strong cords. Like other hypertrophied muscles, those of the 
respiratory apparatus are constantly in a condition of moderate contrac- 
tion; and (just as locksmiths or blacksmiths and the like habitually 
carry their arms slightly flexed, instead of letting them hang loosely), 
so in chronic bronchial catarrh, the chest is as it were drawn up toward 
the head by these muscles. The neck seems shorter and thicker, the 
chest more convex; but we are not warranted in diagnosticating the 
complication of emphysema of the lungs from these symptoms alone, 
although the complication is common enough. 
Sometimes, during long-protracted and severe exacerbations of bron- 
chial catarrh, the jugular veins become distended, cyanosis appears, and CnROXIC BRONCHIAL CATARRH. 
73 
not unfrequently there is general dropsy. As both cyanosis and dropsy 
vanish as the attack subsides, and the jugulars become unloaded, there 
can be no doubt but that the symptoms were really due to the catarrh 
itself, and not to any complication. Their occurrence is by no means 
difficult to account for, if we can only prove to ourselves that patients, 
the calibre of whose bronchial tubes is considerably reduced, always 
contract their abdominal muscles during the act of expiration. Thus, as 
the exit of the air from the vesicles through the narrow tubes is slow, 
a considerable pressure is exerted upon the blood within the thorax, 
and the flow of blood thither from the rest of the body is retarded. 
Hereafter, when treating of emphysema, we shall show that bronchial 
catarrh is one of the main causes of cyanosis and dropsy in that 
disease. 
Alteration in the percussion-sound, if it exist in chronic bronchial 
catarrh, is never on account of the disease itself, but is due to emphy- 
sema, one of the most frequent of its sequelae. Upon auscultation, we 
often hear the sibilant rhonchus, more rarely the sonorous rhonchus, in 
other cases small, moist rales (subcrepitant rales'). At the same time 
there may be normal vesicular respiration, or, as sometimes happens, 
when many of the bronchioles are occluded, the respiration is feeble; 
and again, where the swelling of the mucous membrane has diminished, 
but has not closed the bronchioles, thus increasing the difference be- 
tween their calibre and the capacity of the air-vesicles, the respiratory 
murmur is sharper. 
Few patients ever recover from this malady, yet to very few does it 
ever endanger life. The old man’s cough has become proverbial, and, 
indeed, these patients may attain a very great age ere they succumb to 
pneumonia notha, or other intercurrent malady. In other cases they 
die of the secondary disorders of the pulmonary substance which result 
from chronic catarrh. (See article on emphysema and interstitial pneu- 
monia.) A very different character from that of the “ catarrh sec,” with 
its more or less tough, scanty mucous secretion, is presented by the 
variety of bronchial catarrh attended by copious secretion, and often 
called bronchial blenorrhoea, or bronchorrhcea. In this form the sputum 
is in coherent masses, which, more or less mixed with air, do not sink 
in water. Sometimes a pound or more of this yellowish secretion, full 
of young cells, is coughed up in the course of a day. In winter it is 
profuse; in summer it usually diminishes in quantity. 
The secretion being less adhesive, and hence more easy of expecto- 
ration, the cough is not so persistent and distressing as in the “ dry 
catarrh.” The dyspnoea, too, generally is slighter, the more common 
seat of bronchorrhcea being in the larger tubes, and its tendency being 
rather to produce diffuse dilatation of the finer bronchi. It is only when 74 
DISEASES OF THE TRACHEA AND BRONCHI. 
an acute attack supervenes upon the chronic one that there is much 
dyspnoea, which then depends upon the amount of swelling of the mu- 
cous membranes. 
During these exacerbations the cell-production goes on with less 
activity, so that the secretion of the mucous surface is reduced in quan- 
tity. This causes the patient to imagine that the expectoration has 
become “ tight, and must be loosened,” a view in which, here and there, 
the doctors participate, who, upon increase of the dyspnoea, with arrest 
of secretion, forthwith diving into their arsenal of expectorants, com- 
pose a recipe of the most heterogeneous substances. 
Upon auscultation, in this form of chronic bronchitis, we sometimes 
hear the coarse rhonclii, sometimes coarser, or finer rales. 
This disease, too, upon the whole, is wonderfully well borne. The 
patients not unfrequently attain an advanced age ere pituitary catarrh, 
phthisis pituitosus, develops from blennorrlioea of the bronchi. While 
the dry catarrh is more prone to the production of emphysema of the 
lungs, the tendency of bronchorrhoea is to cause bronchiectasis. The 
patients more frequently die of acute intercurrent disorders than of ex- 
haustion through the persistence and abundance of the discharge. 
The general characteristics of chronic bronchorrhoea are not, in all 
cases, nor even in the majority of cases, so much modified by diffuse 
dilatation of the bronchi as to enable us to recognize this complication 
with certainty. Sometimes, however, the peculiar nature of the sputa 
warrants our forming a diagnosis at least of its probable existence. 
Experience has taught that, as long as the bronchi retain their normal 
calibre, the secretion of their mucous membrane seldom undergoes 
putrefactive decomposition, while in the diffuse and sacculated bronchi- 
ectasis it very often becomes putrid. The fact that the contents of a 
sacculated bronchus frequently’ putrefy, far more frequently, indeed, 
than the contents of a tuberculous cavity, is a matter for our future 
consideration. 
That the secretion formed in tubes which have become diffusely en- 
larged should also show an increased tendency to putrescence would 
seem to indicate, with some plausibility, that besides the ciliary motion 
and the cough (which appears to have little effect in clearing the minuter 
bronchi), contraction of the bronchial muscles also plays a part in ex- 
pectoration, so that palsy of these muscles, which, undoubtedly, is one 
of the main causes of dilatation in the tubes, also favors stagnation, and 
consequent putrescence of the secretion which they contain. If, then, 
the copious puriform sputa hitherto ejected become unusually liquid; if 
both sputa and the breath of the patient begin to emit a penetrating 
stench; if the more solid components of the sputa sink to the bottom 
of the cup, and there form a greenish-yellow sediment, being no longer BRONCHIAL DILATATION. 
75 
held in suspension by the decomposed mucus, which has lost its tenacity; 
if, finally, we find in the sputum a few inspissated whitish, cheesy plugs, 
of particularly evil odor, we may infer the existence of a bronchiectasis 
with great confidence. The microscopic examination of this sputum, 
which, curiously enough, is often less offensive in the vessel than at the 
moment of its ejection, shows it to consist in part of young, well-pre- 
served cells, in part of cells in a state of fatty metamorphosis, with 
some masses of detritus, an appearance which is found elsewhere, where 
pus cells have long lain stagnant. Not uncommonly, too, we find very 
delicately-shaped objects in the cheesy masses, tufts of fine needles, 
which prove, upon employment of ether, etc., to be fat-crystals (marga- 
rine and stearine), and which are observed in the sputa of gangrene of 
the lungs, as well as in that of bronchial dilatation. Absolutely certain 
diagnosis, however, of one form or other of dilatation of the bronchi 
(of whose differential diagnosis we shall treat hereafter), cannot by any 
means be established by the character of the sputa. In some instances, 
as has been proved by Traube, the bronchial secretion takes on a similar 
character, without the existence of any bronchiectasis. This putrefactive 
decomposition of the bronchial contents often has a very prejudicial 
effect upon the wall of the tube, and the adjacent parenchyma of the 
lung. In treating of gangrene of the lungs, we shall find that this 
putrescence of the contents of the bronchial tubes is one of its most 
common exciting causes. In other instances, which, indeed, are even 
more common, it results in the development about the bronchus, or even 
throughout an entire pulmonary lobe, of an extensive pneumonia, with 
a soft, easily-liquefying exudation. 
Diagnosis.—The distinction between simple acute bronchial catarrh 
and catarrh of the larynx is easy. Hoarseness of the voice and of the 
cough always indicates the latter, and that swelling of the mucous mem- 
brane has extended to the vocal chords. 
The points of distinction between acute bronchial catarrh and acute 
disease of the pulmonary parenchyma can be discussed to greater ad- 
vantage after we have studied the symptoms of inflammation of the 
substance of the lung. For the present, we shall merely indicate a few 
important diagnostic points, which we already have had occasion to 
speak of while detailing the course and progress of the disease. 
1. Simple acute bronchial catarrh is never accompanied by darting 
pain in the side. The only painful sensation proper to it is a feeling of 
soreness and burning in the chest, and sensibility at the points of inser- 
tion of the abdominal muscles upon the thorax. When other pains 
arise, complications always exist. 
2. Acute bronchial catarrh, of itself, never changes the sound of 
percussion, so that the presence of the physical signs which indicate 76 
DISEASES OF THE TRACHEA AND BRONCHI. 
condensation of the parenchyma of the lung exclude simple catarrh 
from the diagnosis. 
3. It is true that acute bronchial catarrh may begin with a violent 
rigor, but, as the disease progresses, the tendency shows itself to re- 
peated attacks of chilliness. Hence, when we find an asthenic fever 
without pain in the side, without bloody sputa, and apparently with 
none but catarrhal symptoms, yet, if the attack have commenced with 
but a single rigor, we should not be too hasty in diagnosticating a 
pneumonia notha, or, as we now say “ nervous influenza ” (typhoid in- 
fluenza), lest autopsy should bring to light a pneumonia winch would 
have been recognized, had the single rigor been properly considered 
and the patient been more accurately auscultated. 
In their appropriate chapters we shall explain the mode of distin- 
guishing chronic bronchial catarrh, with scanty secretion and great dys- 
pnoea, from nervous asthma, and shall give the diagnostic points between 
pituitary phthisis and tuberculous phthisis. 
Prognosis.—The danger of bronchitis depends almost entirely upon 
the age of the patient. In early life, the younger the child, the smaller 
the bronchi, so much the more perilous is the disease. In adults, it 
scarcely ever threatens fife, excepting among old persons, where it 
again becomes a dangerous disorder, especially if accompanied by fever. 
The gravest symptoms are those indicative of impeded oxygenation 
in the air-vesicles. The most violent cough, the most intense restless- 
ness, an immense purulent expectoration, and all other symptoms of 
the acute and chronic form, are of far less significance than the first 
token of poisoning by carbonic acid. Never forget that life is not really 
threatened until such symptoms arise. This reflection will form the 
best safeguard against over-active treatment of children with capillary 
bronchitis. As long as the pulse remains full and the countenance 
ruddy, there is no immediate danger. 
Treatment—Prophylaxis.—Upon this head we refer to what has 
been said as to the prophylaxis against laryngeal catarrh. Cautious 
habituation to change of temperature, cold washing, cold baths, are as 
commendable in the one case as in the other. 
Indication as to Cause.—This demands consideration both of the 
predisposing and of the exciting cause. As some of the causes of 
catarrh are unknown, and as others cannot be allayed, the indicatio 
causalis, in many cases, cannot be met; while, in other instances, care- 
ful regard to known exciting agents is rewarded by the best results. 
This applies, above all, to the general tendency to catarrh, and 
especially to bronchial catarrh, engendered by scrofula, and rachitis. 
There are many pigeon-breasted, big-headed children, with open fon- 
tanelle, enlarged epiphyses, retarded dentition, and flabby skin, which TREATMENT OF BRONCHIAL CATARRH. 
77 
flaps like a pair of loose breeches against their bones, who for months 
suffer from bronchial catarrh, and who are often supposed to be tuber- 
culous. Expectorants and derivatives are useless here; but if we place 
such children upon a well-selected diet, giving them milk and under- 
done meat, if we prescribe cod-liver oil and salt baths, the results are 
often brilliant. The children recover, and nothing but the pigeon- 
breast remains to recall to mind the serious illness of childhood. 
Again, we have found the malady to be a very common one in ad- 
vanced life, but particularly so among a class of people of about fifty 
years of age, “ high livers,” who drink freely of wine, sit all day, assim- 
ilating much material, and consuming but little; with haemorrhoids and 
a voluminous paunch, who evince a great tendency to chronic affections 
of the abdomen, as well as to chronic bronchial catarrh. It were folly to 
confine such a person to his room, and set him to taking Seltzer-water 
and milk, sulphuret of antimony or senega. Let him rather institute a 
proper proportion between assimilation and consumption of nutriment, 
cause him to take exercise, forbid spirituous liquors, and set him upon a 
sparing vegetable diet. Finally, let a patient of this class betake him- 
self to Marienbad, Karlsbad, or Kissengen. In such cases, but only in 
cases like them, the alkaline chalybeates have a beneficial effect, not 
upon the cough alone, and other symptoms of catarrh of the bronchi, 
but upon the corpulence and the haemorrhoids. 
Among the exciting causes, mechanical obstacles at the mitral valve, 
which impede the venous circulation of the bronchi, sometimes admit 
of palliation. When the catarrh depends upon insufficience of the 
mitral, the action of digitalis is uncertain, but its effect is very evident, 
where the hyperaemia is due to its contraction. In the latter case, by 
retarding the action of the heart, time is afforded to the auricle to dis- 
charge its entire contents into the ventricle, the engorgement of the 
pulmonary vein subsides, and with it the bronchial catarrh to which it 
has given rise. 
Bronchial catarrh, caused by the collateral fluxion to the lung in 
malarious fever, requires quinine. The collateral fluxion into the bron- 
chial arteries, produced by the pressure of a dropsical effusion upon the 
abdominal aorta, may demand tapping; the more so, as the diaphragm, 
which in these cases is pushed upward into the chest, compresses a 
portion of the lung. After having once witnessed the striking ameliora- 
tion effected by tapping, perhaps even the complete subsidence of a 
bronchial catarrh, which a few days before was the patient’s most griev- 
ous affliction, we shall never permit any case of catarrh whatever to be 
aggravated by collateral fluxion, the result of pressure upon the abdom- 
inal aorta by accumulated fecal matter or by gas, the removal of which 
is still more easy. A teaspoonful of the pulvis liquiritke compositus, 78 
DISEASES OF THE TRACHEA AND BRONCHI. 
taken morning and evening so as to produce a sufficient daily alvine 
evacuation, is a remedy much praised by the patient, and readily taken. 
If the cause be a direct irritant to which we know the mucous mem- 
branes are daily exposed in certain trades or avocations, the causal indi- 
cation cannot be met, as these patients are not usually in position to 
give up their occupations, and to avoid these noxious agents. As we 
have explained above, chronic bronchial catarrh is undoubtedly exacer- 
bated if the patients subject themselves to the action of very cold, dry 
air. We should bear this knowledge conscientiously in mind, and 
make the patient keep his room for weeks or months during a cold win- 
ter, and establish a uniform temperature in his chamber. Experience 
demands our recourse to this procedure all the more, as patients with 
chronic catarrh of the bronchi, after suffering an intercurrent acute 
attack, often indulge in the idle hope that the disease just passed away 
has had some critical influence upon the chronic evil, and that they now 
cough much less, and are much less oppressed about the chest, than 
before. 
Their error becomes evident as soon as they expose themselves anew 
to the air. Chronic bronchial catarrhs, which have arisen under the in- 
fluence of a severe climate, require, where circumstances permit, a change 
of abode. Let the patient avoid the winter—that is, send him, during 
the cold season, into some milder climate. During spring and autumn 
advise residence in some peculiarly-sheltered place, Baden-Baden, Wies- 
baden, Soden, etc., or in the highly-oxygenated atmosphere of the pine- 
woods, in which convenient accommodations have long been established 
for the “ pine-needle-bath institutions.” As a rule, high dry places are 
more suitable for the catarrhus pituitosus, while we must send patients 
who suffer from the dry catarrh to the wooded coasts, or to promenade 
upon the salt-works. In epidemic catarrh, the cause cannot be ob- 
viated. 
Indication in Teeating the Disease.—Even the mighty bleeders 
of the school of JSouillaud, who make little of a pound or two of 
blood, claim nothing for blood-letting in catarrh of the respiratory 
organs. Let us bear this fact in mind, lest we be induced to bleed at 
the sight of severe infantile dyspnoea, from hypersemia, and swelling of 
the bronchial mucous membrane; and let us also remember that the 
danger from the so-called capillary bronchitis of childhood arises merely 
from the situation of the disease. In the vast majority of these cases, 
and it is in these alone, of the many forms of bronchial catarrh, that we 
might be misled into bleeding, instead of averting the danger of car- 
bonic-acid poisoning by so doing, we should enhance it. The swelling 
of the mucous membrane will not subside, and although hitherto, by 
dint of strenuous efforts, the child may have been able to draw air TREATMENT OF BRONCHIAL CATARRH. 
79 
enough through its narrowed bronchi to support life, yet after the 
bleeding his strength may be inadequate to the exertion. He who has 
once seen the altered aspect of a child a few hours after such a bleeding, 
and, on the other hand, has had opportunity of observing how long the 
undepleted powers of nature are able to sustain a respiration, which, if 
laborious, is still sufficient, will readily abstain in these cases from vene- 
section. 
The “ antiphlogistic ” neutral salts of potash and soda are as little 
employed in catarrhal inflammation as depletion by the lancet. Calomel, 
also reckoned an antiphlogistic, is extensively used, both in the bron- 
chial catarrh of teething children and the catarrh of the intestine which 
develops about this period. Incomprehensible as the beneficial effect 
of this drug upon either of these disorders may be, yet experience has 
affirmed it so fully that we cannot have any hesitation in making use of 
the remedy. We give small doses of from the sixth to the quarter of a 
grain, three or four times a day. Certain salts, to which there has been 
ascribed less of an antiphlogistic than of anti-catarrhal virtue, have come 
into very extensive use in bronchial catarrh, either because they excite 
the action of the skin, or because they are supposed to directly modify 
the nutritive condition of the mucous membrane of the bronchi. Among 
these are certain antimonial preparations, golden sulphuret of antimony, 
Kermes mineral, tartar emetic, and, above all, muriate of ammonia. 
The mistura solvens, which consists of muriate of ammonia and liquorice 
aa ( 3 j), with one grain of tartar emetic, or one or two drachms of anti- 
monial wine, dissolved in six ounces of water, forms almost a third of all 
the prescriptions which come into the apothecary’s shop. When I con- 
sider that physicians, and even very clever ones, devoutly order a table- 
spoonful every two hours of this nauseous dose, and even take it them- 
selves upon occasion, I hesitate to declare that it can hardly have any 
other effect than to irritate the gastric mucous membrane and to em- 
barrass the digestion. Perhaps from the sal-ammonias and the anti- 
monials some slight palliative action might be expected in cases where 
the mucus continues to retain an abnormal viscidity. 
The treatment by diaphoresis is highly to be recommended where 
the catarrh is recent, and particularly when cold is the assignable cause. 
Whether determination to the skin act as a derivative to the vessels of 
the mucous membrane, or whether the beneficial action arise from other 
influences, their happy effect upon recent catarrh is established by bril- 
liant experience. The irritability of the mucous membranes can be 
diminished even in a few hours, and in fortunate cases, by profuse 
sweating, we may even succeed in cutting short the catarrh. It seems 
a matter of indifference how we produce the diaphoresis. Copious po- 
tations and warm bed-covering seem to be the most sure means. It is 80 
DISEASES OF THE TRACHEA AND BRONCHI. 
/V 
doubtful, to say the least, if the flores sambuci, spiritus mipidereri, anti- 
monial wine, and other so-called diaphoretics actually do have a diapho- 
retic effect; nay, it seems to be of no consequence as to the result, 
whether we cover up the. patient in a good bed and in warm blankets, 
or whether we wrap him closely in cold wet clothes and then cover him 
up, as these cold applications, from the retained heat of the body itself, 
are very soon converted into warm ones. Perhaps a stronger fluxion to 
the skin is produced by the latter process than by the former. Upon 
similar principles, in chronic catarrh, even where there is no scrofulous 
nor rachitic taint, determination to the skin by the use of salt baths is 
indicated, particularly such baths as contain an extra amount of brine, 
like those of Kreutznach. This treatment is particularly adapted to the 
cases of all patients in whom a protracted acute bronchitis is threat- 
ening to become chronic, but in whom it has not as yet assumed an in- 
veterate character. But, even in inveterate and grave cases of chronic 
bronchial catarrh, I have produced most striking results, at my clinique, 
by means of energetic diaphoresis. I have kept patients for half an 
hour at a time in a bath of a temperature of at least 100° Fahrenheit, 
and then enveloped them in hot blankets, in which they remained from 
one to two hours longer. At first, as long as the dyspnoea was very 
severe, the patient suffered greatly, not only while in the bath, but 
during the sweating. Soon, however, generally toward the end of the 
first week, as the perspiration began to flow more readily and freely, 
they became satisfied at their improved condition, and were wTilIing to 
continue the treatment. After eight or ten baths the dyspnoea had 
abated in the most striking manner, and the cyanosis had disappeared. 
Rash as it may seem to persons unfamiliar with this mode of treat- 
ment, to plunge a patient, panting with dyspnoea and blue with cyanosis, 
into a hot bath, yet such of my pupils as have witnessed the results of 
the procedures described above will be more successful than such as fear 
to resort to forced diaphoresis in treating this distressing malady, which 
often mocks all remedial measures. 
Allied to treatment by general diaphoresis, there is a class of reme- 
dies by means of which a sort of local diaphoresis, or, at all events, a 
local derivation, is set up upon the integument of the chest, and in 
whose favor experience speaks strongly. In cases of protracted catarrh 
of the bronchi, make the patient wear flannel; put a pitch-plaster upon 
his chest. We must not, however, be too hasty in the employment of 
blisters and of sinapisms, the use of which is not indicated by the 
catarrh itself, but only by certain symptoms. While fever exists, they 
are best omitted. 
The introduction of the inhaling apparatus has resulted in a consid- 
erable advance in our mode of treating bronchial catarrh. We refer ACUTE BRONCHIAL CATARRH. 
81 
the reader to what has already been said as to the local treatment of 
laryngeal diseases, that unless the article inhaled be of a volatile na- 
ture, such as oil of turpentine, it will not find its way beyond the 
coarser ramifications of the bronchi. 
Symptomatic Indication's.—We shall now endeavor to lay down 
rules for the exhibition of the so-called expectorants, as we believe that 
the acceptation of this word is somewhat indefinite. 
As we have seen, the abatement of the hyperaemia and a favorable 
termination of the disease are announced by an increase in the amount 
of liquid secretion and by a more copious production of young cells. 
These symptoms, however, are the result, not the cause, of the improve- 
ment ; hence the formation of sputa coda will be best promoted by any 
means which tend to bring about resolution of the catarrh. Then, too, 
when there is an accumulation of sputa in the bronchi, its expulsion may 
be hindered by so many causes, that the various remedies, which may be 
useful in aiding the expulsion, cannot all be placed in the same category. 
The following are the most important symptoms, which must be treat- 
ed in accordance with the pathologico-anatomical phase of the disease: 
1. We have to do with catarrhs in which there has long existed an 
excessive irritability of the mucous membrane, so that the patients are 
tormented by incessant and most distressing cough. Although these 
coughing-fits are only a result of catarrh, yet, from the friction of the 
air upon the irritated mucous membrane, which they occasion, they are 
also one of the causes of its aggravation and persistence. If, then, we 
combat these paroxysms, we not only moderate the individual evil, but 
tend to cut short the general course of the disease. The sweet, muci- 
laginous decoctions and syrups are here both inefficient and injurious to 
the digestion, as are also the cough-bonbons and caramels, in spite of 
the illustrious names on the labels which testify to their efficacy. On 
the other hand, the employment of the alkaline muriatic mineral waters 
of Selters, Ems, Obersaltzbrunnen, is here as urgently to be recom- 
mended as the folly of resorting to them in every bronchial catarrh, as 
in a bronchial blennorrhoea, is to be decried. Of these waters, of whose 
beneficial action upon the irritable mucous membrane we have no phys- 
iological explanation, let five or six glasses be drunk fasting in the 
morning, while promenading; or, in acute catarrh, let them be taken in 
the course of the day instead of the customary ptisane. Be bold, too, 
in administration of narcotics under these circumstances. If rest be dis- 
turbed at night, give ten grains of Dover’s powders in the evening; or, 
when incessant coughing torments the patient, administer, through the 
day, a mixture containing opium or morphine. The cough will then be 
less frequent, and the secretion from the bronchi, having more time for 
accumulation, will, when expectorated, appear in greater quantity, so 
that the patients are apt to praise the powder, which ‘‘has loosened their 82 
DISEASES OF THE TRACHEA AND BRONCHI. 
cough so well,” as the best they have hitherto taken. The application 
of strong, cutaneous irritants, sinapisms, and blisters to the chest, is 
especially adapted to the form of disease in question. 
2. Sometimes a periodically-recurrent dyspnoea, with extensive 
sibillant rhonchi, indicates that the muscles of the finer bronchi are in 
a state of spasm, and that a part of the dyspnoea is to be attributed to 
this circumstance. In these cases there is often great irritability of the 
mucous membrane ; hence, the narcotics are most useful in relaxing 
the bronchial muscles. The nauseants, too, do good service by caus- 
ing muscular relaxation, and we may prescribe infusion of ipecac., or 
small doses of tartar-emetic. Above all, I recommend the iodide of 
potassium in such cases. Its effect is often brilliant, relief following 
the very first spoonful; indeed, having once learned its efficacjq many 
patients require constant warning against the abuse of this some- 
what overactive drug. 
3. Sometimes an opposite condition prevails, the bronchi being 
dilated, their walls relaxed, and their muscular coat half paratyzed. It 
is in just such cases as these that the secretion is apt to be profuse, 
and (owing to the imperfect cooperation of the bronchial muscles) 
difficult to get rid of by coughing. (As already stated, large and soft 
moist rales indicate blennorrhoea of the bronchi.) The appropriate 
remedies in such cases are the stimulant expectorants—an important 
class among the so-called expectorants—namely, senega, squills, pim- 
pinella, carbonate of ammonia, benzoin, liquor ammonia?, anisatus, and 
the like. A very favorite prescription is an infusion of senega? 3 ij— 
3 ss to water 3 vj, with liq. ammon. anisat. 3 ss. The elixir pectoralis,. 
consisting of sacc. liquiritia? § ij, aqua foeniculi 3 vj, liq. ammon. anisat. 
3 ij, to be taken by the teaspoonful. Finally, the use of ptisanes, con- 
taining more or less of aromatic substance, is suitable in these cases, 
although their virtue lies mainly in the warmth they give out when swal- 
lowed while very hot. Preposterous as it may be to prescribe pectoral 
teas to all classes of patients, those who are suffering from bronchial blen- 
norrhcea wTith relaxed bronchial muscles almost always expectorate with 
greater ease after having drunk a few cups of hot ptisane. Besides the 
officinal expectorants, a mixture of mucilaginous, sweet, demulcent (sooth- 
ing ?) articles are ordinarily prescribed as a pectoral tea: rad. althaea, 
fibres malvae, flores et herba verbasci, radix liquiritia?, with the seed of 
plants which contain an ethereal oil, such as semina anisi vulgaris, sem. 
anis. stellati, semina foeniculi, semina phillandrii aquatici. The latter arti- 
cle, which also contains resinous matter, and therefore belongs among the 
remedies to be spoken of in the next class, is in especial repute in bron- 
chorrhoea, in which it is said both to facilitate the expectoration and to ACUTE BRONCHIAL CATARRH. 
83 
restrain the secretion. The stimulants excite the bronchial muscles tc 
more energetic contraction, just as they cause the pulse to rise and the 
heart to beat more vigorously. But it may happen that the bronchial 
muscles become so debilitated as no longer to afford any assistance in 
expectoration, and the cough alone is inadequate for the expulsion of 
the sputa. This state has been called “ incipient palsy of the lung,” but 
the lung takes no active part either in inspiration or expiration. It may 
be detected when, immediately after the act of coughing, the rales, in- 
stead of subsiding for a time, persist with scarcely any diminution. In 
such an emergency, should the expectorants fail, an emetic is impera- 
tively indicated. Let no time be lost, lest the access of air to the alveoli, 
being cut off by the accumulating secretion, and the bronchial palsy 
already commencing, be aggravated by carbonic-acid poisoning. An 
emetic is the surest expectorant. If, during retching, the abdominal 
muscles be energetically shortened, and the thorax powerfully contract- 
ed, the air, which, as we have already explained, is expelled in violent 
puffs, drives the secretion out of the bronchi, or at least out of the 
larger of them. Unfortunately emetics fail us altogether where we 
have to overcome obstruction in the finest bronchial tubes, and this it is 
which renders the latter stage of capillary bronchitis so dangerous. 
Even firmly-adhering croup membranes are often enough loosened and 
expelled by the act of vomiting; but an inspiration of twice the force 
of that which accompanies this act is incapable of driving a current of 
air into the smallest bronchi and of forcing out the mucus contained in 
them. On the other hand, compression of the air-vesicles thus produced 
is accompanied by an equally firm compression of the capillary bronchi, 
by which they are still more firmly closed. 
4. In the treatment of symptoms it may become our task to mod- 
erate the redundant bronchial secretion, which threatens to exhaust the 
patient. A great part of the means recommended for this purpose, the 
lime-water, acetate of lead, tannin, ratanhia, folire uvae ursi, are either 
inert or of doubtful efficacy. The resins and balsams, recommended 
upon the same ground, are more serviceable in diminishing mucous 
secretion, of which their efficienee in treatment of gonorrhoea furnishes 
striking proof. Peruvian balsam, balsam copaibae, myrrh, gum ammo- 
niac, belong to this class. A very favorite prescription is the Griffiths 
mixture: 
I* Myrrha pulv. 3j. 
Potas. carb. et tart. gr. xxv. 
Aqua menth. crisp. § viij. 
Ferri sulpb. crystal. 3j. 
Sacc. alb. § ss. 
S., a tablespoonftu four times a day. 84 
DISEASES OF THE TRACHEA AND BRONCHI. 
It is naturally to be desired that these remedies shall come in as 
direct contact with the bronchial mucous membrane, as they do with 
that of the bladder or urethra, upon which they act immediately, when 
excreted into the urine. Here saccharum myrrhae, taken dry, is recom- 
mended. We may calculate upon a small portion, at least, of the drug 
administered in this way, passing the glottis and reaching the trachea 
and bronchi. The application of remedies in the form of gas is for 
more serviceable. Thus we may boil tar either alone, or mixed with 
water until the atmosphere is entirely impregnated with its fumes; or 
we may put half a drachm of turpentine in a bottle of hot water, and 
cause the patient to inhale, for a quarter of an hour, four times a day, 
through a mouth-piece, attached to the neck of the bottle. Of course 
we can only expect success to follow this treatment when we apply it to 
the cases to which it is adapted; that is, where the mucous membrane 
is the seat of excessive purulent secretion. In all other forms of bron- 
chial catarrh it does harm. The bitters and tonics which are also given, 
especially in bronchorrlioea, and among which are the polygala amara, 
the lichen islandicus, the folia cardui benedicti, may have an influence 
upon the mucous membrane of the stomach, or may improve the appe- 
tite, regulate the digestion, and act beneficially upon the nutrition of 
the body, which is then better able to bear the disease. Upon the 
disease itself they scarcely have any material influence. 
5. In the treatment of bronchial catarrh in young children, who do 
not know how to cough, and who are unequal to the emergency when 
an obstacle in their air-passages requires a corresponding respiratory 
effort, the symptomatic indication requires, first of all, the removal of 
the accumulated secretion by means of an emetic, and secondly measures 
which shall force the child to more vigorous respiratory efforts. Do not 
let him sleep too much, and too profoundly. Put him in a bath, and 
spirt cold water upon lii§ chest while in the bath. Make him scream 
by brushing the soles of the feet, if symptoms of obstruction of the 
bronchi and embarrassed oxygenation in the vesicles set in. 
CHAPTER II. 
CROUPOUS INFLAMMATION OF THE TRACHEAL AND BRONCHIAL 
MUCOUS MEMBRANE. 
Etiology.—Not unfrequently, croupous laryngitis spreads into the 
trachea and bronchi; and in like manner we shall find that croupous in- 
flammation of the pulmonary vesicles almost always is continued into 
terminal branches of the bronchial tubes. Besides this, however, there 
occurs, although rarely, a croupous bronchitis, which appears primarily in CROUP OP THE TRACHEA AXD BROXCHI. 
85 
the bronchi of the third and fourth order; and, as this constitutes a dis- 
tinct disease, it must be spoken of separately. 
This primary croupous bronchitis attacks by preference persons 
during the age of adolescence, but we have not as yet any accurate 
knowledge as to either its predisposing or exciting causes. 
Anatomical Appearances.—The tree-like ramified tubes, already 
described, are formed by the extension of the croupous process from 
the larynx into the trachea and commencements of the bronchi. The 
croupous plugs which fill up the bronchioles in pneumonia we shall find 
to be a constant feature in the sputa of pneumonic patients. 
In primary independent croupous bronchitis the same condition of 
the bronchial mucous membrane is found, and with the same coagulated 
exudation upon it which we have described as existing upon the mucous 
membrane of the larynx in laryngeal croup. In the greater branches the 
calibre of the canal is not completely occluded; the coagula are tubular; 
but in the smaller bronchi they form cylindrical plugs. Croupous 
bronchitis is seldom spread over the whole lung; generally it is partial, 
and confined to a small number of bronchi; but to this tule there are ex- 
ceptions. I know of a young girl, of fifteen years of age, who for years 
has almost daily coughed up a complete cast of the left bronchial tree. 
Symptoms and Course.—The small extent of bronchial croup, as 
well as the absence of the fever, causes the progress of this disease to be 
quite different from that of croupous inflammation in the larynx. In- 
deed, while the latter is an extremely acute disease, croupous inflamma- 
tion of the bronchial mucous membrane is, in some cases, a chronic one, 
which drags on for months, and even years. 
The patients generally suffer from moderate dyspnoea, and nothing 
save the pale countenance and a certain relaxation and sleepiness indi- 
cate that respiration is carried on incompletely, and that the blood is 
not entirely decarbonized. From time to time, convoluted masses are 
ejected, after painful and spasmodic coughing. These become disen- 
tangled in water, and then present regularly-formed casts of the bron- 
chial ramifications, consisting of tree-like, repeatedly-forked coagula, 
generally covered with a little blood. Upon auscultation, we hear ex- 
quisite rhonchus sibilans, corresponding to the extent of the bronchial 
croup; or, as in my case, the respiratory murmur is wanting as long as 
the tubes are filled with exudation, and returns as soon as the membrane 
has been expectorated. From time to time the disease, which, as we 
have said, is usually chronic in its course, takes on exacerbations. These 
often commence with a chill, and are followed by fever. The process 
sometimes spreads throughout other regions; great dyspnoea ensues; 
breathing may become insufficient, and death may take place under the 
often-mentioned symptoms of insufficient respiration. 86 
DISEASES OF THE TRACHEA AND BRONCHI. 
Diagnosis.—Croupous inflammation of the bronchial mucous mem 
brane is easily distinguished from catarrhal inflammation by the expecto- 
ration of characteristic moulds of the bronchial tubes, consisting of 
coagulated fibrin. As the mucus from the finer bronchi may sometimes 
have sufficient tenacity to retain its form, in doubtful cases, we may em- 
ploy the test afforded by the different reactions of fibrin and mucin with 
acetic acid, the fibrinous clot swelling up upon application of the dilute 
acid, the mucus shrinking and becoming firmer. In well-marked cases 
error is impossible. 
Prognosis.—Although the disease seldom attains such magnitude 
as to endanger life, yet the prognosis as to complete recovery is unfa- 
vorable. Bronchial croup is an exceedingly obstinate disease, evincing 
a great tendency to relapse, and often becoming complicated at last by 
tuberculosis, unless, indeed, this disorder accompany it from the outset. 
Treatment.—The treatment is to be conducted upon the principles 
laid down for the management of laryngeal croup. In one case ( Thier- 
f elder), iodide of potassium afforded very marked and brilliant service 
( 3 ss daily), so that this treatment should be imitated. I have never 
observed any benefit resulting from its action in this disorder. 
CHAPTER III. 
SPASM OP TUB BRONCHI—BRONCHIAL ASTHMA NERVOUS OR CON- 
VULSIVE ASTHMA. 
Etiology.—Long before it bad been proved that the bronchi pos- 
sessed muscles, still longer before we had discovered that these muscles 
could be experimentally made to contract by irritation of the par vagum, 
or, still more readily, by irritation of the mucous membrane, a great 
number of forms of asthma had been described in the pathologies. 
True, the causes of the greater part of them have since been traced to 
material alterations in the parenchyma of the lung, especially to emphy- 
sema, organic disease of the heart, etc. Nevertheless, there still remains 
a certain number of cases of motor derangement of the par vagum, in 
which the bronchial muscles contract spasmodically, and the calibre of 
the bronchi becomes narrowed. 
It has already been stated that hypermmia and catarrh are often 
accompanied by contraction of the bronchial muscles, a reflex phe- 
nomenon proceeding from reaction of the sensory fibres of the par 
vagum upon its motor filaments, and furnishing one of the sources of 
dyspnoea in bronchial catarrh. The term nervous asthma, however, is 
not to be applied to cases of spasm of the bronchial muscles, due to 
structural change of its mucous membrane, but merely to those in which 
the point of irritation of the vagus is remote, whether at its root or in NERVOUS ASTHMA. 
87 
its continuity, and to the instances in which we are forced to suppose 
that some irritation of nerve-fibres other than those of the par vagum 
induces a morbid excitement of its motor chords by means of reflex 
action. 
The etiology of nervous asthma is as obscure as is that of spasm of 
the glottis. Disease of the heart and emphysema have been spoken of 
as predisposing causes. It is, doubtful, however, whether, besides the 
dyspnoea which they occasion, these affections ever give rise to abnormal 
action of the bronchial muscles. There are but a very few instances in 
which the source of the malady can be traced to disease of central 
organs, or to pressure upon the par vagum by a tumor. In other in- 
stances, especially in uterine disorders, nervous asthma accompanies 
other nervous derangements. Finally, it may attack persons idiopathi- 
cally, who, in other respects, seem to enjoy perfect health, and in whom, 
after death, none of the above-mentioned abnormities can be found. 
The exciting causes of the paroxysms are, in the majority of in- 
stances, equally obscure. Some persons never suffer from asthma at 
their own abode, but are invariably attacked whenever they spend a 
night in certain localities. In other cases, the inhalation of the dust 
from certain plants, especially ipecacuanha, will occasion a seizure. 
Finally, mental perturbation, sexual excess, inflation of the bowels (the 
laity ascribe a great deal to “ bloating ”), have a somewhat questionable 
claim to rank among the exciting causes of bronchial asthma. 
The attacks of violent dyspnoea, accompanied by suppression of 
urine, which not unfrequently occur in the course of Bright’s disease, 
and sometimes also in disease of the urinary passages, have been called 
urinary asthma. I, too, used formerly to ascribe them to poisoning of 
the blood by the constituents of the urine, or by the results of decom- 
position of these constituents. Recent observations of mine, however, 
which agree with those of Bamberger, seem to show that the dyspnoea 
depends upon oedema of the lung. During the last few years, as long 
as the dyspnoea lasted in such cases, I have always been able, upon 
auscultation, to find moist rales, which subsided together with the 
dyspnoea, upon the ejection of large quantities of watery sputa by 
means of violent vomiting or coughing. It would thus appear that 
urinous asthma is in some degree analogous to many cases of so-called 
uraemic convulsions. (See article, Bright’s disease.) 
Anatomical Appearances.—As we have seen, it is only in the 
rarest instances that we are able to find structural changes in the cada- 
ver, to which the symptoms of bronchial asthma can be attributed with- 
out dispute. Indeed, in order to warrant a diagnosis of pure bronchial 
asthma, the bronchial mucous membrane should appear healthy, nor 
should any other cause for the dyspnoea be discoverable at the autopsy. 88 
DISEASES OF TIIE TRACHEA AND BRONCHI. 
Symptoms and Course.—Bronchial asthma, like other nervous dis- 
eases, has a typical course, in which paroxysms alternate with intervals 
of exemption, although its type is seldom a regular one. Asthmatic 
attacks sometimes follow one another with short pauses, for a while, and 
then subside, often, not again to return for months, or even years. 
Should the paroxysm come on during sleep, the slumber becomes 
restless, and the as yet unrecognized sensation of dyspnoea gives rise to 
the most frightful dreams. When the sufferer awakes, he has, as Rom- 
berg aptly describes it, “ great desire to draw a deep breath, but feels 
that the air does not penetrate into the chest beyond a certain point. 
Hissing, whistling, purring noises are audible, both upon inspiration 
and expiration, which are perceptible to the patient himself, and 
may often be heard even at some distance. The embarrassment in- 
creases ; the respiratory muscles, and even their auxiliaries, are brought 
into action; the alas nasi work; the contour of the sterno-kleido-mas- 
toidei muscles stands out distinctly; the head is thrown back, and the 
arms are braced, so as to expand the chest—but in vain. The vesicular 
murmur ceases, is replaced in some parts by hissing, which suddenly 
comes and goes, while the inspiratory sounds of the larynx and air- 
passages continue, not only undisturbed, but even are louder and 
stronger. Terror is depicted upon the countenance; the eyes are widely 
opened; cold sweat bedews the forehead; the complexion is pale, the 
impulse of the heart violent, unequal, irregular; the radial pulse is 
small and weak; the temperature of the hands and cheeks is depressed. 
Such an attack, after lasting for a quarter of an hour, or perhaps several 
hours with brief remissions, either ceases suddenly, the air rushing 
forcibly into the occluded bronchi and air-cells, causing puerile breath- 
ing, or a cessation comes about gradually, accompanied by eructations, 
yawning, more rarely coughing, with an increased secretion from the 
bronchial mucous membrane, which continues for some time.” 
The latter symptom of this truly classical picture finds a complete 
analogue in the course of a neuralgia of the frontal nerve. As in the 
one case the attack often ends in hypermmia and swelling of the con- 
junctiva, with increased mucous and lachrymal secretion, in the other 
the neurosis of the vagus terminates with hyperaemia, and augmented 
secretion of the mucous membrane of the bronchi. 
Diagnosis.—If we form a distinct conception of nervous asthma, 
distinguishing between it and the spasmodic muscular contractions 
arising as reflex symptoms in bronchial catarrh, its diagnosis is easy. 
The severity of the paroxysms, the free intervals, the absence of symp- 
toms of disease of the mucous membranes, keep us from error. 
Prognosis.—The prognosis as to life is better than the appearances 
would lead one to fear. Although the sufferer, often as he may have safel v NERVOUS ASTHMA. 
89 
undergone an attack, fears that he will not live through the next, yet 
in the disease itself there lies a remedy to allay danger as soon as it 
arises. The moment that signs of carbonic-acid poisoning develop, the 
spasmodically contracted bronchial muscles are relaxed, as are also the 
muscles of the entire body, upon which the poisoning undoubtedly has 
a paralyzing effect. 
Treatment.—Where chronic uterine disease is the cause of nervous 
asthma, the causal indication demands measures corresponding to the 
hvsterical nature of the attack. In general, we are unable to meet the 
causal indication, the cause itself being unknown. 
The indications for treatment of the disease itself are, first, to arrest, 
shorten, or mitigate the paroxysms; and, second, to take measures for 
the prevention of their recurrence. 
To attain the first object, before all else the patient must be freed 
from all tight clothing, and his apartment supplied with pure, dry, warm 
air. The most efficacious of all dietetic remedies (in the widest sense 
of the word) is the respiration of compressed air, but it is rarely that 
a patient has the opportunity to prove its value during an attack. Very 
good results have been observed after a long abode in an institution pro- 
vided with a well-contrived apparatus for this purpose. A gentleman 
of my acquaintance, for many years a sufferer from asthma, has had an 
apparatus constructed in his own house, within which to undergo his 
attacks in greater comfort. The great relief which asthmatic subjects 
experience upon inhaling compressed air is easily accounted for. The 
greater the pressure upon the gas which we respire, so much the more 
of it is taken into the blood; hence a moderate degree of obstruction 
to respiration may be compensated for by augmentation of pressure upon 
the gas respired. It is remarkable that this (in my opinion) principal 
cause for the efficacy of the inhalation of compressed air, the great in- 
fluence of which upon the inspiratory act has been proved by the ex- 
periments of Hoppe-Seyler, is hardly referred to id his writings upon 
this subject. 
The ancient and renowned recipe of a cup or two of strong Mocha 
coffee (two ounces to the cup), and the exhibition of small pieces of 
“ water-ice,” as recommended by Romberg, stand intermediate between 
the dietetic and medicinal remedies. In some cases either one or 
other of these articles will afford considerable relief; in others they fail 
entirely; and it is impossible to predetermine which of these results 
will occur. Among the medicines in the narrower sense of the word, 
the narcotics justly stand highest in repute. When the diagnosis is 
certain, doses of opium or of morphine may be ordered boldly. "Where 
their internal administration fails, the experiment of a subcutaneous in- 
jection of a solution of morphine may be made. My own experience is 90 
DISEASES OF THE TRACHEA AND BRONCHI. 
not in favor of the tincture of lobelia inflata, so famed in treatment of 
asthma (gtt. x—xxx every 15—30 minutes). Nor have I observed 
much of the reputed benefit derived from smoking a pipe containing 
twelve or fifteen grains of stramonium-leaf, mixed -with tobacco or sage- 
leaves, or from the use of the stramonium cigars of the shops, to say 
nothing of the fiict that, in most instances, such procedures result in 
distressing headache. In a few instances, inhalation of chloroform vapor 
affords marked, but, as a rule, only temporary relief. The experiment 
of burning saltpetre-paper (blotting-paper soaked in a saturated solution 
of saltpetre and then dried) may always be made, although the vapors 
thus generated are very unpleasant to many asthmatic patients, and are 
of no benefit to them. In severe attacks we may administer an emetic, 
which often proves of great use. When the paroxysm threatens to 
prolong itself, instead of the emetic we may exhibit tartrate of anti- 
mony, or ipecacuanha, in nauseant doses. (Kohler especially recom- 
mends an infusion of ipecac, gr. v—vi to 3 j, with extract pulsatilla 
3ss.) This internal medication maybe combined to advantage with 
cutaneous stimulation, such as friction upon the chest with warm turpen- 
tine, and the application of sinapisms to the wrists and calves of the 
legs, warm hand and foot baths. The patients, who feel as if in the 
agony of death, beg incessantly that “something more” be done to 
alleviate their sufferings. 
In order to avert future attacks, we should, first of all, caution the 
patient to avoid exposure to any irritants which, according to his expe- 
rience, have been the cause of previous paroxysms. Such instructions 
must be as exact and comprehensive as possible, no matter how odd the 
supposed source of the attacks may seem, and even although the con- 
nection between the cause and effect be altogether unintelligible. For 
instance, if the attack comes on whenever the patient sleeps in a dark 
or close chamber, he must always have a light burning, and leave his 
doors open. It is dhsirable that all asthmatic persons should reside in a 
pure, dry atmosphere; that they should avoid dusty, smoky, and windy 
localities, and that they should not sleep too long. 
Among medicaments especially in repute for the prevention of new 
paroxysms, and for the radical cure of asthma, quinine stands first. The 
shorter and more regular the intervals of the attacks, so much the more 
is to be expected from this drug. It is unsuitable when the pauses be- 
tween the seizures are very long or irregular in their occurrence. In 
such cases we must have recourse to other remedies from the list of the 
so-called nervines. Unfortunately, the mode in which this class of 
medicines modifies the function and nutrition of the nerves is very ob- 
scure, and the indication for the selection of one or other of them is so 
indefinite that we are reduced to a blind empiricism. (We must not, SPASM OF THE DIAPHRAGM. 
91 
however, on this account neglect this disease any more than epilepsy, 
St. Vitus’s dance, etc. As a rule, the metallic nervines (carbonate of 
iron, gr. v—x, in die.; zinci oxid. gr. ij—iv ; argenti. nitrat. gr. 1—4 
in die.; Fowler’s solution, gtt. iij—v in die.) are preferred to tincture 
of valerian, assafoetida, castor, or camphor. 
My experience induces me to doubt the efficacy of Aubr'ee's specific 
in purely nervous asthma. It consists of pot. iod. (twenty-five parts), 
infus. seneg. (two hundred and seventy-five parts liquid to five of 
root), ext. opii (two parts); rectified spirit and simple syrup (each 
one hundred parts). It is colored red with cochineal. Its active part 
is probably iodide of potassium. In two cases it has failed me utterly; 
while in many instances of capillary bronchitis with severe dyspnoea, 
and with or without emphysema, it has proved effective. 
CHAPTER IV. 
SPASM OF THE RESPIRATORY MUSCLES. 
IVintrich and Bamberger describe cases of asthma in which the 
dyspnoea is due to spasm of the diaphragm and not to spasm of 
the bronchi. In this obscure form of asthma the sibillant rhonclii 
of bronchial asthma are absent. The hinderance to respiration in- 
volves the expiratory act alone. The patient must forcibly contract 
the abdominal muscles, so as to force up the diaphragm, then rigid- 
ly fixed in the expiratory attitude. The belly hardens, its muscles 
project, and so forcibly compress its viscera that the urine and 
even the faeces pass involuntarily. The face is blue, the breathing 
but ten or twelve a minute, expiration being twice or thrice as 
slow as inspiration; the epigastrium does not bulge, the lower part 
of the thorax shrinks toward the spine; the upper portion alone 
heaving moderately. Percussion after extreme expiration shows 
abnormal depression of the diaphragm. The clear percussion- 
sound of the lung extends one or two inches too far downward, 
and the heart-shock and cardiac dulness are also displaced one or 
two intercostal spaces. Upon auscultation, the respiratory murmur 
is inaudible. 
The above symptoms are the immediate effects of tonic spasm of 
the diaphragm. Should the attack last long, consciousness fails, from 
disturbance of the cerebral circulation, and incompleteness of respi- 
ration, vffiereby the blood becomes overcharged with carbonic acid; the 92 
DISEASES OF THE TRACHEA AND BRONCHI, 
cyanosis becomes extreme; the pulse grows small, the skin cool, and in 
severe cases death may take place during the seizure. In more fortu- 
nate cases, after a longer or shorter duration, the spasm subsides gradu- 
ally, the cyanosis fades, the dyspnoea ceases, the abatement, however 
being unaccompanied by any cough or expectoration, such as usually 
arises at the end of a fit of bronchial asthma. 
In the cases reported by Bamberger the patient derived relief 
chiefly from use of the cold douche, inhalation of chloroform, and subcu- 
taneous injection of morphia; but he eventually succumbed to the 
disease. 
Bamberger is of the opinion that some forms of asthenia may pro- 
ceed from spasm of other muscles of inspiration, and possibly, too, from 
spasm of the expiratory muscles. 
CHAPTER Y. 
WHOOPING-COUGH.—STICK-HUSTEN.—COQUELUCHE. 
Etiology.—According to our views, wliooping-cough is a catarrh 
of the respiratory mucous membrane, distinguishable, however, from 
other catarrhs of this membrane, both by its mode of origin and by fits 
of spasmodic cough, which depend upon a peculiar hyperaestliesia of the 
air-passages. 
The dependence of whooping-cough upon an unknown, but, un- 
doubtedly specific cause, the frequent epidemic appearance of the dis- 
ease, its propagation by infection, the almost positive protection against 
the malady afforded by a previous attack, remind us in many respects 
of the origin and propagation of measles, scarlet-fever, small-pox, and 
other forms of the so-called acute infectious disorders, of which we shall 
hereafter treat in detail. The circumstance, however, that the sole 
result of the specific exciting cause of whooping-cough is a local affec- 
tion, while the rubeolar, scarlatinous, and typhous poisons involve the 
entire system, is a reason for distinguishing whooping-cough from these 
maladies. At the same time, it is not to be denied that even whooping- 
cough, as well as other epidemic contagious disorders, whose effects are 
merely local, is produced by the action of specific poison. Indeed, we 
regard this mode of origin not only as possible, but even as the proba- 
ble one; but the nature and material of the infection in the disease in 
question must vary essentially from that of infectious diseases, in the 
narrower sense of the term, since their results are so very different. 
Inasmuch, however, as we have no definite knowledge regarding these 
morbid processes, and, since all the symptoms of this disease are easily 
traceable to local disorder of the respiratory mucous membrane, it will WHOOPING-COUGH. 
93 
be more practical, on the whole, in spite of the contagiousness of whoop- 
ing-cough, to treat of it as an affection of the respiratory organs. 
In opposition to our views (namely, that whooping-cough is a catarrh 
of the respiratory mucous membrane, combined with intense hyperes- 
thesia of the air-passages), stand the opinions of physicians, who regard 
it either as a nervous affection of the par vagum, or else believe that it 
is a catarrh of the air-passages complicated by such a nervous affection. 
These views are based partly upon the spasmodic character of the cough- 
ing-fits, and partly upon the fact that the coughing-fits alternate with 
periods of complete exemption, a condition which is certainly suggestive 
of the typical course of the majority of nervous diseases. But coughing- 
spells of the utmost violence, and of the most pronounced spasmodic 
character, arise from reflex action in persons in perfect health, but whose 
respiratory mucous membrane has been exposed to irritation, such as 
contact with some sharp-cornered foreign body, grains of salt, or sugar, 
etc. In whooping-cough patients, coughing-fits, precisely similar, are 
provoked by slight causes, which might easily escape observation; but 
from such a fact we surely are not warranted in assuming the existence 
of a neurosis of the par vagum. The exalted susceptibility (the hyper- 
aesthesia) of the diseased mucous membrane accounts fully for the ready 
occurrence and great violence of these reflex paroxysms of coughing. 
We shall have more to say regarding the typical course of whooping- 
cough when we come to discuss the symptoms. 
Sporadic cases of whooping-cough are exceptional, a proof that 
the specific cause of the malady, if it develop spontaneously, usually 
attacks many persons, and that from a single individual the disease may 
spread to a great number. 
Epidemics of whooping-cough occur most frequently during winter 
and spring, but do not die out upon the approach of warm weather. 
They often succeed epidemics of measles, or of scarlatina, and sometimes 
accompany them. The contagion seems to lie mainly in the secretions 
and exhalations of the diseased mucous membrane. The degree of its 
volatility and its other qualities are unknown. 
Predisposition to whooping-cough is greatest in children, particu- 
larly in such as have attained their second year. It is an important 
fact that this predisposition is enhanced by any causes capable of pro- 
ducing catarrh, and still more so by the presence of any accidental irri- 
tation of the respiratory mucous membrane from cold or other cause. 
“ Colds,” slight but neglected catarrhs, as often furnish the exciting 
cause of an attack of whooping-cough as errors of diet, and catarrhal 
diarrhoeas give rise to cholera. 
Predisposition to whooping-cough always diminishes as age advances, 
and is extinguished almost without exception after one attack of the disease. 94 
DISEASES OF TIIE TRACHEA AND BRONCHI. 
Anatomical Appearances.—Owing to tlie idea that whooping- 
cough is an affection of the nerves, special attention has been paid to 
the post-mortem condition of the par vagum and medulla oblongata. 
In a few cases it has been claimed that the neurilemma of the par 
vagum was relaxed or swollen, or that enlarged bronchial glands have 
been found so situated as to press upon the par vagum, or hyperasmia 
of the medulla oblongata and its membranes has been observed. Such 
observations, however, are but solitary; those, in which anatomical 
investigation fails to find derangement, either of nerves or central 
organs, are vastly more numerous. 
There is no doubt but that, in whooping-cough, the respiratory 
mucous membrane undergoes some anatomical alteration, but to demon- 
strate its existence in the cadaver is a task of great difficulty. Owing to 
the richness in elastic fibres of the mucous membrane of the larger air- 
passages, any hyperasmia, which may have existed during life, disappears 
totally after death, leaving no trace behind. A moderate degree of 
swelling, relaxation, and infiltration of the mucous membrane may 
readily elude close observation, to say nothing of the post-mortem 
changes which may take place in these conditions also. However, the 
contrast between the symptoms during life and the appearances after 
death is no greater nor more puzzling in whooping-cough than it 
is in other catarrhal complaints. As this disorder, when simple and 
uncomplicated, very seldom ends fatally, we find almost always, in the 
cadaver of a whooping-cough patient, gross, palpable lesions, which are 
the results of the complication which has been the cause of death. In 
particular, we find that permanent inspiratory inflation (Alveolarelctasy, 
see above) which even the best recent authorities still persist in con- 
founding with emphysema, wide-spread atelektasis, catarrhal pneumo- 
nia in its several stages, and, far more rarely, croup of the air-passages 
or lungs, meningitis, or hydrocephalus. As these lesions do not depend 
upon the whooping-cough itself, but upon its complications, we refer to 
the appropriate chapters for further discussion upon these subjects. 
Symptoms and Course.—It is customary to recognize three stages 
in whooping-cough: the catarrhal stage, the convulsive stage, and the 
stage of decline. 
The catarrhal stage, in many instances, begins with violent catarrhal 
fever, with reddening of the conjunctiva, and great intolerance of light. 
The patient sneezes incessantly, and is tormented by a distressing cough. 
No one, without knowledge of the prevalence of an epidemic, could 
predict the approach of a whooping-cough at this stage of its develop- 
ment ; nay, so far from receiving recognition as the incipient period of 
the disease, it is often mistaken for an intercurrent accident, in spite of 
its development into whooping-cough at a later period. In a few days WHOOPING-COUGH. 
95 
the fever abates; the redness of the conjunctiva and the photophobia sub- 
side, together with the catarrh of the Schneiderian membrane. But the 
cough becomes more obstinate and persistent, and, at the end of each 
paroxysm, an astonishing quantity of a tenacious, viscid, transparent 
mucus fills the mouth and fauces. This peculiar, adhesive, copious 
secretion is pathognomonic of whooping-cough in its second stage, 
and establishes the diagnosis almost with certainty even at this period. 
Soon, however, the cough assumes a peculiar character; it is accom- 
panied by violent reflex action of the muscles of the larynx, causing 
spasmodic closure of the glottis. From this point we date the begin- 
ning of the convulsive or whooping stage. 
The coughing-fit begins vVith a long-drawn, clear, piping sound 
(produced as the air is slowly drawn into the constricted glottis). 
Then follows a series of short, rapidly-interrupted, expiratory coughs 
(the air, though vigorously expelled, being unable to force open the 
glottis for more than a moment at a time), and tins, in turn, is succeeded 
by the crowing, long-drawn inspiratory act. Thus the “ whoop” alter- 
nates with the cough, the latter finally becoming almost inaudible, until 
at last (though often not until after lapse of some minutes) the viscid 
secretion is brought up, and is removed intuitively by the mother, or 
else, what is more frequent still, is ejected by vomiting, together with* 
some of the contents of the stomach. As shown elsewhere, spasmodic 
closure of the glottis during forced efforts at inspiration impedes the 
current of the jugulars, producing acute cyanosis. The patient grows 
deep red, or bluish, the fauces becomes swollen, the eyes shed tears, 
and seem as if about to burst from their sockets; the tongue looks thick 
and blue; the patient seems to be on the verge of suffocation. Bleed- 
ing from the nose and mouth and ears often takes place, and ruptures 
of vessels occur in the conjunctiva, which becomes infiltrated with blood 
so as to disfigure the patient for days and weeks. Haemorrhage from 
the ear is caused by rupture of the membrana tympani. 
The vomiting, which in bad cases empties the stomach of all its con- 
tents whenever the child coughs, is not always the only indication of 
the forcible compression of the abdomen. Sometimes we may observe 
involuntary evacuations of faeces and urine, although this is rare. At 
others, rupture or prolapsus ani is produced. 
A sensation of tickling in the throat usually precedes each fit of 
coughing, the number of which, in the course of a day and night, may 
amount to twenty-four or upward. The children recognize these pre- 
cursors of an attack with dread. They cling anxiously to their nurses, 
seek a support for the head, or begin to cry. After the paroxysm, 
they remain awhile exhausted, and suffering from pain along the in- 
sertion of the abdominal muscles. Soon, however, they recover, begin 96 
DISEASES OF THE TRACHEA AND BRONCHI. 
to play, or to eat with good appetite, until a new fit interrupts their 
comfort. 
It is upon these alternations of symptoms that the theory is based 
that whooping-cough is a neurosis of the par-yagum nerve. Although 
laughing, crying, loud speaking, insignificant acts of deglutition, often 
give rise to the seizures, yet we cannot deny that they are not always 
the result of demonstrable external provocation. Indeed, we must ad- 
mit that the paroxysms often increase in frequency during the night, 
although the room has not grown colder. It is difficult to assign a 
reason for this circumstance. If, however, we question an observing 
mother, or watch a sleeping child ourselves, until the whooping-cough 
awakens it, we may satisfy ourselves thatr the fit is preceded by a slight 
and very brief, although perceptible, laryngeal rattle, and if we look into 
the child’s throat, as soon as he begins to cough, the pharynx will be 
found filled with that tough mucus the accumulation of which pro 
yokes the attack, and the ejection of which ends it. The secretion 
once discharged, some time elapses before a fresh collection of it pro- 
duces a new coughing-fit, and thus the semblance of intermission is given 
to the apparently rhythmical march of the disease. Every coughing' 
spell is a new source of irritation to the mucous membrane of the larynx. 
The more violent it has been, so much the more rapidly does new secre- 
tion form, and so much the sooner is the next paroxysm to be expected. 
The convulsive stage having lasted three or four weeks, or in other 
cases as many months, the stadium criticum seu decrementi, or stage 
of decline, gradually sets in. The catarrhal secretion loses its tenacious, 
transparent quality, becomes more liquid, yellow, and opaque. The 
sputa cruda become sputa cocta. Here, too, the altered secretion affords 
evidence that the hypermmia and irritability of the mucous membranes 
are subsiding. The paroxysms are no longer provoked by slight exter- 
nal irritants; and the secretion becoming more easy of ejection, and the 
reflex symptoms groAving milder, as irritability of the mucous membranes 
decreases, the fits themselves are shortened. The vomiting, Avliich for- 
merly closed the seizure, ceases to occur, excepting when, the larynx 
chancing to encounter some irritant of unwonted actmty, a coughing- 
spell of the ancient violence is provoked. Relapses are extraordinarily 
apt to occur, if the child be not carefully protected from all pernicious 
influences. The mucous membrane remains extremely sensitive for 
months, although the disease be extinct and the child be recovered. 
Every slight catarrh is attended by spasmodic stricture of the glottis, 
upon coughing, and recalls to mind the old affection from AAdiich it has 
long been free. 
Physical examination made during the interval affords no character- 
istic eAadence. Percussion is normal, and auscultation reveals signs of WnOOPIXG-COUGH. 
97 
catarrh. Other changes depend upon the complications. During the 
paroxysm, according to Wintrich, while the forced expiratory efforts 
continue, the percussion sound is shorter, feebler, and duller. This is 
probably due to the fact that, during the act in question, the air within 
the lungs undergoes considerable compression, and is thus made to press 
so heavily upon the pulmonary tissue and the thoracic walls that the 
latter are brought to so high a degree of tension that they cannot be 
set into vibration by percussion. Upon auscultation, no respiratory 
murmur can be heard during the protracted, sonorous inspiration. 
During the interrupted expiratory act likewise, although the vibration 
of the chest is communicated to the ear, no murmurs are distinctly 
audible. 
Whooping-cough terminates in recovery in a large majority of cases. 
According to popular belief, such an event cannot occur before the 
eighteenth or twentieth week, a prejudice shameful for a physician, and 
highly dangerous to the laity, whom it betrays into a stupid laisser 
otter, and into all sorts of heedlessness. Under judicious treatment and 
systematic nursing, it is almost always possible to bring the disease to a 
close in from four to six weeks. 
In other cases, which are by no means rare, the malady terminates 
in an incomplete recovery; umbilical and inguinal hernia result, and, 
what is still more common, that attenuation of the lung-substance and 
dilatation of the air-vesicles, hereafter to be described as emphysema. 
It is owing to the latter sequel of whooping-cough that many children, 
after having the disease, remain short of breath for the rest of their 
lives. The assertion, so often made, that whooping-cough may leave 
tubercles behind it, is to be accepted with some reserve. So long as the 
terms phthisis and tuberculosis were synonymous, such a statement was 
quite allowable. There is no doubt that a great number of children 
who have suffered from whooping-cough perish, sooner or later, from 
consumption of the lungs; but it is with comparative rarity that the 
form of consumption of which they die is the tuberculous form, due to 
the development and subsequent destruction of miliary nodules in the 
lungs. Most of the children, in whom the signs of phthisis appear, a 
few weeks or months after their having whooping-cough, are suffering 
from chronic catarrhal pneumonia, with cheesy metamorphosis, and sub- 
sequent destruction of the inflamed lung-substance. In such cases, 
catarrhal pneumonia, which has complicated the original disease, instead 
of undergoing resolution, results in the condition above described—a 
form of phthisis much more common than tubercular phthisis. 
When a case terminates fatally it is almost always in consequence 
of complications, some of which consist merely in abnormal extension 
of the disorder, or in the effects of its intensity. If any of the bronchi 98 
DISEASES OF TIIE TRACHEA AND BRONCHI. 
become permanently occluded by the catarrh, so that no more air can 
penetrate to the vesicles in which they terminate, that which they 
already contain becomes absorbed, the vesicles collapse, their walls 
touch, and atelectasis is established. If the catarrh spread from the 
bronchioles into the air-cells, a catarrhal pneumonia is set up. "YVe have 
already stated that nearly all fatal cases show traces of these complica- 
tions. It should always awaken suspicion if the coughing-fits begin to 
lose their characteristic features, if an additional short, dry cough arise, 
if the patient grow short of breath, if the palms of the hands burn, if 
the sleep be troubled, the general health be disturbed, or other febrile 
symptoms appear. In all such cases we must repeatedly and carefully 
search for the signs of capillary bronchitis, of atelectasis, or of catarrhal 
pneumonia. Croup of the larynx or pulmonary vesicles is far easier of 
recognition, partly on account of the acuteness and violence of its initial 
symptoms, and partly because its signs are so obvious and unmistakable. 
This complication, however, is rare. 
The cerebral symptoms which sometimes appear in whooping-cough 
scarcely ever arise from apoplexy, meningitis, or hydrocephalus. The 
vessels of the brain, if normally nourished, are not apt to tear, even 
though subjected to very severe pressure from within; moreover, dis- 
eases like meningitis and acute hydrocephalus are not to be induced by 
a simple and transitory hyperaemia, The convulsions, etc., which take 
place during whooping-cough, and which seldom endanger life, proceed 
either from a temporary venous obstruction with cedematous infiltration 
of the brain, followed by arterial anaemia, or else they are eclamptic 
seizures, caused by reflex action. 
Diagnosis.—As the coughing-fits in this disease are, in my opinion, 
undistinguishable from those of any severe laryngo-bronchial catarrh 
arising from cold, or from the cough produced by the entrance of a 
foreign body into the larynx, or that which may be provoked in an ex- 
tremely susceptible subject (such as an hysterical woman) by the most 
trifling irritation—indeed, as the cough owes its character to physio- 
logical processes, precisely like those which occur in the other varieties 
of cough—we deem it idle to talk of a differential diagnosis of the par- 
oxysms. The epidemic appearance of the disease, its almost exclusive 
occurrence among children, its obstinacy, and long duration will prevent 
error. In infants at the breast, and very little children, the peculiar 
cough and reflex symptoms of the glottic muscles are sometimes absent, 
and, unless the expectoration of copious tenacious secretion and the 
prevalence of an epidemic of whooping-cough be borne in mind, the 
true nature of the affection may be overlooked. 
Prognosis.—One must be aware how rarely children become apo- 
plectic, or die in a whooping-cough fit, ere one can witness a paroxysm WHOOPING-COUGH.—TREATMENT. 
99 
without anxiety. Experience accordingly teaches that the mothers, who 
at first are dreadfully alarmed, by-and-by grow only too careless, and at 
last, without further solicitude or attention, calmly await the advent of 
the twentieth week, when, as they think, the disease is to subside. 
Children who are but a month or two old encounter the greatest danger, 
not because “ their foramen ovales is as yet unclosed,” “ and a com- 
mingling of blood from the two sides of the heart threatens to 
cause acute cyanosis,” but because of obstacles to which they so often 
succumb in other bronchial catarrhs, the facility with which their little 
bronchi become occluded, imperilling life by atelectasis, or by deficient 
oxygenation without atelectasis. The danger arising from these com- 
plications, as well as that occasioned by the sequelae, has already been 
treated of in detail. 
Teeatmext—Prophylaxis.—As whooping-cough scarcely ever oc- 
curs except as an epidemic, and as it is often infectious, prophylaxis 
demands, where circumstances permit, an avoidance of places where the 
epidemic prevails, and separation of the sick from the well, particularly 
from those small, weak, scrofulous children to whom the disease would 
bring great danger. 
As, moreover, the predisposition is augmented by catarrh, and by 
every irritant which can give rise to catarrh, it is well, in seasons of 
epidemic whooping-cough, to protect children with the utmost care from 
taking cold, and to treat the most simple catarrh with the same solici- 
tude and precaution with which, in cholera-times, we put patients upon 
a rigid diet for every trifling diarrhoea, and look upon it as a dangerous 
illness. During epidemics I have kept children continuously confined 
in one room from the moment that any slight unsuspicious cough arose, 
and kept up a uniform temperature day and night for several weeks in 
succession, and have frequently seen children remain free from whoop- 
ing-cough, while it developed among their relatives who had been 
attacked in similar manner, but who had been less carefully nursed. 
The indicatio causalis cannot be met, as we are not able to neu- 
tralize nor to remove the prevalent epidemic influence which excites 
the disease. 
The happy effects which whooping-cough patients often obtain by 
change of abode are perhaps to be accounted for by the exemption from 
continuous or repeated exposure to the exciting cause of the disease, 
which they thus acquire. Whenever an extensive epidemic prevails 
about the dwelling of a patient of mine, I am in the habit of advising a 
temporary migration to some region free from the disorder. 
The indicatio morbi calls for the same general treatment which we 
have recommended for other laryngeal and bronchial catarrhs. Recog- 
nition of the fact, that in whooping-cough we have a catarrh to deal 100 
DISEASES OF THE TRACHEA AND BRONCHI. 
icith, should deter us from a useless and hazardous search for specific 
remedies. Unfortunately, the principles of treatment naturally deducible 
from such knowledge are grossly violated by many physicians. Chil- 
dren are again and again submitted to hurtful exposure, calculated to 
aggravate the catarrh, because the doctor expects to cure it by the ad- 
ministration of preparations of copper and zinc, nitrate of silver, vale- 
rian, assafcetida, castor, or other reputed specific, against whooping- 
cough ; nay, cantharides, phosphorus, arsenic, and even dried vaccine 
crusts, pass for remedies for this disorder in the minds of some men. 
We cannot even ascribe any special curative influence to belladonna, a 
drug which has acquired great reputation, although we have used it 
extensively in the treatment of whooping-cough. (See below.) 
Since, then, the complaint is to be treated upon principles laid down 
for the treatment of other catarrhs, we need not expect great results 
from the use of medicaments. We have already called attention to the 
very questionable virtues of sal-ammoniac, the antimonials, and other 
anti-catarrlial “ remedies,” and hence are decidedly averse to their em- 
ployment in the therapeusis of whooping-cough. On the other hand, 
we attach great value to well-managed treatment by sweating, the 
efficacy of which, in both recent and inveterate catarrhs of other origin, 
I have already insisted upon so urgently. Oppolzer believes it possible 
to bring the malady to a close in a few weeks, by carefully and con- 
tinuously maintaining a uniform temperature in the sick-room. Al- 
though such a statement may be a somewhat exaggerated one, yet I 
have long since adcfpted the practice, and in many instances strictly and 
perseveringly carried it out with the most gratifying results. Alien 
the disease is recent, I put the child to bed, and keep it in a slight but 
continual perspiration. Very young children must not lie in a cradle, 
but should remain in bed alongside of their nurse or mother, where 
they soon get into perspiration. Besides, they should wear a woollen 
sock round the throat, and wear flannel next the skin, upon the chest. 
Throughout the warm season of the year, the patients may be kept in 
the open air; but we should insist upon their returning to their apart- 
ments ere the cool of the evening set in. As a drink, give Seltzer 
water, either warm or mixed with hot milk; in short, treat the catarrh 
as if it proceeded from cold, or had any other non-specific origin. 
Treatment by inhalation of pulverized medicaments may possibly prove 
beneficial; but we have not as yet a sufficient number of observations to 
establish the fact. The symptomatic indication, first of all, calls for 
means of abbreviating the paroxysms of coughing, and of diminishing 
their frequency. It cannot be ignored that the coughing-fits contribute 
materially toward keeping up the irritation of the mucous membrane. 
The longer and more violent the last attack, so much the sooner may WHOOPING-COUGH.—TREATMENT. 
101 
we expect the next one; hence, if we can succeed in rendering the 
seizures milder and less numerous, we not only produce results which 
are palliative but radical, by enabling the disease the sooner to cease 
spontaneously. Reduction of the number, severity, and duration of the 
paroxysms is as important for the cure of whooping-cough, as is prohi- 
bition of loud talking in the treatment of obstinate hoarseness. 
For this purpose I cannot sufficiently urge that the parents, if intel- 
ligent and persevering, be directed to make the child cease from cough- 
ing as soon as possible, and, if necessary, even to enforce this harsh de- 
mand with wholesome sternness and severity, as soon as the mucous 
accumulation is discharged. A portion only of the coughing is invol- 
untary. By an exercise of firmness, a child may withstand the remain- 
ing inclination to cough. The mother, however, must never tire of 
warning, admonishing, and, if need be, threatening, though no imme- 
diate benefit become apparent, even after lapse of days ; for this mental 
dietetic must be maintained for weeks and weeks. 
I have heard the assertion made by the wife of a Prussian general, a 
most determined woman, but an equally tender mother, that whooping- 
cough was only curable by the rod. Such a statement as this, and the 
advice to tell a child to stop coughing, and even to compel it to resist 
the cough as much as it can, have excited objection, here and there, and 
have even given rise to some virtuous indignation. Notwithstanding 
this, however, further personal experience and the approval of other 
judicious practitioners induce me emphatically to reiterate my counsel. 
It is of course inapplicable where the parents are stupid or rude ; but 
the physiological law is well known, that violent reflex symptoms are 
controllable by the will. Perhaps the fact that adults are better able 
to resist the inclination to cough, and do not abandon themselves so 
completely to the irritation, explains why exposure to the same causes 
will, it is true, bring on catarrh, but rarely a catarrh of the intensity and 
persistence observable in the whooping-cough of children. 
This treatment is materially aided, if, as soon as the child perceives a 
fit to be coming on, or when the fine rales in the larynx above described 
give notice of its approach, a moderate dose of carbonate of soda or of 
potash be promptly administered. As the alkaline carbonates reduce 
the viscidity of mucus, and as the secretion collected about the epiglot- 
tis, if deprived of its tenacity, is the more easily expelled, and finally, 
since with the ejection of the mucus the paroxysm usually terminates, 
theory and practice concur with tolerable harmony in approving this 
measure. There is a mixture much employed in whooping-cough 
(R Coccinelke, gr. xij; potas. carb. Sj; aqua? dest. 3 iij; syrup, 
simpl. § j.—rt. S. a teaspoonful when the attack threatens), the effect 
of which in shortening the fits of coughing is often surprising, but 102 
DISEASES OF THE TRACHEA AND BRONCHI. 
which hardly owes its virtue to the cochineal. Half a tumbler of soda 
and water, drunk occasionally, would probably produce about the same 
result. This mixture should not be given as a matter of routine, “ a 
teaspoonful every two hours,” or the like, but only when there is a 
collection of viscid mucus in the throat, and when a paroxysm is ap- 
proaching. Prescribed in the latter way, parents are glad to use it, as 
they soon find out that it renders the attacks milder and shorter, or, as 
they say, “ loosens the cough.” 
Narcotics have also been prescribed to shorten the coughing-fits and 
reduce their number, and there is scarcely an article of this large class 
of drugs which has not been recommended in whooping-cough, and 
even vaunted as a specific. This is especially the case with belladonna. 
We have already expressed ourselves in favor of a bolder use of nar- 
cotics in treatment of catarrhs, and hence approve of their use in whoop- 
ing-cough, which "we regard merely as a catarrh complicated with an 
especially intense hyperesthesia of the air-passages; but we cannot 
admit that any narcotic whatever (belladonna included) has any speci- 
fic action against this disease. If they render the course of whooping- 
cough briefer, they act by mitigating and lessening the frequence of the 
paroxysms, which are perpetuating the irritation. Since, however, as 
as a general rule, narcotics are not well borne by children, being apt to 
cause hyperaemia of the brain, we should restrict their use to those 
cases in which danger from the disease outweighs danger from the 
remedy. Should the treatment, given above, prove ineffective, should 
the child empty its stomach with every paroxysm, should his nutritive 
condition begin to suffer, from constant vomiting and from sleepless 
nights, should convulsions or signs of actual suffocation occur during the 
seizures, the administration of narcotics is indicated. Belladonna enjoys 
this advantage over opium, that, in the condition of the pupil, we have 
an index for regulation of the dose. To children, between the ages of 
two and four years, we may give the eighth of a grain of the drug, night 
and morning, gradually increasing the dose up to half a grain, or until 
the pupil begins to dilate.- Trousseau preferred not to divide the daily 
dose, but gave it all at once, and he thought it useless to push the dose 
to the point of incipient narcotism. For older children, to whom the 
exhibition of opium is less hazardous, we may prescribe small doses of 
morphia (gr. T1^—| in die), dissolve in some liquid like the aqua amyg- 
dalarum, so much lauded by West, or we may give a few drops of lau- 
danum. 
Another and very important indication is, to prevent the secretion 
from accumulating in the minuter bronchial tubes. We have already 
pointed out that such obstructions are a source of danger in themselves, 
being the cause of atelectasis. When we come to discuss the subject WHOOPIXG-COUGII.—TREATMENT. 
103 
of catarrhal pneumonia, we shall show that this disorder depends not 
merely upon a propagation of inflammation from the bronchioles into 
the air-vesicles, but that obstruction of the bronchi and the consequent 
collapse of the lung also play an important part in its etiology. Emet 
ics, therefore, very justly, are highly thought of in the treatment of 
whooping-cough, although we cannot approve of their administration 
every second or third day, without any particular indication, which prac- 
tice is common enough. The smaller the child, the narrower its bron- 
chi, so much the more danger is there of their obstruction, and so much 
the more sedulously must we watch them. If, immediately after the 
cough, there still remain audible rales in the chest, if the child grow 
short of breath, or should the respiration become enfeebled throughout 
a part of the thorax, do not dally until signs of imperfect decarboniza- 
tion of the blood set in, but give an emetic forthwith, and repeat it 
whenever the symptoms recur. We have already explained why it is 
that emetics unfortunately do not always produce the desired effect. 
Finally, especially in the third stage, when impoverishment of the 
blood and general exhaustion furnish the most urgent symptoms, the 
free administration of meat-diet, eggs, wine, and the ferruginous prepa- 
rations is indicated. SECTION III. 
DISEASES OF THE IAEENCIIYMA OF THE L ENG. 
CHAPTER I. 
HYPERTROPHY OP THE LUNG. 
In by far tlie greater number of cases in which the lungs appear to 
be enlarged, their tissue, instead of being hypertrophied, is atrophied 
and wasted—or rarefied, to use a customary expression. Under the 
title of emphysema, we shall treat more fully upon this form of enlarge- 
ment of the lungs in the tliird chapter. 
Rokitansky describes an enlargement of the lung with simultaneous 
increase of tissue, as true pulmonary hypertrophy. This is said to occur 
as a vicarious development of one lung, when the other has been totally 
destroyed. Here the walls of the vesicles are said to be thicker and 
more voluminous, their capillaries multiplied, and their tissue more resist- 
ing, while the vesicles themselves are dilated. 
A second form of hypertrophy of the lung, which Skoda describes, 
and Virchow calls pigmentary induration, consists in an increased vol- 
ume of the pulmonary tissue, at the expense of the air-vesicles. We 
notice it in severe chronic hyperaemia of the lung, particularly in valvu- 
lar disease of the mitral valve, and in hypertrophy of the right side of the 
heart. Here, too, the walls of the vesicles are thickened and their ele- 
ments multiplied, so that, as the lung has not grown larger, the vesicles 
must seem smaller, and the tissues closer and more resistant. The color 
of the tissue is darker and browner, and we notice numerous blackish 
specks in it. This coloring is due to capillary hemorrhages in the tis- 
sues, resulting from the intense engorgement, the pigment which pro- 
ceeds from transformed liematin admitting of demonstration under the 
microscope in the form of brownish and blackish granules, in the inter- 
stitial tissues and in the epithelium of the air-vesicles. 
Either form of hypertrophy of the lung may be suspected to exist 
during life, but neither ever admits of any certain diagnosis. ATROPHY OF THE LUXG. 
105 
CHAPTER II. 
ATROPHY OF THE LUNG. EMPHYSEMA SENILE. 
By atrophy of the lung we mean that attenuation, thinning, and 
gradual wasting of the vesicular 'walls, which results from imperfect 
nutrition of the lung. We most commonly see this wasting of the pul- 
monary tissue in old age, when it is accompanied by atrophy of other 
organs, and by general marasmus. Sometimes the atrophy of the lung 
occurs sooner and more completely than involution of the rest of the 
body, and in these cases the symptoms are more decided. Through 
wasting of their septa, several, and sometimes a great many, of the air- 
vesicles coalesce, and large gaps form, so that, in an aggravated case, 
the entire lung forms a coarse network. The relaxed, bloodless, dry 
tissue feels soft as down to the touch; it is heavily loaded with pig- 
ment, and is sometimes uniformly black. This deposit of pigment is 
not a result of extravasation of blood, but is due to pigmentary meta- 
morphosis of the contents of obliterated capillaries. These nutritive 
derangements of the pulmonary tissue are essentially like those to be 
described in the next chapter, as characteristic of vesicular emphysema 
of the lung, so that the title of senile emphysema is not altogether inap- 
propriate to the disease in question. In senile atrophy, or senile em- 
physema, however, the volume of the lung is diminished, while in em- 
physema, in the stricter sense of the word, it is increased. This impor- 
tant difference, which furnishes a practical distinction between the two 
affections, depends upon the difference in the condition of the thorax. 
The size of the lung manifestly depends upon the capacity of the chest. 
Now, while in true emphysema the thorax is either in a state of chronic 
enlargement, or else in a condition of permanent inflation, in senile 
atrophy the chest is actually contracted, or else it is in a state of per- 
manent expiratory collapse. The thorax of an old man is shortened by 
absorption of the intervertebral substance, and laterally compressed by 
his stooping attitude, and the atrophied muscles of inspiration are inca- 
pable of dilating it effectively. For a similar reason the heart and liver, 
which, in true emphysema, are extensively covered over by the lung, in 
senile atrophy lie in contact with a large part of the thoracic wall. 
This state of the lungs and chest explains why old men become 
short of breath, why their blood is imperfectly decarbonized, and why 
they are so apt to look blue about the lips and cheeks. The shortness 
of breath and the venous state of the blood are due to the diminution 
of breathing-surface by loss of cell-walls, to a decrease in the number of 
capillaries, and, finally, to the incomplete manner in which inspiration is 
effected by the wasted respiratory muscles, and to the absence of that 106 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
important aid to expiration, elasticity of the lung. The cyanotic symp- 
toms occur because the right heart, having fewer efferent channels, 
owing to obliteration of so many pulmonary capillaries, is imperfectly 
emptied, thus causing venous engorgement of the aortic circulation. 
According to this explanation, the more unequally atrophy of other 
organs and general reduction of the volume of the blood keep step with 
the atrophy of the lungs, so much the more marked must the symptoms, 
above described, become. 
As the thin, emaciated, thoracic walls and their flexible ribs are 
easily thrown into vibration, the percussion-sound is remarkably loud 
and full. The dulness over the heart and liver is increased. Upon 
auscultation, the greater the difference is between the capacity of the 
contracted bronchioles and that of the air-vesicles in which they termi- 
nate, so much the harsher is the vesicular murmur. 
Treatment of senile atrophy of the lung is out of the question. 
CHAPTER, III. 
EMPHYSEMxY OP THE LTHSTG. 
By emphysema of the lung is meant either a morbid enlargement 
of the pulmonary vesicles, arising mainly from the blending of several 
vesicles so as to form one great cyst—emphysema vesiculare—or else 
the escape of air into the subpleural and interstitial connective tissue— 
emphysema interlobulare. The latter is analogous to emphysema of 
other organs, such as the subcutaneous areolar tissue; the former, like 
oedema of the lungs, has no analogue elsewhere. 
Etiology.—The opinions of authorities as to the mode of origin of 
vesicular emphysema of the lungs differ materially. Four principal 
theories have been advanced upon the subject. According to the first, 
emphysema arises through immoderate or too protracted inflation of 
the air-cells, by forced and long-continued inspiration—theory of inspi- 
ration. According to the second, likewise, emphysema is the result of 
excessive mechanical distention of the vesicular walls, but is not pro- 
duced by inspiration, but by forced expiration—theory of expiration. 
According to the third, its origin is not mechanical, but it arises from 
nutritive derangement of the lung-substance, which occurs indepen- 
dently of any strain or stretching. Finally, according to a fourth view, 
advanced by Freund, a morbid condition, namely a rigid enlargement 
of the thorax, constitutes the primary disease, to which dilatation of the 
air-cells is only secondary. We believe each view to be true in certain 
cases, but no single one will account for all forms of the disease, and 
consequently adhere to the classification into vicarious and substan- 
tive emphysema. EMPHYSEMA OF THE LUNG. 
107 
Vicarious emphysema arises, first, in all cases in which portions of 
the pulmonary substance become wasted, and shrink without corre- 
sponding reduction of the capacity of the thorax, by collapse of its wall. 
If the capacity of the chest remain constant, the size of the individual 
vesicles which contribute to fill it must, of course, depend upon their 
number. If a portion of them perish, thus reducing the bulk of that 
part of the lung to which they belong, either a vacuum must form in 
the chest, or else the remaining vesicles must dilate. Secondly, vicarious 
emphysema arises where all of the vesicles do not 'participate alike in 
filling out the additional space formed in the thorax by inspiratory 
dilatation. Normally, all the air-vesicles are inflated uniformly by 
atmospheric pressure during inspiratory dilatation of the chest. If, 
then, a part of the air-cells be filled up by exudation or serum, so that 
no more air can enter them, these cells will not dilate during inspiration, 
and hence the remaining and accessible ones must expand for them— 
vicariously—and undergo an abnormal degree of distension. Thus, in 
the bodies of all persons who have died of pneumonia or hypostatic en- 
gorgement, we find vicarious emphysema in the portions of lung spared 
by the original disease. So, too, extensive rigid adhesions between 
the pulmonary and costal pleura give rise to vicarious emphysema. 
Under normal conditions, the air-cells in the apices of the lungs, and 
those placed near the spinal column, although the portion of the thoracic 
wall adjacent to them scarcely takes any part in the inspiratory move- 
ment of the chest, expand equally with the cells in the more movable 
regions of the thorax, and which are situated near to the diaphragm, 
and to the anterior thoracic wall. Of course, for this to take place, the 
adjacent movable parts of the lung must yield and be pushed down- 
ward and forward. Where the costal and pulmonary pleura are firmly 
united, such yielding and displacement become impossible, and the 
vesicles at the apices and along the back-bone cannot fully perform their 
part in occupying the space created in the chest by its inspiratory ex- 
pansion. Hence, other portions of the lung, especially the anterior and 
lower borders, must act for them, and are thus made to undergo an ex- 
cessive and abnormal distention. Finally, chronic catarrh of the smaller 
bronchi is often followed by vicarious emphysema.’ If, in one part of 
the lung, the calibre of the finer tubes be so much narrowed by swell- 
ing, or by accumulation of mucus, that the air enters imperfectly, and 
with difficulty, into the corresponding vesicles, such part of the lung 
will not do its share in filling up the inspiratory expansion of the thorax, 
so that other parts of the lung, which are free from catarrh, must act 
for them, and become abnormally distended. 
From the foregoing representation it is evident enough that the 
“ inspiratory ” theory is a correct one. If vicarious emphysema arise 108 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
acutely during a pneumonia or hypostatic engorgement, the intervesicular 
septa are ruptured. On the other hand, if the affection develop slowly, 
as in a case of adherent pleura, or of tedious catarrh, the vesicular walls 
undergo a gradual atrophy, growing thinner and thinner, and becoming 
perforated, until at length several cells coalesce into one large cyst from 
destruction of their septa. We must decidedly oppose the widely-spread 
impression that the over-distended cell-walls simply lose their elasticity, 
without other change of texture (just as any over-stretched glove or 
caoutchouc-pipe remains permanently enlarged). That an emphysem- 
atous lung has lost its elasticity is true, but the above explanation is 
false. The loss of elasticity is owing solely to the rupture above men 
tioned, or to the gradual wasting of the elastic elements of the tissue. 
Substantive emphysema—that is, a form of vesicular emphysema, 
wherein the enlargement of the pulmonary cells is a more primary and 
independent disease—likewise arises, in many instances, in consequence 
of immoderate and protracted inflation and stretching of the vesicular 
walls. Laennec, who first pointed out the mode of origin of substantive 
emphysema, conceived it to be as follows: If, in consequence of catarrhal 
swelling of the mucous membrane, or owing to viscidity of the bron- 
chial secretion, an obstacle to the passage of air arise in the smaller 
bronchial tubes, such obstacle may be surmounted during inspiration, 
owing to the powerful muscular force by which this act is effected; 
while to expiration, which has fewer auxiliary means at hand, and which 
is effected mainly through the elasticity of the lung and of the thorax, 
and through the counter-pressure exerted by the intestines during inspi- 
ration, such obstacle may prove insuperable. Thus a portion of the air 
is retained in the vesicles. The next inspiratory act adds more, which, 
likewise, is unable to escape completely, so that the vesicles are continu- 
ally becoming more and more over-filled and distended. Two main ob- 
jections have been advanced against this theory: First, it is replied 
that the supposition is erroneous that the auxiliaries to inspiration ex- 
ceed those of expiration—at all events, as regards forced expiration. 
This is true; yet we have already shown that it is chiefly the larger 
bronchi which are emptied by a forced expiratory effort, while it has 
very little action in promoting evacuation of the air-vesicles, especially 
if the bronchioles be obstructed. It is thus that we account for the 
common occurrence of permanent vesicular ectasia of capillary bron- 
chitis. Secondly, it has been urged against the explanation of Laennec, 
that this hypothesis would be satisfactory if the enlargement of the 
pulmonary vesicles were no greater in emphysema than the enlargement 
which they normally undergo in healthy lungs at the height of the in- 
spiratory act, but that it does not account for the abnormal and excessive 
distention of the air-vesicles of an emphysematous lung. This argu- EMPHYSEMA OF THE LUNG. 
109 
rnent ought to have prevented the confusion which exists between per- 
manent inspiratory ectasis and emphysema of the lung. Permanent 
inspiratory ectasis may subside completely; and, indeed, after removal 
of the obstacles to expiration, often does so subside. (These are the 
cases of so-called recovery of emphysema of the authors.) But, if per- 
manent inspiratory vesicular inflation be Jcept up for any great length 
of time, the continuous strain and expansion produce structural 
changes in the vesic/idar walls. They atrophy, grow thin, become per- 
forated, several vesicles blend into one larger cyst, and then emphysema 
really commences. 
This account of the origin of substantive emphysema, from immod- 
erate inspiratory expansion and stretching of the vesicular walls, is not 
applicable to all cases, however, and there are a good many instances in 
which we must give credit to the expiratory theory. It is easy to un- 
derstand how emphysema may arise in the upper part of the lungs as a 
result of often-repeated forcible expiration with simultaneous contraction 
of the glottis. In severe paroxysms of coughing, such as occur in 
whooping-cough and chronic bronchial catarrh, the thorax is vigorously 
contracted, while, at the same time, the escape of air is impeded by con- 
striction of the glottis. In straining, and in playing upon wind-instru- 
ments, the same process occurs. So, too, in lifting heavy weights, and 
in other severe bodily exertions, the air is compressed within the thorax, 
and only allowed to escape at intervals, and with a groaning or panting 
sound. In all these acts contraction of the chest is effected by vigorous 
upheaval of the diaphragm. The result is the expulsion of a strong 
current of air from the lower bronchi, the direction of which is obliquely 
upward, and, if the air be prevented from escaping through the larynx, 
a portion of it, in a compressed state, must be driven into the upper 
bronchi, whose direction is obliquely downward. By the centrifugal 
pressure exerted, by the air thus compressed, upon the vesicles of the 
upper lobes of the lung, and upon the adjacent thoracic wall, the latter 
become distended as far as it is possible for them to yield. In a vigor- 
ous man, whom 1 have had under observation, and in whom the pecto- 
ralis minor and a larger portion of the pectoralis major were absent, I 
have been able to see that, both in coughing and straining, so much air 
was forced into the upper part of the lung as to cause prominence of 
the upper intercostal spaces; and I have often noticed and pointed out 
the same phenomena, though in a lesser degree, in patients with thin 
muscles, and but little subcutaneous fat. 
The occurrence of emphysema, in patients who have not been ex- 
posed to any of the causes hitherto mentioned, is rare, but the fact is 
certain. Hence, in a small number of cases, it would seem that the 
third of the above theories of the origin of emphysema is the correct 110 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
one; according to which, wasting, perforation, and final disappearance of 
the vesicular septa are not always due to a mechanical process, hut may 
proceed from nutritive disturbance, and from other causes at present un- 
known to us. Perhaps most cases of inherited emphysema belong to 
this class. 
The occurrence of rigid dilatation of the thorax as a primary dis- 
ease, causing permanent inspiratory expansion, strain, gradual atrophy 
of the cell-walls, and consequent emphysema, according to the theory 
of Freund, is certainly rare and exceptional. As we shall show by- 
and-by, in a large majority of instances, rigid dilatation of the chest 
and the nutritive disorder characteristic of emphysema occur together, 
and arise from the same causes. I cannot, however, deny having met 
with a few cases which seemed to support the theory of Freund—cases 
in which a marked rigid dilatation of the chest had occurred during the 
period of puberty, without any sign of emphysema, but in which ex- 
treme emphysema had developed a few years later. 
Interstitial emphysema arises from an over-distention and rupture 
of the air-vesicles adjacent to the pleura and interlobular interstices, 
with escape of the air into the sub-pleural and interstitial connective 
tissue. This excessive distention takes place sometimes from very vio- 
lent coughing, like that of whooping-cough, sometimes in cases where 
a large number of air-cells are prevented from taking part in occupation 
of the space created by inflation of the chest. The frequent, though 
somewhat inexplicable, appearance of interstitial emphysema after croup 
is, perhaps, most probably attributable to the bronchitis, which, according 
to JBohn and Gerliardt, constantly complicates laryngeal croup, and 
often causes partial collapse of the lung. 
Predisposition toward emphysema is sometimes congenital. It often 
appears during childhood as a result of whooping-cough (which is almost 
exclusively a disease of that age), as well as in consequence of the fre- 
quent and tedious bronchial catarrhs to which scrofulous and rachitic 
children are so liable. The period of advanced middle life, however, 
furnishes the main portion of emphysematous patients, when the “ ca- 
tarrh sec ” is most prevalent. 
From the above it appears that the exciting causes of the malady 
are chronic inflammation and wasting of the lung, inflammation of the 
pleura, with extensive adhesions, chronic catarrh of the lesser bronchi, 
with contraction of their calibre; frequently-recurring cougliing-fits, 
especially those of whooping-cough and of dry bronchial catarrh; the 
playing upon wind-instruments, and similar procedures; lifting heavy 
burdens, and severe corporeal exertions. In some cases the exciting 
causes are unknown. 
Anatomical Appearances.—The almost universal statement, that, EMPHYSEMA OF THE LUNG. 
111 
upon opening the chest, the emphysematous lungs bulge forcibly out 
of it, is incoirect, or at least inexact. This active projection of the 
lungs from the thorax, when opened, is not the effect of emphysema 
alone, and is only met with in cases where, besides the emphysema, 
there is a wide-spread obstruction of the smaller bronchi, whereby the 
escape of air from the chest is prevented, while, during the last breath 
of the dying patient, the respiratory muscles relax, and the thorax col- 
lapses. True, emphysema is very frequently complicated with capillary 
bronchitis, which is the chief cause of obstruction of the minuter bronchi 
and of the retention of air in the vesicles; and, we may add, that em- 
physema, by- reducing the elasticity of the vesicular walls, and thus 
diminishing their expulsive power, favors the occurrence of permanent 
inspiratory expansion. A very small obstruction in the bronchi of an 
emphysematous lung suffices to hinder evacuation of the air-cells. 
Although the forcible protrusion of emphysematous lungs through 
the opening in the chest is by no means of constant occurrence in em- 
physema, and although it is not due to the latter disease but to one of 
its complications, yet incomplete retraction of the lung, when the thorax 
is opened, is constant and peculiar to this affection. Even where 
there is no complicating contraction nor occlusion of the bronchioles 
(which would likewise prevent retraction of the lungs), emphysematous 
lungs, when removed from the chest, or when merely exposed, remain 
more inflated, and larger than healthy lungs. In order thoroughly to 
comprehend this condition, about which also very erroneous ideas have 
been propagated, we must understand why a healthy lung, upon dissec- 
tion of the thorax, contracts to a certain extent, and then remains with- 
out escape of the rest of the air which is in the vesicles. When, by ex- 
posure of the lungs, upon autopsy, we allow the atmospheric pressure 
to act upon their exterior surface, all air would immediately escape 
from the vesicles, and their walls would collapse like those of an empty 
sack, were it not that their outlets open into those narrow, heavily and 
thickly-walled tubes, the bronchi. Owing to their weight, the bronchi 
soon collapse, and thus prevent further escape of air from the vesicles. 
A simple experiment will demonstrate this fact: If we remove a 
stomach and oesophagus from a body, and, after tying the pylorus, in- 
flate them, only a portion of the air will escape from the stomach after 
we cease blowing, because the heavy walls of the oesophagus collapse 
and oppose its further egress. This would be still more marked, did 
not the elasticity of the air-cells, to some extent, counteract the resist- 
ance set up by the weight of the bronchial wall. The vesicular walls 
of an emphysematous lung are thinner and slighter than those of a 
healthy lung. Besides, they have lost a considerable part of their elas- 
ticity, so that the reason is evident why lungs thus diseased remain 112 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
more puffed up and inflated, when exposed to the atmospheric pressure, 
than do healthy lungs. Since emphysematous lungs, as they do not 
contract, retain about the same volume when the chest is laid open as 
they did when it was closed, we may further understand why, in cases 
of wide-spread and especially of substantive emphysema, in which, 
during life, the dimensions of the lungs had been abnormally large, 
there should also be found an increase in their size, when exposed post 
mortem. This increase in the volume of the lungs, as we shall show 
by-and-by, is the result of an increase in the capacity of the thorax, 
arising in part from depression of the diaphragm, and in part from an 
elongation of the costal cartilages, and a peculiar direction of the ribs. 
If an emphysematous lung were to contract like a normal lung, this in- 
crease in size would disappear if the chest were cut into; actually, 
however, it persists even after the lungs have been removed from the 
body. 
In the circumscribed vicarious emphysema about indurated or 
atrophied parts of the parenchyma, we find groups of tender vesicles, 
varying in size from that of a hemp-seed to that of a pea. They are tightly 
inflated, and always traversed by a delicate network, a remnant of the 
intervesicular septa. The seat of circumscribed vicarious emphysema is 
most frequently at the apex of the lungs. 
When vicarious emphysema has arisen acutely, during a pneumonia 
or hypostatic engorgement, or chronically as in pleural adhesion, the 
affection is limited to the anterior and lower edge of the lungs. This 
will be readily understood, after the explanation of its pathogeny given 
above. On the other hand, where the disease is a result of closure of 
any of the bronchi, the seat of the cellular dilatation is not so constantly 
at the anterior and lower edges, and often occupies the apices and other 
regions. A characteristic of this variety is, that inflated emphysematous 
portions of lung exist alongside of collapsed and shrunken parts. Such 
lungs, when removed from the chest, often present a very irregular con- 
tour, which does not at all correspond with that of the thoracic cavity. 
The emphysematous parts are prominent, and may even appear almost 
bulbous or pedunculated, while the collapsed region is marked by deep 
depressions and rigid bands. If inflated, it of course assumes the shape 
of the cavity of the chest, the hard cords and the pedicles of the bul- 
bous portions retract into the interior, and the projections and lobes 
created by the depressions crowd together. 
If the substantive emphysema arise from forced expiration and con- 
stricted glottis, its seat is always in the upper lobes of the lung and par- 
ticularly in the apices. Where it proceeds from pi'otracted inspiratory 
strain, the vesicular distension is distributed more or less evenly through- 
out the whole organ, and it is a characteristic of this variety, when re- EMPHYSEMA OF THE LUXG. 
113 
moved from the chest, that the lungs maintain their normal contour, in 
contrast to the variety .of vicarious emphysema last described. The 
same conditions obtain, both with regard to the extent of the malady 
and to the maintenance of the natural shape of the lungs, in that form 
of emphysema which arises without mechanical origin, and also in the 
variety whose source lies in a primary ectasis of the thorax. 
If the entire lungs or their upper portions be the seat of emphysema 
of much intensity, the anterior pulmonary walls are pushed far down- 
ward. The left lung often covers the pericardium completely; the 
right reaches down to the seventh rib; the heart, usually much enlarged, 
lies upon the diaphragm in a more horizontal direction. In previous 
editions of this work there are many erroneous statements with regard 
to the position of the heart in emphysema. 
An emphysematous lung feels remarkably soft to the touch, like a 
pillow filled with down. Upon cutting it, a dull, creaking sound is barely 
perceptible. The inflated tissues of acute emphysema are of a strikingly 
bright-red and pale hue; in chronic cases, as a rule, they are exceedingly 
dark, with here and there irregularly-formed black spots, the produce 
of conversion into melanin of hematine contained in the former capil- 
laries. 
Even to a superficial glance, the vesicles are seen to be greatly en- 
larged, sometimes to the size of a pea or bean, and are of irregular 
shape. Upon closer examination (of a dried specimen especially) in 
acute cases, we find, traversing most of the large cysts, a few delicate 
bands, as vestiges of the lacerated interalveolar septa. In mild de- 
grees of chronic emphysema, we find perforations of the septa, varying 
in size and number; in severer cases, the walls are reduced to the con- 
dition of solitary ridges. At first, the atrophy is limited to the septa 
between the vesicles of one infundibulum; but afterward the vesicles 
of one infundibulum blend with those of its neighbors, by wasting of 
the intervening walls; until at last, in the worst stages of the disease, a 
large part of the pulmonary tissue is converted into a coarse network. 
As many of the capillaries perish with the septa, the emphysematous 
tissue is remarkably bloodless and dry. 
Interlobular emphysema forms small cysts, full of air, beneath the 
pleura, which causes the latter to seem as if lifted by froth. These air- 
bubbles may be displaced by pressure, thus furnishing an easy means 
of distinction between vesicular and interlobular emphysema. This dis- 
placement, however, cannot be produced uniformly in all directions, but 
only in lines which mark the boundaries of the lobuli. Single lobules 
are often enclosed, like islands, by a narrow border of minute vesicles. 
This fact alone suffices to refute the assertion of certain French authors, 
that, in vesicular emphysema, the air is not enclosed in the air-cells, but 114 
DISEASES OF TIIE PARENCHYMA OF THE LUNG. 
in their interstices. There is no intervesicular connective tissue in the 
lung1, it exists only between the lobules. More rarely there are larger 
cysts by which the pleura is extensively separated from the lung, and it 
scarcely ever happens that the pleura itself at last gives way, allowing 
air to enter its cavity, or that the air beneath the pleura penetrates 
along the roots of the lungs into the areolar tissue of the mediastinum, 
and thence to that beneath the skin, producing emphysema of the sub- 
cutaneous cellular tissue. 
Symptoms and Course.—Circumscribed, vicarious emphysema, in 
the vicinity of portions of withered and shrunken lung, cannot be recog- 
nized during life, and has more pathological and anatomical than clinical 
interest. 
The more slowly a person has died, the more distinct the symptoms 
of extensive hypostasis have been, the more forcibly the thorax has been 
expanded in the death-agony, so much the more surely may we expect 
to find an acute vicarious emphysema of the anterior and lower pul- 
monary borders at the autopsy. 
The symptoms of extensive vicarious emphysema and those of sub 
stantive emphysema are very similar to one another, as the most promi- 
nent characteristics depend upon a more or less advanced wasting of 
the intervesicular septa, a nutritive derangement common to either 
form. 
By-and-by we shall briefly adduce the points upon which we base a 
differential diagnosis between vicarious and substantive emphysema. In 
many instances the two forms cannot be distinguished from one another 
during life. 
With the enlargement of the air-cells, and the destruction of many 
of the septa, a large number of capillaries have also perished, and the 
breathing-surface is materially diminished. The more points of contact 
the air finds with the blood, so much the more favorable are the condi- 
tions for interchange of gases. On the other hand, the smaller this sur- 
face is, so much the more incompletely, casteris paribus, is the elimina- 
tion of carbonic acid and imbibition of oxygen carried on. The loss of 
the alveolar septa, and the attenuation of the pulmonary tissue is, there- 
fore, the first important factor in the dyspnoea from which emphysem- 
atous persons suffer. A sufficient renovation of the air contained in 
the air-vesicles is as essential to the normal performance of the oxygena- 
tion as is a due extent of respiratory surface. If the thorax and lungs 
do not expand properly during inspiration, or if they contract imper- 
fectly during expiration, the air within the air-cells is not sufficiently 
renewed, and neither can the carbonic acid formed within the body be 
eliminated from the blood, nor can the latter obtain the oxygen required 
by the system. EMPHYSEMA OF THE LUNG. 
115 
That respiratory expansion and contraction of the lungs are embar- 
rassed in emphysematous persons, has been maintained by most authors, 
and they, moreover, have connected the fact with the loss of elasticity 
of the pulmonary tissue; but, on the one hand, they have not suf- 
ficiently understood that the loss of the elasticity of the lung is due to 
certain changes in its structure, that it is dependent simply upon attenu- 
ation of the parenchyma, and loss of the elastic elements of the tissue; 
on the other hand, they have circulated many inaccurate and false 
notions as to the mode in which the respiratory motions are affected by 
decreased elasticity of the lung, so that it behooves us to study this 
influence more closely. It need hardly be mentioned that the inspira- 
tory enlargement of the thorax, by which alone expansion of the lung is 
effected, cannot possibly be impeded by the diminished elasticity of the 
lungs. The inspiratory muscles, among other obstacles, have to over- 
come this pulmonary elasticity. Hence, should this be diminished, in- 
spiration cannot be embarrassed thereby; on the contrary, it should 
now proceed with greater ease than under normal conditions. It is 
much harder to decide the question whether, how, and how much 
decreased resiliency of the lung can interfere with expiratory contrac- 
tion of the thorax. In the first place, when we look at the thorax 
proper, it seems unlikely that the ribs and the sternum need the suction 
of the elastic lung in order to return from their inspiratory to their ex- 
piratory state. The weight of the chest-walls and the spring of the 
ribs, winch is overcome during inspiration by muscular action, seem to 
be quite enough to neutralize the inspiratory expansion of the thorax, 
when this muscular action is suspended. Experiments, which I have 
caused to be made upon the bodies of adults, have at least shown that, 
after perforation of the intercostal spaces, and after entrance of air into 
the pleural cavity, the thorax does not enlarge.* 
There could not fail to be such an expansion, if the traction of the 
elastic lung contributed to the establishment of the position of expira- 
tion ; since, in these procedures, the suction, which it produces upon the 
inner wall of the thorax, is suspended upon the entrance of air into the 
pleural cavity, and the collapse of the lung. Hence, as, in spite of em- 
physema, and in spite of the decreased elasticity of the lung, the thorax 
is still able to return to its expiratory state, as it needs no aid from the 
lungs to accomplish this, an emphysematous lung cannot afford any re- 
sistance to the contraction of the chest. It is very remarkable that we 
see mention made, in most pathologies, of a pressure made by emphysem- 
atous lungs against their neighboring parts, particularly of a displace- 
* In children this may be otherwise. From the greater flexibility of their thorax, 
it is not improbable that it is drawn inward during expiration by the draught of the 
elastic lung, and is contracted more by this means than by the spring of the ribs. 116 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
ment of the heart by the lungs, or of depression of the diaphragm and 
liver. If an emphysematous lung did indeed exercise a pressure inward 
and downward, did it really dislocate the heart and the liver, it is to be 
presumed that this pressure would also act outward upon the inner wall 
of the chest, and oppose an obstacle to its contraction during expiration. 
The supposition of centrifugal pressure of an emphysematous lung1 
against its neighboring parts is due, partly to erroneous physiological, 
pathological, and anatomical assumptions, and in part to confusion of 
emphysema with that condition which we have described as permanent 
inspiratory expansion of the air-cells, and upon whose distinctness from 
emphysema we have already insisted.* 
This demonstration will serve to show that emphysema has no 
influence in impeding either the inspiratory expansion, or the expira- 
tory contraction of the thorax proper. The respiratory movements of 
the diaphragm, however, are very differently affected, in this respect, 
from the movements of the ribs. The diaphragm, which descends dur- 
ing inspiration upon relaxation of its muscles, returns to its inspiratory 
position, partly through the upward pressure of the abdominal viscera, 
partially by the traction of the elastic lung upon its upper surface; but 
it can easily be proved that the latter force plays the most important 
part in this process. In those cases of very relaxed abdominal walls 
occurring after repeated pregnancy, where all pressure upon the dia- 
phragm on the part of the abdominal viscera is out of the question, the 
diaphragm still ascends during expiration, nay, as long as the thorax 
remains closed, it preserves this position in the cadaver, even after all the 
viscera of the belly have been removed. It does not relax and sink until 
the thorax is • opened, because the suction of the lung, upon its upper 
surface, does not cease until then. Hence it is clear that the loss of 
elasticity, which the lung suffers by emphysematous attenuation of its 
tissues, may considerably impede the return of the diaphragm to its 
expiratory state, and sometimes may completely prevent it. Thus the 
cooperation is lost of the most important muscle of respiration, upon the 
tree exercise of which the expansion and contraction of the chest, and 
with it the renovation of air in the vesicles, mainly depend; and we 
may designate, as the second great factor of the dyspnoea of enqthysem- 
atous persons, the permanently inflated condition, or, as more com- 
monly is said, the permanently depressed state of the diaphragm. 
To these, however, in many cases, if not in all, a third cause is to be 
added. In many emphysematous patients the structural alteration of the 
* Iii the permanent inspiratory expansion of the air-cells, resulting from obstruc- 
tion of the more minute bronchi, the air, which is confined in the cells, and com- 
pressed during expiration, does indeed hinder the thorax from returning to its normal 
condition of expiration. EMPIIYSEMA OF TIIE LUYG. 
117 
mng is complicated with deformity of the costal cartilages, to which 
Freund first called attention in his valuable work. This deformity con- 
sists in a hypertrophy, by which each cartilage gains in volume in all 
directions simultaneously, assuming a remarkably firm, brittle, rigid 
character. By elongation of the costal cartilages, not only is the ster- 
num driven farther from the ends of the bony ribs and pushed forward, 
but the ribs are moved upward and outward, and twisted upon their 
long axes in the same manner as they are turned about their axes dur- 
ing inspiration by the traction of the inspiratory muscles. As, however, 
the hypertrophied costal cartilages have become rigid, the thorax can- 
not return to its expiratory state, from this inspiratory ectasis, which 
may much exceed the largest degree of inspiratory expansion which the 
thorax can ever normally attain. A condition arises which Freund very 
aptly calls “ rigid dilatation of the thorax.” I believe that Freund goes 
too far in assuming the alterations of the costal cartilage to be the 
primary disease, and the structural change of the lung to be secondary. 
In a very few cases at most, principally cases of inherited emphysema, 
does this sort of genetic connection seem somewhat probable. 
In the majority of instances, as before said, it would seem to be 
only a complication. True, it is not an accidental one. It would rather 
appear that the same evils which effect the structural changes in the 
lungs also cause hypertrophy and degeneration of the costal cartilages. 
From its analogy to hypertrophy, and to alteration of other bodies, par- 
ticularly to degeneration of the arterial walls, which is of inflammatory 
origin, or at least depends upon processes related to inflammation, we 
may suppose that this alteration of the costal cartilages is a result of 
repeated injury from distention and straining. When emphysema arises 
from forced inspiration, or from forced expiration, with closure of the 
glottis, from violent coughing, or through playing upon wind-instru- 
ments, the ribs also are expanded and strained, and the structural changes 
mentioned above develop in them in consequence of this irritation. If 
forced inspiration have produced the emphysema, the alteration of the 
costal cartilage is general. When forced expiration vTith constriction 
of the glottis is its cause,' the alteration is confined to the upper ribs. 
Finally, costal hypertrophy and rigid dilatation of the chest, as a rule, 
do not take place at all where the emphysema does not appear until 
late in life, after the cartilages have become ossified. The importance 
of the part played by this rigid thoracic dilatation in many cases of 
emphysema is shown, among other W’ays, in our not unfrequently ob- 
serving patients, vrhose dyspnoea decreases when they lie upon their 
bellies, and thereby compress the thorax; and others whose sufferings 
are greatly relieved by exerting a lateral pressure upon the lower part 
of the chest. In such patients I have frequently been able to observe, 118 
DISEASES OF THE PARENCHYMA OF TnE LUNG. 
during life, that, in order the better to compress the thorax during expi- 
ration, they contracted the triangularis sterni, and the upper part of the 
transversus abdominis, and the expiratory gullies in the liver, first accu- 
rately described by Liebermeister, could be seen upon autopsy. When 
rigid dilatation of the thorax is associated with structural change of the 
lung, it constitutes a third factor in the dyspnoea of emphysematous 
persons. 
The entire aspect of the patient betrays obstruction of the respira- 
tion, oppression, dyspnoea, and want of air. They summon all their 
force to open out their thorax; the alee nasi play; the lower part of 
the neck becomes harder and broader from the energetic contraction of 
the scalini with every inspiration. Frequently, and chiefly in the in- 
stances in which the costal cartilages are ossified and their joints atro- 
phied, the forms of the sterno-cleidomastoidei stand out like hard cords. 
The muscular relaxation, the flabbiness, the apathy, which we perceive 
in all patients of this class, are due to imperfect decarbonization and re- 
tarded oxygenation of the blood. When to these constant hinderances 
to respiration a fourth one is added, as when the bronchi are contracted 
by an aggravated catarrh, the dyspnoea rises to an extreme pitch. 
Patients pass entire nights in their arm-chairs, fearing to choke if they 
should lie down. The complexion becomes ashy and muddy, the ex- 
pression of the eye fatigued, the sensorium benumbed, the pulse and 
heart-beat small and irregular, the extremities cool; the manifestations 
of surcharge of the blood with carbonic acid increase to those of acute 
poisoning by this pernicious gas. Before the days of Lciennec, such 
attacks, which recur with greater or less violence and frequence in all 
emphysematous persons, used generally to be considered and described 
as nervous asthma. 
The derangements of circulation which are produced by the ana- 
tomical changes in the pulmonary parenchyma of emphysematous pa- 
tients present a second series of symptoms. With the disappearance 
of the interalveolar septa and the loss of the numerous capillaries, the 
number of efferent channels from the right side of the heart is dimin- 
ished. It follows hence, in the first place, that in that portion of the 
lung spared by the emphysema—usually its lower part—the pressure 
of blood is increased, and it becomes the seat of intense liypenemia, 
and that chronic catarrh takes place in its bronchi, and often chronic 
oedema in its alveoli. Now, we might suppose, the number of capil- 
laries which remain not being sufficient to receive the contents of the 
right ventricle, that the right ventricle, its auricle, and the veins of the' 
aortic circulation would be overloaded with blood, and that cyanosis 
and dropsy would accompany very extensive emphysema. No indica- 
tion, however, of any of these symptoms is usually observed for a long EMPHYSEMA OF THE LUNG. 
119 
time, and if, from time to time, upon aggravation of the bronchial ca- 
tarrh, oedema and cyanosis set in, the symptoms subside as the catarrh 
improves, a proof that the circulatory disturbance depends upon the 
transitory aggravation of the catarrh. The same causes operate in re- 
tarding derangement of the aortic system in emphysema, which often 
so long avert the appearance of cyanosis and dropsy in valvular disease 
of the mitral. In proportion as the circulation becomes embarrassed, a 
complication develops in the right side of the heart, which has the oppo- 
site effect, which counterpoises and compensates for the circulatory im- 
pediment—namely, hypertrophy of the right ventricle of the heart. 
The addition of symptoms of venous derangement about the vena cavae 
does not take place in emphysema until this compensation begins to fail 
through a gradual degeneration of the thickened heart-wall by fatty 
metamorphosis of its muscular fibre. Then the jugular veins swell up 
and throb, with every ventricular impulse, as the vibration, into which 
the valves of the tricuspid are thrown during the systole of the right 
ventricle, is shared by the column of blood which rests upon it. (See 
chap., mitral insufficience.) The face becomes cyanotic, the lips swell 
up and become blue, the cheeks and aim nasi have a varicose appear- 
ance. The obstructed evacuation of the cerebral veins makes the patient 
complain of dizziness and headache. All the signs attain their highest 
pitch when the patient coughs. Symptoms of engorgement in the 
course of the ascending vena cava also set in. The liver swells because its 
outflow of blood is impeded, and the engorgement extends through the 
portal system to the gastric and intestinal veins, giving rise to gastric 
and intestinal catarrh. In the same manner, the veins of the rectum 
often enlarge into varices (blind piles). The latter circumstance is 
almost always greeted with joy by the patient. They believe that they 
have now found the centre, the main root of all their trouble, and are 
all-hopeful for a cure from the critical hremorrhoidal flow, just as they 
are misled by the gastric catarrh, and the loss of appetite which attends 
it, to regard the stomach as the source of their troubles, and to call their 
cough a “ stomach-cough.” 
In the latter stages of emphysema the cyanosis often becomes ex- 
tremely intense. The cheeks, ears, lips, and tongue of the patient are 
literally blue. In no other disease does the cyanosis attain such severity, 
excepting in cases of disorder of the orifices of the right heart, which 
are mostly pongenital, and it is never met with in valvular disease of 
the left ventricle. True, in the latter, the patients generally grow blue 
about the lips and cheeks, but the general color of the countenance 
remains pale, and the blueness is never so pronounced as in emphysem- 
atous persons, or in such as have congenital heart-disfease of the right 
side. This fact, which hitherto has received too little attention, is easy 120 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
of explanation. In valvular affections of the left heart the pulmonary 
circulation is surcharged with blood, w hile the quantity of blood in the 
aortic system is abnormally small. On the other hand, in emphysema 
where many of the pulmonary capillaries have perished, and in con- 
genital malformation of the right heart where the ventricles are usually 
ill developed, or have their orifices contracted, it is the greater circula- 
tion which is overloaded, and the smaller which contains too little 
blood. 
This obstructive engorgement of the great veins extends also to the 
thoracic duct. When the subclavian vein is filled to distention, the flow 
of lymph and chyle must encounter a resistance equal to that opposed to 
the current of any other vessel wThich empties into the subclavian. 
Nay, if lymph be the source of the fibrin in the blood, we see, upon 
simply physical grounds, why the blood of emphysematous patients is 
poor in fibrin, why the “ venous crasis prevents hyperinosis and increase 
of fibrin.” Restricted afflux of chyle must, moreover, prejudice nutri- 
tion both of the blood and of the entire organism. It is one of several 
causes which contribute to the general emaciation and to the premature 
marasmus of emphysematous persons ; perhaps, too, it may account for 
the lack of albumen in the serum of the blood, which produces a ten- 
dency to the establishment of dropsical symptoms. 
As soon as the circulatory derangement ceases to be properly com- 
pensated for, symptoms of insufficient afflux of blood into the left side 
of the heart add to those of venous engorgement. Incomplete filling 
of the left heart produces a small pulse, a pallid complexion, and finally 
distinct diminution in the urine, as the amount of the urine depends 
chiefly upon the filling of the renal arteries and glomeruli of the mal- 
pighian capsules. The scantily secreted urine is concentrated, thick, and 
dark; the urates, which require a great deal of water for their solution, 
precipitate with readiness, in the form of a brickdust-like sediment. 
Precipitation of the urates is not due to concentration of the urine alone, 
nor to a relative increase in the quantity of the salts, but it may also 
depend upon their absolute increase, upon the formation of uric acid 
at the expense of the urea, the scanty supply of oxygen being insuf- 
ficient to oxydize the nitrogenous products of the transmutation of tissue 
so as to produce urea, but only to such a lower degree as to give uric 
acid. 
All other symptoms attributed to emphysema belong to its compli- 
cations. The cough is a symptom of the chronic bronchitis, and often 
disappears altogether during the summer, while the emphysema con- 
tinues as usual. In by no means all cases does physical examination 
give any fixed basis for the recognition of emphysema, and, when of 
small extent, its existence cannot ever be physically proved. EMPHYSEMA OF THE LUXG. 
121 
Inspection, with regard to the formation of the thorax, may give a 
negative result even in very intense emphysema. Individuals with a 
loose, long, so-called paralytic thorax often enough suffer greatly from 
the disease. This will not seem strange after our having shown that 
emphysema has no effect upon the expansion or contraction of the 
thorax proper. In some cases, indeed, the thorax shows characteristic 
abnormities, upon which we have founded the idea of a peculiar form 
of the chest, “ the emphysematous thorax.” In this the circumference 
and the depth, particularly in its upper and middle portion, are consid- 
erably increased. 
Instead of presenting a broken line, the sternum forms a segment of 
a circle; the upper ribs are abnormally crooked, and bulged outward ; 
the shape of the thorax is more spherical or barrel-shaped. It is remark- 
able that absolutely erroneous views as to the mode of origin of the 
emphysematous thorax have prevailed, while the real manner in which 
it is produced is as clear and simple as possible. The deformity of the 
chest is not produced by the emphysema of the lung, for both emphy- 
sema and deformity arise from the same causes. The emphysematous 
thorax is only seen in that species of the disease which arises from 
forced expiration with constricted glottis, as when playing upon wind- 
instruments, coughing, etc. By these acts the diaphragm is forcibly 
driven up by pressure of the abdominal muscles upon the viscera of the 
belly, and the air contained in the lung is strongly compressed. Ac- 
cording to simple physical laws, as long as the costal cartilages retain 
their pliability, the thorax, like any other cavity with yielding walls, 
must become rounded and approximate to the spherical form, wherever 
the pressure upon it from within is augmented. But as the lower part 
of the thorax, to which the abdominal muscles are attached, is fixed, it 
cannot join in the rounding out of the middle and upper portions, and 
this explains why the emphysematous thorax is more barrel-shaped than 
spheroidal. By very deep inspirations, indeed, we can temporarily ex- 
pand the chest to a considerable extept, but the thorax of a healthy 
man in full inspiration is differently shaped from a so-called emphysem- 
atous thorax. We may, for a short time, produce the latter in ourselves 
by making the strongest possible expiratory effort, while at the same 
time holding the nose and mouth. The sole reason for the permanence 
of this condition in emphysematous persons is the hypertrophy and 
alteration of the costal cartilages mentioned above. But this deformity 
of the chest, called par excellence emphysematous thorax, is not the 
only one observed in emphysema. In the cases in which emphysema 
develops in consequence of long-continued forced inspiration, we do not 
find this rounding of the upper and middle portions of the chest, in 
which the lower takes no part; but we find the lower portion dilated, 122 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
and in a permanent inspiratory condition. The augmented contractility 
of the hypertrophied muscles of inspiration may contribute in some de- 
gree to this perpetual condition of dilatation, but it no doubt mainly 
depends upon the disease of the costal cartilages so often referred to. 
Inspection, in many cases of emphysema, further reveals that, with 
every violent cough, a tumor projects through the upper aperture of the 
thorax at the side of the neck, which disappears immediately upon the 
cessation of the coughing-fit. I have recently satisfied myself that this 
tumor very rarely consists of the apex of the lung, which, with the 
pleura, has been driven into the space between the first rib and the 
neck by the violent pressure of the diaphragm, which, as it were, makes 
the chest too small. In the great majority of cases, these tumors are 
formed by enormous enlargements of the sinus of the jugular veins 
which fill up during the cough and empty themselves again when it 
ceases. 
Finally, upon inspection, and, still better, upon palpation, we can 
perceive a strong concussion of the epigastrium, which is synchronous 
with the pulse, and which extends to the lower part of the sternum 
and of the adjoining ribs. This concussion has been usually ascribed to 
the shock of the apex of the heart, displaced toward the middle fine of 
the body, but I agree with Bamberger, that such displacement is 
neither proved by facts nor even physically possible. This concussion 
of the epigastrium is not directly dependent upon emphysema, but 
is due to hypertrophy of the right heart, which complicates that dis- 
ease, and it is found in all considerable cases of hypertrophy, espe- 
daily of the right heart without emphysema. (See Hypertrophy of 
Heart.) Even when the heart of an emphysematous patient has be- 
come considerably enlarged, the shock of its apex is imperceptible, the 
lung having become interposed between it and the thoracic wall. 
Sometimes, however, besides the concussion of the epigastrium, a feeble 
heart-shock is perceptible at a point farther downward and outward 
than is normal. That the apex ris displaced downward, is simply owing 
to the depression of the diaphragm, upon which it rests. But it is not 
only the apex of the heart, but its base too, which rests upon the dia- 
phragm, and, indeed, upon the very part of it which descends the 
furthest in cases of its abnormal depression (farther, at least, than the 
point upon which the apex lies). Hence, as a natural consequence of 
depression of the diaphragm in emphysema, the oblique position of the 
heart becomes more horizontal, and its apex lies farther out. 
Percussion affords an almost certain basis for diagnosis where em- 
physema is of considerable extent. However, we must not expect the 
sound to be unusually loud or full in all cases, as, if the resistance of 
the thoracic wall be augmented, even though the vital capacity of the EMPHYSEMA OF THE LUNG. 
123 
lungs be increased, no very active vibrations, capable of producing any 
very loud or full resonance, can take place. Neither does the sound 
upon percussion become tympanitic, unless there be complications 
through which the pulmonary tissue entirely loses its elasticity. The 
tympanitic ring is a result of regular vibrations. If we make percussion 
upon a bladder, the walls of which are tightly stretched by inflation, the 
sound is not tympanitic, for the compression of the air, which is aug- 
mented or diminished every moment by the vibrations of the Avails, pre- 
A'ents the occurrence of regular vibrations. It is precisely the same in 
a lung, which has become but a cluster of inflated cysts. The tension 
of the alveolar walls generally remains sufficient, even in very intense 
emphysematous disease of the lungs, to prevent the occurrence of reg- 
ular A'ibrations. The only characteristic symptom of the disease, fur- 
nished by percussion, is abnormal extent of the full, clear sound of the 
lungs, as this pro\Tes that the diaphragm is depressed, which, as Ave have 
seen, is a necessary consequence of emphysema. While under normal 
conditions, the percussion-ring, corresponding to the loAver limit of the 
right lung, reaches to the sixth rib at the right mammillary line, and 
passes over at this point into the dull percussive-sound of the liver, 
Avhich here lies against the Avail of the chest. In severe emphysema, 
the right lung pushes back the border of the liver considerably; and 
Ave sometimes hear clear percussion-sound almost as far doAvn as the 
loAver edge of the arch of the ribs. Upon the left, the dulness pro- 
duced upon percussion over the heart commences normally at the level 
of the fourth costal cartilage. In Avell-marked emphysema of the left 
lung it spreads doAvmvard, often to the sixth costal cartilage, and in 
the most extreme cases the heart is so completely covered by the lung 
that the cardiac dulness has disappeared. 
In auscultation, we must discriminate betAveen the phenomena proper 
to the emphysema and those which are to be placed to the account of 
the accompanying bronchial catarrh. As a rule, it is said that the 
A'CSicular breathing is feeble or inaudible, in striking contrast to the in- 
tense percussive resonance. This assertion, howeATer, is only so far cor- 
rect in that, as a rule, besides the emphysema, there is usually a catarrh 
of the minuter bronchi. At the points Avhere these complications coex- 
ist, Ave usually, indeed, hear notliing but rhonchi and fine moist rales, 
or, at the utmost, very feeble vesicular breathing. At points, hoAvever, 
AA’here there is no catarrh, where the air passes freely from the bronchi 
into the dilated cells, the respiratory murmur is generally remarkably 
loud and hissing. It is very commonly found that Ave can only hear 
rhonchi and rdles in the loAver lobes of the lungs; and in a manner strik- 
ingly in contrast with this, particularly at the anterior Avail of the chest 
in the neighborhood of the sternum, the respiration is loud and hissing. 124 
DISEASES OF TIIE PARENCHYMA OF THE LUNG. 
This circumstance, which we had attributed to the collateral oedema 
of the healthy portion of the lung, which is usual in emphysema, is 
ascribed by Seitz, of Giessen, in some degree, to the descent of the 
secretion by gravitation from the upper to the lower regions of the lung 
(a theory which has much to recommend it). The murmurs sometimes 
audible in the heart, even where there is no valvular disease, are to be 
considered in treating of degeneration of the heart; but I may say that 
I fully corroborate the observation of Seitz, that the heart-sounds, though 
remarkably feeble at the level of the third and fourth ribs, where the 
organ is covered by the lungs, are very audible at the epigastrium. The 
explanation is manifest. 
The disease may commence in childhood, and continue throughout 
life. Many emphysematous persons reach even an advanced age, al- 
though their troubles grow with their years, the dyspnoea augmenting, 
the asthmatic attacks increasing in violence and frequency. The suf- 
ferers are never cured. If they feel better in summer, this is because 
of the remission of the accompanying catarrh, and the decrease of the 
dyspnoea, as far as it depends upon these complications. The part which 
chronic catarrh plays, not only in the dyspnoea, but in the cyanosis and 
dropsy of the emphysematous, is, as we have repeatedly explained, a 
very considerable one. Death finally takes place (if the patients do not 
meanwhile succumb to an intercurrent malady), with the symptoms of 
marasmus or of general dropsy. The patients very rarely die of an 
asthmatic attack. 
Diagnosis.—Emphysema of small extent cannot be diagnosticated 
with certainty. Cases of considerable severity, which lead to violent 
dyspnoea and cyanosis, are easily to be distinguished, by physical ex- 
amination, from other conditions which give rise to those symptoms. 
Of the distinction between pneumo-thorax and emphysema we shall 
speak hereafter. 
For the differential diagnosis between vicarious and substantive em- 
physema, the history of the case and the physical signs—in some cases 
at least—furnish ground. If the emphysema have developed after a 
pneumonia or pleurisy, if no particularly violent cough have preceded 
it, or if the patients distinctly affirm that the shortness of breath is of 
earlier date than the cough, we may infer, with a certain degree of confi- 
dence, that a partial wasting of the' lung or adhesion of the pleura has 
occasioned a vicarious emphysema in the anterior and lower part of the 
lung, spared by the atrophy, or that the disease depends upon a primary 
structural wasting. On the other hand, should we find emphysema in 
a person who has been a musician or postilion, who boasts of having 
played well, and of having been able to keep up the note for a long 
while, or if the shortness of breath have arisen after whooping-cough, EMPHYSEMA OF THE LUNG. 
125 
or a tedious catarrh accompanied by violent cough, the presumption is 
warranted that we here have to deal with a substantive emphysema. In 
like manner, a permanent inspiratory state of the thorax argues for the 
former, the barrel-shaped chest more for the latter form of emphysema. 
Prognosis.—The prognosis as to life is, upon the whole, favorable. 
A fatal termination of the disease is rare, and then only occurs after 
long duration. Indeed, it cannot be denied that emphysema sets up a 
certain degree of protection, if not absolute immunity against tuber- 
culosis, depending either upon the “ venous crasis,” or upon the blood- 
lessness of the lung, especially at its apex. Emphysema complicated 
by pneumonia (a somewhat unusual occurrence) should excite our solici- 
tude, lest the pneumonic exudation be not reabsorbed, but should desci- 
cate, and afterward break down, together Avith the cell-Avall, after under- 
going cheesy metamorphosis. (See Croupous Pneumonia.) Prognosis 
as to complete recovery is altogether unfavorable, as shown above. 
Treatment.—The causal indication requires judicious treatment of 
the bronchial catarrh, whooping-cough, etc., so as to set bounds, at least, 
to the progress of the emphysema, though a cure be impossible. In raw 
weather, and in winter, Avhen the temperature is low, make emphysem- 
atous persons keep constantly in their chamber. Observant patients are 
sometimes able to tell precisely what degree of cold is hurtful to them, 
and forbids their going out. To meet the indicatio morbi, the periodical 
administration of emetics has been advised. The object Avas to com- 
press the distended vesicles through the pressure exerted upon the lung 
by active vomiting and retching, in the hope that frequent repetition 
of the process might effect gradual decrease in their size. By others, 
tonics are recommended, to brace the relaxed pulmonary tissue and make 
the alveoli smaller. These, and many other proposed modes of medica- 
tion equally naive, and quite as false in principle, do not deser\re the 
least confidence as radical “ cures ” of emphysema. The nutritive alter- 
ations upon which the disease depends are irreparable, and Ave are totally 
unable to fulfil the indications for the disease itself. 
The symptomatic indication, first of all, requires proper treatment 
of the bronchial catarrh, Avhich almost always accompanies emphysema, 
and greatly adds to the distress of the patient. Habitual Avearing of 
flannel next the skin, stimulants to the chest, Avarm baths of Avater or 
vapor, the alkaline muriatic mineral springs, especially the thermal 
springs of Ems, and other similar treatment, are often signally benefi- 
cial for a Avhile, but their action is all due to their timely application 
against that serious complication, the dry catarrh. The use of iodide 
of potassium is especially efficacious in these cases. 
The next symptomatic indication is to moderate habitual shortness 
of breath of the patient and the attacks of severe dyspnoea, for bre\rity’s 126 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
sake, called asthma. In order to allay the persistent oppression of the 
chest, it is very desirable to send the patient for the summer to the pine- 
wood region, and particularly to places where there is a heavy fall of 
dew. The benefit which they derive in this highly-oxygenated atmos- 
phere is always warmly extolled by them. From experiments made 
with apparatus for inhalation of compressed air, the effect of this unfor- 
tunately somewhat costly remedy, both upon the avidity for air and the 
general health of emphysematous patients, is excellent, although only 
palliative. Many of the patients “feel like new men” while in the 
machine. The explanation of the improvement is easy. We have 
already stated our views of the main element in the benefit derived 
from inspiration of compressed air. 
To avert the asthmatic attacks, the patients must observe a strict 
diet, avoid food likely to induce flatulence, eat little before going to 
bed, and keep the bowels open daily. For the latter purpose, the pul vis 
liquoritiae compos, is a mild and efficient cathartic. During the attack, 
beware of mistaking the blunted sensibility and other “ head-symptoms ” 
for the effects of venous engorgement of the brain, and thus bleeding 
the patient. The symptoms of carbonic-acid poisoning would only be 
promoted by depletion. The narcotics, too, especially opium, must be 
used with caution in these attacks of emphysematous asthma, unless 
called for by bronchial spasm. The more suitable remedies (besides the 
emetics, which are very appropriate) are the stimulants, camphor, musk, 
benzoin, and the large doses of port wine proposed by Waters ( 3 j— 
3 iss every three hours), and when these fail, the use of turpentine 
( 3 i to | ss every three hours) in an aromatic water. 
For the dropsy, as has already been stated, whenever it depends 
upon a capillary bronchitis, I have repeatedly produced excellent results 
by means of vigorous diaphoresis. Later in the disease, when dropsy 
arises from failure of the heart to compensate for the circulatory de- 
rangement of the lungs, it may be relieved for a time by the use of 
digitalis (an infusion 3ss—3 j to water 3 vj), just as in dropsy from 
valvular disease of the heart. Where digitalis fails, squills sometimes 
does excellent, though merely transitory, service. (Acet. sillae. 3 j; pot. 
carb. q. s. ad. saturationem. Aquas destillat. § vj. HI. S. a tablespoonful 
every two hours.) 
CHAPTER IV. 
DIMINISHED CAPACITY OP THE AIR-CELLS—APNEUMATOSIS—ATELECTA- 
SIS—COLLAPSE—COMPRESSION OP THE LUNGS. 
Etiology.—There are conditions under which the capacity of the 
air-vesicles decreases and their walls finally come into contact. This COLLAPSE OF THE LUNG. 
127 
fitter state, which is normal during foetal life, may persist in portions of 
the lung after birth. It is then called congenital atelectasis. In other 
cases the air is absorbed, at a later period, from a number of the vesicles, 
which then collapse. This is called acquired atelectasis, or collapse of 
the lung. In other instances the air is expelled from the vesicles by 
external pressure. We then speak of compression of the lung. Con- 
genital atelectasis is most frequently found in feeble children, particu- 
larly those who have been born prematurely, or who have come into the 
world in a state of apparent death after tedious labor. It would seem 
as though air-vesicles, which do not become filled with air immediately 
after birth, are subsequently more difficult of inflation, so that children, 
which are not induced to cry, and thereby caused to make deep inspi- 
rations during the first hours of their life, very commonly suffer from 
atelectasis. In other instances a catarrh, either congenital or contracted 
in the first hours of life, seems to have given rise to atelectasis by con- 
tracting or occluding some of the bronchi, and thus impeding the sup- 
ply of air to the vesicles to which they lead. Collapse of the lung, or 
acquired atelectasis, is always connected with acute or chronic bronchial 
catarrh, and is of somewhat frequent occurrence in children, as their 
bronchi are small and easily obstructed. In adults it is a peculiarly fre- 
quent complication of the catarrh, which is one of the symptoms of 
typhus (typhoid?). Compression of the lung takes place in conse- 
quence of the presence of liquid or air, more rarely of a tumor in the 
pleural sac, from effusions in the pericardium, from aneurisms, curvature 
of the spine, arrested development of the thorax, and finally, from volu- 
minous effusions in the abdominal cavity, by which the diaphragm is 
driven upward. 
Anatomical Appearances.—In congenital atelectasis circum- 
scribed spots in the parenchyma, more rarely the half or the whole 
lobe of a lung, are found to be depressed somewhat below the level of 
the surrounding parts. These spots are of a dark-blue color, firm, do 
not crackle, and, when cut into, present to view a smooth surface 
abounding in blood. At first they may be readily inflated, afterward 
they become more rigid, contain less blood, and it is no longer always 
possible to inflate them. The areolar walls seem to be fast glued or 
grown together. The alterations of the parenchyma in acquired atelec- 
tasis are essentially the same as those just described. Rokitansky for- 
merly called it catarrhal pneumonia. The blue, depressed spots here 
contrast more against the surrounding emphysematous lung. If we 
cut into the atelectatic spot, we usually come upon a thick, muco-puru- 
lent plug, which has stopped up the bronchus leading to it. When the 
atelectasis is of long standing, other changes take place in the collapsed 
portion of the lung, which belong to that very frequent sequel of this 128 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
disease, catarrhal pneumonia, upon which we shall enlarge more fully in 
Chapter X. Compression of the lung of slighter grade presents an in- 
creased density and consistence, and a condensed condition of the paren- 
chyma, which, however, is not entirely void of air. In the more intense 
forms of compression the air has left the vesicles and bronchi, but the 
pressure has not sufficed to overcome the blood-vessels and expel the 
blood. The condensed lung is red, full of blood, moist, resembling a 
piece of muscle, hence we call it camified. In the highest grade of all, 
the vessels also are compressed, the lung appears bloodless, dry, gray, 
leaden, often converted into a gray, leathery, tough mass. 
Symptoms and Course.—The symptoms of congenital atelectasis 
are essentially those of insufficient breathing and incomplete decarbon- 
ization of the blood, and have often been described. The child breathes 
softly and very quickly, is remarkably drowsy, does not cry as it 
should, but merely whines and whimpers, and cannot suck freely. 
Finally it grows pale, cool, and even cold, the nose becomes peaked, 
the lips livid or lead-color, and it usually perishes in the first few days 
of life; more rarely, not until the third and fourth week, with the 
symptoms of general paralysis, and much less commonly with convul- 
sions. It is but seldom that we can succeed in demonstrating by per- 
cussion that solidified lung lies in contact with the thoracic Avail, as the 
points of atelectasis rarely are \rery large. When collapse of the lung 
accompanies capillary bronchitis of little children, it cannot, in many 
cases, be diagnosticated with certainty. We ha\Te seen, in treating of 
the latter disease, that children may exhibit all the symptoms of insuf- 
ficient breathing and carbonic-acid poisoning from closure of many of 
the little bronchial tubes, and Avithout collapse of the air-vesicles. If, then, 
these symptoms should appear in the course of a capillary bronchitis, 
avc are only Avarranted in diagnosticating an acquired atelectasis, if Ave 
find deadened resonance over a Avide extent of the chest. Generally 
speaking, the collapsed spots are not of sufficient magnitude to make 
the percussion-sound dull. It most frequently arises in measles, in con- 
sequence of very extensive collapse of both loAver lobes of the lungs, 
and presents a symmetrical dulness on each side of the spinal column. 
It is difficult to discriminate between the symptoms of compression 
and those of the diseases Avhich produce compression. The symptoms 
of imperfect respiration, Avhere the pulmonary vessels also are com- 
pressed, are accompanied by derangement of the circulation similar to 
that which Ave have described as attending emphysema; distention, 
dilatation, hypertrophy of the right heart, subsequent distention of the 
veins of the greater circulation, cyanosis, Arenous engorgement of the 
brain, liver, and kidneys. In like manner the left heart, which is sup- 
plied by the uncompressed capillaries alone, receives too little blood, COLLAPSE OF THE LUXG. 
129 
the pulse becomes small, the complexion pale, the urine scanty. In 
severe compression of the lung, the sufferers usually die of dropsy. 
Compression of a large section of a lung has an important influence 
upon the distribution of the blood in the uncompressed parts. If all 
the blood from the right heart be directed to one lung alone, the pres- 
sure in that lung is considerably increased. The greatest danger often 
threatens from oedema of the uncompressed lung, which may even de- 
mand venesection, etc. Should the lower parts of the lung be com- 
pressed by effusions in the peritoneum, the hypenemia thus arising of 
the upper lobes (collateral fluxion) may produce danger and call for 
tapping. In the same way deformed persons, when a part of their 
thorax is contracted and the lung in the narrowed spot compressed, suf-‘ 
fer from hypenemia, catarrh, and oedema of the uncompressed portion. 
It is a curious fact that humpbacked persons can breathe without 
difficulty, show no irregularity of the circulation, and do not evince 
spmptoms of dyspnoea or of cyanosis until the period of puberty. This 
fact is easily accounted for, if we reflect that bones deformed by rachitis 
are retarded in their growth, even after the original disease has become 
extinct. Where the thorax and the thoracic vertebrae have been the 
principal seat of the disease, the crookedness and deformity of these 
parts at the time of its establishment may not, perhaps, have caused any 
loss of room in the chest; but if the rest of the body grow in the nor- 
mal manner, the development of the chest being retarded, a dispropor- 
tion must arise between the space, which, though sufficient for the lungs 
of a child, is insufficient for those of an adult, and for the dimensions of 
the remainder of the body and of the mass of blood belonging to it. De- 
formed persons then acquire the appearance and complexion with which 
we have become familiar in the emphysematous. They seem very short 
of breath, and usually die early in consequence of this respiratory and 
circulatory derangement, although it is exceptional for them also to be- 
come consumptive. 
Treatment.—Take care that newly-born children be made to cry 
properly, and that their mouths be freed from mucus ; and should there 
be any accumulation of mucus in the bronchi, give them an emetic of 
ipecac and oxymel of squills. Should the respiration still remain imper- 
fect, then, placing the child from time to time in a warm bath, apply a 
cold douche to the breast with a clyster-pipe. Do not let such children 
sleep too long and continuously, force them even to cry periodically if 
they do not cry of their own accord, by brushing the soles of their feet, 
etc. If they do not take the breast, see that they receive nourishment 
from the spoon, the mother’s milk being the best. Finally, give a few 
drops of wine occasionally, and, if the child shows a tendency to become 
cool, do not let it sleep in a cradle, but rather in the arms of its nurse 130 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
or mother. Caution and method are not uncommonly rewarded by sur- 
prising success. 
The treatment of acquired atelectasis is the same as has been recom- 
mended for capillary bronchitis, when the latter disease has led to the 
obstruction of the finer bronchial twigs. In most cases, if we succeed 
in overcoming the obstruction, air will reenter the collapsed vesicles. 
Compression of the lung requires mainly a judicious treatment of 
the principal disease, and symptomatic treatment of the more threaten- 
ing derangement of the circulation. 
CHAPTER Y. 
HYPERAEMIA OF THE LUNG—PULMONARY HYPOSTASIS (EDEMA OF 
THE LUNG. 
Etiology.—Hyperremia of the lung must be regarded as of two 
kinds—active and passive. For the first, Virchow has proposed the 
name of “fluxion”—“rush of blood”—(Wallung), while he calls the 
passive form stagnation of the blood—(Blutstockung). These names 
are the more desirable, since the words active and passive do not quite 
correspond to the physiological processes which give rise to the two 
forms of disease. Fluxion, indeed, depends more upon an increased, 
accelerated afflux; stagnation upon an impeded, retarded efflux from the 
capillaries, in whose contents we are especially interested, as it is upon 
the latter that both function and nutrition of organs depend. 
I. Fluxion, or determination of blood to the lungs, is observed— 
1. When the action of the heart is increased. We often see 
young persons at the period of puberty, particularly narrow-chested, 
overgrown subjects, in whom the most trifling causes, as the moderate 
use of stimulants, slight bodily efforts, and the like, produce palpitation 
of the heart, with considerable increase in the force of its impulse, 
accompanied by symptoms of pulmonary hyperaemia. But even with- 
out cardiac erythism, and where there is no special predisposition, over- 
violent bodily efforts, immoderate use of spirits, great mental excite- 
ment, rage, etc., may give rise to dangerous hyperaemia of the lung, 
together with increased and accelerated action of the heart. There are 
cases, unfortunately, as scandalous as they are of frequent recurrence, in 
which delirious persons, or patients with delirium tremens, having been 
brutally strapped to their bed, and intrusted to a rude nurse, are found 
lead the next morning, with bloody foam upon their lips. Such a case 
reveals, upon autopsy, an intense hyperaemia of the lung and pulmonary 
oedema, as the sole cause of death. The symptoms are difficult of ex- 
planation. In most of the organs in the greater or systemic circulation HYPERCEMIA OF THE LUNG. 
131 
mere augmented action of the heart does not produce hyperaemia. The 
fuller the arteries, and the more distended their walls, so much less full 
are the veins, and so much is the tension of their walls lessened. The 
efflux from the capillaries is accelerated in proportion as the afflux is in- 
creased ; the circulation is quickened without any actual increase of the 
quantity of blood in any of the organs. Whether another condition 
exists in the lungs, or whether increased heart-action alone is thus capa- 
ble of giving rise to hyperaemia, we do not attempt to say, as we are 
not sufficiently acquainted with the normal condition of the pulmonary 
circulation, and even the natural degree of pressure of the blood in the 
pulmonary artery when the chest is closed is unknown to us. 
2. The instances of fluxion to the lung produced by direct irritation, 
by the transitory action of cold upon the pulmonary tissue, the inhala- 
tion of very hot air, or of air mingled with irritating matter, are easier 
of comprehension. Here the tissue in which the capillaries are im- 
bedded seems to be relaxed, and to oppose less resistance to the relaxa- 
tion of the capillary walls. The same causes, acting upon the skin, pro- 
duce fluxion upon it in a manner quite similar. The skin reddens if it 
be exposed to cold for a short time, as if a hot poultice or a sinapism had 
been laid upon it. The chronic fluxions, too, which accompany the for- 
mation and softening of neoplastic growths and tubercles, especially 
tuberculosis of the lungs, occur in the same way, and may be traced to 
abnormal relaxation of the connective tissue. 
3. A third form of fluxion, as yet far too little noticed, but which 
we have already alluded to in treating of emphysema and pulmonary 
compression, occurs in all cases of obstruction of the pulmonary circula- 
tion from stasis in its capillaries, or where the latter are compressed or 
destroyed, and, of course, it must develop in portions of the lung where 
the circulation is free from impediment. Such collateral fluxion is a 
physiological sequel to ligation of an arterial trunk, as is proved by the 
appreciable dilatation of the surrounding unobstructed vessels, and it is 
quite indispensable to the symptomatology of most diseases of the lung. 
In the most simple manner it explains symptoms, which otherwise would 
be unintelligible, and it accounts for the action of venesection in pneu- 
monia, pleuritic effusion, etc. 
4. Finally, we have already stated that a rarefaction of the air in the 
alveoli produces determination of blood to the lungs, just as a cupping- 
glass or the boot of Junod causes fluxion to the skin. The suspended 
or diminished pressure to which the capillaries of the air-cells of a child 
with occluded glottis are subjected, when it expands its chest, is, as we 
have seen, the main reason for the consecutive bronchial catarrh and 
pulmonary oedema in croup, and of the poor success of tracheotomy. 
II. Stagnation of the blood, passive hyperaemia, from which we 132 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
illogically separate the mechanical form, takes place in all cases in which 
the pulmonary veins are abnormally filled and their Avails unduly 
stretched. Here the blood flows from the capillaries with difficulty, 
while the arteries continue to convey blood to them, even though 
scantily filled themselves, since even then their walls evince a greater 
degree of tension than the capillary walls. (Blood continues to flow 
from the arteries into the capillaries after the heart has ceased to con- 
tract.) Hence we see that stagnation results in a far greater dilatation 
of capillaries than fluxion does, as when there is much obstruction of 
the venous current in the capillaries, which have become, as it were, 
blind appendices to the arteries, the blood continues to enter them until 
the tension of the capillary Avails is equal to that of the artery, or until 
the delicate membrane can no longer support such a pressure, and be- 
comes ruptured. Stagnation, or engorgement of the pulmonary capil- 
laries, occurs most typically— 
1. From contraction of the left auriculowentricular opening and in- 
sufficience of the mitral valve. Both forms of disease of the heart are 
accompanied by the most intense hypermmia of the lung. We knoAV 
that the brown color of the indurated hypertrophied lung depends upon 
rupture of the dilated capillaries, the chief cause of which Ave have 
found to be Aralvular disease of the mitral. Whether the evacuation of 
the auricle be retarded, or whether the blood be regurgitated during 
the systole into the auricle, either process must impede the emptying of 
the pulmonary vein, and give rise to overcharge of the capillaries. 
2. Enfeebled action of the heart results in imperfect evacuation of 
its cavities, and hence in impeded efflux of blood from the veins. Here 
the supply from the arteries is not diminished in proportion as the out- 
floAV from the capillaries is obstructed, and thus asthenic fevers, in which 
the contractions of the heart are frequent, but incomplete, such as 
typhus, puerperal fever, or pyaemia, are constantly accompanied by en- 
gorgement of the pulmonary capillaries. When the heart’s action is 
Aveakened, gravity furnishes a neAv impediment to the evacuation of the 
capillaries in dependent portions of the body. While such an obstacle 
is easily o\‘ercome Avhen the heart contracts Avith energy, yet Avhen its 
action is depressed, Ave soon see evidences of the effect of gravitation, 
and hyperoemia begins to form at the more dependent places. A liealtliAr 
person may lie in bed for months Avithout the development of this form 
of hypergemia (hypostasis) in the capillaries of the back, or the forma- 
tion of bed-sores, or the different phases of pulmonary hypostasis AAThich 
are the almost constant accompaniment of a typhus of long duration. 
We have learned that swelling and succulence of the mucous mem- 
brane, and increase and alteration of the follicular secretion, are the 
constant result of hyperaemia of a mucous membrane; similar processes IIYPERyEMIA of the lung. 
133 
take place in the alveoli in all cases of severe hyperaemia. Here, too, 
the walls swell up, become more moist and succulent, but the secretion, 
or, more properly, the transudation, which is poured into the cells differs 
from the bronchial secretion, being liquid and serous. If we bear in 
mind that there are but few mucous follicles even in the finer bronchi, 
and none at all in the air-cells, and that the structureless cell-wall is cov- 
ered merely by imperfect pavement epithelium, it must be evident that 
the secretion from the vesicles, which have no mucous membrane proper, 
must be very different from bronchial mucus. While, in other organs, 
the term oedema is applied to an effusion of serum into the interstitial 
tissues, the term oedema of the lung is only used in cases where such 
infiltration is combined with an effusion upon the free surface of the 
lung, i. e., into the pulmonary vesicles. 
CEdema of the lung, however, is not, in all cases, a consequence of 
hypenemia, or of increased pressure of the contents of the capillaries upon 
their walls, but, as in other organs, serum filters out of the pulmonary 
capillaries into the tissue and into the vesicles, under slight pressure, 
whenever the serum of the blood has but very little albumen in solution, 
or whenever a dropsical crasis has developed. We shall consider this 
subject more fully in treating of Bright’s disease. 
If oedema arise from a hypostatic hyperasmia, it is called hypostatic 
oedema. As we have learned, however, there is a double reason for the 
vascular engorgement in hypostatic hypermmia, and hence it is easy to 
understand that in this form the capillaries become extremely overfilled, 
and that their walls undergo an excessive pressure. In this form of 
hyperaemia it is not merely a transudation of a solution of dilute albu- 
men which takes place, but all portions of the serum of the blood, even 
the fibrin, pass through the now porous wall of the vessels, and we call 
this condition hypostatic pneumonia, a process which takes place simply 
from stagnation of the blood, and has nothing in common with inflam- 
mation proper. 
Anatomical Appearances.—When the hyperaemia is moderate, 
the lung is bloated, dark red in color, and its vessels are filled to bursting. 
The tissue is succulent, relaxed, crackles but little, blood flowing freely 
over the cut surface; a bloody, foamy liquid is contained in the bron- 
chi. When of longer duration and greater intensity, the parenchyma 
looks dark, bluish red or blackish red. The interstitial tissue and the 
alveolar walls are so much swollen that the condensed parenchyma 
scarcely gives any indication of its cellular structure. The lung, thus 
solidified, presents a certain similarity of appearance to the tissue of the 
spleen, and is therefore said to be splenified. 
If oedema have developed in the lung, it seems swollen, does not 
collapse when we open the chest, and is tense to the touch. If recent, 134 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
it does not pit on pressure; after longer duration, the parenchyma has 
lost its elasticity, and the lung retains the impression of the finger 
longer and more distinct]}". If the oedema be consequent upon an in- 
tense hyperaemia, the oedematous lung is colored red, but, if it be one of 
the symptoms of a general dropsy, it may appear quite pale. If we cut 
into the oedematous spots, an enormous quantity of liquid, sometimes 
clear, at others of a red color, mixed more or less with blood, flows over 
the surface of the cut. This liquid is full of bubbles, frothy, and copi- 
ously mixed with air, if the air-cells have not been entirely filled up 
with serum and still contain air. In other cases, the liquid hardly con- 
tains any bubbles, except a few from the larger bronchi. Here the serum 
has expelled all the air from the vesicles. In cases of hypostasis we 
find the same conditions; intense liyperaemia, amounting to splenifica- 
tion, or a more or less complete oedema, uniformly occupying the poste- 
rior portion of the lungs next the vertebrae. If the patient have lain 
continually upon one or other side, the hypostasis is often confined to 
this side alone, and may be very extensive, while the other lung may 
be healthy. If the contents of the air-vesicles at the condensed portions 
of the parenchyma cannot be completely evacuated by pressure, if the 
section shows an indistinct granular aspect, if the liquid which flows out 
be clouded by little coagula of fibrin, we have the so-called hypostatic 
pneumonia before us. 
Symptoms and Course.—A moderate degree of fluxion to the 
lungs presents no symptoms. The dilated capillaries present a greater 
surface to the air, the circulation is accelerated, and with this accelera- 
tion the change of the blood in the lung grows more brisk, as both cir- 
cumstances promote and facilitate oxygenation. When, however, the 
fluxion is more considerable, the enlargement of the dense capillary net 
and the swelling of the cell-walls from augmented transudation may 
diminish the capacity of the air-vesicle. An obstacle to respiration is 
thus set up. The lungs cannot inhale so much air. Those narrow- 
chested youths and girls, of whom we have spoken, in their attacks of 
palpitation, complain of shortness of breath, nay, they very correctly 
call the sensation which they experience in the chest a “ fulness ” or 
“ stricture.” A short, dry cough is added to this condition ; far more 
rarely a frothy expectoration, with scattered streaks of blood. There is 
no pain in the chest. Physical examination shows no abnormities. 
We may as well state here that “habitual determination of blood to the 
chest” is sometimes the forerunner of consumprion,though perhaps not 
as often as we are apt to believe. 
The violent hyperaemia of the lungs, mentioned in the pathogeny, 
and which must be regarded as consequent upon excessive action of the 
heart, sometimes arises rapidly, and threatens life with unexpected sud- HYPEREMIA OF THE LUXG. 
135 
denness. Hence such cases are called pulmonary apoplexy (lungen- 
scMagfluss). The shortness of breath quickly increases to a serious ex- 
tent ; the breathing grows hurried and scarcely to be counted. The 
feeling of fulness and compression causes fear of death and a sensa- 
tion of choking; every cough fills the mouth with a copious, frothy, 
bloody expectoration. The heart beats visibly, the radial pulse and 
the carotids betray the tension of the arteries. The face is reddened. 
The oedema, which follows this form of hyperaemia, soon makes itself 
felt. The vesicles, filled with serum, can admit no more air; an acute 
surcharge of the blood with carbonic acid changes the scene. The 
restless patient becomes still and drowsy, the face paler, the muscles of 
the bronchi, palsied with the other muscles, cannot rid the tubes of their 
serous contents. Coarse, moist rales, audible even in the trachea, 
announce the approaching end, the threatening suffocative effusion. 
The symptoms of acute fluxion, brought on by the inhalation of irri- 
tating gases, are modified by the coexistence of irritation of the larynx 
and bronchial mucous membrane, and are accompanied by violent 
coughing-fits. The hyperaemia to which tuberculosis, cancer of the 
lung, etc., give rise, and which most generally produce pulmonary and 
bronchial haemorrhage, are to be treated of in the next chapter. 
Collateral fluxion to the lungs forms a grand feature in the descrip- 
tion which we shall present of pneumonia, pleuritis, and pneumothorax. 
Here a large part of the dyspnoea depends upon the overfilling of the 
capillaries and swelling of the vesicles, in the portions of the lung un- 
affected by the inflammation. Without this complication, or, to speak 
more properly, if no such condition arose when the circulation is im- 
peded, the unaffected vesicles could better obtain their supply of air. 
If the blood pressure be lessened by venesection, the collateral fluxion 
is reduced, the dyspnoea often completely disappears, although the chief 
disease continues unabated. When patients die in the first stages of 
pneumonia or pleuritis, or shortly after air has penetrated into the pleural 
sac, and compressed the lung, they die of collateral hypenemia and 
collateral oedema. If we examine the records of post-mortem examina- 
tions, we shall not fail to find evidence of this form of hypenemia, 
although it is but little appreciated in interpreting the symptoms. 
Passive hypenemia (lUiit-stauung), even when unaccompanied by 
pulmonary oedema, creates greater dyspnoea than fluxion to the lung. 
Patients with insulncience and contraction of the mitral, even if they 
lia\'e no bronchial catarrh, and Avhen the engorgement does not extend 
from the alveolar capillaries into their anastomoses so as to produce 
tumefaction of the mucous membrane and contraction of the tube, 
nevertheless usually suffer from a very distressing shortness of breath, 
aggravated by the slightest movement. This is easily accounted for, 136 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
when we reflect that in passive congestion (Blut-stauung) the circular 
tion is as much retarded as in fluxion it is accelerated, that in the former 
a double cause of dyspnoe aprevails, in the latter but one. Intense 
dyspnoea and all the symptoms of pulmonary apoplexy and suffocative 
effusion, which we have described, are often suddenly and unexpectedly 
added to the constant shortness of breath of disease of the heart. Effu- 
sion into the air-vesicles now exists beside swelling of their walls; the 
respiration, merely impeded hitherto, has now become inadequate. A 
great number of those who have disease of the heart die of acute passive 
congestion and acute oedema, without discoverable cause for the sudden 
increase in the impediment to the circulation. In other cases the symp- 
toms of effusion of serum into the pulmonary vesicles, the inadequate 
respiration, and final death of the patient, take place more gradually in 
cases of disease of the heart. 
If, in the course of an asthenic fever, whether it be a symptom of 
typhus or of pyaemia, the respiration should become shallow and incom- 
plete, should percussion indicate a condensation of the parenchyma of 
the lung, near the spinal column, should sputa be ejected more or less 
tinged with blood, we have to do with an obstructive engorgement of 
the lung with hypostasis or with its sequelae. 
It would be unnatural and artificial to make a distinction between 
the symptoms of liyperaemia and of oedema. If a liyperaemia be intense, 
oedema occurs as one of its most important symptoms. We infer that 
this normal and necessary result has taken place, in the first place, from 
the grade of the dyspnoea, which never becomes so severe from swelling 
of the alveolar walls alone, as from oedema. Almost universally where 
hyperaemia has produced death, serum has been found in the air- 
vesicles. 
The characteristic sputa give a second point for diagnosis. Such 
liquid secretion is seldom or never discharged from the bronchial mu- 
cous membrane, and the expectoration of liquid transparent, profuse, 
sputum, more or less mixed with blood, if it supplant the viscid, scanty 
sputum of pneumonia, is very properly regarded as of serious omen. 
Auscultation also gives information as to the occurrence of oedema. A 
dry rale, that is to say, a rale which is formed in viscid fluid, may easily 
be distinguished from a moist one, that is, from a rattle which takes 
place through the medium of a thin liquid. In the secretion of the 
bronchial mucous membrane we seldom hear such moist rattling sounds 
occur as those which arise when the serous transudation of the vesicles 
fills up the bronchi. In other cases we hear no respiratory sound in 
spots at which the vesicles are filled up by oedema, and where no air 
can enter. Bronchial breathing is only to be heard in rare instances.* 
* Bronchial breathing takes place when the vesicles, filled with serum, do not HYPERAEMIA OF THE LUXG. 
137 
Percussion, finally, which undergoes no change from hyperaemia 
alone, sometimes indicates that oedema has supervened upon hyperaemia. 
The sound upon percussion when the alveolar walls have lost their elas- 
ticity through oedema, and are but lightly stretched over their contents, 
is sometimes distinctly tympanitic. If, however, all the air have been 
driven out of the air-cells by the oedema, and the lung have become 
void of air, the sound upon percussion becomes dull and fiat, as with 
every other condensation of the lung. If these manifestations appear 
in the characteristic places for hypostasis, we have to do with this form, 
or with its sequelae. 
With regard, finally, to that form of oedema of the lung which 
arises in general dropsy, the appearance of dropsical swelling of the 
subcutaneous cellular tissue and of effusions in the serous cavities fur- 
nishes the best grounds for interpretation of the dyspnoea which accom- 
panies these symptoms. Should serous sputa, moist rattles, a tympanitic 
or dull sound, upon percussion, supervene, we are warranted in regard- 
ing pulmonary oedema as their cause. 
Diagnosis.—Hyperaemia and oedema of the lung, if we keep in 
view the symptoms just described, are easily distinguished from other 
diseases of the lung. It may, however, be very difficult (easy as the 
matter may appear in the study) to make a distinction at the bedside 
between active and passive hyperaemia, between fluxion and obstruc- 
tion ; and, moreover, confusion of the two may lead to the worst conse- 
quences, to mistakes which not unfrequently threaten the fife of the 
patient. The confusion occurs most frequently between the collateral 
fluxion, occurring in the course of a pneumonia and pleurisy, and the 
passive hyperaemia, to which enfeebled heart-action and asthenic fever 
give rise. We so frequently notice the occurrence of passive pulmonary 
hyperaemia and oedema of the lung, upon the final exhaustion of the 
patient, upon the diminution of the pulse, upon the delirium, and the 
dry tongue, that we are apt also, in cases of recent pneumonia, if the 
pulse be small, and the patient delirious, to think of passive hyperaemia 
and of obstruction from commencing paralysis of the heart, and instead 
of venesection to prescribe wine, camphor, and musk. 
In treating of croupous pneumonia we shall go more fully into detail 
upon the subject of pulmonary fluxion and engorgement, symptoms of 
the utmost importance in that disease, and demanding especial considera- 
tion in its treatment. 
Prognosis.—The prognosis of hyperaemia and of oedema of the 
contain any air, but where, at the same time, the bronchi, which lead to the con- 
densed spot, are not filled up by the secretion. It is easy to see that the latter con- 
dition, requisite for bronchial respiration (of the origin of which we shall speak more 
'Sully while treating of pneumonia), is almost always wanting in pulmonary oedema. 138 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
lung depends essentially upon its exciting causes. Fluxions, if tliey do 
not proceed from adventitious productions in tlie lung, are generally of 
less serious character, and are more amenable to treatment than obstruc- 
tions, the causes of which are usually difficult to allay. Prognosis of 
the various forms can be derived from the description of the course of 
the disease. 
Treatment—Indicatio causctlis.—As increased action of the heart 
is a frequent cause of fluxion to the lung, and as, in youthful subjects, 
habitual palpitation of the heart, accompanied by hyperaemia of the lung, 
is often the forerunner of tuberculosis, a regimen and treatment suitable 
to such condition are demanded. Strictly forbid the use of spirits, tea, 
coffee, and order all food or drink to be allowed to cool somewhat be- 
fore it is taken. In like manner inexorably forbid dancing and riding, 
and other violent bodily exertion, at the, same time enjoining regular 
and moderate exercise. Shield the patient, as far as possible, from all 
psychical excitement. Besides these precautionary measures, the lung is 
to be protected from injury. Let all hot and smoky rooms and all 
dusty places be avoided, and do not let the patient inhale very cold air. 
Acidulated drinks, lemonade, cream-of-tartar water, are to be recom- 
mended. The milk and whey treatment is especially suitable for such 
cases, and, above all, the “ grape cure ” of Durkheim, Meran, on the 
lake of Geneva, and other places with a mild clime, where sweet grapes, 
which do not purge, are cultivated.* It merely hastens the end of 
patients, in an advanced stage of phthisis, to remove them from the 
quiet and comforts of home in order to try the grape or whey cure. 
On the other hand, these cures often do most brilliant service in the 
instances under discussion, which may not incorrectly be regarded as 
cases of incipient tuberculosis. 
In the collateral form of pulmonary hyperaemia the indicatio causa- 
lis coincides with the treatment of the main disease. In obstruction in 
the lungs the indicatio causalis cannot be met. In disease of the heart, 
above all, in contraction of the mitral valve, the use of digitalis is to be 
recommended as a palliative until the heart’s action have become retard- 
ed. The weaker the action of the heart becomes in the course of an 
asthenic fever, so much the more urgently are stimulants and nourish- 
ing food indicated. In like manner cause the position of patients with 
threatening hypostasis to be changed from time to time, in order to pre- 
vent a settling of the blood. 
With regard to the indicatio morbi, bold venesection from a large 
opening is demanded in fluxion to the lung, arising from excessive car- 
* The very fine sweet grapes, which grow in the better vineyards of mv present 
home, purge so strongly as to be inapplicable to the grape-cure. I have seen a severe 
diarrhoea set in after eating three to four pounds of Wiirtemberg grapes. HYPE PREMIA OF THE LUNG. 
139 
diac action threatening life. The result here is astonishing. As soon 
as the volume of the blood has become lessened, the pressure diminishes 
in the arteries (as it depends upon two forces: first, the energy of the 
cardiac contractions; second, the fulness of the cavities of the heart). 
The patients often become able to breathe more freely, even during the 
operation, the bloody foam which they were expectorating vanishes, 
and life may be rescued from the greatest danger by aid of the phy- 
sician. In cases like these, however, which have been called pulmo- 
nary apoplexy (lungenschlagflms), the danger arises with such light- 
ning rapidity, that the physician usually arrives too late. 
Collateral fluxion, also, when it threatens life, requires venesection. 
If, thereby, the force of the heart be diminished, the pressure, too, in 
the arteries of the hyperaemic parts of the lung is also reduced, the 
capillaries are less full, the transudation of serum, which was threatening, 
or had already set in, does not occur or ceases; and here, too, we often 
see the patient breathe more freely and more deeply, while the blood is 
yet flowing from the open vein. Since, however, in by far the greater 
number of cases, the venesection has an unfavorable effect upon the 
main disease by increasing the danger from exhaustion and impoverish- 
ment of the blood, let us not be led astray by these striking instantaneous 
results, so as to let blood without necessity, that is to say, unless fife 
itself be threatened; but if, in the course of pneumonia, or pleuritis, or 
recent pneumothorax, with intense dyspnoea, a moist rale become audi- 
ble, if the sputa become serous, etc., the danger is imminent; then 
pay no regard to the small pulse, or rather look upon it as a new reason 
for bleeding. The more recent the case, so much is collateral fluxion 
the more easy of recognition, and so much the more surely can we rely 
upon success. 
Should symptoms of oedema threaten in the course of disease of the 
heart, immediate danger to life may demand a diminution of the volume 
of the blood, and the relief consequent upon venesection usually satisfies 
the expectation which has been entertained. In these cases, too, how- 
ever, it is of the utmost importance to restrict blood-letting to the cases 
ot the most urgent necessity. Persons with disease of the heart do not 
bear repeated venesection well; their blood, like that of emphysematous 
persons, and for the same reasons, after long duration of the disease, is 
poor in fibrin and albumen, and has great tendency to form serous 
transudations. Venesection, by diminishing the volume of the blood, 
renders it thinner ; the original mass is soon reestablished by absorption 
of liquid from the tissues and from the intestines; but the tendency to 
dropsical transudation and even to oedema of the lung is aggravated in 
this way. 
In the other forms of hyperaemia of the lung which we have de- 140 
DISEASES OF THE FARENCIIYJIA OF THE LUNG. 
scribed, venesection is absolutely hurtful. Especially is this the case 
with hyperaemia occurring in asthenic fevers, no matter how great it 
may be, and though oedema threaten life. In these cases every thing 
depends upon our supporting the depressed energy of the heart, as by 
this means alone can its cavities be emptied, and blood flow away from 
the pulmonary veins. Blood-letting weakens the energy of the heart 
and augments the danger. As the latter class of cases are by far the 
most frequent, as they close the scene in almost all tedious and exhaust- 
ing diseases, strong soups, fiery wines, camphor, musk, are much more 
frequently indicated for hyperaemia of the lung than is blood-letting. 
The difficulty of distinguishing between approaching heart-palsy and 
collateral fluxion in the course of pneumonia, which, from its great exu- 
dation, leads to intense fever, and at last also to enfeebled contractions 
of the heart, has been discussed above. 
In addition to the procedures just spoken of, oedema of the lung 
may require the employment of emetics, for reasons already explained, 
as soon as the cough lacks energy, and the palsied bronchial muscles 
cease to aid in expelling the serous contents of the bronchi. Should 
the discharge of sputa be arrested, should the rales in the chest be in- 
creased, even if the patient cough, give an emetic of sulphate of copper 
or ipecacuanha, with tartar-emetic, but only when hope of saving life 
has not been extinguished. Traube recommends the use of acetate of 
lead—gr. j every hour—and the application of a very large blister to 
the chest, as a very efficient mode of treating oedema of the lung. 
(Edema of the lung, as a symptom of general dropsy, demands the 
treatment of the main disease, but here, too, in the circumstances alluded 
to, an emetic may be indicated. 
HEMORRHAGES FROM THE RESPIRATORY ORGAN'S. 
In the majority of cases in which blood is coughed up, the bronchial 
mucous membrane is the source of the bleeding, but, as bronchial haemor- 
rhage is almost always the attendant or forerunner of disease of the lung, 
we have preferred to treat of this subject simultaneously with that of 
haemorrhage from the pulmonary substance. 
Under the head of haemorrhage from the respiratory organs, accord- 
ingly, we shall discuss: 1. Bronchial haemorrhage (broncho-hcemorrahie), 
by far the most frequent cause of haemoptysis and pneumorrhagia. 2. 
Haemorrhagic infarction, a haemorrhage of the pulmonary tissue con- 
fined within narrow limits, and which causes no destruction. 3. Pul- 
monary apoplexy proper, an abundant haemorrhage of the pulmonary BRONCHIAL HAEMORRHAGE. 
141 
tissue, caused by rupture of some of its large vessels, and causing de- 
struction of the lung, with the formation of an apoplectic cavity. 
Haemorrhage from cavities and bleeding arising from the opening 
of an aneurism into the air-passages are to be treated of hereafter. 
CHAPTER YI. 
Etiology.—Wounds and erosions of the larger blood-vessels of 
the bronchial mucous membrane are extremely rare. Capillary haemor- 
rhages of the air-passages, too, are seldom of traumatic origin, or due 
to sloughing or ulceration of the membrane. As a rule, haemorrhage 
proceeds from rupture of the capillaries, caused either by over-disten- 
tion, or else by a morbid delicacy of their walls, a result of perverted 
nutrition. The trifling capillary haemorrhages which occur in the first 
stage of acute bronchial catarrh, in cases of violent irritation of the air- 
passages, and in the circulatory disorder attending organic disease of 
the heart, proceed from the first of these causes, while in most of the 
haemoirhages, in which large quantities of blood are poured into the 
bronchi, to be ejected thence by haemoptysis or bronchorrhagia proper, 
they are due to the latter condition. 
The fact, which has been too little appreciated hitherto, that nearly 
all bronchial haemorrhages are mainly owing to a morbid state of the 
vascular walls—to a haemorrhagic diathesis * of the bronchial mucous 
membrane—and do not depend upon over-filling of the vessels, is of 
great practical importance. The truth of this is shown by the fact, not 
only that attacks of haemoptysis and bronchorrhagia are not usually 
preceded by bronchial hyperaemia, but that the spitting of blood almost 
always persists, and, in fact, often does not assume an obstinate char- 
acter until after the patient has lost a good deal of blood, so that his 
vascular system is considerably depleted. 
A tendency to abundant bronchial haemorrhage—to a haemorrhagic 
diathesis, according to the above definition—1. Is met with in rare in- 
stances, occurring unexpectedly in young persons, apparently in bloom- 
ing health, and of vigorous constitution. In such cases, we as yet have 
absolutely no explanation of the disorder, which is usually limited to 
the capillaries of the bronchial mucous membranes, and which is often 
followed by such sad results. 
BRONCHIAL HAEMORRHAGE. 
* We employ this general term merely to signify a morbid tenderness of the vas- 
cular walls, and not a morbid condition of the blood; although we admit that the 
latter may sometimes so modify the nutritive state of the walls of the blood-vessels as 
to impair their resisting power, and thus to lead to a haemorrhagic diathesis* 142 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
2. Much more frequently we find similar tendency to profuse capil- 
lary haemorrhage from the bronchi in young people, between the ages 
of fifteen and twenty-five years, of delicate health, and having marked 
weakness of constitution. Such patients frequently have been orphans 
from an early age, having lost their parents by consumption. They 
have suffered from rickets, or scrofula, in infancy, have often bled at the 
nose, and have rapidly grown tall, without at the same time acquiring 
any corresponding development of the various organs of the body. 
Their long bones are thin, their chest narrow, and even their skin 
seems unusually delicate and transparent; their cheeks redden easily, 
and blue veins may be traced over the ridge of the nose and the tem- 
ples. One might almost be tempted to attribute the remarkable fre- 
quence of bronchial haemorrhage in persons of this type to a deficience 
of vital material, which, having been immoderately expended during the 
maladies of childhood, and by the rapidity of the growth, has proved 
insufficient to maintain normal nutrition of the capillary walls, just as we 
are accustomed to ascribe the occurrence of spontaneous bleeding after 
severe illness, tedious suppuration, or great loss of blood, to a kindred 
source of exhaustion of the nutritive principle. Such an hypothesis, 
however, does not explain why the seat of haemorrhage should first be 
in the nose, and afterward in the bronchi, and why haemorrhage scarcely 
ever occurs into the brain, or into other organs, in patients of this class. 
3. There is a great predisposition to capillary haemorrhage from the 
bronchi in persons suffering from tuberculosis and consumption. The 
frequence of abundant haemorrhage in all stages of these diseases arises 
partly because individuals who are liable to such bronchial bleeding are 
equally liable to tuberculosis, and to consumption of the lungs, and be- 
cause the tendency to bleed does not cease 'when the lungs become 
affected, and partly because deposit of tubercle and chronic inflammation 
cause the pulmonary tissues and the bronchial mucous membranes to 
become relaxed, so that the capillaries which are imbedded in the relaxed 
tissues (now no longer capable of resisting their undue dilatation) suffer 
excessive distention and attenuation of their walls, whereby they be- 
come more easy of rupture. 
Finally, coalescent masses of tubercle and centres of inflammation, 
by compression of vessels, give rise to fluxionary and obstructive hyper- 
remia, by which rupture of the capillaries is favored. 
Prejudice in favor of the narrow views of Laennec and a belief in 
the ancient Hippocratic theorem, Epi aimatos emeto phthoe Tcai ton 
puou katharsis ano, have seriously biased the judgment of physicians as 
to the relation between bronchial bleeding and pulmonary tuberculosis, 
and have given rise to extravagant and erroneous ideas. Many physi- 
cians do. not hesitate to accept a brisk haemoptysis as a sure sign of in- BRONCHIAL HAEMORRHAGE. 
143 
cipient, or even of established tuberculosis, although the patient may 
present no symptoms, either subjective or objective, of disease of the 
lungs, and when, soon after the occurrence of haemoptysis, signs of con- 
sumption have arisen, they confidently assume that the bleeding has 
been caused by the presence of tubercle, or by the process of its deposit 
in the lungs. 
I must earnestly protest against this opinion, as altogether unwar- 
ranted, and fraught with danger to the patient. Cases undoubtedly 
occur, in which tubercles and inflammatory processes form in the lungs, 
in a manner so latent that no tokens of the disease are manifested by 
the individual affected, until he is suddenly attacked by a fit of haemor- 
rhage. Such instances, however, are exceptional. 
In the very great majority of cases in which the first attack of hae- 
moptysis has not been preceded by either cough, dyspnoea, or other 
sign of pulmonary disorder, the lungs are free, and by no means the 
seat of tubecuular deposit, at the commencement of the bleeding. 
It is true that such subjects rarely die of haemorrhage, so that we do 
not often have an opportunity of examining their condition post mortem. 
However, if we collate the reports scattered through our literature and 
compare their statements, we shall assure ourselves that they substan- 
tiate the correctness of the above remarks. I have repeatedly failed to 
find post-mortem traces of pulmonary tubercle, or of any other destruc- 
tive disorder in the lungs of individuals who have died suddenly of 
pneumorrhagia, while in enjoyment of apparent health. 
That bronchial haemorrhage is by no means so rare an event, where 
there is no grave disease of the lungs, is shown, moreover, by the tol- 
erably numerous cases in which persons, after suffering one or more 
attacks of pneumorrhagia, regain their health completely, and indeed 
often live to an advanced age, and after death present no discoverable 
traces of extinct tuberculosis in their lungs. 
That bronchial haemorrhage, as a rule, should precede the disease of 
the lung, in the cases where the initial signs of consumption follow im- 
mediately upon an attack of haemoptysis is also strongly in contradic- 
tion of the theories of Laennec, to which, nevertheless, most modern 
physicians adhere without question. According to Laennec’s view, 
there is but one kind of consumption—tubercular consumption. “ As 
bronchial haemorrhage can never produce a deposit of tubercle, all genetic 
connection between such haemorrhage and the consumption must be 
denied absolutely. Hence, where the first symptoms of consumption 
follow close upon a haemoptysis or pneumorrhagia, we may assume 
confidently that the tubercular deposit has formed either simultaneously 
with or prior to the occurrence of the bleeding.” Such argument, 
though logical, is fallacious, because based upon the erroneous hypoth* 144 
DISEASES OF THE PARENCHYMA OF ME LUNG. 
esis that consumption of the lungs always arises from tubercular de- 
posit. Unbiassed and careful observation of patients, who, without 
warning and often in the midst of exuberant health, have been attacked 
by pneumorrhagia or haemoptysis, and who, without rallying, have per- 
ished in a few months of a phthisis florida, a “galloping consumption,” 
has taught me that such patients scarcely ever succumb to a pulmonary 
tuberculosis in its stricter sense, but that they usually die of a form of 
consumption as yet but little thought of, and of which bronchial haemor- 
rhage is the immediate cause, Laennec to the contrary notwithstanding. 
When, after a bronchial haemorrhage, coagulated blood is retained in 
air-vesicles and bronchi, its irritating effect is quite as great upon sur- 
rounding parts as is that of a thrombus or coagulum within a vein upon 
the vascular tissues. 
The bronchitis and pneumonia arising from such a source may result in 
various ways. (See below.) A very common consequence is, that both 
clot and inflamed pulmonary tissue undergo a caseous metamorphosis, 
with subsequent decay. These pathological and anatomical processes 
agree closely with the type which consumption assumes when it imme- 
diately follows a bronchial haemorrhage in an individual previously vig- 
orous and healthy, and proves fatal in the course of a few months. 
Finally, I may observe that the bronchial haemorrhages which occur 
in an established case of consumption also cause chronic pneumonia 
and destruction of the tissues, and thus hasten the fatal termination. 
The fact that the occurrence of haemoptysis in the course of a pneu- 
monia is a serious event, and that the disease often rapidly grows worse 
immediately afterward, is generally admitted by physicians, although, 
as a rule, it has been falsely interpreted; it being a common supposition 
(but one which is rarely the true one) that fresh tubercles have formed, 
which, by some, are thought to have caused the haemorrhage, and by 
others to have accelerated the consumption. 
As my opinions regarding the relations between bronchial haemor- 
rhage and pulmonary consumption differ in some respects from the 
prevailing views upon this subject, I propose briefly to state them in the 
following paragraphs: 
1. Bronchial haemorrhage occurs oftener than is generally believed, 
in persons who are not consumptive at the time of the bleeding, and 
who never become so. 
2. Copious bronchial haemorrhage frequently precedes consumption, 
there being, however, no relation of cause and effect between the 
haemorrhage and the pulmonary disease. Here both events spring from 
the same source—from a common predisposition on part of the patient 
both to consumption and to bleeding. 
3. Bronchial bleeding may precede the development of consump- BRONCHIAL HAEMORRHAGE. 
145 
tion as its cause, the haemorrhage leading to chronic inflammation and 
destruction of the lung. 
4. Haemorrhage from the bronchi occurs in the course of established 
consumption more frequently than it precedes it. It sometimes, although 
rarely, appears where the disease is as yet latent. 
5. When bronchial haemorrhage takes place during the course of 
consumption, it may accelerate the fatal issue of the disease, by causing 
chronic destructive inflammation. 
Anatomical Appearances.—Upon post-mortem examination of 
those who have died of bleeding from the bronchi, the air-passages are 
found more or less extensively and completely filled up with masses of 
clotted blood. Sometimes -the mucous membrane has a uniform dark- 
red stain, from effusion of blood into its tissues, and it is swollen, re- 
laxed, and bleeds upon pressure. In other cases, again, the entire con- 
tents of the capillaries seem to have been discharged, the mucous 
membrane presenting a pale and bloodless appearance. The source of 
bleeding is never found to be of the nature of a mechanical or ulcera- 
tive lesion. 
The lungs, at points where the blood has descended into the air- 
vesicles, are heavier, denser, and more or less reddened. If the bronchi 
remain filled with their bloody contents, escape of air from the air-cells 
is prevented, and the lungs remain inflated when the chest is opened. 
Where death has been caused by hmmorrhage, there is extreme anaemia 
of all organs. 
In cases where death has taken place some time after the haemor- 
rhage has ceased, either no trace whatever of the former bleeding is 
found in the lungs—and, indeed, this is most commonly the case—or 
else the signs are found of chronic inflammation in its different stages, 
which, however, is never to be ascribed to the haemorrhage, unless a 
greater or less amount of broken-down blood-clots, in a state of fatty 
degeneration, be also found in the bronchi. I have published a case 
from my clinique, in which the post-mortem appearances exhibited the 
entire process, in the most striking manner, in which coagula, bearing a 
perfect resemblance to old thrombosis of the veins,* were found in the 
bronchi. 
Symptoms and Course.—The admixture of small quantities of 
blood in catarrhal expectoration—occurring in the form of minute 
streaks traversing the mass—is a very common and quite harmless 
symptom. The expectoration of a somewhat larger amount of blood— 
either pure or mingled with bloody mucus—which sometimes follows 
upon the inhalation of acrid vapors, or after other severe irritation of 
* “ Upon the relation of bronchial and pulmonary haemorrhage to pulmonary con- 
sumption.” Inaugural dissertation of Doctor Burger. Tubingen, 1864. 146 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
the air-passages, and is of still more frequent occurrence in disease of 
the heart, from obstructive hyperaemia, seldom results seriously, and 
rarely imperils the patient’s life. 
Very profuse haemorrhages, of a very different nature, often arise 
from a morbid inability of the capillary walls to resist the pressure of 
their contents, and it is to these that we usually allude, when we em- 
ploy the terms “spitting of blood” (haemoptysis) and “bursting of a 
blood-vessel ” (pneumorrhagia). In such cases an observant physician 
may long foretell the occurrence of a haemorrhage in patients of the 
constitutional habit above described, especially if they have often bled 
at the nose, and have suffered now and then from palpitation of the 
heart, and oppression of breathing. It is but occasionally, however, 
that the attack itself is preceded by warning symptoms or by sensations 
of constriction of the chest. Far more commonly the long-dreaded 
haemorrhage sets in suddenly. The patient feels as though a warm 
liquid were oozing up from beneath the sternum; lie perceives a strange 
sweetish taste in his mouth, and, upon attempting to clear the throat, 
finds that he expectorates pure blood or bloody mucus,—“ that he is 
raising blood.” Such a discovery generally has a very depressing 
effect, even upon individuals of the utmost courage. The saying of 
Mepliistoplieles, “ Blood is a quite peculiar juice,” stands out here in 
its full reality. Though the bleeding may have been trifling, yet we 
often find the patient tremulous, pale, and almost fainting. Soon after 
“ raising ” the first blood, a sense of titillation induces inclination to 
cough. Coarse, moist rales and a gurgling sound are audible in the 
chest; a short, full, loose cough follows, and frothy, bright-red blood 
gushes from the mouth, and often, too, from the nose. Short pauses 
intervene between the coughing-fits, during which more blood seems to 
be escaping and collecting in the tubes, and, in this manner, larg-e quan- 
tities of it are often ejected in a short time. (The quantity of blood 
lost may vary from an ounce or two to a pound or more.) The attack 
may subside in course of half an hour, sometimes sooner; at times not 
for several hours. The mucus continues to retain a bloody stain, or is 
mixed with blood, but the blood is no longer pure. Attacks of haemop- 
tysis are rarely solitary, however. They almost always recur in course 
of a few hours, or perhaps the next day “ in spite of the most careful 
treatment! ” Indeed, the attacks are generally repeated for two or 
three days, or even a week, until at length the patient, who has grown 
pale and feeble, obtains a respite from his haemorrhage, which may last 
for mouths or even years. 
In such cases, and, indeed, in most others, the course of bronchial 
haemorrhage is singularly uniform, whether it occur in consumption, or 
attack persons whose lungs are exempt from tubercle or any other 
known disease. BRONCHIAL ILEHORRHAGE. 
147 
Very rarely is life directly endangered. It is important that we 
should bear in mind that patients nearly always survive the attack, in 
spite of intense prostration, tendency to syncope, and other signs of im- 
pending dissolution. Death from bronchial obstruction and impeded 
respiration is somewhat more common than death from haemorrhage. 
Physical examination of the chest gives negative results, with the excep- 
tion of a few coarse, moist rales / and it is both useless and imprudent 
to agitate the patient by constant and inconsiderate percussion and 
auscultation. If blood enough pass into the vesicles to expel the air 
from any considerable portion of the lung, the percussion-sound over 
that point is flat and dull, and the respiratory murmur either feeble and 
indistinct, or else bronchial. 
In many cases the patients, after expectorating small masses of 
bloody mucus, and of clotted blood, for a while, recover rapidly. If 
blood have lodged in a bronchus, so as to close it and render it imper- 
meable to air, its color is no longer bright red, but grows dark, inclin- 
ing to black. 
In most patients, and even in those who soon regain their health 
after “ a haemorrhage,” by attentive observation, during the few days 
immediately following the bleeding, we shall discover a more or less 
violent inflammatory condition of the lungs and pleura. I at least, ever 
since my attention has been drawn to the occurrence of this consecutive 
pleuro-pneumonia, have almost always succeeded, two or three days after 
an haemoptysis, in finding an elevation of temperature, and increase in 
the frequence of the pulse, constitutional disturbance, and lancinating 
pains of more or less severity in the sides of the chest Moreover, I 
have frequently found a slight dulness, or a friction sound, with sub- 
crepitant rales. Even in cases where considerable time had elapsed 
since the haemorrhage, I have usually been able to discover, by careful 
examination, that, immediately after the occurrence of the bleeding, 
symptoms, more or less distinct, had arisen, of inflammation of the res- 
piratory organs. I cannot comprehend why these sequel* of bronchial 
h*morrhage, which are almost constant, should hitherto have attracted 
so little attention, and why they are hardly anywhere mentioned in 
books on the subject. 
The most frequent termination by far, of this consecutive inflamma- 
tion, is resolution. The symptoms often vanish in a few days, and the 
patient becomes completely convalescent. 
In other instances the elevation of temperature and increased fre- 
quence of pulse continue. The general health is also influenced by the 
persistence of the fever. The pain in the chest, too, continues in a mild 
form, and is generally ascribed, by the patient, to rheumatism. The 
respiration remains hurried, and the patient coughs, expectorating a 148 
DISEASES OF TILE PARENCHYMA OF THE LUNG. 
mucopurulent sputum. If, besides these signs, we find dulness upon 
percussion at some point in the chest, the respiratory murmur feeble, or 
indistinct, if the patient manifestly be growing thinner and more miser- 
able, we shall have very strong reason to fear that a destructive process 
has been set up in the lung, and that the patient will die of phthisis; 
nevertheless, all hope is not to be abandoned. In many cases, after a 
few weeks, the fever, the pain, the dyspnoea, the cough, and the expec- 
toration, all subside, the patient “ feels as though he had had a severe 
fit of sickness.” His recovery is rapid and complete. Physical exam- 
ination shows a depressed spot in the thorax, in the neighborhood of 
which percussion is somewhat deadened and flat, while the respiratory 
murmur is enfeebled. The pneumonia has resulted in wasting and con- 
traction of the inflamed portion of the lung. In the dissertation before 
referred to, two cases of this kind (one of which concerned a former 
assistant of mine) are carefully detailed, and, since then, I have ascer- 
tained, by a large number of observations, that such a result is a very 
common one. 
If a chronic pneumonia, proceeding from profuse bronchial hemor- 
rhage, do not take a turn for the better; if the patient, on the contrary, 
fail more and more under the effect of intense fever with evening exa- 
cerbations, and profuse night-sweats; if the sputa become more copious 
and purulent; if physical evidence of the formation of caverns arise, we 
may conclude that the chronic pneumonia has terminated in cheesy met- 
amorphosis and disintegration of the inflamedpulmonary tissue. 
I may finally repeat that persons, who have suffered a severe hem- 
orrhage from the lungs, even though it may not have been followed by 
any ill effects, and although they may have recovered from it entirely, 
are, nevertheless, in danger of dying, sooner or later, of pulmonary 
tuberculosis, or of pulmonary consumption. 
Diagnosis.—Haemorrhage from the bronchi, not unfrequently, is 
confounded with epistaxis, particularly if the latter proceed from the 
posterior nares, or if the patient lie upon his back during the bleeding. 
Here the blood flowing into the pharynx reaches the larynx, and is then 
frequently coughed and hawked up, to the great terror of the patient 
and his relatives. Long before the physician makes his appearance, the 
regulation doses of salt and vinegar have been administered, and it is of 
importance, in order that he be not deceived himself in the midst of the 
general consternation, that he should deliberately inspect nose, gums, 
and palate, and inform himself precisely whether the patient have not 
bled at the nose on the previous evening. 
The distinction between haemoptysis and haemorrhage from the 
stomach may also have its difficulties, particularly if we have to decide 
upon the source of a haemorrhage which has taken place years before. BRONCHIAL HAEMORRHAGE. 
149 
In haemoptysis, the irritation of the cough often provokes retching and 
vomiting, or the blood may be swallowed, and afterward thrown up. 
Conversely, violent hasmatemesis is almost always attended by cough- 
ing, small quantities of blood getting into the larynx; hence, the pa- 
tients are not always able to tell, exactly, whether they have coughed 
up the blood or vomited it up. In treating of haemorrhage of the 
stomach, we shall enlarge more fully upon the distinction between the 
two conditions, and merely remark, that we must, first of all, inquire 
whether the cough have been followed by vomiting, or the vomiting by 
cough ; secondly, that we must accurately ascertain whether cardialgie 
distress have preceded the gush of blood or not; thirdly, examine care- 
fully as to whether the bleeding have been followed by black, tar-like 
stools, or whether the patient have voided mucus tinged with blood for 
a few days after the attack. If, moreover, we have opportunity to ex- 
amine the blood which has been discharged, that from the air-passages 
is usually bright red, frothy, with alkaline reaction. Should a clot form, 
it will be soft, and specifically light, as it contains bubbles of air. On 
the other hand, blood which has been vomited is dark, and even black, 
excepting where a great artery of the stomach has been eroded. It is 
not mixed with air-bubbles, but contains remains of food; its reaction 
is usually acid, and the clot, if it forms one, is firm and heavy. 
We have now to add a few words regarding the distinction of haem- 
orrhage of the bronchial capillaries from the bleeding arising from a 
wound in the tissue of one of the'larger vessels, which traverse the walls 
of a cavity. It is admitted, by some authors, that a haemorrhage of 
moderate degree, a haemoptysis, proceeds generally from the capillaries 
of the mucous membrane, but that all profuse bleeding, amounting to a 
pneumorrhagia, springs from rupture, or erosion of larger vessels. So 
convinced are they of the justness of this view, that they assume that 
any one who has had a violent haemorrhage, be he never so healthy in 
appearance, has cavities in his lungs, which have heretofore escaped ob- 
servation. The objection, that so large an effusion of blood cannot pos- 
sibly flow from the bronchial capillaries, is untenable; since capillary 
haemorrhages from the nasal mucous membrane are often so profuse as 
to endanger life, and a haemorrhage from the bronchi of equal activity, 
if it flow from a sufficiently large surface, may very easily yield so much 
blood as to fully warrant application to it of the term “bursting a 
blood-vessel,” instead of “ raising blood.” Moreover, many people who 
have spit blood are prone to exaggeration, and talk of “ gushes of 
blood,” and of “ coughing up blood by the pint,” while the actual 
amount lost has not been nearly so large. Besides, it is highly improb- 
able that there should be undiscovered cavities in the lungs of all per- 
sons who have suffered from severe and profuse bleeding from the air- 150 
DISEASES OF TIIE PARENCHYMA OF THE LUNG. 
passages, but who, in other respects, seem to be in good health ; and if 
would be very extraordinary if haemorrhage from small, latent cavities 
were to be of much more frequent occurrence than from large and 
recognizable ones. But we have direct proof that the blood lost in 
pneumorrhagia does not come from a large vessel; at all events, not 
from a branch of the pulmonary artery. According to the classical pic- 
ture of Rokitansky, the branches of the pulmonary artery, as a rule, 
soon become obliterated in the various forms of consumption. Some- 
times, however, they become perforated by erosion, or suffer rupture. 
In them runs the most venous and darkest blood of the entire body. 
Now, in almost every case, not only of haemoptysis, but of pneumor- 
rhagia, the blood is of a remarkably bright-red color, so that, in the differ- 
ential diagnosis between haemoptysis and haematemesis, great stress is 
laid upon the light color of blood which flows from the lungs and air- 
passages. (See above.) It is only when large quantities of dark blood 
are ejected, that we are justified in inferring that a branch of the pul- 
monary artery has become eroded or ruptured. A striking example 
of this kind occurred in my clinique, and has been made public (see 
Ruryer's treatise). Such accidents, however, are extraordinarily rare, in 
comparison with the frequence of haemorrhages of bright-red blood. 
This bright-red blood can only come from the bronchial mucous mem- 
brane ; or, at all events, either from a branch of the bronchial artery or 
of the pulmonary vein. 
Prognosis.—The prognosis, as regards immediate danger to life, is, 
as we have shown, on the whole, favorable, in spite of the alarming 
character cf the symptoms. The prognosis, however, as to complete re- 
covery, is exceedingly bad. The slighter the provocation, the less ap- 
parent the cause of the haemorrhage, so much the graver is the omen. 
The prognosis is better when rupture of the capillaries has been caused 
by excessive hyperaemia, due to direct injuries, excessive action of the 
heart, or other serious irritants, provided that the irritation thus set up 
can be allayed. Suppressed menstruation and repressed haemorrhoids 
can only be counted among these causes with extreme reserve, much as 
the patients may be inclined to attribute their blood-spitting to such 
anomalies, and readily as they may become satisfied, when the physician 
partakes in their belief. Absence of the menses is much more often the 
consequence of the disease than the cause of it, and the same holds good 
for any hoemorrhoidal bleeding which may have existed prior to the 
attack, and whicn has ceased during or immediately after it. 
Treatment—Indicatio Causalis.—If excessive hyperaemia of the 
bronchial mucous membrane play a material part in the origin of a bron- 
chial haemorrhage, or if it be attributable solely to increased lateral pres- 
sure upon the capillary walls from within, the indicatio causalis may, in BROXCniAL HAEMORRHAGE. 
151 
such cases, but only in such cases, demand venesection. In most cases, 
lateral pressure has but little to do with the bleeding. It does not 
cease, though the pressure be relieved, the vessels empty, and the pa- 
tient be almost dead from haemorrhage. Let us but call to mind those 
waxy, pallid sufferers from epistaxis, whose nostrils we often have to 
tampon, in order to master the bleeding, and our lancet will stay in its 
case as long as the heart’s action is moderate. Indeed, we must restrict 
blood-letting to cases where, in spite of the bronchial haemorrhage, there 
is a persistent and alarming hyperaemia of the lung. 
Since we are unable to assign a reason for the delicacy and thinness 
of the capillary walls, which is the chief source of bronchial bleeding, 
we are forced to admit, that the indicatio causalis cannot generally be 
met—that it is not in our power to combat the haemorrhagic diathesis by 
any rationally specific means. At all events, it is scarcely possible, after 
haemoptysis has set in, to effect any rapid change in the abnormal state 
of the capillary wall. It is preferable, in dealing with patients threat- 
ened with this affection, or who have already suffered an attack, to pre- 
serve them with peculiar care from all hurtful agents which could injure 
their nutritive condition. We should order simple, unexciting, nourish- 
ing food ; moderate bodily exercise in the open air ; should carefully 
regulate the action of the bowels ; should prohibit all excess in baccho 
et venere, and enjoin avoidance of mental excitement. Where there is 
a decided want of red corpuscles in the blood, the exhibition of the 
milder preparations of iron, the employment of Pyrmont-water, or that 
of Driburg or Imnau, are to be recommended, and the neglect of these 
measures is a gross blunder. 
The indicatio morbi, above all things, demands a cautious regimen. 
We should, in the first place, seek to calm the spirits of the patient, 
which are always much excited ; and, inasmuch as these attacks are al- 
most always repeated several times, it is well to save him from further 
agitation, by straightway informing him that there is more blood to 
come, while, at the same time, we should absolutely deny the possibil- 
ity of his bleeding to death. Indeed, we are certainly warranted here 
in deceiving the patient, by affecting to make light of the affair, and 
even to represent the haemorrhage as a salutary process.* 
With a little tact, the physician may leave his patient in a state of 
comfort and peace of mind, whom he has found in the most painful un- 
easiness—a success of no slight importance. Take care that the cham- 
ber be cool; forbid all hot drinks, and let all food be eaten cold. In- 
terdict all conversation, and make the patient stoutly resist the provoca- 
tion to cough. Coughing in haemoptysis is quite as hurtful as is snuf- 
* I here call to mind the effect of conjuration and penance on the spirits, and in* 
directly upon haemorrhage. 152 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
fling and wiping the nose in epistaxis. Finally, remove all portions of 
the clothing which press upon and confine the chest, and cause the 
patient to assume a half-sitting posture in bed. The most powerful 
means of combating the bleeding is the use of cold. We apply this 
in the form of cold compresses, and, when the bleeding is very severe, 
in the shape of frozen compresses.* 
In addition to this, let him swallow small pieces of ice, or give 
small doses of ice-water; or we may apply the cold in the form of clys- 
ters, to which, from time immemorial, a little vinegar has always been 
added. Besides cold, a number of substances have the reputation of ar- 
resting haemorrhage without our being able, physiologically, to explain 
how they act. Under this head, before all others, come two remedies: 
common salt, and the acids, which, curiously enough, when taken in ex- 
cess, occasion a scorbutic state of the blood, a bad nutritive state of the 
capillaries, and lead to haemorrhage. However this may be, we must 
make the patient swallow one or two spoonfuls of finely-powdered, dry 
salt. Sulphuric, or phosphoric acids, are still more preferable, especial- 
ly the elixir acidum Halleri, of which we give ten drops every two 
hours, mixed in a sufficient quantity of water. A series of other haemos- 
tatic remedies follow these, which are not of such generally acknowl- 
edged efficacy as the acids, and which, being less innocent, are therefore 
less highly esteemed. Among these is acetate of lead, of which the 
English physicians maintain that, for internal haemorrhage, there is 
“ nullum simile aut secundum.” Next come secale cornutum, oleum 
terebintliinae, balsam copaivae, ratanhy, and other medicines. 
'Wunderlich particularly recommends the exhibition of secale cornu- 
tum, in doses of from five to ten grains, until a prickling and numb sensa- 
tion in the fingers sets in. A formula, much in use in very obstinate he- 
moptysis, is—1£. Balsam copaiv., syrup balsam, aquas menth. piper, spirit, 
vini rectif. aa 3 j; spirit, ether nitrici 3 ss ; Til. S. 3 ij every two to four 
hours. These various drugs are only to be made use of in very danger- 
ous cases, and we should not forget how impotent all these styptics are 
in severe bleeding of the nose, where, moreover, we are able to apply 
them directly to the bleeding point. Latterly, inhalations of a solu- 
tion of sesquichlorate of iron (3j to 3 ss with § vj) has been recom- 
mended as exceedingly serviceable against haemoptysis. The most 
alarming haemorrhages are said to have been arrested, by this means, in 
the course of four or five minutes. My own experience does not con- 
firm this recommendation. The narcotics should be employed freely. 
The more restless the patient, the more violent his cough, so much the 
* Fill a tin or copper warming-pan with ice, salt, and water, then lay it upon a 
well-squeezed wet compress, the moisture of which soon freezes. These compresses 
are greatly to be preferred to the heavy bladders of ice. HaEMORRHAGIC infarction of the lung. 
153 
more boldly should we order opium. Let a Dover’s powder be taken 
at night, and during the day an emulsion, with half a drachm of lauda- 
num, or half a grain of morphine. 
CHAPTER VII. 
PULMONARY HAEMORRHAGE WITHOUT LACERATION OF THE PAREN- 
CHYMA— IIaEMORRIIAGIC INFARCTION—METASTASIS TO THE LUNGS. 
lx former editions of my text-book I have treated of pulmonary 
haemorrhagic infarction, which occurs from disease of the heart, and the 
so-called metastatic infarction in separate chapters, since, notwithstand- 
ing the complete identity in their essential anatomical lesions, the differ- 
ence in their extent and seat, and, above all, the different manner in which 
they originate, seemed to me to demand it. But from an opinion of Roki- 
tansky, from an excellent essay by Gerhardt, and especially owing to a 
series of observations of my own, published in five dissertation of Doctor 
Hopf* I have become satisfied that my former views were erroneous; 
that the variations in magnitude and in the seat (neither of which are 
constant) constitute no real difference, and that the modes of origin of 
haemorrhagic infarction in heart-disease, and of that of metastatic infarc- 
tion from thrombosis of a vein, or from external suppuration, or sanious 
ulceration, are identical. 
Etiology.—Haemorrhagic infarction consists in a capillary haemor- 
rhage, confined to a small and sharply-defined section of the lung, and 
often bounded by the limits of a single lobule. The blood is effused, 
partly within the cavity of the vesicles and terminal bronchi, and partly 
lies in their interstices between the fibres of elastic tissue by which the 
air-cells are entwined. The haemorrhage does not produce laceration 
of the lung-substance. The abrupt boundary of a haemorrhagic infarction 
is caused by the fact that the bleeding only comes from the capillaries 
pertaining to a single twig of the pulmonary artery. The range of the 
capillary system of an artery depends upon its size; hence haemorrhagic 
infarctions which arise within the capillary limit of a large branch of the 
pulmonary artery are far more extensive than one which forms about a 
smaller twig. As the main trunks of the pulmonary artery enter the 
roots of the lung in company with the great bronchi, and ramify toward 
the surface, constantly growing smaller by repeated subdivision until 
each ultimate twig terminates in a single lobule, the reason is plain why 
the infarctions occurring in the interior of the lung are large, and why 
* Zur Diagnose des Hsemorrhagischen Infarctes. Inaugural Dissertation vorj 
Dr Ilopf. Tubingen, 1865. 154 
DISEASES OF TIIE PARENCHYMA OF THE LUNG. 
peripheral infarctions preserve both the size and the cuneiform shape of 
the superficial lobuli. Upon careful examination of an arterial branch 
within whose range a haemorrhagic infarction has formed, we find in it 
a clot by which its calibre is more or less obstructed. This is easily 
demonstrated in the larger vessels, but in the very small ones it is some- 
times difficult 
That the obstructing coagulum has not formed at the place of its 
lodgment, but that it comes from some remote region of the body, 
whence it has become detached and swept into the current of the blood, 
until, finally, it has become impacted in some branch of the pulmonary 
artery too narrow to admit of its passage, has long been recognized 
as the conditions under which haemorrhagic infarction arises. The 
credit of this valuable discovery is due to Virchow. That investigator, 
by introducing particles of fibrin, muscle, elder-pith, and the like into 
the jugular veins of dogs, demonstrated by dissection that these foreign 
bodies blocked up branches of the pulmonary artery, and produced 
hemorrhagic infarctions, lobular pneumonia, and small abscesses, beyond 
the points obstructed. Conversely, he proved by dissection of bodies, in 
which the diseased spots so long known as metastases had been found, 
that the arteries leading to the affected points were occluded by an 
embolus—a fibrinous plug, which undoubtedly had proceeded from a 
thrombosis of a superficial vein, or frdm particles whose origin was in- 
disputably traceable to some region of suppurative or sanious ulceration 
upon the surface. 
Of late, the doctrines of pyaemia and of septicaemia have undergone 
many revolutions; but that of embolism—that is, of the dependence of 
haemorrhagic infarction upon the introduction of clots, or of particles of 
tissue into the circulation—has remained unshaken. 
It is easy to understand why metastatic infarctions of the lungs are 
caused by emboli from disintegrating thromboses of peripheral veins, or 
from suppurating or sanious surfaces. When an embolus is detached 
from its point of origin by the current of the blood, it meets with no 
obstacle on its way to the heart, as the veins through which it travels 
are constantly growing larger. It passes unhindered into the right heart 
and into the pulmonary artery, and is not arrested nor impacted until it 
arrives at some branch of the latter whose diameter is less than its own. 
Upon similar grounds, it is the rule for emboli, which originate from the 
roots of the portal vein, or which enter the portal vein in cases of ulcera- 
tion or of sanious discharge from the intestines, to pass into the ramifica- 
tions of the portal vein within the liver, causing metastases in that 
organ, and for emboli which come from the lungs on the left side of the 
heart to occlude the arteries of the spleen, kidneys, or brain. Where 
exceptions to this rule occur, as when we sometimes find infarctions in ILEMORRHAGIC INFARCTION OF THE LUNG. 
155 
organs whose arteries an embolus could not hare reached, without first 
passing through the capillaries of another organ (for instance, infarc- 
tion of the liver in thrombosis of a peripheral vein), it seems probable 
that the embolus at first has been minute, but that during its course 
through the system it has grown larger by accretion of fibrin. The 
very common occurrence of haemorrhagic infarctions after injuries of the 
skull, where the diploe have been penetrated, is simply due to the 
gaping of the walls of the veins of this region, which, being adherent 
to the tables of the skull, are prevented from collapsing, so that the 
entrance of coagula into them of course is facilitated. 
In the haemorrhagic infarctions which so often arise in diseases of 
the heart, especially in cases of disease of the mitral valve, the existence 
of clots in the arteries leading to them has long been known. But the 
explanation generally has been that the escape of blood into the vesicles 
and their interstices has compressed the capillaries and prevented the 
outflow of blood from them, and that in consequence of the stagnation 
so produced the arterial contents have coagulated. This was formerly 
my opinion, although I could not ignore that the extreme obstruction 
of the blood in the pulmonary circulation, to which I ascribed the infarc- 
tion in disease of the heart, did not at all account for the restriction of 
the capillary haemorrhage to separate and abruptly-defined sections of 
lung. I am now convinced that, in disease of the heart, haemorrhagic 
infarction also arises from embolism, as has been proved by Rokitansky 
and Gerhardt. The emboli which block the artery in disease of the 
heart do not come from the greater circulation, like the emboli which 
produce metastatic infarction, but from the right side of the heart, 
especially from the right auricle, in which clots usually exist firmly en- 
tangled in the trabeculae, and which are one of the results of the slug- 
gishness of the circulation. If a particle of this clot be tom off and 
washed away by the current of the blood, a branch of the pulmonary 
artery becomes obstructed by it, and haemorrhagic infarction ensues. 
The fibrinous coagula thus detached from cardiac thromboses are gen- 
erally larger than those which come from the aortic circulation. We 
thus find a very simple explanation of why the infarctions of heart-dis- 
ease are more extensive than metastatic infarctions, as well as of why 
the former are often found in the interior of the lung, near its roots, 
while the latter are generally situated near the periphery. As very 
minute particles also may be washed away from the thromboses of 
the right heart, we likewise see how, besides the larger infarctions at the 
roots, smaller peripheral ones also occur in heart-disease. 
The process still remains to be explained by which obstruction of an 
afferent arterial branch produces capillary haemorrhage in the region 
about the obstructed vessel, a process which, at the first glance, seems 156 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
by no means easy of elucidation. The theory of Rokitansky, “ that 
occlusion of the minutest arterial branches of the lung and its capillaries 
causes a collateral hypercemia, which results in hasmorrhage and exuda- 
tion,” is unsatisfactory to me, for the bleeding does not proceed from 
neighboring capillaries, but from those of the obstructed vessel. Nor 
does Virchow give a sufficient explanation of the capillary haemorrhage. 
It is, therefore, all the more welcome and interesting that Ludwig has 
furnished a complete and final solution of the problem, from an entirely 
unbiassed point of view, by showing the influence which the contraction 
of an artery has upon its capillaries. His words are as follows: “ Ten- 
sion within the artery below the point of constriction is diminished, 
since a liquid flowing through a narrow tube loses more of its impetus 
than in flowing through a wide one. But we must not infer from this 
that, when an artery is constricted, the contents of its capillaries are less- 
ened, and that the parts which they traverse grow paler. The sluggish- 
ness of the stream thus produced in the capillaries rather has the effect 
of allowing the heavy blood-corpuscles to collect and become crowded 
together ; now, as two or more blood corpuscles, if brought into contact, 
are apt to become permanently adherent, the blood itself can form a 
plug capable of closing the capillaries. Such an occurrence, winch con- 
verts the capillaries into blind appendices to the artery, must cause an 
increase in its internal pressure.” Let us add that in consequence of 
the pressure, which, after the stoppage, is as severe in the capillaries 
with thin, delicate walls, as in their afferent vessels, a rupture of the 
distended Avails and an escape of blood ensue. This furnishes a simple 
and entirely satisfactory explanation of the origin of the hasmorrhage, 
as Avell as of its limitation to the region supplied by the occluded artery. 
The utmost that can be advanced against the accuracy of this explana- 
tion is, that the artery leading to an infarction not only is narroAved, but 
is entirely closed. Such an objection, lioAvever, is untenable. The in- 
farction of an embolus, which Ave find usually takes place at the bifurca- 
tion of an arteriole, very rarely produces absolute closure of it at first, 
but merely causes in it more or less obstruction. Aftenvard, when the 
infarction has become established—an event requiring but little time— 
fibrin is deposited upon the embolus, and closure of the A7essel becomes 
complete. 
Under conditions similar to those under Avhich metastatic infarctions 
are observed, Ave sometimes find in their stead, or accompanying them, 
circumscribed pneumonic infiltration and small abscesses. As a rule, 
these appearances are manifestly the latter stages, the products of in- 
farction; and it is not surprising that such products should be very 
common, and should form \rery rapidly, AA’hen the emboli consist of 
fragments of sanious or gangrenous tissue, capable of most pernicious HAEMORRHAGIC INFARCTION OF THE LUNG. 
157 
action upon the parts in contact with them. The truth of this idea is 
supported by the fact that in disease of the heart, where the emboli are 
simple fibrinous clots, which are much less dangerous to the parts ad- 
jacent to them, destructive pneumonia and the formation of abscess are 
far more rare. The inflammatory reaction which occurs in the latter 
form is generally more of a nutritive than of a destructive character, 
and often results in a development of connective tissue, by which the 
infarction becomes incapsulated. 
In a few instances, both formation of abscess and circumscribed pul- 
monary gangrene seem to ensue, the latter being a rare termination of 
infarction. Here the extravasation and compression of the capillaries 
above described cause secondary coagula to form, and this time it is in 
the nutritive vessels of the lung, the ramifications of the bronchial arte- 
ries, the pulmonary “ vasa privata.” Nutritive material is thus with- 
held from the point of infarction, which dies and putrefies, or becomes 
gangrenous. 
Anatomical Appearances.—We rarely find the blood liquid in 
dissection of recent infarctions; as a rule, it is coagulated. This circum- 
stance is easy to account for, if we reflect that the locality impedes a 
discharge of the blood, and that, if the patient survive the attack for any 
length of time, the liquid part is absorbed, while the coagulable portion 
is retained. The blood is easily expelled from the bronchi by coughing, 
by the action of the bronchial muscles, and by that of the ciliated epi- 
thelium, but forced expiration can only empty the vesicles in part, and 
they have no muscles nor ciliary epithelium. 
Haemorrhagic infarctions which occur in disease of the heart gener- 
ally vary in size from that of a hazel-nut to that of a hen’s egg. They 
are of a blackish-red or blackish color, completely inelastic, and void of 
air, so that they can be felt from without like hard knots. Their cut 
surface presents an irregular, coarse, granulated aspect, from which a 
brownish-black mass may be scraped off with the scalpel. In the im- 
mediate vicinity of this sharply-defined spot the lung is usually full of 
blood and oedematous from collateral fluxion. Its seat, as already men- 
tioned, is usually at the middle of the lower lobes, or near the roots of 
the lungs; more rarely at the surface. Microscopic examination shows 
the capillaries to be distended by blood-corpuscles, which are also col- 
lected in the tissue outside of the capillaries. 
Where the infarction is of long standing, it looks paler and yellow- 
ish, the fibrin having undergone fatty degeneration, and the coloring 
matter of the blood being partially decomposed. Still later, the fatty 
fibrin is absorbed, and part of the haematin has turned into pigment, 
and the only remaining trace of the infarction is a blackish induration 
in the lung. In the rare instances in which an abscess forms it may be- 158 
DISEASES OF THE PARENCHYMA OF TOE LUNG. 
come incapsulated, and its contents may thicken into a cheesy or calca* 
reous mass. 
Gangrene of the lung, as a result of haemorrhagic infarction, will be 
described in Chapter XII. 
In explaining the pathogeny of metastatic infarction, we have already 
alluded to the small volume, the cuneiform shape, and superficial situa- 
tion which it generally assumes. In color, consistence, and friability, 
metastatic infarctions are entirely similar to those which arise from dis- 
ease of the heart. The microscope also gives the same appearances. 
When metastatic infarction terminates in metastatic pneumonia or 
abscess, discoloration and disintegration generally commence in the 
middle of the diseased part; cavities form, filled with a yellow mass, 
which consists of debris of the pulmonary substance, and of molecular 
decay of the extravasated blood and fibrin, but which at first does not 
contain any j>us. Upon pouring water over its cut surface, we can see 
the vestiges of the lung floating in the hollow. The disintegration 
spreads gradually until scarcely a trace is left of former thickening, 
even at the periphery of the abscess. When situated immediately under 
the pleura, yellow croupous deposits form upon the latter, which cause 
the pleural surfaces to become adherent, and beneath it lies the infarc- 
tion, “ forming a rounded-nodular prominence like a furuncle ” (Roki- 
tansJcy). 
Symptoms and Course.—We shall treat separately of the symp- 
toms of haemorrhagic infarction arising from diseased heart, and of those 
of metastatic infarction; since the appearance of the two forms of dis- 
ease, in spite of their anatomical identity, varies in many respects on 
account of the difference in the diseases which cause them. 
In many cases of chronic disease of the heart, haemorrhagic infarction 
sets in with such well-marked and unequivocal symptoms, that its exist- 
ence can be demonstrated with perfect certainty. In other cases the 
proof is difficult, or quite impossible. 
The characteristic symptoms, from which we can infer the Ijprmation 
of one or more haemorrhagic infarctions in a case of disease of the heart, 
are, a sudden dyspnoea, which may threaten suffocation, and a cough 
with a peculiar sputum tinged with blood. In many instances there are 
the signs of a circumscribed condensation of the lung, which are not un- 
frequently followed by those of pneumonia or of pleurisy. It is manifest 
that the stoppage of one or more branches of the pulmonary artery will 
produce extreme dyspnoea. As the process of respiration can only be 
carried on normally, when both the air in the vesicles and the blood in 
the capillaries are properly renewed, the arrest, either of access of blood, 
or of entrance of air into part of the lung, the obstruction, either of a 
bronchus, or of an arterial branch, must have an equal and extremely HAEMORRHAGIC INFARCTION OF THE LUNG. 
159 
embarrassing' effect upon respiration. The sputa, from the strong admix- 
ture of blood which they contain, bear a certain resemblance to pneu- 
monic sputa, but they are less tough and almost always darker; and, 
moreover, the expectoration of this secretion is continued for a much 
longer time than is the expectoration of pneumonia. The former may 
persist for a week or even a fortnight. Circumscribed condensation of 
the pulmonary tissue can only be detected when the haemorrhagic in- 
farction is of comparatively large size, and has extended to the surface 
of the lung. The sound upon percussion then becomes dull, and crepi- 
tation and bronchial sounds are audible over a limited region of the 
chest. Although such cases occur, they are rare. The diagnosis may 
be confirmed, a few days after the attack of dyspnoea and bloody expec- 
toration, by the development of extensive pneumonic infiltration, or of 
inflammatory effusions into the pleural sac, as we find that haemorrhagic 
infarctions often produce inflammation of the surrounding pulmonary 
tissue, and still more frequently cause inflammation of the pleura. 
Besides the symptoms hitherto described, and which are all imme- 
diately dependent upon stoppage of one or more branches of the pulmo- 
nary artery, there are, in many cases, other symptoms, which proceed 
from the thrombosis of the right heart, and hence are to be regarded 
as indirect tokens of haemorrhagic infarction. These are, a sudden 
irregularity of the pulse, a sudden widening of the cardiac dulness, and 
the sudden cessation of an adventitious murmur, which had previously 
existed. This sudden subsidence of a loud, morbid sound is not only 
a most striking occurrence, but one which is generally very significant. 
My attention was first called to the full meaning of this symptom by the 
work of Gerhardt above alluded to; but I can fully confirm both the 
occurrence of the sign and its full diagnostic importance from my own 
experience. The picture of a haemorrhagic infarction becomes very 
well marked, when the latter group of symptoms coexists with those 
described above. But emboli may break ofF, and be washed away from 
cardiac thromboses so small, that they produce no characteristic phe- 
nomena ; hence, even where there are no signs of cardiac thrombosis, 
where the pulse remains regular, and where the cardiac dulness con- 
tinues unchanged, we may still confidently diagnosticate haemorrhagic 
infarction, whenever unequivocal signs of disorder of the circulation 
and capillary haemorrhage of the lungs suddenly arise in the course of 
disease of the heart. 
Finally, if we bear in mind that the characteristic expectoration of 
the blood from the air-vesicles is not always observed in haemorrhagic 
infarction, and, moreover, that violent fits of dyspnoea may arise from a 
great variety of causes iu disease of the heart, and that infarctions, 
seated deep within the lung, cause no physical signs, it is easy to under- 160 
DISEASES OF THE PARENCHYMA OF THE LUXG. 
stand why the disease, which, in many cases, does not present the small* 
est difficulty of diagnosis, may sometimes elude detection and even sus- 
picion—as, for instance, where the patient is already extremely short of 
breath, and dropsical, and is otherwise wretchedly ill. In the dissection 
of cases of diseased heart, therefore, we should be prepared to find 
hcemorrhagic infarctions as “ accidental discoveries ” where their exist- 
ence has not been suspected. 
The liquid products of inflammation or of ulceration almost always 
pass into the circulation with the emboli; and, while the latter give 
rise to metastatic infarctions, the former result in the symptoms of 
pyaemia, septicasmia, intense fever, rigors, purulent inflammation of 
serous membranes, and the like.* We thus see why most patients with 
metastatic infarction of the lung are extremely depressed, wrhy iheir 
sensorium is blunted by the intensity of the asthenic fever, and why 
they neither complain of pain in the side or breast, nor show any incli- 
nation to cough. In most cases there are neither subjective nor objec- 
tive symptoms of disease of the lung. It is even the rule, at the autopsy 
of persons who have died of pyaemia and septicaemia during some sup- 
purative or ulcerative process, to find metastatic infarction in the lungs, 
which, during life, was quite indistinguishable. These latent metastatic 
infarctions are easily accounted for, if we only call to mind the symp- 
toms upon which diagnosis of the disease is based. The intense dysp- 
noea, which appears in cases where large arterial branches in the lung 
are obstructed, does not exist in metastatic infarction, where the occlud- 
ed arteries are nearly always very small. Dyspnoea of slighter degree 
is not noticed by the patient in his stupefied condition. In like manner 
the characteristic sputum is almost always absent, as generally the 
patient neither coughs nor expectorates. Finally, notwithstanding 
their superficial position, metastatic infarctions scarcely ever occasion 
circumscribed dulness upon percussion, or produce bronchial breathing 
in the affected region. It is only in very rare cases that patients com- 
plain of piercing pain in some point of the chest, and expectorate thin, 
reddish-brown sputa. If, besides, a friction-sound be audible in the 
region of the pain, and if the original malady be one frequently produc- 
tive of metastatic infarction in the lung—as, for instance, an injury of the 
skull affecting the diploe—we may pronounce our diagnosis with con- 
fidence ; but, I repeat, that cases like this are very exceptional. 
* According to recent observations, the introduction into the blood not only of 
decomposed liquids, but even the absorption of liquid inflammatory products which 
are not decomposing, gives rise to violent fever, and to secondary inflammatory pro- 
cesses in distant parts of the body. It would thus seem as though pysemia, which has 
been in some danger of disappearing from the list of diseases, may maintain its place 
by side of septicaemia. PULMONARY APOPLEXY. 
161 
Treatment.—The treatment of haemorrhagic infarction can only 
be a treatment of symptoms. When the affection proceeds from dis- 
ease of the heart, we must beware of attributing the dyspnoea to 
an aggravation of the pulmonary hyperaemia. We are aware that its 
real or chief cause is anaemia of portions of the lung. An injudicious 
venesection might have the effect of increasing a collapse of the lung 
already present, and of hastening a fatal issue. It is only when the 
obstruction of sundry arterial branches in the lung, has given rise to 
collateral hyperaemia, and to collateral oedema of the rest of the lung, 
and when the dyspnoea is plainly due in great measure to this cause, 
that cautious blood-letting, either by cupping or venesection, is ever ad- 
missible. As a general rule, until the pulse, which usually is feeble, 
grows stronger, and until the skin, which usually is cool, becomes 
warmer, we must confine our treatment to stimulation of the patient, 
and to the application of sinapisms and warm baths to the extremities. 
The expectoration of blood is rarely so abundant as to call for exhibition 
of the haemostatic remedies recommended in a previous chapter. The 
inflammation of the lung or pleura, which often sets in at a later period, 
may demand local depletion, the application of cold and other anti- 
phlogistic measures. 
CHAPTER VIII. 
PULMONARY II.EMORRIIAGE WITH LACERATION OF THE PARENCHY- 
MA. APOPLEXY OF THE LUNG. 
Etiology.—In this form of pulmonary haemorrhage the tissues are 
destroyed by extravasated blood, and an abnormal cavity is established. 
Capillary haemorrhage scarcely ever destroys the tissues of the lung. 
It is only erosion or laceration of the larger vessels, especially rupture 
of the arteries, which produces destruction of this kind. In rare cases 
atheromatous degeneration of the pulmonary artery causes its aneuris- 
mal dilatation and final rupture; but, more commonly, wounds, contu- 
sions, or concussions of the thorax, are the causes of pulmonary apoplexy. 
Anatomical Appearances.—A cavity is found in the lung, con- 
taining both liquid and coagulated blood, and surrounded by tatters of 
the lacerated pulmonary substance. If the apoplexy have its seat on 
the periphery, the pleura, too, is often torn, and blood is poured into its 
sac. Such haemorrhages are almost always fatal, so that we have little 
knowledge of the mode of repair of an apoplectic centre. 
Symptoms.—Violent and rapidly-fatal haemoptysis, following serious 
injury of the thorax, or, in other cases, suffocation from effusion of blood 
into the bronchi, faster than it can be expectorated, or sudden death 162 
DISEASES OF THE PARENCHYMA OF TIIE LUNG. 
from infernal haemorrhage, may be the symptoms of this exceedingly rare 
disease, Avhich, being absolutely deadly, is susceptible of no treatment. 
INFLAMMATION OF TIIE LUNGS. 
Inflammation of the lungs may properly be regarded as of three kinds: 
1. Croupous pneumonia, in which the air-cells are involved in a 
process identical with that which attacks the mucous membrane of the 
larynx in laryngeal croup. 
2. Catarrhal pneumonia, a process intimately related to that 
already described as catarrhal bronchitis and laryngitis, producing an 
augmented secretion, and active generation of young cells (pus-cor- 
puscles), but in which no coagulable exudation is formed. In both 
these \7arieties of inflammation the inflammatory products are thrown out 
upon a free surface, the tissue of the lung itself suffering no essential 
disturbance of nutrition. 
3. Interstitial pneumonia, which is an inflammation involving the 
walls of the air-vesicles, and the interlobular connective tissue. As in 
the human subject, this latter form is ahvays a chronic disease; it has 
been also called chronic pneumonia, in contradistinction to the other 
varieties, Avliose course is usually acute. 
CHAP TEE IX. 
Etiology.—With regard to the pathogeny of croupous pneumonia, 
we refer to what has been said in the second chapter of the first section 
concerning croupous inflammation, and of its distinctness from diphthe- 
ria. In croupous pneumonia, also, a fibrinous, rapidly-coagulable exu- 
dation is thrown out upon the free surface of the air-vesicles, involving 
their epithelium, and including the newly-formed cells. Here, too, the 
vesicular Avails become completely restored after expulsion of the exu- 
dation. 
Sometimes pneumonia occurs under the influence of an acute clys- 
crasia, just as catarrh (as we have learned) attacks the air-passages in 
measles, exanthematic typhus, etc. This form of pneumonia, AA'liich ac- 
companies typhus more often than it does other acute infectious dis- 
orders, may be distinguished by the name of secondary pneumonia, 
from the other varieties which arise more independently, and constitute 
a separate disease, which Ave may call primary pneumonia. It is 
CR0UP0TJS PXEUMOXIA. CROUPOUS PNEUMONIA. 
163 
wrong, however, to regard all cases of this disease, which supervene 
upon some chronic malady, as belonging to the secondary form. 
The liability to primary croupous pneumonia exists at all periods of 
life, down to extreme old age. It is rare, however, among infants at the 
breast, and in the first years of childhood. Males are attacked more fre- 
quently than females ; not, however, because vigorous, full-blooded per- 
sons are peculiarly subject to the disease. The latter, indeed, are by 
no means exempt; but feeble and broken-down subjects, convalescents 
from grave diseases, individuals who already have repeatedly suffered 
from pneumonia, are, perhaps, more liable to be attacked than the 
robust; and pneumonia often complicates diseases which have already 
effected an impoverishment of the blood, with emaciation and consti- 
tutional exhaustion. Very many of the inmates of hospitals, sufferers 
from inveterate disease, finally succumb to intercurrent pneumonia. 
Its exciting causes are generally unknown. At times pneumonia 
becomes of very frequent occurrence, while croup, acute articular rheu- 
matism, erysipelas, and other acute inflammatory disorders prevail at the 
same time, attacking their victims without any obvious provocative. 
This prevalence of acute inflammatory disease through the operation of 
unknown atmospheric and telluric agencies is generally spoken of as 
inflammatory epidemic influence. We particularly observe the epi- 
demic occurrence of pneumonia in severe and protracted winters during 
the prevalence of a northeast wind. Sometimes, however, it arises 
under conditions precisely the reverse. The statistical statements as to 
the greater frequence of pneumonia in northerly and elevated localities 
have, of late, been regarded as untrustworthy. 
Direct irritants acting upon the lungs, the inhalation of very cold or 
very hot air, foreign bodies, which have entered the air-passages and 
stopped up a bronchus, fractures of the ribs, wounds of the thorax, may 
be counted as among the exciting causes, although scarcely any of these 
conditions are found to exist in one case of pneumonia out of fifty. Nor 
is the croupous form of the disease often found to attack the parts 
about a morbid growth or around a haemorrhagic infarction. 
With regard to the influence of cold, it is difficult to decide in indi- 
vidual instances whether the attack has been preceded by an exposure 
to cold more severe than that to which the patient has repeatedly 
exposed himself with impunity. Opinions, therefore, are divided as 
to the effect of cold in producing pneumonia. 
Anatomical Appearances.—Croupous pneumonia almost always 
attacks a somewhat extensive portion of the lung, commencing usually 
at the root, and spreading thence to the lower and afterward to the 
upper lobes. Sometimes an entire lung is inflamed, or the process may 
extend into the other lung, producing a double pneumonia. It is 164 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
curious that in old persons and in cachectic individuals the mode of exten- 
sion is usually different, as here the upper lobes are generally the first 
to be attacked, the lower not becoming involved until a later period of 
the disease. We distinguish three anatomical stages in pneumonia: 
1st, the stage of engorgement with blood (engouement); 2d, the stage 
of hepatization; 3d, the stage of purulent infiltration. 
In the first stage the pulmonary parenchyma is dark red, often red- 
dish brown. It is heavier and firmer, has lost its elasticity, and pits upon 
pressure. Upon section, the inflamed portion of the lung does not 
crackle much, and a brownish or reddish liquid, of a strikingly viscid 
and tenacious nature, bathes the surface of the cut. 
In the second stage, the air has disappeared from the air-vesicles, 
and the latter are filled by small, firm plugs of coagulated fibrin, to 
which an admixture of blood imparts a reddish color. A similar exuda- 
tion has taken place in the extremities of the bronchi. The lung has 
now become remarkably heavy, sinks in water, does not crackle, is firm 
to the touch, but is very tender and friable. The appearance of its cut 
surface is granulated, especially when viewed by oblique light, and this 
is most distinct where the air-vesicles are large; less so in children, 
where they are small. The granules (which are merely the fibrinous 
plugs so often mentioned) can no longer be extracted from the lung by 
scraping with the scalpel, but adhere firmly to the walls of the air-cells. 
The granulated aspect of the cut-surface, the rigidity, the friability, the 
redness of the condensed lung, impart to it a considerable resemblance 
to liver, and thus the generally-adopted name of red hepatization has 
arisen. Sometimes, owing to spots of lighter color, and to deposits here 
and there of the black pigment which is secreted in the lung, together 
with the whiteness of the interior of the bisected bronchi and vessels, 
the section, instead of a uniform red, presents a variegated, “ marbled,” 
granite-like appearance. Afterward the redness fades more and more, 
either from cessation of the hyperaemia, or from disintegration of the 
hsematin. The lung assumes a gray or yellowish appearance, while the 
texture continues in other respects, the same, the pulmonary substance 
remaining rigid and granular (yellow hepatization). Besides the amor- 
phous fibrin which fills the air-vesicles, the microscope reveals a very 
active formation of new cells, which probably spring from the epithe- 
lium of the vesicular walls. Should resolution set in, in the stage of 
hepatization, the fibrin and the young cells entangled in it undergo fatty 
metamorphosis and disintegration. An albuminous serum transudes 
from the walls of the vesicles; their contents become liquefied, con- 
verted into an emulsion, and finally are eliminated, by absorp- 
tion, partially by expectoration. There is a slight deviation from the 
above when the pneumonic exudation is less fibrinous and less coagu- CROUrOUS PNEUMONIA. 
165 
lable. The hepatized portion then is softer, its cut is smoother, and 
without distinct granulation. This is most common in the secondary 
pneumonia of typhus, and in that of old persons. When the pneu- 
monia passes into the third stage, that of purulent infiltration, cell-for- 
mation assumes prominence, while the fibrin undergoes disintegration 
as in other cases. The granulated appearance is lost, the cut-surface is 
of a pale gray, or grayish yellow. A reddish-gray matter bathes its 
surface, and may be expressed in large quantities. The tissues are ex- 
ceedingly tender, and are easily torn by the pressure of the finger. The 
minuter structure of the lung, however, is unaltered; the pulmonary 
tissue itself is still intact. Here, too, therefore, complete recovery may 
take place. The purulent contents may be ejected in part, and in part 
may undergo fatty degeneration and become absorbed. 
The rarer sequeke of pneumonia are. 
1. Formation of abscess. The purely croupous form of inflamma- 
tion with which we have here to do essentially excludes the idea of a 
destruction of the inflamed tissue. When abscesses form, the process 
has more of a diphtheritic nature. The proper tissue of the lung be- 
comes infiltrated, and sloughs from the pressure of the fibrinous infiltra- 
tion. In this way small cavities, filled with pus and debris of the pul- 
monary substance, form in the lung, which itself is infiltrated with pus. 
Sometimes they are solitary and sometimes they exist in great number. 
These collections of pus may increase in size from continual melting 
down of the tissues; several of them may coalesce, so that finally a 
huge abscess may occupy the greater part of the lung. These abscesses 
either end fatally through ulcerous phthisis, or else, in rarer instances, 
they open into the pleural sac. In other cases, a reactive interstitial 
pneumonia is set up in the parts adjacent, by which the abscess is in- 
capsulated in a firm cicatricial tissue, its inner wall becoming smooth. 
Should a communication with the bronchi remain, its contents are evacu- 
ated from time to time, but are replaced by fresh matter generated by 
the interior surface. Should the cavity be closed, the pus may become 
thickened, and be converted into a cheesy paste, or, after disappearance 
of the organic substance, may change into a mortar-like or chalky con- 
cretion, which lies imbedded in an indurated firm scar. 
2. Gangrene of the lung is a still rarer sequel to pneumonia. It ap- 
pears only to occur when the supply of blood has been completely cut off 
from the inflamed portion of the lung by the formation of large coagula in 
the pulmonary arteries, and more especially when they form in the bron- 
chial arteries, by whose means nutrition of the lung is carried on. The lung 
may become gangrenous even in the stage of red hepatization. The exu- 
dation then changes into a grayish ichorous liquid, and the pulmonary 
tissue breaks down into a blackish pulp. (See Chapter XII.) 166 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
3. The termination of croupous pneumonia in cheesy infiltration (or, 
as it is still too often called, tuberculous infiltration) is more common. 
If, in the second or third stage of the disease, when the fibrinous effu- 
sion and the cells which fill the vesicles take on fatty degeneration, the 
supply of serum effused by the walls of the vesicles prove insufficient, 
the fatty masses begin to dry up before their liquefaction is completed, 
and are converted into a more or less firm, yellow, cheesy substance. 
Hereafter we shall again refer to the subsequent changes occurring in 
this caseous infiltration of the lung, and shall express ourselves upon 
the inexpedience of permitting the imputation to arise of a sort of iden- 
tity of the products of the latter process with those of tubercular granu- 
lation, by applying a similar title to both. 
4. Cirrhosis of the lung, or induration, is finally to be mentioned 
as a rare termination of tedious pneumonia. This sequel is due to par- 
ticipation of the vesicular walls and the interstitial tissue in the process, 
when the disease is of long standing. Of this we shall treat more in 
detail in Chapter XI. 
That portion of the lung which is not attacked by the inflammation 
is the seat of intense hyperaemia, as before stated; in fact, pulmonary 
oedema is, in many cases, the actual 'cause of death. Wherever the in- 
flammation extends to the periphery of the lung the pleura also becomes 
implicated, showing minute arborescent injection and ecchymosis. It is 
then clouded and opaque, flabby, and covered with a thin layer of fibrin. 
Generally, the right side of the heart, from which the outflow of blood 
has been impeded by the stasis of the capillaries of the lungs, is over- 
flowing with blood; the left heart, its supply being abnormally dimin- 
ished, is less full. In like manner, and for the same reasons, stagnation of 
blood exists in the jugular veins, in the sinuses of the brain, and in the 
liver and kidney. The condition of the blood is exceedingly striking. 
The major part of that which is in the great vessels is not liquid, but 
is coagulated into firln yellow masses. Lumps of curdled fibrin exist in 
the heart, where they are firmly entangled amid the trabeculre and under 
the valves; and long, firm, tough, polypous coagula may be drawn out 
of all the arteries. 
Symptoms and Course.—We shall discuss the subject of secondary 
pneumonia in treating of typhus, etc., as it is impossible to draw up a 
picture of this disorder without making a detailed analysis of the symp- 
toms of the disease upon which it depends. 
The commencement of primary pneumonia, in almost all cases, is 
announced by a rigor which may last for half an hour, or even for sev- 
eral hours, before giving place to a sensation of heat. As is well 
known, the cold is a mere subjective symptom, and the temperature is 
appreciably elevated, even during the algid stage. CROUPOUS PNEUMONIA. 
167 
This rigor is important both in a diagnostic and in a prognostic 
point of view. In no other affections, excepting intermittent fever 
and septicaemia, do we encounter chills of equal violence; and in the 
latter disorders the paroxysms are repeated, while the rigor which 
ushers in pneumonia is almost always the only one throughout the 
entire course of the illness. It is from this chill that we calculate, in 
counting the duration of the disease. In children, convulsions often 
occur instead of a chill. 
The elevation of temperature, which rises to 103° or 105° Fahren- 
heit (rarely higher), even on the first day, is accompanied by accelera- 
tion of the pulse, and by increase of thirst. The countenance is red; 
the patient complains of pain in the back and loins, and of a distressing 
soreness of the limbs. There is great prostration and muscular debility. 
The tongue is coated, and the appetite entirely gone ; occasionally there 
is vomiting. As these symptoms often precede the local manifestations 
by one and even two days, they used formerly to be attributed by many 
to the accumulation of fibrin in the blood (hyperinosis). Some have 
even gone so far as to ascribe a critical significance to pneumonia (Dietl)y 
and to declare that the disorder only disappeared after the elimination 
of the superfluous fibrin from the blood. All these symptoms, however, 
appertain to the fever, and are more or less pronounced in all febrile 
diseases, whether the fibrin of the blood be increased or diminished in 
quantity, or whether its quantity remain unchanged. We need not 
demonstrate more fully, that every fever, by increasing the rate of trans- 
formation and consumption of the tissues, must thereby alter the com- 
position of the blood, and that the products of the interchange of ma- 
terials are mingled with the blood in greater quantity. This febrile 
crasis and the elevated temperature of the blood sufficiently account for 
the perversions of nutrition and function, which take place in febrile 
affections—constitutional disturbance of fever. 
Although fever and derangement of the general health are of earlier 
occurrence than the symptoms of nutritive derangement which the lung 
has suffered, yet we may often observe the same thing in febrile catarrhs 
and other inflammatory fevers. We may assume in such cases that the 
inflammatory disturbances of nutrition commence quite as soon, at least, 
as the fever, but that for a while they do not betray themselves by 
causing pain, cough, or dyspnoea, but remain latent. In other instances, 
symptoms of functional disturbance appear in the lung either simulta- 
neously with the chill or immediately afterward. 
The first of these is shortness of breath, a constant accompaniment 
of pneumonia. Assuming the normal rate of breathing of adults to be 
twelve, sixteen, or twenty breaths a minute, we see it augmented in 
pneumonia to forty and even fifty breaths, and find it to attain a still 168 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
greater frequence in children. The length of each respiration is propor- 
tionately short, the breathing is superficial, a fresh inspiration is required 
during the enunciation of even a short sentence, speech is interrupted. 
As the act of inspiration is executed rapidly, and with a certain degree 
of caution and anxiety, the levatores alas nasi are contracted with every 
breath, and the alee nasi dilated, causing the nostrils to “ work.” The 
shortness of breath is due, 1st, to the slowness with which blood is 
renovated in the inflamed part of the lung; 2d, to the diminution of 
breathing-surface, by exudation into the air-vesicles and consequent ex- 
clusion of air; 3d, to collateral oedema in the uninfiamed part of the 
lung, which causes swelling of the vesicular walls and decrease in their 
capacity; 4th, to the pain which a deep breath causes to the patient, 
who therefore does not breathe deeply; 5th, and above all else, to the 
increased need of air, since, in the augmented combustion and accelerated 
destructive assimilation which goes on during fever, more oxygen is con- 
sumed and more carbonic acid is given out in the organism. We shall 
presently see that, with the abatement of the fever, the dyspnoea ceases 
almost completely, although all the obstacles to respiration still continue. 
Pain is so constant a symptom in pneumonia as to be absent in but 
few instances. In most cases, but not in all, the patients assign the seat 
of the pain to the point at which the inflamed lung comes in contact 
with the thorax. In other cases it is felt at more remote points, and 
even on the other side. It is, therefore, a doubtful matter, at least, 
whether the pneumonic “ stitch ” is solely due to participation of the 
pleura in the inflammation. Every deep inspiration, and especially 
every forcible expiration, such as accompanies coughing or sneezing, 
aggravates the suffering, as do also pressure upon the thorax and move- 
ment of the intercostal muscles. The character of the pain is usually 
described by the patient as piercing or stabbing. Its intensity varies. 
It rarely continues in all its violence for any length of time. It is one 
of the most burdensome symptoms at the commencement of the disease, 
and afterward diminishes or completely ceases. It is apt to be of an 
exceedingly transitory character, or even to be altogether wanting in 
the pneumonia of old persons and very feeble subjects, particularly if the 
seat of the inflammation be the apex of the lung or one of the upper 
lobes. It is of importance to be aware of these facts. 
Cough very soon associates itself with the fever, dyspnoea, and pain 
in the side. It is hardly ever absent, excepting in the cases above 
alluded to, the pneumonia of old men, etc. It is at first short, ringing, 
and harsh. The patients endeavor to repress it; they dread to cough, 
make painful distortions of the countenance while so doing, so that 
observation of the manner of a child, while coughing, furnishes ground 
for a distinction between brouchitis and pneumonia. In almost all CROUPOUS PNEUMONIA. 
169 
cases, a peculiar sputum, pathognomonic of the malady, begins to be 
ejected at an early period. This sputum corresponds essentially to the 
viscid adhesive fluid which, as we have seen, appears in the air-cells 
during the period of engorgement. Like that liquid, it almost always 
contains blood, as pneumonic exudation is almost always attended by 
rupture of capillaries and extravasation of their contents. The pneu- 
monia of old people alone forms an exception to this rule. In these, 
the exudation is often a non-hsemorrhagic one, and the hepatization is 
not red, but yellow, immediately upon its establishment. At the com- 
mencement of the attack, the pneumonic sputa are so tough and adhesive 
that it is difficult to remove them from the mouth, and they are usually 
wiped away with a cloth. They cling so firmly to the receptacle, that 
the latter can often be inverted without spilling its contents. The 
blood which they contain is more intimately mixed than it ever is with 
bronchial mucus. Their color, which always corresponds to the amount 
of blood commingled, may be light red, rusty, brick-red, or reddish 
brown. Microscopic examination usually shows great numbers of intact 
blood-corpuscles, easily recognizable by their form and color, besides a 
small number of young cells, and sometimes a few pigment cells from 
the pulmonary vesicles. Chemical examination shows the existence of 
albumen, which coagulates upon the addition of nitric acid; and of 
mucin, which coagulates upon addition of dilute acetic acid, and forms a 
cloud of mucus upon the surface of the diluted sputa. The fibrinous 
plugs from the vesicles are not expelled; but, upon the entrance of the 
pneumonia into its second stage, small, apparently structureless, lumps 
are found in the expectoration, which are susceptible of being disentan- 
gled, and by the employment of a low magnifying powrer may be recog- 
nized as repeatedly bifurcated and ramifying coagula. These are fibrin- 
ous casts of the minuter bronchi. 
While, as a rule, all these symptoms of pneumonia mature until the 
second day of the disease, when physical examination of the chest leaves 
no further doubt as to its nature, the fever and constitutional symptoms 
continue to increase. 
According to the careful researches of Thomas, of Leipsic, the fever 
is never a continued fever, but is remittent or subremittent, that is to 
say, the daily fluctuation in its exacerbations and remissions may be 
considerable, amounting to 0.75° F. to 1.80° F., or else they may be 
slight, not exceeding 0.4 F. to 0.5 F. The temperature is at its lowest 
during the early morning hours, the exacerbation usually beginning in 
the course of the forenoon, attaining its height usually in the afternoon, 
when, in bad cases, it may rise as high as 105.8° to 107.7° F. In 
most cases, a day or two before the occurrence of the crisis, the remis- 
sion increases. On the other hand, immediately before the fever sub- 170 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
sides, the temperature sometimes reaches a height greater than any pre- 
viously attained. 
The pulse, whose frequence in a pneumonia of average severity 
usually ranges between ninety and a hundred and twenty beats a minute, 
may in severe cases, where the temperature is very high, attain a fre- 
quence of a hundred and thirty, or a hundred and fifty or more. While, 
at the outset of the attack, it usually is large and full, as the malady 
progresses, it often becomes small and soft. In some cases, this is due 
to depression of the heart’s action, by the high temperature (which 
always tends to produce asthenia), so that its feeble strokes scarcely 
overcome the resistance opposed by the aorta to the outflow of the 
blood. Under these circumstances (upon the principle that the effect 
is in proportion to the power, and in inverse proportion to the resist- 
ance), but little blood is expelled from the heart, causing a feeble pulse- 
wave, and a small pulse. In other, and probably in the majority of 
cases, it is not the weakness of the cardiac contractions, but the lack of 
blood in the left ventricle, which causes a deficit in the supply of the 
aortic system, and renders the pulse small and soft. The left ventricle 
is imperfectly filled, because afflux of blood to it is obstructed. In an 
extensive pneumonia, an obstacle to the circulation arises (partly from 
the inflammatory stasis, partly owing to pressure of the exudation upon 
the capillaries), which cannot be fully compensated for by acceleration 
of the capillary circulation in the uninflamed portion of the lung. The 
consequence is, that too little blood enters the left heart, while the right 
heart and the veins of the aortic system are overloaded. (Upon cutting 
into a piece of hepatized lung, but little blood flows from it. The 
redness in the beginning of hepatization depends upon extravasation. 
The lack of blood of the inflamed part is most conspicuous in yellow 
and gray hepatization, and in purulent infiltration.) 
The blueness of the lips and cheeks, which is observed in severe 
pneumonia, is also dependent upon the disturbance of the pulmonary 
circulation, and upon impediment to the outflow of blood from the right 
ventricle, and from the veins of the aortic circulation; but we have no 
acceptable explanation of the reddening of the cheek, which often 
occurs at the side upon which the pneumonia exists. In many in- 
stances a herpetic eruption develops upon the second or third day upon 
the lips, more rarely upon the nose, cheeks, or eyelids; and from the 
frequence of herpes during pneumonia, and its great rarity in abdominal 
typhus, and other diseases, the appearance of vesicles filled with a clear 
liquid may be of diagnostic value in doubtful cases. 
The headache, by which the invasion of pneumonia is accompanied, 
usually continues throughout the attack. It is generally combined with 
sleeplessness, or the sleep is tioubledby dreams; and, if the patient be CROUPOUS PNEUMONIA. 
171 
at all of an irritable temperament, there is apt to be slight delirium. 
These symptoms are mainly due to the fever, and cease as soon as the 
fever subsides. We must beware of inferring the existence of grave 
cerebral disease from the presence of these signs alone. 
Even where there is no complicating gastric disorder, the appetite 
usually is lost, the tongue is lightly coated with white, and shows a 
tendency to dryness, the thirst is considerably augmented, and the 
stools are dry and constipated. These symptoms are also the result of 
fever, and occur in almost every other febrile complaint. The loss of 
appetite is the most difficult to account for. One would suppose, a 
priori, that the augmented destructive assimilation which takes place 
during fever, by means of which the high temperature of the body is 
maintained, would occasion an increased demand on the part of the 
system for a compensating supply of nourishment to replace the waste, 
and we are quite at a loss to understand why no such want is usually 
felt by the patient. The coated tongue, its tendency to dryness, as well 
as the aggravated thirst (see catarrh of the oral mucous membrane), 
and the dryness of the stools, are satisfactorily accounted for by the in- 
creased evaporation of liquid from the skin, in consequence of which 
the tissues become dryer and their secretion is diminished. 
Obstruction to the flow of blood from the liver not unfrequently 
leads to a perceptible enlargement of that organ. Perhaps, in some 
cases, the slight jaundice which occurs during pneumonia is dependent 
upon this obstruction of circulation in the liver, and is analogous to the 
icterus which appears, from the same cause, with tolerable frequence in 
disease of the heart. As the hepatic veins are intertwined with the 
biliary ducts, distention of the former may result in compression of the 
latter, and thus cause retention and absorption of bile. However, this 
theory of the origin of icterus is only to be admitted when the liver is 
greatly swelled and the patient is extremely cyanotic. Far more fre- 
quently, the symptoms of jaundice during pneumonia depend upon a 
catarrh of the duodenum and of the biliary ducts, or else it arises from 
“ dissolution ” of the blood—that is to say, a disintegration of the blood- 
corpuscles, by which free coloring-matter of the blood is converted into 
biliary coloring-matter outside of the liver. 
The pneumonic process and the fever which attends it exercise an 
important influence upon the constitution of the uritie. While the fever 
lasts the proportion of water in the urine is reduced by the insensible 
perspiration. The urine is scanty and concentrated, its color is some- 
what dark, and its specific gravity is high. 
Among the solid constituents of the urine, the urea is considerably 
increased in quantity. As is well known, the ultimate products of de- 
structive assimilation of nitrogenous tissues are eliminated under the form 172 
DISEASES OF TEE PARENCHYMA OF TEE LUNG. 
of urea and uric acid. The elevation of the temperature of the body 
in febrile disease depends upon an abnormal generation of heat from a 
morbidly-active combustion of the constituents of the tissues, in which, 
of course, the nitrogenous elements participate. A short fever reduces 
the weight of the patient far more than does a fast, without fever, of 
much longer duration. But the patient not only grows thin because 
his fat is consumed in overheating his body, but the muscles undergo a 
marked atrophy, and a considerable period of time ekrpses ere a con- 
valescent from fever regains his former strength, and ere his muscles are 
restored to their original volume. The increased destructive assimila- 
tion of the nitrogenous constituents of the body during fever is also 
susceptible of direct proof, by the absolute or relative augmentation in 
the production of urea. Patients suffering from pneumonia, with violent 
fever, even though their diet be absolutely non-nitrogenous, eliminate 
quite as much urea in their urine, if not more, than a healthy person 
does whose food consists almost entirely of meat and eggs. I have 
known pneumonia patients to excrete forty grammes of urea within 
twenty-four hours, while one of my pupils, who was in good health, 
and whose diet was precisely that of the sick man, passed but from 
thirteen to fifteen grammes in the same time. The urine very com- 
monly becomes turbid upon cooling, from precipitation of its urates; 
but it appears to me that this phenomenon is due rather to the reduced 
proportion of water in the urine, which thus becomes incapable of hold- 
ing the urates in solution at a low temperature, than to an excessive 
formation of the salts themselves. By gently warming the urine the 
urates can always be redissolved, and the cloudiness of the urine be 
dissipated. 
While the urea of the urine is increased in quantity, the amount of 
inorganic salts which it contains, especially its alkaline chlorides, is 
diminished, and at the height of the disease they may disappear com- 
pletely. If we add a few drops of a solution of nitrate of silver to 
some of the urine, previously acidulated, the precipitate of chloride of 
silver, so distinct in healthy urine, is scarcely, if at all, observable. 
The greater part of this chloride of sodium depends, no doubt, upon 
the use of food containing salt, and the diet of a pneumonia patient 
might account for the diminution of alkaline chlorides in the secretion; 
but as, even in starving animals, small quantities of alkaline chlorides 
are found in the urine, as a product of transmutation of their tissues, 
its complete disappearance in pneumonia cannot be attributed solely to 
the diet of the patient: and we are warranted in supposing that the 
portion of alkaline chlorides produced by destructive assimilation is ex- 
creted from the blood with the pneumonic exudation. 
The concentration of the urine, the augmentation of urea, the dimi- CROUPOUS PNEUMONIA. 
173 
nution of the chlorides, as well as the appearance of biliary pigment in 
the urine, are simply due to the improper quality of the matter conveyed 
to the kidneys for the of urea. The appearance of albumen 
in the urine, which not unfrequently occurs in severe pneumonia, is de- 
pendent upon other causes. Its presence is sometimes occasioned by 
engorgement of the emulgent veins. As is well known, albuminuria 
may be produced artificially in the low'er animals by ligation of these 
veins. The chief source of the albuminuria of heart-disease is obstruc- 
tion of the venous circulation of the kidney. The presence of albumen 
in the urine of pneumonia, however, is only to be ascribed to such a 
cause when it is accompanied by cyanosis, enlargement of the liver, and 
other evidence of intense venous engorgement of the greater circula- 
tion. In most cases its source is in the parenchymatous degeneration 
of the kidneys, of which we shall speak more fully in our second volump, 
and which consists in a swelling and opacity and molecular destruction of 
the renal epithelium. This parenchymatous degeneration of the kidney, 
with its consequent albuminuria, occurs in a great variety of febrile dis- 
orders, and is apparently a result of excessive elevation of the tempera- 
ture of the body, or febrile crasis. The more intense the fever, so much 
the more probably will albumen be found in the urine of pneumonia 
patients, although there may be scarcely any sign of venous engorge- 
ment of the systemic circulation. The skin, which, at the commence- 
ment of the attack, usually is dry and parched, after a day or two often 
becomes moist, and even bathed in sweat, without, however, affording 
any material relief to the patient. 
Hitherto we have been describing the stadium incrementi, the form- 
ing stage of the disease. Its transition into the stadium decrement i, or 
stage of decline, is not gradual, but takes place with a suddenness with- 
out parallel in any other disorder. 
In former editions of my book I have asserted with great positive- 
ness that the crisis of a pneumonia almost constantly arrived either on 
the fifth, seventh, or, in rare instances, upon the third day, and I believed 
this assertion to be warranted by the results of a large number of ob- 
servations. Meanwhile I have become satisfied that the ancient doctrine, 
that the crisis of pneumonia always occurred on the odd days, is unten- 
able, in spite of the high modern authorities who have pronounced in 
favor of its correctness. If, in calculating the duration of the disease, 
we take accurate notice of the hour at which the initiatory chill began, 
and of that in which the decline of the fever commenced, it will be seen 
that the critical period of pneumonia takes place quite as often upon 
the even days as upon the odd ones. For instance, a pneumonia, which 
begins by a chill on Monday at noon, culminates, no doubt, in many 
cases, in course of the following Sunday; but the crisis occurs quite as 174 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
often during the forenoon (hence during the sixtli day) as in the after- 
noon or seventh day. 
The symptoms continue with constant or increasing intensity until 
the critical day, which generally arrives toward the end, less commonly 
about the middle, of the first week of the disease; and while the con- 
dition of the patient, from the dyspnoea, the thirst, and the intense con- 
stitutional disorder, is beginning to awaken an earnest solicitude, a 
striking change takes place, often within a few hours. The temperature 
and the frequence of the pulse often sink rapidly, the dyspnoea abates, 
the patient feels easier and more free. In course of twenty-four hours 
convalescence is often fully established. The patient sleeps, calls for 
food, and merely complains of extreme debility. From this time the 
recovery of many patients progresses steadily. The temperature not 
unfrequently falls below the normal standard, and I repeatedly have 
seen the pulse sink to forty beats a minute, although the patient had 
not taken a grain of digitalis. The blood disappears from the expecto- 
ration, sometimes gradually, sometimes with suddenness. The sputa 
become somewhat more copious, but generally to so slight a degree that 
we are compelled to suppose that the greater parts of the exudation 
must be absorbed, and that but little of it is expectorated. The tena- 
city and transparence of the sputum disappears with the blood; it 
becomes yellowish—sputa cocta. The yellowness depends upon an 
admixture of young cells, which show more or less trace of fatty 
metamorphosis. Besides slightly granular pus-corpuscles, cells tilled 
with oil-globules, fat granule-cells, and collections of granules, and of 
free oil-molecules, and black pigment-cells in greater or less numbers, 
are found in the expectoration. Although reabsorption commences very 
soon after exudation is complete, yet a considerable period of time usu- 
ally elapses before auscultation and percussion show’ that the pneumon- 
ic infiltration has disappeared. Yet, as the smallest particles of pneu- 
monic exudation are enclosed in their own net-work of capillaries, the 
conditions for their reabsorption are more favorable than for the absorp- 
tion of a pleuritic effusion v’ith but one capillary surface opposed to it. 
In subjects previously healthy, the course of the vast majority of 
pneumonias is as above described. Indeed, with the exception of the 
infectious diseases, there are few maladies whose average course is sq 
remarkably uniform. That we should not, until recently, have perceived 
its evidently cyclical character, is owing to the active manner in which 
we used formerly to attack the disease whereby its typical course be- 
came deranged. One must bear in mind that not very long ago it 
would have been thought a crime to treat a pneumonia without blood- 
letting, and even without repeated venesection. 
In some cases the crisis does not occur at the end of the first week, CROUPOUS PNEUMONIA. 
175 
or there is but a short remission, after which the disease grows worse 
again, and continues into the second week. The pneumonic infiltration 
continues to spread, the temperature remains high, and is sometimes 
higher than ever. Signs of extreme prostration now set it, due in part 
to the elevation of the temperature, partially also to exhaustion pro- 
duced by continuous and excessive calorification, and to the profuseness 
of the exudation, which I have repeatedly estimated at three pounds 
after comparison of the weights of the diseased and healthy lung. The 
fever, formerly of “inflammatory” type, now assumes an asthenic, 
“ nervous ” (typhoid) character. The pulse grows extremely frequent, 
small, and soft; the tongue becomes dry and incrusted; all the senses 
are blunted; the patient not unfrequently voids his urine and faeces in- 
voluntarily, in the bed; some patients lie in a stupor from which they 
can scarcely be roused; others, again, are wildly delirious, so that it is 
scarcely possible to restrain them in bed. In many such cases, especially 
if the patient have not been depleted by blood-letting, a change for 
the better may still take place toward the end of the second week, 
and again the transition from a condition apparently desperate, to one 
of almost complete convalescence, may then occur in the course of a few 
hours. 
The crisis at the end of the first week fails to occur also, when the 
stage of hepatization passes on into that of purulent infiltration, and 
the fever continues into the second week with equal or even aggravated 
intensity. Here, too, the pulse is usually small, and the mouth is dry 
and sticky. The patients are somnolent, or else delirious; the tempera- 
ture, especially in the evening, is greatly elevated, and sometimes there 
are slight chills. The sputa, which are generally profuse, contain great 
quantities of cells in a state of fatty degeneration. It . is clear that aus- 
cultation and percussion alone can distinguish an extension of the pro- 
cess of hepatization from the transition into purulent infiltration. 
When the pneumonia attacks aged persons, or subjects of depraved 
constitution, adynamic symptoms may arise, even though the malady be 
not of unusual duration and although purulent infiltration have not 
occurred. Indeed, so promptly do they sometimes develop, so immedi- 
ately do they appear after the chill, and the first onset of the fever, that 
the signs of pulmonary disorder are entirely eclipsed by those of grave 
asthenic fever. As we have stated already, many patients of this kind 
have no cough and no characteristic sputa / nor do they complain 
either of dyspnoea or of pain. The frequency of respiration is often 
ascribed to the fever, and patients sometimes die Avith the diagnosis of a 
“ typhoid influenza,” a catarrhal fever, or a “ typhoid gastric feArer,” 
whose autopsy reveals extensive pneumonic infiltration; the physician 
having been deceived by external appearances, which really bear greater 176 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
resemblance to typhus than to pneumonia of vigorous adults, and hav- 
ing neglected to make a physical exploration of the chest. 
Asthenic fever may also develop, sometimes, in subjects previously 
healthy and vigorous, where pneumonia is complicated with acute 
gastric or intestinal catarrh. True, such cases, which are not rare, 
differ from the pneumonia of old persons, inasmuch as the pain, cough, 
and characteristic sputa are not at first absent; but the depressing effect 
of the complication as well as the fever, which is usually of great inten- 
sity, soon result in an extreme prostration and in other symptoms, which 
create the terrifying impression upon the minds of the laity that the 
malady has become “ typhoid” (“nervous”), or “ that a nervous fever 
has set in.” The disease is further disguised, and the diagnosis ren- 
dered doubly obscure, by the thickly-coated tonge, which afterward often 
becomes incrusted with black scabs, by the distended abdomen and 
by the watery discharges from the bowels, and—if the intestinal catarrh 
have also involved the ductus clioledochus—by the jaundiced hue of 
the skin, and sclerotica. Here, too, physical examination is our sole 
safeguard against error and mortifying post-mortem disclosures. Pneu- 
monia is apt to assume very peculiar characteristics when it attacks per- 
sons of intemperate habits. The beginning of the attack seems rather 
to be a fit of delirium tremens, and the symptoms of perverted cerebral 
action are so prominent that the pulmonary affection is liable to escape 
notice. The patient can hardly be kept in bed; he is exceedingly 
loquacious, does not complain, but declares that he is perfectly well. He 
is in a most cheerful humor, and his delirium and illusions are of that 
peculiar kind which is almost pathognomonic of delirium tremens. He 
sees small animals, especially mice and beetles, picks with great industry 
and persistance at his bed-clothes, or executes all the manipulations of 
his avocation in pantomime. Even though a patient in this condition 
have no cough, no expectoration, and complain of no pain, yet his chest 
should be explored with great care, especially if he have fever. Many 
a patient has died in a strait-jacket with a diagnosis of delirium tre- 
mens, whose real disease has been pneumonia. At a later period the 
scene changes. It is a well-known fact that drinkers are equally inca- 
pable, or even still less capable, of bearing an increase of calorification 
and an augmentation of their animal heat than aged or debilitated per- 
sons, and that a fever of very moderate intensity and brief duration 
exercises an exceedingly depressing and exhausting influence upon the 
vigor of the heart, the action of the brain, and upon all other functions. 
In a very few days the pulse, originally full, grows small and weak, 
the extreme excitement and bustling demeanor give place to a deep 
apathy, and to rapidly-increasing somnolence, the skin is bathed 
in sweat (from incipient palsy of the cutaneous muscles), gurgling CROUPOUS PXEUMOXIA. 
177 
sounds arise in the chest (from commencing paralysis of the muscles 
of the bronchi)—and the patient dies with the symptoms of oedema of 
the lung. 
With regard to the termination of pneumonia, we have already seen 
that recovery is often rapid, where the exudation liquefies, and is reab- 
sorbed after completion of the stage of hepatization. Complete resto- 
ration may also take place from the stage of purulent infiltration, only, 
as the patients are exhausted by weeks of fever, their convalescence is 
extremely tedious. 
Death, during the first and second stages of pneumonia, usually pro- 
ceeds from hypersemia and collateral oedema, by which the uninfiamed 
air-vesicles are rendered incapable of carrying on respiration. Much 
more rarely it depends upon the excessive extension of the pneumonic 
infiltration alone. The intense dyspnoea, profuse frothy or liquid sputa, 
moist rules in the uninfiamed parts of the lung, the sudden sinking of 
the patient, the drowsiness, the vomiting, the coolness of the skin, are 
all signs of insufficient respiration, and of imminent danger of carbonic- 
acid poisoning. Unless aid be at hand, the symptoms of palsy soon pre- 
vail, and the patient succumbs under symptoms of oedema of the lung, 
palsy of the bronchi, and of suffocative effusion. 
A fatal issue, during the stage of red hepatization, resulting from 
engorgement of the cerebral veins, with consequent effusion, is of far 
rarer occurrence. Simple blueness of the face need not lead us to fear 
cerebral congestion ; nor are even the headache and the delirium sufficient 
to warrant such apprehension, neither do they require the active treat- 
ment imperatively demanded by that condition. If, however, the pa- 
tient fall into somnolence which cannot be ascribed to the embarrass- 
ment of respiration, or if he complain of a sense of formication, or of 
numbness of his limbs, or should slight convulsions occur, life is un- 
doubtedly threatened by oedema of the brain, and death may ensue with 
the symptoms of coma. 
The third and most usual cause of death, during the stage of red 
hepatization in pneumonia, is exhaustion. From this cause a compara- 
tively slight attack of this disorder is extremely dangerous where the pa- 
tient is old or debilitated, or where he is a drunkard whose nerves are 
in constant need of stimulus, who trembles until he has his dram, and in 
whom the privation of the supply, added to the prostration produced by 
the fever, soon brings on paralysis. In like manner, a complication with 
intestinal catarrh and icterus tends to hasten the exhaustion; or, finally, 
the longer duration of the fever, and the magnitude of the exudation in 
a protracted pneumonia, may expend the strength of a person previously 
vigorous and healthy. In all these cases the obtuseness of the senso- 
rium increases to stupor, the pulse becomes smaller and smaller, the 178 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
skin is bedewed with clammy sweat, and the patient dies from passive 
hyperasmia, passive oedema, and suffocative effusion. 
Death takes place with symptoms quite like these in the third stage, 
that of purulent infiltration, when the strength proves insufficient to 
withstand the duration and intensity of the fever. Sometimes the 
asthenic symptoms, which may arise during pneumonia, are accom- 
panied by another group of symptoms of a different kind. The pulse 
grows small and irregular, a slight jaundice appears, which manifestly 
does not depend upon biliary obstruction; the urine becomes albumi- 
nous, the mind of the patient is much disturbed, the delirium being vio- 
lent at first, afterward settling into stupor. When there is much jaun- 
dice, this description corresponds nearly with that of the bilious pneu- 
monia found in many of the ancient pathologies. In these cases we 
probably have to do with a parenchymatous degeneration of the heart, 
liver, kidneys, brain, and blood. In their appropriate sections we shall 
consider in detail the subject of parenchymatous degeneration of these 
organs, as wTell as the relation of icterus to parenchymatous degenera- 
tion of the liver, and then dependence of this degeneration upon an 
increase of the animal heat, and upon intensity of the febrile crasis. 
With regard to the rarer sequeke of pneumonia, we may have good 
reason to suspect the formation of an abscess, when the slight shiver- 
ing fits, which accompany purulent infiltration, change into violent 
rigors; and when a yellow-gray discharge, containing more or less 
pigment, begins to be expectorated in large quantities; but the diag- 
nosis is only sure, when, by means of the microscope, we can discover 
elastic fibres, which, from their structure, are recognizable as belonging 
to the lung, or when physical exploration shows the existence of a 
large cavity in tfie chest. When a pulmonary abscess ends fatally, 
death takes place under conditions similar to those which accompany 
death from purulent infiltration. If the abscess heal, the expectoration 
loses its yellow color, little by little, as the cavity gradually becomes 
enveloped in a capsule of connective tissue; and when the abscess is 
completely closed the sputa cease entirely. Should a permanent cavity 
remain behind, lined with a pyogenic membrane, and surrounded by in- 
durated connective tissue, it affords the same symptoms, runs the same 
course, and gives rise to the same danger as do the bronchiectatic cavi- 
ties of which we have to treat in Chapter XI. The formation of new 
connective tissue and its contraction in the regions about the cavity 
also give rise to those depressions of the thorax which we shall describe 
by-and-by. Gangrene—a very rare sequel to pneumonia—is character- 
ized by most intense collapse, by the expectoration of a blackish sputum 
of a most foul, putrid odor, together with the physical signs of a cavitv 
in the lungs (see Chapter XII.). CROUPOUS PNEUMONIA. 
179 
Caseous infiltration, as a sequel to pneumonia, is by no means con- 
fined to patients in whose lungs old deposits of tubercle already exist, 
but may also take place in subjects previously in good health. Espe- 
cially is this the case with emphysematous persons when attacked by 
croupous pneumonia of the lungs, which is rare. In such cases, 
although the fever moderates somewhat upon the critical day, it does 
not subside so completely as when it terminates in resolution. The pa- 
tients do not improve, the cough and dyspnoea remain. In the evening 
the pulse is more frequent; auscultation and percussion reveal a persist- 
ent condensation of the parenchyma of the lung. After some time, 
the infiltration dissolves, causing vast destruction of the lung, the symp- 
toms of which we shall examine more closely when considering the sub- 
ject of pulmonary consumption. 
For the termination of croupous pneumonia in induration or cirrhosis 
of the lung, see Chapter XII. 
Physical signs of Croupous Pneumonia.—Inspection gives nega- 
tive results as regards the contour of the thorax. Both sides of the 
ehest preserve their normal dimensions, and the intercostal spaces pre- 
sent their proper shape of shallow furrows, a condition of great impor- 
tance in distinguishing pneumonia from pleuritis. There is, however, a 
decided modification of the respiratory movements, since at the begin- 
ning of the attack the patient favors the affected side on account of the 
pain; and, as in the later stages of the disease, the vesicles are filled 
with exudation, and hence are impervious to the air. It is often possi- 
ble to recognize the side upon which the pneumonia has its seat at the 
first glance, as the healthy side heaves normally, while the inflamed 
side, as it were, lags behind. When both lower lobes are infiltrated, 
the diaphragm cannot descend; and the epigastrium does not project 
upon inspiration. The patient breathes by dilatation of the upper part 
of the chest alone (costal type). 
The first point which strikes the attention, upon palpation, is an 
intensification of the impulse of the heart, and (what is very important 
in distinguishing between pleuritis and pneumonia) the heart-shock is 
felt in its normal situation. Palpation also reveals that, during the 
period of engorgement, and often during that of hepatization, the vibra- 
tions of the chest are unusually distinct and strong, when the patient 
speaks—that the pectoral fremitus is strengthened. This important 
diagnostic sign may grossly mislead any one, who is ignorant of the 
fact that, in almost all healthy persons, the pectoral fremitus is stronger 
upon the right side than upon the left. This is probably due to the 
circumstance that the right bronchus is wider, shorter, and stands 
almost at a right angle with the trachea, while the left is longer, and 
narrower, and passes off from the trachea more obliquely. {Seitz.) 180 
DISEASES OF TIIE PARENCHYMA OF THE LUNG. 
The morbid intensity of the pectoral fremitus, during the stage of en- 
gorgement, depends upon the loss of elasticity which the pulmonary 
tissue sustains at this period. Under normal conditions, the transmis- 
sion of the vibrations from the trachea and larger bronchi to the thoracic 
wall is impeded by the tension of the elastic vesicles; moreover, the 
elasticity of the healthy lung exerts a sort of suction upon the inner 
surface of the thorax, whereby thoracic vibrations are held in check. 
These two forces, by which the normal vocal resonance is enfeebled 
during health, are removed when the elasticity of the lung is destroyed. 
The still further increase of the vocal fremitus, which is often observed 
during the stage of hepatization, is owing not only to the loss of elas- 
ticity of the hepatized lung, but also to the fact that the vibrations 
which the vocal chords have imparted to the air within the trachea and 
bronchi pass unimpaired to the walls of the chest, as the medium 
through which they are transmitted is no longer an interrupted one 
(alternations of air and vesicular wall), but a continuous one, the solidi- 
fied pulmonary parenchyma. It sometimes happens that the trans- 
mission of the vibratile waves is checked by a temporary occlusion of 
the bronchi by secretion; but we not unfrequently observe instances, 
in which the pectoral fremitus over a hepatized point is permanently 
weakened or is entirely deadened, when there is neither bronchial 
obstruction nor pleuritic exudation. In such cases we may infer that 
the close contact of a compactly-infiltrated lung prevents the walls of 
the chest from vibrating. 
Percussion during the stage of engorgement often gives rise to a 
purely tympanitic, hollow sound. The elasticity of the normal lung 
may be compared to that of a tightly-inflated bladder; its ring is not 
tympanitic. In the stage of hepatization the vesicles having lost their 
elasticity, its condition is like that of a cluster of imperfectly-inflated 
bladders. Its percussion-sound then is tympanitic. The “hollow” 
percussion-sound depends upon a diminution which the exudation 
causes in the amount of air contained in the vesicles, thereby reducing 
the size of the vibrating body. We regard the expressions “full” and 
“ hollow ” as thoroughly intelligible and practical. By universal cus- 
tom, the sound produced by the vibration of a large voluminous body 
is called a “ full ” tone, and that proceeding from the vibration of a 
small body is called a “ hollow ” tone. Thus, the percussion-sound of 
the stomach sounds full to the ear of the beginner; that of the small 
intestine hollow. I find that there are few practitioners who can recog- 
nize with facility that the tympanitic percussion-sound of engorgement 
also is hollow, while for many it is difficult to make out its higher 
pitch. 
During hepatization, when the solidified point lies in immediate CROUPOUS rXEUMOXIA. 
181 
contact with the side of the chest—but only in such a case—the percus- 
sion-sound is deadened, and during the act of percussion an increase of 
resistance is felt over the point struck. This is because a hepatized 
lung, like any other compact body void of air, cannot be made to 
vibrate. The thicker and wider the hepatized region lying in contact 
with the chest, so much the more marked are the dulness and resist- 
ance. When the dulness is but slight, it will generally be perceived 
that the sound is also hollow; when the sound is perfectly dull, the full 
and hollow tones cannot be appreciated. When the seat of the dis- 
ease is central, that is to say, at the roots of the lung, very extensive 
hepatization of the lung may exist without alteration of the sound upon 
percussion. 
Auscultation during the stage of engorgement usually affords a 
crackling sound to the ear, like that which is heard when one throws 
salt into the fire, or when a few hairs are rubbed between the fingers 
before the ear. This crackling (laennec’s rale crepitant), which is 
formed in the minute spaces of the bronchial terminations and pul- 
monary vesicles, is the finest of all the moist rales, and, as the fluid in 
which it arises is extremely viscid, it is also the dryest of the moist rales. 
Their mode of origin perhaps is, that the vesicular walls, which during 
expiration became glued together, are forcibly separated by the air 
which enters upon inspiration. As soon as that portion of the lung 
which touches the thoracic wall is completely infiltrated, vesicular breath- 
ing is arrested, as the vesicles there are impenetrable to the air. In- 
stead bronchial respiration is heard, that is to say, we hear the sound 
which the to-and-fro movement of the air in the trachea and larger bron- 
chi is always making, but which is not transmitted to the ear through 
the healthy lung, the structure of which, consisting of alternations of 
air and vesicular wall, furnishes a poor conducting medium. When, 
instead of this bad conductor of sound, a uniform medium lies between 
the ear and the bronchi, these bronchial sounds become audible; always 
provided, that the bronchi communicate with the trachea, so that the 
air may either pass to and fro in them, or that the air which they already 
contain may be set in vibration with every breath. Moreover, the bron- 
chi in the condensed part of the lung form better conductors of sound 
than those which traverse the normal lung. If the bronchi should be 
filled up by accumulated secretion, as often happens temporarily in the 
third stage of pneumonia, the bronchial breathing ceases, and does not 
again become audible until the bronchi have become emptied by 
coughing. 
Bronchophony arises under conditions similar to those under which 
bronchial respiration is produced. The vibrations of the vocal chords 
during speech are conducted along the column of air in the larger bron- 182 
DISEASES OF THE FAREXCIIYMA OF THE LUXG. 
chi, but are only perceptible upon the surface of the chest as an indis- 
tinct buzzing, as long as the healthy pulmonary substance lies between 
the ear and the bronchi; the healthy lung-substance being, as we know, 
a bad conductor of sound. If the parenchyma become condensed, and 
its transmitting power thereby improved, the bronchi also becoming 
better conductors of sound, from the thickening of surrounding parts, 
the sound of the voice in the thorax is louder, constituting “ broncho- 
phony ; ” sometimes a tolerably distinct articulate sound is heard, which 
is called “pectoriloquy.” If the sensory nerves of the ear perceive an 
unpleasant jarring sensation from the thoracic wall, we have the “ strong 
bronchophony,” which therefore in part means that the ear when laid 
upon the chest feels an increase of the pectoral fremitus. Some- 
times the voice as heard within the chest has a nasal, bleating tone, for 
which phenomenon (mgophony) there is no satisfactory explanation. 
Like the bronchial breathing sound, bronchophony ceases while the 
tubes are obstructed by secretion, and while their communication with 
the trachea is interrupted. During the process of resolution of pneu- 
monia, moist rales are heard. Sometimes, when the air again begins 
to enter the minuter bronchi and vesicles, the rale is extremely fine, but, 
as the secretion has less viscidity than before, the sound is not so “dry ” 
as that “ crepitation ” heard during the stage of engorgement. This 
sound is called the crepitatio redux. The rales produced in the greater 
bronchi, under conditions like those under which bronchial respiration 
and bronchophony arise, may become bronchial “ consonwit ” [Skoda) 
and “ ringing ” rales (Traube). 
The pleuritis which constantly accompanies pneumonia is not sus- 
ceptible of physical demonstration, excepting when it causes a copious 
effusion. There are scarcely ever any audible friction-sounds in the first 
stage of pneumonia, since the pleural surfaces rub together very little, 
if at all, at that period. They are heard somewhat oftener during reso- 
lution, as the air then reenters the vesicles, and the patients breathe 
with greater freedom, producing friction of the pleural folds. 
The physical signs of a great cavity in the lungs, as a result of ab- 
scess or gangrene, are identical with those of a tubercular cavity. For 
a further description of them we refer to Chapter XIII. 
Diagnosis.—In children, and in greatly prostrated subjects, particu- 
larly in old men, pneumonia is often overlooked. In children this occurs 
chiefly when the disease sets in with convulsions and a violent fever, 
attended by very little cough, as little children do not expectorate, nor 
know how to tell the seat of their pain. Dyspnoea is then attributed 
to the fever, and, if the child have diarrhoea, the fever is often regarded 
as a “ tooth fever,” with inflammatory irritation of the intestinal mucous 
membrane; or, if the bowels be confined, it may be mistaken for acute CROUPOUS PNEUMONIA. 
183 
hydrocephalus. Children with violent fever, brain-symptoms, and hur- 
ried respiration, must be frequently and carefully auscultated. The risk 
of confounding the pneumonia occurring in old and greatly-depressed 
subjects with typhoid fever is guarded against by the absence of the 
tumor of the spleen, the eruption, the tenderness in the ileocsecal region, 
the initiatory chill, above all, by the physical examination of the chest. 
The differential diagnosis between pneumonia and pleurisy will be 
more appropriately considered after we have made ourselves familiar 
with the symptoms and course of the latter. 
Valuable for the diagnosis of pneumonia as we have seen physical 
examination of the chest to be, it nevertheless is not of itself sufficient 
to prove more than the existence of infiltration and filling of the air- 
vesicles. The character of the infiltration is to be ascertained from the 
history of the case. 
Prognosis.—The prognosis, first of all, must depend upon the ex- 
tent of the disease. Double pneumonia is justly regarded as the most 
dreaded form. The prognosis, however, depends much more upon the 
accompanying fever, since, as we have seen, exhaustion from fever ter- 
minating in general palsy is the cause of death in the majority of fatal 
cases. An elevation of temperature above 106° F., an increase in the 
frequence of the pulse above one hundred and twenty beats, renders 
the prognosis bad. 
Pneumonia is an extremely dangerous disease to aged persons and 
to drunkards, owing to their intolerance of even moderate degrees of 
fever; and while but a small proportion of middle-aged patients die of 
it, the mortality from this disease among old people amounts to between 
sixty and seventy per cent. 
Complications of pneumonia with tuberculosis, disease of the heart, 
Bright’s disease, as well as the occurrence of endocarditis and pericar- 
ditis, should cause us to fear an unfavorable result. 
Among the individual symptoms, the sputum furnishes a clew to the 
prognosis. The absence of all sputa must, in the beginning, be regarded 
as unfavorable, as must also the appearance of very dark, brownish-red 
(prune-juice) expectoration. This signifies a poor state of nutrition and 
fragility of the pulmonary capillaries, and, as a rule, denotes a cachectic 
condition of the individual. Very copious liquid cedematous sputa are 
ominous of evil. Scanty expectoration during resolution of pneumonia, 
if the dulness continue to disappear, is of smaller importance; but ab- 
sence of expectoration, accompanied by gurgling sounds in the chest, 
signify palsy of the bronchi, oedema of the lung, and approaching disso- 
lution. Delirium at the beginning of the disease is a matter of no 
gravity, and is due to the derangement of nutrition in the brain, or to 
the high temperature of the blood which flows through the brain. At 184 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
a later period it often accompanies exhaustion, so that, when it is per- 
sistent and intense, it may be regarded as a sign of an adynamic condi- 
tion, and hence may furnish grounds for alarm. The same is true of the 
entire train of symptoms which we are in the habit of calling “ ner- 
vous” (typhoid). It has already been stated that drowsiness, transient 
twitchings, or palsy, are dangerous signs. 
Finally, the prognosis depends upon the sequela? of pneumonia. A 
transition from the stage of hepatization into that of purulent infiltra- 
tion is of far more unfavorable augury than the termination by liquefac- 
tion and absorption. The formation of an abscess, caseous infiltra- 
tion of the exudation, and gangrene, make the prognosis more and 
more grave. 
Treatment.—The indicatio causalis cannot be met in the ma- 
jority of cases, inasmuch as almost every pneumonia arises from 
unknown atmospheric or telluric influences. Indeed, it would be 
highly injudicious to treat a patient with pneumonia by dia- 
phoresis, under the assumption that he had “ taken cold.” Ex- 
perience teaches that in many instances when the sweating is 
abundant throughout the attack, the course of the disease is espe- 
cially severe. 
With regard to the indicatio morbi, we must not forget, in the first 
place, that the natural course of pneumonia is more decidedly cyclical 
than that of almost any other disease, and that, left to itself, in a vigor- 
ous patient, if uncomplicated, and of moderate intensity, it almost always 
ends in recovery. This fact has not been known until recently. We 
have to thank the so-called expectant mode of treatment of the Vienna 
school and the success of the homoeopaths for this important discovery, 
from which the following rules are to be drawn. Simple pneumonia 
attacking persons previously in good health requires no more active 
treatment than does erysipelas, small-pox, measles, or other diseases of 
cyclical course, provided only that the extent of the disease be mod- 
erate, and that there be no complication. Indeed, it has been proved 
that, unless warranted by special indications, active interference has an 
unfavorable effect upon the course of pneumonia; and Dietl is right in 
affirming that this disease, when treated by bleeding, more often termi- 
nates fatally than where no venesection has been employed. It is quite 
a different matter to compare the cases in which we bleed, not because 
of pneumonia, but in spite of pneumonia, and for fear of certain com- 
plications, with those cases in which, upon principle, blood-letting is 
never practised. 
The number of bleedings which used to be practised by Bouillaud 
and other disciples of the “ saign'ee coup sur coup ” school, likewise 
tends to support the experience of Louis, Dietl, and others, that bleeding CROLTOUS PNEUMONIA. 
185 
is no specific, and that it does not even cut the process short. In fact, 
the bleedings had to be repeated and continued until the third, fifth, or 
seventh day—that is to say, until the terminal day arrived—when the 
cycle of the pneumonic process was complete. 
Whichever one of the current theories upon inflammation we may 
adopt, none of them even partially upholds the efficacy of venesection 
in pneumonia. The fact is, unfortunately, forgotten, that the most in 
tense hyperaemia, by itself, cannot occasion croupous inflammation; that 
the enlargement and dilatation of the capillaries, which we see in valvular 
disease of the heart, although they may cause splenification and oedema, 
never produce croup of the air-vesicles. The subject of venesection 
can be more appropriately discussed while considering the symptomatic 
indications for treatment, under which head it, strictly speaking, belongs. 
I have made extensive employment of cold in the treatment of 
pneumonia, and, relying upon a large number of very favorable results, 
can recommend this procedure. In all cases I cover the chest of the 
patient, and the affected side in particular, with cloths -which have been 
dipped in cold water and well wrung out. The compresses must be 
repeated every five minutes. Unpleasant as this procedure is in almost 
all cases, yet even after a few hours the patients assure me that they 
feel a material relief. The pain, the dyspnoea, and often the frequency of 
the pulse, are reduced. Sometimes the temperature goes down an entire 
degree. My patients often retain this surprising condition of improve- 
ment throughout the entire duration of the attack, so that their outward 
symptoms wTould hardly lead one to imagine the grave internal disorder. 
The relatives of the patient, too, who do not fail to perceive the im- 
provement, now readily assist in the treatment to which at first they 
were opposed. In a few cases, and only in a few, the use of cold affords 
no relief, and the troublesome manipulation for its application increases 
the distress of the sufferers so much that they refuse to keep it up. Iu 
such cases I have not insisted upon the further application of cold. 
In the hospital at Prague every pneumonia is treated with cold com- 
presses, and, according to the statements of Smoler, it is exceptional for 
a patient not to feel material relief from this treatment. As, however, 
I have never succeeded in cutting short a pneumonia by means of cold 
applications, I should only ascribe a palliative influence to their use, 
had not the duration of the disease in many instances been decidedly 
shortened and the convalescence hastened by means of their energetic 
and methodical employment. In fact, in but few cases have we seen 
the disease delay its departure until the seventh day. Many have im- 
proved on the fifth, and a very large number as early as the third day; 
nay, I have repeatedly found it impossible to keep patients with recent 
pneumonia in hospital for a longer period than a week. Cold is rightly 186 
DISEASES OF THE PARENCHYMA OF THE XUNG. 
regarded as one of the most efficient antiplilogistics in inflammation of 
external organs. Its action is directly tonic upon the relaxed tissues 
and dilated capillaries. It is harder to comprehend its mode of action 
upon inflammation of parts separated from the point of application, by 
skin, muscle, and bone. However, the contraction of the uterus and 
intestinal muscles, when cold is applied to the abdomen, proves the pos- 
sibility of its operation upon the interior, and ice compresses have long 
and justly been held in repute for meningitis, as have also the cold com- 
presses in peritonitis, by Kiewisch. I have no experience of the effect 
upon pneumonia of the repeated envelopment of the entire body in cold 
wrappings, as has been practised often by hydropaths; although it may 
be assumed that it would reduce the temperature of the body, and tem- 
porarily moderate the fever, even if it were unattended by any great 
direct influence upon the local phenomena. At all events, I am able to 
testify that, in the infectious diseases, active cooling treatment has such 
an effect upon the elevated temperature of the body in a large number 
of cases. All other modes of treatment recommended for pneumonia 
cannot be regarded as addressed directly to the disease, but, like blood- 
letting, belong to the indicatio symptomatica—being required only 
when special symptoms arise. 
Venesection ought to be resorted to in the following three con- 
ditions only: 1st. When the pneumonia has attacked a vigorous and 
hitherto healthy subject, is of recent occurrence, the temperature being 
higher than 105° F., and the frequence of the pulse rating at more than 
one hundred and twenty beats a minute. Here danger threatens from 
the violence of the fever; and free venesection will reduce the tempera- 
ture, and lessen the frequence of the pulse. In those who are already 
debilitated and anaemic, bleeding increases the danger of exhaustion. 
Should the fever be moderate, blood-letting is not indicated, even in 
healthy and vigorous individuals. It cannot cut the fever short, and 
indeed the fever is more apt to persist, although in a somewhat more 
moderate degree, so that the enfeebled patient is thrown into greatei 
danger than if he had had to pass through a more violent fever, but with 
unreduced strength. 
2d. When collateral oedema in the portions of the lung unaffected 
by pneumonia is causing danger to life, the pressure of the blood is re- 
duced by bleeding; and, by prevention of further transudation of serum 
into the vesicles, insufficience of the lung and carbonic-acid poisoning 
are averted. Whenever the great frequence of respiration in the com- 
mencement of a pneumonia cannot be traced to fever, pain, and to the 
extent of the pneumonic process alone, as soon as a serous, foamy 
expectoration appears, together with a respiration of forty or fifty 
breaths a minute, and when the rattle in the chest does not cease for a CROUPOUS PNEUMONIA. 
187 
while after the patient has coughed, we ought at once to practise a 
copious venesection, in order to reduce the mass of blood and to mod- 
erate the collateral pressure. 
The third indication for bleeding arises upon the appearance of 
symptoms of pressure upon the brain, not headache and delirium, but a 
state of stupor or transient paralysis. 
Having determined, for one or other of the above reasons, to bleed, 
the physician must not be misled by the fact that the pulse may be 
small and feeble instead of full and vigorous. Among the practitioners 
of the old school, “ a small, repressed pulse ” was always an indication 
for blood-letting, and a great number of cases may be advanced to show 
that the pulse often improves immediately after, or even during the 
venesection, and indeed the rule obtained that when the physician was 
in doubt as to whether the debility of the patient was genuine or false, 
he must take notice whether the pulse became larger or smaller after 
phlebotomy. The following is the reason why the pulse often grows 
stronger and fuller during or immediately after a bleeding: Ceteris 
paribus, the size and fulness of the pulse depend mainly upon the 
ability of the heart to surmount the resistance opposed by the aorta. 
If the functional vigor of the heart be reduced by the depressing influ- 
ence which results from an immoderate increase of the animal heat, and 
which, in some constitutions, is induced by a very moderate elevation of 
the temperature of the body, the resistance opposed by the aorta remain- 
ing unchanged meanwhile, the volume of blood propelled by the heart 
is diminished and the pulse-wave is small. If, now, we reduce this 
vascular tension by letting blood, we diminish the resistance of the aorta, 
and enable the heart, although actually enfeebled, to propel an increased 
volume of blood, and the pulse rises. True, we may fail in obtaining 
this effect, when, as sometimes happens, the effect of venesection is 
greatly to weaken the action of the heart, so that, although we diminish 
the resistance, we also diminish the propulsive power. 
Digitalis has been extensively employed, and with great justice, in 
the treatment of pneumonia. Like venesection, it is a febrifuge, low'ers 
the temperature, diminishes the frequence of the pulse, without exercis- 
ing so weakening and depressing an effect upon the system as bleeding. 
Its exhibition is indicated in pneumonia with a pulse of from one hun- 
dred to a hundred and twenty in frequence. With a less frequent pulse it 
is not required. We usually combine an infusion of digitalis (3 j— 3 ss. 
to 3 vj) with the neutral salts of nitrate of potassa and soda. If the 
latter have any influence upon the progress of the disease, it is only 
upon the fever; they have no antiphlogistic nor aplastic action. 
Next come the nauseants (antim. et pot. tart. gr. iv—gr. vj to 3 vj. 
S. 3 ss every two hours) and ipecacuanha; after these, quinine, veratrine, 188 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
and inhalation of chloroform. By means of each of these agents, the 
action of the heart and the temperature can be reduced, and the fever 
moderated; but they have no immediate local influence. The use 
of tartar-emetic has of late fallen somewhat into discredit. My re- 
cent experiments with quinine show that, in cases of danger from exces- 
sive fever, quinine should be given in two-grain doses every two hours; 
or, what is better, in two or three ten-grain doses at short intervals. 
According to li termer, veratrin (a remedy spoken of by Voe/t as a 
very effective antipyretic) is one of the surest means of diminishing 
the pulse-rate, and reducing the temperature in pneumonia. Indeed, 
H termer, Kochcr, and others, claim for it a direct influence upon the 
pneumonic process itself, and maintain that, in certain recent cases, 
the disease has been eradicated by its use. Veratrin has this advantage 
over digitalis, that it operates more promptly, both upon pulse and 
temperature, and is less apt to act cumulatively. But, on the other 
hand, reduction of the temperature and lowering of the pulse can only 
be brought about by the exhibition of doses so large as to cause symp- 
toms of poisoning, vomiting, purging, and great prostration. Of pure 
veratrin, the twentieth of a grain may be given for a dose—of the 
resin, veratri viridis, one-sixth of a grain. Of the tincture, from four 
to eight drops may be taken every three hours in a mucilaginous ve- 
hicle. Modern experience fully warrants its use in recent cases and 
robust subjects. 
In most cases of pneumonia all the above-named measures are su- 
perfluous, and the patient will soon improve under cold compresses 
and a placebo of gum-water ; still, the better we remember the indi- 
cation for active treatment, the greater our success will be. 
As the disease advances, the symptoms often demand measures the 
physiological operation of which is exactly the opposite of all those 
hitherto described. AVe have seen that an excessive exudation, a pro- 
traction of the pneumonic fever, or, indejDendently of either of these, 
a debilitated state of constitution prior to the attack, may give rise 
to a state of the most complete adynamia; and, indeed, it is to this ex- 
haustion that most people succumb who die of pneumonia. The feeble 
contractions of the heart tend to produce new dangers from passive 
oedema of the lung, and commencing palsy of the bronchial muscles 
embarrasses the evacuation of the bronchi. Stimulants must now be 
administered; the heart is to be excited into energetic action; the 
contractile power of the bronchial muscles must be raised. Fruitless as 
their extensive employment often is in other diseases, from the transi- 
tory character of their action, yet stimulants may produce very gratify- 
ing results if given in cases where symptoms of exhaustion arise while 
the pneumonic process is still incomplete. By giving large doses CROUPOUS PXEUMOXIA. 
189 
of camphor, musk, and strong wine, we often are able, for about twenty- 
four or tliirtv-six hours, to support the action of the heart, arrest the 
progress of the oedema, and facilitate expectoration. For this purpose 
Benzoic acid (gr. y, every two or three hours) is particularly recom- 
mended. The treatment of all cases of pneumonia by alcohol, as pro- 
posed by Todd, is not approved. 
Compensation for waste of the body by fever is of far greater im- 
portance than the use of stimulants. Do not carry the antiphlogistic 
diet too far, especially in depraved constitutions and enfeebled per- 
sons, but, as soon as distinct indications of asthenia begin to appear, 
in addition to the wine, give concentrated broths, milk, etc. 
The bold administration of the preparations of quinine and iron are 
peculiarly appropriate in these cases. Rademacheds tincture of iron is 
especially applicable ( 3 ss to 3 vj water. S. 3 ss—two hours). There is 
no form of pneumonia which, in the sense of Rademacher, “ eine Eisen- 
affection des gesammt organismus darstellt,” but an impoverishment of 
the blood often sets in during the disease, the obviation of which is 
quite as well promoted by the use of ferruginous preparations as is the 
chronic deterioration of the blood in chlorosis. A physiological explana- 
tion of the undoubted usefulness of the preparations of iron in chronic 
and acute impoverishment of the blood has not as yet been found. We 
only know that, not only is the iron of the blood increased in amount, 
but the protein substances, particularly the globulin of the blood, whose 
quantity always undergoes diminution, increases again under the use of 
iron. We shall easily convince ourselves that the action of the ferru- 
ginous preparations in acute impoverishment of the blood is quite as 
great as in chronic anasmia, if we use them with sufficient boldness in 
cases of exhausting pneumonic and pleuritic exudation; and, without 
assenting to the principles of Rademacher, we cannot deny the success 
which his school has attained by the use of iron in acute febrile diseases. 
Unfortunately, if diarrhoea exist, they are not well borne. 
The employment of stimulants, generous diet, and the preparations 
of quinine and iron, may be indicated from the very outset of the attack, 
when an adynamic state develops early, as in the case of old persons, or 
of cachectic subjects; and it must be regarded as a serious blunder if a 
physician, who, by his stethoscope, has recognized pneumonia in a sup- 
posed “ gastric ” or nervous influenza, should proceed to treat the malady 
upon “antiphlogistic” principles. Local blood-letting, by means of 
leeches or cups, must be resorted to in all cases where the pain is not 
mitigated by the employment of cold, or when the patient cannot bear, 
or will not submit to the latter. It almost always mitigates the pain, 
and as pain is not only a troublesome symptom, but is one of the causes 
of the disturbance of respiration, its removal may have a beneficial effect 190 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
upon the progress of the disease. On the other hand, it is better not 
to employ cutaneous irritants, whether sinapisms or blisters, at all, or at 
least not until a late period, when resolution is going on too slowly. 
Finally, if the patient be plagued by cough or restlessness, or by sleep- 
less nights, the indicatio symptomatica may require the use of narcotics, 
and we must not fear to administer a Dover’s powder at night under 
these circumstances, notwithstanding the persistence of the fever. 
CHAPTER X. 
Etiology.—The catarrhal process is a form of disease peculiar to 
the mucous membranes, and, as no mucous membrane with mucous 
glands exists in the pulmonary vesicles, the name catarrhal pneumonia 
is not quite applicable to the disease in question. Nevertheless, as 
catarrhal pneumonia never arises unless preceded by catarrhal bron- 
chitis, and as its characteristic pathological alterations are entirely 
analogous to those of bronchial catarrh, we shall retain the generally 
adopted title. In many cases catarrhal pneumonia arises solely through 
the extension of the morbid process from the bronchial mucous mem- 
brane into the air vesicles. In the great majority of instances, how- 
ever, this disease develops in pulmonary tissue which has already col- 
lapsed, a circumstance which makes it more than probable that col- 
lapse of the air-cells essentially favors its occurrence. It is not sur- 
prising, moreover, that the capillaries of the alveolar wall, when lib- 
erated from the pressure of the air enclosed in the vesicles, should be- 
come enlarged and surcharged with blood, nor that after long persist- 
ence of this capillary liyperasmia, it should be attended by augmented 
transudation and copious cell-formation. Now these are the very 
alterations which the anatomical appearances of catarrhal pneumonia 
present. 
This disease is most commonly observed as a complication of 
measles, and of whooping-cough; but the reason for this seems to be 
simply, that capillary bronchitis occurs much more frequently in the 
course of the latter complaints than in healthy children. Causes of 
catarrhal pneumonia, other than those from which capillary bronchitis 
and collapse of the lung originate, are unknown. We may very 
properly call it a disease of childhood, as it is in children that capil- 
lary bronchitis, and its sequel, partial pulmonary collapse—the pre- 
cursors and initial stages, as it were, of catarrhal pueumonia—are most 
commonly seen. 
Anatomical Appearances.—While croupous pneumonia extends, 
CATARRHAL PNEUMONIA BRONCHOPNEUMONIA. CATARRHAL PNEUMONIA. 
191 
as a rule, throughout an entire lobe of a lung, or at least throughout a 
large portion of a lobe, catarrhal pneumonia almost always remains 
limited to single lobuli, and hence has also obtained the names of 
lobular, disseminated, insular pneumonia, in contradistinction to the 
lobar or croupous pneumonia. 
If the process, have developed in the midst of pulmonary tissue 
which contains air, we observe in the affected lung distinct scattered firm 
points corresponding to the inflamed lobuli, which lie chiefly upon the 
periphery of the lung, and are then distinctly wedge-shaped. Their 
surfaces lie upon a level with that of the surrounding parts. At first 
they are of a bluish red; later, if the transudation and cell-growth 
predominate, they have a lighter and more grayish color. Upon sec- 
tion, the surface presents a smooth homogeneous appearance, and 
there are none of the granulations characteristic of croupous pneumo- 
nia. Upon lateral pressure upon the inflamed spot, there flows over 
the cut surface an opaque liquid, at first bloody, and afterward pale-gray 
in color, in which, under the microscope, we may see numerous cells, 
some of them already in a state of fatty metamorphosis. In a more 
advanced stage, these inflammatory centres undergo the same changes 
which we have described as taking place in the spots enclosed in col- 
lapsed pulmonary tissue. The gradual transition of atelectasis into 
catarrhal pneumonia has recently been studied and described with 
accuracy by Bartels and Ziemssen. These observers agree in rep- 
resenting that the collapsed portions of lung exhibit alteration of 
structure even when the collapse is quite recent. In slighter cases, 
this alteration is limited to the lower sharp edge of the lungs, and to 
a vertical stripe about two inches wide at their posterior edge upon 
either side. In severer and more protracted cases, the entire lower 
lobes of each side are involved, the process sometimes extending as 
far as the back and inner side of the upper lobes. An attempt to 
inflate them will succeed; but an unusual amount of force is requisite 
for the purpose; and the reinflated portion does not resume its former 
pink color, but becomes of a deep scarlet or vermilion red, a proof 
that the blood in it has increased considerably in quantity. When 
the collapse is of long standing, the collapsed parts become more vo- 
luminous and resistant, and we find in them separate compact knots of 
irregular form and size. If we now inflate the lung, these knots 
remain unchanged while the surrounding parts expand and fill with 
air. Upon section we constantly find in the centre of these spots a 
dilated bronchiole filled with tenacious secretion. The cut surface 
resembles that of the spots of catarrhal inflammation in the uncollapsed 
mng-substance (see above). In a more advanced stage, the numer- 
ous small centres of infiltration often coalesce into voluminous masses 192 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
of induration, so that a large portion of the posterior part of the lung 
exhibits a brownish-red, compact, but friable infiltration, out of which 
only small quantities of purulent but adhesive liquid can be expressed. 
If the disease be of still longer standing, we find that the color of the 
dark-brown infiltration has gradually faded from the centre toward the 
periphery, so that the middle assumes a grayish appearance, its firm- 
ness being at the same time materially diminished. Upon microscopic 
examination, ,we perceive a further advance in the fatty degeneration 
of the cellular elements, and a large admixture of granular multinuclear 
cells (pus-cells). The alterations which we have just described are 
analogous to those of red hepatization and purulent infiltration with 
which we have become acquainted as stages of croupous pneumonia; 
although fibrinous exudation never accompanies the cell-growth in 
catarrhal pneumonia. Abscesses may form as one of the rarer sequelae of 
this disease, while caseous infiltration is a far more common result of 
this disorder than of croupous pneumonia. Finally, catarrhal pneumonia 
often results in neoplastic formation of connective tissue with con- 
secutive wasting and shrinking of the parenchyma. At all events, 
Bartels, in a series of cases, in which the disease had run a more chronic 
course than usual, found, instead of the changes described above, that 
large portions of the lower lobes had acquired a pale, bloodless, strik- 
ingly compact and firm consistence. The cut surface also showed a 
pale-blue color, and presented a homogeneous, smooth, dry appearance. 
The parts of the lung thus altered could not be inflated. The bronchi 
were filled by yellowish caseous plugs. The most striking point was 
the great increase of the interstitial connective tissue. The condensed 
portions were traversed by thick grayish-white cords, and bands of 
connective tissue, which ran in different directions, crossing one another 
repeatedly, and forming a well-defined network. This termination of 
catarrhal pneumonia is analogous to the induration which we have 
described as occurring in croupous pneumonia. 
Symptoms and Course.—It is difficult to draw up a comprehen- 
sive picture of catarrhal pneumonia, as the disease is never of primary 
origin, but always supervenes upon a catarrhal bronchitis or a collapse 
of the lung proceeding from bronchitis, and its only symptoms consist 
in modifications more or less distinct of the symptoms of the disorder 
by which it has been preceded. With the exception of the physical 
signs, which, however, are not always characteristic, the kind and man- 
ner of the cough and the character of the fever furnish the most im- 
portant data for the recognition of the complication which has set in. 
It is highly suspicious if the sick child fear to cough, or when we find, 
by its complaints, or, in a very young child, by the distressed expression 
of its countenance, during coughing, that coughing gives it pain. We CATARRHAL PXEUMONIA. 
193 
have already stated, while speaking of whooping-cough, that the cessa- 
tion of the protracted coughing-spells and the occurrence, in their stead, 
of short, harsh, painful “ hacks,” are very serious symptoms; but, in 
the catarrh of measles, and in a genuine capillary broncliitis, attentive 
observers will rarely miss the modification of the cough just mentioned. 
A fact established by Ziemssen is of great diagnostic value, namely, 
that the temperature of the body always becomes elevated upon the 
supervention of a catarrhal pneumonia upon a catarrhal bronchitis. 
While the temperature of the body, according to Ziemssen, seldom 
reaches the height of 102.2° F. in simple capillary bronchitis, upon the 
development of a catarrhal pneumonia, it often mounts, in a few hours, 
to 105° F. and sometimes still higher. At the same time the pulse 
becomes more frequent, the face redder, and the child evinces great 
terror and restlessness, or, in severe cases, soon falls into a state of 
apathy and somnolence. Upon examining the chest of a child suf- 
fering from measles, whooping-cough, or genuine bronchial catarrh, 
whose cough has begun to grow painful, or whose fever has suddenly 
grown worse, or in whom intense fever has arisen where none has pre- 
viously existed, we must not expect for the first day or two to discover 
the characteristic physical signs of catarrhal pneumonia. When the 
pneumonic spots are surrounded by healthy parenchyma, and are of no 
very great magnitude, neither auscultation nor percussion furnishes any 
diagnostic data throughout the whole course of the disease. On the 
other hand, if the complaint have developed from an extensive atelec- 
tasis in a few days, an adept in percussion will find a dulness, which is 
almost always symmetrical, ascending posteriorly upon both sides of 
the spinal column in a narrow stripe, which is characteristic of it, and 
which does not extend toward the lateral regions of the thorax until a 
late period. As the collapsed portion of the lung at first presents but 
a thin layer, void of air, we must percuss with feeble, short stroke, in 
order to recognize the dulness. The pectoral fremitus and the respi- 
ratory sounds are not as yet altered. At most, the rhonchi and rales 
of the capillary bronchitis, in the vicinity of the collapsed region, are 
somewhat less loud and less distinctly audible than in other parts of 
the lung. Should the collapse extend, and should the collapsed part 
become more voluminous and dense, the dulness becomes more distinct, 
extends more outwardly, the pectoral fremitus becomes stronger. The 
breathing is bronchial, any rales which may be heard have a ringing char- 
acter ; in brief, the signs of auscultation and percussion are now iden- 
tical with those of a croupous pneumonia at the stage of hepatization. 
If not called to see the sick child until this period, it may be difficult and 
even impossible to decide whether we have to do with a croupous pneu- 
monia or wfith an extensive catarrhal inflammation of collapsed lung. 194 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
(Physical exploration, as we have repeatedly stated, never gives infor- 
mation as to the quality of the condensation of a lung, or of effusion 
into the pleura.) If, on the other hand, we have had opportunity to 
observe the progress of the malady from its commencement, the dis- 
tinction between the two is, as a rule, easy: as the occurrence ol 
double symmetrical condensation and the tardy lateral extension of the 
narrow condensed stripes indicate collapse of the lung and catarrha* 
pneumonia; while, on the other hand, a condensation at first confined 
to one side, and, afterward, spreading over the whole of one of the 
pulmonary lobes, denotes croupous inflammation of the lung. 
The progress of catarrhal pneumonia is sometimes, although not 
often, a very acute one. The disease may prove fatal in a few days, 
especially if it attack feeble children. In such an event the counte- 
nance, previously red, becomes pale and livid. The lips assume a 
bluish hue; the eyes grow dull and lustreless; the restlessness gives 
place to apathy, and to a continually augmenting somnolence. Owing 
to the serious disturbance of respiration, the pernicious effects of 
incomplete oxygenation and overcharge of the blood with carbonic 
acid soon become apparent. It is also rare for a rapid resolution to 
occur in catarrhal pneumonia, and, even when it does take place, the 
sudden decline of the fever so characteristic of croupous pneumonia 
is scarcely ever seen; so that, in doubtful cases, the termination 
of the attack by a lysis or a crisis may decide the question as 
to the distinction between catarrhal and croupous pneumonia. 
It is much more common for catarrhal pneumonia to take on a 
subacute, and even chronic course. This is especially true of those 
cases which set in upon a whooping-cough or chronic catarrhal bron- 
chitis. Here, as a rule, not only does the consolidation form slowly 
and gradually, but it continues stationary with great persistence often 
for many weeks. The child becomes extremely emaciated, until death 
finally ensues with the symptoms above given; or, perhaps, after hope 
has almost ceased, resolution of the infiltration and complete recovery 
follow. 
Tubercular infiltration, abscess, and induration of the lunjrs following 
catarrhal pneumonia, present the same symptoms as when they appear 
as sequelae of croupous inflammation of the lung. 
Treatment.—It is easy to understand that if, in the course of 
capillary bronchitis, the disease extend from the *mucous membrane of 
the bronchi into the air-cells, producing catarrhal pneumonia, the same 
general directions already given will apply for the treatment of this 
disease. This is especially the case with regard to local and general 
blood-letting. According to the recent experience of Bartels and 
Ziemssen, the latter never proves of service, and often does con- CHRONIC INTERSTITIAL PNEUMONIA. 
195 
siderable harm by reducing the strength of the patient, lowering the 
energy of the inspirations, and thus tending to encourage the spread 
of pulmonary collapse; and here I will again briefly call to mind the 
value of emetics, transitory as it may be, and the frequent lack of suc- 
cess in their use. It has been of great interest to me, that both 
Bartels and Ziemssen strongly commend the application of cold com- 
presses to the chest (proposed by me in croupous pneumonia), as by 
far the most efficient mode of treatment. 
CHAPTER XI. 
CHRONIC INTERSTITIAL PNEUMONIA—INDURATION OF THE LUNG— 
BRONCIIIECTATIC CAVITIES. 
Etiology.—The lung, when healthy, has but little connective tis- 
sue in its composition. A portion of this combines with numerous 
elastic fibres to form the pulmonary air-cells; another portion serves 
to bind together the lobules, while a third belongs to the walls of the 
blood-vessels and bronchi. There is a large class of cases in which, 
instead of these mere rudiments of connective tissue, we find large 
sections of the lung converted into a callous, fibrous mass, the product 
of a chronic interstitial pneumonia, which must be regarded as one of 
the most frequent of diseases. 
In chronic pneumonia there is no free exudation either into the air- 
cells, or their interstices, excepting in that form of the affection known 
as caseous infiltration, of which we shall speak by-and-by, while treat- 
ing of pulmonary consumption. While in croupous and catarrhal 
pneumonia the pulmonary tissues themselves suffer little or no nutri- 
tive disturbance, in the form of inflammation at present under con- 
sideration it is precisely this pulmonary intercellular and interlobular 
connective tissue which is attacked. The process consists in a hyper- 
plasia of the connective tissue, resulting in an augmentation of the 
substance of the lung, and in a diminution of its cavities for the recep- 
tion of air. The newly-formed material, by which the lung is solidified, 
then undergoes further changes, as do all other neoplastic formations 
of connective tissue arising from inflammation. At first soft and filled 
with blood, it afterward contracts, and is transformed into a callous, 
bloodless substance, occupying a smaller amount of space than was 
formerly filled by the healthy lung. 
Chronic interstitial pneumonia scarcely ever occurs as an indepen- 
dent and primary disease. Even in the interesting cases observed to 
follow the inhalation of iron or coal-dust, the induration is not a direct 
result of such inhalation of irritating substances, but only appears 196 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
secondarily, as a consequence of the bronchitis induced by the irri- 
tant : 
1. We have seen that interstitial pneumonia is one of the compli- 
cations of prolonged croupous or catarrhal inflammation of the lungs, 
and that it results in induration of the latter. 
2. Simple collapse of the lung appears sometimes to give rise to an 
inflammatory proliferation of the interstitial substance, resulting in in- 
duration of the lung. 
3. The deposit of tubercle, and especially the softening of tubercu- 
lous deposits, cancer of the lung, haemorrhagic infarctions, pulmonary 
apoplexy, and pulmonary abscess, all produce interstitial pneumonia 
with “ nutritive ” exudation ( Virchow). It is thus that the capsules 
of connective tissue are found, which separate the products and residue 
of the processes, above named, from the healthy lung. 
4. Interstitial pneumonia not unfrequently forms a complication of 
chronic bronchitis, when it first involves the parts immediately around 
the bronchus, but may extend thence, forming extensive solidification 
of the lung. 
The occurrence of bronchiectasis as a result of chronic interstitial 
pneumonia is easy of explanation. The space created in the thorax 
by contraction of the lung must be compensated for by atmospheric 
pressure. The thoracic wall sinks in as far as it is possible for it to 
yield; but, from the structure of the chest, this collapse is restricted 
within somewhat narrow limits, so that a vacuum would form within 
its cavity were it not that the bronchi become dilated by pressure of 
the atmosphere. This process is usually described as if the contract- 
ing tissue of the lung exerted a traction upon the bronchial wall, thus 
dilating the tubes into spacious canals and extensive cavities. But 
the extra bronchial traction, which the contracting connective tissue 
exercises upon the bronchial Avail, is not the only cause of bronchiectasis. 
The discoA’ery of diffuse or sacculated dilatations in the midst of tissue 
Avhich is simply collapsed, or which still contains air, compels us to 
ascribe the origin of some cases of bronchiectasis to other sources. 
Unfortunately, the condition in question is an extremely complicated 
one; and, in spite of the excellent work of liiermer upon the patho- 
geny and anatomy of bronchial dilatation, its origin is, as yet, by no 
means satisfactorily explained. We must, therefore, content ourselves 
by briefly stating that, in some cases, probably the calibre of the bron- 
chus is enlarged by the pressure of stagnant secretion upon its inner 
surface, especially Avhen the resilience of the bronchial Avail is impaired. 
In other cases bronchiectasis, perhaps, is a result of atmospheric pres- 
sure during the act of inspiration, in cases Avhere portions of the lung 
are incapable of expansion, other portions suffering abnormal compen- CHRONIC INTERSTITIAL PNEUMONIA. 
197 
satory dilatation. In such a case, if the resisting power of the bron- 
chial Avail be less than that of the pulmonary substance, or if an ob- 
struction in the smaller bronchi, or other impediment, hinder proper 
expansion of the vesicles, it would seem that compensatory bronclii- 
ectasis may arise in place of pulmonary emphysema. 
Finally, it is possible that some bronchiectases may be the result 
of dilatation of the bronchial wall at points in the upper lobes of the 
lung, where the tubes yield before the centripetal rush of air dri\Ten 
into them from the ah’eoli by the act of coughing, and, while giving 
way before the pressure, cause bronchiectasis instead of emphy- 
sema. 
Anatomical Appearances.—We rarely have the opportunity of 
examining interstitial pneumonia before it begins to contract. We 
then find the pulmonary substance solidified and void of air, in conse- 
quence of swelling of the vesicular walls and scanty intervesicular and 
interlobular connective tissue. At first it is hyperaemic and reddened; 
afterward of a paler, bluish-gray color. In several cases in which 
bronchiectatic cavities have been found at the base of the lung in the 
midst of indurated tissue, I have had an opportunity of observing ex- 
tensive tracts of pale-red homogeneous substance, composed of young 
connective tissue, and situated between portions of the lung which 
contained air. 
Products of a later stage of the disease are much more frequently 
met with. They consist of bands, or irregularly-shaped masses en- 
twined in the pulmonary substance, are of a Avhitish color, or else are 
blackened by pigment, and of a dense structure which “ cries ” under 
the knife. They surround old masses of tubercle, which have already 
become caseous, and tuberculous ca\’ities, abscesses of long standing, 
and the residue of the latter sometimes found in the lung in the shape 
of calcified concretions. When croupous pneumonia terminates in in- 
duration, entire lobes of a lung may become converted into this black- 
ish, callous substance. 
In the autopsy of individuals who have worked in coal-mines, or 
who ha\re inhaled coal-dust in other occupations, the lungs and bron- 
chial glands are often found to be of a deeply-black hue. From the 
results of recent investigation, there is no doubt that this coloration 
depends upon the penetration into the lung of particles of coal. As a 
rule, the pulmonary tissues sustain this intrusion of coal-dust remark- 
ably well, and there are cases in which this anthracosis (that is, black- 
ness resulting from deposit of coal-dust) has been the only lesion 
found in the lung. In other cases, the black discoloration is combined 
with an interstitial pneumonia, originating from the bronchial walls, 
but often extending Avidely. In other instances, again, cavities are 198 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
found in the indurated tissue, which are undoubtedly to be regarded 
as suppurating bronchiectases. 
Zenlcer, in a valuable treatise, shows that disease of the lungs may 
also arise from the inhalation of iron-dust, which, in all essential par- 
ticulars, is similar to antliracosis, differing merely in the nature of the 
dust inhaled, and in the color of the lung, which is of a slate-color 
instead of black. In one of the cases of this disease, reported by 
Zenker, for which he proposes the name of siderosis, or of pneumono- 
koniosis siderotica (/), the oxide of iron, which had entered the lung, 
had given rise to extensive induration and to the formation of large 
cavities. 
Rokitansky describes saccular dilatation of the bronchi as follows : 
We find a bronchial tube widened into a fusiform, or rounded pouch ; 
in the latter case the dilatation often being greater upon one side than 
another, so that a greater part of the bronchial sac lies out of the 
axis of the bronchial tube. In rare cases, the size of such a pouch 
may equal that of a hen’s egg. They will often contain a bean, a 
hazelnut or a walnut. We further find either that any one of the 
bronchial tubes may become expanded into a pouch of this kind, the 
tube retaining its normal calibre upon either side of the dilatation, or 
else quite a large tract of the bronchial ramifications may undergo 
enlargement. Then, many such sacs of different size are so grouped 
together that they form, as it were, a vast sinuous cave with many 
branches, whose individual pouches are bounded and separated from 
one another by ledges or valvular folds of the bronchial wall.” 
The inner surface of bronchiectatic cavities is at first smooth, the 
mucous crypts haying flattened out and disappeared through excessive 
extension. The mucous membrane having thus gradually lost its char- 
acter, becoming more like a serous membrane, its secretion also at first 
bears some resemblance to that of a serous sac. We find in bronchi- 
ectatic cavities a synovia-like liquid, resembling that found in a greatly 
over-distended gall-bladder, or in an obstructed processus vermiformis. 
At a more advanced stage, however, the inner surface often loses its 
smooth character, and the contents of the cavity undergo change. 
Owing to the unyielding condition of the surrounding parenchyma, 
which is not compressed even by the most violent coughing, and par- 
ticularly if the cavities are situated in the lower lobes of the lung, it 
becomes extremely difficult to get rid of the secretion. Hence, the 
latter, exposed to an elevated temperature, and in communication with 
the atmosphere, is converted into a foul, yellow, stinking ichor, which 
often acts as a corrosive upon the walls of the cavity, producing 
sloughs and depriving the walls of their smoothness. It is not un- 
common for severe haemorrhage to take place when these sloughs CHRONIC INTERSTITIAL PNEUMONIA. 
199 
separate. In other cases, the putrid contents of the dilated tubes 
cause inflammation or diffuse putrescence of the lung. In the very- 
rarest instances, the bronchus leading to a cavity becomes obliterated, 
when its contents may be transformed into a cheesy or calcified 
paste. 
Symptoms and Course.—In its first stage interstitial pneumonia 
can hardly be recognized with certainty. Should the resolution of a 
croupous pneumonia be very tardy; if we find, after the lapse of weeks, 
that the percussion-sound continues dull and the respiration bronchial 
or indistinct, we may anticipate that the disease will terminate in indu- 
ration, particularly if the patient have no fever, and gradually recover 
his health, so that we may exclude the idea of cheesy infiltration. We 
cannot diagnose the disease with certainty until the thorax commences 
to sink in at the affected side, and the signs of bronchiectasis appear. 
It is quite the same with regard to the interstitial pneumonia 
which accompanies tuberculosis, and caseous infiltration of the lung. 
As this is one of the constant complications of the above diseases, we 
may reasonably infer that the dulness at the apex of the lung observed 
in consumption is due in part to interstitial pneumonia. The depres- 
sion of the supra and infra clavicular regions, which sometimes accom- 
panies pulmonary consumption, can only be ascribed to this interstitial 
pneumonic induration, since neither reduction of the dimensions of 
the lung, nor depression of the thoracic wall, is produced either by 
tubercular deposit, caseous infiltration, destruction of the pulmonary 
substance, or by the establishment of cavities. Although this symptom 
(which is often erroneously called a pathognomonic sign of consumption) 
is a very common one among consumptive patients, yet this is only 
because the process by which the lung is destroyed is almost always 
accompanied by a chronic pneumonia, which causes its induration and 
contraction. When chronic pneumonia is associated with chronic 
bronchitis and emphysema, depression of the thoracic wall is less com- 
mon. In such cases the only diagnostic signs are the coughing-fits, 
characteristic of the existence of cavities with rigid Avails, and the na- 
ture of the sputa. 
When the disease is someAvhat extensive, signs of dilatation and 
hypertrophy of the right side of the heart are added to the symptoms 
above described; and at a later period, where hypertrophy of the heart 
is no longer capable of counteracting the effects of obstructed circula- 
tion, cyanosis appears, with blueness of the lips, puffiness of the face, 
enlargement of the liver, and finally dropsy, symptoms Avhich, as we 
have learned, also accompany emphysema. An explanation of this is 
easy; the obstacle to evacuation of the right heart manifestly pro- 
ceeding from atrophy of the pulmonary capillaries. We rarely observe 200 
DISEASES OF TIIE PARENCHYMA OF THE LUNG. 
cyanosis in the pulmonary induration which accompanies consumption, 
although in such cases there is a double hinderance to the pulmonary 
circulation. This is attributable to the circumstance that, simultane- 
ously with the destruction of the pulmonary capillaries, the volume of 
the blood is reduced by hectic fever. 
Easy as it often is to recognize bronchiectatic cavities of the lung 
with certainty, the diagnosis in other instances is extremely obscure. 
The signs usually described as pathognomonic of bronchiectatic cavi- 
ties are only met with in cases which are uncomplicated with tubercu- 
losis or cheesy infiltration, and where the cavities are situated in the 
lower lobes of the lungs. Bronchiectatic cavities at the apex of the 
lung, lying side by side with tuberculous cavities, cannot be distin- 
guished from the latter even upon dissection, to say nothing about 
recognizing a difference between them during life. The manifestation 
afforded by a bronchiectasis in the lower lobes of the lungs is readily 
explicable, if we only know the extreme difficulty of discharging the 
contents of cavities in such dependent positions. The liquid contents 
of a vomica at the apex of the lung has no difficulty in flowing away 
through the obliquely descending bronchi, but the discharge from a 
similar cavity situate in one of the lower lobes, through bronchi whose 
direction is obliquely upward, is either quite impracticable, or, at least, 
only practicable while the body is in particular attitudes. (Cases occur 
in which copious volumes of the thick, yellowish-green fetid contents 
of a bronchiectatic cavity pour from the mouth of a patient, even be- 
fore he has coughed, whenever he stoops forward or allows the upper 
part of the body to sink laterally while lying in bed.) 
Owing to the difficulty and incompleteness with which bronchial 
cavities in the lower lobes of the lung are emptied, and to other un- 
known causes, the contents of the cavities often undergo putrefaction. 
This putrid sputum has an extremely penetrating, fetid odor (particu- 
larly at the moment of its expectoration), and is less viscid than most 
catarrhal sputa, often containing caseous plugs, in which clusters of 
margarine crystals are found. When collected and allowed to stand, 
it separates into three strata, an upper frothy layer, a middle layer of 
whitish-gray liquid, and a thick grayish-green sediment; in short, it 
completely resembles the sputa of diffuse bronchial dilatation, and of 
putrid bronchitis. Nevertheless, in most cases, it is easy to decide 
whether we have to do with the latter form of disease, or with a sac- 
culated bronchus. In the former, the coughs follow with short inter- 
vals, and all the sputa which the patient ejects are of similar quality. 
On the other hand, patients with a bronchiectatic sac often announce, 
of their own accord, that they “ have two kinds of cough.” Indeed, 
half a day, or even a whole day, may pass, and the patient will cough CHRONIC INTERSTITIAL PNEUMONIA. 
201 
but little, expectorating small quantities of catarrhal sputa. This will 
be followed by a violent paroxysm of coughing, in which, in course of 
a short time, the patient will eject enormous quantities of putrid secre- 
tion. "When the fit is over, another long period of exemption begins, 
the spit-cup remaining empty for six or eight hours, or receiving but a 
few expectorations of mucus, when another attack will soon fill it to 
overflowing. The walls of bronchiectatic cavities seem to be tolerably 
insensible, and the irritation of the putrefying secretion does not appear 
to give rise to cough. It is only when the sac is completely full, and 
when its contents reach the neighboring bronchi, which still retain 
their normal sensitiveness, that the cough begins. We may, therefore, 
assert that violent coughing-fits, which recur at long intervals, and 
during which large quantities of putrid sputa are expelled, are pathog- 
nomonic of the existence of a bronchiectatic cavity. 
In addition to the symptoms hitherto described, there is usually 
well-marked cyanosis, and, at a later period, dropsy. In bronchiectasis 
of long standing, I have hardly ever failed to find the clubbed enlarge- 
ment of the terminal phalanges such as usually forms in cases of per- 
sistent cyanosis. These signs of venous engorgement are not, however, 
directly dependent upon bronchiectasis, being due rather to the con- 
comitant induration of the lungs (see above), and hence they are absent 
in the very rare instances in which bronchiectasis is not accompanied 
by extensive induration. 
Physical examination always affords very characteristic results 
when the bronchial sacculation lies close beneath the thoracic wall. 
When the pulmonary substance about the cavity is consolidated and 
contracted, the thorax is also depressed at the point corresponding, 
the percussion sound is exceedingly dull, and the sensation of resist- 
ance considerably increased. Upon auscultation, if the patient have 
not coughed for some time, we hear either an enfeebled respiratory 
murmur or else indistinct moist redes. Upon compelling him to cough, 
so as to provoke copious expectoration, the enfeebled respiration is 
often replaced by loud bronchial or even cavernous breathing. On 
the other hand, there are some cases in which physical examination 
furnishes no aid to diagnosis, because the cavity is situated more 
toward the centre of the lung, and is surrounded by normal paren- 
chyma. In spite, however, of the absence of physical signs of a cavity, 
we may diagnose its existence with positive certainty when a patient, 
without suffering any precursory dyspnoea, expectorates half a pint or 
more of purulent secretion in the course of a few minutes. Such enor- 
mous quantities of matter could only come from a large cavity, as its 
presence in the bronchi would render respiration extremely difficult, if 
not impossible. 202 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
Diagnosis.—It is often by no means easy to distinguish a diminu- 
tion and consolidation of the lung, resulting from interstitial pneu- 
monia, from a similar condition arising from continued compression. 
The thoracic wall sinks in after either process, and the heart, liver, and 
spleen are displaced, so that the history of the case is often our sole 
guide. If it cannot be determined whether the primary disease have 
been pleurisy or pneumonia, the question often remains unsolved, al- 
though bronchiectasis is far oftener a consequence of interstitial pneu- 
monia than of compression of the lung. 
In distinguishing bronchiectatic caverns from tuberculous excava- 
tions, besides the difference of their situation, the following points are 
to be taken into consideration: 1. Patients with bronchiectasis are 
generally free from fever, and hence often long retain a tolerable de- 
gree of strength, and suffer but little emaciation. 2. Secondary dis- 
ease of the larynx and intestine is of rare occurrence in cases of bron- 
chial dilatation; hence, hoarseness and diarrhoea, in a doubtful case, 
would indicate the tuberculous nature of the disease, although the 
coexistence of bronchiectasis is by no means excluded. 3. Saccular 
dilatation of the bronchi is so often accompanied by emphysema that, 
in forming a differential diagnosis between bronchiectasis and tuber- 
cular excavation, the evidence of the existence of emphysema would 
turn the scale in favor of the former. 
Prognosis.—As interstitial pneumonia scarcely ever is an inde- 
pendent affection, the prognosis depends essentially upon the original 
disease. This is especially the case when the malady accompanies 
tuberculosis. Extensive wasting of the lung, consequent upon tedious 
pneumonia, or accompanying chronic bronchial catarrh and emphysema, 
is often endured for a long time, even after bronchiectatic cavities 
have formed, the patients only succumbing at a late period, upon the 
establishment of marasmus and dropsy. At other times, life is sud- 
denly endangered by haemorrhage from the walls of the caverns, or by 
pneumonia from diffuse putrescence of the lung. 
Treatment.—In the stage at which interstitial pneumonia becomes 
recognizable, it is as impossible to do any tiling for its relief as it is to 
soften and resolve any other form of cicatricial tissue. We are equally 
powerless to effect the closure and obliteration of bronchiectatic vomica?. 
It only remains, therefore, for us to see to the emptying of these cavities, 
so that the foul secretion may not occasion still greater corrosion of 
the bronchial walls or parenchyma of the lungs. As a second indica- 
tion, we must endeavor to limit the secretion, both of the cavity itself 
and of the bronchi, from which secretion seems to flow into the cavity. 
Both indications are best met by the inhalation of oil of turpentine, as 
recommended above. It has already been mentioned that this pro- GANGRENE OF THE LUNGS. 
203 
cedure actually represses the secretion, and we can easily convince our- 
selves that, after an inhalation of a quarter of an hour, violent coughing 
follows, and evacuation of the cavities is effected. The inhalations are 
repeated three or four times daily, and I have seen patients raised by 
this means from a condition of extreme misery to one of tolerable 
comfort, which lasted for some time. 
CHAPTER XII. 
GANGEENE OF THE LUNGS. 
Etiology.—Various forms of mortification have already come under 
our notice in the foregoing chapters, among others, that of abscess as a 
sequel of pneumonia, and disintegration of the pulmonary parenchyma 
as a consequence of haemorrhagic infarction. Mortification proper, 
gangrene of the lung, differs from these forms of necrosis, inasmuch as 
the dead part putrefies and undergoes chemical decomposition. Putre- 
factive decomposition of necrotic parts of the economy occurs most 
commonly in organs which are exposed to contact with the air, such as 
the skin and the lungs, while in the brain, the liver, and the spleen, 
as long as they remain within their normal envelopes, putrefaction of 
dead tissue is not so apt to occur. The transition of necrosis into 
gangrene is materially promoted if a “ ferment ” (a bit of putrid ma- 
terial) come in contact with the mortified part. This explains why, 
though circumscribed gangrene of the lungs may be produced by 
haemorrhagic infarction in disease of the heart, through obstruction of 
the nutrient arteries (the bronchial arteries), it is that such a result is 
far more common in metastatic infarction, caused by an embolus from 
some region where putrefaction is going on. 
Diffuse pulmonary gangrene arises, in rare instances, during the 
culminating period of pneumonia, the inflammatory stasis causing the 
absolute arrest, both of circulation and nutrition, in the inflamed region. 
Such an occurrence is the more likely when stagnation of the blood in 
the capillaries causes coagulation of that which is in the bronchial 
arteries. 
Pneumonia caused by entrance into the air-passages of food, or the 
residua of food, is especially prone to run into gangrene, owing to the 
putrefaction of these foreign bodies. 
Gangrene may also arise with or without previous inflammation, 
from corrosion of the tissues surrounding a diffuse or saccular bronchi- 
ectasis, and their implication in the putrefaction of its contents. 
It is difficult to explain the occurrence of diffuse gangrene of the 
lungs in drunkards, and in persons whose constitution has been much 204 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
debilitated by misery and deficient nourishment; as is also its frequent 
appearance in lunatics, even where no foreign body has entered their 
air-passages, and its occurrence in the course of severe asthenic fever, 
measles, small-pox, and typhus. It would seem, indeed, as if a part, 
which already has suffered derangement of its nutrition, were espe- 
cially liable to die when its tissues are exposed to further inflammatory 
disturbance (Virchow). 
Anatomical Appearances.—According to the distinction of 
Lacnnec, there are two forms of pulmonary gangrene, the circum- 
scribed and the diffuse: 
1. Circumscribed gangrene is the more common form. At isolated 
points varying in size, from that of a hazelnut to that of a walnut, we 
find the parenchyma of the lung converted into a bluish-green, moist, 
frightfully fetid slough, resembling the eschar of the skin produced by 
caustic potash. It is abruptly limited, and surrounded by cedematous 
tissue alone. This sphacelous spot, which is at first tolerably firm, and 
adherent to the adjacent parts, soon decomposes into an ichorous liquid, 
which merely contains in its interior a somewhat hard greenish-black 
core, mixed up with rotten and ragged debris of the tissue. 
The seat of circumscribed pulmonary gangrene is generally the 
periphery of the lung, and the lower lobes. Not unfrequently a bron- 
chus opens into the gangrenous spot; the ichor of the slough enters 
the tube, and an intense bronchitis is the result. 
In a few cases, the pleura also mortifies; the slough softens, the 
ichor flows into the cavity of the sac, and thus a dangerous pleuritis is 
set up; and if the gangrenous centre at the same time communicates 
with a bronchus, pyopneumothorax may occur. In other instances, 
diffuse gangrene arises from circumscribed gangrene of the lungs. In 
very rare cases indeed, interstitial pneumonia arises in the surrounding 
parts, resulting in incapsulation of the gangrenous point; the sloughs 
are ejected and cicatrization follows, such as we see in pulmonary 
abscess. 
2. Diffuse gangrene of the lung not unfrequently attacks an entire 
lobe. We then find the parenchyma decomposed and converted into 
a putrid, tinder-like, black, stinking substance, saturated with blackish- 
gray ichor. Unlike the preceding form, the process is not abruptly 
limited, but is gradually merged in the oedematous or liepatized paren- 
chyma. If the mortification reach the pleura, it too is destroyed. 
Recovery never takes place, the patient dying of general constitutional 
disturbance. 
Either form of gangrene may lead to introduction of decomposed 
tissue into the veins, to embolism, and to metastatic abscess in the 
various organs of the greater circulation. GANGRENE OF THE LUNGS. 
205 
Symptoms and Course.—We have seen that the signs of haemor- 
rhagic infarction and metastatic deposits in the lungs are very obscure. 
Even circumscribed gangrene, which develops from haemorrhagic 
infarction and metastatic deposits, cannot generally be diagnosed until 
the gangrenous discharge reaches a bronchus and is ejected. Then, 
indeed, the foul odor of the breath, the blackish-gray liquid, and also 
the very ill-smelling sputa, leave no doubt about the nature of the case. 
Sometimes the fetid smell of the breath precedes the characteristic 
expectoration by some days. The sputa, like those of the decomposing 
contents of a bronchiectatic cavity, soon separate into several layers, 
a frothy superficial one, a liquid middle stratum, and a thicker sedi- 
ment. The color of the expectoration is of a dirty blackish or brown- 
ish color. It contains black, tinder-like masses, and frequently soft 
cores, containing acicular crystals of fat. In rare cases, it also con- 
tains fibres of wavy, elastic tissue. Sometimes, physical exploration 
affords further information. The sound upon percussion is tympanitic, 
more rarely dull, and in a few instances cavernous sounds may arise. 
Some patients evince the greatest prostration from the beginning; 
the countenance is “ pinched ” and livid, the pulse small and extremely 
frequent, and the patient soon perishes from asthenic (putrid) fever. 
Others bear this serious disorder wonderfully well. Their general 
condition is scarcely changed; they walk about, are without fever, and 
the disease goes on for weeks. In these cases haemorrhage may arise 
at a later period, which may exhaust the patient; or, after a time, 
asthenic fever may develop, to which the patient may succumb, after 
lingering, now better, now worse, for a long time. Should recovery 
take place (a very rare event indeed), the odor of the sputum dis- 
appears, it gradually becomes yellow, and at last, if the gangrenous 
spot be incapsulated and atrophied, it may cease altogether. 
When diffuse pulmonary gangrene arises from pneumonia, we 
observe a sudden loss of strength during the progress of the latter 
disease, with a small irregular pulse, a disturbed countenance, and 
soon the fetid breath and blackish liquid sputum, with its penetrating 
odor, are added to the above symptoms. When diffuse gangrene arises 
independently of pneumonia, it is attended from the outset by signs 
of extreme adynamia, and by symptoms like those which accompany 
the entrance of septic matter into the blood, rigors, delirium, stupor, 
hiccough, etc. The expectoration then often ceases entirely, either 
because the bronchial mucous membrane itself has become gangrenous 
and insensible, or else because the patient no longer can respond to 
any irritation whatever. They now not unfrequently swallow what 
sputum still reaches the fauces, and thus bring on an obstinate diar- 
rhoea in lieu of the expectoration. 206 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
Physical examination in diffuse pulmonary gangrene at first affords 
well-marked tympanitic sound, and afterward a dull one on percussion. 
Upon auscultation, we hear indistinct breathing and rales, and after- 
ward bronchial or even cavernous sounds. 
Treatment.—The treatment of gangrene of the lungs is some- 
what ineffectual. The inhalations of turpentine, recommended by 
Skoda, deserve consideration, as being recommended by an author 
distinguished by his skepticism in therapeutics. Whether it be of 
service in other forms of pulmonary gangrene than those which arise 
about bronchiectatic cavities, may be doubted. Nourishing diet, 
wine, infusion of bark, and stimulants may be required by the gen- 
eral condition of the patient. They are of no avail against the gan- 
grene itself, any more than is acetate of lead, creasote, or charcoal. 
TUBERCULOSIS OF TIIE LUXG. 
The term pulmonary tuberculosis continues to be the expression 
most commonly used to signify consumption of the lungs, a proof that 
the majority of modern physicians and clinical teachers still adhere to 
the teachings of Laennec, and only recognize one form of pulmonary 
consumption, the tuberculous form. I have long contested this doc- 
trine, and, upon various occasions, have declared, in direct contradic- 
tion to it, that destruction of the pulmonary tissues, the establishment 
of cavities and consumption of the lung are much more frequently a 
result of chronic inflammation than of tubercular deposit. And I hope 
that these views, of whose justness any one may easily satisfy himself 
who will only study the subject with calmness and without prejudice, 
will ultimately obtain general acceptation. 
The error into which Laennec and his disciples have fallen is not 
that they regard tubercle as a neoplasm, but that they look upon 
solidifications of the lung, due to entirely different causes, as products 
of tuberculosis. Even according to modern views tubercle still ranks 
among the pathological neoplasms, although, however, but one form, 
the miliary form, and one mode of origin, miliary tuberculosis, is rec- 
ognized. It is one of the characteristics of tubercle, that it always 
appears in the form of small nodules, scarcely as large as a millet-seed, 
and that the individual nodules never grow into voluminous tumors. 
The larger so-called tubercular nodules consist always of an aggrega- 
tion of many small miliary tubercles. All the extensive indurations 
and enlargements formerly described as tuberculous infiltration, or as 
infiltrated tubercle, depend neither upon infiltration of the tissues with TUBERCULOSIS OF THE LUNGS. 
207 
tubercular matter, nor upon diffuse development of tubeicle, but upon 
morbid processes of a different nature. 
In the lungs it is more especially the residua of chronic inflamma- 
tion which Lciennec and his pupils have regarded as tubercular infiltra- 
tion. The main source of their error was the idea that caseous meta- 
morphosis, to which tubercle of long standing almost invariably is 
subjected, was a specific peculiarity of the disease, and that it might 
be regarded as a diagnostic mark, by which the tuberculous nature of 
a growth, wherein the process arose, might be determined. Accord- 
ing to such views, the product of chronic pneumonia, which often ap- 
pears in phthisical lungs independent of tubercle, was ascribable to 
tuberculosis, since, generally speaking, this inflammatory product at 
first is moist, transparent, and of a grayish or grayish-red color, and, 
after a lapse of time, becomes transformed into dry, opaque, yellow, 
cheesy masses, and, subsequently, into a creamy or curdy, flocculent 
liquid (“ tubercular ” pus). 
But the point of view, from which caseous metamorphosis was con- 
sidered a characteristic sign of tuberculosis, is obsolete. It is well 
established that not only tubercle but many other formations with 
which it has nothing in common, such as old, cancerous nodules, lym- 
phatic glands enlarged by hyperplastic cell-growth, hcemorrhagic in- 
farctions, incapsulated collections of pus, may all undergo caseous 
metamorphosis, and the term tuberculization, which has been produc- 
tive of great confusion, and against which I have long protested, has 
fallen into disuse. 
By this important step in pathological anatomy, for which we are 
chiefly indebted to Virchow, the very foundation of the teachings of 
Laennec is swept away. His fundamental idea that all pulmonary 
consumption depends upon neoplasm, after having exercised a most 
baneful influence both upon the prophylaxis and the treatment of the 
disease, is no longer tenable, and it is really incomprehensible that the 
majority of physicians of the present day should still adhere to his 
views. 
Although the consolidation and destruction of the pulmonary tis- 
sue in consumption is mainly a result of inflammation, yet the frequent 
coexistence in phthisical lungs of the products of chronic pneumonia 
and tubercle renders it improbable that the presence of the latter 
should be purely accidental, and suggests a causative connection be- 
tween tubercle and the inflammatory lesions. According to the com- 
mon opinion, this connection is, that tuberculosis is the primary affec- 
tion, to which the pneumonic process is secondary and dependent. It 
cannot be denied that this view is right in certain cases; in a great 
majority of instances, however, the converse is true; the tuberculosis 208 
DISEASES OF TIIE PARENCHYMA OF TIIE LUNG. 
supervening as a secondary process upon a preexisting pneumonia. It 
is, indeed, rare for tubercles to form in a lung which does not contain 
products of chronic inflammation. 
As the formation of tubercle never takes place unless preceded by 
a pneumonia terminating in caseous infiltration of the pulmonary tis- 
sue, and, as it occurs with equal frequence, whether the infiltration be 
a sequel to croupous, catarrhal, or to chronic inflammation, we may as- 
sume that there is no direct and immediate relationship, or community 
of origin, between tuberculosis and the inflammatory disorders •which 
generally precede it, but that their connection is indirect, arising from 
the caseous metamorphosis of the pneumonic product. The truth of 
this supposition is materially supported by the fact that, in the rare 
instances in which tubercles have developed in lungs which were in 
other respects healthy, caseous deposits have almost always been 
found in other organs, and no less so by the observation that, in exten- 
sive tuberculosis, the oldest and most numerous tubercles are always 
found in the immediate vicinity of masses of cheesy degeneration. The 
peculiarly frequent occurrence of tubercle in the lungs is manifestly 
because there is no other organ in which diseases arise which so often 
terminate in caseous metamorphosis. 
Having thus distinctly stated my belief in a causative relationship 
between caseous infiltration of the lung and pulmonary tuberculosis, 
and having called attention to their frequent coexistence, in our next 
chapter, we may, without impropriety, discuss the subjects of chronic 
pneumonia with caseous infiltration, and of chronic pulmonary tubercu- 
losis, under a common heading, as the two diseases which play the 
principal part in pulmonary consumption. In Chapter XIV. we shall 
speak of acute miliary tuberculosis, which is not accompanied by 
chronic pneumonia, and which never gives rise to destruction or con- 
sumption of the lungs. 
CHAPTER XIII. 
CASEOUS INFILTRATION" AND CHRONIC TUBERCULOSIS OF TIIE LUNGS— 
PULMONARY CONSUMPTION. 
Etiology.—When pneumonia terminates in resolution, the inflam- 
matory product undergoes fatty metamorphosis; then liquifies, and is 
absorbed. When the disease is followed by caseous infiltration, the 
fatty metamorphosis is incomplete. The infiltration dries up; the 
cells are atrophied; they lose their rounded form, and shrink, through 
loss of their water, into irregularly-shaped clots ( Virchow). 
It is a fact that in the lungs the product of simple inflammation 
often undergoes caseous degeneration, whereas in the compact organs DISEASES OF THE PARENCHYMA OF THE LUNG. 
209 
this result is rare, and only occurs when a pathological cavity has 
formed, enclosing the inflammatory products. The explanation is, that, 
in the lungs, natural cavities already exist, and it is in these that in- 
flammatory products are usually deposited. 
We must emphatically express our dissent from the theory that 
caseous infiltration of the lung, with its concomitant formation of 
vomicae, has its source in a form of primary inflammation of peculiar 
nature, which is distinguishable from other varieties of pneumonia. 
The hypothesis of a “tuberculous or caseous inflammation of the 
lung ” is entirely untenable, and only tends to cause fresh confusion. 
On the contrary, it may be said, with perfect truth, that all forms of 
pneumonia may end in caseous infiltration under certain conditions, 
and that there is no form of pneumonia of which caseous infiltration 
is a sole and constant termination. It is true that the difference is 
very great in the frequence with which the inflammatory products of 
the various forms of pneumonia undergo cheesy transformation instead 
of liquefaction and absorption. In croupous pneumonia such a result 
is rare; in acute catarrhal pneumonia it is somewhat more frequent, 
while in the chronic catarrhal form it is almost the rule. 
I regard the name chronic catarrhal pneumonia as the only title 
appropriate to the form of disease usually called infiltrated tubercu- 
losis, and gelatinous or tuberculous infiltration, and which latterly and 
with equal impropriety has sometimes received the name of tubercu- 
lous or of cheesy pneumonia. This lobular infiltration, or (when the 
disease is extensive, as it often is) this lobar infiltration of the lungs, 
with its homogeneous section and its color and glitter of frog-spawn, is 
not dependent simply upon a filling of the air-vesicles with young 
spherical cells of indeterminate nature, that is to say, with the ana- 
tomical products of catarrhal pneumonia, but arises, with rare excep- 
tions, through extension of a chronic catarrh, with a copious secretion 
of young cells, into the finer terminal bronchioles, and thence into the 
pulmonary vesicles. I certainly should attach little weight to the 
application of the name chronic catarrhal pneumonia to the so-called 
gelatinous pneumonia, did I not believe that, by calling the disease by 
its proper name, not only is our comprehension of the etiology and 
pathology of the malady facilitated, but its prophylaxis and thera- 
peusis are promoted. It is not difficult to understand why chronic 
catarrhal pneumonia should generally give rise to caseous infiltration, 
far more frequently, indeed, than the acute form of the disease, or than 
croupous pneumonia. Owing to the slowness and tedious nature of its 
progress, the tendency of which is to a perpetual accumulation of 
young cells in the air-vesicles, perhaps also by an inhalation of cells 
from the smaller bronchi, thus adding still more to those already 210 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
generated in the vesicles, the cells are more and more crowded to- 
gether, thus becoming mutually injurious, and undergoing degen- 
eration. 
The knowledge that the majority of cases of consumption are not 
the result of neoplasm but of inflammation, and that, when tubercles 
exist in phthisical lungs, the tuberculosis is almost always preceded by 
a pneumonic process, which, by caseous degeneration of its products, 
has prepared the soil for the growth of tubercle, has been of material 
assistance in explaining the etiology of consumption. Numerous 
well-established facts, which had hitherto defied all interpretation (as 
long as consumption was always ascribed to neoplasm), are now fully 
reconcilable to the generally acknowledged laws of pathology. 
Predisposition to pulmonary consumption or, to speak more pre- 
cisely, the predisposition toward pneumonia terminating in cheesy in- 
filtration, is strongest in persons of feeble and delicate constitution. 
It is by no means meant by this that vigorous persons, possessing 
normal resisting power against noxious influences, enjoy an immunity 
from this disease. Indeed, although it is somewhat rare, even croup- 
ous pneumonia sometimes terminates in caseous infiltration, with sub- 
sequent disintegration of the lung, in individuals who, prior to the 
attack, were in perfect health, and gave no signs whatever of weakness 
or delicacy of constitution. In similar manner the most vigorous and 
blooming children may be attacked by acute catarrhal pneumonia, 
during the measles or whooping-cough, and may soon perish through 
caseous metamorphosis of the pneumonic product. The origin of the 
many deaths which have been observed to take jllace after an epi- 
demic of measles or of whooping-cough, and which, until recently, has 
been chiefly ascribed to tuberculosis, is, in most cases, really traceable 
to the effect of a catarrhal pneumonia contracted during the course of 
the above-named disorders. 
But even a simple, genuine catarrh may extend into the air-vesicles 
in a person of apparently perfect health and vigor. Healthy men 
should never feel sure that they will not die of an acute or chronic 
catarrhal pneumonia, proceeding from a cold, and resulting* in caseous 
infiltration and destruction of the pulmonary substance. 
That feeble and ill-nourished persons should be in far greater dan- 
ger of becoming consumptive than vigorous, well-nourished ones, will 
not appear extraordinary from this point of view. 
Daily experience teaches us that a bad state of nutrition is usually 
accompanied by a feeble power of endurance of noxious influences. 
Even without especial knowledge of the fact, it is usually assumed, 
a priori, that feeble, badly-fed persons are “ sickly ”—that they are 
especially prone to disease, and that they do not recover as rapidly CONSUMPTION OF THE LUNGS. 
211 
from its attacks. The frequence with which the various organs of the 
body are affected by disease differs according to the age of the indi- 
vidual. Persons who, during childhood, have often suffered from croup, 
pseudo-croup, cerebral irritation, and moist eruptions, are liable during 
and after the period of puberty to bronchial haemorrhage and to in- 
flammatory disorders of the lungs. 
But delicacy and a liability to pneumonic and other inflammatory 
disorders are not the only distinctive marks between feeble, ill-nourished 
subjects and those who are well nourished and strong. All the inflam- 
matory derangements of nutrition occurring in the former class give 
rise to a very profuse formation of young, indeterminate and perish- 
able cells. It is said of such persons, that their “ flesh does not heal,” 
that is, that a trifling wound is apt to be followed by severe irritation, 
and copious suppuration of the wounded part. This peculiarity is 
partially attributable to an increased irritability which accompanies 
constitutional weakness, and partially to the fact that badly-nourished 
or ill-developed organs, when inflamed, are more prone to the formation 
of cells of a decrepit and perishable nature, than to the formation of 
such as are capable of development into new tissue. 
The main points of the subject hitherto discussed may, then, be 
summed up as follows: The consolidation and destruction of the 
lungs, which form the anatomical basis for consumption, are 
usually the products of inflammatory action, and the greater the 
quantity of cellular elements collected in the vesicles, and the longer 
the duration of the inflammation, so much the more readily will 
pneumonia lead to consumption, since these are the conditions most 
favorable for the production of caseous infiltration. Secondly: 
pneumonia resulting in caseous infiltration occurs most f requently, 
but not exclusively, in puny, badly-nourished subjects. This is par- 
tially because such persons are especially delicate, and, in part, because 
all inflammatory nutritive disorders by which they may be affected 
show great tendency to copious cell-formation, with subsequent caseous 
degeneration. 
We may now, in few words, define our position with regard to 
that greatly-vexed question, the relations of scrofula and pulmonary 
consumption. 
It very frequently happens, especially during childhood, that the 
lymphatic glands participate in this morbid tenderness, which, as a 
rule, is accompanied by augmentation of irritability and a strong ten- 
dency to profuse cell-production. While, in persons exempt from this 
peculiar tendency, the lymphatic glands neither enlarge, inflame, nor 
suppurate, excepting in case of intense and malignant inflammation of 
the parts from which they derive their lymph, very trifling irritants, 212 
DISEASES OF THE PAREXCHYMA OF THE LUXG. 
and mild and innocent inflammation of the region whence the lym- 
phatic vessels originate, suffice to excite the glands, of individuals who 
are thus affected, into an active production of new cells. Inflamma- 
tion and suppuration of the glands do not take place in all or even 
in the majority of cases, the morbid action usually limiting itself to a 
simple cellular hyperplasia, that is to say, to an enlargement of the 
glands, from multiplication of their normal cellular elements. But, as 
the retrogression of all morbid processes in individuals of this class is 
extremely tedious, the glandular enlargements are exceedingly obsti- 
nate in character, and in many instances (and, the greater the mass of 
cells, so much the more apt is it to happen) a partial or diffuse caseous 
degeneration of the swollen gland is the result. 
Persons whose lymphatic glands participate in the general delicacy 
of the tissues, and in their tendency to this profuse cell-formation un- 
der the stimulus of inflammation, are said to be scrofulous. 
We lay especial stress upon the circumstance that, in scrofulous 
individuals, the tendency to glandular enlargement by cellular hyper- 
plasia is constantly combined with a general tendency to disease, par- 
ticularly to inflammatory disease. This is so very marked as a rule, 
that the exciting causes of “ scrofulous eruptions,” “ scrofulous ophthal- 
mia,” “ scrofulous catarrh,” and other so-called scrofulous disorders, are 
apt to escape observation. It often appears as if such inflammations 
came on spontaneously (“ of themselves,” as the laity say). There is 
no anatomical sign by means of which a “ scrofulous ” ophthalmia or a 
scrofulous eruption can be distinguished from similar non-scrofulous 
disorders, and, with the exception of the implication of the lymphatic 
glands, it is only from the insignificance of the causes from which the 
affections proceed, the frequence of their recurrence, and their obsti- 
nate persistence, that we can infer their scrofulous nature. 
Now, if this feeble power of resisting noxious agents, this suscepti- 
bility of scrofulous individuals, have not subsided at the period when 
the lungs become more especially liable to disease, although the fre- 
quence of the moist eruption, the obstinate affections of the cornea and 
conjunctiva and the like, meantime have diminished, yet pneumonic 
processes are now apt to occur from causes equally trifling with those 
which formerly gave rise to the ophthalmia and the eruptions, etc.; 
and such pneumonic affections evince the same obstinacy which the 
other so-called scrofulous diseases used to show, a circumstance which 
greatly favors their termination in caseous degeneration. 
Upon glancing over the various causes which experience points 
out to us as predisponents toward consumption, it will be strikingly 
apparent that they all agree in one particular, that they all retard 01 
disturb the normal development and conservation of the oryanism. CONSUMPTION OF THE LUNGS. 
213 
The tendency to consumption is, in many cases, congenital. When 
the congenital tendency is due to the fact that the parents were con- 
sumptive at the time of begetting the offspring, it may properly be 
spoken of as inherited. But it is not (as is often asserted) the malady 
which causes the inheritance, but the weakness and vulnerability of 
constitution which had already laid the foundation of the consumption 
in the parents, or which had arisen in them in consequence of that 
disease. The hereditary constitutional feebleness of the offspring may 
proceed from other disease of the parent instead of consumption. 
Parents afflicted by other exhausting maladies, or who are ruined by 
debauchery, or who are far advanced in years, are quite as liable as 
consumptive parents to beget children who come into the world with 
a predisposition to consumption. 
Among the influences by wrhich a liability to consumption is ac- 
quired, or by which a congenital predisposition to it is aggravated, 
that of an insufficient or improper diet stands first. Feeding a suck- 
ling-babe with bread, pap, etc., instead of the mother’s milk, may sow 
the seeds of the malady. An erroneous regimen is often kept up 
throughout the entire period of childhood. The child is ill-fed (“ ver- 
futtert ”) as the laity say, and consequently acquires a feebleness and 
susceptibility to disease identical with a scrofulous predisposition. 
The comparatively greater prevalence of consumption among the poor 
than among the more well-to-do classes is in great measure dependent 
upon the wretched diet of the former, which consists chiefly of vege- 
tables. [Germany.] This also accounts for the increased frequence 
of consumption, according to the size of towns, or, what amounts to 
the same thing, the number of its pauper population. Hunger and 
want, as is wrell known, are less common in the country than in great 
cities. The influence of a wTant of fresh air is quite as baneful as is 
that of an insufficient or improper supply of nourishment. We have 
no satisfactory explanation of the mode in which continuous sedentary 
life, and especially an abode in a close atpiosphere charged with effluvia, 
produces its pernicious effect upon the organism; but the fact has long 
been established that both scrofula and consumption are far more com- 
mon in asylums for foundlings and for orphans, in houses of correction, 
prisons, and among factory operatives who spend the entire day at 
work in a close room, than among persons who take much exercise in 
the open air. The objection, that the prevalence of scrofula and con- 
sumption in such institutions proceeds from other causes than lack of 
fresh air, is untenable. The average diet of the populations of many 
poor villages is much worse, and the number of prejudicial influences 
far greater, than is the case among the occupants of prisons and houses 
of correction, and yet they are not equally subject to these diseases. 214 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
Not unfrequently, persons born with well-nourished, vigorous con- 
stitutions evince a decided tendency to consumption from the effect 
of some other disease, whereby the prehension or assimilation of their 
food is prevented, or which is undermining their health in some other 
way. Many patients with ulcers of the stomach, with strictures of 
the oesophagus, lunatics who persistently refuse their food, finally die 
consumptive. In like manner persons afflicted with diabetes mellitus, 
obstinate chlorosis, or tertiary syphilis, ultimately die of pulmonary 
phthisis. Among acute disorders, typhus is apt, when protracted, to 
leave behind it a predisposition to this disease. 
To these predisposing causes, acquired through other affections, 
may be added those which are provoked by persistent suckling, 
onanism, venereal excess, by depressing or exciting mental influences, 
immoderate study, and inconsolable grief. 
I regard the wide-spread doctrine that consumption is solely 
dependent upon a diathesis, from which it proceeds independently of 
all so-called “exciting causes,” as equally gratuitous and dangerous. 
The circumstance that the admission of the origin of this disease 
from external irritation stood in direct conflict with a theory which 
no one dared to gainsay, has manifestly prevented an unbiassed inter- 
pretation of facts. The deliberate assertions of Laennec and his 
pupils, that “ catching cold,” and other irritation, had no influence in 
producing pulmonary consumption, and that it never arose from a 
neglected catarrh, has had the most pernicious effect, both upon 
prophylaxis and treatment of the disease. 
The exciting causes which give rise to consumption, where predis- 
position to it exists, consist, as I believe, in all influences capable 
of producing fluxionary hyperaemia of the lungs and bronchial catarrh. 
I therefore refer to what has l>een stated already as to the etiology 
of the latter. 
The popular idea, that consumption is often the consequence of 
indulging in cold beverages while the body is overheated, I used 
formerly to look upon as a fable, or at least as a badly-interpreted 
fact. But, as I gradually emancipate myself from the teachings of 
Laennec, I dare no longer maintain such absolute views, and am 
forced to admit that a sudden chilling of the stomach is quite as ca- 
pable of inducing catarrhal and pneumonic processes, and hence con- 
sumption, as is a sudden cooling of the skin. The fact that large 
draughts of cold water have been swallowed with impunity by innu- 
merable persons in an overheated condition, by no means contradicts 
the suppostion that such a cause may now and then be followed by 
serious results. So, too, sudden chilling of the skin is not followed 
by sickness in all cases, but only occasionally; and since it is not 
understood how this result occasions derangement in remote organs, CONSUMPTION OF THE LUNGS. 
215 
we are not warranted in denying the possibility of a chilling of the 
stomach having the same effect. 
Numerous examples exist in the practice of every experienced 
physician, in which the cough has commenced on some particular day 
following a severe cold, soon after which the other symptoms of con- 
sumption have made their appearance. 
A proof of the extremely important role played by the presence 
of foreign substances in the air-passages, as an exciting cause of con- 
sumption, is found in the great prevalence of the malady among opera- 
tives and other persons who constantly live in a dusty atmosphere, 
such as stone-cutters, file-grinders, hatters, wool-carders, cigar-makers, 
etc. Of all foreign bodies which, by irritation of the bronchial walls, 
and of the pulmonary substance itself, give rise to consumption, the 
blood which is retained in the air-vesicles and bronchi after a hemop- 
tysis or pneumorrhagia most frequently has that effect, as we have 
already explained while treating of bleeding from the bronchi and lungs. 
Having discussed the etiology of the pneumonic process which 
plays the most important role in the production of pulmonary phthisis, 
we must now add a few words regarding the etiology of pulmonary 
tuberculosis. 
The development of tubercles in the lung, without the preexistence 
of caseous degeneration of the inflammatory products, is less common 
in chronic pulmonary tuberculosis, which is complicated with chronic 
pneumonia, and terminates in consumption, than in acute miliary tuber- 
culosis (see Chapter XIV.). The etiology of these exceptional cases 
is utterly obscure, although it would seem that persons predisposed to 
inflammation, ending in caseous degeneration, suffer from primary 
tuberculosis of the lung, in the stricter sense of the word, with greater 
relative frequence. 
The caseous masses, upon which the consecutive (secondary) devel- 
opment of tubercles in the lungs depends, are situated, in the great ma- 
jority of cases, in the lungs themselves, and consist of the products of 
chronic pneumonia, in a state of caseous degeneration. We have no 
hesitation in staling that the greatest danger, for the majority of con- 
sumptives, is, that they are apt to become tuberculous. The conditions 
which cause tuberculosis to accompany many cases of caseous infiltration 
with formation of cavities, but not all such cases, and the reason why 
the complication is sometimes early and sometimes late in its appear- 
ance, are at present unknown to us, but it seems that incapsulation of the 
caseous mass affords a certain degree of protection against tuberculosis. 
Next to the caseous products of pneumonia, the exudation of pleu- 
risy and pericarditis in a state of caseous degeneration, and bronchial 
glands in similar condition, most frequently give rise to tuberculosis. 216 
DISEASES OF TIIE PARENCHYMA OF THE LUNG. 
Under this category those cases may also be included in which the 
cheesy inflammatory products of the results of tuberculosis of the 
genito-urinary apparatus, the intestines, mesenteric glands, joints, 
bones, or superficial lymphatics, are followed by tubercular disease. 
In cases of doubt, the discovery of cheesy residua in these organs 
may decide the question in favor of tuberculosis. It is quite possible 
that in the future, the danger of pulmonary tubercle, which the pres- 
ence of the cheesy residua of enlarged lymphatic glands produces, will 
rank among the indications for the extirpation of peripheral lymphatic 
tumors, and even for the performance of resections and of amputations. 
With regard to the frequency of consumption, it is supposed that 
from a seventh to a fifth of all deaths are the result of this disease, 
.and that in nearly the half of all cadavers we find traces of the nutri- 
tive disorders from which pulmonary consumption proceeds. 
During foetal life and early childhood, consumption is rare. Even 
in later childhood, bronchial catarrh, with swelling and cheesy meta- 
morphosis of the glands, or “ consumption of the bowels,” is far more 
common than pulmonary phthisis. 
Toward the period of puberty, and still more so between the twen- 
tieth and thirtieth years, the malady attains its greatest frequence, be- 
coming rarer as life advances, without becoming quite unknown even 
in extreme old age. Males and females seem to be equally liable. 
The former belief in the prevalence of the disease in cold climates, 
and its comparative rarity in warm ones, is not borne out; regions 
situated far to the north being wellnigh free from it. Ilirsch declares 
that the mean temperature due to the geographical and territorial 
situation of a place has absolutely no influence upon the production or 
frequence of consumption; that great alternations of temperature and 
a high degree of moisture favor its development, while in elevated re- 
gions its appearance is rare. The rarity of consumption in malarious 
regions is not constant, and is scarcely due to the influence of the ma- 
laria, but it depends rather upon other causes, such as the paucity of 
the population and lack of culture in many regions afflicted by malaria. 
Persons with heart-disease enjoy a certain immunity from consump- 
tion. Probably this does not depend upon the more venous quality 
of their blood, but is rather because the products of the pneumonias, 
from which they suffer with comparative frequence, have but little 
tendency to cheesy degeneration, owing to the moist and engorged 
state of their lungs. Emphysematous persons are seldom consump- 
tive, but for a different reason: their dry, bloodless lungs rarely in- 
flame ; but, once attacked, the danger of degeneration is great. 
Anatomical Appearances.—A great variety of lesions are found 
in the lungs, especially pathological cavities, extensive infiltration and CONSUMPTION OF T1IE LUNGS. 
217 
other forms of solidification of the parenchyma, which, when cut into, 
nearly always exhibit small points which suggest the idea of miliary 
tubercles. 
It is only in rare cases that the diffuse consolidation of the lung- 
substance presents the granular aspect and other characteristics of a 
lung hepatized by croupous pneumonia. Far more commonly, there is 
that homogeneous, dull-looking infiltration with smooth section, which 
we have described as the product of acute and especially of chronic 
catarrhal pneumonia. As a rule, the gelatinous infiltration has already 
undergone the transformation peculiar to cheesy degeneration of 
inflammatory products. If the latter have but recently commenced, 
we see, upon the gray or grayish-red dead lustre of the cut surface, a 
few yellow, lustreless marblings. If the caseous metamorphosis be 
further advanced, the yellow places are larger, until at last the entire 
solidified portion of the lung is converted into a yellow, cheesy mass. 
After the infiltration has become caseous, it may undergo immediate 
liquefaction, and, together with the tissues, break down into a creamy 
puruloid matter. Thus cavities filled with the so-called tubercular pus 
are formed. At last a communication is set up with a neighboring 
bronchus, through which its contents are discharged by coughing. 
The walls of these cavities are irregular and interrupted; the pul- 
monary parenchyma about them is infiltrated with caseous matter, and 
is in a more or less advanced state of disintegration. 
The gelatinous or catarrhal infiltration, which, when attacked by 
cheesy metamorphosis, and softening of the infiltrated lung-substance, 
leads to the formation of these cavities, is at first generally confined to 
single lobules. If the diseased lobule be situated near the surface, 
the solidified spots bear the peculiar wedge-shape of the peripheral 
lobules. When seated more deeply within the lung, they form rounded 
indurations, or, where the process is restricted to the immediate vicin- 
ity of separate bronchi, the consolidation runs along the course of the 
tube. By repetition of the process, and by confluence of many of the 
lobular centres, a whole lobe or even an entire lung may be solidified 
and become the seat of vast destruction. 
But caseous infiltration of the pulmonary tissues, from whatever 
form of pneumonia it may proceed, does not in all, nor even in the 
majority of cases, result in immediate disintegration of the seat of the 
cheesy infiltration, and in formation of a cavity. Such an event only 
takes place under peculiar circumstances, and perhaps when the dis- 
order is of extreme severity. It is probably brought about through 
the crowding together of the accumulated cells in the air-vesicles, 
whereby they not only encroach one upon another, but exert a pres- 
sure upon the surrounding tissues and their vessels, thus depriving the 218 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
alveolar walls of their nutritive fluid, and causing them to perish and 
break down. Perhaps the anaemia and necrosis of the pulmonary tissue 
are favored in severe cases by an extension of the process of prolifera- 
tion of cells from the surface into the tissues themselves. 
If the cell-growth be not of sufficient volume seriously to compress 
the vesicular walls and their vessels, the caseous masses gradually 
become still more inspissated, and the shrunken atrophied cells 
break down into a detritus. Little by little their organic matter dis- 
appears, while calcareous salts are deposited until there finally is left 
a chalky or mortar-like concretion. In other cases, again, the arrested 
fatty metamorphosis of the cells is reestablished: they become lique- 
fied, and capable of reabsorption. 
While one or other of these processes is progressing in the cellular 
elements involved in the caseous degeneration, an extensive prolifera- 
tion of the connective tissue is going on in the lung. The calcified 
deposits are incapsulated, and the space rendered vacant by the cells, 
which have suffered fatty degeneration and liquefaction, is filled up by 
connective tissue. In such cases, the lung-substance does not again 
become penetrable by the air, but is converted into a dense callous 
mass; and as the connective tissue, which continues to shrink more 
and more, occupies less room than the healthy parenchyma which it 
replaces, the lung becomes reduced in size and the thorax sinks in. 
But, as depression of the thorax can only take place to a limited extent, 
the bronchi become dilated into rounded and elongated cavities. This 
is the most common form of cavity in phthisis where it runs a chronic 
course. The absorption of the caseous masses, through supplementary 
fatty degeneration and liquefaction, may be so complete that, upon dis- 
section, we may find nothing except pulmonary tissue in a state of 
induration from interstitial pneumonia, perfectly void of air, traversed 
by (broncliiectatic) cavities, and without a trace of caseous deposit. 
While the apex of the lung usually contains cavities of greater or 
less capacity, and while a large portion of its upper lobes is solidified 
—partly by gelatinous or caseous infiltration, and in part through indu- 
ration and consolidation—upon section of the remainder of the lung 
which still remains permeable to the air, the small points of induration 
before alluded to are almost always found projecting above the sur- 
face of the cut in the shape of yellow nodules. We must beware of 
immediately assuming such minute solid spots to be tubercles. Ex- 
perience teaches that many objects which at the first glance seem to 
be miliary tubercles, and which were formerly regarded as such, prove, 
upon closer examination, to be transversely-divided bronchi with case- 
ous contents, or bronchi surrounded by alveoli, with thickened walls and 
infiltrated with caseous matter. By avoiding such errors in £>ost-mor CONSUMPTION OP THE LUNGS. 
219 
tem examination, we shall arrive at the conclusion that not a single 
tubercle exists in very many phthisical lungs, and that consolidation 
and destruction are solely due to a disorganizing pneumonia. 
We believe, however, that Virchow goes too far in asserting that 
the doctrine of miliary tuberculosis of the lung is also almost entirely 
erroneous, and that nearly all so-called miliary tubercles of the lung 
are foci of bronchitic, peribroncliitic, or pneumonic inflammation. It 
not unfrequently happens that these translucent grayish nodules which 
are scattered through the lungs, as well as in most other organs in 
acute miliary tuberculosis, and of whose tuberculous nature there can- 
not well be any doubt, are also met with in phthisical lungs. Hence, 
we must also acknowledge the yellow caseous deposits found in the 
lungs (notoriously regarded as miliary nodules) to be of tubercular na- 
ture, when they coexist with the gray miliary tubercles, and when the 
latter, together with caseous tubercles, are found in other organs at 
the same time. There are no means of proving that the caseous 
nodules are the product of vesicular pneumonia, and not tubercle, as 
we have no criterion for the distinction between caseous tubercles and 
caseous miliary nodules of inflammatory origin. I again express my 
opinion that, exclusive of tuberculosis of the bronchial mucous mem- 
brane, the development of secondary tuberculosis in phthisical lungs is 
of very frequent occurrence. 
Hitherto we have been describing the anatomical lesions found in 
pulmonary consumption, as it occurs in the vast majority of cases, 
wherein the malady, throughout its whole course, is solely dependent 
upon chronic pneumonia, or in which tuberculosis does not appear until 
at an advanced stage of the phthisis, when, although it must be re- 
garded as a most serious complication, it takes but little part in the 
disorganization of the lungs. 
In tubercular consumption, in our acceptation of the term— 
that is, in the form of phthisis in which destruction of the lung is 
caused by the breaking down of tubercles, and by secondary pneu- 
monia dependent upon the tuberculosis—the tubercle generally first 
develops in the mucous membrane of the bronchi, as was first shown 
by Virchow. Even in the trachea and larger bronchial tubes we 
often find extensive granular patches, consisting of innumerable miliary 
tubercles, or ulcers with the characteristic marks, according to Roki- 
tansky, of primary or secondary tuberculous ulceration. In addition 
to this, however, in the finer bronchi, besides the evidences of purulent 
catarrh, we find small whitish or yellow nodules, and, upon examina- 
tion of a successfully-prepared fine section, we may satisfy ourselves 
that the development of the tubercle has spread from the bronchus to 
its lateral and terminal alveoli. According to the line of the section, 220 
DISEASES OF THE PAKEXCIIYJIA OF THE LUXO. 
tubercular groups formed in this manner present the appearance of 
rounded or wedge-shaped conglomerations of miliary nodules, an ap- 
pearance rarely or never found in acute miliary tuberculosis where the 
development of tubercle does not begin in the bronchial mucous mem- 
brane. The pneumonic process by which the tuberculosis is attended 
in tuberculous consumption is much less extensive, as a rule, than that 
which accompanies the consumption which is solely due to chronic 
pneumonia, or than the form in which secondary tuberculosis super- 
venes, at a late period, upon the process of induration and destruction, 
a circumstance of some importance in the diagnosis of tuberculous con- 
sumption. It is also quite an exceptional occurrence for a large part, 
or, perhaps, an entire lobe of a lung, to become solidified by pneumonic 
infiltration, nor does caseous infiltration often advance to the stage of 
induration and contraction. The cheesy infiltration almost always 
breaks down at an early period, so as to allow cavities to form. It is 
true that we now and then find the apex of the lung to be the seat of 
callous induration, or of a deposit of thickened caseous matter, or a 
bronchiectasis, but it is easy to satisfy one’s self that these lesions 
have no connection with the final disease, and that they are the results 
of some morbid process of prior date. 
As it appears from what has been stated above, the bronchi of 
phthisical lungs exhibit a great variety of conditions. Gelatinous and 
caseous infiltration is preceded and accompanied by purulent catarrh 
of the finer bronchi, with dilatation of their cavity. Disintegration of 
a deposit of caseous infiltration is ushered in by ulceration of the bron- 
chial wall, and the liquefaction almost always begins in the immediate 
vicinity of the bronchus. In tubercular consumption, the eruption of 
miliary nodules appears upon the mucous membrane of the bronchi. 
The majority of the cavities found in chronic consumption are of bron- 
chiectatic origin, while, on the other side, many of the minuter tubes 
which traverse the infiltrated and indurated lung-tissue become oblit- 
erated. The purulent contents of a closed cavity, resulting from the 
breaking down of caseous infiltration, are discharged by perforation 
into a large open bronchus. We not unfrequently see several bronchi, 
with round or oval mouths, running either squarely or obliquely into 
such a cavity, but their entrance is always abrupt, and never gradual 
or imperceptible. Finally, where the bronchial surface has suffered no 
profound or structural change, it is the seat of a catarrh whose profuse 
secretion is full of young cells. This bronchial catarrh is the main 
source of the expectoration of phthisical persons. 
Many of the blood-vessels, especially many branches of the pulmo- 
nary artery of the infiltrated and hardened tissue, are obliterated. In 
the walls of cavities the obliterated vessels often form prominent CONSUMPTION OF TILE LUNGS. 
221 
ridges, and sometimes stretch from one wall to the other in the form 
of ligamentous bridges. It is very seldom that, prior to obliteration 
of the walls of a vessel, they become so eroded as to cause dangerous 
haemorrhage. We shall take this opportunity to call attention to a 
peculiarity in the circulation of the lungs which frequently arises in 
phthisis. Many branches of the pulmonary artery becoming destroyed, 
those of the bronchial dilate, and conduct arterial blood to the lungs. 
Many newly-formed vessels, springing from the intercostal arteries, 
also advance through pleuritic exudations into the lung. Thus the 
phthisical lung receives more arterial blood than the sound lung. Part 
of it passes into the pulmonary veins, a part into the bronchial veins, 
and a third portion passes through the pleuritic adhesions into the in- 
tercostal veins. As the discharge of blood from the cutaneous veins 
into the overloaded intercostal veins is thereby impeded, they, too, are 
apt to become overfilled and distended, and a blue net-work of veins 
appears upon the skin of the thorax. A chronic form of inflammation 
of the pleura almost always occurs as soon as the affection of the pul- 
monary substance commences to approach the periphery of the lung. 
The pleural surfaces become thickened and adherent. The thickening 
may be so great, especially at the apex of the lung, that it may be 
covered, as by a cap, with a thick, compact fibrous rind, and at such 
places it is generally impossible to separate the two pleural surfaces 
without tearing the lung. In many cases the two pleural surfaces 
grow together throughout the entire extent of the lung, so that a 
pleural cavity no longer exists, and so that pneumothorax cannot occur, 
though the process of destruction advance to the pleura itself. It is 
only through the rapid disorganization of superficially-seated caseous 
deposits that perforation sometimes occurs before adhesion is estab- 
lished, or before the adhesions have grown strong enough to prevent 
air and debris of tissue from entering the pleural cavity. In tubercu- 
lous consumption, and in secondary tuberculosis, miliary tubercles are 
often found, both in the pleura itself and in the pseudo-membrane, re- 
sulting from the chronic pleuritis. The cavities rarely enlarge in what 
was formerly supposed to be their most frequent mode of enlargement, 
that is to say, by caseous disorganization of secondary tubercular de- 
posit in their walls. Generally speaking, no matter in what manner 
the cavities have formed, their increase in size is the result of a 
diphtheritic process, an infiltration of their walls, with subsequent 
decay. 
The frequent coexistence of laryngeal disease with pulmonary con- 
sumption has been already spoken of in detail. The equally common 
complication of pulmonary phthisis with ulcer of the bowels, intestinal 
tubercle, with fatty liver, with amyloid liver, with parenchymatous in- 222 
DISEASES OF TI1E PARENCHYMA OF THE LUNG. 
flammation, and amyloid degeneration of the kidney, will be again 
referred to under their appropriate headings. 
In recent cases, the right heart, whose outflow is always impeded, is 
found to be hypertrophied and dilated. In protracted cases, in which 
the volume of the blood is much reduced, the heart is generally flabby, 
small, and atrophied. A white coating, like curdled milk, is often 
found upon the tongue and palate, which microscopically consists of 
vegetable spores and filaments. The cadaver is usually in a state of 
extreme emaciation; the skin is thin, remarkably white, and not unfre- 
quently covered with scales of epidermis (pityriasis tabescentium). 
The feet are often oedematous, and one or other crural vein is fre- 
quently stopped up by a thrombus, the corresponding leg being tume- 
fied and dropsical. The entire body is bloodless, excepting the right 
heart, which, when dissolution takes place gradually, contains tolerably 
large and soft coagula. 
Symptoms and Course.—The course of pulmonary consumption 
varies in type according as its symptoms are dependent upon pneu- 
monia alone from beginning to end of the disease, or as they become 
complicated with tuberculosis at a later stage, or are tuberculous from 
the outset. In most instances these three forms may be distinguished 
from one another with tolerable precision. 
We shall first make a brief analysis of the various symptoms ob- 
served in the generality of cases of consumption, with especial refer- 
ence to the particular morbid process to which each symptom belongs, 
and shall then endeavor to draw a comprehensive picture of the prog- 
ress, of each of the three main forms of the disease. 
Increased frequence of respiration, in greater or less degree, occurs 
in all forms of consumption, and proceeds from a variety of causes. 
Moderate acceleration of the rate of breathing is not always accom- 
panied by that distressing sense of shortness of breath requiring con- 
tinual forced inspiration for its relief, known as dyspnoea. Even pa- 
tients far gone in the disease often have no dyspnoea at all, excepting 
when some transient increase of the destructive assimilation going on 
in the system demands an additional supply of air. While at rest 
they are fully capable of supplying their blood with oxygen, and of 
eliminating the carbonic acid formed in the system, without any 
fatiguing exertion. On the other hand, the increased respiratory fre- 
quence may be combined with a severe and persistent dyspnoea, which 
of course is liable occasionally to still further aggravation, and is one 
of the most burdensome symptoms of the malady. 
The augmented frequence of the respiration and dyspnoea of phthis- 
ical patients is due, in part, to a diminution of the breathing surface of 
the lung, in part to obstruction of the bronchi by the attendant catarrh; CONSUMPTION OF THE LUNGS. 
223 
partly, although rarely, to pain during respiration; and partly, and in- 
deed chiefly, to fever. As a rule, dyspnoea is only caused by the joint 
action of several of these factors. Thus the breathing surface may be 
excessively reduced in area without the patient’s feeling any dyspnoea, 
and without any acceleration of the breathing while the patient is at 
rest, provided only that neither severe catarrh, pain, nor fever be pres- 
ent at the same time. Many patients, whose lungs are so much con- 
solidated and disorganized that scarcely half of their capillaries remain 
to carry on the process of oxygenation, still breathe at the normal rate 
as long as they sit still or are lying in bed. This is simply because a 
healthy person, under ordinary circumstances, needs to employ but a 
very small portion of his respiratory apparatus, in order to obtain his 
proper supply of air. Nor ought w'e to overlook the fact that, where 
the lung is indurated and disorganized, the surviving vesicles are more 
strongly distended by an inspiration of ordinary depth, and allow more 
air to escape upon expiration than do the air-cells of a healthy lung. 
The increased activity of oxygenation which thus goes on in the re- 
maining air-cells manifestly compensates, in a great measure, for the 
deficiency of those which have perished. 
The breathing-surface may be seriously diminished by the presence 
of miliary tubercles, which, though they may elude physical demonstra- 
tion, fill up a large number of the disorganized alveoli, and close many 
of the smaller bronchi. Hence, great rapidity of breathing without 
dulness on percussion, or bronchial respiration, is one of the most im- 
portant signs of tuberculous consumption, in the narrower sense of the 
word. If we find that a patient, whose lungs are more or less solidi- 
fied and destroyed, but who hitherto has suffered but little, if at all, 
from shortness of breath, begins to exhibit an increase in frequence of 
respiration and a distressing dyspnoea, there being no increase in the 
solidification or destruction of the lung or aggravation of the fever to 
account for it, there is strong reason to fear the addition of a tubercu- 
losis to the phthisis which already exists. Cases arise in which we 
can infer the existence of such a complication, solely from the dispro- 
portion between the small degree of dulness upon percussion and the 
extreme frequence of the respiration. 
It would be superfluous to explain in detail why the respiratory 
frequence of a phthisical subject is aggravated by pleuritic pain and 
by exacerbation or extension of the bronchial catarrh, which accom- 
panies the malady, or by its complication with the pleuritic effusion, 
hydrothorax, pneumothorax, etc. That respiration is accelerated by 
fever is evident. Fever consists of a morbid increase of calorification 
whereby the body becomes overheated. The necessity for air is aug- 
mented in fever just as it is augmented by every bodily exertion; since 224 
DISEASES OF THE PARENCHYMA OF TnE LUNG. 
in either process, an extra amount of carbonic acid is formed, and an 
extra quantity of oxygen is consumed in the system. If we compare 
the rate of breathing with the elevation of temperature and the fre- 
quence of the pulse in phthisis, it will be seen that the want of air is 
partially relieved by the greater depth of the breaths drawn; for the 
steep curves which generally are used to mark the character of the very 
considerable fluctuations of the morning and evening temperature 
hardly ever correspond to similar abrupt curves representing the rate of 
respiration. The evening acceleration of the latter seldom exceeds 
above six or eight breaths a minute, and in many cases is not more 
than three or four breaths. In some cases no acceleration at all can 
be detected. 
Pain in the chest and shoulders is a symptom which is often absent 
throughout the entire course of the disease. It more commonly accom- 
panies the pneumonic form than the tuberculous form of the malady. 
In cases where physical examination leaves us in doubt, whether we 
have to do with tubercle or with small scattered pneumonic deposits, 
pleuritic pains may be of service both in the diagnosis and prognosis, 
especially when accompanied by sputa tinged with blood. 
Consumption is preceded, in a large number of cases, by a more or 
less protracted period of cough and expectoration, depending upon the 
precursory catarrh, which afterward leads to catarrhal pneumonia by 
extension into the air-vesicles; and, subsequently, to consumption of the 
lungs by caseous degeneration and disintegration of the inflammatory 
products. It is highly important to endeavor to ascertain of every 
patient whether his pallor, fever, and emaciation, have been preceded 
for some time by cough and profuse expectoration, or whether these 
symptoms have all appeared simultaneously and before the expecto- 
ration became copious. In the first case, formerly ascribed to a post- 
ponement of the fever and emaciation until an advanced stage of the 
tuberculosis (according to Louis, this is the case in four-fifths of all 
cases, while in one-fifth only do the cough and fever begin together), 
it is more probable, ceteris paribus, that the disease is of pneumonic 
nature, while the latter class of cases are probably of tuberculous 
origin. 
The duration of the precursory catarrh varies. Distinct evidence 
of propagation of the process into the alveoli and of incipient phthisis 
is sometimes discernible as early as the second or third week. Most 
of the instances in which consumption is an immediate consequence of 
measles and of whooping-cough are of this kind, as well as those in 
which tuberculosis develops under the disguise of a catarrhal fever or 
influenza. Conversely, a catarrh may have existed for months and 
years, growing worse in winter and improving during the summer, and CONSUMPTION OF TEE LUNGS. 
225 
may ultimately attack the air-vesicles. In such cases the physician is 
often entirely at his ease about his patient, as, in spite of the cough 
and expectoration, the latter has no fever, maintains his strength, and 
is in a fair nutritive condition, when the scene suddenly changes and 
the symptoms of consumption appear. 
There is also some variety as to the original seat of this treacherous 
catarrh. Sometimes it is situated in the smaller bronchi from the very 
outset; but it by no means rarely commences in the larynx or trachea, 
whence the process gradually extends into the air-vesicles. The fre- 
quence with which such cases occur is shown in the following descrip- 
tion by Andral-—an unqualified adherent of Laennec’s—from the 
fourth volume of his “ Clinique Medicale: ” “ The phlegmasia of the 
air-passages, the symptoms of which precede those of tubercle, does 
not always commence in the minuter bronchial ramifications, nor even 
in the greater bronchi. So far from it, indeed, that we have more than 
once found its point of departure to be in the upper portion of the air- 
passage, and to consist at first of a simple laryngitis. Persons of this 
class (who are to be distinguished from those in whom laryngitis only 
supervenes at a more advanced period of tubercular consumption) do 
not at this time present any symptoms whatever indicating disease of 
the lungs, until they are attacked by an angina, which at first seems of 
but little gravity. The voice, however, remains hoarse; the larynx is 
the seat of a feeling of uneasiness rather than of pain. Sooner or 
later, the cough returns in more fatiguing paroxysms. The unpleasant 
sensation formerly confined to the larynx, now extends successively to 
the trachea and to the bronchi. Each fit of coughing occasions an un- 
pleasant pricking sensation and a disagreeable feeling of heat, and 
sometimes a genuine pain beneath the sternum. Thus we may, in a 
measure, follow the phlegmasia, step by step, in its progress from the 
organs of deglutition through that of the voice and through the trachea 
to the bronchi and their ramifications. It is only at this period that 
the malady assumes a graver aspect. Circulation becomes disturbed, 
nutrition is impaired, and it becomes evident that tubercles hgve de- 
veloped in the pulmonary parenchyma.” 
In badly-nourished, delicate persons, the extension of the catarrh 
into the air-vesicles and caseous metamorphosis of the infiltration are 
more to be dreaded than they are in well-developed and robust ones. 
Individuals are especially threatened whom we know have often suf- 
fered from a catarrh, and whose previous catarrhs have been of very 
protracted character. 
Finally the sputa expelled duing the precursory catarrh sometimes 
furnish a means of estimating the danger. It is a bad sign if the 
sputa contain sharply-defined, deep-fellow streaks; for it shows that 226 
DISEASES OF TIIE PARENCHYMA OF TnE LUNG. 
the catarrh is seated in the finer bronchi, and that its product is full 
of cells. It is when thus situated and of this character, that its 
implication of the air-vesicles is most to be dreaded. According to 
most clinical teachers and physicians who do not share our views, 
and who ascribe all consumption to tuberculosis, this “ expectoration 
streaked with yellow” {Louis) is of course regarded as a symp- 
tom of an incipient phthisis or tuberculosis, instead of a sign of a mere 
preliminary catarrh. 
Absence of cough and expectoration during the disease itself is 
very rare; yet instances are met with now and then, in which infiltra- 
tion of the lung and caseous degeneration have taken place without 
previous or concomitant disease of the bronchial mucous membrane. 
Such patients, at first, often have neither cough nor expectoration. 
Fever, general malaise, loss of appetite, debility, and emaciation, form 
a group of symptoms which are often difficult to account for, until 
physical examination reveals the actual condition. When the pul- 
monary disease is accompanied by intestinal consumption with violent 
diarrhoea, the cough and expectoration may decrease or cease entirely, 
even in advanced stages of consumption of the lungs. This may in 
some degree be ascribed to the derivative action from the bronchi, 
caused by the intense intestinal irritation. 
A hoarse or inaudible cough is one of the chief signs of tuberculous 
consumption, or of the complication with tuberculosis of a consumption 
originating in destructive inflammation. The exceedingly interesting 
cases in which alteration of the voice or of the tone of the cough of 
phthisical patients results from palsy of the vocal chords, from pres- 
sure upon the recurrent nerve by indurated pleuritic membranes, are 
of extreme rarity, in comparison with the instances in which similar 
symptoms arise from tuberculous ulceration of the mucous membrane. 
The non-occurrence of hoarseness and inaudibleness of the cough, until 
an advanced period of the malady, is indicative of consecutive tuber- 
culosis. On the contrary, if the cough have been hoarse from the 
beginning, especially while the sputa were still viscid and transparent, 
and before physical examination showed any irregularity, the exist- 
ence of primary tuberculosis may be suspected. As we have said 
already, tuberculosis often begins in the trachea or larynx, and only 
extends into the finer bronchi at a later period. 
Although the sputa of consumption are mainly the products of the 
catarrh which complicates the disease, yet they may exhibit certain 
peculiarities which serve materially to help the diagnosis. 
We thoroughly indorse the assertion of Canstatt, that it is a most 
suspicious sign, and one highly calculated to awaken our apprehension 
of tuberculosis, when the sputa of a persistent cough, accompanied by CONSUMPTION' OF THE LUNGS. 
227 
fever, long retain the crude character of the expectoration of acute 
bronchitis. The development of tubercle in the bronchial mucous 
membrane is generally attended by precisely such obstinate and dis- 
tressing cough, and by that scanty sputa which contains few organic 
forms, the “ sputum crudum ” of the ancients, the “ purely mucous 
sputum ” of more modern writers. 
Should microscopic examination reveal that the deep-yellow, sharply- 
defined streaks above referred to contain elastic fibres, recognizable 
through their arrangement and curve as belonging to the air-cells, we 
know that the event has happened which the appearance of such sputa 
would lead us to dread. The profuse formation of cells has extended 
from the surface of the bronchial mucous membrane into its walls, and 
the parts surrounding. The discovery of such elastic fibres is a sure 
sign of phthisis. 
The intimate admixture of blood with the muco-purulent sputa, 
whereby the latter acquire a uniform yellowish-red color, is pathog- 
nomonic of chronic pneumonia, and we have good grounds for inferring, 
from the appearance of such sputa in the course of a chronic catarrh, 
that the air-vesicles have also become involved. 
When cavities have formed in the lungs, a peculiar form of expec- 
toration appears, which is generally described as pathognomonic of con- 
sumption, and is often and erroneously supposed to be characteristic 
of tuberculosis. Rounded, numulated grayish masses are found in the 
spit-cup, separated one from another, by a greater or less quantity of 
clear bronchial mucus. If the sputa have been collected in a some- 
what deep glass, we see irregularly-rounded opaque lumps, having a 
ragged outline, sink slowly to the bottom. These sputa globosa fun- 
dum petentia of the ancients are an almost positive indication that 
cavities exist in the lungs. Under the microscope the lumps are found 
to consist of young granular cells, showing evidence of fatty metamor- 
phosis, together with a very considerable quantity of irregular angular 
bodies, and granular detritus. They also often contain elastic fibres 
from the walls of the air-vesicles. Their opacity and greenish-gray color 
are due to the unusual amount of definitely-formed solid constituents 
which they contain, which has been incorporated with them during their 
long sojourn in the cavity. The rotundity of form is owing to the gen- 
eral tendency of the sputa, after their ejection, to preserve the shape of 
the space in the lung whence they have been expelled. They tend to 
sink to the bottom of the vessel containing the bronchial secretion, 
because but little air becomes mixed with them in the cavity while 
the bronchial secretion, being agitated by the inspiration and expira- 
tion of air, encloses numerous bubbles, and is of lighter weight. The 
small, rounded, ill-smelling fragments of caseous matter sometimes 228 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
found in the expectoration, and which are often thought to be actual 
tubercles by the laity, consist almost always of thickened secretion 
from the tonsils, although now and then they are small diphtheritic 
sloughs from the walls of the cavities. 
Chemical examination furnishes no test for the distinction between 
the sputa of simple bronchial catarrh and that of consumption. 
Fever is one of the most constant symptoms of consumption both 
in the tuberculous form and that which proceeds from chronic pneumo- 
nia. Ziemssen has demonstrated that in children the invasion of the 
air-vesicles by catarrh is always accompanied by considerable elevation 
of temperature and acceleration of pulse. This is equally true of the 
commencement of catarrhal pneumonia in adults. The statement of 
Louis, that, in the majority of cases of tuberculosis (four-fifths), fever 
only arises at a more or less advanced stage of the malady, is based 
upon the observations of that author, taken from Laennec’s point of 
view, according to which the precursory catarrh itself is due to the 
presence of tubercle. We have repeatedly called attention to the 
dangerous consequences of this error, and believe that we may declare 
that, by precise observation of the temperature and the frequence of 
the pulse, and by the most careful treatment of all cases, in which fever 
arises during the course of a protracted catarrh, the development of pul- 
monary consumption may often be averted. 
Not only is the fever an important sign of the extension of the 
catarrh from the bronchi to the air-cells, but its continuance furnishes 
the main evidence that the pneumonic process has not subsided. The 
curves, by means of which we represent upon paper the morning and 
evening fluctuations of temperature, usually show a wonderful degree 
of similarity, and we may infer the existence of a consumption from 
them with the same certainty with which we diagnose abdominal 
typhus or pneumonia. The difference between the morning and even- 
ing temperature is about a degree and a half or two degrees Fahren- 
heit ; very seldom less, and frequently much more. In the morning 
the temperature is often almost normal, while in the afternoon and 
evening it may rise to 102° F., or even higher. Such fluctuations of 
temperature are not peculiar to all kinds of exhausting fever. Upon 
comparison of the thermal curve of a patient with pulmonary consump- 
tion with that of one who is suffering from a tedious peripheral caries, 
a great difference will be observable, particularly in regard to the 
regularity of the morning remission and evening exacerbation. After 
extended study of the hectic fever of phthisis, especially as to the 
cause which interrupts its regular march, we have as yet come tc 
no conclusion upon the subject. We may mention, however, that the 
variations in the morning and evening temperature of a true tubercu- CONSUMPTION OF THE LUNGS. 
229 
losis (in the narrow sense of the word), and of a tuberculosis superven- 
ing upon chronic pneumonia, are generally much less. Hence, if the 
fever be a remitting fever approaching the intermittent type, the prog- 
nosis will be better than if the fever assume a more continued form. 
In the former case we have often succeeded in moderating, or even in 
completely allaying the febrile action, and thereby greatly improving 
the strength and nutritive condition of the patient; but we cannot 
claim any such results where there was no morning remission. When 
the caseous masses become incapsulated, or liquefy, and are absorbed, 
the fever may cease altogether. Patients are often seen who have 
large cavities in the apices of their lungs, but no fever whatever. In 
such cases (the pneumonia having resulted in induration) the physical 
signs presented, and the globular masses of sputa, which the patient 
spits up morning after morning, form a striking contrast with his 
apparent good health, his fresh, vigorous look, his nutritive condition 
and strength. We have already shown that, in spite of their partial 
recovery, such persons are still liable to die of consumption, either 
through recurrence of the pneumonia or through consecutive tubercu- 
losis ; and we would advise that the condition of the patient as to 
weight and temperature be still kept under observation, that we may 
be apprised of it, in case either event occur. We see, then, that, in 
the diagnosis, prognosis, and treatment of consumption, the use of the 
thermometer is as great as, if not greater than, in any other disease. 
The subjects of emaciation and deterioration of the blood, the 
symptoms to which consumption owes its name, properly succeed 
that of fever, since there can be no doubt that it is to fever that they 
are mainly due. A most striking proof of the soundness of the theory, 
that the elevation of temperature in fever is dependent upon an in- 
crease in the calorification, consists in the rapid loss of weight which 
the body sustains even in a fever of short duration. For years, at my 
clinic, the fact has been established, by dint of innumerable measure- 
ments and weighings of consumptive patients, that their loss and gain 
in weight stood in direct proportion to the increase or diminution of 
their fever. There is a very pretty theory, that a continued fever of 
moderate intensity consumes less (especially if the patient keep his 
bed) than a hectic fever like that of phthisis, in which the temperature 
fluctuates daily between a condition almost normal and one of a con- 
siderable degree of intensity. There is no doubt that both calorifica- 
tion and consumption of the constituents of the body go on with great 
rapidity during the rapid rise in the temperature, as has been proved 
by Immermann, but we still hesitate to accept the absolute truth of 
the above hypothesis. Knowledge of the fact, that it is the fever 
which consumes both the strength and substance of phthisical pa- 230 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
tients, is a matter of tlie utmost importance in the treatment of the 
disease. 
Physical Signs.—Inspection of the chest reveals the existence of a 
“ phthisical habit ” in many persons who suffer from phthisis, or who 
are threatened by it. This term is used to signify that peculiar build 
of the body indicative of a want of proper nutrition and development, 
and which is found in persons who have been subjected to debilitating 
influence capable of stunting the healthy growth of the system before 
their bodies have become fully developed. The bones of such persons 
are slender, their skin is thin, their cheeks have a delicate redness, the 
sclerotica is bluish, the subcutaneous connective tissue contains but 
little fat. The muscles are ill-developed; those of the neck allow the 
thorax to sink, causing the neck to seem too long. The intercostal 
muscles permit the ribs to spread widely apart, making the intercostal 
spaces broader; the angle at which the ribs are attached to the ster- 
num is acuter; the entire chest is flatter, narrower, and longer than in 
robust, muscular persons. The shoulders also are apt to sink forward, 
and the inner edges of the scapulas are tipped up like wings. 
The diagnostic and prognostic significance of the phthisical habitus 
has been a good deal underrated of late, and, no doubt, many persons 
possessing such a conformation do live exempt from phthisis and attain 
a good old age. But such a circumstance does not in the least conflict 
with the belief that the phthisical habit is a valuable index of feeble- 
ness and delicacy of constitution, hence of a tendency to consumption. 
There is greater danger that a catarrh at the apex of the lung will in- 
vade the air-vesicles in a patient of this kind, than in a muscular and 
robust man. 
Depression of the supra and infra-clavicular fossos upon one oi 
both sides, which, hitherto, has always played a great role in the 
symptomatology of phthisis, is indicative neither of tuberculosis, noi 
of caseous infiltration, nor of disorganization of the tissues; but is 
always and solely due to decrease in size of the apex of the lung, by 
induration and shrinking. As this is the only process capable of caus- 
ing depression of the thoracic wall, the symptom is rather a favorable 
sign, indicating a comparative cure of the nutritive derangements which 
are the chief causes of consumption. We are not warranted, therefore, 
in forming a diagnosis of consumption, unless signs of an advancing 
destruction of the lung be also present, besides the symptom in 
question. « 
Feebleness of the respiratory movement, when it corresponds to a 
depressed point in the chest, is of similar import. In such a case the 
contracted lung is impermeable to air, and cannot yield to the traction 
of the inspiratory muscles. If the spot, which remains stationary upon CONSUMPTION OF THE LUNGS. 
231 
inspiration, retains its normal convexity, the percussion-sound over it, 
however, being dull and flat, we may infer the existence of an extensive 
solidification of the lung, which is most probably a pneumonic infiltra- 
tion. A feeble respiratory movement at a point where the percussion- 
sound, instead of being dull, is normal, or somewhat hollow and tym- 
panitic, is a suspicious sign of tubercle, but not a conclusive one, as 
small scattered spots of lobular pneumonia may also weaken the move- 
ments of respiration without causing any dulness upon percussion. 
There is often an unusually wide extension of the shock of the car- 
diac impulse, and an outward dislocation of the apex of the heart, when 
the upper lobe of the left lung is indurated and contracted, thus laying 
bare the pericardium and drawing the heart to the left. This symp- 
tom, like depression of the thoracic wall, denotes a partial recovery 
from the pneumonic process, and a patient is not to be pronounced 
consumptive unless it be accompanied by fever, loss of flesh, or other 
sign of inflammatory or tubercular destruction of the lung. 
Palpation, besides being serviceable in estimating the movements 
of respiration, and the degree of dislocation of the apex of the heart, 
often exhibits abnormity of the pectoral fremitus in phthisis. Over 
large cavities, containing air, and communicating with an open bron- 
chus, the fremitus generally is intensified. It is also rendered stronger 
by lobular infiltration and by extensive tuberculosis, which has occa- 
sioned a relaxation of the pulmonary tissue. According to Seitz, how- 
ever, for whose opinion I have great respect, the vocal resonance is of 
little diagnostic value in consumption. 
Percussion furnishes several diagnostic points of the utmost im- 
portance. 
Since Seitz first caused me to observe that it was easy to mark out 
the upper boundary of the lungs, and that this was easier to do in 
front than behind, and when the mouth is open than when shut (since 
the tympanitic sound of the trachea is then more definitely distinguish- 
able from the non-tympanitic sound of the apex), I never neglect this 
mode of examination of patients with chronic pulmonary affections. I 
can assert that the height of the pulmonary apex, which, under normal 
conditions, is equal upon each side, and which extends from three to 
five centimetres beyond the collar bone, is often found to be much 
lower, especially upon one side, when the lungs are in a state of 
chronic disease. A depression of the upper boundary, therefore, like 
the depression of the supra and infra-clavicular regions indicates indu- 
ration and contraction of the apex of the lung. 
A dulness upon percussion, in the supra and infra-clavicular region, 
extending over the clavicle itself, and posteriorly over the supra- 
scapular and supra-spinatus regions, is recognized even by many of 232 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
the laity as pathognomonic of plithisis. Most patients, when they 
consult a new physician, can state precisely what the size and extent of 
the dulness was at the last exploration. Dulness in these regions sig- 
nifies that a large tract of the parenchyma is infiltrated or consolidated 
by growth of connective tissue. Tuberculosis never gives rise to a 
consolidation of sufficient magnitude to render the percussive sound 
dull. Hence, as a general rule, it is a favorable sign when the area 
of dulness accords with the other symptoms, and when it extends its 
limits in proportion as the malady advances. If it be otherwise, there 
is reason to fear the existence of tuberculosis. 
The presence of lobular infiltration and of miliary tubercles, by 
which the lungs’ capacity for air is reduced, may give rise to a percus- 
sion-sound which is not dull, but hollow and tympanitic. Much more 
commonly, however, the percussion is not affected by such a condition 
of the lungs. A distinctly tympanitic sound is most frequently heard 
over a cavity containing air. If the pitch of the ring be altered by 
opening and shutting the mouth, it is a sure sign of a cavity. 
From the metallic, tinkling sound upon percussion, which is of very 
rare occurrence in consumption, it may be inferred that beneath the 
point struck upon there is a large empty cavity, with smooth, regular, 
and baggy walls, but we must first make sure that there is no pneu- 
mothorax. 
The cracked-pot sound is produced upon percussion, over the seat 
of a superficial cavity with thin walls, whereby the air is expelled into 
a neighboring cavity, or into a bronchus with a hiss, which is charac- 
teristic of the “ bruit de pot fele.” 
Auscultation, at the commencement of the disorder, and indeed 
often in its more advanced stages, shows no irregularity beyond the 
signs of a catarrh at the apex of the lung. There is a feebleness of 
respiration, at other times it is extremely harsh, or the breath may be 
drawn in a series of jerks (saccade). But, above all, there is the 
greatest variety of moist rales and peculiar squeaking rhonclii. Some- 
times, after the patient has coughed, the moist rales and the crackling, 
squealing sounds cease. More frequently they are only heard after 
the first breaths which follow a cough (Seitz). It is, therefore, always 
advisable, in ausculting a patient, to make him cough from time to 
time. It is easy to understand why peribronchial and pneumonic 
deposits, which have not caused much solidification, and why tubercles 
and tubercular masses, and cavities enveloped in parenchyma, still per- 
vious to air, do not produce other symptoms than those of catarrh; but 
I must most decidedly express my disapprobation of that prevalent 
belief, according to which the signs of catarrh of the summit of the 
lung are pathognomonic of consumption, as being both false and pre- CONSUMPTION OF THE LUNGS. 
233 
judicial to the patient. I certainly regard catarrh of the apex of the 
lung as a serious symptom, and the longer it lasts, so much the more 
have we to fear that it may lead, or that it has already led, to those 
derangements of nutrition from which consumption so often proceeds; 
but, we are not at liberty to conclude that the catarrh has involved 
the substance of the lungs themselves, until fever, emaciation, pallor 
of the skin, the presence of elastic fibres in the expectoration, and 
other evidences of phthisis arise, besides the catarrhal signs. 
Bronchial respiration, bronchophony, and sonorous rales are heard 
in cases of consumption, when extensive induration enclosing large 
open bronchi, or cavities, has formed near the surface of the lung-. 
Indurations of such magnitude never proceed from tubercle or tubercu- 
lar conglomeration alone. Whether they are the result of infiltration 
or of induration, whether they contain bronchi or cavities with air in 
them, must be determined from the other symptoms. When the cavi- 
ties or bronchi which traverse the solid part of the lung are filled 
with secretion, no respiration is audible. 
Sounds are heard sometimes which place the existence of cavities 
beyond all doubt, and which therefore are called cavernous sounds. 
The cavernous sounds include—1st. Coarse moist rales, audible over 
places where there are no large bronchi, where large bubbles can 
form, as at the apex of the lung. 2d. The sudden transition (called 
metamorphosing by Seitz) from a sharp hissing or sucking sound to 
bronchial respiration, or into indistinct murmurs and sonorous rales. 
This very common and very characteristic sign is probably produced 
by the entrance of air into a cavity through an opening which at the 
commencement of the respiratory act is narrow, but which is enlarged 
as the chest becomes inflated. 3d. Amphoric breathing, the rale with 
metallic resonance, a sound like the bursting of single bubbles with a 
metallic ring, the metallic tinkling. These noises may be produced 
artificially by blowing over the open mouth of a bottle, or by agitating 
a liquid in a bottle held before the ear, or by letting fall a drop into 
the bottle, the ear being placed against it. It is only when there is a 
similar condition of the lung, when it contains a capacious cavity with 
symmetrical concave walls, capable of producing uniform reflection of 
the sound-waves, that amphoric breathing and metallic sounds are 
audible. 
It but rarely happens that diagnostic information of any value in 
consumption is obtained by use of the spirometer, and by measurement 
of the capacity of the lungs, that is, of the volume of air expelled from 
the chest after drawing as deep a breath as possible. There are cases 
of obstinate cough, where percussion and auscultation, giving nega- 
tive results, excite the suspicion of the existence of lobular infiltra* 234 
DISEASES OF TEE PARENCHYMA OF THE LUNG. 
tion, or of tubercle in the lung. In Germany, the vital capacity of 
adult healthy men is about 3,300 cubic centimetres, but it varies 
according to sex, age, weight, and size, so that, when the stature is 
between five and six feet, every additional inch increases the vital 
capacity by about 130 cubic centimetres. But even after making due 
allowance for all these conditions, there still remains considerable 
variation, depending upon whether the patient be skilful and prac* 
tised, or awkward and inexperienced. Hence, although a normal 
or remarkably great capacity of the lungs indicates that they are 
healthy, no conclusions can be drawn from a slight reduction of their 
capacity below the normal standard, and it is only when the decrease 
amounts to several hundred centimetres, and when it cannot be 
ascribed to want of skill, or to lack of power, and after excluding all 
other sources of impediment to respiration, that spirometry can con- 
tribute toward the diagnosis of an incipient phthisis. 
We shall now endeavor to describe the main features which char- 
acterize the separate varieties of pulmonary consumption, beginning 
with that form in which the symptoms and termination are solely due 
to inflammatory action. 
At the outset it not unfrequently assumes the aspect of an acute 
disorder, with symptoms of greater or less violence. This is the case 
when a croupous pneumonia, instead of ending by resolution, passes 
into caseous infiltration, followed by consumption. It also occurs when 
the blood effused into and coagulated within the bronchi and air-cells 
during a hemoptysis causes intense and extensive pneumonia, as well 
as in cases of invasion of the pulmonary vesicles by acute catarrh of 
the bronchi. 
In a croupous pneumonia, when the fever persists beyond the end 
of the first or beginning of the second week of the disease, when it 
becomes considerably aggravated toward evening, and remits toward 
morning, with profuse perspiration; when the dulness in the thorax 
continues, and when moist rales still remain audible over the affected 
region, and when the expectoration is profuse and muco-purulent, it is 
to be feared that the malady has terminated in caseous infiltration and 
consumption, which is a somewhat rare occurrence. The discovery of 
elastic fibres in the sputa, and of cavernous sounds, dispels all doubt 
that the tissues are in a state of cheesy infiltration and decay. The 
majority of patients die in a few weeks, consumed by the intensity of 
the fever. Far more rarely, 4he malady subsides after exciting the 
very worst apprehensions; the sputa become scanty, and the patient 
slowly begins to improve. The dulness, however, remains. The 
thorax sinks in over the affected region, and, after a while, well-marked 
evidence arises of induration and contraction of the diseased portion CONSUMPTION OF THE LUNGS. 
235 
of the lung, as well as of bronchiectatic cavities. The pneumonia 
which follows immediately upon a haemoptysis or a pneumorrhagia, 
and which, in my opinion, is caused by effusion and coagulation of the 
blood within the bronchi and air-vesicles, is of a very similar character. 
The greater the area of dulness which develops after an attack of 
haemoptysis, and the longer it lasts, the more pronounced the pleuritic 
symptoms, the more intense and persistent the fever, so much the more 
reason is there to fear that the retained blood and the inflamed paren- 
chyma have undergone cheesy metamorphosis, involving serious disor- 
ganization of the lung. As we have already explained, however, sub- 
sequent liquefaction and absorption of the caseous mass are still possible, 
as are also its incapsulation and induration of the affected lung through 
profuse proliferation of the connective tissue, followed by contraction. 
The invasion of a considerable number of air-cells by an acute 
catarrh is sometimes attended by such serious symptoms, especially 
violent fever and a rapid decline of the strength and nutritive condi- 
tion, that the diagnosis is sometimes difficult. It is excusable in such 
cases if for a while, and until reliable data can be obtained, the phy- 
sician ascribe the catarrh and intense fever to infection, or to acute 
tuberculosis of the lung. The case soon clears up, however. The 
sputa begin to assume the characteristic admixture of blood peculiar 
to pneumonia, pleuritic pains, of varying severity and extent, are felt, 
the percussion-sound becomes hollow and tympanitic in the upper part 
of the chest, and, if the points of solidification, originally lobular, coa- 
lesce into one voluminous mass, the percussion-sound is dull. At the 
same time the rales, which at first were indefinite, become ringing, 
and the respiratory murmur becomes bronchial. It is possible that an 
acute catarrhal infiltration may undergo complete resolution; far more 
generally, however, the infiltrated tissue suffers caseous metamorphosis, 
and soon disintegrates. Most cases of galloping consumption, where 
wide-spread destruction takes place in a lung within a few weeks, the 
patient quickly wasting away and sinking under violent fever, arise 
from the extension into the vesicles of an acute catarrh, involving a 
considerable portion of the lung, and which may be called an acute 
phthisis, resulting from acute or subacute catarrhal pneumonia. When 
an entire lobe of a lung is involved in a process of this kind, subse- 
quent absorption or incapsulation of the caseous deposit, with indura- 
tion and wasting of the affected part, rarely occurs. Such a termination 
is much more frequent where the disease is less extended. We may 
often trace back a depression of the supra and infra-clavicular region, 
with sinking of the summit of the lung, to an attack of acute catarrhal 
pneumonia, which has become chronic, and resulted in induration and 
contraction. We not unfrequently have the opportunity of observing 236 
DISEASES OF TEE PARENCHYMA OF THE LUNG. 
patients who have survived such attacks again and again, at varying 
intervals, the area of dulness and depression of the thoracic wall ex 
tending itself on each occasion, and who are finally carried off by a 
tuberculosis, or a less fortunate repetition of the pneumonia. 
In contrast to the fonn of disease hitherto described, the implica- 
tion of the air-cells in the bronchial catarrh may be unattended by any 
violent symptoms, and may even be entirely latent. Upon dissection, 
we often find the apex of the lung to be the seat of cicatricial con- 
tractions, of incapsulated caseous deposits, and callous indurations, 
resulting from a, pneumonia which has totally escaped observation. 
And we find many persons whose supra and infra-clavicular regions are 
sunken in, and the summit of whose lungs is in a state of abnormal 
depression, without any clew as to the date of the pneumonia by which 
the apex of the lung has become solidified and wasted. Still, when- 
ever the inflammatory process is at all extensive, even chronic catarrhal 
pneumonia is almost always accompanied by fever. True, for a while, 
this insidious fever is generally unobserved, or else misunderstood by 
the patient, and sometimes, too, by the physician, as the more obvious 
subjective febrile symptoms, the shivering, sense of heat, thirst, and 
the like, are slight, and are thrown into the background by the wasting, 
and the pernicious influence of the fever upon the appetite, the diges- 
tion, the licematosis, and general nutrition. When a patient with 
chronic bronchial catarrh, which has no ill effect upon his general 
health and activity, begins to lose appetite, to grow pale and thin, and 
to perceive a marked decline in his strength, there is reason to suspect 
that the pulmonary vesicles have become involved in the catarrh, and 
it is our imperative duty to ascertain the existence of fever, and of 
solidification of the lung, by careful measurement of the temperature, 
and by repeated physical examination of the chest. The chronic form 
of catarrhal pneumonia shows a decided tendency, under favoring cir- 
cumstances, to end in induration and shrinking, as well as to relapse 
under pernicious irritation. This is the reason why so many persons, 
in spite of the callosities and bronchiectatic cavities in the summit of 
their lungs, feel tolerably well during the summer months, and gain in 
strength and weight, while in winter, especially if obliged to work, 
and to expose themselves to cold, they grow feverish, thin, and pale, 
and suffer further induration of their lungs. Such alternations often 
go on for a number of years. Patients of this class furnish a large 
contingent to the hospitals, where (unless they present some physical 
signs of especial rarity) they are apt to be unwelcome guests, “ chronic 
pulmonary tuberculosis,” as it is called, being generally regarded as a 
somewhat uninteresting disease. The striking manner in which this 
form, which is by far the most common form of phthisis, yields to CONSUMPTION OF TIIE LUNGS. 
237 
treatment, and especially to dietetic treatment, in the wider sense of 
the word, is perfectly comprehensible when looked at from our point 
of view, and furnishes an argument in favor of the theory. 
The development of tuberculosis in lungs which are already con- 
sumptive, as a result of inflammatory action, sometimes takes place in 
a manner so latent as to make it extremely difficult, if not quite im- 
possible, to recognize the fact with certainty. On the other hand, 
there are many instances, especially where the lungs are the seat of 
very numerous tubercles, and 'when the tuberculosis involves other 
organs, in which the diagnosis presents no difficulty. Where we find 
a consumptive patient to be growing very short of breath, there being 
no perceptible increase in the dulness upon percussion to account for it; 
if, in spite of the most careful treatment the fever continue, and if it 
change from the remitting to the continued form; should diarrhoea set in 
in a patient who hitherto has been somewhat inclined to constipation; 
if hoarseness and aphonia be combined with the other symptoms of 
consumption, or if signs appear of disease of the meninges of the 
brain, we may confidently infer that tuberculosis has developed in the 
already consumptive lung. In young subjects, who are peculiarly 
liable to tuberculosis of the cerebral membranes, brain-symptoms may 
aid in forming a diagnosis, while in persons of more advanced years 
the appearance of intestinal or laryngeal symptoms may do the same. 
The development and progress of a tuberculous consumption differ 
essentially in type from any thing hitherto described, and its symptoms 
are so characteristic that the diagnosis of this form of consumption 
(which is not common) is, as a rule, easy. In the first place, it has no 
precursory catarrh. The fever and wasting are not deferred until the 
sputa become profuse and purulent, the tubercular eruption being ac- 
companied by a marked elevation of the temperature and rapid emaci- 
ation of the body from excessive calorification. If we are informed 
that a patient did not begin to cough and expectorate until several 
weeks after he had begun to decline in strength, and to grow pale and 
thin, there is always reason to fear that he has tuberculous consump- 
tion. Our suspicion will receive confirmation if the patient be un- 
wontedly short of breath, and if, at first, physical examination of the 
chest give negative results. At a later period the percussion-sound 
may grow dull from consecutive pneumonia, the respiratory murmur 
becoming bronchial, and the rales ringing, but the solidification is 
rarely as extensive as in the forms of consumption previously described. 
The sound of the voice and of the cough soon grows hoarse, and 
if there be much tuberculous disease of the larynx, and if it spread 
rapidly, the well-known distressing symptoms of laryngeal consump- 
tion make their appearance. Nor is it long before the signs of intes- 238 
DISEASES OF TEE PARENCHYMA OF THE LUNG. 
tinal tuberculosis and intestinal consumption set in. Exhaustion is 
accelerated by profuse diarrhoea. The abdomen becomes sensitive to 
pressure. The malady seldom lasts over a few months, and most pa- 
tients succumb even sooner. 
It would lead us too far were we to attempt to make a detailed 
description of the numerous modifications to which the different forms 
of consumption are subjected by the manifold changes of acute and 
chronic disease, and the various intercurrent accidents and complica- 
tions. I am sure, however, that most cases of consumption which we 
observe ourselves, or which are properly reported to us, may be as- 
signed without difficulty to one or other of the above-given categories. 
It follows, from what has been said, that death is the most frequent 
result of all forms of pulmonary consumption, and that it is the sole 
termination of tuberculosis, but that, in the forms of the malady which 
are dependent upon pneumonia, an improvement and approximative 
recovery are not as rare an occurrence as is usually supposed. It has 
been satisfactorily established, moreover, that even persons in whom 
all evidences of consumption have disappeared, and who are completely 
well of the malady, are still in greater danger than other persons of 
dying of a fresh attack of the pneumonic process or of tuberculosis. 
The fatal termination usually takes place through gradual con- 
sumption, “ wasting away,” “ decline.” The emaciation of the patient 
finally becomes extreme. The skin seems too loose for the body, 
owing to disappearance of the fat and atrophy of the muscles. The 
zygomatic bones project from the sunken cheeks, the nose seems 
longer and more pointed, the orbits from which all the fat has disap- 
peared seem too large for the eyes, the nails become incurved, the pad 
of fat upon the last phalanges being gone. Not unfrequently the tem- 
per of the patient, which at first was sullen and perverse, now grows 
cheerful and kindly. Many have perfect confidence in their recovery 
up to the moment of death, and expire in the midst of plans looking 
far into the future. Toward the last, however, the suffering is often 
severe. If the larynx be also “ consumptive,” there is an incessant 
cough which robs the patient of his rest at night; aphthae form in the 
mouth and pharynx, rendering chewing and deglutition difficult; the 
decubitus causes severe pain; one or both of the feet become the seat 
of an extremely painful oedema, owing to thrombosis of the femoral 
vein. In such cases the final stage seems extremely wearisome to the 
physician and attendants, and even to the patient himself, who often 
longs for his release. 
Very much more rarely consumption results in death from haemor- 
rhage. This is most usually the consequence of erosion of an unoblit- 
erated vessel in the wall of a cavity, or else of an aneurismal expansion CONSUMPTION OF THE LUNGS. 
239 
of a blood-vessel, which, being so situated in the wall of a cavity as to 
be deprived of support of the indurated pulmonary substance, yields 
to the pressure of the blood and finally bursts. In these cases of 
pneumorrhagia the patient either rapidly bleeds to death or else suffo- 
cates, the trachea and bronchi becoming filled with blood, thus cutting 
off entrance of the air into the lungs. The occurrence of pneumotho- 
rax, which we shall describe in detail hereafter, is a more common 
cause of death than haemorrhage, as are also secondary degeneration of 
the kidneys, intestinal phthisis, tubercle of the bowels, pneumonia, 
pleurisy, and other acute diseases. 
Treatment.—The treatment of consumption has made great ad- 
vance since recognition of the fact that the disease depends, as a rule, 
upon inflammatory action, and is only now and then due to neo- 
plasm. This view of the case has not led to the introduction of any 
new remedies for consumption, but it has enabled us more definitely 
to establish indications for remedies already long in use, so that by 
their methodical application, better results have been attained than 
were formerly gained at a time when consumption and cancer were 
regarded as equally incurable, and were somewhat similarly treated. 
Prophylaxis against consumption requires, in the first place, that, 
when an individual shows signs of defective nutrition and a feeble con- 
stitution, especially if already he have given positive evidence of un- 
usual delicacy, with a tendency to diseases which result in caseous 
products, he should be placed, if possible, under influences calculated 
to invigorate the constitution, and to extinguish such morbid ten- 
dency. 
Delicate children, especially such as are born of consumptive or 
otherwise decrepit parents, should not be suckled by their own moth- 
ers ; still less ought they to be reared artificially on “ pap,” but should 
be confided to good w'et-nurses. After weaning the child, let its diet 
consist almost exclusively of cow’s milk, instead of the customary pap 
of meal or bread, and after it has done teething let it eat a little meat. 
This diet must be kept up throughout the whole period of childhood, 
whenever there is any indication of glandular enlargement, moist cuta- 
neous eruption, or any other so-called scrofulous affection, or even 
when they merely give evidence of a so-called scrofulous habit. It is 
better to prescribe the exact amount of milk the child must take (after 
drinking which it may eat what bread, potatoes, or the like, it pleases), 
than merely to warn the parents in general terms against the immoder- 
ate use of bread and potatoes. When the child has drunk milk enough, 
the other food will do no harm. The common direction, that a “ child 
shall not eat dry food,” is wrong. It is better that it should chew and 
eat its bread dry, so that the amylum which it contains may be prop- 240 
DISEASES OF TIIE PARENCHYMA OF TnE LUNG. 
erly combined with saliva, whereby it is more thoroughly converted 
into sugar and is easier of assimilation. Besides this, however, it will 
drink all the more milk if it eat its bread plain. A similar plan of 
treatment is of course proper for children, who, instead of inheriting, 
have acquired a feebleness of constitution which often shows itself at 
an early date in the form of scrofula, and occasions a predisposition to 
consumption. 
A proper supply of fresh air is of equal importance with regula 
tion of the diet. The facts adduced above, illustrating the baneful 
effect of continual in-door life in producing scrofula and consumption, 
are not sufficiently taken into account by many physicians. They very 
often suffer delicate, sickly children to sit day after day and six hours 
at a time upon the benches of a crowded school-room, after which they 
have their tasks at home to prepare, private lessons to take, the piano 
to play, etc. Cod-liver oil and an occasional month at a watering- 
place cannot possibly repair the injurious effects of such a mode of life. 
As soon as the influence of this immoderate “ schooling ” begins to 
“ tell,” a reduction of it, or even a total cessation of it, should be im- 
peratively insisted on. Obstinate opposition to such demands will be 
often met with, but, in a series of instances in which I have obtained a 
complete and prolonged respite from education, and made the children 
spend most of their time in the open air, I have obtained effects at 
which I was myself astonished, and which completely satisfied their 
parents that results fully outweighed the serious sacrifices which they 
had made. People in easy circumstances, who have delicate and scrof- 
ulous children, especially if subject to croup and bronchitis, should be 
induced to spend their winters in the South, so that the children may 
also pass those months in the open air, which in our climate would be 
too cold. This is a very common practice in Russia, where the per- 
nicious effects of in-door life during the long winter are very con- 
spicuous. 
In adults, when the signs of delicacy and weakness, combined with 
deterioration of the blood, appear, the use of ferruginous preparations 
is to be recommended, particularly the chalybeate springs of Pyrmont, 
Driburg, Imnau, etc. I think that this treatment deserves a more gen- 
eral adoption, as a prophylactic measure against consumption, than it 
has received hitherto. 
Prophylactic treatment of consumption further demands a careful 
avoidance of all agents calculated to cause hyperaemia of the lungs and 
bronchial catarrh, and which we have enumerated as exciting causes of 
phthisis. Persons in whom a tendency to consumption is suspected 
should be strictly forbidden to inhale an atmosphere charged with 
smoke or dust, or which is too hot or too cold, as well as to make CONSUMPTION OF THE LUNGS. 
241 
great efforts in running, singing, dancing, or to drink hot or spirituous 
beverages. Chilling of the skin is to be guarded against with the ut- 
most care, and the patient should be made to wear flannel next the 
skin. What we have already said regarding the prophylaxis against 
pulmonary hypasremia and bronchial catarrh is equally applicable in 
the present instance. 
Finally, whenever there is the slightest suspicion of a predispo- 
sition to consumption, every catarrh, no matter how slight, is to be 
treated with the utmost care, which is not to be relaxed until the 
catarrh is entirely well. This rule, so obvious from our point of view, 
is very frequently violated. Many patients fall a victim to the deeply- 
rooted prejudice, that a neglected catarrh never leads to consumption. 
The rules which we have laid down for the prevention of phthisis 
must be carried out with equal strictness, whether the disease have 
merely just commenced, or whether it already have made some prog- 
ress. It is, therefore, superfluous to make separate mention of the 
indications derived from the cause, as they are identical with those of 
prophylaxis. 
When the air-vesicles of the lung become involved in the bronchial 
catarrh, the indicatio morbi calls for the usual remedies applicable to 
chronic inflammation. Above all, the affected lung, like any other in- 
flamed organ, is to be shielded from the action of any new irritation. 
It is incredible how much this simple rule (so obvious where the nature 
of phthisis is rightly understood) is disregarded by many physicians. 
It is a matter of daily occurrence that patients from the better class, 
suffering from advanced consumption, are not sufficiently urged by 
their physician to withdraw from their occupation, to throw up their 
position at the counting-house or office, and to keep away from club- 
rooms, with their over-heated and tobacco-laden atmosphere. It is 
often by exposure to irritants like the above, whose effect is so very 
injurious to the inflamed lung, that the extension of the inflammatory 
product is aggravated and made to terminate in disorganization, while, 
by their careful avoidance, the disease is often promptly arrested and 
brought to a favorable issue. The beneficial effect obtained in con- 
sumption, by protecting the affected lung from further detriment, is 
still more marked among the poorer classes, who seek aid at the hos- 
pitals. Many patients are received in a condition so wretched that a 
speedy death seems imminent, and yet they leave the institution, in 
the course of a few weeks or months, in much stronger and better con- 
dition, and often with a material increase in weight. Soon, however, 
they return, seeking readmission, their condition having grown rapidly 
worse again, owing to inclemency of the weather, and to other noxious 
influences, to which they have been exposed. 242 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
Were it not for tlie very grave objections already detailed, I should 
counsel most consumptive patients to keep the house during our North- 
ern winter, and to maintain the utmost uniformity of temperature in 
their chamber, in order to preserve their lungs from further harm. 
This dilemma may be obviated by making the patient avoid the North- 
ern winter, by sending him to some place where he can spend the 
greater part of the day in the open air, without risk of taking cold, or 
of inhaling a raw, inclement atmosphere. This, in my opinion, is the 
real benefit derivable from change of climate. When a patient has 
the means, we should never omit to enjoin upon him to make the sacri- 
fice, but the matter must be made plain to him, so that he may not 
suppose the air of the place to which he is sent has any special cura- 
tive power upon his lungs. We need not expect any benefit from a 
residence in Nizza, Mentone, Pau, Pisa, Algiers, Cairo, or Madeira, 
unless the patient fully understands that he must take care of himself. 
Otherwise, it were often better that he remained at home. Acting 
upon this principle, the patient should be sent during the autumn, and 
before the harsh winter sets in, to Soden, Badenweiler, Wiesbaden, 
and, above all, to the lake of Geneva, where he may try the grape-cure, 
and where he is as well protected as he is at home during the summer. 
None but very intelligent and prudent persons, who we may be sure 
will stay at home in bad weather, should be allowed to spend the 
winter at Nizza, Mentone, Pisa, or Pau. When the patients have the 
means, it is always better to send them to Algiers, Cairo, or Madeira. 
The comparative merit of these winter abodes is not as yet positively 
deternlined, and the indications for preferring Madeira, Algiers, or 
Cairo, in particular cases, or for certain stages of the disease, are so 
indefinite as to be of little value. One principle, however, always ob- 
tains : that the patient, wherever he may be, must live circumspectly, 
and remain under the charge of an intelligent and strict physician. 
For patients who are unable to seek a milder climate, the use of a 
“ respirator,” a wire gauze, warmed by the breath, through which the 
external air is inhaled, is advisable. A handkerchief held before the 
mouth, however, which also is soon warmed by the expired air, will 
answer the same purpose, and, indeed, is really better than a “ respi- 
rator,” as it is not, like the latter, liable to become too warm. 
Wlien the invasion of the air-vesicles by acute catarrh, or the rapid 
spreading of a catarrhal pneumonia, is accompanied by violent symp- 
toms, when high fever sets in, when the sputa become bloody, and the 
patient complains of lancinating pain upon drawing breath, and upon 
coughing, local depletion, by means of leeches or cups, and the appli- 
cation of cataplasms, should be resorted to. At the same time, the 
patient must be required to keep his bed until all symptoms of the CONSUMPTION OF THE LUNGS. 
243 
acute attack, or of the exacerbation of the old inflammatory disorder 
of the lung, be past. The fits of shivering, which come on regularly 
every evening, in many cases of phthisis, and which sometimes actually 
amount to rigors, have often been observed to cease if the patient re- 
main in bed. And, upon closer observation, it has been found that not 
only does the chill which heralds the evening access of fever, but all 
the other febrile symptoms, especially the rise in temperature, undergo 
marked improvement while the patient remains in bed for a few days. 
There is nothing strange about this, if, instead of regarding the hectic 
fever of consumptives as something peculiar, as an ens sui generis, we 
look upon it as a fever due to chronic inflammation. The fever which 
accompanies bronchial catarrh, pneumonia, or inflammation of any other 
organ, increases and diminishes as the disease grows better or worse, 
and it is just the same with the hectic fever of phthisis. Hence, if 
resting in bed, such as we generally recommend in other inflamma- 
tory disorders, have a beneficial effect upon the pneumonia of con- 
sumptives, it will tend also to mitigate their fever. 
The use of the alkaline muriate mineral wTaters, which is often so 
beneficial in simple catarrh, is equally useful in some cases of consump- 
tion. According to our view of the disease, this effect (which of 
course all believers in the theories of Laennec will deny) is not more 
enigmatical than that which these waters produce upon a simple 
catarrhal inflammation, wliich does not involve the substance of the 
lung-. The idea, that the use of the waters of Ems and Obersaltzbrun- 
ner is contraindicated by the presence of fever, is merely one of the 
results of imperfect observation. It is not the mineral waters which 
disagree with the fever, but the journey to the watering-place, and 
the promenades at the springs. As we have said before, a patient 
with any appreciable degree of fever ought to be in his room or in his 
bed. 
A continued abode in elevated regions, where, without any appar- 
ent reason, consumption is rare, is also advisable for consumptives, 
when their disease depends upon chronic pneumonia. I fully approve 
of the customary practice of sending phthisical patients to spend their 
summer at Heiden, Gais, Weissbad, Kreuth, etc., although I think but 
little of the “ curds and whey treatment ” which is practised there. 
In tuberculous phthisis, and in secondary tuberculosis, it is out of 
our power to meet the indications derived from the disease itself. 
Indicatio Symptomatica.—Fever is the symptom which principally 
demands treatment, whenever it persists at all severely, in spite of 
the remedies directed against the main disease. Anti-pyretics very 
properly play a most important part in the therapeusis of consumption. 
It is not that these remedies exert any more direct influence upon 244 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
chronic pneumonia than they do upon croupous pneumonia or typhus, 
or upon any other of the many maladies in which they are so much 
prescribed, often, indeed, without any very clear idea as to what is to 
be expected of them. But, if we know that the discharge of mucus 
and of pus-cells has but little to do with the exhaustion of the patient 
(indeed, it is often far more profuse in a simple bronchial catarrh), and 
that the fever is really his most formidable enemy, it follows, of course, 
that we must use every means at hand of combating this enemy. 
Digitalis and quinia have a well-merited reputation, as means 
whereby we often succeed in arresting the abnormal calorification, 
and reducing the animal heat, in spite of the continuation of the dis- 
ease. Digitalis is the principal ingredient of the much-employed 
Heim’s pill. (TjL pulv. herb, digitalis 3 ss., pulv. rad. ipecac., pulv. 
opii puri aa. gr. v., extract helenii q. s. u. f. pil. no. XX. consp. 
pulv. rad. irid. flor. S. a pill three times daily.) 
The addition of a scruple of quinine to the above prescription be- 
comes all the more appropriate, the more periodical the type assumed 
by the fever, the more severe its evening exacerbations become, and 
the more pronounced the chills by which they are ushered in. I am 
so much in the habit of using Heim’s pill with or without quinine, in 
consumption, whenever the fever proves refractory to the other rem- 
edies heretofore mentioned, that it has become a very common pre- 
scription at my clinic. Now and then, when I am a good deal consult- 
ed by phthisical patients, I prescribe it three or four times in one day. 
At the clinic, exhibition of the pills is suspended whenever a distinct 
reduction of the temperature and of the frequence of the pulse becomes 
apparent, and is resumed as soon as the effect subsides. In consulta- 
tion practice, I have repeatedly found that the patients pretty soon 
learn to judge for themselves when it is time to stop the pills, and when 
to resume them. 
The subject of antipyretic treatment of consumption may, with 
great propriety, be immediately followed by that of the diet of phthis- 
ical patients, for the same reason which induced us to treat the sub- 
jects of fever and emaciation in immediate conjunction. A man who 
has fever which is rapidly consuming him, stands in far greater need 
of a supply of nutriment than one who has no fever. The fever of a 
consumptive patient often lasts for months, so that the danger that it 
will wear him out is greater in his case than in one of acute febrile 
disease of brief duration. Hence it follows that phthisical patients 
require the richest possible diet which will agree with them. It is 
often said, but without any proof whatever, that food excites the fever, 
and (independently of the English practice) even here (in Germany) 
we only keep a patient on fever-diet—that is, we only deprive him of CONSUMPTION OF THE LUNGS. 
245 
nourishing food until it becomes evidently dangerous to persist in so 
doing. As soon as this is evident, the so-called law of nutrition is 
utterly ignored, or, rather, it is flagrantly violated. In selecting suit- 
able nourishment for consumptives, articles commended, time out of 
mind, by rude experience, are found to be in complete agreement with 
the current physiological laws of assimilation and nutrition. All the 
food which is regarded as especially proper for phthisical patients con- 
tains large quantities of fat or of fat-generating matter, and a compara- 
tively small portion of protein substances. This accords with our 
experience, that the production of urea, and hence the destructive 
assimilation of nitrogenous constituents, is augmented by an increase 
of the supply of protein substances, while, by a simultaneous free sup- 
ply of fat or fattening food, the destructive assimilation and consump- 
tion of the organs of most importance in the body are diminished. Thus 
the use of milk, to which little children owe the plumpness of their 
limbs, and from which corpulent persons do well to abstain, cannot be 
sufficiently urged upon consumptive persons. It is altogether useless, 
however, and indeed wrong, to remove the casein of the milk, and to 
give it in the form of whey, unless, indeed, the whey agree with the 
patient better than the milk, which is rarely the case. I often order 
my patients to drink a pint of milk “ warm from the cow,” three times 
a day, but have no other object in so doing than that of preventing 
the milk from being skimmed, which is impossible immediately after 
milking. The milk of animals which pasture in the mountains, such as 
goat’s milk, but, above all, ass’s milk, is in especial repute, and it is 
desirable to send patients, who can travel without danger, to places 
where there are dairies where a supply of good fresh milk is to 
be obtained. Where this cannot be done, the “ milk-cure ” must be 
practised at home. The name is of importance, in order that the 
patients may have faith in the treatment, and follow it out punctually. 
I have treated a great number of patients who, as soon as they found 
that they increased appreciably in weight, for half a year at a time 
drank three or four pints of milk daily without repugnance. 
The use of cod-liver oil is also highly commendable, and, when it 
agrees well with the patient, may be combined with plenty of milk. 
It is more than doubtful whether this oil, which is hardly ever with- 
held in phthisis, at all events in Germany, exerts any specific influence 
upon the disease. The quantity of iodine in it is so trifling, that it 
cannot be taken into account, hence it is probable that all its beneficial 
effects are solely due to the large amount of fat which it affords. This 
is all the more likely, as dog's fat is a popular remedy for consumption, 
as ancient and well-tried as cod-liver oil. 
Of late years I have obtained very good effects from an extract of DISEASES OF THE PARENCHYMA OF THE LUNG. 
246 
malt, prepared by Trommer. This preparation of Trommer is not 
a strong beer, containing a large amount of alcohol and carbonic acid, 
like the Hoff's malt extract so greatly extolled, but is a genuine 
extract resembling other officinal extracts, and consists of the soluble 
constituents of the malt, and of the bitter extractive matter of the 
hops, and can be prepared by every apothecary. One hundred parts 
of it contain about seventy-six parts of grape sugar, or malt sugar, dex- 
trin, bitter of hops, resin of hops, and tannin, seven parts of albuminous 
or protein substance, eighty-two hundredths of a part of phosphate of 
lime and magnesia, eighteen hundredths of alkaline salts, and sixteen 
parts of water. The patients almost always enjoy two or three table- 
spoonsful of it daily, and it usually agrees well with them. It may be 
diluted in spring-water, mineral water, or warm milk or other liquid. 
Broth, made of coarsely-broken rye-meal, which contains a good 
deal of gluten, besides the amylum, is a good food for consumptives, 
and has long enjoyed such a reputation. Soup of lentils and bean- 
tneal (revalenta arabica), as well as the various preparations of choco- 
late, mixed with cacao-meal, and sold under various names, is also 
appropriate. 
Jellies of animal or vegetable substance are much less desirable, 
such as the snail-soup, and the jelly from the Iceland moss. 
With respect to the symptomatic treatment of the cough and ex- 
pectoration, wTe simply refer to what has already been said regarding 
the treatment of bronchial catarrh. An indiscriminate use, one after 
another, of the so-called expectorants is as absurd in the treatment of 
the chronic bronchial catarrh which accompanies phthisis as it is in any 
other form of catarrh. The sweet, mucilaginous, “ soothing,” demul- 
cent articles are least serviceable of all. Precisely according to the 
conditions laid down above, the alkaline chlorides may be required at 
one time, at another senega, squills, or other stimulants may be indi- 
cated, and at still another the articles which diminish secretion. As we 
have already expressed our preference for the balsams and resins for the 
latter purpose, I must again say a word or two in favor of the saccha- 
rum myrrh®, and of Griffith’s mixture, adding, however, that acetate 
of lead is held in great esteem by many authorities as a remedy for the 
condition in question. (In almost every case where acetate of lead is 
used it is given in combination with opium, to which some of the effect 
attributed to the lead is certainly due.) 
The narcotics are to be employed in order to allay the cough, and 
are quite indispensable in consumption. As we have said already, it 
is not the soothing, soporific action of the first few doses of the opium 
or morphine which gratifies the patients, but it is because they find 
that they cough less and more easily, “ that their cough is looser; ” ACUTE MILIARY TUBERCULOSIS. 
247 
and, indeed, when we consider that coughing is an irritant to the bron- 
chial mucous membrane, which is the principal source of the secretion, 
it seems quite probable that a diminution of the inclination to cough 
may result in a decrease of the expectoration. Nevertheless, it is best 
not to commence using the narcotics too soon, and, instead of opium, 
we should begin with small doses of something else, as, extract of 
lactucaria virosa, gr. ss to gr. j, in powder, or in the form of a syrup. 
By a too early resort to narcotics, it may happen that they fail of 
effect at a later period, when the need for them has become most 
urgent, as when the tormenting cough of a laryngeal phthisis deprives 
the patient of rest both by night and by day. It seems also, that, as 
soon as it becomes necessary to give large doses of opium, the progress 
of the consumption becomes more rapid, an additional reason against 
a too hasty employment of a remedy which becomes indispensable to 
the patient. When the narcotics are not tolerated by the stomach, 
they must be injected subcutaneously. 
For the night-sweats we may order small doses of “ Haller’s acid,” 
or the patient may drink a cup of cold sage-tea, if the antipyretic 
treatment fails to do good. The efficacy of the above articles is some- 
what questionable, no doubt, but it would be cruel to tell the patient 
that there are no means of relief from this distressing symptom. Some 
physicians recommend the boletus laricis (a very unsafe article), as a 
most efficient remedy against the night-sweats of consumption. 
With regard to the treatment required by the complication of 
laryngeal and intestinal phthisis with consumption of the lungs, as 
well as that demanded by the secondary diseases of the liver and kid- 
neys, etc., we must refer to the sections in which affections of those 
organs are described. 
ACUTE MILIARY TUBERCULOSIS. 
CHAPTER XIY. 
Etiology.—Acute miliary tuberculosis, which is not to be con- 
founded with acute (“galloping”) consumption, depends upon an 
eruption of tubercles in the lungs as well as in most other organs, 
and is accompanied by the symptoms of an acute disease. In the 
great majority of cases the disease is seen in persons whose lungs 
or other organs contain old caseous deposits. This fact, and the cir- 
cumstance that the symptoms and course of acute miliary tuberculosis 
bear a strong resemblance to those of the acute infectious diseases, 
would make it appear highly probable that the malady arose from in- 
fection of the blood by the caseous products {Buhl), were it not that 
the occasional although rare occurrence of the disorder, unpreceded by 248 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
caseous deposit, contradicts tliis plausible hypothesis. We must, 
therefore, content ourselves by stating that, in most cases, acute 
miliary tuberculosis is a secondary disease, arising, in some manner 
as yet unknown to us, from the pernicious effect of the cheesy deposit, 
but that may also proceed from other causes, of whose nature we are 
equally ignorant. 
Anatomical Appearances.—If we find, upon dissection, that the 
lungs are studded uniformly from top to bottom with miliary tubercles, 
if the miliary nodules present that gray, translucent appearance of 
fresh tubercle, if the surfaces of the pleura be also strewed with 
miliary tubercles, we may decide with positive certainty that the 
patient has had acute miliary tuberculosis, even though we know 
nothing of what the course of the disease has been. In chronic tuber- 
culosis this uniform dissemination of the tubercle is never found, and 
yellow, caseous granulations always coexist with the new gray tuber- 
cles, showing that the deposit has been a gradual one. In most cases 
of the acute disease, the peritonaeum, the liver, the spleen, the kidneys 
are covered by miliary tubercles. Finally, especially in young per- 
sons, numerous granulations are Often found in the pia mater, particu- 
larly at the base of the brain, about the pons, and the chiasm of the 
optic nerves, together with acute hydrocephalus of the ventricles. 
The parenchyma looks injected and more or less infiltrated with 
serum, otherwise it is generally free from inflammatory or other nutri- 
tive disturbance, with the exception of the traces of former disease 
which may be there. The corpse of a person who has died of acute 
miliary tuberculosis resembles that of one who lias died of an acute 
febrile disease, the resemblance commencing during life and con- 
tinuing after death. The blood is dark and liquid, and settles to the 
most dependent points, giving rise to extensive pulmonary hypostasis. 
The muscles are red, and even the spleen is often somewhat swollen 
and softened. 
Symptoms and Course.—When an acute miliary tuberculosis de- 
velops at an advanced stage of consumption, complicated with hectic 
and night-sweats, it is very difficult of recognition, inasmuch as it can 
hardly be decided whether the fever and the rapid decline of the pa- 
tient are due to the original complaint or to the complication. Physical 
examination of the chest gives negative information as to the new 
deposit of miliary tubercles; as the innumerable little granules, being 
everywhere enclosed in tissue containing air, do not modify either the 
sound upon percussion or the respiratory murmur, although the dis- 
proportion between the intense dyspnoea and the trifling extension of 
some old point of induration perhaps may aid the diagnosis. 
The disease assumes a different guise when it attacks persons in ACUTE MILIARY TUBERCULOSIS. 
249 
good health, or those whose chronic pulmonary affection has hitherto 
escaped attention. It then not unfrequently begins with repeated 
rigors, great frequence of the pulse, and severe constitutional disturb- 
ance, symptoms often hard to interpret, as they are attended by no 
tokens of local disorder. The frequence of the pulse often becomes 
exceedingly great, abundant sweats set in, the patient sinks visibly 
from day to day, the tongue becomes dry, the sensorium deranged, he 
becomes delirious or lies supine in a state of stupor. A rapidly-increas- 
ing prostration, cough, and dyspnoea accompany these symptoms, it is 
true, but the most persistent physical examination of the chest reveals 
nowhere that the substance of the lung is infiltrated. No sounds can 
be perceived, save a few fine rhonchi and scanty rales. The symp- 
toms which we have depicted are so very like those of typhus, that 
the most experienced diagnosticians acknowledge to having met with 
instances in which a diagnosis between the two was absolutely impos- 
sible, and where patients dying with a diagnosis of typhus really had 
died of tuberculosis, and conversely. The less violent the symptoms 
of catarrh in acute miliary tuberculosis, the smaller the clew afforded 
by the spleen, the more rapid the march of the malady, so much the 
more difficult does the distinction become. The patient may succumb 
to miliary tuberculosis, after the lapse of a fortnight,.or a few' days 
longer, or about in the same time in which patients usually die of 
typhus. More rarely death does not take place until the end of the 
fifth or sixth week. The patient perishes, as we have said, consumed 
by fever, just as he falls a prey to fever, too, as a rule, wffien he dies 
of typhus. The pulse becomes smaller and more and more frequent; 
finally, the pulmonary veins are no longer able to pour their blood into 
the imperfectly-emptied heart, and oedema of the lungs, palsy of the 
bronchi, and suffocative effusion are established. If tuberculous basilar 
meningitis accompany the attack, its course is modified (see appro- 
priate chapter) and the fatal termination takes place with even still 
greater rapidity. 
Diagnosis.—At the outset of the disease, if the chills recur with 
some degree of regularity, it may be mistaken for intermittent fever. 
We shall soon observe, howrever, that the intermissions are not com- 
plete, that quinine fails in its effect, that the complaint is attended 
by a disturbance in the respiratory function, which is unusual in inter- 
mittent ; that the frequence of the pulse is constantly on the increase, 
and that the entire character of the complaint is more pernicious than 
that of simple intermitting fever. 
In other cases the disease, at its commencement, resembles an ex- 
tensive bronchial catarrh, accompanied by fever, especially if the cough 
be very violent and distressing; but here, too, all difficulty of distinc- 250 
DISEASES OF THE PARENCHYMA OF THE LUNG. 
tion soon vanishes, as the violence of the fever, the rapid collapse, and 
the malignant course of the malady, but especially the shortness of 
breath which often renders it impossible for the patient to breathe in a 
recumbent position, and which is in striking contrast with the absence 
of physical signs of disease, afford data for diagnosis. 
A differential diagnosis between miliary tuberculosis and typhus 
is based upon the following points : 
1. In tuberculosis, the cough and dyspnoea appear, as a rule, at an 
earlier period and with far greater intensity than in typhus. In exan- 
thematic typhus, it is true, we likewise find early and violent bron- 
chitic symptoms; but here the distinction is easy, as the eruption of 
exantliematic typhus is highly characteristic and scarcely to be over- 
looked, while there is no eruption in acute miliary tuberculosis. 
2. In abdominal typhus (typhoid), likewise, we rarely fail, after 
careful and repeated search, to discover a few spots of roseola upon the 
upper region of the abdomen, which do not exist in acute miliary tu- 
berculosis. 
3. Enlargement of the spleen can rarely be found in acute miliary 
tuberculosis, and when found scarcely ever is an enlargement of much 
magnitude, while we hardly ever fail to find it in abdominal typhus : 
and even though it were not found, in exanthematous typhus the ex- 
istence of the eruption would render this clew almost unnecessary. 
4. Meteorism, liquid stools, tenderness in the ileo-ccecal region, 
are seldom absent in abdominal typhus. These symptoms are not ob- 
served in acute miliary tuberculosis. 
5. Typhus rarely supervenes upon chronic disease of the lungs, 
while acute miliary tuberculosis seldom attacks any save those who 
are suffering from such disease. Dulness at the apex of either lung 
is therefore of great diagnostic significance. 
6. Wunderlich has observed that the temperature in acute mil- 
iary tuberculosis is much lower than in typhus, seldom reaching 104° 
F., and is out of ajl proportion to the enormous rapidity of the pulse. 
Prognosis.—Prognosis as to the issue of acute miliary tuberculo- 
sis must be almost absolutely unfavorable. Only a very few observa- 
tions ('Wunderlich) allow us to suppose that tubercles thus deposited 
may become atrophied, and the malady terminate in recovery. The 
cases, too, in which the acute disease has become arrested, and chronic 
tuberculosis and phthisis have followed, certainly must be considered 
as among the greatest of rarities. The more violent the fever, the 
more pronounced the brain-symptoms, so much the sooner is the end 
to be expected. 
Treatment.—The treatment of acute miliary tuberculosis is of 
course a mere treatment of symptoms. The most important symptom CANCER OF THE LUNG. 
251 
is the fever; for it is of the fever alone that the majority of those at- 
tacked perish. Large doses of quinine should be given, particularly at 
the outset of the disease and as long as the rigors continue to occur, 
and at a later period use digitalis, nitre, and the acids. Little success, 
however, is to be anticipated. For the dyspnoea, cold is to be applied. 
Combat the cough with narcotics; and, should appearances lead us to 
suspect the existence of meningeal tuberculosis, apply ice to the 
head. 
CHAPTER XV. 
CANCER OF THE LUNG. 
Etiology.—The pathogeny and etiology of this malady are as ob- 
scure as those of the malignant neoplasms in general. 
Cancer of the lung is a somewhat rare disease, and primary cancer 
of this organ is of especially unusual occurrence; that is to say, the 
substance of the lung is scarcely ever the point at which the first 
traces of it develop themselves. Cancer of other organs, particularly 
of the breast, almost always precedes cancer of the lungs. 
Anatomical Appearances.—In the lung, cancer assumes almost 
exclusively the medullary form, far more rarely that of the scirrhus or 
of alveolar degeneration. It sometimes assumes the form of rounded 
isolated masses, varying from the size of a hemp-seed to that of a fist, 
constituting cancerous nodules of a marrowy appearance and soft con- 
sistence, which, when they touch the pleura, are apt to show a flattened 
or umbilicated depression. Sometimes the disease appears as the so- 
called infiltrated cancer. Unlike the previous variety, the latter form 
does not present a distinct limit between the cancer and the surround- 
ing parenchyma, but makes a gradual transition; nor does the disease 
present the rounded contour of cancerous nodules. 
The old hypothesis, that, in the latter case, we had to do with a 
conversion of an infiltration into cancer, has been abandoned; and it is 
now believed that, in the origin of infiltrated cancer, after the trans- 
formation into cancer-cells of a few of the connective tissue-cells of the 
matrix of the lung, and of a few of the epithelial cells of the vesicles, 
this conversion is propagated into the neighboring connective tissue, 
and into the connective tissue-cells of the adjacent alveoli. On the 
other hand, with regard to the appearance of isolated cancerous nodules 
in the lung, w'e must suppose that here, too, the cancer-cells originate 
from the elements of the tissue, and then proliferate without further 
implication of the contiguous tissues in the disease. The enlargement 
of the tumor, therefore, is due to proliferation of the original cancer-cell 252 
DISEASES OF TIIE PARENCHYMA OF THE LUNG. 
alone; the surrounding pulmonary substance being pushed aside and 
compressed. 
It is exceedingly rare for medullary fungus of the lung to soften, 
and break down, so as to form cavities. The disease is much more 
liable to extend into the pleura, and, as the pleural folds rapidly adhere, 
to spread through them into the walls of the chest, which it often 
penetrates. 
Symptoms and Course.—In the great majority of instances, no 
characteristic marks of cancer of the lung are to be observed, and it is 
hardly ever possible to prove the existence of the disease with cer- 
tainty, except in cases wherein a carcinomatous breast has been extir- 
pated, or in which extensive cancerous disease of other parts of the 
body can be discovered. Should dyspnoea, cough, blood-spitting, and 
pain in the chest, symptoms indicative of chronic disease of the lung, 
appear in such a case, instead of apprehending the formation of tuber- 
cle, we should bear in mind the rarity of tuberculosis in cancerous per- 
sons, and of the frequent relapses of the malady, in the form of pul- 
monary carcinoma, after extirpation of cancerous masses. 
Diagnosis will be confirmed if percussion and auscultation show a 
consolidation of the substance of the lung, especially as, unlike tubercle, 
cancer is not habitually situated at the summit of the lungs. 
We are very seldom able to prove the existence of any character- 
istic objects in the sputa. The diagnosis is more commonly rendered 
certain by the perforation of the thorax by the disease and its extension 
into the integument. 
Treatment.—Of course, there can be no idea of treating a cancer 
of the lung. The hyperaemia in its adjacent parts, the cedema, the 
hemoptysis, must be treated according to directions already given. SECTION IV. 
DISEASES OF THE PLEURA, 
CHAPTER I. 
INFLAMMATION OF THE PLEURA—PLEURITIS, PLEURISY. 
Etiology.—As we shall find presently, there are two forms of pleu- 
risy. The first form merely causes thickening of the pleura, and 
adhesion of its opposing surfaces. The second also produces thick- 
ening, but at the same time gives rise to an effusion into the pleural 
sac, containing more or less of fibrin and of young cells. The thick- 
ening and adhesion of the pleural surfaces are due to proliferation of the 
normal connective tissue of the pleura. The pleuritic effusion is the 
result of an interstitial exudation. The young cells, which the effusion 
contains, owe their origin to a proliferation of the connective tissue cor- 
puscles of the pleura, and of the epithelial cells which cover its surface. 
Regarding the essential points in the etiology of pleurisy, we may 
refer to what has already been said with regard to the etiology of 
pneumonia. 
We must here denounce the impropriety of calling all cases of 
pleurisy secondary pleurisy, which, instead of attacking robust and 
vigorous persons, occur in subjects with broken-down constitution, or 
in individuals who have already suffered from some other disease. 
Even the pleurisy which so often occurs in Bright’s disease is not, in 
my opinion, a secondary disease, dependent upon ihe renal affection, 
but should rather be looked upon as a complication. The frequence of 
such complications, and the especially common occurrence of pleuritis 
in debilitated and depraved constitutions, and among convalescents 
after protracted disease, depend upon the increased predisposition, 
which such individuals possess, for all kinds of inflammatory diseases, 
and especially for the one in question. A very trifling exciting cause 
is requisite in this class of persons to provoke the malady; but it never 
arises without provocation of some kind. 254 
DISEASES OF TEE PLEURA. 
The case is different in the pleurisy which sometimes accompanies 
septicaemia, puerperal fever, scarlet fever, and other infectious dis- 
orders. Such a pleurisy arises independently of the action of any new 
irritant, and forms one of the nutritive derangements which proceed 
from infection of the organism by putrid matter, scarlatinous poison, or 
the like. This secondary pleurisy, which generally produces a puru- 
loid exudation full of young cells, is attended by inflammation of other 
serous membranes. 
The exciting causes of pleurisy are— 
1. Injuries of the ribs and pleura, and the entrance into the latter 
of foreign bodies, such as pus, blood, air, and the contents of cavities. 
Such exciting causes generally give rise to a form of pleurisy, accom- 
panied by a very profuse sero-fibrinous exudation into the pleural sac. 
2. Pleuritis often arises through propagation of inflammation from 
neighboring organs, as from the lungs to the substance of the pleura. 
In these cases the exudation generally is scanty and fibrinous, although 
it sometimes is very copious and sero-fibrinous. 
3. Next in order come the very numerous instances in which pleu- 
risy is caused by the advance to the pleura of neoplasms, especially of 
tubercle and carcinoma. Here the pleurisy is dry, or else it results in 
adhesions of the opposing surfaces of the pleura, or else a more or less 
plentiful effusion into the sac may form, or, finally, tubercle or cancer 
may develop in the pseudo-membrane. 
4. Pleurisy is often the consequence of exposure to cold, or to the 
action of other atmospheric or telluric influences, of which we have no 
definite knowledge. In this form, which is an independent, idiopathic 
disease, and which is usually called rheumatic pleurisy, there is a 
great deal of variety as to the quantity and character of the effusion. 
Anatomical Appearances.—In commencing pleuritis, the pleura 
is reddened by injection proceeding from the sub-serous connective 
tissue, and producing fine rose-red points and stripes upon its surface. 
Besides this distention of the capillaries, we often find slight extrava- 
sations of blood, ecchymoses, forming irregular dark spots, in which 
the ramifications of small vessels are visible. The tissue of the pleura 
is infiltrated, the epithelium is nearly all cast off, the surface, formerly 
smooth and glossy, looks dull, the pleura itself is somewhat swollen. 
Gradually the free surface begins to assume a rough, shaggy appear- 
ance. This is due to the development of minute delicate folds, and 
papillary granulations, which are firmly attached to the surface, and 
are not to be confounded with fibrinous deposits. Microscopically, 
these granulations consist of newly-formed fusiform cells, and tender 
filaments of wavy connective tissue, with considerably-elongated capil- 
laries, which are coiled into loops within them (Foerster). INFLAMMATION OF THE PLEURA. 
255 
These changes occur in every form of pleuritis, whether effusion 
take place in the pleural cavity or not, whether the latter be profuse 
or scanty, contain much or little fibrin, or many or few pus-corpuscles. 
It is to this source alone that pseudo-membranes and adhesions of the 
pleura owe their origin. 
The most common forms of pleurisy are— 
1. That in which no symptoms occur, excepting those just de- 
scribed, and to which we may give the name of pleuritis sicca, dry 
pleurisy, or pleurisy with purely nutritive exudation. It is true, that 
we but rarely have opportunity to make anatomical examination of a 
dry pleurisy in its earliest stage. However, whenever this has been 
possible (Foerster), no free exudation has been found to exist, the out- 
growths from the pleura just described forming the sole abnormity. 
Besides this, however, very extensive adhesions of the pleura are often 
found, which have formed almost without giving rise to any symptoms, 
and this fact wTould indicate that they must occur without exudation, 
for we find that very small exudations are accompanied by very great 
pain. 
2. Pleurisy with scanty, but very fibrinous, exudation. Such a 
pleurisy we almost always see accompanying croupous pneumonia or 
complicating chronic affections of the lungs. It may also occur as an 
independent disease. Here the inflamed pleura, having undergone the 
alterations above described, soon becomes coated by an extremely deli- 
cate membranous coagulum of fibrin, which causes it to appear more 
opaque, so that we cannot discern the injection, or ecchymosis of the 
pleura itself, until we have scraped off the fibrin with the scalpel-handle. 
In other cases, this very fibrinous effusion is somewhat more profuse, 
and we may then observe upon the pleura a white deposit, half a line 
or more in thickness, somewhat soft, and very much like a croup mem- 
brane. Of course, the exudation in these cases was originally liquid, 
and only coagulates at a later period; nevertheless, we are often unable 
to find any liquid effusion besides the coagulated one in the cavity of 
the pleura, When this form of pleuritis recovers, the fibrinous de- 
posit, after undergoing fatty degeneration and liquefaction, is absorbed, 
the outgrowths of the opposing surfaces of the pleura are brought into 
contact, and adhesions generally ensue. 
3. Pleurisy with abundant serofibrinous exudation. The altera- 
tions in the tissues of the pleura are usually very extensive in this 
form of the disease, both upon the pulmonary and costal surfaces; but, 
in addition to this, an effusion of serum takes place in the pleural sac, 
amounting, not unfrequently, to two or three, and, indeed, even to ten 
pounds or more. This exudation consists of two components—a yel- 
lowish-green serum, and a quantity of coagulated fibrinous masses. 256 
DISEASES OF THE PLEURA. 
Part of the latter floats in the serum in the form of flakes and lumps, 
another part traverses the serum in the form of a loose net-work, while 
a third portion is precipitated upon the pleura, upon which it lies in 
the form of a membrane. The longer tlie effusion remains, so much 
the stronger and more rigid do the masses become, until they finally 
grow fibrous, without, however, taking on any organization. Both 
in the serum and in the fibrinous deposit we find a few pus-corpuscles, 
so that the transition from this form of pleurisy to the next, in which 
pus-corpuscles are far more abundant, is quite gradual. The greater 
the quantity of pus, so much the more turbid is the serum, and the 
more yellow the deposit. The proportion between the serum and the 
fibrin varies, although here, too, we are not warranted in regarding 
fibrinous exudation as the consequence of a hyperinosis (augmentation 
of fibrin in the blood). Indeed, according to the old-fashioned theory, 
it is far more probable that a pleurisy, in which a great amount of 
fibrin is secreted in the pleura, also causes the increased quantity of 
fibrin in the blood. The exudation often seems to receive accessions, 
and to increase by fits and starts. As these after-flows do not come 
immediately from the vessels of the pleura, but from the tliin-walled 
vessels of the young connective tissue, we often find an admixture of 
blood in the serous effusion of chronic pleuritis, in consequence of rup- 
ture of the delicate capillary walls, thus forming pleurisy with haemor- 
rhagic exudation. We constantly find agglutinations of the opposing 
surfaces by fibrinous exudation, as well as commencing adhesions, sur- 
rounding the effusion, whereby the latter is often incapsulated. This 
is a condition of great importance in the symptomatology of the 
disease. 
According to the lucid and concise account of Rokitansky, the 
changes which take place in the thorax and its contents, in consequence 
of extensive effusion, are as follows: “The thorax is dilated in a 
manner more or less apparent, the intercostal spaces are widened and 
prominent, the diaphragm is forced down into the abdomen, the medi- 
astinum and heart are displaced to the other side, or, when the effusion 
is symmetrical, lie in the middle of the chest. The lung itself is com- 
pressed to a degree corresponding to the amount of the effusion, and, 
unless old adhesions offer resistance, it is constantly pushed upward 
and inward against the mediastinum and back-bone. We find it re- 
duced to the fourth, sixth, and even to the eighth part of its normal 
volume, and flattened into a cake, its color is pale reddish or bluish 
gray, or lead color, and its consistence is leathery, tough, and void of 
blood and air, and in a state of atrophy at the edges and surface. It 
is coated externally by the coagulum of fibrin, which extends from the 
costal to the pulmonary pleura. In partial pleuritis, the displacement INFLAMMATION OF THE TLEURA. 
257 
and compression are limited to a portion of lung corresponding to its 
seat and extent.” 
The lung upon the unaffected side is always the seat of intense 
collateral fluxion, and, in fatal cases, of collateral oedema. Should re- 
covery take place in this form of pleuritis, the exudation gradually 
becomes more and more concentrated (so that the absorption proceeds 
at first far more rapidly than it afterward does). The liquid portion 
may at length disappear completely; the pleural surfaces, roughened 
by fibrinous deposit, coming into contact. The fibrin also undergoes 
fatty metamorphosis, liquefies, and is absorbed, and then an adhesion 
of the pleural surfaces, which are usually much thickened, always takes 
place. Sometimes yellow, cheesy masses, consisting of remnants of 
unabsorbed fibrinous deposit and cellular elements of the exudation, 
are found imbedded between the adhesions. 
When absorption takes place early, the compressed lung may again 
become pervious to the air, and may expand; the intercostal spaces 
may return to their normal state, and the mediastinum, diaphragm, 
and the dislocated heart and liver, may all regain their proper places. 
In other cases the alveoli become agglutinated or adherent by con- 
tinued pressure, or else dense fibrinous deposits upon the compressed 
lung prevent its reinflation. The time required for the production of 
this condition cannot be given with accuracy. If absorption of the 
exudation should afterward take place, a vacuum tends to form, to fill 
up which, the thoracic wall and the adjacent organs suffer displace- 
ment. The affected side of the chest sinks in, and may present a con- 
cave instead of a convex surface; the intercostal spaces become Nar- 
rower, until the ribs finally touch; the shoulder sinks, and even the 
spinal column becomes curved. In pleuritis of the right side, the 
liver, previously deeply depressed, is now dislocated far in the opposite 
direction, sometimes as high as the third rib. In pleurisy of the left 
side, the heart, at first often displaced to beyond the right edge of the 
sternum, now is drawn back as far as the left axillary line. 
4. Pleuritis with purulent effusion. Empyema, Pyothorax.—The 
liquid part of the effusion is here so rich in pus-corpuscles as to form 
an opaque, yellow, thick fluid. The fibrinous portion also contains 
great quantities of pus-cells and seems soft, and of a very yellow color. 
Here too, the exudation, and not only the serous part of it, but the 
fibrin and pus, after undergoing the often-mentioned metamorphosis, 
may be absorbed; but there is another sequel to pleuritis sometimes, 
and it most frequently follows this form of the malady. Not only are 
pus-corpuscles generated upon the free surface, but they are also 
formed within the tissue of the pleura itself. The latter becomes 
opaque and softens, and irregular losses of substance occur. Should 258 
DISEASES OF TIIE FLEURA. 
they be situated upon the costal pleura and penetrate deeply, external 
perforation of the empyema may take place, and in fortunate cases, 
especially if the lung remain capable of redistention, recovery may be 
the result. In similar manner, a penetration of the empyema into the 
lung and its discharge by way of the bronchi sometimes happen, but a 
recovery in such instances is rare. 
Symptoms and Course.—Dry pleurisy has no symptoms, or, at 
least, if it have symptoms, they cannot be distinguished from those of 
the disease which it accompanies. We sometimes find adhesion of the 
entire pleural surface in the bodies of persons who never have been 
seriously ill. Extensive and rigid adhesions of the pulmonary and costal 
pleurre hinder the two surfaces from sliding upon one another, and 
thus prevent a uniform expansion of the lung during inspiration (see 
vicarious emphysema). The consequence often is a slight dyspnoea, 
which is only felt, when unusual bodily exertion or other cause excites 
a demand for an increased supply of oxygen. 
Pleurisy with scanty fibrinous exudation is accompanied by 
severe piercing pain when a breath is drawn; the suffering produced 
by the limited and slow movement of the pleura, during ordinary 
breathing, is far greater than that arising from the strong and rapid 
motion of forced respiration. Coughing and sneezing are especially 
painful to the patient, as these acts compress the inflamed pleura from 
within. In like manner a pressure upon the ribs and intercostal mus- 
cles affects the pleura immediately, and greatly increases the pain. 
The respiration of the patient is shallow and cautious. The body is 
generally bent toward the affected side, as this attitude lessens the 
tension of the intercostal muscles and its inflamed covering. Besides 
the pain, some patients have a distinct sensation of friction, or of 
scratching at some point of the thorax. There is also cough, as a rule; 
although cases now and then are observed where there is absolutely 
no cough, and it has not as yet been determined satisfactorily whether 
the cough is a result of reflex action from the inflammatory irritation 
of the pleura, similar to that arising from irritation of the bronchial 
mucous membrane, or whether it is due to a complication of pneu- 
monia or bronchitis with the pleurisy. The pleurisy with scanty 
fibrinous exudation, unless accompanied by extensive and severe 
inflammation of the lung, is usually unattended by fever, or other 
serious derangement of the health. Many patients never even keep 
their room, and often go on foot to the clinic, or to the office of their 
physician, for medical aid. 
We have already stated that the pleuritic stitch, which is one of 
the most painful symptoms of croupous pneumonia, and which indubi- 
tably owes its origin.to the almost constant complication of the latter INFLAMMATION OF THE PLEUKA. 
259 
disease with the form of pleuritis now under consideration, is generally 
of briefer duration than the other symptoms of pneumonia. Perhaps 
this is because the pleural surfaces cease sliding upon one another, 
where a large portion of the lung has become infiltrated. But even 
when the disease occurs spontaneously, or when it supervenes in 
chronic disease of the lung, the pain usually ceases in a few days, 
especially if properly treated. Its persistence for weeks is an excep- 
tional occurrence, and should cause suspicion of grave disease of the 
lung. 
Pleurisy with profuse serofibrinous exudation sets in quite often, 
with violent general phenomena, and severe symptoms of local disease, 
in a manner very like the commencement of pneumonia. The malady 
begins acutely, and runs an acute course. Ushered in by a severe 
rigor, it is followed by intense fever, with the full and frequent pulse, 
the headache, and pain in the back and limbs, the coated tongue, and 
the parching thirst, which we see in almost all violent inflammatory 
diseases. There may, however, be more than one chill, and there are 
often several, the succession of which may take on so well-marked a 
tertian type, that it is quite possible to mistake an incipient pleurisy 
for an intermitting fever. A sharp pain, usually referred to the side 
of the chest, is also felt at the beginning of this variety of pleurisy, 
into which the form last described often passes, the exudation becom- 
ing more copious and richer in serum. As the disease advances, the 
pain abates somewhat, and often ceases altogether, before the pleurisy 
has attained its climax, or, especially before the effusion is complete. 
The cough, which scarcely ever fails, and which is often extremely 
distressing and persistent, is sometimes plainly attributable to the col- 
lateral hyperaemia, and collateral oedema of the uncompressed part of 
the lung. At other times its source is obscure. Besides these symp- 
toms, there is dyspnoea, which becomes aggravated as the effusion 
increases, and which often becomes extremely severe. It is important 
to bear in mind the fact that a part only of the dyspnoea is caused by 
pressure of the effusion upon a portion of the lung, and that the col- 
lateral hyperaemia and oedema arising in the uncompressed portion, and 
by which the breathing surface of the latter is materially diminished, 
play an important part in the production of dyspnoea. At all events, 
even where the effusion is very large, the difficulty of breathing dimin- 
ishes, and often ceases altogether, just as it does in croupous pneumo- 
nia, as soon as the fever abates, and with it the need of additional 
oxygen. 
After increasing in intensity for six or eight days, a sudden im- 
provement may take place, just as in croupous pneumonia, the general 
disturbance and dyspnoea undergoing a marked decrease, or even ceas- 260 
DISEASES OF THE PLEURA. 
ing totally within a few hours. This depends upon a rapid abatement 
of the fever. In fortunate cases the reabsorption of the effusion also 
begins immediately and progresses rapidly. As already stated, the 
absorption goes on most rapidly at the outset, and, as the volume of 
the liquid decreases, and its concentration becomes greater, absorption 
grows slower and slower, so that, even weeks after the patient has 
apparently entirely recovered, a remnant of the exudation can still be 
found. 
Next to these cases, which are acute from beginning to end, come 
those which, being acute at the outset, afterward take on a slow and 
tedious character. The fever moderates at the end of the first week, 
or a little later. The exudation makes no further progress; but we 
wait in vain for a complete subsidence of the febrile general disturb- 
ance, and for absorption. At last the exudation begins to diminish; 
the air once more enters the compressed parts of the lung; but, in the 
midst of this apparently favorable prospect, we again one day find the 
patient short of breath, coughing hard, anew spitting bloody froth. 
The fever, too, has grown worse; and, if we now examine the chest, 
we find that the effusion has increased by a hand’s breadth, and ex- 
tends higher than ever. In this way the disease, originally acute, 
drags on with fluctuating symptoms for months, and, as a rule, termi- 
nates fatally. 
Thirdly and lastly, there are a great many patients in whom this 
form of pleuritis develops slowly, and often without attracting atten- 
tion, its subsequent progress being of an equally tedious character. 
There is no inflammatory fever, and often no pain, at least none of 
that severe pain which ushers in all varieties of the disease hitherto 
described. Not unfrequently the comparatively slight shortness of 
breath under which the patient labors escapes the notice of the patient 
himself, and he only seeks assistance of a physician because he “ for 
some time past has become aware of a falling off in strength, and of 
having become pale and thin ; ” or he pbrliaps may think that he has 
some chronic disease of the abdomen, the more so as, in pleurisy of 
the right side, the depressed position of the liver may cause the right 
liypochondrium to bulge, and create tension in that region. Every 
physician in good practice must have seen cases of this kind, in which 
the patient has never been confined to the house, where he is unable 
precisely to fix the date of the commencement of his attack, and in 
which physical examination demonstrates the existence of enormous 
quantities of effusion in the pleural cavity. The extreme prostration 
and debility of these patients are easy of explanation, when we con- 
sider tha tthey are seldom free from fever, and that their pleura? are 
filled up by an exceedingly albuminous effusion, which may amount to INFLAMMATION OF THE PLEURA. 
261 
a weight of twelve or fifteen pounds. Such an effusion, under the most 
favorable circumstances, would only be very slowly reabsorbed ; but it 
is very apt, as before said, alternately to decrease and to be repro- 
duced, and finally, as we shall see, it terminates in most cases in con- 
sumption of the lung. 
Pleuritis with purulent exudation, empyema, pyothorax, when 
it occurs by the gradual multiplication of young cells (which are never 
entirely absent in any case, in effusions of the form already described), 
can hardly be diagnosticated otherwise than by the long duration of 
the disease. The symptoms of compression, etc., are just the same as 
in effusions containing little pus. As already mentioned, pleuritic 
effusions often form during septicaemia and other diseases arising from 
blood-poisoning, in which an abundant cell-formation takes place from 
the commencement. However, it is not on account of its insidious 
attack, but owing to the serious implication of the system and to the 
blunted condition of the sensorium, that patients frequently make no 
complaint whatever, so that all subjective symptoms are wanting, and 
we must rely upon the objective ones. 
With regard to the termination of pleurisy, all forms of the disease 
may end in recovery. Adhesions of the pleural surfaces, which always 
or nearly always remain, are hardly to be regarded as rendering the 
recovery incomplete, as patients may attain a very great age without 
suffering any serious inconvenience on this account. It has already 
been mentioned that the reabsorption of large effusions, even if rapid 
at first, is apt to be extremely tedious toward the last. We must be 
careful of diagnosticating a diminution of the exudation in all cases 
where the line of dulness sinks in the chest. A decrease of the dul- 
ness may also be due to the fact that the thoracic wall and intercostal 
muscles have become more yielding, or that the diaphragm has become 
relaxed and forced farther downward. These facts must always be 
borne in mind in judging of the condition of the patient. An obstinate 
exudation, which is very hard of reabsorption, should not be despaired 
of too soon, as its absorption may at last take place after we have 
given up all hopes of such an event. 
When the compressed lung, either being enclosed in a firm fibrin- 
ous sheath, or its alveoli being occluded or adherent, is no longer able 
to admit air and to expand, and when the thorax collapses, the neigh- 
boring organs being employed to fill up the vacancy arising from 
absorption of the effused liquid, the pleurisy must be regarded as ter- 
minating in incomplete recovery. In persons thus affected, if other- 
wise in good health, the remaining portions of the lung can always 
oxygenate the blood sufficiently, and eliminate the carbonic acid, as 
long as the patient abstains from an overactive bodily exertion; and, 262 
DISEASES OF THE PLEURA. 
notwithstanding that a part of the pulmonary capillaries has perished, 
the right side of the heart, which is then always somewhat hypertro- 
phied and dilated, is still capable of so accelerating the current of the 
blood in the sound parts of the lung as to avert derangement of the 
circulation. 
When an empyema “ points ” or opens externally, an cedematous 
swelling of the integument makes its appearance, not, however, at the 
most dependent part of the chest, but generally in the neighborhood 
of the fourth or fifth rib. Soon a hard, firm tumor protrudes through 
the intercostal space, which, after a time, begins to show fluctuation, 
and finally discharges a large amount of pus. This termination very 
rarely results in complete recovery, and in reinflation of the lung and 
reoccupation of the space restored by discharge of the pus. It is 
much more common in such cases for the thorax to collapse, and for 
secondary displacements of the organs to occur. Still more commonly 
there remains an imperfect closure of the thoracic opening (after point- 
ing of an empyema), and a thoracic fistula forms, from which pus con- 
stantly flows, either in a continuous stream or in occasional profuse 
gushes. A patient with such a fistula may live for many years. 
When empyema points inwardly, that is to say, into- the lung, the 
perforation is sometimes preceded by the symptoms of a slight pneu- 
monia, bloody sputa, a renewal of the stitch in the side, etc. At other 
times it takes place without warning, the patient suddenly discharg- 
ing an enormous amount of purulent sputa after a violent fit of cough- 
ing. Here, too, in very rare instances, recovery with or -without retrac- 
tion of the thorax may ensue, but symptoms of suffocation, or of pyo- 
pneumothorax, are the more usual result (see Chapter III.). 
Perforation of empyema through the diaphragm, or into neighbor- 
ing organs, produces violent peritonitis. 
A fatal result in recent pleurisy generally arises from collateral hy- 
persemia, leading to intense oedema in the healthy portions of the lung. 
Rattling sounds, frothy and often bloody sputa, and great dyspnoea 
arise; carbonic-acid poisoning follows; the sensorium becomes be- 
numbed, the action of the heart is weakened, the pulse grows small, 
the extremities cool, and the sufferer soon expires. 
In other cases, compression of the lung and its capillaries gives rise 
to incomplete filling of the left ventricle, and to engorgement and ob- 
struction of the right ventricle and the veins of the aortic system. 
Bartels points out that, in displacement of the heart to the right, the 
vena cava suffers flexure at its point of emergence from the foramen 
quadrilaterum of the diaphragm, causing disturbance of the circulation. 
This imperfect filling of the aortic system frequently gives rise, not 
only to a small pulse, but to an excessive diminution and concentration. INFLAMMATION OF THE PLEURA. 
263 
of the urine (Traube). Distention of the veins leads to cyanosis and 
dropsy. Finally, owing to obstruction to the outflow' from the renal 
veins, albumen, blood, and fibrinous cylinders frequently appear in the 
urine. 
In other cases death ensues in consequence of bursting of empy- 
ema into the lungs, abdomen, etc. Death results still more frequently 
in unabsorbed effusions, in consequence of persistent, although mod- 
erate, fever, which consumes the organism, and which, therefore, is 
called hectic. 
Finally, and, indeed, most commonly of all, tedious or imperfect ab- 
sorption of empyema results in tuberculosis, or in chronic destructive 
pneumonia, the patient succumbing to the symptoms of consumption. 
Physical Signs op Pleurisy.— When the exudation is scanty, 
forming a thin membranous coating upon the pleural surfaces, or when 
it is liquid, and sinks to the more dependent part of the pleural sac, 
■without, however, materially encroaching upon its space, the results 
of inspection usually are negative. It is only when respiration is ex- 
tremely painful that we can perceive that the patients spare the af- 
fected side, and that its respiratory motion is not as free as upon the 
other side. 
When the pleuritic effusion is large, inspection reveals a series of 
appearances, depending upon the fact that the inner surface of the 
chest is no longer affected by the traction of the elastic lung (as it 
should be), but is exposed to the pressure of the exudation. 
1. The intercostal spaces over the area of the effusion are no longer 
shallow grooves, but are upon a level with the ribs, “ they are effaced,” 
and, indeed, are sometimes somewhat prominent. 
2. Where the effusion fills up the entire pleura, the affected half 
of the chest appears enlarged in all directions, but chiefly in the’line 
of the vertebro-mammillary diameter. When the effusion is not so 
large, when it is usually incapsulated in the posterior and lower re- 
gions of the pleural sac, dilatation of the thorax is limited to the region 
which contains the effusion. Very much more rarely, incapsulated exu- 
dations in the pleura produce prominence of some other portion of the 
thoracic wall. 
3. In effusion of the left side, displacements of the heart can often 
be made out by inspection alone, and it is the same with displacement 
Df the liver when the effusion is upon the right side; in the former 
case the impulse of the heart being too low, and too much toward the 
median line (sometimes, indeed, being perceptible to the right of the 
sternum); in the latter, the right hypochondriac region shows an un- 
natural prominence. Besides this evidence of presshre from within, 
exerted by the effusion upon the surrounding parts, inspection shows 264 
DISEASES OF THE PLEURA. 
that, as far as the effusion reaches, the thoracic wall does not take pari 
in the respiratory movement. This is, in some degree, owing to in- 
filtration and palsy of the intercostal muscles from collateral fluxion, 
and partly because the dilatation of the chest is physically impossible 
when the lung cannot expand. If the diaphragm be so much de- 
pressed as to form a projection into the abdomen, and if its muscles 
be not paralyzed, the contraction of the organ, with every inspiratory 
act, tends to flatten the convexity, which now, of course, is on its lower 
surface, so that, in these very rare instances, the epigastrium, instead 
of rising, sinks, during inspiration, upon the side where the effusion is 
situated. 
If, as absorption of a pleuritic effusion progresses, the compressed 
lung again undergoes perfect expansion, there generally remains no 
sign of the disease which has just passed away. When the absorption 
is complete, the intercostal spaces again form shallow furrows, being 
once more exposed to the elastic traction of the lung. The dilatation 
of the thorax is corrected, the derangement of the respiratory move- 
ments has ceased, and the dislocated heart and liver have returned to 
their proper situations. Sometimes, however, after perfect absorption 
of the effusion, the heart, having become fixed by adhesions, remains 
out of place. If, however, the lung do not expand as the effusion be- 
comes absorbed, all the dimensions of the chest seem to undergo reduc- 
tion, and, more especially, its length and antero-posterior diameter, 
the ribs coming close together, and even overlying one another. The 
more the thorax loses its rounded form, and the more it becomes flat- 
tened, so much the more is its capacity diminished, even although its 
circumference remain the same. Hence, in cases where absorption of 
the exudation has commenced, if we wish to watch the progress of the 
reabsorption, and of the restoration of the lung, it is urgently recom- 
mended not only, from time to time, to measure the two halves of the 
chest, but to ascertain the length of the two vertebro-mammillary diam- 
eters by means of the callipers, and to compare the results of the two 
measurements. A still surer method is to draw accurate ideal sec- 
tions of the two halves of the thorax, by means of the Kyrtometer of 
TVoillez, which can be laid one upon the other and accurately compared 
at leisure. The more the ribs of the affected side are pressed together, 
so much the lower will the shoulder of that side descend, and so much 
the greater is the curvature of the spine. The collapse of one half of 
the chest, the depression of the shoulder, and the lateral curvature of 
the spinal column, the convexity of which is toward the sound side, 
are often so great as seriously to deform the patient, who is said to 
be “ grown out of shape.” 
Finally, in cases where the lung has not reexpanded after absorp- INFLAMMATION OF THE PLEURA. 
265 
tion of the effusion, inspection will often show that the heart beats fin 
to the left, and even as far as the axillary line. The cause of this is 
that the heart, which at first was pushed to the right by the pleuritic 
effusion, upon reabsorption of the latter, is now drawn as far into the 
left pleural cavity, in order to fill up the vacant space caused by the 
disappearance of the liquid. 
We may finally observe that the restoration of the normal dimen- 
sions of the chest, and even the secondary contraction of a chest pre- 
viously distended by effusion, is not, by itself, a sufficient proof of the 
complete absorption of the exudation. A compressed lung occupies 
very little space, and, even after the pleural cavity has been greatly 
reduced in size, there is always room for a considerable quantity of 
liquid effusion. Upon palpation, a sensation of friction is perceptible 
in a large number of cases of pleurisy. The characteristics and pecu- 
liarities which distinguish this sensation from other sensible signs, as 
well as the conditions under which it arises, will be discussed while 
treating of the auscultatory phenomena. 
Palpation, moreover, often furnishes important diagnostic signs of 
pleurisy with profuse effusion, from the peculiar character which the 
vocal fremitus exhibits in cases of pleuritic exudation. In general 
terms, it may be asserted that the pectoral fremitus is much weakened, 
or entirely suspended, wherever a liquid pleuritic effusion is in contact 
with the thoracic wall; but, above the limit of the effusion, where the 
compressed lung touches the side of the chest, the fremitus is intensi- 
fied. It is quite manifest that a profuse liquid effusion will impede 
the conduction of sound-waves to the thoracic wall, and that it will 
also act as a powerful damper upon the vibrations of the latter, and it 
is equally plain that the retracted pulmonary tissue forms a better con- 
ductor for the passage of the vibrations to the chest-wall, and disturbs 
them less, than does the normal unretracted lung. As, under normal 
conditions, the vocal resonance is more plainly felt upon the right side 
of the chest than upon the left, feebleness or absence of pectoral fre- 
mitus upon the right side is of greater diagnostic importance than the 
occurrence of the same symptom upon the left side. In the anterior 
and lateral regions of the chest, the abrupt transition from absence to 
exaggeration of the fremitus is a valuable means of determining the 
limit of the exudation. Posteriorly, however, the signs change in a 
more gradual manner. According to some very accurate observations 
of Seitz, when the exudation is slight, the fremitus is only more or less 
weakened; when it is extensive, the fremitus is lost over the lower 
portion, but over the upper it is merely lessened, and even this dimi- 
nution decreases gradually toward the level of the liquid. When the 
patient has a weak, high-pitched voice, whose wave-sounds hardly 266 
DISEASES OF THE PLEURA. 
reach the thoracic Avail under any circumstances, Ave lack an important 
aid to the diagnosis of pleuritic effusion. 
Finally, palpation is of use in ascertaining the existence of the 
displacements of the heart and liver, alluded to in speaking of inspeo 
tion, and Avhich result from the effusion and its subsequent reabsorp 
tion. In cases of copious exudation into the right pleura, the edge of 
the liver may often be felt several fingers’ breadth beloAV the border 
of the ribs, or even loAver. 
Percussion affords no information of the presence of exudation 
when it is scanty and lies upon the pleura in the form of a thin, coagu- 
lated coating. On the other hand, large effusions, by Avhich a consid- 
erable part of the lung is separated from the diaphragm and thoracic 
wall, furnish very characteristic signs upon percussion: 1. Over the 
region where the bulk of the liquid effusion lies in contact with the 
side of the chest, all vibration is checked, and the percussion-sound is 
dull. 2. Over the space into which the retracted lung (which, how- 
ever, may still contain air) touches the thoracic Avail, percussion is 
holloAV and tympanitic. The conditions under which the dull, liolloAV, 
and tympanitic sounds arise have already been fully and repeatedly 
explained. No disease is better adapted for the demonstration of the 
difference between the dull and the liolloAV percussion-sounds than 
pleurisy AA'ith copious effusion. The dulness proceeding from pleuritic 
effusion generally first becomes perceptible in the region of the back 
and below the scapulas. As it ascends it spreads toAvard the front. 
The dulness scarcely e\Ter extends as far upAvard in front as it does 
behind. In many cases the dulness Avhich reaches far up the back is 
not found at all over the breast, but only reaches as far as the axillary 
line. At other times, AA'hen nearly the whole pleural sac is occupied 
by the effusion, the upper boundary of the dull sound is but little 
loAver in front than behind. Anteriorly, the dull percussion-sound 
changes abruptly to the empty tympanitic sound; posteriorly, as the 
upper limit of the effusion is approached, the dulness gradually be- 
comes fainter and less distinct. The reason for this is, that the 
thickness of the body of effusion upon which the dull sound depends 
gradually diminishes from beloAV upAvard. The form and boundaries 
of the dulness are not generally altered by changing the attitude of 
the patient, as agglutination and' adhesions soon form about the effu- 
sion, which, although they still alloAV the pleural surfaces to slide upon 
each other, oppose their separation by the pressure of the exudation. 
Upon auscultation, friction-sounds are heard whenever the sur- 
faces of the pleura lose their smoothness through fibrinous deposit or 
the growth of rugged vegetations; but of course these sounds are 
only audible Avhen the roughened surfaces are in contact, and Avhen INFLAMMATION OF THE PLEUKA. 
267 
the respiratory movement causes them to rub together with a certain 
degree of rapidity. They are usually perceptible both upon inspira- 
tion and expiration, and give a distinct impression of scraping or of 
scratching, calling to mind the creaking of new leather, and there are 
often little jarring interruptions. It is most liable to be mistaken for 
a buzzing rhonchus, which is likewise often perceptible to the touch. 
A friction-sound, however, is scarcely ever as loud as a rhonchus, and, 
besides, is not altered by coughing; whereas a rhonchus almost 
always ceases after a vigorous cough, or, at all events, undergoes a 
change. It is also somewhat characteristic of a friction-sound, that it 
is heard more distinctly when the stethoscope is pressed rather firmly 
against the chest. This sound is rarely heard in the beginning of the 
disease, as the fibrinous deposit is not rough enough at first, and the 
patients, while they continue to suffer pain, breathe cautiously, so that 
the pleural surfaces do not rub together with sufficient quickness. 
The time at which it is audible most frequently is when the exu- 
dation begins to be reabsorbed, when the faces of the pleura, which 
previously were separated by the serum, now once more come into 
contact. They also become audible after evacuation of the liquid by 
tapping. 
When the exudation is not very large, faint vesicular breathing, 
transmitted by the surrounding parts, can be heard over the whole 
region of dulness. When the effusion is very profuse, and when not 
only the air-cells but the bronchi are compressed by it, no respiratory 
murmur whatever is heard over the dull region, or, at the utmost, the 
sound is very faint and indistinct. It is only between the scapulas and 
the spinal column, where the compressed lung lies close to the thoracic 
wall, that we can hear a feeble bronchial respiration and a faint bron- 
chophony, the latter sometimes having a bleating tone, known as 
cegophony. In a few instances, where there is severe dyspnoea, in 
spite of the compression of the lung, and although we are obliged to 
suppose that the greater part of the bronchi are compressed and do 
not contain air, loud bronchial breathing is heard over the whole chest, 
even at points where there is a large mass of liquid between the ear 
and the lung, that is to say, at the sides of the thorax. Over the un- 
compressed lung, both upon the diseased and healthy sides, the respi- 
ration is loud and puerile, unless it be the seat of collateral hypersemia 
and catarrh, when rhonchi and rdles are to be heard. 
Of course, the physical signs of pleuritis are greatly modified when- 
ever old adhesions of the pleura prevent the exudation from collecting 
in the most dependent part of the chest. It would lead us too far to 
detail all these modifications, and we shall merely state that incapsu- 
lated effusion of very considerable magnitude may form between the 268 
DISEASES OF THE PLEURA. 
diaphragm and the base of the lungs, and be very difficult of recog- 
nition, and often remain quite unrecognizable. 
Diagnosis.—It is not always easy to distinguish a pleuritis with 
abundant exudation from a pneumonia, and the following are the chief 
points upon which we may rely for the purpose : 1. Pleurisy scarcely 
ever begins with a single violent chill, while in pneumonia this is the 
rule. 2. The course of a pleurisy is never so cyclic, nor is there that 
sudden and complete change for the better, or crisis, which we observe 
in pneumonia. 3. In pleurisy the sputa are indicative of catarrh or of 
oedema, and sometimes contain streaks of blood; but there never is 
that peculiar tough expectoration, stained yellow or yellowish-red, by 
intimate admixture of blood, which is pathognomonic of pneumonia. 
4. The principal physical signs indicative of pleuritic exudation are, 
dilatation of the thorax, effacement of the intercostal furrows, displace- 
ment of the heart and liver, faintness or absence of pectoral fremitus, 
absolute dulness upon percussion, feebleness or absence of the respi- 
ratory murmur; whereas, in pneumonic infiltration, the chest is not 
enlarged, the intercostal spaces are not effaced, the heart and liver 
retain their situation, the pectoral fremitus is seldom enfeebled, and, 
indeed, is often intensified, the dulness upon percussion is not so abso- 
lute, and the respiratory murmur is almost always bronchial. 
Patients having pleuritic effusions in their right side are not unfre- 
quently supposed to have disease of the liver, and when we have ascer- 
tained by palpation that the liver reaches below the border of the ribs, 
and fills up the right hypochondrium, it is important that we should 
be able to tell -whether the organ is enlarged or merely depressed. 
The following are the points of distinction between the two con- 
ditions : 1. The liver rarely pushes the diaphragm upward ; hence, 
when the liver extends below the border of the ribs, and we at the 
same time find a dulness in the thorax which reaches farther upward 
than the normal hepatic dulness should do, we may reasonably infer 
that there is an effusion in the pleura and that the liver is pressed 
downward. 2. In the very rare instances in which, through enlarge- 
ment of the liver (usually from an abscess, or a cyst of echinococcus), 
the diaphragm is abnormally pressed upward, and made to project 
into the cavity of the thorax, the dulness reaches farther up in the 
front of the chest, while in nearly every case of pleuritic effusion the 
opposite condition obtains. 3. When the liver is enlarged, its lower 
border, and with it the line of percussive dulness, moves downward 
upon inspiration and upward upon expiration. This does not take 
place when there is large effusion in the pleural sac, as the diaphragm 
is then depressed, and kept in a state of permanent expiratory exten- 
sion. 4. The transition from the feeling of resistance, presented by the INFLAMMATION OF THE FLEUR A. 
269 
thoracic wall, to that produced by the enlarged liver, is immediate; 
whereas a small yielding interval is usually discoverable between the 
border of the ribs and the surface of a liver which has been displaced 
downward. 5. In enlargement of the liver, the lower ribs not unfre- 
quently are somewhat bowed outward, the intercostal spaces, how- 
ever, still remaining uneffaced, excepting in the rare instances in which 
a huge cyst of echinococci, or an abscess of the liver projecting far into 
the thoracic cavity, lies in contact with the side of the chest. 
The main point of distinction between a small pleuritic effusion of 
the left side and an enlarged spleen consists in the change which 
takes place in the line of dulness during respiration, and which does 
not occur in pleurisy, but is easily perceptible in enlargement of the 
spleen. 
Finally, the persistence of the fever, the emaciation and pallor of 
the patient, may awaken the suspicion that phthisis is developing. It 
should not be forgotten that both fever and wasting may be solely 
dependent upon a latent pleurisy, but the threatening phantom of in- 
cipient consumption should always be kept in view, and physical ex- 
ploration of the thorax should be repeated again and again. 
Prognosis.—Dry pleurisy is an altogether insignificant affection, 
nor does pleurisy with scanty sero-fibrinous effusion, of itself, ever 
cause danger, although the pain which attends it, being a main cause 
of the dyspnoea, augments the danger from the pneumonia or tubercu- 
losis, or whatever the primary disease may be. Among the varieties 
of pleurisy with profuse sero-fibrinous effusion, that which runs an 
acute course from the outset admits of the most favorable prognosis. 
"YVhen the malady is of a creeping, insidious type, the prospect is 
much more grave, as, even after complete absorption, tuberculosis fre- 
quently appears as a sequel. This is also true of empyema when it 
develops from the foregoing variety, while the effusions which are 
purulent from the commencement involve a bad prognosis, from the 
nature of the diseases which give rise to them, namely, septicaemia, 
puerperal fever, etc. 
Decrease of the effusion is to be regarded as a favorable sign, in 
the diagnosis of which, however, we must beware of the sources of 
error already alluded to. As there is more or less danger from con- 
sumption in the majority of cases, it is to be regarded as of favorable 
augury when the patient possesses a vigorous constitution. Finally, 
the earlier reabsorption commences, so much the more reason have we 
to hope that the lung may expand again, so that no deformity of the 
thorax may remain behind. 
Symptoms of oedema of the lung and imperfect decarbonization of 
the blood at the commencement of the disease are to be viewed as un- 270 
DISEASES OF TIIE PLEURA. 
favorable prognostic signs; as is also a diminution in the amount of 
urine secreted, which indicates that the arteries are incompletely filled 
Still worse are the symptoms of over-distention of the veins, with cya- 
nosis, dropsy, and the appearance of albumen, casts, and blood in the 
urine. The longer the effusion lasts, the more persistent the fever 
which accompanies it, the greater the wasting of the patient, so much 
the worse should our predictions be. Finally, all sequelae, other than 
that of reabsorption, must be considered as prognostically unfavorable, 
although, as shown above, the danger may vary in degree. 
Treatment.—The causal indications can no more be met in treat- 
ment of pleurisy than they can in treating pneumonia. In fact, even 
if we were aware that an attack of pleurisy were caused by “ catching 
cold,” if the fever wTere at all intense, a treatment by diaphoresis would 
be absolutely injurious. 
Indicatio morbi.—The “antiphlogistic system,” with its general 
and local blood-letting, its exhibition of calomel, and inunction of mer- 
curial ointment until salivation is produced, and its subsequent deriva- 
tion by blistering, etc., which formerly used to be the general practice 
in the treatment of pleurisy, but which, in the last ten years, has grad- 
ually fallen into discredit, recently has again been urgently recom- 
mended by Joseph Meyer, in a work which gives evidence of great in- 
dustry. The arguments of this author in favor of the former method 
of treatment, and against the less active modes of procedure, are, how- 
ever, based upon a very slender foundation. Thus great weight is laid 
upon the fact that a certain number of patients, with large pleuritic 
exudations, have been received into the Berlin Charity Hospital, who 
have not been bled, and who have never taken any mercury ; and it 
is inferred that the profuseness of the effusion is a consequence of 
a neglect of active treatment. The enumeration of such cases as 
these proves nothing, unless the number of cases who were not 
bled, and yet who did not have large effusions, and who therefore 
did not seek admission at the Charity, be also given. But even 
the somewhat limited number of cases observed by Myer and 
others, in which recent cases of pleurisy, being treated by copious 
blood-letting, did not result in effusion, have not converted me. The 
assertion that pleurisy which is ushered in and accompanied by very 
acute symptoms, if left to itself, almost always terminates in profuse 
effusion difficult of reabsorption, I consider as quite erroneous. In- 
deed, the greatest danger in this respect is to be apprehended from 
the pleurisies which come on in a manner almost imperceptible, and 
whose duration is extremely tedious. 
1 still believe that venesection can be dispensed with in the treat- 
ment of pleurisy, with exception of a few rare cases, where certain INFLAMMATION OF THE FLEURA. 
271 
symptoms demand it. I am convinced that it neither cuts short the 
malady, nor prevents the effusion; and, as this disease, owing to its 
tedious course, is always liable to lead to deterioration of the blood, 
and to consumption, I regard the practice of bleeding as still more dan- 
gerous in pleurisy than in pneumonia. 
At the commencement of an attack of pleurisy, however, I cannot 
sufficiently recommend the use of cold and of local blood-letting. It is 
highly essential that the proper moment for employing this impor- 
tant treatment should not be neglected, as much evil may then be pre- 
vented, which, at an after-period, is difficult to repair. When the pa- 
tients dread the application of cold compresses, or if the latter do not 
relieve the pain and dyspnoea in an hour or two, a tolerably large num- 
ber of leeches, or cut-cups, should be applied; and, if the pain, which 
is almost always relieved by the depletion, recurs in the course of a 
day or two, we should not hesitate to repeat the local blood-letting 
until the relief becomes permanent. 
Besides this, and for want of remedies of more certain action, half 
a drachm of mercurial ointment may be rubbed into the affected side 
of the chest twice daily, but the inunction must be at once suspended 
the moment that signs of mercurial sore mouth appear. As a decided 
benefit is sometimes obtained from the inunction of mercurial ointment 
in inflammation of other serous membranes, particularly inflammation 
of the articular capsules, its efficacy should always be tested in cases 
of recent pleurisy, although its action is then far less easy to observe. 
Having convinced myself, from my own observation and from the 
cases reported in the work of Meyer above alluded to, that the fever 
is not materially aggravated by the use of blisters, I now retract my 
former advice not to resort to vesication while fever lasts. Indeed, the 
application of large vesicatories seems to be of service in certain cases, 
but, when used at all, they must be used early. 
In protracted cases, large hot poultices, which, however, must not 
be too heavy, do good service. 
Internal medication, save when called for by special symptoms, is 
unnecessary in treatment of pleurisy. The antiphlogistic action of 
nitrate of potash, of tartar emetic, and of calomel, I regard as highly 
problematic ; and, moreover, the exhibition of calomel is not without 
its dangers, as it tends to augment the impoverishment of the blood, 
and the tendency to exhaustion which already exists. 
Indicatio Symptomatica.—Antipyretic treatment is always proper 
when the fever is very high at the commencement of the attack, or 
when it is so persistent that there is reason to fear that it will exhaust 
the patient. With this object in view, the very customary use of 
digitalis is to be recommended in certain cases. It does not affect the 272 
DISEASES OF THE PLEURA. 
primary disease at all. In recent cases, where the fever is high, I 
•usually give digitalis in the form of infusion (3 ss to § vj); in tedious 
cases, where the fever is of a more latent character, I give it in sub- 
stance (gr. j for a dose, usually combined with equal parts of quinine). 
Dyspnoea, when it arises from collateral hyperaemia of the uncom- 
pressed parts of the lung, especially when signs of commencing collat- 
eral oedema already exist, imperatively demands venesection. Under 
such circumstances I have often ordered three or four successive bleed- 
ings, and as I did not bleed to cure the pleurisy, but on account of the 
danger arising from the hyperaemia, I have not laid myself open to the 
charge of inconsistency. 
It is far more rare for cyanosis, dropsy, and other symptoms of 
venous engorgement of the aortic system depending upon disturbance 
of the pulmonary circulation, to require venesection. 
Especial attention is to be paid to the deterioration of the blood, 
which often becomes apparent at an early period, owing to the volume 
of the effusion, and to the wasting induced by the fever. There should 
be no hesitation about administration of the ferruginous preparations, 
and of a nourishing diet. The old prejudice, that iron causes conges- 
tion, is entirely void of foundation. 
Remedies for the promoting of reabsorption of the effusion deserve 
little reliance. It is, indeed, questionable whether it be possible, by 
any therapeutic means, to bring about the conditions upon which the 
absorption of pleuritic effusion depends. If, after the inflammatory 
symptoms have subsided, the effusion remain undiminished, all medi- 
cation, both external and internal, is to be rejected, and the applica- 
tion of blisters is of very doubtful use. The fact that pleuritic or other 
pathological effusion has been rapidly absorbed during an attack of 
cholera, when the blood had become thickened by loss of its water, 
makes it seem rational to attempt to reduce the water of the blood by 
the administration of diuretics and drastics, in order to promote ab- 
sorption of the effusion. Unfortunately, the action of the diuretics, of 
which bitartrate of potash, boracic cream of tartar, and the juniper- 
berry are the best, is very uncertain, so that we cannot promise our- 
selves much from their use, and the pernicious effect of the drastics 
upon digestion and assimilation forms a serious objection to their em- 
ployment. In one case, which I did not treat myself, but which I 
watched with attention, a pleuritic effusion, which had withstood all 
efforts to remove it, diminished rapidly under what is known as 
Schrot/i’s treatment; the physician in charge, conceiving the idea of 
producing inspissation of the blood by diminishing the supply of water 
coming to it, instead of attempting to abstract the water from it, fed 
the patient upon the driest possible diet, and almost entirely deprived HYDRO THORAX. 
273 
him of drink. I have seen other cases, where this treatment failed, as, 
contrary to all reason, the patient was allowed a copious supply of 
wine on certain days. An attempt may also be made to excite reab- 
sorption by the outward and inward administration of iodine, which 
has a well-known reputation as an absorbent. I have seen such re- 
markably rapid absorption take place under the internal use of syrup 
ferri iodidi ( 3 ij) with syrup simplic. ( 3 ij), a teaspoonful being taken 
every two hours, in conjunction with the external application of a 
weak compound solution of iodine (iodini. 3 ss, potass, iodid. 3 ij, aquse 
destil. | ij), upon the affected side of the chest, that I cannot help re- 
garding the beneficial action of this prescription as probable, although 
I do not regard it as proved. 
Considering our slender ability to excite or even to hasten reab- 
sorption of pleuritic effusions by means of internal medication, the dis- 
covery that their evacuation by surgical means is attended by much 
less danger than was formerly supposed, and the frequent and early 
practice of such operations in cases of pleurisy with effusion, must be 
considered an important advance in therapeutics. Every additional 
day, during which the lung is exposed to pressure, and time is allowed 
for cells to multiply in the exudation, the chances of complete recovery 
diminish, and the danger of a fatal termination increase. It is to 
be hoped that the experience of Kussmaul, Bartels, and Ziemssen, 
will promote the introduction of paracentesis thoracis, both in cases 
of empyema and of serofibrinous effusion. Indications for the proced- 
ure of tapping and its various details are given in the hand-books 
of surgery. 
CHAPTER II. 
Etiology.—Hydrothorax is not the result of an exudation, but of 
a dropsical transudation into the pleural sac. In most instances its 
source is easily traceable to one or other of the well-known condi- 
tions under which pathological transudations arise, namely, increase of 
the lateral pressure within the veins, and decrease in the amount of 
albumen in the serum of the blood, the so-called dropsical crasis. 
“Water on the chest,” which, to the minds of the laity, is one of 
the most formidable of maladies, in which view the older pathologists 
participated, is never an independent and primary affection, but is 
always secondary, being the result of some morbid process, which has 
given rise to the conditions necessary for the production of a patho- 
logical transudation. Hydrothorax, therefore, no more deserves the 
name of a disease than does dropsy of the subcutaneous tissue, or 
dropsical effusions into other large cavities of the body. It is merely 
HYDROTIIORAX. 274 
DISEASES OF THE FLEURA. 
as a matter of convenience, and in compliance with ancient custom, 
that I have included it in the list of disorders of the pleura. 
Hydrothorax, caused by augmented pressure within the veins of 
the pleura, is one of the more formidable accidents occurring in diseases 
of the lung which (as we have shown in a previous chapter) obstruct 
the action of the right side of the heart, and produce venous engorge- 
ment of the aortic circulation. It occurs with equal frequence in cer- 
tain diseases of the heart, namely, derangement of its valves and 
degeneration of its muscular substance, which, as we shall show by- 
and-by, also impede the outflow of the blood from the right side of the 
heart, and from the veins of the aortic system. 
Hydrothorax, dependent upon diminution of the amount of albu- 
men in the serum of the blood, whose pathogeny is somewhat obscure, 
as we shall show while treating of Bright’s disease, is one of the ac- 
companiments of grave cachectic conditions, and especially of inflam- 
mations occurring in chronic degeneration of the kidney with albumi- 
nuria, in malignant malarious disease, and in dysentery of long standing. 
Whether hydrothorax be a consequence of venous engorgement, 
or of a morbid state of the blood, it is usually but one of the symptoms 
of a general dropsy. When arising from the former condition, it 
sometimes precedes the effusion into other cavities, whereas it almost 
always appears at a late period when due to the latter. 
Anatomical Appearances.—Hydrothorax is almost always dou- 
ble, but one pleura sometimes contains more liquid than the other. 
Its amount varies from a few ounces to many pounds. It usually is 
movable, but is sometimes incapsulated by old adhesions. The trans- 
udation contained in the pleura is a clear, yellowish liquid, consisting 
of water, albumen, and the salts of the serum of the blood. It is easily 
distinguishable from a pleuritic effusion, by the absence of the fibrinous 
coagula and inflammatory changes in the pleural surfaces. The latter 
have lost their polished appearance, and have a milky opacity, and 
both they and the subserous tissue are slightly swollen by serous infil- 
tration. When the effusion is very large, the lungs, unless they are 
held down by old adhesions, are driven up against the spinal column, 
large portions of them being in a state of compression. 
Symptoms and Course.—From the most ancient times down to 
the beginning of the present century, the symptoms and course of 
water on the chest, as an independent disease, have not only been 
described with great fulness and accuracy, but, in many instances, the 
diagnosis has been confirmed by post-mortem dissection. Tliis was be- 
cause the symptoms ascribed to the disease by the ancients apply to 
the class of affections of the lungs and heart which ultimately results 
in dropsical transudations of all kinds, and in effusions into the pleura, HYDROTHORAX. 
275 
among others. There is no doubt that emphysema, a disease which 
formerly must have been as common as it is now, but the existence of 
which was entirely unknown and overlooked, post mortem, until the 
days of laennee, was generally supposed to be a dropsy of the chest, 
and was described as such. 
In the present state of science we know that such symptoms as se- 
vere dyspnoea, aggravated by every slight exertion, and which compels 
the patient to sit upright in bed, suddenly starting in terror from sleep, 
and oedematous swelling of the malleoli and eyelids, do not always 
denote the existence of hydrothorax, as similar symptoms occur from 
diseases of the lungs or heart, without dropsy of the pleura. But, as 
we know that hydrothorax is a very common event in diseases which 
give rise to these symptoms, and that the distress of the patient is 
greatly aggravated by such a complication, it behooves us to make 
repeated physical exploration of the chest, that we may be aware of 
the fact of its appearance. 
Physical exploration of the chest likewise furnishes the only certain 
means of recognizing the existence of the hydrothorax occurring in 
Bright’s disease, or in any other malady, accompanied by general dropsi- 
cal cachexia, as the symptoms of dyspnoea, which attend its develop- 
ment and progress, are equally attributable to other sources, particu- 
larly to incipient oedema of the lungs. The physical signs of hydro- 
thorax bear great similarity to those of pleuritic effusion, although the 
resemblance is not complete. 
Inspection reveals a dilatation of the chest in the region of the 
transudation, but the intercostal furrows are not obliterated, since the 
intercostal muscles, not being paralyzed by collateral oedema, offer 
resistance to the pressure of the liquid. The liver, which is often en- 
larged by venous engorgement, is depressed when the effusion is large, 
but the heart is hardly ever displaced, as the pressure upon the medi- 
astinum is usually tolerably equal upon each side. 
Palpation gives an enfeeblement or total arrest of the pectoral 
fremitus wherever the effusion touches the thoracic wall, while above 
the effusion its intensity is increased. 
The percussion-souncl is dull over the effusion, above it it is hollow 
and tympanitic. The dulness does not extend itself in the peculiar 
manner which is almost pathognomonic of pleuritic exudation. When 
the patient stands or sits upright, its upper limits are upon the same 
level both before and behind. Moreover, the boundaries and shape 
of the area of dulness change slowly when the patient alters his atti- 
tude. Upon auscultation over the region of dulness, the respiratory 
sound is weak, indistinct, or even absent. Between the scapulae and 
the spine there is feeble bronchial respiration. 276 
DISEASES OE THE PLEURA. 
Treatment.—Treatment of hydrothorax is identical with a treat- 
ment of the main disease, and, as usually but little can be effected to 
benefit the latter, our success is seldom good. When the dyspnoea is 
very intense, and is manifestly dependent upon the profusion of the 
transudation, its evacuation by tapping is indicated. The benefit tem- 
porarily obtained in such circumstances is often very marked. 
CHAPTER III. 
PNEUMOTHORAX. 
Etiology.—We are not at liberty to suppose that under any cir- 
cumstances gases are secreted by the surfaces of the pleura and collect 
in its sac. It is manifest that the facts, upon which such a theory of 
the origin of pneumothorax is based, have been falsely interpreted. I 
will not absolutely deny that decomposition of a pleuritic effusion may 
give rise to the development of gases in the pleura without the en- 
trance to it of air; but such occurrences are, at least, very rare. The 
most common source of pneumothorax is the entrance of air into the 
pleural cavity through an opening in the pulmonary surface, or through 
perforation of the thoracic wall. 
Perforation of the pulmonary pleura may take place from within, 
the destructive disease of the lung attacking the pleura; or from with- 
out, an injury or gradual degeneration of the tissues upon the surface 
of the pleura penetrating the lung. It is by the first of these methods 
that pneumothorax arises in pulmonary abscess, gangrene of the lung, 
and consumption. Most of the cases of pneumothorax, which have 
been reported, have occurred in phthisis (not in tuberculosis, as is com- 
monly said), in consequence of the opening of a vomica into the pleural 
sac. I would here remark that a tedious chronic consumption is far 
less liable to result in pneumothorax than a consumption whose prog- 
ress is rapid and subacute. When the disorganization of the lung pro- 
ceeds slowly, the pleural surfaces usually become firmly adherent to 
one another as the morbid process approaches the surface, so that, if 
perforated, air cannot enter the cavity of the pleura. Quite often the 
pneumonia, upon which the consumption depends, is of recent origin; 
no dulness, upon percussion, or bronchial breathing, at the apex of the 
lungs, as yet being discoverable, the strength and nutritive condition 
of the patient having suffered but slightly when the pneumothorax 
forms. The rapid destruction of but a single lobule in a state of 
caseous infiltration, and lying at the surface of the lung, might induce 
the catastrophe. Besides the pneumothorax, arising from destructive 
disease of the lung, there are other rare but well-authenticated cases PXEUMOTHOEAX. 
277 
in which the disease has resulted from a rupture of dilated emphysem- 
atous subpleural pulmonary vesicles. 
The majority of cases of traumatic pneumothorax are not, as a 
rule, the result of entrance of air into the pleural sac, through a mere 
penetrating wound of the thoracic wall, but of a stab or gun-shot 
wound, which also involves the pulmonary pleura, thus permitting the 
escape of air from the lung into the pleural sac. In fracture of the 
ribs, it sometimes happens that the pulmonary pleura is lacerated by 
spicula of bone, causing pneumothorax, without perforation or appre- 
ciable wound of the wall of the chest. A gradual perforation of the 
pulmonary pleura, by ulceration of its external surface, is a much more 
frequent occurrence than this acute traumatic perforation. As we have 
already stated, the bursting of an empyema into the lungs and its 
evacuation through the bronchi take place in a similar manner. After 
a certain amount of pus has been discharged by the coughing-fit which 
follows the perforation of the empyema, a corresponding quantity of 
air naturally enters the sac with the next inspiratory act. The pyo- 
thorax is thus converted into a pneumo-pyothorax. In this form of 
disease the air scarcely ever passes freely into the pleura, but merely 
enters a space firmly bounded by adhesions, by which the empyema is 
incapsulated, and which separate it from the rest of the cavity, a con- 
dition to which we shall allude again while discussing the symptoms. 
We have already stated that all perforations of the thoracic wall 
do not cause pneumothorax. If the track of the wound through the 
wall of the chest be tolerably narrow, and if its direction be oblique, 
the integument forms a sort of valve at its outer end, which prevents 
the air from entering the chest. It is the same with the fistulous 
passages, which usually remain after the spontaneous external opening 
of an empyema. On the contrary, if the thoracic wall be penetrated 
perpendicularly, and the opening be sufficiently large, pneumothorax 
does occur, air flowing in and out of the pleura, through the orifice, as 
the chest heaves and falls. It may be mentioned, finally, that in ex- 
ceedingly rare instances, pneumothorax arises through the perforation 
of the pleural sac by ulceration or degeneration of growths within the 
stomach or oesophagus. 
Anatomical Appearances.—The existence of pneumothorax may 
often be guessed upon simple inspection of the cadaver, owing to the 
enormous distention of one or other side of the chest, with obliteration 
or prominence of the intercostal spaces. If the abdomen be opened 
first, we find that the convexity of the diaphragm faces downward, 
and that the liver or the spleen is deeply displaced. If a knife or 
trocar be thrust into the distended side of the chest, the air gushes out 
with a hissing sound, capable of extinguishing a light held before the 278 
DISEASES OF THE PLEURA. 
orifice. The gas which escapes consists principally of carbonic acid 
and nitrogen, and contains but little oxygen. Its quantity varies, but 
is usually sufficient to produce the monstrous dilatation of the chest 
above alluded to. It is rare for the pleural sac to contain air alone. 
Even though the patient only survive the pneumothorax a day or two, 
pleurisy develops, and we find sero-purulent or purulent exudation in 
the pleura besides the air. The quantity of the effusion is variable, 
and generally is largest when the pneumothorax is of longest standing. 
Again, the effusion may almost fill up the pleura, while the amount of 
air it contains may be very small. Finally, all the air may disappear 
from the sac, so that it contains nothing except the effusion. 
Whether the pleura contain air alone, or both air and pleuritic exu- 
dation, the lung is compressed into a very small volume, completely 
void of air, and is pushed up against the spinal column. And it is 
only when it is partially attached by adhesions to the thoracic wall 
that it occupies any other position. In many cases it is only with great 
trouble, and by inflating the lung under water, that the point of perfo- 
ration, which is usually covered by fibrinous deposit, can be discovered. 
In other instances the orifice is already closed. Besides the above- 
mentioned downward displacement of the diaphragm, a considerable 
lateral displacement of the heart and mediastinum is generally found 
in pneumothorax. 
Many important variations from the anatomical alterations de- 
scribed above take place when uniform retraction of the lung on all 
sides is prevented by extensive and firm adhesions of the pleural sur- 
faces. Sometimes the air which has escaped is contained in spaces of 
small capacity, and enclosed by adhesions upon all sides. Then, only, 
the adjacent parts of the lung are compressed, and the thorax is only 
partially dilated; the liver and heart are not displaced. This latter condi- 
tion is the rule in pneumothorax from perforation of an empyema, but it 
occasionally is met with also in cases of perforation of a superficial cavity. 
Symptoms and Course.—The symptoms of pneumothorax are 
generally very striking and characteristic, and are easily understood, 
if we bear in mind the consequences which necessarily must ensue after 
perforation of the pulmonary pleura, or of the thoracic wall. 
The pleural cavity being no longer hermetically sealed, the lung 
retracts by virtue of its elasticity. A retraction of the lung, such as 
we find upon opening the thorax upon the dissecting-table, occurs 
during life, at the moment when the air enters the pleural sac through 
a perforation, either externally or internally. Even the lung of the 
uninjured side retracts as far as the mediastinum can yield to the 
traction, now exerted upon one side of it alone. Immediately after 
the establishment of the pneumothorax, the cavity only contains the PNEUMOTHORAX. 
279 
air which has been expelled from the lung by virtue of its elasticity. 
With the next inspiratory movement of the chest an additional quan- 
tity of air enters the pleural sac, and, if this air can pass out again 
with the succeeding expiration, the thorax returns to its expiratory 
state, and the lung does not suffer compression. If, however, the air 
which enters the pleura during inspiration cannot escape with the next 
act of expiration, the thorax remains dilated, and the lung is com- 
pressed. This process is repeated until the thorax attains the utmost 
dilatation which a forced inspiratory act can produce in it, and until 
all air has been driven out of the lung, and its compression is com- 
plete. Owing to the peculiar ragged character of the opening in the 
pulmonary pleura, through which the air enters the pleural sac in most 
cases of pneumothorax, it generally happens that the air which gets 
in cannot get out again. The orifice opens like a valve during inspi- 
ration, and is closed by the pressure of the compressed air when expi- 
ration commences. Finally, after the tension of the air within the 
pleura has reached a sufficient degree of intensity, the valve is perma- 
nently shut, even during inspiration, and, although there is no aggluti- 
nation or adhesion of the point of perforation, no more air enters the 
cavity. In pure pneumothorax, the dilatation of the chest does not 
exceed the normal expansion which forced inspiration can produce in it. 
The extraordinary degree to which this normal limit is often exceeded, 
and the excessive distention which the walls of the chest frequently 
undergo, are due to a consecutive effusion of liquid, which also takes up 
room, or, in other words, the pneumothorax has become a pyo-pneumo- 
thorax. In the rare instances in which the air passes freely in and out 
of the thorax, as occurs in large wounds or fistulous openings which 
penetrate perpendicularly, and in spacious fistulous communications, 
with rigid resisting walls running between the pleural cavity and a 
large bronchus, there is no dilatation of the chest, and no compression 
of the lung, which, however, has generally been emptied of its air by 
other causes. 
When a vomica perforates the pleural sac, the moment of perfora- 
tion is usually distinctly perceptible to the patient. He feels as if 
“ something had given way, or burst, in his chest.” Immediately after- 
ward a dyspnoea commences, which rapidly assumes the utmost in- 
tensity. The patient can only lie upon the affected side, or else is 
compelled to sit upright, so as to give the freest play possible to the 
sound side of his chest. This dyspnoea is partially owing to the sudden 
compression of one lung, and in part to the collateral hypersemia and 
collateral oedema, and obstruction of the alveoli in the sound lung, 
consequent upon the compression of the vessels of the diseased one. 
In all the cases of sudde.n pneumothorax which I have seen, the pa- 280 
DISEASES OF THE PLEURA. 
tients soon began to complain of severe pain in the region of the lower 
ribs, wliich is to be attributed either to the strain upon the diaphragm, 
or else to the pleurisy which is excited by the escape of air, and of the 
contents of the vomica into the pleura. If the patient be not very 
anaemic already, marked signs of engorgement of the right side of the 
heart, which is deprived of half its efferent channels by compression 
of the vessels of the lung, soon are added to the above symptoms. 
The patient becomes cyanotic and dropsical; swelling of the face and 
extremities is often observable from the very commencement. The 
pulse is small, the urine scanty, the skin cool, partly because the left 
side of the heart receives blood from one lung only, and hence is not 
completely filled, partly in consequence of the collapse which accom- 
panies bursting of a vomica into the pleural sac, and other serious in- 
juries, such as the perforation of ulcers of the stomach. 
Some patients die in a few hours, or even sooner, from the com- 
bined effects of want of breath and collapse. In other instances, death 
does not take place for days or even weeks. The collapse then sub- 
sides, the patient grows warm again; but the dyspnoea continues, and 
grows worse, as the pleuritic effusion increases, and pushes the heart 
and mediastinum more and more against the sound lung. The cyano- 
sis and dropsy also increase. The patients finally succumb to pul- 
monary oedema and to insufficient decarbonization of the blood, or 
perhaps die of the consecutive pleurisy, exhausted by fever and by the 
profuseness of the effusion. 
Recovery from pneumothorax is rare. When it occurs, the pneu- 
mothorax first changes into a simple pyothorax, the liquid exudation 
accumulating in the chest, and so augmenting the pressure upon the 
air contained in the pleural sac, that it is diffused among the adjacent 
vessels. Then, if circumstances favor, the effusion itself may be reab- 
sorbed, and, if meantime the orifice of the perforation be closed, the 
lung may expand again. I treated a patient in Magdeburg, who, 
after lying for weeks in a condition of the utmost misery, so that her 
death was daily expected, so far recovered in the course of three 
months as to marry, and to carry on a somewhat extensive business. 
In other cases, a wide communication forms between the pleural cav- 
ity and some large bronchus, which still remains patulous in the com- 
press*cd lung, and from time to time—but only when the patient 
assumes particular attitudes (as has been related in a very interesting 
case in Romberg's clinic, reported by Henoch)—a part of the liquid 
contents of the cavity which has entered the bronclii is discharged by 
coughing. When the perforation of a cavity causes the admission of 
air into a space which has been enclosed in old and firm adhesions, 
or where an empyema has pointed into the lung, and where air has PNEUMOTHORAX. 
281 
entered to take the place of the pus which has been evacuated by the 
bronchi, the symptoms and course of pneumothorax are altogether 
different from those described above. In such cases, especially in the 
latter instance, there often are no subjective symptoms whatever, and 
the malady is only discovered accidentally when the chest of the 
patient is examined. When the quantity of air in the pleural sac is 
large, physical examination gives the following results : 
Inspection.—If we find that a consumptive patient (whom a few 
days ago we left walking about, or whose attitude as he lay in bed 
was perfectly unconstrained) now exhibits signs of great dyspnoea, 
that lie lies upon one side, anxiously avoiding all alteration of this 
position, these symptoms alone (particularly if the change have taken 
place suddenly) should awaken a strong suspicion that pneumothorax 
has been established. Upon looking at the chest, even an unprac- 
tised eye can mark the dilatation which it has undergone, the oblit- 
eration of the intercostal furrows, and the absence of respiratory move- 
ment upon the affected side, and, when the pneumothorax is in the left 
pleura, that the cardiac impulse is visible to the right of the sternum. 
Palpation.—Displacement of the heart toward the sound side, as 
well as downward displacement of the liver, in pneumothorax of the 
right side, is still more perceptible upon palpation. The pectoral fre- 
mitus is generally quite imperceptible, and is always fainter upon the 
affected side than upon the sound one. 
Percussion.—Over the region of the pneumothorax the percussion- 
sound is full, clear, and tympanitic, and when the pneumothorax is of 
the right side it extends too far downward, and when of the left too 
far inward. When the thoracic wall is very much disturbed, the 
intensity of the pressure hinders the formation of regular vibrations, 
and the sound is not tympanitic. So tense does the thoracic wall 
sometimes become, that percussion does not produce any sonorous 
waves at all, and, even when practised with heavy strokes, only gives 
rise to a feeble, dull sound. Great stress has recently been laid upon 
the change of pitch in the percussion-sound of pneumothorax occa- 
sioned by the patient’s lying down or sitting up (Biermer), it being 
supposed that the diaphragm is depressed by the effusion, and the long 
diameter of the pleural sac is increased, while in the erect attitude 
(Biermer, Gerhardt). I cannot help doubting the constancy of this 
increase in the long diameter of the pleural cavity in the erect posture, 
and indeed believe that, sometimes, the very reverse occurs, that is, 
when there is a certain amount of exudation in the cavity. Finally, a 
metallic clang is often heard upon percussion, especially when the 
ear is laid upon the chest during the operation. The percussion-sound 
becomes dull, as far as the effusion extends, in a very few days. A 282 
DISEASES OF THE PLEURA. 
characteristic sign of pyo-pneumothorax is, that the limits of the dul- 
ness change as the patient alters his posture. When he lies upon his 
back, the sound in front may be full, down to the border of the lower 
ribs; if he stands up, the dulness may extend far up his chest. 
Auscultation.—When there are both air and liquid in the pleural 
sac, a distinct metallic splashing (like the sound of water, shaken up 
in a half-filled bottle) is often audible, even without putting the ear to 
the chest, whenever the patient suddenly changes his position, or when 
he is shaken (succussion). No vesicular respiration is to be heard, 
which, in conjunction with the full percussion-sound, is a symptom of 
great significance. In its stead, we hear metallic sounds and am- 
phoric breathing, and especially the metallic rattling (the tintement 
metallique) sounds which are also heard over large vomicae with smooth, 
regular, concave walls. We are not at liberty to infer, from the exist- 
ence of metallic sounds, that air flows into and out of the pleural sac, 
as such sounds may also arise when the communication is closed, the 
murmurs generated in the lung giving a metallic reverberation. While 
the above signs arise with great completeness and harmony, in most 
cases where the air is capable of free movement in the cavity of the 
pleura, after perforation of a vomica, so that the affection is then very 
easy of recognition, many of them may be absent when the pneumo- 
thorax is incapsulated. If the space containing the air be too small, 
or too irregular in shape, to be capable of assuming a regular bulbous 
form under pressure of the air and exudation, no metallic sounds are 
heard, either upon percussion or auscultation. The most constant and 
trustworthy sign of incapsulated pneumothorax is a full percussion- 
sound, with absence of respiratory murmur. 
Besides this, in a few cases, in which, after bursting of an empyema 
into the lungs, the cavity containing the air and effusion was extreme- 
ly irregular, I have been able, by laying my hand upon the thorax, 
to feel the liquid wash against the anterior side of the chest, when the 
patient raised himself quickly and with energy. 
Diagnosis.—It is only when we are suddenly called to the bedside 
of a patient, or when we receive him into hospital in such a condition 
of suffocation that he is unable to give any account of his previous ill- 
ness, that pneumothorax is liable to be confounded with emphysema. 
In all other instances, the rapid development of the dyspnoea in pneu- 
mothorax and its extremely gradual establishment in emphysema 
place the matter beyond a doubt. 
In the less obscure cases we may rely upon the following tokens. 
1. In emphysema, both sides of the chest, in pneumothorax but one is 
dilated (emphysema is bilateral, pneumothorax is almost always mono- 
lateral). 2. In emphysema the intercostal spaces are shallow furrows; TUBERCULOSIS OF THE PLEURA. 
283 
in pneumothorax they have disappeared, or become prominent. 3. In 
emphysema the vesicular breathing is weak, but is not absolutely want- 
ing ; or we hear the sounds of bronchitis in its place. In pneumotho- 
rax we never hear vesicular murmur, but metallic sounds are frequent- 
ly audible. 4. In emphysema the pectoral fremitus is perceptible ; in 
pneumothorax it is hardly ever present. 
Pneumothorax is to be distinguished from large, empty, superficial- 
ly situated cavities—over which upon percussion we hear the metallic 
ring, and in which amphoric breathing and metallic tinkling are audi- 
ble upon auscultation—by the following points of difference : 1. The 
thorax is depressed over a large superficial cavern; over a pneumo- 
thorax it is dilated. 2. Where a cavity exists, the pectoral fremitus 
frequently is strengthened; in pneumothorax it is imperceptible. 3. 
The rules in a cavity are usually loud and numerous ; in pneumothorax 
they are few and faintly audible. 4. Where there is only a cavity, 
the neighboring organs are not dislocated; in pneumothorax the dis- 
placement is generally well marked. 5. In a cavity the pitch of the 
tympanitic percussion-sound is altered by opening and shutting the 
mouth. This is not the case in pneumothorax. 
Treatment.—The treatment of pneumothorax can only be a pallia- 
tive one, and a treatment of symptoms. In many cases, particularly 
where the volume of the blood is not as yet diminished, as in the trau- 
matic form of the malady, venesection may be urgently demanded at 
the outset. We may even be required to repeat the venesection, 
should the uncompressed lung become so intensely hypercemic as to be 
unable to fulfil its function. The pain which arises from straining of 
the diaphragm and commencing pleuritis should be treated by local 
blood-letting and cold applications. Opiates are indispensable, for the 
mitigation of the distress of the patient, and to procure him rest. 
Puncture of the thorax with a fine trocar is indispensable, as a 
means of relieving the dyspnoea of the patient, although the effect ob- 
tained is merely palliative. The operation does not benefit the lung 
of the affected side, but rather the sound lung, when the mediastinum 
is displaced by pressure of the accumulated air and exudation, and 
hence encroaches upon the unperforated pleura. 
The principles laid down for the treatment of pleuritis are appli- 
cable to the treatment of the more advanced stages of pneumothorax. 
CHAPTER IY. 
TUBERCULOSIS OE THE PLEURA. 
I. Gray miliary tubercle of the pleura occurs almost exclusively in 
acute miliary tuberculosis, simultaneously with miliary tubercles of the 284 
DISEASES OF THE PLEURA. 
lung, spleen, liver, and meninges. As we have already seen, the pa- 
tient succumbs to the intensity of the fever in this malady, before the 
tubercles undergo further metamorphosis. Miliary tuberculosis of the 
pleura gives rise to no peculiar local symptoms. 
II. Tubercular granulations develop with far greater frequence in 
the young false membranes which grow from the pleura after repeated 
relapses of pleurisy. We have seen that rupture of small blood-ves- 
sels is liable to occur during the inflammation which the new vegeta- 
tions (profusely supplied as they are with large and delicately-walled 
capillaries) have to undergo in a relapse of pleurisy. This accounts for 
the haemorrhagic character of the exudation, which accompanies tuber- 
culosis of pseudomembranes. It appears in the form of numerous nodu- 
lar prominences, of about the size of a hemp-seed, which at first are 
white, afterward acquiring, a yellow color. It is this tuberculosis of 
pseudomembrane which is best adapted for the study of the origin and 
metamorphosis of tubercle ( Virchow). The symptoms of this form of 
tuberculosis of the pleura are indistinguishable from those of a pleurisy 
with haemorrhagic exudation. 
CHAPTER Y. 
CANCER OP THE PLEURA. 
Cancer of the pleura never occurs primarily, and only is met with 
in advanced general cancerous infection, and where cancer has arisen 
in other organs, and particularly in those adjacent to it. It most fre- 
quently complicates cancer of the mamma, of the mediastinum, and 
of the lungs, and arises with especial frequence after extirpation of 
cancer of the breast. The pleura is then either perforated from with- 
out, by cancerous deposits of the vicinity which sprout inward, in the 
form of bulbous swellings, or else independent cancerous nodules 
spring up upon the pleura, attaining the size of a fist, and presenting 
a lardy, marrowy appearance, and a nodulated or more or less level 
surface. Cancers of the pleura are full of cells, have very little con- 
nective tissue, And belong to the class of medullary sarcoma. 
When the cancerous degeneration is somewhat extensive, a liquid 
collects in the cavity of the pleura, which, as it were, stands midway 
between inflammatory and dropsical exudation. It contains fibrin in- 
deed, just as we find it in other serous sacs, which have become the 
seat of cancerous disease, but it does not coagulate until a late period; 
that is to say, we find no fibrinous deposit in the effusion, but, upon al- 
lowing the liquid to stand after evacuation, it gradually precipitates 
coagulating masses, often continuing so to do for days.—(Hydrops lym- 
phaticus, Virchow)—(Hydrops fibrinous of Vogel.) CANCER OF THE PLEURA. 
285 
In the very great majority of cases, cancer of the pleura cannot be 
diagnosticated. Should an effusion gradually form in the pleural sac 
in a case of long-standing cancer of the breast, which is immovably at- 
tached to the thorax, or after extirpation of a mammary cancer, we 
are entitled to suppose that a cancerous growth exists upon the inner 
wall of the thorax. Large tumors may cause compression of the lung 
or greater bronchi; may displace the heart, or exert pressure upon the 
great vessels. Thus dyspnoea, cyanosis, and dizziness may arise, 
symptoms whose meaning, however, is seldom rightly interpreted. 
When large cancerous tumors reach the wall of the chest, the percus- 
sion-sound at the point involved becomes absolutely dull; and, if the 
tumor lie against the thorax posteriorly, with the aorta in front of it, 
pulsation may arise, and the cancer be mistaken for an aneurism of the 
aorta. This may happen all the more easily, as a spurious murmur 
may be produced in the aorta at the point where it is compressed, 
which may be perceptible at the feebly pulsating point of dulness. 
However, the pulsation as aforesaid is always weak and the false mur- 
mur is always merely a systolic one. We never hear the double, false 
murmur which we seldom fail to hear in an aneurism lying in contact 
with the chest. Finally, the history of the case, particularly that of 
previous extirpation of a cancerous tumor of the breast, will assist the 
diagnosis. 
We cannot consistently speak of any treatment of cancer of the 
pleura, as we must confine our efforts to palliation of its more distress- 
ing symptoms. APPENDIX 
TO THE 
DISEASES OF THE RESPIRATORY ORGANS. 
DISEASE OF TIIE NASAL CAVITIES. 
CHAPTER I. 
HYPEREMIA AND CATARRH OF THE NASAL MUCOUS MEMBRANE— 
CORYZA, GRAVEDO, COLD IN THE HEAD. 
Etiology.—The nutritive and functional disorders characteristic 
of catarrh are to be seen with extreme frequence in the nasal mucous 
membrane, where they are called “ cold in the head” (Schnupfen). 
Far more rarely, and almost solely in the course of infectious maladies, 
the nasal mucous membrane is attacked by croupous or by diphtheritic 
inflammation. 
The same remarks apply, with regard to the etiology of nasal 
catarrh, which we have already made in treating of catarrh of the 
larynx and bronchi. Predisposition to cold in the head varies greatly 
in different individuals. In general, it is greater in children and in 
feeble, delicate, and, above all, in scrofulous persons, than in adults 
and in individuals who are muscular and robust. Gradual “ harden- 
ing ” diminishes the predisposition, so that it is comparatively rare for 
inveterate snuff-takers, who are in the habit of irritating their nasal 
membranes almost constantly, to suffer much from catarrh. Besides 
these, however, there are sources of predisposition which are quite un- 
known to us, or, in' other words, we find a remarkable tendency to 
coryza in persons in whom we are not able to detect any peculiarity 
by which they may be distinguished from other less predisposed in- 
dividuals. 
The causes which occasion catarrh of the nose are very numerous, 
and the almost universal impression which prevails among the laity, 
that “ colds ” always proceed from chilling of the skin, is erroneous; CORYZA. 
287 
although, indeed, most cases of coryza do depend upon exposure to 
cold, and particularly upon exposure of the feet. 
Next in frequence, local irritants cause catarrh of the nasal pas- 
sages, such as the entrance of hot air, dust, acrid gases or foreign 
bodies; or the snuffing of tobacco by persons unaccustomed to it; 
likewise blows or shocks which the nose may encounter, and often re- 
peated and violent blowing of the nose, etc. Nasal catarrh may also 
be an accompaniment of other diseases, ulcers, outgrowths (Neubil- 
dung), caries, necrosis of the nasal bones. Inflammation from neigh- 
boring organs often spreads into the mucous membranes of the nose; 
thus, a very troublesome and intense coryza always accompanies a boil 
of the upper lip, and an abscess of the gum of the superior incisors. 
Nasal catarrh, too, is frequently a symptom of constitutional disease. 
The coryza which accompanies measles and exanthematic typhus 
belongs to this class, as do also the milder form of scarlatinous co- 
ryza, the coryza of congenital syphilis (see syphilis, vol. ii.), and 
probably also the nasal catarrh, which attacks a great number of per- 
sons during the prevalence of the influenza-epidemics, forming one of 
the symptoms of very general catarrh. In some respects, also, the 
iodine coryza, which constitutes one of the chief symptoms of iodic 
poisoning, comes in this category. 
The somewhat common opinion, that a cold in the head is conta- 
gious, is contradicted by the experiments of Friedrich, who could not 
succeed in implanting the disease upon the mucous membranes of 
healthy persons by transferring to them secretions of persons suffering 
from catarrh in its several stages. 
Anatomical Appearances.—At the commencement of an acute 
nasal catarrh, the capillaries of the nasal mucous membranes are sur- 
charged with blood, the tissues are infiltrated, and the membrane, 
swollen by hyperaemia and oedema, gives out a colorless, thin, saline 
secretion. At a later period, while the hyperemia and swelling of the 
mucous membrane diminish, the secretion becomes thicker and less 
transparent, from a copious admixture of young cells. 
In chronic catarrh the nasal membrane is considerably swollen; it 
discharges a secretion, scanty in a few instances, but usually profuse 
and purulent, from the number of young cells which it contains. This 
often dries up within the nose into hard, dirty, dark-green crusts, and in 
some persons it evinces a great tendency to putrefaction without any 
assignable cause. 
In many instances chronic nasal catarrh produces catarrhal ulcers, 
the cell-formation not confining itself to the surface, but spreading into 
the substance of the mucous membrane. They remain superficial, as a 
rule, but sometimes, particularly in scrofulous and cachectic subjects, 288 
DISEASE OF TIIE NASAL CAVITIES. 
they penetrate more deeply, and may destroy the perichondrium and 
periosteum, and give rise to caries and necrosis of the cartilages and 
bones of the nose. In the secretion from the ulcer, especially one 
which has caused a caries, and necrosis of the cartilage and bones, a 
foul decomposition is almost constantly going on, which produces an 
extremely bad odor, an occurrence only occasionally observed in the 
secretion of simple chronic nasal catarrh. 
In other cases, chronic nasal catarrh gives rise to polypous out- 
growths. According to Rokitansky, “ the latter sometimes appear, 
first, as a diffuse thickening over a large surface of the mucous mem- 
brane, particularly on the turbinated bones, growing with an uneven 
surface, and developing wart-like protuberances and fold-like ridges. 
Sometimes the growths are more circumscribed, assuming a rounded, 
pedunculated, pyriform shape. They consist of a gelatinous growth 
from the matrix of connective tissue of the mucous membrane, and 
from its glands, which frequently degenerates into cysts. Gradually, 
the material of which the growths are constituted is converted into 
firm, fibrous tissue. They contract or block up the air-passages, and 
finally may become visible in the openings of the nostrils.” 
Symptoms and Course.—The symptoms of acute nasal catarrh 
may be presumed to be generally known ; and everybody, probably, 
having had personal experience of them, they need but very brief no- 
tice here. The patient first complains of a feeling of dryness and of a 
more or less complete obstruction in one or both nostrils, which induces 
a very prejudicial inclination to blow the nose. From time to time, at 
short intervals, there arises a titillating or prickling sensation within 
the nostril, which usually precedes the complicated group of reflex 
symptoms known as sneezing, but which may also occur every now and 
then without being followed by the sneeze. This dryness of the nos- 
tril is soon succeeded by a very abundant secretion, a colorless, trans- 
parent watery liquid, of saltish taste, flowing almost incessantly from 
the nose, and sometimes producing excoriation of the upper lip. Ac- 
cording to Ronders, the irritating quality of the now strongly-alkaline 
secretion is due to the quantity of ammonia which it contains, while 
the proportion of chloride of sodium in it is less than its salt taste 
would lead one to suppose. 
The senses of smell and taste become perverted, the tone of the 
voice is nasal. In almost all instances the catarrh extends into the 
mucous membranes of the frontal sinus, and, if the attack be severe, 
the patients complain of a feeling of pressure or of distressing pain in 
the forehead. We can perceive the redness and swelling of the mu- 
cous membrane as far as the eye is able to reach. In catarrhs of 
greater intensity, the redness and swelling extend from the mucous CORYZA. 
289 
membranes to the skin of the nose and cheeks. A cold in the head is 
often complicated by a conjunctivitis. The patients avoid the light, 
and copious tears flow from their reddened eyes into the nostrils and 
over the cheeks. Should the fauces participate in the nasal catarrh, 
there is difficulty of swallowing; if the air-passages be implicated, 
cough and hoarseness accompany the symptoms. Propagation of the 
disease into the eustachian tube induces slight pain and roaring in the 
ears, or a temporary hardness of hearing. 
The group of symptoms which we have just described is almost 
always accompanied by fever and general constitutional disturbance ; 
particularly if the catarrh have acquired great intensity or be spread 
over a wide extent of surface. It may be slight in many persons, 
who are but little predisposed to febrile reaction; in others, who are 
usually spoken of as irritable persons, it is highly oppressive. 
We have already depicted the symptoms of catarrhal fever, the 
often-recurring chill provoked by every change of temperature, the 
painful bruised sensation of the limbs, the loss of appetite, etc., while 
treating of bronchial catarrh. 
The duration of acute nasal catarrh is usually short; indeed, the 
secretion generally becomes less profuse, and grows thicker and more 
opaque, even on the second or third day. It then loses its salt taste ; 
the alkaline reaction is less marked; it takes on a yellowish or yellow- 
ish-green tinge, and dries, especially during the night, into hard crusts, 
which adhere firmly to the mucous membrane. The titillation in the 
nostrils and the sneezing are less frequent, the frontal headache 
abates, the swelling of the mucous membrane subsides, and, all liquid 
or inspissated secretion having been discharged, the nasal passages be- 
come free again. The febrile constitutional disturbance seldom lasts 
longer than a day or two. Those symptoms, too, which appertain to 
the spreading of the catarrh into the neighboring mucous membranes, 
generally begin to lose their intensity or even cease entirely toward 
the end of the first week ; and in most cases the disease terminates in 
complete recovery on the fifth, sixth, or eighth day. It is very rarely, 
and only in scrofulous subjects, that a cold in the head becomes pro- 
tracted and changes from an acute into a chronic affection. 
While acute nasal catarrh is a complaint as common as it is harm- 
less, it sometimes proves dangerous to infants at the breast, because 
the obstruction of their nasal passages, which are at all times narrow, 
makes it difficult for them to suck. If we do not feed with a spoon 
in such cases, life itself may be endangered in ill-nourished or feeble 
children. 
In chronic nasal catarrh we do not usually find the feeling of prick- 
ling in the nose, the sneezing and the frontal pain, and the febrile 290 
DISEASE OF THE NASAL CAVITIES. 
general suffering. The swelling of the mucous membrane, however, 
creates a permanent narrowing of the nasal passages. 
This disease owes its vulgar name of “ snuffles,” or “ Stockschnup- 
fen,” to the more or less complete closure of one or both halves of 
the nose, by which inhalation of the air is impeded, and the voice ac- 
quires a nasal tone. The secretion of the diseased mucous membrane 
is sometimes purely mucous and sometimes muco-purulent, and its 
quantity varies. It is not always the more profuse and purulent secre- 
tion which shows the greatest tendency to putrefy. In fact, the so- 
called “ stinknase,” “punaisie,” ozcena, is sometimes observed where 
the secretion is so scanty, even in chronic catarrh, that the existence 
of such catarrh has been overlooked, and it has been asserted that 
punaisie depends upon a fetid exhalation from the mucous membrane, 
and not upon the stench from putrid secretion. That the secretion 
should decompose more readily where the nostrils are unusually con- 
tracted is not improbable; and an analogous condition may, at all 
events, be adduced in young children who suffer from intertrigo behind 
the ears, in whom the secretion from the sore in the narrow cleft be- 
tween the ear and the head is very apt to putrefy, and to emit a foul 
odor. If the secretion be copious and purulent, the blackish-green 
crusts, of stony hardness, above mentioned, frequently form, some of 
which are expelled by blowing the nose, while others are sucked into 
the pharynx through the posterior nares, and are then hawked up. In 
many instances we find the posterior wall of the pharynx covered with 
similar crusts. Chronic catarrh of the nose is an extremely obstinate 
disorder, often defying all treatment, and continuing for years, with 
varying intensity. It is often difficult, or even impossible, to determine 
whether the malady have led to ulceration and to ozoena, in the nar- 
rowest sense of the word. The very fact that the fetid odor of the 
secretion is not pathognomonic of ulceration of the nasal mucous mem- 
brane, and that it may be present also in simple chronic coryza, has 
made it necessary for those physicians who include all diseases of the 
nose, accompanied by an offensive discharge, under the term ozasna, to 
suppose the existence of two forms of ozsena, an ulcerous and a non- 
ulcerous form. It is only when the ulcers are situated so low down 
that we are able to see them by means of suitable dilatation and illu- 
mination of the nostrils, that a positive diagnosis is possible. Even 
the superficial ulcers of the nasal mucous membrane, which do not 
penetrate to the periosteum or perichondrium, are very refractory to 
treatment. Apart from the constantly-repeated provocations which 
they suffer upon blowing the nose, the close adhesion of the mucous 
membrane to the bone or nasal cartilages renders it almost impossible 
for the edges of the ulcers to approach one another, a condition which OZ.EXA 
291 
greatly impedes cicatrization. We shall speak of syphilitic ozcena in 
our second volume, where destruction of the nose by lupus, often called 
scrofulous ozmna, up to the point at which it passes into the province 
of surgery, is also to be discussed. 
The question whether the nasal passages are obstructed by swelling 
and hypertrophy of the mucous membrane, or by a polypous growth, 
always remains doubtful until the polypus becomes accessible to 
sight or touch. In patients suffering from obstructive catarrh (Stock- 
schnupfen) of one or both nostrils, particularly when the secretion is 
more or less covered by blood after violent blowing of the nose, we 
should never neglect exploring the cavities of the nose, both in front 
and rear, with the utmost care. 
The method of examining large polypi and the symptomatology 
of such affections belong to the domain of surgery. I therefore pass 
by this subject, as well as that of the other growths in the nose, and 
the affections of its adjacent cavities, referring to the surgical text- 
books, and, above all, to the classical work of my colleague, Bruns. 
Treatment.—Various abortive methods of treatment for acute 
nasal catarrh have been proposed, but none of them, neither swabbing 
the nostrils with sponges or charpie, nor syringing, nor touching the 
mucous membrane with a pencil dipped in solution of astringent or 
narcotic medicament, nor the application of narcotics in the form of 
powder, nor the inhalation of the vapor of vinegar, nor the so-called 
dicta sicca, have obtained general approval. The production of active 
diaphoresis, which has, indeed, in many instances, cut short acute nasal 
catarrh, is the only procedure worthy of adoption. Where the oppor- 
tunity offers for a Russian bath, direct a patient, who is beginning to 
suffer from a cold in the head, to make use of one, observing all the 
precautions, upon which the success of this somewhat heroic procedure 
depends. In most cases, we should confine ourselves to advising the 
patient to keep his room for a day or two, and to swallow some hot 
drink from time to time, to keep the head and feet warm, not to use 
silken or cotton, but linen, pocket-handkerchiefs, and to change them 
frequently; to smear the upper lip with lip-salve, in order to protect it, 
by means of a film of grease, from the irritating action of the acrid 
secretion. The inhalation of warm vapor at the outset of a cold, while 
the nose is still dry, is advised by many. The snuffing of cold water 
into the nostril is not dangerous, as is vulgarly supposed, but it fails 
to afford a lasting relief, and sometimes even appears to protract the 
morbid process. In the latter stages of acute coryza, after the irrita- 
bility of the mucous membrane has given place to a more torpid con- 
dition, a long walk in the fresh air, or even an occasional pinch of snuff, 
accelerates the cure. In infants at the breast, who are as yet unable 292 
DISEASE OF THE NASAL CAVITIES. 
to clear their nostrils, it is necessary to free them of the obstructing 
secretion by syringing out the nose with lukewarm water, and to feed 
them by the bottle, or with a teaspoon, as long as the obstacles to 
sucking continue. 
In the treatment of chronic nasal catarrh, particular attention must 
be paid to any constitutional defect which may exist. The exhibition of 
cod-liver oil is indicated where there seems to be a scrofulous condition 
(presently to be described). In bloated, flabby subjects, with an over- 
tendency to obesity, a depletive treatment by the systematic exhibition 
of laxatives, as well as the cold-water cure, is suitable. Local treat- 
ment is of the utmost importance in the cure of chronic coryza. The 
most effective measure is pencilling the swollen mucous membrane 
with a solution of nitrate of silver (gr. iv— 3 ss to § j), or cauteriza- 
tion with the lunar caustic in substance, repeated from time to time. 
The local employment of mercurials, in the form of snuffs, is in great 
repute in such cases (calomel, liyd. precip. rub., aa gr. xij, sacch. alb. 
§ ss), as are also dilute solutions of corrosive sublimate injected into 
the nostrils. The preparations of alum, zinc, lead, tannin, etc., are less 
to be recommended. When the discharge is offensive, and should this 
condition not be corrected by the treatment above suggested, we may 
try whether the injection of weak solutions of chlorine, or of iodine or 
creasote (iodini puri, gr. ij—iv, potas. iodid. gr. iv—viij, aqua 3 vj), 
will not give more satisfactory results. 
Catarrhal ulcers require essentially the same treatment as chronic 
catarrh. Local treatment, however, especially the touching of the 
ulcers with caustic, is demanded where there is ulceration, even still 
more imperatively than in simple catarrh. 
The management of polypous growths belongs to the province of 
the surgeon. 
CHAPTER II. 
HAEMORRHAGE PROM THE NASAL MUCOUS MEMBRANE—BLEEDING AT 
THE NOSE EPISTAXIS. 
Etiology.—Rupture of tlie capillaries of tlie nasal mucous mem- 
brane, from internal pressure, is of far more common occurrence than 
rupture of the capillaries of other mucous membranes, or of other 
organs. 
Most people have never suffered from any spontaneous bleeding, 
save bleeding at the nose. One person may be more liable than 
another is to such haemorrhage; but few have never suffered from it at 
all. Hence, as bleeding at the nose is the most common of all forms 
of spontaneous haemorrhage, it is not surprising that, Avhen a morbid HEMORRHAGE FROM THE NASAL MUCOUS MEMBRANE. 
293 
tendency to spontaneous bleeding arises, it should be these very 
capillaries of the nasal mucous membrane which generally, and indeed 
almost always, give way. The morbid state of the capillary walls, 
which renders them apt to tear—the haemorrhagic diathesis—therefore, 
is probably more or less diffused over the entire vascular system of 
the body; but it is in the nose alone, the organ whose vessels at all 
times evince a diminished power of resistance, that the nutritive dis- 
order of the vascular wall suffices to occasion rupture from simple pres- 
sure of the blood. 
Predisposition to nasal bleeding is, on the whole, far greater in 
youth than in more advanced life; but it rarely appears before the 
period of the second dentition, and does not occur in very young chil- 
dren. It is, moreover, the fragile constitutions, with slender bones, 
relaxed muscles, delicate skin, rather than big-boned, muscular persons, 
who are troubled by bleeding of the nose. The nutrition of the capil- 
lary walls is especially liable to suffer from exhausting diseases, 
whether acute or chronic, and we see epistaxis occur with striking 
frequence, as one of the symptoms of acute or chronic marasmus, in 
the course of typhus, of tedious intermitting fever, of the acute exan- 
themata, pleurisy, peritonitis (particularly that insidious inflammation 
within the abdomen, which originates in the cascum or colon), and also 
in the course of tuberculosis, caries, etc. 
The opinion here advanced, that the capillaries of the nose are 
more prone to rupture than those of other organs, is materially sup- 
ported by the phenomenon that bleeding of the nose is seen nine 
times ere bleeding from other organs is seen once, in diseases which 
undoubtedly affect the condition of the entire body, and not the nasal 
mucous membrane alone. We must also mention that, in nearly all 
affections of the spleen, nasal haemorrhage is a common symptom, and 
that among ancient physicians, and to this day among the people, 
repeated bleeding of the nose, especially if from the left nostril, is 
taken for an almost pathognomonic symptom of such diease. Affec- 
tions of the spleen, however, occur so often in connection with exhaust- 
ing maladies, and these maladies again, when uncomplicated by dis- 
ease of that organ, so frequently show a tendency to epistaxis, that 
the gepetic connection between nasal haemorrhage and disease of the 
spleen remains a matter of doubt. This is true as regards hyperaemia, 
simple hypertrophy, and lardaceous degeneration of the spleen; and 
it is only when diseases of this viscus give rise to leuchaemia that we 
can consider it as demonstrated that bleeding at the nose depends 
immediately upon an affection of the spleen, or, at all events, that it is 
brought about by disorders of nutrition, to which disease of the latter 
organ gives rise. 294 
DISEASE OF TIIE XASAL CAVITIES. 
The exciting causes of epistaxis are usually of so trifling a char- 
acter as generally to escape detection. Haemorrhage from the nose, 
indeed, sometimes occurs in consequence of blows, or other injuries 
sustained by that organ, and is a frequent concomitant of catarrh, 
ulceration, and the development of morbid growths in the nasal pas- 
sages ; but such haemorrhages occurring in subjects exempt from mor- 
bid predisposition are rarely of great magnitude, and scarcely ever 
require any active treatment. On the other hand, in individuals 
afflicted by a morbid tendency to bleeding, the plethora arising after a 
full meal often gives rise to epistaxis. Sometimes the use of spirits, 
or of coffee, tea, or other hot drink, as well as violent bodily efforts, 
acute mental excitement, and other influences which excite the action 
of the heart, may have the same effect. In another series of cases, 
rupture of the capillaiies is induced by some trifling obstacle to the 
outflow of the blood from the head; but, as we have already remarked, 
in predisposed individuals, the exciting cause of the bleeding is not 
generally determinable; and although theoretically we may classify 
the causes of nasal haemorrhages into plethoric, fluxionary, and obstruc- 
tive, it is often difficult to decide, in particular instances, to which of 
these three categories a case belongs. 
The frequent occurrence of instances where patients with habitual 
epistaxis always bleed from one and the same nostril, from which nos- 
tril a brisk haemorrhage may always be made to spring by thrusting 
any thing into it, while no such result is obtained by a similar proce- 
dure at the other nostril, makes it seem likely that bleedings of this 
kind proceed from dilatation of some small blood-vessel in the lower 
and anterior part of the nasal cavity. If Ave consider that the vascular 
net-work of the lower turbinated’bones and their mucous membrane is 
extremely Avell developed, there being a vascular plexus there of some 
magnitude, containing both arteries and veins ; and if Ave reflect that, 
in some persons, such haemorrhages come on Avith suddenness and A’io- 
lence, a continuous jet of blood spirting all at once from the nose, there 
can hardly be any doubt (in spite of our lack of anatomical proof of the 
fact) that the source of the epistaxis, from Avhich some people suffer 
upon every trifling occasion, consists in a A'aricose dilatation and thin- 
ning of one or more of these blood-vessels. The remarkable fact that 
A’cry violent Hemorrhage can often be stanched by merely plugging 
the nose in front, and that it is not often necessary also to tampon the 
posterior nares, A\rould likeAvise seem to indicate that the source of the 
bleeding lies Ioav doAvn and in front {Seitz). 
Anatomical Appearances.—The bodies of persons aaIio have 
died of epistaxis putrefy very rapidly, and upon autopsy exhibit signs 
of the most complete anosmia. In other respects, the results of post• HAEMORRHAGE FROM THE NASAL MUCOUS MEMBRANE. 
295 
mortem examination are negative, that is, we neither can find patulous 
vessels as the source of the bleeding, nor can we, under the microscope, 
demonstrate any anatomical change in the condition of the vascular 
walls, to account for their liability to rupture. 
Symptoms and Course.—In many instances the haemorrhages 
are preceded by certain premonitory symptoms. These consist simply 
in the sensations which are peculiar to hyperaemia and swelling of the 
nasal mucous membrane, so that, for some time before the bleeding be- 
gins, the patients complain of stoppage of the nose, or of pressure in 
the region of the frontal sinus, or else there may be signs of fluxion- 
ary or obstructive hyperaemia of the brain, or general vascular pleth- 
ora. In either case, soon after the establishment of the haemorrhage, 
the prodromal symptoms usually abate, and, as they are often more dis- 
tressing than the haemorrhage itself, the latter is generally regarded 
as “ critical.” 
The symptoms of the actual bleeding, when once it has set in, re- 
quire no detailed description. Blood flows from both, or (as is more 
common) from one nostril, either in drops, or in a continuous stream 
of greater or less profusion. Should the haemorrhage begin while the 
patient lies sleeping upon his back, the blood readily flows through the 
posterior nares into the pharynx. Part of it may enter the larynx 
and excite a cough, and the patient, upon awaking, fancies, to his great 
terror, that he has had a haemorrhage from the lungs. 
In other cases, the blood is swallowed, enters the stomach, and, 
when afterward voided by vomiting, may give rise to confusion with 
gastric haemorrhage. The blood first lost has almost always a some- 
what dark color, and shows great tendency to coagulate in the vessel 
into which it is received, or upon the lips, and even within the nose. 
This coagulation generally checks the bleeding in a short time, acting 
either as a spontaneous tampon, or by spreading from the effused blood 
to within the capillaries themselves. In other instances, however, in 
which the blood shows little tendency to coagulate from the first, or in 
which the tendency diminishes more and more, the haemorrhage lasts 
longer, and exhausts the patient, particularly if he • already be enfee- 
bled prior to the loss of blood. 
It is a matter of daily experience that, the longer an epistaxis lasts, 
the more obstinate it becomes ; and often, after a duration of three or 
four days, it can only be subdued by means of the tampon. In some 
cases, it becomes apparent that loss of blood aggravates the haem- 
orrhagic diathesis more than any other debilitating cause, since, after 
an exhausting epistaxis of several days’ duration, haemorrhages from 
other mucous membranes and bleedings into the structure of the skin 
(petectia) supervene. In such cases of abundant and persistent bleed- 296 
DISEASE OF THE NASAL CAVITIES. 
ing from the nose, the visible mucous membranes, especially the lips 
and the conjunctiva, assume a marked pallor; the skin acquires a dirty- 
white, waxy hue; the patients are extremely prostrate, complain of 
pain in the head and back of the neck, of uneasiness, and of palpitation 
of the heart, and readily faint away; and, should it not be possible to 
arrest the bleeding, a task which, under such circumstances, is only tc 
be accomplished by the most energetic interference, death from loss of 
blood may ensue. 
Treatment.—A moderate epistaxis occurring in a vigorous person, 
particularly when preceded by symptoms which abate when the bleed- 
ing begins, may be left to itself, as it will, generally, soon cease spon- 
taneously. If the haemorrhage be more profuse, and begin to tell upon 
the patient, or if the latter be already in a depressed condition, so that 
we may dread evil consequences from even a slight loss of blood, we 
should warn the patient against aggravating the flow by frequent 
snuffing and wiping the nose, and should apply cold to the nose and 
forehead in the form of cold compresses, or else cause him cautiously 
to snuff cold water, containing a little vinegar or alum, into the nos- 
trils. As long as the bleeding continues, we should also forbid all 
violent bodily motion, as also the use of coffee, tea, hot soup, and 
other heating substances, and advise that his drink be cool and acidu- 
lated. Should this treatment be unsuccessful—if the patient, in spite 
of it, become perceptibly weaker; should the blood begin to assume a 
brighter color, or coagulate slowly or incompletely, do not lose too 
much time in the trial of other styptics, as sulphate of zinc, creasote, 
liquor ferri sesquichlorat, but proceed at once to the simple tampon ; 
or, if this be insufficient, to the double tamponade, by means of the 
canula of Belloc. 
The application of ice to the testicles in men, and to the breasts in 
women ; of dry or wet cups to the nape of the neck ; ligation of the 
extremities; holding up the arms over the head—all procedures fol- 
lowed by decided success in some instances—are only to be resorted to 
as long as the bleeding still remains within limits which do not threaten 
danger. The same holds good of the internal administration of acids, 
of secale comutum, and of gallic acid. The longer we delay the tam- 
ponade, not only will it be so much the harder to arrest the bleeding 
of the nose, but, as the hannorrhagic diathesis increases with the dura- 
tion of the bleeding (see above), other haemorrhages are all the more 
apt to complicate the epistaxis, and against these we possess less cer- 
tain remedies than the use of the tampon. I know of several cases in 
which a fatal result was almost indubitably owing to the too dilatory 
employment of the tamponade. DISEASES OF THE CIRCULATORY ORGANS 
SECTION I. 
DISEASES OF TIIE HEAD! 
CHAPTER I. 
HYPERTROPHY OP THE HEART. 
Etiology.—The term hypertrophy of the heart is applied exclu- 
sively to a thickening’ of the cardiac wall, arising from an increase in 
the volume of its muscular tissue. It is of importance to observe a 
sharp distinction between this true hypertrophy of the heart and other 
enlargements of the cardiac wall, due to heterologous deposits, which 
may be called false hypertrophy, since the effect which the one dis- 
ease has upon the circulation and the symptoms to which it conse- 
quently gives rise are entirely different from those of the other. If, 
as not unfrequently happens, the hypertrophied heart undergo de- 
generation, and if the genuine hypertrophy be converted into a spu- 
rious one, we find that the effects of the former disorder gradually sub- 
side, and that, if at length the degeneration preponderate over the 
hypertrophy, a group of symptoms arise which are almost directly the 
reverse of those which formerly existed. We know that the muscles 
of the heart, as well as those of the rest of the body, waste away and 
become atrophied from insufficient supply of nourishment, or in dis- 
eases attended by consumption; and we also know that a most abun- 
dant supply of nourishment has but little effect in augmenting the bulk 
of the muscles. On the other hand, it is a matter of daily remark that 
the external more visible muscles of the body undergo hypertrophy 
whenever they are subjected to constantly recurrent and vigorous con- 
traction. The muscles of the blacksmith’s arm, and of the leg of the 
mountaineer, are thus hypeHrophied, and, as we have told in a previous 298 
DISEASES OF THE HEART. 
section of the work, hypertrophy of the unnaturally-tasked muscles of 
respiration is one of the chief causes of the permanent expiratory con- 
dition of the thorax of emphysema. We have not as yet any satisfac- 
tory explanation of this fact; but an interesting discovery has been 
made, that a muscle, kept for some time in a state of tetanic contraction 
by the application of electricity, maintains an increase of its volume 
for several hours. 
Upon analysis of the conditions under which hypertrophy of the 
heart arises, it will be found that most of them consist in disorders by 
which both the vigor and the frequence of the cardiac contractions are 
increased. (According to the measurements of Bizot, the thickness of 
the ventricular wall continues to increase until late in life [unless gen- 
eral marasmus arise], which is only ascribable to the constant exercise 
of the cardiac muscles.) 
It is admitted by the physiologists that there must be some regu- 
lator of the action of the heart, which is still unknown to us, and by 
which the energy of the organ is adjusted to meet the wants of the 
system, and its activity increased as obstacles, which the heart has to 
overcome, become augmented. It is a matter of importance, then, to 
be able to demonstrate that hypertrophy of the heart occurs whenever 
the function of the organ is permanently or repeatedly overtasked, 
and when the resistance, which it should normally encounter, is in- 
creased. To prove this is easy: 
1. Hypertrophy of the heart almost always accompanies abnormal 
enlargement of its cavity (dilatation). When the heart is dilated, its 
capacity is increased, and, as the organ cannot discharge its normal 
load without expenditure of a certain degree of force, the effort re- 
quisite for the expulsion of its abnormal increase of contents must be 
proportionately greater, even though the resistance at the orifices and 
in the arteries be normal. 
When we come to study pericarditis, we shall learn that there is a 
form of hypertrophy of the heart which is purely the result of dilata- 
tion. The immediate effect of the infiltration of the cardiac wall, which 
takes place in this disease, is dilatation; very soon, however, this is 
followed by hypertrophy, although no fresh obstacle to the outflow 
from the heart has arisen meantime. The first result of defective 
closure of the valves of the heart is also dilatation; and it is not until 
afterward that hypertrophy develops in the portion of the heart imme- 
diately before the diseased valve, and which is caused by the greater 
effort now required to expel the increased amount of blood which the 
heart contains. 
2. Hypertrophy of the heart accompanies stricture of its outlets, 
and contraction of the great vascular trunks. No detailed explanation HYPERTROPHY OF THE HEART. 
299 
is needed to show that, under such circumstances, the resistance which 
the organ has to surmount must be augmented. Obstruction of the 
arterial outlets of the heart and insufficient calibre of the aorta, whether 
congenital or acquired, is accompanied by hypertrophy of the ventri- 
cles. Stenosis of the auriculo-ventricular orifices is attended by hyper- 
trophy of the auricles. 
3. Hypertrophy of the heart occurs in aneurism of the aorta and 
of the pulmonary artery. It is a fact in physics that the resistance 
encountered by a liquid, flowing through a tube, is increased if the 
tube be contracted or expanded suddenly. Now, whenever the great 
vessels which spring from the heart have undergone any considerable 
aneurismal dilatation, particularly if the dilatation be of the circum- 
scribed form, both of these conditions exist in the vessels, and thus an 
additional tax is imposed upon the function of the heart. 
4. Hypertrophy of the heart is an accompaniment of obstruction 
occurring in the range of the aortic current, or of the current of the 
pulmonary artery. The greater and more extensive this obstruction, 
so much the fuller must the aorta or pulmonary artery become, so 
much the more intense the strain upon their coats, and so much the 
greater the resistance which the heart has to surmount. 
The great majority of obstacles to the circulation, which give rise 
to hypertrophy of the heart, are met with in the pulmonary circulation, 
and hence cause hypertrophy of the right side of the organ. In a 
previous section, a large number of diseases of the lungs and pleura 
have come under our notice, in which hypertrophy of the right heart 
has been shown to be not only a necessary consequence of anatomical 
changes brought about by the affections of the lungs, but was even 
counted as a symptom of these diseases themselves. In one case 
evacuation of the pulmonary arteries is impeded, a part of its efferent 
vessels, the capillaries of the air-vesicles, having perished through em- 
physema. We have seen, too, how the capillaries are obliterated from 
the shrunken tissues of a cirrhosed lung; and that, in pleurisy, some- 
times one-half of the vessels into which the pulmonary artery should 
discharge its contents are compressed and have become impervious. 
But strain upon the pulmonary artery is not dependent upon diminu- 
tion of the number of its efferent channels alone. A mere impediment 
of the outflow of blood from the capillaries into the veins will produce 
the same effect; hence, to the catalogue of pulmonary diseases above 
mentioned, we must add that of the affections of the left side of the 
heart, which give rise to obstruction in the pulmonary vein. In treat- 
ing of valvular deficiency of the left auriculo-ventricular passage, we 
shall consider the subject of “ compensating ” hypertrophy of the right 
ventricle more in detail. 300 
DISEASES OF TIIE HEART. 
Disorders of the greater (aortic) circulation, which give rise to 
hypertrophy of the left ventricle, are more rare. This is due to the 
fact that, in its vast system of vessels, the obliteration of a very great 
number of capillaries, and even the ligation and compression of the 
great vascular trunks, is compensated for by dilatation of the vessels 
of other regions. The impediment to the aortic circulation which 
most commonly embarrasses the action of the left side of the heart, and 
to which most cases of hypertrophy of the left side are commonly due 
(when they are not the result of disease of the aortic valves), is a de- 
generation of the arterial walls, generally known as “ atheroma in its 
widest sense,” and which we shall by-and-by describe in detail as 
endarteritis deformans. In this affection, which is often widely dif- 
fused throughout the wall of the arteries, the vessels not only become 
elongated and tortuous, so that the friction of the blood against the 
sides of the arteries is increased, but the elasticity of the arterial tunics 
(a most important auxiliary element of the circulation) is seriously 
diminished. In the obliteration of the aorta, which sometimes occurs 
close below the point of entrance of the ductus botalli (see Section III., 
Chapter IV.), the left ventricle is also found in a state of considerable 
hypertrophy. Occupations which require violent muscular exertion 
have likewise been enumerated among the causes of this disease. If 
this be true, such hypertrophy also belongs in this category. The 
n umber and size of the efferent vessels of the aorta are reduced by the 
pressure to which the capillaries within the contracted muscles are 
subjected, and thus the contents of the aorta and the tension of its 
coats are increased. Traube has shown by experiment, that an aug- 
mentation of pressure takes place in the aortic system during general 
contraction of the muscles. Traube finally counts the hypertrophies 
usually found on the left side of the heart, which (even according to 
Bright) often complicate the third stage of Bright'’s disease, as among 
those which proceed from disturbance of the aortic circulation. He 
supposes that an increase of tension within the aorta arises, partly 
from atrophy of the vessels, partly from abnormal fulness of the aorta, 
from which a reduced amount of liquid is withdrawn into the kidneys, 
which, by augmenting the obstacles to the evacuation of the left ven- 
tricle, give rise to hypertrophy. Bamberger brings forward serious 
objections to this explanation. He shows that the hypertrophy begins 
in the earlier stages of Bright's disease, that it does not affect the left 
heart alone, but often involves the whole organ; that we sometimes 
find the aorta not only undilated, but even narrowed, that it is im- 
probable, and that there is no precedent for the supposition that the 
destruction of a few renal capillaries should produce a hypertrophy of 
the heart, to which the ligation of large arterial trunks cannot give rise. IIYPERTROrilY OF TI1E HEART. 
301 
5. Hypertrophy accompanies general plethora. It is easy to com- 
prehend that, if the vascular system at large be overfilled, the obsta- 
cles which the heart has to overcome must be increased. It may, how- 
ever, very properly be questioned, whether a permanent and general 
increase of the contents of the vascular system be possible. Such a 
condition would immediately be compensated for by augmented secre- 
tion, especially from the kidneys, as urine always continues to form as 
long as lateral pressure upon the renal arteries and vascular tufts of 
Malpighi is kept up. 
A transient plethora, however, undoubtedly arises both after every 
hearty meal and after copious drinking. Persons who, by immoderate 
eating and drinking, often bring upon themselves this merely transitory 
plethora, persons who lead a gluttonous life (for example, travelling 
wine-sellers, who often eat and drink all day long), furnish no incon- 
siderable contingent to the general mass of cardiac hypertrophy. 
In all cases, mentioned hitherto, it has been more or less distinctly 
demonstrable that the augmented action of the heart, which gives rise 
to hypertrophy, proceeds from increased resistance and from the re- 
quirements of the general organism for such increase of action. To 
this class of cases another must be added, in which hypertrophy is a 
result of increased cardiac action without increased resistance. The 
action of the heart is accelerated by excitement of the passions. In 
many persons we are forced to assume the existence of an exalted 
irritability, an erythism of the nervous system, particularly of the 
nerves of the heart, so that trifling causes serve to excite and 
strengthen its action. The use of strong coffee, tea, and spirits, has 
a similar effect, thus furnishing a fresh exciting cause to the class of hy- 
pertrophies treated of under our fifth heading. Such agencies, however, 
are far less productive of hypertrophy than those previously mentioned. 
Finally, it must be admitted that we are ignorant of the pathogeny 
of quite a large number of cases of hypertrophy of the heart* and (in 
accordance with the objections of Bamberger to the views of Traube) 
we must reckon among these the hypertrophies which so often com- 
plicate Bright's disease without the coexistence of any valvular lesion, 
or other structural changes in the heart or blood-vessels. 
We sometimes notice that cardiac hypertrophy confines itself to 
one side of the heart, or even to one ventricle or auricle. It can 
nearly always be shown that the cavity, whose walls are hyper- 
trophied, has an unusual task to perform. It is more common, how- 
ever, even though but one orifice be contracted, for the hypertrophy to 
extend more or less over the entire heart. The former condition is 
probably the more difficult of explanation, when we reflect that part 
of the muscular fibres of one ventricle pass over to the other. 302 
DISEASES OF THE HEART. 
Anatomical Appearances.—The weight of the normal heart 
amounts .in adult males to about ten ounces, in females to about 
eight. A hypertrophied heart may weigh from one to two pounds. 
According to Bizat, the thickness of the left ventricular wall is computed, 
in the male at five, in the female at four and a half lines; the thick- 
ness of the right ventricle in males being almost two lines, in females 
one and two-thirds lines. The right auricular wall is one line in 
thickness, the left one and a half lines. Hypertrophy of the right 
ventricle may be considered to commence when the thickness attains 
six lines in the male, and five in the female. The right ventricle is 
hypertrophied if its thickness amount to three lines in the male, or 
two and a half in the female. In the most extreme cases of hypertro- 
phy, the left ventricular wall may acquire a thickness of an inch or an 
inch and a half; and the right may be six or nine lines in thickness, 
while that of the auricles may amount to two lines, or in the left au- 
ricle even three lines. 
This increase in volume sometimes is most marked in the fleshy wall 
proper, sometimes in the trabecula? and papillary muscles. The former 
is most often found upon the left ventricle, the latter in the right 
ventricle. Hypertrophy may be total, that is to say, extending all 
over the heart, or partial, that is, limited to certain portions of it. 
We distinguish three forms of hypertrophy, according to the capacity 
of the hypertrophied portion—where the capacity is normal, simple 
hypertrophy / where the cavity of the heart is enlarged, excentrie 
hypertrophy; where it is diminished, concentric hypertrophy. In 
the first and second forms, the size of the heart is increased; in the 
third, if the diminution of the cavity exceed the hypertrophy of the 
wall, the organ actually may be smaller than is natural. 
Simple hypertrophy is not common. In many cases in which the 
hypertrophied heart seems to have its normal capacity, its cavity has 
been dilated during life, but has contracted energetically during the 
agony of death, so as to cause the dilatation to disappear in the ca- 
daver. This form is confined to the left heart, particularly to cases in 
which hypertrophy of the heart complicates Bright’s disease. 
Excentrie hypertrophy is the most common form, and is often met 
with extending over the entire heart, and should the hypertrophy and 
dilatation attain any great degree of magnitude, it may occasion the 
establishment of an “ enormitas cordis,” of a “ cor taurinum.” In 
some cases excentrie hypertrophy is restricted more to the left side of 
the heart; in others, to the right. In the former case, the capacity of 
the right ventricle often suffers, as the septum, the muscles of which 
belong, in great part, to the left ventricle, is made to project into the 
cavity of the right ventricle. HYPERTROPHY OF THE HEART. 
303 
Concentric hypertrophy is exceedingly rare, although a normal 
heart, which has contracted strongly at the moment of death, has often 
been mistaken by inexperienced persons for such a condition. The 
very existence of this form has been doubted by Cruveilhier. Roki- 
tansky and Bamberger express their opinion that, although rare, it 
sometimes occurs. 
The shape of a heart in a state of general hypertrophy is that of 
an obtuse-angled triangle. If the hypertrophy be limited to the left 
side, the organ is usually longer, and has a more conical form. The 
lower end of the right side does not extend as far downward toward 
the apex as it otherwise should. In excentric hypertrophy of the right 
ventricle, the heart grows broader, and assumes a more spherical form. 
The right ventricle lies farther forward; the left is, as it were, pushed 
away from the thoracic wall. Hie apex is often small, consisting 
principally of the right ventricle. 
The heavier the heart becomes, so much the deeper does it lie. 
The diaphragm is pressed downward, and the heart generally inclines 
more to the left side of the thorax. When the hypertrophy is exces- 
sive, and accompanied by dilatation, the base always keeps sinking 
deeper, and the organ assumes a transverse attitude, the base toward 
the right, the apex toward the left. When the right ventricle alone 
is affected, the heart projects more into the right side of the thorax. 
If the left alone is involved, the prominence is rather into the left side 
of the thorax. Hypertrophy of the heart depends, probably, upon a 
multiplication of the muscular fibres and primitive fasciculi of which its 
walls are formed, as Foerster has never been able to demonstrate the 
existence of any “ thickening ” in them.* 
The color of the substance of the heart is a dark, brownish red. 
The consistence is often considerably increased, so that the walls of a 
hypertrophied heart do not collapse when cut open, as they otherwise 
should do. 
Symptoms a yd Course.—It is difficult to furnish a picture of pure 
hypertrophy c f the heart, since this affection, as we have seen, scarcely 
ever exists independently, but is almost always an accompaniment of 
other grave diseases of the organ, or of the great vessels, etc. In fact, 
these complications often completely neutralize the effect which the 
hypertrophy would have, were it to exist alone. A great number of 
the phenomena set down as symptoms of cardiac hypertrophy certainly 
are not dependent upon that cause; and indeed would exist in a much 
more marked degree were it not for the coexistence of the hypertrophy 
of the heart with the main disease. This is especially true of cyanosis 
* RoJcitansTcy and Bamberger certainly speak of an increase in bulk of the primitive 
muscular bundles. 304 
DISEASES OF THE HEART. 
and dropsy. Often as we see these symptoms in such cases, they are 
always to be ascribed to the complications, and never to the disease 
itself, if the hypertrophy be genuine ; that is, if it depend upon multi- 
plication of the normal muscular fibres of the heart. JBouillaud justly 
denounces the statements of authors, according to whom a hypertro- 
phy of the heart gives rise to cyanosis and dropsy. He says: “ Can 
any one, according to sound physiology, suppose that a true and sim- 
ple hypertrophy of the heart can be capable, by itself, of producing 
phenomena which indicate embarrassment and weakening of the func- 
tion of the heart ? ” In spite of this clear and vigorous protest, cyano- 
sis and dropsy are still set down among the symptoms of hypertrophy 
of the heart. , 
Let us first suppose a hypertrophy of both ventricles. The blood 
must then be propelled into the arteries with unwonted energy upon 
every stroke of the systole, and if (as is usually the case) the ventri- 
cles be at the same time dilated, the arteries will become abnormally 
full. But just as, during the systole, the hypertrophied ventricle com- 
pletely expels its contents, so during diastole the efflux of the blood 
to the heart from the veins must be made easier. The veins become 
more empty, while the arteries fill. Nor can the capillaries ever un- 
dergo any undue distention, for the outflow from them becomes easy 
in proportion as the vis a tergo is increased. The effect, then, of a 
general hypertrophy of the heart is, that the arteries become fuller, 
the veins less full, and that the circulation is accelerated. 
If the left side alone be hypertrophied, its contents must be more 
completely expelled than if its walls possessed merely their normal 
thickness. Hence (and all the more so if dilatation also exist) the 
aortic system becomes over-filled, while the volume of blood in the 
pulmonary system must be correspondingly reduced. In spite, how- 
ever, of the over-filling of the aortic system, it can never become so 
great as to cause dropsy or cyanosis by over-distention of the capil- 
laries and veins. This is prevented by the depletion which takes place 
in the vessels of the pulmonary circulation. The vessels of the lung, 
being imperfectly filled, offer but little resistance to the entrance into 
them of blood from the right ventricle, which, although not hyper- 
trophied, can propel its blood with unusual ease. Thus the engorge- 
ment of the vena cava subsides, its blood, under the increased pressure 
from behind, flowing readily into the empty right heart; and the right 
ventricle, being well supplied with blood, and its contents readily pass- 
ing out into the meagrely-filled vessels, soon is propelling quite as 
much blood as the left ventricle, into which the blood runs, under a 
reduced pressure, and which discharges its contents into the over-filled 
aorta with difficulty. Hence the effect of hypertrophy, especially of nYPERTROFHY OF THE HEART. 
305 
exceutric hypertrophy of the left ventricle, is to produce an abnormal 
fulness and engorgement of the vessels of the aortic circulation, which 
does not extend into the veins (the outflow from which, indeed, is 
facilitated), to diminish the fulness of the vessels of the smaller circu- 
lation, and to accelerate the current in both systems. The latter fact 
is easy to account for, if we remember that both ventricles set an ab- 
normally large amount of blood in motion with every systole; the left, 
because it is hypertrophied, the right, because it sends its blood through 
scantily-filled vessels. 
Should the right ventricle alone be hypertrophied, then, conversely, 
the volume of blood in the lesser circuit is increased, and that of the 
greater is diminished. But here, no sooner does the right ventricle 
discharge more blood than the left, than the flow from the right ven- 
tricle into the over-distended pulmonary artery becomes embarrassed, 
while the flow from the unhypertropliied left ventricle into the scantily- 
charged aorta is rendered easier. Upon the other side the blood pours 
into the left heart from heavily-charged veins, and into the right from 
veins which are imperfectly filled, so that here, too, both ventricles 
soon begin to propel an equal amount of blood, without which the 
whole of the blood would collect in the pulmonary system. Hence, 
hypertrophy of the right ventricle would result in augmentation of 
the contents of the pulmonary system, reduction of that of the aortic 
system, acceleration of the circulation, with easier outflow from the 
pulmonary veins than from the vena cava. 
From the foregoing, in which we have mainly adopted the lucid 
analysis of Frey, it is easy to perceive what symptoms hypertrophy 
of the heart occasions, and what variations must arise, according as 
the entire heart is involved, or portions of it. We are treating now, 
however, of uncomplicated hypertrophy, where there is no obstacle to 
the current of the blood, the effects of which, hypertrophy would tend 
to counteract, and can only consider the subject of consecutive hyper- 
trophy when we discuss the subject of valvular diseases, the symptoms 
of which they modify. 
Total excentric hypertrophy of the heart is the form which most 
frequently arises without complication. In most instances, persons 
thus affected feel perfectly well, and it often happens that the exist- 
ence of the malady is not detected until the physician makes a phys- 
ical exploration of the chest, after the occurrence of an apoplectic 
stroke, or that it is first observed post mortem, after an apoplexy which 
has cost the patient his life. The patient has had no occasion to con- 
sult the doctor, the doctor none to examine the chest. Thus it is with 
the majority of cases, which, though really under observation, are not 
understood. The pulse of such patients is full and strong, the carotids 306 
DISEASES OF THE HEART. 
pulsate visibly; in all the greater arteries we hear, during the systole 
of the ventricle, a distinct ring. The face is reddened, the eye glitters, 
and sometimes is remarkably prominent. The functions are normal. 
Respiration, as long as the heart has not attained an excessive develop- 
ment, is not materially embarrassed in pure hypertrophy. However, 
when a “ cor bovinum ” displaces the lungs to either side, and de- 
presses the diaphragm, there may be a sensation of fulness in the chest, 
of pressure in the epigastrium, and often a considerable degree of short- 
ness of breath. In many instances, the patients complain of palpita- 
tion of the heart, particularly when excited, although these are not, 
by any means, constant signs. We must often wonder that the im- 
pulse of a heart, strong enough to jar the chest like the blow of a 
hammer, should cause the patient so little inconvenience, or afford ab- 
solutely no subjective symptoms whatever. 
In the course of total excentric hypertrophy, especially if any par- 
ticular cause excite the action of the heart, symptoms of active liyper- 
oemia and fluxions arise in those organs whose vascular walls, possessing 
but a feeble power of resistance, are liable to an increased afflux of 
blood into them whenever pressure of the whole arterial system is 
augmented, as in the brain and the bronchi. In consequence of the 
fluxion to the brain, if the patient run, make use of heating drink, or 
undergo any physical excitement, headaches arise, or spots before the 
eyes, buzzing in the ears, dizziness, formication, etc., and fluxion to 
the bronchial arteries occasions swelling of the bronchial mucous mem- 
branes, wide-spread sibilant rhonchi, great dyspnoea, attacks of asthma, 
which often soon subside after the patient has lost a little blood, or 
after the administration of a cathartic, which, by relieving pressure 
upon the abdominal arteries, facilitates the circulation in the thoracic 
and abdominal aorta. These attacks must not be attributed to hyper- 
semia in the region of the pulmonary artery. The symptoms, especially 
the wide-spread cooing in the chest, and the character of the dyspnoea, 
which strikingly resembles that of a bronchial asthma, show distinctly 
that the fluxion has taken place in the province of the bronchial arteries. 
It is by no means rare for cerebral apoplexy to occur in a case of 
total excentric hypertrophy; indeed, we shall see that, in the majority 
of cases of ruptured blood-vessels of the brain which have been ob- 
served in young subjects, hypertrophy of the heart, either total or left- 
sided, was the assignable cause. The frequence of apoplexies of the 
brain is in part due to the fact that the vessels of the brain are thinner 
than those of other organs, and hence are more liable to rupture when 
unduly distended; and in part, also, to the circumstance that the coats 
of the arteries in hypertrophy of the heart are often atheromatous, 
and hence give way easily. That there is a genetic connection between HYrERTROrilY OF THE HEART. 
307 
atheroma of the arteries and cardiac hypertrophy (which Rokitansky 
and Virchow also admit) can hardly be longer called in question, after 
the observations of Dittrich, according to whom the pulmonary artery, 
which is otherwise rarely the seat of atheroma, is often found to be 
atheromatous where there is a hypertrophy of the right side of the 
heart. Should the patient survive the first or second attack of apoplexy, 
he may attain a tolerably advanced age. In other cases the hyper- 
trophied heart degenerates, when the malady assumes a very different 
aspect. Venous obstruction, dropsy, etc., arise, symptoms which we 
shall discuss more in detail in treating of degeneration of the sub- 
stance of the heart. 
The symptoms of total, simple, uncomplicated, excentric hypertro- 
phy of the left side of the heart, which is next in frequence of occur- 
rence, must, of course, closely resemble those of total hypertrophy. 
Here, too, the circulation is accelerated, the arteries are extremely full, 
and there is no engorgement of the veins or capillaries, the blood flow- 
ing into the right side of the heart with ease and rapidity. The res- 
piration is not injuriously affected by diminution of the contents of the 
pulmonary system, as the negative influence exerted upon oxygenation 
by emptiness of the vessels is fully counterbalanced by the positive 
one of acceleration of the circulation. Here, too, we seldom hear any 
complaint from the patient. The pulse is full and strong, the com- 
plexion healthy, and the functions normal. Derangement of the respi- 
ration is even still more rare in this form of disease than in total hy- 
pertrophy of the heart, as, in these cases, the heart seldom encroaches 
upon the cavity of the thorax. Palpitation is a frequent, but by no 
means constant, symptom. The malady usually terminates in apo- 
plexy. 
Often as the right ventricle takes part in an excentric hypertrophy 
of the left ventricle, and extremely often as hypertrophy of the right 
side of the heart accompanies derangements in the pulmonary circula- 
tion, and lesions of the valves of the heart, yet simple hypertrophy is 
extremely rare in the right ventricle, indeed it is questionable whether 
it ever has been seen. Any description of simple hypertrophy of the 
right side of the heart which we might make, must be a fictitious one, 
not based upon actual observation. At all events, intense dyspnoea 
and oedema of the lung, which have been set down among its symp- 
toms, are as little dependent upon hypertrophy of the right ventricle 
as are cyanosis and dropsy caused by hypertrophy of the left; indeed, 
as we shall see, hypertrophy actually diminishes the dyspnoea which 
the main disease has occasioned, just as hypertrophy of the left side, 
when complicating valvular derangement, long averts the occurrence of 
cyanosis and dropsy. 308 
DISEASES OF THE HEART. 
With regard to concentric hypertrophy, from the great rarity o>1 
this form of the disease, the very existence of which has been doubted 
by authors of merit, we have no available clinical data whereon to base 
an account of its symptomatology. If the capacity of a concentrically 
hypertrophied heart be considerably reduced, symptoms essentially 
different from those hitherto described must arise. In spite of the in- 
crease of muscular development, the quantity of blood thrown into 
the arteries can only be small; the outflow from the veins into the 
narrowed heart must be impeded, so that cyanosis and dropsy may 
ensue. 
Physical Signs.—In young subjects suffering from excentric hy- 
pertrophy of considerable extent, we may sometimes observe a distinct 
prominence over the region of the heart, which is not to be confounded 
with the deformity which proceeds from rachitis. In older persons, 
whose costal cartilages have become ossified, this symptom is not met 
with even in cases of “ enormitas cordis.” Besides this, the shock of 
the heart is observed to extend widely over the thorax, and is visible 
at unusual places. We shall consider this more attentively while 
speaking of palpation. 
Palpation.—In the majority of healthy persons, we see and feel, 
during systole of the ventricle, that the spot in the thoracic wall cor- 
responding to the apex of the heart receives a concussion, is shaken, 
and that a limited space between the two adjacent ribs is then made to 
bulge forward. This phenomenon, the impulse of the heart, arises from 
the force with which the heart is depressed and pressed against the 
thoracic Avail when the Arentricle contracts. Although the views of the 
different investigators may Arary as to the cause of the systolic descent 
of the heart, one side asserting it to be due to elongation, and stretch- 
ing of the great vessels ; another that it depends upon the recoil which 
the heart makes Avhen the blood is forcibly expelled from it, somewhat 
like that of an exploding gun ; yet all agree that the heart descends 
during the systole. Now, if Ave bear in mind that the heart does not 
hang free in the chest, but lies upon the diaphragm, a surface which 
slopes forward, it Avill become apparent that the heart, Avhen pressed 
doAvmvard, must also be pushed fonvard against the Avail of the chest. 
If the apex of the heart then strike upon an intercostal space, it is 
driven into it, and causes it to bulge. If, however, it meet a rib, or if 
the intercostal spaces be too narroAV to admit the apex between the 
adjoining ribs, then, instead of the impulse of the apex, a feeble cir- 
cumscribed shock is felt upon the ribs or intercostal spaces. It is A’cry 
plain, that the beat of the apex Avill be most often \Tisible in persons 
aaIio have wide intercostal spaces, and the point of Avhose heart in- 
clines more outAvardly; AA'hereas the circumscribed concussion is more HYPERTROPHY OF THE HEART. 
309 
commonly felt in individuals with narrow spaces, and whose apices 
point more inwardly. Even in the healthy subject, if the heart be 
stimulated into more vigorous action, a feeble jar may be noticed, not 
only over the apex, but throughout all that part of the chest which 
comes into contact with the heart. So, too, when the heart is excited, 
other conditions being normal, a shock may be observed in the epigas 
trium, which, however, is not to be confounded with the so-called pul- 
satio epigastrica. This epigastric pulsation is produced by the left 
lobe of the liver, which is driven downward a little by every systolic 
movement. 
In hypertrophy of the heart, various deviations from this normal 
cardiac impulse are met with. Very great intensity of impulse is 
almost peculiar to hypertrophy, while a less violent pulsation may 
arise from mere excited action of a heart of normal size. Skoda 
recognizes two degrees of abnormal intensity in the beat of the heart, 
one in which the head of the auscultator, when laid upon the chest of 
the patient, perceives a strong, jarring sensation, but in which the 
thoracic wall and the head of the listener are not lifted by the shock; 
the other, in which the thoracic wall is distinctly elevated during the 
systole, and sinks again with the diastole. Here, too, if this lifting of 
the thoracic wall take place rapidly, a shock is imparted to the head. 
It is this second degree, this distinctly heaving heart-shock, which is 
pathognomonic of hypertrophy, and which does not occur in any other 
disease. (This heaving cardiac impulse, however, must extend over a 
large area of the thoracic wall, to warrant a certain diagnosis of hyper- 
trophy ; as the apex of a normal heart, when it beats upon an inter- 
costal space, will produce distinct elevation of the point of impact, and 
will lift the finger when laid upon it.) The jarring impulse, if a con- 
stant and not merely a transitory symptom, is also decidedly indicative 
of hypertrophy. As a rule, the beat of a healthy heart is only felt 
over a spot covering one or two intercostal spaces, while the shock 
caused by the organ when hypertrophied is often perceptible over a 
region including several of these spaces. In total excentric hypertro- 
phy it is diffused both longitudinally and transversely. In hypertrophy 
of the left ventricle the heaving pulsation is most distinct at the apex, 
and thence spreads somewhat longitudinally, less so in the transverse 
direction of the organ. 
In excentric hypertrophy of the right side of the heart, the thoracic 
wall between the apex and the lower edge of the sternum, or even the 
sternum itself, is shaken. All these variations are attributable to dis- 
placement of the lung, and to the more perfect contact thus existing 
between the heart and the parietes of the chest. Observation of the 
beat of a hypertrophied heart, moreover, reveals a displacement of its 310 
DISEASES OF THE HEART. 
apex. Under normal conditions the apex almost always beats at the 
fifth intercostal space, and it is only when the spaces are very wide, or 
when the abdomen is distended, that the apex beats at the fourth 
space, and when the spaces are narrow, at the sixth space. According 
to Seitz, it is more often felt in the fourth than in the fifth space in 
children. The point in the fifth intercostal space, at which the apex is 
usually felt, is from half an inch to an inch below the nipple, at the 
parasternal line (that is, a vertical line running midway between the 
nipple and the left border of the sternum). Sometimes the beat is a 
little without this line, more rarely somewhat within it. If the heart 
be considerably enlarged, the impulse is not exclusively visible at the 
apex, as the chest suffers a jar from contact with other portions of the 
organ. Hence, we must know how to find the apex. The rule is, to 
assume that the lowest and most external point at which the impulse 
is distinctly felt corresponds to the apex. In all forms of excentric hy- 
pertrophy—the total form, as well as that of either side—the apex may 
be displaced to the left, and in total or left-sided hypertrophy it may 
likewise move farther downward, and be found in the sixth or even the 
seventh intercostal space. This very seldom happens when the right 
side is affected, and only when the right ventricle projects beyond the 
apex. With a little care and practice it is easy to distinguish the 
sensation arising from pressure of the heart against the thoracic wall 
(which is the sole guide for estimating the extension of the cardiac 
impulse) from that caused by participation of the surrounding region in 
the shock. 
Percussion.—The normal region of dulness over the heart forms a 
triangle which is bounded inwardly by the left border of the sternum, 
from the fourth rib downward; externally by an imaginary line drawn 
from the sternal edge of the fourth rib to the point at which the apex 
beats. Below, the dulness is usually merged in that of the left lobe 
of the liver, and ft is only in cases where the latter extends less to the 
left than usual that the cardiac dulness is bounded on the lower side 
by the sixth rib or seventh intercostal space. 
This normal dulness of the cardiac region becomes greater in excen- 
tric hypertrophy of the heart. In hypertrophy of the left side it 
becomes longer, in that of the right broader, and in total hypertrophy 
it is increased both in the vertical and transverse directions, i. e., is both 
longer and broader. In hypertrophy of the left ventricle, wherein the 
cardiac dulness extends downward rather than upward, observation 
of the situation of the heart-stroke is of more moment, in diagnosis, 
than percussion, which here often fails. 
Besides the cardiac dulness, that is, the dulness upon percussion 
arising from contact of the compact heart with the wall of the chest, HYPERTROPIIY OF THE HEART. 
311 
many authorities also describe a region of flatness, which is found 
where a thin layer of lung lies between the heart and the thoracic 
wall, and indeed a dispute has arisen between them, as to which of 
these percussion-signs is entitled to the name of cardiac dulness, and 
which that of cardiac flatness. Such niceties and disputes over names 
are of no practical use. They neither benefit the patient nor promote 
the progress of science. 
Auscultation.—We follow Bamberger's account of the normal 
sounds of the heart. According to him, the first sound, that which is 
heard simultaneously with the heart-stroke, and which corresponds with 
the systole of the ventricle, is produced both in the ventricles and in 
the arteries: in the ventricles, by the sonorous vibrations into which 
the tricuspid and mitral valves are thrown, when placed in a state of 
tension by the blood as it is forcibly expelled; in the pulmonary artery 
and aorta, by the sound created by the distention and stretching of the 
walls of those vessels by the passage of the blood-wave. We are 
forced to the latter supposition, by the circumstance that we can hear 
a systolic sound in all the larger arteries, even at a distance from the 
heart, which could not possibly be propagated from the ventricles, 
whenever the vessels are much distended. The second heart-sound, 
which is heard during the diastole of the ventricle, and which is sepa- 
rated from the previous one by a short pause, and from the sound 
which follows by a more extended interval, is produced in the arteries 
alone. Although it is audible in the region of the heart, yet it is con- 
ducted thither, as no sound can well arise in the heart itself during its 
diastole. Its source is in the arteries, where it is created by the flap- 
ping of the semilunar valves, which are put on the stretch by the 
diastole, and receive a shock from the blood which is driven against 
them. The heart-sounds are never altered nor converted into mur- 
murs by simple hypertrophy. On the contrary, when the heart is 
hypertrophied, the sounds are more distinct and louder, the mitral and 
tricuspid valves being exposed to heavier concussion and thrown into 
stronger vibration, the aorta and pulmonary artery being fuller, and 
hence vibrating more actively, owing to the additional flow of blood 
which they receive, and to the greater shock falling upon the semilunar 
valves from increase of the arterial contents. When there is much 
hypertrophy, a peculiar metallic sound is audible (cliquetis metallique) 
during systole, which appears to come from vibration of the thorax. 
Diagnosis.—Not only are the subjective signs of hypertrophy of 
the heart, and their concomitant derangements of the circulation, liable 
to be overlooked, but even the physical signs may fail to reveal the 
existence of the malady. When the left lung is emphysematous, and 
intervenes between an enlarged heart and the thoracic wall, there is 312 
DISEASES OF TIIE HEART. 
often no abnormal increase of the cardiac impulse, which, indeed, may 
actually become diminished in strength, or even be quite imperceptible. 
In similar manner, the cardiac dulness may be reduced in area, rather 
than increased, and even the heart-sounds themselves, when muffled 
by an emphysematous lung, may fall feebly upon the ear. 
The following are the diagnostic points deduced by grouping the 
subjective and objective signs of excentric hypertrophy of the left 
ventricle : Visible pulsation of the carotids, loud systolic sound in the 
larger arteries, and a full pulse, visible even in the smaller arteries; an 
abnormally strong heart-stroke, extending over the length of the heart; 
a depression of the apex, extension of the cardiac dulness, intensifica- 
tion of the heart-sounds in the left ventricle and in the aorta, and some- 
times a metallic click. 
Excentric hypertrophy of the right heart declares itself by the 
following objective signs: Augmented heart-stroke, which often ex- 
tends along the sternum and the left lobe of the liver; dislocation of 
the apex, which extends outward, but hardly ever downward; exten- 
sion in width of the cardiac dulness, intensification of the cardiac sounds 
in the right ventricle, and in the pulmonary artery. The difference in 
the strength of the heart-sounds is most distinctly perceptible in the 
arteries, and particularly in the second sound, so that a stronger second 
sound from the pulmonary artery, which is easily recognizable, even in 
extreme emphysema, is a most important token of hypertrophy of the 
right side of the heart. 
The sum of the objective symptoms of hypertrophy of either side 
of the heart furnishes the physical signs of total hypertrophy. The 
arteries and the pulse make the same manifestations as in hypertrophy 
of the left side; the heart-stroke is considerably stronger, extending 
both longitudinally and transversely; the apex is situated low down, 
and far to the left; the cardiac dulness is extended in all directions, and 
all the heart-sounds are louder. 
As it is of importance, in diagnosticating the several forms of this 
disease, to be able to compare the sounds which are audible at the 
origins of the arteries and auriculo-ventricular orifices, we must obtain 
an exact knowledge of the points in the thorax which correspond to 
the arterial and venous openings, or at which, at all events, each sound 
may be most distinctly heard and isolated from the others. The rule 
here is to seek for the aortic sounds at the right edge of the sternum, 
at the level of the third costal cartilage. This sound, it is true, is 
usually more audible upon the left of the sternum than upon the right, 
but at the left side, where the pulmonary artery lies directly over the 
aorta, it is often difficult to determine whether a sound proceeds from 
the aorta or pulmonary artery. For the sound of the pulmonary arterv HYPERTROPHY OF THE HEART. 
313 
we listen at the middle of the third costal cartilage; for that of the 
tricuspid, at the lower end of the sternum, on a level with the fourth 
intercostal space. 
The mitral sounds are less distinctly audible at the spot in the 
thorax corresponding to the situation of the mitral valve, but can be 
heard and isolated better at the region of the apex, which lies about 
in the third intercostal space, an inch and a half from the left border 
of the sternum. This is owing to the fact that the mitral valve is 
separated from the anterior wall of the chest by the right side of the 
heart, and from the lateral wall by the lung. These media are poorly 
adapted for the transmission of the sounds of the mitral to the ear, or 
for their isolation from the sounds arising in the right side of the heart. 
On the other hand, the apex, which belongs to the left ventricle alone, 
and which lies immediately in contact with the wall of the thorax, is 
well calculated to isolate the tones of the mitral, and to conduct them 
to the ear. 
The sounds and murmurs which arise in the various orifices of the 
heart are often heard, with greater distinctness, at other points than 
those just mentioned. This is sometimes owing to an elevated or de- 
pressed attitude of the diaphragm, or to displacement of the medias- 
tinum, and sometimes, indeed, no reason for the variation can be 
assigned. In order not to be led into error of diagnosis by such 
irregularities in determining the source of a murmur, we must not 
attach too much diagnostic importance to the situation of the point 
where the sound is most plainly audible, but should rather rely upon 
the concomitant signs of enlargement of one or other portion of the 
heart. 
To save repetition, we shall defer the discussion of the differential 
diagnosis of hypertrophy and dilatation of the heart, and of pericardial 
exudation, etc., until we shall have learned the symptoms of the latter 
diseases. 
Prognosis.—Of all diseases of the heart, hypertrophy admits of 
the best prognosis, if we accept the narrowest meaning of the term 
which we have assigned to it. In many instances, in which we shall 
find hypertrophy as a complication of other diseases of the heart, the 
compensatory hypertrophy actually mitigates the danger of the chief 
disease. 
Patients with simple hypertrophy of the heart may live to a great 
age. If they die early, death is generally due to hoemorrhagic effu- 
sions into the brain or lungs, for the prevention of which occurrences 
a careful treatment and a judicious regimen do not seem to be with- 
out efficacy. The prognosis, however, is often rendered more grave 
by the occurrence of a consecutive degeneration of the substance of 314 
DISEASES OF THE HEART. 
the heart. With the transition from genuine to spurious hypertrophy, 
the picture changes, and many dangers arise. 
Treatment.—It is certainly out of our power to cure a hypertro- 
phied heart by any mode of treatment, although we do not deny that 
such a heart may undergo atrophy quite as well as a normal one. 
Much, however, may be accomplished in the way of checking the ad- 
vance of the disease, and in moderating the dangers to which it gives 
rise. We are not now referring, of course, to the cases in which hyper- 
trophy is a complication of another malady of the heart or lungs, but 
to that form of the disease which exists in a certain degree indepen- 
dently, such as we see in drunkards, gluttons, etc. Here the disease 
generally remains unrecognized, until the enlargement of the heart 
begins to encroach upon the lungs, or until dizziness, muscse volitantes, 
or other symptoms of fluxion to the brain, arise, or, what is still more 
common, until an apoplectic attack calls attention to the state of the 
organ. If we now give our orders with decision, we may reckon upon 
punctual obedience upon the part of the patient, who previously would 
scarcely have paid them any attention, but to whom the inconven- 
iences just alluded to become a source of the greatest solicitude. Patho- 
geny makes the treatment clear. Such patients must beware of im- 
moderate eating and drinking, in. order to avoid the plethora which, 
although but transient, always follows upon a free use of food or drink. 
How often does the long-threatening apoplexy set in in the midst of 
the plethora which has developed after a long and hearty meal! Here 
too, we must insist upon the rule of issuing the most precise orders, 
and of exactly regulating the quantity and quality of the meals of 
which the patient is to partake in future. In this connection I may 
mention an act of folly which I have often seen practised by tavern- 
keepers and itinerant wine-dealers. The latter often suppose that, by 
a free use of water, they can counteract the pernicious influences to 
which they expose themselves, although it is evident that the pleth- 
ora arising after a full meal would only be increased by an immod- 
erate addition of liquid. Besides this, however, the patient must 
avoid all the causes which, independently of plethora, stimulate the 
action of the heart, and further distend the already overcharged 
arteries. Under this head come the use of stimulating drinks, mental 
excitement, and immoderate bodily exertion. Hot water must be in- 
cluded in this class, and there is no wonder that the use of the Karls- 
bad Spradel should make victims every year who die of apoplexy. 
Besides these dietetic measures, we should see that there be no ob- 
stacle to the current of blood in the abdominal aorta, and thus remove 
pressure from the endangered vessels of the brain and bronchi. Be- 
sides forbidding all food that can cause flatulence, take care that the HYPERTROPHY OF THE HEART. 
315 
bowels be regularly moved, thus relieving the aorta and its branches 
from the pressure of the abdominal viscera. The practice of repeated 
and systematic blood-letting in treatment of hypertrophy of the heart, 
which originated with Valsalva and Albertini, is still adhered to by 
the French, but with us is falling more and more into disuse. Vene- 
section diminishes the volume of blood for a short time only, and is 
apt to be followed by an erythism of the heart, and seems to favor 
degeneration of the substance of the organ. We do not mean that 
there never is any indication for bleeding, as in case of a threatened 
apoplexy proceeding from hypertrophy, of the heart. The application 
of a seton in the region of the heart is more customary with us, as 
soon as a hypertrophy or in fact any trouble whatever about the heart, 
becomes apparent. This procedure must also be pronounced useless, 
and even dangerous, although commanded by classical authority. 
Iodine and mercury are of course both inadmissible and useless. The 
patients often do well under the use of the “ whey-cure.” The grape- 
cure also has a good effect, but not unless we restrict the supply of 
other kinds of food. If we permit the patients to take their ordinary 
meals, and then daily to eat three or four pounds of grapes besides, 
dangers may easily arise, particularly that of congestion of the brain 
and apoplexy. I once saw a fresh attack of apoplexy occur in a per- 
son, who, after having been for four weeks at Marienbad, where he 
had done very well, was then daily eating four pounds of grapes at 
Vevay, as an “ after-treatment,” without, however, making any reduc- 
tion in the amount of his other food. 
Digitalis in pure uncomplicated hypertrophy is unsuitable. As has 
been brilliantly demonstrated by Dr. JReich, the results of experiments 
made with this medicine upon dogs stand in glaring contradiction to 
the conclusions drawn from experience at the bedside. (On the em- 
ployment of digitalis in disease of the heart. Inaugural address under 
President Prof. Niemeyer, Tubingen, 1864.) The action of digitalis, 
under the use of which, in innumerable cases of disease of the heart, 
cyanosis, dropsy, hepatic engorgement, and suppression of urine have 
been made to subside, is not to lower the centrifugal pressure of the 
arteries, but rather to increase it. Its use is indicated in diseases in 
which the action of the heart is weakened, but never in cases where it 
is augmented. The application of cold, in the form of a tin flask filled 
with ice-water, and worn upon the region of the heart, is of great 
benefit to many patients. 316 
DISEASES OF THE HEART. 
CHAPTER II. 
Lx exeentrie hypertrophy of the heart, the cavities of the organ 
become enlarged, but, as its walls at the same time are thickened by 
development of their muscular substance, the heart does not suifer any 
impairment of its functional power, which, indeed, is augmented. Al- 
though excentric hypertrophy has been called “ active dilatation ” by 
the pathological anatomists, yet, from a clinical point of view, it can- 
not be regarded as a dilatation of the heart. According to the gen- 
eral usage both of physicians and laity, the term dilatation is exclu- 
sively applied to a morbid condition of the heart, in which its cavities 
are enlarged, but in which there is no corresponding growth of the 
muscular substance of its walls, so that the contractile power of the 
organ is diminished. This condition corresponds to the “ passive dilata- 
tion ” of the pathological anatomists. 
There are three recognizable forms of cardiac dilatation, although 
the transition of the first variety into the second is not abruptly defined: 
1. The cavity is dilated, the wall of the heart retaining its normal 
thickness, and being merely comparatively too thin. 
2. The cavity is dilated and the cardiac wall is positively thinner 
than is normal. 
3. The cavity is dilated, while the heart-wall is thickened ; not, 
however, by augmentation of its muscular substance, but through a 
spurious hypertrophy. 
Etiology.—The causes of dilatation of the heart are— 
1. When the organ is subjected to an unnaturally severe internal 
pressure during its diastole, causing its wall to yield to a certain de- 
gree, the fact, that contractions of the orifices of the heart, and other ob- 
stacles to the circulation, cause dilatation of the portion of the organ from 
which the efflux of blood is impeded, might give rise to the erroneous 
supposition that an abnormal resistance, encountered by the heart 
during its systolic movement, may result in dilatation. It is manifest, 
however, that, the moment that the contractile force of the heart be- 
comes incapable of overcoming the resistance opposed by its contents, 
and it yields to internal pressure, the circulation of the blood will 
stop. The explanation of the mode in which dilatation is produced, 
when one of the cardiac orifices has become contracted, is as follows : 
The first consequence of an obstacle to the circulation is, that the 
affected cavity is incompletely emptied of its blood. The gush of 
blood which enters the heart upon diastole, instead of finding the cav- 
ity empty, finds it almost as full at the beginning of the diastolic move- 
DILATATION OP TIIE HEART. DILATATION OF THE HEART. 
317 
ment as it should be when that movement is complete. Blood 
continues to enter as long as the pressure of the afferent vessels upon 
their contents exceeds the power of resistance of the walls of the 
cardiac cavity. Let us, for instance, suppose an obstacle to exist at the 
root of the pulmonary artery, or, what is more likely, an obstruction in 
the current of the capillary system of the lungs. Such obstacle can- 
not prevent a systolic contraction of the right ventricle, although no 
doubt it may have the effect of preventing the ventricle from expel- 
ling the whole of its contents. Now, as long as the pressure upon the 
blood within the vena cava is greater than the resisting power of the 
thin walls of the right ventricle, the ventricle will be distended by 
an abnormal influx of blood. Moreover the diastolic relaxation is ter- 
minated by a contraction of the right auricle, whose contents are forci- 
bly propelled into the right ventricle. As the blood enters the heart 
by the veins, and enters it under quite a moderate pressure, it is mani- 
fest that the right auricle and ventricle, the thickness of whose walls 
is only one and two lines, respectively, should be much more liable 
to dilatation than the left ventricle, whose ventricular wall has a thick- 
ness of five lines; and, in fact, we find that the auricles are the most 
frequent seat of dilatation; next to these, the right ventricle, while di- 
latation of the left ventricle is the rarest of all. 
A considerable degree of dilatation of the left ventricle arises in 
cases of deficience of the aortic valves, and a smaller degree in de- 
ficience of the mitral; and this circumstance, -which is taught in every 
text-book on pathological anatomy, also argues in favor of the correct- 
ness of the above deductions. Let us suppose that the aortic valves are 
insufficient, and that blood regurgitates from the aorta into the left ven- 
tricle during its period of diastole, the pressure which the blood exerts 
upon the relaxed cardiac wall is then a very considerable one, and 
capable of overcoming the resisting power of the latter. Bamberger 
has made a careful examination of fifty hearts with valvular disease of 
the aorta, with regard to the coexistence of dilatation and hypertrophy 
of the left ventricle, and has arrived at the following conclusions, 
which fully agree with our views as to the pathogeny of dilatation of 
the heart. He found that, in simple contraction at the root of the 
aorta, there is no dilatation, or else only a very slight dilatation of the 
left ventricle. Although the obstacle to the circulation is very great in 
these cases, there is no increase of that internal pressure, during dias- 
tole, by which alone the dilatation of the ventricle is caused. On the 
other hand, in insufficience of the aortic valves, there is always a con- 
siderable dilatation of the left ventricle, which predominates over the 
coexisting hypertrophy. There is often room enough in the dilated 
ventricle to contain a full-sized fist. In such cases, as we have 318 
DISEASES OF TIIE HEART. 
shown, the wall of the ventricle is subjected to an extreme pres- 
sure. Bamberger found that the greatest degree of dilatation of the 
left ventricle arose when the aortic valves were the seat of simultane- 
ous contraction and insufficience, as then such a condition would natu 
rally be the most favorable one for the occurrence of dilatation; since 
the stenosis prevents a complete emptying of the ventricle during 
systole, while, owing to the insufficience, the blood regurgitates into the 
ventricle during the diastole, with all the force which the pressure of 
the aorta can impart. 
The occurrence of a slighter degree of dilatation in insufficience of 
the mitral is likewise easy to account for. When the mitral valve is 
not effectually closed, a considerable amount of blood regurgitates 
from the ventricle during the systolic movement, so that the auricle and 
pulmonary veins become overloaded and their walls tightly stretched. 
Blood consequently pours into the left ventricle with unnatural 
force during diastole. Perhaps the hypertrophy of the left auricle 
and the increased energy of its contractile power also aid in causing 
the left ventricle to yield to the abnormal pressure, when the mitral 
valve is insufficient. 
In stricture of the left auriculo-ventricular orifice also, there is a con- 
siderable degree of engorgement of the left auricle, and pulmonary 
vein, and the auricle itself becomes hypertrophied, but the augmenta- 
tion of propulsive power is neutralized by the obstacle to the 
entrance of the blood. This is plainly the reason why the left ventricle 
is dilated when the mitral valve is insufficient, but does not dilate 
where the valve is only contracted. 
Dilatation of the heart, when arising solely from an increase of the 
pressure of the blood within the cardiac cavities, as a rule, is soon fol- 
lowed by excentric hypertrophy, the continuous and abnormally active 
contractions of the organ giving rise to a multiplication of its muscu- 
lar fibres. When we come to treat of valvular disease, we shall ex- 
plain more in detail that it is by this transition from dilatation into 
excentric hypertrophy that the effect of obstruction to the circulation, 
arising from derangement of the valves, is counteracted. 
2. Dilatation of the heart may arise from the loss of tone of the 
cardiac wall, owing to disease of its substance, in consequence of which 
the wall gives way even before the normal internal pressure exerted 
upon it during diastole. Even the simple serous infiltration to which 
the heart is subject in the various forms of inflammation which affect 
it, especially in pericarditis, diminishes the resisting power of the or- 
gan and causes it to dilate. Sometimes its muscles seem to undergo 
an atrophy, like that suffered by the muscles of the rest of the body 
after severe and protracted illness, and in consequence of which the dilatation or the heart. 
319 
svall yields to the pressure of the blood; but the cause which most 
frequently deprives the cardiac parietes of their tenacity is degeneia- 
tion of its tissues and in particular fatty degeneration. 
After the subsidence of the collateral oedema which remains after 
the abatement of an inflammatory affection of the heart, the muscles 
of the organ may regain their power of resistance, and the dilatation 
may be repaired. In other instances hypertrophy follows upon dilata- 
tion. The dilatation arising from typhus, or protracted chlorosis, usual- 
ly disappears when the attenuated muscular fibres of the heart, with 
the rest of the muscles, recover their proper condition. On the con- 
trary, the dilatation proceeding from degeneration of the substance of 
the heart, is incapable of repair, and, indeed, always grows worse as it 
grows older. . 
3. Dilatation may proceed from the degeneration of the substance 
of an excentrically hypertrophied heart. This transition from hyper- 
trophy to dilatation occurs quite as often as does the transformation 
above alluded to from dilatation to hypertrophy ; and, indeed, it often 
happens that both metamorphoses take place in the same patient at 
different periods of the disease. Thus it can be shown that a valvular 
derangement first gives rise to dilatation ; and that this is subsequent- 
ly converted into a hypertrophy, which compensates for the deficiency 
of the valve; and that at last the substance of the heart undergoes 
degeneration, and the hypertrophy is again replaced by dilatation, 
whereupon the compensatory action ceases. The latter dangerous 
transformation often does not take place until long after the valvular 
disease has been established. So, too, in emphysema; years may 
elapse ere the excentric hypertrophy of the right ventricle, which com- 
pensates for the obstruction of the pulmonary circulation, changes into 
dilatation, to the great detriment of the patient. Nevertheless, it 
would seem that a certain period of continued overaction of the heart 
suffices to determine the conversion of a true hypertrophy into a spuri- 
ous one, a circumstance which has not been observed to occur in other 
overworked muscles. Degeneration of the hypertrophied cardiac mus- 
cles is much accelerated if the patient’s nutritive condition be allowed 
to deteriorate. One of the most common of the diseases of aged and 
decrepit people is an excentric hypertrophy of the left side of the heart, 
caused by endarteritis deformans, which, when of long standing, grad- 
ually changes into dilatation by degeneration of its muscular sub- 
stance. These are the cases to which people allude when they speak 
of enlargement of the heart as being one of the most severe and dan- 
gerous of the maladies of that organ, and which is the most terrible 
bugbear of many old people. 
Anatomical Appearances.—Care must always be taken not to 320 
. DISEASES OF THE HEART. 
mistake a heart distended by blood and relaxed from putrefaction for 
a dilated heart. Advanced decomposition of the rest of the body, ex- 
treme softness of the substance of the heart, and its saturation with 
the coloring matter of the blood, are the distinctive marks in such 
cases. When the dilatation involves the entire organ, its form is 
changed in the manner described in speaking of hypertrophy of the 
heart. As, however, in most cases the dilatation is partial, and far more 
frequently involves the right side of the heart than the left, a dilated 
heart usually appears wider without any corresponding increase in 
length. When the wall of the dilated organ seems thinned, the de- 
gree of thinning must be accurately determined by measurement, as 
otherwise there will be danger of error. General statements, such as 
“ moderate thinning ” or “ moderate thickening ” of the walls of the 
heart, are of no value whatever. When the wall of the left ventricle 
is thinned, it collapses when cut open. This does not occur when the 
organ is in normal condition. In cases of great dilatation of the auri- 
cles, the muscular fasciculi may be so widely separated that the walls, 
in places, have a membranous appearance. When the ventricles are 
much dilated, with wasting of the muscular substance, we sometimes 
find some of the trabecul® reduced to the condition of fleshless ten- 
dinous cords. 
When the wall of a dilated ventricle is thickened, it is sometimes 
possible to recognize that the hypertrophy is of the spurious kind, 
merely from the color and resistance of its substance. In other in- 
stances, the tissues of the heart appear normal upon cursory examina- 
tion ; but the general dropsy, and other signs of engorgement, which 
are not ascribable to valvular disease, or to other obstacle to the circu- 
lation, give proof of the abnormal state of the muscular substance of 
the heart, and microscopic examination reveals its degeneration. At 
other times the microscope exhibits a much slighter degree of degen- 
eration of the substance of the cardiac wall than the intensity of the 
venous engorgement would lead one to suspect. As this latter condi- 
tion, when unaccompanied by obstruction to the course of the circula- 
tion, is a most positive sign of lack of functional pow'er in the heart, I 
feel warranted in making the following assertion, based upon a large 
number of accurate observations: that it is not possible, by means of 
the microscope, to recognize all the alterations of the muscular fibrill®, 
which diminish the functional power of the heart. 
Notwithstanding that the orifices of the heart also take part in the 
dilatation, the valves still remain capable of closing perfectly, in con- 
sequence of their enlargement, which keeps pace with their thinning, 
and owing to elongation of the chord® tendine®. 
Symptoms and Course.—Dilatation of the heart renders its ac- DILATATION OF THE HEART. 
321 
tion more laborious, since, although its power is not diminished, the 
amount of blood which it must expel is increased. Hence, the effect 
of dilatation upon the distribution and force of the circulation is pre- 
cisely the reverse of that of hypertrophy. However, as long as the 
substance of its walls remains healthy, the organ still continues capa- 
ble of fulfilling its function, by dint of increased exertion, just as a 
healthy heart overcomes obstacles to the circulation by greater energy 
of its contraction. It is very different, however, when dilatation of the 
heart is accompanied by degeneration of its muscles, as it is then un- 
able to sustain such augmentation of its functional energy. Its action 
is insufficient, and the consequences of this defective action become 
recognizable in derangement of the circulation which ensues. The 
amount of blood expelled from the heart being too small, the arteries 
are inadequately filled, their walls contract, and the size of the indi- 
vidual vessels is reduced. The consequence of the diminution of the 
arterial contents is an augmentation of that of the veins ; but, as the 
number of the veins exceeds that of the arteries, the filling of the in- 
dividual veins never increases in proportion as that of the arteries di- 
minishes. Moreover, a part of the blood which should occupy the 
arteries is in the dilated and half-emptied heart. Accordingly, the 
signs of deficience of blood in the arterial system appear earlier and 
in slighter degrees of the disease than do the symptoms of engorge- 
ment of the venous system. The capillaries also become abnormally 
full, owing to the impediment to their circulation offered by the en- 
gorgement of the veins, while the tension of the arterial walls, even 
when the vessels are imperfectly filled, still exceeds that of the capil- 
laries, so that the blood continues to flow into them. Finally, the 
quantity of blood set in motion by each systole being abnormally 
small, the circulation is retarded, and the blood acquires a more venous 
character, owing to the greater quantity of carbonic acid which it re- 
ceives, and because it does not return so often to the lungs to obtain 
oxygen. 
When dilatation of a part of the heart is complicated by valvular 
disease, emphysema, or any other affection of the lungs by which the 
circulation is impeded, it is often difficult to decide whether and how 
much the lack of blood in the arteries, the venous engorgement, the 
retardation of the circulation, and the venous state of the blood, de- 
pend upon the primitive disease, and how much upon the dilatation. 
(Thus, Traube ascribes the dropsy of pulmonary emphysema to dilata- 
tion and degeneration of the right heart alone, and not to destruction 
of a large number of the pulmonary capillaries ; while, in my opinion, 
both of these causes are to be taken into account, and the dropsy of 
emphysema is only to be dreaded when disorder of the pulmonary cir- 322 
DISEASES OF THE HEART. 
culation ceases to be compensated for by the hypertrophy of the right 
heart.) But the fact that all derangement of the circulation is averted 
in valvular disease or emphysema, as long as the portion of the heart 
involved is hypertrophied, instead of being dilated, warrants the con- 
clusion, whenever .there is much embarrassment of circulation, that 
either the original dilatation has not been followed by any great de- 
gree of hypertrophy, or else that the hypertrophy has turned into a 
dilatation through degeneration of the substance of the heart. Of 
course the extent of the disorders which arise in the circulatory system 
varies with the seat of the dilatation. In treating of valvular disease, 
we propose to describe more fully the conditions which result from dil- 
atation of the various parts of the heart, just as we have made a de- 
tailed description of the effect which the state of the right ventricle 
exerts upon emphysema, in treating of that disease. There is but one 
symptom (palpitation of the heart) to which we shall draw attention at 
present, since its occurrence is quite as common in partial dilatation 
as in the complete dilatation. This distressing subjective symptom, 
consisting of a painful sense of pulsation in the region of the heart, 
often ceases when the dilated heart becomes hypertrophied, and re- 
turns when the hypertrophy begins to undergo degeneration. It is 
not the beat of a hypertrophied heart—which, though it often jars the 
chest like the blow of a hammer, is nevertheless performed without 
effort—which gives rise to the sense of palpitation. This sensation is 
rather the result of the laborious contractions of an unhypertropliied 
organ. Thin-blooded and chlorotic persons complain much more of 
palpitation than those whose heart is actually diseased; and, of all the 
varied disorders of the organ, dilatation, inflammation, and degenera- 
tion of the cardiac substance, are the ones which are most generally 
accompanied by palpitation. 
In the total dilatation which generally is due to a morbid flaccidity 
of a degenerate heart-wall, it is often difficult to say how much of the 
derangement of the circulation depends upon the degeneration and 
how much upon the dilatation. The latter, however, plays an im- 
portant part in their production, as it is found that degeneration of the 
heart, without dilatation (which is common enough in anaemic persons), 
is much better borne, and deranges the circulation much less, than 
when it is accompanied by dilatation. 
The first symptoms which are observed in this form of dilatation 
consist, as we have said, of a complaint of palpitation of the heart, 
which form a striking contrast with the faintness of its objective and 
visible pulsation, and which soon is accompanied by a slight dyspnoea. 
The cause of the dyspnoea is easily traceable to the overloading of the 
pulmonary veins and capillaries, and to the retardation of the circula- DILATATION OF THE HEART. 
323 
tion. It is aggravated upon ascending stairs, walking up-hill, and 
similar causes, and at first is scarcely perceptible when the body is at 
rest. The aspect of the patient at this period is pale, owing to the 
lack of blood in his arteries; but the overloaded state of the veins is 
not at first sufficient to produce cyanosis and dropsy, although the lips 
may be somewhat livid. Besides this, there are a certain languor and 
apathy, with liability to fatigue upon slight exertion, symptoms which, 
as we have repeatedly said, indicate a venous condition of the blood. 
If the disease advance, the palpitation and dyspnoea become more dis- 
tressing, the patient fears to make any exertion, because it “ puts 
him out of breath.” The lips and cheeks assume a distinctly blue 
tinge, the liver begins to swell, from the venous engorgement, and a 
slight oedema of the extremities begins to appear toward evening. In 
the most aggravated stage of the disease the patient complains of 
great shortness of breath, even when in a state of complete repose, 
which becomes almost intolerable upon his making the slightest effort. 
The pulse is small, and often is irregular and intermittent. The 
urine, which is extremely scanty and concentrated, deposits a copious 
sediment of urate of soda upon cooling, the small amount of water 
which it contains being insufficient to retain the salts in solution at a 
reduced temperature. At this period more or less albumen usually 
appears in the urine, and both lips and cheeks are decidedly cyanotic. 
The dropsy spreads from the ankles to the legs, thighs, scrotum, 
and abdominal integument. The upper extremities and face become 
oedematous, dropsical effusions also forming in the cavity of the abdo- 
men and the serous sacs of the chest. At length the patient suc- 
cumbs to the symptoms of bronchial palsy and oedema of the lungs. 
Every busy practitioner has repeated opportunities to witness cases 
where old people die of this malady with precisely such symptoms, or 
with symptoms but slightly different. The smallness of the pulse 
and the diminution of the urine are the result of the constant de- 
crease of the arterial contents; the cyanosis, dropsy, and albumin- 
uria are necessary consequences of the ever-increasing venous engorge- 
ment. 
The symptoms of dilatation supervening upon an excentric hyper- 
trophy, arising from endarteritis deformans, are essentially the same as 
those described above. It is often impossible to determine with which 
of these two forms we have to deal. This will not seem strange, when 
we consider that endarteritis deformans does not occasion any derange- 
ment of the circulation as long as the heart remains in a state of excen- 
tric hypertrophy, and that the evidence of disease only becomes appar- 
ent after the hypertrophy has become spurious by secondary degener- 
ation, and after its compensatory action has become imperfect. When 324 
DISEASES OF THE HEART. 
we find, by physical exploration, that an old person, suffering from cya- 
nosis and dropsy, has a dilated heart, that his superficial arteries are 
tortuous, pulsate visibly, and feel hard to the touch, the case is prob- 
ably one of endarteritis deformans with secondary degeneration of a 
heart which was once hypertrophied. If, on the other hand, there be 
no such condition of the peripheral arteries, the degeneration is prob- 
ably the primary disease to which the dilatation is secondary. 
Physical /Signs.—Inspection never reveals the prominence of the 
precordial region sometimes seen in excentric hyper tropin-. 
When there is much enlargement, the apex of the heart is found, 
upon palpation, to beat abnormally low dow-n, and too much to the 
outer side of the chest. Its impulse is often extremely feeble, and 
may even be quite imperceptible. In other cases, particularly during 
moments of excitement, it may be unnaturally strong {Skoda), and 
may even be equal to that of an exeentrically hypertrophied heart, 
although, indeed, the heaving pulsation is never seen in cases of sim- 
ple dilatation. 
Percussion shows an extension of the cardiac dulness like that 
arising in hypertrophy, so that in general an extension of the cardiac 
dulness with intensification of the impulse is indicative of hypertrophy, 
while a similar extension with diminution of the force of the impulse 
signifies dilatation. Dilatation of the left ventricle, which accompanies 
the first stage of insufficience of the aortic valve, produces the same 
alterations of the percussion-sound which accompany the subsequent 
hypertrophy of the ventricle. The same is true of the right ventricle. 
In dilatation of the right auricle, the sound of percussion is dull under 
the sternum, and at its right edge, from the second rib to the fifth or 
sixth rib. Dilatation of the left auricle cannot be demonstrated by 
percussion, as the auricle lies too far to the rear. Upon auscultation, 
the normal sounds, which are loud and strong in hypertrophy, in 
dilatation are found to be unusually feeble, although pure; since both 
the auriculo-ventricular valves and the arterial walls are set into very 
languid vibrations by the feeble action of the heart. In other cases, 
the sounds are muffled; perhaps because the papillary muscles, which 
are atrophied as well as the wall of the heart, produce a less vigorous 
tension of the valves. Finally, and very frequently, too, we hear 
murmurs over a dilated heart instead of the normal sounds, from 
which, however, we are not warranted in concluding that the valves 
have suffered alteration in their structure. These murmurs depend 
rather upon the. irregularity of the vibrations, into which the ill- 
stretched valves are thrown by the current of the blood. They are 
nearly allied to those which we notice in cases of abnormal innervation 
of the organ, where there is no dilatation of the heart, in febrile disease, ATROPHY OF THE HEART. 
325 
or in relaxation of the cardiac muscles, such as occurs in anaemia, com- 
bined with general loss of tone of the muscular system. 
Tkeatment.—In cases of dilatation, we have to see that the 
nutrition of the body goes on normally, this being the best preventive 
of flaccidity of the cardiac walls, and the patient is to be protected 
from all causes which render the action of the heart more laborious. 
Thus, a nutritious diet is very proper; but the meals should be light 
though frequent. Eggs, meat, and, above all, milk, are particu- 
larly commendable. Sometimes milk may be used exclusively for a 
while. 
Iron should always be prescribed when any signs of anaemia or of 
liydnemia are shown. On the other hand, all violent muscular effort 
should be forbidden, and the use of spirituous liquors ought to be 
restricted, without entirely forbidding them, to patients habituated 
to their use. When the liver swells, if the feet become cedematous, 
or the patient become cyanotic, digitalis should be given. I formerly 
looked upon the use of this remedy in dilatation of the heart as idle 
and even dangerous. Of late years I am satisfied that digitalis is a 
very efficient means of temporarily strengthening the heart’s contrac- 
tile power, and of thus allaying cyanosis and dropsy. In dilatation, 
digitalis, combined with an exclusively milk diet, is invaluable. By 
it I have often removed huge dropsical effusions and given great tem- 
porary relief. I usually employ the infusion of digitalis. The effi- 
cacy of this drug varies greatly according to the region where it has 
grown. In Wiirtemberg, although giving smaller doses than I for- 
merly gave elsewhere, I have seen grave signs of poisoning arise. I 
generally prescribe ten grains of it to five ounces of water, giving 
a tablespoonful for a dose, and do not repeat the medicine more than 
twice. 
In desperate cases only I substitute the ethereal tincture for the 
infusion, giving twelve or fifteen drops four times daily. Accord- 
ing to JPapillaud, arsenic and antimony have effects similar to that of 
digitalis, and are valuable remedies for diseases which depress the 
power of the heart. He prescribes the thirtieth of a grain of arseni- 
ous acid daily, and recommends still more the sixtieth of a grain of 
arsenite of antimony in pill twice a day. 
CHAPTER III. 
ATROPHY OF THE HEART. 
Etiology.—Congenital, or original diminutiveness of the heart, 
which, strictly speaking, cannot be called atrophy, occurs by preference 326 
DISEASES OF THE HEART. 
in the female sex (.RokitansJcy), accompanied by retarded develop- 
ment in general, but especially of the sexual organs. We know nothing 
of the manner in which it originates. 
Acquired atrophy occurs— 
1. In general marasmus, such as is developed in the course of tuber- 
cular consumption, cancerous cachexia, and cancerous suppuration, or 
in consequence of old age. Even attacks of acute disease, of long 
duration, such as protracted typhus, may cause atrophy of the heart. 
We also find that, although an abundant supply of nourishment is not 
sufficient, of itself alone, to cause the muscular tissue of the heart to 
grow, yet a scanty supply, or an abnormal consumption of it, may give 
rise to atrophy of the cardiac muscles, as well as to wasting of the 
muscular system at large. 
2. The heart atrophies when exposed to unusual pressure from 
without, just as the muscles of the extremities waste away under con- 
tinued compression of shackles or bandages. Atrophy of the heart 
also accompanies extensive pericardial effusion, fibrous thickening of 
the epicardium, and may even result from large accumulations of fat 
upon the organ. 
3. Contraction of the coronary arteries causes atrophy of the heart, 
by limiting the supply of nutritive fluid. 
Anatomical Appearances.—In congenital smallness of the heart, 
the heart of an adult may be like that of a child of five or six years of 
age, with thin walls, small cavities, and delicate valves (Rokitansky). 
Acquired atrophy is almost always concentric—that is, the thinning 
of the wall of the organ is accompanied by contraction of its cavities. 
Another characteristic sign, besides the reduction in size, and by which 
it may be distinguished from congenital smallness, consists in the dis- 
appearance of the fat of the heart, and in the serous infiltration of the 
connective tissue, in which the fat formerly lay. The pericardium is 
opaque, the white specks, which we so often find in the heart (Sehnen- 
flecke), are wrinkled, and the coronary arteries remarkably tortuous. 
The endocardium is also clouded, the valves of the veins swollen. 
The substance of the heart is usually pale, and its consistence less 
firm; in other cases, it is hard and dark. Ramberger very properly 
calls to our attention that, in many cases of concentric atrophy of the 
heart, there is a considerable quantity of liquid in the pericardial sac. 
This bears a certain analogy with the collections of water in the skull 
in atrophy of the brain—with hydrocephalus ex vacuo. 
Simple atrophy of the heart is much more rare. Here the organ 
is of normal size, but its walls are thinned. Hence the normal size 
can only be the result of dilatation of the cavities, so that this form 
of disease is allied to that described in a previous chapter. This ap- ATROPHY OP THE HEART. 
327 
plies still more forcibly to the excentric atropliy. The latter almost 
completely coincides with simple dilatation. Indeed, it would be almost 
impossible to decide whether the walls have been thinned by excessive 
distention alone (dilatation), or whether atrophy of their elements 
have contributed to their attenuation (excentric atrophy). True, the 
effect of the two conditions is not quite the same, for, if the walls of a 
dilated heart be also thinned (as they sometimes are by accumulation 
of fat about the heart, and as is observed most typically in the indu- 
rated thickening of the epicardium which remains after a chronic peri- 
carditis), we find the propulsive power of the organ to be much more 
reduced than is the case in simple dilatation. We have, finally, to 
mention that, when the contents of the left ventricle have been reduced 
as a result of contraction of the left auriculo-ventricular orifice, a most 
classical diminution in size and atrophy of the left ventricle is often 
observed. 
Symptoms ajto Course.—According to Laennec, congenital atro- 
phy of the heart is the cause of frequent attacks of fainting. Accord- 
ing to Hope, besides the tendency to faintness, the signs of defective 
nutrition of the body, great muscular debility, palpitation of the heart, 
signs of ancemia, and chlorosis, are to be found in persons suffering 
from congenital smallness of the heart. 
Acquired cardiac atrophy varies in its symptoms, according as it 
forms a part of a general state of marasmus, or stands alone, indepen- 
dent of poverty of blood or wasting of the general system. In the 
first instance, the symptoms are not very prominent. In fact, in certain 
cases, it can hardly be decided whether the enfeebled propulsive power 
of the heart depend upon lack of energy in its contraction, or upon 
atrophy of its muscles. In either case, the arteries are incompletely 
filled, and the blood accumulates in the veins. As, however, the blood 
itself is reduced in quantity, there are no signs of extreme venous en- 
gorgement. Severe dropsy, or well-marked cyanosis, is hardly ever 
met with in this form of atrophy of the heart. The bluish hue of the 
lips, the varicosities upon the cheeks of old men, the small effusions 
into the subcutaneous tissue in the hands and feet, which are usually 
cool and slightly bluish, are only partially dependent upon feeble pro- 
pulsive power. Atrophy of the lungs, as we have already seen, con- 
tributes largely to the establishment of these symptoms. 
Atrophy of the heart, arising in consequence of local derangements 
of nutrition, long-continued compression of the heart, or stricture of 
the coronary arteries, has a very different character. In the first place, 
the patient often complains of a distressing palpitation, a symptom 
which, as stated in a previous chapter, generally exists when the heart 
is unable to keep up the circulation without very great exertion. 328 
DISEASES OF THE HEART. 
Moreover, in consequence of the emptiness of the arteries, the veins 
are over-filled, and the retardation of the current of the blood gives a 
venous character to the latter, and occasions shortness of breath. The 
patients may become exquisitely cyanotic. General dropsy appears, 
and with it there is often great dyspnoea. If the atrophied heart be 
also dilated, an additional cause of engorgement of the veins and im- 
pediment of the circulation comes into play, and all the symptoms are 
much aggravated. But the progress of the malady is still more rapid 
and serious upon addition of a third cause—fatty degeneration of the 
cardiac muscles—the effects of which are quite similar to those of the 
first two, and which usually accompanies them. Such cases are tolera- 
bly common, and when old and feeble persons become blue and drop- 
sical, without having any valvular disease, it is generally owing to 
dilatation and degeneration of the substance of the heart, or else to 
extensive endarteritis deformans. An approximate diagnosis, at least, 
may be made sometimes by physical exploration. As long as the pa- 
tient remains at rest the heart-shock may be very feeble, or quite im- 
perceptible. The pulse is remarkably small. In some cases, the area 
of cardiac dulness has decreased with the diminution of the heart, a 
symptom which is only of value when it can be proved that diminution 
of the heart has caused vicarious emphysema, distending the lungs. 
In other cases, instead of extension of the lung, a large effusion into 
the pericardium fills the vacuum caused by shrinking of the heart, and 
the cardiac dulness is normal. In other cases, in which the lungs are 
also reduced in size, the pericardial effusion may be so profuse as to 
render the cardiac dulness abnormally large. The same is the case in 
atrophy of the wall of the heart with dilatation of its cavity. As, in 
hypertrophy, the heart-sounds are stronger and louder, so in atrophy 
they are either feebler or indistinct, or else they are muffled, and some- 
times murmurs are audible, which depend upon the conditions winch 
we have already mentioned, as causes of modification of the sounds of 
the heart. 
Treatment.—A real treatment of atrophy of the heart is out of 
the question. Of course, all violent efforts must be avoided, rich food 
be provided, and even the moderate employment of wine, “ vinum lao 
serum” may be permitted. 
CHAPTER IV. 
ENDOCARDITIS. 
Etiology.—We entirely agree with Virchow as to the pathogeny 
of endocarditis. He regards the hypothesis of the formation of a free 
exudation in this disease as not proven and even doubtful, and counts ENDOCARDITIS. 
329 
both this malady and the inflammation of the inner arterial tunics, 
from which the so-called atheroma proceeds, among the parenchyma- 
tous inflammations. This term is applied by Virchow to the active 
disturbances of nutrition which are provoked by an irritation, but 
which, instead of producing an exudation between the elements of the 
tissues, causes a swelling of the normal elements themselves, and a 
proliferation of their cells. In endocarditis the inflammation does not 
originate in the deeper layers of the endocardium, but upon its more 
superficial portions. They become enlarged, are infiltrated by a liquid 
■whose chemical properties resemble that of mucin, that is, it coagu- 
lates into the form of threads upon addition of acetic acid. In addition 
to this, a vast formation of new cells takes place, which immediately 
organize into connective tissue. It is only in very rare cases, in the 
so-called ulcerative endocarditis, that the proliferation of young cells 
goes forward with such activity that the tissue breaks down under 
their pressure, producing a loss of substance, an ulceration of the 
endocardium. 
The cause of endocarditis is somewhat obscure. It is seldom the 
result of direct irritation. Bamberger has only seen two cases of 
traumatic origin. The frequence with which the orifices and valves of 
the heart suffer from this disease scarcely leaves any doubt that endo- 
carditis, arising from internal causes, attacks those portions of the endo- 
cardium by preference which are especially exposed to strain and fric- 
tion from the action of the heart. Just as the pulmonary artery, which, 
though otherwise rarely atheromatous, if exposed to abnormal tension 
by hypertrophy of the right ventricle^is often attacked by atheroma; 
and just as the veins even undergo atheromatous degeneration when 
distended by a current of blood from a communicating artery, so in the 
heart, it is the narrow places, the outlets, which are most often dis- 
eased, but especially those portions of the valves which strike against 
one another in closing, the auricular surfaces of the mitral, and tricus- 
pid, and the convex faces of the semilunar valves. 
Whether primary idiopathic endocarditis ever occurs, and whether 
the disease independently can attack a previously healthy person who 
has been exposed perhaps to cold, may be doubted, yet it is not impos- 
sible. The great frequence of valvular disease, in individuals who pro- 
fess never to have suffered from any acute sickness, makes it probable 
that an idiopathic chronic endocarditis is not uncommon. In the vast 
majority of cases endocarditis arises in the course of acute articular 
rheumatism (Bamberger), and all the more readily the greater the 
number of joints attacked. It is idle to indulge in speculations as to 
how this complication comes about, as they cannot lead to any ser- 
viceable explanation. Although, however, acute articular rheumatism 330 
DISEASES OF THE HEART. 
is the most frequent cause of endocarditis, yet the number of cases in 
which rheumatism runs its course without it is far greater than was 
supposed for a long time, after the frequent coexistence of the two 
maladies had been recognized. 
The fact that a blowing sound can be heard in the heart, during an 
attack of acute rheumatism, is not by any means a sufficient evidence 
of the existence of endocarditis. Such a sound, which may be heard 
in at least one-half of all rheumatic attacks, depends, in a very great 
degree, upon the irregular tension of the valves, to which the excited 
and uneven action of the heart gives rise. According to the careful 
statistical compilations of Bamberger, the frequence of the complica 
tion of acute articular rheumatism with endocarditis may be rated at 
about twenty per cent. 
Next in frequence, endocarditis complicates Bright’s disease, ac- 
companying the acute form which develops after scarlatina, as well as 
the chronic form. Here, too, the tendency to inflammation in the 
heart, serous membranes, and lungs, set up by this affection of the 
substance of the kidney, remains inexplicable. 
The endocarditis which comes on during acute febrile maladies, 
especially acute infectious disorders, is closely allied to the above 
mentioned forms. The disease seems to arise frequently from puer- 
peral fever, while Wunderlich regards measles as the most prolific 
cause of endocarditis next to rheumatism. According to the experi- 
ments of Billroth and Weber, it seems not improbable that the blood 
of a fever patient acts as an inflammatory irritant, and that individuals 
laboring under violent fever, no matter what its cause may be, are 
liable to secondary inflammation of various organs, and especially to 
inflammation of the endocardium. If this supposition be true, the fre- 
quence of the complication of articular rheumatism and endocarditis is 
attributable to the intensity which rheumatic fever often acquires. 
The existence of a diseased valve is frequently the cause of endo- 
carditis. It is a matter of common experience, that a patient, at first, 
may have a simple valvular disease arising from acute rheumatism, 
but after a time, and without his having had any fresh rheumatic at- 
tack, the valvular affection become a complicated one, compelling us 
to infer that it is the result of a latent endocarditis. 
The endocarditis which accompanies myocarditis, and pericarditis, 
must be considered as the result of extension of the disease by con- 
tiguity. As a very great rarity, inflammation of the lungs or pleura 
also spreads to the endocardium. 
Anatomical Appearances.—As nearly all the congenital defects 
of the heart which are attributable to a former endocarditis are found 
in the right side of the organ, it would seem that the right side of the ENDOCARDITIS. 
331 
heart is especially liable to this disease during foetal life. On the other 
hand, in extra-uterine life, it is almost as exclusively the left heart in 
which we find endocarditis. Inflammation hardly ever affects the 
whole lining of the organ, but confines itself rather to patches of vary- 
ing size. As we have already remarked, however, it is from the valves, 
and especially from the parts of them already alluded to, that the in- 
flammation is apt to proceed. 
It has been customary to mention reddening and injection of the 
endocardium as the first sign of endocarditis. Rokitansky, however, 
observes, that it is only possible in rare instances to obtain a view of 
an endocarditis in this stage, and warns against confounding the red- 
ness of injection with the infiltration of the endocardium which takes 
place after death. Foerster points out that this reddening by injection, 
which we find surrounding points which have already undergone fur- 
ther derangement of texture, may be distinguished from the reddening 
of post-mortem imbibition, as the latter is darker and merely involves 
the superficial coats, while the reddening from injection exists in the 
deeper layers only, in which, by means of the microscope, we may see 
the capillaries filled with blood to bursting. 
Very soon we find a puffiness and swelling of the endocardium, as 
its external layer thickens and enlarges. Virchow describes this in- 
crease in volume as “ consisting of a homogeneous, translucent, toler- 
ably clear ground-substance, in which so many cells are imbedded, that 
it might seem, at first sight, as though it were an accumulation of 
growing epithelium.” 
Besides this diffuse swelling of the endocardium, reddish or grayish- 
red delicate villi often develop as the disease advances, which give the 
endocardium a fine, granulated aspect, and which, sometimes, rapidly 
grow into tolerably thick, coarsely granular papillae and warts. These 
are very hard and firm at their base, while their round, bulbous, free ex- 
tremities appear soft and gelatinous. At the base we find perfectly- 
formed connective tissue, while the apex is still filled up by elements 
which have not as yet organized into connective tissue. These excres- 
cences, known as valvular vegetations, are outgrowths from the endocar- 
dium, from proliferation of its connective tissue. Upon the auriculo- 
ventricular valves, these excrescences often form a border of varying 
width, close to the free edge of the valve, and spread hence, particu- 
larly upon the chordae tendineae. On the semilunar valves, they 
generally proceed from the noduli Morganii. We must beware of 
mistaking the fibrinous deposits, which are apt to form upon the rough 
and uneven surfaces of the valves, and almost always cover them, 
for the vegetations themselves. 
This swelling of the endocardium, which is afterward converted 332 
DISEASES OF THE HEART. 
from a gelatinous to a semi-cartilaginous consistence, and leads to per- 
manent tliickening and rigidity of the valves, and the retraction and 
shrinking of the thickened valves, in which chalky masses often form, 
are much the most common causes of valvular disease of the heart. 
When the vegetations grow old, calcification may also take place in 
them, so that irregular lobulated masses, of stony hardness, cover the 
shapeless valves. While the anatomical alterations hitherto described 
are the most common results of endocarditis, there may appear as less 
usual accompaniments of the disease— 
1. Laceration of the endocardium. This may readily be accounted 
for, from the relaxation and softening which the endocardium under- 
goes. It is the chordae tendineae which give way with the greatest 
frequence; and it is easy to see that the proper tension of the valve 
during systole must then be materially interfered with. In other 
cases the valve itself tears; in others, one surface of a valve alone is 
torn ; the blood which penetrates through the rent, causing the oppo- 
site surface of the endocardium to bulge in the form of a sac, consti- 
tuting an aneurism of the valve. It is rare for the endocardium to give 
way at any point in the muscular wall of the heart—although, should 
this happen (but only in such a case), it may be possible for the sub- 
stance of the heart-wall to take part in the inflammation—for the blood 
to force its way into the rupture, and more or less to tear asunder the* 
cardiac muscles, so as to produce an acute aneurism of the heart, a 
rounded, circumscribed sac, seated upon the wall of the heart, as an 
appendage, bounded at its entrance by torn and ragged endocardium, 
its wall consisting of the forcibly separated fibres of the muscular sub- 
stance of the organ. 
2. The adhesions of the chordae tendineae, and of the edges of the 
valves either to one another or to the wall of the heart, to which en- 
docarditis sometimes gives rise, are of quite as much importance, and 
produce consequences quite as grave, as do the lacerations; for, by 
adhesion of the edges of the valves, or of the chordae tendineae to 
one another, the auriculo-ventricular orifice becomes very much con- 
tracted ; and, by adhesion of the valves or chordae tendineae with the 
heart-wall, closure of the mitral orifice during systole of the ventri- 
cle is rendered impracticable. We shall discuss this subject more fully 
while treating of valvular disease. If we reflect that the heart is in 
constant action, and that during the formation of these adhesions the 
parts must have been in a constant state of alternate contact and sep- 
aration, the formation of these adhesions will appear more difficult to 
account for than any other anatomical change which occurs in endo- 
carditis. 
In ulcerative endocarditis there are irregularly-shaped, abruptly- ENDOCARDITIS. 
333 
defined losses of substance in the endocardium, which, immediately 
around the ulcer, is swollen and thickened. The floor of the ulcer 
is formed by the muscular substance of the heart, which is infiltrated 
with pus. 
Endocarditis is accompanied by myocarditis, that is to say, the car- 
diac muscles take part in the inflammation with far greater frequence 
than was formerly supposed. At other times, the inner layers of the 
cardiac wall which lie next to the inflamed endocardium become the 
seat of infiltration, which fully explains why the cardiac wall loses 
its tone, and why endocarditis is apt to be followed by dilatation of the 
heart. 
The fibrinous deposits, which almost always cover the vegetations 
upon the valves, may, if broken loose by the current of the blood, occa- 
sion disorder of a different kind; and baneful as the ulterior effects of 
endocarditis are upon the system, yet almost the only source of dan- 
ger, during the height of the disease, consists in the liability of these 
little coagula (emboli) to wash away. Should any of them be broken 
off by the current and borne into the circulation, haemorrhagic infarction 
and metastatic abscess will be the result. We have discussed the pa- 
thogeny of these processes in detail, while treating of metastasis into the 
lung. Here, however, it is not the lungs in which the infarctions arise, 
but, in the vast majority of cases, the embolus gets into the artery of the 
spleen, blocks up some one of its minuter branches, and, a wedge- 
shaped spot, with the apex pointing inward and the base outward, is 
established, which is at first of a blackish red, afterward assumes a 
yellow hue, and passes into a state of caseous degeneration. 
We sometimes see spots of this kind in the kidney; but they are 
far more rare than haemorrhagic infarction of the spleen, which is met 
with post mortem, with extraordinary frequence. In the liver they 
are still less common, and, as we have just observed, they are rarest 
of all in the lungs. In the two latter organs indeed, one could hardly 
conceive of the occurrence of infarction, unless a branch of the hepatic 
artery or bronchial artery, but not of the portal vein or pulmonary 
artery, were to be obstructed. 
That abscesses, instead of infarction, should be so rarely found in 
endocarditis, is explained from what we have said already upon the 
pathogeny of metastasis. The embolus which here obstructs the 
artery does not come from a collection of putrefying material, as 
emboli of the lungs so often do, but consists of coagulated fibrin, a 
fact which is unfavorable for the conversion of the infarction into an 
abscess. 
Should a somewhat large fibrinous clot pass into one of the caro- 
tids, or vertebral arteries, then, accordingly as the artery of the brain is 334 
DISEASES OF THE HEART. 
totally or partially occluded, it causes the formation of haemorrhagic 
foci (capillary apoplexy) with their consequences, or else gives rise to 
partial anaemia, and consequent necrosis of the anaemic portion of the 
brain (yellow softening). Indeed, occlusion of the greater vessels of 
the extremities, by a large embolus, may even occasion spontaneous 
gangrene of the toes. 
We are entirely unauthorized, by the occurrence of metastasis, to 
infer that perforation of an exudation from the deeper layers of the 
endocardium to its free surface has taken place, as the coagula entirely 
suffice to account for the symptoms. Nor are we warranted in diag- 
nosing a septicaemia, from the appearance in an endocarditis of signs 
suggestive of septic poisoning, since it is not to be supposed that any 
exudation which might make its way to the free surface of the endo- 
cardium could be a septic one, or could infect the blood. 
Symptoms and Course.—When endocarditis supervenes upon an 
attack of acute inflammatory rheumatism (and, as stated above, this is 
by far its most common commencement), there are often no subjective 
symptoms to warn the patient of the new enemy which is stealing 
upon him, and who frequently does not declare himself in all his malig- 
nance for weeks, months, nay, for years afterward. If we ask a patient, 
with valvular disease, whether he has ever had articular rheumatism, 
he often answers in the affirmative; if, however, we ask him whether 
during his attack he has ever suffered from pain in the region of the 
heart, or from oppression or palpitation, he almost always will deny 
it. It is not very different if we watch the patient ourselves. Gen- 
erally he does not complain, even when we make special inquiry as to 
the existence of this kind of trouble; and we must depend for our 
diagnosis upon physical examination alone. 
In other instances, however, functional disturbance, more or less dis- 
tinct in character, certainly does arise. Pain in the cardiac region, how- 
ever, never appears to proceed from simple, uncomplicated endocar- 
ditis, even although we make pressure upon the thorax or epigastrium. 
In a few, but very rare instances, the frequence of the pulse increases 
with the commencement of the endocarditis, and may even become 
extremely great. We shall not lose ourselves in speculations as to 
the cause of this augmented frequence of the heart’s action, which is 
sometimes enormous, nor shall we attempt to decide whether it be due 
to sympathy of the muscular portion of the heart, or to irritation of 
the ganglia seated in its walls, but shall confine ourselves to announ- 
cing the fact. It is at least equally hypothetical to assume that there 
is an ulcerative form of the disease in the cases of endocarditis marked 
by acceleration of the pulse. 
As increased frequence of the heart and pulse-stroke often coex- ENDOCARDITIS. 
335 
ist with a reduction of the energy of the heart, which may fairly be at- 
tributed to its infiltration with serum, the pulse is frequently small, and 
the fever assumes the character of extreme adynamy, so that it be- 
comes liable to be mistaken for other asthenic fevers, typhus, etc. 
The statement that an unobserved endocarditis is the source of many 
fevers spoken of as nervous, febris simplex, versatilis, torpida, putrida, 
etc., is an exaggeration, as the disease seldom takes the latter form. 
When endocarditis is attended by metastasis, especially metastasis to 
the spleen, the fever becomes aggravated, and rigors occur, but the 
presence of septicaemia cannot be inferred from such symptoms alone, 
since both of them arise (although they are not constant) when 
metastases form in the spleen, from the detachment of clots, or frag- 
ments of the valves, in cases of long-standing valvular disease, where 
septicaemia is out of the question. 
Palpitation of the heart is a more common symptom than excite- 
ment of the pulse. The reason for this is at once clear, when we re- 
member that the action of the heart is always embarrassed by infiltra- 
tion of its muscular substance, and that palpitation is usually comp 
plained of the most when the performance of its function has become 
laborious, as well as excessive, and that it does not proceed from the 
abnormally vigorous action of the hypertrophied heart. This serous 
infiltration of the cardiac muscles, which sometimes arises in endocar- 
ditis, and the consequent debility and imperfect action of the heart, 
also account for the dyspnoea which accompanies the palpitation. 
In the chapter upon hyperaemia of the lung, we have explained 
why these symptoms are attended by passive hyperaemia. If insuffi- 
cience of the mitral actually be established while the endocarditis is 
still in progress, if blood be regurgitated into the auricle during the 
systole of the ventricle, the Venous engorgement of the lungs and the 
dyspnoea are all the more severe. 
From what we have said regarding the symptoms of endocarditis, 
especially from the fact that, in a great number of cases, there is abso- 
lutely no disturbance of the functions, it will readily be perceived that 
the malady seldom runs its course in a well-defined manner, like in- 
flammation of other important organs. Neither does the commence- 
ment of the disease often admit of detection, nor can its progress often 
be followed up, nor, to say the truth, can we well fix the point where 
endocarditis ceases, and that malady begins which we call valvular 
disease. Disease of the valves is indisputably the most common 
sequel of endocarditis, the valves either remaining thickened, and 
afterward shrinking, or the chordae tendinece and edges of the valves 
adhering, or rupture of one or other of these parts occurring. As re- 
traction of the thickened valves commences gradually, and progresses 336 
DISEASES OF THE HEART. 
slowly, and as adhesions of the valve-tips and chord® tendine® only 
take place by degrees, it may happen that, immediately after an attack 
of endocarditis, there may be no perceptible defect of the valve ; yet 
valvular disease may become apparent after the lapse of some months. 
If, however, the chord® tendine® suffer rupture, or if an orifice be 
blocked up by vegetations, the transition from endocarditis into val- 
vular disease is immediate. In a previous chapter we have shown how 
endocarditis may cause dilatation, and afterward lead to hypertrophy 
of the heart. 
The usual termination of endocarditis is death from disease of the 
valves, which is almost always its sequel; but this fatal result does 
not generally ensue until years have elapsed, and it is rare for a 
patient to die suddenly of endocarditis alone. Such a termination 
hardly ever takes place in the form of disease, which complicates acute 
articular rheumatism. It is somewhat more common in the variety 
which accompanies Bright’s disease, or the infectious maladies, and 
here it usually is difficult to determine what part in the fatal issue the 
original disease has played, and what the complication. Palsy of the 
heart, engorgement of the lungs with consequent oedema, in very rare 
instances exhaustion through fever, symptoms of softening of the brain, 
of metastasis into the spleen, kidneys, and liver, even gangrene of the 
toes, are symptoms with which death may then take place. Recovery 
from endocarditis may occur often enough if the valves be spared by 
the inflammation. White, thickened, and opaque spots, upon the 
interior of the wall of the heart, are often found post mortem, without 
having produced any symptoms during life. Even inflammation of the 
valves may terminate in recovery, if the thickening, which probably 
always remains, does not derange their function. Experience does 
not show this termination to be common. Although the valves may 
act normally at first, yet they are afterward liable to become the seat 
of fresh irritation, until, at last, deformities arise capable of deranging 
their function. 
We have hitherto described endocarditis such as complicates rheu- 
matism of the joints. The functional symptoms, the progress, and the 
consequences of an endocarditis which complicates an existing disease 
of the valves present no new feature to the picture. This is also the 
case in that form of the malady which complicates acute infectious 
diseases. Here the symptoms of the main affection mask those of the 
complication so fully, that an exact clinical description of them can 
scarcely be given; in particular, the delirium, stupor, albuminuria, 
jaundice, etc., which certainly are very common accompaniments of 
this form of endocarditis, do not depend upon the endocardial disorder 
for their cause, but rather are a result of the infection of the blood and ENDOCARDITIS. 
337 
of the intense fever arising from such infection. Physical examination 
alone can give us the required information, and it should never be neg- 
lected, though no special signs demand such investigation. With 
regard to the origin and course of endocarditis complicating chronic 
Bright’s disease, as this form too usually presents no subjective symp- 
toms, it is overlooked in most cases if physical exploration be neg- 
lected. 
Physical Signs.—The impulse of the heart in the commencement 
of the attack is almost always stronger and more extended than 
natural. The smallness and softness of the pulse, when the muscles 
of the heart are infiltrated with serum and contract feebly, in spite of 
their furious action, bear striking contrast to the above. The cardiac 
dulness is normal at first; but, after a few days (Skoda), the outflow 
from the pulmonary veins may be so much embarrassed that the 
blood accumulates in the left auricle, and the obstruction extends 
through the vessels of the lungs into the right heart. The right 
heart is imperfectly emptied, and soon becomes dilated by the blood 
entering from the vena cava. Hence, as we have already seen, the 
dulness is rendered abnormally broad. If the tissue of the valves be- 
come softened, and the valves themselves thickened by the inflamma- 
tion, it is easy to see that the heart-sounds must also undergo modifi- 
cation. It is impossible for the softened and thickened valve to 
vibrate, like the hard and delicate valve. As the first sound of the 
heart in the left ventricle proceeds from vibration of the mitral, the 
substitution of an abnormal murmur at the apex for the first cardiac 
sound is the most frequent and important sign of endocarditis, which 
usually has its seat in the left heart. Besides, the thickening of the 
delicate web on the outer edge of the mitral prevents it from unfold- 
ing freely, and keeps the softened chordae tendineae from completely 
fixing the valve, which, if the chordae tendineae be broken, may even 
be folded backward toward the auricle during the systole of the ven- 
tricle. All these forces combine to render it impossible for the valve 
to perform its function during systole of the ventricle, and to prevent 
regurgitation of blood into the auricle. That condition, where the 
valve loses the power of acting as a valve, is called “ insujfi- 
cience.'>'> If, however, the valve be but partially fixed, if part of it 
be free to flap in either direction, if some of the blood pressing against 
it be opposed by a portion only of its lower surface, while the rest, 
flowing back into the auricle, bathes its upper face, the vibrations of 
the mitral become entirely abnormal and irregular, and give rise to 
another murmur, which takes the place of the first sound of the left 
ventricle. We have seen that the second sound that we hear at the 
apex is, under normal conditions, produced by vibration of the semi- 338 
DISEASES OF TIIE HEART. 
lunar valves of the aorta, whence it is conducted to the apex. In the 
normal heart, the entrance of blood into the ventricle is unaccompanied 
by any murmur or other sound. If, however, in endocarditis, the 
auricular face of the mitral-valve be studded with warty excrescences, 
and if the blood have to flow over a rugged surface instead of a smooth 
one, friction of the blood-stream produces a murmur which is audible 
at the apex during the diastole of the ventricle. The second tone, 
propagated from the aorta, may also be heard with it, or the latter 
may be drowned by the intensity of the new murmur, and thus be im- 
perceptible. The larger the excrescences, and the more they encroach 
upon the orifice, so much the more intense is the friction of the blood, 
and so much the louder the murmur. In the extremely rare cases in 
which the right ventricle is the seat of endocarditis, similar symptoms 
may be made out at the lower part of the sternum, where we listen to 
the -sounds of the tricuspid. It would be exceedingly difficult, how- 
ever, to make a diagnosis here, as the right ventricle is hardly ever the 
sole seat of disease, and we should scarcely be able to distinguish 
whether the sounds were conducted from elsewhere or actually origi- 
nated at the tricuspid. The sounds of the aorta are usually pure, as its 
valves are far more seldom attacked by endocarditis. Should it occur, 
however, should warty growths form upon the lower sides of the semi- 
lunar valves, a murmur, produced by friction of the blood upon these 
asperities, arises during systole of the ventricle, which is best heard at 
the root of the aorta—i. e., at the sternum, on a level with the second 
intercostal space, and which is conducted hence along the carotids. It 
is much less common to hear a diastolic murmur at this point than a 
systolic one. 
We hear normal heart-sounds at the pulmonary artery almost 
always, as the disease hardly ever extends as far as this. On the 
other hand, we often hear a remarkably loud and sharp accentuation 
of the second sound of the pulmonary artery, which is a sign of im- 
portance. The fuller the pulmonary artery becomes, so much the 
stronger does the shock grow which its semilunar valves must sustain 
during diastole. Now, as an acute insufficience of the mitral develops 
in the majority of cases of endocarditis, the pulmonary artery must 
puffer distention and its second sound must become intensified. 
Diagnosis.—Endocarditis occurring in the course of acute rheuma- 
tism is often overlooked, and quite as often its presence is diagnosti- 
cated where it does not exist. In order to avoid the former error, 
never fail to auscult all patients with acute articular rheumatism daily, 
even in the absence of all complaint or constitutional disturbance. 
That you may not rush from Scylla into Charybdis, however, beware 
how you declare an endocarditis upon the mere occurrence of a blow- ENDOCARDITIS. 
339 
ing sound, audible at the apex. The symptom may, indeed, be due to 
thickening of the valve by inflammation, but it is quite as likely to be 
dependent upon mere abnormal tension of a healthy valve, caused by 
violence of fever or irregular action of the heart. Neither condition 
can be determined from the quality of the murmur, and diagnosis re- 
mains a matter of doubt until the signs of dilatation of the right ven- 
tricle and overloading of the pulmonary artery, lateral extension of 
cardiac dulness and intensification of the second pulmonary sound, 
supervene upon the murmur. 
The differential diagnosis is still more difficult between a recent 
endocarditis complicating articular rheumatism and an old valvular de- 
rangement, which happens to preexist, especially insufficience of the 
mitral. Such cases are by no means rare. There are few maladies 
which have so great a tendency to relapse as acute articular rheuma- 
tism ; indeed, we meet with sufferers who have had attacks of it, of 
more or less severity, every year since its first onslaught. If we have 
not previously seen or examined them, and if upon some fresh relapse 
we hear a systolic blowing at the apex, the cardiac dulness extending 
laterally, and the second pulmonary tone being sharply accented, we 
must remain in doubt, unless the signs of dilatation of the right ven- 
tricle have attained such a height as cannot be ascribed to acute in- 
sufficience. In other cases we may perhaps ascertain if, after any of 
his previous illnosses, the patient have remained short of breath, etc. 
Prognosis.—Rarely as life is threatened by endocarditis itself, the 
prognosis of this malady as to complete recovery is bad. Indeed, in 
the cases in which the disease is recognized; it almost always leaves 
derangements behind it, which sooner or later imperil life. Endocar- 
ditis, which attacks the wall of the heart, is, no doubt, far less dan- 
gerous ; but it occurs rarely, and, moreover, is quite unrecognizable. 
Symptoms which would lead us to fear an unfavorable termination 
to this disease are those which indicate considerable implication of the 
muscle of the heart in the inflammation, such as an extremely frequent 
pulse with scanty filling of the arteries. Rigors are quite as ominous, 
ndeed more so, as well as acute swelling of the spleen, or pain in that 
region, vomiting, or the appearance of blood or albumen in the urine, 
or symptoms of hemiplegia, in short, the signs of metastasis. 
Treatment.—The indication as to cause in treatment of endocar- 
ditis cannot, as a rule, be met. A genetic connection undoubtedly ex- 
ists between acute articular rheumatism and this disease, whether the 
former merely predispose to the latter, or whether the alliance be still 
more intimate. Great, however, as is the number of remedies and 
modes of cure recommended for rheumatism, it is only equalled by 
their untrustworthiness. "VVe are no less helpless against the morbus 340 
DISEASES OF THE HEART. 
Brightii, the acute exanthemata, and the other infectious maladies, 
which give rise to endocarditis, or, at least, predispose toward it. 
With regard to the indications from the disease and the antiphlo- 
gistic apparatus, we have already and repeatedly declared that the 
majority of the so-called “ antiphlogistics,” and, above all, venesection, 
often as they are employed in inflammation, have no right to the name. 
But, in spite of contrary assertions on the part of French and English 
physicians, there is, perhaps, no affection in which the practice of 
bleeding without special occasion, as well as the employment of 
calomel and “blue ointment to reduce the plasticity of the blood,” is 
so dangerous as in endocarditis; and we must entirely agree with 
Bamberger, when he states his belief that most patients, who die 
during an attack of this malady, have perished less from the disease 
than from the treatment. 
Even local blood-letting should only be resorted to where there is 
pain about the heart, and here we generally have to do with complica- 
tions. With regard to cold, which we have employed against inflam- 
mation of internal organs as freely as it has been used in inflammation 
of external parts, we do not apply it in these cases, unless especially 
demanded by extreme excitement of the heart’s action, inasmuch as, 
according to our experience, even when applied upon inflamed joints in 
rheumatism, it has but trifling palliative effect. Indeed, although 
many cases of endocarditis, which used formerly to escape diagnosis, 
are now recognized through pleximeter and stethoscope, yet their 
treatment is no more successful than before; nay, if the physician find 
the evidence of the presence of endocarditis an occasion for meddle- 
some treatment, it were better for the patient had the doctor never 
learned auscultation. 
The indication as to symptoms calls for venesection in cases where- 
in overcharge of the pulmonary circulation imperils life by threatening 
oedema of the lungs, and demands prompt relief by diminution of the 
volume of the blood. A great acceleration of the pulse and signs of 
feebleness in the action of the heart, cyanosis, etc., indicate the exhi- 
bition of digitalis. Should palsy of the heart threaten, stimulants 
must be used. 
CHAPTER Y. 
Etiology.—Myocarditis consists of an inflammation of the muscu- 
lar fibres of the heart, whereby they are softened, become flabby, and 
finally disintegrate. This destructive process is accompanied by pro- 
liferation of the perimysium; the gaps formed by absorption of the 
MYOCARDITIS. MYOCARDITIS. 
341 
primitive fasciculi are filled up by connective tissue, and thus a scar is 
formed in the heart-wall; or else the perimysium breaks down simul- 
taneously with the muscular fibrillae, and a mass of debris collects in 
the substance of the wall. This is called an abscess of the heart. 
Myocarditis is not a rare affection, and we find post-mortem signs 
of its former existence in many cases of valvular disease of the heart 
resulting from endocarditis. Indeed, the etiology of myocarditis is, in 
a great measure, identical with that of endocarditis, acute articular 
rheumatism acting most frequently as the cause in either disease. 
Myocarditis, thus excited, usually appears in the form of mere circum- 
scribed spots, which terminate in scar-like alterations of a portion of the 
cardiac wall; but in more rare instances it may result either in extensive 
degeneration, which may give rise to a chronic aneurism of the heart, 
or else may produce cardiac abscess. In most cases we may regard 
myocarditis accompanying acute rheumatism as an extension of a con- 
comitant endo- or pericarditis. In other cases, however, the disease 
runs a more independent course, is more extensive than any attendant 
endo- or pericarditis, which, in their turn, may then be considered as de- 
pending upon the inflammation of the heart’s substance. 
Chronic disease of the heart, particularly valvular disease, leads to 
myocarditis, and to formation of scars in the heart quite as often as 
to endocarditis. 
Emboli, proceeding from gangrenous lungs, not unfrequently enter 
the coronary arteries of the heart, and we then see numerous abscesses 
in its wall, as well as abscesses in many other organs of the aortic 
circulation. 
Septicaemia, protracted typhus, tedious and malignant scarlatina, 
even though the occurrence of embolism be not proved, nay, though it 
be very unlikely, may also give rise to abscess of the heart. The 
pathogeny of such abscesses is obscure. 
In the second volume we shall treat of syphilitic myocarditis, when 
we come to treat of syphilis in general. Traumatic myocarditis, like 
traumatic endocarditis, is one of the greatest of rarities. 
Ax atomical Appearances.—The seat of myocarditis is almost ex- 
clusively the left ventricle, especially the apex; but quite as frequently 
(according to Dittrich) it occurs in the septum just below the aorta. 
The papillary muscles, however, are often affected by the disease, 
which fact is of importance to the pathogeny of deformity of the valves. 
At the outset of the malady, the muscular substance appears of a 
dark bluish-red hue. Soon, however, the injection disappears, and dis- 
coloration of the muscular fibre arises, the diseased place becoming of 
a grayish color and softened. Under the microscope, after the trans- 
verse and longitudinal striae have disappeared, we see the fibrillae 342 
DISEASES OF THE HEART. 
broken down into a finely-granular detritus, with a few fat-globules. 
We can rarely get opportunity to observe myocarditis in this stage. 
Much more commonly we find its results, in the form of irregular, rami- 
fying collections, varying in size, of a reddish-white or white color, and 
of a scar-like density, scattered through the muscular substance of the 
heart. Sometimes this indurated tissue is spread over a large portion 
of the heart-wall, and forms its sole component. Here the degener- 
ated wall may yield to the pressure of the blood; a protrusion may 
form, and a true aneurism of the heart result, which is to be distin- 
guished as chronic cardiac aneurism from that form described as acute 
cardiac aneurism, in treating of endocarditis. Such sacs may attain 
the size of a hazel-nut or even that of a hen’s egg, or larger. The 
scar-like walls usually grow thin from distention; they sometimes 
ossify, and quite often their cavity contains masses of stratified fibrin, 
such as wre find in aneurism of arteries. The entire heart is generally 
dilated as well as the aneurism, and, even when there is no aneurismal 
pouch, numerous scars in the heart-wall will cause dilatation of the 
organ. On the other hand, large scars in particular situations, as at 
the approach to the aorta, may cause diminution of the capacity of the 
heart (Dittrich)s true cardiac stricture). 
When endocarditis terminates in abscess, discoloration and soften- 
ing prevails more and more in the muscle, until at last a collection of 
yellow, purulent liquid, surrounded by softened and discolored muscu- 
lar substance, is formed. Such an abscess rarely becomes incapsulated 
and dries up; perforation nearly always takes place, unless death occur 
beforehand. If the perforation be into the pericardium, pericarditis 
follows; if into the cavity of the heart, the debris of its broken-down 
tissue passes into the circulation, and numerous metastases are often 
the consequence. The insertion of an aortic valve may be torn away 
by the inward pointing of an abscess ; or communication between the 
two sides of the heart may be set up; even the entire cardiac wall 
may suffer rupture. Tearing up of the muscular structure of the 
heart by infiltration of the blood, which we have described in a pre- 
vious chapter as acute cardiac aneurism, may, of course, occur with 
equal or even greater ease in consequence of the pointing of such an 
abscess to the interior. 
Symptoms and Course.—Myocarditis is but seldom diagnosticated 
with certainty during life. As a mild form of the disease complicates 
almost every case of endocarditis, we seem warranted in the inference 
that the substance of the heart is more seriously inflamed when the 
region around it appears unduly sensitive (which it never is in pure en- 
docarditis), still more so if there be great acceleration of the pulse, if 
the pulse grow small, or, above all, if the heart’s action become irreg MYOCARDITIS. 
343 
ular. Even then, however, our opinion will only amount to a some- 
what vague suspicion. Diagnosis of myocarditis grows more sure, but 
not certain, when symptoms appear in the course of acute rheumatism 
which suggest diseases of the heart, while physical examination affords 
negative evidence of endo- or pericarditis. If, now, rigors should set 
in, or swelling of the spleen, or pain in the region of the spleen, vomit- 
ing, or pain in the region of the kidneys, with the presence of albumen 
and blood in the urine ; in short, if metastases be established, the diag- 
nosis becomes tolerably certain: but such cases are not common. 
If cicatrices have formed at numerous points in the heart, and if 
the heart be dilated in consequence, symptoms of dilatation appear, 
such as we have already described, only they are more severe; and it 
is impossible to say, in most cases, what parts the dilatation and de- 
generation respectively play in retarding the circulation and overload- 
ing the venous system. Thus, in the diagnosis of mitral insufficience, 
we may bear in mind that it may possibly have been induced by de- 
generation of the papillary muscles. Extensive scar-like degeneration 
of the heart-wall, as well as true cardiac stenosis of Dittrich and 
chronic cardiac aneurism, causes symptoms of extremely depressed ac- 
tion of the heart. The beat is scarcely perceptible, the arterial pulse 
is extremely small and weak as well as very irregular and intermittent. 
Extreme cyanosis and general dropsy accompany these symptoms. If 
called upon for a diagnosis in a case of this kind, after exclusion of 
valvular deformity as a cause of the derangement of circulation, we 
must count diffuse cicatricial formation as one of the alterations of 
structure capable of producing the train of symptoms above described; 
but we shall hardly ever make an absolutely certain diagnosis by the 
system of exclusion of other anatomical changes, such as dilatation 
with atrophy, extensive fatty degeneration, etc., etc. 
As for abscess of the heart and the various results of perforation, 
we are rarely able to form more than a vague diagnosis after the nu- 
merous metastases have arisen. We have no means of ascertaining 
this condition with certainty. 
Treatment.—We can hardly speak of the treatment of myocardi- 
tis, having almost denied the possibility of recognizing its existence. 
Should it be possible to diagnosticate the disease, the treatment would 
not differ from that of endocarditis. It is, of course, out of our power 
to remove the cicatrices, or to avert the embolism from perforation of 
an abscess, or to allay its effects. A mere treatment of symptoms id 
all that can be effected. 344 
DISEASES OF THE HEART. 
VALVULAR DISEASE OF THE HEART. 
By valvular disease of the heart, in its narrowest sense, we mean 
merely those anomalies of its valves which affect the function of the 
organ, and thus react upon the circulation. Valvular anomalies which 
give rise to no symptoms, and which hence are purely matters of pa- 
thologico-anatomical curiosity, and not of clinical interest, need but 
little notice in the following chapter. They are— 
The so-called simple hypertrophies of the valves, which are found 
chiefly upon the mitral near its free border, whence is found growing 
a series of little lumps of a jelly-like connective tissue. The fine web 
on the lower border, upon whose unfolding the valvular action mainly 
depends, remains intact in hypertrophy, while endocarditis usually has 
the effect of thickening it, and, as it were, rolling it up. 
The next deformity of the valves, which does not derange their 
action, is enlargement, which often occurs in them with simultaneous 
thinning, when the ostium is abnormally dilated. Most cases of per- 
foration of the valves also belong under this head. Small oval fissures 
or holes are often seen in them, which, however, do not seem to impair 
their efficiency. 
The most important valvular changes are those known as insuffir 
cience and contraction. These two alterations nearly always coexist, 
one usually prevailing over the other, however, in degree. By insuffi- 
cience, we mean that condition of a valve which renders it incapable 
of preventing regurgitation of blood into the cavity which, as a valve, 
it should close. If the entire contents of the ventricles be not thrown 
into the aorta and pulmonary artery during systole, and if a portion 
of the blood regurgitate into the auricles, the mitral or tricuspid are 
insufficient. Again, if, during diastole of the ventricle, part of the 
blood which had entered the aorta and pulmonary artery flow back 
into the ventricle, the semilunar valves are insufficient. 
By stenosis (constriction) of a valve, or, more properly speaking, 
of an orifice, we mean that condition by which the effluent blood 
meets 'with abnormal resistance through contraction of the outlet of 
the heart. 
Although valvular deformities have, in common, the effect of re- 
tarding the circulation, the influence upon the distribution of the blood 
varies according to the seat of the affection. The system can endure 
valvular deficience at one point much better than at another; hence 
we deem it better at once specially to describe its effects at the differ- 
ent outlets, rather than to go into a further general discussion of the 
subject. We cannot altogether avoid repetition, by this method of SEMILUNAR YALYES— THE AORTIC ORIFICE. 
345 
treating the subject, but shall thus have less to repeat, and, moreover, 
less to retract, than by any other mode. As the pathogeny of valvular 
defect of the aorta is much more simple than that of mitral disorder, 
as its symptoms are easier of comprehension, and as its consequence? 
are much longer and better withstood than are those of mitral defi* 
cience, we shall first take up the subject of aortic valvular disease. 
Derangement of the valves is of far less common occurrence in the 
right than in the left heart, so that we shall reserve the discussion of 
the former until the last. 
CHAPTER YI. 
INSUFFICIENCE OF THE SEMILUNAR VALVES, AND CONSTRICTION OF 
THE AORTIC ORIFICE. 
Etiology.—Closure of the semilunar valves takes place in a man- 
ner purely mechanical, while a certain vital action is required to effect 
closure of the valves between ventricle and auricle, namely, contrac- 
tion of the papillary muscles. If the mere pressure of the blood during 
diastole of the left ventricle do not suffice to deploy and press together 
the leaves of the semilunar valve, which were pushed up against the 
wall of the aorta during systole, there will be regurgitation of blood 
into the ventricle, and the valve is insufficient. If, however, during 
systole, the semilunar valves do not yield to the current of the blood, 
and lie back against the aortic wall as it emerges from the left ven- 
tricle, but stand projecting into its outlet, we have constriction (steno- 
sis). Much more rarely the latter occurs from contraction of the aorta 
at the point of insertion of the valves, whereby the outlet is dimin- 
ished. 
The alterations which cause insufficience and constriction of the 
aortic valves are the results of inflammation, but less often of endocar- 
ditis, which we have described in Chapter IV., than of a more chronic 
form of inflammation, which attacks the arteries, and whose results are 
known as atheroma of the arteries. Hence it follows, although not 
without exception, that valvular disease of the aorta is found at a more 
advanced period of life, when arterial atheroma is far more frequent 
than during youth, and that its development is more slow and gradual 
than that of the disorders caused by endocarditis. 
Anatomical Appearances.—If, upon autopsy, we remove the 
heart and aorta ; and if, upon filling the latter with water sufficient to 
distend its walls, the water flow into the ventricle because the edges 
of the valves do not touch, we may assume that such regurgitation has 
also occurred during life, and must regard the valves as insufficient. 346 
DISEASES OF THE HEART. 
Tlie anatomical changes which cause insufficience are usually 
shrinking and shortening of the valves, so that, even if spread out by 
the blood, they would not meet. But thickening, and rigidity too, may 
prevent closure, the pressure of the blood becoming insufficient to make 
the leaves flap together. Much more rarely we find adhesion of the 
valve to the arterial wall, or laceration or detachment of one of the 
leaves from its insertion, as a palpable cause of insufficience. 
Besides these changes at the root of the aorta, we constantly find 
in the cadaver a degree of excentric hypertrophy of the left ventricle 
greater than is observed under almost any other circumstances. The 
wall of the ventricle may be an inch in thickness, its cavity is often 
capable of containing a fist. We have already seen that dilatation of 
the left ventricle is the necessary result of severe pressure sustained by 
it from within while in a state of relaxation, and that hypertrophy fol- 
lows in consequence of the augmented effort which it must make in 
order to propel the increased volume of blood which it holds. A large 
number of the signs of aortic insufficience are due to this enormous hy- 
pertrophy of the left ventricle. In a former chapter we have fully de- 
tailed all the alteration which the shape of the heart undergoes from 
this enlargement. We have seen that the rest of the organ participates 
in a less degree in the affection, and that bulging of the septum into the 
right ventricle materially encroaches upon the capacity of that chamber. 
The mouth of the aorta may contract to such a degree as barely to 
admit the insertion of the end of the little finger into the narrowed open- 
ing. The anatomical changes which occasion such strictures are gen- 
erally the thickening and shrinking of the flaps described above. These 
flaps may form unyielding prominences at the root of the aorta; so 
that it becomes equally impossible for the stream of blood to lay them 
back against the aortic wall during systole, and for the weight of the 
blood during diastole to force them together again. Cohesion of the 
semilunar flaps is the next cause of stenosis, and is the more marked 
the more the point of adhesion approaches the centre of the valve. Old 
vegetations on the valves, of cartilaginous hardness, and which are often 
the seat of calcareous deposit, assist in blocking up the constricted pas- 
sage, although they rarely constitute the sole cause. 
In simple stricture of the aortic valve, the left ventricle has no in- 
crease of pressure to support during diastole, and hence does not be- 
come dilated; it has, however, to propel its blood through a contracted 
orifice, and becomes hypertrophied on account of the greater amount 
of effort thus required from it. In contradistinction, then, to what we 
meet with in insufficience of the semilunar valves, we find a simple hy- 
pertrophy, instead of excentric hypertrophy of the left ventricle, when 
the aortic outlet is contracted. DISEASE OF THE SEMILUNAR VALVES. 
347 
We have said above, that the two forms of valvular derangement 
usually coexist; as, however, insufficience soon predominates over ste- 
nosis, we find a gradual transition from simple to the most intense ex< 
centric hypertrophy taking place in the left ventricle. 
Symptoms axd Course.—The ultimate effect both of stenosis and 
of insufficience of the aortic valves must always be a retardation of 
the circulation; the blood returns to the lung with diminished fre- 
quence, and hence assumes a more venous character. (Of course, with 
every systole, an abnormally small amount of blood is discharged from 
the ventricle, or a portion of it flows back again during diastole.) The 
consequences are, that the aorta and its branches are inadequately 
filled, while, on the other hand, the pulmonary vein is gorged with 
blood, which is prevented from flowing away into the left auricle, 
already almost full. Thus the entire pulmonary system becomes over- 
loaded; but, being incapable of containing the whole of the blood 
which should properly fill the aorta, the remainder gradually accumu- 
lates in the veins of the aortic system, and gives rise to cyanosis, 
dropsy, etc. 
As a rule, however, nothing of this kind takes place, until after the 
lapse of considerable time; inasmuch as simultaneous hypertrophy of 
the left ventricle has the opposite effect, and neutralizes the baneful 
influence of the defective valves. While the latter tends to retard the 
circulation of the blood, and to render it venous, hypertrophy accel- 
erates its course and makes it arterial. While valvular deformity 
causes decrease of the contents of the aorta, hypertrophy renders the 
aorta fuller; while deficience of the valves hinders the outflow from 
the pulmonary veins, and lets the lesser circulation overcharge itself 
with blood, hypertrophy facilitates such outflow, and relieves the pres- 
sure upon the pulmonary system. 
By keeping these facts in view, it is easy to understand how it 
happens that persons with extreme deficience of the valves of the aorta 
enjoy comparatively good health, if only there be a compensatory 
hypertrophy of the left ventricle; and, indeed, such persons are fre- 
quently not even short of breath, a symptom never missed in cases of 
valvular disease of the mitral.* 
There may be some palpitation of the heart, but it is not constant. 
It is very remarkable, too, that the patients complain so little of jarring 
of the thorax. Sometimes attacks of pain in the chest and left arm 
occur, which we shall describe more closely in the chapter upon angina 
pectoris. 
* A huntsman in Greifswald, who suffered from extensive stenosis and insufficience, 
and immense excentric hypertrophy of the left ventricle, performed all the manoeu- 
vres and forced marches of the army without difficulty. 348 
DISEASES OF THE HEART. 
This state of comparative good health is common to both stenosis 
and insufficience; in general, however, the symptoms differ widely, 
those of one or other malady usually predominating. Insufficience 
gives rise to symptoms, and dangers which proceed from the consec- 
utive excentric hypertrophy, which, no longer merely compensating the 
disorder of the valves, produces an excessive action of the heart. The 
patients then usually complain of dizziness, headache, and of spots 
before the eyes. In other cases, they suddenly perish from apoplexy. 
More rarely asthmatic attacks occur, but all these symptoms are due 
to the hypertrophy (Chap. I.), and not to the valvular disorder. 
In stenosis, on the other hand, the symptoms of the circulatory 
impediment outweigh those coming from the hypertrophy, and although 
a patient may do well for a considerable length of time, evincing no 
signs of venous engorgement, yet there will be tokens that the arteries 
are but scantily filled, a symptom which must always precede those 
which indicate overcharge of the veins. The patients look pale, are 
prone to fainting-fits, and present signs of anasmia of the brain; just as 
others, who suffer from insufficience of the valves, seem to incline to 
cerebral hypercemia and to apoplexy. 
This period of comparative comfort, enjoyed by patients with dis- 
ease of the aortic valves, often ceases in a somewhat sudden and 
remarkable manner, after having lasted, perhaps, for many years. 
Either because the hypertrophied heart has degenerated, or else from 
insufficience of the mitral, caused by chronic endocarditis, which so 
often complicates valvular disease, or through increase of the original 
aortic defect, or finally because extensive atheroma of the aorta has 
set in, thus giving rise to a new liinderance to the circulation, the 
hypertrophy of the left ventricle is at last no longer able to compen- 
sate for the deficience of the valves, and to overcome the impediments 
to the circulation. Then the symptoms appear which we have men- 
tioned at the beginning of this article. The patients grow short of 
breath, the veins of the aortic system become overloaded, cyanosis 
and dropsy arise. These symptoms set in much sooner in mitral dis- 
ease, and hence shall be described in the next chapter. 
Death takes place either from oedema of the lungs (or else, when 
there is insufficience, by apoplexy). Frequently, too, death results 
from embolism, to which valvular disease of the aorta gives rise with 
a frequence next to that of endo- and myocarditis. In most of the 
cases wherein embolism of the arteria fossae Sylvii has been found to 
have caused necrosis of the brain, valvular disease of the aorta has 
existed. 
Physical signs of insufficience of the aortic valves.—Inspection 
and palpation furnish the usual signs of hypertrophy of the left ven- DISEASE OF THE AORTIC YALYES. 
349 
tricle, namely, prominence of the cardiac region, an impulse often 
enormously increased, and which shakes a broad tract of the thoracic 
wall and sometimes actually lifts it; considerable descent of the apex, 
even as far as the eighth rib, with displacement outward. Percussion 
also shows an elongation of the heart, where the lower limit of dulness 
is not obscured by the position of the left lobe of the liver. Upon 
auscultation (best at the right edge of the sternum, at the second in- 
tercostal space), instead of the second sound, we hear a murmur, aris- 
ing from irregular vibrations caused by imperfect tension of the rough- 
ened, misshapen valves. In very rare instances, besides the murmur, 
we hear the normal second sound of the heart, although but feebly, 
and this occurs, as it would seem, when one or other of the valves con- 
tinues sound, and is thrown by the blood into its normal state of vibra- 
tion. The murmur is usually conducted both to the apex and along 
the sternum, and may even be heard at the sides of the chest and along 
the back-bone. The first sound, as heard at the aorta, is pure in the 
few cases in which insufficience exists without constriction of the valve 
or roughness upon its under surface. In the majority of cases, how- 
ever, it has undergone the modifications peculiar to constriction of the 
aortic orifice. The first sound of the mitral is inaudible in many cases, 
a fact accounted for by the following excellent explanation of Traube: 
As the left ventricle is supplied from two sources during diastole, as it 
receives blood both from the auricle and from the aorta, the force of its 
internal pressure soon exceeds that with which the blood enters the 
ventricle from the auricle. A reversed current is thus established, 
flowing from ventricle to auricle, and which shuts the mitral valve be- 
fore the diastolic movement is complete. Sometimes, besides the dias- 
tolic murmur, another sound is heard, caused by the premature closure 
of the mitral valve. Unless there be some complication, the sounds of 
the pulmonary artery are normal. The phenomena observed in the 
peripheral arteries, although chiefly dependent upon the consecutive 
hypertrophy of the left ventricle, are very characteristic in insufficience 
of the aortic valves. The carotids often pulsate in a remarkable man- 
ner. If we listen, we do not hear two distinct tones, as we should do 
under normal conditions (one supposed to proceed from the vibrations 
of the wall of the carotid, expanded by the blood-wave; the second, 
attributable to conduction of the second sound of the semilunar 
valves). The second sound is not heard, as the semilunar valves 
do not vibrate normally, or, as more rarely happens, we hear a 
murmur which fakes its place. According to Bamberger, the first 
sound is also deadened in the carotids or turned into a murmur, a 
phenomenon which he attributes to immoderate tension of the carotid 
walls. Even the smaller arteries at a distance from the heart produce 350 
DISEASES OF TEE HEART. 
a sound, during their expansion, by the vibration of their walls. Their 
tortuous course and their pulsation, visible at the radial artery, and 
even in smaller arteries, are also strikingly characteristic symptoms of 
aortic insufficience. • All these phenomena, excepting the diastolic 
murmur conducted to the carotids, occur also in hypertrophy of the 
left side of the heart, when there is no insufficience of the aortic valves; 
but there is one symptom appearing in the arteries which is pathog- 
nomic of the valvular disorder in question. This consists in a re- 
markably rapid subsidence of the arterial expansion, which, indeed, is 
of but momentary duration. This jerking pulse (pulsus celerrimus) 
depends upon the fact that the artery, distended during systole of the 
ventricle, is emptied in two directions during diastole. In some cases 
of insufficience of the aortic valves the physical signs of excentric hy- 
pertrophy of the left heart are less distinctly marked. The apex beats 
in the fifth or sixth intercostal space, the impulse is not of a heaving 
character. Such patients usually suffer from dyspnoea because the 
valvular disease is not compensated for, and the lungs are loaded with 
blood. We are unable to account for this exception to the rule, which 
is not uncommon. 
* 
Physical signs of stricture of the aortic valves.—Inspection 
and palpation show signs of simple hypertrophy of the left heart. 
The impulse is stronger, the apex dislocated downward and outward, 
but not as much so as in insufficience. Upon palpation we often feel 
a distinct whizzing about the aorta accompanying systole, which is 
rare in insufficience. Upon auscultation we hear a systolic murmur 
over the valves of the aorta, which is usually very loud, and extends 
so as to be heard all over the region of the heart, masking the other 
signs. During diastole of the ventricle, as the stricture is seldom 
uncomplicated, sometimes we hear a feeble sound, but far oftener a 
murmur. In the carotids, the systolic murmur is sometimes, but not 
always, conducted to the ear from the aorta; or we sometimes hear a 
short, ringing sound in its place. The second sound, too, is usually 
inaudible in the carotid. The pulse is as small and compressible as 
it is hard and full in insufficience. 
Treatment.—Treatment of insufficience of the aortic valves is 
essentially like treatment of cardiac hypertrophy. Immoderate eating 
and drinking, and bodily and mental excitement, are to be avoided with 
care; determination to the head is to be averted, by daily evacuations 
of the bowels; venesection is never to be practised, unless the brain 
be endangered by immoderate “ rush of blood.” In this respect wre 
should be the more cautious, as it is almost certain that the practice 
of bleeding favors degeneration of the heart; and attenuation of the 
blood undoubtedly promotes the tendency to dropsy. DISEASE OF THE MITRAL VALVE. 
351 
Stricture of the aortic outlet requires measures of quite a differen 
nature. Here we have no threatening hypereemia to alia}’, or over- 
action of the heart to moderate. Much more depends upon furthering 
the nutritive state of the system, and, with it, that of the heart, so 
that its contractions may have force enough to prevail over the resist- 
ance at the outlet. Rich animal food, and even the moderate use 
of wine, are quite as strongly indicated here as they are contraindi- 
cated in insufficience. Blood-letting must never be practised. Use 
of digitalis is to be confined to those cases in which compensation be- 
gins to become imperfect. It is most effective in the cases in which 
the action of the heart is so accelerated that the left ventricle appar- 
ently has not the time to expel its contents through the narrowed 
opening during the short period of systole. 
CHAPTER VII. 
INSUFFICIENCE OF THE MITRAL VALVE, AND CONSTRICTION OF THE 
LEFT AURICULO-VENTRICULAR ORIFICE. 
Etiology.—The mode of origin of insufficience of the mitral is, in 
many cases, quite analogous to that of insufficience of the aortic valve; 
in other cases, however, it depends upon a morbid state of the papillary 
muscles and chord® tendine®; and, indeed, there have been instances 
in which, although during life the valve was deficient, yet after death 
no palpable alteration in it could be detected. Stenosis of the auric- 
ulo-ventricular passage, winch is often found to accompany insuffi- 
cience, arises partially through contraction of the ring of valvular 
insertion, partially through adhesions of the valve-tips, or chord® 
tendine®. 
Valvular disorder of the mitral is almost always a consequence of 
endocarditis, or of myocarditis; more rarely of atheromatous degen- 
eration. It is only when valvular disease of the aorta accompanies 
similar disease of the mitral that the latter depends upon the chronic 
form of inflammation caused by atheroma. 
Anatomical Appearances.—The most common lesion found in 
mitral insufficience is a marked shortening of the valve-tips, the valve 
itself being thickened and indurated, often enclosing large, flat plates 
of calcareous matter. The delicate, tender web on the free edge of 
the valve has disappeared, the edge forming a thick, clumsy pad, upon 
winch the chord® tendine® originating from the papillary muscles are in- 
serted. Of the secondary chord® tendine®, which, springing from the 
primary set, are inserted into the web of the valve, there is hardly any 
trace. In other cases, instead of these lesions, or, in addition to them, 352 
DISEASES OF TIIE HEART. 
the valve is torn. Still oftener, it is the chorda? tendinea? that have 
given way, and it can be distinctly recognized that the latter, which 
are usually thickly covered by the vegetations previously described, 
are inverted by the regurgitating stream of blood, and made to flap 
backward into the auricle. More rarely, the tendons are adherent to 
the wall of the heart, so as to prevent the valve-tips from approaching 
one another. Finally, as more or less extensive tendinous degenera- 
tion of the papillary muscles not unfrequently constitutes a minor 
source of the disorder, and where neither these nor other anatomical 
alterations are found to account for an insufficience which has notori- 
ously existed, it is most probable that some invisible change in these 
muscles has been the cause of the symptoms. The lesions, which the 
cavities and walls of the heart exhibit in cases of insufficience, are 
equally characteristic and interesting. The left auricle, into which the 
blood is first driven during systole, is always a good deal enlarged, and 
its walls are considerably thickened. The pulmonary artery and vein 
are in like manner dilated, as is also the right heart, both ventricle and 
auricle. The right ventricle, whose task is enormously increased, be- 
comes so much hypertrophied that its walls grow as thick as those of 
the left. If cut open, they do not collapse as before, but the cut gapes 
as it would do if iqade in the left ventricle. There is almost always a 
moderate degree of dilatation of the left ventricle, into which, as we 
have seen, the blood pours under greatly-increased pressure. 
In insufficience of the mitral valve, the valve-tips are shortened; 
in constriction of the orifice, they have generally grown narrower, and 
this contraction of the valvular ring is the most common cause of im- 
pediment to the flow of the blood from auricle to ventricle. It rarely 
happens, however that the valves thus thickened by endocarditis, and 
in which new connective tissue is growing, contract in one direction 
alone; they almost always become narrowed and shorter simultane- 
ously, so that stenosis and insufficience appear together. In other 
cases, the lower edges of the valve-tips, or of the chorda? tendineae, 
are so intimately united, that the valve takes the shape of a funnel, 
broad toward the auricle, and ending toward the ventricle in a narrow 
opening, through which it is often almost impossible to pass the tip of 
the finger. The vegetations, which often cover the valve in the form 
of hard, wart-like concretions, may also contribute to occlusion of the 
orifice. 
Dilatation of the left auricle, and of the pulmonary arteries and 
veins, is also a constant accompaniment of stenosis of the mitral, and 
the walls of the dilated chambers exhibit hypertrophy similar to what 
we have described above. The left ventricle, however, is in a condi- 
tion opposite to that which we find in insufficience. Instead of being DISEASE OF THE MITRAL VALVE. 
353 
Hypertrophied and dilated, it is generally small, and its walls are 
thinner, rather than thicker. We have already accounted for this cir- 
cumstance. In spite of the violent pressure under which the blood is 
thrown into the ventricle, its walls encounter a moderate pressure 
only from within, as the increased propulsive power is neutralized by 
the greater resistance met with in the contracted ostium. 
Symptoms and Course.—The effect of mitral disease upon the 
circulation must, in the main, be the same as that which we have de- 
scribed as occurring in uncompensated aortic valvular disorder. 
If, in case of insufficience, a part only of the blood enter the aorta 
upon systole, the rest regurgitating into the auricle; or, in a case of 
constriction, if too little of it flow into the ventricle, upon diastole, it 
is clear that in either case the amount of blood propelled must be 
smaller than normal, and its flow must be retarded. In like manner 
the arteries of the aortic circuit contain too little blood, and contract 
by virtue of their elasticity, while the blood by which they should be 
filled is overloading the pulmonary system. If the latter be incapable 
of accommodating all the blood, engorgement of the venous system of 
the aorta must follow. We have seen that hypertrophy of the left 
ventricle neutralizes all these circulatory derangements in disease of 
the aorta. A greater pcg-tion of them, but not all, may also be reme- 
died for a time in mitral disease, by hypertrophy of the right ventricle. 
The dilated and hypertrophied right heart propels so large a mass 
of blood, and propels it with so much power into the vessels of the 
pulmonary circuit, that the blood in the pulmonary veins is subjected 
to heavy pressure. In consequence of this, to say nothing of the 
action of the auricle, the blood pours with such force and rapidity into 
the left ventricle as to completely neutralize the effect of the constric- 
tion of the valve. In spite of the constriction, the ventricle receives 
blood enough ; the aortic contents are not lessened, nor is the circula- 
tion retarded. In the same way, the fulness and tension of the pul- 
monary vein prevent any considerable regurgitation into the ventricle, 
notwithstanding the insufficience of the valve ; indeed, as we have seen, 
the left ventricle is usually both hypertrophied and dilated, so that, in 
spite of the regurgitation of a considerable amount of blood, it still re- 
mains capable of filling the aorta. Retardation of the circulation, with 
engorgement of the venous system, and a corresponding emptiness of 
the arteries, is thus averted by a compensating hypertrophy of the 
right ventricle ; but there is one anomaly, which, in aortic disease, is 
corrected by hypertrophy of the left ventricle, but which hypertrophy 
of the right ventricle is unable to obviate when the mitral is diseased. 
This affection is overcharge of the vessels of the pulmonary circuit. 
Clinical experience entirely corroborates this physiological, or, 354 
DISEASES OF THE HEART. 
rather, physical demonstration. Patients with mitral disease are al- 
ways short of breath, in consequence of hyperaemia of the lung. As 
the vessels of the bronchi are less affected than those of the air-cells 
by this engorgement, the dyspnoea is not always combined with bron- 
chial catarrh ; as, however, the bronchial and pulmonary arteries anas- 
tomose, nay, as part of the blood of the capillaries and bronchial 
arteries flows into those of the pulmonary artery, the dyspnoea is gen- 
erally accompanied by bronchial catarrh. Even at this early stage of 
the disease, unusual exertion, or other stimulant to the action of the 
hypertrophied right heart, may cause the death of the patient from 
acute pulmonary oedema, although such an event is of more common 
occurrence at a later period, after obstruction of the aortic veins and of 
the thoracic duct has thinned the serum of the blood. 
Patients with insufficience and constriction of the mitral valve often 
enjoy tolerable health, excepting that they are short of breath, and 
we should err greatly in supposing that disease of the mitral valve is 
always accompanied by cyanosis. In constriction of the valve, par- 
ticularly if combined with insufficience, the compensation soon becomes 
imperfect. The patients look pale from lack of blood in their arte- 
ries ; but this derangement of distribution does not cause engorgement 
of the veins, mainly because most of the blood is collected into the 
pulmonary circulation. 
Sooner or later, the picture changes. Compensating hypertrophy 
of the right ventricle has its limits, while deformity of the valves grows 
worse and worse from fresh endocarditis, or else the conditions de- 
scribed in the previous chapter arise, and compensation becomes im- 
perfect. Then the contents of the aorta and its branches diminish 
more and more, the secretion of urine is lessened, the veins and 
capillaries become overloaded, the lips and cheeks assume a bluish or 
even a deep-blue hue. The embarrassed outflow of the cerebral veins 
creates heaviness in the head, headache, etc. The liver soon becomes 
enlarged, the patient complains of fulness and oppression in the right 
liypochondrium; the liver forms a tumor, distinctly demonstrable by 
percussion and palpation, and which may extend down almost to the 
navel. Obstruction of the hepatic veins may so increase that the re- 
pleted vessels compress the biliary passages, so as to give rise to re- 
tention and reabsorption of the bile. The mucous membrane of these 
passages may also become the seat of a catarrh, and the flow of mucus 
thus produced may so obstruct the bile-ducts as to cause biliary ab- 
sorption. A yellow color is thus added to the previous cyanotic as- 
pect, which may impart a greenish tint to the complexion. Chronic 
gastric and intestinal catarrh arises from obstruction of the gastric and 
intestinal veins; the haemorrhoidal veins swell; engorgement of the DISEASE OF THE MITRAL VALVE. 
355 
uterine veins occasions menstrual derangement. Finally, should any 
considerable congestion of the kidneys set in, there is derangement of 
the secretion of urine, such as may be produced by ligation of the 
emulgent veins. The urine is scanty, and contains albumen, blood- 
corpuscles, and the so-called fibrinous or exudation cylinders, that is, 
microscopic casts of the urinary tubules, the diagnostic importance of 
which is to be considered more in detail when we come to study dis- 
eases of the kidney. 
Venous engorgement, moreover, leads to one of the most impor- 
tant, and, in long-standing cases, one of the most constant symptoms 
of mitral disease, namely, dropsy. As before observed, an impoverish- 
ment of the blood, particularly a diminution of its albumen, contributes 
essentially to the establishment of transudation of serum. This im- 
poverishment is easily traceable to engorgement. Embarrassment to 
the outflow from the veins extends itself to the thoracic duct, and ob- 
struction of this duct, of course, impedes the supply of nutritive mate- 
rial to the blood. The dropsy almost always begins in the extremi- 
ties, generally in the region of the ankles ; thence it gradually extends 
over the thighs, the external genitals, the integuments of the abdomen, 
and so to the rest of the body. The serous sacs also become the seat 
of dropsical effusions, producing ascites, hydrothorax, and hydroperi- 
cardium. Years may elapse after the first appearance of oedema about 
the ankles, the patient alternately improving and growing worse ; his 
feet now swelling and now growing smaller again, ere the general 
dropsy is established, of which he, in most cases, ultimately dies. In 
other cases, he rapidly declines as soon as the first signs of serous effu- 
sion show themselves. In many cases an erythema is set up about 
the genitals, the groins, etc., which is very distressing to the patient, 
and which, not uncommonly, terminates in diffuse gangrene of the 
skin. When hydrothorax and hydropericardium develop, his condition 
grows desperate. The dyspnoea becomes extreme; he can no longer 
lie down. The serum finally so fills up the air-cells of the lungs, that 
the blood becomes surcharged with carbonic acid, and his last hours, 
at least, are relieved by a merciful stupefaction. While the majority 
of cases thus terminate by dropsy and final oedema of the lung, death 
takes place, in a smaller number, in consequence of metastases, haemor- 
rhagic infarction of the lung, or of intercurrent maladies. How much 
Bright’s disease contributes in producing a speedy death is difficult to 
decide ; at all events, whether due to it or not, albuminuria certainly 
promotes the tendency to dropsy. 
Physical signs of insufficience of the mitral—Inspection and, 
Palpation.—We often see and feel a strong shock, or even a rise and 
fall of the thoracic wall over all the region which is in contact with 356 
DISEASES OF THE HEART. 
the left ventricle. The apex is displaced outward and somewhat 
downward. Simultaneously with the shock against the thorax, the 
epigastrium is also shaken rhythmically. We have considered each of 
these symptoms while treating of hypertrophy of the right side of the 
heart, to which they are due. Percussion reveals an extension in 
width of the cardiac dulness. Upon auscultation, instead of the first 
sound, we hear at the apex a murmur, generally somewhat loud, which 
arises from the irregular vibrations of the valve, which, being rough- 
ened and uneven, is in a very unfavorable state to vibrate normally. 
Sometimes we hear the murmur better, if we listen more above and to 
the outer side of the apex, as, from hypertrophy of the right heart, the 
left ventricle of which the apex is formed is, as it were, pushed off 
from the thoracic Avail. As the second sound heard o\rer the ventricle 
is merely transmitted from the arteries, it presents no abnormity in 
pure mitral insufficience. Above the aorta, the sounds are feeble; 
over the pulmonary artery, they are remarkably loud, especially the 
second, and this intensification, which is still more marked by contrast, 
is of great diagnostic value. Sometimes, even, Ave feel a distinct shock 
at the root of the pulmonary artery, during diastole of the Arentricle. 
Pulsation of the veins, with rhythmical dilatation, does not occur in mitral 
insufficience, unless complicated by valvular derangement of the tri- 
cuspid ; although Ave often may observe a rhythmical undulation of the 
jugulars, isochronic Avith systole of the ventricle. 
This proceeds from transmission, the strong shock suffered by the 
tricuspid’s being conducted along the column of blood above it, and 
continues uninterrupted, excepting by the delicate valves, as far as the 
jugulars. Although the valves in the veins pre\Tent regurgitation of 
the blood, they cannot check the transmission of a Avave of A'ibration 
along their contents (P ambergei*). 
Physical signs of stenosis of the mitral.—Here, too, inspection 
and palpation sIioav the signs of excentric hypertrophy of the right side 
of the heart. The impulse is not usually as strong as it is in insuf- 
ficience, as the left side of the heart does not take part in the hyper- 
trophy. Besides this, it is much more common in insufficience than in 
hypertrophy to perceive the fr'emissement cataire, that slight, AA'hizzing 
sound at the apex, Avhich immediately precedes the beat of the heart, 
and which ceases suddenly as the beat commences. This phenomenon, 
the priesystolic purring, is often perceptible through thick clothing, and 
is so characteristic as in itself almost to suffice to establish the diagno- 
sis of stenosis of the mitral. Upon auscultation Ave almost always 
hear a long-drawn murmur at the apex during diastole. Although the 
blood, as it pours through the normal spacious orifice, occasions no 
sound, this is by no means the case Avhen it has to be driven forcibly DISEASE OF THE MITRAL VALVE. 
357 
through the narrow passage produced in this disease. The sound is 
all the louder, the more rapidly the blood pours in, and the rougher 
and more uneven the surface over which it flows. As a longer time is 
needed for it to pass through the contracted auriculo-ventricular orifice 
to fill the ventricle, the murmur heard in mitral stenosis is of longer 
duration than others, and almost always extends over the whole pause, 
until cut short, as it were, by the next systolic sound. Traube there- 
fore calls a “ praesystolic ” murmur at the apex a pathognomonic 
symptom of stenosis of the mitral valve. If the contracted orifice be 
not also roughened, if the stenosis be moderate, if the volume of the 
blood be reduced, there may be no sound. In addition, we can, of 
course, hear the second sound propagated from the arteries, unless the 
murmur be too loud. Whether we hear the first sound, or a murmur 
be audible in its stead, depends upon the efficience of the valve. The 
second sound of the pulmonary artery is naturally considerably inten- 
sified. 
Treatment.—It is not to be supposed that we can cure valvular 
disease of the mitral by any therapeutical interference whatever. We 
are equally helpless against the consecutive hypertrophy of the right 
ventricle, which, however, has a beneficial action upon the distribution 
of the blood. We are, therefore, reduced to a treatment of the more 
prominent and dangerous of the symptoms. 
Hyperaemia of the lung is an inevitable consequence of mitral dis- 
ease ; it cannot be averted nor permanently relieved. We should, 
therefore, never interfere actively unless it be severe, or unless there 
be danger of oedema of the lung. This is the more important, as 
blood-letting, the only active remedy against hyperaemia, although for 
the time it may ward off the peril, is extremely dangerous for the 
patient. Perhaps, prior to the bleeding, there may have been no effu- 
sion into the subcutaneous areolar tissue. Soon after it the blood will 
have regained its former volume; but its serum has now become so 
much attenuated as to transude under a pressure which would not pre- 
viously have caused transudation. The symptoms of dropsy often 
first set in immediately after the first phlebotomy. Such “ curae pos- 
teriores,” however, should not make us hold our hand, if the preserva- 
tion of life really demand venesection (see chapter on pulmonary 
hyperaemia and oedema of the lung). 
In digitalis we possess a very powerful means of moderating, not 
only hyperaemia of the lungs, but also engorgement of the aortic 
venous system ■which arises in mitral disease. If we can succeed in 
retarding the action of the heart by means of digitalis, we afford time 
to the auricle to drive its contents into the ventricle through the con- 
tracted passage. Sometimes systole and diastole can be so greatly 358 
DISEASES OF THE HEART. 
prolonged (Traube) that a pause intervenes between the murmur and 
the next systolic sound, so that it can no longer be called praesystolie. 
A marked improvement often accompanies such a result; the breath- 
ing grows more free, the swelling of the liver subsides, and the cyano- 
sis and dropsy abate. Latterly, since I have grown bolder in the 
use of digitalis, and rid myself of the theory of Traube, even in 
cases of insufficience of the mitral, particularly if the heart’s action be 
much accelerated, I have seen the dropsy, cyanosis, and tumefaction 
of the liver diminish or disappear, while the urine became more copious 
after the use of an infusion of digitalis. I have come to the conclusion 
that, by proper administration of this drug, compensation, which is be- 
ginning to fail, may, for a time, be reestablished. Arsenic and anti- 
mony, likewise, may be employed in valvular disease of the heart. 
The action of diuretics upon dropsy, resulting from heart-disease, is. 
at least, a doubtful matter. If digitalis act here as a diuretic, it is 
probably because it readjusts the circulatory derangement, and thus 
permits more blood to fill the arteries, thereby affecting the glomeruli 
of the Malpighian capsules. An agent, intended to relieve sup- 
pression of urine, caused by disease of the heart, must either have a 
special action upon the circulation like digitalis, or it must cause dila- 
tation of the arterioles of the kidney, so that more blood may enter 
them from the scantily-filled aorta; or else it must so alter the struc- 
ture of the walls of the renal vessels, as to facilitate the transfusion of 
liquids through them. True, as long as the class of diuretics has any 
reputation left, it will be difficult to refrain from prescribing cream of 
tartar, the alkaline carbonates, squills, etc., when we see the urine 
daily diminishing, while the serous effusion augments; but, at all 
events, their action upon the diuresis and dropsy of cardiac disease is 
inexplicable and remarkably small. 
Preparations of iron, on the other hand, are of signal efficacy in 
dropsy, as is also a nourishment rich in albumen and other protein 
substances. As already observed, we are totally unable to explain the 
effect of iron upon the composition of the blood, which consists in an 
increase in the number of its red corpuscles and of the amount of albu- 
men. However, just as bleeding, by thinning the blood, favors drop- 
sy, so iron and a nitrogenous diet, by rendering the serum more con- 
centrated, have an antihydropic action, and deserve the utmost reliance 
in treatment of both mitral and aortic disease. 
We may afford great assistance, by the institution of a treatment 
of the symptoms adapted to the phase of the disease, while all exclu- 
sive treatment will do harm. DISEASE OF THE PULMONARY VALVES. 
359 
CHAPTER VIII. 
INSUFFICIENCE OF THE SEMILUNAR VALVES AND CONTRACTION OF 
THE MOUTH OF THE PULMONARY ARTERY. 
As endocarditis scarcely ever attacks the right heart during extra- 
uterine life, and as atheroma of the pulmonary arteries is rare, it is 
easy to see that valvular deformities, which are almost always the con- 
sequence of one or other of these morbid processes, have been met with 
in the pulmonary artery in but few solitary instances. In these the 
insufficience depended upon the same causes which occasion valvular 
disease of the aorta. The few cases of stenosis on record do not 
always affect the valve ring, some of them arising from annular indu- 
ration of the conus arteriosus. 
The symptoms of valvular insufficience of the pulmonary artery 
seem to be mainly those of hypertrophy of the right ventricle, just as 
the excentric hypertrophy of the left ventricle forms the chief sign of 
corresponding aortic disease. In the cases which have been observed, 
the quantity of blood in the lungs was not abnormally small, indeed 
was abnormally great. Dyspnoea, haemorrhagic infarction, and even 
consumption of the lungs, followed upon the insufficience. Stricture, 
at this point, too, seems to be less perfectly neutralized by consecu- 
tive hypertrophy, so that cyanosis, dropsy, and other tokens of venous 
engorgement of the greater circulation soon set in in cases of contrac- 
tion at the root of the pulmonary artery. Diagnosis of valvular dis- 
ease of this artery is only possible by means of physical examination; 
as the functional disturbances, to which the malady gives rise, admit 
of a too manifold interpretation. In either case, but more especially 
in insufficience, we find the signs of enlargement of the right heart, so 
often described; and over the region of the pulmonary artery (that is, 
over the third left costal cartilage) a murmur during systole is audible 
in stenosis, while in insufficience it is heard during diastole. These 
murmurs are produced just as those are which occur in the aorta; 
they are heard most distinctly over the right ventricle, and over the 
left upper region of the chest, but are inaudible in the carotids. On 
account of the extreme rarity of valvular disease at this point, we must 
employ the utmost caution in diagnosis, and make sure that the mur- 
mur heard in the region of the pulmonary is actually loudest at that 
point, and is not conducted from the aorta. 
The treatment can only be symptomatic, and the same rules which 
we have set forth in the foregoing chapter are applicable here in man- 
agement of the more threatening manifestations. 360 
DISEASES OF THE HEART. 
CHAPTER IX. 
INSUFFICIENCE OF THE TRICUSPID, AND STRICTURE OF THE RIGHT 
OSTIUM ATRIO VENTRICULARE. 
A so-called relative insufficience of the tricuspid used formerly, 
upon theoretical grounds, to be regarded as a very common form of 
valvular disease. The ostium was seen to be enormously widened, 
and it was assumed that the valve was incapable of closure. This 
relative insufficience, if it ever occurs, is rare. When the ostium 
dilates, the valve grows in breadth and length, almost always remain- 
ing competent to close the widened orifice. Primary and independent 
disease—thickening, shrinking, etc.—of this valve is also quite rare. 
It is more common for it to accompany similar disorder of the mitral. 
Bamberger, indeed, regards the combination of mitral and tricuspid 
deficience as the most frequent of all combinations of valvular defect, 
and I, too, have repeatedly observed contraction of the tricuspid, with 
rupture of the chordae tendineae, as an accompaniment of severe stric- 
ture of the mitral. 
In insufficience of the tricuspid, which is in general pure (stenosis 
being extraordinarily rare), the blood regurgitates into the vena cava 
during systole of the ventricle; but, as the right ventricle is generally 
hypertrophied in consequence of mitral disease, this regurgitation takes 
place with great violence. The vena cava and the jugulars become 
enormously dilated. The valves of the jugular, which, if its calibre 
were normal, would set a limit to the regurgitation, become insuffi- 
cient from dilatation, and it is transmitted as far as the vessels of the 
neck. Ileal pulsation of the dilated jugulars, perceptible both to 
touch and sight, is a pathognostic symptom of insufficience of the 
tricuspid. Besides this, we hear a distinct systolic murmur at the 
lower part of the sternum, which, in conjunction with the venous pul- 
sation, makes the diagnosis certain; but here also we must make sure 
that the murmur is really strongest at this point, and is not conducted 
thither from the aorta. 
As insufficience of the tricuspid causes the most intense engorge- 
ment of the veins of the aortic circulation, so, of all valvular disorders, 
this leads most rapidly to cyanosis and dropsy.* 
* When one valvular defect complicates another, the symptoms of the former one 
are modified. The modifications vary according as the complication has a similar or 
an opposite effect upon the circulation; and according as one or other defect predom- 
inates. The signs of complex valvular disease may easily be deduced from the analy- 
sis of the foregoing chapters. FATTY DEGENERATION- OF THE HEART. 
361 
CHAPTER X. 
DEGENERATION OF THE SUBSTANCE OF THE HEART, GROWTHS, 
PARASITES. 
Etiology and Pathological Anatomy.—1. An abnormal soft- 
ness, relaxation, and flabbiness of the substance of the heart, impart- 
ing to it “a parboiled look” (Rokitansky), are not uncommon in the 
bodies of those who have died of typhus, septicaemia, puerperal fever, 
etc. No important alteration can be detected in its structure, and we 
must beware of mistaking the relaxation resulting from decomposition 
for that which has taken place during life. The state of other organs 
must form our criterion in this case. 
2. Fatty Heart must be regarded as of two kinds: 
a. Increase of the amount of fat normally found upon the surface 
of the heart. 
b. Fatty metamorphosis of the primitive fasciculi of the muscular 
substance. 
In the former we find a layer of fat, half an inch thick, covering 
the heart, particularly along the course of the coronary arteries, upon 
its edges, and in the sulcus between the two chambers. Beneath this 
fatty layer the muscle is either normal or has undergone atrophy and 
thinning from pressure of the superimposed fat. In many cases, atro- 
phy of the muscle occurs while the fat-tissue is forming, and with- 
out the growth of the latter having become very remarkable. This 
growth, then, takes place at the expense of the substance of the heart, 
so that a cardiac wall of normal thickness may at last consist only of 
adipose tissue. This excessive production of fat in the heart often 
accompanies general obesity, especially that of advanced age, and in 
subjects otherwise healthy. It is also seen, however, in cancer, and 
in other, cachexia, and especially among drunkards. 
Fatty metamorphosis of the pyrimitive fasciculi consists in conver- 
sion of the fibrillae into fat-granules, which gradually fill the entire 
sarcolemma, and afterward combine to form large drops. Thus the 
substance of the heart becomes discolored, and is converted into a pale- 
yellowish mass which tears readily. Sometimes the metamorphosis 
pervades large tracts of the organ, while in other cases particular 
parts only are affected, as, for instance, the papillary muscles. Accom- 
panied by arcus senilis, and fatty degeneration of the arteries, it often 
forms one of the signs of marasmus senilis, or of other marasmic states, 
which arise in cancer, Bright’s disease, etc. Ossification of the cor- 
onary arteries, pressure of pericardial exudation, or even that accu- 
mulation of fat upon the surface of the heart just mentioned, may give 362 
DISEASES OF THE HEART. 
rise to fatty degeneration of its walls. Finally, in many cases of val- 
vular disease, with consecutive hypertrophy, a partial fatty metamor- 
phosis takes place. 
The origin of this “ spurious hypertrophy ” is somewhat obscure, 
and almost without parallel; while fatty degeneration of the cardiac 
muscles, in consequence of defective nutrition or pressure, etc., finds 
many analogies in the metamorphosis of other organs whose nutrition 
is impaired. 
3. Amyloid degeneration, according to Hokitanslcy, occurs espe- 
cially in the hypertrophied right side of the heart, causing its cut sur- 
face to resemble that of a piece of bacon, and occasioning great rigid- 
ity of its wall. The sarcolemma is filled up by nodules, which glitter 
dimly and show the peculiar reaction of amyloid degeneration, turning 
blue upon application of a dilute solution of iodine and weakened 
sulphuric acid. 
4. Cancer is very rare in the heart, occurring only in general can- 
cerous infection, or by extension from the mediastinum or pericardium. 
It forms circumscribed tumors, usually of the medullary, or else of the 
melanotic kind, which project either inward or outward, and may 
sprout into the cavity of the organ. In other cases, especially where 
propagated from cancer of neighboring parts, wide tracts of the sub- 
stance of the hearts become transformed into cancer (infiltrated cancer, 
see cancer of the lungs). 
5. Tubercles scarcely ever occur in the heart. Yellow, cheesy 
nodules, sometimes found embedded in its walls, are not to be regarded 
as tubercles, and shall be accounted for when we come to treat of 
pericarditis. 
6. Parasites.—The cysticercus has been found in the heart, enor- 
mous numbers of them existing at the same time in other muscles of 
the body. The echinococcus has also been met with. 
Symptoms and Course.—Relaxation of the cardiac substance, after 
typhus, exanthematic disease, etc., of course reduces the efficience of 
the organ, and is very apt to occasion dilatation. It is only in the 
latter case that we are able to recognize it with certainty. If, after an 
attack of some exhausting disease, we find that the impulse of the 
heart is extraordinarily feeble, the area of cardiac dulness having in- 
creased, we may also attribute the small pulse, the dropsical aspect, 
the spontaneous coagula in the veins, in part, at least, to the structural 
changes which the substance of the organ has undergone.* 
If the existence of dilatation cannot be proved, we must remain in 
* In such instances cyanosis is rare, as the volume of the blood is reduced and 
its quality is very poor; so that, even though it were to overfill the veins, it would not 
give rise to the bluish complexion. FATTY DEGENERATION OF THE HEART. 
363 
doubt as to whether the retarded circulation and the scanty arterial 
supply be due to general exhaustion or to relaxation of the heart. 
Growth of fat about the heart plays an important role among the 
people, in accounting for shortness of breath and other troubles arising 
among fat, pot-bellied individuals. Unless the accumulation cause 
atrophy of the muscular substance, -which is by no means frequent, it 
it does not seem to occasion any functional disturbance whatever. 
Should atrophy result, the symptoms already mentioned (see atrophy 
of heart) will arise. 
Fatty degeneration of the cardiac substance, like simple relaxation 
of it, depresses the action of the organ, and in like manner, when it 
affects the whole heart, occasions dilatation. All the circulatory dis- 
turbance which we have so repeatedly described may ensue from fatty 
degeneration. We find a feeble heart-shock, a small and remarkably 
slow pulse, a tendency to faintness, from an imperfect supply of blood 
to the brain. If the volume of the blood be not diminished, that is, if 
the degeneration depend upon local rather than upon general nutritive 
disorder, there may also be cyanosis and intense dropsy. In the latter 
case, when the disease is usually combined with other affections capable 
of reducing the propulsive power of the heart (such as pericardial ex- 
udations, induration and thickening of the pericardium, etc.), it is 
difficult to determine what part is taken by these disorders, and what 
the degeneration plays in producing the train of symptoms; so that a 
positive diagnosis is impossible in most instances. The same thing 
holds good with regard to the transition from genuine to spurious hy- 
pertrophy, through fatty degeneration of the muscular fibres. If the 
impulse and contractile force of a hypertrophied heart become mani- 
festly weaker, or if compensation for an imperfect valve begin to fail, 
we may assume that the change from true to false hypertrophy has 
taken place. Fatty metamorphosis of the papillary muscles is also to 
be reckoned among the possible consequences of insufficience of the 
mitral or tricuspid. 
Of rupture of the heart, as a result of fatty degeneration, we shall 
treat hereafter. 
As for amyloid degeneration of the substance of the heart, evi- 
dence, often easy to obtain, of existence of the disease in the liver, 
spleen, or kidney, affords our only but uncertain clew as to its presence 
in the heart; and we can never do more than vaguely suspect it. 
Cancer, tubercles, and parasites of the heart, also have the effect of 
depressing its action, but their diagnosis is almost always impossible. 
Treatment.—If the heart be relaxed by debility following acute 
disease, the remedies so often named are called for which have the 
effect of improving nutrition, together with mild stimulants. 364 
DISEASES OF THE HEART. 
Persons in whom a general obesity has developed, through luxuri- 
ous living, and in -whom an accumulation of fat may also be suspected 
about the heart, should be sent to Karlsbad, Marienbad, etc. It is an 
indisputable fact that, during treatment at these baths, the fat decreases 
and the garments of patients grow too loose for them, although we 
have no better physiological explanation of the circumstance than a 
somewhat feeble hypothesis. 
In true fatty degeneration of the heart we must confine ourselves 
to a treatment of symptoms, and, if it form one of the accompaniments 
of general marasmus, we should prescribe a generous diet and cor- 
responding medicines. We may, perhaps, succeed in restraining the 
progress of the malady, if we do not entirely allay it. 
Treatment of amyloid degeneration, cancer, tubercle, and parasites, 
is out of the question, as the diseases are never recognizable. 
CHAPTER XI. 
RUPTURE OP THE HEART. 
We refer exclusively to the so-called spontaneous ruptures, and 
shall not allude to traumatic solutions of continuity of the heart. A 
healthy heart never bursts, in spite of the greatest strain. If the organ 
be diseased, strains of any kind may, no doubt, aid in causing its rup- 
ture. The most frequent cause of rupture is fatty degeneration; more 
rarely, myocarditis, cardiac abscess, and acute and chronic cardiac 
aneurism. As all of these affections usually arise in the left side of 
the organ, rupture nearly always occurs there also. Upon autopsy, 
we find the pericardium distended by blood, and, if fatty metamorphosis 
have occasioned the rupture, an irregular but outwardly smooth rent, 
of variable length, is found; while at a deeper point the flesh is torn 
asunder and mangled. The rent is occasionally filled throughout by 
coagirla; again more than one rupture is found. 
Sometimes the heart bursts during some unusual exertion, or it may 
give way without any apparent cause, and death usually ensues sud- 
denly with the symptoms of internal limmorrhage. The pressure of the 
extravasated blood, however, also seems to have some effect in pro- 
moting speedy death. In rare instances the rupture has been preceded 
by a brief period of violent pain under the sternum, shooting toward 
the left shoulder and along the arm. In cases equally rare, patients 
have survived rupture of the heart for several hours. This seems to 
happen -when the extravasation consists, at first, of a mere filtration of 
the blood through the broken-down, disintegrated cardiac wall, the 
rent gradually growing larger. Symptoms then appear of a less active FIBRINOUS DEPOSITS IN TILE IIEART. 
365 
nnemorrhage; and it is sometimes possible to make out the physical 
signs which mark the progress of the flow into the pericardium. 
CHAPTER XII. 
We seldom dissect a body without finding in its heart a clot of 
fibrin, especially in the right side of the organ. Sometimes the clot is 
yellow, consisting entirely of fibrin, which has separated from the red 
portion of the blood; sometimes it contains red corpuscles, and is more 
or less colored. Their tenacity is variable, and they are usually en- 
tangled among the trabeculae, but may easily be separated from the 
endocardium. In the bodies of persons who have died of pneumonia, 
or other disease in which the fibrin of the blood is increased in quan- 
tity, these coagula are found especially large, and, if removed from the 
heart, long clots, forming prolongations into the arteries, are drawn 
after them. These fibrinous clots, or false polypi of the heart, have 
formed after death, or during the period of dissolution. The more pro- 
tracted the latter, so much the longer is the blood, as it were, whipped 
up in the heart, so much the more completely is the fibrin separated 
from the red blood, and so much the more colorless and intimately en- 
tangled in the trabecula? is the resulting clot. In other instances, the 
coagula seem to have formed some time before death. The fibrin has 
lost the elasticity and glitter of fresh fibrin, and is firmer, drier, and 
yellower. The clots are tightly adherent to the endocardium, and we 
sometimes find their interior decomposed into a puruloid, yellowish, or 
brownish-red emulsion, or conyerted into a yellowish, cheesy mass. 
No real pus is formed, but a mess of debris, in which colorless blood- 
corpuscles must not be mistaken for pus-corpuscles. 
Sometimes we find fibrinous deposits in the heart, in the form of 
rounded, wedge-shaped masses, in size from that of a millet-seed to 
that of a nut (Laennec’s vegetations globuleuse). If we examine their 
mode of attachment more attentively, we perceive numerous roots pro- 
ceeding from the spherical vegetations, which are prolonged deeply into 
and entangled among the meshes of the trabeculae. The source of the 
vegetations is to be sought there; the spherical form is the result of 
subsequent deposit upon the clots first formed. Here, too, the soften- 
ing just mentioned is found sometimes in the interior of the coagulum, 
so that at last they may assume the appearance of sacs, with thin walls 
and puruloid contents. We have already spoken of the deposits which 
form upon roughened places on the endocardium, from endocarditis, 
acute or chronic aneurism of the heart, and valvular disease. 
FIBRINOUS DEPOSITS IN THE HEART. 366 
DISEASES OF THE IIEART. 
The coagula which form prior to death are mainly the result of the 
feeble manner in which the heart contracts. Hence, they are com- 
monly found among marasmic subjects, and in persons who have de- 
generation of the heart. Their points of origin are always the shallow 
recesses between the trabeculae, which readily dilate when the heart is 
relaxed or softened, so that, if its contractions be incomplete, the blood 
in them stagnates and coagulates. In very rare instances an embolus 
may, perhaps, form the nucleus of a clot. 
When coagula form in the heart during the death-throes, they may, 
no doubt, occasion some obstruction to the circulation, but it is impos- 
sible to know how much of the feebleness of the circulation is due to 
the palsy of the heart, and how much to obstruction of the orifices by 
clots. Even if the clots produce murmurs, they cannot be distin- 
guished from the murmurs caused by irregular and imperfect action 
of the heart. This is true also for the clots which form prior to the 
death-agony, as they, too, form in case of feeble cardiac action and 
impeded circulation. 
CHAPTER XIII. 
CONGENITAL ANOMALIES OF THE HEAET. 
Etiology.—The majority of congenital defects of the heart are 
due either to arrest of development (the organ remaining in a condi- 
tion which was normal during foetal life), or else to foetal endocarditis 
or myocarditis. We are unacquainted with the causes of this arrest 
of development, as well as with the causes of the foetal inflammation. 
Prominently in the former class of congenital deformities of the 
heart stands incompleteness of the septa; in the second class, the in- 
durated strictures produced by inflammation, and congenital stricture 
and insufficience of the valves, are the most important. The latter 
occur generally in the right heart, which, after birth, is very rarely 
attacked by endocarditis or myocarditis. 
The causes of congenital malformation in position of the heart may 
be similarly classified. Sometimes they are to be regarded as cases of 
arrested development, the ribs, the sternum, and the clavicles being 
imperfectly formed, so that a greater or smaller portion of the heart is 
covered by soft parts alone. In other cases they depend upon inflam- 
mation during foetal life, which has given rise to adhesions with neigh- 
boring organs. 
The pathogeny of dextro-cardia, in which the heart lies on the 
right side of the thorax, the liver generally occupying the left hvpo- 
chondrium, and the spleen the right, etc., is altogether obscure. CONGENITAL ANOMALIES OF THE HEART. 
367 
Anatomical Appearances.—Congenital deformities of the heart, 
which are incompatible with life, and which cause children to die either 
immediately, or else very soon after birth, belong rather to the province 
of pathological anatomy than to that of special pathology and thera- 
peutics. Entire absence of the heart, or of one of its chambers, is one 
of these. In anomalies which permit the continuance of life, even for 
a short time, we generally find every part of the organ represented, 
although some portions of it are only rudimentary. In most instances 
the aorta or the pulmonary artery is stunted, or quite undeveloped. 
If the pulmonary artery be deficient, the blood pours from the right 
heart directly into the left, as such cases are always combined with 
imperfection of the septa. The aorta then supplies the lungs with 
blood through the dilated bronchial arteries, or through the ductus 
Botalli, in which it sets up a current counter to the foetal blood-stream. 
If the aorta be contracted or closed immediately above the opening of 
the ductus Botalli, it then can only supply the head and upper ex- 
tremities, while the pulmonary artery conveys blood to the lower half 
of the body through the ductus Botalli. If the aorta be closed at its 
origin, the blood which comes to the left heart passes directly through 
the open septum into the right heart, the pulmonary artery then fur- 
nishing blood to the whole aortic system. When the septum between 
the ventricles is imperfect, it may seem as if the aorta and pulmonary 
arteries sprang from both of them. If the septum stand too far to 
the right or left, the right or left ventricle will be too large, and both 
arterial trunks will originate from it, while the stunted ventricle has 
to discharge its blood into it through the open septum. In very rare 
instances, the aorta has been found to spring from the right, the pul- 
monary artery from the left ventricles. There also are anomalies of 
the veins discharging into the heart, to describe which, however, would 
carry us too far. 
Insufficience and stenosis of the orifices, and cicatricial strictures of 
the heart consequent upon foetal endocarditis and myocarditis, differ from 
those acquired after birth, in that their situation is in the right heart. 
Valvular disease is more common at the pulmonary valves than at the 
tricuspid. In these cases, too, the septum is not closed, so that trans- 
fusion of the blood takes place from one side of the heart to the other. 
Defects may exist in the septa of greater or less extent, but they 
do not afford complications and results like those just described, which 
are of far less importance, and, indeed, may be without any material 
influence whatever upon the circulation, and, hence, are to be regarded 
as independent, and proceeding from arrested formation due to un- 
known causes. In particular, we very often make post-mortem dis- 
covery of slit-like openings, or even great holes, in the foramen ovale 368 
DISEASES OF THE HEART. 
which openings have never occasioned any symptoms whatever during 
life. In the septum of the ventricles, likewise, especially at a point 
at the upper end, which normally is very thin, it is not uncommon to 
find imperfections, of more or less magnitude, which have never given 
rise to any inconvenience. 
In the higher grades of ektopia, in which a greater part of the wall 
of the chest or belly is wanting, the heart lying in the abdomen or 
upon the neck, continuance of life is impossible. There are persons 
alive, however, with smaller imperfections of the bony thorax, fissures 
in the sternum, etc., and who even have attained an advanced age. 
In such cases the deformity is covered by the skin, and the subject 
suffers little inconvenience. 
Symptoms and Course.—If we keep the effect in dew, which 
congenital malformations of the heart exert upon the circulation, turn- 
ing first to the most frequent and important of them, that namely, in 
which the aorta or pulmonary artery with its ventricles is undeveloped, 
so that the blood passes through the open septum, from one side of the 
heart to the other, and is carried into the body through the more per- 
fect trunk alone, it will be apparent that the following derangements 
in the distribution of the blood must occur. 
First, the current of the blood-stream is greatly retarded, and hence 
the blood, tarrying long in the body and rarely returning to the lungs, 
is overloaded with carbonic acid, and assumes an intensely venous char- 
acter. Ceteris paribus, the rapidity of the circulation depends upon 
the volume of blood set in motion by every heart-beat. If the aorta or 
pulmonary artery be missing, if but one outlet from the heart remain, 
then, notwithstanding hypertrophy of the ventricle, the volume of 
blood set in motion must be far too small. The retardation of the cir- 
culation thus resulting sufficiently explains a series of symptoms ob- 
servable in congenital imperfections of the heart—the lassitude, lan- 
guor, intellectual apathy, depressed spirits, and, above all, the low 
temperature of the body. 
If, however, the supply of blood to the greater and lesser circula- 
tion be furnished by only one of the ventricles, it must follow that the 
arteries are very scantily filled, and that venous engorgement of great 
intensity arises, as in all other cases, where the arteries have not their 
due supply. Accordingly, we find the pulse small, the breathing very 
short, and, above all, we observe cyanosis, the symptom which we 
have so often designated as the characteristic one of overloading of 
the veins. Since cyanosis arises here, as it does elsewhere, from obstruc- 
tion to the course of the blood through the capillaries and veins, the 
extreme intensity which it here exhibits must be owing to some other 
cause, which is to be sought in the excessively dark hue of the blood. CONGENITAL ANOMALIES OF THE HEART. 
369 
This blackness of the blood is not in itself capable of producing cyano- 
sis (as is shown by a case, related by JBreschet, in which the color of a 
left arm was perfectly normal, although it contained none save venous 
blood, the left subclavian artery springing from the pulmonary artery). 
It cannot be denied, however, that where venous engorgement exists, 
the degree of cyanosis depends upon the blackness or redness of the 
blood. Thin-blooded people never exhibit much cyanosis. In cases 
of congenital imperfection of the heart, in which the pulmonary artery 
is undeveloped, the dark color of the blood may be ascribed to the 
mixture of venous and arterial blood which then takes place. In the 
converse cases, wherein the arterial part of the blood is thrown into 
the venous portion, the cause of the darkness of hue cannot be found 
in the mixture, but is to be attributed rather to the extreme retarda- 
tion of the current.* 
Induration and stricture at the conus arteriosus of the right heart, 
and the extensive valvular deformities which affect the pulmonary 
artery, have an effect quite similar to that of arrested development of 
the arterial trunks, especially as in these cases, too, the septa remain 
open. 
The deep-blue color of the skin, particularly that of the face, the 
lips, cheeks, and the tips of the fingers and toes, is the most con- 
spicuous symptom of congenital deformity of the heart. The collec- 
tion of venous blood in certain parts also causes their enlargement, 
due (as has been ascertained by the careful observation of- Foerster) to 
serous infiltration, moderate thickening, and hypertrophy. The nose 
becomes bulbous, the bluish lips swollen, and the terminal phalanges 
of the fingers and toes so much thickened as to look like the knobs 
of drumsticks. The nails are wide and arched. 
Most patients have puny frames with long limbs, and show great 
tendency to profuse haemorrhage. They are susceptible to cold; are 
sluggish, languid, and irritable. They often have imperfect develop- 
ment of the genitals and feeble sexual power. They suffer attacks of 
palpitation, oppression, and syncope, and rarely attain the age of 
forty or fifty years. They nearly always die early of intercurrent dis- 
ease, which they are ill able to resist, or else they perish from oedema 
of the lung, dropsy, etc. 
It is remarkable that sometimes the cyanosis and functional dis- 
turbance just described do not manifest themselves until the period of 
* That the great cyanosis of persons with congenital malformation of the heart is 
due to an especial cause, becomes evident from the fact that individuals with congeni- 
tal cyanosis do not become dropsical nearly so soon as those suffering from acquired 
cyanosis. This would not be the case if the cyanosis were due to venous engorge- 
ment alone. 370 
DISEASES OF THE HEART. 
puberty. It may be that, for a time, compensation for the congenital 
deformity is effected by consecutive hypertrophy, but that insufficience 
of the heart only appears after the development and growth of the 
body and the increase of the volume of the blood have advanced so 
fast that the puny heart can no longer keep pace with it. Physical 
examination is of little value in the diagnosis, owing to the great 
diversity of form which such malformations assume. The impulse 
of the heart is usually strengthened and extended, the dulness greater; 
we feel the fremissement cataire and hear confused murmurs. In 
other cases the heart-sounds are normal. 
The ancient assumption, that imperfection in the septa caused cya- 
nosis, is erroneous. This defect, alone, never occasions blueness, etc., 
but is a harmless anomaly, which gives no evidence of its existence 
during life. 
Treatment.—Treatment of congenital deformity of the heart must, 
of course, be purely symptomatic, and confined to combating the more 
dangerous manifestations. The same rules hold good here which we 
have laid down for the management of acquired disease of the heart. 
CHAPTER XIY. 
NEUEOSES OF THE HEART. 
Etiology.—There are a number of influences which tend to modify 
the functional energy of the healthy human heart, as well as the num- 
ber of its beats. We may assume that the greater force and frequence 
of the heart-beat, caused by mental or bodily excitement, or by the 
use of ardent spirits, are not the effect of any structural change in the 
muscles of the organ, but rather are due to a perversion of its inner- 
vation. The term neurosis of the heart, however, is not applied to 
functional derangements proceeding from causes of this nature, but 
only to those forms of perversion of its action or abnormity of its sen- 
sation which, without depending upon any structural change, arise 
either without preceptible cause or else upon occasions which, in most 
persons, would not give rise to any functional disturbance. Under 
this head stand the so-called nervous palpitation and the train of 
symptoms known as angina pectoris. The character of these two affeo- 
tions, particularly the paroxysms and the free intervals observed in 
their course, entitle us in some measure to count them among: the neu- 
roses of motion and sensibility. It would be somewhat rash, however, 
to ascribe them as yet to any particular class of these complaints, as 
long as our knowledge regarding the influence of the cardiac nerves 
upon the function of the heart remains in its present imperfect state. NEUROSES OF THE HEART. 
371 
The nerves of the heart consist of branches of the par vagum and sym- 
pathetic, and, besides these, it has its peculiar ganglia. If we sepa- 
rate the organ from the nerves, and cut it out of the body, it still will 
continue to contract rhythmically for some time ; and, even after ceas- 
ing to beat, will recommence, if we inject blood into the coronary arte- 
ries, or supply it with oxygen. Rhythmical contraction, then, is not 
dependent upon the pneumogastric or sympathetic nerves, but seems to 
be brought about solely by the cardiac ganglia, although this too has 
been doubted. As to the effect of the pneumogastric upon the beat 
of the heart, we know that irritation of this nerve retards its action, 
while section accelerates it, so that we may regard the nerve as a 
moderator of the activity of the heart. We know but little in this 
respect, and nothing of certainty, concerning the influence of the sym- 
pathetic nerve. 
It would, therefore, seem rash to count palpitation among the 
hypercineses, a condition due to extreme excitement of the motor 
nerves, as has been done by Romberg, and more lately by Bam- 
berger. It is quite as possible that palpitation of the heart might 
proceed from reduced energy of the pneumogastric as from over-excite- 
ment of the sympathetic or cardiac ganglia. Besides, in many cases 
of nervous palpitation, an increased force of the heart’s action cannot 
be observed, the symptom being merely subjective, and perceptible 
only to the patient. Such cases should more properly come under the 
head of hyperaesthesi®, and be regarded as an extreme excitement of 
the sensory nerves of the organs.* 
Romberg defines angina pectoris as hyper®sthesia of the cardiac 
plexus. Bamberger calls it a hypercinesis with hyperesthesia. The 
cardiac plexus is assumed to be the source of the pain ; but this, too, 
must be pronounced a matter of theory only. At all events, the pain 
which attends this “ cardiac neuralgia ” extends with great intensity 
along the brachial plexus. 
Ignorant as we are regarding the pathogeny of neuroses of the 
heart, we still have some idea as to their cause. Nervous palpitation is 
principally seen in anaemic subjects, and is one of the most constant 
manifestations of chlorosis. Next in frequence, we find it in derange- 
ment of the sexual system, not only among females, where it plays an 
important part in hysteria, but also among males addicted to venereal 
excess, above all, among onanists. Palpitation is also common in hy- 
* We should be equally warranted in calling every fainting-fit an acinesi3 of the 
heart. When a person swoons from psychical or other causes, the scene always com- 
mences by a depression of the heart’s action, smallness of the pulse, and pallor of the 
skin; and it is not until then that the consequences of diminution of the supply of 
arterial blood to the brain, loss of consciousness, etc., appear. It is quite the same in 
a too-protracted inhalation of chloroform or ether. 372 
DISEASES OF THE HEART. 
pochondriasis. As a striking instance of this hypochondriac palpita- 
tion, Romberg relates the example of Peter Frank, who, while en- 
gaged in study of disease of the heart, thought himself suffering from 
aneurism. We very often see palpitation accompany rapid growth 
about the time of puberty. It affects other persons, in whom no defi- 
nite exciting cause can be discovered. 
Angina pectoris is found almost exclusively in persons suffering 
from organic disease of the heart. Either ossification of the coronary 
arteries, valvular defects, hypertrophy, degeneration, or aneurism of the 
aorta, has been found upon autopsy of most persons who have been 
afflicted in this manner. Nevertheless, we cannot regard angina pec- 
toris as indicative of any of these lesions. Not one of them is con- 
stant ; and the malady always takes the same form while the structural 
alterations differ most widely. It is always marked by paroxysm and 
intervals of immunity, so that we are forced to set it down as a ner- 
vous disorder of the heart, to which organic changes merely afford a 
predisposition. In rare instances it has occurred where no organic 
disease existed, particularly in old and obese persons, males being 
affected oftener than females. 
Symptoms and Course.—Nervous palpitation is characterized by 
an accelerated and sometimes unrhythmical beating of the heart, ac- 
companied usually by a feeling of dread and dyspnoea. The impulse 
is generally short and bounding; in many cases without perceptible 
increase of force, and in others so violent as to shake the hand at each 
stroke. Even in the latter cases the subjective feeling of palpitation 
experienced by the patient is greater than what the apparent force of 
impulse would lead us to expect. The pulse and aspect of the patient 
are not always the same. Sometimes the pulse is full, and the face red; 
sometimes it is small and intermitting, and the countenance is pale, 
apparently as if the beats lacked energy, or as though they were of 
too brief duration effectually to fill the arteries. The length of an at- 
tack of this kind varies, lasting from twenty minutes to an hour or 
more. It is not unfrequently accompanied by nervous derangement 
of other kinds, dizziness, buzzing in the ears, trembling, etc. Its ter- 
mination may be sudden or gradual, the action of the heart returning 
to its normal condition, and weeks or months may pass without the 
occurrence of a new attack, while in other cases the seizure recurs at 
very short intervals. 
The intermission and recurrence of the paroxysms without known 
cause, their appearance under conditions which do not, as a rule, give 
rise to exaggerated action of the heart, its association with other ner- 
vous disorders, and, above all, the results of physical exploration, will 
serve to prevent error, and yet the disease is not always easy of re- NEUROSES OF THE HEART. 
373 
cognition. If the exciting cause be obvious and amenable to treat- 
ment, the malady will disappear sooner or later. This is especially 
the case with chlorotic girls, hysteric women with curable disease of 
the womb, and even in palpitation induced by excess in venery. At 
other times it is extremely obstinate, and persists throughout life. 
During the intermission, physical exploration reveals nothing 
anomalous; during the paroxysm, we often hear abnormal murmurs 
attributable to unnatural tension of the valves and arterial walls. 
In angina pectoris, the patient suddenly experiences beneath the 
sternum a feeling of strangulation and pain, which almost always 
shoots in the direction of the left arm, less frequently toward the right. 
This is accompanied by a distressing feeling of dread and sense of im- 
pending dissolution. The sufferer imagines that he cannot breathe; 
but, if forced to do so, succeeds in making a deep inspiration. He does 
not dare to speak, but groans and sighs. If the attack come upon 
him while walking, he stands still, seeking a support, and clasping 
his breast. The hands are cool, the countenance pale, the features 
perturbed. After the lapse of a few minutes, or in a quarter or half an 
hour, the paroxysm gradually abates, nearly always with eructations 
of gas. These attacks are repeated at first with long intervals ; after- 
ward they become so frequent as to be of almost daily occurrence. As 
an exciting cause, mental emotion seems to be the most common agent; 
physical exertion and error of diet produce it more rarely. Between 
the attacks health may seem unimpaired, while in other cases evidence 
of serious disease of the heart may be detected. 
Treatment.—Treatment of nervous palpitation demands, above 
all else, the removal of every recognizable and remediable predispos- 
ing cause. In chlorotic or anaemic subjects, the preparations of iron 
often render signal service. Hysterical palpitation may require the 
application of leeches to the os uteri, and of lunar caustic to the ori- 
fice ; a treatment which, as we shall see in the proper chapter, will 
often effect a cure in a case previously hopeless. Hypochondriacs, 
with varicosities of the anus, if affected by palpitation, often find great 
relief from the application of leeches to the fundament. Fuller details 
of the appropriate remedies in this affection would occupy us too long, 
as it would include the treatment of all the maladies of which palpita- 
tion is an accompaniment. Patients, in wrhom no special cause for the 
disease can be found, should be ordered to bathe in cold water, be sent 
into the country, made to travel, and forbidden all over-exertion and 
luxurious living. 
During the attack, the effervescent powders, vegetable and mineral 
acids, cream of tartar, “ eau sucre,” enjoy a certain reputation. It 
would be foolish to carry one’s skepticism so far as to slight these 374 
DISEASES OF TELE HEAR! 
medicines, because they are superfluous and impotent; as it is, the 
mental preoccupation afforded by the preparation of an effervescent 
powder, etc., is often of the greatest relief to any person afflicted with 
palpitation, and even shortens the paroxysms. The application of cold 
over the heart seems to be of decided efficacy in abbreviating the fits. 
The nervines, tincture of castor, tinctura valerian® setherea, often have 
the same effect. On the contrary, narcotics, especially digitalis, if 
used, must always be employed with the greatest caution in cases of 
nervous palpitation, in the narrow acceptation of the term which we 
employ. 
It is doubtful whether it be in our power to relieve paroxysms of 
angina pectoris by means of any medication; but, after having once 
witnessed the impatient and hurried clutch of the sufferer for his medi- 
cine-glass, as the attack comes on, the physician will readily acknowl- 
edge that the “ laisser alter ” mode of treatment is sheer cruelty. 
Romberg advises the inhalation of sulphuric and acetic ether, a couple 
of teaspoonsful of it being poured into a saucer, and its edge held to 
the mouth of the patient while it evaporates. Complete narcosis must 
not be permitted. In these cases, too, I have seen decided abbrevia- 
tion of the fit by the use of tincture of valerian and castor setherea. 
Opiates, and other narcotics, are to be avoided. During the intervals, 
treatment must be limited to combating whatever recognizable and 
remediable predisposing cause may exist. Fontanelles, setons, etc., 
much as they have been made use of, ought not to be employed. 
' CHAPTER, XV. 
basedow’s disease. 
The term JBasedoitfs disease is applied to a train of symptoms of 
tolerably frequent occurrence, consisting of a subjective sense of pal- 
pitation, accompanied by acceleration of the action of the heart, beat- 
ing of the veins of the neck and head, swelling of the thyroid gland, 
and exophthalmos. This peculiar series of symptoms is sometimes 
seen in patients with valvular disease of the heart, but is more fre- 
quently observed in persons free from any organic cardiac disease. 
The tumefaction of the thyroid body, which is not .often very large, 
arises partially from dilatation of its vessels, and in part from infiltra- 
tion of its tissues with serum, and from simple hyperplasia. More 
rarely cysts, with serous or colloid contents, are found in the gland. 
The swelling of the intra-orbital fat, which is the cause of the ex- 
ophthalmos, seems in most cases to be due to hyperaemia and oedema, 
or to simple hyperplasia of the adipose tissue ; since, when recovery BASEDOW’S DISEASE. 
375 
takes place, the prominence of the eyes subsides as completely as do 
the thyroid enlargement and the disturbance of circulation. 
That this it not a mere coincidence of morbid conditions, and that 
it is fully entitled to be regarded as a separate and distinct disease, is 
evident from the circumstance already alluded to, that the changes in 
the thyroid and eyes, not only appear simultaneously with the derange- 
ment of the circulation, but that they also subside together. 
In seeking for a common source to which the individual symptoms 
of Basedoic's disease may be attributed, the idea of a derangement of 
innervation of the vascular walls naturally suggests itself. Palsy of 
the vaso-motor nerves fully accounts for the dilatation and increased 
pulsation of the carotids and thyroid arteries, as well as for the oedem- 
atous swelling of the thyroid gland and intra-orbital fat. The sub- 
ject of the innervation of the heart, indeed, is by no means satisfac- 
torily understood, in spite of the labor expended upon the subject; yet 
it is perfectly supposable that variation in the degree of fulness of 
the blood-vessels, which traverse the substance of this organ, may have 
an important influence upon its function; and that palsy of the vaso- 
motor nerves of the cardiac vessels will cause them to dilate, thus aug- 
menting the supply of blood to the cardiac muscles, and producing 
essential modification of the heart’s action. We have no hesitation in 
declaring our belief that the probable cause of the symptoms of Base- 
dow's disease consists in a subparalytic state of the vessels of the mus- 
cles of the heart. At the same time we deem it rash, or at least pre- 
mature, to ascribe such palsy of the vascular walls to coarse structural 
changes of the cervical ganglia of the sympathetic nerve. Apart 
from the fact that the lesions of the ganglia in some cases are entirely 
different from those found in others, and that in other instances again, 
in spite of the most careful search, no lesion whatever has been found 
in the ganglia, it is improbable that the nervous disorder of the vas- 
cular wall should depend upon coarse and palpable alterations of tex- 
ture of the nerve-fibres and ganglion-cells, simply because such nervous 
derangement often subsides entirely. 
Basedow's disease is far more common among women than among 
men; menstrual disorder, or perhaps the lack of red corpuscles in the 
blood, which so often accompanies such disorder, also seems to have 
some part in its production; but it is altogether inadmissible to regard 
such disease of the vaso-motor nerves as a mere part of that wide- 
spread disorder of innervation, which occurs in hysteria, and to attrib- 
ute the relaxed state of the vessels to faulty nutrition, either of the 
vessels or of their nerves, proceeding from the want of red corpuscles 
in the blood. Indeed, Basedow's disease is not especially prevalent in 
cases of severe hysteria or intense chlorosis, and in some cases even 376 
DISEASES OF TIIE HEART. 
appears in persons free from both menstrual disturbance and impov- 
erishment of the blood. Men who are affected by this malady are 
usually somewhat advanced in life, while among women it generally 
appears during youth. 
The patients generally have long suffered from palpitation, with a 
remarkable frequence of the pulse, which sometimes rises as high as 
120 or 140 beats, when the patient and his friends become aware 
that his eyes are more prominent than formerly, and that the neck is 
enlarged. If the hand be laid upon the thyroid gland, or the steth- 
oscope be applied to it, a remarkable rustling is perceptible both to 
ear and touch. Sometimes a blowing sound is also heard at the heart. 
Generally these sounds are easily recognizable as “ blood-murmurs,” 
as there is no secondary dilatation, nor hypertrophy of the organ, 
without which it is impossible to ascribe a false murmur to valvular 
derangement. At a more aggravated stage of the malady, the prom- 
inence of the eye-balls increases to such an extent as to render the 
eyelids incapable of covering the eyes completely. This inability to 
close the eyes may have the most disastrous consequences. In some 
instances, infiltration, abscess, and perforation of the cornea, and even 
complete destruction of the eye, have been known to follow. Such acci- 
dents are no doubt due in a great degree to a -want of proper cover- 
ing, and lubrication of the bulb, although it would seem that the 
graver degree of destruction does not occur until after the establish- 
ment of a certain amount of anaesthesia of the cornea (attributable to 
strain upon the ciliary nerves), rendering the eye incapable of protect- 
ing itself properly. Sometimes the motion of the bulb is embarrassed, 
probably in consequence of palsy of the ocular muscles, resulting from 
stretching; but, excepting the affections of the cornea above alluded 
to, there is scarcely ever any other derangement of vision. Graefe 
speaks of a spasmodic contraction of the levatores palpebrae superioris 
as a very characteristic symptom which sometimes precedes the exoph- 
thalmos. It becomes recognized by the hesitating and imperfect 
manner in which the upper-lid is depressed when the eye is made to 
look downward. In severe cases, the pulsation of the thyroid and 
carotids is so marked as to be apparent to the eye even at a distance. 
Most patients complain of oppression; some of dizziness and headache, 
and of other irregular symptoms. 
Generally the disease drags on for months and years. Instances 
when its course has been acute and rapid are exceptional. If the 
result is to be unfavorable, it is generally on account of a gradual 
dilatation of the heart with diminution of its functional power. The 
patient becomes cyanotic, and dropsical, the obstruction in the veins 
of the pulmonary circulation gives rise to extreme dyspnoea, and at BASEDOW’S DISEASE. 
377 
last to oedema of the lungs. More rarely death takes place with cere- 
bral symptoms, or in consequence of intercurrent disease. An im- 
provement terminating in complete restoration is by no means an 
uncommon occurrence. Indeed, recovery is a much more common end- 
ing of the disorder than is death. 
JBcisedow's disease often recovers under a treatment consisting 
in a strengthening diet, and in the use of iron. The secale cornutum 
has also been prescribed as having a reputed power of causing con- 
traction of the walls of blood-vessels, and a reduction of their oalibre. 
Whether the improvement be really in consequence of this mode 
of treatment, or not, remains a matter of doubt. At all events, it would 
be well to try this remedy, or some similar one, and for the time to 
disregard the application of a constant and induced current applied to 
the cervical portion of the sympathetic, which has been proposed upon 
purely hypothetical grounds. 
When the exophthalmos is very great, Graefe advises the use of a 
light bandage, and in extreme cases the diminution of the opening ot 
the eyelids by means of a surgical operation. SECTION II. 
DISEASES OF TIIE PEE ICA EDI UM. 
CHAPTER I. 
PERICARDITIS. 
Etiology.—With regard to the pathogeny of pericarditis, we may 
refer to what we have already said concerning its kindred affection, 
pleuritis. In many cases, where the disease is partial, the inflammatory 
derangement of nutrition is not such as to produce interstitial exuda- 
tion and effusion into the sac; but a proliferation of the pericardium 
takes place, so that its normal tissue forms offshoots, and becomes 
thickened. Thus the so-called tendinous spots, etc. (Sehnenflecke) 
originate. In other cases, the cell-growth in the pericardium is accom- 
panied by a free exudation. This always contains fibrin, but in vari- 
able quantity, and we are not warranted in attributing this variation 
to differences in the crasis of the blood; indeed, accumulation of fibrin 
in the blood must be regarded rather as a consecutive and not as a 
primary alteration of its composition. 
Pericarditis may be caused, although rarely, by injuries, penetrat- 
ing wounds, blows, concussions, etc.; to this class of cases we naturally 
annex those in which inflammation has spread to the pericardium from 
a neighboring organ. It is extraordinarily rare for this malady to 
attack previously healthy persons as an independent isolated disease. 
When it does occur, it is chiefly at times when pneumonia, pleurisy, 
croup, and other inflammatory complaints are rife, and epidemic influ- 
ence prevails. In such cases it is customary to assume that cold has 
been allowed to act upon the organism, although this is generally diffi- 
cult to prove. 
Pericarditis occurs much more frequently, allied to other acute or 
chronic diseases. The most important of these is acute articular rheu- 
matism, particularly when several joints are successively affected. 
According to Bamberger’s carefully-collected statistics, about thirty PERICARDITIS. 
379 
per cent, of the cases observed have been complicated with acute rheu- 
matism. 
Next in frequence, pericarditis complicates Bright’s disease, tuber- 
culosis, particularly tuberculosis of the lungs, chronic disease of the 
heart, and aneurism of the aorta. In all these cases, as it seems to 
me, the primary disease gives rise to a predisposition to pericarditis; 
but the latter is not a sequel, only a complication of the primitive com- 
plaint, and is not to be regarded as secondary in the narrow sense 
of the word. 
It is otherwise in the pericarditis which attends septicaemia and 
kindred conditions, puerperal fever, severe scarlatina, small-pox, etc. 
Here the disease belongs to the consequences, and is not a complica- 
tion ; the infection manifests itself by a series of inflammatory disturb- 
ances, attacking the skin, the joints, and the pericardium. 
Anatomical Appearances.—In the bodies of many, and especially 
of old persons, we find upon the visceral surface of the pericardium a 
number of fine papillae, consisting of delicate, vascular connective tissue. 
Still more frequently we find irregular, whitish, flat tendinous deposits, 
called maculae albidce, lactce (Sehnenflecke). These, likewise, consist 
of new connective tissue, springing directly from that of the pericar- 
dium, from which they can only be detached by force, and by whose 
epithelium they are covered. If the pericardial proliferation be of in- 
flammatory origin (a matter still sub judice), like the thickening and 
adhesions of the pleurae, they appear to proceed from inflammation, 
which produces a merely nutritive exudation, a pericarditis sicca. 
As the growth of villi and the formation of maculae albidae are not 
recognizable during life, but are mere accidental post-mortem discover- 
ies, we shall give them no further attention. 
In discussion of the subject of exudative pericarditis, our attention 
will be occupied, first, with the changes undergone by the pericardium; 
second, the quality and quantity of the exudation. 
At the commencement of the disease the pericardium appears more 
or less reddened, in consequence of a dense capillary injection spring- 
ing from the deeper parts, with here and there extravasations in the 
form of irregular, dark-colored, homogeneous red spots. The tissue is 
relaxed by serous infiltration, and can be very readily torn; the sur- 
face, the epithelium having fallen, is dull and void of glitter. The 
membrane soon takes on a shaggy appearance; fine villi, papillae, and 
folds develop by the proliferation and generation of young connective 
tissue-cells, constituting the first step in the formation of pseudo-mem- 
branes, and of the adhesions of the pericardium, which remain after 
pericarditis. 
Pericardial effusions present all the modifications which we have 380 
DISEASES OF THE PERICARDIUM. 
described as occurring in pleurisy. The exudation soon separates into 
a liquid and a solid portion. The former may be very scanty in quantity, 
or may amount to several pounds. Small accumulations of it form in 
the upper and anterior part of the sac, at the root of the great vessels, 
while the heart gravitates to the lower portion. When in larger 
amount, the entire sac is distended, the lungs compressed, particularly 
the lower lobes of the left lung; even dilatation of the thorax, in the 
region of the heart, may be the consequence. 
Although the exudation always contains some young cells or pus- 
corpuscles, their quantity is often extremely small, and the liquid is 
then tolerably clear, and either colorless or of a yellowish tinge. If 
more or less of coagulated fibrin be found in the liquid, it is called 
sero-fibrinous. A smaller quantity of fibrin imparts a slightly-flaky 
opacity to the liquid part of the exudation, or may produce a slimy 
turbid deposit upon the pericardium. Sometimes delicate fibres, like 
cobwebs, pass across from one surface to another. This we find, chiefly, 
in cases in which inflammation has been transmitted from some neigh- 
boring organ to the pericardium. 
In other cases, the exudation is very heavily charged with fibrin, 
which is extensively precipitated upon the walls of the pericardium, 
forming reticulated and villous masses. The surface of the heart ac- 
quires the aspect of a cut sponge, or of one of two surfaces smeared 
with butter, which have been quickly pulled asunder after having been 
brought into contact. A heart upon which this sort of villous, ragged 
precipitate has formed, is called cor villosum or hirsutum. This is the 
kind of exudation most commonly met with in the pericarditis of acute 
articular rheumatism. 
In many cases an escape of blood from the ruptured capillaries 
accompanies the exudation, thus producing a haemorrhagic exudation. 
If there be but little blood mixed with it, the serum has a reddish color; 
if the flow of blood be considerable, the effused mass may resemble a 
pure extravasation, and assume a blackish hue. Even the fibrinous 
deposit, otherwise whitish yellow in color, is stained, either dark or 
bright-red, by admixture of the blood. Haemorrhagic exudation some- 
times occurs in recent pericarditis, which has attacked cachectic sub- 
jects, topers, tuberculous persons, or those suffering from advanced 
Height's disease. It is still more frequently observed when the in- 
flammation, instead of invading the true pericardium, has attacked the 
young connective tissue which has developed upon it, and in which 
very large but delicate and thin-walled vessels form, which are very 
liable to rupture. In these cases we often find miliary tubercles de- 
veloped in the young adventitious membrane, besides the haemorrhagic 
exudation ; and this is what we commonly find in the form known as PERICARDITIS. 
381 
chronic pericarditis, a disease which, during life, permits of our recog- 
nizing repeated outbreaks of the inflammation. 
If young cells (pus-corpuscles) be commingled in any great amount 
with the exudation, the effused liquid becomes yellow and opaque, like 
thin pus. The fibrinous deposits are remarkably yellow, unelastic, 
rotten, and even pasty. This we call purulent exudation (pyopericar- 
dium). It arises precisely like empyema, sometimes from protracted 
pericarditis, with sero-fibrinous exudation; sometimes the inflammation 
shows strong tendency to formation of pus-cells from the outset, so 
that even the recent exudation is purulent. Such a disposition is often 
seen in the pericarditis of septicaemia, puerperal fever, etc. In pyo- 
pericardium, pus-cells sometimes form in the substance of the serous 
membrane, producing ulceration; although this is more rare than in 
empyema. 
In cases of extraordinary rarity, pericardial effusion becomes putrid, 
fetid, discolored, emits gas ; and here, too, erosion may take place in 
the membranes. Ichorous exudation is the product of such decom- 
position. 
In recent cases, the substance of the heart often suffers no material 
alteration. In cases of longer standing, however, or when the disease 
has been very intense, it appears soon to become sodden with serum, 
softened, and flabby, so that extensive dilatation of the heart super- 
venes upon the pericarditis. In cases of htemorrhagic and purulent 
exudation, the muscles of the heart become very much discolored, 
flabby, and softened, the epicardial surface undergoing fatty degenera- 
tion ( Virchow). Myocarditis, too, is a not unfrequent accompaniment 
of the disease. 
The effects of pericarditis depend greatly upon the degree of thick- 
ening of the pericardium, and the quantity of coagulated matter con- 
tained in the effusion. If the thickening be slight, and the amount of 
fibrin in the effusion small, it is soon absorbed, the liquid first, and 
then the solids, undergoing fatty degeneration, and thus becoming 
capable of absorption. Thickening of the pericardium leaves behind 
it thick tendinous spots, or else adhesions from between the two sur- 
faces, a circumstance of but little moment if the pericardium be but 
moderately thickened, so that such a termination of the disease may 
be regarded as a recovery. If the pericarditis be of long standing, 
the thickening generally becomes so great that permanent and serious 
disorder remains, even after the exudation has been absorbed. The 
young connective tissue is converted into a firm fibrous mass, so that 
the epicardium at last forms a dense indurated capsule around the 
neart. The parietal surface is usually less thickened, and here, too, if 
the effusion be fully absorbed, it may be firmly joined to the visceral 382 
DISEASES OF THE PERICARDIUM. 
portion. Frequently, absorption is incomplete; the folds of the peri- 
cardium are then only partially adherent; in other places, the residua 
of the exudation appear in the form of puruloid or cheesy masses, 
which afterward not unfrequently are converted into a chalky paste, 
which may seem embedded or impacted in the flesh. 
When death occurs at the height of acute pericarditis, or in the 
course of the chronic form, we find the traces of cyanosis, and not un- 
commonly discover dropsical effusions in the body. 
Symptoms and Course.—As pericarditis hardly ever attacks a 
person in good health, or appears as a solitary and independent disease, 
it is difficult to describe its course distinctly. Moreover, when this 
malady sets in upon some preexisting disorder, its symptoms often 
modify those of the latter so little that they are exceedingly apt to be 
overlooked. When pleuritis or pneumonia extends into the pericar- 
dium, a diagnosis, or even a suspicion, of the complication is often im- 
possible without physical examination; and, as the latter too often fails 
us here, “ a participation of the pericardium in the inflammation ” often 
remains undiscovered until the autopsy is made. 
When acute articular rheumatism is the complicating disease, it is 
quite rare for attention to be called to the existence of pericarditis by 
any rigor, aggravation of the fever, acceleration or retardation of the 
pulse, pain in the region of the heart, palpitation, dyspnoea, or terror. 
It should be our invariable rule daily to auscult the chest of a rheu- 
matic patient, even though he do not complain, for all the above-named 
symptoms may be wanting, and yet pericarditis, and even a copious 
effusion, may exist. When subjective symptoms do occur, however, 
pain and palpitation are the more frequent of the signs. The pain 
usually affects the left side of the epigastrium, and spreads more or 
less over the chest. It is sometimes piercing, sometimes duller, and is 
almost always aggravated by a firm pressure upward upon the epi- 
gastrium. Excessive pain almost always signifies implication of the 
pleura or lung in the inflammation. Palpitation is generally met with 
where the action of the heart is embarrassed, and where the organ has 
difficulty in fulfilling its task. It is easy to understand that pericarditis 
can impede the function of the heart through pressure upon it by the 
exudation, by serous infiltration of its muscles, and by participation of 
the latter in the inflammation. On the other hand, it is singular that 
palpitation, and other symptoms indicative of embarrassment of the 
heart’s action, should not be a more common source of complaint. 
Sometimes the pulse becomes very frequent when the disease sets in 
in other cases, it is temporarily retarded. We have already spoken of 
this latter symptom while upon the subject of endocarditis, and have 
there expressed our view that it is a matter of pure theory to ascribe PERICARDITIS. 
383 
these phenomena to irritation of the cardiac ganglia. If the pulse be 
both frequent and small, pericarditis may assume a strong resemblance 
to typhus and other asthenic fevers. The sick man is collapsed, is ex- 
tremely restless, sleeps badly, and starts from his sleep; he becomes 
delirious, until at last somnolence sets in. The more imperfect and 
hurried the action of the heart becomes, so much the more marked are 
the symptoms of circulatory obstruction; the countenance becomes 
congested and cyanotic, and the breathing rapid. If a fresh obstacle 
to respiration be added to this passive hyperaemia of the lung, should 
the lung be compressed by a huge pericardial effusion, the dyspnoea 
may become intense. The patient lies upon the left side, as it is the 
left lung which is the most compressed, and freer play is thus afforded 
to the right side of the thorax, or else he sits upright, or bent forward 
in bed. Even when the function of the heart is not suffering mate- 
rially from the effects of the pericarditis, dyspnoea, and very severe 
dyspnoea, too, may arise through compression of the lung, so that, as 
acceleration of pulse is not a very common symptom, 'pain in the car- 
diac region, palpitation, and subsequent dyspnoea, must be pronounced 
its most frequent subjective signs, if it produce any functional derange- 
ment at all. 
If pericarditis be a complication of tuberculosis, Bright’s disease, 
chronic disease of the heart, or aortic aneurism, its invasion is equally as 
insidious as, if not more so than, when it arises in rheumatism. With- 
out physical examination, its diagnosis would be impossible. After long 
duration, the malady develops a series of symptoms, which we shall 
describe as chronic pericarditis. If it set in in the course of grave 
blood-disease, there are absolutely no subjective symptoms. In such 
maladies the sensorium is usually much benumbed by the asthenic 
fever, and the great apathy of the patient renders him insensible to 
pain and distress far more violent than any arising in pericarditis. It 
would seem that depression of the cardiac action is most intense in 
cases of purulent effusion, but, without physical proof, we are unable 
to decide with certainty whether the acceleration and contraction of 
the pulse, already rapid and small, be due to the prostration or to the 
pericarditis. 
With regard to its course and termination, the forms of the disease 
which accompany pneumonia, pleurisy, and acute articular rheumatism 
generally have a favorable issue; the disease is acute, and ends in 
complete recovery. If, as often happens, it have not given rise to any 
subjective symptoms, the change for the better is only to be recognized 
by physical examination. Palpitation, pain, and dyspnoea, if present, 
usually soon subside, as also does any frequence of the pulse which 
may appear. This favorable result is far less common in the forms of 384 
DISEASES OF THE PERICARDIUM. 
the disorder which complicate Bright’s disease, disease of the heart, 
tuberculosis, and, rarest of all, in the purulent pericarditis accompany- 
ing septicaemia, etc. 
Death is not a common consequence of acute pericarditis; that is 
to say, the disease is not often the sole and immediate cause of death. 
When it occurs in a rheumatic case, the disordered action of the heart 
suddenly, or else gradually, increases to cardiac palsy; the pulse be- 
comes small and irregular; the consciousness is completely lost; en- 
gorgement of the pulmonary veins produces oedema of the lungs, and 
the patient dies. Death may be all the more speedy, if the pericarditis 
be complicated by pleuritis or pneumonia. The termination of tuber- 
culosis, Bright’s disease, etc., may also be accelerated by such a com- 
plication, but the disease then almost always assumes a chronic form. 
Cases in which, from the beginning, the effusion has been purulent, 
almost always end fatally; but it is difficult to decide how much of 
this evil result is due to the local affection, the pericarditis, and how 
much to the constitutional disorder which it complicates. 
As a third mode of termination, acute pericarditis may pass into 
a chronic state. A small number of cases of chronic pericarditis pro- 
ceed from the acute rheumatic form of the disease. It is more com- 
mon, however, as an accompaniment of the cachectic conditions and 
cardiac disease which we have so often spoken of. The malady, which 
probably always at first assumes the acute form, does not get entirely 
well, and sooner or later (just as in many cases of pleurisy), the in- 
flammation breaks out afresh. The exudation is extremely profuse, 
the dyspnoea severe. After a while the symptoms abate again; but 
new relapses often follow, and the disease goes on for months. We 
have said that the substance of the heart becomes extremely soft, re- 
laxed, and discolored; and, accordingly, we often find the pulse very 
small and irregular, the veins overloaded, and the patient dropsical. 
The more copious the exudation in the pericardium, so much the more 
severe not only does the dyspnoea become, but the cyanosis and drop- 
sy. Much of the blood which ought to be in the arteries is crowded 
into the veins, and cannot gain access to the right heart; for the lat- 
ter, compressed by exudation, is unable to dilate, as in other cardiac 
diseases. It is only in very rare instances that chronic pericarditis 
terminates in complete recovery. Death by oedema of the lungs and 
slow suffocation is the most frequent ending, and, in almost every case, 
the disease is attended by sequelae: 
1. First among the sequelae of pericarditis stands adhesion of 
heart and pericardium, to be treated of in the next chapter. 
2. We have already learned how dilatation of the heart becomes a 
sequel of this disease (Chap. II.), and that the longer the attack lasts 
so much the more is this likely to happen. PERICARDITIS. 
385 
3. If the substance of the heart be not degenerated, the dilatation 
turns into hypertrophy, which is usually total, and is to be set down 
as a not unfrequent sequel. 
4. The nutritive state of the organ suffers under the perpetual 
pressure of the pericardial exudation, and the constant infiltration of 
its substance, resulting in atrophy and fatty degeneration. 
Physical Signs—Inspection.—If the thoracic wall be yielding, and 
the effusion large, inspection often reveals a distinct bulging of the 
cardiac region. Ossification of the costal cartilages tends to prevent 
this prominence, which, therefore, is to be found principally in children 
and youthful persons. 
Palpation at the outset of the disease often enables us to feel that 
the beat of the heart is in its proper position, and frequently, too, that 
the vigor of the beat is increased. When the exudation is more copi 
ous, the impulse is usually weaker than normal, unless the heart be 
hypertrophied or violently excited. Sometimes the beat is quite im- 
perceptible. It may frequently be felt while the patient is standing 
upright, but is lost as soon as he lies down, as the heart then sinks 
back into the liquid, and is separated from the thoracic wall. The im- 
pulse often is situated too low down, the diaphragm having become 
depressed by the accumulation of liquids. Oppolzer’s statement, that 
the shifting of the heart-beat as the patient alters his attitude is a 
characteristic token of pericardial effusion, is incorrect. According to 
a number of observations of Gerhardt, the truth of which I can fully 
vouch for, the apex of the heart of a healthy person generally moves 
to the left about two centimetres when he lies upon his left side. 
Sometimes the hand laid upon the chest perceives a distinct sensation 
of friction, caused by the rubbing together of the rugged surfaces of 
the pericardium. 
Percussion.—If the lung intervene between the pericardium and 
the thoracic wall, percussion will reveal nothing abnormal even when 
the exudation is tolerably large (half a pound). At other times an un- 
natural dulness arises early, which, from the point at which it first be- 
comes perceptible, and the form which it afterward assumes, is one of 
the most important signs of the disease. At first, as the liquid rises, 
and the heart takes the deepest position possible, we find a dulness 
upon percussion at the root of the aorta and pulmonary vessels. It 
extends upward to the second rib, or even higher, and passes beyond 
the right edge of the sternum. When very copious, the exudation 
bathes the entire organ, and the dulness forms a triangle with the 
base downward, and with an obtuse apex above. The dulness, which 
always grows broader as it extends lower, often passes far beyond the 
left mammillary line and the right border of the sternum. 386 
DISEASES OF THE PERICARDIUM. 
Extension of the dulness to the left, beyond the point at which the 
apex beats, is a positive sign of the existence of a collection of liquid 
in the pericardium. Gerhardt has pointed out that pericardial effusion 
forms an important exception to the rule according to which cardiac 
dulness remains the same, whether the attitude be erect or recum- 
bent, as in the latter case its limits become from one-third to one-half 
larger. 
Upon auscultation, unless the heart be hypertrophied, or in violent 
action, its sounds are remarkably feeble, and often nearly inaudible. 
The disproportion between the extensive dulness and the feeble im- 
pulse and lowness of the heart-sounds is an important indication of pe- 
ricardial effusion. In addition to this, there are, in most cases, friction- 
sounds which suggest the idea of scraping, rubbing, and scratching. 
These friction-sounds are unlike those of pleuritis, which are only audi- 
ble before the pleural surfaces are separated by the liquid, or after the 
liquid part of the effusion has been absorbed, as they sometimes may 
be heard when there is a great deal of water in the pericardial sac. 
As the sounds are produced both by the rubbing up and down of the 
heart against the thoracic wall and its rotation upon its long axis, 
after the opposing surfaces have lost their primitive smoothness, and 
as the movements of the heart are of far longeu duration than the nor- 
mal sounds which it causes, these friction-sounds, although rhythmical, 
are hardly ever isochronic with the normal cardiac tones, but outlast 
them, making a prolongation, or sometimes preceding them. 
About the lower lobe of the left lung the percussion-sound is often 
flat, from pressure, and we must beware of mistaking it for pleuritis. 
The presence of pectoral fremitus will guard against error. 
Diagnosis.—Pericarditis is most apt to be mistaken for endocar- 
ditis. The functional disturbances, when they occur, are very much 
alike in the two diseases, although pain about the heart is far more 
common in pericarditis, as is also the case with dyspnoea and the cyano- 
sis. As it often happens, however, that neither of them furnishes any 
subjective symptoms whatever, differential diagnosis must mainly de- 
pend upon physical exploration : 1. In the first place, in endocarditis, 
we never find prominence of the cardiac region, which, although not 
common, does sometimes appear in pericarditis. 2. The form of the 
tract of abnormal dulness affords an important clew. In endocarditis 
the dulness may become abnormally widened in a few days, as when 
dilatation of the right ventricle occurs early. In pericarditis the dul- 
ness almost always begins in the vicinity of the great vessels, and 
afterward assumes a triangular form. If the left border of the dul- 
ness reach beyond the apex, the right considerably surpassing the 
right edge of the sternum, effusion is present in the sac. We have PERICARDITIS. 
387 
already dwelt upon the significant fact that, notwithstanding the ex- 
tent of the dulness, the heart-tones are low, and the beat feeble and 
inaudible when the patient lies down. If the dulness commence at 
the second rib, we must take notice whether or not the diaphragm and 
heart be pushed upward. If so, it will be impossible to form any 
positive conclusion as to the presence of liquid in the pericardium. 
The possibility of the existence of aneurism of the aorta, of excessive 
dilatation of the right auricle, of infiltration of the anterior edges of 
the lung, and of retraction of the lung, which allows a larger portion 
of the pericardium to come into contact with the thoracic wall, must 
also be excluded ere the diagnosis of pericardial effusion can be re- 
garded as established. Sometimes, notwithstanding the existence of 
a very large effusion, the cardiac dulness is not increased, although in 
the vicinity of the area of dulness the percussion-sound is somewhat flat. 
In these cases the anterior edge of the lung has become immovable, 
owing to adhesion of the pulmonary and costal pleurae. 
3. The murmurs heard in the heart, usually permit of a conclu- 
sion as to the nature of the existing disease. In the first place, their 
quality affords some information. Not only the pericardial sounds, but 
many of those arising in the heart are friction-sounds. In the one 
case, the roughened surfaces of the pericardium rub together; in the 
other, the roughened endocardial surface is rubbed by the current of 
the blood; but, in many instances, the sounds are so distinctly those 
of scraping or scratching, that we can have no doubt but that they 
proceed from the pericardium. The points at which they are best 
audible is of more importance. As it is mainly the right side of the 
heart which lies in contact with the side of the chest, and rubs against 
it during its diastole and systole, pericardial sounds are very often 
heard over the right ventricle, where endocarditis and valvular disease 
are very rare. The time at which the sounds are heard is of great mo- 
ment. In endocarditis, they are isochronic with the heart-sounds, and 
supplant them. In pericarditis they precede the normal sounds, or 
come after them. When the beat of the heart is very rapid, it is hard 
to say if the false sounds be isochronic with the normal ones or not. 
The extension of the sounds exhibits a further difference (Bam- 
berger). In pericarditis they are sometimes confined to a very small 
spot; in endocarditis they are transmitted along the current of the 
blood. Lastly, as the heart rises and falls in the liquid around it, 
pericardial sounds are much more liable to change with alteration of 
attitude in the patient than the endocardial murmurs. 
Rhythmical friction-sound of the pleura may arise in consequence 
of inflammation of that portion of the pleura which overlies the peri- 
cardium, the roughened costal pleura being made to rub against the 388 
DISEASES OF THE PERICARDIUM. 
pulmonary pleura by the beating of the heart. This extra-pericardial 
friction can only be distinguished from the intra-pericardial sounds 
when it ceases entirely during inspiration. I have seen one very well- 
marked case, in which it could be demonstrated, by means of ausculta- 
tion and percussion, that the expanded lung entered the mediastino- 
costal sinus during inspiration, and separated the roughened surfaces 
of the pericardium and costal pleura. 
It is not always easy to determine the character of the exudation 
in the cases in question, although the cause of the disease and its 
duration may enable us to form an opinion. The pericarditis which 
complicates rheumatism is, if recent, almost always accompanied by a 
sero-fibrinous effusion. That of septicaemia is nearly always purulent; 
the chronic variety often has a haemorrhagic exudation. It would be 
unsafe to infer the nature of the effusion from the character of the con- 
stitutional disorder, as the latter depends more upon the primitive dis- 
ease than upon the form of exudation. Even physical research only 
informs us, by means of friction-sounds, of the presence of rugged layers 
of fibrin. When the exudation is purulent, the surfaces are not rough 
enough to give rise to friction sounds. 
Prognosis.—As we have already said, pericarditis, supervening 
upon rheumatism, very rarely causes death, and this is also the case with 
primary idiopathic and traumatic forms of the disease. Out of twenty 
cases, seventeen of which were rheumatic, Bamberger did not find one 
fatal case. The prognosis is favorable also where the malady proceeds 
from pneumonia or pleuritis, as is shown by Bamberger's statistics. 
It is quite otherwise where it complicates incurable disease, as it then 
nearly always hastens, if it does not actually bring about, a fatal ter- 
mination. 
In discussing the terminations of pericarditis, we have seen how 
great the number of sequelae is, by which it is liable to be succeeded. 
According to their nature, these exert more or less influence upon after- 
life. 
Treatment.—Upon the subject of treatment of pericarditis, we 
may refer in great part to what we have already said regarding pleu- 
ritis and endocarditis. 
General blood-letting is never required in pericarditis as such. Its 
employment is to be confined to the very few cases in which the re- 
pressed outflow from the veins into the heart causes symptoms of pres 
sure upon the brain, and demands a reduction of volume in the circula- 
tion. Local blood-letting moderates the pain somewhat, and is indi- 
cated where it is troublesome. It is best to apply from ten to twenty 
leeches, according to circumstances, to the left edge of the sternum. 
The effect is astonishing in most cases. The use of cold deserves ADHESION OF THE HEART AND FERICARDIUM. 
389 
great reliance. Even ice-bladders have been applied upon the cardiac 
region. Digitalis is suitable in cases where the beat of the heart is 
very frequent and insufficient, causing cyanotic and dropsical symp- 
toms. Its effect here is often very marked. Calomel and blue oint- 
ment, in spite of the praise of English physicians, are not only useless 
but hurtful. As to the employment of diuretics, drastics, preparations 
of iodine, and blisters, what we have said, while treating of pleuritis, 
applies equally well here. Impoverishment of the blood, which occurs 
in protracted cases, requires nourishing diet and iron. Threatening 
heart-palsy demands stimulus. 
When a recent pericarditis comes on in acute rheumatism, we may 
assume that it will do as well, and perhaps better, without treatment. 
As long, therefore, as nothing save the physical signs betrays its exist- 
ence, it is better to refrain from active interference. The astonishing 
number of recoveries in JBamberger’s collection of cases occurred under 
a thoroughly expectant treatment. It is only under conditions men- 
tioned above that we should apply leeches, cold, etc. In order to pro- 
mote absorption, Bamberger lays stress upon the application of warmth 
and moisture, and especially upon flying blisters. Paracentesis is to 
be performed when the distress of the patient, especially from the 
dyspnoea, imperatively demands aid. The result is merely palliative, 
as a rule ; but, even to afford the sufferer opportunity, after the opera- 
tion, to pass the night in his bed (perhaps fox the first time in a long- 
period) and to enable him to sleep a little, is a great gain. Whether 
in other cases the operation can effect a radical cure, our limited ex- 
perience does not permit us to decide. Particulars of the operation 
are to be found in the hand-books on surgery. 
CHAPTER II. 
adhesion’ of the heart and pericardium. 
Anatomical Appearances.—Adhesion of the pericardium and 
heart is one of the consequences of pericarditis. Its pathogeny and 
etiology have "been given in the previous chapter. The adhesion is 
sometimes partial, sometimes total. Sometimes it consists in a firm 
agglutination of the surfaces, sometimes long bands and fibres are the 
media of connection. In a clinical point of view, the condition of the 
epicardium is of much more importance. There is occasionally so 
little thickening of the adherent pericardial faces that the pericardium 
seems to have disappeared; in other cases the epicardium is converted 
into an indurated, unyielding case, in which we find masses of even a 
bony hardness. Again, in circumscribed spots where the fusion of the 390 
DISEASES OF THE PERICARDIUM. 
two surfaces is incomplete, remnants of effusion now and then exist, as 
we have already described. 
Symptoms and Course.—As but a small portion of the pericar- 
dium is attached to the thoracic wall, and even that is held by loose 
cellular tissue, a simple adhesion of the two surfaces does not seem 
materially to interfere with the movements of the heart. Functional 
disturbances, observed to accompany this condition, usually depend 
upon a concomitant degeneration of the heart, valvular disease, or, per- 
haps, upon a former carditis. The effect is very different when the 
organ is enclosed within and adherent to a dense fibrous case, often 
of the consistence of cartilage. Such a condition reduces the pro- 
pulsive power of the heart in the very highest degree. The pulse be- 
comes extremely small and almost always is very irregular. Dysp- 
noea, cyanosis, and dropsy appear all the earlier, as the substance of 
the heart is nearly always degenerated. Physical examination must 
decide to what source disorders of the circulation are due. 
A lack of difference between the percussion-sounds during inspira- 
tion and those during expiration has been given as one of the physi- 
cal signs of pericardial adhesion; but, whether heart and pericardium 
be or be not adherent, the lung will still intervene between the latter 
and the side of the chest with every deep inspiration, and, conversely,- 
will recede when a forced expiration is made. In this respect, then, 
the signs will remain unaltered, unless, indeed, the outer surfaces of 
the pleura and pericardium be grown together (CejJcd). There is a 
second symptom, of greater value. Sometimes, at the point whereat 
we ought to feel the beat of the apex, instead of rising, we see the 
intercostal space sink with every beat. This phenomenon we explain 
as follows : The heart is shortened during systole, and a vacuum 
would form, wrere not the space filled, either by the descent of the 
heart or the depression of the intercostal space; but, if heart and peri- 
cardium be adherent, no descent can take place, hence depression of 
the intercostal place must substitute it. This symptom is all the more 
important, if, during diastole, we find the space rise again, when, upon 
cessation of the systolic suction, the heart again becomes elongated, 
and the apex returns to its position. This symptom, too, is often 
wanting in many cases of pericardial adhesion. If the pleura and peri- 
cardium be not adherent, the lungs may occupy the vacancy left by 
the withdrawal of the apex during systole, and vice versa. 
On the other hand, a systolic depression of the region over the 
apex may depend upon other causes than that of adhesion of the heart 
and pericardium. If the latter be likewise attached to the spinal col- 
umn, the lower half of the sternum will also be drawn down by the 
systole of the ventricle. Moreover, according to Friedreich, in such HYDROPERICARDIUM. 
391 
cases there sometimes is a peculiarity observable about the veins of the 
neck. We see, namely, when the sternum, after having been drawn 
down by the systolic movement, springs back again with the diastole, 
thereby creating an expansion of the chest, that the veins collapse. 
In Friedreich's case this phenomenon only lasted for a limited time, 
and ceased as the action of the heart, and with it the systolic depres- 
sion, grew more feeble. Thus, in solitary cases, physical examination 
may inform us of the existence of pericardial adhesion. In the major- 
ity of instances, however, the statement of Skoda, in the first edition 
of his book, still holds good, that “ no symptoms are discoverable, 
through percussion and auscultation, which can be ascribed to adhe- 
sion of the heart and pericardia.” 
CHAPTER III. 
HYDKOPEEICAEDIUM. 
Etiology.—Hydropericardium depends upon an increase of the 
normal liquor pericardii, a transudation which contains but little albu- 
men. We have already seen how a decrease in the size of the heart, 
by reducing the pressure upon the pericardium from within, results in 
an increase in quantity of the liquid in the sac. The same thing takes 
place when the lungs become adherent to the pericardium and are 
reduced in volume, either from atrophy, failure to regain their normal 
size after absorption of a pleuritic effusion, or contraction from chronic 
pneumonia. This form of hydropericardium is analogous to the in- 
crease in the amount of cerebro-spinal liquid which takes place in 
atrophy of the brain, and, as the latter is called hydrocephalus ex 
vacuo, so hydropericardium ex vacuo would be a suitable name for 
the former. 
A second form of hydropericardium is that which arises from an 
obstruction of the veins of the right heart. An abnormal pressure is 
thus thrown upon the pericardial veins, and dropsy of the sac results 
just as it takes place in other serous sacs, or in the subcutaneous cel- 
lular tissue. The collections of water in the pericardium arising in 
valvular disease of the mitral, emphysema, cirrhosis of the lungs, and 
m other diseases in which the right side of the heart is overloaded, 
all belong under this head. In all these cases dropsy may be of earlier 
occurrence in the pericardium than in any other part of the body. 
It is otherwise in the third form, in which dropsy of the pericar- 
dium, like that of other organs and structures, is to be regarded as the 
effect of a “ dropsical crasis.” Appearing in diseases in which the 
blood has a tendency to lose its albumen, and for its serum to trans- 392 
DISEASES OF THE PERICARDIUM. 
ude, as in Bright’s disease, chronic affections of the spleen, cancerous 
cachexia, etc., the pericardium is not usually affected until a late 
period. 
Anatomical Appearances.—According to the explanation of the 
foregoing paragraph, only collections in the pericardium, of a liquid 
containing but little albumen, are to be regarded as hydropericardium. 
If the liquid contain fibrin, it belongs to the inflammatory effusions. 
Sometimes small quantities of disintegrated blood are mingled with 
the serum. In such cases the nutritive state of the capillary walls has 
deteriorated so that they become ruptured. The frequent occurrence 
of small haemorrhages into the skin (petechioe), in general dropsy, is 
an analogous condition.* 
The quantity of the liquid effused is very variable. A collection 
of an ounce or an ounce and a half of liquid in the sac is not to be 
regarded as pathological. In cases which are not rare, the amount 
may be as much as four or six ounces; in others, particularly when 
the affection arises from disturbance of the circulation, it may exceed 
several pounds. When the effusion is very large, the pericardium is 
dull-white and lustreless, the fat has disappeared from about the heart. 
Sometimes its connective tissue is oedematous. 
Copious dropsical effusion into the pericardium distends it, com- 
presses the lungs, and dilates the thorax exactly like pericardial ex- 
udations. 
Symptoms and Course. — Our remarks upon the subject of 
liydrothorax are equally applicable to that of hydropericardium. 
Although, to the minds of the ancient physicians, “ water on the 
heart ” used to be a most formidable malady, as even now is the case 
among the laity, yet it has no real title to rank as an independent 
disease. But not only is accumulation of liquid in the pericardium al- 
ways a secondary affection, depending either upon some derangement 
of the circulatory or respiratory apparatus, or else upon a morbid con- 
dition of the blood, but the very symptoms imputed to water on the 
chest, and so much dreaded, proceed chiefly from the primary disease, 
and are not caused by the pericardial effusion. When, prior to the 
introduction of physical examination, a diagnosis of hydropericardium 
was often confirmed %>ost mortem, it was due to the fact that the 
symptoms upon which the diagnosis was based nearly always arose 
from such diseases as emphysema and valvular disease of the heart, 
which ultimately resulted in dropsical affections, and therefore in effu- 
sion into the pericardium. 
A large serous effusion into the pericardium undoubtedly has the 
* We shall treat of fibrinous dropsy in cancer of the pericardium, just as we have 
spoken of it in cancer of the pleura. PNEUMOPERICARDIUM. 
393 
effect of aggravating the dyspnoea arising from the primary disease. 
Such an effusion often helps to prevent the patient from lying down 
without danger of suffocation, and compels him to sit day and night 
leaning forward upon his chair or bed. Moreover, the pressure exerted 
by the liquid upon the heart and mouths of the great vessels impedes 
the systemic circulation, causing the jugular veins to swell up, and 
aggravating the cyanosis and dropsy. Frequent as is the coexistence 
of such symptoms with hydrops pericardii, yet the presence of every 
one of them does not afford sufficient ground for a positive diagnosis 
of hydropericardium, unless supported by the evidence drawn from 
physical exploration. All these symptoms may be present without 
there being any increase in the amount of the pericardial liquid. 
Upon physical examination, the prominence of the region of the heart 
is observable, although in a less degree than in cases of inflammatory 
effusion. The depression of the intercostal spaces is not obliterated. 
The impulse of the heart is very feeble, and is often quite impercep- 
tible, especially when the patient lies upon his back. When the effu- 
sion is large, and provided that the lungs are capable of retraction, 
the cardiac dulness is extended, and has the same shape and exhibits 
the same modifications, upon change from the upright to the recum- 
bent attitude, which already have been described as characteristic of 
pericardial effusion. It happens more frequently in this affection than 
it does in pericarditis, that the lung is unable to retract, owing either 
to emphysema or to adhesions of the costal and pulmonary pleurae. 
In such cases, notwithstanding the existence of a very large effusion, 
the area of dulness is not extended.' Upon auscultation, unless the 
valves of the heart be diseased, the heart-sounds are pure though 
feeble. Friction-sounds are never heard. 
Treatment.—All the measures recommended for the treatment of 
hydrothorax are equally applicable to that of hydropericardium. The 
only rational procedure is to treat the primary disease. It rarely is 
practicable to reduce the liquid in the pericardium by means of diuretics 
and drastics. 
CHAPTER IV. 
PNEUMOPERICARDIUM. 
Air sometimes enters the pericardium through a perforating wound 
of the thorax; in other cases the pericardial sac suffers perforation by 
some destructive morbid process, and air is admitted into it from some 
organ wliich naturally contains air. I have observed one instance of 
this kind (which has been reported by Dr. T'utel, my assistant at the 394 
DISEASES OF THE PERICARDIUM. 
time, in the German Clinic), in which pneumopericardium arose after 
perforation of the pericardium by carcinoma of the oesophagus. Other 
cases have been reported of perforation of the pericardium by ulcers of 
the stomach, cancer of the stomach, or superficial cavities in the lungs. 
Finally, gas sometimes is generated in the pericardium, by the decom- 
position of the effusion which it contains. 
Upon post-mortem examination, the pericardium is usually much 
distended, partly by air and partly by a purulent or sanious liquid. 
The latter is the product either of a recent pericarditis, caused by the 
entrance of air, or cancerous discharge, or of broken-down pulmonary 
tissue, into the pericardial sac, or else, if the pneumopericardium be 
the result of a generation of gas from a putrefying exudation, of a peri- 
carditis of long standing. Upon puncture of the distended sac, the air 
usually escapes with a hissing sound. 
Pneumopericardium is far less common than pneumothorax, and 
nearly always is easy of recognition. It is true, the subjective symp- 
toms, arising from perforation of the sac and of entrance into it of air 
and debris of the tissue, are not very characteristic. Besides, the oc- 
currence is usually attended by severe collapse, in which the patient 
lies in a state of apathy, making no complaint, and, if questioned, re- 
plying with hesitation and incompleteness. Even at some distance 
from the patient a peculiar, clear, splashing sound can be heard, which 
comes and goes with short, rhythmical intervening pauses, and which, 
beyond all question, is caused by the agitation produced in the liquid 
contents of the pericardium by the movements of the heart. In my 
case this splashing sound was distinctly audible to the room-mates of 
the patient, who lay at the other end of the ward. Upon inspection, 
if the thorax still be flexible, the prominence of the cardiac region and 
the obliteration of the intercostal depressions are very marked. The 
cardiac impulse is indistinct or imperceptible. Upon percussion, there 
is no cardiac dulness, and, indeed, the percussion-sound about the re- 
gion of the heart is extremely full, clear, and tympanitic, often having 
a distinct metallic ring. Upon making the patient sit up, or upon 
making him bend forward, the beat of the heart becomes somewhat 
more perceptible, and, as the air now rises and the liquid presses for- 
ward, the former clear sound is replaced by a dull one. Upon auscul- 
tation, either nothing can be heard excepting the above-named metallic 
splashing, or else we may also hear feeble heart-sounds and friction- 
sounds. 
With exception of cases of traumatic origin, this disease, as a rule, 
rapidly proves fatal. The collapse and severe pericarditis which 
almost always accompany pneumopericarditis sufficiently account for 
this. Recovery from traumatic pneumopericardium has been observed TUBERCULOSIS AND CANCER OF THE PERICARDIUM. 
395 
repeatedly. Of course, the treatment of this affection can only be a 
treatment of symptoms, and in most cases it is limited to an exhibition 
of stimulants. 
CHAPTER V. 
TUBERCULOSIS OF THE PERICARDIUM. 
Tubercles in the tissue of the pericardium are only seen in acute 
miliary tuberculosis. The grayish nodules here visible do not undergo 
further metamorphosis, and the patient dies, consumed by fever, with- 
out betraying any symptoms of the existence of tubercles in the peri- 
cardium. 
It is far more common for tubercles to form in the young pseudo- 
membranes which develop on the pericardium in the course of a chronic 
pericarditis. We nearly always find a haemorrhagic effusion in the 
sac in these cases, and observe its walls to be studded with drusy 
prominences, which are at first translucent, but may afterward become 
yellow and cheesy, although they rarely soften into “ tubercular pus.” 
The symptoms of this form of tubercle of the pericardium are undistin- 
guishable from those of chronic pericarditis. 
CHAPTER VI. 
CANCER OF THE PERICARDIUM. 
Cancer of the pericardium is almost always an extension of can- 
cerous disease from the sternum or mediastinum. Sometimes it grows 
diffusely, so that a large part of the sac degenerates into cancer; some- 
times it forms solitary rounded masses, or flat nodules upon the mem- 
brane. More rarely it appears independently after extirpation of an 
external cancer; and then other nodules upon other organs and upon 
other serous membranes are nearly always found. The formation of 
cancer in the pericardium is nearly always combined with a collection 
of liquid within the sac, which, like the liquid found in cancer of the 
peritonaeum or pleura, contains “ fibrin of tardy coagulation.” It is pos- 
sible, only in the very rarest instances after removal of a cancer of the 
breast, to diagnosticate the formation of cancer of the pericardium by 
the evidence of a gradually increasing effusion in the sac. SECTION III. 
DISEASES OF THE GREAT VESSELS. 
CHAPTER I. 
INFLAMMATION OF THE COATS OF TUB AORTA. 
Etiology.—Inflammation of each of the three tissues of the aorta, 
the adventitia, the media, and the intima, is best studied by itself, just 
as we have already successively discussed pericarditis, myocarditis, and 
endocarditis. 
Acute inflammation of the tunica adventitia is rare, and hardly ever 
occurs, excepting when inflammation or ulceration of the lymphatic 
glands, the oesophagus, the trachea, or other neighboring organ, ex- 
tends into the aorta. Chronic inflammation is far more common; but 
neither is it primary, being allied almost always to pericarditis and at- 
tacking the root of the aorta; or else to endarteritis, when its action 
may be very extensively diffused. 
The tunica media often takes part in inflammation of the adventitia. 
In chronic inflammation of the intima, too, the media is almost always 
diseased, but is not often inflamed. It is much more commonly the 
seat of simple atrophy or of fatty degeneration. 
From 'Virchow's point of view, chronic inflammation of the internal 
coat of the arteries is to be regarded as one of the most frequent of 
diseases. The reason for classing the gelatinous and semicartilaginous 
thickening of the inner arterial tunic (see below), which forms the in- 
cipient stage of ossification and atheroma of the arterial walls, among 
the parenchymatous inflammations, is due to the fact that, in this dis- 
ease, we undoubtedly have to do with an active process, with genera- 
tion of cells, and that in many cases it can be shown that these nutri- 
tive disturbances owe their origin to certain irritants which have acted 
upon the tunics; as, undue strain, or distention (see pathogeny of 
endocarditis). In other cases, indeed, it cannot be proved that the 
arteries have been subjected to special irritants; as, however, the INFLAMMATION OF THE COATS OF TIIE AORTA. 
397 
anatomical changes are precisely the same, we may assume that the 
sources of irritation exist, but have escaped our observation. 
Endarteriitis deformans, as we may call chronic inflammation of the 
intima, according to Virchow, is an extremely common disease of ad- 
vanced age; and it is always at the points most exposed to strain or 
distention, such as the ascending portion and arch of the aorta and 
the places of origin of the vessels which pass olf laterally, that the 
disease is most apt to occur. In the second place, the malady is most 
frequently found to affect gouty, rheumatic, or syphilitic persons, as 
well as drunkards. We are not at liberty, however, to go so far as to 
suppose that in these cachectic subjects the disease proceeds from 
the composition of the blood, that an irritant circulates in the latter 
which excites the internal coat of the artery to the point of inflamma- 
tion. 
Finally, endarteriitis accompanies hypertrophy of the heart in young 
subjects who are not cachectic, and here it seems to attack by prefer 
ence dilated portions of the arteries. These cases furnish strong evi 
dence of dependence of the disease upon local injury to the vessels. 
Anatomical Appearances.—We rarely have opportunity to see 
purulent and ichorous collections in the tissue of the adventitia. In 
durated thickening of the cellular tissue, as a residue of chronic in- 
flammation, is a far more common discovery. At first the calibre 
of the artery usually is narrowed; afterward it generally becomes 
widened. 
Inflammation of the tunica media begins with a speckled redness, 
which has its seat beneath the internal coat. The spots soon become 
of a whitish or yellow color, are elevated above the inner surface, and 
resemble small pustules. At first a mere sprinkling of the infiltration, 
in the form of amorphous granules, takes place upon the tissue, which 
still remains firm. It afterward liquefies, and pus forms, so that actual 
abscesses are established in the wall of the artery. 
Chronic endarteriitis commences with relaxation and infiltration of 
the tunica intima. Two forms of it occur, distinguishable according 
to the grade of infiltration, and which have often been described as 
different stages of the same disease. In the first form, that of gela- 
tinous thickening of the inner coat, a gelatinous, moist, pale-reddish 
layer seems to lie upon the inner surface of the artery, sometimes in 
circumscribed spots, sometimes spread over a wider surface. These 
apparent deposits readily admit of being crushed or displaced in the 
form of jelly. They consist mainly of a liquid resembling mucus, in 
which fine elastic fibres and round or spindle-shaped cells lie embedded. 
They are immediately connected with the tunica intima, and are cov- 
ered by its epithelium. 398 
DISEASES OF THE GREAT VESSELS. 
In the second form, that of semi-cartilaginous induration, we find 
opaque, bluish-white plates, like boiled white of egg, lying upon the 
inner surface of the artery. Here, too, the tissue of the tunica intima 
is softened and infiltrated, but it remains firmer and more consistent 
than in the other form, and it afterward assumes a cartilaginous hard- 
ness. Under the microscope, numerous fusiform and reticulate cells 
can be seen in the semi-cartilaginous variety, but, above all, broad 
fasciculi of connective tissue are visible, which plainly form an imme- 
diate continuation of the lamellar fibres of the tunica intima. 
The further changes which these inflammatory products undergo 
are: 1. Fatty metamorphosis; 2. Calcification or ossification. 
In the gelatinous thickening, fatty metamorphosis begins chiefly in 
the superficial portion, commencing in these cells, while the interme- 
diate substance breaks down, and the surface becomes rough and 
tufted. This process is called “fettige TJsur ”—“ fatty consumption.” 
In semi-cartilaginous thickening, fatty metamorphosis begins in the 
deeper layers. At first, numerous drops of fat are deposited around 
the nuclei of the connective-tissue cells, which become transformed into 
star-shaped cells of fatty granules. These ultimately perish, and the 
fat-molecules are liberated. The bundles of connective tissue also break 
down, and thus, deep in the interior, a pea-soup colored, fatty paste is 
formed, consisting of fat-molecules, numerous crystals of cholesterin, and 
debris of connective tissue, constituting true atheroma. As long as the 
greasy paste remains separated from the current of the blood by a thin 
film of the internal coat, it is called an atheromatous pustule.* After- 
ward, when the covering has broken down, after its contents have been 
washed away, and an irregular loss of substance, with ragged edges, 
has formed, we speak of an atheromatous ulceration. Atheroma and 
“ usur ” bear the same relation to one another as abscess and ulcer. 
Calcification depends upon a deposit of salts of lime in the deeper 
layers of the semi-cartilaginous thickening. In the plates of lime thus 
formed we sometimes find bodies analogous to bone-corpuscles, jagged 
in form, and furnished with prolongations, which are the residua of 
connective tissue-cells, so that we then are warranted in employing the 
term ossification. "While the smaller arteries may become converted 
into tubes, with rigid walls, from deposit of earthy matter, ossification 
of the aorta usually appears in the shape of separate plates and scales, 
of variable size, wliich form shallow depressions upon the inner surface 
of the vessel, and which are separated from the blood by the interven- 
tion of a thin film of the tunica intima. By-and-by the ossification 
reaches the surface itself; the scales of bone are completely exposed, 
* The term “ pustule ” is not used here in its proper sense, and is solely applicable 
to the macroscopic-appearance of these little inflammatory foci. INFLAMMATION OF THE COATS OF THE AORTA. 
399 
ancl are sometimes washed loose by the blood, and then form projec- 
tions, upon which the fibrin of the blood is very apt to precipitate itself. 
At the outset of endarteriitis, the tunica media does not become 
perceptibly altered. In advanced atheroma it grows yellow, relaxed, 
and fissured. Large deposits of fat form between its lamella?. The 
media is generally atrophied, and thinned by ossification of the intima. 
In the beginning of the process the adventitia is also normal, but after- 
ward becomes swollen, thickened, and indurated. 
In many cases we find all the various phases of the disease along- 
side of one another in the aorta: in one place gelatinous or semi-carti- 
laginous induration; in another, atheromatous pustules; here again 
ulceration; there calcification, in a slight depression, covered by the 
tunica intima; and at some other point we find plates of bone pro- 
jecting free into the aorta. 
Symptoms and Course.—No clinical description of acute inflam- 
mation and ulceration of the adventitia can be given, as, in the few in- 
stances in which the process has been watched, the disease has always 
been complicated by other grave disorders. This is also the case in 
chronic inflammation of the adventitia, and in the instances of abscesses 
observed now and then in the tunica media. 
Chronic inflammation of the tunica intima and its results, generally 
comprehended under the term atheroma, in its wider sense, furnish but 
few symptoms as long as they do not cause aneurism, rupture, or stop- 
page of one of the smaller arteries by detachment of a clot. We 
shall consider the subjects of aneurism and rupture in the second and 
third chapters. The results of embolism, as far as they affect internal 
organs, are treated of in various chapters of this work. 
If, in consequence of degeneration of its coats, the aorta have lost 
its elasticity, and if, too, its branches take part in the disease, the de- 
mands upon the heart are increased, and hypertrophy arises (see hyper- 
trophy of heart). If the chronic inflammation spread from the arterial 
wall to the valves, insufficience and stenosis may be the result. Hyper- 
trophy often fails to take place, owing to depression of the general 
nutritive condition, or it is not sufficiently pronounced to compensate 
for the impediment which degeneration of the aorta and its ramifica- 
tions presents to the circulation, or else the hypertrophy is soon con- 
verted from a genuine to a false hypertrophy, from degeneration of the 
substance of the heart. Symptoms of retarded circulation and over- 
loading of the venous system then arise, cyanosis, dropsy, and sup- 
pression of urine, as described in a previous chapter. 
The most important token in the diagnosis of chronic inflammation 
of the inner coat of the aorta is the evidence of the existence of 
similar disease in the peripheral arteries, as the inference is thus war- 400 
DISEASES OF TIIE GREAT VESSELS. 
ranted that the affection is also present in the aorta, in a still more 
advanced stage of development. As the vessels have become dilated, 
and their walls more rigid, the pulse generally feels hard and full; the 
course of the elongated arteries is remarkably sinuous, their curvature 
increasing with the beat of the pulse, which becomes visible. The 
artery, even when undistended by the current of the blood, can usually 
be felt as a hard, irregular cord. 
As long as there is no aneurismal dilatation of the aorta, percussion 
and auscultation do not aid the diagnosis. In rare cases, false mur- 
murs arise, in consequence of roughness of the inner coat of the aorta, 
and where there is no deformity at the ostia. 
According to Bamberger, the first sound of the aorta is often dull, 
muffled, or even inaudible ; the second, particularly if the walls of the 
great vessels be studded with bony plates, and as long as the valves 
retain their efficiency, has a remarkably loud and metallic ring. 
CHAPTER II. 
ANEURISM OF THE AORTA. 
Aneurisms, produced by wounds, belong to the province of surgery. 
Spontaneous aneurism, that is to say, partial dilatation of a vessel 
caused by degeneration of its walls, is the only form of the disease 
which occurs in the aorta. 
Uniform dilatations of the entire tube, such as arise in hypertrophy, 
and which take place above stricture of the vessel, are not regarded 
as aneurisms. 
Etiology.—The degeneration of the aortic wall, which most fre- 
quently gives rise to aneurism, is the result of the chronic endarteriitis 
described in the previous chapter, and known as atheroma. 
Next in frequence, as a cause of aneurism, is simple fatty degenera- 
tion of the inner and middle arterial tunics, a disease which we have 
purposely avoided mentioning hitherto, as it has nothing in common 
with the inflammatory affection previously described. In simple fatty 
metamorphosis there is no preliminary thickening, and cell-growth in 
the tunica intima; but, from the very outset, we find opaque, whitish 
or yellowish-white spots, grouped in a peculiar manner, and but slight- 
ly prominent above the surface, which consist of deposits of fat mole- 
cules in the tissue of the arterial coats. 
Thirdly, simple atrophy, and thinning of the aortic wall, which 
seems to be by no means uncommon among elderly people, may be a 
cause of aneurism. 
Whether palsy of the vaso-motor nerves be also a cause of this ANEURISM OF TEE AORTA. 
401 
disease (Rokitansky), is questionable, at all events, as regards tlie 
aorta, which is but poorly provided with contractile elements. 
In consequence of these changes, particularly in the middle coat, 
the aorta loses its elasticity, sometimes at a circumscribed spot, some- 
times throughout a larger portion of its extent, and gradually yields 
and becomes dilated by the pressure of the blood. Not unfrequently, 
however, upon the occasion of some sudden strain, the tunic of circular 
fibres seems to give way suddenly, and the dilatation of the wall, which 
now consists only of the adventitia and intima, goes on more rapidly. 
Many persons suffering from aneurism believe that they know the 
period, or even the moment, from which their malady dates, assigning, 
as a cause, some violent muscular effort, the lifting of a heavy burden, 
etc. It has already been remarked that a general contraction of the 
muscles, by compressing many of the capillaries, must throw an in- 
creased strain upon the aorta. A violent jar of the frame seems to 
have a similar effect; at least, many patients date their affection from 
some fall from a great height, or the like. Such accidents will not 
cause aneurism in a healthy subject; and, in many cases, an acknowl 
edgment of the immediate causes of the complaint is only forced upon 
the patient by the examiner. 
Aneurisms are rare in young people. They occur chiefly in per- 
sons of somewhat advanced age, in whom chronic inflammation of the 
arterial coats is a very common affection. Men are much more fre- 
quently attacked than women; but as the majority of aneurisms are 
found in persons who habitually make' violent muscular efforts, this 
difference may be accounted for by the difference in the occupations 
of the sexes. 
Anatomical Appearances.—Scarpa's classification was mainly 
based upon the number of coats which could be counted in the wall 
of an aneurism. If the wall contained all three tunics, it was an 
aneurisma verum • if covered by the adventitia alone, it was an 
aneurisma spurium, or mixtum externum. If, again, the wall con- 
sisted of a protrusion of the intima through an opening in the media, 
the pouch being either bare or covered by the adventitia, it was an 
aneurisma mixtum internum seu herniosum. This classification has 
been abandoned as unpractical. An aneurism may belong to the first 
class (aneurisma vera) at the period of its commencement, and, as it 
grows, become an aneurisma spuria ; and, indeed, in the same tumor, 
one half of it may be of the true kind, and the other of the false. 
Classification of aneurisms, according to their form, is of more im- 
portance. Thus we distinguish the circumscribed and the diffuse 
aneurism. 
A diffuse aneurism involves a considerable portion of the vessel, 402 
DISEASES OF THE GREAT VESSELS. 
and its entire calibre. If the dilatation terminate abruptly, it is called 
a cylindrical aneurism. If it decrease gradually, it is a fusiform 
aneurism. Diffuse aneurism is always a true one, in Scarpa's sense, 
and is most commonly met with in the ascending and transverse por- 
tion of the arch of the aorta. It is very often combined with the form 
next to be described, that is to say, circumscribed pouches often form 
upon the dilated portion of the artery. 
Circumscribed aneurism consists in the dilatation of a shorter por- 
tion of the artery. Here, too, the artery is sometimes widened in all 
directions, the tumor involving its entire diameter. Far more fre- 
quently, however, one side alone is dilated, and the aneurism, whose 
walls form an angle with those of the normal part of the vessel, as- 
sumes the appearance of a tumor situated on its side. Secondary 
pouches, in the form of elevations of varying size, are often observed 
upon these sac-like dilatations, just as in the other kind. At the out- 
set, the disease almost always bears the character of a true aneurism 
of Scarpa, consisting of all three of the aortic coats ; but, when the 
sac has attained some magnitude, the inner tunic only extends for a 
short distance into it. When at its period of fullest development, the 
middle tunic, too, dwindles, and finally disappears totally, while there 
still remain traces here and there of the tunica intima, in a state of 
degeneration. 
Aneurisms attached by a neck must be regarded as a peculiar 
species of the sac-like form. In these cases, a very small spot on the 
arterial wall gives way. If the dilatation be large, the wall of the 
aneurism wraps itself around that of the artery. Thus a duplicature 
is formed, which, looked at from within, presents a prominent ridge, 
while, from without, the tumor seems to have been constricted at its 
base. In these saccular aneurisms, the tunica media can only be 
traced for a short distance, and soon disappears on the far side of the 
neck, the wall then consisting of the intima and adventitia (aneurisma 
mixtum internum seu kerniosum). When very large, all the tissues 
gradually disappear under the pressure; and the adjacent structures, 
to which the aneurism becomes adherent, finally furnish its Avail. If 
the enlargement be s1oaat, the new Avail may become very firm by pro- 
liferation of the connective tissue ; but, if rapid, the Avail remains thin, 
and soon bursts. If the tumor encounter any resisting body, such as 
bone, the latter undergoes absorption (usur), just like the sac-Avall, and, 
after destruction of the periosteum, the bone is laid bare, and projects 
naked into the pouch. 
In the cfivities of aneurisms of large size, especially in the sac- 
shaped ones, we almost always find deposits of fibrin arranged in sep- 
arate layers. Those attached to the Avails are yelloAV, dry, and firm; ANEURISM OF THE AORTA. 
403 
those next the blood are reddened and soft. Here and there, between 
their layers, there are frequently deposits of brownish-red or chocolate- 
colored blood. 
The vessels proceeding from the sac, independently of the contrac- 
tion to which they are liable by ossification, are not unfrequently 
blocked up by clots of fibrin, and are impervious to blood. In other 
cases, their mouths are stretched into narrow slits, and in others again 
they may be narrowed or closed by pressure of the tumor. The con- 
dition of the vessels springing from an aneurism is important in a diag- 
nostic point of view. 
The size of aortic aneurism varies. Within the pericardium they 
rarely attain any great magnitude, but soon give way. When they 
originate beyond the pericardium, however, they may grow to the size 
of a man’s head. 
The effect of an aneurism of the aorta upon the parts about it de- 
pends upon the amount of displacement and pressure which it inflicts. 
The trachea, the bronchi, the oesophagus, the great vessels of the 
thorax, or the nerves, may be dislocated or atrophied by the compres- 
sion to which they are exposed. Atrophy, or “ usur,” of the bones 
may even open the spinal canal, and destruction of the bone and carti- 
lage of the thorax may permit the aneurism to emerge as a prominent 
tumor, covered only by soft parts. 
As partial dilatation of the aorta augments the labor of the heart, 
that organ is almost always hypertrophied. 
Spontaneous cure of an aortic aneurism, by complete solidification 
of the sac by means of coagula and subsequent atrophy, is one of the 
greatest of rarities. Other forms of spontaneous cure, which some- 
times occur in peripheral aneurism, are impossible in the aorta. 
When death does not result from the effect of the tumor upon the 
circulation, and its pressure upon neighboring organs, the aneurism 
usually bursts spontaneously, a mode of termination vastly more fre- 
quent than that by recovery. If it open into the pericardium, or 
pleura, a genuine rupture at the thinnest point takes place; if into the 
oesophagus, trachea, or one of the bronchi, it gives way at some point 
of adhesion which forms between the tumor and one or other of these 
organs, and which, gradually growing thinner, at last breaks; or else a 
slough forms and separates, thus making an aperture into the sac. 
Opening into a neighboring vessel takes place after its walls have 
become adherent, and communication is established by a gradual wast- 
ing of the septum thus formed. More rarely, it is only the adventitia 
of the vessel that becomes adherent, and, after perforation at the ad- 
herent spot, blood is injected between the adventitia and media of the 
vessel. The external rupture of an aneurism, which has penetrated 404 
DISEASES OF THE GREAT VESSELS. 
the wall of the chest, occurs either by gradual atrophy and final lacera- 
tion of the integument, or else, which is most common, by loosening 
and detachment of a slough induced by immoderate and incessant 
strain. 
Aneurism of the aorta is most frequently situated upon its ascend- 
ing branch, before the departure of the innominata, and is more com- 
mon upon its convex than upon its concave side. Those which arise 
outside of the pericardium, and which are generally very large, usually 
project toward the right half of the sternum, and become visible in the 
region of the upper ribs, and costal cartilages of the right side. In 
the majority of cases, they break into the right pleural sac, or else 
burst externally. Aneurisms which spring from the concavity of the 
ascending aorta grow in the direction of the trunk of the pulmonary 
artery, or toward the right auricle, which they may perforate. Those 
which arise from the convexity of the arch also extend to the right, 
forward, and upward, and make their appearance in the neighborhood 
of the right sterno-clavicular articulation. Those which proceed from 
the concavity of the arch press upon the trachea, the bronchi, and the 
oesophagus, which they may perforate. Aneurisms of the descending 
limb of the aorta often compress the left bronchus, more rarely the 
oesophagus, and usually open into the left pleural cavity; they may 
destroy the back-bone, and may come to the surface at the left side of 
the back. Aneurisms of the abdominal artery often attain an immense 
size, may also erode the spinal column, and burst into the peritonaeum 
or retroperitoneal connective tissue. 
Symptoms axd Course.—Persons suffering from aneurism of the 
aorta often perish suddenly and unexpectedly of internal haemorrhage, 
before the disease has given rise to any great degree of distress. At 
other times the symptoms are so obscure as to render a positive diag- 
nosis impossible. In other instances, again, it admits of a more or less 
certain recognition from the subjective and objective manifestations 
which it occasions. 
The signs to which aortic aneurism gives rise depend, in part, upon 
the crowding and compression of the adjacent organs in the thorax, 
as described in a previous section; and in part, also, upon obstruction 
of the circulation, which is one of the necessary consequences of any 
large aneurism. 
As a result of compression of the lung or greater bronchi, dyspnoea 
arises, which is often extremely severe. The most intense dyspnoea, 
accompanied by a peculiar whistling upon breathing and coughing, 
attends aneurism of the arch pressing upon the trachea. If the pneu- 
mogastric nerve or its recurrent branch be stretched or irritated, the 
dyspnoea may assume a spasmodic, asthmatic character, and appears ANEURISM OF THE AORTA. 
405 
to proceed from the larynx, and comes on in paroxysms. Dyspnoea is 
one of the most common and distressing symptoms of aneurism. 
A second set of signs proceeds from compression of the right auri- 
cle, the vena cava, or the vena anonyma. If the auricle or vena cava 
be compressed, the jugular veins swell, blue networks of veins appear 
upon the skin of the chest, the veins of the arms become distended 
with blood; indeed, it is not uncommon for dropsy soon to develop in 
the upper half of the body. The patient may complain of headache, 
dizziness, buzzing in the ears, and fits of unconsciousness may be ob- 
served. If but one of the vena innominata be compressed, the venous 
dilatation is limited to the corresponding side of the head and chest. 
In consequence of the pressure and strain to which the intercostal 
nerves and brachial plexus are subjected, most violent pain often arises 
in the right side of the chest, the armpit, and right arm. Like most 
other of the troubles to which aneurism gives rise, this pain is often 
paroxsymal, and may deprive the patient of his sleep, and is reckoned 
by Lauth among the agents which tend to produce speedy death by 
exhaustion. 
Compression of the arteria innominata, or of the left subclavian, 
may render the radial pulse extremely small or quite imperceptible. 
Inequality between the pulsations at the wrist of either side may also 
be a result of distortion of the arterial mouths, or of their stoppage by 
clots. 
To these symptoms of compression of adjacent organs, are added 
those of retarded circulation. Foremost among the latter is the pause, 
often so distinctly perceptible, which occurs beticeen the beat of the 
heart and the wave of the arterial pxdse, at a point below the aneu- 
rism. This phenomenon is most striking when the aneurism is sit- 
uated between the points of origin of the great vessels of the arch. 
The pulse is then felt later at one wrist than at the other; or, if the 
tumor involve the descending aorta, the pulse below the tumor cannot 
be felt until after that of the upper extremity. 
As hypertrophy can only temporarily compensate the impediment 
to the circulation, not only does palpitation eventually set in, such as 
we encounter wherever the heart’s action is overtasked, but the de- 
rangement in the blood’s distribution, so often described, finally is 
established; the arteries are ill supplied, the veins and capillaries are 
gorged, and general marasmus and dropsy ensue. If the patient do 
not die of disordered circulation or of embarrassed breathing, and 
should he not succumb to some other intercurrent disease, the aneurism 
finally bursts. It would be erroneous, however, to regard this mode of 
termination as constant or even as the most common mode of death. 
When, after coming to the surface in the form of a tumor, it breaks 406 
DISEASES OF THE GREAT VESSELS. 
externally, the integument gradually grows thinner, turns dark blue, 
then black, and at last sloughs. After a time, the eschar separates. 
The blood, however, does not always escape in a stream. Sometimes 
it is restrained by the coagula, so that there is only a gradual trickling 
flow; and it may even be possible to stanch the first haemorrhages 
by means of the tampon, so that death may not occur until after re- 
peated outbursts of blood. 
It is otherwise when rupture takes place into the pleura, pericar- 
dium, trachea, or oesophagus. The patient then sinks, often with ex- 
treme rapidity and in the midst of great suffering, with the signs of an 
internal haemorrhage or of profuse haemoptysis or haematemesis. 
Life has been known to continue for some time after perforation of 
the pulmonary artery, or vena cava. The symptoms observed were 
those of extreme obstruction of the veins of the aortic circulatory 
system. 
Although the most important symptoms of aortic aneurism are de- 
rived from physical exploration, yet dyspnoea, cyanosis, varicosity of 
the veins, and dropsy of the upper half of the body, severe pain in the 
right side and arm, inequality of pulse at the wrists, the long pause 
between the beat of the heart and that of the pulse at the wrist, permit 
us to infer the existence of this disease with great certainty. The signs 
vary, of course, according to the position of the tumor upon the aorta. 
In aneurism of the ascending a orta, the vena cava and lungs are 
more especially encroached upon, so that cyanosis and dropsy of the 
upper half of the body, with intense dyspnoea, form the most constant 
symptoms. 
In aneurism of the arch, it is mainly the trachea and the par vagum 
nerve which are compressed, and corresponding functional disturbance 
ensues. In many cases, also, there is dysphagia, from pressure upon 
the oesophagus. Inequality in the pulses at the wrists, also, is most 
frequent in these cases. 
In aneurism of the descending thoracic aorta there is often severe 
pain in the back, sometimes inability to extend the spinal column, and, 
if destruction of the vertebrae be extensive, there may be paraplegia. 
There are also sometimes difficulty in deglutition and severe dyspnoea 
from compression of the lungs. 
The functional derangements and subjective symptoms, to which 
aneurism of the abdominal aorta gives rise, are manifold. It may 
cause the most violent neuralgic pain, and, at a later period, palsy of 
the lower extremities, by pressure upon the nerves and erosion of the 
vertebrae. Compression of the digestive apparatus occasions colic, con- 
stipation, and vomiting. Pressure upon the liver and its excretory 
ducts may produce obstinate jaundice; while suppression of urine ANEURISM OF THE AORTA. 
407 
may result from similar action upon the kidneys. If the aneurism be 
situated immediately beneath the diaphragm, the latter will be pushed 
upward in a painful manner, and the heart will be dislocated upward 
and outward. 
Physical Signs.—As long as the aneurism remains enclosed within 
the thorax, without touching its wall, diagnosis is not assisted by 
physical examination. The respiratory murmur may, perhaps, be di- 
minished upon one side or the other, or a constant whistling sound 
oyer a compressed bronchus may be audible; but such signs admit of 
too many and too different interpretations to warrant our founding a 
decided opinion upon them. 
When the aneurism touches the thoracic wall, upon inspection, we 
can almost always perceive a distinct pulsation at the point of contact, 
and this becomes still more evident upon palpation. The pulse is 
isochronic with the beat of the heart, or follows close upon it. It is 
usually stronger, also, and is almost always accompanied by a peculiar 
whirring “ fremissement cataire.” The point at which pulsation ap- 
pears in aneurism of the ascending aorta is usually on the right border 
of the sternum at the second intercostal space. In aneurism of the 
arch it is at the manubrium sterni; in the descending aorta, it is seen 
upon the left side of the lower thoracic vertebrae. Where the aneu- 
rism has perforated the thoracic wall, inspection and palpation dis- 
cover new symptoms. At first, one intercostal space projects in the 
form of a hemisphere. The tumor soon extends, admitting of no ar- 
rest of its progress. It sits firmly and immovably upon the chest, and 
fully conveys the impression that it has sprung from within the thorax. 
Sometimes the hemispherical form afterward gives place to an irreg- 
ular shape. In cases of great rarity, where there is an inordinate ac- 
cumulation of clot in the sac, there is no pulsation. 
Percussion is absolutely dull and flat all over the tumor, or over 
the region where it lies in contact with the chest. The sense of re- 
sistance upon percussion also seems considerably increased. 
Upon auscultation of aneurisms which lie in contact with the side 
of the chest, we hear either a murmur or a simple or a double “ tone.” 
Explanation of these symptoms is obscure. 
The main cause of the systolic murmur and systolic sound is vibra- 
tion of the aneurismal wall. When the vibrations, into which the 
latter is thrown by the entrance of the blood, are regular, a systolic 
sound is the result; when it is otherwise, there is a murmur. Perhaps, 
too, a systolic murmur sometimes arises when the aorta or pulmonary 
artery is compressed by the aneurismal sac, and when the blood enters 
the aneurism from the aorta through a narrow aperture. Diastolic 
sounds and diastolic murmurs are respectively the result of healthy, 408 
DISEASES OF THE GREAT VESSELS. 
regular vibrations, and inefficient irregular vibrations of the aortic 
valves, which are transmitted to the aneurism. Generally speaking, 
however, even when the aortic valves are healthy, a diastolic murmur 
is heard above the aneurism, and not a normal diastolic sound. This, 
probably, is due to the recoil of a blood-wave, or to the actual regurgi- 
tation of blood from the aneurismal sac into the aorta, owing to the 
narrowness and roughness of the aperture of communication. 
Diagnosis.—The diseases for which an aneurism is most liable tc 
be mistaken are carcinomatous tumors of the pleura and mediastinum. 
Like aneurism, the latter may encroach upon the interior of the thorax, 
may compress and distort the adjacent organs, and, if in contact with 
the aorta upon one side and with the thoracic wall upon the other, 
may even present a circumscribed pulsating point and afterward a 
pulsating tumor. Distinction between the two affections is based upon 
the following points: 
1. Carcinoma of the pleura scarcely ever appears primarily, but its 
occurrence is almost always consecutive to the development of cancer 
elsewhere, particularly after extirpation of cancer of the breast. If the 
etiological conditions for cancer of the pleura be absent, we may infer 
the existence of aneurism with great certainty. 
2. Pulsation m a cancerous tumor of the thoracic wall never ex- 
hibits any lateral dilatation, while an aneurism swells up visibly with 
every beat. 
3. A systolic murmur may proceed from pressure of a cancer upon 
the aorta, just as it may occur in any artery pressed upon by the 
stethoscope; but we never hear the double sound or double murmur 
in cancer of the pleura, which is so common in aneurism. 
4. We rarely or never discover difference between the pulses at 
the Avrist, when a tumor presses upon the aorta. 
5. The symptoms of aortic aneurism just described are distin- 
guished by alternate paroxysms and intervals. The symptoms of 
cancerous tumors, on the contrary, are steady. 
The diagnosis between an aortic aneurism and an aneurism of the 
innominata cannot be made Avith certainty. The symptoms ascribed 
to the latter—pressure upon the vena cava superior, upon the right 
bronchus, the right bronchial plexus, feebleness and retardation of the 
right radial pulse, dulness, pulsation, and a tumor in the right sterno- 
clavicular region—all occur in aneurism of the aortic arch. 
Prognosis.—Aortic aneurisms rarely recover. Cure has never 
been observed in a case A\rhere the disease has been recognized. On 
the other hand, life has sometimes been preserved for years, AA'here 
early exhaustion of the patient has not been brought about by debil- 
itating treatment. RUPTURE OF THE AORTA. 
409 
Treatment.—Venesection repeated at short intervals, a treatment 
formerly much in vogue, is entirely without benefit in the treatment of 
aneurism. This is true also with regard to digitalis, which, like vene- 
section, was supposed to reduce the pressure from within, and to re- 
strain further expansion of the sac. Nor is it otherwise with the plan 
of placing a patient, with aneurism, upon a “ vita minima; ” that is, 
almost starving him to death, so as to reduce the volume of the blood. 
The action of this method, formerly much in use, can only be to aid in 
rendering the sufferer dropsical, and in hastening his death. The sug- 
gestion of acetate of lead, and of drugs containing tannin as a means 
to promote coagulation of the blood, and to fill the sac with clots, is 
founded upon theory alone, and deserves no reliance. 
Having recognized the existence of an aneurism, we must see that 
the patient shun all agents which tend to increase the action of the 
heart. Let him live moderately; guard him from the temporary 
plethora which follows every excess; prescribing, however, a nourish- 
ing nitrogenous diet to counteract the threatening impoverishment of 
the blood. 
When a tumor develops upon the wall of the thorax, and when 
the skin upon it begins to redden, let the patient wear a tin vessel 
upon the prominence, shaped according to the shape of the tumor, and 
filled with cold water. Electro-puncture, which has been employed a 
few times even against aortic aneurism, in order to produce coagulation 
of its contents, has hitherto had too little success to warrant repetition 
of the operation. To allay the pain, we are reduced to the exhibition 
of narcotics. 
CHAPTER III. 
RUPTURE OP THE AORTA 
The aorta seldom bursts, if its tunics be sound. In most cases of 
its spontaneous rupture, its coats are the seat of the degeneration de- 
scribed in the previous chapter, or of the simple fatty metamorphosis 
mentioned while treating of aneurism. This is the case, even when 
an excessively-distended aorta gives way above a stricture, for then, 
too, the coats are almost always diseased. 
In some cases the rupture at first involves the inner and middle 
tunics alone, while the adventitia, which is more yielding, and more 
easily distensible, remains for a time unbroken. The blood then flows 
in between the tunica media and adventitia, and forces them asunder; 
and thus a fusiform tumor, filled with blood, is formed, which commu- 
nicates with the artery through the opening in the media and intima— 
aneurisma dissecans. According to the observation of HokitansTcy 410 
DISEASES OF THE GREAT VESSELS. 
recovery from this condition is possible. Far more frequently, in the 
course even of a few hours or days, death ensues from bursting of the 
adventitia, and escape of the blood into the pericardium, mediastinum, 
or pleura. At the moment of rupture the patient sometimes suffers 
violent pain; but soon becomes pale, cold, and pulseless, singultus 
appearing with profound syncope, and other symptoms of internal 
haemorrhage. 
CHAPTER IV. 
STRICTURE AND OBLITERATION OF THE AORTA. 
According to Rokitansky, congenital narrowness of the aortic 
system is sometimes found, and principally in the female sex. It is 
accompanied by pallor, tendency to syncope, retarded development of 
the entire frame, but especially of the sexual organs, symptoms simi- 
lar to those which attend congenital smallness of the heart. 
We sometimes see a partial contraction of the aorta as a persist- 
ence of the so-called isthmus aorta? at a point between the left sub- 
clavian and the ductus Botalli. In other instances there is an obliter- 
ation of the vessel at this point instead of a contraction. In these 
cases we have no sufficient knowledge of the conditions occasioning 
the permanent narrowness, or even obliteration of the isthmus aorta?, 
which exists during foetal life as a narrow communication between the 
arch and the descending aorta, but which becomes dilated soon after 
birth. It has been supposed that the ductus arteriosus Botalli might 
become obstructed by a thrombus, and that this thrombus might ex- 
tend into the aorta; or that the ductus Botalli, while in process of 
obliteration, might, during its contraction, also constrict the aorta. 
Neither explanation is satisfactory, as both constriction and oblitera- 
tion of the aorta have been observed where the duct of Botalli re- 
mained open. 
The immediate consequence of contraction of the aorta is hyper- 
trophy of the left ventricle and dilatation of that part of the aorta 
which lies between the heart and the point of constriction. The enor- 
mous dilatation which takes place in the branches of the subclavian, 
and its anastomoses with the intercostal arteries, are of great impor- 
tance. The finest ramifications are converted into large branches with 
firm walls, and a collateral circulation so complete is set up, that the 
blood, in ample quantity, is conveyed around the seat of stricture into 
the descending aorta. The principal of these collateral channels is 
formed by anastomosis between the first intercostal, arising from the 
subclavian, and the second, which springs from the descending aorta; 
but extensive anastomotic communication also forms from the dorsalis DISEASES OF THE PULMONARY ARTERY. 
411 
scapuli, subscapularis, transversalis colli, and the intercostals. The in- 
ternal mammary becomes immensely enlarged, as do the anterior inter- 
costals which proceed from it. Its terminal branch, the superior epi- 
gastric, also dilates, and, by its communication with the inferior epi- 
gastrics, conveys blood to the iliacs. 
Obliteration of the aorta, serious as the malformation appears to be, 
is, nevertheless, a tolerably endurable one. It may long remain latent, 
and the patient may attain a very great age (ninety-two years). In 
other instances, in course of time, palpitation of the heart, distressing 
pulsation of the carotids, or symptoms of hypersemia of the brain, may 
manifest themselves. By-and-by a cachectic condition develops, and, 
in nearly half the cases reported, death has ensued with symptoms of 
marasmus and dropsy. Thus we see that an obstruction to circulation 
as grave even as that presented by obliteration of the aorta may be 
compensated for, temporarily, by hypertrophy of the heart, but that it 
finally becomes imperfect, and that symptoms then set in of retarded 
circulation, venous engorgement, and impoverishment of the blood, 
such as we have so often described. In other instances, death, by rup- 
ture of the heart or aorta, is the result, the walls, probably, always 
undergoing previous degeneration. 
Diagnosis of this affection is based mainly upon the signs of the 
anastomotic circulation above described, and upon the absence of pul- 
sation in the ramifications of the abdominal aorta. In such subjects 
we see varicose, worm-like, sinuous arteries, and groups of arteries, 
distinctly pulsating on the back along the shoulder-blade, and upon 
the arch of the ribs. At a point corresponding to the course of the 
internal mammary, we hear, near the sternum, a blowing sound, which 
is audible, also, at all points where the existence of dilated arteries is 
perceptible to sight and touch. On the other hand, in the tibials, or 
even in the popliteals and femorals, the pulse is feeble or even imper- 
ceptible. Bamberger considers that the deformity can always be 
recognized with certainty from these diagnostic points. Treatment 
of stenosis of the aorta is entirely analogous to that of stenosis of the 
aortic orifices, to which we therefore refer. 
CHAPTER V. 
Acute inflammation, terminating in suppuration, is quite as rare in 
the pulmonary artery as in the aorta. The alterations of the tunica 
intima, described by us as chronic endarteriitis, are often absent in this 
artery, where the entire aortic system is far advanced in the disease. 
DISEASES OP THE PULMONARY ARTERY. 412 
DISEASES OF THE GREAT VESSELS. 
On the other hand, it is tolerably common even when the aorta is 
sound in cases of deficience of the mitral valve, with consecutive hyper- 
trophy of the right ventricle. To it Dittrich attributes the frequence 
of haemorrhagic infarction in the lungs of persons with heart-disease. 
Aneurisms of the pulmonary artery are exceedingly rare, and never 
attain any considerable size. In a case observed by Skoda there was 
found in this artery an aneurism as large as a goose-egg. During life 
the patient had labored under signs of grave circulatory disturbance, 
was cyanotic and dropsical; but no diagnosis could be formed by 
physical exploration. 
Diffuse dilatation of the pulmonary artery occurs with extraordi- 
nary frequence in cases which cause hypertrophy and dilatation of the 
right heart. It never produces any change in the percussion-sound 
over the chest [Skoda), but not unfrequently, and usually upon dias- 
tole, we perceive a shock, and, indeed, a distinct pulsation, in the 
vicinity of the root of the pulmonary artery. 
While treating of metastases of the lung, we have already learned 
that the minuter branches of the pulmonary artery may become ob- 
structed by the intrusion into them of wandering emboli. When one 
of the larger branches is thus occluded, intense dyspnoea arises, and 
even death may suddenly ensue from the extent of breathing-surface 
thus thrown out of action from interruption of its circulation. Within 
the last few years I have seen two cases in which death occurred in the 
course of a few hours, with all the signs of extreme dyspnoea and col- 
lapse, and in which it was found post mortem that a large thrombus 
had been detached from the femoral vein, had passed into the circula- 
tion, and, by obstruction of the main branch of the pulmonary artery, 
had occasioned this peculiar kind of suffocation. One of these cases 
is reported in the Wiirtemberger Correspondenzblatt by my then as- 
sistant, Dr. Spdth. 
CHAPTER YI. 
DISEASES OF THE GREAT VEXOUS TRTJXKS. 
It is of disorders affecting' the vena cava and the pulmonary veins 
alone that we now treat, as diseases of the peripheral veins are 
treated of in the hand-books of surgery; those of the portal vein and 
veins of other organs are more appropriately discussed as diseases of 
the liver, etc. 
Primary inflammation does not occur in the vena cava, and it is 
rare to observe inflammation and perforation of the coats of the as- 
cending portion of it by an abscess of the liver, or of the cellular tissue DISEASES OF THE GREAT VENOUS TRUNKS. 
413 
behind the peritonaeum. Inflammation of the pulmonary veins, termi- 
nating in abscess, is equally rare. 
Dilatation of the great venous trunks takes place in diseases of the 
heart, which occasion engorgement of the venous system. Their con- 
striction is almost solely the result of compression by adjacent tumors. 
Primary thrombosis—that is, coagulation of the contents of a vein, 
with consequent inflammation of its walls—has been seen occasionally 
in the vena cava ascendens, but then the coagulum almost always forms 
first in one of the femoral veins, and afterward spreads to the vena 
cava. Such a formation of thrombus may be recognized by the follow- 
ing signs: If, in addition to the tense painful oedema of a phlegmasia 
alba dolens of the leg, there suddenly set in a painful swelling of the 
other limb, if the secretion of urine be suddenly repressed, or should 
it become scanty and bloody, we may infer that the thrombus has in- 
volved the vena cava and emulgent veins. DISEASES OF THE ORGANS OF DIGESTION. 
SECTION I. 
DISEASES OF THE MOUTH. 
CHAPTER I. 
CATARRH OF THE MOUTH. 
Etiology.—The mucous membrane of the mouth is peculiarly ex- 
posed to the sources of injury which excite catarrh elsewhere. Hence 
catarrh of the mouth is a very frequent affection, but it is only recently 
that the name “ catarrh of the mouth ” has been given to those changes 
which, occurring in other mucous membranes, are termed catarrh. It 
is remarkable that this affection is rarely induced by exposure of the 
skin to cold, a cause which so frequently excites catarrh of other mu- 
cous membranes. 
Among the injurious influences that may excite catarrh of the 
mouth are— 
1. Irritation which acts on the mucous membrane. Dentition fre- 
quently causes catarrhal stomatitis, which often attains great severity. 
Rough teeth, ulcerated teeth, wounds in the mouth, very hot, very 
cold, or chemically injurious ingesta, smoking and chewing tobacco, 
etc., excite catarrh. The same effect is produced by the use of mer- 
curial preparations, not only when mercurial salve is rubbed on the 
gums, or when mercurial preparations, in powder or solution, aye taken 
by the mouth, but by inunction of mercurial ointment, and by taking 
mercurial pills, well covered up. For since the mercury, absorbed from 
the skin or the intestinal canal, is excreted by the salivary glands, it 
still causes direct irritation of the oral mucous membrane. Often, 
very small amounts of mercury will induce mercurial stomatitis; we 
can readily understand this, if we bear in mind that the mercurial 
swallowed with the saliva is again absorbed from the intestine, and 
reaches the mouth repeatedly before escaping from the economy. The CATARRH OF THE MOUTH. 
415 
sensitiveness of the mouth to mercury varies with the individual; 
lienee, in one patient stomatitis may occur sooner than in another, just 
as, after frictions on the skin with mercurial ointment, one person is 
affected earlier than another with the superficial dermatitis, which we 
shall hereafter describe as eczema mercuriale. 
2. In many cases, oral catarrh is a propagation of inflammation 
from neighboring organs to the mucous membrane of the mouth. 
Wounds and inflammations of the face, particularly facial erysipelas, 
also inflammations of the fauces, are almost always complicated with 
oral catarrh. Less constantly, nasal and bronchial catarrh extends to 
the mouth. While a thickly-coated tongue was considered a certain 
sign of disturbance of digestion, this secondary catarrh caused facial 
erysipelas and angina to be almost always regarded as manifestations 
of gastric disturbance, and to be treated accordingly. Acute and 
chronic catarrh of the stomach is surprisingly often complicated with 
catarrh of the mouth. JBeaumont, who had the opportunity of com- 
paring the gastric mucous membrane with that of the mouth, in the 
case of the Canadian, St. Martin, found that changes in the former 
instantly excited analogous changes in the latter, and daily experience 
supports this observation. But, although catarrh of the mouth very 
frequently accompanies catarrh of the stomach, we must not sup- 
pose, on the other hand, that gastric catarrh occurs with every oral 
catarrh. 
3. Catarrh of the mouth is not unfrequently a symptom of consti- 
tutional affection. Among the acute infectious diseases, typhus and 
scarlatina especially are accompanied by peculiar changes of the mu- 
cous membrane of the mouth, which are essentially catarrhal; these 
will be more accurately described when speaking of the diseases in 
question. Coated tongue is found in almost all feverish affections; 
but it would be going too far, to say catarrh of the mouth occurs in 
every fever (see treatment). 
Finally, in many cases we do not know the exciting causes. 
Pfeuffer gives sitting up at night, and other observers give mental 
excitement, as a cause. 
It is remarkable that in some patients oral catarrh obstinately per- 
sists for years, without our being able to find any continuous cause. 
Anatomical Appearances.—We seldom have the opportunity 
of observing oral catarrh in its incipient stage. Only after severe irri- 
tation, and occasionally during difficult dentition, we see the oral mu- 
cous membrane at first dark red and very dry, till, finally, in the stage 
of decline, there is a copious secretion, which is clouded by contain- 
ing young cells. After less severe irritation, and in the oral catarrh 
which usually complicates catarrh of the stomach, the intense redness 416 
DISEASES OF TIIE MOUTH. 
and. dryness of the mouth are either unobserved, or are seen only tem- 
porarily. 
Quite early in the affection there is decided swelling of the mucous 
membrane and submucous tissue, increased secretion, and excessive 
formation of young cells. The swelling is most evident at the edges 
of the tongue and over the cheeks. The tongue appears too broad to 
lie between the teeth, and its sides show impressions of the teeth. A 
turbid mucus covers the cheeks, gums, and especially the tongue. The 
mucus and young cells most readily adhere to the filiform papillae, thus 
giving a coated tongue. 
Chronic oral catarrh has similar symptoms. The swelling of the 
mucous membrane is usually even more decided ; on the inner surface 
of the lips and cheeks, and on the roof of the mouth, we not unfre- 
quently find small nodules as large as a barley-corn (swelled mucous 
glands) ; thick yellow mucus covers the gums, especially about the 
teeth ; the elongated processes of the filiform papillae appear as small 
white threads, and give the tongue a felty or hairy look (lingua hir- 
sute/). On microscopical examination (Miqud), it is found that the 
coating of the tongue, even in chronic oral catarrh, consists mostly of 
epithelial cells. These contain fat globules and brown granules, and 
not unfrequently unite together into brown plaques. At the same 
time we see rod-like formations, the broken epithelial processes of the 
filiform papilla? (Kolliker). Felt-like formations grow on these, their 
matrix forming a granular border to the hardened epithelial cells. 
We also find fat-globules, vibrioncs, and usually some remains of 
food. 
Symttoms and Course.—Besides what we have said in the pre- 
ceding paragraph, there is little to add to the objective symptoms. In 
the severe forms of acute oral catarrh, which we first described, there 
is a feeling of burning and tension in the mouth. Babies no longer 
bite the ivory ring or orris-root, which is usually given them to facili- 
tate the cutting of the teeth. They cry when we touch their mouths, 
and, on attempting to nurse, they soon let go of the nipple, as if it hurt 
them. In some cases, whose frequency is magnified by the laity, so-called 
“ teething convulsions ” occur, which may prove fatal without leaving 
any material changes in the central organs to be seen on post-mortem 
examination. From our present knowledge of the subject, these con- 
vulsions must be considered as reflex symptoms, which are caused by 
the severe irritation of the sensitive nerves of the mouth being trans- 
ferred through the central organs to the motor nerves. Indeed, it is 
doubtful whether these attacks are caused by the acute oral catarrh, 
or are the result of direct irritation of the sensitive nerves from the 
pressure of the teeth. (See chapter on Eclampsia.) CATARRH OF THE MOUTH. 
417 
In moderate eases of acute oral catarrh, characterized by increased 
mucous secretion and excessive cellular formation, the patients com- 
plain particularly of a “ bad taste,” which they generally describe as 
slimy or clammy. Accurately speaking, this “ slimy, clammy taste ” 
is a misnomer, as physiologists only recognize bitter, sour, sweet, and 
salty tastes. The patients feel a slimy substance on the oral mucous 
membrane, and attempt to remove it by hawking and spitting. But 
the sense of taste itself is also influenced by oral catarrh. Usually the 
disturbance only causes the taste to be less acute, and not so sensitive. 
Since an insensitive layer lies between the.substance to be tasted and 
the peripheral ends of the nerves of taste, only very irritant substances 
excite distinct sensations. In such cases, the patients usually say their 
taste is bad or stale. When they chew hard substances, and thus re- 
move the insensitive layer from the mucous membrane, the sense of 
taste is for a time better. In some cases, patients suffering from oral 
catarrh complain of a bitter taste. The laity consider this a sure 
sign of “ biliousness,” and some physicians think there is a status 
biliosus, and not a status pituitosus. In far the greater number of 
cases the bitter taste is a subjective symptom; it is not excited 
by bitter substances, but must depend on a perversion of the nerves 
of taste. 
Lastly, the patients not unfrequently complain of a “ foul ” taste; 
this term is also unphysiological and incomplete. This foul taste is 
caused by excitement, not of the nerves of taste, but of the olfactory 
nerves, with whose peripheral expansions in the Schneiderian mem- 
brane the gaseous emanations from the coating of the tongue come 
in contact through the posterior nares. The foul taste, or, more cor- 
rectly, the foul smell, is not solely a subjective symptom; generally, 
other persons perceive a fetor from the mouth of the patient, especially 
in the morning, before breakfast; this disappears when eating has re- 
moved the foul epithelial coating from the tongue. It is doubtful 
whether pain in the forehead, so frequent a symptom in acute catarrh 
of the stomach, occurs in simple oral catarrh. The above symptoms 
are by no means always accompanied by disturbance of the stomach 
digestion. The patients often have a normal feeling of hunger; but, 
it is true, they usually choose very sour and salty, or highly-flavored 
articles of food, which can excite the nerves of taste even through the 
epithelial covering. Frequently there is no evidence that the stomach 
lias not properly digested the food taken into it. After meals, there 
is no pressure in the epigastrium, no eructation, or other symptom of 
disordered digestion. It is often difficult, indeed, to persuade the pa- 
tient that his stomach is sound, and not filled with decomposing sub- 
stances. The thickly-coated tongue, the slimy, bitter, or foul taste, 418 
DISEASES OF THE MOUTH. 
and the smell from the mouth, appear to him sc distinctly to indicate 
an emetic, that he considers advice unnecessary. 
The milder grades of oral catarrh, such as occur in most smokers, 
cause but slight subjective symptoms. In the morning the epithelium, 
which has collected during the night, usually causes a slimy taste and 
disagreeable odor from the mouth ; but these soon pass off, and, during 
the day, the patients have nothing to complain of; nevertheless, they 
usually prefer the most piquant, to the bland and unirritating kinds 
of food. 
In severe cases, chronic oral catarrh is a most annoying affection. 
The victims of it occupy a considerable time in the morning in hawk- 
ing and spitting, in scraping the tongue and rubbing the teeth and 
gums with a hard brush to clear off the adherent mucus. The sensa- 
tion, taste, and smell of the mouth are perverted all day; the odor from 
the mouth does not pass away. The patients consult the physician on 
account of the “ slimy taste,” for which they have in vain taken va- 
rious kinds of spring water, StrahVs and Morrison's pills, and which 
occasionally gives them severe hypochondriasis. The healthy appear- 
ance and w'ell-nourished state of the patients usually contrast with 
their complaints. On questioning them, we find that even articles of 
difficult digestion are eaten with impunity. It is necessary to under- 
stand these states, in order to recognize them in special cases and to 
treat them successfully. 
Diagnosis.—The coating on the tongue, observed in oral catarrh, 
must not be confounded with that which is found in healthy persons, 
especially in the morning, on the back part of the tongue, and which is 
called the normal coating. According to Miquel, this is caused by 
the air passing through the nose and fauces during the night, inducing 
evaporation from the neighboring parts of the mouth, so that the epi- 
thelium, which, under normal circumstances, is thrown off, becomes dry 
and forms an opaque coating. According to Neidliart, who, in a disser- 
tation, written under Seitz’s supervision, makes serious objections to this 
explanation of the coating of the tongue, other causes have much to do 
with its production. The epithelium of the mouth and tongue under- 
goes continuous desquamation, which is to be regarded as a result of 
the mechanical action of speaking and chewing. It is evident that 
where the movement of the tongue is greatest, and where it is most 
brought in contact with other parts, the epithelium will be soonest and 
most effectually cleaned off. Now, this occurs particularly in the an- 
terior part of the tongue, which, with every movement, is brought in 
contact with the roof of the mouth, and in the sides, which lie directly 
against the teeth. The back part of the tongue, on the contrary, 
where the normal coating mostly occurs, does not lie against the roof CATARRH OF THE MOUTH. 
419 
of the mouth, and only touches it in the act of swallowing. Hence it 
follows, on the one hand, that the most superficial epithelial patches 
on the anterior part are soonest and most completely loosened, and 
also that they are soon removed; but, on the other hand, that they 
should remain attached longer at the base, and even when loosened 
should remain longer in position, especially as the elongated processes 
of the papillae afford them a great protection. 
In most feverish complaints the whole top of the tongue appears 
whitish. This does not generally depend on an increased formation of 
cells due to oral catarrh, but occurs because, while there is an increased 
loss of fluid through the skin, the secretions of the mouth are dimin- 
ished, so that the epithelium is less moist and transparent. Besides 
this, patients with fever suffer from loss of appetite, and do not chew 
hard substances, such as best remove the epithelium. Just as, in ma- 
rasmic persons with dry skin, there is continued apparent desquama- 
tion of the epidermis without its formation or removal being actually 
increased, so in fever the homy processes of the papilla? and the 
epithelium of the mouth become more evident without their being 
formed or removed in greater amounts. The presence of the swelling 
and moisture of the mucous membrance, which exist in oral catarrh, 
prevents our mistaking the coating of the tongue, that occurs in it, for 
that which we find in fevers, where the tongue is flat, small, and some- 
times even very pointed, the mouth dry, and consequently the patient 
thirsty. If the tongue of a fever-patient is dry, without the epitheli- 
um and processes of the filiform papilla? being at least of normal 
amount, of course the tongue does not appear coated. 
For the difference between simple oral catarrh and that accompany- 
ing gastric catarrh, see Section III., Chapter I. 
Prognosis.—If we except the spasms during dentition, which are 
sometimes dangerous to life, and whose dependence on oral catarrh is 
still doubtful, the prognosis as regards life is favorable. The progno- 
sis for a perfect cure, especially in chronic oral catarrh, is less favora- 
ble, although even here a suitable, judicious treatment, if carefully fol- 
lowed by the patient, which is rarely done, may give a favorable 
result. 
Treatment.—The causal indications cannot be fulfilled in all 
cases. In difficult dentition, cutting the gums is of doubtful benefit; 
occasionally the incisions inflame and cause the catarrh to become 
worse. Sharp edges of the teeth, which are easily overlooked, are to 
be carefully removed, wounds of the mouth and ulcerated gums are to 
be properly treated. Where smoking, especially the use of strong 
cigars, causes troublesome oral catarrh, it must be totally forbidden, 
or at least weak cigars only should be smoked through a cigar-holder, 420 
DISEASES OF THE MOUTH. 
or, still better, a long pipe should be used. Oral catarrh, caused by the 
use of mercurials, requires their discontinuance, and in such cases all 
traces of blue ointment are to be carefully removed from the skin. The 
secondary oral catarrh usually disappears with the cure of the erysipe- 
las, angina, gastritis, etc. We shall hereafter see that the latter does 
not require emetics nearly so often as these are ordinarily used in 
practice. The fact of the tongue being for a time cleaner after the 
vomiting depends altogether on mechanical causes, and does not at all 
prove that the oral and gastric catarrh are benefited. When caused 
by some infectious disease, the indications are the same as those for 
the treatment of the original affection. 
The treatment of the disease itself is essentially local, just as for 
affections of other mucous membranes that are within easy reach. 
This direct treatment is especially required in those cases of chronic 
oral catarrh which prove very obstinate even after the exciting cause 
has disappeared. For this obstinate clamminess I can strongly recom- 
mend a well-known domestic remedy; namely, slowly chewing small 
pieces of rhubarb before going to bed. I cannot ascribe the very gen- 
eral improvement to the direct action of the rhubarb on the gastric 
mucous membrane, since it does not produce the same effect when 
given in very soluble pills. 
In chronic catarrh persisting without cause, rinsing the mouth 
with solution of carboilate of soda, or slowly drinking a bottle of soda- 
water, on an empty stomach, is very useful. This evidently depends 
on the well-known power of the carbonates of the alkalies to diminish 
the tenacity of the mucus and render it more fluid. If this treatment 
is inefficacious, we may confidently order the mouth to be pencilled 
with a solution of corrosive sublimate (gr. j—ij, to the pound of water), 
as recommended by Pfeuffer, or with a solution of nitrate of silver 
(gr. j to 3 ss water), as advised by Henoch. The effect of these pre- 
scriptions in oral catarrh is not inferior to that in other catarrhs from 
the same remedies. 
CHAPTER II.- 
cuourous STOMATITIS—APHTHAE. 
Etiology.—On tlie mucous membrane of the mouth we often see 
small white spots, surrounded by a red border, which look like flat 
vesicles; after a short time these are thrown off, and an excoriation, 
which heals readily, is left. This affection of the oral mucous mem- 
brane is designated by most authors as “ aphthae,” a name which is 
also used for other diseases of the mouth, especially cancrum oris and CROUPOUS STOMATITIS.—APHTILE. 
421 
thrush. From numerous careful observations, Bohn has shown that, 
when these white spots are punctured even in their earliest stage, no 
fluid can be evacuated from them, and hence that they are not vesicles, 
but solid thickenings, consisting of exudation on the free surface of 
the mucous membrane under the epithelium. I consider this view, 
which in the main corresponds with that of Rokitansky and Foerster, 
as correct; but I think that, to be consistent, the affection, which on 
other mucous membranes we call croupous inflammation, should have 
the same name when it attacks the oral mucous membrane; hence, 1 
do not hesitate to define aphthae as a croupous stomatitis limited to a 
circumscribed portion of the oral mucous membrane. 
Aphthae are chiefly observed in children. During the first few 
months, however, they are rarer than during dentition. Weakly, 
badly-nourished children are more disposed to them than strong and 
well-nourished ones. Among the exciting causes, cutting the teeth is 
the chief. Aphthae often accompany the affection of the skin in the 
acute exanthemata, especially measles. Occasionally also they occur 
as small epidemics, without any perceptible cause, and it then appears 
as if they spread by contagion. Lastly, aphthae accompany other 
severe affections of the mouth, particularly cancrum oris. 
Anatomical Appearances.—Aphthae chiefly occur on the anterior 
half of the tongue, and the inner surface of the lips, cheeks, and hard 
palate. They are about the size of a lentil, round, often quite numer- 
ous, and are either disseminated or run together into irregular figures. 
The grayish or yellowish-white deposits separate gradually from the 
periphery toward the centre, making the red border broader. When 
the exudation has entirely separated, there is no ulceration, only an 
excoriation; this is characteristic of a croupous affection, and distin- 
guishes it from a diphtheritic. The excoriated place is soon covered 
with epithelium again ; aphthae leave no cicatrix. Catarrh, with copi- 
ous production of mucus and cells, affects the rest of the mouth. 
Symptoms and Course.—The eruption of aphthae is often pre- 
ceded for several days by fever, restlessness, loss of appetite, and the 
symptoms of oral catarrh. The disease itself is accompanied by pain, 
which is increased by nursing, and in older children by speaking and 
chewing. At the same time the secretion of saliva is so much in- 
creased, that a clear fluid almost constantly run3 from the half-open 
mouth. From the decomposition of the accumulated epithelium and 
the exudation thrown off, there is a disagreeable, penetrating fetor 
from the mouth, especially in the not unfrequent complication of the 
croupous with diphtheritic stomatitis (see Chapter III.). By repeated 
relapses the affection may last several weeks. Of itself it is scarcely 
ever dangerous. 422 
DISEASES OF THE MOUTH. 
Treatment.—Chlorate of potash has very properly attained the 
reputation of a specific for aphthae. In almost all cases, under the use 
of a watery solution of this remedy (gr. jv—vj. at a dose), improvement 
and cure very soon occur. If, contrary to our expectation, the chlorate 
of potash does not produce this result, we may paint the aphthae with 
dilute muriatic acid, or with nitrate of silver. 
‘CHAPTER III. 
DIPHTHERITIC STOMATITIS, STOMACACE, CANCRUM ORIS, MUNDFAULE. 
Etiology.—As lias been repeatedly said, in diphtheritic inflam- 
mation a fibrinous exudation is deposited in the tissue of the mucous 
membrane, and the part of the membrane affected sloughs from the 
compression to which its vessels are subjected by exudation. After 
the detachment of the diphtheritic slough thus formed, which is some- 
times dry, sometimes moist, a loss of substance remains. 
Diphtheritic stomatitis results—1. From the too continued or too 
excessive use of mercurials. 2. It not unfrequently occurs without 
perceptible cause, especially among people living under unfavorable 
circumstances (mal loges, mal vetus, mal nourris, Taupin, J3ohn). 
The latter form is usually called stomacace or cancrum oris; exten- 
sive epidemics of it occur in foundling hospitals, orphan asylums, bar- 
racks, and other institutions, and also in armies not in barracks, but in 
the field, or otherwise living in the open air; it is not improbably ex- 
tended by contagion. 
Anatomical Appearances.—In the milder grades of the diph- 
theritic form of mercurial stomatitis, at certain parts of the mouth, 
along the lateral borders of the tongue, and on the parts of the cheeks 
and lips which lie against the teeth, we at first find a whitish or some- 
what dirty discoloration of the mucous membrane. These white spots 
cannot be wiped off, but after a few days the superficial layer of 
mucous membrane, with the exudation infiltrating it, falls off, and in 
its place is left an unhealthy-looking ulcer, which cleans off slowlv 
and finally cicatrizes from the margins. In more severe cases, where 
the exudation infiltrates and destroys the whole thickness of the 
mucous membrane, a large portion of the inner surface of the mouth 
is often converted into a soft, discolored slough. If this separates, a 
deep ulcer with irregular borders and uneven base is left. The loss 
of substance is but slowly filled with granulations, and as the lost 
mucous membrane is not regenerated, but is replaced by cicatricial 
tissue, contracted cicatrices, or even adhesions and false anchylosis, not 
unfrequently remain. DIPHTHERITIC STOMATITIS, ETC. 
423 
In cancrum oris the infiltration and ulceration always begin on the 
gums, usually at their upper border on the anterior surface. In severe 
cases it advances to the posterior surface of the gums, and the adjacent 
parts of the lips, cheeks, and tongue. The teeth become loosened, 
and occasionally the periosteum of the jaw is exposed and destroyed. 
In consequence of this, in some cases there are caries and necrosis of 
the maxillary bones. 
Symptoms and Course.—The diphtheritic form of mercurial sto- 
matitis is accompanied by severe pain, particularly when the sloughs 
have separated and left ulcers. Chewing, or even speaking, will ren. 
der this pain unbearable. The secretion from the salivary and mucous 
glands is enormously increased, the patients cannot sleep, as the secre- 
tion, if not ejected, runs into the larynx, and induces cough or suffoca- 
tion ; if they lie on the side and succeed in sleeping, they soon wake 
to find the pillow cold, wet, and saturated with saliva. On the parts 
of the tongue and gums, but especially along the edges of the teeth, 
which are free from sloughs or ulcers, there is an unusually thick, yel- 
low, soft coating. There is a very penetrating bad odor from the 
mouth, caused by the decomposition of this coating, and of the slough 
of the mucous membrane. It is not decided whether or not this 
smell is caused by the formation of sulphuret of ammonium from the 
disintegration of the sulpho-cyanide of potassium, which is a normal 
constituent of the saliva, by the decomposition going on in the mouth. 
Even when the mercurials have been stopped, the pain, flow of saliva, 
and smell, pass off slowly, and even in mild cases it is usually from 
eight to fourteen days before the patient feels well. In severe cases 
the cure progresses even more slowly; as was mentioned above, there 
may even be permanent injury. 
At the commencement of cancrum oris, according to the excellent 
description of Bohn, the gums are dark red and greatly swelled by 
excessive hyperaemia. They appear loosened from the teeth, and bleed 
on the slightest pressure. After this stage has lasted two to four 
days, a gray membranous deposit almost always appears on the upper 
border of the gums, particularly about the incisor teeth of one side of 
the lower jaw. On careful examination, we find that this deposit, 
which is a pulpy substance, does not lie on the gums, but consists of the 
gangrenous tissue of the gums. After the separation of the pulpy 
mass which we, in opposition to Bohn, must consider a diphtheritic 
slough, there is found a loss of substance of the gums, on the surface 
and periphery of which the same process is repeated as long as the 
affection lasts, until in severe cases the contours of the gums are lost, 
the teeth loosened, and the other evils described above have resulted. 
At the same time the neighboring lymphatic glands are swelled and 424 
DISEASES OF THE MOUTH. 
painful; the parts of the lips and cheeks corresponding to the affected 
part are oedematous; the breath has a cadaverous odor; the saliva, 
which is often bloody and discolored, flows constantly from the mouth; 
and every attempt to swallow, or even to drink, causes severe pain. The 
patients avoid closing the mouth and even keep the jaws apart, to 
prevent rubbing. Strange to say, the general condition and even the 
appetite are affected but little ; fever is slight or even absent; when 
properly treated, the disease almost always runs a favorable course, the 
diphtheritic sloughs separate, and the ulcers under them heal in a 
relatively short time. Neglected and improperly treated, the affection 
may exist for months, but it rarely endangers life. Fatal results 
probably always depend on complications. 
Treatment.—In the diphtheritic form of mercurial stomatitis we 
must not neglect to tell the patient how slow his cure will be. He 
will bear his sufferings much better if he does not find his hopes dis- 
appointed from day to day ; but if we promise him that, if not cured 
sooner, he will, at least, be comfortable by the eighth or ninth day, he 
will be patient and submit to what is unavoidable. Frequently wash- 
ing the mouth with cold water, or with water and red wine, at the 
commencement, subsequently painting the ulcers with dilute muriatic 
acid, or, still better, with the solution of nitrate of silver, described in 
Chapter I., but especially the use of solution of chlorate of potash, are 
far preferable to the internal administration of iodide of potassium and 
mercurial antidotes, or painting the mouth with spirits of camphor, 
which is as painful as useless. Touching the ulcers occasionally with 
solid nitrate of silver is very beneficial, but exceedingly painful. 
Chlorate of potash is just as certain a specific against cancrum oris 
as against aphthae. To children under one year we may give one, scruple 
daily, to older ones half a drachm, to adults one to two drachms, dis- 
solved in six ounces of water. Under this treatment the bad odor very 
quickly disappears; the ulcers also commence to clean up in a few 
days and heal rapidly. We are very rarely obliged to touch the ulcers 
with nitrate of silver. 
CHAPTER IV. 
EXCORIATIONS AND ULCERS OF TIIE MOUTH. 
Etiology.—The rapidly-healing excoriations which remain after 
aphthae, and the ulcers caused by mercurial stomatitis and cancrum 
oris, were discussed in the last chapter and the one before it. 
Small vesicles, followed by very painful excoriations about the 
point of the tongue, appear to be caused by local injuries; at least, the EXCORIATIONS AND ULCERS OF THE MOUTH. 
425 
patients suffering from them always say they must have burnt them- 
selves, smoked too much, etc. 
Diffuse catarrhal ulcers rarely occur in the oral mucous membrane; 
still I have observed them in some cases. In one instance the greater 
part of the surface of the tongue was the seat of an obstinate catarrhal 
ulceration. 
Follicular ulcers not unfrequently occur from stoppage, swelling, 
and ulceration of the large mucous glands, which are particularly plen- 
tiful on the inner surface of the lips. In some females these almost 
always occur at the menstrual periods; in others, during pregnancy or 
lactation (stomatitis vesicularis materna). They are also seen in men 
without any apparent cause. 
Irregular ulcers at the angles of {he upper or lower jaw occur quite 
often. According to JBednar and Bamberger, they result from the 
destruction of a fibrinous exudation, infiltrating the mucous membrane, 
but by their limitation to the above-named locality are distinguished 
from the ulcers left by cancrum oris. 
Variolous ulcers result from the eruption in variola passing from 
the skin to the mucous membrane of the mouth. Herpetic vesicles 
may attack the mouth and cause small herpetic ulcers. The callous 
ulcers on the tongue caused by sharp edges of teeth, and those of the 
gums resulting from the formation of tartar, belong to surgery. Syph- 
ilitic and scorbutic ulcers will be treated of in separate chapters. 
Anatomical Appearances.—The small vesicles and excoriations 
at the end of the tongue are only discovered on careful examination. 
If the vesicle has ruptured, it looks as if the epithelial processes of 
one or more filiform papillae were broken off; we see only a small, 
slightly-excavated red spot. In diffuse catarrhal ulcers, there is a loss, 
not only of the epithelial covering of the mucous membrane, but also 
a superficial loss of substance of the mucous membrane itself, of varia- 
ble extent, and usually of irregular shape. The rest of the mucous 
membrane of the mouth shows the above-described changes of cataixhal 
inflammation with extensive production of cells. 
Follicular ulcers are rarely numerous; frequently there is only one. 
This usually starts as a bright, pearly vesicle, which subsequently 
breaks, and becomes an oval ulcer, several lines long. The base of 
this ulcer is quite yellow, or lardaceous, and covered with a thin secre- 
tion ; the edges are somewhat elevated, hard, and red. 
The irregular ulcers at the angle of the jaw are occasionally sym- 
metrical on both sides; they may be several lines long, are irregularly 
shaped, and present a loss of substance of the mucous membrane, 
which even extends into the submucous tissue. They often cause ob- 
stinate swellings of the cervical glands. 426 
DISEASES OF THE MOUTH. 
The variolous ulcers occur particularly on the roof of the mouth. 
After the rupture of the flat pustules, with which the eruption begins, 
superficial, round, easily-healing ulcers are left. Herpetic ulcers usually 
occur on the insides of the cheeks, and on the roof of the mouth. The 
vesicles, which form groups like the herpes vesicles on the lips, break 
early, and leave flat ulcers, which soon heal. 
Symptoms and Course.—The small vesicles and excoriations on 
the point of the tongue are annoying, but perfectly free from danger. 
They disappear without treatment in a few days. The inconvenience 
they cause contrasts strongly with the very slight anatomical changes. 
The diffuse catarrhal ulcers render the motions of the mouth, es- 
pecially of the tongue, very painful. After they have lasted some 
time, this pain seems to diminish, even if the objective symptoms con- 
tinue unchanged. 
Follicular ulcers also are accompanied by pain in speaking and 
chewing, and by the symptoms of oral catarrh. The lardaceous base 
and hard edges of these ulcers greatly frighten half-initiated non-pro- 
fessionals, who have suffered from syphilis, because, from these appear- 
ances, they make up their minds that the ulcers are of specific nature. 
The ulcers at the angle of the jaw render chewing and swallowing 
difficult, and, in some patients, cause severe pain, while in others they 
are not discovered till the mouth is carefully examined. They are 
rarely dangerous, although they sometimes last for weeks. 
Variolous and herpetic ulcers rarely cause much pain. 
Treatment.—The small vesicles and excoriations at the point of 
the tongue disappear if the mouth is kept free from injuries for a few 
days, smoking and the use of hot food, etc., being avoided. 
Chlorate of potash is not so serviceable in diffuse catarrhal ulcera- 
tion as in other affections of the mouth. Continued and energetic 
local treatment with nitrate of silver, and particularly with a weak 
solution of corrosive sublimate, is most serviceable. The beneficial 
effects of the latter are analogous to those attained by the treatment 
of some skin affections with mercurials. 
In treating follicular ulcerations, we must look out for any disturb- 
ances of digestion. If these have been removed, or are not discover- 
able, we confine ourselves to the use of chlorate of potash and energetic 
local treatment. Touching the ulcer with solid nitrate of silver is very 
painful, it is true, but it acts surely and quickly. 
The ulcers at the angle of the jaw require no internal treatment, 
but chlorate of potash is recommended for them also. Locally, we 
may use nitrate of silver or concentrated acetic acid, as recommended 
by Hilliet and JBavtliez. 
Variolous and herpetic ulcers require no special treatment. SYPHILITIC AFFECTIONS OF TIIE MOUTH. 
427 
CHAPTER Y. 
SYPHILITIC AFFECTIONS OF THE MOUTH. 
Etiology.—Primary ulcers and condylomata—that is, those de- 
veloping at the point where the transfer of the syphilitic poison has 
taken place—occur, according to my observation during the last few 
years, much more frequently than I had formerly supposed. In some 
cases the contagion passes from the nipple of a syphilitic nurse to the 
mouth of the nursling. Occasionally the infection is caused by un- 
natural debauchery; most frequently through so-called sugar-teats, 
which pass from the mouth of a syphilitic to that of a non-syphilitic 
person. From one town in the vicinity of Tubingen, I have treated, 
and shown in the clinic, a family of ten persons, children, parents, and 
grandparents, who all had syphilitic ulcers and condylomata of the 
oral mucous membrane from this cause. 
Among the secondary syphilitic affections (by which term we mean 
those that occur in the early stages of the disease only, not at the 
point of infection, but at other parts of the body), condylomata and 
ulcers often occur together in the mouth. Among the tertiary forms 
(those which occur in the later periods), we have the gummy tumors, 
or nodular syphilomata (Wagner) of the tongue, which are often mis- 
taken for cancer of the tongue. 
Anatomical Appearances.—Both the primary and secondary 
syphilitic ulcers and condylomata spring from circumscribed indura- 
tions, or from syphilitic papules of the mucous membrane. Then an 
excessive collection and milky cloudiness of the epithelium give a pe- 
culiar white appearance (as if it had been touched with nitrate of 
silver) to the surface of the affected part. Subsequently the papules 
of the mucous membrane form syphilitic erosions or ulcerations by 
molecular disintegration, or condylomata by papillary proliferation, or 
both together. The ulcers occur most frequently at the corners of the 
mouth; here they are usually superficial, and it looks as if the com- 
misure of the lips were torn. On the edges of these ulcers there are 
almost always small condylomata. The ulcers occurring on the tongue, 
especially on its upper surface or sides, which are exposed to many 
sources of injury, form more or less deep fissures, or extensive losses 
of substance, whose uneven base is covered with a whitish-gray de- 
tritus. On the lateral edges of the tongue, the condylomata usually 
form elongated, shallow excrescences; on the dorsum of the tongue, 
on the contrary, they form round or oval warty vegetations, with broad 
bases, often separated by fissures. Not unfrequently, patients who 
have a bad conscience, and occasionally, also, inexperienced physicians 428 
DISEASES OF THE MOUTH. 
mistake the circumvallate papillae at the base of the tongue for syphi 
litic condylomata. 
Gummy tumors, or nodular syphilomata of the tongue, usually 
come on the anterior third. At first only an indurated spot is noticed; 
this soon swells to the size of a bean or hazel-nut, and subsequently 
softens and ruptures. After the rupture of the nodule there is left a 
deep, sharply-bounded ulcer, with inverted, thickened borders. 
Symptoms and Course.—The primary and secondary ulcers in the 
mouth cause pain in chewing and speaking, and are accompanied by 
the symptoms of chronic oral catarrh, described in the first chapter. 
The diagnosis rests partly on the history, partly on the objective symp- 
toms above given. 
When condylomata occur at the edges of the tongue, they cause 
little annoyance, and would be easily overlooked, if patients who have 
long suffered from syphilis did not pay such attention to themselves. 
They often recede at one place, while new ones come at another. In 
other cases, without any treatment, they disappear for a longer or 
shorter time, but come back again, and, with any treatment, show great 
tendency to relapse. Condylomata on the dorsum of the tongue impede 
its movements, and thus become annoying. Inspection of the mouth 
renders the diagnosis certain, as the affection is not easily mistaken. 
The nodular syphilomata of the tongue develop without pain, 
and even their ulceration does not cause much, but they render the 
tongue unwieldy and rigid, and thus interfere with speaking and 
chewing. But the ulcers left, after their breaking down, are very sen- 
sitive to the touch of the teeth, and to hard articles of food. 
Treatment.—The principles for treating syphilitic affections of 
the mouth will be given hereafter. 
The effect of preparations of mercury on primary and secondary 
ulcers and condylomata of the mouth is, as a rule, very striking. We 
may, almost with certainty, reckon that, under mercurial treatment, 
they will very shortly improve, and entirely disappear. Nevertheless, 
we must guard against the misuse of mercurials, especially in repeated 
relapses of syphilitic papules of the mouth, when they are the sole 
symptoms of syphilis. Even the nodular syphilomata of the tongue 
may disappear at any stage, under proper treatment. 
CHAPTER VI. 
SCORBUTIC AFFECTIONS OF THE MOUTH. 
Etiology.—The affection of the gums is among the most constant 
and among the first symptoms of scorbutis. The changes in the gums 
are exactly analogous to those caused by the disease in other tissues. SCORBUTIC AFFECTIONS OF THE MOUTH. 
429 
They compel us to suppose an abnormal condition of the capillary 
walls, which explains the various exudations and inclination to haemor- 
rhage, seen in scorbutis, better than would be done by an abnormal 
condition of the blood, the nature of which is entirely unknown, and 
whose presence even has not been proved. 
For the causes of scorbutis, and hence almost always of this affec- 
tion of the gums, see chapter on scorbutis. 
Anatomical Appearances.—The seat of the scorbutic affection 
of the mouth is exclusively in the gums, but, where any of the teeth 
have been lost, the gums are just as free from the affection as other 
parts of the mouth, and, where all the teeth are gone, the patients do 
not have any scorbutic affection of the mouth. Occasionally the affec- 
tion is limited to one side, and in some cases to the parts around a 
few teeth. At the commencement there is a red border to the upper 
margin of the gums; these soon begin to swell, and to become dark 
blue. The pointed processes between the teeth especially swell out, 
and their attachment to the teeth is loosened. The swelling, which 
depends on oedema and the escape of blood into the parenchyma of 
the gums, may become so great that the gums press over the teeth 
and hide them, or that spongy swellings, half an inch or more thick, 
form on the gums. About the teeth, and at the top of the swelling, 
the surface subsequently disintegrates to a soft, discolored mass, after 
the separation of which there is left a loss of substance. This sloughing 
appears to be caused partly by the excessive tension of the infiltrated 
portion, partly by the pressure it is subjected to by the teeth. When 
improvement begins, the swelling of the gums subsides; they again 
become attached to the teeth, and finally attain their normal color. In 
a few cases, a new formation of connective tissue seems to occur during 
the affection; after the swelling has subsided, the gums retain a cica- 
tricial solidity, are uneven and nodular. 
Symptoms and Course.—Chewing is very painful, and often im- 
possible, on account of the swelling of the gums. The secretion of 
mucus and saliva in the mouth is greatly increased. Hemorrhages 
occur on attempting to chew, as well as from slight pressure on the 
gums. The decomposition of the contents of the mouth, which are 
mingled with blood, and subsequently with dead tissue, causes a very 
penetrating and disagreeable odor. These symptoms, and the exami- 
nation of the mouth, in which we find the above-described changes, 
together with the observance of the other symptoms of scorbutis, con- 
firm the diagnosis of a scorbutic affection of the mouth. 
Treatment.—With proper treatment of the original affection, the 
affected gums often return to a normal state in a surprisingly short 
time. Along with the dietetic and therapeutic remedies for the original 430 
DISEASES OF TIIE MOUTH. 
disease, which will be described hereafter, it is customary to use astrin- 
gent mouth-washes, such as spiritus cochlcarias, tinctura myrrhae, rhata- 
niae, or decoctions of willow, oak, or Peruvian bark. In an epidemic 
in Prague, observed and described by GejJca, washing the mouth with 
warm vinegar, containing more or less brandy, was found beneficial 
where there was loosening of the gums. Where the affection of the 
gums was more severe, a linctus, with muriatic acid, was prescribed. 
Subsequent relaxation was treated by astringent decoctions and solu- 
tions of alum. 
CHAPTER YII. 
SOOK — MUGUET — THRUSH. 
Etiology.—Thrush was considered as a peculiar form of exudative 
stomatitis until it was discovered that a parasitic plant, growing on the 
mucous membrane of the mouth, caused the disease, or at least had a 
great deal to do with it. The tlirusli-fungus, oidium albicans {Robin), 
is not found outside of the organism, hence we do not know how its 
germs reach the mouth. But there is no doubt about certain circum- 
stances being required for the germs to reach the mouth and the fun- 
gus to grow there. In children the affection is only seen during the 
first days and weeks of life, rarely in the second month; in adults it 
only occurs in protracted, exhausting diseases a short time before death. 
Hence it appears probable that the germs become attached most 
readily, and the fungus grows best, where the acts of chewing and 
swallowing are not very energetically performed, and the fungus can 
remain quiet and find nourishment in the disintegrating product of the 
epithelium and remains of food adherent to it. The layer of mucus, 
lining the mouth, appears to interfere with the implantation of the 
fungus. In the newly-born or in moribund patients we may often 
foretell appearance of the thrush fungus, from a certain amount of dry- 
ness of the mouth. It is not probable, at least for all cases, that the 
diminished secretion from the mouth is due to the first stage of catarrh, 
even though the unaccustomed irritation in the delicate oral mucous 
membrane of a newly-born child may readily cause catarrhal irritation. 
Neglect of cleansing the mouth greatly favors the development of 
thrush. In large lying-in and foundling hospitals, where the care, by 
which thrush can almost always be prevented, is not exercised, the 
affection often attacks almost all the children. Although thrush has, 
in some cases, been transferred directly from the oral mucous mem- 
brane of one person to that of another, still the affection cannot be 
reckoned among those that spread by contagion. It is not necessary 
for a patient with thrush to be in the vicinity, for another to be affect- THRUSH. 
431 
ed with it; but the germs of thrush, like those of mould, seem to be 
very plenty and widely-spread, and to develop wherever they find a 
suitable place and favorable circumstances. 
Anatomical Appearances.—Whitish points, or a delicate frosty 
coating, in severe cases a cheesy, smeary mass, looking much like cur- 
dled milk, are found on the inner surface of the lips, tongue, and roof 
of the mouth. At first these may be readily removed, subsequently 
they are more firmly attached. From the mouth the coating occasion- 
ally advances to the larynx, more frequently to the oesophagus; in 
some cases the latter has even been found filled with thrush deposit. 
The disease scarcely ever extends to the stomach. On microscopical 
examination of the milky deposit it is found to consist of young and 
old epithelial cells, fat-globules, etc., between which peculiar round 
granules and filaments may be seen. The first are known to be spores 
of fungi by their oval form, sharp outlines, by the excavation which 
is evident in the larger ones, and by their difference in size, indicating 
their growth. The filaments starting from the spores are of variable 
thickness ; they have sheaths and constrictions; where the latter occur 
they have branches, which go off from them at acute angles, and have 
the same calibre as the trunks. These fungoid filaments form beauti- 
ful tree-shaped figures, or, when very numerous, form a thick felt. It 
often looks as if they perforated the epithelial cells, located at their 
joints. At first the thrush-spores are in the most superficial layers of 
the epithelium; later they press in between them. They may even, 
although this rarely occurs, grow into the mucous membrane itself. 
Symptoms and Course.—Children suffering from thrush almost 
always show that nursing pains them. Patients dying of phthisis, car- 
cinoma, etc., complain of painful burning in the mouth, when they are 
affected with sprue. It is uncertain whether these difficulties depend 
on the injuries that the deposit causes to the mucous membrane, or 
whether a coincident slight inflammation of the oral mucous membrane 
excites these pains and causes the growth of the fungus. In children, 
suffering from thrush, we often see diarrhoea, accompanied by pain in 
the abdomen, with fluid, green, acid stools. At the same time there 
are not unfrequently redness and excoriations about the anus, inside of 
the thighs apd nates. As this symptom also occurs in nursing infants 
without thrush, and as many children having thrush have no diarrhoea, 
many consider it as an accidental complication, while others, especially 
French observers ( Valleix), have considered diarrhoea among the symp- 
toms of thrush. It is difficult to decide which is right. In many cases 
the diarrhoea may be independent of the thrush. But, as we have to 
ascribe so many cases of infantile diarrhoea to abnormal decomposition 
of the ingesta, and as we know that, where microscopical germs fonn, 432 
DISEASES OF THE MOUTII. 
there is usually abnormal decomposition, it does not appear very im- 
probable that part of these diarrhoeas are caused by the presence of 
thrush-deposit in the mouth and its passage into the stomach and in- 
testine. 
Treatment.—Mothers rarely use an amount of care in cleaning 
the baby’s mouth sufficient to prevent the development of thrush. It 
is true the mouth is washed out in the morning, and at night when 
undressing it; but during the day they let it go to sleep on the breast, 
carefully withdraw the nipple from the mouth so as not to awake it, 
and lay it in the cradle, while the last portions of milk, not yet swal- 
lowed, remain in the mouth and decompose, preparing the mouth for 
the thrush-fungus. The physician should strongly urge his patients to 
carefully wash the baby’s mouth with a linen rag dipped in water, or a 
mixture of water and wine, after each feeding, whether it is to go to 
sleep or not, and they will almost certainly remain free from thrush. 
Even after the development of thrush we may limit ourselves to 
carefully removing the creamy deposit and washing the mouth. The 
home remedies, such as sprinkling the mouth with sugar, painting it 
with borax and mel rosie, which are advised by the nurses, are to be 
avoided; they render the mouth sticky, give new material for decom- 
position, and do not at all interfere with the development of the 
thrush. The accompanying diarrhoea must be treated according to 
principles hereafter set down. 
CHAPTER YIII. 
PARENCHYMATOUS INFLAMMATION OF THE TONGUE—GLOSSITIS. 
Etiology.—In most cases of glossitis an exudation is deposited 
between the muscular filaments of the tongue while they themselves 
are rarely inflamed or destroyed (see pathogenesis of myocarditis). 
Acute parenchymatous glossitis is a rare affection, it is only induced 
by severe injuries affecting the tongue; such as burns and injuries 
from acrid or caustic substances, and especially from bee and wasp 
stings. Chronic partial glossitis results most frequently from the pres- 
sure of sharp edges of the teeth and rough pipe-stems. We do not 
know the causes of dissecting glossitis, nor that of a superficial glos- 
sitis, which very properly has been termed psoriasis of the mouth, in- 
asmuch as it is marked by an infiltration of the lingual mucous mem- 
brane with morbid production of epithelium. The only good descrip- 
tion of this affection which I have been able to find is in Rayers’s work 
on cutaneous diseases under the title “ Pityriasis of the Mouth; ” al- 
though I myself have met with it three times in the past year. PARENCHYMATOUS INFLAMMATION OF THE TONGUE. 
433 
Anatomical Appearances.—In acute glossitis the whole tongue 
is usually affected; very rarely one side alone. The tongue doubles 
in size, its surface is dark red, and smooth or fissured, and covered with 
tough, often bloody exudation. Its substance is infiltrated, soft, and 
pale. Sometimes it returns rapidly to its normal size and structure; 
in other cases it remains for a long while, or permanently, indurated 
and enlarged. In severe glossitis, small abscesses form; these enlarge, 
unite, and may burst through the mucous membrane and heal, leaving 
a depressed scar. 
In chronic partial glossitis wre find, particularly at the edge of the 
tongue, circumscribed hard spots, which project slightly or not at all, 
and which often retract the neighboring parts of the tongue just like 
cicatrices. At these points the muscular substance has disappeared, 
and is replaced by connective tissue. 
In glossitis dissecans, the tongue’s surface is divided into lobules 
by deep furrow's. Remaiiy; of food and epithelium collect in these 
furrows and cause ulceration. Many apparent cracks in the tongue 
are mere wrinkles like those on the faces of the old. In the superficial 
glossitis described above as analogous to psoriasis of the skin, the lin- 
gual mucous membrane is thickened, rigid, and extensively cracked. 
In some spots there is a morbid luxuriance of the epithelial coating, 
while in other parts of the surface it is entirely absent, and the whole 
tongue looks smooth and shining, as though it were varnished. 
Symptoms and Course.—In acute glossitis there is not room 
enough in the mouth for the enlarged tongue, which projects almost 
an inch beyond the teeth, which are kept apart. The upper surface is 
whitish, or, if the exudation covering it is mixed with blood, it is dirty 
brown; the under surface is dark red. The deep impressions made by 
the teeth in the sides soon change to ulcers with fatty coatings. 
The tension of the tongue caused by the great swelling excites severe 
pain. The movements of the tongue are impaired by the pressure 
caused by the exudation on the muscular fibres, speech becomes unin- 
telligible and soon impossible, chewing and swallowing the same way. 
The saliva constantly runs out of the mouth at both sides of the tongue, 
while, the mouth being open, evaporation constantly goes on, and the 
surface of the tongue, not being moistened, becomes dry and incrusted. 
The submaxillary and the lymphatic glands of the neck enlarge, the 
circulation in the jugular vein is obstructed; the face appears blue 
and swollen. The entrance to the larynx may be contracted by the 
swelling at the root of the tongue, and respiration be very much im- 
paired ; hence attacks of suffocation often occur at the height of the 
affection; these may cause death. Acute glossitis is accompanied by 
high fever, full pulse, great anxiety and restlessness, and severe con- 434 
DISEASES OF THE MOUTH. 
stitutional disturbancesubsequently the pulse becomes small, the 
patient listless, and signs of asphyxia may arise. Left to itself the 
disease may gradually subside; sound treatment often relieves it 
promptly. "When an abscess forms, all the symptoms increase; but 
subside almost instantly when it breaks. 
Chronic partial glossitis causes a circumscribed dull pain, which 
becomes burning when the mucous membrane is ulcerated. The in- 
duration impairs the movement of the tongue. The affection may last 
for years, and is often mistaken for cancer. In glossitis dissecans 
the ulcerated fissures are painful. When these have healed, the tongue 
remains lobulated but free from pain. 
Psoriasis of the lingual mucous membrane is a very distressing and 
obstinate affection, and lasts with varying intensity for years. The 
patient is often quite incapable of chewing solid food and smoking 
tobacco, for every motion of the tongue occasions acute pain. 
Treatment.—Acute glossitis the promptest treatment. 
Bleeding, blisters, and purging, are useless; leeches to the tongue in- 
crease the evil. We should rather scarify it deeply and boldly, for 
the swelling will protect the ranine artery. We may also lay pieces 
of ice in the mouth, and give soothing mouth-washes when the symp- 
toms have moderated. If deep incisions fail, and suffocation threaten, 
tracheotomy may be necessary. 
In chronic partial glossitis wre must first of all remove the sharp 
edges of teeth, etc. But frequently this fails, and operation is the 
only resource. Iodine, wrater from mineral springs, and systematic 
purgation, have been recommended on theoretical grounds; experi- 
ence has not proved their advantage. 
In glossitis dissecans we may limit ourselves to the treatment of 
the ulcers by nitrate of silver in substance or solution. 
Psoriasis of the lingual mucous membrane will be aggravated by 
the use of mercury, given under the false impression that the affection 
is syphilitic. In one of my three cases, after applying all manner of 
treatment without advantage, a permanent and material improvement 
was effected by persistently rinsing, the mouth with a very dilute 
solution of carbolic acid, and touching the fissures with the same acid 
pure. 
CHAPTER IX. 
NOMA—WATER CANKER—GANGRENOUS SORE MOUTH. 
Etiology.—Noma is that form of gangrene which results from an 
asthenic inflammation, that is, from an inflammation occurring in a de- 
bilitated person. “If a nutritive change of destructive character af- NOMA, WATER CANKER, ETC. 
435 
fects parts which have been greatly altered by previous changes of their 
nutrition, entire death of the part may quickly result.” ( Virchow.) 
The disease is almost exclusively encountered among children, 
especially among those who have become cachectic from want of care, 
insufficient or spoiled food, and bad dwellings; or among those who 
have just recovered from severe illness that has greatly weakened 
them. Noma is most frequently seen as a result of measles, more 
rarely after other acute exanthematous affections, or after typhus, 
pneumonia, etc. Misuse of mercurials in the treatment of the above 
affections appears to have much to do with the occurrence of noma as 
a sequel; it often begins simultaneously with mercurial stomatitis. 
In the north of Germany, and especially in Holland, it is more fre- 
quent than in the south. It seems never to be epidemic. 
Anatomical Appearances.—The affection almost always begins 
on the inside of the cheeks. Over a spot hardened by infiltration, the 
mucous membrane becomes red, then discolored ; a vesicle filled with 
cloudy serum, often forms on this. The affected part soon blackens, 
softens, and disintegrates. The gangrene spreads, destroys the gums, 
the lips, the base and edges of the tongue on the affected side; the 
maxillary bones are exposed and exfoliate, the teeth become loose and 
fall out. Progressing, the gangrene reaches the outer surface of the 
cheeks, spreads rapidly, and finally changes the entire cheek, part of 
the nose, the lower eyelid, often even half the face, into a ragged, 
pulpy, moist mass, or to a dry, black slough. The blood-vessels resist 
the destruction longest; on post-mortem examination, they are found 
still preserved, but filled with fibrinous coagula. In the few cases that 
recover, the gangrenous masses are thrown off and the loss of sub- 
stance is filled with granulations, so that a firm, fibrous cicatrix finally 
results from a new formation of connective tissue. Adhesions in the 
mouth and frightful disfigurement always remain. 
Symptoms and Course.—According to the excellent description 
of Hilliet and Barthez, while the gangrene commences, usually with- 
out pain, on the inner surface of the oral mucous membrane, a soft, 
regular, circumscribed oedema occurs in the affected cheek and lip, 
and gradually spreads. A hard, round nucleus forms in its centre, over 
which the skin appears shining, pale, or mottled violet. Even when 
the inside of the cheeks and a great part of the gums have become 
gangrenous, the child often sits quietly in bed. A sanguineous, or 
even black saliva, runs out of his mouth ; but he plays, demands food, 
takes it eagerly, and with the food swallow’s the sloughs that fall off 
from the gangrenous parts. At the same time the skin is pale and 
cool, the pulse small and moderately frequent, and there'is delirium at 
night. Occasionally, mostly at the fifth or sixth day of the disease, a 436 
DISEASES OF THE MOUTH. 
circumscribed, dry, black slough forms on the cheeks or under-lip ; tliis 
increases daily, till it affects half the face. Occasionally, even at this 
stage, the child is tolerably strong, demands food, and tears gangre- 
nous pieces out of the mouth. The appearance becomes more hideous 
when the slough separates, and tags hang from the cheeks, between 
which we can see the bare, loosened teeth, and blackened jaw-bone. 
Then the smell is excessively disagreeable, the patient very weak, and 
diarrhoea usually comes on; thirst is almost unquenchable; the skin 
is cool and dry ; the pulse small and imperceptible ; finally, the child 
dies of exhaustion. Occasionally, the disease begins to recover from 
the first stage; but, even after detachment of the external slough, 
the gangrene may be limited, the swelling diminish, the general health 
improve, the surfaces of the wound clean off, and healthy suppuration 
occur. 
Treatment.—Quinine, chlorine-water, charcoal, and other antisep- 
tics, have been recommended as internal remedies; but they are of 
little service ; they are recommended more on theoretical grounds than 
from experience of their benefit. We should give the patient fresh 
air, good nourishment, a small amount of wine, and treat the gangrene 
locally, according to surgical principles. Almost all caustics have been 
advised for noma ; the actual cautery has obtained the greatest repu- 
tation. The object of these applications is to destroy the gangrenous 
parts, and to excite inflammatory reaction in the surrounding parts. 
CHAPTER X. 
PAROTITIS—INFLAMMATION OF TIIE PAROTID AND ITS VICINITY— 
MUMPS. 
Etiology.—Besides the cases caused by wounds of the parotid, by 
the entrance of foreign bodies into its excretory duct, or by calcareous 
deposits, which cases belong to the surgeon, we distinguish two forms 
of parotitis: 1. Idiopathic parotitis, parotitis polymorplia (mumps); 
2. Symptomatic or metastatic parotitis. 
In opposition to the generally-received opinion, Virchow maintains 
that the affection starts in the gland-ducts of the parotid. He has di- 
rectly proved this in the case of symptomatic parotitis, and in the idio- 
pathic form also it appears to us much more probable that the inflam- 
mation should begin in the gland-ducts than in the interstitial tissue. 
If, with Virchow, we consider idiopathic parotitis as resulting from a 
simple catarrh, which has no tendency to suppurate, and the sympto- 
matic or metastatic form, as caused by catarrhal inflammation of the 
gland-ducts, that has a tendency to suppurate, the symptoms, course, INFLAMMATION OF THE PAROTID, ETC. 
437 
and so-called metastases of the affection are less inexplicable than if 
we follow the old view, which considered the intercellular substance 
of the gland as the starting-point and peculiar seat of the affection. 
Idiopathic parotitis is rarely sporadic ; it almost always occurs in 
epidemics; these usually come in the spring and autumn, that is, in 
cold, damp weather, rarely in the dry, warm weather of summer. They 
vary in duration and extent; occasionally they are confined to certain 
institutions, foundling houses, barracks, etc. Trustworthy observations 
render it most probable that the disease spreads by contagion. It does 
not appear to us justifiable (with liilliei) to consider mumps as an in- 
fectious disease, and the inflammation of the parotid as the local ex- 
pression of a constitutional disease, and to regard it as analogous to 
the affections of the skin that accompany the acute infectious diseases. 
The same objections that we have raised to considering whooping- 
cough among the infectious diseases, in the ordinary sense of the term, 
urge us to separate mumps from them also, in spite of its contagious- 
ness. Infants and old persons usually escape epidemic parotitis; males 
are more frequently attacked than females. 
Symptomatic parotitis results from severe diseases, like typhus ; 
in some epidemics of this disease it follows almost all cases. More 
rarely it is seen in the course of cholera, septicasmia, measles, small- 
pox, dysentery, or as an accompaniment of pneumonia. We do not 
exactly know the relation of such cases of parotitis to these diseases. 
The oral catarrh, which always accompanies abdominal typhus, might 
excite the suspicion that the parotitis accompanying this disease was 
induced by a propagation of the catarrh of the mucous membrane of 
the mouth along the excretory ducts of the glands. But, opposed to 
this view is the fact, that the frequency with which it occurs in typhus 
is not proportionate to the intensity of the affection of the oral mucous 
membrane, as well as the circumstance that parotitis, running the same 
course, occurs in other affections that are not complicated by oral ca- 
tarrh. Since symptomatic parotitis is seen not only in infectious dis- 
eases, but also in pneumonia, we cannot say that it is induced by an 
irritation of the gland from infected blood. The hypothesis, that under 
some circumstances it has a critical indication, and exercises a favorable 
influence on the course of the original disease, is disproved by facts; 
it always forms an unpleasant and undesirable complication. 
Anatomical Appearances.—We do not exactly know the ulti- 
mate anatomical changes of parotitis. As the course of the disease is 
almost always favorable, there is rarely an opportunity for anatomical 
examinations. Nevertheless, from the softness of the swelling, and 
the slight amount of pain that it causes, and especially from its usually 
rapid disappearance, without leaving any traces, we may believe that 438 
DISEASES OF THE MOUTH. 
it is cliiefly or solely caused by serous exudation. Although we have 
said above that the affection probably proceeds from a cataixh of the 
gland-duct, still there is no doubt that the swelling chiefly affects the 
interstitial substance and the connective tissue about the gland. The 
swelling usually extends far beyond the borders of the gland. The 
development of oedema about the inflamed gland-ducts is not at all 
strange ; it corresponds exactly with observations made in analogous 
conditions. Infiltration, with firm fibrinous exudations and suppura- 
tion, rarely occur in parotitis. We do not know whether the suppura- 
tion proceeds from the gland itself or the interstitial substance ; but it 
is most probable that there is just the same state of affairs as in sup- 
purating symptomatic parotitis. (See below.) 
Symptomatic parotitis begins, according to the careful observa- 
tions of Virchow, with decided hypencmia, which causes the gland 
and interstitial substance to appear infiltrated and swelled. Changes 
in the gland-ducts soon begin; a tough, filamentous, whitish, or yellow- 
ish substance, which soon becomes purulent, collects in them. Even 
at the second or third day the microscope shows that it contains pus- 
corpuscles, with numerous salivary corpuscles. If the disease pro- 
ceeds, the lobules of the gland soften and break down; this process 
begins within, so that at one time the lobules represent cavities filled 
with pus. Finally, the tunica propria is also destroyed, and the inter- 
stitial tissue begins to suppurate; this suppuration may extend rap- 
idly, and become a diffuse phlegmonous inflammation. In this case a 
large parotid abscess forms; more frequently the gland-tissue only is 
destroyed, and as the interstitial tissue remains intact, numerous small 
abscesses are formed. Occasionally also there are extensive destruc- 
tion and gangrene of the gland-tissue and interstitial substance; the 
inflammation and suppuration may spread from its original seat in vari- 
ous directions and cause dangerous results. It most frequently attacks 
the neighboring connective tissue, and the masticatory muscles lying 
in it, the periosteum of the maxillary, temporal, and sphenoid bones, or 
even the bones themselves. Where the disease is very severe, it 
occasionally passes from the bones to the membranes of the brain, and 
the brain itself, or to the internal and middle ear. This propagation 
of inflammation and suppuration to the cerebral membranes and the 
internal ear may take place along the blood-vessels and nerve-sheaths, 
as well as through the bones. Finally, in some cases parotitis induces 
phlebitis and thrombus of neighboring veins, especially of the anterior 
and posterior facial and external jugular veins; the disintegration of 
these thrombi may cause embolism and septicaemia. 
Symptoms and Course.—In idiopathic parotitis, as in other in- 
flammations, the 'iocal symptoms are often preceded by slight fever INFLAMMATION OF THE PAROTID, ETC. 
439 
The general disturbance, depression, headache, loss of appetite, rest- 
less sleep, etc., accompanying this as other fevers, are usually called 
the premonitory symptoms of idiopathic parotitis. After the fever has 
lasted two or three days, or in some cases simultaneously with its 
occurrence, a swelling forms, which, beginning near the lobe of the ear, 
rapidly extends over the cheek and to the neck; usually only one side 
is at first affected. In the middle it is firmer, at the periphery softer; 
the skin over it is pale or only slightly reddened. This swelling is 
accompanied by a feeling of tension and pressure, but by no severe 
pain; the motions of the head are impaired, tl\e mouth can only be 
slightly opened, and chewing and swallowing are difficult. The secre- 
tion of saliva may be increased, diminished, or unaltered. These 
annoyances are so slight in proportion to the disfigurement which 
gives the name to the disease, that the patients excite more laughter 
than sympathy. The swelling almost always soon extends to the 
other side of the face, and is often greatest there when it has gone 
from the side first affected and the fever has subsided. About the 
fifth or sixth day, occasionally even earlier, rarely later, the fever 
ceases, and after eight or ten days the face appears natural. But 
sometimes a circumscribed, painless, hard swelling remains for a while 
in the region of the parotid. Far more rarely about the fifth or sixth 
day the swelling becomes very painful, hard, dark red, and abscesses 
form, which open outwardly or into the external auditory meatus. 
Occasionally, in the course of the disease, one of the testicles is 
affected by an inflammation similar to that of the parotid ; this occurs 
more frequently in men than in boys; it is usually accompanied by 
pain in the sacral and inguinal regions and exacerbation of fever. 
The scrotum also becomes oedematous and forms an inelastic, doughy 
tumor, which is not often reddened; on careful examination we readily 
find that there is a serous exudation in the tunica vaginalis. Inflam- 
mation of this part usually runs as favorable a course as that of the 
parotid does, and after a few days terminates in resolution. Occasion- 
ally the parotitis and orchitis seem to alternate, as it were; the for- 
mer disappears as the latter comes on, and the reverse: hence we speak 
of parotitis polymorpha being “fugitive,” and of its inclination to 
metastasis to the testicle. In other cases, however, the two inflam- 
mations run on together, which renders it probable that both are due 
to the same cause, and that the occurrence of the one is not to be 
regarded as due to the disappearance of the other. As in men the 
scrotum is sometimes affected, so in women the vulva or breasts are 
occasionally attacked with inflammatory oedema. In other cases, pain 
in the region of the ovaries, increased by pressure, shows that an ovary 
is inflamed, just as the testicles are in men. Cases have also been 440 
DISEASES OF THE MOUTH. 
recorded, where, in the course of idiopathic parotitis, fatal meningitis 
has been developed. 
When symptomatic parotitis occurs at the height of typhus or any 
of the above-mentioned diseases, the apathetic patients do not usually 
complain of pain or any other symptom. Occasionally slight chills or 
an exacerbation of fever precede the formation of the parotid tumor. 
This sometimes forms gradually, at others very rapidly, and generally 
affects only one side. If parotitis comes on during convalescence from 
typhus, etc., it is accompanied by the same symptoms that we have 
described for idiopathic parotitis. Symptomatic parotitis also may end 
in resolution. This occurs most readily when the tumor has formed 
gradually and attained only a moderate hardness and extent. The 
diminution in size is sometimes slow, sometimes rapid. When about 
to suppurate, the swelling becomes uneven, nodulated, and very red; 
it usually shows fluctuation at several points, and, when opened 
spontaneously or artificially, benign pus is evacuated. Occasionally 
the opening occurs simultaneously outward, and into the external 
auditory meatus, more rarely into the mouth or pharynx. Finally the 
pus may burrow along the sterno-cleido-mastoid muscle, or the oesoph- 
agus and trachea, and form abscesses at the lower part of the neck 
or even enter the chest (Bruns). While mortifying, the skin cover- 
ing the tumor becomes dark blue and discolored; the tumor, which 
was previously hard, becomes doughy and sinks in; after a spontaneous 
or artificial opening, a discolored pus, mixed with shreds of tissue, is 
evacuated. 
Treatment.—As idiopathic parotitis almost always ends in a cure, 
if left to itself, we have little to do but protect the patient from inju- 
rious influences, and to regulate the digestion and bowels, while the 
disease lasts. We keep the patient in his chamber, cover the swell- 
ing with wadding or a spice-bag, and as long as the fever lasts let him 
avoid eating much meat or other protein substances which would not 
be readily digested (see diseases of the stomach). In some cases an 
emetic or laxative may be necessary. If hardness and greater sen- 
sibility of the swelling, with increase of the fever, excite fears of sup- 
puration, we may attempt to check it by applying leeches. If we find 
fluctuation, we should apply cataplasms, and open the abscess early, to 
prevent further destruction of the parotid, or perforation of the pus 
into the external auditory meatus. Irritant applications have been 
used to prevent metastases, and sinapisms and blisters have even been 
applied to the parotid region, to induce a return thither of the inflam- 
mation that had affected the scrotum and testicles. As experience 
has shown, such treatment can only prove injurious. 
In symptomatic parotitis even local blood-letting is badly borne, on SALIVATION—PTYALISM. 
441 
account of the severity of the original disease. If the swelling be red, 
and the patient winces when we press on the tumor, we should apply 
compresses of cold water or ice. When there is fluctuation, warm 
poultices and early opening of the abscess are indicated. 
CHAPTER XI. 
Strictly speaking, we have no right to consider salivation as a 
distinct disease (it forms a symptom of a great variety of affections), 
but we follow custom in giving a separate chapter to the anomalies of 
secretion of the salivary glands. The quantity of saliva secreted in 
twenty-four hours is usually estimated at ten to twelve ounces, but it 
varies considerably even during health. It is best, with Wunderlich, 
to consider the increased secretion as disease or salivation, when it 
ceases to pass into the stomach with the ingesta; but some of it flows 
out of the mouth, some is spit out, or is swallowed by itself, because 
it becomes troublesome. 
Etiology.—Physiology sufficiently explains the causes of most 
forms of salivation ; in other cases we do not know them. 
Salivation is caused—1. By irritation of the mucous membrane of 
the mouth or pharynx. Introduction of irritating substances into the 
mouth excites the flow of saliva, which consequently occurs in most of 
the affections of the mouth described in the preceding chapters, as 
well as in almost all surgical affections of the mouth. According to 
the beautiful experiments of Ludwig, the flow of saliva is increased 
by irritation of certain nerves, such as the lingual branch of the tri- 
facial or the glossopharyngeal; this increase also occurs when these 
nerves are divided and their central ends irritated. Of course the 
irritation of the divided nerves must be transferred to the nerve fil- 
aments governing the secretion of saliva, which is then to be regarded 
as a reflex symptom. In the same way we may regard the flow of 
saliva caused by the irritation of the peripheral expansions of the 
glossopharyngeal and lingual nerves induced by acrid ingesta, by 
wounds or ulcers, as a reflex symptom. Probably the salivation ob- 
served in neuralgias of the trifacial results from the same cause. The 
increase of saliva due to the use of mercurial and iodine preparations 
appears to depend not on the simple addition of these substances to 
the secretion, but to the irritation of the mouth, produced by excreting 
them for a long time. For they must be long taken before the secre- 
tion of 'saliva is greatly increased; salivation does not begin till the 
mouth becomes diseased from their continued action. Corresponding 
SALIVATIO N—P TYALISM. 442 
DISEASES OF THE MOUTH. 
to this, Lehmann found that at the commencement of mercurial pty- 
alism the excretion was not saliva but mucus, mingled with shreds of 
epithelium from the oral mucous membrane. The preparations of iodine, 
which induce stomatitis less frequently, cause salivation far more rarely, 
although we can detect their presence in the saliva quite early. We 
do not know whether the salivation produced by muriate of gold 
and other metallic and vegetable substances originates in the same 
way. 
2. In many cases, salivation appears to depend on irritation, affect- 
ing the gastric or intestinal mucous membrane, perhaps also the uterus 
or other organs. Frerichs has shown, by experiment, that irritation of 
the gastric mucous membrane increases the secretion of saliva; for, 
when he introduced food into the stomachs of dogs through fistulous 
openings, there was profuse salivation; if he used common salt, quan- 
tities of saliva flowed from the mouth. These experiments appear 
to prove that irritation of the gastric nerves is also reflected to the 
nerves governing salivation, and they at least partly explain the 
increased flow of saliva accompanying many pathological states of the 
stomach, such as ulcer or cancer of the stomach, and preceding vomit- 
ing, whether induced by emetics, overloading, or disease of the stom- 
ach. It seems probable, also, that the same cause induces the saliva- 
tion so constantly accompanying the pains produced by worms in the 
intestines, that the laity who are aware of this symptom have the 
most wonderful hypotheses about the flow of water into the mouth 
from the irritation of worms. We have less reason for referring the 
salivation which not unfrequently occurs during the first months of 
pregnancy, or in hysteria, to an excitement of the genital nerves re- 
flected to the secretory nerves of the salivary glands. 
3. Salivation depends on certain mental influences. We see how 
the secretion is increased in disgust or desire. As a proof that abnor- 
mal excitement of the brain may directly increase the secretion of sa- 
liva, we may note the fact that physiologists have been obliged to 
locate the origin of the nerves, governing the secretion of saliva, in the 
brain. The activity of the salivary glands is increased in the same 
way by irritation of the trigeminus and facial nerves, even at points 
where no sympathetic filaments are mingled with them, that is, above 
the ganglia. 
4. Occasionally salivation occurs in the course of diseases, such as 
typhus, intermittent, etc., without other perceptible cause; its occur- 
rence in these diseases has even been regarded as critical. 
Finally, some apparently healthy persons suffer from obstinate sali- 
vation without perceptible cause. In insane and old people, the flow 
of saliva from the mouth does not appear to depend on its increased SALIVATION—PTYALISM. 
443 
secretion, but on neglecting to swallow that which is produced in nor- 
mal amount. 
Anatomical Appearances.—We do not know the anatomical 
changes undergone by the salivary glands in increased salivation. In 
continued and excessive salivation, slight swelling of the parotid occurs 
in some rare cases. The fact, that the secretion may still be obtained 
after the heart has ceased to beat, proves that overloading of the ves- 
sels, or hypersemia of the salivary glands, which instantly causes their 
infiltration and swelling, is not the sole cause inducing increased secre- 
tion. 
Symptoms and Course.—The pains in the mouth, and painful 
swellings of the neighboring lymphatics, which occur in salivation, be- 
long to the various forms of stomatitis exciting it; salivation itself 
causes no pain, but it greatly inconveniences the patient. The fre- 
quent collection of fluid in the mouth obliges him to spit constantly; 
frequently he cannot speak two words without interruption. Rest at 
night is also disturbed, partly by the saliva flowing from the mouth 
and wetting the pillow, partly by that which, flowing backward, passes 
into the pharynx and larynx. The escaping fluid may reach the 
amount of six or eight pounds in twenty-four hours. Lehmann and 
other observers have found it, at first, more mucous, cloudy, of greater 
specific gravity, and richer in solid constituents (young and old epi- 
thelial cells), than normal saliva. The fluid is alkaline, contains much 
fat and little ptyaline, and only rarely perceptible amounts of sulpho- 
cyanide of potassium. Subsequently, the secretion was less cloudy, 
and, like the saliva that Ludwig obtained, by continued irritation of 
nerves influencing the secretion, it contained less solid constituents 
than normal saliva. This fluid was also alkaline, rich in fat and so- 
called mucous corpuscles ; it contained no sulpho-cyanide of potassium. 
When salivation has continued a long while, albumen may occasional- 
ly be found in the fluid. The patients usually emaciate ; the loss of 
water and organic constituents has little to do with this, but, as the 
accompanying stomatitis interferes with chewing, the patients take 
little nourishment, and what they do take is badly assimilated, be- 
cause the quantity of saliva swallowed interferes with digestion. 
Treatment.—The causal indications require a careful treatment 
of the original disease when the salivation is caused by affections of 
the mouth. When resulting from the misuse of mercurials, slight laxa- 
tives are to be recommended. Gullerier calls constipation “ one of the 
best known of the exciting causes of salivation,” and, indeed, it is more 
rational to suppose that the mercurials which reach the mouth through 
the salivary glands, and are swallowed, would be more readily removed 
by purgatives than by remedies directed to the skin or kidneys. Sali- 444 
DISEASES OF TIIE MOUTH. 
vation caused by affections of the stomach, intestines, uterus, etc., is 
also most readily improved by proper treatment of the original affec- 
tion ; in other forms the causal indications cannot be fulfilled. 
For the indications of the disease, derivatives, “ general baths, ap- 
plication of blisters and mustard to the throat and nape of the neck,” 
astringent mouth-washes of alum, sulphate of zinc, sage, or oak-bark, 
have been recommended. The use of opium deserves most confidence. 
It is always satisfactory when, as in this case, theory and practice 
agree in supporting a therapeutic measure. The use of opium in sali- 
vation was recommended by the first practitioners of medicine; and, 
since salivation depends on excitement of the nerves, it appears ra- 
tional to use for it remedies which, like the narcotics, diminish the ex- 
citability of the nerves. There are cases of spontaneous salivation that 
defy all treatment. SECTION II. 
AFFECTION'S OF THE PHARYNX. 
CHAPTER I. 
CATARRHAL INFLAMMATION OF THE PHARYNGEAL MUCOUS MEM- 
BRANE—ANGINA CATARRIIALIS. 
Etiology.—The disturbances of function and nutrition, which we 
have frequently designated as characteristic of catarrhal inflammation, 
are often observed in the mucous membrane of the pharynx, the soft 
palate, the uvula, and tonsils, and are usually termed angina catar- 
rhalis. In this section, the tissues of the soft palate are considered as 
belonging to the pharynx, since they participate in almost all the dis- 
eases of the pharynx. 
The predisposition for catarrhal inflammation of the pharynx varies 
with the individual. If exposed to the slightest injurious influences, 
some persons are immediately attacked with affections of this part, 
while others, exposed to the same influences, remain well, or have dis- 
ease of some other part. Some persons are troubled several times a 
year with catarrhal angina, while others live for years without having 
it. The causes of the increased predisposition to catarrhal angina are 
mostly unknown. It is customary to say that a lymphatic constitu- 
tion predisposes to the disease, or that it is more apt to occur in scrofu- 
lous persons. But we often see robust individuals, who show no con- 
stitutional anomalies, affected with catarrhal angina at every exposure. 
In general, we may say that the disease is more common in children 
and young persons than in those more advanced in life ; that repeated 
attacks leave an increased predisposition; that patients who have had 
syphilis, or who have used mercurials for a long time, are peculiarly 
liable to acute and chronic pharyngeal catarrh. 
Among the exciting causes are : 1. Direct irritation; such as hot 
or corrosive substances, rough, ragged bones, which stick in the fauces, 
and other injuries to the pharyngeal mucous membrane. Perhaps the 446 
AFFECTIONS OF THE PHARYNX. 
catarrli induced by spirituous liquors depends on their direct action. 
2. In other cases, the catarrh undoubtedly depends on catching cold. 
3. Not unfrequently it is propagated from neighboring parts to the 
pharyngeal mucous membrane. In this class belong the catarrhs oc- 
curring in mercurial stomatitis, and those difficulties of swallowing 
which accompany the later stages of laryngeal catarrh. Sometimes it 
accompanies catarrh of the stomach; but every angina is not, as was 
formerly supposed, of gastric origin. Not unfrequently catarrhal an- 
gina must be regarded as the result of a blood-disorder. It is not a 
complication, but a symptom of scarlatina, which is just as constant as 
the exanthema. More rarely in exanthematous typhus, or measles, 
which are always accompanied by catarrh of the respiratory organs, 
there is also pharyngeal catarrh. Among the chronic infectious dis- 
eases, constitutional syphilis often makes its appearance as pharyngeal 
catarrh ; but other changes in the tissues of the pharynx usually occur 
soon, which will be spoken of hereafter. 5. Sometimes catarrhal angi- 
na is epidemic. A large number of persons are taken sick without our 
knowing the influences inducing the affection. In many other cases, 
also, the exciting causes are unknown. 
Anatomical Appearances.—In acute catarrhal angina, the mu- 
cous membrane, especially that of the soft palate, appears dark red. 
The swelling of the mucous and sub-mucous tissue is most evident at 
the uvula, which has plenty of relaxed sub-mucous tissue. The uvula 
is thicker, but especially longer, and often rests on the root of the 
tongue (“the palate is down”). The tonsils also are more or less 
swollen. At first the mucous membrane is dry ; later, it is covered 
with cloudy secretion, particularly about the tonsils and posterior wall 
of the pharynx. 
In chronic catarrh of the fauces, the membrane does not appear 
regularly reddened; it is traversed by varicose veins, and is darker-col- 
ored. The swelling is greater and more irregular than in the preced- 
ing variety. The diseased mucous membrane sometimes appears dry 
and glistening, sometimes covered with a cloudy secretion. On the 
soft palate and uvula the swollen and closed glands often appear as 
small granules, or they form small yellow vesicles, which soon rupture, 
and leave round (follicular) ulcers. In the dilated openings of the 
tonsils there are occasionally found cheesy, badly-smelling plugs or 
stony concretions, which are the putrefied or petrified contents of the 
follicles. 
Recently, chronic pharyngeal catarrh has received a great deal of 
attention in the journals and treatises on baths, but it has not been 
sufficiently considered in the text-books on pathology. Occasionally 
it is limited to the pharyngeal mucous membrane; again, it extends to CATARRHAL INFLAMMATION—ANGINA CATARRHALIS. 
447 
that of the larynx or nares. The changes consist in an irregular hy- 
peraemia, so that sometimes we see only a few varicose vessels in the 
otherwise pale membrane; in a thickening, or hypertrophy, which is 
either diffuse, or limited to undefined spots ; and, in a perverted secre- 
tion of the mucous membrane. From the partial thickening of the 
mucous membrane, in which the sub-mucous tissue also participates, the 
posterior wall of the pharynx acquires a peculiar nodulated appear- 
ance ; there are numerous round, or oval, sometimes confluent promi- 
nences, whence the disease is called 'pharyngitis granulosa. Some 
authors designate it pharyngitis follicularis, because they consider that 
the partial hypertrophy of the mucous membrane is chiefly limited to 
the vicinity of diseased mucous glands. This view is probably correct, 
but has not yet been anatomically proved. In some cases the secre- 
tion of the mucous glands is very abundant, and then it sometimes 
shows an inclination to dry into disgusting yellow or green crusts ; in 
other cases it is scanty, and then also shows the inclination to dry, and 
the posterior wall of the pharynx looks as if covered with a thin coat 
of varnish. For this form of the affection, Lewin has proposed the 
very suitable name of pharyngitis sicca. 
Symptoms and Course.—Acute catarrhal angina is usually ac- 
companied by a fever, which has the symptoms of catarrhal fever, as 
previously described; this occasionally precedes the local difficulties, 
but it is sometimes, though rarely, entirely absent. At first the secre- 
tion from the mucous membrane is diminished; hence the patients 
complain of dryness in the throat. From the tension of the mucous 
membrane, especially at the half arches of the palate, where it is 
closely attached to the subjacent muscles by a scanty connective tissue, 
there is great pain, which is so increased at every attempt to swallow 
that the patients make wry faces whenever they attempt it. When, 
as frequently happens, the elongated uvula touches the tongue, there 
is a sensation of a foreign body in the throat and a constant inclina- 
tion to swallow. In very severe forms of catarrhal angina, which are 
often called erysipelatous or erythematous angina, the muscles of the 
palate are often infiltrated with serum and their functions lim- 
ited. Under normal circumstances, as is well known, the contrac- 
tion of the muscles of the anterior half arches of the palate prevents 
the return of food into the mouth; contraction of the muscles of the 
posterior half arches closes the passage to the nose, as the uvula fills 
up the opening that is left. If the function of these muscles be im- 
paired, fluids would be driven through the nose or back into the mouth 
by the contractions of the pharynx in the attempt to swallow. If the 
mucous membrane of the pharynx be the seat of an intense catarrh, 
and, as a consequence, the muscles be paralyzed by serous infiltration, 448 
AFFECTIONS OF THE PHARYNX. 
the patient suffers still more. As soon as a morsel of food, or, still 
more, any liquid, has passed the anterior half arches, the patient is 
greatly terrified, as he cannot pass it either forward or backward. As 
the substance in the pharynx would pass into the larynx on any at- 
tempt to breathe, the patients hold their breath and attempt, in every 
conceivable manner, to evacuate the contents of the pharynx through 
the mouth ; they bend far forward and let the head hang over the side 
of the bed. Nevertheless, some of the contents of the pharynx often 
enter the larynx, and are again expelled by spasmodic coughing. The 
patients at last become timid, and, with terror, wave back the drink or 
medicine offered to them, they pass day and night in the most uncom- 
fortable postures, so that the saliva may flow out of the mouth, and 
they may not be obliged to swallow it. A “ nasal ” tone of the voice 
is a pathognostic symptom of all affections of the pharynx, where the 
functions of the muscles of the half arches of the palate are affected, 
and consequently for all the intense forms of catarrhal angina. As is 
well known, it is only in saying JV and M that we allow the air to pass 
through the nose; while pronouncing other letters, the nasal cavities 
are closed. When patients are unable to shut off the nose in this way, 
from inability to contract their posterior half arches, the resonance of 
the nose gives to all sounds a peculiar tone, which is called “ nasal,” 
and the person is said to “ speak through the nose.” Besides this dif- 
ference of tone, there is a certain difficulty of speech. The patients 
speak slower and more carefully, because it pains them, especially 
when saying JV, in doing which the root of the tongue is for a moment 
pressed against the roof of the mouth. A last characteristic is, that 
the pronunciation of guttural It, in' which the uvula is made to vi- 
brate, becomes difficult or even impossible, if the uvula is much swollen 
and elongated. 
As we said in the first chapter of the previous section, the milder 
as well as the more severe forms of catarrhal angina are almost always 
accompanied by catarrhal stomatitis. The patients have a coated 
tongue, bad taste, foul breath, and the mouth is always full of saliva. 
Not unfrequently acute pharyngeal catarrh extends to the Eustachian 
tubes and the tympanum; the patients become deaf, have piercing 
pains in the ears, which may be excessive, until perforation of the 
drum permits the escape of pus from the middle ear, when a remission 
suddenly occurs. 
Catarrhal angina almost always terminates in recovery after a few 
days. While the pain and difficulty in swallowing subside, quantities 
of mucus are removed from the pharynx by hawking and spitting; at 
the same time the symptoms of oral catarrh pass away. 
In chronic catarrh of the fauces, the pain and difficulty of swallow- CATARRHAL INFLAMMATION—ANGINA CATARRHALIS. 
449 
mg are usually slight, and only become worse occasionally when the 
chronic catarrh is exacerbated by slight injuries. This is particularly 
true of the chronic catarrh of the soft palate, which is very frequent in 
patients who have suffered from syphilis, or who have used mercurials 
for a long while. The slight difficulties that these patients experience 
in swallowing, and the temporary exacerbations which occur, are a 
source of unceasing care. They usually soon attain great skill in 
looking at their own throats in the mirror; the smallest phlyctenula 
coming on the soft palate does not escape their notice; they constantly 
run after the doctor, who must again look in their mouth, and again 
assure them that they are not syphilitic. The cheesy plugs which 
form in the tonsils are occasionally ejected by hawking. This symptom 
also troubles the patient a great deal; the yellow, round bodies, which 
smell horribly when squeezed, are to them a sure sign that they have 
tubercles; and it is as difficult to convince the latter patients that they 
are not consumptive as to satisfy the former that they are not syphi- 
litic. Chalky concretions from the tonsils, which are fyawked up, are 
usually represented as lung-stones. The milder cases of chronic pha- 
ryngeal catarrh, from which most habitual drinkers suffer, usually 
trouble the patients only in the morning, when the mucous membrane 
secretes most abundantly a tough mucus, or when it is covered with 
the mucus secreted during the night, Tfrie patients attempt to remove 
this secretion by continued hawking and spitting, and this straining, 
which not unfrequently causes nausea and vomiting, is one of the causes 
of the notorious morning vomiting of drunkards. The severe forms 
of chronic pharyngeal catarrh, especially of the follicular or granular 
varieties, are far more troublesome. They do not render swallowing 
actually difficult, but the patients complain of an irritation, a disagree- 
able sensation of prickling, also of dryness in the throat, which leads 
them unwillingly to make the motion of swallowing, or, more fre- 
quently, to hawk and hack for a long while. It is thought, too, that 
this repeated hawking is a bad habit. The voice often becomes husky 
also, as the laryngeal mucous membrane usually participates in the 
affection. When the follicular pharyngeal and laryngeal catarrh is 
exacerbated, the hacking increases to a troublesome spasmodic cough, 
and the husky voice becomes actually hoarse. If the affection extends 
to the nasal mucous membrane, the nose becomes stopped at night; 
hence the patients sleep with the mouth -open, and by morning the 
pharynx and back of the tongue have become so dry that moving them 
causes cracks in the dry coating, or even in the membrane itself, and 
then there are slight haemorrhages. Many patients are greatly worried 
by this spitting of blood, whose origin can hardly be discovered, unless 
we see the patient just after he has awakened; and thus follicular 450 
AFFECTIONS OF THE PHARYNX. 
catarrh of the pharynx and larynx, which is a very obstinate, although 
not dangerous disease, has a very depressing effect on most patients. 
Treatment.—When of moderate intensity, acute catarrhal angina 
does not require any particular treatment. Often the patients do not 
apply to a physician, but go to some old woman, who knows howT to 
raise the “fallen palate” by certain hairs at the top of the head. 
These foolish ideas have a serious as well as a ridiculous side. The 
apparent success of this and similar senseless procedures must teach 
us to abstain from energetic treatment in affections where they have a 
great reputation. This teaching is much opposed in the treatment of 
catarrhal angina. We might say that more than half the physicians 
superfluously give an emetic, partly with the idea that it will act as a 
revulsive, partly to combat the gastric disorder, which is diagnosticated 
from the symptoms of oral catarrh, on which the angina is thought to 
depend. As the tongue is cleaner the day after the emetic, and the 
angina has improved, as it w'ould have done at any rate, the remedy 
receives the credit of it. 
In catarrhal angina, the use of an emetic is only admissible under 
certain circumstances, as when there are substances in the stomach 
that have excited, or are keeping up, a gastric catarrh. In severe cases 
it is well to let the patient apply moist compresses, well wrung out, 
and carefully covered with a dry cloth, to the throat, every few minutes. 
In persons who are afraid of the cold compresses, or where, for any 
reason, we do not wish to use these, we may employ warm poultices. 
At the same time, we may have the mouth frequently washed with 
cold water, or with a solution of alum, sulphate of zinc, acetate of 
lead, etc. Occasionally, by covering the inflamed spots with powdered 
alum, or painting them with a solution of nitrate of silver, 3 j to 3 j, 
we may abort the disease. 
Chronic catarrh of the fauces is best treated by the above-named 
astringent mouth-washes, and particularly by painting the inflamed 
spots with solution of nitrate of silver. 
Chronic pharyngeal catarrh must be very carefully and continu- 
ously treated; in many cases it defies medical skill. In the blennor- 
rhoeal form even, which offers the best prognosis, treatment often fails, 
because the patients cannot decide to give up the use of liquor, or to 
smoke less. The best treatment in these cases is the local application 
of solutions of nitrate of silver, alum, or tannin, and these seem to be 
more efficacious when given in a nebulized form than when applied 
with a brush. In the forms where there is little secretion, and par- 
ticularly in the follicular and granular pharyngeal catarrh, it occasion- 
ally appears as if the application of the above solutions caused a 
‘ toning up ” of the affected mucous membrane, and an improvement CROUPOUS INFLAMMATION—PHARYNGEAL CROUP. 
451 
of the disease, but in the cases that I have seen, this improvement has 
only been apparent, or, at least, only temporary. Solutions of corro- 
sive sublimate or sulphuret of lime have not proved more beneficial. 
Recently, as recommended by Leicin, I have, in some cases, tried a 
LucjoVs solution (I£ iodin. gr. vj; potass, iodid. gr. xij; aquas § vj), 
for painting the pharyngeal mucous membrane, and, although I have 
not used it in a great many cases, it seems preferable to other remedies 
in dry catarrh of the pharynx, with or without granulations. In this 
form of chronic pharyngeal catarrh the alkaline muriatic mineral waters 
have the best reputation, particularly those of Ems and the sulphur 
springs, especially those of Weilbach, and some Pyrenean springs. 
CHAPTER II. 
CROUPOUS INFLAMMATION OF THE PHARYNGEAL MUCOUS MEMBRANE 
—PHARYNGEAL CROUP. 
Etiology.—In the croupous inflammation of the pharyngeal mu- 
cous membrane, the croup membrane often adheres so firmly to the 
inflamed mucous membrane that, on detaching it, a bloody, superficial 
loss of substance remains. Then the affection shows a change from 
croupous to diphtheritic inflammation. 
1. Pharyngeal croup occurs as an independent disease, from the 
same causes as pharyngeal catarrh, and it almost seems as if it were 
occasionally only a more intense form of catarrh. 2. The croupous 
deposits on the tonsils, so often seen in parenchymatous angina, are 
explained by the intense participation of the mucous membrane in the 
inflammation of the subjacent tissues. 3. Pharyngeal croup, which 
appears as a symptom of a sporadic, or, more frequently, epidemic 
croupous inflammation, affecting the mucous membrane of the palate, 
pharynx, larynx, and trachea, is very important. In this form the croup 
sometimes seems to spread from the larynx to the pharynx (croup as- 
cendant), sometimes the reverse (croup descendant). 4. Lastly, pha- 
ryngeal croup occurs with croupous and diphtheritic inflammations of 
other mucous membranes in the later stages of typhus, in septicaemia, 
and similar diseases, a form which we shall not consider further at 
present. 
Anatomical Appearances.—We see white or grayish-white mem- 
branous masses on the reddened mucous membrane of the soft palate, 
tonsils, and pharynx. They usually form small, irregular, roundish 
islands; more rarely extensive membranes. Under these there is no 
loss of substance. 
Symptoms and Course.—Idiopathic, uncomplicated croupous an- 452 
AFFECTIONS of the pharynx. 
gina causes the same annoyances as severe catarrhal angina; we only 
discover the form of the inflammation by inspecting the pharynx. On 
careless examination, the gray patches may be mistaken for ulcers, 
with fatty bases. 
The subjective symptoms of parenchymatous angina are not altered 
by croup, so that, in this case also, the croup is first recognized on in- 
specting the pharynx. 
Croupous angina, which usually occurs epidemically with croupous 
laryngitis, is easily overlooked, as it causes proportionately little diffi- 
culty, which, moreover, will probably be misunderstood, as it affects 
children almost exclusively. If we examine the fauces of children sick 
with croup, we often find them covered with croup membrane, although 
the parents may not have noticed that the children had any difficulty 
in swallowing. We have before said how important for diagnosis and 
prognosis it is to examine the throat of every child affected with 
hoarseness. 
Treatment.—The treatment of croup occurring idiopathically, after 
catching cold, etc., is the same as that for the severe forms of pharyn- 
geal catarrh. 
Pharyngeal croup accompanying croupous laryngitis requires, as we 
have already said, the prompt removal of the membrane, and energetic 
cauterization of the affected mucous membrane, with a concentrated 
solution of nitrate of silver. 
CHAPTER III. 
DIPHTHERITIC INFLAMMATION OF THE PHARYNGEAL MUCOUS MEM- 
BRANE. 
Diphtheritic inflammation, in which a fibrinous exudation is de- 
posited in the tissue of the mucous membrane, and presses on its ves- 
sels so as to cause it to slough, attacks the pharynx very frequently. 
Diphtheritic pharyngitis, however, does not occur as a primary and in- 
dependent affection, but in almost all cases depends on infection of 
the blood from the poison of scarlatina, or of the disease we call epi- 
demic diphtheria and class among the infectious diseases. (We speak of 
croupous and diphtheritic inflammations of the different mucous mem- 
branes ; but when we speak of “ croup,” or “ diphtheria,” we always 
mean croupous inflammation of the laryngeal mucous membrane or 
diphtheritic inflammation of the pharyngeal mucous membrane.) We 
shall hereafter give a detailed account of diphtheria, when speaking 
of scarlatina and epidemic diphtheria. PHLEGMONOUS INFLAMMATION OF THE PHARYNX. 
453 
CHAPTER IV. 
Etiology.—The submucous tissue of the pharynx and the inter- 
stitial tissue of the tonsils, which are the seat of simple oedema in ca- 
tarrhal and croupous inflammation, may also suffer from inflammatory 
disturbances of nutrition. These often consist in infiltration of the 
tissue with fibrinous exudation, and in proliferation of the connective 
tissue; in other cases pus is formed, the tissues melt away, and ab- 
scesses result; diffuse mortification and phagedaena of the affected 
parts occur in some rare cases. 
The same causes, according to their intensity, or the predisposition 
of the patient, appear capable of exciting the catarrhal and parenchym- 
atous forms of pharyngeal inflammation; hence we refer to the etiol- 
ogy of the catarrhal form. Parenchymatous pharyngitis also leaves 
great tendency to relapse; the more frequently it has affected a per- 
son, the more liable he is to have it again. Many persons have it 
yearly, or even oftener. Once having ended in suppuration, it seems 
disposed to take the same course on subsequent occasions, so that, in 
such cases, in new attacks, there is little hope of causing the disease to 
end in resolution. 
Anatomical Appearances.—Acute parenchymatous pharyngitis 
usually attacks the tonsils; one or both may be inflamed, sometimes 
the inflammation passes from one to the other. From the exudation, 
with which they are infiltrated, the tonsils often swell to the size of a 
walnut; their surface appears nodulated, dark red, covered with glu- 
tinous exudation or croupous deposits. As the inflammation passes 
on to suppuration, some circumscribed spot usually becomes softer and 
more prominent, and finally the pus perforates the thinned walls of 
the abscess. More rarely the acute parenchymatous inflammation oc- 
curs in the submucous tissue of the soft palate; a hard swelling forms 
here, and fluctuation gradually occurs; finally, in this case also, the 
pus is evacuated into the mouth or pharynx. 
Chronic parenchymatous pharyngitis also almost exclusively affects 
the tonsils; more rarely the uvula, or the soft palate, is permanently 
thickened by inflammatory hypertrophy of the submucous connective 
tissue. From this cause the tonsils may become very large and hard; 
their surface is often uneven and nodulated, and has depressions where 
there was formerly a loss of substance from suppuration. The mu- 
cous membrane is but slightly reddened, or is even pale. We often 
find the above-described cheesy plugs in the gaping openings on the 
surface of the tonsils. 
PHLEGMONOUS INFLAMMATION OF THE PHARYNX. 454 
AFFECTIONS OF TIIE l'HARTNX. 
Symptoms and Course.—Acute parenchymatous pharyngitis gen- 
erally begins with a high fever, which may be preceded by a severe 
chill. The general condition of the patient is much affected, the pulse 
full and frequent, the temperature 104°, or over. In this case we have 
not, as in pharyngeal catarrh, a catarrhal, but we have an inflamma- 
tory fever, such as accompanies pneumonia and other inflammations of 
important organs. It is only in rare cases, where the disease is not 
severe and runs a very sluggish course, that the fever is moderate. 
With the commencement of the fever, or, perhaps, not till next day, 
the patients complain of a feeling of tension and soreness in the throat, 
and often of piercing pain, extending toward the ear; it feels to them 
as if there were a foreign body in the pharynx, hence they make con- 
stant attempts to swallow, although the motion increases their pain. 
Sometimes all the painful and terrifying symptoms occur, which we 
described in the first chapter of this section as accompanying the se- 
verer forms of catarrhal pharyngitis. Not only does swallowing be- 
come very painful, so that, when the patient attempts to swallow a 
little saliva, he distorts the face; but, from the imbibition and paraly- 
sis of the muscles of the palate and pharynx, when he attempts to 
swallow, both solids and fluids come back through the mouth and nose, 
or else Ave have the painful and dangerous condition that we have be- 
fore described (p. 448) as caused by the impossibility of getting the 
morsel out of the pharynx. The secretion of saliva is often enormous- 
ly increased; if the patient opens the mouth, Avithout spitting, the 
saliva runs from the corners of the mouth. The tongue is thickly 
coated, the odor from the mouth very unpleasant; there is also the 
characteristic modification of the voice; its resonance is changed, the 
speech has the peculiar nasal tAvang, from which alone we may often 
suspect the disease as soon as the patient speaks. Other characteris- 
tics of parenchymatous angina are the difficulty and pain caused by 
opening the mouth; frequently the patient cannot separate the teeth 
more than a few lines; this difficulty is apparently caused by the ex- 
cessive tension of the bucco-pharyngeal fascia. Respiration is affected 
far less frequently than speech and the opening of the mouth. Any 
considerable Avant of breath, added to the symptoms of parenchyma- 
tous angina, is always a serious symptom, and must arouse the suspicion 
that there is oedema glottidis. On examining the mouth and pharynx, 
which is done Avith difficulty, Ave often find the tonsils so swollen as to 
touch each other or to squeeze the oedematous uvula betAveen them. 
If only one tonsil be inflamed, Ave often see the uvula pressed entirely 
to the opposite side. We find the soft palate pressed forward into 
the middle of the mouth. At the part of the neck corresponding to 
the tonsil, that is, behind and beloAv the angle of the loAver jaw, Ave PHLEGMONOUS INFLAMMATION OF THE PHARYNX. 
455 
find a hard, painful swelling. Even more frequently than in catarrhal 
pharyngitis, the inflammation extends, with severe pain, to the Eusta- 
chian tube and tympanum. While the local symptoms thus increase 
for three or four days, the fever grows higher, and symptoms of hyper- 
semia of the brain occur; the patient has severe headache, is sleepless, 
tormented by horrible dreams, or even becomes delirious. When the 
inflammation ends in resolution, the local and general symptoms usu- 
ally subside toward the end of the week, and the patient generally re- 
covers in eight to fourteen days. "When suppuration occurs, and ab- 
scesses form, there is a sudden remission after the symptoms have 
reached their highest point. The patients often perceive the opening 
of the abscess only by the sudden relief they experience, as the pus 
may be swallowed or overlooked; in other cases the opening may be 
instantly recognized by the fetid odor and the yellow color of the sub- 
stance thrown out. It is doubtful how the pus, which has been com- 
pletely enclosed and protected from the air, acquires this very disagree- 
able smell. After the opening of the abscess convalescence is gener- 
ally rapid. 
Acute parenchymatous inflammation of the soft palate gives sub- 
jective symptoms similar to those of acute tonsillitis, and we can only 
decide on the presence of one or the other by the objective appear- 
ances. 
Chronic parenchymatous angina either results from protracted at- 
tacks of the acute form, or comes on gradually and independently. It 
generally causes very little trouble; there is little or no pain, the in- 
creased mucus is due to the accompanying catarrh; but the slightest 
irritation causes the chronic to relapse into the acute form again. The 
speech is often changed by the hypertrophy of the tonsils; in other 
cases pressure on the Eustachian tubes causes permanent deafness. 
The enlarged and elongated uvula may irritate the entrance to the 
glottis, and so excite habitual spasmodic cough. 
Treatment.—General and local blood-letting are recommended 
in acute parenchymatous angina. The former, which JBouillaud em- 
ployed as “ coup sur coup,” is never required by the disease 
itself, and but rarely by its complications. Leeches, applied to the 
neck, give little ease, and even scarification of the tonsils has not done 
as much good as was expected of it. 
If called the first or second day of the disease, we may employ the 
treatment advised by 'Velpeau ’ that is, apply powdered alum to the 
inflamed part two or three times daily, and advise the patient to rinse 
his mouth frequently with a solution of alum ( 3 iij— 3 ss to 3 vj of 
barley-water). Instead of alum, solid nitrate of silver has been recom- 
mended to cut short the disease. 456 
AFFECTIONS OF THE PHARYNX. 
If called in later, or if the Velpeau treatment has been unsuccess- 
ful, the energetic use of cold is a rational treatment, whose benefit is 
proved by experience. We let the patient take ice and cold water in 
the mouth, and cover the throat with cold compresses, which must be 
frequently renewed. 
If fluctuation occurs, we should apply warm poultices to the throat, 
wash out the mouth frequently with camomile-tea, and open the 
abscess early with the finger nail, or with a bistoury, covered to near 
the point with adhesive plaster. 
Emetics are not indicated by the disease, and should only be used 
where the abscess cannot be opened any other way. Laxatives are 
more advisable, especially where there are marked symptoms of cere- 
bral hyperamiia. 
Purgatives, mustard-plasters, foot-baths, as well as some remedies 
called specifics (tincture of pimpinella, borax, guaiac), have no effect on 
the disease. 
In chronic parenchymatous angina, internal remedies are of no 
avail. As long as the swelling of the tonsils depends on their infiltra- 
tion, we may paint solutions of alum, nitrate of silver, or dilute tinc- 
ture of iodine on them, and apply cold compresses to the throat. Any 
remaining hypertrophy of the tonsils can only be removed by oper- 
ation. 
CHAPTER Y. 
SYPHILITIC AFFECTIONS OF THE FIIARYNX. 
Etiology.—The disturbances of nutrition in the pharyngeal tissue, 
caused by syphilis, occasionally consist only in liypercemia, swelling, 
succulence, and perverted secretion of the mucous membrane, that is, 
in the characteristic symptoms of catarrh. In other cases, as a result 
of infection with syphilitic poison, we find the mucous papules, de- 
scribed when speaking of syphilitic affections of the mouth, which 
afterward become superficial ulcers or condylomata. Lastly we have, 
in the fauces and pharynx, gummy tumors, nodular tumors, and, by 
the breaking down of these, deep and often extensive loss of sub- 
stance. 
As syphilitic catarrh of the pharynx and syphilitic mucous papules 
come soon after the infection, they are classed among the secondary 
symptoms, while the gummy tumors, which do not appear till late, are 
classed among the tertiary symptoms. 
Anatomical Appeaeances.—Syphilitic catarrh of the pharynx 
particularly affects the soft palate and tonsils. The generally sharp SYPHILITIC AFFECTIONS OF THE PHARYNX. 
457 
boundary of the redness, at the line where the soft palate becomes the 
hard, is as little characteristic of this disease as is a bluish-red (copper) 
color of the mucous membrane; we find both of these appearances in 
non-syphilitic cases of catarrhal angina. 
Syphilitic mucous papules also come chiefly on the arches of the 
palate and the tonsils, which are sometimes extensively covered with 
them. In such cases, if the epithelial covering be milky, on superficial 
observation it looks as if the mucous membrane were covered with a 
croup membrane, and, if the white coating be present only in the space 
between the half arches of the palate, it seems as if there were an 
ulcer covered with a fatty base. The ulcers caused by the breaking 
down of syphilitic papules present losses of substance, reddened or 
covered with gray detritus, and bleeding easily, which gradually 
spread, by the breaking down of more recent papules that come 
around the edges, but show no tendency to become deeper. Condylo- 
mata form, small pedunculated excrescences, particularly on the uvula. 
Gummy tumors occur in all parts of the pharynx. If they develop 
on the tonsils, these at first appear decidedly swollen, with smooth red 
surfaces. The breaking down of the nodules causes deep ulcers, of the 
size of a pea or a bean, with fatty floors. Not unfrequently gummy 
tumors form on the posterior wall of the velum, and then sometimes 
cause perforation before they are recognized. Gummy nodules, and 
the ulcers caused by their breaking down, occur most frequently on 
the uvula and the parts of the soft palate bordering it. At first the 
uvula looks as if gnawed, later it only hangs by a small pedicle, finally 
it and a large part of the soft palate may be destroyed. Under prop- 
er treatment, gummy tumors may be resolved. In such cases there 
is proliferation of connective tissue at the former seat of the nodule; 
this subsequently shrinks, and there is a cicatricial contraction. If ex- 
tensive ulcers heal, there remain radiated, firm, white cicatrices—occa- 
sionally also adhesions of the soft palate to neighboring parts, con- 
strictions and distortions of the pharynx, or closure of the Eustachian 
tube. 
Symptoms and Course.—Syphilitic catarrh of the pharynx can- 
not at first be distinguished from other pharyngeal catarrhs; diagnosis 
is only possible later in the disease. If a patient has had difficulty of 
swallowing for weeks, if this difficulty has come on gradually, not sud- 
denly, and if it obstinately resists all treatment, we may strongly 
suspect that the existing catarrh is of syphilitic nature. If these 
difficulties are found in a person who had a chancre a few weeks pre- 
viously, and if they improve rapidly under the use of mercurials, the 
diagnosis may be considered as certain. 
Syphilitic mucous papules often develop without pain or other 458 
AFFECTIONS OF TIIE PHARYNX. 
inconvenience. Sometimes we find them accidentally, when examining 
the throat of a patient who has other symptoms of syphilis. If they 
have changed to ulcers, they cause pain in swallowing. The objective 
symptoms are given above. 
Gummy tumors do not cause pain or difficulty of swallowing till 
they have softened and ulcerated. When patients that we suspect of 
syphilis complain of difficulty in swallowing, we should never neglect 
to examine the posterior surface of the velum with the finger or the 
rhinoscope, when inspecting the throat. Occasionally our attention is 
called to ulcerated nodules at the above locality, by a circumscribed 
dark-red spot on the anterior surface of the velum. The acts of swal- 
lowing and speaking are impaired, as before described, by perforation 
of the velum; tliis impairment is the greater the farther forward the 
perforation has occurred. In eating and drinking, solids and fluids 
return into the nose ; and as soon as the patient speaks, we hear the 
nasal twang to his voice. For the objective symptoms, we may refer 
to the last paragraph. 
Treatment.—Syphilitic affections of the throat must be treated 
according to the rules to be hereafter laid down when speaking of 
syphilis. In recent cases, the favorable action of mercurials is very 
striking. When there is danger in delay, I often employ IVeinholcVs 
treatment (which is of late very unpopular), with the modification that, 
for several evenings in succession, I give ten to twenty grains of calo- 
mel, until the ulceration is arrested, which is usually by the third or 
fourth day. 
CHAPTER VI. 
retropharyngeal abscess. 
Etiology.—Inflammations terminating in suppuration are oc- 
casionally seen, especially among children, in the connective tissue 
between the spinal column and the pharynx. This affection is usually 
caused by caries of the spine, or a “ scrofulous ” inflammation and 
suppuration of the lymphatic glands at the back of the pharynx ; at 
other times it develops with secondary inflammation of other organs, 
late in typhus, measles, the septicaemias, and other infectious diseases; 
lastly, it appears to occur occasionally as an idiopathic inflammation. 
Anatomical Appearances.—The posterior wall of the pharynx 
is often pressed forward by the collection of pus, and the pharynx con- 
tracted or entirely closed; the pus may subsequently perforate the 
wall of the pharynx, or even sink into the breast, and there perforate 
,he oesophagus, trachea, or pleura. 
Symptoms and Course.—When disease of the cervical vertebral ANGINA LUDOVICI. 
459 
accompanies retropharyngeal abscess, the affection is preceded for a 
time by peculiar stiffness of the neck and other symptoms of the verte- 
bral disease; in this case we cannot easily make a mistake, for, as soon 
as there is difficulty of swallowing, the inside of the throat will be 
carefully examined. It is otherwise, especially in small children, when 
the affection begins without these preliminary symptoms. The rest- 
lessness of the child, its refusal to take the breast, its anxiety when 
compelled to drink, and the attacks of coughing and choking which 
interrupt the drinking, are occasionally referred to some primary affec- 
tion of the larynx, as croup, laryngismus, etc. This is particularly 
liable to be the case when, besides the above symptoms, there is con- 
tinued dyspnoea, the child is hoarse or voiceless, and the cough has 
a croupy sound. With the above symptoms it would be unpardon- 
able not to examine the pharynx carefully; this examination quickly 
certifies the diagnosis: the finger usually encounters, close behind the 
soft palate, a tense, elastic tumor, which usually fluctuates distinctly 
and cannot be readily mistaken. Sometimes the abscess breaks spon- 
taneously into the pharynx, its contents being swallowed or vomited 
up, and there is immediate relief of the symptoms. More frequently, 
if aid be not given at the proper time, the patient dies. There may 
be complete closure of the glottis by the swelling or the occurrence of 
oedema glottidis, or the opening of the abscess during sleep, and the 
entrance of its contents into the larynx, may choke the patient. In 
other cases the abscess sinks into the breast and causes pleuritis, pneu- 
monia, pericarditis, etc. 
Treatment.—The abscess is to be opened as early as possible. 
My old preceptor, Peter Kruckenberg, of Halle, said, in his hu- 
morous way, which* always had a substratum of earnest, that every 
physician should allow one of his finger-nails to grow long, and sharpen 
it like a lancet, so that it would be always ready to open immediately 
any retropharyngeal abscess that he might run against. Probably 
none of his pupils ever followed this advice of “ old Peter,” but doubt- 
less some of them have to thank him for the symptoms of retropharyn- 
geal abscess always remaining fresh in their minds, and that no cases 
of it have escaped them. 
CHAPTER VII. 
ANGINA LUDOVICI. 
The floor of the mouth and the intermuscular and subcutaneous 
connective tissue of the submaxillary region are occasionally the seat 
of a phlegmonous inflammation, which may readily lead to diffuse 460 
AFFECTIONS OF ME PHARYNX. 
gangrene and sloughing, but in other cases ends in formation of abscess 
or not unfrequently in resolution. This disease (which is often improp- 
erly called “ gangrenous ” inflammation of the neck, and which we 
name Angina Ludovici, after the deceased Ludwig, of Stuttgard, who 
first fully described it) is said by reliable observers to occur as a pri- 
mary and idiopathic disease, and sometimes to be epidemic. In the 
few cases that I have observed, the inflammation of the connective 
tissue undoubtedly proceeded from periostitis of the lower jaw. Last- 
ly, there is a form of the disease which comes with symptomatic or 
metastatic parotitis occurring in typhus and other infectious diseases; 
this probably starts from the submaxillary glands. 
The disease begins with a more or less painful, very hard swelling 
in the vicinity of one or other submaxillary gland. We may feel this 
swelling from the mouth, as well as from the outside; the skin cover- 
ing it is of normal color. The swelling soon extends over the entire 
submaxillary region, and upward toward the parotid; sometimes also 
downward, toward the larynx and trachea. The floor of the mouth is 
pressed far upward. Chewing and speaking become very difficult; the 
movements of the tongue are almost arrested, and the patient cannot 
open the mouth, because the muscles by which this is done are partly 
embedded in the infiltrated cellular tissue, and partly participate in the 
inflammation. The affection is usually accompanied by moderate fever 
and slight general disturbance; at other times the fe.ver is high, and 
there is great constitutional sympathy. 
Even in favorable cases, when resolution has occurred, the hardness 
disappears very slowly. When an abscess forms, the skin becomes red 
at some points, and fluctuation occurs; finally the pus breaks through 
the thinned covering. Quite as often the abscess opens into the mouth. 
When it terminates in gangrene, and there is perforation, instead of 
healthy pus, we have a fetid, discolored fluid, containing shreds of 
tissue. Death may result, at the height of the disease, from oedema 
glottidis and suffocation; at the termination, in gangrene from septi- 
caemia ; in the metastatic forms death usually results from the original 
disease. 
At the commencement of the affection we attempt to secure reso- 
lution by the application of a large number of leeches near the tumor. 
Later we should continuously apply warm cataplasms. As soon as 
there is fluctuation we evacuate the matter through a large incision. 
Where there is danger of suffocation, we should scarify freely, and, if 
this does not answer, we should proceed to tracheotomy. If a hard, 
indolent swelling of the maxillary region remain for a long while, I 
find that repeated blisters do more good than rubbing in iodine or 
mercurial salves, or painting on tincture of iodine or LugoTs solution. SECTION III. 
AFFECTIONS OF THE (ESOPHAGUS. 
CHAPTER I. 
INFLAMMATION OF THE (ESOPHAGUS—(ESOPHAGITIS—DYSPHAGIA 
INFLAMMATOEIA. 
Etiology.—Catarrhal, croupous (diphtheritic), and pustular inflam- 
mations may affect the mucous membrane of the oesophagus, which 
may also be the seat of ulcers, or even mortify from the action of strong 
chemical agents; lastly, there are inflammations and suppurations of 
the submucous tissue. 
Catarrhal inflammation is most frequently caused by the action of 
local irritants, such as acrid or too hot food, awkwardly-introduced 
oesophageal sounds; in other cases, the catarrh extends from the 
stomach or pharynx to the oesophagus; in still others, it may depend 
on venous congestion, which, in diseases of the heart and lungs, often 
exists throughout the whole intestinal canal. 
Croupous inflammation of the oesophagus is rarely seen, and, when 
it does occur, it is almost always in company with similar inflamma- 
tions of the larynx and pharynx, or in protracted typhus, cholera, and 
the acute exanthemata. 
Pustular inflammation comes in some rare cases of variola, or after 
the use of tartar emetic. 
Ulcers of the oesophagus are mostly caused by pointed bodies, 
which penetrate the mucous membrane, or by angular bodies that have 
become lodged at some spot in the oesophagus; more rarely, -it comes 
from corrosion of the mucous membrane, or in the course of chronic 
catarrh. The same causes may excite inflammations and suppurations 
of the submucous tissue. 
Lastly, the mucous membrane is sometimes burned by corrosive 
substances, particularly by concentrated acids. 
Anatomical Appearances.—Acute catarrhal inflammation of the 462 
AFFECTIONS OF THE (ESOPHAGUS. 
oesophagus is rarely found on post-mortem examination; when it is 
seen, the mucous membrane appears very red, swollen, readily torn, 
and is covered with a mucous secretion. In chronic catarrh, the mu- 
cous membrane, particularly that of the lower third of the oesophagus, 
appears thickened, dirty brown, or slate-gray, and is covered with 
tough mucus. Chronic catarrh may cause dilatation of the oesophagus 
by relaxation of its muscles, or stricture, by partial hypertrophy of the 
muscles and submucous tissue (see Chapter III.). 
In croupous inflammation of the oesophagus we find the mucous 
membrane dark red, and covered with thick layers of exudation, in 
spots, or spread out widely. 
In pustular inflammation slight elevations form, fill with pus, burst, 
and leave a superficial loss of substance; when caused by tartar emetic, 
the disease is limited to the lower third of the oesophagus. 
Ulcers of the oesophagus are mostly superficial excoriations, but 
they may also destroy the entire thickness of the mucous membrane, 
and attack the muscles and surrounding connective tissue. When 
chronic, inflammation of the submucous tissue may lead to thickening 
of the walls of the oesophagus and stricture; when acute, it may ter- 
minate in abscess. 
In inflammation of the oesophagus from corrosive substances, the 
parts affected are changed to a discolored, brown, or black slough, in 
whose vicinity injection and extensive serous exudation are quickly de- 
veloped. The sloughs become detached, the loss of substance may be 
filled up; if the destruction was extensive, stricture of the oesophagus 
always remains as a result of the contraction of the cicatricial tissue. 
Symptoms and Course.—In swallowing a hot mouthful, we may 
notice how little sensibility the oesophagus has, particularly at the 
lower portion. Hence we only have pain in very severe inflammations 
of the oesophagus, when caused by burns, injuries from pointed or 
angular bodies, but particularly after corrosion from caustic substances. 
This pain is felt deep in the breast, and at the back, between the 
shoulder-blades. In these cases we also find difficulty of swallowing; 
for, as soon as the muscles of the oesophagus are inflamed or infiltrated 
with serum, they cannot pass the morsel downward. This condition, 
which was formerly described as dysphagia infiammatoria, is always 
accompanied by oppression and great anxiety. The higher up the 
morsel is arrested, the more distinctly the patient feels it. If he makes 
new attempts to swallow, the contractions of the oesophagus may 
drive upward its contents, which cannot pass downward, so that there 
will be a regurgitation of the partly-swallowed substance, bloody 
mucus, and masses of exudation (see Chapter II.). These symptoms 
are always accompanied by excessive thirst, and, where the inflamma- STRICTUEES OF THE (ESOPHAGUS. 
463 
tion is extensive, there may also be fever. When the disease runs a 
favorable course, the symptoms disappear gradually; after the perfora- 
tion of a submucous abscess, they may pass away suddenly; in other 
cases stricture remains; occasionally, even death is caused by perfora- 
tion or rupture of the oesophagus (see Chapter V.). 
During life, the slighter cases of acute and chronic catarrh do not 
have any recognizable symptoms. The same is true of pustular in- 
flammation. The croupous form also is usually overlooked, unless 
pseudomembranes are vomited up; if it accompanies croup of the 
larynx and fauces, the dyspnoea and other symptoms of these affec- 
tions throw into the background the pain and difficulty of swallowing; 
when it comes as a secondary croup in typhus and similar diseases, 
the patients usually lie in a perfectly apathetic state, so that they 
utter no complaints. 
Chronic ulcers occasionally cause pain at some circumscribed spot, 
and permanently interfere with swallowing ; they can only be distin- 
guished from strictures by introducing an oesophageal bougie, which, 
in case of ulcers, finds no obstruction, and often brings up mucous, 
bloody masses. As the ulcers cicatrize, the symptoms of stricture 
may occur. 
Treatment.—The question of treatment can only arise in the 
more severe forms of oesophagitis, as the slighter cases are not recog- 
nized. Foreign bodies exciting the inflammation are to be removed 
according to the laws of surgery. In corrosion by mineral acids and 
caustic alkalies, antidotes can only be used in very recent cases. For 
the rest, in acute catarrh, we may limit ourselves to giving the patient 
ice-water to swallow, or let him take pieces of ice in the mouth. Gen- 
eral and local bleeding are only injurious ; the employment of medi- 
cines is difficult, and promises little benefit. If the patient can swal- 
low, he should take only fluids. If swallowing be totally impossible, 
the patient may be nourished through the stomach-tube, or by ene- 
mata. In chronic ulcers of the oesophagus, the numerous remedies 
recommended remain without effect, and careful nourishment of the 
patient is the chief object of treatment. 
CHAPTER II. 
STRICTURES OF THE CESOPHAGUS. 
Etiology.—Contractions of the oesophagus may be due—1, to com- 
pression ; 2, to the protrusion of new growths into its canal; 3, to 
structural changes of its walls. The latter form are strictures in the 
exact sense of the word; they result from the inflammations described 
in the last chapter. 464 
AFFECTIONS OF TIIE (ESOPHAGUS. 
Anatomical Appearances.—Compression of the oesophagus may 
arise in various ways. Among the most frequent causes we may men- 
tion : swelling of the thyroid bodies or of the lymphatic glands of the 
neck or mediastinum ; dislocation of the hyoid bone ; exostoses of the 
vertebrae; abscesses or tumors between the trachea and oesophagus ; 
carcinoma of the lungs or pleura; aneurism. Not unfrequently the 
diverticuli, to be described in the. next chapter, compress the section of 
the oesophagus immediately below them. In some cases where, during 
life, there were signs of compression of the oesophagus, on post-mortem 
examination, the right subclavian artery has been found morbidly di- 
lated, arising from behind the left subclavian, and running to the right 
between the oesophagus and trachea, or oesophagus and vertebrae. 
The difficulty of swallowing thus caused has been named dysphagia 
lusoria. 
In Chapter IV. we shall speak of the new formations on the inner, 
wall of the oesophagus, which are the most frequent causes of its con- 
traction. 
Strictures of the oesophagus, in the exact sense of the word, de 
pend—1, on cicatricial contractions of the membrane which have oc- 
curred after considerable losses of substance; they remain most fre- 
quently after corrosion or extensive ulceration ; 2, on hypertrophy of 
the muscular and intermuscular connective tissue, induced by chronic 
catarrh of the oesophagus. On a longitudinal section through the wall 
of the oesophagus, which, in such cases, is frequently much thickened, 
there is often a peculiar fan-like appearance, as the hypertrophied mus- 
cular filaments are grayish red, while the hypertrophied connective 
tissue between them presents white fibrous bands, and the mucous 
membrane is thickened and irregular. Lastly, strictures may be due 
to hypertrophy and subsequent cicatricial shrinkage of the submucous 
tissue. 
Sometimes the contraction is almost unnoticeable, at others so de- 
cided that the oesophagus is completely closed. The most frequent 
seat of stricture is the lower third, but it may occur in any part. 
Above the stricture, the walls are almost always hypertrophied, and 
the canal dilated; below it, the Avails are often thinned, and the canal 
collapsed. 
Symptoms and Course.—As strictures of the oesophagus from 
any cause develop gradually, the disease is at first apparently without 
danger, and does not cause much inconvenience. For a long time the 
sole symptom is a slight impediment in SAvalloAving large morsels, 
which is overcome Avhen the patient drinks or makes new efforts to 
swallow. Although the patients become more careful, and chew all 
their food very fine, they gradually find it more and more difficult to STRICTURES OF THE (ESOPHAGUS. 
465 
swallow. Even when the stricture is near the cardiac orifice of the 
stomach, they almost always indicate the region beneath the manu- 
brium stemi as the place where the food sticks; finally, they cannot 
even swallow liquids. 
The greater the obstacle, the less the patient succeeds in overcom- 
ing it by drinking, or by renewed attempts to swallow ; and the more 
frequently the food regurgitates. An antiperistaltic movement, in 
which the contraction of a lower segment of the oesophagus is followed 
by the contraction of the segment just above it, has not been physiologi- 
cally observed, it is true; on the contrary, the contractions which are 
voluntarily begun in the pharynx always go from above downward; 
but these facts do not exclude the possibility of a morsel of food, which 
cannot pass downward, being pressed upward by contractions which 
have proceeded peristaltically from above down to the point of stric- 
ture, or of a regurgitation in the same way, into the mouth, of the con- 
tents of the oesophagus, which has been filled up to a certain point. 
Occasionally there is no abdominal pressure in this form of vomiting; 
in other cases there is spasmodic contraction of the muscles of the ab- 
domen without any influence on the evacuation of the oesophagus. 
When the contraction has increased still further, after every attempt 
to eat or drink; often after a few mouthfuls, occasionally not till a 
good deal has been swallowed (Chapter III.), there is a feeling of 
pressure deep in the breast, accompanied with great unpleasantness 
and anxiety, which increases until, with intentional or instinctive at- 
tempts to swallow, the food is slowly evacuated from the mouth, little 
changed, but largely mixed with mucus. The introduction of a bougie 
affords the best diagnostic sign, as it shows not only the existence of 
the stricture, but also its grade, locality, and even its form. 
Besides the appearances described, and the other symptoms that a 
carcinoma or other tumor causes, the impaired nutrition induces grad- 
ual emaciation, and the belly sinks in; there may be no passage from the 
bowels for weeks, the patient starves, and, as Boerhaave aptly says, 
“ tandem post Tantali pcenas diu toleratas lento marasmo conta- 
bescunt.” 
Treatment.—The treatment of stricture of the oesophagus belongs 
to surgery. By skill, patience, and persistence, surprising results are 
sometimes attained. In the surgical clinic at Griefswald there was a 
patient who, without perceptible cause, had a stricture of the oesopha- 
gus ; at first only a common elastic catheter could be passed through 
it, but after four weeks it was so dilated that not only could the 
largest oesophageal sounds be passed, but ordinary morsels of food 
could be swallowed with ease. 466 
AFFECTIONS OF THE (ESOPHAGUS 
CHAPTER III. 
Etiology.—The dilatation of the oesophagus is sometimes total, af- 
fecting the entire organ, sometimes partial, limited to a short section. In 
partial dilatation sometimes only one wall is affected, then enlargements 
form which often develop to large sacs, communicating with the oesoph- 
agus ; they are called diverticuli; their walls are sometimes formed 
of the mucous membrane, which protrudes hernia-like between the mus- 
cular filaments, and of the external connective tissue layer. 
Besides the diverticuli, dilatations of the oesophagus are most fre- 
quently found:—1. Above a constricted portion; in stricture of the 
cardiac orifice there is total, when the stricture is higher up there is 
partial dilatation. 2. In other cases the total dilatation appears to de- 
pend on a chronic catarrh and on the muscular paralysis induced by it. 
3. In many cases the causes are unknown. Rokitansky's hypothesis, 
that concussions of the body, and Oppolzer's, that the treatment of 
gout with large quantities of warm water, may cause enormous dilata- 
tion of the whole oesophagus, appear to me very problematical. 
The diverticuli are formed—1. By foreign bodies which have stuck 
in the wTalls of the oesophagus, and are constantly driven farther in by 
the food which passes down. 2. They are sometimes formed by the 
shrinkage of bronchial glands, which have become adherent to the mu- 
cous membrane, while they were swollen, and which on contracting 
draw the mucous membrane after them. 3. In other cases we can dis- 
cover no cause. 
Anatomical Appearances.—In total dilatation of the oesopha- 
gus, the entire canal has been found dilated to the size of a man’s arm; 
the walls are usually hypertrophied, more rarely thinned. 
In partial dilatation, the portion immediately above the constriction 
is usually largest. The dilatation gradually decreases as we go up- 
ward, so that an elongated sac is formed, at whose fundus there is a 
second, narrow exit. 
Diverticuli usually form near the bifurcation of the trachea, or at 
the point where the pharynx becomes the oesophagus; they are at 
first roundish, but later they form cylindrical or conical appendages to 
the oesophagus, lying between it and the spine. Such diverticuli 
sometimes only communicate with the oesophagus by a narrow fissure; 
in other cases, they seem to be prolongations of the oesophagus itself, 
with a blind end, which the food enters, while alongside of it the 
lower part of the oesophagus lies empty, constricted, collapsed. 
Symptoms and Course.—Total dilatation exists without the 
DILATATION OP THE (ESOPHAGUS. MORBID GROWTHS IX THE (ESOPHAGUS. 
467 
presence of any symptoms by which the affection may be recognized. 
The partial dilatation that forms above a contracted part modifies 
the symptoms, so that the food remains in the oesophagus for a longer 
time and in greater quantities before regurgitating. When the food 
is finally vomited, it is softened, mixed with mucus, sometimes decom- 
posed, but it is undigested and almost always of alkaline reaction. 
This circumstance may be useful in deciding whether the food comes 
from the stomach or oesophagus. 
When the diverticuli are so large that food goes into them instead 
of into the stomach, they excite the same symptoms as stricture with 
partial dilatation. The food that has been swallowed sometimes re- 
gurgitates hours afterward, and may then be much decomposed, so 
that there will be a very bad smell from the mouth of the patient. 
Occasionally introducing the bougie renders the diagnosis certain, since 
we may at one time meet an insurmountable obstacle to its passage, 
while at another it may readily pass the diverticulum, and enter the 
stomach. If the diverticulum be at the commencement of the oesoph- 
agus, a soft tumor may be found in the neck behind the larynx, 
which increases in size after eating and drinking, and diminishes when 
the food and drink have been evacuated; if it be farther down, by 
pressure on the trachea and great vessels, it may cause dyspnoea, and 
disturbance of the circulation. In these cases, also, the patient may 
finally die of starvation. 
Treatment is of no use in dilatation of the oesophagus. If we can 
pass a stomach tube through the diverticulum into the stomach, we 
may attempt to feed the patient in this way for a while, with a very 
slight hope that, if the food no longer enter the diverticulum, it may 
decrease in size. 
CHAPTER IV. 
MORBID GROWTHS IN THE (ESOPHAGUS. 
Etiology.—Fibroid tumors are rarely, and tubercles almost never, 
seen in the oesophagus; but carcinomata occur quite often. They 
are usually primary, more rarely carcinomatous growths spread from 
the mediastinum to the oesophagus. 
The cause of cancerous degeneration of the oesophagus is just as 
unknown as that of cancer elsewhere. It has been claimed that brandy- 
drinkers are particularly liable to the disease. 
Anatomical Appearances.—The fibroid tumors form movable, 
bluish-white concretions of the size of a lentil or bean, in the submu- 
cous tissue, or they appear as pedunculated polypi, often lobulated at 468 
AFFECTIONS OF THE (ESOPHAGUS. 
tlie free end, which usually originate from the cricoid cartilage (HoJci- 
tansJcy). 
Of the carcinomatous growths, scirrhus and medullary cancer, and 
very rarely epithelioma, occur in the oesophagus. They generally 
affect the upper or lower third, more rarely the middle third; the whole 
circumference is usually comprised in the degeneration forming a can- 
cerous stricture. The degeneration always begins in the submucous 
tissue, but soon attacks the mucous membrane. If the cancer softens 
and disintegrates, uneven ulcers form, surrounded by a medullary in- 
filtrated wall, and covered with sanies, and bleeding fungous growths, 
or black ragged masses. From the external connective tissue mem- 
brane of the oesophagus, the cancer may extend to the neighboring 
structures, and, when breaking down, cause perforation of the ti’acliea, 
bronchi, or even of the aorta and pulmonary arteries. 
Symptoms and Course.—The small movable fibroids of the 
oesophagus cause no symptoms; pedunculated fibrous polypi cause 
the symptoms of stricture of the oesophagus, and may induce haemor- 
rhage ; the oesophageal sound may be passed around them, and, when 
they are high enough up, they may be reached with the finger. 
Cancer of the oesophagus is not easily mistaken. If, in a person 
of advanced age, particularly in one who has been in the habit of 
drinking strong liquor, difficulty of swallowing gradually occurs, with- 
out any other known cause, and increases slowly till it produces the 
very painful symptoms described in the second chapter, we may very 
strongly suspect carcinoma, for we know that this is by far the most 
frequent cause of stricture of the oesophagus, and that all other forms 
are proportionately very rare. The presumption that the disease is 
cancerous increases in probability when there are lancinating pains at 
various places, particularly between the shoulder-blades, when the 
patient emaciates rapidly, and the dirty-yellow, cachectic appearance 
of the face, common to cancer-patients, occurs. The diagnosis be- 
comes absolutely certain when we find fragments of cancer in the mu- 
cous, sanious, or bloody masses, that are vomited or brought up with 
the oesophageal sound. Subsequently, when the cancer sloughs, the 
symptoms of stricture subside; nevertheless, the emaciation continues, 
the feet swell, coagula often form in the femoral veins, and, finally, 
the patient dies from exhaustion, or from perforation of one of the 
above-named organs. 
Treatment.—Dilatation of the cancerous stricture by bougies is 
dangerous, and should never be tried when the diagnosis is certain. 
In the earlier stages it may hasten the sloughing of the cancer, and 
later it may cause perforation of the oesophagus. The treatment must 
be symptomatic. If there is great pain, we may give opium; when PERFORATION AND RUPTURE OF THE (ESOPHAGUS. 
469 
there is inability to swallow, we may make the almost hopeless at- 
tempt to nourish the patient by enemata. 
CHAPTER Y. 
PERFORATION AND RUPTURE OF THE OESOPHAGUS. 
Perforation of the oesophagus may take place from within out- 
ward, or the reverse. The first form most frequently results from the 
breaking down of cancer, more rarely from ulcers caused by splinters of 
bone, or from deep sloughs, excited by corrosion with caustic sub- 
stances. So-called perforating ulcers, such as are found in the 
stomach and duodenum, are never seen in the oesophagus. The 
oesophagus may be perforated from without inward by aneurisms of 
the aorta, by the breaking down of tuberculous bronchial glands, espe- 
cially of those located at the bifurcation of the trachea, by abscesses on 
the anterior surface of the spine, by caries of the vertebrae, even by 
tuberculous cavities in the lungs, etc. 
Rupture of the oesophagus without precedent disease has only been 
observed in a very few cases (.Boerhaave, Oppolzer). It more fre- 
quently happens that the wall of the oesophagus, which has been 
almost destroyed by carcinoma, corrosion, or ulcers, and nearly per- 
forated, is suddenly ruptured by severe retching and vomiting. 
If the wall of the oesophagus is opened in any way, its contents pass 
into the surrounding connective tissue, or communication is opened with 
the trachea, pleural or pericardial sacs, or with the great vessels. 
Before perforation or rupture of the oesophagus occurs, the advan- 
cing destruction may cause adhesive inflammation of the adjacent or- 
gans, the symptoms of which precede the perforation. I have seen 
double pleurisy and pericarditis gradually develop in a man with car- 
cinoma of the oesophagus; on post-mortem examination I found the 
parts of the pleura and pericardium lying next the cancer discolored 
and mortified, but no escape of the contents of the oesophagus into 
those cavities. Sudden, severe pain, deep in the breast, usually indi- 
cates the moment of perforation ; besides this there are chill, paleness, 
and coolness of the extremities, fainting, and sometimes, depending on 
the seat of the perforation, attacks of suffocation, or symptoms of se- 
vere pleurisy, or profuse vomiting of blood. Death sometimes occurs 
jnmediately. There can be no treatment. 470 
AFFECTIONS OF THE (ESOFUAGUS. 
CHAPTER VI. 
NERVOUS AFFECTIONS OF THE (ESOPHAGUS. 
Globus hystericus, or the feeling of a ball rising to a certain point 
in the oesophagus and remaining there, has been called hyperwsthesia, 
i. e., increased excitability of the sensory nerves, of the oesophagus. 
We have already mentioned globus hystericus when speaking of the 
nervous affections of the larynx. Some cases that are described as 
spasm of the oesophagus should also be reckoned among the liyperaes- 
thesiae; such as those where the patient feels as if the oesophagus 
were ligated, and thinks he cannot swallow. This state not unfre- 
quently occurs in persons that have been bitten by dogs. Andral re- 
lates a case where Boyer was obliged to stay with a patient at meal- 
times for a whole month, because she thought she would suffocate as 
soon as she attempted to swallow. 
There can hardly be anesthesia, that is, diminished or lost excita- 
bility of the sensory nerves of the oesophagus, because the normal sen- 
sitiveness is so very slight. 
IlyperJchiesis, increased excitability of the motor nerves, oesopha- 
gismus, or dysphagia spastica, occurs more frequently, although, doubt- 
less, many cases, classed under this head, have been misinterpreted. 
Spasm of the oesophagus is most frequently of reflex origin; it is often 
excited by irritation of the uterus, hence is most frequently met in 
hysterical women; occasionally it is of central origin and forms one 
symptom of disease of the brain or upper part of the spinal marrow; 
it may also be induced by poisoning with narcotic substances or alco- 
hol. Like most neuroses, spasm of the oesophagus runs its course 
with paroxysms and free intervals. The attacks most frequently occur 
during eating; the patient suddenly becomes unable to swallow, and 
feels as if there were a foreign body in the oesophagus. If the spasm 
be at the upper end of the organ, the food returns as soon as intro- 
duced ; if at the lower end, it does not regurgitate for a short time. 
There are, usually, at the same time, attacks of oppression and suffo- 
cation, and sometimes spasmodic contractions of the muscles of the 
neck. After lasting for a while, the attack usually passes off; in other 
cases, a slight amount of spasm remains for weeks or months as a per- 
manent affection, called “ spastic stricture.” During the interval, if 
we examine with the bougie, we find no obstacle; if we examine dur- 
ing the attack, the stricture occasionally disappears during the probing. 
Besides a proper treatment of the original disease, it is advisable to 
use narcotics, particularly belladonna, or the so-called antispasmodics. NERVOUS AFFECTIONS OF THE (ESOPHAGUS. 
471 
such as valerian, asafcetida, musk, etc. If the patient cannot swallow, 
these remedies should be used by enema. Repeated careful introduc- 
tion of the oesophageal bougie promises the best results. 
Akinesis, diminished excitability of the motor nerves of the oesoph- 
agus, is not unfrequently seen along with the signs of general paral- 
ysis shortly before death. In other cases, the paralysis is of central 
origin, and accompanies diseases of the brain, or of the cervical por- 
tion of the spinal marrow. In complete paralysis of the oesophagus, 
swallowing is impossible; often, when the bystanders wish to refresh 
the dying patient, they are horrified that he cannot swallow, and be- 
cause the food or drink they offer returns out of the mouth, or passes 
into the larynx, and excites attacks of suffocation. When the paraly- 
sis is incomplete, food does not return, btit large morsels and firm sub- 
stances are most easily swallowed. Swallowing is facilitated by the 
upright position and by drinking. In this dysphagia the patient does 
not usually complain of pain, and the probe meets no obstacle. Treat- 
ment is almost always hopeless, on account of the severity of the origi- 
nal disease. The repeated use of the probe, the employment of strych- 
nia and electricity, have been recommended, and it has been claimed 
that they have sometimes proved serviceable. SECTION IV. 
DISEASES OF TIIE STOMACH. 
CHAPTER I. 
ACUTE CATARRHAL INFLAMMATION OF TIIE MUCOUS MEMBRANE OF 
THE STOMACH—ACUTE GASTRIC CATARRH. 
Etiology.—During normal digestion changes occur in the gastric 
mucous membrane, which, if found in other mucous membranes, would 
be called catarrh. The secretion of the gastric juice is always accom- 
panied by considerable hypercemia of the mucous membrane, which is 
regularly followed by an abundant flow of mucus, and a considerable 
detachment of epithelium. This physiological process, like the analo- 
gous pathological one, is accompanied by a slight general disturbance, 
the so-called digestive fever. Hence, the definition, that we have given 
for catarrh of mucous membranes generally, does not answer for gas- 
tric catarrh; what in them is pathological is here normal, and we can 
only speak of gastric catarrh when the physiological process increases 
beyond normal bounds. It will be readily understood that, as the act 
of digestion is repeated several times during the day, and our food is 
complicated and sometimes of improper character, the process may 
readily become abnormal; hence, as may easily be conceived, acute 
gastric catarrh is one of the most frequent of diseases. On the other 
hand, it is just as evident that a morbid augmentation of normal pro- 
cesses may subside more readily and quickly than other more material 
deviations from the normal state. Hence, under favorable circum- 
stances, gastric catarrh usually lasts a shorter time than that of other 
mucous membranes. 
The indisposition to this affection varies with the individual; in 
some persons it is induced by exciting causes, which would have no 
effect on others. In many cases increased predisposition to gastric 
catarrh depends on too scanty a secretion of gastric juice, as this favors 
abnormal decomposition in the stomach, which is the most frequent ACUTE GASTRIC CATARRH. 
473 
cause ot the disease. On this diminution of the gastric juice depends 
the great inclination to gastric catarrh observed: 
1. In all fever patients. It is going too far to say that every fever 
is accompanied by catarrh of the stomach; neither the coated tongue 
nor the loss of appetite of fever patients justifies this view. But, as in 
every fever, in consequence of the increased temperature, the amount 
of water lost through the skin and lungs is excessively increased, it 
may be concluded a priori that less gastric juice will be secreted; 
this supposition is confirmed not only by the analogous condition of 
other secretions, but. by actual observations [Beaumont). (It is possi- 
ble that in fever the composition of the gastric juice is also changed; 
but this hypothesis is not necessary to explain the results of slight 
errors of diet on the part of the fever patients.) If the patients do 
not bear this in mind, and adapt their diet to the diminished secretion 
of the stomach, very distressing gastric catarrh will result. A large 
portion of the gastric complications in pneumonia and other inflam- 
matory affections result from neglect of this simple dietetic rule. 
2. The increased predisposition to acute gastric catarrh, which we 
see in debilitated and badly-nourished persons, appears also to depend 
on diminished quantity or inferior quality of gastric juice, which favors 
the decomposition of the ingesta. If the amount of blood be decreased, 
it is probable that the quantity of gastric juice as well as of the other 
secretions is diminished. As, in hydrasmia, there is a diminution of the 
albuminates of the blood, which we must regard as the material of 
which pepsin, the organic constituent of the gastric juice, is formed, 
the supposition is warranted that a juice, deficient in pepsin, is formed 
in such cases. From the diminished action of the gastric juice, part 
of the ingesta remain undissolved and decomposed; hence many con- 
valescents have gastric catarrh from eating what would not have 
harmed them at another time. In the same way puny children have 
this disease when they take the same amount of mother’s milk, or the 
same quantity of cow’s milk diluted to the same extent, as healthy 
children of the same age can take without harm. 
3. Although we have many analogous facts in other organs, it is 
not easy to explain the increased predisposition to gastric catarrh in 
persons who are very careful about their stomach, and carefully protect 
it from irritation. Catarrh of the stomach is more readily induced by 
a slight excess in drinking, in persons unaccustomed to the use of 
"liquor, than in those who take a moderate amount daily; and by a 
slight error of diet in children whose diet is usually carefully watched, 
than in those accustomed to complicated and indigestible food. 
4. Lastly, we find an increased predisposition to gastric catarrh in 
persons who have suffered from it repeatedly. 474 
DISEASES OF THE STOMACH. 
1. Among its exciting causes is the use of very large quantities 
of food, even of that which is very easily digested. We have already 
pointed out that in these cases acute gastric catarrh is not induced so 
much by the overfilling of the stomach as by the action of the products of 
decomposition, formed when the gastric juice does not suffice for the sub- 
stances to be digested. Hence, after overloading the stomach, the symp- 
toms of acute catarrh do not occur immediately, but come on next day. 
In grown-up and sensible people it does not often happen that 
they have simply eaten too much ; this is far more frequently seen in 
children, especially among such as have their diet very much restricted, 
and hence are never satisfied, but seize every opportunity to overload 
the stomach. Children at the breast hardly have any feeling of satiety; 
when nourishment is plenty, they usually drink till the stomach is 
overfilled. If they vomit easily, the overloading is soon removed, and 
only so much nourishment remains as they can readily digest; if they 
do not vomit easily, the stomach remains overfilled, and they are 
affected with gastric catarrh, although they have taken the most suit- 
able nourishment. Nurses know very well that children which vomit 
often and easily (“ spei-kinder ”) sicken less readily and thrive better 
than others. 
2. Gastric catarrh may be excited by moderate use of food difficult 
of digestion. In this case, also, it is not the food itself, but the prod- 
ucts of its decomposition, when partly undigested, that cause the dif- 
ficulty. The indigestibility of food often depends on its shape. Per- 
sons who eat with avidity, or who have no teeth, often introduce 
perfectly digestible food into their stomachs in a state which offers 
little surface to the gastric juice, which is consequently slowly absorbed 
and digestion is retarded. It is well known that the yolk of a hard- 
boiled egg is far more easily digested than the white; this is simply 
because the former is far more readily broken into fine morsels in the 
mouth than the latter is. The use of fat meat, or greasy sauces mixed 
with the meat, often causes gastric catarrh, not, as the laity suppose, 
because fat is indigestible, but because, when mixed with the meat, it 
hinders its imbibition and so diminishes its digestibility. It would 
lead us too far if we were to mention all the substances that are indi- 
gestible, and may cause gastric catarrh, even when used in moderate 
quantities. 
3. Gastric catarrh is often caused by the use of substances that 
have begun to decompose before entering the stomach. It may be 
thus caused in adults by spoiled meat, or by new beer; but it most 
frequently occurs in children from the use of milk that has begun to 
sour. This is what renders the artificial nourishment of infants so dif- 
ficult in hot weather, when milk begins to spoil very soon. If children ACUTE GASTRIC CATARRH. 
475 
do not have their mouths regularly cleaned, or if a sugar-teat be given 
them to prevent their crying, the decomposition of good fresh cow’s 
milk, or even of the mother’s milk, may be commenced in the mouth 
itself. (It is well known how carefully milk-cans must be cleansed and 
purified of all decomposing substances in order to prevent the milk 
from spoiling.) If decomposition has once begun in the milk in the 
stomach, the best milk taken subsequently will act as a poison, as it 
also soon begins to decompose. We shall hereafter see that ferment- 
ing substances in the stomach, after death, may destroy and dissolve 
its walls. Even if such an action on the walls of the stomach be pre- 
vented during life by the circulation and the rapid change of tissue in 
them, it is nevertheless not improbable that the epithelium, where nu- 
trition is less active, may be destroyed, even during life, by the fer- 
menting substance; and that the deprivation of the mucous membrane 
of its protection may cause extensive transudations. It appears not 
to be the lactic acid, the product of the souring of the milk, but the 
process of fermentation itself, which excites the symptoms of cholera 
infantum, and after death causes the softening of the stomach. We 
come to this conclusion because milk, which has already curdled, and 
whose sugar has been transformed into lactic acid, may be eaten 
even in large quantities by older children and by adults, without dele- 
terious influence; and because the so-called softening of the stom- 
ach may be more readily induced in that organ, when cut out of an 
animal, by filling it with fresh milk and exposing it to a moderate tem- 
perature, than by filling it with dilute acid. 
4. Acute catarrh of the stomach may also be caused by irritation, 
from taking into it very hot or cold articles, some medicines, alcohol, 
or spices. Alcohol acts most injuriously when it is but slightly diluted. 
Spices and similar substances, in small quantities, excite the normal 
processes, and hence may improve digestion; in larger quantities, 
however, they increase these processes beyond the normal limits, and 
lead to gastric catarrh. 
5. Acute gastric catarrh is excited by the introduction of sub- 
stances that weaken the digestive power of the gastric juice, or retard 
the movements of the stomach. It is evident that, in either case, there 
may be abnormal decomposition of the contents of the stomach. Apart 
from the direct irritation of the gastric mucous membrane, the misuse of 
alcoholic stimulants acts injuriously in this way. In the matter vomited 
the day after a debauch, much to the astonishment of the patient, he 
often finds some of the food eaten the previous day, which is hardly 
changed. The narcotics, particularly opium, seem to cause the gas- 
tric catarrh, which is so often seen after large doses of them, by impair- 
ing the movements of the stomach and thus preventing the food from 476 
DISEASES OF THE STOMACH. 
being sufficiently mixed with gastric juice, and keeping it too long in 
the organ. 
6. Catching cold also leads to gastric catarrh, though less fre- 
quently than to catarrh of the respiratory organs. 
7. Lastly, at certain times, without known cause, from a “ genius 
epidemicus gastricus,” gastric catarrh occurs surprisingly often; and 
at such times other affections are complicated with it, without there 
having been any error of diet. In this class belong the feverish, gas- 
tric, and intestinal catarrhs and cholera morbus, which are occasionally 
epidemic. 
When speaking of infectious diseases, we shall treat of those cases 
of gastric catarrh which, like other catarrhs, are symptomatic of an in- 
fection. 
Anatomical Appearances.—We seldom have the opportunity 
of seeing the remains of acute gastric catarrh on post-mortem examina- 
tion ; where we do, the gastric mucous membrane is found reddened in 
spots by a fine injection, its tissue is relaxed, and its surface covered 
with a layer of tough mucus. But more frequently, especially among 
children who die with the symptoms of cholera infantum, the autopsy 
gives negative results, except as to appearances that will be described 
hereafter. This does not appear strange, when we remember that the 
capillary hyperaemias of other mucous membranes, which we have 
been able to observe directly during life, leave no trace after death ; 
and that a relaxation and partial loss of epithelium, which we have re- 
garded as the most probable cause of the extensive transudation in 
cholera infantum, may be very readily overlooked in the dead body, 
and can very rarely be observed with certainty. Hence, the observa- 
tions that Beaumont made on his Canadian St. Martin, when he had 
catarrh of the stomach after overloading that organ with indigestible 
substances, or after the excessive use of liquor, are very important. 
At the commencement of the affection the gastric mucous membrane 
appeared intensely reddened, had aphthous (?) spots on it, and was 
covered with tough mucus, here and there mixed with traces of blood. 
Later, the mucous covering was thicker, and the secretion of gastric 
juice was suppressed. The fluid taken out through the fistula con- 
sisted mostly of mucus and muco-pus, which showed an alkaline reac- 
tion. In a few days the mucous secretion and the alkaline reaction 
of the contents of the stomach ceased; and, at the same time, the 
mucous membrane regained its normal appearance. 
The gastromalacia, or softening of the walls of the stomach, found 
on autopsy of children, was often diagnosticated during life, so that it 
appeared as if the diagnosis were confirmed by the post mortem. An 
exhaustive description of the symptoms of gastromalacia has also been ACUTE GASTRIC CATARRH. 
477 
given (Jaeger), and we often meet with cases answering the descrip- 
tion. Nevertheless, there can be no doubt (Elsciesser) that gastroma- 
lacia is always a post-mortem appearance. The description of soften- 
ing of the stomach is precisely that of cholera infantum, and thus there 
is a simple explanation of the apparent confirmation of the diagnosis 
by the autopsy. For, if a child dies who has had vomiting and 
purging from abnormal fermentation in the stomach, and if there are 
still fermenting substances left there, the fermentation will not be 
arrested by the gradual cooling of the body. "When the circulation 
ceases, the stomach can no longer resist the decomposition, which then 
extends to it also, just as the stomach, that has been cut out of an ani- 
mal and filled with milk, softens if left only for a short time in a warm 
place. Hence physicians, who consider softening of the stomach as a 
post-mortem appearance, may also predict it with certainty, when a 
child that has died of cholera infantum had eaten milk, or any other 
easily-decomposed substance, shortly before death. 
Rokitansky, who does not consider softening of the stomach as a 
post-mortem appearance in all cases, distinguishes two forms, the 
gelatinous and the black. According to his description, the former 
almost always begins at the fundus of the stomach, and gradually ex- 
tends along the greater curvature ; the mucous membrane is first soft- 
ened, but the softening soon extends to the muscular coat, and finally 
to the peritonaeum. The membranes altogether change to a grayish 
or yellowish-red translucent gelatin, which occasionally has some 
blackish-brown striae through it; these are the blood-vessels that are 
also softened. When the softened inner layer is detached, the fundus 
consists of a thin, easily-torn peritonaeum. The softened stomach tears 
on the slightest touch, and comes to pieces between the fingers, or 
else we find that rupture has already occurred, and the contents have 
escaped int6 the abdomen. The process is not always limited to the 
stomach, but may attack the neighboring organs, especially the dia- 
phragm ; this may even be perforated, and the contents of the stomach 
may pass into the left side of the thorax. In the black softening of 
the stomach, the walls are not changed to a translucent gelatin, but 
to a blackish brown or black pulp. This modification occurs if the cap- 
illaries of the stomach are overfilled when the softening begins. The 
blackish-brown stria? in the gelatinous softening represent the same 
changes of the large vessels and of the blood contained in them, which, 
m this case, affect the capillaries and their contents. 
The theory that gastromalacia does not occur till after death, or, at 
least, till a short time before it, when the circulation and the change 
of tissue in the walls of the stomach have almost ceased, is supported— 
1, by the fact that the softening is almost always found in the fundus 478 
DISEASES OF THE STOMACH. 
of the stomach, where the acid contents are collected together, and it 
only attacks the pyloric portion, when, from the position of the body 
on the right side, the contents have settled to that portion ; 2, by the 
circumstance that it is also found in the bodies of children who showed 
no signs of gastric disturbance during life, but who had taken milk, 
sugar-water, or other easily-fermenting substances, during the last 
hours of life; 3, because, even in cases where the walls of the stomach 
are found torn, and its contents have entered the abdominal cavity, 
there have been no symptoms of peritonitis during life, nor have any 
remains of it been found on autopsy; finally, 4, another proof is the 
above-mentioned experiments, where artificial softening was induced 
in stomachs that had been removed from animals. 
(The cases where softening of the stomach has been found, while 
that organ was empty, do not belong here. It has been attempted 
to explain this by citing the digestive power of the gastric juice, and 
asserting that there was a self-digestion of the stomach, and that the 
gastric juice secreted shortly before death had digested the stomach 
just as it -would digest any other membranous tissue. It is, however, 
improbable that gastric juice would be secreted into an empty stomach, 
and it is possible that a decomposition of mucus (which also sets free 
lactic acid) would have the same effect on the Avails of the stomach as 
fermenting ingesta do.) 
Symptoms and Course.—We shall first speak of the symptoms 
of acute gastric catarrh when it is accompanied by moderate fever, and 
often constitutes only an ephemeral affection. This form, the most 
frequent result of errors of diet, is usually called status gastricus, gas- 
tricismus, gastrosis, “ disordered stomach.” 
E\ren the physiological process of digestion is accompanied by a 
certain depression, sluggishness, and disinclination to bodily or mental 
exertion; and the hyperaemia and production of mucus, Avhen increased 
to acute catarrh, are accompanied by a general malaise and sick feel- 
ing that seem out of proportion to the slight and evanescent disease. 
The patients feel dull, are fretful, complain alternately of heat and 
cold; have a hot head, cold extremities, but particularly a pressing, 
tormenting pain in the forehead, Avhich extends toAvard the occiput; 
on stooping, they have flashes before their eyes, and feel as if their 
heads Avould burst. The affection of the mucous membrane of the 
stomach causes a feeling of pressure and fulness, even Avhen that organ 
is empty; the “ pit of the stomach ” is sensitive to pressure; there is 
loss of appetite, but increased thirst; there is usually distaste for food, 
and qualmishness. Besides these, there are symptoms caused by ab- 
normal decomposition of the contents of the stomach; gastric catarrh 
is often the result of abnormal decomposition of the ingesta, and, on ACUTE GASTRIC CATARRH. 
479 
the other hand, it is sometimes the cause. Bidder and Schmidt have 
shown that when the gastric juice is rendered alkaline by admixture 
of mucus, it loses its power of dissolving protein substances, which 
then undergo spontaneous decomposition, and give out a putrid odor. 
Daily experience in practice confirms this experiment. But those sub- 
stances also, that are not digested by the gastric juice, undergo abnor- 
mal decomposition in gastric catarrh. The amylaceous substances, 
whose change had already begun in the mouth from the admixture of 
saliva, under normal circumstances, are not converted into sugar until 
they enter the stomach. But, in gastric catarrh, the mucus secreted 
acts as a ferment, and induces a change of a large portion of the sugar 
into lactic acid, and often also into butyric acid. If, during gastric 
catarrh, fermented substances, such as beer or wine, be taken, or if ex- 
cessive use of these has induced the affection, acetic fermentation takes 
place ; if fatty substances be swallowed, fatty acids appear to be de- 
veloped from them. In all of these decompositions of the contents of 
the stomach, except the lactic acid fermentation, gases are set free. 
In the breaking up of albuminous substances, stinking, sulphuretted, 
hydrogen gases are freed; hydrogen and carbonic acid are formed 
in butyric-acid fermentation; in acetic fermentation, carbonic acid is 
freed. This explains why the epigastrium is slightly prominent in pa- 
tients with acute catarrh, and why, from time to time, they belch up 
gases which sometimes smell disagreeably, at others are odorless, ac- 
cording to the quality of the food that has been taken. At the same 
time, sour or rancid substances often rise into the mouth. 
Since gastric catarrh, as before mentioned, is usually complicated 
with oral catarrh, the tongue is generally coated, the taste stale and 
slimy, and there is a bad breath. 
If the patients fast, and do not expose themselves to any new 
sources of injury until the stomach is able to fulfil its normal functions, 
the above symptoms usually disappear quickly. The abnormally-de- 
composed contents of the stomach pass through the pylorus into the 
intestine; there further decomposition seems to be arrested sometimes 
by the admixture of bile, but more frequently, although moderated, it 
still continues; the secretion of the irritated intestinal mucous mem- 
brane increases, the movements of the intestines are hastened, flatu- 
lence, rumbling, etc., with griping pains in the belly, occur, and are 
relieved by the passage of badly-smelling gas; finally, one or more 
pulpy stools occur, and the trouble ends. If the patient sleeps the 
following night, his general health is usually improved, or fully restored. 
We may also mention that, during the affection, the urine usually con- 
tains quantities of pigment and urates, and that herpetic vesicles not 
unfrequently come on the lips. 480 
DISEASES OF THE STOMACH. 
When the injuries that excite the acute gastric catarrh are more 
intense, or the patient more sensitive, there is greater nausea, which 
finally increases to retching and vomiting. By the latter the contents 
of the stomach are evacuated, more or less changed, with a very acid 
smell and taste, and usually mixed with quantities of mucus. The 
vomiting may be repeated at varying intervals; the longer it lasts, the 
more the matter vomited is mixed with bile, which gives it a bitter 
taste and green color. These severe forms of the status gastricus are 
almost always accompanied by great irritation of the intestinal mucous 
membrane. Then there is severe diarrhoea, by which green masses are 
passed, with or without pain. After the vomiting and purging, the 
patient is almost always relieved, and, although perhaps a little feeble, 
is usually well otherwise in a couple of days. In other cases, the 
vomiting and diarrhoea are very bad, and present the symptoms of 
cholera morbus. 
By cholera morbus we mean that form of acute gastric catarrh 
which extends to the intestinal mucous membrane, and is characterized 
by profuse transudation of a fluid, containing little albumen, into the 
stomach and intestines. These watery transudations occur so fre- 
quently in the first stage of acute catarrhs of other mucous membrane, 
especially of the nasal, that we cannot hesitate to designate as a ca- 
tarrh the gastric and intestinal affection, on which depend the symp- 
toms of cholera morbus, and mostly, also, those of Asiatic cholera, 
which will be hereafter described, and which only leads to symptoms 
that other catarrhs do not have, on account of its extent. 
The disease prevails most during the hot weather of summer, and 
then often attacks a number of persons simultaneously; it is more 
rarely excited, at other times, by errors of diet. The cholera attacks 
are rarely preceded by premonitory symptoms; on the contrary, the 
patient is usually attacked suddenly, often during the night, with a 
disagreeable feeling of pressure at the pit of the stomach, which is 
soon followed by nausea and vomiting. At first the food last eaten is 
vomited, little changed, but the vomiting is soon repeated, and quan- 
tities of a pale-yellow or greenish bitter fluid are thrown up. After 
this, or, in some cases, even previously, there are borbyrigmi, followed 
by pulpy stools, -which soon become thin and liquid. In a short time 
enormous quantities of fluid are evacuated; the greater the amount, 
the less color it has, as the bile, even if of normal amount, no longer 
suffices to color all the transudation. The loss of water from the blood 
excites intense thirst, which is only temporarily quenched by large 
quantities of drink. The fluid taken into the stomach is rapidly evacu- 
ated, up-ward or downward, being voided every quarter of an hour, or 
oftener, as long as the diarrhoea and vomiting continue. The blood CHOLERA MORBUS. 
481 
constantly becomes thicker; the secretions, particularly that of urine, 
are diminished, or cease entirely, for want of fluid to maintain them; 
the interstitial liquid is absorbed from all the tissues; hence the skin 
appears dry and shrivelled, the patient looks collapsed and disfigured, 
the nose is pointed, the eyes are sunken, because the connective tissue 
in the orbit has become dry, and has hence actually lost in volume. 
While there is rarely pain in the abdomen, there are very painful con- 
tractions of the muscles, especially of the calf of the leg. If these 
occur, and the evacuations of the patient consist only of colorless fluid, 
containing shreds of intestinal epithelium, so that they resemble rice, 
water, or oat-meal gruel, the cholera morbus will very much resemble 
Asiatic cholera; nevertheless, it rarely goes on to the complete disap- 
pearance of the heart-beat and the pulse, to the cyanotic hue, and rep- 
tile temperature of the skin, which is seen in the so-called asphyxiated 
stage of the Asiatic cholera. No matter how threatening the symp- 
toms, how great the collapse and depression of the patient, how dis- 
pirited he and his attendants may appear, the physician must not feel 
discouraged if he is sure that epidemic cholera is not raging, for he 
must know that a previously healthy adult very seldom dies of cholera 
morbus. Usually, after a few hours, rarely not till the next day, the 
vomiting and purging subside; the skin becomes warm, and acquires 
its fulness again, the exhausted patient falls asleep, and only suffers 
from great depression. More rarely, the symptoms of gastric fever 
join on to the cholera morbus. In the rarest cases, and only in sickly 
and weak persons, or in children or old persons, do we see a fatal ter- 
mination ; then the bowels are paralyzed, the vomiting and purging 
cease, while the transudation continues; the pulse disappears, the move- 
ments of the heart become weaker, the intellect cloudy, and the patient 
dies of exhaustion. 
The acute gastric catarrh of children, during the first years of life, 
presents certain peculiarities, which are due to the fact of such children 
being almost exclusively nourished with mother’s or cow’s milk. Bed- 
nar considers the fermentation of the ingesta as the sole cause of this 
disturbance of digestion, and denies either a primary or secondary par- 
ticipation of the walls of the stomach in the affection; he designates 
the milder forms of the affection as dyspepsia / according to the classic 
description of this author, the appearance of the child is little changed, 
at most it only looks a little pale and has a slight ring around the 
eyes. Almost always, shortly after nursing, there is vomiting, and the 
milk evacuated is no longer curdled. This sort of vomiting is an im- 
portant symptom; even the nurses recognize it as such, and readily 
distinguish it from the healthy evacuations of an overfilled stomach. 
The curdling of the milk in the so-called “ puking of children ” does 482 
DISEASES OF THE STOMACH. 
not show that the milk has become sour, but that the gastric juice has 
acted normally on it, and curdled the casein; when the vomited milk 
is not curdled, it shows that there is an abnormal secretion in the stom- 
ach, and this must excite the suspicion of gastric catarrh. Soon after 
the vomiting, or even at the same time, the passages from the bowels 
become abnormal, or there may be no vomiting, and the appearance 
of the passages may form the sole symptom of gastric catarrh. The 
evacuations consist of a very acid, green or greenish-yellow fluid, con- 
taining more or less firm lumps; they remind us of the changes that 
the milk undergoes after standing for some time out of the body, and 
show that the gastric juice has not even digested it enough to cause 
its sudden coagulation. The vomiting and purging, which are usually 
preceded by restlessness of the child, by crying and drawing the legs 
up toward the belly, occur more or less frequently; the evacuations 
often change their color and consistence. In many cases, the vomiting 
ceases after a few days, the undigested milk disappears from the evac- 
uations, the children improve and pick up; but in other cases, from time 
to time, quantities of acid milk, partly unchanged, partly curdled and 
mixed with mucus, are vomited; the purging increases, the evacuations 
become thin, liquid, and very free; at first they are bright yellow or 
green, but at last almost white. Some yellow or greenish flocculi swim 
in the colorless fluid; these remain on the diaper, while the fluid partly 
filters through, partly leaves large, damp, discolored spots in it. Even 
now both the smell and reaction of the evacuations are acid. Occasion- 
ally the appearance of the dejections changes suddenly, without our 
being able to say why; they become dark brown or clayey, and softer 
masses of disagreeable smell are evacuated in large quantities. These 
severer forms of acute gastric and intestinal catarrh reduce the child rap- 
idly ; its face falls and is contracted with pain, it may even become wrin- 
kled in a few days, the eyes are usually half opened and deep set, the lips 
as well as the hands and feet are often bluish, the rest of the body, es- 
pecially the back, is mottled. The temperature is uneven, the trunk, 
especially the belly, is burning hot, while the face and limbs are cool. 
From the diminution of cerebral pressure the fontanelles become de- 
pressed, occasionally even the frontal and occipital bones sink slightly 
below the parietal bones, the movements of the children become sluggish, 
even nursing troubles them; they let go of the breast, but eagerly drink 
water when it is offered to them. The cries of pain which usually pre- 
cede the evacuations gradually change to weak whimpering; in the 
interval the child lies half asleep. As the exhaustion increases, many 
die; occasionally, shortly before death, convulsions (liydrocephaloid) 
and other symptoms of anaemia of the brain appear. When the disease 
runs a favorable course, the evacuations gradually become fewer and CHOLERA INFANTUM. 
483 
more normal, the collapse disappears, the temperature becomes more 
even, the child improves and convalesces, but a great tendency to re- 
lapse remains. 
If the symptoms above described appear very rapidly, and the evac- 
uations come one right after the other, if decided collapse occurs in a 
few hours, with great depression of the bodily temperature, and signs 
of thickening of the blood, before emaciation has resulted, we call it 
cholera infantum. The thickening of the blood is shown by the un- 
quenchable thirst; older children follow the glass of water with eager 
eyes, and when it is offered to them seize it with both hands and hold 
it tightly till it is emptied; it further betrays itself by the increasing 
cyanosis, and by a peculiar dyspnoea, in which the thorax and dia- 
phragm make extensive movements, without there being any apparent 
obstruction to the breathing, except the difficulty of the thickened 
blood passing through the capillaries of the lungs. The patients may 
die in a few hours of cholera infantum, with the above symptoms; 
in other cases, the cholera proper passes off, and a milder form of the 
disease remains; and finally, in other cases, rapid and complete re- 
covery take place from conditions which are apparently utterly hope- 
less. 
Diagnosis.—In Chapter X. of this section we shall speak of the 
distinction between gastric catarrhs, occurring as the status gastricus, 
and other disturbances of digestion. 
During an epidemic of Asiatic cholera it is impossible to distinguish 
cases of cholera morbus from those caused by the cholera miasm, for 
the symptoms are not only similar, but are absolutely the same as those 
of the milder cases of Asiatic cholera. The chief difference is, that of 
those attacked’with Asiatic cholera about half the patients die, while 
almost all recover from cholera morbus. The disease may much more 
readily be mistaken for poisoning; but cholera morbus is rarely accom- 
panied by sych severe pain as poisoning with acids and metallic salts 
induce, and they seldom cause such copious evacuations as characterize 
cholera morbus. If the disease lasts unusually long, or if its course 
shows any other peculiarity, we should carefully examine every circum- 
stance that could indicate the presence of poison. 
Acute gastric catarrh of children in the first years of life and 
the diarrhoea of children cannot easily be mistaken for other dis- 
eases. 
Prognosis.—The prognosis is evident from the description we have 
just given of the course. Previously healthy adults rarely die of this 
disease; but chronic catarrh may result from repeated attacks, weakly 
and decrepit persons may die of gastric fever, or still more readily of 
catarrhal fever (see this disease). In children, acute gastric catarrh, 484 
DISEASES OF THE STOMACH. 
with its results, is a very dangerous disease, which may end fatally 
even under the most careful treatment. 
Treatment.—To speak with only moderate exactness of acute 
gastric catarrh, would lead too far, as we should have to mention all the 
rules for diet. From the remarks on etiology, we may see that, in 
order to avoid gastric catarrh, the diet of some persons, as of fever 
patients and convalescents, but particularly of infants, must be carefully 
watched. In the latter case, where it is impossible to give the child 
the breast of the mother, or a healthy nurse, certain precautions must be 
exercised in the choice of cow’s milk; these were mentioned under etiolo- 
gy : 1. The milk must be fresh; even in the city it should be brought 
twice daily. If it shows the least indication of acidity, it should be 
boiled immediately, to prevent further transformation of the sugar into 
lactic acid; carbonates of the alkalies may also be advantageously 
added to such milk, till it becomes neutral or slightly alkaline [small 
quantities of sulphite of soda are very good for this purpose]. 2. Milk 
from cows fed on oil-cake or distillery swill should not be used. In 
large cities, the best milk is that from brewery cows which are fed 
on grains. 3. The milk should be sufficiently diluted, the first three 
months, with about two parts of water, the second quarter with one 
part. 4. It should be given at regular, and not too short, intervals. 
During the first weeks, the bottle may be given every two hours, later 
every three or four hours. The shorter the intervals, the less milk 
should be given at each time. 5. The vessels from which the child 
drinks, as well as its mouth, should be carefully cleansed. Neglect of 
any of these rules may lead to gastric catarrh, while their observance 
may prove, at least, some protection for the child, against the disease. 
The causal indications may require the administration of an emetic, 
where injurious or decomposing food in the stomach keeps up the ca- 
tarrh. Some carry the use of emetics in gastric catarrh too far, while 
others neglect them too much. If we accede to the request of the 
patient, or, from the feeling of pressure and fulness in the epigastrium, 
the coated tongue and the odor from the mouth, conclude that the stom- 
ach is coated also, and, in all such cases, give an emetic of ipecacu- 
anha or tartrate of antimony, we shall often protract the disease by 
letting a new injury act unnecessarily on the already diseased mucous 
membrane of the stomach. But just as much harm is done by the ex- 
cessive fear of the injurious effects of emetics, induced by their acting 
also as purgatives, and by the pustular inflammation of the stomach, 
occasionally caused by the continued use of tartrate of antimony, but 
particularly by a false theory of their action. It is forgotten that 
the irritation of the gastric mucous membrane by the emetic, as is 
proved by daily experience, is not very malignant or injurious, and that ACUTE GASTRIC CATARRH. 
485 
the beautiful experiments of Magendie and liudge have proved that 
the emetic influence of ipecac, and tartrate of antimony do not result 
from irritation of the gastric mucous membrane, but from absorption 
into the blood. By injecting tartar emetic into the veins, Magendie 
proved that vomiting could be excited even where a bladder had been 
substituted for the stomach. 
If the prominence of the epigastrium, percussion over the stomach, 
eructations of gases and fluids whose smell and taste are like those of 
the food that has been eaten, render it certain that there are decom- 
posing substances in the stomach, and if the sufferings of the patient 
justify such active treatment, it will be best to give a sure emetic, 
such as ipecacuanha 3 j with tartrate of antimony gr. j. In the para- 
graph on symptoms we have shown that, even in such cases, without 
the use of an emetic, the undigested and decomposed ingesta may be 
occasionally passed from the body quickly and uninjuriously; but this 
is not by any means an absolute rule. The injurious substances often 
remain a long while in the stomach, and when they pass into the intes- 
tines cause severe and lasting disturbance. If we can rid the stomach 
of the substance causing a continued irritation and protect the bowels 
from its action, we should not dread the temporary irritation of the 
gastric mucous membrane by the emetic. If, in such a case, we do 
nothing, or, instead of an emetic, prescribe the popular mixture of 
magnesia usta, we may just as readily cause a prolongation of the at- 
tack as if we gave an emetic at the wrong time, or without sufficient 
cause. Moderate fever, accompanying the gastric catarrh, does not 
contraindicate an emetic; but if the fever is more severe, and we have 
the faintest suspicion of a commencing typhus, it should not be used, 
for typhus almost always runs a severe course, when emetics or laxa- 
tives have been used at its commencement. 
The causal indications never require the use of laxatives in the 
treatment of simple acute gastric catarrh. It is different when the 
injurious ingesta have passed into the bowels and caused flatulence, 
colicky pains, escape of flatus, and other symptoms which are called 
the passage of the gastric turgescence downward. In such cases 
mild laxatives, such as rhubarb or compound infusion of senna, may be 
prescribed; if there is excess of acid, we may use a mixture of mag- 
nesia usta (| ss to f viij water, a tablespoonful every hour or two), 
which, in these cases, acts as a mild and efficient laxative; the purga- 
tive neutral salts are less suitable. 
If there be an excessive formation of acid in the stomach that 
seems to keep up the catarrh, whether it be caused by the transforma- 
tion of the amylacea into lactic or butyric acids, or if acetic fermenta- 
tion has been induced by the use of beer or wine, and if the very 486 
DISEASES OF TIIE STOMACH. 
moderate sufferings of the patient do not justify the use of an emetic, 
we should give a carbonate of one of the alkalies. The most used is 
the bicarbonate of soda, in doses of gr. v-x, in powder or solution; if 
we wish to employ it in the popular form of mineral water, we should 
first assure ourselves that the water furnished actually contains bicar- 
bonate of soda, and does not simply consist of carbonic acid and 
water. 
In spite of numerous evacuations upward and downward, small 
amounts of the decomposing substances not unfrequently remain in the 
stomach. The alkalies prescribed can neutralize the acids already 
formed, it is true, but they cannot entirely arrest the process of decom- 
position and the formation of new acid products. The substances re- 
maining in the stomach and undergoing decomposition transfer their 
chemical action to the fresh and unspoiled food, and render the most 
harmless food injurious and even dangerous for the gastric mucous 
membrane of children, in whom this state most frequently occurs. In 
such cases it is necessary to arrest the decomposition of the contents 
of the stomach remaining after the vomiting and purging. It is diffi- 
cult to fulfil this indication, and all the skill of the physician often fails 
in the attempt. If we recognize the abnormal decomposition of the 
contents of the stomach and intestines as the most frequent cause of 
infantile diarrhoea, we can at least understand the unfortunate results 
of its treatment, which we cannot do if we regard the gastric and in- 
testinal catarrh as(the sole disease. Even outside of the body, as is 
well known, it is often difficult to arrest a fermentation or other de- 
composition that has once begun. But the means that answer for this, 
outside of the body, cannot always be used in it. We cannot perfectly 
dry the contents of the stomach or keep them at so high or so low a 
temperature as to arrest decomposition; and certain substances that 
prevent fermentation are poisonous to the organism. But, if we regard 
the numerous remedies (often exactly opposite in their other qualities) 
which physicians employ in the diarrhasa and vomiting of children, with 
or without clear ideas of the reasons for so doing, and Avliich are some- 
times unmistakably serviceable, we find that they are such substances 
as are used outside of the organism for arresting fermentation and 
other decompositions. The remedies most frequently given in infantile 
diarrhoea are carbonates of the alkalies; mineral acids, particularly 
muriatic; metallic salts, especially calomel and nitrate of silver; also 
tannin, creasote, and nux vomica. Possibly part of these, such as the 
nitrate of silver and tannin, have, at the same time, a favorable effect 
on the irritated mucous membrane of the stomach and intestines, by 
their astringent action on the liypercemia. But the greater part of 
these remedies, especially the one most used, calomel, cannot be said ACUTE GASTRIC CATARMI. 
487 
to act in this way, and their effect is only to be explained by their 
power of arresting decomposition. If a child is suffering from a slight 
gastric catarrh, which only show’s itself by the characteristic vomiting 
and the presence of undigested milk in the acid dejections, besides strict 
diet (of which we will hereafter speak), we should use the mildest of 
the above remedies, such as the carbonates of the alkalies, with small 
doses of rhubarb; a well-known and popular form of these is the pulv. 
rhei comp.; if the diarrhoea is more severe, we may give the tine, rhei 
aquosa. An old and extensively used mode of giving the latter is in a 
mixture of tinctura rhei aquosa 3 ij, with liq. potassii carbonici gtt. xij, 
aqua foeniculi 3 ij, and syrupus simplex 3 ij, of which a teaspoonful is 
to be taken several times daily. If this treatment is inefficacious, if 
the decomposition in the stomach continues, and the passages become 
more frequent, we may give small doses of calomel, a plan that 
has long been justly popular in the treatment of infantile diarrhoea. 
I usually give £ to £ gr. two or three times daily. JBednar, who pre- 
fers calomel to all other remedies in this disease, gives it combined 
with jalap, in larger and more frequent doses. His prescription is: 
“ IJ, calomel, gr. iv; pulv. jalap, gr. ij; sacchar. alb. 3 ss; iq,. ft. pulv. 
no. viij. S. Take one povrder in water every twTo hours.” Even this 
treatment is not always successful. The evacuations often persist in 
spite of the most rigid diet and the free employment of calomel, until 
we fear to use any more mercury, although, from the continuance of 
the vomiting and purging, but little of it seems to be absorbed, and 
hence mercurial, stomatitis rarely occurs. In such cases, every prac- 
tising physician sometimes finds himself in a position where he is 
obliged to give up the remedy from wdiich he has seen the best effects 
and which he usually trusts most, and try one in which he has less 
confidence. He may even feel around from one remedy to another. 
There are no definite and certain indications for the cases where nitrate 
of silver, tannin, muriatic acid, tincture of nux vomica, etc., are re- 
spectively advantageous. Usually the remedy that was efficacious in 
the last attack is given ; if it fails, others are tried. Without laying 
particular stress on it, I would recommend very small doses of nitrate 
of silver ( fil argent, nitrat. gr. -j-; aquae distillat. ? ij. HI. S. Take 
a teaspoonful every half hour or hour), and frequent potions of ice- 
water, in those cases where there are excessive vomiting, great thirst, 
and copious watery evacuations. If there be no vomiting, but great 
purging, and calomel does not answer the purpose, I usually give tan- 
nin (I£ tannin, 3ss; aquas distillat. 3 iij. lit. S. A teaspoonful 
every two hours). In mild but prolonged cases I give muriatic acid 
in mucilage. I have not much experience in the use of tincture of nux 
vomica, creasote, or tincture of muriate of iron. 488 
DISEASES OF THE STOMACH. 
In gastric catarrh, caused by catching cold, the causal indications 
demand diaphoretic treatment. 
When induced by unknown epidemic influences, there are no causal 
indications to fulfil. 
For the fulfilment of the indications of the disease, it is just as ne- 
cessary to follow out the strictest dietetic rules, as it is unnecessary to 
give medicine. Experience teaches that the abnormal hyperaemia, mu- 
cous secretion, etc., of the gastric mucous membrane readily and speedi- 
ly disappear on the removal of the causes which had induced or kept it 
up. But, as there is no doubt that even the mildest ingesta may main- 
tain catarrhal hyperaemia, it is safest to keep patients with acute gastric 
catarrh without food for a while—to let them fast entirely. This is 
particularly advisable in the form called status gastricus. This order 
is often objected to; anxious mothers can hardly make up their minds 
to refuse their children all nourishment, even for a short time; adults 
with acute gastric catarrh do not feel hungry, it is true; but they 
have a longing for salty, piquant food. The more we insist on the 
fasting, the better results we shall have. If the disease is protracted, 
if it is accompanied by fever, or if, on account of the consumption of 
tissue, caused by the fever, we fear continuing the starvation, we 
should give nourishment in the fluid form, as that causes least irrita- 
tion. In choosing this nourishment, .we must remember that the gas- 
tric secretion is rendered alkaline from the admixture of mucus, and its 
digestive power greatly impaired. Hence we should usually forbid 
milk, eggs, and meats, which require acid gastric juice.for their assimi- 
lation, and, as long as there are no signs of abnormal formation of 
acid, we should only permit amylaceous food. The so-called water- 
soups are very suitable nourishment for persons with protracted gas- 
tric catarrh. 
It is exceedingly difficult to manage the diet of children with acute 
gastric catarrh, which has been caused, and is kept up, by decomposi- 
tion of the contents of the stomach, that it is difficult to arrest. Milk, 
which is the most suitable and natural food for children, is injurious to 
them in these cases, because it quickly decomposes; then arises the 
difficult question : What shall we give them instead of milk ? Under 
these circumstances, what nutriment will not be decomposed and trans- 
formed into injurious substances? We may easily satisfy ourselves 
that oat and barley gruel, as well as arrow-root and panada, are 
changed, and become sour as quickly as milk. 
For the successful treatment of the disease in question, we should 
carefully remember that the children do not suffer from hunger, even 
if we withdraw all nourishment for a day or two, and feed them on 
fresh water alone, avoiding even the addition of sugar. If, under this ACUTE GASTRIC CATARRH. 
489 
treatment, the vomiting and purging cease, if the water be restored to 
the thickened blood, the collapse often disappears quickly, and it looks 
as if the fasting child were recovering, then we commence gradually 
with small quantities of diluted milk. If this be rejected again and 
again, and it appears dangerous to subject the children to a longer ab- 
stinence, I can recommend teaspoonful doses of beef-essence, which is 
prepared by cutting the flesh into small cubes, placing these in a bot- 
tle (without adding water), closing this securely, and leaving it in a 
vessel of boiling water for several hours. 
The indicatio morbi very rarely calls for the so-called antiphlo- 
gistic remedies. Abstraction of blood, general as well as local, may 
be dispensed with. In severe cases, characterized by excessive vomit- 
ing and thirst, cold is serviceable. Both in cholera morbus and cholera 
infantum the use of ice-water and small pieces of ice is beneficial, as 
is also the application of cold compresses to the abdomen; these should 
be frequently renewed. 
We can speak even more decidedly against the use of muriate of 
ammonia in the treatment of acute gastric catarrh than we did of 
its use in bronchial catarrh. We cannot depend on its anticatarrlial 
action, and its employment can only increase the difficulty. 
Carbonic acid is very popular in the treatment of this disease; it is 
given as effervescing powder, or effervescing mixture, or as carbonic- 
acid water. It usually causes eructation very soon, and this appears 
to bring up other gases from the stomach, so that there is almost 
always momentary relief. It is not claimed, however, that carbonic 
acid, which everywhere acts as an irritant, moderates the hyperaemia 
of the stomach, and has any direct influence on the rapid cure of the 
disease. 
It is different with the use of the carbonates of the alkalies; they 
lessen the toughness of the secreted mucus, and facilitate its evacua- 
tion ; hence, independent of their use for fulfilling the causal indica- 
tions (see above), they deserve full consideration in the later stages 
of acute gastric catarrh. Moreover, the alkaline carbonates appear to 
assist the secretion of the gastric juice; at least JBlondlot and Fre- 
richs observed that, after giving carbonates of the alkalies, enough 
acid gastric juice was formed, not only to neutralize the alkali, but to 
give the contents of the stomach an acid reaction. In the status gas- 
tricus they are usually given in the form of soda-water, or tinctura rliei 
aquosa. 
Further rules are rarely required for the treatment of symptoms. 
Among the symptoms that most frequently call for treatment is vom- 
iting, and, where the bowels are affected at the same time, diarrhoea. 
If moderate, these may be regarded as favorable symptoms, and re^ 490 
DISEASES OF THE STOMACH. 
quire no special treatment; but sometimes, as in cholera morbus, or 
cholera infantum, they may be so severe that the blood will be much 
thickened by the loss of water, and life be endangered. Opium is the 
most usual prescription for the excessive vomiting and purging. We 
do not know exactly how opium arrests these symptoms. If it only 
paralyzed the intestines, and so diminished the number of the stools 
without decreasing the secretion of the mucous membrane, it would be 
of little real benefit; but it really seems as if, besides the influence it 
has on the movements of the intestines, and perhaps as a direct result 
of this, it also limited the secretion of the intestinal mucous membrane. 
Hence, if, in cholera morbus, ice-water do not arrest vomiting, and the 
passages become more numerous, we should give gr. ss of opium in 
powder, or its equivalent of laudanum, alone or with analeptics. In 
spite of our dislike to give opium to children, and in spite of our be- 
lief that it answers neither the indicatio rnorbi, nor the causal indica- 
tions, we may be obliged to give small doses of it in cholera infantum. 
In cholera morbus, or cholera infantum, the greater the collapse, the 
weaker the pulse, and the lower the temperature, the more necessary 
it becomes to use stimulants; inwardly we may give small doses of 
wine, ether, coffee; outwardly we may use sinapisms. 
On the other hand, in the course of acute gastric catarrh, in spite 
of the alkalies that have been exhibited, a quantity of mucus may col- 
lect as a product of the disease, and by its decomposition cause an 
obstinate continuance of the affection, or, after this has run its course, 
may retard convalescence and disturb digestion. If, in the later stages 
of gastric catarrh, the painful attacks of vomiting, which, from time to 
time, throw out quantities of mucus, the loss of appetite, or the slow 
recovery, render it probable that such a state of affairs exists in the 
stomach, it may be necessary to give an emetic. 
CHAPTER II. 
CHRONIC GASTRIC CATARRH. 
Etiology.—Chronic gastric catarrh sometimes occurs as a result 
of the acute affection; when this is protracted or relapses frequently, 
sometimes it originates as a chronic disease. Hence the etiology 
is mostly the same as that of acute gastric catarrh. It may be 
caused: 
1. By all injurious influences tfyat excite the above disease, 
when they act continuously or repeatedly. But the habitual mis- 
use of spirituous liquors deserves particular mention, as it is by 
far the most frequent cause of chronic gastric catarrh. We also ob- CHRONIC GASTRIC CATARRH. 
491 
serve that alcohol acts the more injuriously the more undiluted it is 
taken; hence brandy-drinkers are most liable to the affection. 
2. In many cases chronic gastric catarrh depends on congestion of 
the gastric mucous membrane. The obstruction of the circulation in- 
ducing this congestion may be located in the portal vein; hence we 
find that all affections of the liver, by which the portal vein or its 
branches are compressed, are always accompanied by chronic gastric 
catarrh. But more frequently the obstruction lies beyond the liver; 
all affections of the heart, lungs, or pleura, that cause an overfilling 
of the heart and obstruction of the vena cava, also obstruct the escape 
of blood from the liver, and hence from the stomach; consequently, in 
emphysema, cirrhosis of the lungs, valvular disease of the heart, etc., 
we meet chronic gastric catarrh just as often as we do cyanosis of the 
skin, and both affections must be induced in the same way. 
3. Chronic gastric catarrh often accompanies phthisis and other 
chronic diseases. In part I., we showed that patients with incipient 
phthisis often complain more of their gastric catarrh than of the lung 
trouble, and that is what first induces them to apply for aid. 
4. It always accompanies cancerous or other degeneration of the 
stomach. 
Anatomical Appearances.—In chronic gastric catarrh, the mu- 
cous membrane is often reddish brown or slate gray, just as it is else- 
where when it is the seat of chronic catarrh. This is caused by small 
capillary haemorrhages in the tissue of the mucous membrane, and the 
transformation of the haematin into pigment. Instead of the fine 
injection seen in acute catarrh, we usually find a coarse anastomosis, 
and in some places dilatations of the vessels. Moreover, the mucous 
membrane has become hypertrophied, it is thicker and firmer, and, even 
when the muscles are not contracted by rigor mortis, we find the 
mucous membrane forming numerous folds, and some parts of it are 
occasionally elevated to soft spongy nodules by a velvety hypertrophy. 
We often find innumerable small prominences, separated by super- 
ficial furrow's, a state described as the etat rnamelonne. The mam- 
millated appearance most frequently depends on partial hypertrophy 
of the gastric mucous membrane, by which some of the glands and 
their insterstitial connective tissue have been enlarged. Frerichs 
asserts that it is also caused by roundish collections of fat in the sub- 
mucous tissue, or by the development of closely-crowded closed fol- 
licles ; according to Budd, they result in some cases from overfilling 
of the gastric glands with retained secretion. These changes are 
found most frequently and farthest advanced in the pyloric end of the 
stomach. The inner surface of the stomach is covered with a grayish- 
white, tough mucus, which clings firmly to it. 492 
DISEASES OF THE STOMACH. 
The thickening is not always limited to the mucous membrane; 
sometimes the submucous and muscular tissues are changed to a fatty 
mass, several lines or even half an inch thick. This thickening of the 
wall of the stomach also depends on simple hypertrophy, in which 
there is both a new formation of muscular cells, and an increase of the 
submucous and intermuscular connective tissue. On the cut surface 
the thickened muscular tissue shows a pale grayish-red, soft, fleshy 
mass, traversed by parallel connective-tissue striae, running from with- 
out inward, and having a peculiar fan-like appearance. Occasionally 
the whole pyloric end of the stomach, and especially the pylorus itself, 
is changed in this way; in other cases the thickening of the wralls of 
the stomach is more circumscribed, and forms certain prominent nod- 
ules (Foerster). The pylorus may be greatly constricted by thicken- 
ing of the walls of the stomach from simple hypertrophy, and this con- 
striction may cause great dilatation of the part of the stomacli above 
the stricture. 
Symptoms and Course.—In chronic gastric catarrh, the patients 
complain most of a disagreeable feeling of pressure and fulness in the 
stomach, which is increased by eating, but rarely amounts to severe 
pain. Where the latter occurs after eating, and the epigastrium is 
sensitive to pressure, we must always suspect that there is not simply 
chronic gastric catarrh, but that it is complicated by some more serious 
disease. With the feeling of fulness there is almost always a promi- 
nence of the epigastrium, caused by the filling of the stomach with 
gas, and by the ingesta remaining in it for a long while. The gases 
in the stomach are formed in chronic catarrh also by the decomposition 
that the ingesta undergo when the gastric juice, which has become 
alkaline, no longer causes normal digestion, and the mucus in the 
stomach acts as a ferment on its contents. The abnormal decomposi- 
tion is assisted, however, by the fact that, although the muscular coat 
of the stomach has increased in thickness, its functions are paralyzed 
by serous infiltration. When the movements of the stomach are 
retarded, food remains in it a great while, and undergoes abnormal 
decomposition. From time to time there is eructation of gases having 
the same composition as those formed in acute gastric catarrh. With 
the eructation, which is a constant symptom of chronic gastric catarrh, 
besides the gases, small quantities of sour or rancid fluid often rise 
into the mouth, and are either spit out or swallowed again. The for- 
mation of lactic and butyric acids from the transformation of the amy- 
lacea is often very extensive, and the sour and acrid fluids, rising into 
the oesophagus and pharynx on belching, cause the burning feeling 
called heartburn. 
Occasionally, beside the above symptoms there is vomiting ; this, CIIROXIC GASTRIC CATARRH. 
493 
however, is not constant; on the contrary, it is rather rare. According 
to the observations of Frerichs, to whom we owe most of what we 
know concerning the anomalies of digestion, the hydrocarbons are 
occasionally changed into a tough filamentous mass resembling gum, 
and which is not unfrequently formed by lactic-acid fermentation out- 
side of the body. The vomited substances not unfrequently consist 
of large quantities of this non-nitrogenous material, which is thrown 
up in mucous filamentous masses after painful retching. In other 
cases, pure mucus with an insipid fluid is thrown up; this form of 
vomiting occurs chiefly in the chronic catarrh of drunkards, and con- 
stitutes the celebrated vomitus matutinus (water-brash). Frerichs, 
who has carefully examined these masses, found that they were usually 
alkaline, had a low specific gravity, always contained sulphurets, and 
that alcohol added in excess threw down a white flocculent precipitate 
which rapidly converted starch into sugar. This peculiarity of the 
fluid showed that it was not formed in the stomach but in the salivary 
glands. We have before said that irritations and diseases of the 
stomach increased the salivary secretion; hence it appears that in 
drunkard’s chronic gastric catarrh, the saliva swallowed during the 
night is thrown off in the morning as vomitus matutinus. In simple, 
non-complicated chronic gastric catarrh, unaltered food is very rarely 
vomited. If this does occur, it is usually mixed with a Quantity of 
mucus, and from admixture of butyric acid has a disagreeable, acrid 
smell and taste, and occasionally contains a peculiar microscopic for- 
mation, the so-called sarcina ventriculi. It can scarcely be doubted 
that the sarcina, which, when it occurs in the stomach, is always found 
in great numbers, is an algoid growth. It presents cells of the to 
yj-g- of a line in diameter, with square surfaces divided into four regular 
parts; usually several, sometimes very many of these, are united into 
smaller or larger squares. It is not to be supposed that it is this par- 
asitic plant which, acting as a ferment, causes an abnormal decomposi- 
tion of the contents of the stomach, for, in healthy stomachs (though 
it rarely occurs there, it is true), its presence does not induce this ab- 
normal decomposition. 
The sensation of hunger is almost lost, even when the patient is 
much emaciated, and the body is very much in need of support; fre- 
quently the patients can hardly be persuaded to take nourishment. In 
other cases there is a feeling of hunger, but even a few mouthfuls 
satisfy it. Finally, in some cases, particularly where much acid is 
formed, there is occasionally pain in the stomach, accompanied by faint- 
ness. As this is generally relieved by eating, it is commonly called 
“wolfish appetite” (heiss-hunger). As there is no feATer, the thirst is 
not increased; it is often less, like the appetite. 494 
DISEASES OF THE STOMACH. 
If the chronic catarrh extends from the stomach to the mouth, we 
have, at the same time, the symptoms of chronic oral catarrh: the 
tongue is coated, shows the impression of the teeth along its sides; 
there is a stale, slimy taste, and a more or less fetid smell from the 
mouth. But a clean tongue and absence of the other symptoms of oral 
catarrh do not at all prove that the stomach is healthy. 
Not unfrequently the chronic gastric catarrh extends to the intes- 
tines, and, besides the symptoms above described, we have those of 
chronic intestinal catarrh. We must, however, bear in mind that every 
intestinal catarrh does not cause diarrhoea, because it is not always 
accompanied by fluid secretions, or large quantities of mucus. There 
is more apt to be somewhat obstinate constipation, because the move- 
ments of the intestines, like those of the stomach in chronic gastric 
catarrh, are greatly impeded. Decomposition of the contents, which 
thus remain a long time in the intestines, continues; there is flatu- 
lence, which renders the belly tense, and the patients, who feel relieved 
by the escape of flatus, usually ascribe their difficulty to the “ move- 
ments of the flatus.” 
Occasionally, also, the catarrh extends from the duodenum to the 
ductus clioledochus, and there are retention and absorption of bile. We 
shall find that the jaundice caused by gastro-duodenal catarrh is the 
most frequfint form of icterus. 
In regard to the general state of the patient, the severe headache, 
pain and weakness of the limbs, and other general symptoms which 
accompany acute gastric catarrh, are usually absent in the chronic form; 
but, on the other hand, there is usually some mental depression. If 
this state be designated as hypochondria, because the abnormal excite- 
ment of the brain depends on abnormal conditions of the abdominal 
viscera, there can be no objection to it; but the mental disturbance 
accompanying gastro-intestinal catarrh should not be distinguished 
from other forms of melancholia by the fact that the bodily state is 
the sole object of the gloomy thoughts. I have seen a general dis- 
couragement, an under-valuation of mental power, despair as to busi- 
ness, etc., induced by chronic gastric catarrh, and have seen these 
symptoms disappear on the cure of the disease. Only a few years 
since I treated a very wealthy man for chronic gastric and intestinal 
catarrh, who, during the disease, thought he was near bankruptcy, and 
left unfinished a building that he had begun, because he thought he 
had not sufficient money to continue it. After spending four weeks at 
Carlsbad, his old strength and feelings returned, he finished his house 
with great splendor, and has been well ever since. 
When the disease lasts a long while, the nutrition of the patient 
suffers from the disturbance of chymification, as well as from the in- CHRONIC GASTRIC CATARRH. 
495 
terference with resorption, caused by the tough mucus on the gastric 
and intestinal mucous membrane; the fat disappears, the muscles be- 
come relaxed, and the skin dry. Not unfrequently, scorbutic affec- 
tions, loosening of the gums, bleeding from them, and even ecchymoses 
on the extremities, are seen. Excessive emaciation is suspicious; when 
it occurs, we may fear that the gastric catarrh is a secondary or symp- 
tomatic affection, which is caused or maintained by carcinoma. 
The frequent change observed in the urine in this disease is pecu- 
liar, and difficult to understand. Even taking into consideration the 
fact that disturbed absorption must excite a change in the excretions, 
we cannot explain the high color, the sediments of urates, or the 
frequent appearance of quantities of oxalate of lime in the urine 
of patients who have chronic gastric catarrh (see chapter on dys- 
pepsia). 
As to the course and remits of chronic* gastric catarrh, the symp- 
tomspibove described may run on for months, or even.years, with more 
or less severity, and often with frequent variations of intensity. When 
the causes can be removed by proper treatment, the disease is often 
cured; in other, not very frequent, cases, it induces severer lesions of 
the stomach, particularly chronic ulcer of the stomach (?), and, when 
induced by mechanical disturbances, it may cause haemorrhage from 
the stomach. Not counting the secondary affections, this disease is 
rarely fatal; although cases do occur where the patients finally die of 
marasmus and dropsy, but they more frequently die of the diseases 
complicating or causing the gastric catarrh. 
Hypertrophy of the membranes of the stomach cannot be recog- 
nized during life, unless the calibre of the pylorus is diminished. This 
may result from the villous hypertrophy of the gastric mucous mem- 
brane which we described among the anatomical appearances. 
Stricture of the pylorus, from hypertrophy of the mucous mem- 
brane, impedes the exit of the contents of the stomach; a new cause 
of abnormal decomposition is thus added to those resulting from the 
catarrh. This explains why, in stricture of the pylorus, the symptoms 
that we deduced from abnormal decomposition of the contents of the 
stomach (such as eructation of gases and badly-tasting fluids, heart- 
bum, etc.) reach even a higher grade, and are more distressing than 
in simple chronic gastric catarrh. Besides this, we have vomiting, 
which does not occur, or comes only occasionally, in many, or even in 
most cases of simple chronic gastric catarrh, as one of the most con- 
stant symptoms of pyloric obstruction; it usually comes quite regu- 
larly two or three hours after eating. This is occasionally different 
when the stomach is much distended, and hence can hold a large 
quantity ; then there may be no vomiting for two or three days j aftef 496 
DISEASES OF THE STOMACH. 
such pauses, enormous quantities are evacuated at one time. In such 
cases there may be a certain regularity. 
In stricture of the pylorus, the vomited masses almost always con- 
sist of more or less digested food embedded in mucus, which smell dis- 
agreeably sour and rancid ; they usually contain quantities of lactic 
and butyric acids, and frequently sarcina. If there be decided acidity 
which cannot be checked, with frequent and regular vomiting, there is 
very probably pyloric obstruction ; the diagnosis becomes more certain 
.f we can make out a consecutive dilatation of the stomach (which 
may become large enough to fill the greater part of the abdomen) ; 
this may sometimes be done by inspection of the abdomen, when the 
distended stomach may be seen as a convex prominence, extending 
down to the navel, or even below it. Bamberger calls attention to 
the fact that where the stomach is very low down, not only the greater, 
but also the lesser curvature, may be made out as a prominence extend- 
ing from the cartilages of the false ribs on one side to those on the 
other, just below the so-called “ pit of the stomach,” which is sunk in. 
On moving the skin in the epigastrium, we occasionally observe the 
region of the stomach to swell up and form a tense tumor. This ap- 
pearance, along with which the contours of the stomach may be felt, 
is doubtless due to the tension of the organ over its fluid and gas- 
eous contents which cannot escape, and to its consequent change from 
its usual relaxed state to a more spherical shape. The most elevated 
segments of this sphere become visible on the abdomen, while those 
lying deeper are perceived only by the touch. This change of the 
stomach from a relaxed, loose bag, to an elastic, tense, spherical blad- 
der, is usually accompanied by a disagreeable and more or less painful 
sensation. Apart from the transitory symptom just described, we 
notice the slight resistance of the epigastric region, which Bamberger 
has so well described as feeling like an air-cushion. The prominence 
of the epigastrium decreases or disappears wdien the patient has vom- 
ited freely. In one case, treated at the Greifswalder clinic, on giving 
the patient an effervescing powder, the region over the stomach, and as 
far down as the navel, swelled considerably, and the contours of the 
stomach were clearly marked. Then, if part of the carbonic acid 
were belched up, the swelling subsided. When the stomach is full 
of food, the percussion dulness is very extensive ; but if, as is usually 
the case, it contains a quantity of gas at the same time, the percussion- 
sound is particularly full and tympanitic at the prominent places. If 
the patient changes his position, the solid substances always go to the 
lower parts of the stomach, and the bounds of the dull and clear per- 
cussion change. 
The above symptoms render the existence of pyloric constriction CHRONIC GASTRIC CATARRH. 
497 
very probable, but we can only ascribe this to simple hypertrophy of 
the walls of the stomach, when we can exclude the other and more 
frequent forms of stricture, particularly the cancerous and the cica- 
tricial stricture, not unfrequently left after the healing of a chronic 
ulcer. 
The prognosis of chronic gastric catarrh agrees with what we have 
said of its course. Stricture of the pylorus must be classed among the 
frequently fatal diseases, for patients with this disease always die, 
sooner or later, of marasmus or dropsy. 
Treatment.—Of all serious chronic diseases, chronic gastric catarrh 
probably gives the best result from rational treatment. 
As we have described, in the first part of this chapter, the injuries 
which, according to the duration of their action, induce acute or chronic 
gastric catarrh, we may, in speaking of the causal indications for treat- 
ment, refer to that description, and we have little to add to it. These in- 
dications are rarely fulfilled by the use of an emetic, as there are rarely 
any injurious substances in the stomach that can be considered as 
keeping up the disease. On this point we often meet opposition. It 
is difficult to convince the patients that the pressure they feel is not 
excited by “ something heavy on the stomach,” and that an emetic 
would bring no relief, but rather would make matters worse. The 
causal indications urgently require the forbidding of all spirituous 
liquors, if their continued use has caused, and is keeping up, the affec- 
tion. This command will rarely be obeyed; nevertheless, we must 
not weary of repeating it. Temperance lecturers, who also demon- 
strate the terrifying results of brandy-drinking on the stomachs of 
topers, usually preach to deaf ears, it is true, but they attain some un- 
deniable results, and these should encourage the physician to persist 
in his advice. In the chronic catarrh caused by repeatedly catching 
cold, or by the action of a moist, cold climate, the indication is to ex- 
cite the activity of the skin by warm clothes, warm baths, and similar 
means. Such cases are not at all rare; and, even at Greifswald, pa- 
tients who have come here without preparing for the damp, windy 
climate, by dressing more warmly, are often affected with chronic gas- 
tric catarrh, Which is better in summer, worse in winter, and is not 
cured till the causal indications are properly attended to. When the 
disease results from congestion, the causal indications can rarely be 
fulfilled. 
Dietetic rules are also of the greatest importance in fulfilling the 
indications of the disease. It is not possible to keep the patients 
fasting throughout this tedious complaint, but we should most care- 
fully select their food, and urgently insist on its exclusive use. The 
more precise the rules, the more carefully they will be followed, and, 498 
DISEASES OF THE STOMACH. 
if the prescribed diet be considered as a regular treatment, it is usually 
observed by the patient with painful conscientiousness. Since the use 
of meat, and other animal food, particularly requires activity of the 
stomach, one might suppose that the indication was to allow only vege- 
table diet to a patient with chronic catarrh of the stomach, the diges- 
tive power of whose gastric juice has become weakened, but experi- 
ence teaches the contrary. The power of the gastric juice to convert 
the protein substances into peptone (Lehman), or albuminose (.Mialhe), 
is diminished in chronic catarrh, it is true, but it is not entirely lost. 
If they be given judiciously and in proper form, the patients improve 
more than if fed only on amylacea, from which quantities of lactic and 
butyric acids are formed in the stomach. From what has been said 
above, it follows, of course, that fat meat and sauces are to be for- 
bidden ; that the food is to be carefully chewed, and only small por- 
tions of it swallowed at a time. Some patients get along very well 
when they only eat concentrated, unskimmed meat broth; others do 
so when they only eat cold meat, and but little white bread. The 
latter prescription is especially useful in patients who suffer from ex- 
cessive acidity, and, in very obstinate cases of this kind, instead of the 
“ cold-meat treatment,” we may recommend the use of salt or smoked 
meat. If it be considered curious that some patients bear meat better 
when in this indigestible form than otherwise, it is because the fact is 
overlooked that smoked and salt meat, even if indigestible, has this 
advantage over fresh meat, that it is not so readily decomposed as 
fresh meat. In one case that I treated, the patient, who had chronic 
gastric catarrh, with great inclination to acidity, knew exactly when 
he must abandon all other food (because it increased the gastric juice), 
and limit himself to the use of lean smoked ham, sea-biscuit, and a 
little Hungarian wine. The exclusive use of milk, the so-called milk- 
cure, agrees wonderfully with some patients, while others cannot stand 
it at all, and we cannot certainly tell beforehand which will be the 
case. Butter-milk suits many patients better than fresh milk. In 
Krukeriburg1s clinic I have seen very brilliant results from the pre- 
scription, “ when the patient is hungry, let him eat butter-milk; when 
ne is thirsty, let him drink butter-milk.” Perhaps fresh milk is not so 
well borne, because it readily curdles in the stomach, and forms large, 
firm lumps, while in the butter-milk the casein is already curdled, but 
finely divided. 
Dietetic treatment does not succeed so often in chronic as in acute 
gastric catarrh, but we have some very efficient remedies for the former 
disease. The chief among these are the alkaline carbonates. We 
have already recommended bicarbonate of soda, in divided doses, and 
tinctura rhei aquosa, in prolonged attacks of acute gastric catarrh. CHRONIC GASTRIC CATARRH. 
499 
Where chronic gastric catarrh is obstinate, we should try soda water, 
or the natural soda waters of Ems, Salzbrun, Selters, and Bilin, as well 
as the waters which, besides carbonate of soda, contain sulphates of the 
alkalies and earths or chloride of sodium. The use of the waters of 
Karlsbad and Marienbad has the most wonderful results. The highest 
recommendation that could be given for them is the fact that they are 
recommended by parties whom no one can accuse of being easily de- 
ceived by therapeutic results: the learned professors of the Vienna 
and Prague schools prize the use of the warm springs of Karlsbad as 
the best remedy for chronic gastric catarrh, and even for chronic ulcer 
of the stomach. Moreover, the numerous cases where obstinate jaun- 
dice was cured by the use of the waters of Karlsbad were almost 
always those where it was due to gastro-duodenal catarrh. There is 
no reason to delay this treatment until the catarrh of the stomach and 
duodenum has caused jaundice, or to suppose that it will be less effi- 
cacious if this complication be wanting. If the circumstances of the 
patient permit, the treatment may be followed out at Karlsbad or 
Marienbad; at these places the anecdotes of the frightful results from 
errors of diet during the use of the waters so terrify the patients that 
the diet required by chronic gastric catarrh will be certainly adhered 
to while there. Even after returning home, the patients subject them- 
selves to the strictest regimen for months, fearing that the waters 
may revenge themselves even yet for the slightest errors of diet. If 
obliged to use the waters at home, it makes little difference from which 
of the Karlsbad springs they come, as they vary little except in their 
temperature, and they may be warmed to any desired extent. In 
Karlsbad the springs of lower temperature, as the Schlossbrunnen and 
Theresienbrunnen, are most frequently used in chronic gastric catarrli. 
If there be no coincident obstinate constipation, soda water will often 
succeed quite as well, provided it be properly used, i. e., if the patient 
diets the same as at Karlsbad. After eating but little, and not very 
late, the night previous, he must drink the soda water in the morning 
while fasting, and must not breakfast for an hour after the last glass 
of water, so that the medicament may not be mixed with the ingesta, 
but may act undiluted on the gastric mucous membrane, and on the 
mucus covering it. The results from this treatment are the most bril- 
liant that are ever attained in medicine. 
The ter-nitrate of bismuth and the nitrate of silver have a great 
reputation in the treatment of chronic gastric catarrh. These metallic 
salts may be beneficial, both by arresting decomposition in the stomach 
and by their great astringent action on the hyperaemic and relaxed 
mucous membrane. I have used these remedies in my clinic in very 
large doses (bismuth nitrat. gr. x, argenti nitrat. gr. j—ij, at once), 500 
DISEASES OF THE STOMACH. 
given like the alkaline carbonates, on an empty stomach, before break- 
fast. Most patients bore these doses very well; severe pain, nausea, 
or vomiting never occurred, and there was diarrhoea in only a few cases. 
But the results were very varied; while in some cases there was very 
rapid improvement, in others there was none, and I was unable to find 
any cause for difference between them. 
In chronic gastric catarrh we sometimes dare not continue the mild 
diet; on the contrary, slightly-seasoned and salty food is much better 
borne than unseasoned and unirritating. When this state of “ atony 
of the gastric mucous membrane ” occurs, we should carefully prescribe 
preparations of iron and mild stimulants. The Eger Franzbrunnen, 
and even the chalybeate waters of Pyrmont, Driburg; or Cudowa, are 
better borne, and do more good than those of Karlsbad and Marienbad. 
When the mucous membrane is in this state, the best remedy is, ipe- 
cacuanha, gr. ss—j, pulv. rliei, gr. iij—iv, in pill, to be taken before 
meals, as recommended by JBudd. The tinctura rhei vinosa, Hoff- 
mann’s visceral elixir, ginger, calamus, etc., do good in these cases; 
but we must beware of going too far in the use of these remedies, or 
of giving them in improper cases, or too large doses. 
The symptoms rarely require the application of leeches or cups to 
the epigastrium; they are only to be used when there is great pain. 
Difficult as it is to understand, the pain is almost always relieved by 
the abstraction of blood. In those cases where the hyperaemia and 
catarrh of the stomach are symptomatic of great abdominal plethora, 
depending on compression of the portal vein, or obstruction to the 
flow of blood from the hepatic veins, surprising results are often ob- 
tained by an abstraction of blood from the anastomoses of the portal 
vein by applying leeches at the anus. Narcotics, which are almost in- 
dispensable in treating ulcers of the stomach, are rarely required in 
cfironic gastric catarrh. Emetics may be employed under the circum- 
stances in which they were advised in acute gastric catarrh, but we 
must be more careful with them, as we do not know that ulceration 
may not have occurred already. The constipation which almost always 
exists is to be treated by enemata or laxatives; the medicines most 
used are rhubarb and aloes, and, in obstinate cases, extract of colo- 
cynth. Several of these articles are usually combined; the officinal 
(in Germany) and much-used compound extract of rhubarb contains 
aloes, rhubarb, and jalap. J3udd says, also, that aloes and colocyntli 
act chiefly on the rectum, and irritate the stomach but little, so that 
they are the best purgatives in chronic gastric catarrh; he warns 
against the use of senna and castor-oil. DISEASES OF THE STOMACH. 
501 
The treatment of dilatation of the stomach lias latterly made 
great progress. In some instances happy results have been obtained 
by a modification of “ Schroth’s cure,” in which the patient’s supply 
of water and of liquid food is reduced to the smallest endurable 
limit. 
In other and more numerous cases great improvement, and often 
complete cure has been brought about by repeatedly pumping out the 
stomach by means of Wyman’s stomach-pump, and by rinsing out 
the organ with soda-water or the alkaline-muriatic mineral waters. 
Kussmaul has done great service by introducing this mode of treat- 
ment. 
After a somewhat extensive experience of my own, I can fully sub- 
stantiate the striking results which Kussmaul has obtained. Even 
the first application of the pump generally gives the patients such 
relief, that, so far from dreading a repetition of this, in itself, by no 
means pleasant operation, they clamorously beg for it; and the first 
timidity once over, the introduction of the stomach-tube—which at 
the outset inspires almost all patients with fear—no longer is dis- 
tressing ; moreover, they soon learn to introduce the tube for them- 
selves, and I have met with several instances when the patient would 
scarcely wait for my visit, but earnestly besought my assistant to 
pump his stomach out .or “ acidulate ” it forthwith. In one instance, 
where all previous treatment had been fruitless, the patient gained 
thirty pounds in weight, and was fully restored to his strength; 
although, when received at my clinique, he was reduced to the extreme 
of emaciation, and was quite incapable of any labor. 
In this patient the sarcinm, which were very numerous in the 
matter vomited, under treatment, disappeared entirely from the con- 
tents of the stomach evacuated by the pump. 
It is remarkable that even after a very few sittings the stomach re- 
acquires the power of propelling the greater part of its contents into 
the duodenum. It is easy to verify this, firstly, from yielding of the 
previously-obstinate constipation, and from a more regular occurrence 
of the stools; secondly, because the patient’s urine, which before was 
scanty, now so augments in quantity as to impress the attention of 
the patient himself. The latter observation proves conclusively 
that very little indeed of the fluid contents of a dilated stomach is 
absorbed. 
This complete restoration of apparently desperate cases of gastric 
dilatation might give rise to the impression that this affection occurs 
as an independent malady, more often than has been supposed. But, 
both in my cases and in those of Kussmaul, the evidences of a pre- 502 
CHRONIC GASTRIC CATARRH. 
existing ulcer of the stomach were almost always so plain that the 
dependence of the dilatation upon a cicatricial stricture of the pylorus 
could not well be doubted; moreover, Kussmaul has seen cases of 
unmistakable cancerous stricture of the pylorus, in which decided 
benefit, although no cure, has been derived by.this treatment. Com- 
plete closure of the pylorus is never seen, even when every thing has 
ceased to pass from the dilated stomach into the duodenum, and 
when the patients remain for weeks without alvine evacuations, and 
every second or third day vomit immense volumes of acid liquid, 
sometimes mixed with blood, we find post mortem that the pylorus 
is still sufficiently patulous, so that it seems strange that liquid should 
not have passed through it during life. 
We may at least infer, from this observation, that the enfeebled 
condition of the gastric muscles has much to do with the retention 
of the contents of a dilated stomach. The internal pressure sustained 
by an ektatic and overfilled stomach is so great that the demands 
upon its muscular coat are considerably increased. Now, a continu- 
ous strain induces myopathic palsy of the gastric muscles just as in any 
other muscles; and, moreover, the chronic catarrh of the stomach, 
which exists in nearly all such affections, also in many cases results 
in myopathic disease of its walls. 
Whether the benefit derived from use of the stomach-pump be due 
to the unloading of the gastric walls, or to the improvement of the gas- 
tric catarrh with consequent restoration of muscular tone, this much is 
certain, that in the course of a few days or weeks the necessity for the 
pumping diminishes. 
The only untoward event that I have observed during applica- 
tion of the instrument—and this is extremely rare—is the sucking 
of a bit of the mucous membrane into the openings of the tube. 
To protect the patient from the injury which might thus be inflict- 
ed, as soon as traction upon the piston becomes in the least degree 
impeded, it must be pushed forward again, and a little water or air 
must be thrown into the stomach before the pumping may be re- 
sumed. INFLAMMATION OF THE CONNECTIVE TISSUE, ETC. 
503 
CHAPTER III. 
CROUPOUS AND DIPHTHERITIC INFLAMMATION OF THE GASTRIC 
MUCOUS MEMBRANE. 
Croupous and diphtheritic inflammation of the gastric mucous 
membrane is rarely observed, unless poisonous substances have acted 
on it (see Chapter V.). In some cases, in infants, the catarrhal form 
of inflammation increases to the croupous; in others, croupous and 
diphtheritic gastritis belongs to the secondary inflammations occurring 
in the acute infectious diseases, especially in typhus, septicaemia, and 
small-pox. 
Croup membranes rarely spread over a great extent of the gastric 
mucous membrane; they are usually limited to small circumscribed 
spots. The diphtheritic sloughs also form isolated patches; on falling 
off, they leave losses of substance with discolored ragged bases. 
Unless pseudomembranes are vomited up, the disease is rarely, if 
ever, recognized during life. The difficulties the disease causes in 
children can never be rightly interpreted, and the severe symptoms of 
septicaemia, typhus, etc., are so little modified by an intercurrent croup- 
ous or diphtheritic gastritis, that in such cases also diagnosis is impos- 
sible. 
CHAPTER IV. 
INFLAMMATION OF THE SUBMUCOUS CONNECTIVE TISSUE—GASTRITIS 
PHLEGMONOSA. 
Inflammation of the submucous connective tissue, which Hold- 
tansky compares to pseudoerysipelas, is also rare. It occurs either 
as a primary affection, without perceptible cause in previously healthy 
persons, or, like the above, it is a so-called secondary or metastatic in- 
flammation, and, as such, accompanies typhus, septicaemia, and similar 
diseases. 
The submucous tissue of the stomach is diffusely infiltrated with 
pus, which collects in its distended meshes ; more rarely there are cir-. 
cumscribed abscesses in the submucous connective tissue. The under- 
mined mucous membrane is thinned, and subsequently it has numerous 
small openings, from which the pus trickles out as through a sieve. 
The inflammation soon extends to the muscular layer, the submucous 
tissue, and peritonaeum. If the patient recovers, cicatricial tissue may 
form in the meshes of the submucous, and strictures may thus result, 
as is shown by specimens in the Erlangen Museum. 504 
DISEASES OF THE STOMACH. 
The most important symptoms of the disease are severe pain in the 
epigastrium, vomiting, great anxiety, high fever; later, there are 
symptoms of peritonitis, the patient collapses, and usually dies in a 
few days. Of course, a diagnosis can only be certainly made in a few 
cases, where, with the above symptoms and vomiting of pus, we are 
able to exclude other forms of gastritis, particularly those caused by 
poisons. The treatment can only be symptomatic. 
INFLAMMATIONS AND OTHER CHANGES IN THE STOMACH FROM CAUS- 
TICS AND POISONS. 
CHAPTER Y. 
Etiology.—The changes in the stomach caused by the action of 
concentrated acids, caustic alkalies, and some metallic salts, depend on 
the fact that these substances unite chemically with the tissue of the 
walls of the stomach, whose organic structure is consequently de- 
stroyed. The changes that vegetable or animal poisons excite in the 
gastric mucous membrane, on the contrary, cannot be traced to chem- 
ical processes. 
Poisoning by carelessness is most frequently induced by copper- 
salts, sulphuric acid, or vegetable poisons being taken into the stom- 
ach ; while intentional poisoning occurs most frequently from arsenic 
or sulphuric acid. 
Anatomical Appearances.—If dilute mineral acids have acted 
on the mucous membrane, only the epithelial and superficial mucous 
layers are changed to a soft, brownish or black slough. If a quantity 
of concentrated acid has reached the stomach, all the layers of the 
mucous membrane are converted into a soft black mass, which may 
become several lines thick from imbibition with bloody watery fluid. 
The muscular tissue becomes softened or gelatinous, and very friable ; 
more rarely both it and the serous membrane are entirely decomposed, 
and the stomach perforated. These changes are usually limited to a 
few longitudinal folds of the mucous membrane, running from the car- 
diac end toward the pylorus, while the rest of the membrane is red- 
dened by hypersemia and ecchymosis, and swollen by serous infiltra- 
tion ; the blood in the vessels of the stomach, and often even in the 
neighboring large vascular trunks, is transformed into a black, smeary, 
tar-like substance. Only the milder cases recover, for the parts de- 
stroyed slough off, and the loss of tissue is replaced by callous cicatri- 
cial substance. The caustic alkalies change the epithelium and the 
superficial, or even the deeper layers of the mucous membrane, into a 
pulpy, discolored mass. In these cases, more frequently than in cases EFFECTS OF POISONS ON THE STOMACH. 
505 
of poisoning' from acids, the destruction extends to the muscular and 
serous tissues, and so leads to perforation. When the destruction is 
superficial, cure may result even in such cases, after the sloughing of 
the necrosed parts. 
Brown or black sloughs are formed by the action of corrosive sub- 
limate, copper, or other metallic salts ; these are surrounded by active 
injection and serous swelling of the mucous membrane. Phosphorus 
excites similar changes. 
If gastritis occurs after poisoning from arsenic, we find one or more 
spots of the mucous membrane covered with a powdered, white sub- 
stance, swollen, reddened, and softened to a pulp, or transformed to a 
yellowish or greenish-brown slough. From these sloughs extend red- 
dened folds of mucous membrane, between which the walls of the 
stomach are often unaltered. 
After the action of ethereal oils, or acrid vegetable or animal poi- 
sons, the remains of severe catarrhal, croupous, or diphtheritic inflam- 
mation are seen. 
Symptoms and Course.—Gastritis from poisoning is peculiar, be- 
cause, even where the poison used has no directly paralyzing effect on 
the nervous system, besides the local symptoms, there is a general de- 
pression, and particularly an almost complete arrest of the circulation. 
These paralytic symptoms are also seen in other severe injuries of the 
stomach or other abdominal viscera, but especially in perforation of the 
stomach from ulceration. 
If a previously healthy person be suddenly attacked with severe 
pain, which spreads from the epigastrium over the abdomen; if this 
be accompanied by vomiting of mucus or bloody mucus ; if there be 
also purging of mucus and blood, preceded by severe colicky pains and 
tenesmus, and the patient be at the same time collapsed, and his fea- 
tures distorted, his extremities cool, pulse small, and skin covered with 
cold, clammy sweat; there is strong ground for suspecting the action 
of a corrosive substance or some other poison on the gastric mucous 
membrane. If concentrated acids or strong alkalies have been taken, 
there are almost always characteristic sloughs about the mouth ; the 
oral mucous membrane is destroyed in some places; there are severe 
pains in the mouth and throat; swallowing is very difficult, or impos 
sible. After taking the metallic salts or arsenic in a diluted form, the 
signs of corrosion of the mouth and throat do not appear, and the 
symptoms of gastritis do not occur for some time. The symptoms ob- 
served in the different organs, but particularly the examination of the 
evacuations, show what kind of poison has been taken. In the most 
severe cases there is nausea, but the paralyzed stomach cannot evac- 
nate its contents; an icy coldness spreads over the body, the paralysis 506 
DISEASES OF TIIE STOMACH. 
becomes total, and the patient may die in a few hours. In milder cases 
death does not occur till later, and, when a quantity of the poison has 
been vomited, the symptoms of paralysis may gradually disappear, and 
the circulation may be reestablished ; but convalescence is usually very 
slow, and the patient often suffers for life from strictures in the oesoph- 
agus or stomach, or else because the poison taken has undermined the 
constitution in some other way. 
Treatment.—The antidotes given in books on toxicology can only 
be givOn in recent cases, that is, within a few hours after acids, caus- 
tic alkalies, or metallic salts have been taken. If these substances 
have already been vomited, or have already united with the elements 
of the gastric mucous membrane, antidotes can do no possible good, 
and may prove injurious by exciting new irritation in the inflamed gas- 
tric mucous membrane. It is different with arsenic and the acrid vege- 
table and animal poisons, whose action continues longer, and for which 
the customary antidotes may be used for a longer time after they have 
been taken. If there be no vomiting, or if this do not suffice to rid 
the stomach of the poison, we may give an emetic of ipecacuanha. 
Besides these rules for fulfilling the causal indication, the indications 
from the disease itself are to use cold, as blood-letting does little or no 
good. We may cover the abdomen with cold compresses, which are 
to be frequently changed, and give small quantities of ice-water; or, 
if the patient can swallow, let him have small pieces of ice. For fur- 
ther treatment, we refer the reader to works on toxicology. 
CHAPTER \i. 
CHRONIC (round, perforating) ulcer op the stomach—ULCUS 
VENTRICULI CIIRONICUM (rOTUNDUM, PERFORANs). 
Etiology.—Perforating ulcer of the stomach is probably always 
acute; even its extension appears to be due to an acute process of 
destruction at its periphery and base. However, as the ulcer in ques- 
tion often gives the patient great trouble for years, it may rightly keep 
its name of “ chronic ulcer.” The sharp borders of the round ulcer, 
the absence of signs of inflammation or suppuration at its periphery, 
the direct observation of very recent cases, as well as the strik- 
ing results of a series of experiments on animals, prove, beyond 
doubt, that the destruction of the wall of the stomach is not due to a 
gradual breaking down from suppuration, but to the formation of a 
slough, to a partial necrosis, and that this usually, if not always, de- 
pends on an obstruction of the blood-vessels running in the walls of 
the stomach and nourishing it. The death of a circumscribed portion CHRONIC ULCER OF THE STOMACH. 
507 
of the wall of the stomach from cutting off its nourishment is analo- 
gous to the localized softening of the brain, infarction of the lungs, 
spontaneous gangrene of the toes, caused by cutting off the circula- 
tion. In the above-mentioned experiments on animals, the obstruc- 
tion of the gastric vessels was induced by introduction of emboli. 
This mode of development of the round ulcer is rare in man, but there 
are some cases where certainly it has been observed. (I myself have 
seen a most exquisite example of it within a few years.) The ob- 
structing clots usually form at the very site of the ulcer, and their 
formation seems to depend on disease of the walls of the vessel. The 
gastric juice quickly causes softening and entire dissolution of the 
dead portion of the wall of the stomach, which cannot withstand its 
action, so that we rarely have the opportunity of seeing the first stage 
of the process on post-mortem examination. The predisposition to 
chronic ulcer of the stomach is very extended. Jaksch and others 
have given us statistics of its frequency at different ages, in different 
sexes, and in different employments, etc. In the accounts of two thou- 
sand three hundred and thirty post-mortem examinations, Jaksch 
found round ulcers mentioned fifty-seven times, and cicatrices fifty-six 
times; so that, to about every twenty bodies, there was either an 
ulcer or a cicatrix. TVilligan, JBrinton, and others came to similar 
conclusions. Round ulcer is rarely found in children, but, on the other 
hand, it is quite frequent about puberty. Females are much more dis- 
posed to it than males. I think there is no doubt that poverty of the 
blood and chlorosis, those frequent results of sexual disturbances, have 
great influence in causing the round ulcer, and that they do so because 
abnormal states of the blood induce diseases of the walls of the ves- 
sels, and hence favor the formation of thrombi. In other cases acute 
or chronic catarrh of the gastric mucous membrane appears to cause 
disease of the walls of the vessels, and consequently thrombosis. 
The exciting causes of round ulcer are entirely unknown. We can- 
not deny the possibility of its being induced by the injuries usually 
named; such as the use of very hot of very cold food and drink, the 
misuse of liquor, and other errors of diet. But it is very remarkable 
that, in spite of the frequency of chronic gastric catarrh in topers, they 
rarely have the round ulcer. 
Anatomical Appearances.—The ulcer which we are considering 
occurs almost exclusively in the stomach or upper part of the duodenum, 
while it is only rarely seen in other parts of the intestinal canal. It is 
most frequently situated in the pyloric portion of the stomach, oftener 
in the posterior than in the anterior wall; and almost always at the 
small curvature or its vicinity; it is rarely seen at the fundus. Usual- 
ly there is only one ulcer, occasionally two or more, and not unfre- 508 
DISEASES OF THE STOMACH. 
quently a recent ulcer near the cicatrices of some that have healed. In 
typical cases, according to Rokitansky's classical description, there is 
a circular hole with sharp borders in the serous coat of the stomach, 
as if a piece had been cut out with a punch. Regarded from within, 
the loss of substance is greater in the mucous membrane than in the 
muscular coat, and greater in this than in the serous coat, so that the 
ulcer is in terraces and looks like a shallow funnel. The ulcers vary 
from |j inch in diameter; old ulcers attain the size of a thaler or the 
palm of the hand. At first they are round, after they have existed 
some time they become elliptical, or bulge out in some places, and so 
become irregular. They spread transversely in the course of the ves- 
sels, so that the stomach is occasionally surrounded by a girdle as it 
were. 
Sometimes the ulcer heals before it has perforated all the coats of 
the stomach. If the loss of substance has been limited to the mucous 
and submucous tissue it is replaced by granulations ; these are trans- 
formed to shrinking cicatricial tissue; they draw the edges of the ulcer 
together, and a stellate cicatrix of variable size forms on the inner sur- 
face of the stomach. If the ulcer has penetrated deeper and destroyed 
the muscular coat also, when it heals up, the cicatricial contraction of 
the neoplastic connective tissue will contract the peritonaeum also into 
a stellate figure; its inner surface may even be retracted into the form 
of a fold in the stomach. If the ulcer were very large, its healing may 
cause a stricture, as the diameter of the stomach will be much dimin- 
ished by the cicatricial contraction; this will remain as an incurable 
obstacle to the passage of the contents of the stomach into the bowels. 
If the ulcer be located in the small curvature, as is usually the case, 
even if all the walls of the stomach be destroyed, escape of the contents 
into the peritoneal cavity may be temporarily or permanently prevent- 
ed. For, while the ulceration progresses outwardly, local peritonitis 
occurs at the affected part; the threatened portion of serous membrane 
becomes attached to the neighboring organs; if it then be destroyed, 
these organs (most frequently the pancreas', the left lobe of the liver 
or the omentum), which are firmly attached to the edges of the ulcer, 
fill up the resulting opening in the walls of the stomach. The destruc- 
tion sometimes extends to the organ which covers the ulcer, but more 
frequently a thick layer of connective tissue develops on the sin-face of 
this organ, and forms the floor of the ulcer. The covering organ never 
lies in the same plane with the inner wall or projects into the stomach. 
But, after the muscular coat has retracted, the mucous coat becomes 
everted at the edge of the ulcer, and comes in contact with the organ 
in question. If, in such cases, the ulcer heal, the connective-tissue 
layer on the organ contracts, the edges approach each other, and, CHRONIC ULCER OF THE STOMACH. 
509 
if the opening be not too large, may finally unite so as to form a firm, 
hard cicatrix. 
When the ulcer first forms, and still more frequently while an ulcer 
already formed is spreading, the vessels of the stomach, or of the 
neighboring organ into which the ulcer has perforated, are destroyed, 
and there is considerable haemorrhage into the stomach. Perforations 
of the coronary, pyloric, gastro-epiploic sinistra, gastro-duodenal arte- 
ries and their branches, of the splenic artery, but most frequently of its 
branches going to the pancreas, and of the pancreatico-duodenalis, have 
been observed. 
The gastric mucous membrane also exhibits the changes character- 
istic of chronic gastric catarrh, which were described above. Sometimes 
these are absent or very slight. 
Symptoms axd Course.—Sometimes, by perforating all the coats, 
and thus permitting the escape of the contents of the stomach into the 
peritonaeum, ulcer of the stomach may cause fatal peritonitis; or, by 
erosion of a large vessel, may cause abundant haematemesis before the 
disease has been recognized, or before its recognition was possible. It 
is going too far, however, to say that in such cases the signs of the 
suddenly occurring peritonitis, or the haematemesis, were the first symp- 
toms of the ulcer of the stomach. On more careful inquiry, we almost 
always find that slight disturbances of digestion, and some oppres- 
sion in the epigastrium, increased by eating, have gone before, and that 
the patient had been troubled by wearing any thing tight about the 
waist. Between the first appearances of these insignificant difficulties 
and the fatal termination, there is sometimes only an interval of a few 
days or weeks, so there can be no doubt that, in this short time, all the 
coats of the stomach have been perforated. (I have had a very sorrow- 
ful opportunity of satisfying myself of the rapid course of a perforating 
ulcer; in Magdeburg, Dr. Brunnemann, a very distinguished and prom- 
ising young physician, died of such an ulcer. When the perforation 
occurred, he was not for an instant in doubt about the diagnosis, and 
most decidedly said that he had not suffered over eight days from slight 
trouble, which he thought proceeded from a slight gastric catarrh.) It 
even seems as if perforation, with escape of the contents of the stom- 
ach into the abdomen, occurred most frequently in the cases beginning 
in this concealed manner, and running a rapid course; that, on the 
other hand, in the cases which begin with severe and pathognomonic 
symptoms, and run on for months or years, the stomach has time, as it 
were, to unite to the neighboring organs, and so prevent the escape of 
its contents into the abdomen. I would remind my readers that the 
cheesy infiltrations of the lungs, which run a rapid course, lead to per- 
foration of the pleura and pneumothorax far more frequently than 510 
DISEASES OF THE STOMACH. 
miliary tuberculosis, which has a slow course, and where the folds of 
the pleura almost always become adherent, if the destruction goes as 
far as the pleura. The cases where the inconvenience is so slight that 
a certain diagnosis of ulcer of the stomach is impossible, or where the 
patient is so little troubled that he does not seek medical aid before 
the occurrence of the perforation, or the hcematemesis, are, however, 
rare when compared to those wdiere the disease is readily recognized, and 
where it excites very annoying symptoms. Among the most frequent 
and troublesome symptoms of chronic ulcer of the stomach are pains in 
the epigastrium. The patients complain partly of a steady pain in the 
pit of the stomach, which is increased by pressure, and is generally par- 
ticularly severe at some circumscribed spot; partly of paroxysms of se- 
vere pain, which, starting from the epigastrium, extend toward the back, 
and are designated as attacks of cardialgia. The sensitiveness to 
pressure in the epigastrium, when the ulcer is extending in breadth or 
depth, is sometimes so great that the patient can hardly bear even the 
pressure of light bed-clothes; this is because there is slight peritonitis 
over the affected part. The cardialgic attacks generally occur soon 
after meal-times, and are severe in proportion to the coarseness and 
roughness of the food that has been taken. The patients sigh, groan, 
double themselves up, and often do not find ease till the stomach has 
been emptied by vomiting; if there be no emesis, the attacks of pain 
may last for hours. The seat of the ulcer may be determined with 
some certainty from the length of time at which the pains folloAV the 
meal; if they come immediately after eating, we may suppose that the 
ulcer is near the cardiac orifice; if they come an hour or two later, it 
will probably be in the pyloric portion. Although, as a general rule, 
the attacks of pain occur after eating, and are the more severe the 
more indigestible and the rougher the food, there are some exceptions, 
and it is important that wTe should know these even if we cannot ex- 
plain them. In these exceptional cases, while the stomach is empty 
there is pain, which is relieved by taking food; or after eating indiges- 
tible food the patient remains free from pain, while it becomes very 
severe if he eat easily-digested articles. The attacks of pain are usually 
attributed to the irritation of the surface of the ulcer by the motion of 
the contents of the stomach; while in an empty stomach such causes 
are absent. Another explanation is that the gastric juice secreted on 
the introduction of food irritates the ulcer and excites the pain, while 
there are intermissions, because, while the stomach is empty, a mucus 
which is but slightly irritating covers the ulcer. But when wTe consider 
that perforation of all the coats of the stomach may occur without ex- 
citing these attacks of pain, and that, on the other hand, the most se- 
vere pain often continues when the ulcer has healed, but the stomach CHRONIC ULCER OF THE STOMACH 
511 
has become adherent to other organs, there seems no doubt that the 
chief if not the only cause of pain is the obstruction to the peristaltic 
movements of the stomach, due to cicatricial contraction, or the adhe- 
sion of its wall to neighboring organs. The larger and rougher the in- 
gesta, the more energetic and continued are the movements of the 
stomach they excite; hence the severity and long duration of the 
paroxysms of pain after eating large pieces of bread, potatoes, and 
other vegetables, and the comparative ease of the patient after eating 
soup, milk, and other fluid and mild nutriment. 
Vomiting is almost as constant a symptom as the sensitiveness of 
the epigastrium and the cardialgic attacks. It is caused by the same 
circumstances as the attacks of pain, and often terminates these, as it 
were. Vomiting also occurs a longer or shorter time after meals, ac- 
cording as the ulcer is near the cardiac or pyloric orifice. It is the 
more apt to occur, the nearer the ulcer is to the orifice of the stomach. 
Henoch calls attention to the fact that the same holds good in other 
hollow organs ; that is, reflex movements are particularly liable to be 
excited in them by affections near their openings ; he reminds us that 
severe spasm of the bladder is most apt to occur from inflammatory 
irritation about its neck; that tenesmus, depending on affections of 
the rectum, is more distressing the nearer the disease is to the anus. 
Patients usually vomit their food more or less changed, and mixed 
with mucus and sour fluids. The state of the substances vomited, in 
which there are often sarcina, depends principally on the intensity and 
extent of the coexistent gastric catarrh. Sometimes only quantities 
of mucus and acid fluids are vomited, while the food remains in the 
stomach. 
Severe cardialgia and vomiting, occurring regularly after meals, 
render it very probable that there is a chronic ulcer of the stomach ; 
the diagnosis is rendered certain, if there be also vomiting of blood. 
The hsematemesis may have various sources: sometimes it is due to 
capillary haemorrhage, induced by the spreading of the ulcer; more 
frequently it is caused by the erosion of a large vessel, and this form 
is pathognomonic of ulcer of the stomach. We shall speak more in 
detail of haemorrhage from the stomach in Chapter VIII. 
The symptoms of the chronic gastric catarrh which accompanies ul- 
cer of the stomach unite with the characteristic symptoms of the latter, 
it is true, but they are more or less decided according to the grade and 
extent of the catarrh, sometimes being just apparent. Some patients 
have decided swelling in the epigastrium, frequent eructation, severe 
heartburn, complete loss of appetite; others feel very well during the 
intervals of their pain ; even their appetite is scarcely impaired. 
The signs of oral catarrh, which also complicates ulcers of the stom- 512 
DISEASES OF THE STOMACH. 
acb, are somewhat different from the usual state of the mouth in 
chronic oral catarrh. The acid fluids that rise into the mouth appear 
to dissolve the epithelium and the vomiting to clear it away; at least, 
instead of the thickly-coated tongue, which is rarely absent in simple 
chronic catarrh of the stomach, we usually find the tongue red and 
furrowed, and this state is almost always accompanied by increased 
thirst and habitual constipation. 
Regarding the general health of the patient, chronic ulcer of the 
stomach may soon impair the nutrition, so that the patient is rapidly 
debilitated, and has a pale, cachectic look; in other cases, the nutri- 
tion is very little deranged. 
Except in the first-mentioned cases, where the round ulcer proves 
fatal in a few days or weeks, the course of the disease is usually very 
tedious; and it may run on for years, the patient suffering many 
alternations of comfort and distress. Not unfrequently, in the midst 
of apparent convalescence, vomiting of blood suddenly occurs; or the 
affection returns with its former severity years after it had disappeared. 
Recovery is the most frequent termination of chronic ulcer of the 
stomach. The sufferings of the patient gradually subside, the nutri- 
tion is fully restored, all disturbance ceases, and, when the patient has 
died of some other disease, we find the characteristic cicatrix as the 
sole remains of the ulcer. 
Secondly, the result in incomplete cure is not infrequent. The 
symptoms of chronic gastric catarrh disappear, it-is true; often also 
the periodical vomiting; the patient may become fresh and healthy- 
looking; but every meal is followed by cardialgia, which occasionally 
becomes more severe than usual. In such cases the ulcer has healed, 
and the gastric mucous membrane has become relatively healthy; but 
there is a cicatrix or more frequently an adhesion of the stomach to 
some neighboring organ, which limits its movements at some point, 
and keeps up the cardialgic attacks. Stricture of the pylorus, with 
dilatation of the stomach, is a common sequel to chronic gastric ulcer, 
whenever the seat of the ulcer has been near the pyloric orifice, or 
when the disease has been complicated by chronic catarrh with hyper- 
trophy of the gastric Avails. 
In other cases ulcer of the stomach causes death. This may occur 
(a), from perforation of the walls of the stomach, and escape of its 
contents into the abdominal cavity. In such cases patients sometimes 
die before the occurrence of peritonitis,' or before this has developed 
sufficiently to be regarded as the cause of death. Along with the sud- 
den occurrence of fearful pain in the abdomen the skin becomes cool, 
the pulse small, the countenance sunken; and the patient collapses and 
dies in this state. If the heart’s action becomes weaker, the filling of CHRONIC ULCER OF THE STOMACH. 
513 
the arteries less complete, typical cyanosis may result from the collec- 
tion of blood in the veins, and the patient looks like one in the col- 
lapsed stage of cholera. In these cases the perforation appears to cause 
a paralysis in the sympathetic nervous system, analogous to what oc- 
curs in other severe injuries. Although such cases are not rare, it is 
more common for the patient not to die during the first day or two, 
but for the symptoms of a fatal peritonitis to combine with the above. 
(5.) In rare instances death results from haemorrhage from the stomach. 
Even when the patient appears quite bloodless and waxy-looking, 
where every attempt to raise the head induces fainting, where oppres- 
sion, palpitation, dizziness, tinnitus, and other symptoms of loss of 
blood, are present, the patient often recovers, contrary to all expecta- 
tion. Death may result very quickly, however, from erosion of large 
arteries. I saw one case where the splenic artery was perforated, and 
the patient suddenly fell and died before there was any vomiting of 
blood, (c.) Death may result from gradual exhaustion, and this may 
take place even where the ulcer has healed, but there is a stricture of 
the stomach from cicatricial contraction. In such cases not only is 
there the severest cardialgia, but every thing that the patient eats is 
vomited; he may have no passage from his bowels for weeks, the belly 
sinks in, he wastes away to a skeleton, and dies from inanition. 
Diagnosis.—In the rare cases of ulcer of the stomach, where it 
runs its course without any pathognomonic symptoms, it cannot be 
distinguished from chronic gastric catarrh; but in most cases the dif- 
ferential diagnosis between the two affections presents no difficulty. 
Great sensitiveness of the stomach at a circumscribed spot, severe 
cardialgic attacks, but particularly vomiting of blood, exclude simple 
catarrh with great certainty. A far less certain sign is the appearance 
of the tongue, which is red and smooth in cases of round ulcer, and 
almost always coated in cases of simple catarrh. It may be difficult 
to distinguish it from stricture of the pylorus due to hypertrophy of 
the membranes of the stomach. The slightness of the cardialgic attacks, 
which are not in proportion to the frequency of the vomiting, the reg- 
ular occurrence of the latter, and the presence of consecutive dilatation 
of the stomach, aid somewhat in the diagnosis, as they indicate stric- 
ture rather than ulcer. 
Where, with great severity of the cardialgic attacks, there are no 
dyspeptic symptoms, and, in spite of the long continuance of their dis- 
ease, the patients preserve a blooming appearance, we may suspect a 
cicatrix, which impairs the motions of the stomach. The probability 
of this is still greater if there have formerly been for a long time sure 
signs of an ulcer of the stomach, which, except the cardialgia, have 
subsequently entirely disappeared. Where the symptoms of stricture 514 
DISEASES OF THE STOMACH. 
have developed and slowly increased after there has been chronic 
ulcer of the stomach, we must suspect that a cicatricial stricture has 
formed. 
We will speak in the following chapter of the diagnosis of chronic 
ulcer of the stomach, from cancer and nervous cardialgia. 
Prognosis.—In accordance with what we have said of the course 
and results, the prognosis of chronic ulcer of the stomach is, on the 
whole, favorable; we must not forget, however, that the disease often 
has remissions followed by exacerbations, that in the midst of apparent 
improvement hemorrhages will occur, and that, even after recovery 
has begun, relapses are always imminent. 
Treatment.—The disease of the blood-vessels, which, as we have 
said, gives rise to the partial necrosis of the walls of the stomach which 
results in round ulcer, can rarely be referred to chronic gastric catarrh; 
for topers, who have the most obstinate forms of this disease, rarely 
have ulcer of the stomach. As we do not know the causes of these 
affections of the blood-vessels, we have no hesitation in saying that, in 
the treatment of chronic ulcer of the stomach, we cannot fulfil the 
causal indications. 
Dietetic rules best answer the indications from the disease. The 
result of the treatment mostly depends on their being strictly followed 
out. It is true, we cannot protect the affected portion of the wall of 
the stomach from injury, as we would an ulcer of the skin; the intro- 
duction ©f even the mildest food excites a hypenemia of the gastric 
mucous membrane and irritates the affected part; however, the coarser 
and rougher the ingesta, the greater the irritation they excite. From 
this fact, proved by experiment and confirmed by practice, we deduce 
the rule that the patients should have the mildest possible, and, pref- 
erably, a liquid diet. We should then try if an exclusively milk diet 
will be borne; unfortunately, this is not always the case. If fresh 
milk curdles in the stomach to hard, tough lumps, we should always 
give it with white bread, as advised by Budd. Some patients, who 
cannot use fresh milk, have no difficulty with buttermilk, or sour milk. 
If the patient has a great distaste for milk-diet, or if he cannot take 
sour or buttermilk, we may give rich unskimmed soups, with an addi- 
tion of Liebig's meat-extract. The nutrition in the small quantities 
of these extracts that the patient takes is not great, it is true, but 
they are strong analeptics. Trommer's malt-extract, which has been 
before described, contains the nutritious constituents of malt in a state 
of solution, and is to be recommended because several spoonfuls of it 
may be taken daily without difficulty; hence it must be regarded as a 
valuable remedy. I know patients who have taken one or two ounces 
of Trommer's malt-extract daily for years. Vegetables, bread from CHRONIC ULCER OF THE STOMACH. 
515 
unbolted flour, roast potatoes, potato salad, etc., are particularly to be 
avoided, while puree of potatoes does well. 
The therapeutic use of the alkaline carbonates has a wonderful 
effect in chronic ulcer of the stomach. Among the mineral waters con- 
taining alkaline carbonates and purgative salts, the warm springs are 
preferable to the cold. Patients whose circumstances allow it may be 
sent to Karlsbad. If there be insuperable obstacles to a trip to the 
springs, Karlsbad, Marienbad, Tarasper, and similar waters may be 
prescribed at home; they should be properly warmed before drinking. 
In some cases I have seen patients wonderfully improved by the treat- 
ment at Wildbad, and other Akrato-therma, after they had taken the 
waters of Karlsbad and Marienbad without benefit; but am not con- 
vinced that the use of water from warm springs can replace the treat- 
ment at Karlsbad, as Professor Bock claims in the “ Gartenlaube.” I 
am sorry that so clear and shrewd a person as Bock should permit 
himself to spread a dangerous half-knowledge among the laity; I have 
more than once found that people, under the impression that they had 
learned enough from Bock's writings to judge of their cases and treat 
themselves, have done themselves great injury. The rules of the 
water-cures contain some superfluous and finikin regulations, but it is 
not well to shake faith in these, or else even the rational rules may be 
less carefully followed. Among the latter I place in the first rank, 
that patients should not eat later than seven o’clock, and then only 
soups, that they should not breakfast for at least half an hour or an 
hour after their last glass of water. It is certain that very much 
depends on the warm mineral water going into an empty stomach. 
If under the treatment just described, contrary to our expectations, 
there be no improvement, we may give nitrate of silver, or subnitrate 
of bismuth. From the effect that these remedies, particularly the for- 
mer, are seen to have on ulcers of the skin, or of other mucous mem- 
branes, their use appears perfectly rational, and in some cases the 
results attained with them are surprising. In other cases, on the con- 
trary, they do no good. For the mode of administering these rem- 
edies and their dose, we refer to what was said in the treatment of 
chronic gastric catarrh. 
The treatment of symptoms, first of all, requires the relief of the 
cardialgic attacks. There are but few cases of chronic ulcer of the 
stomach where we can dispense with the use of narcotics; these usually 
have an instantaneous and brilliant effect on the attacks of pain. 
Even a few minutes after the administration of a small dose of mor- 
phia, there is relief or even complete freedom from pain. This seems 
to show that the pain is chiefly induced by tension of the stomach. If 
it depended on irritation of the walls of the stomach by the ingesta, or 516 
DISEASES OF THE STOMACH. 
the gastric juice, we could not explain the action of the narcotics, 
which JaJcsch says is often magical; but, if it depends on tension of 
the walls of the stomach, wre can readily understand the effect of nar- 
cotics, which, besides their anaesthetic effect, retard the movements of 
the stomach. Stokes declares that morphia is the only trustworthy 
remedy in the treatment of chronic ulcer of the stomach, and thinks 
that all the other remedies which are highly spoken of are only effect- 
ual when combined with a narcotic, as is generally done in using sub- 
nitrate of bismuth. Very small doses {fa—gr.) of morphia usually 
suffice, and it is not necessary to increase these. JaJcsch saw a woman 
take the same sized dose of morphia more than a hundred times with- 
out its efficacy diminishing. Morphia is preferable to extract of hyoscy- 
amus or belladonna, which are also recommended. When the epigas- 
trium is very sensitive to pressure, a few leeches or wet cups fulfil the 
indications. If these do not answer the purpose, blisters or pustulat- 
ing plasters left for some time on the pit of the stomach may be of 
use. Among the symptoms deserving particular attention, we may 
have obstinate vomiting. The narcotics, particularly morphia, seem 
to be of aid in this symptom also. If they do no good, small pieces 
of ice or mouthfuls of ice-water are sometimes beneficial, and occasion- 
ally where all else fails we may give creasote (gtt. jv. to 3 vj. of 
wrater, in tablespoonful doses), or tincture of iodine (gtt. ii.—iii. in 
sweetened water). Finally, in the course of chronic ulcer of the stom- 
ach, hcematemesis or peritonitis may require special treatment; but 
we will speak of this in the chapters devoted to these subjects. 
CHAPTER YII. 
CARCINOMA OR THE STOMACH. 
Etiology.—Among the internal organs, the stomach is the one 
most frequently affected with carcinoma; it is usually affected pri- 
marily ; more rarely it is secondary to cancerous degeneration of other 
organs, or is propagated from them to the stomach. 
The cause of cancer of the stomach is just as obscure as that of 
cancer elsewhere. In some families it seems to be hereditary: the 
father of Napoleon I., his sister, and himself, died of this disease. In 
regard to the influence of sex, age, and employment, we may say that 
men are more frequently affected than women; that it is most frequent 
between the ages of forty and sixty years, while before forty it is rare, 
and before thirty it very exceptionally occurs ; finally, that no class of 
people escape it entirely. If cancer of the stomach be more frequent 
in the inferior classes than in the higher, it is because the former are CARCINOMA OF THE STOMACH. 
517 
more numerous. There is no proof of what has been said of the in- 
fluence of strong liquors, mental depression, the suppression of erup- 
tions, or the cure of ulcers (J. Frank). 
Anatomical Appearances.—Cancer of the stomach most fre- 
quently attacks the pyloric portion of the stomach, less often the 
cardiac portion or the small curvature, and most rarely the fundus 
and greater curvature. It always shows a tendency to spread trans- 
versely, so that cancer of the small curvature extends toward the 
greater, and that of the pyloric or cardiac portions readily causes annu- 
lar stricture. Cancerous stricture of the pyloric portion is usually 
sharply limited by the pylorus, while that of the cardiac almost always 
affects more or less of the oesophagus. 
Of the various forms of carcinoma of the stomach, the most fre- 
quent is scirrhus, medullary next, and the least frequent are alveolar 
or colloid; the various forms often combine—the union of scirrhus and 
medullary is most common. 
Scirrhus almost always begins in the submucous tissue; it occasion- 
ally forms small nodules, sometimes diffuse thickening, which, grow- 
ing irregularly, gives an uneven appearance. The growth has the char- 
acteristics of hard cancer, and presents a dull, whitish, dense mass of 
cartilaginous hardness. The mucous membrane soon unites with the 
subjacent neoplasia; it subsequently softens to a black pulp, sloughs 
off, and the bare surface of the cancer is left. The muscular coat usu- 
ally becomes hypertrophied, and shows the previously-described fan- 
like appearance; it may subsequently atrophy under the pressure of 
the growth, or may be destroyed by the latter. The serous coat be- 
comes thickened and clouded by local peritonitis, often unites with 
adjacent parts, and is frequently covered with milky, laminated de- 
posits. After the destruction of the mucous membrane, the exposed 
cancer begins to ulcerate; at first shallow, later deep excavations are 
formed, and we have an irregular cancerous ulcer, with hard, callous 
edges, like those occurring on the skin. In other cases medullary 
masses spring from the floor and borders of the scirrhous ulcer. 
If the affection of the stomach commence as medullary cancer, the 
nodules and diffuse thickening of the submucous tissue are softer from 
the first; they look like brain-substance, and, after a section through 
them, we may press out a quantity of the so-called “ cancer-juice.” 
Medullary cancer spreads much more rapidly than scirrhous, and soon 
projects from the inner surface of the stomach as soft, easily-bleeding, 
spongy excrescences. The middle of the growth usually breaks down 
into black, soft, ragged masses, while the proliferation continues 
the periphery. If the dead masses be thrown off, there is left an ex- 
cavated ulcer, surrounded by elevated, everted, cauliflower edges. 518 
DISEASES OF THE STOMACH. 
Such a cancerous ulcer may attain twice the size of the hand, and 
the proliferations be sufficient to encroach considerably upon the space 
in the stomach. 
Alveolar or colloid cancer rarely appears as scattered nodules; it 
more frequently occurs as diffuse degeneration. It also usually com- 
mences in the submucous tissue, but soon induces degeneration of all 
the coats of the stomach; in the wall, which has become several lines, 
or even half an inch thick, no trace of the original structure can be 
found; it consists almost entirely of innumerable small cavities (al- 
veoli), which contain a gelatinous fluid. Microscopic examination of 
the latter shows the cellular formation characteristic of gelatinous can- 
cer. In alveolar cancer, also, the mucous membrane is destroyed, the 
alveoli are evacuated, the free surface appears ragged and discolored ; 
but the loss of substance never becomes very deep, for, while the 
destruction goes on above, there is new production below. 
The cancerous degeneration often extends to other organs, particu- 
larly to the lymphatic glands, the pancreas, liver, transverse colon, or 
omentum. The breaking down of the growth may also extend beyond 
the stomach to these organs, and give rise to communication between 
the stomach and the intestines, or, after adhesion of the stomach to the 
anterior wall of the abdomen, perforation outwardly may occur. Al- 
veolar cancer alone rarely affects the organs above mentioned; but it 
frequently induces diffuse degeneration of the peritonaeum and conse- 
quent ascites. 
If the breaking down of the cancer advances to the peritonaeum be- 
fore the stomach has become adherent to the neighboring parts, its 
contents may escape into the abdomen, and fatal peritonitis result. 
If the cancerous degeneration leads to stricture of the pylorus, 
which, by nodular prominences and angular curvature of the contracted 
portion may still more increase the difficulty of the escape of the con- 
tents of the stomach, dilatation of the stomach will result. If, on the 
other hand, the cancer be located at the cardiac portion, or, if there be 
degeneration of a large portion of the wall of the stomach, as happens 
particularly in alveolar cancer, the stomach may become smaller. 
In many cases the diseased pylorus remains at its normal locality, 
being attached by adhesions; but in many others it moves freely, and, 
from its weight, sinks down in the abdomen even as low as the sym- 
physis pubis. 
Symptoms and Course.—Cases occur where it is impossible to 
recognize cancer of the stomach with certainty during life. In elee- 
mosynary and hospital practice, patients not unfrequently come under 
ireatment who are emaciated to skeletons, indifferent, and so apathetic, 
that they make no complaints, and cannot give any history of their CARCINOMA OF THE STOMACn. 
519 
case. At the same time they have no pain on pressure in the epigas- 
trium ; they have little appetite, but the food taken is not vomited, and 
examination of the abdomen reveals no tumor. It is necessary to 
know that cancer of the stomach may occur without the last-mentioned 
symptoms, and remember the possibility of its being the cause of the 
excessive marasmus; but an absolute diagnosis is impossible. If such 
a patient die and at the autopsy a large cancerous ulcer of the stom- 
ach be found, inexperienced physicians are usually greatly astonished, 
and cannot understand how a disease so severe and so far advanced 
could be mistaken. 
In other cases we can make an approximative diagnosis of cancer 
of the stomach. A patient, far advanced in life, complains of loss of 
appetite, of a feeling of pressure and fulness in the epigastrium, of 
eructation and other dyspeptic symptoms; but, along with these mild 
symptoms, the patient rapidly loses his strength, acquires a dirty-yel- 
low cachectic color of the face, and finally oedema of the ankles occurs. 
If, in such a case, we- can exclude other diseases, which might explain 
the cachexia and marasmus, we have cause to suspect that there is not 
a chronic catarrh, but a malignant disease of the stomach, even if there 
be no actual pain, vomiting, or characteristic tumor. 
In most cases the symptoms of cancer of the stomach are much 
more decided, and can scarcely be mistaken. Besides the dyspepsia 
and symptoms of cachexia and marasmus, there is tenderness in the 
region of the stomach. This is increased by pressure, and also after 
eating; but does not usually attain the severity of cardialgic attacks. 
Almost as often there is vomiting. When the cancer is in the smaller 
curvature, the vomiting only occurs now and then, but comes after 
every meal, when it constricts the pyloric or cardiac orifices. In stric- 
ture of the pylorus the vomiting does not usually come on till several 
hours after eating; in stricture of the cardiac orifice it occurs imme- 
diately after or during eating. Occasionally it happens that, after the 
vomiting has recurred regularly for a time, it gradually becomes less 
frequent, ceases altogether, or is replaced by a sort of chewing the 
cud. This occurrence is explained when the autopsy shows that by 
breaking down of the cancer the contracted part has become larger, or 
that the stomach, being enormously dilated or structurally changed, is 
evidently not in condition to contract and perform its part in the act 
of vomiting. In other cases the autopsy gives no explanation of the 
cessation of vomiting. The vomited masses consist sometimes of the 
food, enveloped in a thick coat of mucus, which is little changed, if the 
cancer be at the cardiac extremity, but is often greatly altered when 
the pylorus is affected; sometimes they consist only of quantities of 
mucus and variously-colored sour and bitter liquid. The presence of 520 
DISEASES OF THE STOMACH. 
lactic, butyric, or acetic acids in the vomited matters depends on the 
causes that we investigated when speaking of simple stricture of the 
pylorus. Sarcina ventriculi very often occur in the vomited matters, 
while portions of the cancerous growth are rarely found. This is be- 
cause, while the cancer ulcerates and breaks down, the characteristic 
form of its elements is destroyed. Capillary haemorrhage readily re- 
sults from the breaking down of the vascular growth. The blood 
poured into the stomach is quickly altered by its acid contents and 
converted into a black, grumous mass. Hence the presence of “ cof 
fee-ground ” masses in the vomited matters is a frequent and impor- 
tant symptom in cancer of the stomach; but its diagnostic significance 
has been much overestimated. The erosion of large vessels, causing 
copious haemorrhage, is much more rare; in doubtful cases this symp- 
tom indicates chronic ulcer of the stomach (see Chapter VIII.) rather 
than cancerous disease. 
The most important symptom of cancer of the stomach is the pres- 
ence of a tumor in the epigastrium. It is necessary to know that this 
symptom may be wholly absent; this may be readily understood when 
we remember the relation of the stomach to the liver and ribs. Can- 
cer of the cardiac portion never causes a perceptible tumor, even when 
it attains a great size; that of the small curvature is not felt till it has 
advanced to the greater curvature. Most of the tumors that can be 
felt are located at or near the pylorus, the pyloric part of the stomach; 
and it is only because cancer affects this portion most frequently, that 
we almost always find a tumor in this disease of the stomach. HyrtVs 
description of the position of the stomach is not true; this is particu- 
larly the case in the assertion that, on expiration, the point of the ster- 
num corresponds to the middle of the anterior wall of the stomach. 
LuscKka, says, in his classical work (on every page of which the prac- 
titioner will find valuable information), that an incision made through 
the median line of the body will divide the stomach, so that five-sixths 
will lie on the left side, and at most one-sixth on the right. When the 
itomach is in a normal position, even cancer of the pylorus will give a 
tumor of the left side. When the diseased pylorus sinks down from its 
weight, the tumor may be near the navel, usually somewhat above and 
rather to the right than to the left of this. If it be still farther down, 
it may be mistaken for ovarian tumor. The size of the tumor varies 
from that of a pigeon’s egg to that of the fist; if it be very large, it 
may form a visible prominence in the abdomen; the surface is usually 
uneven and nodular. In many cases the tumor is movable, and it 
changes position according as the stomach is full or empty; in other 
cases, where there are adhesions, it is immovable. In the same way 
the sensitiveness of the tumor varies greatly. Sometimes, instead ot CARCINOMA OF THE STOMACH. 
521 
a circumscribed, nodular tumor, we find a regular, more or less exten- 
sive prominence and resistance of the epigastrium. Percussion of the 
tumor, caused by cancer of the stomach, almost always gives a not 
quite clear and decidedly tympanitic sound. 
In cancerous stricture of the pylorus, besides showing the presence 
of a tumor, physical examination may prove a dilatation of the stomach, 
whose symptoms we described while speaking of simple stricture of 
the pylorus; if, on the other hand, the stomach be contracted, and, as 
often happens, the bowels be empty, the lower margin of the ribs be- 
comes very prominent, while the belly is sunken, so that we can dis- 
tinctly feel the vertebral column and the pulsating aorta. The symp- 
toms of cancer of the stomach are modified by the development of 
cancer in other organs, particularly in the liver. Occasionally, also, 
cancer of the lymphatic glands of the stomach spreads to the retro- 
peritoneal glands, to those of the mediastinum, thence to those of the 
neck, so that a hard swelling of the supra-clavicular glands may be of 
diagnostic importance in cases of cancer of the stomach (I have seen 
such cases). The symptoms of alveolar cancer are often modified by 
the occurrence of ascites. 
During the course of cancer of the stomach the symptoms gener- 
ally increase regularly; more rarely, the patient improves for a time, 
pain and vomiting cease for a while, and even the appetite returns. 
These remissions do not usually continue long; the difficulties increase 
again, the appetite is entirely lost; constipation, which has existed 
from the first, can hardly be overcome; emaciation makes giant strides. 
If the cancer be medullary, the disease usually runs its course in a few 
months, while scirrhus, and particularly alveolar cancer, may run on 
for years. 
The only termination of cancer of the stomach is in death. In 
those cases where cure of cancer has been claimed from the clinical 
course of a disease of the stomach, there may have been a mistake in 
diagnosis. Those observations, where autopsy is said to have revealed 
the cicatrix of a cancerous ulcer, also are not perfectly trustworthy; 
for if fresh cancerous growths are found in the vicinity of the cicatrix, 
the disease has not truly disappeared; but if this support be wanting, 
the cicatrix from a cancer cannot be certainly distinguished from that 
of a simple ulcer. In most cases, death occurs with the symptoms of 
exhaustion. As there is no accompanying fever, the last stage of the 
disease is usually much protracted, and patients may live for days, 
while we hourly expect their death. In these cases the tongue usually 
becomes red, inclined to dryness, and covered with aphthous deposits. 
Besides this painful affection, there is not unfrequently a painful tense 
oedema of one of the legs shortly before death. This symptom do 522 
DISEASES OF THE STOMACH. 
pends on obstruction of the femoral vein, and shows that, in conse- 
quence of the retarded circulation, a clot has formed in it. More rarely 
death occurs from a rapid peritonitis, after perforation of the stomach. 
Still more rarely, copious haemorrhage from the stomach hastens the 
exhaustion, or, by its extent, causes sudden death. Finally, death 
may be caused or hastened by complications and secondary diseases. 
Diagnosis.—In cases where the epigastrium is painful, where there 
is frequent vomiting, occasionally of substance looking like coffee- 
grounds, where there is a tumor in the epigastrium, the diagnosis of 
cancer of the stomach from chronic catarrh is easy. If these symp- 
toms be absent, particularly the tumor, which Andral maintains is the 
only certain sign of cancer of the stomach, the differential diagnosis 
of these two diseases may be very difficult. In forming an opinion, 
the age of the patient is important; besides this, we often can only 
judge from the general condition. 
The diagnosis from chronic ulcer of the stomach, also, is sometimes 
easy, again very difficult. In one well-known case, two medical celeb- 
rities, Oppolzer and Schoenlein, could not agree whether there was 
cancer or ulcer of the stomach. In the differential diagnosis, the factors 
chiefly to be regarded are the following: 1. The age of the patient; 
in young persons, cancer may be excluded almost with certainty. 2. 
The duration of the disease; if it has existed more than a year, the 
probabilities are against cancer. 3. The strength and condition of the 
patient; in ulcer, these are often affected but little, and not till late in 
the disease, while in cancer they are greatly impaired very early. 4. 
The character of the pain; cardialgic attacks indicate ulcer rather than 
cancer. 5. The condition of the blood vomited; in ulcer of the stomach, 
it is in large quantities, and hence slightly changed, while in cancer the 
amount is usually scanty, it is black, and looks like coffee-grounds; 
still, in some cases of cancer, there is abundant vomiting of blood, and 
with an ulcer of the stomach there may be ejection of black, grumous 
masses. 6. The presence or absence of a tumor; the former proves 
almost certainly that there is cancer, for the cases where thickening of 
the walls of the stomach and connective-tissue growths, in the vicinity 
of an ulcer, cause a tumor, are exceedingly rare. But, on the other 
hand, we must not forget that absence of a tumor does not prove that 
there is no cancer. 
The variety of the cancer can rarely be determined with any cer- 
tainty during life. Alveolar cancer, being the rarest variety, is only 
to be suspected where the disease runs a very sIoav course, and when 
there is ascites. The diagnosis becomes more certain if, after tapping, 
nodular masses can be felt in the omentum. If these symptoms are 
absent, we must suspect scirrlius or medullary cancer. The more acute HEMORRHAGE FROM THE STOMACH. 
523 
the course, the larger the tumor becomes and the more rapidly it 
grows, the more probable it is that the new formation is medullary 
cancer. 
Treatment.—As the indications from the cause and from the dis- 
ease cannot be fulfilled, we must restrict ourselves to the treatment 
of symptoms. The diet must be regulated according to the rules pre- 
scribed in the treatment of chronic gastric catarrh; if milk be well 
borne, it is the most suitable nourishment; if milk cannot be used, con- 
centrated broths, yolk of egg, and other nutritious substances may be 
ordered, but always in small quantities, and where there is stricture 
they should be given in fluid form or finely divided. Wine also, par- 
ticularly red wine, may be given, and it is usually well borne. For 
the excessive acidity, the alkaline carbonates do well, especially in 
the form of soda-water; they often fail, however, and sometimes, 
as in stricture of the pylorus, we cannot in any way prevent the 
acidity. In such cases it is well at each meal to give pills containing 
gtt. 1— of creasote, as recommended by JSudd. Pills of aloes and 
colocynth may be given for the obstinate constipation. For the severe 
pain and the sleeplessness, narcotics, particularly morphia, must be 
given. 
CHAPTER VIII. 
HEMORRHAGE FROM THE STOMACH. 
Etiology.—1. Haemorrhage from the stomach results from rupture 
of the over-filled blood-vessels without previous change of texture. 
Arterial fluxion is rarely so decided as to cause rupture; besides the 
slight haemorrhage seen in inflammation of the stomach, this occasion- 
ally occurs in anomalies of menstruation. It cannot be denied that 
ripening and detachment of an ovum are sometimes accompanied by 
fluxions and haemorrhages in other organs and not in the uterus, 
although we can give no explanation of the fact. Venous congestion 
of the gastric mucous membrane is a much more frequent cause of 
haemorrhage. The most decided congestions result from impediments 
to the circulation in the liver. Haemorrhage from the stomach may be 
caused by obstructions of the portal vein by blood-clots ; by pressure 
on its branches due to cirrhosis of the liver, or to the enlargement of 
the gall-ducts, caused by closure of the ductus hepaticus or choledochus; 
by plugging of the capillary vessels of the liver with clumps of pig- 
ment in pernicious fever (Frerichs); finally, by destruction of the 
capillaries, in the so-called yellow atrophy of the liver. The hyper- 
semiaof the gastric mucous membrane, due to obstruction of the cir- 
culation in the chest by diseases of the lungs, pleura, heart, or pericar- 524 
DISEASES OF THE STOMACH. 
dium, is rarely sufficient to cause a rupture of the vessels; but 
haemorrhage from the stomach is sometimes seen from these causes. 
The haemorrhages which sometimes occur in new-born infants most 
likely belong in this class. It is most probable that these depend on 
imperfect expansion of the lungs, and the obstruction thus induced tc 
the flow of blood from the stomach. 
2. Haemorrhage from the stomach may result from the rupture of 
diseased vessels. In rare cases varices burst or aneurisms open into 
the stomach. More frequently disease of the walls of the vessels must be 
suspected, without our being able to prove it either with or without the 
microscope. Under this head come the haemorrhages occurring in the 
so-called haemorrhagic diathesis; those coming after exhausting dis- 
eases, in the course of yellow fever and other severe diseases; finally, 
those arising from improper living, especially abstinence from fresh 
meat and vegetables, which form one of the symptoms of scorbutis. 
In these cases it is insufficient to ascribe the bleeding immediately to 
an abnormal quality of the blood; this can only act by disturbing the 
nutrition of the walls of the vessels. 
3. Finally, haemorrhage from the stomach may arise from erosion 
and other injuries of the walls of the vessels. In this class belong the 
cases where chronic ulcer or ulcerating carcinoma leads to haemorrhage 
from the capillaries or larger vessels; those where corrosive substances 
and sharp, foreign bodies open vessels of the stomach; lastly, those 
where a blow over the stomach has caused rupture of one of the 
vessels. 
Anatomical Appearances.—Even after decided haemorrhages 
from the gastric mucous membrane, we often seek in vain, on post- 
mortem examination, for its source; when the patient has died from 
loss of blood, after washing off the stomach, we find it just as pale and 
bloodless as the rest of the body. In other cases there has been coin- 
cident capillary haemorrhage in the mucous membrane, in which we 
find bluish-red or blackish-red spots, from which blood oozes out on 
slight pressure. This haemorrhagic infiltration of circumscribed por- 
tions of mucous membrane generally leads to superficial softening and 
throwing off of the softened portion; superficial excavations thus oc- 
cur, which are not discovered till the dirty-brown blood particles cling- 
ing to them are washed off. The superficial bleeding fossae, called 
haemorrhagic erosions, are usually numerous, small, of round or elon- 
gated form, and are chiefly found at the summit of the longitudinal 
folds formed by the mucous membrane. If large vessels have been 
eroded by ulcer or cancer of the stomach, or if ruptured varices or 
aneurisms have caused the haemorrhage, we may in many cases find 
the gaping mouth of the vessel. HAEMORRHAGE FROM THE STOMACH. 
525 
When the patient dies soon after the haemorrhage, and if this has 
been very copious and occurred rapidly, the blood contained in the 
stomach forms red, clotted masses. If it has escaped slowly, and has 
been retained in the stomach a long while, so that the gastric juice and 
the acid contents of the stomach have had a chance to act on it, it ap- 
pears brown or black. Where the haemorrhage has been very slight, 
we find only a few black striae and flocculi, or masses like coffee-grounds, 
in the stomach. 
Symptoms and Course.—If the haemorrhage from the stomach be 
not abundant and the blood be not vomited, the haemorrhage is not 
usually recognized during life. According to Beaumont's observations, 
small haemorrhages usually occur in the stomach during acute gastric 
catarrh; but blood mixed with mucus is very rarely vomited. The 
haemorrhagic erosions also, which, as proved by autopsies, quite fre- 
quently accompany chronic catarrh, cancer, and ulcer, rarely cause 
haematemesis and consequently are rarely recognized during life. 
In other cases, it is true, the mixture of small quantities of blood 
with the vomited matters leaves no doubt that there has been a haem- 
orrhage from the stomach, when it is certain that the blood has not 
been previously swallowed; but frequently haematemesis is the only 
symptom of the bleeding. This is daily observed in patients with 
cancer of the stomach, who are neither better nor worse when they 
vomit the “ coffee-ground ” masses. 
If there has been a quantity of blood poured into the stomach, 
there are usually some symptoms preceding the haematemesis. These 
depend partly on the stomach being full of blood, partly on the empti- 
ness of the blood-vessels of the body. The patients have a feeling of 
pressure about the stomach, a desire to loosen the clothes, feel con- 
stricted and nauseated; they become pale, the pulse is small, the skin 
cool, they see sparks before the eyes, have noises in the ears, become 
dizzy, or they even faint. I knew one case where a surgeon opened 
a vein for his mother, while she was in such a state, thinking that she 
was apoplectic. In robust, strong persons the faint feelings do not 
occur, and the premonitory symptoms are limited to the feeling of 
pressure and fulness in the epigastrium. After there has been nausea 
for a time, accompanied by the feeling of a warm fluid rising in the 
oesophagus, and a sweetish, stale taste, there is violent vomiting, and, 
to the great terror of the patient, blood, partly fluid, partly clotted, 
and usually dark brown, is evacuated through the mouth and nose. 
Small portions of blood often enter the larynx and induce coughing, 
and, as blood is brought up by this also, the patients relate that they 
have “ broken a blood-vessel,” but they cannot say whether they vom- 
ited or coughed up the blood. Sooner or later, after the haematemesis, 526 
DISEASES OF THE STOMACH. 
there is a passage of blood from the bowels. If the haemorrhage were 
very copious, blood is passed at stool very soon afterward, and it 
appears in black, clotted masses; if it be not passed for two or three 
days after the liaematemesis, it is usually changed to a black, tar-like 
mass. In exceptional cases the blood poured into the stomach is 
evacuated by stool alone, and there is no vomiting. If patients, suffer- 
ing from chronic ulcer of the stomach, become very pale in a shorl 
time, and show other symptoms that may depend on internal haemor- 
rhage, we should not neglect to examine the passages repeatedly. 
Many pounds of blood may be withdrawn from the circulation in a 
short time by haemorrhage of the stomach; and even the strongest 
persons will then become pale, cool, and faint. In severe cases, every 
attempt of the patient to sit up, or even to raise the head, causes 
nausea, blackness before the eyes, and dizziness; every attempt to 
rise brings on fainting. Terrifying as it usually is to the patient and 
those around him, the fainting undoubtedly has a beneficial effect on 
the attack, for it momentarily arrests the haemorrhage and favors the 
formation of coagula. It appears entirely due to this fact that the 
affection usually terminates more favorably than we should expect 
from the appearance of the patient. Indeed, proportionately few 
patients die of haemorrhage from the stomach, that is, by bleeding to 
death, or suffocating from the blood entering the larynx. Much more 
frequently, after the patients have become deathly pale and exces- 
sively exhausted, and have lain for days in an apparently hopeless 
state, the vomiting ceases, blood gradually disappears from the stools, 
and a very slow convalescence begins. The patients long remain with- 
out appetite, complain of foul eructations and an unpleasant taste. As 
the great loss of blood is replaced by water, the patients become very 
liydraemic, and often dropsical; but these symptoms may also disap- 
pear, although, perhaps, somewhat slowly, and the patients recover. 
Finally, we must mention those cases where the haemorrhage is so 
profuse that the patient dies before the blood is evacuated either up- 
ward or downward. We must remember this when a patient, who has 
had the symptoms of chronic ulcer or cancer of the stomach, suddenly 
sinks with the symptoms of internal haemorrhage and dies in a few 
minutes. 
Diagnosis.—Since patients with haemoptysis often vomit at the 
same time, and those with haematemesis frequently nave a coincident 
cough, it is not always easy to distinguish haemorrhage of the stomach 
from that coming from the lungs or bronchi, particularly if we are not 
present at the time, or if it is a question of a “ haemorrhage ” that has 
occurred some years before. The following points are important in 
the differential diagnosis. HAEMORRHAGE FROM THE STOMACH. 
527 
1. The appearance of the blood ejected. Vomited blood is usually 
dark, blackish, clotted, mixed with food; the coagula, containing no 
air, are heavier; sometimes it has an acid reaction from the gastric, 
juice. On the other hand, blood coming from the lungs and bronchi 
is usually bright-red, frothy, mixed with mucus, not coagulated at first, 
and if a coagulum does form, it contains air-bubbles and is light; its 
reaction is always alkaline. But we must know that blood, which has 
been but a short time in the stomach, and has been little affected by 
the gastric juice, may be bright red, and, on subsequent hasmatemesis, 
small portions of black blood may be thrown off. 
2. Vomiting of blood is, in most cases, preceded by cardialgic at- 
tacks and other symptoms of ulcer or cancer of the stomach; in the 
much rarer cases caused by congestions and fluxions, there are symp- 
toms of hyperaemia of all the organs in the abdomen; haemoptysis, on 
the other hand, is usually preceded by disturbance of the respiration, 
and of the circulation in the thoracic viscera. 
3. Intelligent patients can generally tell whether vomiting occurred 
first and was followed by coughing, or whether, on the other hand, 
nausea, retching, and vomiting have been excited by the coughing. 
4. In hasmatemesis percussion generally shows fulness of the 
stomach, while physical examination of the chest shows no changes 
there. In haemoptysis there is no epigastric dulness on percussion, 
and in the thorax we almost always hear moist rales, if there be no 
other sounds present. 
5. After vomiting of blood, there are almost always bloody stools 
for a few days; after coughing of blood, instead of these, there is just 
as often a bloody mucous expectoration. 
We cannot tell, from the vomited matters or from the. stools, 
whether the blood vomited really comes from the stomach or whether 
it has been swallowed. In doubtful cases we should carefully exam- 
ine the nose and pharynx, and ask the patient if he noticed any signs 
of nose-bleed before going to bed the previous night. A careful 
inquiry about premonitory symptoms may clear up the matter here 
also, particularly when we suspect intentional deception. In the 
description of the symptoms preceding the vomiting, malingerers usu- 
ally overdraw the picture, and this fact, with the contradictory state- 
ments they make, often assists to expose them. 
It is generally easy to decide whether the vomited matters be 
really blood or not, although there are cases where the physician has 
lost his presence of mind, and mistaken stewed cherries for blood. 
Even in the black coffee-ground masses some shrunken and misshapen 
blood-corpuscles can almost always be recognized with the microscope, 
and a chemical examination to prove the presence of iron in the black 528 
DISEASES OF THE STOMACH. 
masses, will very rarely be necessary to determine that it is really 
altered blood. 
It is usually easy to decide whether the bleeding depends on the 
erosion of large vessels or the rupture of capillaries. Besides the fact 
that in the first case the bleeding is usually more abundant than in 
the latter, a review of the premonitory symptoms almost always gives 
a certain means of diagnosis. If there have been cardialgic attacks, 
chronic vomiting, and other symptoms of ulcer of the stomach, there 
is probably erosion of a large vessel, which is by far the most frequent 
cause of haemorrhage from the stomach. If, on the contrary, there have 
been ascites, enlargement of the spleen, or other signs of obstruction 
to the portal circulation, the haemorrhage is most probably from the 
smaller vessels, and was caused by venous congestion. If the hemor- 
rhages occur regularly every four weeks while there is amenorrhoea, we 
must suspect extensive fluxion to the stomach; if it come during yel- 
low fever, or scorbutis, or after exhausting diseases, we must suspect 
disturbance of nutrition of the walls of the vessels. 
Prognosis.—We have already mentioned that only a small pro- 
portion of patients die from hematemesis, and that in spite of the 
waxy color of the skin, and even of the long-continued faintness, we 
may give a favorable prognosis. It is doubtful whether hcemorrhage 
from the stomach has under any circumstances a beneficial influence 
on chronic ulcer of the stomach; if the patients are occasionally better 
for a long time after it, it is probably because the severe attack has 
frightened them, and they have become more careful in their diet. 
The haemorrhages caused by congestion may temporarily have a good 
effect on the other symptoms of abdominal plethora. On the other 
hand, in scorbutis and other exhausting diseases, haemorrhage from 
the stomach always renders the prognosis more grave. 
Treatment.—The prophylactic and causal indications are fulfilled 
by the treatment of the original disease. If patients, with cirrhosis or 
other disturbance of the circulation of the liver, show premonitory 
symptoms of haemorrhage from the stomach, we may with advantage 
apply a few leeches to the anus; in women, who with amenorrhoea 
have periodical vomiting of blood, we may from time to time apply a 
few leeches to the os uteri. 
The indications from the disease require a less energetic treatment 
in haemorrhage from the capillaries, than in that depending on erosion 
of a large vessel. At the commencement of the latter, JdJcsch recom- 
mends a venesection; but this is rarely beneficial, and when not so, 
increases the danger. The employment of Junod's cupping-boot 
would be much more advisable, but never after faintness has come on; 
lor, after this, the use of hacmospastics, which may cause even robusf SPASM OF THE STOMACH—NERVOUS CARDIALGIA. 
529 
patients to faint, is very dangerous. Cold must be regarded as the 
most efficacious remedy in haemorrhage from the stomach; we may 
let the patients swallow small quantities of ice-water or small pieces 
of ice, from time to time, and we may cover the epigastrium with cold 
water or ice-compresses, and renew them frequently. Styptic medi- 
cines are not always well borne, but are often vomited up; the best 
of these are mistura sulphurica acida or alum, particularly in the form 
of serum lactis aluminatum. We should always give these remedies 
in small quantities and keep them on ice. Acetate of lead, sulphate 
of iron, and ergotin, may be dispensed with. 
The indications from the symptoms, first of all, require attention 
to the syncope. The patient must lie flat in bed; must not rise to 
stool, but use a bed-pan. If syncope occur, we may hold eau de cologne 
or hartshorn to the nose, and sprinkle the face with water, but be 
very careful about the internal administration of restoratives. Among 
these cold champagne is best, as it is less apt to cause vomiting than 
the analeptic medicines. The unceasing inclination to vomit, which is 
partly due to the attacks of syncope, partly to the blood in the stom- 
ach, is the most annoying symptom that the patient has. In trying 
to arrest it, we should be careful about the use of narcotics, and should 
preferably apply a sinapism to the pit of the stomach occasionally, 
and give a pinch of effervescing powder. Since P. Frank has an- 
nounced that it is necessary to purge patients with haemorrhage from 
the stomach, to prevent the blood from exciting low and putrid fever, 
clysters and slight cooling laxatives are almost universally prescribed. 
My observations correspond with those of Bamberger, according to 
whom even enemata are injurious for the first few days after a haemor- 
rhage. 
CHAPTER IX. 
SPASM OF THE STOMACH—NERVOUS CARDIALGIA. 
Etiology.—By nervous cardialgia, we mean painful affections of 
the stomach, not dependent on perceptible changes of structure. Rom- 
berg distinguishes two forms of this disease, one of which, he says, de- 
pends on a hyperaesthesia of the pneumogastric, the other on hyperaes- 
thesia of the solar plexus. The former he calls gastrodynia neuralgica, 
the latter neuralgia coeliaca. But it can probably never be determined 
in any given case whether the pains be located in the filaments of the 
pneumogastric or in those of the sympathetic; and Henoch says, with 
truth, that this distinction is practically worthless, though it may be 
theoretically correct. 530 
DISEASES OF THE STOMACH. 
1. Like other nervous diseases, this affection is often observed in 
anaemic persons. If in chlorotic females, who have more or less se- 
vere attacks of spasm of the stomach as a constant symptom, the blood 
be enriched by preparations of iron, the cardialgia disappears, even in 
those cases where the amenorrhoea continues, and the quick recurrence 
of the chlorosis proves that the original disease has not been removed. 
It follows, from these observations, that the cardialgia of chlorotic pa- 
tients depends solely on the poverty of the blood; not, as in hysterical 
women, on affections of the sexual organs. The cardialgia not unfre- 
quently observed in tuberculous persons, convalescents, and onanists, 
probably, also, depends on poverty of the blood. 
2. Diseases of the uterus, such as dislocations, flexions, or chrome 
inflammation, and follicular ulcers of the os uteri, as well as affections 
of the ovaries, induce cardialgia. It is among the most frequent symp- 
toms of hysteria. The dependence of spasm of the stomach on affec- 
tions of the female sexual organs is most evident when the attacks 
occur exclusively, or are most severe, at the menstrual periods. I 
treated one woman for amenorrhoea with retroflexion of the uterus and 
catarrhal erosions of the os uteri, whose cardialgic attacks recurred 
regularly every four weeks and lasted three days; but during the in- 
tervals they only appeared when leeches were applied to the cervix 
uteri, and they only lasted during the time of the application. 
3. In other cases, nervous cardialgia depends on diseases of the spinal 
marrow or brain; and from analogy with other neuroses, it is probable, 
although it has not been proved by observations, that it may be caused 
by organic changes in the pneumogastric, or sympathetic "nerves, 
swelling of their neurilemma, or tumors pressing on them. 
4. Cardialgia may depend on dyscrasia. Infection of the blood, with 
malarial poison, occasionally seems to excite spasm of the stomach in- 
stead of the paroxysm of intermittent fever. Romberg attaches par- 
ticular importance to arthritis as a cause, and in his own first attack 
of gout he suffered severely from spasm of the stomach. 
5. Finally, we frequently cannot find, either during life, or on au- 
topsy, any cause for cardialgia that has existed for years. 
From the description above given, the attacks of pain caused by 
certain contents of the stomach, without any structural change, must 
be considered as nervous cardialgia. Among these are the cases of 
spasm of the stomach induced by excessive acidity, by the presence of 
worms in the stomach, by the exhibition of certain medicines, and oc- 
casionally after a cold drink and similar causes. 
Symptoms akd Course.—Like most neuroses, nervous cardialgia 
is distinguished from other diseases by its typical course, i. e., after in- 
tervals of freedom, follow paroxysms of the severest pain. Occasion- SPASM OF THE STOMACH—NERVOUS CARDIALGIA. 
531 
ally there is a regular type, so that the attacks recur at the same hour 
daily, or every second or third day. 
It is impossible to describe a cardialgic attack more strikingly, or 
briefly, than has been done by Romberg. 
“ Suddenly, or after a precedent feeling of pressure, there is severe, 
griping pain in the pit of the stomach, usually extending to the back, 
with a feeling of faintness, shrunken countenance, cold hands and feet, 
and small intermittent pulse. The pain becomes so excessive that the 
patient cries out. The epigastrium is either puffed out, like a ball, or, 
as is more frequently the case, retracted, with tension of the abdominal 
walls. There is often pulsation in the epigastrium. External pres- 
sure is well borne, and not unfrequently the patient presses the pit of 
the stomach against some firm substance, or compresses it with his 
bands. Sympathetic pains often occur in the thorax under the ster- 
num, in the oesophageal branches of the pneumogastric, while they 
are rare in the exterior of the body.” 
“ The attack lasts from a few minutes to half an hour; then the 
pain gradually subsides, leaving the patient much exhausted; or else 
it ceases suddenly with eructation of gas or watery fluid, with vomit- 
ing, with a gentle soft perspiration, or with the passage of reddish 
urine.” 
Besides these severe attacks, we often see painful sensations, of 
various varieties and degrees of intensity, in the stomach, which also 
alternate with intervals of rest and freedom from pain, which are less- 
ened, not increased, by external pressure, or by the introduction of 
food; these also are accompanied by sympathetic pain in the breast 
and back, reflex motions of the abdominal muscles, etc. It is these 
mild attacks, without “ the feeling of faintness and impending death,” 
that Romberg styles neuralgia of the pneumogastric, in contradistinc- 
tion to neuralgia coeliaca.” 
Diagnosis.—The character of the pain gives no aid in distinguish- 
ing cardialgic attacks, accompanying an ulcer of the stomach, from 
those due to neuralgia of the gastric nerves. In the former we also 
see the extension of the pain to the back and breast, and see them 
subside with vomiting and eructation, and the depressing effect of the 
pain on the patient. The following factors are important in judging 
between the two states: 1. In most cases, pains induced by ulcer of 
the stomach are increased by external pressure or by introduction of food 
(“ pressure from within ”); while, on the other hand, nervous cardialgia 
is usually relieved by pressure over the stomach, and by eating. 2. In 
chronic ulcer of the stomach, dyspepsia and other symptoms of dis- 
turbance of the functions of the stomach are present during the in- 
tervals ; these do not appear in nervous cardialgia. In accordance with 532 
DISEASES OF THE STOMACH. 
this, nutrition is little impaired in the latter disease, and, when the 
neuralgia is not due to anosmia, the patient may look strong and 
healthy. 3. Dysmenorrhoea, metrorrhagia, sterility, and other symp- 
toms which betray affection of the sexual organs, as well as decided 
chlorosis, render it probable that the affection is nervous in character; 
but too much weight must not be attached to these symptoms, for it is 
in just such cases that ulcer of the stomach is apt to occur. 4. The 
simultaneous occurrence of other neuralgic affections speaks for a 
similar nature in these attacks of pain. 5. Finally, genuine neuralgia 
of the stomach is excited by unknown causes, and often occurs while 
the stomach is empty; the attacks of pain in ulcer of the stomach 
almost always come after eating. 
Prognosis.—The prognosis is favorable in cardialgia dependent on 
poverty of the blood, which is not due to cancer, tuberculosis, or some 
other incurable disease. Those cases, also, that are caused by uterine 
complaints disappear with the cure of the original disease, if this be 
amenable to treatment. The prognosis is generally favorable, also, in 
those cases resulting from the influence of malaria or arthritis. On 
the other hand, treatment is almost always unavailing in the cases 
depending on affections of the brain or spinal marrow, and in those 
arising from unknown causes. 
Treatment.—The indications from the cause require the energetic 
and early employment of the preparations of iron in chlorotic and 
anasmic cases. It is a great error to delay the use of iron in the treat- 
ment of chlorosis until the stomach is prepared for it, and the cardialgic 
attacks have passed away. The dyspepsia and cardialgia of chlorotic 
patients do not yield sooner to any remedies than to those which 
improve the state of the blood. The springs of Pyrmont, Driburg, 
and Cudowa are wonderfully beneficial in this affection. Among the 
officinal preparations of iron, the best is the ferri carbonas saccharata 
(Br.). Blaud's pills are also an excellent prescription (see treatment 
of chlorosis). In hysterical cardialgia, applications of leeches to the 
os uteri, touching ulcers on it with nitrate of silver, and other treat- 
ment, which we shall learn when speaking of uterine diseases, may be 
indicated, and may have a striking effect. In cardialgia excited by 
malaria or arthritis, the fulfilment of the causal indications answers for 
the treatment of the original disease. 
The indications from the disease are best answered by the narcotics, 
and, among these, acetate of morphia is preferable to the extracts of 
hyoscyamus, belladonna, etc., which have also been recommended. 
This remedy is usually given in combination with the so-called anti- 
spasmodics, particularly with valerian, asafoetida, and castoreum. Re- 
cently, a mixture of equal parts of tincture of nux vomica and tincture DYSPEPSIA. 
533 
of castor (dose, 12 drops during the attack) has been much used, and 
apparently with good effect. Metallic remedies also, particularly 
nitrate of bismuth, nitrate of silver, cyanide of zinc, have been recom 
mended in spasm of the stomach; however, as they are scarcely ever 
given alone, but are used in combination with narcotics, their efficacy 
is problematical. Finally, llomberg recommends aiding the treatment 
by applying belladonna or galbanum plasters over the stomach, or rub- 
bing in a mixture of mixtura oleosa-balsamicae ( § j) with tinctura 
opii ( 3 ij). 
CHAPTER X. 
DYSPEPSIA. 
In the preceding chapters we have often spoken of dyspeptic symp- 
toms, i. e., of signs of impaired digestion. Hence, while giving a sepa- 
rate chapter to dyspepsia, we shall only speak of those disturbances of 
digestion which arise without perceptible change of structure of the 
stomach. The different forms of this dyspepsia may be included under 
two heads: the digestion is impaired either because the gastric juice 
secreted is of abnormal quality, or because the movements of the 
stomach are diminished, and, consequently, the ingesta are not suffi- 
ciently mixed with the gastric juice. Digestion, which is a purely 
chemical process, can only be influenced by the nerves when they 
modify the secretions, or the movements of the stomach, and only in 
this sense is it proper to speak of nervous dyspepsia. 
The change in the gastric juice may be either qualitative or quan- 
titative. We know very little about the qualitative changes. They 
may consist in alteration of the proportion of the normal constituents 
to each other; thus we know that too slight an amount of free acid 
weakens the solvent power of the gastric juice; or in the fact that for- 
eign substances are mixed with the gastric juice, such as urea in cases 
of retention of urine; or because, under certain circumstances, the con- 
stitution of the gastric juice is totally changed, some constituents 
being added and others disappearing. The symptoms caused by quali- 
tative changes of the gastric juice are entirely unknown, and still less 
do we know the remedies for treating the state in question. 
As to the quantitative changes of the gastric juice, the very un- 
suitable name of “ atonic indigestion ” has been given to the symp- 
toms induced, where the gastric juice is insufficient, or where it is not 
sufficiently concentrated. In the etiology of gastric catarrh we men- 
tioned that too scanty a secretion, or too poor a quality of the gastric 
juice, existed in anaemic and chlorotic persons. We there explained 534 
DISEASES OF THE STOMACH. 
that this anomaly increased the inclination to chronic catarrh of the 
stomach, because, as the ingesta readily decomposed, their products 
excited intense irritation of the mucous membrane. To what has been 
said, we must add that the gastric mucous membrane is not affected in 
all the cases where the contents are abnormally decomposed, and that 
the cases where this membrane remains healthy should be carefully 
distinguished from those where it becomes diseased. The symptoms 
induced by restricted secretion of gastric juice are, it is' true, frequently 
similar to those occurring in chronic catarrh, and even to those of 
chronic ulcer of the stomach. In this form of dyspepsia, also, the ap- 
petite is less, or is satisfied after eating very little. After eating, the 
epigastrium swells, and there is eructation of gases, or sour and rancid 
liquids; the patients suffer from flatulence, and are disturbed and 
anxious about their condition. Besides the nervous cardialgia occur- 
ring in anaemic and chlorotic patients, the excessive formation of acid 
may cause griping pain in the stomach (in the substances vomited by 
chlorotic patients, Frerichs found acetic acid and quantities of yeast 
fungus), and these cases may very readily be mistaken for chronic ulcer 
of the stomach. The diagnosis of this form of dyspepsia depends 
chiefly on the etiology. If the symptoms occur in chlorotic girls, about 
the age of puberty, or in persons weakened by venereal excesses, par- 
ticularly onanism, or in those exhausted by care and anxiety, by con- 
tinued work, or night watching, or if they come during convalescence, 
from protracted and exhausting diseases, and particularly if we can 
find that the nutrition was impaired before the appearance of the 
digestive difficulties, the chances are in favor of its being the so-called 
atonic dyspepsia, and against the existence of structural change of the 
stomach. 
The condition of the tongue gives another point in diagnosis. 
While in chronic gastric catarrh there is a coated tongue and other 
signs of oral catarrh, in the dyspepsia of anaemic patients the tongue 
is usually clean, the taste unchanged, and there is no fetor from the 
mouth. In many cases the diagnosis is decided by the effect of fast- 
ing and of eating. Spiced and irritating substances, which increase 
the difficulty in chronic catarrh and chronic ulcer of the stomach, are 
Avell borne in atonic dyspepsia, and ease the painful symptoms which 
accompany it. 
Above all, a mode of life that improves nutrition, the administra- 
tion of iron, and sea-bathing, which have but little effect on chronic 
gastric catarrh, or chronic ulcer of the stomach, produce most brilliant 
results in dyspepsia dependent on anaemia or hydraemia. In some of 
these cases, particularly where the dyspepsia is accompanied by irrita- 
bility or sensitiveness of the stomach, the pure bitters, such as quassia DYSPEPSIA. 
535 
or hops, are very serviceable. We cannot explain the unmistakably 
favorable influence of these remedies on the gastric mucous mem- 
brane ; for, while they are very irritant to the gustatory nerves, they 
have no effect when applied to the other mucous membranes, or to the 
skin. Quassia is generally ordered as a cold infusion. In the evening 
we may pour a cupful of cold water over about a teaspoonful of 
quassia-chips ; by the next morning a bitter infusion will have formed, 
which is to be drunk fasting, or else water may be left for a while in 
a cup, turned from quassia-wood, and then drunk. Hop-bitter is gen- 
erally used in the form of Bavarian beer, wrhich is now brewed all over 
Germany; but we must take care that it comes from a trustworthy 
brewery, where, instead of hops, some injurious substitute is not used. 
The strong malt-extract, of which we previously spoke (page 246), has 
proved very efficient, in my hands, in several cases of dyspepsia, char- 
acterized by irritable indigestion. Occasionally it was almost the only 
nourishment the patients bore. It is not improbable that the prepara- 
tions of nux vomica, which have a great reputation as stomachics, act 
like the above remedies, by their bitterness. The preparations most 
used in dyspepsia are the aqueous extract (gr. %—1), alcoholic extract 
(gr. —|), and the tincture (gtt. x—xii). 
Too scanty a secretion of gastric juice, and the symptoms depend- 
ent on it, occur also in persons accustomed to great irritation of the 
stomach, as soon as they change their mode of life, and take their food 
without the addition of any stimulants. Unable as we are to explain 
how an organ becomes accustomed to irritation, there is no doubt of 
the fact. We may aptly compare the gastric mucous membrane of 
persons who daily use quantities of pepper, mustard, and other spices, 
to the nasal mucous membrane of habitual snuff-takers. In most per- 
sons small quantities of snuff excite great reflex symptoms, when 
taken into the nose, while the habitual snuff-taker can fill the nose 
with snuff without sneezing. Moreover, the secretion of gastric juice 
must be regarded as a reflex symptom, excited by the irritation of the 
ingesta on the mucous membrane. In the persons in question, the 
irritation from ordinary food is insufficient to produce a sufficient sup- 
ply of gastric juice. Part of the ingesta remains undigested; it is de- 
composed, and we have the symptoms above described. If, on the 
other hand, the food be taken with a strong addition of spices, the 
patients do quite well, their nutrition goes on all right, and there is 
nothing to induce us to think that they have chronic gastric catarrh, or 
other organic change of the stomach, till finally symptoms occur which 
prove that the stomach has not borne these insults without injury. We 
must go very carefully to work in the treatment of these patients 
we cannot allow them to retain their bad habits, but we should only 536 
DISEASES OF THE STOMACH. 
break them off gradually. If we break either of these precepts, 
we may readily induce gastric catarrh or some other disease of the 
stomach. 
Among the stomachics, which are indicated in the last-described 
form of dyspepsia (well called “torpid indigestion”), rhubarb is the 
best; it is given as powder or pills, or as the aqueous tincture ( 3 j), 
but best as the vinous tincture (gtt. xx—xxx). In torpid dyspepsia, 
ipecac, (gr. \—-J) has also a good reputation, particularly with English 
physicians. Finally, the bitter medicines containing an ethereal oil 
are good in torpid indigestion; among the most popular remedies of 
this class is elixir aurantiorum comp. (gtt. xxx—xl). 
The dyspepsia of old persons also appears to be caused by too 
scanty a secretion of gastric juice, which partly depends on a lack of 
die materials necessary to its formation, and partly on diminished 
excitability of the gastric nerves. It is difficult to decide how far the 
disturbance of digestion in this, as well as in the first-mentioned form 
of dyspepsia, depends on bad nutrition of the muscles of the stomach ; 
and it is sufficient to call attention to the fact that the retarded move- 
ments of the stomach consequent on this deficient nutrition may lead 
to incomplete mixture of the ingesta with the gastric juice, and hence 
to dyspepsia. 
Abnormally-increased secretion of gastric juice does not cause dys- 
pepsia, it is true; nevertheless, we will here relate the symptoms that 
it appears to excite, particularly when the stomach is empty. Vomit- 
ing is seen to result from irritations which do not affect the walls of 
the stomach itself, but neighboring organs, particularly the ureters or 
the ductus choledochus, or even distant organs, as the uterus. This is 
usually considered as depending simply on reflex movements. Rudd, 
however, in a spirited and striking manner, calls attention to the fact 
that in such cases the nerves causing secretion of the gastric juice have 
become more active from the reflex irritation. When Spallanzani 
induced vomiting in himself before breakfast, by tickling the fauces, 
he threw up an acid fluid, which dissolved meat; this shows that 
mechanical irritation of the fauces may excite secretion of gastric 
juice, even when the stomach is empty. Rudd further says that, 
where there is impaction of biliary or urinary calculi, the vojnited 
masses are often very acid, even when the stomach was previously 
quite empty of food, and that the acid they contained was found by 
JProut to be muriatic. This circumstance and the decided and rapid 
removal of these gastric difficulties by alkaline remedies render it 
probable to him that part of the pain, and perhaps also the vomiting, 
depended on the irritation of the gastric mucous membrane by the 
juice poured into the empty stomach. At all events, the urgent DYSPEPSIA. 
537 
advice of Hudd and Trout, to give large doses of bicarbonate of soda 
( 3 ij in a pint of warm water), is worthy of attention. 
A number of renowned physicians, particularly in England and 
France, maintain the opinion that the occurrence of oxalic acid in the 
blood, along with some other symptoms of disease, results in a peculiar 
form of dyspepsia, which can only be cured by removing the oxalic 
diathesis. As the doctrine of the oxalic diathesis, and of the dys- 
pepsia caused by it, has lately found many supporters as well as 
many opponents in Germany also, I will briefly state my position in 
regard to this still debatable question. 
Traces of oxalate of lime are so often found in the urine of healthy 
persons, that it forms, as it were, a transition from the normal to the 
abnormal constituents of urine. 
Quantities of this salt are found in the urine when the affected 
persons have eaten substances containing oxalates, such as certain 
vegetables, sorrel, sheep-sorrel, or rhubarb-stalks; they also occur 
temporarily after the free use of carbonated drinks, such as cham- 
pagne, seltzer-water, soda-water, etc. In all of these cases no disturb- 
ance of digestion or of the general health is observed. 
It is different in those cases where large quantities of oxalate of 
lime occur for a length of time in the urine; here there are almost al- 
ways other morbid symptoms. Sometimes, along with the oxalate of 
lime, wre find spermatozoa and quantities of mucus in the urine, which 
render it probable that, in these cases, the oxalate of lime is not ex- 
creted by the kidneys, but forms in the urine during its stay in the 
urinary passages. Since Gallois and Hoppe-Seyler have shown that 
the characteristic crystals of oxalate of lime (octohedrons, so-called 
envelope-shaped) increase in size after the urine stands awhile, we 
cannot doubt that this salt probably also forms in secreted urine from 
the decomposition of mucus. We must dismiss the idea that the 
insoluble salt formed in the urinary passages can have an injurious 
influence on the stomach and the rest of the organism; then the 
symptoms of this form of oxaluria, disturbance of the general health, 
melancholia, paleness, etc., will be naturally explained by the coincident 
spermatorrhoea and the catarrh of the urinary passages. But, finally, 
there are a greater number of cases where the oxaluria cannot be de- 
duced from a decomposition of the secreted urine, but we are obliged to 
refer the presence of the oxalates in the urine to an increased formation 
of oxalic acid in the blood, that is, to an oxalic diathesis. Now, what 
causes the proportionately rich formation of this substance in the blood 
and its proportionate abundance in the excrements of the body, where, 
normally, only traces of it can be found ? At present, tins question 
cannot be satisfactorily answered. However, there is no doubt that 538 
DISEASES OF THE STOMACH. 
oxaluria is more frequent in England, where the people cat and drink 
more and better food and liquor than in Germany, and that in the 
latter country it is almost only seen among people of the better 
classes, who enjoy the pleasures of the table. Little inclination as I 
have for chemico-physiological hypotheses, I still believe that, from 
these facts, we may consider it as probable that the oxalic diathesis 
and oxaluria are to some extent caused by the supply of nutriment to 
the body exceeding the requirements. At the same time, I will not 
dwell on the question as to whether, while this misproportion exists, 
the consumed products can only be brought to a low degree of oxida- 
tion ; or whether the abnormal increase of substances at a low grade 
of oxidation in the excrements of the body, such as oxalic acid, uric 
acid, etc., depends upon other complicated and still wholly unknown 
causes. I think I can support the observation that, in general, persons 
who become fat with good living remain healthier than those who pro- 
duce but little fat under like circumstances, and particularly more so 
than those who, continuing their mode of life, lose fat. While, as a rule, 
the former only suffer from certain inconveniences dependent on their 
corpulence, the latter often complain of all kinds of distresses, which 
physicians usually associate with portal obstructions or hemorrhoids, or 
deduce from gouty, rheumatic, or catarrhal diseases. This renders it 
probable that, in many cases where there is the above-mentioned dis- 
proportion between the supply and demand, and this is not at once 
removed by increased production of fat, the products of the change of 
tissue are modified, and that the above-described difficulties depend on 
an abnormal nutrition of the different organs by the blood, which is 
overloaded with quantitatively or qualitatively abnormal excremental 
material. After a long continuance of the hypochondriasis, the dis- 
turbance of digestion, the pharyngeal and bronchial catarrh, pain in 
the joints, especially the smaller ones (of which groups of symptoms, 
first one, then another becomes prominent, or is even exclusively pres- 
ent), such persons usually become feeble, pale, and thin, so that they 
appear to have a severe and grave affection. The urine, which is usually 
concentrated and acid, does not always show characteristic changes. But, 
in most cases, abundant sediments of uric-acid salts are occasionally de- 
posited. According to my experience, tonic treatment, and the use of 
wine, and preparations of quinine and iron, to which we may be tempted 
by the weakness, pallidity, and emaciation of the patient, are almost al- 
ways injurious; while the use of alkaline-saline mineral waters has 
the happiest results, particularly when combined with cold washing, 
or cold tlouclies (as is often done by Dr. Muller, in Ilomburg), or if sea- 
bathing be tried after the water-treatment. I have no great experi- 
ence in oxaluria and the oxalic diathesis, but those cases that I have DYSPEPSIA. 
539 
met resembled most closely those I have just described, although I 
will not consider them as exactly identical; they had the same etiol- 
ogy, the same varied complaints (not exactly corresponding to any of 
the usually-described forms of disease), the same sleepiness, paleness, 
and emaciation, only the urine, which is usually acid, contained no 
sediment of urates, but had crystals of oxalate of lime. Hence I deem 
it most proper to regard the dyspepsia, which occurs as one of the 
many symptoms of oxaluria, as the result of a constitutional derange- 
ment, and that this derangement is developed in persons predisposed 
to it, by the manner of living above described. At present we have 
no idea which link in the long chain of processes between assimilation 
of nourishment and the excretion of the used-up constituents of the 
body, is first changed by this injurious influence, which induces the 
formation of quantitatively or qualitatively abnormal products. 
In this affection we should employ the treatment which I above 
recommended for the diseases allied to, if not identical with, the oxalic 
diathesis. (The occurrence of oxalate of lime, as a final product of the 
change of tissue in the oxalic diathesis alone, is opposed to their com- 
plete identity.) The administration of nitric acid (twenty drops of the 
dilute acid two or three times daily), recommended by English physi- 
cians for the oxalic diathesis, and the forbidding of all saccharine arti- 
cles of food, appear to depend more on theory than on the results of 
practical experience. 
Before closing the consideration of dyspepsia, I wish to speak of a 
peculiar form of dizziness which is a very frequent but inexplicable 
symptom. Trousseau, who considered that it arose from the dyspepsia, 
called it vertige stomacale. Almost any practitioner can refer to some 
case among his patients that will correspond with the true and life-like 
description given by Trousseau of the vertige stomacale, the vertigo a 
stomacho laeso, or, as our people call it, abdominal dizziness (bauch- 
schwindels). The disease, which subsequently becomes very obstinate 
and tedious, usually begins acutely without any premonition. The 
patient, who just previously felt perfectly well, complains of great diz- 
ziness ; it seems to him as if every thing around him, or as if he him- 
self, were whirling or rolling about. Besides this hallucination, there 
are usually abnormal sensations in the head, which, the patient says, 
he cannot call pain, but which he in vain attempts to describe. Some- 
times patients say their heads feel “ empty,” or “ light; ” others speak 
of a “ numbness,” of a “ sensation of undefined pressure,” of a “ cloud 
arising in the head; ” besides this, there are usually sparks before the 
eyes, noises in the ears; the patients are afraid of falling, seek sup 
port, want to sit down or lie down. These attacks, during which the 
color is either unchanged or becomes pale, usually pass off after a few 540 
DISEASES OF THE STOMACH. 
minutes; but, while they last, they greatly terrify the patients and 
those around them. They often, but not always, teiminate with gap- 
ing and eructations. 
Sometimes there is only one such attack, but more frequently 
there is a recurrence, sooner or later. It is, at the same time, very re- 
markable that the new attacks are excited by apparently insignificant 
causes, such as walking on a polished floor, or a smooth sidewalk, or 
by passing a grating ; also, that on such occasions the patient does not 
become dizzy if he holds the hand of even a small child, or rests on a 
slender cane; lastly, that there is no dizziness if he is engaged in 
something that occupies his whole attention, or if he be mentally ex- 
cited. I knew one patient who could on no consideration walk alone 
through a hall, or across an open square, while he could dance without 
trouble in the same hall, and unconcernedly rode a spirited horse across 
the same square. The longer the affection lasts, the more the thoughts 
of the patient are directed to his enigmatical and curious state. 
He becomes greatly depressed by the idea that he has disease of the 
brain, and particularly when he hears that dizziness was one symptom 
in some other patient who actually had cerebral disease, who perhaps 
died of softening of the brain, that most terrible bugbear of the laity. 
Physicians also are often mistaken, and order bleeding, derivatives, 
preparations of iodine, saline springs, and forbid wine and beer, and 
restrict the diet as much as possible. If this treatment be ineffec- 
tual, and under it the patient becomes pale and thin, the physician 
often changes his opinion: he suspects that the dizziness is caused 
by anaemia of the brain ; then he prescribes iron, advises the use of 
wine and beer, and places the patient on a nutritious animal diet. 
However, this treatment also proves unavailing, and the patient re- 
turns unimproved from the Alps, from the cold-water cures, and from 
the sea-shore. As above mentioned, Trousseau believes that these 
attacks of dizziness depend on dyspepsia; at the same time he ac- 
knowledges that in many cases the signs of dyspepsia are so slight as 
to be readily overlooked. He relates cases of the successful treatment 
of “ vertige stomacale ” by the alternate administration of infusion of 
quassia and a composition of carbonates of the alkalies. Even from 
this prescription I have never seen any benefit; and while I must ac- 
knowledge that the first attacks of dizziness, affecting the patients that 
I have seen, usually occurred after an indigestion, and were accompa- 
nied by dyspeptic symptoms, still, in none of them were there evident 
signs of indigestion during the subsequent attacks, which often con- 
tinued for years. I believe the repetition of the attacks of dizziness to 
be due to psychical causes. As there are persons who become dizzy 
when they stand on the edge of a precipice, or on a high tower; and DYSPEPSIA. 
541 
as one who has once become dizzy on such an occasion, is almost cer- 
tain to become so again in a similar position; so, a person, who has 
once become dizzy in his chamber, or while walking oyer an open 
square, is in the greatest danger of becoming so again on a similar oc- 
casion. The fear of the dizziness is a strong predisposing cause for it 
in this form, just as it is in that where people have it from standing 
on a high place. On the other hand, concentrated attention on any 
point, mental emotion, or even a slight noise, may, to a certain extent, 
prevent attacks from either cause. As a proof of the correctness of 
this view, I may mention the case of a clergyman, who, while going to 
the pulpit in his church, had a severe attack of dizziness, and fell to 
the floor. For years, as long as I had a chance to observe him, this 
patient never had another attack of severe dizziness; but he never en- 
tered his pulpit after the first attack. On two or three attempts, he 
thought he noticed premonitions of the dizziness, which induced him 
to give up further attempts ; he had to give up his employment, just 
as a tower-keeper or a roofer would have to abandon his, if, while 
engaged in his avocation, he had one or two severe attacks of dizzi- 
ness. SECTION 
AFFECTIONS OF THE INTESTINAL CANAL. 
CHAPTER I. 
CATAREIIAL INFLAMMATION OF THE INTESTINAL MUCOUS MEMBRANE 
ENTERITIS CATARRHALIS, CATARRIIUS INTESTINALIS. 
Etiology.—In tlie mucous membrane of tlie intestines also catarrh 
is tlie constant result of every liypersemia, whether the vascular fulness 
depend on purely mechanical causes, or on other injurious influences. 
At the commencement of the disease, and in acute cases, the liyperse- 
mia induces more particularly extensive transudations of a salty fluid, 
deficient in albumen ; subsequently, and in chronic cases, on the other 
hand, it generally leads to abnormal production of mucus and cells. 
Intestinal catarrh, and particularly the chronic variety, is one of the 
most frequent of diseases : 
1. It constantly accompanies obstruction of the circulation of the 
liver. The impeded escape of the blood from the portal vein must 
necessarily cause overfilling of the intestinal veins, and so produce 
catarrh of the intestines. 
2. It frequently, but less constantly, accompanies the diseases of 
the respiratory and circulatory organs, which cause obstruction to the 
evacuation of the vena cava. As in these affections there is venous 
congestion throughout the circulation, it also occurs in the intestinal 
mucous membrane; in these cases the liypersemia and catarrh of the 
intestine represent, as it were, the cyanosis of the skin. 
3. More rarely, disturbance of the external circulation appears to 
cause active liypersemia and catarrh of the intestines. In this class 
appear to belong the excessive liypersemia of the intestines, which ac- 
company severe inflammation of the skin, caused by bums, as well as 
the evanescent liypersemia writh copious serous exudation induced by 
sudden exposure of the skin to low temperature, as by travelling in 
the mountains (Bidder and Schmidt). We will not attempt to say INTESTINAL CATARRH. 
543 
whether cases of catarrh caused by coldness of the feet and of the 
lower part of the body, which depends on the continued action of 
cold, and the chronic cases induced by damp, cold climates, belong in 
this class. 
4. The severe intestinal catarrh frequently occurring in peritonitis, 
particularly puerperal peritonitis, must also be considered as due to 
excessive active hyperaemia. In these cases the intense inflammation 
leads to oedema of the subserous tissue, of the muscular coat, and of 
the intestinal mucous membrane. We see similar oedema occur in the 
vicinity of all inflammatory disturbances of circulation, and we have 
repeatedly described it as collateral oedema, or oedema from collateral 
fluxion. It readily explains the watery passages, which often accom- 
pany peritonitis, in spite of the paralysis of the muscular coat of the 
intestines. 
5. Fluxion to the intestinal capillaries with consecutive serous 
transudation appears also to be the cause of diarrhoea induced by men- 
tal excitement. In these cases we must suppose that the afferent ves- 
sels are dilated by nervous influence, and this hypothesis has at least 
received some support, since Budge showed that there is constant 
diarrhoea after extirpation of the coeliac ganglion in rabbits. 
6. In most cases hyperaemia and catarrh of the intestinal mucous 
membrane are the results of local irritation. Most purgatives act in 
this way, for very few of them purge, by acting as concentrated solu- 
tions of salt, i. e., by endosmotically inducing a copious flow of liquid 
from the intestinal vessels into the intestines, without exciting hyper- 
aemia. Catarrh of the intestines is caused much less frequently than 
was formerly supposed by large quantities of bile, and not very often 
by the presence of parasites. In this class belong the cases of intesti- 
nal catarrh occurring after the use of certain non-medicinal substances, 
such as some kinds of vegetables, but particularly those cases due 
to the passage of undigested and decomposing substances from the 
stomach into the intestines (see etiology of gastric catarrh). It is 
very frequently caused by the retention of fecal masses; if these 
remain for a length of time at any part of the intestines, they decom- 
pose, and form products which have a very injurious and irritant influ- 
ence on the intestinal mucous membrane. To Virchow is due the 
credit of calling attention to the frequent occurrence of local peritonitis 
and the change of position, constriction, and twisting of the intestines 
dependent on it. Indeed, these are in many cases the causes of habit- 
ual constipation; and some chronic ailments, which in general terms 
are called “ chronic abdominal difficulty,” depend solely on distortion 
and constriction of the intestinal canal, on the development of gases 
from the decomposed faeces, or on consecutive intestinal catarrh. 544 
AFFECTIONS OF THE INTESTINAL CANAL. 
7. At certain times intestinal catarrhs prevail from unknown causes, 
which, without our exactly understanding, are usually called genius 
epidemicus gastricus. 
Finally, it is frequently only a symptom of a general disease. In 
the lower animals it may always be excited by the injection of putrid 
substances into the veins (/Stick), it always accompanies typhoid fever, 
and is the severest symptom in Asiatic cholera. We shall hereafter 
speak of these symptomatic forms, as well as of those accompanying 
ulceration and degeneration of the intestinal canal. 
Anatomical Appearances.—Catarrh rarely affects the entire 
intestinal canal. It is most frequent in the large intestine, less so in 
the ileum, and rarest in the jejunum and duodenum. The anatomical 
changes left in the cadaver by acute catarrh are sometimes pale, at 
others dark, redness, swelling, relaxation, and friability of the mucous 
membrane, which is sometimes diffuse, at others limited to the vicin- 
ity of the solitary glands, and of Peyer’s patches, and a serous infil- 
tration of the submucous tissue. Occasionally, after death, the injec- 
tion has entirely disappeared, and the mucous membrane appears pale 
and bloodless. Swelling of the solitary glands and glands of Peyer 
is an almost constant appearance; they distinctly project above the 
surface of the mucous membrane. The mesenteric glands also are 
usually found hypersemic and somewhat enlarged. The contents of 
the intestines consist at first of plentiful serous fluid, mixed with 
detached epithelial and young cells, subsequently of a cloudy mucus, 
which is adherent to the wall of the intestine, and contains epithelial 
structures. 
In chronic intestinal catarrh the mucous membrane looks more 
brownish-red or slate-gray; it appears puffed up, and, particularly in 
the rectum, forms polypoid protrusions. The enlarged follicles usually 
project even more distinctly than in acute catarrh, as white nodules 
above the surface, covered with tough, gray, or puriform mucus. Some- 
times, though more rarely than in chronic gastric catarrh, there is 
hypertrophy of the muscular coat, which may cause a constriction of 
the intestinal canal analogous to simple stricture of the pylorus. 
In some cases catarrhal inflammation has a diphtheritic character. 
Then superficial sloughs form on the very red mucous membrane, so 
that it looks as if sprinkled with bran. After the sloughs have been 
thrown off, shallow erosions, which bleed readily, are left. This 
anatomical appearance, which is almost exclusively found at the lower 
part of the large intestine and in the rectum, and occurs there from a 
collection of hardened feces at that place, answers to the clinical pic- 
ture of a mild catarrhal dysentery. 
The severe forms of intestinal catarrh may lead to ulceration; we INTESTINAL CATARRH. 
545 
may have either diffuse catarrhal or follicular ulcers in the intestine. 
Diffuse catarrhal ulcers result from acute or still more frequently 
from chronic inflammation, to which an acute attack supervenes. The 
most frequent cause is foreign bodies in the intestine or retained faeces. 
Hence they most frequently occur where the contents of the intestines 
are most readily arrested; in the ccecum, ascending colon (typhlitis 
stercoralis), processus vermiformis, then in the rectum and colon, above 
constricted or distorted places. The dark-red and swollen mucous 
membrane softens, and is destroyed by suppuration in its tissue; the 
result is a loss of substance which exposes the submucous or muscular 
tissue. If the ulcer heal at this stage, the loss of substance is filled 
with granulations, and a firm cicatrix remains, which almost always 
constricts the intestine. In other cases the muscular and serous coats 
are also destroyed and the intestine perforated. While the destruc- 
tion proceeds from within outward, a partial peritonitis may occur, and 
cause a union with neighboring portions of intestine, thus preventing 
the escape of the contents of the bowels into the abdomen. This 
course is most frequently seen in perforation of the vermiform append- 
age. Perityphlitis (a phlegmonous inflammation of the loose connec- 
tive tissue attaching the ccecum and ascending colon to the iliac 
fascia) occurs as frequently as peritonitis in inflammation and ulcera- 
tion of the ccecum, which is called typhlitis stercoralis. As this may 
also occur independently of disease of the intestines, we will speak of 
it in a separate chapter. 
The second form of catarrhal ulceration, the follicular ulcer, occurs 
almost exclusively in the large intestine, particularly at its lower part. 
It causes great destruction, and is characterized by the slight reaction 
shown by the mucous membrane, in the vicinity of the ulcer. Accord- 
ing to Rolcitansfofs masterly description, it comes in this way: At 
first the follicles are greatly swollen, surrounded by a dark-red vascu- 
lar ring; subsequently they ulcerate from within; the pus breaks 
through; there is a small, follicular abscess, which has red, spongy 
walls, and a small, ulcerated, finely-fringed opening. While the ulcer- 
ation gradually destroys the whole follicle, the hyperaemia of the adja- 
cent mucous membrane gradually disappears; the ulcer is then about 
the size of a lentil-seed, round or oval. The ulceration soon extends 
to the surrounding mucous membrane ; the round form of the ulcer is 
lost; large, irregular ulcerations occur, or, for a considerable distance 
of the intestine only, some islands and irregular projections of the 
membrane are preserved, while elsewhere the submucous or the mus- 
cular tissue is exposed. In the intestine we usually find a grayish- 
red, half-fluid, floccular substance, mixed with undigested ingesta. 
Symptoms ayd Course.—In acute intestinal catarrh, besides the 546 
AFFECTIONS OF THE INTESTINAL CANAL. 
serous transudation, there is acceleration of the movements of the in- 
testines, so that the passages are not only more fluid, but they become 
more frequent. Diarrhoea, which is often preceded by rumbling in the 
intestines, is the most constant, and occasionally the only symptom of 
acute intestinal catarrh. Pain and other symptoms may be absent, 
the strength and nutrition of the patient may remain normal, if the 
evacuations be not too copious and long continued. In such cases the 
laity usually regard the diarrhoea as a favorable symptom, from which 
they anticipate a cleansing of the body and all sorts of benefit. At 
first the evacuations consist of thin fecal matters (diarrhoea stercoralis). 
If the serous transudation and the accelerated peristaltic movement 
continue after all the faeces present in the bowels have been evacuated, 
the dejections gradually lose the peculiar fecal odor, and consist of 
salty transudations mixed with epithelial masses (cylindrical epithe- 
lium), young cells, and more or less undigested and slightly-changed 
ingesta (diarrhoea serosa). The color of fluid stools is usually some 
shade of green; this does not depend on an abnormal quantity of bile 
being poured into the intestines, but on the bile being evacuated with 
the fluid and the intestinal secretions, before it has undergone the 
normal changes. The more copious the transudations, the paler they 
become, because the bile, mixed with them, is insufficient to color the 
whole. There is scarcely a trace of albumen in these catarrhal evacua- 
tions ; but there are not unfrequently crystals of phosphate of mag 
nesia and ammonia, whose presence was long considered as character- 
istic of typhous passages, and there is usually plenty of chloride of 
sodium. Generally, after the diarrhoea has lasted a day or two, or 
even longer, the normal transformations of the ingesta begin again: 
the evacuations become less frequent, and again acquire their feculent 
appearance and smell. A more or less obstinate constipation gener- 
ally follows the diarrhoea. 
In other cases, besides the diarrhoea, there are pains in the abdomen. 
These are chiefly periodical attacks of griping pain or colic, during 
which, if the pain be severe, the patient becomes very pale and cool. 
These colicky pains usually subside when a discharge from the bowels 
has just taken place, or is about to occur. A continued feeling of 
pressure or soreness, and of sensitiveness to pressure, in the abdomen, 
is seen far more rarely than the above-mentioned attacks of pain. It 
is only in the rare cases, where acute intestinal catarrh accompanies 
extensive burns of the skin, that the latter pains become very severe. 
This peculiarity and the presence of blood in the evacuations distin- 
guish this form from all others. 
In acute intestinal catarrh the abdomen is often somewhat promi- 
nent, and quantities of badly-smelling gases escape with the passages. INTESTINAL CATARRH. 
547 
The development of gas in the intestines cannot be regarded as a symp- 
tom, or as the result of acute intestinal catarrh, as long as this is in 
the stage of moderate transudation and increased peristaltic motion; 
it more frequently depends on the same causes as the catarrh itself, 
particularly on the passage of undigested and decomposing food from 
the stomach into the intestines. 
Finally, acute intestinal catarrh is not unfrequently accompanied by 
fever. If it was caused by catching cold, it generally shows the pecu- 
liarities of so-called catarrhal fever; in other cases the fever is more 
severe, and, if the stomach be affected at the same time, we have the 
symptoms of a gastric, bilious, or catarrhal fever, which we shall here- 
after describe. 
Acute intestinal catarrh runs the above course when it affects a 
large portion of the intestines, or if, as is usually the case, it be located 
in the lower part of the ileum and colon. Catarrh of the duodenum 
often accompanies catarrh of the stomach; but it can only be recog- 
nized when it extends to the ductus choledochus, and so causes obstruc- 
tion of the gall-ducts and jaundice; in all other cases it modifies the 
symptoms of gastric catarrh too little to be recognized. 
Catarrh of the small intestines may run its course without diar- 
rhoea, if the fluid contents of the small intestine remain for some time 
in the large intestine, and become thickened by resorption of the 
watery portions. If, with the symptoms of gastric catarrh, we have 
loud gurgling and rumbling in the abdomen, showing that there are 
gases and liquids moving about in the bowels, but if the anticipated 
discharge do not occur, we are justified in supposing that the gastric 
catarrh has extended to the small intestines, but not to the large. 
There is often catarrh of the lower part of the large intestine and 
of the rectum without coincident disease of the other parts of the 
intestinal canal. When the inflammation is very severe, and shows a 
change from the catarrhal to the diphtheritic form, the symptoms are 
peculiar. Just as in dysentery, the passages are preceded by severe 
cutting pains, which spread from the navel toward the sacrum. Then 
there are spasmodic contractions of the sphincter, burning sensations 
at the anus, and, with severe pressure and straining, more or less 
white and glassy mucus, often mixed with blood, is evacuated. After 
this there is generally relief for a while, when the pains begin again, 
and the scene is repeated. Occasionally masses of hard feces arc 
passed, and the patient is left at rest for some time. Under proper 
treatment, i. e., if wre immediately remove the hardened feces, which 
excite and maintain the disease, catarrhal dysentery (as this disease 
is properly called) may be quickly cured. Improperly treated, it may 
be protracted, and lead to follicular ulcerations. 548 
AFFECTIONS OF THE INTESTINAL CANAL. 
Finally, if the acute catarrh be confined to the rectum, there is 
also a constant desire to go to stool; the passages are mucous, or 
bloody mucus without any feces; but there are none of the char- 
acteristic pains in the belly that precede the stools in catarrhal dys- 
entery. 
In adults, chronic intestinal catarrh rarely leads to extensive serous 
transudations into the bowels; in most cases the secretion from the 
mucous membrane is scanty and mucous. Hence, in adults, this dis- 
ease is rarely or only temporarily accompanied by diarrhoea; on the 
contrary, the patients are usually constipated. The tough mucous 
coating over the wall of the intestine hinders resorption, and inter- 
feres with the nutrition; patients become debilitated and emaciated, 
and their complexion assumes a pale or dirty-gray color. Moreover, 
the mucus in the intestines acts as a ferment on the other contents, in- 
ducing decomposition, thus setting free quantities of gas, which inflate 
the bowels, and cause great annoyance ; the belly becomes tense, the 
diaphragm is pressed upward, the respiration impaired; compression 
of the arteries causes congestion of other organs, particularly of the 
brain. Under such circumstances the passage of flatus is a great event 
for the patient, and it affords him much gratification. Besides the 
habitual constipation, the distui'bance of the nutrition, and the flatu- 
lence with its results, there is almost always great mental disturbance, 
like that which we have already described among the symptoms of 
chronic gastric catarrh. The patients either occupy themselves entire- 
ly with their physical state, and have no brains or time for any thing 
else, or they are subject to a total indifference and despair. In this 
connection it is well worth attention, that, on autopsy of lunatics and 
suicides, we often find flexions and abnormal positions of the intestines, 
which are the most frequent causes of chronic intestinal catarah. Oc- 
casionally the habitual constipation is temporarily interrupted by 
severe colicky pain and a diarrhoea, by which quantities of mucus and 
badly-smelling feces are evacuated. As this interlude often occurs 
without perceptible cause, it appears as if the decomposition of the 
contents of the intestines occasionally formed products which were 
particularly injurious and irritating to the mucous membrane of the 
bowels, and increased the chronic to an acute catarrh. Chronic ca- 
tarrhs, running the above course, are among the most frequent, trouble- 
some, and obstinate of diseases. From the inefficacy of the remedies 
prescribed, many patients despair of medical aid, and fall into the 
hands of charlatans, or use Jtforrisori’s pills, JOeroi’s herbs, StrahFs 
pills, or other domestic remedies. We shall hereafter show that these 
remedies, being laxative, undoubtedly have a favorable influence on the 
difficulties that accompany chronic intestinal catarrh, and that they INTESTINAL CATARRH. 
549 
owe their reputation as universal remedies to the great frequency of 
this affection. 
Occasionally, however, chronic intestinal catarrh is accompanied by 
increased secretion from the mucous membrane and accelerated peri- 
staltic movement of the bowels, and then runs its course as chronic 
diarrhoea. But in adults these cases are very rare; hence, diarrhoea, 
lasting a week or a month, must always excite the suspicion that there 
are more severs lesions of the intestines, and we should not consider 
simple catarrh as the cause of such cases till we have excluded other 
lesions. In such cases the dejections consist of quantities of glairy or 
puriform mucus, mixed sometimes with softened fasces, or sometimes 
with undigested food, if the catarrh be very extensive (diarrhoea lien- 
terica). If colorless masses of mucus or puriform fluids be passed at 
some times, while at others hard scybola are evacuated, wTe may decide 
that the lower part of the large intestine is the seat of the disease, 
and that there is danger of the catarrh passing into follicular ulcera- 
tion. Occasionally the diarrhoea ceases for a few days, giving place to 
obstruction, and then begins again more severely. Sometimes patients 
die of exhaustion from the chronic diarrhoea; bur then we usually find 
some further disease or change in the intestines. 
The case is quite different in the chronic intestinal catarrh of chil- 
dren. This almost always runs its course as an obstinate and exhaust- 
ing diarrhoea, and we must be careful not too hastily to diagnosticate 
tuberculosis of the intestines, or mesentery, or a catarrhal ulcer, from 
this symptom. In the intestines of most children who die of chronic 
diarrhoea, usually with the imperfect diagnosis of “marasmus,” on 
'post-mortem examination, we find only the traces of a chronic catarrh, 
which may readily escape notice. This disease most frequently occurs 
toward the end of the first year, shortly after weaning (diarrhoea ab- 
lactatorum). At first the evacuations are more mucous and less copious 
than natural, have an acid reaction, and either immediately after being 
passed, or after being exposed to the air for a while, they have a 
greenish color. This depends on the admixture of unchanged bile, 
and on higher oxidation of the still retained coloring matter of the 
bile. Subsequently the dejections are very copious, watery, occasion- 
ally clay-colored, fetid, and mixed with undigested food. The previ- 
ously healthy, well-nourished child is at first but little affected by this 
diarrhoea, but some fatal judgment often asserts it to be a safety-valve 
that protects the child from convulsions during teething, and that 
must not be stopped. Hence it often happens that the doctor is not 
sailed till the child has become flabby and relaxed, and then it is fre- 
quently difficult to master the disease; the diarrhoea continues, the 
child emaciates more and more; and a large number of children die 550 
AFFECTIONS OF THE INTESTINAL CANAL. 
during their second year from chronic catarrh of the intestines. In 
babies put out to board, chronic intestinal catarrh usually appears 
earlier and runs its course quicker. The mother of such a child, which 
has previously been healthy and plump, and whose appearance was 
the best recommendation for the fitness of the mother as a nurse, often 
takes a position as wet nurse even six or eight weeks after her confine- 
ment. The child is given over to some old woman, who feeds him 
with bad milk and spoiled pap, and, to prevent his crying too much, 
gives him a sugar teat or crust of bread during the intervals between 
meals. Diarrhoea soon occurs, emaciation goes on rapidly, and soon 
becomes extreme; fat and muscles disappear, the child becomes 
wrinkled, and looks like a little old woman; his flabby skin flaps 
about him like a loose pair of trousers ; there are excoriations about 
the anus, and the oral mucous membrane is covered with thrush depos- 
it. While the child which the nurse suckles flourishes, her own child 
usually wastes away and dies in the third or fourth month. In large 
cities, women who gain a living by taking children to board bury three 
or four, or even more, every year. Even in these cases, on autopsy, 
nothing is usually found but the signs of excessive wasting, and the 
slight remains of chronic intestinal catarrh. The latter may be consid- 
ered, in the diarrhoea ablactatoruin, as a series of daily returning acute 
catarrhs, which are daily excited by the passage of undigested and 
decomposed ingesta into the intestines. 
We shall next speak of the most frequent form of the severe ca- 
tarrhal inflammations that lead to ulceration of the mucous membrane, 
and not unfrequently of the entire wall of the intestine, viz., typhlitis, 
or, as it is usually called, typhlitis stercoralis. Sometimes there are 
premonitory symptoms, before attaining the stage of severe inflam- 
mation, that we call typhlitis; collections of faeces in the ccecum and as- 
cending colon cause repeated attacks of colic and catarrh; so that from 
time to time the patient complains of stomach-ache, and has alternate 
constipation and diarrhoea. In other cases there are no premonitions, 
and even the first retention of faeces in the coecum or ascending colon 
leads to severe inflammation and ulceration of the wall of the intestine. 
When this occurs, the muscular coat loses its power of contraction, and 
there is almost as great obstruction to the advance of the contents of 
the intestines as there is in constriction or adhesions of the bowels. 
Mucous or bloody mucous masses, the result of catarrh in the loAver 
portion of the rectum, are passed, but there is no proper defecation. 
The contents of the small intestine cannot pass downward, hence are 
driven upward by the contractions of the intestinal muscles; there are 
so-called anti-peristaltic movements. The contents of the small intes- 
tines entering the stomach ca use severe irritation • nausea and vomiting INTESTINAL CATARRH. 
551 
occur; at first the food in the stomach is vomited, then green, bitter, 
bilious masses, and in rare cases a brownish fluid of disagreeable taste 
and feculent odor (Ileus, miserere). From these symptoms, we may 
be certain that an obstruction to the progress of the contents of the 
intestines has occurred at some point; in the few cases where the 
pains in the right iliac fossa are slight, and when no tumor can be 
found there, we may be unable to determine the nature of this obstruc- 
tion ; but, in most cases, besides the constipation, there are severe pain 
and a characteristic tumor, which put an end to all doubt. The pains 
spread over the right lower part of the abdomen are marked by severe 
exacerbations, with intervals of comparative ease, and are increased by 
the slightest pressure in this region, as well as by every motion. On 
palpation, which the patients usually fear greatly, we feel a tumor, 
which has a sausage-like shape, and extends from the right iliac fossa 
toward the lower margin of the ribs. This tumor corresponds so 
exactly to the shape and position of the coecum and ascending colon 
that it may be readily distinguished. Improvement begins in the 
above stage in favorable cases; the patient has several passages, with 
severe griping pains in the bowels, large masses of badly-smelling 
faeces are evacuated; vomiting subsides, the tumor decreases and dis- 
appears gradually, as only part of it is due to the contents of the in- 
testine, the rest depending on the swelling of the wall of the intestine. 
But the disease does not always take this favorable course; on the 
contrary, in most cases, the inflammation extends from the serous cov- 
ering of the coecum and ascending colon to the peritonaeum of the 
neighboring intestine and abdominal wall, and to the connective tissue 
uniting the ascending colon to the iliac fascia. From the extension of 
the peritonitis, the abdominal tenderness becomes more diffuse, the 
swelling loses its peculiar sausage shape and grows broader; from the 
perityphlitis (inflammation of the connective tissue behind the colon), 
there are pains in the right thigh, or a feeling of numbness; the psoas 
and iliacus muscles are infiltrated and cannot contract, so that the pa- 
tient cannot raise his thigh. In these cases, the patient usually lies 
on the right side with the body bent forward, and dreads every move- 
ment, for in this position the abdominal muscles are less tense, and the 
psoas and iliacus are most relaxed. With the above symptoms the 
disease has not unfrequently attained its acme, and now gradually im- 
proves. As the typhlitis disappears, the secondary inflammations 
cease, and the exudation is gradually absorbed. In such cases, the 
pain in the abdomen subsides; the tumor, which had been regularly 
advancing toward the median line of the body, again becomes smaller, 
and finally disappears altogether. In the same way the pain and feel- 
ing of numbness in the right thigh pass off, the psoas and iliacus may 552 
AFFECTIONS OF THE INTESTINAL CANAL. 
again be contracted, and the thigh again raised. In unfavorable cases, 
the inflammation gradually affects the whole peritonaeum or the incap- 
sulated exudation is not absorbed, but keeps up a chronic peritonitis, 
and the patient succumbs to the protracted fever accompanying this 
disease. Finally, the walls of incapsulated exudation may gradually 
ulcerate, and there may be perforation outwardly, into neighboring 
parts of the intestines, or into other organs; we shall enter into this 
more particularly when speaking of peritonitis. Bad termination of 
the peritonitis, particularly its rapid spread over the entire peritomeum, 
should excite the suspicion that the ulceration of the coecum has led to 
perforation; however, perforation is quite rare in this form, and there 
are very few cases where it can be certainly recognized during life. 
When perityphlitis results in formation of abscess and burrowing of 
the pus, its terminations are very varied (see Chapter VI.). 
Ulceration of the processus vermiformis is usually accompanied by 
pain in the right iliac region ; but this is usually so undecided that it 
is almost always impossible to interpret it correctly. It is not till the 
ulceration has reached the peritonaeum, or when this has been destroyed 
and the above-described symptoms of partial peritonitis or those of 
perityphlitis occur, that the disease can be recognized. We could not 
at all determine whether the vermiform process or the coecum was the 
starting-point of the consecutive inflammations, were it not for the ab- 
sence of premonitory symptoms and of the obstruction and vomiting, 
but particularly of the characteristic tumor. If we are called to a case 
in a patient where there is already extensive peritonitis or formation 
of pus as a result of advanced perityphlitis, and who can give only a 
very incomplete history of his disease, the two affections cannot be 
distinguished. Although the peritonitis and perityphlitis in ulceration 
of the processus vermiformis are in most cases caused by its perfora- 
tion and escape of its contents, these diseases may nevertheless run 
the above-described favorable course. This is most frequently the case 
when the perforation takes place gradually, so that the intestine be- 
comes attached to the surrounding parts and the rest of the peritonaeum 
is thus protected from injury by the escaping contents. Finally, firm 
adhesions may form; the pus and escaped masses may be incapsulated 
in a dense tissue, or they may perforate outwardly, while the point of 
perforation in the processus vermiformis is closed by a dense cicatricial 
'issue, so that no further escape takes place. 
Severe inflammations and ulcerations of the intestines at other 
points than those above mentioned are much more rare; their most 
frequent seats, however, are in the transverse colon and sigmoid flexure. 
The symptoms are similar to those of typhlitis, and consist in obstinate 
constipation, pain in a circumscribed spot in the abdomen, and the oo- INTESTINAL CATARRH. 
553 
eurrence of the characteristic tumor. They very rarely induce genera, 
peritonitis, as it is much easier to remove the collections of faeces at 
these points and thus arrest the inflammation. 
Follicular ulcers of the intestines are most frequently met in cachec- 
tic individuals. At first the symptoms are those of protracted catarrh 
of the large intestine; but we soon find peculiar translucent lumps, 
resembling swelled sago, in the mucous, white, and transparent masses, 
whose passage is preceded by slight tormina, and accompanied by mod- 
erate tenesmus. Occasionally there are passages of faeces with whitish 
or bloody mucus and the sago-like lumps. The mucous masses now 
become more opaque, fluid, yellowish white, and purulent, and we have 
the form of diarrhoea that was formerly called fluxus coeliacus, or diar- 
rhoea chylosa. In this stage, also, the passages may sometimes be of 
normal color and consistence. If the follicular ulcers heal, strictures 
almost always result, and hence there are obstinate constipation, great 
inclination to flatulence, and the above-described symptoms of chronic 
catarrh. 
Diagnosis.—Acute intestinal catarrh, unaccompanied by fever, is 
not readily mistaken for other diseases. 
We shall hereafter speak of the diagnosis of idiopathic gastric 
and intestinal catarrh, occurring in the commencing stage of typhoid 
fever. 
Those cases of chronic intestinal catarrh, where constipation, flatu- 
lence, and mental disturbance are the prominent symptoms, are often 
mistaken. Not long since it was almost universally believed that these 
symptoms depended mostly on disease of the large abdominal glands, 
particularly of the liver. The patients were sent to Karlsbad to be 
cured of their “ biliousness,” and, when they returned improved, it was 
considered as an evidence that the diagnosis had been correct. After 
accurate and unprejudiced autopsies had shown that chronic abdominal 
derangements, as the above symptoms were characterized, were rarely 
caused by perceptible changes of the liver, spleen, or pancreas, and, 
on the other hand, that great degeneration of these organs, as found 
on autopsy, had not always been accompanied during life by severe 
indigestion, a new error crept in. Many physicians, with JRademacher, 
considered it as proved that there are numerous diseases of the liver, 
spleen, and pancreas, which leave no perceptible changes of structure. 
It is unnecessary to enter into an argument against such a hypothesis, 
and we shall only call attention to the unheard-of method by which 
these diseases of the liver, spleen, pancreas, etc., are diagnosticated. 
If an affection, which, according to our physiological knowledge, has 
not the most remote connection with any organic or functional derange- 
ment of these organs, is improved by the use of St. Mary’s thistle, nux 554 
AFFECTIONS OF TIIE INTESTINAL CANAL. 
vomica, or nut-galls, jRademacher and his followers consider it as a 
proof of the dependence of the disease on a primary affection of the or- 
gans in question, in spite of the fact that none of these remedies have 
been proved to have any specific action on these organs whose diseases 
they are said to cure. The recognition of chronic catarrh with obstruc- 
tion is facilitated, if there be at the same time a chronic gastric catarrh ; 
but there are cases where the gastric digestion is intact. In the latter 
cases, the good appetite, the comfort of the patient after eating, and the 
clean tongue, readily mislead us into seeking the cause of the trouble 
in other anomalies than in disturbances of digestion. If there be also 
pain in one or more circumscribed spots in the right hypochondrium, it 
is often difficult for the physician to make his patient believe that there 
is chronic intestinal disease. Just at the first flexure of the colon are 
most frequently found adhesions with the liver, which induce distor- 
tions and constrictions, and hence sensitiveness to pressure in this 
region rather confirms than opposes the diagnosis of chronic intestinal 
catarrh. The diagnosis of this form of chronic catarrh is materially 
assisted by the symptoms growing worse if the patient remain consti- 
pated for some time. We shall hereafter have frequent occasion to 
speak of the diagnosis of chronic intestinal catarrh from other abdom- 
inal diseases, and will therefore simply again call attention to the fact 
that it is a very frequent disease, and that in making a diagnosis we 
should accustom ourselves to first think of ordinary every-day diseases. 
If this were more commonly done, there would be fewer of those pa- 
tients who now say that no physician could aid them, and that they 
did not improve till they began to take Morrison's pills. 
Prognosis.—The prognosis of intestinal catarrh may be deduced, 
for the most part, from what we have said of its course. An acute 
case, causing copious transudation and accelerated movements of the 
intestines, is usually of not much importance or danger; the diarrhoea 
may even prove advantageous, by removing irritant substances that 
have reached the intestines. Moderate intestinal catarrh may also 
prove beneficial at the period of dentition, in children inclined to hy- 
percemia of the brain and lungs; but we should disabuse our patients 
of the belief that all patients must have diarrhoea while cutting the 
teeth, and that at this time we should never try to arrest a diarrhoea. 
This superstition is widely prevalent and very dangerous ; this is why 
the physician is often not sent for till the child is debilitated and 
emaciated, and in a very dangerous condition. Under well-timed and 
suitable treatment even the chronic diarrhoeas of children usually offer 
a favorable prognosis. In accordance with what we have said of its 
course, even typhlitis and its sequelm do not often endanger life. The 
prognosis is worst in the follicular ulcers of the large intestine, par* INTESTINAL CATARRH. 
555 
tieularly when they occur in a person already cachectic, as is usually 
the case. 
Treatment.—The causal indications can rarely be fulfilled in in- 
testinal catarrhs depending on congestion, as we can rarely succeed in 
removing the obstruction to the flow of blood from the intestinal veins. 
But we can frequently give palliative aid in these cases by attention to 
the exciting causes; when patients suffer from chronic intestinal ca- 
tarrh as a result of congestion, we may occasionally, particularly during 
exacerbations, apply a few leeches at the anus. Sometimes, after repeat- 
ing this abstraction of blood, at regular intervals, perhaps every four 
weeks, there may subsequently be periodical loss of blood from the 
hasmorrhoidal veins, which will greatly relieve the patient. If acute 
intestinal catarrh has resulted from catching cold, the patient should be 
put to bed, he should drink a few cups of warm peppermint or camo- 
mile-tea, and have the abdomen covered with warm cloths. Patients 
who suffer from chronic intestinal catarrh, caused by a damp, cold 
climate, should wear woollen stockings, and change these whenever 
they have cold feet. Abdominal bandages of flannel, also, are very 
good in such cases; where women suffer from this disease, they should 
wear drawers, and in winter these should be made of Canton flannel 
or some other thick material. (In Greifswald, even the neediest women 
wear drawers, an article of clothing which elsewhere is only customary 
among women of the upper classes.) If we neglect this precaution, or 
if we have too much false modesty, we shall neglect a remedy that is 
often more important for the welfare of the patient than all other 
dietetic or medicinal prescriptions. 
When chronic intestinal catarrh in children is due to improper nour- 
ishment, the causal indications require the regulation of the diet, and 
attention to this will often be crowned by brilliant success. While 
the diarrhoea lasts, as has already been explained, the child will rarely 
stand a milk diet; meat broths suit him best, but still better, finely- 
shaved raw beef, taken with a little white bread, and a small quantity 
of good wine, such as pure Tokay or Malaga. Under this treatment, 
the diarrhoea, which had previously withstood all remedies, often ceases 
in a short time, and the emaciated child soon recovers its appearance. 
Concerning the use of calomel, and other customary remedies in gas- 
tric and intestinal catarrh, see treatment of gastric catarrh. If the 
retention of hardened faeces in the colon, or any other part of the in- 
testines, be the cause of the catarrh, the treatment should be com- 
menced with a purgative. If we would treat intestinal catarrh success- 
fully, we should ourselves examine the passages, to see whether there 
are no hard scybola along with the liquid discharges. The rule of 
commencing the treatment with a laxative is particularly applicable to 556 
AFFECTIONS OF*THE INTESTINAL CANAL. 
the catarrhal inflammation of the colon, which we have designated as 
catarrhal dysentery. In such cases, one rather large dose of oil often 
suffices to entirely remove, in a few hours, the abdominal pain, tenes- 
mus, and even the mucous and bloody appearance of the passages. 
This result is the more striking when the patient has been for days 
taking mucilaginous soups and opiates, and when, under this treatment, 
the disease has gradually been growing worse. We can only partly 
fulfil the causal indications in those cases, also, where twisting and 
distortion of the intestines, or constrictions, which will be spoken 
of in the next chapter, lead to habitual constipation, and this again to 
intestinal catarrh; for, although we can remove the constipation, we 
cannot get rid of its cause. Such patients only feel well, and can only 
feel well, while constantly using purgatives, and we have to exercise 
great care in the choice and composition of the laxatives prescribed. 
The rule of giving as simple a prescription as possible does not answer 
in those cases where we wish to prescribe a purgative that will act 
well for months. Compositions of rhubarb, jalap, aloes, and colocynth 
answer better than either of these remedies alone; but, as patients 
often have copious stools, which are, at most, pulpy, not watery, we 
are often obliged to try for a long while before we find the proper 
remedy and the suitable dose. Practitioners can obtain at Berlin 
several packages of StrcihPs domestic pills, No. II. and III.; then the 
patient can try for himself how many of each he must take to produce 
the desired result. By careful attention to keeping the bowels regular, 
wonderful results are sometimes attained in this disease. Enemata 
alone, particularly of cold water, rarely answer the purpose, at least 
for a length of time, but they may be used as adjuvants. The action 
of laxatives is greatly facilitated by certain dietetic rules, which, how- 
ever, are not always explicable. Some patients find it advantageous 
to drink a few glasses of water, or to smoke before breakfast; others 
to eat bread and butter with their coffee, and most persons are bene- 
fited by stewed vegetables, particularly stewed prunes, with their 
dinner. Regular exercise, on foot or horseback, and other bodily move- 
ments, aid the treatment, but we should not over-estimate their value. 
Finally, we should constantly urge the patient to at least attempt to 
have a stool at a regular hour every day. 
Bretonneau and Trousseau praise belladonna as the most efficient 
remedy in habitual constipation, and “ dyspepsia accompanied by slug- 
gishness of the large intestine.” They give belladonna alone (pulv. 
belladonnce, extract belladonnas, each gr. —gr. |), not, as some phy- 
sicians do, in combination with drastic purges. Although I cannot 
agree with all the laudations which Trousseau expends on belladonna, 
not having witnessed its “ efficacit6 merveilleuse ” in all patients with INTESTINAL CATARRH. 
557 
habitual constipation, I have, nevertheless, been agreeably surprised 
by its decided effect in many cases of this affection. Some patients 
have assured me that, from the time they began to take the belladonna 
pills, they had felt like new beings, and, particularly with the last pre- 
scription, they had less disagreeable sensations than with the former 
ones. Unfortunately, I cannot at present distinguish the cases of 
habitual constipation where belladonna is indicated from those where 
it is not. It is to be hoped that future observations will determine the 
cases proper for the use of this remedy, which is so excellent in some 
forms of habitual constipation. 
In typhlitis stercoralis, the causal indications also require the re- 
moval of the masses collected in the coecum and ascending colon, it is 
true, but this is to be done with care. If the case be recent, and un- 
accompanied by vomiting, we may give a full dose of castor-oil ( 3 ss— 
3 j), but if vomiting has begun, and the oil administered be rejected, 
we should cease the attempt of giving internal remedies to cause a 
passage, and, above all, we should not be led into the error of giving 
drastic purges. As long as there is an insuperable obstacle to the 
passage downward of the contents of the intestines, all remedies that 
increase the movements of the bowels cause their contents to move 
upward, and induce vomiting. In the latter cases, the clysopompe 
[Davidson’s syringe] is an invaluable remedy; it cannot be replaced 
by a simple syringe, even if we give several injections in succession. 
We may inject as much as four pints of liquid; as pure water is readily 
absorbed in the large intestine, we should add to it salt, oil, milk, or 
honey. Vomiting usually ceases after a moderate evacuation, or even 
when the passage of a few badly-smelling, crumbly masses shows that 
the fluid has reached the fecal collections, and has softened and set 
them in motion. But if there has been a free evacuation, we must not 
be misled, by the swelling in the coecal region, into continuing the 
evacuant treatment. If the intestinal wall or the peritonaeum be ex- 
tensively inflamed, we shall increase the pain and inflammation by con- 
tinuing to excite the movements of the intestines. 
The indications from the disease never require bleeding in acute 
intestinal catarrh, and even leeching may be dispensed with, except in 
the treatment of typhlitis. But, in the latter disease, the application 
of 10—20 leeches in the right iliac region, and the employment of 
cataplasms, to keep up the bleeding, are usually very beneficial, and 
the operation should be repeated if the pains recur. As we mentioned 
when speaking of cholera morbus, cold suits those cases where the 
hypercemia is excessive, and is accompanied by moderate transudation 
into the intestine, as well as in the severe forms of catarrhal enteritis, 
which occur after extensive burns, and are accompanied by great pain. 558 
AFFECTIONS OF THE INTESTINAL CANAL. 
The best mode of using cold is by applying cloths, wrung out of cold 
water, to the abdomen. In the chronic forms of intestinal catarrh, par- 
ticularly those combined with obstruction, irritating and warming com- 
presses are suitable; among these, Preissnitz’s compress is extensively 
used. We let the patient wear a wet towel, covered with a dry one, 
during the night only, or renew it several times daily. In those cases 
of chronic intestinal catarrh accompanied by the production of tough 
mucus, the same mineral waters are indicated as in the analogous form 
of gastric catarrh. The astringents, also, particularly nitrate of silver 
and tannin, may, by their astringent action, moderate the relaxation 
of the mucous membrane, decrease the hyperaemia, and so answer the 
indications from the disease. Besides these remedies, of which nitrate 
of silver, in small doses, particularly deserves trial in the chronic ca- 
tarrh of young children, we may use catechu, kino, Colombo, casca- 
rilla, etc.; but the circumstances where any particular one of these 
remedies deserves the preference are still obscure, and we employ one 
when we find another unserviceable. Employment of astringents, in 
the form of enemata, is only advisable when the catarrh affects the 
large intestine, as even large enemata will not pass the ileo-coecal 
valve and enter the small intestine. In follicular ulcers, which par- 
ticularly occur in the lower part of the large intestine, enemata of 
nitrate of silver (gr. ij—vj to 3 vj), sulphate of zinc, or tannin ( 3 ss 
to 3 vj), are very useful, and are preferable to all other remedies, but, 
unfortunately, they are not well borne in all cases. 
In cases where the diarrhoea is to be regarded as an injurious, 
rather than as a favorable symptom, the indications are to arrest it. 
It is easy to tell, in each case, when the time has come for arresting 
the discharges. No general rules for this can be given. We usually 
first attempt to attain our end by dietetic rules, by prescribing mucila- 
ginous drinks, oat-meal, rice, or barley-water, or give soups made of 
parched meal; and these prescriptions are worth trying. I will not dis- 
cuss the question as to whether mutton-broth, particularly when fat, will 
cure diarrhoea, as is popularly believed. Besides mucilaginous drinks, 
slightly astringent liquids, which are not exactly medicines, are usually 
prescribed; red wine, infusions of dried whortleberries, roasted acorns, 
etc. These also may prove serviceable, and are worthy of trial in slight 
cases. The astringents mentioned above, when speaking of the indi- 
cations from the disease, may also be named among diarrhoea remedies. 
As we have already said, nitrate of silver is particularly serviceable in 
the chronic diarrhoea of children, while catechu in large doses (3 ij to 
3 vj of mucilage, a tablespoonful every hour or two) is often surprising- 
ly efficacious in the diarrhoea of adults. In proportion to the advantage 
from its use, acetate of lead is too dangerous a remedy to merit exten- PERFORATING DUODENAL ULCER. 
559 
sive employment. By far the most certain and useful remedy is opium, 
little as we positively know of its manner of action. If a diarrhoea 
seem dangerous, and we wish to check it quickly and certainly, we 
may use laudanum (3j— 3 ss to 3 vj of mucilage, or weak infusion, 
of ipecac. Give a tablespoonful every hour). Opium given by enema 
is not less serviceable than when given by the mouth. 
Intestinal disease is only one symptom, and is not even a constant 
symptom, in typhus fever [Professor N. divides typhus fever into exan- 
thematous or typhus, and abdominal or typhoid fever. This explains 
why he does not consider the bowel affection as by any means a con- 
stant symptom]; hence it is impossible to fully describe the typhous 
disease of the intestine without depicting typhus fever. Moreover, 
typhous bowel affections are the result of the specific infection, 
which we are compelled to admit in typhus. On this account, when 
considering the infectious diseases, we shall speak both of typhus 
and the accompanying intestinal affection. 
The case is somewhat different with the intestinal affections in Asi- 
atic cholera and dysentery, induced by miasma; for, in these affections, 
disease of the intestines is very rarely absent, and all the symptoms of 
cholera and dysentery may be deduced from the bowel lesions. Hence, 
we have spoken of cholera morbus and catarrhal dysentery in the 
present section, and will treat of epidemic cholera and epidemic dys- 
entery in a future one, because we believe that, from a proper inter- 
pretation of the etiological causes, the latter must be regarded as 
infectious diseases. 
CHAPTER II. 
PERFORATING DUODENAL ULCER. 
The cases of perforating1 ulcer of the duodenum, scattered through 
the journals, hand-books of practice, and monographs, on the diseases 
of the duodenum, or of the intestine, were first collected by the indus- 
trious and meritorious labor of Krauss, and were so carefully analyzed 
that it is now possible to state something positive about this disease 
which is probably not very rare. 
Etiology.—From the great resemblance, as well of the anatom- 
ical appearances as of the symptoms, course, and results, it is more than 
probable that perforating duodenal ulcer is due to the same processes 
that cause perforating ulcer of the stomach; hence, that it is not a 
proper ulceration, but a necrosis, and a solution of the necrosed part of 
intestine by the gastric juice. 
It is difficult to give any thing definite concerning the frequency 
of duodenal ulcer, for doubtless some cases that have not led to perfo- 560 
AFFECTIONS OF THE INTESTINAL CANAL. 
ration, and still more, some cicatrices of healed duodenal ulcers, have 
been overlooked at the autopsy. In one thousand post-mortem ex- 
aminations made at the Prague institute for pathological anatomy, 
WilligJc found perforating duodenal ulcer only twice, while in seventy 
four cases he found either ulcers or their cicatrices. Perforating duo- 
denal ulcers appear to be more frequent in men than in women; just 
the opposite of what occurs in ulcer of the stomach. It is hardly ever 
seen during childhood; most of the cases collected by Krauss occurred 
during middle age. It does not appear, from the analysis of the cases 
known, whether certain causes, particularly burns of the skin, induce 
this disease. 
Anatomical Appearances.—The most frequent seat of the ulcer 
is the upper horizontal portion of the duodenum; in some few cases 
it has been observed in the descending portion, and in one case in the 
lower horizontal portion (Krauss). lebert says that perforating 
ulcers may occur in any portion of the intestinal canal. I myself have 
seen an ulcer, with all the characteristics of simple perforating ulcer, 
in the upper third of the small intestine, in a public officer, aged fifty- 
six years. In recent cases the edges of the ulcer are sharp and not 
swollen, the loss of substance in the mucous membrane is more exten- 
sive than in the muscular coat, and greater in this than in the serous. 
Ulcers that have existed some time are surrounded by thickened edges, 
indurated by newly-formed connective tissue. In some cases the floor 
of the ulcer is formed by neighboring organs to which the duodenum 
has become adherent before its complete perforation. The liver, pan- 
creas, gall-bladder, and posterior wall of the abdomen, have been ob- 
served as coverings of duodenal ulcers. The progress of the destruc- 
tion from the duodenum to the adherent gall-bladder occasionally 
causes a fistulous communication between the two. A continuation of 
the destruction to the adherent abdominal wall may lead to perfo- 
ration outwardly. Occasionally this, like the perforating ulcer of the 
stomach, heals, with great retraction of the cicatricial tissue. It 
may thus lead to stricture of the duodenum. Finally, obliteration of 
the ductus choledochus has been observed as a result of cicatricial 
contraction of a healing duodenal ulcer. 
Symptoms and Course.—When speaking of round ulcers of the 
stomach, we mentioned cases where peritonitis which ivas rapidly fatal, 
or severe vomiting of blood, was the first symptom from which that 
severe and dangerous disease could be diagnosticated. Perforating 
ulcer of the duodenum appears to remain latent until the fatal ter- 
mination, more frequently than similar ulcers of the stomach. At the 
same time it should not be said that the patients have been perfectly 
well until the appearance of these fatal symptoms; on the contrary, it PERFORATING DUODENAL ULCER. 
561 
seems that slight dyspepsia, a feeling of fulness after eating, and sen- 
sitiveness to pressure in the upper part of the abdomen, have preceded 
the perforation or the vomiting of blood for a few days; but these 
symptoms have remained unnoticed, or have not led to the diagnosis. 
In another series of cases, the symptoms were as nearly as possible 
those common to perforating ulcers of the stomach. The cases that 
have been published do not by any means prove that cardialgia and 
vomiting occur later in perforating ulcer of the duodenum than in the 
same disease of the stomach, and only in a few cases did it appear 
that the pains were seated rather farther to the right side. In the 
same way the analysis of published cases shows that duodenal ulcer 
does not induce icterus more frequently, so that this symptom does not 
aid in the diagnosis between gastric and duodenal ulcers. The rare 
occurrence of icterus appears to prove that perforating ulcer of the 
duodenum is not accompanied by extensive catarrh any more fre- 
quently than ulcer of the stomach is. If the catarrh did occur, nutri- 
tion would be sooner affected from ulcer of the stomach, and obstruc- 
tion of the gall-ducts with resorption of bile (icterus), from ulcer of 
the duodenum. The sudden occurrence of peritonitis after slight dis- 
turbance of digestion gives us no more certainty, in the diagnosis be- 
tween a perforating ulcer of the duodenum and one of the stomach, 
than does the following group of symptoms, viz., feeling of pressure 
and fulness after eating, sensitiveness in the epigastrium, cardialgia and 
vomiting. Perforating ulcer of the stomach being far the more fre- 
quent, the probabilities are in its favor. Finally, a number of cases are 
reported, where duodenal ulcers ran their course with periodical attacks 
of pain, and where, from the pain being in the right hypochondrium, 
from their occurrence several hours after meals, and the accompanying 
symptoms of dyspepsia and acidity, and occasionally from decided 
enlargement of the stomach, the diagnosis of duodenal ulcer could be 
made with great probability. But even in such cases we cannot 
always be certain there is not a cancerous or a simple stricture of the 
pylorus. At the present time, I am treating two patients who, besides 
having a dull pressure in the right hypochondrium, complain of an in- 
sufferable feeling of fulness after eating, also of a belching sometimes of 
gases without smell or taste, sometimes of sour and rancid substances. 
One of these patients never vomits, the other rarely; but both appear 
convinced that there must be an obstruction to the exit of food from 
the stomach, both insist that the food escapes from the stomach more 
readily when they remain upright for a few hours after eating; and, in 
spite of their emaciation and debility, they persist in sitting up for 
several hours after their meals. No tumor can be found in the hypo- 
chondrium : the prominence in the epigastrium can be perceived after 562 
AFFECTIONS OF THE INTESTINAL CANAL. 
a large meal. In both patients the disease has lasted several years. 
I consider it as not improbable that these patients have an ulcer or a 
cicatrix in the duodenum. 
Absence of vomiting speaks against stricture of the pylorus, but I 
cannot with certainty exclude a constriction of the duodenum or com- 
mencement of the jejunum caused by chronic partial peritonitis (see 
Chapter III.). 
If it be difficult to diagnosticate an open ulcer of the stomach from 
one that has healed and left a contracting cicatrix, it is impossible to 
distinguish between an open duodenal ulcer and a cicatrix. The peri- 
tonitis caused by the perforation of a duodenal ulcer runs the same 
course as one depending on perforation of an ulcer of the stomach, 
only it appears to run its course more rapidly, perhaps from the mix- 
ture of bile with the contents that escape into the abdomen. For the 
symptoms resulting from perforation into the gall-bladder, or exter- 
nally, I refer to the monograph of Krauss. 
Tkeatment.—Perforating ulcers of the duodenum are to be treated 
in the same way as perforating ulcers of the stomach; by strict regula- 
tion of the diet, the use of alkaline and alkaline-saline mineral waters, 
particularly the warm springs of Karlsbad and Eins, and under some 
circumstances by nitrate of bismuth, and nitrate of silver. If there be 
severe cardialgia, narcotics are indispensable. 
CHAPTER III. 
CONTRACTIONS AND CLOSURES OP THE INTESTINAL CANAL. 
The varied processes which induce constriction or closure of the 
intestine are best treated of in the same chapter, as the greater part 
of the symptoms excited by them are common to all. 
Etiology.—1. Contraction or closure of the intestine may result 
from compression. The rectum is most frequently compressed either 
by a retroverted uterus or a pelvic tumor, such as fibroid of the uterus, 
ovarian cysts having an unusual location, or by tumors and abscesses 
starting from the pelvic bones or other tissue. Occasionally an over- 
filled or cancerous portion of intestine compresses the portions of in- 
testine lying under it; or a piece of mesentery, drawn down by the 
intestine belonging to it, being in a large hernial sac, compresses por- 
tions of intestine lying between it and the spinal column. 
2. Constriction of the intestine may be caused by structural 
changes of the wall of the intestine. The different forms of stricture 
of the bowel come under this head. Those resulting from cicatrization 
of intestinal ulcers, particularly the catarrhal, follicular, or dysenteric, CONTRACTIONS AND CLOSURES OF THE INTESTINAL CANAL. 
563 
arc the most frequent. Cicatrization of tuberculous (scrofulous) ulcers 
rarely, and of typhoid ulcers never, leads to stricture of the intestine. 
Cicatricial strictures occur in the rectum also, after the healing1 of 
syphilitic ulcers or of wounds. Simple stricture due to hypertrophy 
of the walls of the intestine is. more rare than that which occurs in the 
oesophagus and pylorus from the same cause. Lastly, we must men- 
tion those strictures induced by neoplasia, particularly carcinoma, of 
which we shall hereafter speak. 
3. The intestine may be closed by rotation on its axis; even half a 
rotation closes its calibre. The closure may result either from a por- 
tion of intestine rotating on its own axis, or from the mesentery, or 
part of it with the intestine attached to it, being twisted on itself, or 
from a portion of mesentery with its intestine being wound around 
another loop of intestine. A long and relaxed mesentery predisposes 
to the occurrence of rotation on the axis; the mechanism of this is 
obscure. 
4. Closure of the intestine may result from internal strangulation, 
or incarceration. This occurs when a portion of intestine enters any 
fissure in the abdomen, or gets behind a ligament stretched there, and 
thus becomes constricted. A portion of intestine may be thus stran- 
gulated in the foramen of Winslow, or in a congenital or developed 
fissure in the omentum or mesentery. The bands which most fre- 
quently cause strangulation are those resulting from peritonitis; they 
occur between the most different organs, but particularly between the 
uterus and its surroundings. A portion of intestine may be thrown 
around the omentum which is drawn downward strongly, or around 
the vermiform process which has become adherent at its point, and 
may thus be constricted. 
5. The intestine may be closed by one portion of intestine entering 
another portion; this almost always takes place from above downward. 
This is called invagination, or intussusception, as it consists of an in- 
version of the intestine into itself. When this occurs, there are three 
layers of intestine, one over the other; the outer one is called the 
sheath, or intussuscipiens; the middle and inner one are called the in- 
tussusceptum. The mucous surface of the external and middle layers 
and the serous coat of the middle and internal layers are brought in 
apposition. The mesentery lies between the middle and internal lay- 
ers. As this is attached at its root, it is rendered tense by this inver- 
sion, tind hence exercises traction where it is inserted into the intes- 
tine. In consequence of this one-sided traction, the invaginated portion 
of intestine is distorted ; its opening is drawn from the middle toward 
the side of the sheath, and it is elongated to a narrow fissure. If there 
be quantities of intestinal contents pressing downward, the invaginated 564 
AFFECTIONS OF THE INTESTINAL CANAL. 
portion is constantly driven deeper in, and tlie inversion becomes more 
complete. Intussusception is found in botli the small and large intes- 
tine. The lower end of the small intestine not unfrequently enters 
the large intestine ; and cases have been observed where the ileo-cmcal 
valve was close to, or even projected out of, the anus. Intussuscep- 
tions mostly occur in the course of chronic diarrhoeas ; it is most prob- 
able that they are caused by a portion of intestine contracting strongly, 
and, by elongating and moving forward at the same time, entering the 
non-contracted portion just below ; part of the latter is drawn along 
and inverted with the contracted portion. New peristaltic movements 
force the invaginated portion of intestine farther and farther into the 
outer portion, until the resistance from the mesentery, or the adhesion 
of the parts pushed into one another, arrests the progress of the inner 
portion. Occasionally, particularly in the bodies of children who have 
died of hydrocephalus, we often find one or more intussusceptions, 
which are usually short; these have occurred during the death-agony, 
as is shown by the absence of all signs of inflammation. They also 
appear to be caused by increased and unequal contraction of the intes- 
tines, by which the contracted portions are forced into the larger. It 
is worthy of remark that increased movements of the intestines, which 
may even be perceived through the abdominal walls, are seen just be- 
fore death in animals, even after paralysis of the cerebro-spinal system 
has occurred. 
6. Finally, the intestines may be closed by extensive accumulations 
of hard and dry faeces, or by stony concretions consisting of hardened 
faeces, or precipitates of the triple phosphates and lime-salts. This form 
of closure may be just as complete, and the symptoms durinig life may be 
just as threatening, as in those caused by rotation of the intestine on its 
axis, by internal strangulation, or by invagination. Cases where fecal 
vomiting and obstinate constipation were overcome by large doses of 
metallic mercury and similar remedies are not to be blindly taken as 
examples of cures of internal strangulated hernia, etc., but rather prove 
that retained feces may excite the combination of symptoms, which is 
usually designated as ileus or miserere. Complete closure of the in- 
testines by masses of feces occurs most readily at those places where 
mechanical obstructions constantly oppose and retard the progress of 
the contents of the intestines; hence it is more likely to take place 
above the bent portions and the adhesions, of which we spoke in a 
previous chapter, above compressed portions, or above the various 
forms of stricture of the intestine. In other cases a sub-paralytic state 
of the intestinal muscles, or a diminution of the secretion from the in- 
testinal mucous membrane, appears to favor the collection of the ob- 
structing feces. Lastly, the use of food which forms a great quantitv CONTRACTIONS AND CLOSURES OF THE INTESTINAL CANAL. 
565 
of hard faeces, such as vegetables, or bread containing much bran, or 
even of badly-prepared asparagus, may induce this form of obstruction 
of the intestines. 
Anatomical Appearances.—It would take too long to speak in 
detail of the different tumors that may compress the intestine. The 
pathological anatomy of strictures of the intestine is entered into when 
speaking of the different diseases that cause them. The change of 
position of the intestines that causes closure of the intestines has been 
previously described. 
Above contracted places we usually find the intestine dilated, and, 
as it is at the same time elongated, it is abnormally curved. The 
walls of these portions of intestine are usually hypertrophied, or at 
least thickened ; the cavities are filled with gases and faeces. Below 
the contraction the bowel appears empty and collapsed. Where gas 
and faeces have rested for a time, the mucous membrane is usually in a 
state of chronic catarrh, which, from time to time, becomes acute (see 
previous chapter). 
In closure of the intestine, its vessels, and in some cases those of 
the mesentery also, are compressed; in consequence of which there is 
great capillary congestion, which induces decided swelling of the wall 
of the intestine, severe catarrh of the intestinal mucous membrane, 
transudations and small haemorrhages in the serous coat. More or less 
extensive peritonitis usually accompanies these changes. If the pres- 
sure and tension of the vessels be not removed, absolute stasis occurs 
in the capillaries, and, in consequence of this, mortification of the wall 
of the intestine. In the latter case there may be a perforation, which 
almost always causes death from peritonitis. In some few cases the 
intestine becomes adherent to the abdominal wall before perforation, 
and a fecal fistula or so-called artificial anus results; these diseases 
belong to the domain of surgery. In intussusception the mortification 
of the invaginated part, and its passage through the anus, may effect 
a relative cure, if a firm adhesion between the external and middle 
layers of the intussusception have previously taken place; but this 
place usually remains permanently constricted. This is still more apt 
to be the case if only the lower part of the invaginated intestine slough 
off while the upper part becomes firmly adherent to the sheath, so that 
at this point the intestinal wall shall permanently consist of several 
superimposed layers. 
Symptoms and Course.—The most important symptom of con- 
striction of the intestine is difficult and tedious defecation. But, as 
many persons suffer from sluggish bowels without any mechanical ob- 
stacle impeding the progress of the contents of their bowels, it does 
not appear improper to insert here some remarks on “ habitual con- 
stipation.” 566 
AFFECTIONS OF THE INTESTINAL CANAL. 
Henoch, who, in his clinic of abdominal diseases, treats very ex- 
haustively of habitual constipation, and gives a very lifelike and accu- 
rate account of the inconvenience to which it leads, says very truly that 
“ suffering from constipation ” is a very relative term. Some persons 
habitually only have a passage every second or third day, and still feel 
very well, or feel worse when they have more; on the other hand, 
others feel sick if they do not have one or two stools daily. The 
cause of this difference depends partly on the fact that the former form 
but little keces, as they eat food containing but little indigestible ma- 
terial, and as they perfectly assimilate the digestible part of the food; 
while the latter have a quantity of feces, because their food contains 
much indigestible material, or because their power of digestion is im- 
paired. But even persons eating similar food and digesting equally 
well show the same difference in the number of evacuations required 
to keep them feeling well. It is difficult to give a satisfactory explana- 
tion of these symptoms, but in most cases they seem to depend on the 
fact that in some persons the irritation of the mucous membrane, by the 
retained feces and the products of decomposition, leads to intestinal 
catarrh, while in other less susceptible persons the intestine remains 
healthy. In the latter cases only small amounts of gases form from 
the feces contained in the intestines, the abdomen does not become 
tense, and the diaphragm is not pressed upward, even when the person 
has no passage for two or three days or more. In the former cases 
the mucus covering the walls of the intestine acts on the contents of 
the bowels as a ferment, and by their rapid decomposition quan- 
tities of gas are formed; the abdomen is puffed up, and, even after a 
short retention of feces, we have the inconvenience described in a pre- 
vious chapter. To this description we have to add a few symptoms 
that depend more directly on collection of feces in the lower portions 
of the bowels, particularly in the flexure of the colon and in the rectum. 
Occasionally patients have an “unsatisfactory feeling,” as Henoch 
aptly calls it, after stool; they feel as if there were still masses in the 
intestines, which should have been passed. This feeling alone gives 
them great discomfort, and puts them in a disagreeable frame of mind. 
But, besides this, there are often symptoms resulting from the pressure 
of the full intestines on the neighboring blood-vessels and nerves. 
Pressure on the iliac veins rarely causes oedema of the feet; but 
patients with habitual constipation usually suffer from cold feet, a very 
annoying symptom, which is most readily explained by the impeded 
return of the blood from the feet. Dilatation of tne vessels in the 
walls of the rectum most frequently result from pressure on the hypo- 
gastric veins, and occasionally there are ruptures of these dilated ves- 
sels. The significance of these varicose vessels and the haemorrhages CONTRACTIONS AND CLOSURES OF THE INTESTINAL CANAL. 
567 
(blind and bleeding piles) is overvalued by the laity, who usually 
regard them as the cause and not as the result of their trouble. In 
the same way the escape of blood from the pudic veins, or, in women, 
from the uterine veins, may be impeded. In consequence of this, in 
most women who are habitually constipated, there is hypersemia of the 
uterus, which shows itself by very abundant menstruation and uterine 
catarrh, and which subsequently often leads to important disorders of 
nutrition of the uterus. Thus we see that the notorious Morrison’s 
pills may nqt incorrectly be said to benefit menstrual difficulties and 
fluor albus. Men with habitual constipation may have frequent erec- 
tions and seminal emissions, induced by the impeded escape of blood 
from the pudic veins ; if they were previously worried about their feel- 
ings, they are absolutely frightened by this symptom. Lastly, the 
pressure of the loaded intestines on the sacral plexus may cause neu- 
ralgic pains in the legs, or, what is more frequent, a feeling of numbness. 
The causes of habitual constipation, which does not depend on curva- 
tures and adhesions of the intestines, or on the various forms of con- 
striction, are rather obscure. The disease occurs more frequently in 
women than in men, and not un frequently develops in growing chil- 
dren. A slow movement of the intestine appears most frequently to 
induce it; but there is scarcely any explanation of this sluggishness of 
the intestinal muscles. The bad habit, of repeatedly restraining the 
faeces forcibly, induces habitual constipation in some cases. “ Sedentary 
habits,” also, such as are common to students and persons of certain 
occupations, are likewise properly classed among the exciting causes 
of this affection. Still it is remarkable that perseveringly walking 
does not, by any means, render defecation as easy as might be ex- 
pected. Patients with habitual constipation usually become indefat- 
igable walkers, without thereby attaining the goal which is often the 
object of their whole desire and endeavor [Henoch). In some cases, 
the habitual constipation is due to chronic intestinal catarrh, which, 
like chronic gastric catarrh, as we have shown, induces a sub-paralytic 
state of the intestinal muscles, in spite of the thickening of the walls 
of the intestines that it causes. Hence people who have led a luxu- 
rious life often suffer from habitual constipation. We often meet per- 
sons who, at the university, were great beer-drinkers, and were most 
jovial and popular fellows, who, a few years later, have become ill- 
tempered and peevish, and have no thoughts beyond whether they 
“ will have the longed-for passage to-day.” Recently, inactivity of the 
abdominal muscles has been classed among the causes of habitual con- 
stipation, and cases have been described where the patients accustomed 
the abdominal muscles to exercise, and were thus cured of their consti- 
pation. The excessive stretching and relaxation of the abdomen re- 568 
AFFECTIONS OF THE INTESTINAL CANAL. 
maining after frequent pregnancies, particularly after twins, appear to 
me much more injurious than the diminished activity of the abdominal 
muscles. Such women, upon whose abdomen it seems cruel to press, 
from a feeling that we should break through the walls, almost always 
suffer from habitual constipation, and they cannot strain much; and in 
these same women there is always abdominal plethora and chronic 
intestinal catarrh, which alone would sufficiently explain the retarded 
defecation. (We may readily understand that, under these circum- 
stances, a dilatation of the blood-vessels in the abdomen can easily 
occur; when we consider that, normally, they are subjected not only 
to the pressure of the atmosphere, but to that caused by the tension 
of the abdominal walls, and consequently, when the latter are relaxed, 
they are deprived of one important aid to the preservation of their 
normal condition.) 
As habitual constipation, then, has so many causes, that its presence 
alone does not justify the diagnosis of stricture of the intestine, the 
question arises, How shall we recognize such a cause of constipation ? 
The observation of the feces may aid us here. In the ordinary forms 
of constipation, sausage-shaped feces, of extraordinary size, are often 
passed; in stricture of the intestine, on the contrary, particularly when 
seated at the lower part of the intestine, they often have a very small 
calibre, and consist of small rolls, scarcely as thick as the finger, or of 
small round masses, like sheep’s dung. Important as this symptom is 
for the diagnosis of stricture of the intestine, Ave must still remember 
that it may also occur after long starvation, particularly after long-con 
tinued disease. The empty intestine, which is tightly contracted at 
such times, appears to expand only gradually to its former calibre. 
Even spasmodic contractions of the sphincter occasionally cause this 
form of feces. Hence, before we can diagnosticate stricture of the in- 
testines from this symptom, the above states must be excluded. The 
history may give another aid in diagnosis. We have already explained 
that cicatricial contraction is the most frequent cause of stricture. 
Hence, if habitual constipation and a peculiar form of the feces occur 
after a long attack of dysentery, or after diarrhoeas which seemed to 
depend on ulcers of the intestine, the presumption is in favor of stric- 
ture. In the same Avay, in other cases, Ave may suspect, from the his- 
tory, that there is a retroversion of the uterus, or some kind of tumor 
in the pelvis, which is compressing the intestine. In forming a diag- 
nosis, Ave should also aArail ourselves of physical examination. Promi- 
nence of the abdomen at any part, and a remarkably full percussion- 
sound at this point, if found at repeated examinations, sIioav that part 
of the intestine, above a constricted portion, is dilated. Finally, when 
Ave suspect stricture of the intestine, Ave should never neglect to ex- CONTRACTIONS AND CLOSURES OF THE INTESTINAL CANAL. 
569 
amine the rectum with the finger. If we can reach no stricture with 
the finger, we should use an elastic catheter. We may be deceived by 
the catheter striking against the promontory of the sacrum, or by a 
fold in the wall of the intestine, preventing the further entrance of the 
instrument. Spasmodic contractions of the rectum may also deceive 
unaccustomed observers. In women it is just as important to make a 
vaginal examination, to satisfy ourselves about the position, size, and 
form of the uterus, and find if there be any tumors in the pelvis. 
The symptoms of closure of the intestines, which subsequently be- 
come terrible, and very dangerous, are often slight, and apparently 
free from danger at the outset. The patients feel puffed up, have colic, 
periodically appearing and disappearing, think they have made some 
error in diet, and take some camomile-tea, or a slight laxative. The 
physician is not usually called till these remedies fail, and, in spite of 
them, the pains increase, and the bowels do not move, or when nausea 
and vomiting occur. A careful and experienced physician always con- 
siders this combination of symptoms as disagreeable and threatening. 
The first thing to do is carefully, without over-modesty or forbearance, 
to examine those parts of the body where hernia may occur. Woe to 
him who trusts that the patient will, unquestioned, tell him he has a 
rupture, or who rests contented with his simple denial of the question ! 
'The rectum and vagina should be explored just as carefully as the in- 
guinal regions, to find if there be any obstructions to the evacuation 
of the bowels. In spite of the anxiety that the case causes him, the 
physician, of course, hopes, at this time, that the symptoms are excited 
by a retention of faeces, somewhat obstinate, perhaps, but one which 
may, nevertheless, be overcome. He prescribes enemata, and large 
doses of castor-oil, with the addition of a little croton-oil. After a few 
hours he returns, uncalled for, to the bedside of the patient, for the 
purpose of satisfying his own anxiety. Meanwhile, the enemata have 
occasionally brought away a little faeces from the lower part of the in- 
testine, but, in most cases, they have had no effect, or it has been im- 
possible to give the patient an enema. In spite of the addition of 
croton-oil, the castor-oil has remained ineffectual; after taking it, the 
patient has had great pain, and frequently vomited green masses. At 
the same time, his appearance has changed; his face is distorted and 
pale, the skin, particularly on the hands, is cool, the pulse small. Now 
the sorrowful conclusion becomes more and more certain, that the in- 
testine is closed, and, perhaps, is so obstructed that medical aid can 
give no relief. The abdomen gradually becomes more prominent; 
there are severe, straining, bearing-down pains, which the patient calls 
cramps. These paroxysms of pain are usually followed by nausea, and, 
to the terror of the patient and those around him, the vomited masses 570 
AFFECTIONS OF THE INTESTINAL CANAL. 
constantly become browner and more discolored, and the smell more 
distinctly feculent. There has been much dispute as to whether ster- 
coraceous vomiting could result from obstruction of the small intestine, 
or if it could only occur in closure of the large intestine, where the 
formation of the faeces proper begins. We should bear in mind that 
even the contents of the ileum, particularly if they have been there 
long, may have a feculent odor, and that in so-called fecal vomiting 
actual faeces are rarely, if ever, vomited. I consider it improbable that 
the contents of the large intestine should pass the ileo-coecal valve, 
and enter the small intestine and stomach. There are various views, 
even, concerning the origin of retrograde movements of the contents 
of the intestine. Betz not only denies all influence of the contractions 
of the intestines on the backward movement of the contents, but he 
even believes that they rather impede than aid the normal progress of 
the contents from the stomach toward the rectum. In the act of 
vomiting, abdominal pressure unmistakably plays the chief part; it is 
this, aided by the above-mentioned contraction of the pyloric portion 
of the stomach, which evacuates its contents. The contents of the in- 
testines appear to enter the stomach, because, during the contraction 
of the intestines, the masses cannot pass downward, and are driven 
upward. We will not discuss the question as to whether this occurs 
regularly, or whether the contraction of one portion of intestine imme- 
diately follows the contraction of the portion just below it—that is, 
whether there be an actual antiperistaltic motion. At all events, it is 
evident that, as long as the obstruction exists, all drastics, by increasing 
the contraction of the intestines, must induce vomiting. In some cases 
the disease runs along for eight to fourteen days, or longer, with these 
symptoms, which may even temporarily remit. During the attacks of 
pain which usually precede the vomiting, according to Watson's graphic 
description, we may feel or see in the abdomen “ immense coils of in- 
testine, as big, perhaps, as one’s arm, rise and roll over, like some huge 
snake, with loud roarings and flatulence. The distended bowel strives 
with all its poAver, but strives in \*ain, to overcome the opposing bar- 
rier.” The patient, noAv fearfully disfigured, has a ghostly look, a dirty 
color, his face is co\rered with cold SAveat, his hands cool, his pulse im- 
perceptible, Avhile the mind remains long unclouded; finally, lie dies 
exhausted, with the symptoms of general paralysis. 
The picture is somewhat different AAdien extensive peritonitis occurs 
early in the obstruction. Then the abdomen is puffed up much sooner; 
it becomes excessively tense, and so painful that even the slightest 
pressure is not borne. As the exudation occurs almost exclusively be- 
tAveen the inflated intestines, it can rarely be recognized by the dull 
percussion-sound at the dependent parts of the abdomen. The patients CONTRACTIONS AND CLOSURES OF THE INTESTINAL CANAL. 
571 
do not toss around on the bed, like those above described, but lie still 
on their back, carefully avoiding all movement, because it increases 
their pain. The pulse is very frequent, the temperature very high; 
the diaphragm, pressed upward, compresses the lungs, and the respira- 
tion is hastened; the obstructed flow of blood from the right side of 
the heart gives the patient a cyanotic look. In comparison with the 
symptoms above mentioned, which even now continue, those of peri- 
tonitis are so prominent that the former are not sufficiently noticed, 
and, while the peritonitis is recognized, the internal strangulation, or 
other obstruction of the intestine causing it, escapes observation. We 
should make it a rule to consider “ rheumatic peritonitis ” a very rare 
disease, and, when peritonitis occurs in a non-puerperal patient, to think 
of perforation, particularly of perforation of the stomach by an ulcer, 
or of acute obstruction of the intestine. If the disease has occurred 
quite suddenly, and is not accompanied by vomiting, the chances are 
in favor of perforation. If it has come on gradually, and there was 
.vomiting at the very first, which continues obstinately, or if fecal 
vomiting occurs, there is, most probably, obstruction of the intestine. 
In the latter case, the course is usually much more rapid; even after a 
few days, there is usually great collapse, general paralysis, and almost 
always a fatal termination. 
During life it can hardly be said, in any case, whether the group 
of symptoms that we have described depends on a rotation, internal 
strangulation, intussusception, or an obstruction of the intestine by 
hardened faeces or stony concretions. We have the least certainty in 
diagnosticating rotation of the intestine on its axis. The suspicion of 
internal strangulation is somewhat supported, if the patient has had a 
previous attack of peritonitis, as the bands, which are the most fre- 
quent cause of the strangulation, are almost always remains of former 
peritonitis. Intussusception occasionally shows peculiarities of symp- 
toms by which it may readily be distinguished from other forms of ob- 
struction of the intestine. Among these is a sausage-shaped tumor, 
usually of only moderate resistance, which may sometimes be felt in 
the abdomen, particularly when the walls are not very tense. This 
tumor cannot be moved much; it is painful, and, on percussion, gives a 
sound not quite dull. In intussusception, moreover, the calibre of the 
intestine is often not closed so completely as in other forms, so that, 
occasionally, small quantities of faeces, or intestinal gases, are evacu- 
ated. Moreover, from the compression of the veins of the mesentery, 
which is likewise invaginated, there is great congestion of the invagi- 
nated portion of intestine, which may readily induce rupture of vessels 
in the mucous membrane, and bloody or bloody-mucous passages. This 
symptom is peculiarly important in the diagnosis of intussusception in 572 
AFFECTIONS OF THE INTESTINAL CANAL. 
small children, in whom the disease occurs, proportionately, very often. 
(In these cases the coecum and ascending1 colon are almost always in- 
verted into the lower part of the large intestine, and into the rectum; 
the constipation is not always absolute; vomiting rarely becomes fecal, 
and the puffing up of the abdomen is usually moderate as peritonitis 
is rare. On the other hand, the bloody or bloody-mucous dejections 
are rarely absent.) The diagnosis of intussusception is beyond doubt, 
•when, from the rectum, we can feel the slit-sliaped mouth of the in- 
vaginated portion of intestine, which is usually turned toward the wall 
of the rectum, or, if this sloughs off, and is evacuated, somewhat mor- 
tified, but still recognizable. Obstruction of the bowels by hard fecal 
masses is readily recognized when these can be felt in the rectum. In 
other cases, a hard movable tumor in the abdomen leaves little doubt 
that it is formed of hard fecal masses or stony concretions, and that 
these obstruct the intestines. If the patient has previously suffered 
from the symptoms of constriction of the intestines, and if these have 
suddenly increased to those of absolute obstruction, according to what 
was above said, it is probable that the sudden obstruction has been in- 
duced by hard masses of faeces. Above all, the favorable course of the 
disease, the sudden disappearance of the symptoms after the passages 
of a quantity of faeces, speaks in favor of the latter variety of ob- 
struction. 
The diagnosis and prognosis of obstruction of the intestine are 
evident from what avo have said of the symptoms and course of the 
disease. 
Treatment.—The treatment of habitual constipation has been as 
fully discussed as the plan of this work allows, when speaking of the 
causal indications in the previous chapter; a discussion of the advan- 
tages of and objections to individual laxatives does not come within 
its scope. I have no personal experience of the result of the Swedish 
movement-cure in habitual constipation. Electricity, which has also 
been recommended, comes under the head of gymnastics; contractions 
of the abdominal muscles may be caused by applying the electrodes 
to the skin of the abdomen, and they may be strengthened by repeated 
applications. Application of the electrodes to the abdomen has no 
effect on the movements of the intestines themselves. The proposal 
to place one electrode in the mouth, the other in the anus, must be 
regarded as very naive. 
If stricture of the intestine be located in the rectum, the treatment 
consists in the removal of tumors, or dilatation of strictures, and, where 
these procedures will not answer, in the formation of an artificial anus; 
hence it belongs to surgery. Contractions of the intestine higher up 
can never be radically cured. We have to limit ourselves to placing CONTRACTIONS AND CLOSURES OF THE INTESTINAL CANAL. 
573 
the patient on a diet which will leave as little faces as possible. The 
more threatening the symptoms of the constriction, the more necessary 
it becomes that the patient should live on eggs, strong broths, and 
pure muscular meat, with delicate fibre. At the same time, we must 
secure regular evacuations by enemata and laxatives. 
Those cases of obstruction of the intestine that are caused by hard- 
ened faces and stony concretions are far more amenable to treatment 
than those caused by changed position of the intestines. This is par- 
ticularly true of the obstructions of the rectum by faces, which are 
often collected in astonishing masses above the sphincter. A prudish 
physician, who does not venture to ask for a local examination, will 
prescribe laxative after laxative for days, in such cases, without any 
benefit; while a physician who has no false modesty, and takes no 
refusal wThen it is a question of knowing the disease more thoroughly, 
obtains wonderful results. It often requires great pains and untiring 
patience to make a passage with the finger, the handle of a spoon, or 
corn-tongs, for enemata which, at first, would not enter, and to pass an 
elastic tube through these masses, and give softening enemata. The 
task becomes more difficult if the hardened feces be higher up. We 
may here refer to what we said of the removal of impacted feces when 
speaking of the treatment of typhlitis stercoralis. At first we attempt 
to induce a passage by a few spoonfuls of castor-oil, or by large doses 
of calomel; to each dose of the former we may add half a drop of 
croton-oil. If these remedies prove ineffectual, and increase the vomit- 
ing, we should confine ourselves to the use of the clysopompe [Davi- 
son’s syringe], which certainly offers the most chance of softening the 
hard masses which are usually in the large intestine. We must not 
be discouraged if the first injection does not produce an effect, but 
must repeat it two or three times daily. In one case that I have seen, 
it was not till after four days’ assiduous use of the pump that small, 
friable, greatly-discolored masses of feces, which had a horrible odor, 
were mixed with the fluid injected. And not till the following day 
were there large quantities of similar appearance. In desperate cases 
we may use pure quicksilver; from a few ounces to a pound or more 
of this article may be swallowed. It cannot be denied that, in some 
cases, where all other remedies failed, the weight of the mercury broke 
through the obstruction. Rotations and internal strangulations can 
rarely be diagnosticated with sufficient certainty to justify gastrotomy, 
which, to be successful, should be performed as early as possible. It 
is not impossible that quicksilver may, by its weight, remove a rota- 
tion of the intestine, or cause the reposition of a strangulated part by 
the traction that it exercises on it before reaching it; however, there 
is some doubt about the diagnosis of the cases where this result is said 574 
AFFECTIONS OF THE INTESTINAL CANAL. 
to have been attained. Since, in intussusception, the inversion of the 
intestine almost invariably takes place from above downward, there is 
a contraindication to the exhibition of laxatives, which would force the 
invaginated portion still deeper into the sheath. This is still more 
true of quicksilver. When the intussusception has been recognized 
early, we may perform gastrotomy, as has been successfully done in 
some cases. If we can reach the invaginated intestine through the 
rectum, we should attempt to replace it by carefully introducing an 
oesophageal bougie that has a sponge fastened to its end. This pro- 
cedure has been particularly successful in some cases in children. If 
we cannot reach the invaginated part, we may inject large quantities 
of liquid, or blow air into the rectum with an air-bag, so as to press 
back the invaginated portion, if possible. As soon as severe perito- 
nitis has occurred, these procedures can be of no use, but may do harm, 
as the portions of intestine have become glued together. Then we 
should confine ourselves to large doses of opium, and to covering the 
abdomen with cold compresses. The same treatment should be fol- 
lowed where the symptoms of extensive peritonitis occur with other 
forms of obstruction of the intestine. 
CHAPTER IV. 
SCROFULOUS AND TUBERCULOUS DISEASES OF THE INTESTINES AND 
MESENTERIC GLANDS. 
Etiology.—Tuberculosis of the intestine and mesenteric glands is 
not, by any means, so frequent as is taught; many so-called tubercu- 
lous diseases of these parts are not at all due to the formation of mili- 
ary tubercle, the only form of tubercle that we recognize, but to a 
cheesy degeneration of the intestinal follicles and mesenteric glands. 
The solitary glands, and glands of Peyer of the intestine, which 
are known not to be secretory organs, but elementary lymphatics, are 
sympathetically affected in the different diseases of the intestinal mu- 
cous membrane. In acute and chronic catarrhs of the intestine they are 
always found more or less swelled, and projecting above the surround- 
ing parts. This swelling of the follicle, which depends partly on the 
increase of cellular elements, and still more on increased absorption of 
fluid, usually disappears without leaving a trace, on the subsidence of 
the catarrh. But, under some circumstances, it becomes more decided 
and obstinate; the cellular hyperplasia particularly attains a high 
grade,, and then, as occurs elsewhere, when there is an extensive collec- 
tion of cellular elements, atrophy, or an incomplete metamorphosis into 
fat (cheesy degeneration), readily occurs. The mesenteric glands that SCROFULOUS DISEASE OF THE MESENTERIC GLANDS. 
575 
derive tlieir lymph from the intestinal mucous membrane usually par- 
ticipate in its diseases, just as the small lymphatics located in the walls 
of the intestine itself do. In acute and chronic catarrh of the intestine 
and cellular hyperplasia, the increased absorption of fluid causes them 
also to swell, but this swelling is usually slight and temporary; but, 
under some circumstances, it becomes more decided and obstinate, and 
as, in such cases, there is also a large collection of cellular elements in 
the mesenteric glands, they readily undergo cheesy degeneration. 
The caseously degenerated intestinal follicles deliquesce after a 
time, and form small abscesses, filled with cheesy pus, in the walls of 
the intestine; when the covering of these is perforated small ulcers 
are left, which may subsequently enlarge by the continuation of the 
cell-production and the disintegration. 
In the caseously degenerated mesenteric glands, deliquescence and 
perforation of the capsule of the gland and of the peritonaeum are more 
rare ; but, on the other hand, condensation and final transformation of 
the cheesy mass to a chalky pulp, or to a hard chalky concrement, are 
very frequent. 
If we more attentively regard the persons in whom decided and 
obstinate swelling and cheesy degeneration of the intestinal follicles 
and mesenteric glands particularly occur, we find that the larger part 
of them are children, and especially those children in whom the periph- 
eral lymphatic glands and the bronchial glands incline to swell and 
undergo cheesy degeneration during the course of moist exanthe- 
mata, otorrhoea, bronchial catarrh, etc., and which are usually called 
scrofulous. This circumstance and the entire correspondence of the 
pathological changes render it consistent to designate this swelling 
and degeneration of the intestinal follicles and mesenteric glands and 
intestinal ulcers, consequent upon the former, as scrofulous diseases of 
the intestines and mesenteric glands. 
The wide-spread error, that scrofulous ulcers of the intestines are 
due to tuberculosis, is easily explained : firstly, the caseously infiltrated 
solitary glands have the greatest similarity to cheesy miliary tubercles; 
and, secondly, on post-mortem examinations, we often find miliary tu- 
bercles in the portion of peritonaeum corresponding to the ulcers of the 
intestine. But, if we examine these free from prejudice, and then ask 
ourselves when the ulcers and when the tubercles probably occurred, 
we shall often come to the conclusion that the ulcers have existed for 
a long while, perhaps for years, while the tubercles have been depos- 
ited shortly before death. Hence it is just the same in the intestines 
as in the lungs, where tubercles are finally added to cheesy infiltra- 
tions and cavities. 
As we have previously explained at length, in some persons the 576 
AFFECTIONS OF THE INTESTINAL CANAL. 
excessive susceptibility and the tendency of the tissues to become the 
seat of extensive production of indifferent cells, on inflammatory irrita- 
tion, last beyond the age of childhood. But, as in grown persons dif- 
ferent organs are apt to be diseased from those affected in children, 
the peculiar forms of the disease vary with advancing age. Even at 
the commencement of puberty, the intestinal catarrhs which were 
previously so frequent give way to affections of the lungs, etc. Hence, 
in many autopsies we find calcareous mesenteric glands and cicatrizing 
intestinal ulcers, while in the lungs there are fresh cheesy masses and 
progressing destruction. But, very remarkably and inexplicably, ex- 
perience shows that adults, who are rarely affected by these diseases 
of the intestinal follicles and mesenteric glands, are often afflicted 
by them when analogous diseases attack or have already affected their 
lungs. We may express this bit of experience in another way, by 
saying : caseous degeneration of the intestinal follicles and mesenteric 
glands is rare as a primary and idiopathic disease in adults, but occurs 
quite frequently secondarily, and as a complication of consumption of 
the lungs. 
Except as a secondary tuberculous eruption in the vicinity of scrof- 
ulous ulcers of the intestines, tuberculosis of the intestines and mesen- 
teric glands is rare. This is still more true of tuberculosis of the in- 
testines, in the strict sense. It appears in many cases as if the sec- 
ondary tuberculosis of the intestines occurred simultaneously with sec- 
ondary tuberculosis of the lungs, and as if the proper tuberculous con- 
sumption of the intestine affected particularly those who had also the 
tuberculous form of consumption of the lungs. 
Anatomical Appearances.—Caseously infiltrated intestinal folli- 
cles and the ulcers resulting from their breaking down are most fre- 
quently found in the ileum. Not un frequently the disease extends 
thence to the colon, and remarkably often to the processus vermiformis. 
In some cases the colon alone is affected, while the ileum remains free. 
These appearances are rarely found in the jejunum, and very seldom 
in the duodenum or stomach. The number of follicles affected varies. 
Occasionally a considerable extent of intestine is regularly covered 
with them; far more frequently the disease is limited to several small 
spots at some distance apart. In the earliest stage the swollen fol- 
licles form sliglitly-prominent, rather hard gray nodules, about the 
size of a millet-seed. These become yellow and less hard as the 
cheesy metamorphosis commences. If the mucous covering have been 
perforated by the pus, we find round “ crater-shaped ” ulcers (Roki- 
tansky’s primitive tuberculous ulcer). In advanced stages the mucous 
membrane and submucous tissue in the vicinity of the primitive ulcer 
are the seat of a gray and subsequently of a yellow infiltration. Ex- SCROFULOUS DISEASE OF THE MESENTERIC GLANDS. 
577 
tensive losses of substance result from the breaking doAvn of the 
cheesy infiltration and of the infiltrated tissue itself, and the union of 
several primitive ulcers (Rokitansky’s secondary tuberculous ulcer). 
The ulcer extends particularly in the circumference of the intestine, so 
that finally the ulcers form bands of various width around the interior 
of the bowel. Infiltration and destruction sometimes go on in the 
floor of the ulcer, so that it extends in depth also, and may finally 
perforate the wall of the intestine. As the destruction advances 
toward the serous coat, a circumscribed peritonitis occurs at the part 
about to be attacked. Even on external examination of the intestine 
we can usually tell the points where the ulcers are located, as the 
serous coat is there cloudy and thickened, and occasionally covered 
with scanty fibrinous exudations, or attached by these to neighboring- 
loops of intestines. These adhesions of portions of intestine to each 
other not unfrequently prevent the escape of the contents of the intes- 
tine into the abdominal cavity when perforation of the intestine takes 
place. In such cases the contents do not gush out through the perfo- 
ration till we break up the adhesions at the autopsy. If capillary 
haemorrhage have occurred from the extension of the ulcer, we find the 
edges and base of the ulcer suffused with blood and covered with dark 
clots. Complete cure of these ulcers of the intestine is rarely seen. 
On the other hand, we often find undoubted signs of incomplete cica- 
trization as a callous, darkly-pigmented or non-pigmented connective 
tissue forms the floor of the ulcer, and by its retraction appears to 
have approximated the edges. If the edges of the ulcer approach 
each other so nearly as to come in contact, they unite together. In 
such cases a ridge-shaped resistant swelling always remains on the 
inner surface, while there is a cicatricial retraction on the outer surface 
of the intestine. 
The swelling of the mesenteric glands may be so decided that the 
individual glands will attain the size of a pigeon’s egg, and a collec- 
tion of them may form a tumor as large as the fist. As long as the 
increase in size depends on simple cellular hyperplasia, a section will 
show the glands to be succulent and of a grayish-red color. We often 
find only a few points of the swollen glands changed to a yellow 
cheesy mass ; in other cases, one or more glands are caseously degen- 
erated throughout. On post-mortem examination we frequently find 
ehalky, irregular, sometimes branched, concretions, surrounded by nor- 
mal or atrophied parenchyma in these mesenteric glands, as a result 
of cheesy degeneration which may have run its course years before. 
In genuine tuberculosis of the intestinal mucous membrane, small 
gray nodules, either discrete or united into groups, appear in the early 
stages. If we find such groups of miliary bodies at parts where there 578 
AFFECTIONS OF THE INTESTINAL CANAL. 
are no Payer's glands, it gives the best means of making the very 
difficult diagnosis between miliary tubercles and swelled follicles. 
Tuberculous ulcers result from the cheesy degeneration, softening, and 
breaking down of miliary tubercle; these never become so extensive 
as the ulcerations dependent on caseous degeneration of the follicles, 
and in their vicinity we find fresh tuberculous granulations, instead of 
cheesy infiltration of the tissue. 
In the numerous cases of secondary tuberculosis of the peritonaeum, 
we find those portions corresponding to the intestinal ulcer thickened 
by proliferation of connective tissue, and covered with numerous small 
nodules. The eruption of tubercles has often spread from these points 
along the lymphatics to the mesentery. 
Symptoms and Course.—It is generally difficult to decide whether 
a scrofulous child has simple intestinal catarrh, or if there be cheesy 
degeneration of the intestinal follicles and ulceration of the intestine. 
The case is suspicious when the passages are preceded by pain, when the 
abdomen is sensitive to pressure, and particularly when these symp- 
toms are accompanied by a lingering fever. Not unfrequently the 
diarrhoea disappears for a time, although the intestinal ulcers may 
remain; the child appears to improve; but some slight error in diet, 
catching cold, or some other undiscoverable cause, again induces fre- 
quent, copious, fluid evacuations. If these renewals of the intestinal 
affection be accompanied by an increase of the fever, the child soon 
loses again what strength and flesh he had gained during the interval. 
Occasionally this variation from good to bad continues for years, and, 
even when the diarrhoea has ceased for months, we are not at all cer- 
tain that the ulcers have healed. On autopsy we often find the mu- 
cous membrane of the small and even of the large intestine covered 
with numerous ulcers, when, perhaps, there has been constipation 
instead of diarrhoea. This is not strange, when we remember that the 
thinness of the dejections depends solely on the catarrh accompanying 
the intestinal ulcers, and that the severity of the catarrh varies just as 
much as the hyperaemia and oedema in the vicinity of a cutaneous 
ulcer. When the large intestine is free from ulcers and consequently 
from catarrh, the fluid contents of the intestines entering them become 
of normal consistence, so that consistent stools are passed during life, 
and on autopsy we find the lower part of the intestine filled with firm 
faeces. The longer the disease lasts, the more nutrition is affected by 
it. The patients are often considered much younger than they really 
are. Young men of twenty look like boys; girls attain the age of 
nineteen or twenty without the breasts developing or the menses 
appearing. Frequently, we do not discover the cause of this retarded 
development, till, on careful examination, we find that for years they SCROFULOUS DISEASE OF THE MESENTERIC GLANDS. 
579 
have had repeated attacks of diarrhoea accompanied by fever. Death 
as a result of scrofulous ulcers of the intestine is far rarer than we 
might suppose. It most frequently depends on a subsequent consump- 
tion of the lungs, or a secondary tuberculosis. 
If obstinate diarrhoea join itself to the symptoms of consumption 
of the lungs, or if it occur as the chest symptoms begin, it is very 
probable that the intestinal follicles are caseously degenerated, and 
that ulcers have developed. Even in such cases the diagnosis is not 
certain, for so-called colliquative diarrhoea occurs during disease of the 
kidney and consumption of the lungs, without our being able to find 
any evident structural changes of the intestine on autopsy. Perhaps 
these diarrhoeas are the analogues of the abundant sweatings of the 
phthisis patient, and of the oedema of the subcutaneous connective tis- 
sue ; and it is not improbable that thinning of the serum of the blood, 
a so-called “ dropsical crasis,” favors the occurrence of serous transu- 
dations into the intestines. If the diarrhoea cease, and be replaced 
by constipation, and great sensitiveness of the abdomen to pressure, 
there is still greater probability that the previous diarrhoea was caused 
by intestinal ulcers, for from the above symptoms we may decide that 
there is peritonitis, and we know that this very frequently accompanies 
ulcers, which are advancing toward the serous coat. 
Caseous degeneration limited to the mesenteric glands, whose 
remains are often found on autopsy, can hardly be recognized with 
certainty during life. The intestinal catarrh may long since have dis- 
appeared, while the swelling and change of the mesenteric glands con- 
tinue, just as the swelling of the peripheral glands in many cases out- 
lasts the exanthemata that have caused it. It is very rare for con- 
volutions of glands, even when considerably swollen, to become 
evident to the touch. We may always suspect this disease when we 
find a person who has had obstinate diarrhoea, and scrofulous swelling 
of the peripheral lymphatic glands, with a protuberant belly. In 
scrofulous catarrh, as we designate intestinal catarrh, which is accom- 
panied by cheesy degeneration and swelling of the mesenteric glands, 
the nutrition and development of the patient are also affected; the so- 
called tabes mesenterica does not appear to be due to the impermeabil- 
ity of the mesenteric glands, but solely to the intestinal catarrh. If 
this be removed, the patients may recover perfectly, and on autopsies 
we often find chalky masses embedded in the mesenteric glands of 
robust individuals who have died of acute disease. 
We should suspect proper tuberculous ulcers when diarrhoea 
occurs during decided tuberculosis of the lungs. The secondary erup- 
tion of tubercles on the covering of the intestines has no symptoms, 
except the partial peritonitis which usually accompanies it. 580 
AFFECTIONS OF THE INTESTINAL CANAL. 
Treatment.—In the treatment of scrofulous diseases of the intes- 
tinal follicles and mesenteric glands, we should first of all combat 
the morbid predisposition which excites and maintains them. On this 
point we may refer to what we have said concerning the prophylaxis 
and causal treatment of pulmonary consumption, and will only call 
attention to the important rule, so often neglected, that the patient 
should be kept in the fresh air as much as possible. When speaking 
of the treatment of scrofula, we shall treat particularly of the indica- 
tions for cod-liver oil, acorn-coffee, walnut-leaf-tea, as well as of the 
use of alkaline springs. Cod-liver oil does not by any means increase 
the diarrhoea in all cases, so that, when its use is indicated, we may try 
if it will be borne. In other respects the treatment of scrofulous and 
intestinal ulcers corresponds with that of chronic intestinal catarrh. 
If the diarrhoea become exhausting, opium will be indispensable, but, 
before employing this remedy, we should try the astringents and bit- 
ters recommended for the treatment of catarrhal diarrhoea. If the 
abdomen become sensitive to pressure, we may use warm poultices. 
If the pains increase greatly, we may apply a few leeches to the pain- 
ful part. 
CHAPTER Y. 
CARCINOMA OF THE INTESTINES. 
Etiology.—Cancer of the intestines is far rarer than that of the 
stomach; it is almost always primary, and is even generally isolated; 
it is only in solitary cases that the cancer advances from neighboring 
organs to the intestine. The etiology is perfectly obscure. 
Anatomical Appearances.—Cancer of the intestines affects the 
large intestines almost exclusively, and particularly the sigmoid flexure 
and the rectum. Only in rare cases do we find numerous cancerous 
nodules affecting both the large and small intestine ; in the latter case 
they correspond to Peyer’s glands. 
As in the stomach, so in the intestine, we have scirrhus, medullary 
and alveolar or colloid cancer. We also find the same combinations of 
different forms of cancer; the degeneration often begins in the submu- 
cous connective tissue as scirrhus, and, after it has perforated the mu- 
cous membrane, medullary masses arise from the scirrhus base. Cancer 
of the intestine has a great inclination to spread in the transverse di- 
rection, and so form ring-like strictures. The diseased portion of in- 
testine often sinks down in the abdomen from its weight; at first it 
remains movable, but subsequently usually becomes fixed by adhesions 
between it and neighboring organs, caused by partial peritonitis, or CARCINOMA OF THE INTESTINES. 
581 
by the cancer spreading from the intestine to neighboring organs. 
The development of the tumor may contract the calibre of the intes- 
tine to the size of a quill; the stricture is not usually over a few inches 
in length. Above the stricture the intestine is often enormously dilated 
and filled with faeces and gas, its walls are hypertrophied, and the mu- 
cous membrane is inflamed in various degrees ; below the stricture the 
intestine is empty and collapsed. As we have stated, when speaking 
of cancer of the oesophagus and pylorus, the stricture may be enlarged 
by the breaking down of the cancer. Occasionally the destruction of 
the cancer extends to the peritonaeum; when this has been destroyed, 
the contents of the intestine enter the abdomen, or, if there have been 
previous adhesions, the destruction attacks neighboring organs. In 
the latter case, there may be abnormal communications between differ- 
ent portions of intestine, or, if the affected portion of intestine have be- 
come adherent to the abdominal wall, there may be a fecal fistula; 
perforation of the vagina or bladder may be caused by the breaking 
down of cancer of the rectum. Ulceration of the inflamed part of in- 
testine above the stricture may also cause perforation, and permit the 
escape of the contents into the abdomen, or lead to abnormal commu- 
nications. 
Symptoms and Course.—In many cases it is impossible to recog- 
nize cancer of the intestines with certainty. Patients in whom it de- 
velops complain of dull pain, sometimes continuous, sometimes occur- 
ring at intervals at a circumscribed part of the abdomen. Besides this, 
there is habitual constipation, which usually begins before the stricture 
exists, and is then due to the degeneration of the muscular coat and 
the interruption of the movements of the intestines at that part. From 
time to time the constipation becomes peculiarly obstinate; the pain 
increases, the belly is puffed up, and nausea, vomiting, and other symp- 
toms of obstruction of the intestines occur. If constipation be relieved, 
the patient feels pretty well again. These attacks recur at shorter in- 
tervals, increase in severity, and threaten life more and more. Finally, 
the constipation cannot be relieved, and the patient dies with the 
symptoms of ileus. If, up to that time, the appearance and nutrition 
of the patient had not suffered, if there were no tumor to be felt in the 
abdomen, and the form of the faeces gave no clew for diagnosis, the 
disease would be very obscure. It might be known that there was a 
gradually increasing obstacle to the progress of the contents of the 
intestines, but the nature of this obstruction would not be certainly 
known till revealed by autopsy. 
In other cases the patients do not die so soon from an acute attack 
of obstruction of the bowels, but, besides the gradually increasing con- 
stipation and the dull pain in the abdomen, the signs of a severe ca- 582 
AFFECTIONS OF THE INTESTINAL CANAL. 
chexia appear ; there are a rapid loss of strength, great emaciation, and 
a dirty complexion. These symptoms give a presumption for the can- 
cerous nature of the obstruction. If the emaciation increases, and an 
uneven, nodular, hard, painful tumor, which is at first movable, can be 
felt deep in the abdomen, through the thin abdominal walls, there will 
no longer be any doubt about the diagnosis. 
If, as is frequently the case, the cancer be in the rectum, or even a 
few inches above it, the patients complain of severe pain about the 
sacrum, extending to the back and thighs. The significance of these 
sacral and spinal pains is often undervalued for a long while, and they 
are regarded as symptoms of a disease free from danger, particularly 
when there is at the same time varicose dilatation of the haemorrhoidal 
veins, and a passage of bloody mucus from the intestine. But, grad- 
ually, the increasing constipation and the peculiar appearance of the 
faeces become suspicious. The latter have a very small diameter, are 
sometimes round, again flat and ribbon-like, or are small balls, like 
sheep’s dung. These passages are at first mucous and glairy, subse- 
quently they are covered with blood and pus, and they are evacuated 
with constantly-increasing pain, which finally becomes excessive. Oc- 
casionally the passages occur more readily, after the cancer breaks 
down, or, instead of constipation, there may be diarrhoea, which can- 
not be checked. At the same time there are often abundant haemor- 
rhages, and during the intervals between defecation a discolored, stink- 
ing fluid flows from the rectum, corroding the anus and its vicinity. 
If the wall of the rectum be perforated, and the ulceration advance to 
the vagina and bladder, there is a most fearful destruction and a most 
miserable condition. The description of this and the directions for ex- 
amining the rectum with the finger and the speculum, which give the 
most reliable information, we leave to works on surgery. 
With few exceptions, of which we have already spoken, the course 
of cancer of the intestine is rather tedious; it always terminates in 
death. The latter sometimes occurs with the symptoms of ileus, which 
appear gradually or suddenly; sometimes with the symptoms of ex- 
cessive marasmus, which is occasionally accompanied, at the last, by 
dropsy and thrombus of the veins; sometimes death is hastened by 
peritonitis, which may occur with or without perforation of the intes- 
tine. 
Treatment.—The treatment of cancer of the intestine can only be 
palliative. We must try to regulate the diet, so that as little faeces 
as possible shall be formed; it is best to nourish the patient with con- 
centrated broths, soft-boiled eggs, and milk. We should most stren- 
uously insist on a daily evacuation of the bowels, and, for this purpose, 
should prescribe laxatives which act certainly, and with as little irri- PERITYPHLITIS AND PERIPROCTITIS. 
583 
lation as possible. Castor-oil seems to suit best, and, according to 
Henoch's observation, after it has been used a long time, the disgust 
which most patients have for it subsides. For other points we refer 
to the treatment of stricture of the intestine as described in Chapter II.; 
and for operative procedures, to works on surgery. 
CHAPTER YI. 
INFLAMMATION OF THE CONNECTIVE TISSUE IN THE VICINITY OF THE 
INTESTINES ; PERITYPHLITIS AND PERIPROCTITIS. 
By perityphlitis we understand the inflammation of the connective 
tissue which attaches the ascending colon to the iliac fascia. In far 
the greater number of cases this inflammation is propagated from the 
coecum and ascending colon; in other cases it is an independent dis- 
ease ; it is then usually called rheumatic perityphlitis ; lastly, it occurs 
late in typhus, septicaemia, puerperal fevers, etc., and then belongs 
to the so-called metastatic inflammations. The exudation deposited 
may be absorbed, and the disease end in recovery ; but more frequent- 
ly the inflammation leads to diffuse necrosis of the inflamed connective 
tissue, and large abscesses form which may extend upward to the kid- 
neys, and downward even below Poupart’s ligament, to the inner part 
of the thigh. Lastly, the posterior wall of the coecum and of the as- 
cending colon, the anterior wall of the abdomen or the skin of the 
thigh, may be perforated ; or the contents of the abscess may escape 
into the abdomen and cause peritonitis. 
If the disease develops from a typhlitis, after the superficial tumor 
due to the inflamed coecum has disappeared, there remains a painful 
tumor lying farther back. This is covered by the inflated coecum, and 
hence gives a clear percussion-sound. Frem the pressure of the tumor 
on the nerve-trunks, there is often pain, or a dull feeling in the corre- 
sponding leg, and from the pressure on the veins there is oedema. If 
there be resolution of the inflammation, the tumor becomes smaller, 
the pain less, and the patient quickly recovers. If it leads to suppura- 
tion and formation of abscesses, the tumor increases; in favorable cases, 
fluctuation appears sooner or later in the abdomen or thigh ; when the 
abscess opens, purulent masses, mixed with mortified connective tissue, 
are evacuated, and if the strength of the patient hold out, cure may 
result in these cases also; in other cases death results from exhaus- 
tion. If the contents of the abscess escape into the ascending colon 
after perforation of its posterior wall, the result is usually favorable ; 
but if, on the contrary, they break through into the abdominal cavity, 584 
AFFECTIONS OF ME INTESTINAL CANAL. 
the resulting peritonitis soon causes death. The course of rheumatic 
perityphlitis is perfectly similar, while in the metastatic form death 
usually results from the constitutional disease before suppuration and 
perforation take place. 
At the commencement of the disease, as in typhlitis, we apply 
leeches ; this application may be repeated several times ; subsequently 
warm poultices may be used. The abscess should be opened as soon 
as there is fluctuation. 
Periproctitis is an inflammation of the connective tissue surround- 
ing the rectum; sometimes it develops in the course of acute and 
chronic inflammations and degenerations of the rectum; again it ac- 
companies affections of the pelvis, or of the organs situated in the pel- 
vis ; at other times, like perityphlitis, it is one symptom of extensive 
metastatic inflammations. We also see periproctitis develop very often 
in patients who have consumption of the lungs and intestines. The 
cause of this complication is obscure, for the dependence of the inflam- 
mation of the connective tissue on a suppuration of caseously degener- 
ated lymphatic glands has not been proved. 
Acute periproctitis may end in resolution, but more frequently 
leads to abscesses which may subsequently perforate outwardly or into 
the intestine. Chronic periproctitis leads to decided thickening and 
induration of the inflamed connective tissue, but it also almost always 
ends in partial suppuration, and fistulous ulcers form and are difficult 
to heal. 
At the commencement of acute periproctitis we find a hard, pain- 
ful tumor in the perinasum, or in the vicinity of the coccyx. On intro- 
ducing the finger into the rectum, we often recognize infiltration of the 
connective tissue by the feeling. The patient cannot sit up, and has 
the severest pain on defecation ; if the inflammation terminates in sup- 
puration, and the abscess perforates inwardly, the pain at stool in- 
creases, there is severe tenesmus, and, finally, purulent, stinking masses 
are evacuated per anum. This is the way that internal incomplete 
rectal fistulas are formed. If the abscess perforates externally, fluc- 
tuation occurs in the middle of the hard swelling in the perinaeum, or 
near the coccyx, and, after the covering has been pierced, the above- 
described masses are evacuated. This process may cause an external 
incomplete rectal fistula. The symptoms of chronic periproctitis are 
usually obscure till the disease induces stricture of the rectum, and are 
hidden by the symptoms of disease of the mucous membrane, or other 
original disease. If abscesses form, there is severe pain along with the 
symptoms above described. 
At first, we should attempt to bring the imflammation to resolution, 
particularly by the use of cold ; later, we should apply cataplasms and HAEMORRHAGES FROM THE INTESTINES. 
585 
fomentations, and open the abscess early to prevent perforation of the 
rectum or bladder. 
CHAPTER VII. 
HAEMORRHAGES AND VASCULAR DILATATIONS OF THE INTESTINE. 
Etiology.—Haemorrhages from the upper part of the intestinal 
canal occur from the same causes as haemorrhages of the stomach. 
They most frequently result from excessive congestion of the portal 
circulation, such as occurs particularly in cirrhosis of the liver. In 
other cases, vessels of the intestinal mucous membrane are eroded by 
ulceration ; such haemorrhages occur during typhoid fever, dysentery, 
and in some few cases of consumption of the intestines. Lastly, there 
are haemorrhages in the intestinal canal which must be referred to dis- 
ease of the walls of the vessels, although the microscope shows no 
change of structure; among these are to be classed the intestinal 
haemorrhages in yellow fever (?), scorbutus, etc. 
Varicose dilatations of the haemorrhoidal veins (blind piles, haemor- 
rhoids) and bleeding from the vessels of the rectum (bleeding piles) 
are among the most frequent of affections. It is not long since these 
were regarded as symptoms of a specific constitutional disease, haemor- 
rhoidal disease, and, according to the former opinion, they were the 
most favorable shape that the disease could assume; the case wTas far 
more serious if the disease were “ misplaced,” that is, affected the 
head, breast, or abdomen. This view has been generally given up, 
since it has been found how much the occurrence of venous dilatation 
and bleeding in the rectum is due to mechanical causes, and how little 
tenable is the idea of “ misplaced haemorrhoids.” Nevertheless, the 
pathogeny and etiology are still somewhat obscure. 
Obstruction of the circulation, which is the most frequent cause of 
congestion everywhere, must be regarded as the most common cause 
of haemorrhoids, with which general name we shall designate the ve- 
nous dilatations and haemorrhages occurring in the rectum. 
The escape of blood from the haemorrhoidal veins may be caused: 
1. By collections of faeces in the rectum, by tumors in the pelvis 
or the gravid uterus ; and these are the most frequent causes of haemor- 
rhoids. 
2. The escape of blood may be impeded by obstruction of the por- 
tal vein. Hence we shall mention haemorrhoids as one of the most 
frequent symptoms due to the congestion in cirrhosis of the liver. 
Overfilling of the portal veins appears to have a similar effect, and 
perhaps this best explains the frequent occurrence of haemorrhoids in 
drunkards. During digestion there is an increased flow of fluids from 586 
AFFECTIONS OF TIIE INTESTINAL CANAL. 
the intestines into the intestinal veins; we know that the increased 
fulness of the portal vein, from this cause, obstructs the escape of blood 
from the splenic vein, and that consequently the spleen is enlarged 
every time that digestion goes on. But it readily follows that from 
excess in eating and drinking the fulness of the portal veins is in- 
creased, and is more permanent, and that consequently other veins 
which open into the portal veins may dilate, and from repeated ex- 
cesses may remain dilated. This explanation is hypothetical, it is true, 
but it is not more so than other explanations that have been offered for 
the occurrence of haemorrhoids from excess in eating and drinking. 
3. The obstruction which impedes the escape of blood from the 
haemorrhoidal plexus may lie beyond the liver, in the chest. Thus 
we often see haemorrhoids develop in lung-diseases where the capilla- 
ries are compressed or atrophied; the patients considering them as the 
cause, not as the result, of their chest-disease. In the same way 
haemorrhoids develop from heart-affections, along with other results of 
overfilling of the veins. 
The above-mentioned obstructions to the circulation do not usually 
suffice to cause haemorrhoids; their frequency is not proportionate to 
the amount of the obstruction; they are often absent when the escape 
of blood from the haemorrhoidal plexus is greatly interfered with, 
while in other cases, where there is no perceptible obstruction except a 
temporary constipation, they become excessive. There is an analo- 
gous condition in the varicose veins of the legs of women during 
pregnancy; in some women the varicose veins appear during the first 
months, in others they do not occur even during the latter months, in 
spite of large amounts of liquor amnii, large children, or the most un- 
favorable position of the child. This goes to prove that the walls of 
the veins are less resistant in some persons than in others, and that 
this diminished tonicity of the walls of the vessels is most important 
for the occurrence of phlebectasias anywhere, and of haemorrhoids in 
particular. This abnormal lack of resistance in the walls of the veins 
is in many cases congenital. The fact, that in certain families all the 
members for several generations suffer from haemorrhoids, cannot be 
denied, and can only be explained by the supposition that a peculiar 
state of the vessels is hereditary. In other cases the want of resist- 
ance is undoubtedly acquired, and is probably induced by the disturb- 
ance of nutrition in the walls of the vessels from the chronic catarrh 
of the rectum. We have learned that dilatation of the veins is one of 
the anatomical appearances of chronic catarrh in all the mucous mem- 
branes, and hence can understand that the veins of the rectum, which 
from their position are peculiarly disposed to dilatation, should in a 
similar way become varicose from catarrh of the mucous membrane of HAEMORRHAGE FROM THE INTESTINES. 
587 
the rectum. The variety of injuries that the rectum has to bear, the 
frequency of acute and chronic diseases of neighboring organs, in which 
the rectum is implicated, abundantly explain the frequency of chronic 
catarrh, and at the same time the frequency of relaxation of the hmrnor- 
rhoidal veins. 
It is usually supposed that general plethora induces haemorrhoids, 
and that bleeding piles are of critical significance in plethoric condi- 
tions. It cannot be denied that persons, who, particularly after they 
have attained their growth, consume more than is required for the 
support of the body, are often affected with haemorrhoids; and also 
that gout, chronic catarrh, and other diseases, which are also frequent 
in such persons, are usually better after liaemorrhoidal haemorrhage. 
Nevertheless, we should hesitate about referring either the haemor- 
rhoids or the other diseases, in these cases, to a general plethora, to an 
absolute increase of the contents of the vessels, as the permanent 
occurrence of such a state has not been fully proved; and there is 
good reason to suppose that the overfilling of the vessels leads to 
increased excretion till the disproportion has been removed. The 
changes that the blood undergoes from too great a supply of nourish- 
ment (abnormal concentration?) are not thoroughly understood, and 
hence the pathogeny of the diseases developing under such circum- 
stances is quite obscure. 
Haemorrhoids are rarer in children than in adults; this is explained 
by the greater rarity of the above-mentioned obstructions to the cir- 
culation, and of chronic gastric catarrh, during childhood. On the 
other hand, it is evident how a sedentary life, the use of irritating food, 
the misuse of drastic purges, the frequent and clumsy use of enemata, 
may rank among the exciting causes of haemorrhoids. If it be true, as 
is said, that piles are less frequent in women than in men, and in tem- 
perate climates than in hot ones, and that they are induced by exces- 
sive venery, we cannot so readily explain the fact by the causes above 
given. 
Anatomical Appearances.—As the haemorrhages from the upper 
part of the intestine are almost always capillary, their source can rarely 
be recognized on autopsy. Occasionally, after capillary haemorrhages, 
a considerable extent of the mucous membrane is found sulfused with 
blood, which is a sign that the haemorrhage has taken place into the 
tissue of the membrane and not on its free surface. After haemor- 
rhages caused by ulcers in the intestine, coagula generally adhere to 
the ulcers which have bled, and the edges and base of the ulcer are 
suffused with blood. The blood is sometimes fluid, sometimes slightly 
coagulated, rarely red, but usually chocolate-brown, or transformed to 
an adhesive, black, tarry mass. 588 
AFFECTIONS OF TIIE INTESTINAL CANAL. 
The varicosities of the rectum, which are termed blind piles, usually 
occur at the end of the rectum, above the sphincter and at the edge 
of the anus. The former are called internal, the latter external piles. 
At first the venous dilatation is diffuse and forms a thick blue net, 
afterward single varices appear, and not unfrequently the anus is sur- 
rounded by a wreath of the latter. At first the varices are small and 
have a broad base, they appear and disappear at intervals; later they 
may attain the size of a cherry or even become larger. As the inter- 
nal varices are pressed through the anus, when the bowels are evacu- 
ated, and draw the mucous membrane after them, the latter often 
forms a pedicle for them and they remain outside of the anus; even 
then they sometimes appear tense, at others relaxed; but the sacs 
once formed never disappear. The appearance and structure of the 
haemorrhoidal tumors change in the course of time. At first they are 
bluish and their walls are thin and delicate; if repeated chronic inflam- 
mations subsequently cause them to adhere to the mucous membrane, 
they lose their bluish look, and become hard and thick-walled. Not 
unfrequently neighboring varices coalesce, only rudiments of their par- 
titions remain, and thus large, sinuous sacs are formed, into which 
several veins open. Occasionally a thrombus forms in the varices, 
filling them up and causing their obliteration and ulceration. Large 
varices which are extruded during defecation may inflame and even 
mortify from the pressure; in other cases there is inflammation and 
ulceration of the mucous membrane at the root of the haemorrhoidal 
tumor and haemorrhoidal ulcers result; in still other cases the inflam- 
mation attacks the surrounding connective tissue, and we have peri- 
proctitis, and, as a result of this, may have rectal fistula. 
Bleeding piles result sometimes from the rupture of varices, but 
small haemorrhages are mostly caused by overfilled capillaries. 
According to Vir chore’s description, on anatomical examination of 
the rectal mucous membrane, we find it “ relaxed, often in puffs and 
folds, slightly thickened, grayish-white; the submucous tissue is in- 
creased and relaxed; both are very vascular. It is usually covered 
with tough, whitish mucus, which chiefly consists of detached epithe- 
lium, with a mixture of mucus.” 
Symptoms and Course.—Haemorrhages in the upper part of the 
intestine are, as above stated, symptoms of severe diseases, and must 
be described when speaking of these. 
The description of haemorrhoids given in the old text-books, and 
which still corresponds to the popular idea, distinguishes three groups 
of symptoms: 1. The local difficulties which are caused by the catarrh, 
the varices, and the haemorrhages, “mucous or blind and bleeding 
piles; ” 2. Periodical difficulties, both local and general, which precede HAEMORRHAGE FROM THE INTESTINES. 
589 
the swelling of the varices and the haemorrhage from the rectum, and 
are relieved by the latter, “ molimina haemorrhoidalia; ” 3. Permanent 
difficulties, which indicate constitutional disease, or disease of some dis- 
tant organ, but which are also relieved by the liaemorrhoidal bleeding, 
“ misplaced haemorrhoids,” or, if haemorrhages occur elsewhere, “ vica- 
rious haemorrhoids.” 
We should strike the latter from the list of haemorrhoids. If a 
venous abdominal plethora, dependent on cirrhosis of the liver, is im- 
proved by liaemorrhoidal bleeding, and the dyspepsia, flatulence, and 
hypochondria disappear for a time, this does not justify us in regarding 
these symptoms as signs of a haemorrhoidal disease. We have just 
as little right to regard bronchial catarrh, or attacks of gout occurring 
in a plethoric person, as anomalous or misplaced haemorrhoids, because 
these diseases remit after a haemorrhoidal bleeding. 
In regard to molimina haemorrhoidalia, we must agree with Virchow, 
who regards it as a symptom of returning rectal catarrh. The patient 
has a feeling of burning and tension in the rectum, just as occurs in 
other mucous membranes in acute catarrh or relapsing chronic catarrh. 
There are also severe sacral and dorsal pains, which remind us of the 
headache in catarrh of the nose and frontal sinus. The general state 
of the patient is disturbed in the same way by catarrh of the rectum 
as it is by catarrh of other parts; the patients become relaxed, slug- 
gish, and depressed. The inconveniences which the varices, swelled 
by the increased hyperaemia, cause, complete the picture of haemor- 
rhoidal hyperaemia. In many cases, at the height of the attack, there 
is a haemorrhage, which has a favorable influence on the catarrh and 
the fulness of the varices, so that the patient feels relieved, or even 
free from all trouble. If, after a time, he be again affected with mo- 
limina, we cannot blame him for longing for the haemorrhage that re- 
lieves him. If we can remove the catarrh and swelling of the varices 
in any other way, as by removing constipation, -which has caused the 
increased congestion and hyperaemia of the rectum, the molimina dis- 
appear without a haemorrhage. 
The local difficulties that the haemorrhoids excite vary with the 
number, size, and fulness of the varices. At first they are slight, the 
patients have the feeling of a foreign body in the anus, and pain only 
occurs when there is a hard stool. When the anus is surrounded by 
large varices, or when individual tumors have become very large, and 
are very tense, the patients have constant pain, cannot sit down, and 
even a soft passage gives them great suffering, which only disappears 
slowly, and which not unfrequently causes the patients foolishly to retain 
their passages. The pain becomes most severe when large varices are 
protruded through the anus, strangulated there, and become inflamed. 590 
AFFECTIONS OF THE INTESTINAL CANAL. 
ILx'morrhoidal bleedings usually occur during defecation; if they 
are of capillary origin, only a small quantity of blood adheres to the 
feces; if they come from ruptured varices, several ounces of blood are 
often lost. It is only in rare cases that there is sufficient haemorrhage 
to cause danger. 
The so-called mucous haemorrhoids consist of the passage of the 
above-described catarrhal secretion; this is sometimes evacuated with 
the feces, sometimes squeezed out of the rectum without any admix 
ture of feces. Frequently only the symptoms of mucous piles are 
present, and it is only subsequently that those of blind and bleeding 
piles occur. 
From the usually prolonged action of the injurious influences causing 
them, it may be readily understood that the course of this disease is 
usually tedious. If the causes act only for a time, the haemorrhoids 
may disappear forever, after lasting only a short time. 
The variation of the symptoms of hemorrhoids, after they have 
lasted a long time, has led to the most varied hypotheses. They have 
been compared to menstruation, and even the changes of the moon 
were claimed to have an influence on their course. The causes of the 
unpleasant feelings of the patient at one time, and his comfort at an- 
other, may often be discovered; the occurrence of constipation has ob- 
structed the escape of blood from the rectum; or a debauch has caused 
an overfilling of the portal vein, and a consequent congestion of the 
haemorrhoidal vessels; or they have been exposed to some other source 
of injury, which in them has not induced a nasal or bronchial catarrh, 
but has excited an increase of the rectal catarrh, because the rectum 
was the locus minoris resistentfe. In other cases, the exciting causes 
cannot be discovered, but this also happens in the temporary exacerba- 
tions of other diseases, and so we are not justified in any adventurous 
hypotheses. 
We hear a great deal about the dangerous effect of the arrest of 
habitual bleeding from haemorrhoids. This belief is not altogether 
without grounds, but we should not consider the bleeding as Nature’s 
attempt at a cure. The rectum is probably the part whose diseases 
have least effect on the organism, and patients in whom the rectum is 
the part soonest affected, when they are exposed to injurious influences, 
are better off than those whose stomach or bronchi are affected under 
similar circumstances. If they be affected with disease of one of the 
last-mentioned organs, when exposed to injury, we may deplore it, but 
if they have haemorrhoids, they are just as correct in saying “ all right ” 
as one is who, having been exposed, begins to sneeze, and thereupon 
concludes he is only going to have a cold in the head, and not a worse 
disease. In cases where abdominal plethora, dependent on mechanical HAEMORRHAGE FROM THE INTESTINES. 
591 
obstruction, is relieved by an occasional haemorrhoidal bleeding, or 
where there is a remission of bronchial catarrh, or other disease, which 
usually exists in patients of forty years or upward, who lead a luxu- 
rious life, the cessation of the bleeding may prove serious. But, as in 
these cases the relief depends solely on the loss of blood, and as this 
can be replaced by local blood-letting, the injury practically only occurs 
when the physician fails to see that the latter is indicated. 
Treatment.—Where the repeated collection of hard feces excites 
the catarrh and varices of the rectum, the causal indications require 
the regular evacuation of the bowels ; but we should only use drastic 
purges, such as aloes and colocynth, when absolutely necessary, as we 
fear their irritant effect on the mucous membrane of the rectum, and 
should generally prefer llowers of sulphur or precipitated sulphur, 
which have long been used in the treatment of haemorrhoids; sulphur 
is generally given in combination with tartrate of potash. One of the 
commonest prescriptions is Ijfc. sulphur, depur. 3 ij, potass, bitart. 3 ss, 
syrup, limonis, sacch. albi ana 3 iij, HI. ft. pulv. S. A teaspoonful two 
or three times daily. 
If we do not succeed with this prescription, we may add some 
senna or rhubarb to it. Another popular way of prescribing sulphur 
is the pulvis glycyrrhiza compositus, of which a few teaspoonfuls may 
be taken during the day. Enemata are not generally advisable; for, 
even if carefully used, they are liable to irritate the rectum. Where 
cirrhosis of the liver, or diseases of the lungs or heart, cause the 
haemorrhoids, we cannot usually fulfil the causal indications. In these 
cases, also, the administration of sulphur is advisable, so that a second 
evil may not be added to the first. As we have mentioned overfilling 
of the portal veins, from excess in eating and drinking, as among the 
causes of haemorrhoids, so the casual indications require that such 
patients should not eat too frequently or too much. Finally, in those 
patients who, besides other troubles, have haemorrhoids from excessive 
eating, we must lay down the most stringent rules. If there be a true 
plethora in such cases, it can only be explained on the supposition that, 
when the serum of the blood contains an increased amount of protein 
substances, particularly of albumen, it requires an abnormal fulness 
of the blood-vessels to cause the separation of the same amounts of 
fluid that are excreted with a normal fulness of the vessels. If the 
normal amount of albumen exists in the blood, we may regard it as 
proved that the amount of urine excreted diminishes with the increase 
of albumen in the serum of the blood. The above hypothesis also 
corresponds to the general belief of the laity and physicians: a man 
does not become full-blooded by eating or drinking too much, but by 
eating nourishing food and drinking spirituous liquors. Without en- 592 
AFFECTIONS OF TIIE INTESTINAL CANAL. 
tering into the question whether, in so-called plethora, there is actually 
an increase of the amount of blood, or only an increase of the blood- 
cells, or of the albumen in the blood (polycythaemia and hyperalbumi- 
nosis, Vogel), certain rules of life may be laid down for the affected 
persons which correspond to the physiological and practical view of 
the affection: 1. The use of protein substances must be limited; the 
patient should only eat a little meat or egg once a day, but should 
eat vegetables, fruit, rice, etc. 2. The consumption should be increased; 
the recommendation of long walks and energetic muscular exercise, 
and drinking plenty of water, which hasten the transformation of ma- 
terial, is just as rational as forbidding spirituous liquors, and tea and 
coffee, which seem to retard the transformation. 3. Such patients 
are very greatly benefited by saline purgatives, particularly by the 
moderate and continued use of glauber salts and chloride of sodium, 
as they occur in the waters of Marienbad, Kissengen, Homburg, 
Soden, etc. The use of the waters at Karlsbad requires great precau- 
tions, on account of the high temperature of the springs. If it be 
proved that, by this treatment, the blood grows richer in salts, and 
poorer in albumen (C. Schmidt, Vogel), there would be a rational ex- 
planation of its brilliant results in the treatment of plethora. 
The indications from the disease do not present any further rules 
in cases where occasional moderate suffering is speedily relieved by the 
occurrence of spontaneous haemorrhage; we content ourselves with ful- 
filling the causal indications as well as possible. But if the patients are 
tormented with severe molimina, which do not disappear after the re- 
moval of any existing constipation, we should apply from four to six 
leeches about the anus. After the leeches drop off, we should encour- 
age the bleeding, by placing the patient on a night-stool, with a vase 
of warm water under it. The same proceeding is advisable when great 
fulness and excessive tension of the varices cause severe pain, or if 
haemorrhoids are accompanied by painful tenesmus. "VYe should let 
moderate bleeding continue, particularly when it promises relief from 
troublesome symptoms, and should only use cold or styptics when the 
loss of blood is considerable. Haemorrhoids that have come down and 
been strangulated should be replaced by continued careful pressure 
with a bit of oiled linen, while the patient rests on his knees and 
elbows, with the body bent far forward. Inflamed haemorrhoids should 
be covered with cold-water compresses, or bladders filled with cold 
water. We will not discuss the operative treatment. 
With our view of haemorrhoids, we cannot follow* the ruling custom, 
and speak also of remedies for “ bringing on suppressed piles.” Luckily 
for the patients, the remedies recommended for this end, such as peri- 
odical abstraction of blood, warm sitz-baths, irritating suppositories, ENTERALGIA. 
593 
and the administration of so-called pellentia, rarely cause haemorrhoids, 
while the periodical abstraction of blood attains the only object that it 
was sensible to aim at. 
CHAPTER VIII. 
NERVOUS AFFECTIONS OF THE INTESTINES COLIC—ENTERALGIA. 
Affections of the sensory nerves of the mesenteric plexus— 
colic, in the strict sense of the word—are not by any means frequent. 
Analogy leads us to suspect their occasional occurrence from structural 
diseases of the ganglia and plexuses of the sympathetic nerve; but 
this has not been proved. The frequent occurrence of mesenteric 
neuralgia in hysterical females speaks for its reflex origin. Lastly, lead- 
colic is the most striking instance of a nervous affection caused by 
poisoning. In the latter case, however, there appears to be not a sim- 
ple affection of the sensory nerves—a hypenesthesia—but, at the same 
time, there seems to be a disturbance of the motor nerves—a hyper- 
cinesis—as the painful intestine is always contracted. The lead, 
whose absorption into the body causes lead-colic—one symptom of 
lead poisoning—is partly breathed in as fine powder, and partly ab- 
sorbed from the intestinal and Schneiderian mucous membrane. Hence 
we find the disease among white-lead paint-makers, lead and silver- 
smiths, painters, color-grinders, potters, type-founders, compositors, 
and others who work in an atmosphere loaded with particles of lead. 
The misuse of medicinal preparations of lead, the adulteration of wine 
and other liquors with sugar of lead, or by the accidental addition of 
lead to them, is at present a much rarer cause of lead-colic than those 
above mentioned. Still the celebrated colic of Devonshire, Poitou, and 
other epidemic and endemic colics, which very much resembled lead- 
colic, appeared due to poisoning from some drink containing lead, and 
not to poisoning by vegetable substances. In some rare but authen- 
tic cases, lead-colic has occurred from using snuff that had been packed 
in lead-foil. The predisposition to lead-colic is very varied, but among 
the predisposing causes we only know the great tendency to the dis- 
ease left by a previous attack; all the other causes which are blamed, 
as increasing the predisposition to lead-colic, such as debauchery, 
drunkenness, etc., can hardly be denied, for they are found everywhere, 
Avhen no other causes can be detected. 
But by colic, in the wider sense, we understand, besides the nervous 
affections of the mesenteric plexus, all painful affections of the intes- 
tines which are not caused by inflammation or textural changes of the 
intestinal walls. So, among the symptoms of helminthiasis, we shall 594 
AFFECTIONS OF THE INTESTINAL CANAL. 
speak of colicky pains, just as we mentioned them when speaking of 
the premonitory symptoms of typhlitis stercoracea, and of contraction 
and obstruction of the intestines. But we have already distinguished 
the colicky pains which precede the inflammation from those which 
accompany and depend on it. The same cause which has to-day in- 
duced a colic, may to-morrow excite a colitis. We cannot always ex- 
plain how these colics can induce increased excitability in the sensory 
nerves of the intestines; but we may suppose that the pains are always 
caused by irritation of the peripheral extremities of the intestinal 
nerves; so that this form of colic must be distinguished from the proper 
nervous affection of the intestine. The most frequent cause of colicky 
pain is, unmistakably, excessive distention of a portion of intestine, 
causing stretching of the walls of the intestine, and gases enclosed at 
some circumscribed part appear particularly to cause this distention. 
We may often clearly perceive that the gas is driven forward against 
the fasces, or some other obstruction, and, there arrived, it excites the 
most severe pains; and, in other cases, that the gases are driven by 
the contraction of the intestines, from one place to another, and, with 
their change of location, the position of the pain also changes. It is 
just as improbable that the pain in this colica flatulenta is caused by 
the irritation of the intestinal gases on the intestinal mucous mem- 
brane, as that it depends on the pressure from the contraction of the 
intestinal muscles on the nerves of the intestine. As the decompo- 
sition of the contents of the intestines is the most frequent cause of 
the collection of gas, it becomes evident that the diseases in which the 
contents undergo abnormal decomposition are often accompanied by 
the symptoms of wind-colic. This is particularly true of intestinal 
catarrh, which is excited by the passage of undigested food from the 
stomach into the intestine, or by the long retention of faeces. As in 
children, undigested and decomposing milk very frequently enters the 
intestines, colica infantum is an exceedingly frequent disease. If the 
decomposing substances be removed from the intestines before the in- 
testinal mucous membrane is affected with catarrh, colic may be the 
sole symptom of the abnormal process. Just as colica flatulenta ap- 
pears to be caused by a collection of gas in the intestine, colica stereo- 
racea appears due to a distention of the intestines by feces, and colica 
verminosa to a distention of the intestine by a coil of tape-worm, or 
a bundle of round worms. The abdominal pains following the em- 
ployment of drastics or injurious ingesta are also usually described as 
colic, but the changes in the secretions of the intestine after the use 
of these medicines, or after eating unripe fruit, and many other sub- 
stances, tend to show that there is slight inflammation, which is of 
short duration, and disappears with the removal of the injurious sub* COLIC. 
595 
stances. We may well compare these pains to those that result when 
a sinapism is applied to the skin, and which disappear as soon as the 
sinapism is removed. Perhaps some cases of colica verminosa also be- 
long here, particularly of those where the attacks of pain are followed 
by the discharge of large mucous masses—so-called worm-nests. In 
the painful and long-continued attacks of colic occurring after ex- 
posure of the skin, particularly that of the feet and abdomen, to cold, 
the muscular coat of the intestines appears to suffer in the same way 
as muscles elsewhere do in rheumatic affections; hence the affection is 
well-named colica rheumatica. 
Symptoms and Course.—Romberg describes neuralgia mesen- 
terica as follows: “ There are attacks of pain spreading from the navel 
over the abdomen, alternating with intervals of ease. The pain is 
tearing, cutting, pressing, most frequently twisting, pinching, intro- 
duced and accompanied by peculiar bearing-down pains. The patient 
is restless, and seeks relief in changing his position, and in compressing 
the abdomen; his hands, feet, and cheeks are cold; his features are 
pinched; the wrinkled brows and contracted lips betray his agony. 
The pulse is small and hard. The skin of the abdomen is tense, 
whether puffed up or drawn inward. There are often nausea, vomiting, 
and desire for stool; sometimes there is also tenesmus. There is usu- 
ally constipation, but sometimes the bowels are regular, or even too 
loose. Such an attack may last from a few minutes to several hours, 
relaxing at intervals. It ceases suddenly, as if cut off short, and there 
is a feeling of the greatest relief. The course is periodical, but less 
regularly so than in other neuralgias.” 
Lead-colic is almost always preceded by the symptoms of lead- 
poisoning. The patients are thin and badly nourished, their skin looks 
dirty and earthy, the gums are dark, almost slate-gray, the teeth them- 
selves discolored, and the breath bad; the patients have a sweetish, 
metallic taste in the mouth. Then there are periodical pains, which 
are at first dull, and extend from the epigastrium toward the back and 
extremities. The pain soon becomes more severe, so that, during the 
attack, the patients moan and groan, toss themselves about on the bed, 
or else leave the bed in despair, and do the most foolish things. At 
the same time, the pulse becomes much slower, the voice is lost, and 
strangury, nausea and vomiting often occur, showing that the abnormal 
excitement of the intestinal nerves has spread to other nerves. There 
is almost always obstinate constipation, and, in spite of the most pow- 
erful drastics, eight to fourteen days may pass before the evacuation 
of a small amount of dry, hard, spherical faeces. The abdominal walls 
are in a very peculiar state; they are strongly contracted, and the 
belly seems as hard as a board, and is drawn in. With few excep- 596 
AFFECTIONS OF THE INTESTINAL CANAL. 
tions, the course of the disease shows a distinctly remitting type, so 
that paroxysms of the severest torture are varied with intervals of 
comparative ease. The duration of the disease varies: under suitable 
treatment, the first attack of lead-colic usually subsides in a few days 
or weeks; after repeated returns, the attacks may last for months. 
When the disease terminates in recovery, this may occur suddenly or 
gradually; the pains subside, there are free evacuations, and strength 
soon returns. The cure is often incomplete, and, after the lead-colic 
has been removed, symptoms of chronic lead-poisoning may remain. 
The disease rarely causes death, and, even in such cases, the patients 
do not die of the lead-colic, but of some of its complications. 
The above description of a mesenteric neuralgia will also answer 
for that of colic in the wider sense. Ilenocli is correct in saying that 
the quality of a pain is the same, whether caused by the irritation of a 
nerve at its peripheral expansion, at its origin, or during its course. 
In colica flatulenta, and other colics of this class, the pain may become 
very severe, and then its intensity is depicted in the changed appear- 
ance of the patient; he is near fainting, the body is covered with cold 
sweat, the visage is pale and distorted, the pulse small; occasionally 
there are also nausea, vomiting, strangury, and other similar circum- 
stances. We should know these symptoms, so as not to be deceived 
and unnecessarily worried. We can often hear and distinctly feel, on 
the abdomen of the patient, that the gas is freed from its imprison- 
ment, and passes into other parts of the intestine. This is an important 
event; with its occurrence the pain often disappears instantly. In 
other cases, there is no improvement till the patient has a passage, and 
the faeces, which distended the intestine, or behind which the gases were 
collected, are evacuated. 
Treatment.—In the neuralgic form, the causal indications may 
require treatment of the uterine disease that has induced the neuralgia. 
In lead-colic, the attempt has been made to fulfil the causal indications 
by chemically precipitating the lead that has been taken into the body. 
With this view, sulphuric acid and sulphates, particularly alum and 
glauber salts, have been prescribed. Although we can do little by 
this, or any other treatment, to remove lead-poisoning, wTe may do 
much to prevent its occurrence. With this view, we should avoid the 
use of lead in making pipes and vessels for conducting or holding water 
and other fluids for drinking. The workers in founderies, and other 
places where particles of lead fill the air, should bathe and wash care- 
fully, and change their linen frequently; they should not eat in their 
workshop, and the latter should be very airy, and wrell ventilated. 
Zinc-paint should be used, instead of lead-paint, for painting doors and 
windows, and it should be a penal offence to pack snuff in sheet-lead. COLIC. 
597 
In colic caused by something abnormal in the intestines, evacuants 
are indicated, particularly those which do not, like the drastics them- 
selves, cause colicky pains. The internal administration of castor-oil, 
and the use of enemata, are most advantageous. If exposure of the 
feet or abdomen were the cause of the colic, the causal indications 
require a diaphoretic treatment; and the popular aromatic teas, the 
bottles of warm water and warm stones applied to the abdomen, are 
very suitable in these cases. 
In all forms of the affection, the indications from the disease require 
the administration of narcotics, particularly of opium. In the neuralgic 
form, the action of opium is explained by its anaesthetic effect. In 
colica stercoracea, flatulenta, etc., there seems to be also a second ac- 
tion. The contractions of the intestinal muscles, which drive the gases 
and faeces toward certain parts of the intestines, or confine them there, 
are removed by the use of opium, and thus the contents are enabled 
to spread out over large portions of the intestines. In colica flatulenta 
and stercoracea, warm teas of camomile, peppermint, and valerian, 
drunk by the cupful, or used as enemata, have great reputation, as 
have also some other carminatives, and long and continued friction of 
the abdomen with warm oil. Opium is the most effectual remedy 
against lead-colic, and is used, even by the homoeopaths, in full doses, 
in this disease. We should not be afraid of using it, under the im- 
pression that it will increase the constipation already existing. There 
is no remedy more successful than opium in relieving the constipation 
in lead-colic. This seems to favor the idea that, in that disease, be- 
sides the hyperassthesia, there is a spasmodic contraction of the intes- 
tine, and that this causes the constipation. (.Romberg considers this 
hypothesis improbable, as we cannot believe in a spasm lasting a week, 
and he considers the immobility of the bowels to be due to the pain, 
just as in sciatica the movements of the leg affected are restricted.) 
But, although opium is the most important remedy for the constipa- 
tion, and is of more benefit than laxatives, when it is given alone, still 
we should not neglect to use them with opium. Recently, croton-oil 
is the cathartic most frequently given in lead-colic. In most cases, we 
shall have a good result from the administration of —1 gr. opium, 
three times daily, and every two hours one tablespoonful of a mixture 
of croton-oil (gtt. iij) and castor-oil ( § ij). Warm baths, narcotic cata- 
plasms, and the alternate use of laxative and narcotic enemata, aid 
this treatment. Besides this simple treatment, and slight modifica- 
tions of it, consisting in the use of other laxatives, such as epsom salts, 
senna, calomel, and a bolder or more careful use of opium, there is a 
series of complicated methods, among which the treatment at La 
Charite is particularly celebrated. In all these methods of treatment, 598 
AFFECTIONS OF TIIE INTESTINAL CANAL. 
among the numerous remedies administered, there are always laxatives 
and opium, and their effect seems to depend on these remedies. 
CHAPTER IX. 
WORMS IN THE INTESTINAL CANAL HELMINTHIASIS. 
Toe worms most frequently found in the human intestines are the 
taenia solium, the taenia mediocanellata, the bothriocephalus latus, the 
ascaris lumbricoides, the oxyuris vermicularis, and the trichocephalus 
dispar. 
The taenia solium, the long tape-worm or chain-worm, is from ten 
to twenty feet long, yellowish-white, thin and round at its anterior 
end, and broader and flatter posteriorly. It is divided into head, neck, 
and body, the latter consisting of many hundreds of links. The head 
forms a blunt, square, bulbous enlargement; it consists of a slightly- 
prominent conical snout, which is surrounded by a double row of hooks, 
and farther back by four round suckers symmetrically placed. The 
neck is very slender and about half an inch long. Then come the 
youngest links, which are scarcely quarter of a line broad, while the 
terminal and at the same time the oldest links may be half an inch 
wide or even wider. The individual links, which in shape remind us 
of a pumpkin-seed with the ends cut off, have different structure 
according to their age. The younger ones have a single, slightly 
brownish-yellow median canal, with short lateral ofl-shoots, the first 
indications of sexual organs. The older links have a small prominence 
at the edge, sometimes on one side, sometimes on the other, but not 
regularly alternating, from which the sickle-shaped penis projects, and 
into which the tortuous seminiferous tubes and the oviducts empty. 
The interior of the older links is almost wholly occupied by a uterus 
branching out to both sides or by the ovary. In the oldest links, the 
latter is filled with eggs, and the small embryos with their six small 
hooks may often be distinctly recognized. Vessels start from a vas- 
cular ring within the head, and run down the side of the links; accord- 
ing to some observers, these communicate by transverse canals. Thus 
far no other organs have been observed in the taenia. 
The taenia solium inhabits the small intestine, but may enter the 
large. There is usually only one, but there may be two or more, 
in one person. Taenia solium occurs in Europe, America, Asia, and 
Africa; and, very curiously, it is not found, except in Switzerland, in 
countries where the bothriocephalus latus occurs. 
Until within a few years, the taenia mediocanellata has been con- 
founded with the taenia solium, and in fact its individual links are vcn WORMS IX THE INTESTINAL CANAL—HELMINTHIASIS. 
599 
similar to those of the taenia solium. They have the lateral sexual open- 
ings, but the links are broader and thicker; and the sexual organs are 
more fully developed, and more branched than in the links of the 
taenia solium. The difference in the head is more decided. The head 
of the mediocanellata has neither snout nor the row of hooks, but is flat, 
with four large suckers. This species has remained unknown so long, 
because we rarely succeed in expelling the head, and it has been 
customary when we found links where the sexual openings were on 
the side, to consider them as cases of tenia solium, and when the links 
had the openings in the middle, to regard them as bothriocephalus 
latus. 
The bothriocephalus latus, the broad tape-worm, resembles tenia, 
but may readily be distinguished from it. In its head, instead of the 
snout, the hooks, and suckers, Ave find only two lateral slit-shaped 
fossae. The neck is scarcely to be seen. The breadth of the links is 
much greater than the length; they are about in the proportion of 
three to one. The most important distinguishing mark between single 
links of the two varieties is the position of the sexual openings. In 
the bothriocephalus these are not to the side but in the middle of the 
links, so that in them we may speak of a belly and back. The both- 
riocephalus also inhabits the small intestine. It occurs in eastern Eu- 
rope as far as the Vistula, and in Switzerland it is found with the 
tenia solium. 
The ascaris lumbricoides, the round worm, is cylindrical, pointed 
at both ends, from six to twelve inches long, and from two to three 
lines thick. The body is so transparent that we may see the intesti- 
nal canal, extending from one end to the other, and the sexual organs. 
There is a circular depression behind the head; the latter has three 
small elevations, between which lies the mouth. The sexes are in 
different individuals. In the female there are large ovaries and ovi- 
ducts ; the male is smaller and somewhat crooked at its tail-end, which 
contains the long, tortuous, seminiferous tubes and the testicles. At 
the tail-end of the male we may see the hair-like, sometimes doubled, 
penis. In the upper third of the female is a fissure six to eight lines 
long, the opening of the sexual organs. The round worm inhabits the 
small and large intestine, but makes excursions in various directions 
and may enter the stomach, oesophagus, or even the larynx. From 
the duodenum it occasionally makes it Avay into the ductus choledo- 
chus. It does not seem probable that it can perforate the intestine; 
but if the intestine be perforated by any disease, we not unfrequently 
find round worms in the cavity of the abdomen. They often occur in 
incredible numbers. 
The oxyuris vermicularis, thread or maw-worm, is a small Avorm 600 
AFFECTIONS OF THE INTESTINAL CANAL. 
about as thick: as twine. The males are rare, about a line to a line 
and a half long, and rolled up at the tail-end. The females are larger 
and straight, or only slightly bent. The head of the thread-worm is 
enlarged by wing-like attachments. The penis is at the tail-end of 
the male. The sexual opening of the female is near the head. The 
usual seat of this worm is the lower part of the intestine, particularly 
the rectum, but they may even enter the lower part of the small intes- 
tine. They often crawl out of the anus and enter the vagina, etc. 
The tricJiocephalus dispar, the hair-headed or whip-worm, is about 
an inch and a half or two inches long; the posterior part is quite thick, 
the anterior hair-like. In the male, which is the smaller, the posterior 
part is wound into a spiral, and has at its end the hook-shaped penis 
surrounded by a bell. The female is thicker and straight, and its pos- 
terior end is full of eggs. The trichocephalus inhabits the large intes- 
tine, particularly the coecum. 
Development of Intestinal Worms, and Etiology of Helminthi- 
asis.—The time for believing in spontaneous generation, and in the 
formation of intestinal worms by a collection and alteration of intes- 
tinal mucus, has passed. The parasites living in the intestinal canal 
originate from eggs, and have reached the intestines in that state, or 
one further advanced. Of the taenia solium and taenia mediocanellata 
alone, we more accurately know the mode of development. The last 
links (proglottides) of the tape-worm, which contain the ripe eggs, 
occasionally drop off, and are evacuated. In order to develop further, 
the embryos from the eggs must enter some other animal. If they are 
swallowed by some animal, they pass from the intestines into the tissues 
of the body, till they find a suitable place; then they throw off the 
little hooks, and a neck and head (scolex), resembling those of the 
tape-worm, grow from their wall. At first the scolex is enclosed within 
the embryo; it subsequently becomes free, and the swollen body of 
the embryo hangs to it like a bladder. At this stage of development 
the scolices constitute the parasites known as cysticerci, or bladder- 
worms ; the most common variety of them, those found in swine, called 
cysticercus cellulosus, is the scolex of taenia solium. If this cysticercus 
enters the intestines of a human being, it becomes attached to the 
wall, drops the bladder-like tail, forms links, and becomes a tape-AVorm. 
Taenia mediocanellata develops in the same Avay Avlien a cysticercus 
living in beef enters the intestines of man. The scolices of bothrio- 
ceplialus latus are unknown, as are also the first stages of ascaris lum- 
bricoides, oxyuris vermicularis, and of trichocephalus dispar; but it is 
certain that the young worms are not directly developed from the eggs 
of worms existing in the intestines. Hence Ave must suspect that the 
young of these Avorms also are taken into the body Avith the food. WORMS IN THE INTESTINAL CANAL—HELMINTHIASIS. 
601 
Our ideas of the etiology of helminthiasis have been totally changed 
by the discoveries of recent times; most causes to which it was for- 
merly attributed are now recognized to be without effect. It even ap- 
pears improbable that any decided change of the intestinal mucous 
membrane, or any peculiarity of the contents of the intestines, is 
necessary for the development and future life of the worms. The eti- 
ology of taenia solium is frequently discoverable. K'dchenmeister found 
young taenia in the intestines of a decapitated criminal, to whom he 
had administered cysticerci a few days before death. Of the animals 
whose flesh we eat, swine are the most apt to have the scolex of taenia 
solium. It also occurs in the meat of the goat, and, although more 
rarely, in beef. In Jews and Mohammedans, who eat no pork, taenia 
are very rarely found; and, while in Abyssinia almost every one has 
tape-worm, the Carthusian fathers, who eat only fish, remain exempt 
from them. Taenia are much more frequent in regions where pork- 
raising flourishes, while they are rare where swine are scarce. Cysti- 
cerci cannot withstand boiling, roasting, or smoking, and tape-worm 
never results from the use of measly meat prepared in these modes. 
On the other hand, they are most likely to occur in persons who eat or 
chew raw flesh, or put knives, soiled with cysticerci, in their mouths, 
as is not unfrequently done by waiters, cooks, and butchers. The 
latter may greatly aid the spread of tape-worm by cutting the sausage 
or ham that they sell with a dirty knife, as these articles are often 
eaten without further cooking. The practice of giving badly-nour- 
ished children raw shaved meat to eat is not devoid of danger, for cases 
have occurred where children have undoubtedly acquired tape-worm 
(taenia mediocanellata) in this way. 
The supposition, that the use of meat, containing trichina spiralis, 
led to the development of trichocephalus dispar, has been disproved. 
If, as has been supposed, ascaris and oxyuris are most frequently found 
in persons who subsisted cliiefly on amylaceous food, this might be ex- 
plained by the observations of Stein, who found entozoae in weevils. 
It is possible that, by using bad flour, eggs or lame of ascaris or ox- 
yuris may reach the intestines. 
Symptomatology.—The symptoms excited by intestinal worms 
vary greatly with the peculiarities of the person affected. Frequently 
there are no signs till worms, or fragments of worms, are passed at 
stool. This is chiefly true of tape-worms. Many patients with taenia, 
or bothriocephalus, enjoy the best health, have neither stomach-ache 
nor any reflex symptoms, and the links that pass away, from time to 
time, alone call attention to their disease. Frequently it is difficult for 
the physician to recognize the dried proglottides that are brought to 
him wrapped in paper. In other cases, the patients complain, from 602 
AFFECTIONS OF TI1E INTESTINAL CANAL. 
time to time, of severe pain in tlie abdomen, which they describe as 
twisting and turning (but, perhaps, they may not do so until they 
know they have a tape-worm) ; they double themselves up, or press 
the abdomen against some hard substance, have nausea, and, occasion- 
ally, vomiting. The secretion of saliva is almost always increased, so 
that the saliva flows out of the mouth. The attacks above described, 
particularly when they occur after the use of herring, onions, horse- 
radish, or large-grained fruits, are by the laity considered as a certain 
sign of worms, and should excite in the physician also a suspicion of 
tape-worm; but there is no certainty about it till links of the tape- 
worm have been passed, either spontaneously or after the use of laxa- 
tive or anthelmintic remedies. In other cases, the presence of the 
parasite is not so well borne; occasionally, particularly after eating 
salty or spiced food, there is diarrhoea; the patient becomes weak, 
pale, and thin. This occurs particularly in persons previously debili- 
tated, especially in children and young girls. Lastly, the irritation of 
the intestines, caused by tape-worm, may be reflected to other nerves; 
but the frequency of nervous affections from this cause has been much 
exaggerated, and this exaggeration has led to numerous errors. The 
sensation of tickling in the nose, which induces the patient to rub and 
pick that organ, the dilatation of the pupil, squinting, grating the 
teeth, and other unimportant and more isolated disturbances of inner- 
vation, are rather attributed to the round worm, while the tape-worm 
is blamed with severer and more extensive nervous affections, particu- 
larly epilepsy and St. Vitus’s dance. We may entertain a faint hope 
that epilepsy, occurring without any perceptible cause, depends on irri- 
tation from worms, but we should avoid the belief that the passage of 
links of tape-worm from an epileptic patient proves that the disease 
depends on the presence of the worm, and will disappear with its re- 
moval. Cases where this occurs are very rare, compared to those where 
the epilepsy remains the same after the removal of the tape-worm as it 
was before. 
As a rule, the presence of round worms in the intestines excites no 
symptoms. They are so very common that, if the intestinal canal were 
much irritated, and nutrition greatly impaired by their presence, there 
would not be so many healthy and blooming children. If there be a 
large number of them in the bowels, they may curl up together, and 
form an obstruction, as hard fasces sometimes do, or cause colicky 
pains; if they do not again uncurl, or cannot be removed by cathartics, 
fhey may induce the symptoms of ileus. In other cases, active move- 
ments of the round worms seem to excite abdominal pains, similar to 
those caused by tape-worms. The causes of this disquiet of the worms 
is unknown, and JCttchenmeister''s suggestion, that perhaps the round WORMS IN THE INTESTINAL CANAL—-HELMINTHIASIS. 
603 
worms become more lively during coitus, appears to be meant as a joke. 
To infer, from a pale, cachectic appearance, and from the nervous 
symptoms above mentioned, that a child is suffering from round worms, 
is an error even more common than that of diagnosticating a tape- 
worm in an adult who has the same symptoms. If such a child pass 
round worms from the bowels, or vomit them, it is only too common 
to consider the diagnosis as verified, and to neglect more careful ex- 
amination. By and by, when too late, the discovery is made that the 
symptoms do not depend upon worms, but upon acute hydrocephalus 
or some other dangerous malady. The same is true of worm fever. 
Bound worms may occasionally induce intestinal catarrh, with slight 
febrile reaction, but, in most cases, worms have nothing to do with the 
fever ascribed to them. They may enter the stomach, exciting great 
nausea and discomfort; the little patient cannot describe his feelings, 
and the doctor is perplexed, until a vomited worm solves the riddle. 
Again, a worm in the stomach may be quite unfelt, and may even crawl, 
unperceived, from the mouth during sleep. If it wander into the larynx, 
there will be a spasm of the glottis. Children have even suffocated 
as a result of this accident. If the round w'orm finds its way into 
the ductus choledochus, there may be biliary obstruction, and, if it 
pass on still farther into the gall-ducts of the liver, there may be par- 
tial hepatitis; but we can rarely interpret the symptoms correctly. 
The signs usually ascribed to the presence of ascarides are so little 
to be trusted that Houchut advises the microscopic examination of the 
mucus which covers the feces, in search of the eggs. 
When the oxyuris approaches the anus, or crawls out of it, its in- 
cessant motions cause a very troublesome itching. This usually in- 
creases late in the evening and during the night, and interferes with 
sleeping. Besides the itching, there is usually an incessant desire to 
go to stool. In the evacuations, which are often mixed with mucus, 
the worms continue their snaky movements. If they crawl over the 
perinaeum to the vulva and vagina, they cause annoying prickling and 
itching there also. The irritation from the worms, and from the rub- 
bing that they induce, may cause catarrh of those parts, and the 
frightened mother brings the child to the doctor, saying “ it has the 
whites already.” In such cases a careful examination quiets all fears. 
The trichocephalus dispar causes no symptoms. 
Treatment.—The prophylactic treatment for taenia solium follows, 
as a matter of course, from what has been said. No pork should be 
eaten that has not previously been subjected to the procedures by 
which any cysticerci in it would be killed. Cooks should be forbidden 
to taste raw sausage, or to hold the kitchen-knife in the mouth. 
Butchers should be instructed not to cut sausage or ham with the knife 604 
AFFECTIONS OF TIIE INTESTINAL CANAL. 
they use for raw meat. We can offer no prophylactic treatment for 
the other varieties of worms, as we do not know their mode of 
origin. 
Of the numerous remedies which were formerly used for removing 
tape-worm, we now only employ male fern, pomegranate-rind, koosso, 
and oil of turpentine [pumpkin-seeds]. 
Male fern—Radix filicis mavis—appears to be chiefly efficacious 
against bothriocephalus, and often fails when given for taenia solium. 
Half a drachm or a drachm of the powdered root is given at a dose, and 
two or three such doses are taken in the morning, fasting, or at bed- 
time. A few hours later, or, if the powder be taken at bed-time, the 
next morning, we give a sharp laxative of gamboge, scammony, or 
calomel, or an ounce or more of castor-oil. The ethereal extract of 
male fern, which is usually made into pills, with equal parts of the 
powdered root, and given in doses of a scruple or half drachm, divided 
into two portions, is more certain and more easily taken. Male fern 
enters into most of the numerous and complicated worm-medicines, 
which are of late more and more neglected. 
Pomegranate-rind—Cortex radicis punicce granati—when fresh, 
appears to be one of the most certain remedies against taenia solium. 
We pour a pint or two of water over two or four ounces of it, and, 
after macerating for twenty-four hours, boil it down to one-half. This 
decoction is generally divided into three doses, and used in the morn- 
ing, fasting, and, although very usually efficacious, it is occasionally 
vomited by the patient, and always causes excessive pain in the abdo- 
men for hours. I can urgently recommend that, before using the de- 
coction, the simple maceration should be tried; this is also made from 
two or four ounces of the rind. This maceration acts much more 
mildly; the patients suffer scarcely any, and after its use I have fre- 
quently seen one tape-worm passed, and, in one case three, with their 
heads, were passed. If the maceration fails, the decoction may be 
tried in a few days. After the exhibition of pomegranate-rind, the 
worm usually passes, unbroken, and is often rolled into a ball. If it 
be not passed in from one to three hours after the last dose, we may 
give one or two ounces of castor-oil. Kilchenmeister recommends 
making an extract from four or six ounces of pomegranate-rind, and 
adding this, with from four to six ounces of hot water, to a scruple or 
half a drachm of ethereal extract of male fern, and four to six grains of 
gamboge. Two cups of this mixture taken, with an interval of three- 
quarters of an hour, are said to expel the worm. If this do not re- 
sult in an hour and a half, the third should be administered. 
Koosso—the dried and powdered flowers of Rrayera anthelmin- 
tica—a remedy recently introduced from Abyssinia, has not fulfilled WORMS IN THE INTESTINAL CANAL—HELMINTHIASIS. 
605 
the expectations entertained of it; at least, the brilliant results at- 
tested by some observers have not been attained by others. From two 
drachms to half an ounce may be macerated in water, or made into 
an electuary with honey, and given in two doses, with an interval of 
half an hour, in the morning, after a cup of coffee has been taken. If 
nausea occur, we may give some lemon-juice. If the patient do not 
have a passage in three hours, we may give a dose of castor-oil or 
senna. 
Although oil of turpentine is among the most certain remedies for 
tape-worm, it should only be used in case of necessity, not only on ac- 
count of its disagreeable taste, but because in the requisite doses it is 
apt to irritate the urinary organs. One or two ounces of oil of turpen- 
tine alone, or mixed with honey or castor-oil, or in emulsion, are to be 
given in one dose, at bed-time. 
It is best to use any of these remedies at times when some of the 
links of the tape-worm have been passed spontaneously; but it is quite 
unnecessary to delay treatment till certain phases of the moon, when, 
according to popular belief, the worms may be more readily dislodged. 
We should employ some preparatory treatment: let the patient live 
moderately, keep his bowels open with castor-oil, and let him live for a 
few days almost exclusively on herring, ham, onions, and other salty 
and spicy food. Instead of the above, the patient may eat freely of 
wild strawberries, huckleberries, etc., as the numerous seeds of these 
fruits appear to sicken the worm (KttchenmeisterJ. The cure cannot 
be regarded as perfect till we find the head of the animal; nor must 
we forget that there may be more than one tape-worm in the intes- 
tines. Kameela, a powder obtained from the capsules of llottera tinc- 
toria ( 3 ij—iij, rubbed up with water), cortex musence (§ i—ij, with 
honey), radix pounce ( 3 j—ij), and a few other medicines, have been 
more or less lauded as remedies for tape-worm, but after repeated 
trials no one of them has proved peculiarly efficacious. 
For ascaris lumbricoides, semina cynce vel santonici, the buds of 
Artemisia contra, justly enjoy the best reputation. The practice of 
giving an electuary, made of the powdered seeds of -worm-seed, jalap, 
valerian, honey, and other substances, by which children were formerly 
tortured several times a year, as well as its exhibition in the shape of 
worm-chocolate or cakes, is now almost displaced by the more certain 
and agreeable preparations, such as the ethereal extract, and particu- 
larly santonin. Of the former we may give a child gr. v—x during 
the day, of the latter, gr. iij—jv. Apothecaries often keep troches of 
santonin, containing gr. ss—j each, which taste pleasantly. Kilchen- 
meister advises dissolving santonin, gr. ij—iv, in castor-oil § i, and 
giving a teaspoonful of this solution every hour till it acts; he had 606 
AFFECTIONS OF THE INTESTINAL CANAL. 
still better results from the santonate of soda, in doses of gr. ij—iv, 
given morning and evening for several days. A laxative should al- 
ways be given after the use of worm-seed, or its preparations. Othei 
anthelmintics for expelling round worms may be dispensed with. 
Enemata suffice to drive the oxyuris from the rectum. Even in- 
jections of cold water, with a little vinegar, are very efficacious ; but 
they should be very large, so as to reach any of the worms that may 
be up in the sigmoid flexure, and they should be used for a long time. 
In obstinate cases we may add a weak solution of corrosive sublimate 
(gr. i to 3 ij) to the enema. 
(In my last edition, tricliiniasis was considered at this place, but in 
this one I shall speak of it among the infectious diseases; the reasons 
for this will be stated when speaking of its etiology.) 
CHAPTER X. 
GASTRIC FEVER, CATARRHAL AND BILE-FEVER. 
Many physicians, particularly among the Germans, describe as 
gastric fever a disease running an acute course, in which high fever is 
only accompanied by dyspeptic symptoms, and generally by diarrhoea, 
while there are usually no symptoms that would indicate severe dis- 
ease of any important organ. Celebrated authorities, particularly 
those clinical observers who have developed in hospital, and have had 
only hospital practice, consider all cases of so-called gastric fever as 
mild cases of typhus. I cannot at all agree with this view. Every 
physician in private practice often has the opportunity of seeing, after 
errors of diet, without any suspicion of infection, symptoms of variable 
duration, which exactly answer to those of gastric fever. If this be so, 
even where we can find no error of diet, wre must be careful about in- 
ferring that there is an infection, and must acknowledge the possibility 
that catching cold, atmospheric and telluric influences, and other 
sources of injury, may excite a similar set of symptoms. But I will 
not attempt to deny that numerous slight cases of typhus are diagnos- 
ticated as gastric fever. 
As a rule, gastric fever begins with several slight chills, rarely with 
one severe one. The pulse quickly rises to 100 or more. According 
to the few observations that have been made, the temperature is some- 
times normal, in other cases it is decidedly increased; it may reach 
from 102° to 105°. The constitutional disturbance is very marked. 
The faintness is so great that the patient remains in bed; the limbs, 
particularly at the joints, pain “ as if they would burst.” The insup- 
portable headache is usually increased by laying the head on a feather GASTRIC FEYER, CATARRHAL AND BILE-FEVER. 
607 
pillow, while it is occasionally relieved by binding a towel firmly 
around the head. The patient does not sleep at all, or is disturbed by 
dreams. The symptoms of disease of the stomach or intestines vary. 
Usually the appetite is lost, the tongue coated, the taste slimy or bit- 
ter, the breath is bad, the patients complain of a feeling of pressure and 
fulness in the epigastrium, and are sensitive to pressure there. There 
is also eructation of gases and fluids, usually acid products of abnor- 
mal gastric digestion. Occasionally there is repeated vomiting. At 
first there is usually constipation; but later, particularly when the dis- 
ease is protracted, there is diarrhoea, preceded by more or less colicky 
pain; the stools are fluid, and colored green by bile, and are sometimes 
mucous. 
Occasionally these symptoms pass off quickly, and the patient, who 
is one day in a sad plight, feels quite well the next (ephemera). At 
the same time herpetic vesicles not unfrequently come on the lips. 
We should not consider tliis a distinct disease, a febris herpetica. 
Herpes labialis accompanies gastric fever as often or perhaps oftener 
than it does pneumonic or intermittent fever, and has the same sig- 
nificance in the former disease as in the latter. But the disease does 
not by any means always terminate in one day; it often continues 
several days, but rarely longer than a week. In persons who do not 
bear well the feverish increase of temperature, or the consumption 
caused by the increased development of heat (we have frequently said 
that individual peculiarities vary greatly in regard to this), there is 
great depression, the mind is affected ; instead of dreams, the patient 
has delirium; and, if at the same time the tongue become dry, the 
similarity with typhus is very great. It often happens that the true 
nature of the case is only explained at the sixth or eighth day, by the 
sudden improvement and the rapid convalescence. 
In consideration of the difficulty of diagnosticating gastric fever 
from a commencing typhus, it is advisable to be very guarded in diag- 
nosis and prognosis during the first week. It would be very danger- 
ous for the reputation of the physician, if, after he has pronounced the 
disease to be gastric fever, and promised improvement from day to 
day, it should develop with all its terrors in the second or third week. 
But it will compromise the doctor just as much if the supposed nervous 
fever terminate in cure at the end of the first week, and the patient 
be able to walk out a few days later. Even the laity no longer believe 
that under certain circumstances “ gastric fever ” may become “ gas- 
tric nervous,” and this again develop into “nervous fever.” They 
know that these two diseases are of different nature from the first. 
In making a differential diagnosis during the first week, great atten- 
tion should be given to the etiology. If there have been injurious 608 
AFFECTIONS OF TIIE INTESTINAL CANAL. 
influences that could cause gastric and intestinal catarrh, in doubtful 
cases the presumption will be in favor of gastric fever. If, on the 
other hand, there have been numerous cases of typhus in the city or 
vicinity, and no errors of diet can be discovered as causes of the dis- 
ease, we should suspect typhus. Secondly, the increase of the bodily 
temperature is not so regular in gastric fever as in typhus. Thirdly, 
catarrh of the finer bronchial tubes, with cough and sibilant rhonclii, 
indicates typhus rather than gastric fever, although bronchial catarrh 
may occur in the latter also; such cases are usually termed gastro- 
catarrhal. Fourthly, an eruption of herpetic vesicles about the mouth 
almost certainly excludes typhus. Fifthly, and lastly, a perceptible 
enlargement of the spleen, and the appearance of roseola spots on the 
upper part of the abdomen at the end of the first week, speak against 
gastric and in favor of typhus [typhoid] fever. 
Cases occur where from the great general disturbance the gastric 
symptoms are thrown so much in the background, that we may doubt 
whether the disease is venting itself in the intestinal canal, and 
whether the fever and the symptoms caused by it can really be re- 
garded as symptoms of gastric and intestinal catarrh. It is such cases 
that have led to the formation of the class called simple (essential) 
fever, fiime simple continue, or synoeha. I doubt the propriety of 
believing that fever can occur as the sole effect of the action of any 
injurious influence on the body. It seems much more probable that 
even in such cases there is structural change, which we cannot at 
present discover, in some organ or other. I consider this hypothesis 
justifiable from the well-known fact that, in numerous cases of pneu- 
monia, erysipelas, and severe nasal and bronchial catarrhs, the fever 
and great general disturbance appear before the local symptoms. It 
is very difficult for me to believe that here also there is at first an 
essential fever, to which a local affection is subsequently added; and 
the more so, as, after this occurs, the fever and local disease keep step, 
and the former disappears when the latter has run its course. Now, 
if the delicate organic disease do not reach so high a grade as to 
cause evident functional disturbances, according to my hypothesis we 
have the state usually called essential fever. In any fever there is 
slight dyspepsia; and simple want of appetite, slightly-coated tongue, 
etc., do not justify us in designating a febrile affection as gastric fever. 
Even more decidedly than in the case of gastric fevers does 
Griesmger say that the rare but very regular and characteristic 
disease called catarrhal fever, febris pituitosa, is also a typhus dis- 
ease, which has, it is true, a peculiar and unusual course. I do not 
know whether Griesinger himself has made a large number of autop- 
sies in cases of this disease, or whence he derives his authority for say- GASTRIC FEVER, CATARRHAL AND BILE-FEVER. 
609 
mg “ that we find open or even cicatrizing intestinal ulcers in these 
cases.” The long duration of the disease, the slightness of the fever, 
the great extent of the catarrh, the excessive production of mucus, and 
other points, decide me to doubt the correctness of Griesinger's belief 
till I have learned the facts on which he bases it. The description 
which I shall now give of the symptoms and course of catarrhal fever, 
I take partly from my own observation, partly from the excellent 
description of this disease, given in Schonlein’s lectures, and which 
exactly corresponds with my own observation. 
This disease does not begin with frequent pulse, pain in the limbs, 
severe headache, and restlessness, as gastric fever does. The pulse 
is usually moderately increased, the temperature slightly elevated, but 
the patients feel very dull and heavy, are apathetic, constantly sleepy, 
and disgusted at all food. If the patient be compelled to eat some- 
thing, he soon has a distressing feeling of fulness ; then vomiting oc- 
curs, and the food is thrown up, enveloped in large quantities of tough 
mucus. The accompanying oral and pharyngeal catarrh is also pecu- 
liar : the coating of the tongue is, at first, thick and yellowish ; teeth 
and gums, palate and pharynx are covered with tough mucus ; later 
the whole epithelial covering of the tongue is often thrown off, and it 
then looks red, like a piece of raw meat, or as if coated with varnish. 
In the morning, especially, the patients raise so much mucus, by spit- 
ting, hawking, vomiting, and coughing, that a spittoon will hardly con- 
tain it all; quantities of mucus are mixed with the undigested food, in 
the passages from the bowels, while the urine contains a mucous 
deposit. Even in the subsequent course, the fever remains moderate, 
and has sometimes a remittent, sometimes a continued type. The 
patients become very feeble; their apathy increases so, that while 
they do not sleep, they lie without any interest in their own state, or 
in things about them. If the disease begins to mend, which frequently 
does not occur till the third or fourth week, the production of mucus 
gradually ceases, the appetite slowly returns, the pulse becomes very 
sluggish, and the exhausted patients do not recover strength for a long 
time. The slightest cause induces a relapse; then the process begins 
anew, and months may pass before a perfect cure, or, in weak, decrepit 
persons, death may result. 
It is difficult to determine what disease the older physicians meant 
by bilious, or gall-fever. I hope, however, by my observations during 
the last few years, to have arrived at a better understanding of those 
fevers accompanied by icteric symptoms. I no longer believe that 
this icterus is due to a polycholia, where more bile is produced than 
can be expelled from the gall-ducts, and that, consequently, part of it 
is reabsorbed. I rather consider the icterus accompanying excessive 610 
AFFECTIONS OF THE INTESTINAL CANAL. 
fever, as a “ hmmotogene,” that is, as one resulting from disintegration 
of the blood-corpuscles, and transformation of the released coloring 
matter of the blood into coloring matter of the bile. When speaking 
of diseases of the liver, I shall return to the subject, and will here 
confine myself to the following remarks. In pyaemia, in puerperal 
fever, and in other infectious diseases, probably as a result of the ex- 
cessive increase of bodily temperature, there is often parenchymatous 
degeneration of the most varied organs, in wdiich the blood also par- 
ticipates. More rarely, in the course of inflammatory affections, such 
as pneumonia, there is a dissolutio sanguinis (which -was recognized 
by the older physicians), and, as a consequence of this, haemotogenous 
icterus. But lastly, even catarrhal diseases, affecting the intestinal 
or bronchial mucous membrane, may lead to parenchymatous degenera- 
tion of the liver, heart, kidneys, or blood. During the last few years I 
have seen many patients with simple bronchial or intestinal catarrh 
die with severe nervous symptoms, icterus, moderate swelling of the 
liver, irregular and retarded pulse, albuminuria, etc., without there be- 
ing any suspicion of an infectious disease. Such cases, which, like 
“ bilious pneumonia,” are more frequent at certain times, and occur 
oftener in certain regions, particularly in the tropics, doubtless form 
part of the bilious fevers of old writers, while another part of them 
were certainly cases of pyaemia and other infectious diseases. 
Muriatic acid has a great reputation in the treatment of gastric 
fever. We are undecided as to whether the common prescription of 
half a drachm of concentrated muriatic acid to six ounces of muci- 
lage, or of a weak infusion of ipecacuanha (gr. viij— 3 vj), has the 
favorable effect ascribed to it. At all events, patients usually take 
this remedy willingly, and it moderates the thirst; and it is worthy 
of remark, that this prescription furnishes the gastric juice with the 
acid to which, as physiology shows, it owes its digestive powers. 
In catarrhal fever we prescribe the alkaline carbonates, particu- 
larly the tinctura rliei aquosa. I have used this prescription, just as 
advised by /Schonlein, in rather large doses, i. e., a teaspoonful every 
two hours, with excellent effect; and can fully support its recom- 
mendation as almost a specific in this disease. I have also observed 
that the patients do not 'well bear the customary soups, and get along 
better if wre give them, from time to time, a small piece of black 
bread, sprinkled with salt. 
In febris biliosa the mineral acids are usually prescribed. Perhaps 
an antipyretic treatment, such.as quinine, in large doses, and the en- 
ergetic abstraction of heat by cool baths, or repeatedly wrapping the 
body in wet sheets, will do still better. SECTION VI. 
DISEASES OF THE PER IT 0 FEE UM. 
CHAPTER I. 
INFLAMMATION OF THE PERITONAEUM, PERITONITIS. 
Etiology.—For the pathogeny of peritonitis we may refer to 
what was said of the pathogeny of pleuritis and pericarditis. The 
same course that we have described as occurring in the pleura and 
pericardium during those diseases is repeated in the peritonaeum during 
peritonitis; while there is a new formation of young connective tissue, 
a proliferation in the peritonaeum, its surface is covered by a fibrinous 
exudation, containing a variable number of young cells—pus-cor- 
puscles. In some cases of chronic peritonitis, however, the inflamma- 
tion seems to remain limited to the proliferation of the peritoneal con- 
nective tissue, and there is no free exudation. It is most probable 
that the thickenings and adhesions of the peritonaeum, which exactly 
resemble those of the pleura, and, like these, are formed without symp- 
toms, occur in this manner. 
The predisposition for peritonitis, at least for the acute and diffuse 
form, is not great in strong, healthy persons. Slight causes, such as 
frequently induce inflammations of other serous and of mucous mem- 
branes, scarcely ever cause peritonitis. Hence, when a previously 
healthy person is attacked with peritonitis, we should suspect that it 
is due to one of the serious difficulties below mentioned, and should not 
consider it as a case of so-called rheumatic peritonitis till these other 
causes have been excluded, which is sometimes a difficult task. The 
tendency to peritonitis is much greater in persons affected with tuber- 
culosis, morbus Brightii, and other exhausting diseases, as well as 
in -women at the menstrual periods, than in healthy persons. Among 
the former, slight causes not unfrequently suffice to induce peritonitis. 
We have frequently given our reasons for not considering these 
cases of peritonitis as secondary symptoms, just as we have done the 612 
DISEASES OF THE PERITONAEUM. 
pneumonia and pleurisy which so frequently occur under the same cir- 
cumstances. Finally, in not a few cases, peritonitis is the immediate 
result of an infection, and comes under the same category as the inflam- 
mations of the skin in exanthematous diseases. This form will be de- 
scribed when speaking of puerperal fever, and other infectious diseases 
which are “ localized in the peritonaeum.” Among the exciting causes 
of peritonitis are: 
1. Severe contusions and penetrating wounds of the abdomen. 
Among the surgical operations, paracentesis rarely leads to diffuse 
peritonitis, operations for hernia do so more frequently, while gastrot- 
omy always causes it. 
2. In the same way it may be caused by ruptures or perforations 
of organs covered by the peritonaeum, and the consequent entrance of 
foreign bodies into the peritoneal sac. Thus perforating ulcer or can- 
cer of the stomach, ulceration of the vermiform process, or of the 
coecum, typhoid or scrofulous ulcers of the intestine, perforation of the 
gall or urinary bladder, opening of abscesses of the liver or spleen, 
etc., may cause peritonitis. In all these cases the inflammation usu- 
ally spreads rapidly over the entire peritonaeum. It is only rarely 
circumscribed by old attachments, or recent adhesions of the intestines, 
protecting other parts of the peritonaeum from contact with the escaped 
substances. 
3. Peritonitis may result from propagation of inflammation from 
other organs; the peritonaeum participates in the inflammation of or- 
gans covered by it, just as often as the pleura does in inflammation of 
the lungs. Of this nature is the peritonitis in typhlitis stercoracea, 
strangulated hernia, internal strangulations, rotations, and intussuscep- 
tions of the intestines. Inflammation often extends from the female 
sexual organs to the peritonaeum. In the same way hepatitis or sple- 
nitis may cause peritonitis. In these cases the inflammation is usually 
circumscribed at first; and in many cases it remains so during its sub- 
sequent course; in others, particularly in those caused by incarcera- 
tion and similar processes, it becomes diffuse. 
4. As we have already said, peritonitis very rarely occurs in per- 
sons previously healthy, from catching cold, or from unknown atmos- 
pheric influences. When it does occur, it is called rheumatic perito- 
nitis. 
Anatomical Appearances.—We shall first speak of the appear- 
ances in acute diffuse peritonitis. 
At the commencement of this disease the peritonaeum is reddened 
partly by hyperaemia, partly by the escape of blood into the tissue. 
But, to discover this redness, it is usually necessary, first, to remove 
from the peritonaeum the deposits which will be described hereafter. INFLAMMATION OF THE PERITONAEUM, PERITONITIS. 
613 
Subsequently this redness disappears, apparently because the capil- 
laries are compressed by the occurrence of oedema in the tissue of the 
peritonaeum. The surface soon becomes cloudy from loss of its epithe- 
lium, and has the velvety appearance which, as we have fully described 
in pleuritis, depends on a proliferation of the connective tissue compos- 
ing the peritonaeum. 
Far more noticeable than these structural changes of the perito- 
naeum, are the exudations which never fail even after a short duration 
of the peritonitis. Their shape and amount vary greatly. Occasion- 
ally a thin transparent layer of coagulated fibrin, which may be peeled 
off like a delicate membrane, coats over the inflamed peritonaeum, and 
unites the loops of intestine loosely together; fluid exudation is no- 
where to be found. In other cases the deposit is thicker, less trans- 
parent, yellow, like croup membrane, and, in the dependent parts of 
the abdomen, there is a moderate amount of cloudy flocculent serum. 
In other cases there is a great quantity of exudation; when the abdo- 
men is opened, an immense amount of turbid, flocculent fluid escapes, 
while a still greater quantity remains among the intestines, in the pel- 
vis, and along the spine. Then, besides the membranous deposits cov- 
ering the peritonaeum, we find numerous yellow clumps of coagulated 
fibrin which partly swim in the fluid, partly sink, and collect in the 
dependent parts of the abdomen. 
The scanty, very fibrinous exudation is chiefly found in peritonitis 
due to injuries or to propagation of inflammation from neighboring 
organs. On the contrary, the abundant sero-fibrinous exudations are 
more frequent in peritonitis from perforations, or dependent on infec- 
tion, particularly puerperal, and lastly in the so-called rheumatic 
peritonitis. 
All the coats of the intestines are the seat of collateral oedema, 
particularly in those cases accompanied by profuse exudation. Con- 
sequently the intestinal wall appears thicker; the oedema of the mu- 
cous membrane has caused serous transudation into the intestine, and 
the oedema and paralysis of the muscular coat have often led to enor- 
mous collections of gas in the intestine. The superficial layers of 
the liver, spleen, and abdominal walls, are often infiltrated and discol- 
ored. Finally, we must mention (more particularly as this partly 
explains the early death), that the exudation, and still more the dis- 
tention of the intestines, may press the diaphragm up to the third or 
second rib, and compress a great part of both lungs. 
If the patient does not die at the height of the inflammation, the 
appearances change. In the most favorable cases the fluid part of 
the exudation is rapidly absorbed. Subsequently the coagula and pus 
corpuscles, which are partly enclosed in them and partly suspended in 614 
DISEASES OF THE PERITONEUM. 
the fluid, also disappear after they have undergone a fatty metamor- 
phosis, become fluid, and ready for absorption; but partial thickenings 
and adhesions of the peritonaeum always remain. In less favorable 
cases the absorption of the fluid part of the exudation is incomplete. 
The pus-corpuscles, which were at first rare in the exudation, now in- 
crease so as to give it a purulent appearance, and the fibrinous deposits 
also become yellower and softer. At some places the intestines ad- 
here quite firmly and enclose the fluid, thus limiting its motions. If 
the patient survive this stage also, which is usually found in persons 
who have died in the fourth to sixth week of peritonitis, the capsulated 
fluid may be absorbed or thickened, and changed to a yellow cheesy 
or even chalky mass, which, enclosed in tough connective tissue, re- 
mains in the abdominal cavity. In other cases the extensive cell-for- 
mation occurring in the free surface of the peritonaeum attacks the tis- 
sue itself, causing ulceration and perforation of the peritonaeum; accord- 
ing to the location of this perforation, the capsulated fluid reaches the 
intestines or bladder, breaks through the abdominal Avails, or descends 
into the cellular tissue of the pelvis, and escapes outwardly at some 
deeper point. 
In acute partial peritonitis, the changes that we have described 
are limited to the serous coating of the liver, of the spleen, of a portion 
of intestine, or of several loops lying near together, and to the immedi- 
ate vicinity of these parts. If the exudation be scanty and fibrinous, 
the process usually terminates with the adhesion of the inflamed parts. 
If the exudation be more copious and sero-fibrinous, portions may be 
capsulated between the inflamed parts, as in the diffuse form, and these 
capsulations run the course above described. 
By chronic peritonitis is usually meant, first those cases which, 
beginning acutely, run a protracted course, and lead to the formation 
of the collections of pus above described. Secondly, those cases occur- 
ring, particularly in children, in connection with tuberculosis of the 
intestine and mesenteric glands, which are chronic from the start, and 
spread over the whole or the greater part of the peritonaeum. This 
form is characterized by the excessive proliferation of connective tis- 
sue, as a result of which there are gelatinous or indurated thickenings 
of the peritonreum. The intestines usually adhere in shapeless masses, 
and between the various convolutions there are cavities filled with 
serous, purulent, or bloody fluid. The admixture of blood depends on 
the rupture of vessels, which usually occurs where a chronic inflamma- 
tion is repeatedly lighted up, for not only the original tissue, but that 
which has recently formed on it, and is rich in large and thin-walled 
eapillaries, becomes the seat of the new inflammation. Tubercles are 
often found in the thickened peritonaeum, in this form of peritonitis; this INFLAMMATION OF THE PERITONAEUM, PERITONITIS. 
615 
is most apt to occur where there is haemorrhagic exudation. Thirdly, 
and lastly, there is very frequently a partial chronic peritonitis, which 
we know better in its results than in its first stages. It occurs in 
chronic inflammations and degenerations of the abdominal viscera, and 
causes partial cloudiness and thickening of the peritonaeum, adhesions 
of neighboring organs to each other, and distortions and folds of the 
intestines. 
Symptoms and Course.—The symptoms of acute diffuse perito- 
nitis at its commencement vary with the causes which induce it. 
Traumatic peritonitis usually begins with severe pain at the seat of 
the injury, which quickly spreads over the entire abdomen. In peri- 
tonitis from perforation also, excessive pain over the whole abdomen 
is the first symptom, if the perforation has occurred suddenly, and 
foreign substances have entered the peritonaeum. At first, along with 
the pain there are symptoms of great general depression, and subse- 
quently there is severe fever. If the perforation occurs gradually, and 
only a slight amount of foreign substances enters the peritonaeum, the 
symptoms of general peritonitis are preceded by those of partial peri- 
tonitis. The commencement of an acute diffuse peritonitis, where the 
inflammation is propagated from neighboring organs, is far less strik- 
ing. The pain already existing gradually increases ; it is at first re- 
stricted to the seat of the affected organ, and thence spreads gradually 
over the entire abdomen. It is only in rheumatic peritonitis, and 
those cases resulting from infections, that we have a severe chill and 
intense fever at the onset of the disease, as in other severe inflamma- 
tions. 
No matter how the disease begins, whether there is fever at first, 
or it does not come on till late, pain is always the most troublesome 
and the most characteristic symptom. Any slight pressure on the ab- 
domen increases it; even the pressure of the bed-clothes may become 
unbearable. The patient does not toss about the bed, as he does 
in colic, but lies on his back with the knees drawn up, and dreads 
every change of position. The slightest cough causes a distortion of 
the countenance, from pain ; the patient speaks low and carefully, and 
does not breathe deep, fearing the pressure of the descending dia- 
phragm. The abdomen soon becomes tense and puffed up. At first 
the distention depends but little on filling of the abdomen with exuda- 
tion, and is mostly caused by distention of the intestines, which are 
filled with gas. This tympanitis is not easily explained ; it is proba- 
ble that it is not due to an increased formation of gas, for we can find 
no cause for a more rapid decomposition of the contents of the intes- 
tines ; and it is just as unlikely that air should be exhaled from the 
-vail of the intestine in peritonitis. Hence the meteorismus seems to 616 
DISEASES OF TIIE PERITONAEUM. 
depend, to a small degree, on the expansion of the gases due to relax- 
ation of the intestinal walls ; to a greater degree on obstructed escape 
of the gases due to paralysis of the muscular coat. The belly may 
soon become very much distended. But of course the exudation and 
the inflated intestines press upward against the diaphragm in the same 
way that they press against the abdominal walls, and so cause symp- 
toms which, next to the pain, are the most distressing and most dan- 
gerous. The compression of the lower lobes of the lung by the up- 
ward pressure of the diaphragm, as well as the excessive hyperaemia 
of the non-compressed portions of lung (resulting from the disturbance 
of circulation in the compressed portions), induces excessive dyspnoea 
and a frequency of respiration of 40 to 60 inspirations in a minute. The 
effect of the disturbance of the circulation of the lungs may extend be- 
yond the right side of the heart to the veins of the general circulation, 
and give the patient a cyanotic look. In most cases of acute diffuse 
peritonitis the patient is obstinately constipated; this symptom is ex- 
plained by paralysis of the muscular coat of the intestines by collateral 
oedema. In puerperal peritonitis alone there is usually watery diar- 
rhoea ; for in this form the oedema extends to the mucous coat, and 
causes copious transudation into the intestines, and, if they become 
somewhat full, it flows away in spite of the paralysis of the muscular coat. 
If we set such patients up in bed, or if we press strongly on the abdomen, 
watery, slightly-colored masses pass from the anus. Besides the above 
symptoms, there is often vomiting, provided the peritonitis has not 
been caused by the perforation of a chronic ulcer of the stomach. At 
first the vomited masses .are mucous and colorless, later they are more 
watery, greenish, or even intensely green. The causes of the vomit- 
ing, and the circumstances under which it is absent, are obscure. This 
difference is not explained by the participation of the covering of the 
stomach in the inflammation, or by its freedom from it. If the inflam- 
mation extend to the peritoneal covering of the bladder, there arises 
an incessant desire to urinate, and a feeling of fulness in the bladder. 
If an inexperienced physician be deceived by this, and be induced, by 
the patient’s desire to urinate, to introduce a catheter, only a few drops 
of concentrated urine will be withdrawn. Fever is one of the symp- 
toms of acute diffuse peritonitis, and, where this does not begin with 
the disease, it occurs very early. The pulse is very frequent and small; 
the temperature rises to 105° or more. As in any severe fever, the 
general state of the patient is much affected—the mind is unusually 
clear. 
In severe cases the above symptoms become very decided in a few 
days. But the pain is usually worse at first, and subsequently dimin- 
ishes. The belly is inflated like a drum; the liver and the point of the INFLAMMATION OF THE PERITONAEUM, PERITONITIS. 
617 
heart are often pressed up as high as the third rib. While at the com- 
mencement of the disease percussion gave a full tympanitic sound, after 
the exudation has become abundant, there is a distinct but rarely ab- 
solute dulness. The anxiety of the patient is pitiful; he beseeches 
aid, and looks perfectly desperate. If a quantity of blood be not ab- 
stracted, or the volume of blood be not diminished by extensive exuda- 
tions, the countenance may become excessively cyanotic. Finally, the 
mind becomes cloudy, the patient grows apathetic and delirious, the 
pulse is smaller and more frequent, the body covered with cold sweat, 
and occasionally on the third or fourth day after the commencement of 
the affection, or more frequently at the end of the first week, the patient 
succumbs to his disease. 
If the malady take a favorable course, which usually occurs only 
when we succeed in removing the exciting causes, or when these are 
not very grave, the pain, tympanites, and fever gradually subside, the 
respiration becomes freer, and the patient may recover rapidly. But 
very often, as a result of the adhesions and flexions of the intestines, 
habitual constipation, and occasionally colicky pains before stool, re- 
main for life. 
If the patient does not die during the first week, and if there be 
no decided improvement during this time, the character of the disease 
usually changes : it takes on a more chronic course. The pain moder- 
ates, the abdomen is only sensitive on hard pressure, the tympanitis 
decreases without disappearing entirely. If, up to this time, the pa- 
tient has suffered from constipation, he now has movements from the 
bowels ; if, on the contrary, there was diarrhoea as a result of the ex- 
cessive transudation into the bowels, this disappears, or constipation 
and diarrhoea alternate. The pulse and temperature also sink some- 
what, without, however, becoming normal. As the tympanites sub- 
sides, the dulness at the dependent parts of the abdomen usually be- 
comes more distinct, and at the dull spots we perceive a gradually 
increasing resistance ; by degrees the abdomen becomes unsyminetrical 
and nodular, and the capsulated exudations appear like irregular tu- 
mors. The fever, although moderated, continues and exacerbates from 
time to time, and it consumes not only the strength of the patient, but 
his blood and tissues. The fat disappears, the muscles become flabby 
and relaxed, the skin dry and scaly; not unfrequently there is oedema 
of the legs, and in the fourth, fifth, or sixth week, the patient dies of 
exhaustion. If, contrary to our expectation, there be reabsorption of 
the fluid, convalescence is very slow, and the symptoms of contraction 
and distortions of the intestines, which remain more constantly after 
these cases, are the sources of long and severe sufferings. If there be 
ulceration and perforation of the peritonaeum, the fever increases, and, 618 
DISEASES OF THE PERITONEUM. 
at some circumscribed spot, the abdominal walls become infiltrated, 
reddened, and finally the pus breaks through, or abscesses form and 
point at the most varied places, or, in fortunate cases, the abscesses 
perforate into the intestine, and the pus is passed at stool. In these 
cases, also, the patients usually die of exhaustion, and but few recover 
after .tedious convalescence. 
Acute partial peritonitis is usually preceded by premonitory symp- 
toms, due to the disease of the organs, from which the inflammation 
extends to the peritonaeum. Thus acute partial peritonitis, beginning 
in the right iliac fossa, is usually preceded by the symptoms of typh- 
litis ; that commencing in the hypogastric, epigastric, or right hypo- 
chondriac regions, by the symptoms of ulcer of the intestines or 
stomach, or of abscess of the liver. The commencement of the disease 
itself is characterized by pain extending over the entire abdomen, but 
the great sensitiveness of the abdomen to pressure, which is almost 
characteristic of peritonitis, is limited to a circumscribed portion. Tym- 
panites is wanting, or is, at least, partial, and the fever is more moder- 
ate than in the diffuse form. If the exudation be not extensive, these 
symptoms usually disappear rapidly, and the disease ends in perfect 
cure, unless adhesions form to disturb the movements of the intes- 
tines, or the original disease cause some other termination. AVhen 
the exudation is more extensive, acute partial peritonitis runs a dif- 
ferent course. In the vicinity of the peritonitis the percussion gradu- 
ally becomes duller, the resistance of the abdominal walls more de- 
cided, till finally, in this case also, palpation shows a tumor in the ab- 
domen. Such masses occur rarely after perforation of ulcer of the 
stomach; more frequently in the slow perforation of tuberculous in- 
testinal ulcers, and in ulcerations of the coecum, and the vermiform 
process. Its subsequent course is the same as that of capsulated ab- 
scesses, after protracted diffuse peritonitis. 
In his clinic of abdominal diseases, Henoch gives a very true de- 
scription of the chronic peritonitis which occurs, particularly in child- 
hood, along with tuberculosis of the intestines and mesentery. He 
pictures the children as weak, scrofulous individuals, in whom the occa- 
sional colicky pains, the diarrhoea, alternating with constipation, and 
the increasing emaciation, often excite the suspicion of worms, or of 
tabes mesenterica. On careful examination of the abdomen, during 
which we must guard against mistaking the signs of displeasure for 
those of pain, we find it more sensitive at certain points. Sometimes 
even the pressure of the abdominal muscles causes pain, so that the 
child cries when going to stool. While the emaciation progresses rap- 
idly, and becomes very great in a few months, while fever, toward even- 
ing, occurs regularly, the belly of the child becomes more protuberant, INFLAMMATION OF THE PERITONAEUM, PERITONITIS. 
619 
and gradually assumes a spherical shape. Finally, the abdominal walls 
become tense, even shining, and are often traversed by enlarged veins. 
By pressure on the abdomen, which is still painful for the child, we 
find an elastic resistance. The results from percussion of the abdomen 
vary. Only in rare cases can a free exudation be recognized by dulness 
in the dependent portions of the abdomen, which changes its locality 
with the change in position of the patient. More frequently the entire 
abdomen gives a dull sound, as the intestines are drawn back against 
the spine by the atrophying mesentery, and the exudation lies on the 
abdominal wall. In most cases the percussion is tympanitic at some 
places (where the intestines lie), and dull at others (where the fluid is). 
If we bear in mind this description, we shall rarely mistake this disease, 
which does not often occur, and which alone, or by its complications, 
always causes death. 
Chronic 'partial peritonitis, whose remains, in the shape of thick- 
enings, adhesions, and cicatricial contractions of the peritonaeum, are 
found in the cadaver just as often as thickenings and adhesions of the 
pleura, develops just as latently as the pleuritis does, from which the 
pleuritic adhesions arise, and we cannot give any description of it. 
Diagnosis.—Peritonitis is not readily mistaken for any other dis- 
ease, as the great sensitiveness of the abdomen to the slightest pres- 
sure, the tympanites, and, in the acute form, the fever, give almost 
certain points for the diagnosis. Those cases dependent on perforation 
of ulcers of the stomach or intestines, that have not been recognized, 
present some difficulties of diagnosis. The sunken countenance, cool 
skin, small pulse, retracted abdomen, and other symptoms of severe 
general depression, remind us more of colie than of a severe inflam- 
mation. But if we bear in mind how insignificant the symptoms of 
gastric and duodenal ulcers may be, and if we observe how sensitive 
the abdomen is to pressure from the commencement, we shall avoid error. 
On the other hand, colic, and the impaction of bilious and urinary 
calculi, may be erroneously considered as peritonitis; but the diag- 
nosis is only difficult in those cases where, in hysterical women, mesen- 
teric neuralgia is complicated with hyperaesthesia of the skin of the 
abdomen, in the so-called rheumatic colic, and in that from gall-stones, 
when the right hypochondrium is very sensitive to pressure. In these 
cases it may be necessary to wait for further developments before form- 
ing a diagnosis. In all other cases, the insensibility of the abdomen 
to pressure, or even the relief afforded by this, renders the diagnosis 
certain very early in the disease. 
Prognosis.—Although most of the patients attacked with perito- 
nitis die of the disease, it is not because this affection is particularly 
ill borne by the organism, but because it almost always depends on 620 
DISEASES OF THE PERITONAEUM. 
grave injuries or severe blood-disease, or occurs in persons previously 
ill, and having little power of resistance. If peritonitis be induced by 
the same causes on which most cases of pleuritis depend, the prognosis 
is unmistakably better than it is in the latter disease. Thus we fre- 
quently see the rheumatic peritonitis, which exceptionally occurs in 
otherwise healthy persons, particularly in menstruating women, as well 
as that which accompanies retention of faeces, typhlitis, or even strangu- 
lated hernia, terminate in cure, provided the exciting causes can be 
removed soon enough. Still less dangerous is the circumscribed chronic 
peritonitis, which complicates chronic inflammations and degenerations 
of the abdominal organs. We might regard the final object of this 
inflammation as an attempt of Nature to guard against future injury. 
Among the symptoms on which the prognosis depends, in each 
case, are, in the commencement of the disease, tympanites, and the 
dyspnoea that it causes; the more oppressive the latter, the greater the 
danger. Subsequently, particularly in protracted cases, the fever and 
the strength and nutrition of the patient affect the prognosis more 
than most of the other symptoms. 
Treatment.—Where retention of fasces, and consequent ulceration 
of the intestines, particularly typhlitis stercoracea, or where strangu- 
lated hernia has caused peritonitis, the causal indication may be an- 
swered by the treatment for the original disease and by operation, 
respectively. In all other cases we cannot fulfil it. This, however, is 
the proper place to speak of the treatment of perforation by large and 
repeated doses of opium; by arresting, as much as possible, the move- 
ments of the intestines, this prevents, to some extent, the contact of 
the escaped substances with large portions of peritonaeum; and, more 
particularly when these foreign substances are shut off from the rest of 
the peritoneal cavity by adhesions, it prevents their breaking through. 
Statistics show favorable results for this treatment, and, in cases where, 
instead of opium, purely symptomatic treatment was used, and the 
constipation was treated by enemata and purgatives immediately after 
the use of these remedies, I have often seen a peritonitis, which was 
previously circumscribed, and might have remained so, spread over the 
entire peritonmum. At first we give gr. ss—j of the opium every hour, 
and later do not give it so often. 
Concerning the indications from the disease, views have changed 
greatly of late. Formerly every patient treated lege artis was bled 
a pound or two; then the abdomen was covered with leeches, and one 
to two grains of calomel given every two hours, and at the same time 
i quantity of mercurial ointment was rubbed into the skin of the 
thighs and abdomen. “ That was the proper treatment; the patients 
died, and no one thought of asking who recovered.” It is true, we INFLAMMATION OF THE PERITONAEUM, PERITONITIS. 
621 
cannot claim any brilliant results from the treatment now in vogue • 
but that above given was just as irrational as it was injurious. On 
examining the bodies of persons who had died of peritonitis with 
abundant effusion, even when no blood had been taken, the tissues 
were found uncommonly bloodless, as a result of the excessive 
exudations. But, on examining the bodies of persons dying from 
a peritonitis treated lege artis, we find so very little blood in the 
heart and arteries, that we are tempted to ascribe death to the 
treatment rather than' to the disease. If to this we add the fact 
that experience shows that a great loss of blood during labor 
proves to be no protection against an epidemic puerperal fever, and 
that all injurious influences which generally act as causes of peri- 
tonitis are just as active in debilitated, bloodless persons as in the 
strong and well-nourished, we silently pass over other reasons for 
avoiding venesection. (Nevertheless, we shall hereafter see that the 
symptomatic indications occasionally demand bleeding.) Of late 
scarcely any one believes in the antiphlogistic and antiplastic action 
of mercury, and we do not hesitate to say that we consider calomel 
and mercurial ointment as at least superfluous in the treatment of 
peritonitis, and that in purgative doses we regard calomel as directly 
injurious. It is far different with local blood-letting, which is much 
less dangerous than venesection, and of whose beneficial effect on the 
pain, at least, there is no doubt; this effect does not fail even in those 
cases where the peritonitis is caused by perforating ulcer of the 
stomach. The employment of cold acts in the same way, and perhaps 
it has even more effect on the inflammation itself. If the patient can 
bear it—which, unfortunately, is not always the case—we may cover the 
entire abdomen with cold compresses, and renew them every ten minutes. 
From this treatment, which is recommended by Abercrombie, Kiwisch, 
and others, I have seen the best results in cases that were amenable 
to any treatment; but I cannot deny that warm cataplasms were bet- 
ter borne than cold compresses by many patients. Recently the re- 
sults of the opium-treatment in peritonitis, caused by perforation, and 
the belief that the inflamed parts needed rest more than any thing else, 
have rendered opium popular in the treatment of all forms of peri- 
tonitis. We agree fully with those who consider the application of 
leeches to the abdomen, the use of cold, and the internal administra- 
tion of opium as the most effective treatment. Opium is invaluable 
in all forms of peritonitis. By the peristaltic motion of the gut the 
exudation—an intense irritant—is constantly brought in fresh contact 
with uninflamed parts of the peritoneum. Hence, by checking this 
motion with opium, we remove a main cause of spreading of the dis- 
ease. In protracted cases, any incapsulated collections of pus which 622 
DISEASES OF THE PERITONaEUM. 
may form, must be steadily poulticed and opened early. Like treat- 
ment and the use of iodine externally and internally are indicated in 
chronic peritonitis. 
In regard to the symptomatic indications, an early cyanosis, and 
still more excessive dyspnoea, if accompanied by symptoms of oedema 
of the lungs, requires venesection. It is true, this only temporarily 
removes the danger to life; but we know of no other remedy to fulfil 
this urgent indication. The administration of oil of turpentine, long 
since recommended in England, benefits the cause of the dyspnoea, the 
tympanites, just as little as the absorbents and other remedies, by 
which it has been attempted to carry gases off from the intestines. 
The introduction of a small trocar into the abdomen, to draw off the 
gas, should be avoided, as we may attain just as much by the introduc- 
tion of a tube through the rectum (Bamberger). The vomiting is 
most benefited by swallowing small pieces of ice. Even the mildest 
eccoprotics should not be used for the constipation until the inflamma- 
tion has ceased; generally, opium is as useless as the astringents in the 
diarrhoea depending on the oedema of the mucous membrane. In pro- 
tracted cases, where there seems to be danger from the consumption 
caused by the fever, we should give sulphate of quinine in large doses, 
small quantities of wine, and a nutritious and easily-digested diet. 
CHAPTER II. 
DROPSY OF THE PERITONAEUM ASCITES. 
Etiology.—Dropsy of the peritonaeum—ascites—is a transudation 
into the abdominal cavity, resembling the normal transudations of the 
body. The circumstances under which ascites develops are the same as 
those under which increase of the transudations occurs elsewhere, and 
may either be referred to increased lateral pressure in the vessels, or 
to a diminished amount of albumen in the blood, or, lastly, to a degen- 
eration of the peritonaeum: 
1. Ascites is very often one symptom of general dropsy, whether 
this depend on obstruction to the flow of blood from the veins, by dis- 
ease of the heart and lungs, or on degeneration of the kidneys, of the 
spleen, or any other disease inducing poverty of the blood. In all 
these cases the ascites is usually one of the last in the series of dropsi- 
cal symptoms, and does not occur till dropsical effusions in the sub- 
cutaneous tissue (anasarca) of the extremities, face, etc., have existed 
for some time. 
2. In other cases, the ascites is the result of a congestion confined DROPSY OF THE PERITONAEUM—ASCITES. 
623 
to the vessels of the peritonaeum. As this can only occur from an ob- 
struction of the portal vein, it is evident that ascites occurring alone, 
without dropsy of any other part, accompanies diseases of the liver 
and its blood-vessels. 
3. Lastly, ascites not unfrequently accompanies extensive degenera- 
tion of the peritonaeum, such as carcinomatous or tuberculous. Of the 
various forms of carcinoma, however, the alveolar carcinoma of the 
peritonaeum alone appears to be accompanied by extensive ascites. 
Anatomical Appearances.—The amount of serum found in the 
abdomen varies. In some cases it is only a few pounds, in others it is 
forty or more. The fluid is sometimes clear, sometimes slightly cloudy, 
from containing cast-off and fatty epithelium. It is usually bright yellow, 
rich in albumen and salts, and only rarely contains flocculi of coagulated 
fibrin. In the fluid which is poured into the abdomen, particularly in de- 
generation of the peritomeum, precipitates of “ late coagulating fibrin ” 
(fibrin spiitergerimiling) form after it stands awhile in the air. 
The peritomeum itself is usually dull and whitish; the superficial 
layers of the liver and spleen are slightly discolored. Under the pres- 
sure of large effusions, the liver, spleen, and kidneys may become 
bloodless and smaller. Lastly, the diaphragm is occasionally pressed 
upward, to the third or second rib, by the fluid. 
Symptoms and Course.—It is scarcely possible to give a descrip- 
tion of ascites, as it is never an independent disease, and as its symp- 
toms can only be artificially separated from those of the original af- 
fection. 
If ascites occur during general dropsy, the subjective symptoms of 
the new disease, when compared with the other troubles of the patient, 
are usually too unimportant at first to direct attention to the ascites. 
Then the physical examination, induced by the suspicion that there 
may be ascites, gives the first certain knowledge of its existence. The 
case is different in the ascites accompanying disturbance of the portal 
circulation or degeneration of the peritomeum. When cirrhosis of the 
liver or cancer of the peritomeum occurs latently, the gradually in- 
creasing troubles caused by the ascites may be the first anomalies 
noticed, and may first excite a suspicion of the original disease. As 
long as the abdomen is moderately filled with fluid, the patients only 
complain of a feeling of fulness, and are inconvenienced by the tight- 
ness of clothes which were previously comfortable. They also notice 
slight difficulty on deep inspiration. If the fulness of the abdomen 
increase, the sensation of fulness becomes painful, and the slight diffi- 
culty of breathing increases to severe dyspnoea. The pressure of the 
fluid on the rectum may cause constipation, and the flatulence induced 624 
DISEASES OF THE TERITON^EUM. 
by this may increase the dyspnoea. Still more frequently the secretion 
of urine is diminished by the pressure of the fluid on the kidneys. It 
is an old belief that, after diuretics have lost their effect, they reacquire 
it after tapping the abdomen. This supposition apparently depends 
on a false interpretation of the fact that ascites adds a new difficulty 
to an already existing obstruction to the urinary secretion, and when 
it is removed the obstruction is diminished. The pressure on the vena 
cava and the iliac veins, where there is much effusion, causes obstruc- 
tion of the circulation in the lower extremities, external genitals, and 
the abdominal walls. This explains the venous dilatation of those 
parts, and the dropsy of the subcutaneous tissue, which may become 
very great, and lead to mistaken ideas of the disease. We should 
never neglect to ask whether the legs and scrotum, or the abdomen, be- 
gan to swell first. 
Almost all patients with ascites are in great danger; most of 
them, however, do not die of the ascites, but of the original disease. 
The obstruction of the respiration or the excoriations and super- 
ficial gangrenes, which occasionally result from the excessive ten- 
sion of the skin of the external genitals and thighs, may hasten the 
fatal result. 
Physical examination ’ of the abdomen is most important in the 
diagnosis of ascites. On inspection, the first thing noticed is the dis- 
tention and peculiar form of the abdomen. As long as the effu- 
sion is moderate, the shape of the belly changes with every change of 
position of the body. If we examine the patient while he is standing, 
the lower part of the abdomen appears prominent; if he be lying 
down, the belly appears very broad. But if the transudation be ex- 
cessive, the abdomen is protruded everywhere as far as the lower ribs; 
the false ribs themselves are elevated and pressed outwardly. Then 
the abdomen maintains its shape in all positions. In excessive ascites, 
inspection almost always shows thick networks of blue veins in the 
thinned coverings of the abdomen. The navel is protruded, and rap- 
tures in the tissue of the corium form bluish-white translucent striae, 
which also occur during pregnancy, if the abdomen be very much dis- 
tended. If the level of the fluid rise above the brim of the pelvis, we 
may feel fluctuation by placing one hand flat on the abdomen and 
smartly tapping on the opposite side with the fingers of the other 
hand. Lastly, wherever the fluid is in contact with the abdominal 
wall, percussion is absolutely dull. At the same time it is important 
to notice that, except in those cases where the whole anterior surface 
gives a dull percussion-sound, the dulness varies with any change in 
position of the patient, because the fluid always goes to the most de- 
pendent part. DROPSY OF THE PERITONAEUM—ASCITES. 
625 
Diagnosis.—To distinguish free dropsy from ovarian dropsy, it is 
imperatively necessary to obtain a perfect history of the case by a 
careful examination of the patient, and to pay particular attention to 
any possible causes of dropsy that may be discovered. The circum- 
stances under which ovarian dropsy occurs are little known; we only 
know that it is often found in apparently healthy women without be- 
ing complicated with any other disease. It is quite different with 
ascites. If we can determine that none of the anomalies of composi- 
tion or distribution of the blood, described under etiology, have pre- 
ceded the collection of fluid in the abdomen, and if degeneration of 
the peritonaeum can also be excluded, in doubtful cases, the chances 
will be most in favor of ovarian dropsy. There are cases where the 
differential diagnosis depends entirely on the above factors, as the 
physical examination gives no decided evidence. In small ovarian cysts, 
it is true, the characteristic form and position of the sac, the lateral 
deviation of the os uteri, the similar results of percussion while the 
patient is in different positions, readily distinguish ovarian dropsy 
from ascites. But*, when the cyst is very large, the peculiar form of 
the sac is lost; it lies in the middle of the belly, the uterus is pressed 
downward by the weight of the sac, but is not laterally displaced; as 
in extensive ascites, the percussion is dull over the entire anterior ab- 
dominal wall. Bamberger advises us to pay particular attention to 
the spot between the crest of the ilium and the twelfth rib, for, in 
ovarian tumors at that point, we generally find the full sound of the 
large intestine, in ascites we do not. Still he acknowledges that this 
sign occasionally fails. 
After ascites has been recognized, the most important question is, 
what is its cause? We have already mentioned that ascites, occurring 
as one symptom of general dropsy, is never its first symptom. Hence, 
if ascites occurs in a person who has#no oedema, it either depends on 
obstruction of the portal circulation or on degeneration of the perito- 
naeum ; it is often difficult to decide which of the two is the case. In 
general we may say that the coincident occurrence of symptoms of 
congestion in other branches of the portal vein, or the signs of dis- 
turbed action of the liver, indicate the first form ; while cachexia, signs 
of cancer, or tuberculosis in other organs, but, above all, the presence 
of tumors in the abdomen, indicate the latter form. The color of the 
urine is very important in the differential diagnosis. For, in those 
diseases of the liver that lead to ascites, the urine, as a rule, contains 
either traces of the coloring matter of the bile or abnormal pigment; 
in degeneration of the peritonaeum, on the contrary, it is almost always 
of normal color. 
Treatment.—When the ascites is a partial symptom of general 626 
DISEASES OF THE PERITONAEUM. 
dropsy, and depends on obstructed evacuation of the vena cava, the 
causal indications require a treatment of the often-mentioned heart 
and lung diseases; and when it is the result of excessive hydrmmia, a 
suitable treatment of the exhausting original disease and an improve- 
ment of the quality of blood. In the former case w'e are generally 
unable to fulfil the indications. In dropsy resulting from intermittent, 
morbus Brightii, and the convalescence from severe disease, the fulfil- 
ment of the latter indications usually has the best result and does much 
more good than the old-fashioned routine administration of liydra- 
.gogues. When the portal or hepatic veins are compressed or obliter- 
ated, we cannot render them pervious again, nor can we cause an ex- 
pansion of the contracting parenchyma of the liver'which constricts 
the vessels in cirrhosis of the liver. In regard to the causal indica- 
tions in ascites resulting from tuberculosis or carcinoma, we are just 
as powerless. 
The indications from the disease demand the removal of the fluid 
in the abdomen. Almost all patients with ascites have diuretics pre- 
scribed them, but the number cured by these is hardly worth mention- 
ing. If the ascites be one symptom of general dropsy, diuretics may 
very properly be given, but, if the result of portal obstruction, they do 
no more good than they would in oedema of the leg from obstruction 
of the crural vein by a thrombus. The case is different with drastics. 
Practitioners have long preferred these to diuretics in the treatment of 
ascites; and, in obstruction of the portal vein, we can readily see why 
they should be more efficient, as they cause a depletion of the branches 
of the portal vein, and hence diminish the increased lateral pressure, 
which is the cause of the ascites. In ascites, the most active among 
the drastics are usually chosen, and of the various compositions that 
have gained a reputation as hydragogues, we may mention lie ini’s 
pill, which, besides squills and golden sulphuret of antimony, contains 
chiefly gamboge. As long as the strength of the patient and the con- 
dition of his abdominal canal permit the use of drastics, they are bene- 
ficial, but if the strength fail decidedly, or the bowels become irritated, 
they must be given up. The operation of tapping is almost always 
free from danger, and it removes the fluid from the abdomen more cer- 
tainly than any other method of treatment. But the more the slight 
danger and certain effect of tapping speak in its favor, the more neces- 
sary it becomes to enumerate its bad subsequent results. We should 
never forget that we do not remove water, but an albuminous fluid, 
from the abdomen, and that the fluid evacuated is almost always soon 
replaced try a new effusion. This is a severe tax on the patient’s 
strength and supply of blood. Daily experience teaches that, after 
the first tapping, emaciation progresses much more rapidly than previ- TUBERCULOSIS AND CANCER OF THE PERITONAEUM. 
627 
ously. From what has been said, it follows that, in ascites, the abdo- 
men should only be tapped where life is immediately endangered by 
obstruction of the respiration, or by threatened gangrene of the skin. 
CHAPTER III. 
TUBERCULOSIS AND CANCER OF THE PERITONAEUM. 
Tuberculosis of the peritonaeum hardly ever occurs primarily, but 
accompanies tuberculosis of either the lungs, intestines, urinary or 
sexual organs. In other cases it is one symptom of acute miliary 
tuberculosis. The latter form has no clinical interest; for the deposit 
of the few small, translucent nodules in the peritonaeum causes no 
symptoms, and has no perceptible influence on the course of acute 
miliary tuberculosis. The few small white nodules found in the thick- 
ened serous membrane of the intestines over scrofulous ulcers are also 
of more pathological than clinical interest. The extensive develop- 
ment of the proportionately large, whitish tubercles, which are occa- 
sionally scattered through the peritonaeum, is more important. The 
vicinity of the different nodules is either suffused with blood, or the 
escaped haematin has been changed to pigment, and the white tubercle 
is surrounded by a black areola. The omentum is usually rolled up, 
and strewn with tubercles; it forms a nodular swelling, resembling a 
sausage. Besides the tuberculous formations, there is usually thick- 
ening of the peritonaeum from inflammatory proliferation, and there is 
a large quantity of fluid, sometimes bloody, in its sac. 
Cancer of the peritonaeum is also rare, as a primary disease, but is 
usually propagated from neighboring organs, as the liver, stomach, 
female sexual organs, and, more rarely, from the intestines. Scirrhus 
and medullary cancer usually occur as numerous granulations and 
nodules, scarcely so large as a pea, and scattered over the entire peri- 
tonaeum, or as diffuse, flat degenerations of the peritoneal tissue. Al- 
veolar cancer occasionally forms large, or even immense, tumors. But 
along with these, which are usually located in the omentum, almost all 
the organs of the abdomen, as well as the parietal portion of perito- 
naeum, are also covered with small, gelatinous-looking tumors. In 
alveolar cancer, the intestines often adhere together in places, and the 
fluid in the peritoneal sac is consequently capsulated. 
The symptoms accompanying tuberculosis and cancer of the intes- 
tines closely resemble those of simple ascites. The most important 
symptom is the gradual distention of the abdomen by the increasing 
collection of fluid within it. The unusual sensitiveness of the abdomen 
to pressure, which is absent in other forms of ascites, the rapid occur- 628 
DISEASES OF THE PERITONAEUM. 
rence of cachexia, and the exclusion of all other causes for the collec- 
tion of fluid in the abdomen, render it probable that there is a degen- 
eration of the peritonaeum. This suspicion can only be rendered a 
certainty by the discovery of one or more tumors. From the shape 
and extent of these tumors, from the age of the patient, and from the 
coincident occurrence of tuberculosis or of cancer in other organs, we 
decide which form of degeneration exists in the case before us. DISEASES OF THE LIVER AND BILE-DUCTS 
SECTION I. 
DISEASES OF THE LIVER. 
CHAPTER I. 
Etiology.—The amount of blood in the liver may be increased by 
greater afflux or by impeded efflux. The hypercemia due to increased 
afflux we term fluxion [determination], that due to obstructed efflux, 
congestion. 
Fluxion to the liver results— 
1. From increase of the lateral pressure in the portal vein. Under 
normal circumstances, there is fluxion to the liver at each digestion. 
The passage of fluids from the intestines to the intestinal capillaries 
causes an increased fulness of the intestinal veins; consequently their 
contents are subjected to greater pressure, and are impelled more 
strongly toward the liver. In persons who eat and drink immoder- 
ately, this physiological fluxion becomes excessive, continues longer, is 
often repeated, and, like other frequently-recurring hyperaemias, may 
cause permanent dilatation of the vessels. 
2. There is fluxion to the liver, because its capillaries, which, under 
normal circumstances, find a support in the parenchyma, dilate when 
fjiis parenchyma becomes relaxed, and then offer an abnormally slight 
resistance to the blood entering the organ. The hyperiemia of the 
liver occurring after injuries of that viscus, or in the vicinity of inflam- 
mations and neoplasia?, appears to develop in this way. Perhaps those 
cases induced by the use of spirituous liquors also belong in this class. 
In all of these cases we have to do with an irritation of the liver, as 
the alcohol is conducted directly to the liver by the portal vein; the 
first action of an irritant appears to consist in changes of the paren- 
IIYPERiEMIA OF THE LITER. 630 
DISEASES OF THE LIVER. 
chvma of the irritated organ; this is usually accompanied by a diminu- 
tion of resistance of the parenchyma. This diminution of resistance 
must result in dilatation of the capillaries, and increased flow of blood 
to the part. This explanation of the fact, “ ubi irritatio ibi affluxus,” 
which is so apparent in the action of warmth on the skin, is here hypo- 
thetical, it is true, but it is certainly that which best agrees with our 
present knowledge of the subject. 
3. We are just as ignorant as to whether the cases of hyperaemia 
of the liver from infection of the blood with miasm, particularly with 
malaria, or those occurring so frequently in the tropics, depend on re- 
laxation of the parenchyma, or whether they are due to paralysis of 
the muscular fibres of the efferent blood-vessels, or to a textural change 
of their walls, or how else they occur, as we are about the pathogeny 
of the hypermmias and textural changes in the other infectious dis- 
eases. Among the cases of apparently fluxional hyperaemia of the 
liver, for which we can give no full explanation, are those which occur 
in some women just before menstruation, and are particularly marked 
in amenorrhoea. 
Congestion of the liver is far more frequent than fluxion; all the blood 
which flows from the liver through the hepatic vein has passed through 
a double set of capillaries. (This is also true of the blood supplied by 
the hepatic artery. The capillaries formed from the hepatic artery and 
spreading out in the serous covering of the liver, and in its substance 
between the vessels and bile-ducts, unite to small venous trunks, which 
do not empty into the hepatic veins but into the portal veins, and, with 
these, again break up into capillaries.) Hence the lateral pressure in 
the hepatic veins is very slight. But the hepatic vein opens into the 
vena cava at a point where, under normal circumstances, the flow of 
blood meets proportionately no obstruction, as it can pour freely into 
the empty auricle, and particularly since during each inspiration there 
is a tendency of the blood toward the thorax. If there be a disturb- 
ance of these very favorable conditions for the escape of the blood, if 
the obstruction to its entrance from the hepatic vein into the vena cava 
be increased, it collects in the liver. Only a slight obstruction is 
necessary, for the lateral pressure in the hepatic vein is too insignifi- 
cant to overcome even a very slight obstruction. # 
According to what we have just said, the circumstances which induce 
congestion of the liver are those which interfere with emptying of the 
right auricle. Thus it occurs— 
1. In all valvular diseases of the heart, it appears soonest in affec- 
tions of the right side, later in those of the mitral, and latest of all in 
those of the aortic valves. The date of the appearance of congestion 
of the liver in valvular disease depends, as we have previously fully IIYFEIwEMIA OF THE L1YER. 
631 
explained, on the complete or incomplete occurrence and on the longer 
or shorter duration of compensatory hypertrophy of the heart. 
2. We may readily understand the congestions accompanying all 
organic diseases of the heart and pericardium, which induce obstruction 
to the escape of blood from the veins. 
3. Under the same class would come congestions, occurring with 
enfeebled action of the heart, without perceptible organic change of 
that organ, either when appearing late in the course of exhausting 
acute diseases or in chronic marasmus. The effect on the distribution 
of the blood is the same in commencing paralysis of the heart as in 
degeneration of its substance. 
4. Congestion of the liver is often induced by acute and chronic 
diseases of the lung, by which the pulmonary capillaries are atrophied 
or compressed, and the right side of the heart and vena cava overfilled, 
as in emphysema, cirrhosis, compression from pleuritic effusions, etc. 
5. Lastly, in some few cases, compression of the vena cava by tu- 
mors, particularly aneurisms of the aorta, has been observed as the 
cause of congestion of the liver. 
Anatomical Appearances.—According to the degree of the hy- 
perremia, the liver is more or less swollen ; sometimes it is very much 
so; its shape is unchanged, except that it is more increased in thick- 
ness than in length. When the swelling is decided, the peritoneal 
coating is smooth, glistening and tense, the resistance of the liver is 
increased. When cut, quantities of blood flow over the cut surfaces. 
The latter either appear evenly dark or are spotted; this is particularly 
apt to occur when there has been congestion for a long time; dark 
spots, corresponding to the dilated venae centrales, the commencement 
of the hepatic veins, and varying in shape with the direction of the 
cut, alternate with brighter-colored ones which do not contain so much 
blood, and which represent the termination of the portal vessels. The 
spotted appearance, which has given rise to the much misused name 
of nutmeg liver, becomes still more marked, when the more bloodless 
spots in the vicinity of the dilated central veins appear decidedly yel- 
low from obstruction of the bile-ducts. The latter may be partly due 
to catarrh of the gall-ducts, induced by the hyperremia of their mucous 
membrane; partly to the pressure of the enlarged vessels obstructing 
the free escape of bile from the small bile-ducts; and it may be partly 
due to gastroduodenal catarrh, induced by the same causes that excite 
the hyperremia of the liver. 
The enlarged liver may subsequently become smaller, and acquire 
a granular appearance, so that, on superficial examination, it may 
be confounded with granular liver. This is usually termed the atro- 
phied form of nutmeg-liver. According to Frerichs, the atrophy 632 
DISEASES OF THE LIVER. 
and granular appearance are caused by “ the venae centrales lobu- 
loruxn, and the capillaries opening into them, dilating under the 
strong pressure of the obstructed blood, and thus inducing atrophy of 
the liver-cells, lying in their network. The cells lying in the midst of 
the lobuli atrophy, and, in their place, appears a soft, vascular tissue, 
consisting of dilated capillaries, and neoplastic connective tissue.” 
This explanation is not exactly correct, or, at least, not entirely com- 
plete. The liver cannot be diminished in size by a substitution of con- 
nective tissue, and dilated vessels for liver-cells. The diminution does 
not occur till the neoplastic tissue shrinks, and is reduced to a small 
volume. Moreover, according to Liebermeister, the assertion that, in 
congestive liyperaemias, the proliferation of connective tissue occurs 
particularly in the vicinity of the venae centrales, is based on theoreti- 
cal grounds, and not on direct observation. On the contrary, Lieber- 
meister found that, in the atrophic form of nutmeg-liver, as well as in 
cirrhosis, the proliferation affected chiefly the vicinity of the venae in- 
terlobulares, and in some cases led to a typical development of inter- 
lobular tissue, which, as is well known, hardly exists in healthy human 
livers. 
Symptoms and Course.—There are neither subjective nor objective 
symptoms of the disease until the hyperaemia of the liver has attained 
a high grade, and the organ has considerably increased in size. Where 
the liver is decidedly enlarged, the patients feel that their right liypo- 
chondrium is unusually full, and this sensation of fulness not unfre- 
quently increases to a painful feeling of tension, which spreads from 
the right hypochondrium over the abdomen. The pressure in the right 
hypocliondrium, or the sensation of having a firm hoop around the ab- 
domen is often, next to the dyspnoea, the chief complaint of patients 
with heart-disease. And when the liver swells, the sufferings of em- 
physematous patients, and of those affected with cirrhosis of the 
lungs, or curvature of the spine, are decidedly increased. Patients 
with extensive hyperaemic swelling of the liver cannot bear tight 
clothes, as they interfere with deep inspiration. If, from the causes 
above mentioned, a slight obstruction of the gall-ducts accompany the 
nyperasmia of the liver, there will be some icterus; and, as the patient’s 
color is already somewhat bluish (cyanotic), from the obstruction of the 
venous circulation, he will have the peculiar greenish color character- 
istic of patients with heart-disease shortly before death. Besides the 
symptoms just mentioned, and the physical observation that the liver 
is enlarged, in simple hyperasmia there may be no symptoms of 
disturbed hepatic function. A slight increase or diminution of the 
secretion of bile may escape our observation during life; even in the 
cadaver, where there was excessive congestive hyperamiia, Frerichs HYPERAEMIA OF THE LIVER. 
633 
could not make out such a change. In some few cases only, did he 
find the bile albuminous. Patients with hyperaemia of the liver have 
other complaints, it is true; they suffer from headache, difficulty of di- 
gestion, irregularity of the bowels, hemorrhoids, etc. These troubles, 
however, are not the result of the hepatic engorgement, but may have 
no connection with it, or, as is more frequently the case, they depend 
on the same causes. Diseases of the heart not only induce hyperaemia 
of the liver, but also lead to gastric and intestinal catarrh; in the 
same way, excess in eating and drinking excites gastric and intestinal 
catarrh even sooner than it does hyperaemia of the liver. It appears 
to be different with those cases of hyperaemia of the liver which fre- 
quently occur in the tropics, probably from malaria. These begin 
with great constitutional disturbance, severe headache, bilious evacua- 
tions upward and downward, and often with the passage of bloody 
mucous masses. These symptoms of this disease—which is but little 
known—decidedly favor the idea that it is not a simple hyperaemia, 
but either a coincident anomaly of secretion of the liver, independent 
of the hyperaemia, or the first stage of a severe organic disease, which, 
in fact, not unfrequently develops more fully. But perhaps in these 
cases, also, the hyperaemia of the liver is only the partial expression 
of a disease affecting all the abdominal organs, particularly the intes- 
tines ; and this view would best explain the constitutional affection, 
and the other symptoms. 
When the hyperaemia has reached a high grade, physical examina- 
tion very clearly shows the swelling of the liver. As we now, for the 
first time, speak of the physical signs of enlargement of the liver, we 
must give some account of them. 
As physical aids for recognizing enlargement of the liver, we have 
inspection, palpation, and percussion. 
In decided swelling of the liver, inspection shows a prominence in 
the right hypochondrium, extending more or less toward the left side, 
and gradually disappearing interiorly. At the same time, the right 
side of the thorax, which even normally is from half an inch to an inch 
larger than the left, becomes more prominent at its lower part. Lastly, 
the inferior ribs may be elevated by the enlarged liver, pressed close 
together, and their lower edges turned forward. 
If we do not undertake the examination very quietly and carefully, 
the contractions of the abdominal muscles, which usually occur, greatly 
interfere with palpation. The inexperienced often mistake contracted 
portions of the rectus abdominis for tumors of the liver. We should 
never undertake the examination while the patient is standing or sitting. 
He should lie down, and draw up the knees a little. At the same 
time, we should tell him to respire regularly, and should distract his 634 
DISEASES OF THE LIVER. 
attention from tlie examination, by questions, etc. In many cases of 
enlargement of the liver, that can be certainly recognized by percus- 
sion, it is true, we find great resistance in the right hypochondrium, 
but we cannot clearly make out the edge of the liver. This is particu- 
larly the case where the resistance of the liver is not increased, and 
still more so when it is diminished. In other cases, palpation gives 
the best evidence concerning the amount of enlargement, and also, 
about the shape of the margin and surface ; and this is the more dis- 
tinct the greater the resistance of the enlarged organ. 
Percussion is the most important physical aid in the diagnosis of 
the enlargement of the liver. In determining the upper boundary, it 
is not customary to decide by the commencing flatness of percussion 
at those points where there is a thin layer of lung between the liver 
and the walls of the thorax, but by the absolute dulness where the 
liver comes in contact with the thoracic wall. Hereafter, in speaking 
of the upper border of the liver, we shall always mean the line of ab- 
solute dulness. The highest point of the liver lies about 3 cm., 
above this line. Normally, on the mammillary line, the upper margin 
of the liver lies at the lower border of the sixth rib ; on deep inspira- 
tion it descends to the seventh rib, on complete expiration it ascends 
to the fifth. In the axillary line the upper margin lies about the 
eighth rib, near the spine about the level of the eleventh rib. 
In the median line, the upper margin of the liver lies on a level 
with the union of the xiphoid cartilage and the body of the ster- 
num, but its position cannot usually be determined, as the liver dul- 
ness passes into that of the heart. Normally, in the mammillary line, 
the lower border of the liver lies at the margin of the ribs or a little 
below; in the axillary line it is usually above the eleventh rib; in the 
median line about half way between the xiphoid cartilage and the 
navel; near the spine its position cannot be determined. As the 
thorax is shorter in women and children, the lower border of the liver 
lies somewhat below the edge of the ribs. Neither the sharp border 
of the liver, which extends a few centimeters below the ribs, nor its 
left lobe, if not thickened, causes any decided dulness on percussion. 
In forty-nine cases, of persons between twenty and forty years of age, 
examined by Frerichs, the distance from the upper line of dulness to 
the lower averaged, in the mammillary line, 9.5 cm., in the axillary 
line, 9.36 cm., in the sternal line, 5.82 cm. (The observations of 
Bamberger differ decidedly from these: in thirty measurements made 
in adults, he found in the mammillary line, in Avomen, 9 cm., in men, 
11 cm., in the axillary line, in Avomen, 10.5 cm., in men, 12 cm., and 
in a line one inch to the right of the median line, in Avomen, 8.5 cm., 
in men, 11 cm., as the average extension of dulness.) HYPERiEMIA OF THE LIVER. 
635 
If the liver be enlarged, the liver dulness will extend into the right 
hypochondrium and epigastrium. Near the edge of the liver the dul- 
ness becomes indistinct or disappears entirely, a fact which we must 
know, or we shall suppose the organ is smaller than it really is. Be- 
fore deciding, from the extension of dulness into the right hypochon- 
drium, that the liver is enlarged, we must determine that it is not 
displaced downward. We have already spoken at length of some im- 
portant points for the diagnosis between enlargement and displace- 
ment of the liver. Moreover, without being enlarged, a greater part 
of the liver may lie in contact with the abdominal walls, if it has sunk 
downward from pressure on the lower part of the thorax or from re- 
laxation of its tissue, or if it has an abnormal form. Among the 
anomalies of form the most frequent are those induced in women by 
tight-lacing and still more by wearing their waistbands tight. As a 
result of this constant pressure on it, without increase of its volume, 
the liver may become much flattened and so elongated as to descend 
several finger-breadths below the ribs, or in some few cases even down 
to the crest of the ilium. We must bear in mind these deviations in 
position and form of the liver, if we would rightly interpret the results 
of physical examination. 
Hyperacmic swelling of the liver can rarely be perceived by simple 
inspection. From the decided increase of thickness of the organ, per- 
cussion gives great dulness, which may extend from the right to the left 
hypochondrium, and as far down as the navel or even below it. And 
as the resistance of the liver is increased, we can usually feel its mar- 
gin, and satisfy ourselves that its form is unchanged and its surface 
smooth. A characteristic of hepatic enlargements caused by liyper- 
mmia is that they grow more rapidly than any other form, and decrease 
again rapidly. 
It is remarkable that the symptoms of atrophic nutmeg-liver 
have not received proper attention until lately, when Liebermeister 
has paid a great attention to them. As the symptoms of this disease 
are characteristic, it may be quickly sketched. The patients affected 
have disease of the heart or emphysema, or some other disease of the 
lung, which impedes the flow of blood through the right side of the 
heart. This obstruction of the circulation has caused enlargement of 
the liver, cyanosis, and general dropsy. As is usual in heart and lung 
diseases, the dropsy began in the lower extremities, and afterward in- 
vaded the serous cavities. Subsequently the state of affairs is changed: 
the ascites becomes more decided than the anasarca; or the ascites 
continues, while we may succeed in removing the other symptoms of 
dropsy for a time by suitable remedies. On examining the liver, we 
find it smaller than at first, its lower border is some finger-breadths 636 
DISEASES OF THE LIVER. 
higher than it was some weeks or months previously. Not unfre- 
quently, Avliile the anasarca is moderate, the ascites increases, so that 
we are compelled to tap the patient. In the cases that I have ob- 
served, where in heart and lung diseases I have been able to diagnose 
atrophic nutmeg-liver from the disproportion between the ascites and 
anasarca and from the perceptible diminution in size of the enlarged liver, 
I have not found the spleen enlarged. If we rightly understand 
atrophic nutmeg-liver, the explanation of the above symptoms is not 
difficult. The contraction of the connective tissue of the liver com- 
presses the vessels, hence the flow of blood from the veins of the peri- 
toneum is opposed in two ways : first, by the heart or lung affection ; 
secondly, by the compression of the hepatic vessels. The absence of 
enlargement of the spleen is the only thing that could appear remark- 
able ; as, by compression of the vessels of the liver, the flow of blood 
from the spleen is also obstructed, and since in cirrhosis of the liver 
(see Chapter III.), where the same circumstances prevail, we almost 
always find enlargement of the spleen, and usually ascribe this en- 
largement to obstruction of the blood in the splenic vein. I propose, 
when speaking of cirrhosis of the liver and hyperaemia of the spleen, 
to discuss this apparent contradiction more fully. 
Tkeatment.—The causal indications require the removal of the 
circumstances inducing the fluxion to or the congestion of the liver. 
In the fluxions caused by excess in eating and drinking, the diet is to 
be regulated; in those cases resulting from misuse of spirituous liquors, 
alcohol should be forbidden. In the same way it may be necessary 
to advise a change of residence wThen persons in the tropics, or from 
the influence of malaria, suffer repeatedly from hypereemia of the liver. 
Finally, if severe fluxions to the liver occur just before the menses or 
during their absence at the time they are expected, the causal indica- 
tions require the application of leeches to the os uteri or of cups to the 
inner surface of the thighs. In congestion of the liver we are either 
unable to fulfil the indicatio causalis or, where we can do so, it is al- 
most always some other trouble than the hyperaemia of the liver, which 
decides us. to interfere. For instance, when we bleed in pneumonia, and 
thus moderate a congestion of the liver, the venesection has not been 
induced by the latter, but by the congestion in the brain, or some 
other cause. 
For the fulfilment of the indications from the disease, the abstrac- 
tion of blood from the region of the liver, which is so frequently recom- 
mended, is just as irrational as it is inefficacious, and Ilenoch is right 
in saying that the leeches would do just as much good if applied to 
the wrist or ankle-joints as when applied to the right hypochondrium. 
On the contrary, leeches about the anus are strongly to be recom SUPPURATIVE HEPATITIS. 
637 
mended, if the sufferings of the patient render it worth while to use 
them at all. They draw blood from the anastomoses of the branches 
of the portal vein, and thus lessen the lateral pressure in the portal 
vein, and consequently the supply of blood to the liver. Laxatives 
have a similar influence, particularly the neutral salts, as, by abstract 
ing water, they also cause depletion of the intestinal veins, and thus 
diminish the lateral pressure in the portal veins. For patients who 
habitually suffer from hyperaemia of the liver, the mineral springs at 
Homburg, Kissengen, Marienbad, etc., are particularly beneficial, for 
the salts, in the form in which they there enter the body, can undoubt- 
edly be used for a long time without injury. 
INFLAMMATIONS OF THE LIVER. 
For sake of convenience, we shall make a general division of five 
forms of inflammation of the liver, of each of which we shall hereafter 
give a more accurate description: 1. Suppurative hepatitis ; 2. Chronic 
interstitial hepatitis, which, in its later stages is called cirrhosis hepa- 
tis; 3. Syphilitic hepatitis; 4. Pylephlebitis; and 5. Acute yellow 
atrophy of the liver, which is reckoned among the inflammations of the 
liver, at least by most recent pathologists. We shall not treat of the 
last form till we have considered other affections of the liver, accom- 
panied by jaundice, that are more readily understood. . 
CHAPTER II. 
SUPPUEATIVE HEPATITIS. 
Etiology.—According to Virchow, the processes observed in this 
form of hepatitis originally affect the liver-cells themselves. At first 
these swell from imbibition of an albuminous substance ; subsequently 
there is disintegration of the cells, and consequently of the parenchyma 
of the liver; finally, there are cavities in the liver which are filled with 
the disintegrated elements of the tissue. On the other hand, Lieber- 
meister thinks that his examinations prove that, in suppurative hepati- 
tis, the process starts from the interstitial tissue, and that the disinte- 
gration of the liver-cells is secondary. The etiology of parenchymatous 
nepatitis is obscure. It is rare in the temperate zones, but more fre- 
quent in the tropics, particularly in India, although the old accounts 
of its frequency there are overdrawn. 
Among the exciting causes, we may mention— 638 
DISEASES OF THE LIVER. 
1. Wounds and contusions of the liver; but among sixty cases 
that he observed himself, or collected from other observers, JJudd found 
only one case due to injury. 
2. Yery similar to the above are the cases induced by impaction 
of angular concrements in the gall-ducts, but these must be considered 
as very rare. 
3. Suppurative hepatitis develops more frequently from ulceration 
or other gangrenous affections of the abdominal organs. It has been 
found complicating ulcers of the stomach, intestines, and gall-bladder 
and, in some few cases, abscesses of the liver have been seen to follow 
operations for hernia or about the rectum. In these cases it is most 
natural to suspect an embolus of the branches of the portal vein or the 
transfer of injurious irritating matter to the liver by the portal blood ; 
but, so far, it has been impossible to obtain any positive proof of this. 
liudd believes, and most authors agree with him, that the majority of 
cases of hepatitis of the tropics belong in this class. It is true that it 
is very rarely a primary disease, but is almost always secondary to the 
dysentery endemic in the tropics; but it has not been proved in this 
form either, that the transfer of particles of gangrenous mucous mem- 
brane or of putrid fluid, from the large intestine to the liver, has induced 
the inflammation in the latter, and still less that this is the sole cause 
of hepatitis in the tropics. The fact that epidemic dysentery in our 
country is hardly ever complicated by hepatitis, although with us also 
there are extensive gangrene of the mucous membrane and putrid de- 
composition of the contents of the large intestine, rather militates 
against JBudd's view of the subject. 
4. Lastly, among the exciting causes of parenchymatous hepatitis, 
we must mention injuries, suppurations, thromboses, and inflammations 
of the veins. The explanation of this form, which, together with the 
above, is usually called metastatic hepatitis, is very difficult. We 
have given the views at present prevalent concerning the formation of 
metastases in the lungs. According to the explanations there given, 
the occurrence of metastases in the liver from peripheral suppurations 
should induce the belief that emboli which have passed through the 
capillaries of the lungs may plug up the hepatic artery. We must 
content ourselves with having mentioned the fact, and called attention 
to the difficulty of its explanation. The sympathy between the head 
and the liver, of which we have already spoken a good deal, can only 
be explained by the fact that wounds of the skull affecting the diphoc 
very readily induce metastases, and, under some circumstances, metas- 
tases to the liver. 
An atomic at. Appearances.—In parenchymatous hepatitis, the 
entire organ is never inflamed, but there are always inflamed spots. SUPPURATIVE HEPATITIS. 
639 
These vary in size; often there is only one; in other cases, numbers 
of them are scattered through the liver. 
We rarely see the 'post-mortem appearances of the disease in the 
commencing stage. The description of the inflamed parts as dark-red, 
resistant places, which become slightly prominent when we cut into 
the engorged liver, is probably taken more from analogy than from 
actual observation. On the other hand, in commencing hepatitis, we 
do find discolored, yellowish, and very soft spots in the hyperaemic 
liver. When these are superficial, before opening them, we may readily 
mistake them for abscesses. At these spots, on microscopical exami- 
nation, Virchow found, according to the degree of discoloration and 
softening, either that the liver-cells were cloudy, transparent, and gran- 
ular, or that their number was decreased, and between those still ex- 
isting there was effused a finely-granular mass, or, lastly (at the most 
discolored and softened spots), that the liver-cells had entirely disap- 
peared, and in their place there was only a finely-granular detritus. 
Far more frequently, parenchymatous hepatitis is not seen till its 
later stages. Then we find abscesses in the liver, from the size of a 
pea to that of a hen’s egg; if several of these have united, or if the 
disintegration has progressed further, these form irregular collections 
of pus, which are often very large. They are surrounded by disinte- 
grating, discolored parenchymatous substance, and contain a creamy 
pus, which is often greenish from admixture of bile. When the de- 
struction advances to the surface, these abscesses of the liver may 
break. This may occur into the abdominal cavity, or, if there has been 
previous adhesion of the liver to the abdominal wall, the perforation 
may be outwardly; in other cases, after the liver has become adherent 
to the diaphragm, the latter is perforated, and the pus enters the 
pleural sac or the lung, if that be adherent to the pleura costarum. 
In rare cases, abscesses of the liver have been known to perforate into 
the pericardium, stomach, intestines, gall-bladder, even into the portal 
vein, and into the ascending vena cava. 
If the patient lives after the opening of the abscess, in favorable 
cases, the walls may unite; then there is a proliferation of connective 
tissue, and finally a hard cicatrix forms, which often contains thickened 
and calcified masses of pus. And where perforation does not occur, 
after an abscess has existed a long time, there is usually a proliferation 
of connective tissue in the wall and vicinity of the abscess; its inner 
surface becomes smooth, the pus is incapsulated, and gradually thick- 
ened by reabsorption of its fluid constituents. Then the abscess may 
be diminished in size by the shrinking of the surrounding connective 
tissue, till finally only a dense cicatrix remains, enclosing a calcareous 
mass. 640 
DISEASES OF THE LIVER. 
Symptoms and Course.—The typical description usually given of 
parenchymatous hepatitis answers, as Budcl aptly says, only for the 
traumatic cases, including those induced by impacted gall-stones; but, 
as we have already stated, this is the rarest form of the disease. If, 
after a blow, or some other violence, affecting the region of the liver, 
there be severe pain there, if the liver swells, and there be high fever 
with general suffering, there is no difficulty in the diagnosis. 
The case is altogether different when hepatitis comes on during 
some gangrenous process in the abdomen, when it complicates a dysen- 
tery, or when it develops during peripheral suppuration, after injuries 
of the head, great surgical operations, etc. The cases related by Budcl, 
Andral, and others, show a number of instances where abscesses of 
the liver, occurring in this way, were recognized very late, or not at all. 
In chronic ulcerations of the intestines, in perityphlitis, and similar dis- 
eases, as well as after operations on the rectum or abdomen, we may 
suspect the occurrence of hepatitis, if the patient has a chill, if the 
liver swells and becomes painful, and there be icterus. But none of 
these symptoms are constant; and cases where local symptoms of 
hepatic disease are absent, in metastases starting from one of the ab- 
dominal organs, are at least as frequent as those of metastases in the 
lungs, which run their course without pain in the chest or bloody ex- 
pectoration. The chills and fever may also depend on other causes, 
and cannot, by any means, be regarded as sure signs of secondary hepa- 
titis. It is still more difficult to recognize the occurrence of hepatitis 
during endemic dysentery. For, in this disease, the liver is not unfre- 
quently swollen and painful, even when it is not inflamed; the fever 
present does not decide the question, for it is present in dysentery 
alone; in many cases there is no icterus, and, when it occurs, it is no 
sure sign of hepatitis. The parenchymatous hepatitis which occurs in 
peripheral suppurations, or after surgical operations, and is one symp- 
tom of the so-called pyaemia, is the most difficult to recognize. Under 
such circumstances, we should not expect the prostrate patient, who is 
much depressed mentally, to complain of pain about the liver; the 
chills and high fever, and even excessive icterus, do not render it abso- 
lutely certain that there is disease of the liver. 
If we add, to what has already been said, that the abscesses, which 
have formed during the above-named diseases, always enlarge slowly, 
and are accompanied by very unimportant symptoms, it may readily be 
understood that a subsequent chronic disease, with the symptoms here- 
after mentioned, may first excite the suspicion, or render it certain that 
the original disease has been complicated with hepatitis. 
The symptoms of the abscess which remains and gradually in- 
creases are quite varied. There is almost alwavs a dull pain in the SUPPURATIVE HEPATITIS. 
641 
right hypochondrium, which is increased by pressure. Occasionally 
there is also a peculiar “ sympathetic ” pain in the right shoulder, 
whose frequency and diagnostic importance were formerly much over- 
rated. The liver almost always projects below' the ribs, and in cases 
where the abscesses are large or numerous, or the hyperaemia is great, 
the liver may be double its normal size, and bulge out the right half 
of the thorax, render the hypochonclrium prominent, and project deep 
into the abdomen. When the abscesses are on the convex surface of 
the liver and are somewhat prominent, we may sometimes, on careful 
palpation, find slight protuberances or even fluctuation. Icterus is not 
at all a constant symptom of abscess of the liver, being absent even in 
the majority of cases. The accumulation and absorption of bile, on 
which icterus depends, are partly the result of compression of the gall- 
ducts, and partly due to their obstruction by albuminous and fibrinous 
coagula (.Rokitansky). Large abscesses may compress the ramifica- 
tions of the portal vein; such as project from the concave surface may 
compress its trunk. In such cases, besides the symptoms above de- 
scribed, there are usually swelling of the spleen and serous effusion 
into the abdomen. While the abscesses are small there is little or no 
accompanying fever, and at this time the general health of the patient 
is little affected, his strength is good, and he may live for years in 
passable health. But as soon as the abscess has attained some size 
the fever becomes higher, chills come on from time to time, as we 
have seen that they do in chronic suppurations elsewhere, the strength 
and nutrition of the patient suffer, he becomes cachectic and exces- 
sively emaciated, and in most cases finally dies exhausted and dropsical, 
of “ consumption of the liver.” 
If the abscess of the liver perforate into the abdomen, the symp- 
toms of peritonitis soon set in and quickly cause the death of the 
patient. If the abscess become adherent to the anterior abdominal 
wall, this at first becomes cedematous and finally infiltrated; this 
renders any formerly perceptible fluctuation indistinct, but a super- 
ficial fluctuation gradually occurs in the abdominal wall, and this is 
finally perforated by the pus. If the perforation take place through 
the diaphragm, we either have the symptoms of pleurisy, or, more fre- 
quently (as the pleural surfaces have become adherent), dark-red or 
brown purulent masses are suddenly thrown off, from whose appear- 
ance Budd claims to have frequently made a diagnosis of abscess of 
the liver. From perforation into the pericardium, pericarditis rapidly 
develops and soon causes death. In perforation of the stomach, the 
peculiarly colored masses are vomited. In perforation of the intestine, 
on the other hand, there are purulent passages from the bowels. 
When the pus is evacuated outwardly or into the stomach, or intes- 642 
DISEASES OF TIIE LIVER. 
tines, or even Avhen it enters the bronchi and is coughed up, the pa- 
tients usually feel instantaneously relieved; the improvement rarely 
remains permanent, however, and, when it does so, it is only in cases 
where the abscess was small. Budd only saw closure of the abscess 
and perfect cure of the patient in one case after the evacuation of the 
pus. The abscess usually continues to suppurate, and the patients 
sooner or later die of exhaustion from the suppuration and fever. 
Cases of cure after capsulation and gradual decrease in size of the 
abscess, with inspissation of its contents, are very rare, and during life 
it must be difficult to decide that this has occurred. 
Treatment.—It is only in the rare cases of traumatic hepatitis 
that we can hope to induce resolution of the inflammation by the use 
of cold compresses, and the application of leeches about the anus. In 
the subsequent course of the disease, blisters over the liver, and the 
internal administration of calomel, are very generally employed, but are 
of doubtful efficacy. 
In all other forms of parenchymatous hepatitis, we have to confine 
ourselves to the treatment of symptoms, particularly as they are rarely 
recognized until abscesses have formed. Fortunately for the patient, 
the views on which it was formerly maintained, that the reabsorption 
of pus was aided by the internal and external use of mercurials, are 
no longer held; although it is said that patients with liver-disease are 
just the ones who can take large doses of calomel without injury. 
As long as there is no perceptible fluctuation, and we cannot open 
the abscess, we must limit ourselves to keeping up the strength of the 
patient by suitable diet, Avine, and preparations of iron. For the chills 
Ave prescribe quinine, Avhich not unfrequently has a very decided anti- 
periodical action. 
As experience shows that those abscesses heal best from Avhich 
pus mixed Avith blood and broken-doAvn parenchyma of the liver have 
been evacuated, while those containing good or laudable pus rarely 
healed, we should make it a rule to open the abscesses as early as pos- 
sible, before a so-called pyogenic membrane has formed in them. Sur- 
gery teaches us to be peculiarly careful in opening abscesses of the 
liver, and that Ave should use caustics instead of the knife, Avhere Ave 
cannot certainly determine that the liver has become adherent to the 
abdominal Avails. 
CHAPTER III. 
CHRONIC INTERSTITIAL HEPATITIS, CIRRHOSIS OP THE LIVER, GRANU- 
LAR LIVER. 
Etiology.—Interstitial hepatitis affects the fibrous covering of the 
liver and the scanty connective tissue, which, as the continuation of CIRRHOSIS OF THE LIVER. 
643 
Glissoti’s capsule, accompanies the hepatic vessels and traverses the 
parenchyma of the liver. In this form of inflammation there is neither 
free exudation, suppuration, nor formation of abscesses. The inflam- 
matory process rather consists in a proliferation of the tissue above 
named, by the formation of young connective-tissue elements from 
those already existing. While the connective tissue of the liver in- 
creases, its parenchyma proper is more and more displaced. In the 
later stages of the disease the neoplastic tissue undergoes a cicatricial 
retraction, which strangulates and partly destroys the parenchyma of 
the liver. The blood-vessels and bile-ducts not unfrequently become 
impervious throughout a considerable extent, and a large part of the 
liver-cells atrophy and die. 
Alcohol is the irritant which most frequently induces interstitial 
hepatitis. Hence English physicians give granular liver the vulgar 
name of “gin-drinker’s liver.” Corresponding to the extent to which 
alcohol is used by the sexes and at different ages, the disease is more 
frequent in men than in women, and is very rarely seen during child- 
hood. Even the apparent exceptions support the rule. Thus 
derlich found typical cases of the disease in two sisters aged eleven 
and twelve years; but on careful inquiry it was found that both of 
them were great schnapps-drinkers. 
The use of alcohol, however, is not the only cause of interstitial 
hepatitis, and all persons affected with this disease, who deny the ha- 
bitual use of liquor, are not to be regarded as secret topers. Simple 
congestive hyperasmia, which so often occurs in heart-disease, has fre- 
quently been blamed as a cause of cirrhosis; but, according to Bam- 
berger's numerous observations, this is probably an error, which was 
due to the atrophic form of nutmeg-liver being confounded with cirrho- 
sis. We are unacquainted with the other causes of interstitial hepa- 
titis. Budd (as quoted by Bamberger and Henoch) says: “ There 
may be other substances, among the immense variety of matters taken 
into the stomach, or among the products of faulty digestion, which, on 
being absorbed into the portal blood, cause, like alcohol, adhesive in- 
flammation of the liver.” Budd himself, however, terms this view 
hypothetical. I have seen one case where biliary calculi caused chronic 
interstitial hepatitis. In this case, which was fully detailed by Lieber- 
meister, most of the large bile-ducts were filled with stony concrements, 
and the liver was most strikingly cirrhotic in character. 
Anatomical Appearances.—In the first stage, which we rarely 
see, the liver is increased in size, particularly in thickness ; its perito- 
neal covering is slightly thickened and clouded; except some slight 
elevations, the surface is smooth and even. On section, the parenchyma 
is seen to be interspersed by a vascular, succulent, grayish-red mass, 644 
DISEASES OF THE LIVER. 
which gives the liver a fleshy look, and which is shown by the micro- 
scope to consist of delicate connective-tissue striae with spindle-shaped 
cells. Between this tissue, the original parenchyma appears as large 
and only slightly-prominent granulations. 
The second stage, into which the first gradually passes, is excel- 
lently described by Rokitansky. According to him, in typical cases, 
the liver is much smaller than normal; its form is altered,’the edges 
becoming thinned, and finally changed to an indurated border, which 
contains no liver-tissue: on the other hand, the thickness, particularly 
of the right lobe, is relatively greater. Lastly, the whole organ often 
consists of the spherical right lobe, to which the left is attached as a 
flat appendix. In this stage we may see granular or watery projec- 
tions (granulations) on the surface, to which the disease owes its name 
of “ granular liver.” If the granulations are all of the same size, as 
large as a hemp-seed, for instance, the surface appears regularly gran- 
ular ; if they vary in size, it is irregularly granular. Between the 
prominences the serous coat is whitish, tendinous, shrunken, and re- 
tracted ; if deep retractions separate large portions of the liver from 
each other, it appears lobular. The serous coat is also usually attached 
to the surrounding parts, particularly to the diaphragm, by short, firm 
adhesions, or by bands. The substance of the cirrhotic liver is very 
hard and of leathery toughness. On section, there is often as much 
resistance as on cutting into scirrhus, and on the cut surface we find 
the same granulations as on the surface of the liver. They are embed- 
ded in a dirty-white, dense, non-vascular tissue. At some places the 
parenchyma has entirely disappeared, and the dense tissue alone re- 
mains. On microscopic examination in this stage, we no longer find 
the first elements of connective tissue, but this is fully formed, and en- 
closes in concentric layers groups of liver-cells (the granulations). The 
still existing liver-cells are partly affected with fatty degeneration and 
partly intensely yellow, as a result of the retention of bile induced by 
obstruction of the bile-ducts. The fatty metamorphosis of the liver- 
cells, and still more the pigment in them, gives the entire liver, but 
particularly the granulations, the yellow color to which it gives its 
name, “ cirrhosis.” 
Symptoms and Course.—The symptoms of the first stage of cir- 
rhosis are very similar to those of simple hyperremia of the liver; the 
inflammatory process within the liver and in its covering is usually ac- 
companied by little pain, although the patient may be more sensitive 
to pressure over the liver than is the case in simple hypermmia. In 
some cases, however, the feeling of fulness in the right liypochondrium 
increases to painful tension or even to burning pain. Besides these 
symptoms, there are various troubles in the first stage of cirrhosis. CIRRHOSIS OF THE LIVER. 
645 
The patients complain of loss of appetite, of a feeling- of pressure and 
fulness after eating; they suffer from flatulence and constipation. The 
nutrition may be already affected and the appearance cachectic; but 
the same is true of these appearances as has been said of several of the 
accompaniments of simple hyperasmia of the liver, that, although they 
accompany the disease, they are not symptoms of it. The habitual use 
of liquor almost always causes chronic catarrh of the stomach, and the 
symptoms depend on this, not on the interstitial hepatitis. 
The symptoms of the second stage depend almost entirely on me- 
chanical conditions. Compression of the branches of the portal vein 
must cause symptoms of congestion in those organs from which the 
portal vein conducts the blood to the liver; the compression of the 
bile-ducts (as long as the liver-cells to which they belong prepare bile) 
induces absorption of bile and icterus. 
Symptoms of congestion are seen soonest and most frequently in 
the gastric and intestinal mucous membrane. The chronic gastric 
catarrh accompanying the second stage of cirrhosis is not, as in the first 
stage, a complication, but is a necessary result of the disease. The 
symptoms it causes have already been described. Intestinal catarrh, 
which is just as frequent an accompaniment of cirrhosis, rarely leads to 
excessive transudations of fluid into the intestines, but, like most chronic 
catarrhs, to a copious production of cells and to the secretion of tough 
mucus. We have learned that constipation, tympanites, cachectic 
appearance, etc., are among the symptoms of this form of chronic in- 
testinal catarrh, hence we readily understand why they should take a 
prominent part among the symptoms of cirrhosis of the liver. Not un- 
frequently the capillaries of the gastric and intestinal mucous mem- 
brane become so full as to rupture. Hence, next to ulcer of the 
stomach, cirrhosis of the liver is the most frequent cause of gastric and 
intestinal haemorrhages; and as the obstructed evacuation of the portal 
vein causes overfilling of the inferior mesenteric artery and the haemor- 
rhoidal plexus, it is to be mentioned among the causes of haemorrhoids, 
and these form one of the most frequent symptoms of cirrhosis. 
As the splenic vein also empties into the portal vein, compression 
of the branches of the latter will impede the escape of blood from the 
former ; hence symptoms of congestion of the spleen unite with those 
of the gastric and intestinal congestion. In the later stages of inter- 
stitial hepatitis the spleen has so often been found enlarged to two or 
three times its natural size, or even more, that Oppolzer, Bamberger, 
and others, give enlargement of the spleen as one of the most important 
symptoms of cirrhosis of the liver. Out of thirty-six cases, Frerichs 
found the spleen enlarged eighteen times. We cannot agree, however, 
in referring the enlargement of the spleen solely to obstruction of the 646 
DISEASES OF THE LIVER. 
blood: on the one hand, because it sometimes comes very early, at 
others very late, without any corresponding change in the other symp- 
toms of congestion; secondly, because in some cases of cirrhosis, and 
in all the cases of atrophic nutmeg-liver that we have observed, in spite 
of the excessive compression of the hepatic vessels, there has been no' 
enlargement of the spleen, or it has been only slightly enlarged. 
Probably the swelling of the spleen depends, partly at least, on a 
process similar to that affecting the liver. But, that part of the splenic 
enlargement is due to obstruction of the flow of blood, is shown by the 
constant diminution in size of the spleen, when a hasmatemesis, from 
rupture of the capillaries of the stomach, has facilitated the escape of 
blood from the spleen. 
As the veins of the peritonaeum also, particularly those of its visceral 
folds, empty into the portal vein, we may readily understand the occur- 
rence of ascites, which is the most apparent symptom of cirrhosis. We 
may refer to the chapter next to the last of the previous section, where 
the increased lateral pressure in the veins of the peritonaeum was 
shown to be the most important cause of serous transudations into the 
abdomen. As rupture of the capillaries of the peritonaeum occasion- 
ally occurs, in some cases, we find small quantities of blood mixed with 
the transudation. In other cases, there are fiocculi of fibrin in the 
fluid, which tend to prove that, while the inflammation is going on in 
the liver and its vicinity, small quantities of free exudation are formed. 
The ascites, which forms a symptom of cirrhosis of the liver, is particu- 
larly extensive; hence in it, more frequently than in any other form of 
abdominal dropsy, we find the blue veins over the abdomen, oedema of 
the lower extremities, genital organs, and abdominal walls, resulting 
from compression of the vena cava and iliac veins, as well as the super- 
ficial gangrene of these parts that we have previously described. 
Now that we have mentioned chronic gastric and intestinal catarrh, 
gastric-and intestinal haemorrhages, hemorrhoids, enlargement of the 
spleen, and, lastly, ascites, as the almost constant symptoms of cirrhosis, 
and as the mechanical results of compression of the branches of the 
portal vein, it may be asked how we explain the exceptions, where 
these symptoms do not exist, or are insignificant. We shall first re- 
mark that, occasionally, in spite of advanced cirrhosis, the branches of 
the portal vein remain quite pervious, so that, according to the obser- 
vations of Foerster, in some cases, they may be traced a considerable 
distance in the cadaver. But, besides this, the escape of blood from 
the stomach, intestines, spleen, and peritonaeum may be facilitated, and 
the congestion in these organs avoided, by the blood seeking other 
passages, and the development of a collateral circulation. This may 
result: 1. From the connection between the inferior mesenteric and CIRRHOSIS OF THE LIVER. 
647 
the hypogastric veins, through the haemorrhoidal plexus; 2. From the 
anastomoses between the portal veins and those veins of the perito- 
naeum which open into the diaphragmatic and oesophageal veins; 3. 
Through newly-formed vessels in the adhesions between the liver and 
diaphragm. Besides these ways, and other occasional abnormal com- 
munications, by which the blood from the portal vein may elude the 
hepatic vein and reach the vena cava, in some cases, 4, a very peculiar 
form of collateral circulation is set up, which may be recognized, even 
during life, by very evident symptoms. It was formerly supposed that 
this form only occurred when the umbilical vein was incompletely 
closed after birth, and that a fine canal remained in the ligamentum 
teres during after-life. If considerable congestion of the liver occur 
in such cases, this fine canal is gradually distended by the pressure of 
the blood, and may become so pervious as to conduct the blood to the 
anterior abdominal wall, where it empties into the ramifications of the 
internal mammary veins. The consequent overfilling of the internal 
mammary veins impedes the escape of blood from the cutaneous veins, 
so that these may be excessively dilated, and surround the navel as a 
blue cushion. The deformity thus induced, the caput Medusas, does 
not, however, depend on dilatation of the incompletely obliterated um- 
bilical vein, but on dilatation of the branches of the portal vein run- 
ning from the liver to the anterior abdominal wall, between the folds 
of the falciform ligament, which anastomose wfith the roots of the epi- 
gastric and internal mammary veins (Sappey). 
It is more difficult to explain why some of the symptoms of con- 
gestion occur, while others are absent, than it is why none of them 
exist. We only partly know (see above) why the spleen (which Bam- 
berger found enlarged in fifty-eight cases out of sixty-four, and Frerichs 
in eighteen cases out of thirty-six) remains small in some cases, and why 
some patients have haematemesis frequently, while others do not have 
it throughout the disease; and we shall not attempt to explain these 
irregularities. 
Although, in cirrhosis of the liver, the gall-ducts are subjected to 
the same pressure as the portal veins, there is rarely much biliary ob- 
struction. It is true, most of the patients have a dirty-yellow color, a 
yellow tinge of the sclerotic and dark urine; but intense icterus is by 
no means a frequent symptom of cirrhosis. This symptom is readily 
explained by the physiology of the formation of bile. There is no 
bile in the blood going to the liver, but it is prepared there from the 
materials supplied. Hence obstruction and reabsorption of bile always 
presuppose that at least part of the liver-cells is preserved, and acts 
normally. In cirrhosis of the liver, on the one hand, the bile-ducts are 
compressed, and the conditions are induced which most frequently lead 648 
DISEASES OF THE LIVER. 
to obstruction and reabsorption of bile; on the other hand, numbers 
of the liver-cells have been destroyed, and the formation of bile is thus 
greatly limited. Hence we may readily see why icterus is hardly ever 
absent in cirrhosis, and, at the same time, why it rarely attains a high 
grade. Generally, a slight degree of icterus, in advanced cirrhosis, is 
an indication that one factor, the destruction of the liver-cells, prevails; 
a higher grade of icterus indicates that the other factor, compression 
of the gall-ducts, is in excess, or that, from complication, there is some 
new obstruction to the flow of bile. These complications, particularly 
catarrh of the bile-ducts, or their obstruction by gall-stones, occur quite 
frequently in cirrhosis. If the escape of the bile be entirely prevented, 
even the slight amount formed by the remaining cells is sufficient to 
cause intense icterus. The light-gray color of the faeces also depends 
mostly on the compression of the gall-ducts; as this compression 
hardly ever causes their absolute closure, perfectly pale, clay-colored 
stools, such as occur in other forms of icterus, are not seen in cirrhosis. 
The urine usually contains traces of bile pigment, but is far more re- 
markable for its richness in urates, and in peculiar coloring matters, to 
which we shall again refer. 
Besides the symptoms due to compression of the portal vein and 
bile-ducts, there are others which depend on the extensive destruction 
of the liver-cells. When speaking of the icteroid symptoms, we said 
that the atrophy of the liver-cells diminished the production of bile; 
and, probably, the discoloration of the feces depends as much on lim- 
ited formation as on retention of the bile. Little as we know of all of 
the functions of the liver, we are, nevertheless, certain that the forma- 
tion of bile is not the sole function of the cells of the liver. (The 
times when l'el tauri inspissatum was given in pill, or the patient took 
fresh ox-gall by the spoonful, “ to replace the functions of the liver,” 
are not long past, it is true, but the belief from which such prescrip- 
tions started is obsolete.) The liver is very important for the general 
nutrition, and particularly for the blood, and it is certain that an ex- 
tensive destruction of liver-cells affects the general health very severely. 
The affection of the nutrition in patients with cirrhosis of the liver de- 
pends partly on the existing gastric and intestinal catarrh; perhaps, 
also, the excessive fulness of the intestinal veins prevents the entrance 
of substances from the intestines into these vessels; but there must be 
another cause for the disturbance of nutrition, for the patients become 
weaker, more emaciated, and have a dryer skin and more cachectic ap- 
pearance than those have who are suffering from simple gastric and 
intestinal catarrh, and in whom the escape of blood from the intestinal 
veins is obstructed in some other way. Physiology does not, at present, 
teach us whether the affection of the nutrition depends on arrest of CIRRHOSIS OF THE LIVER. 
649 
the formation of sugar in the liver, or on the arrest of some other un- 
known function. In isolated cases, severe brain symptoms appear 
shortly before death; some patients fall into delirium, and finally into 
deep sopor; others have symptoms of depression, coma, or sopor, from 
the commencement. On autopsy, we find no palpable changes in the 
brain to explain these symptoms; hence we are justified in referring 
them to an intoxication; but we do not know wrhat substances cause 
the intoxication. Formerly it was universally supposed that these 
brain-symptoms depended on the absorption of the constituents of the 
bile, and they were, consequently, termed cholcemic intoxications. But 
the fact that their frequency is not at all in proportion to the icterus, 
that, on the contrary, where there is but little jaundice, convulsions, 
coma, and sopor not unfrequently occur suddenly, while they are often 
absent in the severest cases where the overloading of the blood with 
the absorbed constituents of the bile is much more evident, speaks very 
strongly against the correctness of this explanation. Frerichs has 
advanced the hypothesis that it is not the reabsorption of bile, the so- 
called cholmmia, which is dangerous, but the acholia, occurring in ex- 
tensive degeneration of the liver, i. e., that condition where the exten- 
sively-diseased liver can no longer prepare bile from the materials 
supplied to it. When this important process fails, instead of the nor- 
mal products of interchange of tissue, we have abnormal products of 
decomposition and poisonous substances. The above severe disturb- 
ances of innervation are induced by these substances. The correctness 
of this hypothesis of Frerichs is by no means beyond doubt. When 
speaking of icterus, we shall return to the relation of the brain-symp- 
toms in question, to cholaemia, or acholia, and show that some recent 
observers incline to the first theory, as they regard the reabsorbed bile- 
acids as the poisonous substances. 
The occurrence of quantities of abnormal coloring matter, and of 
urates in the urine of patients suffering from cirrhosis, also appears to 
depend on the destruction of the liver-cells, and the diminished or 
altered action of the liver. We do not know what modifications of the 
change of tissue induce this condition of the urine. The most we can 
determine is that, if the coloring matter of the urine be derived from 
the coloring matter of the bile, and this be a derivative from the color- 
ing matter of the blood, in extensive degeneration of the liver, where 
the coloring matter of the blood is no longer normally transformed into 
the coloring matter of the bile, this anomaly must influence the forma- 
tion of the coloring matter of the urine and its modifications. 
Lastly, as to the physical signs of interstitial hepatitis, in the 
first stage, palpation and percussion usually show a very decided in- 
crease in size and resistance. In the second stage, also, the liver is 650 
DISEASES OF TILE LIVER. 
not so much out of the reach of palpation as is generally asserted. If, 
by placing the patient on the left side, and so removing the fluid in the 
abdomen from the liver, we succeed in reaching the edge of the liver, 
we perceive that its resistance is even greater than in the first stage, 
and on the surface we may feel hard, roundish prominences of unequal 
size. If the ascites be not too great, in the second stage also percus- 
sion shows in some cases an increase, in others (but, according to my 
experience, not at all frequently) a decrease of the normal liver dul- 
ness. In estimating the latter symptom, we must be more careful than 
when the extent of the dulness is abnormally great; for, as the numer- 
ous measurements of Frerichs prove, the size of the liver and the ex- 
tent of its dulness vary greatly within certain bounds. Moreover, any 
abnormal position of the liver, such as occurs by decided inflation of 
the abdomen, causes the organ to come in contact with the anterior wall 
of the abdomen and thorax only by its sharp border. Finally, portions 
of the intestines, filled with gases, pressing between the liver and the 
abdominal wall, may diminish or entirely remove the normal liver dul- 
ness. If we bear these facts in mind, the diminution of liver dulness is 
a very important symptom in cirrhosis. As the left lobe of the liver is 
the first to decrease in size, the abnormally clear percussion-sound in 
the epigastrium is first noticed; subsequently the dulness over the right 
lobe may so decrease that it will be reduced to one or two inches in the 
mammillary line (Bamberger). The most certain point in diagnosis is 
the gradual decrease in size of the previously enlarged organ, as shown 
by repeated examinations. 
Having introduced the symptoms of interstitial hepatitis individ- 
ually, and weighed them as a whole, we will add a short and general 
description of the disease. The patients are mostly men in middle or 
advanced life, and addicted to drink. In the commencement the symp- 
toms are slight and obscure; the patients complain of pressure and ful- 
ness in the right hypochondrium; more rarely, when the serous cover- 
ing is more affected and intensely inflamed; there is pain in the region 
of the liver. In this stage, the most prominent symptoms are enlarge- 
ment of the liver, dyspepsia, flatulence, and emaciation. Gradually, 
often not for years, the abdomen swells, from an effusion of fluid into 
the peritonaeum, while there is no simultaneous oedema of the feet. 
The skin becomes dirty yellow, the urine dark red, and rich in urates, 
the faeces slate-colored; the dyspepsia and emaciation increase. In 
this stage, the liver is sometimes smaller, the spleen almost always en- 
larged. In some patients there is bleeding from the intestinal canal; 
in almost all, haemorrhoids. The increasing ascites interferes with 
breathing, and induces oedema of the legs, genitals, and abdominal 
walls. Finally, after months or years, the patients die, excessively CIRRHOSIS OF THE LIVER. 
651 
emaciated and exhausted. During the last days of life, delirium and 
sopor not unfrequently develop. 
Diagnosis.—Cirrhosis would not readily be mistaken for any of the 
previously described diseases of the liver, but its diagnosis from cancer 
or tuberculosis of the peritonaeum may be very difficult. In these de- 
generations, as in cirrhosis, there is often ascites, which has been pre- 
ceded by no other symptoms of dropsy. The patients also soon be- 
come emaciated and cachectic, and, as the tumors not unfrequently com- 
press the ductus choledochus, we may have icterus accompanying them. 
The following points are particularly important in the diagnosis be- 
tween cirrhosis and these diseases of the peritonaeum : 
In doubtful cases the dependence of the ascites and other symp- 
toms common to the two diseases on cirrhosis may be suspected— 
1. When there is swelling of the spleen. We have learned that this 
is an almost constant symptom of cirrhosis; on the other hand, the 
spleen is almost always unaffected by tuberculosis and carcinoma, and 
these are not more likely to cause any other form of enlargement of 
the spleen. 2. The urine is saturated with abnormal coloring matter, 
and urates. While this symptom also is rarely absent in cirrhosis, the 
urine of cancerous or tuberculous patients, like that of all hydraemic 
persons, is usually very clear and watery. When the degeneration of 
the peritonaeum is accompanied by fever, or when compression of the 
kidneys and renal blood-vessels by the ascites limits the secretion of 
urine, the scanty urine may, it is true, be quite concentrated, but there is 
usually no sediment, and the urine is not so dark as in cirrhosis. 3. The 
knowledge that the patient was given to drinking. In far the greater 
number of cases, as we have seen, cirrhosis may be referred to the 
misuse of spirits, while this has no influence on the development of 
cancer or tuberculosis. 
On the other hand, the following symptoms speak for degeneration 
of the peritonaeum, and against cirrhosis: 1. Extensive sensibility of 
the abdomen to pressure. 2. Rapid development of ascites. 3. Rapid 
loss of strength. 4. Recognition of cancer, or tubercles in other or- 
gans. 5. Tumors in the abdomen, which may not be felt till after 
‘apping. 6. Occurrence of fibrin, which does not coagulate for a long 
time, in the fluid evacuated by tapping. 
The peculiar color, usual in cancerous persons—which is of some 
importance in distinguishing cancerous degenerations from other 
diseases—is of little value in diagnosing carcinomatous degeneration 
of the peritonaeum from cirrhosis; for in the latter also the patient 
has the dirty-yellow, so-called cancerous hue. 
Treatment.—If, as rarely happens, interstitial hepatitis be recog- 
nized or suspected in its first stage, we should attempt to arrest its 652 
DISEASES OF THE LIFER. 
progress by strictly forbidding the use of spirituous liquors. The 
treatment recommended for hyperaemia of the liver is also suited to 
these cases, particularly the occasional application of leeches about the 
anus, and the administration of saline laxatives. The latter are best 
prescribed as natural or artificial mineral waters of Karlsbad, Marien- 
bad, Tarasp, etc., in which they are better borne than they are without 
the addition of carbonic acid and the alkaline carbonates. If the 
nutrition of the patient have already suffered much, we give the prefer- 
ence to springs containing small quantities of iron, such as the Eger, 
Franzenbrunnen, Kissengen, Ragoczy, and Homburg springs. 
In the second stage, even at its commencement, -we can no longer 
hope to arrest the disease. As the neoplastic tissue, which fdls a loss 
of substance in the skin, continues to shrink till a firm cicatrix has 
formed, so the neoplastic connective tissue in the liver unceasingly 
contracts till the evil results arise which were depicted under the head 
of symptoms. But then radical aid is entirely impossible, for the dense 
tissue can never expand again. Subsequently the treatment of cir- 
rhosis can only be symptomatic. Among the symptoms of congestion, 
the gastric and intestinal catarrh demand particular attention, as they 
increase the emaciation and debility of the patient. According to the 
rules previously given, it is just in this form of gastric and intestinal 
catarrh that the administration of the alkaline carbonates is most bene- 
ficial ; they appear to decrease the toughness of the mucus, and thus 
to enable the mucous membrane to get rid of its mucous coating more 
readily. The haemorrhage from the stomach and intestines should 
also be treated according to the rules previously laid down, although 
we cannot hope for very favorable results. We should only tap the 
patient when it is imperatively necessary, for the ascites, dependent 
on obstruction in the portal vein, is particularly liable to return very 
quickly, as soon as the pressure of the fluid, which has impeded the 
transudation, has been removed. But, if we have been obliged to tap, 
we may hope to retard the fresh collection of fluid by compressing the 
abdomen with a proper bandage. The assertion previously made, that 
diuretics are as useless as they are irrational in the treatment of ascites, 
is particularly true of this form of the disease. The most important 
.ndication in the treatment of cirrhosis is, to improve the strength and 
nutrition of the patient. While the state of the digestive organs per- 
mits it, we should give him nutritious diet and preparations of iron, 
which are not unfrequently well borne and very beneficial. In one 
patient, with cirrhosis of the liver, who afterward died of hasmate- 
mesis, under free use of iron, and a diet consisting mostly of milk and 
eggs, I have frequently seen the fluid in the abdomen diminish, while 
it increased again when the patient was removed from the hospital, SYPHILITIC HEPATITIS, SYPHILOMA OF THE LIVER. 
653 
or was not so well cared for, or when he had hfemorrhage from the 
stomach. 
CHAPTER IY. 
SYPHILITIC HEPATITIS, SYPHILOMA OF THE LIVER (Wagner). 
Etiology.—Among the internal organs of the body, the liver ap- 
pears to be the one most frequently affected by constitutional syphilis. 
At all events, syphilitic hepatitis or syphiloma of the liver is correctly 
interpreted earlier than the syphilitic affections of any other organ. 
Syphilitic disease of the liver is not unfrequently found in the 
bodies of children who have had congenital syphilis. Among the dis- 
turbances of nutrition due to acquired syphilis, syphilitic hepatitis 
comes rather late, so that it is classed among the tertiary rather than 
among the secondary syphilitic diseases. 
Anatomical Appearances.—From numerous microscropic ex- 
aminations of organs affected with syphilitic disease, it is true 
Wagner has come to the conclusion that not only the form ap- 
pearing as circumscribed deposits (gummy tumors of Virchow), but 
also the diffuse syphilitic degenerations of the organs, depend on the 
development of a specific neoplasia, syphiloma, but the appearance to 
the naked eye of livers in which structural change has resulted from 
constitutional disease varies so greatly, in different cases, that it still 
appears proper to describe different forms of syphilitic hepatitis. We 
may distinguish a syphilitic perihepatitis, a simple interstitial syphi- 
litic hepatitis leading to diffuse induration, and a third form called by 
Virchow gummous hepatitis. The latter, whose syphilitic nature 
was long since recognized by Dittrich, is most readily recognized and 
distinguished from other forms of liver disease. In it we find spots, 
from the size of a hemp-seed to that of a hazel-nut, or even -walnut, in 
the liver, which in recent cases have a medullary appearance, but, 
after they have existed a long while, form yellow, cheesy masses. 
These spots, which, previous to Dittrich's explanation, were regarded 
as cancer in the stage of recovery (which they greatly resemble), are 
enclosed by a dense tissue, and dense connective-tissue strife extend 
from them in various directions toward the surface of the liver. On 
the surface even we may notice deep furrows, which give the liver a 
peculiar lobulated appearance, and which are caused by the paren- 
chyma of the liver being destroyed in some places and being replaced 
by contracting connective tissue. In the diffuse syphilitic indurations 
of the liver, we find more or less extensive parts transformed into a 
hard, dense tissue. The gland-substance is mostly destroyed and re- 
placed by connective tissue. The simultaneous occurrence of the 654 
DISEASES OF THE LIVER. 
above-described spots is almost the only symptom which will prevent 
our mistaking syphilitic induration of the liver for cirrhosis; but the 
more regular homogeneous appearance of the cut surface and the ab- 
sence of the granulations, which are rarely never wanting in cirrhosis, 
furnish some points for the diagnosis. Besides the fact that syphilitic 
perihepatitis usually complicates the above-described parenchymatous 
diseases, it is somewhat characteristic of this affection that the thick- 
enings of the serous covering caused by it are more decided than in 
other forms of perihepatitis, and that they are peculiarly hard and 
tough. 
Symptoms and Course.—In many cases syphilitic hepatitis can- 
not be recognized or suspected during life. Occasionally we may make 
the diagnosis from the peculiar form of the enlarged liver, on whose 
surface prominences and retractions may be distinguished, and from 
the coexistence of other symptoms of constitutional syphilis. In one 
patient in Greifswald, who complained of the symptoms of chronic 
peritonitis, from the peculiar form of the liver I was able to diagnose 
the probable existence of hepatitis, before the patient acknowledged 
to being infected, and before examination of the throat had shown a 
decided defect in both sides of the soft palate. This patient has since 
died, and, according to a notice that I have found in the Grief swalder 
Medicinischen Beitrdyen, the autopsy confirmed my diagnosis. In 
the former editions of my book I asserted that it was not improbable 
that, where the process was very extensive, compression of the portal 
vein and bile-ducts might induce a series of symptoms similar to those 
from cirrhosis. I was then obliged to add that, in the cases then pub- 
lished, there had been a moderate ascites in only one, while icterus 
had not occurred in any case. Since then I have had the opportunity 
of observing one case that has fully sustained my conjecture: A pa- 
tient, who denied ever having had syphilis, was received into the 
clinic with icterus, excessive ascites (which required repeated tapping), 
and very dark urine, which contained quantities of abnormal coloring 
matter. The liver was enlarged, and on its surface could be felt distinct 
round protuberances, which were not puffy or in the form of ridges. 
The diagnosis of carcinoma of the liver, with consecutive closure of the 
portal vein, was not confirmed by the autopsy. The liver Avas typi- 
cally lobulated, its covering much thickened in some places, a large 
amount of its parenchyma diffusely indurated; deep in the right lobe 
of the liver were three or four still fresh, medullary-looking gummy 
tumors. 
Treatment.—There can hardly be a question of treatment in syph- 
ilitic hepatitis, for, even in those cases Avhere the disease is recognized 
during life, it is only toAvard its end. We cannot depend on relaxing INFLAMMATION OF THE PORTAL VEIN—PYLEPHLEBITIS. 
655 
or removing the shrunken connective tissue by iodine or mercurial 
preparations, and consequently are limited to a symptomatic treatment. 
CHAPTER V. 
INFLAMMATION OF THE PORTAL VEIN PYLEPHLEBITIS. 
Etiology.—By pylephlebitis we understand not only those con- 
ditions where an inflammation of the wall of the vein induces a clot in 
the portal vein, but also those where coagulation of the contents of 
the portal vein occurs independently of inflammation in the walls of 
the vessel. 
The first form—primary phlebitis—is far rarer than the latter. Its 
exciting causes are partly injuries of the portal vein, partly inflamma- 
tion of the parts about it, which extends to the wall of the vein. 
Secondary phlebitis, or, as it is now called, thrombus of the portal 
vein, cannot always be referred to any evident causes: 1. In some 
cases it is due to compression of the trunk of the portab vein, by lym- 
phatic glands, caseously or cancerously degenerated, or by thickened 
or cicatricially contracted peritonaeum. 2. In other cases, compression 
of the branches of the portal vein, as by cirrhosis, so retards the cur- 
rent of the blood, that coagula form in the trunk or ramifications of 
the portal vein. 3. It appears to result much more frequently from the 
gradual increase and extension of a thrombus that has formed in some 
branch of the portal vein. In the same way, where there is thrombus 
of one of the crural veins, not unfrequently a clot occurs not only in 
the vein of the corresponding leg, but the thrombus often extends up- 
ward also into the vena cava, or even into the renal veins. In such 
cases there is a primary thrombosis in the portal vein and its branches, 
even when the original coagulum in one of the roots of the portal 
vein resulted from inflammation of its walls. In this way are most 
readily explained the thromboses of the portal vein, due to ulcerations 
and suppurations in the abdomen, to inflammation of the umbilical 
vein in newly-born children, to abscesses of the spleen, ulcers of the 
stomach, to inflamed and suppurating haemorrhoidal tumors, and to 
similar causes. 4. It has not been determined whether emboli, from 
collections of pus reaching the liver, can give rise to a coagulum at 
first circumscribed, subsequently diffuse, in the portal vein. 
Anatomical Appearances.—In the first stage of both forms 
of pylephlebitis there is always coagulation of the contents of the 
vein. It is important to note this, to avoid error: suppurative phle- 
bitis begins with suppuration in the vein. The clot adheres firmly 
to the wall of the vein. In primary phlebitis this is from the first 656 
DISEASES OF THE LIVER. 
thickened, infiltrated with serum, and shows a cloudiness of the mucous 
coat, and an injection of the fibrous. In thrombosis, the wall of the 
vein is at first normal, but it is soon changed in the manner above de- 
scribed. The coagulation of the contents may be limited to some twigs 
of the portal vein, but in other cases it extends to the trunk, roots, 
and branches. The tei ruinations of pylephlebitis vary, and, according 
to the difference of its termination, it is called adhesive or suppurative. 
In adhesive pylephlebitis, while the thrombus gradually shrinks, 
undergoes fatty degeneration, and is partly or entirely absorbed, there 
is inflammatory proliferation of the wall of the vein, which terminates 
in its obliteration, although we cannot follow the different phases of 
the process. If we examine a liver that has been the seat of adhesive 
pylephlebitis, we find on its surface cicatricial retractions, and within 
it, corresponding to these retracted places, we find a hard tissue, in 
which may still be recognized the atrophied branches of the portal 
vein. Occasionally these contain remains of the thromboses, colored 
more or less yellow by haematin. 
In suppurative pylephlebitis, instead of atrophying gradually, the 
thrombus dissolves into a puruloid fluid. This is, for the most part, a 
finely-granular detritus, containing only a few roundish cells, which may 
be either white blood-corpuscles or newly-formed pus-corpuscles. The 
whole thrombus rarely breaks down at the same time. In the trunk 
of the vein there is often a firm coagulum, while there is a puruloid 
fluid in the branches and roots. But more frequently there is no dis- 
integration in the finer branches of the portal vein, so that the coagula 
there prevent the disintegrated masses entering the hepatic vein, and 
reaching the pulmonary circulation. I have had the opportunity of 
carefully observing this “ sequestration ” in two cases of suppurative 
pylephlebitis. It readily explains the frequent escape of the lungs 
from secondary disease, which could scarcely fail to occur if the termi- 
nations of the portal vein were not closed. 
But, in phlebitis of the peripheral veins, the inflammation not un- 
frequently extends from the adventitia to the surrounding parts, in- 
ducing suppuration and formation of abscesses, so that inflammation 
of the parenchyma of the liver, which terminates in the formation of 
abscesses, often accompanies suppurative pylephlebitis. Then we often 
find in the liver numerous deposits of pus, which surround the portal 
vein, and often communicate with it. 
Symptoms and Course.—When adhesive pylephlebitis is limited 
to individual twigs of the portal vein, it runs its course without show- 
ing any symptoms during life. The pervious branches suffice to trans- 
fer the blood from the abdominal organs to the hepatic vein. If the 
trunk of the portal vein, or all or most of its branches, be obliterated, FATTY LIVER—IIEPAR ADIPOSUM. 
657 
the symptoms greatly resemble those of cirrhosis. In both cases the 
obstruction to the escape of blood from the roots of the portal vein 
leads to gastric and intestinal catarrh and haemorrhage, to haemor- 
rhoids, enlargement of the spleen (not constantly), and to ascites. 
Biliary retention and icterus result more frequently from compression 
of the gall-ducts in adhesive pylephlebitis than in cirrhosis, because a 
greater number of the liver-cells are preserved to prepare bile. The 
continued secretion of bile and the occurrence of icterus in pylephlebi- 
tis appear to show that the hepatic artery, as well as the portal vein, 
furnishes the liver with material for the formation of bile. The course 
of the disease is chronic. Recovery is impossible; but it often lasts 
for months before death occurs from the same symptoms as it does in 
cirrhosis. Hence it appears that the disease can only be recognized 
and distinguished from cirrhosis by aid of the history of the case. If 
it be found that the patient was not given to drinking, and if the above 
symptoms were preceded by chronic inflammation and suppuration in 
the abdomen, the chances are in favor of adhesive pylephlebitis, par- 
ticularly if the disease have run its course more rapidly than is custom- 
ary with cirrhosis. 
Hitherto suppurative pylephlebitis has rarely been recognized dur- 
ing life. Its symptoms are pain in the right hypochondrium, enlarge- 
ment and tenderness of the liver, chills recurring at irregular intervals, 
high fever, and almost always icterus. If these symptoms join them- 
selves to an inflammation or ulceration of one of the abdominal organs, 
we may, with some certainty, conclude that there is an acute inflam- 
mation of the liver; but we cannot yet say whether the parenchyma 
or the portal vein be inflamed. We are only justified in the latter 
supposition, when, besides the other symptoms, we have those of ob- 
struction of the portal vein, particularly when there is enlargement of 
the spleen, slight ascites, and haemorrhage from the stomach. Schonlein 
was the first to recognize a case of suppurative pylephlebitis during 
life, from the above symptoms; thereby showing great diagnostic acu- 
men and anatomico-physiological knowledge. 
Treatment.—Concerning the treatment of adhesive pylephlebitis 
we may refer to what has been said of cirrhosis; while that of sup- 
purative pylephlebitis corresponds exactly with that of suppurative 
hepatitis. 
CHAPTER VI. 
Etiology.—There are two forms of fatty liver. In one, superfluous 
fat is deposited in the liver-cells from the blood of the portal vein; in 
the other, the nutrition of the liver-cells is disturbed by disease of the 
FATTY LITER IIEPAB ADIPOSUM. 658 
DISEASES OF THE LIVER. 
parenchyma of the liver, and they undergo retrogressive metamorpho- 
sis, during which fat granules appear in them, as happens under sim- 
ilar circumstances in other cells and other tissues. This second form, 
fatty degeneration, is one symptom of many structural changes of the 
liver; we have already mentioned it in cirrhosis, and shall often refer 
to it again. Here we shall only consider the first form, fatty liver in 
the strict sense, or, as we may call it with Frerichs, fatty infiltration. 
On superficial observation, the circumstances under which fatty 
liver occurs appear very varied: for, on the one hand we find it, along 
with an excessive production of fat throughout the body, where the 
supply of nutriment is excessive and its consumption limited; and, on 
the other hand, it occurs with excessive emaciation, where there is in- 
creased consumption of the body. This contrast is, however, only 
apparent; both circumstances agree in causing an abnormal amount 
of fat in the liver. In the one case, fat or the substances from which 
it is formed in the body are supplied from without; in the other case, 
fat is reabsorbed from the subcutaneous and other tissues rich in fat, 
and taken into the blood. 
If we inquire more minutely into the first-mentioned mode of de- 
velopment of fat, we find that the persons affected with fatty liver are 
chiefly those who exercise but little, while they eat and drink freely. 
But by this mode of life they are subjected to conditions analogous to 
those under which we place animals when we wish to fatten them. 
We do not let the latter work, but shut them up in a pen, and give 
them plenty of hydrocarbons. But, under this treatment, one animal 
will become fat readily and quickly, while another will do so slowly 
or not at all; in the same way, of two persons living alike, one will 
become fat and have fatty liver, while the other will remain lean and 
his liver will be healthy. We do not know the causes of the individ- 
ual predispositions, which appear to be sometimes congenital and he- 
reditary in some families, or the causes of immunity of other persons to 
fat bellies and livers. They may depend either on easy or difficult 
assimilation of nutritive materials; or on slow or rapid consumption of 
tissue. If there be a decided predisposition, the disease appears to 
develop on ordinary mixed diet, if more of it be consumed than is re- 
quired to supply the place of what has been used up; if the predis- 
position to fat be slight, it only occurs where there is an excessive 
supply of fats, hydrocarbons, and particularly of spirituous liquors. 
It is probable, but not absolutely certain, that the latter act by retard 
ing the transformation of tissue. 
The frequent occurrence of fatty liver with tuberculosis of the lungs 
has long been remarked; their connection has been ascribed to incom- 
plete oxidation of the hydrocarbons, and their transformation into fat, FATTY LIVER—HEFAR ADIPOSUM. 
659 
due to impaired respiration. But as fatty liver rarely occurs in other 
lung-diseases where the respiration is also affected, and as it often re- 
sults from tuberculosis of the bones and intestines, and from carci- 
nomatous and other diseases in which the patients emaciate, the ob- 
structed respiration cannot be the sole cause of its occurrence in tuber- 
culosis of the lungs. Budd and Frerichs agree with the theory first 
advanced by larrey, that it depends on too much fat in the blood, 
and that this was due to the emaciation and reabsorption of fat from 
other parts of the body. Perhaps the grade of the fatty liver is 
somewhat influenced by the cod-liver oil so much given of late for 
tuberculosis of the lungs. 
Anatomical Appearances.—Slight amounts of fatty infiltration 
do not alter the size or appearance of the liver, and can only be recog- 
nized by the microscope. In higher grades the liver is enlarged, but 
usually appears flattened; the edges are generally thickened and 
rounded off. In many cases the increase in size and weight is but 
slight, in some it is very decided. The peritoneal covering of the 
fatty liver is transparent, smooth, and shining; occasionally it is trav- 
ersed by varicose vessels. According to the grade of the fatty infil- 
tration, the surface of the liver is yellowish red, or distinctly yellow. 
We often notice that the yellow color is interrupted by reddish spots 
and figures, which correspond to the vicinity of the central veins. The 
consistence of the liver is diminished; it feels doughy, and pits on 
pressure with the finger. On incision, we meet little resistance; a 
coating of fat remains on the warmed knife-blade. But little blood 
flows from the cut surface, which is also yellowish red or yellow, and 
shows the red spots and figures above mentioned. 
On microscopic examination, according to the grade of the disease, 
the enlarged and usually rounded liver-cells appear either filled with 
fine fat globules, or these have united to form single larger drops, or, 
lastly, individual liver-cells are entirely or mostly filled by one large 
drop of fat. The infiltration always begins at the periphery of the 
lobules of the liver, that is, near the interlobular veins, the termina- 
tions of the portal vein; it rarely extends to the vicinity of the central 
vein (whose freedom causes the red spots in the yellow liver), and 
even then the liver-cells in the centre are usually less infiltrated than 
those at the periphery. The chemical examination of the liver often 
shows enormous quantities of fat. In one very fatty liver, Vauquelin 
found 45 per cent, of fat, in one case Frerichs found 43 per cent., 
and when the substance of the liver was freed from water he found 78 
per cent. According to Frerichs, the fat consists of olein and mar- 
garin in variable proportions, with traces of cholesterin. 
One variety of fatty liver is what Home and Bokitansky call waxy 660 
DISEASES OF THE LIVER. 
liver. It depends on tlie same structural changes, but is distinguished 
by a waxy dryness, a peculiar brilliance and intense yellow color. 
Symptoms and Course.—In most cases of fatty liver there are no 
subjective symptoms, and, on objective examination also, only high 
grades of the disease can be recognized. In fat persons, and in those 
with consumption of the lungs, we should examine the region of the liver 
from time to time, even without their complaining. If, in these cases, 
we find an enlargement of the liver, which is the more readily recog- 
nized as the liver is usually elongated, has thickened edges, and from 
the relaxation of its parenchyma hangs far down (Frerichs), and if the 
enlarged liver be painless, its surface smooth, its resistance slight, so 
that we cannot readily feel the lower border, these symptoms suffice 
to complete the diagnosis, on account of the frequent coincidence of 
fatty liver with these states. 
If the fatty liver be of high grade, as occurs particularly in topers, 
as in any other enlargement of the liver, there may be a feeling of 
fulness in the right hypocliondrium. If the abdominal walls, the 
omentum, $nd mesentery be also very fatty, the fulness of the abdo- 
men and the tension of its walls may impede the movements of the 
diaphragm and interfere with respiration. In such persons the secre- 
tion from the sebaceous glands is usually so increased that their skin 
shines with fat, and, when they sweat, the sweat runs from their skin 
in large pearls; this condition of the skin, which is due to the same 
state of affairs as the fatty liver, is often mentioned as one of its 
symptoms. 
As fatty livers rarely cause any trouble, as on post-mortem ex- 
amination the bile is usually found in normal amount and quality, as 
they can be generally well injected, and as there are usually no symp- 
toms of congestion in the abdominal organs, the belief has gradually 
gained ground that the fatty infiltration neither impairs the functions 
of the organ nor interferes with its circulation. But this supposition 
only appears correct for the lower and medium grades of the disease. 
In the highest grades, after death, we often find but little bile in the 
bile-ducts, and the fasces in the intestines are but slightly colored. 
The weakly constitution of such patients, particularly their known in- 
tolerance of bleeding, also indicates disturbance of the function of the 
liver. From the varicosities not unfrequently found on the capsule of 
the liver, Frerichs concluded that the compression of the blood-vessels 
Also caused a slight congestion of the vessels before they enter the 
liver. It is true there is no enlargement of the spleen or ascites, but 
the gastric and the intestinal catarrh appear to depend, at least partly, 
on this congestion. Ililliet and Fart hex consider it not improbable 
that the profuse diarrhoea which occurs without perceptible structural FATTY LIVER—HEPAR ADIPOSUM. 
661 
change of the intestines, in phthisical patients who have fatty liver, is 
caused by the latter. Schonlein and Frerichs speak in the same way. 
I have seen obstinate diarrhoea in non-phthisical patients, where exces- 
sively fatty liver was the only anomaly found in the abdominal organs 
on post-mortem examination. 
Treatment.—In gluttons and topers, the causal indications im- 
peratively demand a change of the mode of life. General advice is of 
no use, as it is badly followed. For such patients we should prescribe 
the hours of exercise, forbid afternoon naps, give careful directions 
about their meals, forbidding all gravies and other fatty substances; 
for supper we should only allow water-soup and a little stewed fruit. 
The use of coffee and tea should be limited, that of liquor entirely for- 
bidden. In the fatty liver occurring in consumptive diseases, particu- 
larly in pulmonary consumption, we can rarely fulfil the causal indica- 
tions. 
The indications from the disease have long been supposed to 
require remedies for increasing the secretion of bile. And, in the 
present state of physiology, we must suppose that the success of this 
intention would have the best effect on fatty liver. We find less fat in 
the hepatic vein than in the portal vein. Frerichs saw the secretory ac- 
tivity of the liver-cells diminish as their fatty contents increased; hence 
we can hardly doubt that the fat going to the liver is used up in the 
production of bile, and that the superfluous fat must disappear from the 
liver-cells when the secretion of bile is increased. But our knowledge 
of the difficulty of fulfilling this indication increases in proportion with 
our comprehension of its urgency. At present we can scarcely hope 
that an inert indifferent vegetable extract will decidedly increase the 
secretion of bile, since we no longer regard the bile as a secretion 
necessary for digestion, or, at least, only secondarily so, but as a prod- 
uct whose quantity and quality vary with the acceleration or retardation 
of the change of tissue, or with its other modifications. It is possible 
that the freshly-expressed juices of taraxacum, chelidonium, etc., have 
a curative influence when used as “spring cures” (Friihlingscuren), 
while the patients rise early, live moderately, and exercise freely; but 
it is probable that the benefit is mostly due to the change in the mode 
of life. The case is different with the treatment at Karlsbad, Marien- 
bad, Homburg, Kissengen, etc. In the results there obtained, the 
favorable mode of life must be taken into consideration; but the free 
and continued use of the different solutions of salts must have just as 
much effect on the change of tissue. It is certain that the superfluous 
fat of the body soon disappears under the use of these mineral waters, 
and after a month’s residence in Karlsbad most patients return home 
much thinner than when they went there. Simple pedestrian excur- 662 
DISEASES OF TIIE LIVER. 
sions, with the most moderate manner of living, have not, by any 
means, the same effect. Several very crude hypotheses have been ad- 
vanced concerning the action of the alkaline-saline' springs; the body 
of a Karlsbad patient has even been compared to a soap-factory, and 
the characteristic passages have been regarded as soap, which was said 
to be formed from the soda of the waters and the fat from the body. 
We should not, however, wait to find a better explanation, but should 
send fatty patients with fatty infiltrations of the liver to those water- 
ing-places. This is occasionally very erroneously done with patients 
whose fatty liver depends on decided emaciation, because the patients 
or the physician do not recognize the significance of the disease. It 
is unnecessary to state the contraindications to the use of the alkaline- 
muriatic springs. If the blood be impoverished, we should carefully 
try if the Eger Franzensbrunnen, or the Kissengen Ragoczy waters, 
are borne, and, if they are not, we should be satisfied with regulating 
the diet and mode of life. This rule refers also to those cases where 
patients with fatty liver are inclined to diarrhoea. 
CHAPTER VII. 
LARDACEOUS (OR WAXY) LIVER AMYLOID DEGENERATION OF THE 
liver—(Virchow). 
Etiology.—Lardaceous degeneration of the liver depends on a 
deposit in the liver-cells and in the walls of the hepatic vessels ( Wag- 
ner) of a substance whose nature we do not yet know, but whose re- 
action to iodine and sulphuric acid closely resembles that of amylum 
and cellulose. From this similarity of chemical reaction, which may 
perhaps, be accidental, the title of “ amyloid degeneration ” has of late 
been given to that state which was formerly called “ lardaceous degen- 
eration,” from its external resemblance, but particularly from its pecu- 
liar lustre. 
Lardaceous liver never occurs in persons otherwise healthy; it is 
more apt to occur in advanced cachexia, particularly in cases resulting 
from scrofulous, cachectic, or syphilitic affections, from mercurialism, 
tedious suppurations, and caries of the bones; it is also occasionally 
found in patients with pulmonary consumption ; in some cases it is in- 
duced by malaria. 
Anatomical Appearances.—A lardaceous liver is usually de- 
cidedly increased in size and weight, and resembles fatty liver in form, 
as it appears elongated, flattened, and thickened at the edges. The 
peritoneal covering is smooth and tense, and the liver is hard as a 
board. The cut surface is very dry and bloodless, smooth, almost ho- LARDACEOUS LIVER. 
663 
mogeneous, with a gray color and very lardaceous lustre. When there 
is a coincident fatty degeneration, the knife-blade is covered with fat. 
There is almost always a similar degeneration of the spleen, and not 
unfrequently of the kidneys also. 
On microscopic examination, the polygonal liver-cells appear round 
and enlarged; the fine granular contents, and usually also their nuclei, 
are atrophied, and the cells filled with a translucent, homogeneous 
substance. If there be at the same time fatty degeneration, we find 
small discrete fat globules in the degenerated cells, particularly at the 
periphery of the lobules of the liver. On the addition of a solution of 
iodine, there is not a yellowish-brown but a peculiar reddish-brown 
color; after the addition of sulphuric acid, there is a violet and subse- 
quently a blue color of the preparation. 
Symptoms and Course.—The very gradual enlargement of the 
liver causes no pain; and the patient’s attention is first called to his 
disease, when the enlarged organ fills the right hypochondrium, and 
causes a feeling of pressure and tension. Budd considers ascites as a 
constant symptom of lardaceous liver, and refers it to the compression 
of the portal vessels. He also believes that, in children debilitated 
by scrofulous diseases of the glands and joints, the recognition of a 
painless enlargement of the liver, accompanied by ascites, is sufficient 
for the diagnosis of the disease in question. In opposition to the view 
that ascites accompanying lardaceous liver is due to obstruction of the 
portal vein, Bamberger very correctly says that in such a case there 
should also be symptoms of congestion in the other abdominal organs, 
but these never occur. It is far more probable that the dropsy is due 
to the general cachexia and hydrremia, from which all patients with 
lardaceous liver suffer. In the cases observed by Bamberger, the 
ascites was always preceded by oedema of the feet, and in those re- 
lated by Budd it does not appear that the ascites preceded the oedema 
of the feet. The enlarged liver-cells do not compress the bile-ducts 
any more than they do the blood-vessels, and icterus is absent as a 
rule. Icterus may, however, result from complications, such as lar- 
daceous enlargement of the lymphatic glands at the porta hepatis, so 
that Frerichs warns us against considering the absence of icterus as 
a diagnostic criterion of lardaceous liver. The faeces have little color, 
on account of the impaired function of the diseased liver-cells. It is 
difficult to decide how far the bad nutrition of the patient, the pale- 
ness of his skin and mucous membranes, the hydroemia and dropsy, de- 
pend on the degeneration of the liver, as this disease only occurs in 
those who are cachectic at any rate, and as the spleen is almost al- 
ways diseased at the same time, and the kidneys are very frequently 
so. The etiology, the hard liver-tumor readily felt on palpation, 664 
DISEASES OF THE LIYEK. 
the usually coincident enlargement of the spleen, and, lastly, albumi- 
nuria, when it exists, are important in the diagnosis of lardaceous 
liver. By paying attention to these points, the higher grades of the 
disease may be readily recognized. 
Treatment.—It has not been proved, nor is it probable, that lar- 
daceous degeneration is capable of restoration; and, although cases 
are said to have been observed where lardaceous livers have become 
smaller and normal, further proof is needed on this subject before we 
can believe the statement. The long-continued inunction of iodine 
salve over the liver, although strongly recommended by Rudd, de- 
serves little confidence. The preparations of iodine, particularly 
syrupus ferri iodidi, are extensively used in lardaceous liver, as are 
also alkaline baths and preparations of iron. Although these may not 
improve the liver-disease, they may do much to arrest its progress. 
Iodine justly holds the reputation of being a specific for tertiary syph- 
ilitic affections, and in other dyscrasias also its beneficial effects have 
been proved; the preparations of iron are indicated by the great pov- 
erty of the blood. The peculiarities of each case should decide which 
of these remedies is to be employed. 
CHAPTER VIII. 
CANCER OP THE LIVER CARCINOMA IIEPATIS. 
Etiology.—The liver is so frequently affected with carcinoma 
that, according to Rokitansky, there is about one case of cancer of 
the liver to every five cases in all parts of the body, and Oppolzer 
found it fifty-three times in four thousand autopsies, or in about 
every eightieth patient. In many cases it is primary7, in others it is 
preceded by cancer of the stomach, rectum, or other organs ; it is pe- 
culiarly apt to develop after extirpation of peripheral cancerous tu- 
mors. 
The causes of carcinoma of the liver are just as obscure as those 
of carcinoma elsewhere. It is true that, when asked, the patients are 
rarely puzzled to tell what caused their disease, but their accounts 
give us no true information as to its etiology. 
Anatomical Appearances.—Medullary cancer is the form most 
frequently found in the liver. It sometimes forms circumscribed, 
sharply-bounded tumors; sometimes it spreads out diffusely between 
the liver-cells, and has no sharp borders. 
In the former case we find roundish or glandular and lobulated 
tumors in the liver; these are enclosed by a delicate, vascular connec- 
tive tissue capsule, and, where they touch the peritonaeum, are often CANCER OF THE LITER—CARCINOMA HEPATIS. 
665 
flattened, or have a shallow excavation, a so-called “cancer navel.” 
The size and number of the tumors vary; they are found from the 
size of a pea to that of a child’s head; sometimes they are solitary, 
again innumerable. The nearer they lie to the periphery of the liver, 
the more readily do knobbed protuberances appear. Their consistence 
varies from that of firm brawn to that of soft brain-matter. A large 
amount of “ cancer-juice ” may be pressed out of the softer cancers, 
while only a small amount can be expressed from the harder ones. 
Lastly, the color of the tumor is milk-white or reddish, according as it 
has few or many vessels; it may also be dark red, from effusions of 
blood, or black from deposits of pigment. In the unaffected parts of 
the liver there is usually great hypersemia, which has something to do 
with the enlargement of the organ, which is often very great. Not 
unfrequently the liver is rendered intensely yellow by compression cf 
the gall-ducts and retention of the bile. In the immediate vicinity of 
the cancerous tumors, the liver-cells have usually undergone fatty de- 
generation. Chronic partial peritonitis almost always occurs quite 
early in the covering just over the tumors, causing thickening and ad- 
hesion with the neighboring parts; in other cases cancerous masses 
develop in this part, and spread over the entire peritonaeum. The for- 
mation of the “ cancer navel ” in carcinoma of the liver, as in carcino- 
ma elsewhere, depends on atrophy of the oldest parts of the neoplasia, 
in which the cellular elements undergo fatty degeneration and atrophy; 
but occasionally we meet cases of cancer of the liver where this retro- 
gression extends to the entire tumor, which is finally reduced to a 
yellow crumbly mass, enclosed in a cicatricial connective tissue (the 
remains of the cancerous framework). If young cancer be found with 
these cicatricial masses in the liver, there can be no doubt about the 
nature of the latter; but if this be not the case, it will be difficult to 
decide whether it be indeed cancer that has recovered or the remains 
of some other process. In rare cases medullary cancer softens, and, by 
disintegrating, leads to acute peritonitis, or to dangerous haemorrhage. 
In the second form, which Rokitansky calls infiltrated cancer, we 
find large portions of the liver converted into a white cancerous mass. 
The obliterated vessels and gall-ducts, which are surrounded by rudi- 
mentary liver-cells atrophied, fattily degenerated and colored by bile, 
often traverse this white mass as a coarse yellow framework. Toward 
the periphery the infiltrated cancer gradually passes into the normal 
parenchyma, as there are places where cancerous masses, and others 
where the liver-cells, are in excess. 
The alveolar or gelatinous cancer, which almost exclusively attacks 
the stomach, intestines, and peritonaeum, in some few cases extends 
from the latter to the parenchyma of the liver. In one case, observed 666 
DISEASES OF TIIE LIVER. 
by JLuschka, almost the whole of the liver was transformed into a 
shapeless mass of the structure of alveolar cancer. 
Still more rarely small nodules of the structure of epithelial cancer 
are found in the liver. 
Occasionally cancer of the liver is accompanied by cancer of the 
portal vein, the trunk, roots, and branches of the latter being filled by 
a loosely-connected thrombus of cancerous substance. I have seen 
one case where the contrary occurred: cancer of the portal vein first 
complicated cancer of the stomach, and the cancer of the liver found 
on autopsy had evidently resulted from the extension of the degen 
eration from the portal vein to the tissue of the liver. 
Symptoms and Course.—The symptoms of cancer of the liver 
are always obscure at first; later they are usually quite distinctive, 
but cases do occur where a certain diagnosis cannot be made till death. 
The first complaints of the patient are almost always of a feeling of 
pressure and fulness in the right liypochondrium, such as accompanies 
all enlargements of the liver when they occur rapidly and become great. 
When the tumors are near the surface of the liver, and hence induce 
partial peritonitis early, there is pain in the region of the liver even at 
the commencement of the disease; this pain often spreads to the right 
shoulder. Even from the first the region of the liver is usually more 
sensitive to pressure than in any of the diseases of the organ hitherto 
described, except suppurative hepatitis. After a time the patients 
themselves notice that their right side is prominent, and that there is 
a hard tumor in the right liypochondrium. If the tumors compress 
large branches of the portal vein, there is moderate ascites ; if, on the 
other hand, they grow on the concavity of the liver and compress the 
portal vein itself, the ascites becomes considerable; in other cases 
there is none, but this is rare; for, besides the obstruction of the ves- 
sels, consecutive disease of the peritonaeum causes ascites. Gastric 
and intestinal catarrh, which often complicate cancer of the liver with- 
out the stomach or intestines being affected with cancer, are to be 
regarded as due to the obstruction of the circulation. The spleen is 
rarely enlarged, perhaps because the hydrsemia favors the early occur- 
rence of dropsy, and the pressure of the dropsical fluid interferes with 
the swelling of the spleen. The same is true of icterus as of ascites. 
Compression of the large bile-ducts causes partial obstruction of bile 
and moderate jaundice; but, from the gall-ducts that are not com- 
pressed, sufficient bile flows into the duodenum to color the feces nor- 
mally. If the ductus choledochus be compressed, however, the obstruc- 
tion of bile becomes general, the icterus great, and the fieces are col- 
orless. Lastly, the jaundice and discoloration of the feces occasion- 
ally depend on catarrh of the gall-ducts. In more than half of the CANCER OF THE LIYER—CARCINOMA IIEPATIS. 
667 
cases there is no jaundice. As icterus does not occur in most of the 
organic diseases of the liver, its presence with enlargement of the liver 
is strong evidence that this is due to carcinoma rather than to other 
diseases; but its absence cannot be regarded as proof against carcino- 
ma. Where the cancer of the liver is extensive, the urine shows the 
peculiarities before mentioned, and appears peculiarly red or bluish 
from the presence of abnormal coloring matter, resulting from the de- 
struction of numerous liver-cells. 
While the above symptoms gradually occur, the diseases may gen- 
erally be suspected from the appearance of the patient, who looks 
cachectic, is wasted away, has a relaxed skin, and oedema about the 
ankles. In some patients the cancerous marasmus does not appear 
till very late, and, even when large tumors may be felt in the liver, 
they appear as well nourished and fresh as many patients with carci- 
noma of the breast, before it has ulcerated. But even these patients 
do not escape the injurious effects on the general health, which are 
difficult to understand when the cancer does not suppurate. They 
gradually become marasmic ; and, when the emaciation and exhaustion 
have reached the highest grade, they generally die of dropsy. Among 
the final symptoms we not only unfrequently have thrombus of the 
femoral veins, follicular catarrh of the large intestine, and shortly be- 
fore death thrush not unfrequently comes in the mouth. 
Where there are large tumors in the liver, the physical examina- 
tion not unfrequently gives important aid in diagnosis. In none of the 
diseases of the liver, so far described, does the organ attain the size that 
it may reach in carcinomatous degeneration. The liver, exdarged by 
this disease, most frequently elevates the lower ribs, pushes them out- 
ward, and forms a visible prominence in the abdomen, which often has 
the outline of the liver, and may extend from the right hypochondrium 
to below the navel and into the left hypochondrium. On palpation, 
we usually distinctly feel the edge of the indurated organ, and on its 
surface we find larger or smaller protuberances, which are almost pa- 
thognomonic of the disease. 
If the peritoneal covering of the tumor be the seat of a recent in- 
flammation, we sometimes feel and hear a distinct friction from the 
movements of the liver during respiration. If there be considerable 
ascites, it may prevent exact examination of the surface of the liver; 
but if, by pushing the finger in quickly, we displace the fluid, we may 
at least convince ourselves of its increased size and consistence. 
In most cases the above-described symptoms and course render the 
diagnosis of cancer of the liver quite easy; but, as we have before said, 
it is occasionally difficult or even impossible. Where the cancer is in- 
filtrated, or a few small cancerous nodules develop deep in the liver, 668 
DISEASES OF THE LIVER. 
this is often only slightly enlarged, and even when it projects from 
beneath the ribs we do not find the characteristic peculiarities of its 
surface, on palpation. There is little or no pain, as the serous covering 
is not inflamed, and there is usually no ascites or icterus, as neither the 
branches of the portal vein nor the gall-ducts are much compressed. In 
such cases we often have no sufficient grounds for suspecting the dis- 
ease, till our suspicion of cancer is awakened by a gradually increasing 
cachexia, for which we can find no other explanation, as all the func- 
tions are undisturbed; and when cancer of the uterus, stomach, etc., 
where it is more readily recognized, can be excluded. The probability 
is still greater when the suspicious marasmus has developed after the 
operative removal of an external cancer. If, besides the cancer of the 
liver, which runs its course without decided enlargement and pain of 
the liver, or icterus, or ascites, there be cancer of the stomach, morbus 
Brightii, or some other disease, to explain the marasmus, the disease 
may often escape suspicion. 
Treatment.—We cannot expect any successful radical treatment 
of cancer of the liver. In most cases we must satisfy ourselves with 
maintaining the strength of the patient as long as possible by careful 
nourishment. If the liver become very painful from intense hepatitis, 
we apply a few leeches, and cover the region of the liver with warm 
poultices; these means almost always remove or at least relieve the 
pains. The ascites complicating cancer of the liver may require tap- 
ping under the previously-mentioned conditions. 
CHAPTER IX. 
TUBERCULOSIS OF THE LIVER. 
Tuberculosis of the liver is never primary, but always accompa- 
nies an already existing tuberculosis of other organs, or else forms one 
symptom of miliary tuberculosis. In the latter case, we only find dui], 
translucent granulations, as large as grains of sand, which occur par- 
ticularly on the surface of the liver, with advanced tuberculosis of the 
intestines and lungs. On the other hand, we occasionally find yellow, 
cheesy, tuberculous masses, as large as a hemp-seed, pea, or even 
larger. These very rarely break down into small vomicae, filled with 
tuberculous pus. But they often compress capillary bile-ducts, and 
lead to their dilatation behind the compressed parts; thus forming 
cavities as large as a hemp-seed or pea, which are filled with bile and 
mucus, and which we must not confound with tuberculous cavities. 
Tuberculosis of the liver cannot be recognized during life. ECniXOCOCCI OF THE LIVER. 
669 
CHAPTER X. 
ECHINOCOCCI OP THE LIVER. 
Etiology.—Echinococci hold the same relation to taenia echinococ- 
cus (Siehold) that cysticercus cellulosae does to taenia solium; i. e., 
they are the young, sexless brood of the mature tape-worm. Experi- 
ments of feeding animals with echinococci from man have given no 
decided results, it is true ; but the taenia echinococcus has been found 
in the intestines of animals that had been fed on echinococci from 
other animals. 
It is doubtful how the egg and embryo of the taenia echinococci 
reaches the human liver, there to develop to echinococcus vesicles. 
In Iceland they are so common, that physicians there say that one- 
eighth of all the diseases of that island are due to this disease, and 
that about every seventh person contains echinococci (Kdchenmeister). 
From analogy, it is supposed that the migration takes place as follows: 
Animals affected with the taenia echinococcus evacuate mature links 
from the bowels; the eggs or embryos contained in these in some way 
get into the drinking-water, or come in contact with some food that is 
eaten raw. Entering the intestinal canal with these, the small em- 
bryos with their six hooks bore into the wall of the stomach or intes- 
tine, and, wandering farther, they finally reach the liver. There the 
microscopic embryo swells to a large vesicle, on whose inner wall a 
colony of young, immature tmniae or scoleces is developed. In most 
cases, besides the scoleces, daughter vesicles develop in the mother 
vesicle, or rather wet nurse ; in these, a second generation of vesicles 
is formed, whose inner wall is also covered with scoleces. 
Ktichenmeister refers the endemic occurrence of echinococci in Ice 
land principally to the number of dogs kept there, and to the warmth 
of the river-water, which is much used for drinking. The dogs prob- 
ably eat the vesicles that have been evacuated from the mouth, anus, 
or suppurating sacs that have not been taken care of. The warm tem- 
perature of the water is favorable for the embryos of the echinococcus, 
as it is for all the lower animals. KiXchenmeister considers it as not 
improbable that, when the echinococci reach the bowels of the person 
in whom they exist, they there develop to tcenia, and conversely that 
the embryo escaping into the intestines of persons affected with taenia 
may become echinococci. 
Anatomical Appearances.—Echinococcus sacs are sometimes 
solitary, sometimes very numerous in the liver, and occur more fre- 
quently in the right lobe than in the left. Their size varies from that 
of a pea to that of a fist or a child’s head. If they are large and 670 
DISEASES OF THE LITER. 
numerous, the liver is usually decidedly enlarged. Sacs, deep in the 
organ, and surrounded by liver parenchyma, change the form but little; 
very large sacs, or those near the surface, are generally elevated above 
the liver, and cause decided deformity of the organ. Over the periph- 
eral cysts the peritoneal covering of the liver is decidedly thickened, 
and is attached to the parts around by firm pseudo-membranes. The 
parenchyma of the liver is displaced by the parasites, and, when these 
are large and numerous, it is extensively destroyed; the parenchyma 
still preserved not unfrequently appears very vascular, as a result of 
partial congestions. The echinococcus vesicle itself is enclosed by a 
hard fibrous capsule, which is formed by proliferation of connective tis- 
sue, but may readily be removed from this. The envelope of the ves- 
icle itself is a delicate, half-transparent membrane, resembling coagu- 
lated albumen, which, by the microscope, is shown to consist of numerous 
fine, concentric lamelhe. If we open the vesicle, a clear serous fluid 
escapes; this almost always contains numbers of smaller vesicles. The 
fluid contains about 15 parts of firm constituent to the 1,000; no albu- 
men, but chiefly salts, mostly chloride of sodium, and, according to 
Heintz, 3 parts of succinate of soda to the 1,000. The daughter ves- 
icles are like the mother sac; they are as large as a hemp-seed or a 
large hazel-nut. The larger ones float about freely in the mother sac; 
the smaller ones are firmly attached to its inner wall. The grand- 
child vesicles, which are only found in the larger daughter vesicles, are 
usually about the size of a pin’s head. On careful examination, we 
may discover a whitish, gritty coating on the inner surface of the 
mother, daughter, and grandchild vesicles. The microscope shows 
this to be a colony of young, immature taeniae or scoleces. The indi- 
vidual animals are about \ mm. long, and mm. broad; they have a 
thick head, with four suckers, and a snout which is surrounded by a 
double row of hooks. The head is separated by a constriction from 
the short body, in which there are numerous round and oval chalk con- 
crements. The head is generally drawn into the body. The animals 
are then usually round or heart-shaped, and the circle of hooks is in the 
middle. At the posterior end of the body is a short pedicle, by which 
the animal is firmly held till he subsequently breaks loose and floats 
about in the fluid. The echinococci often die. The mother and 
daughter vesicles collapse, their contents become cloudy, fatty, and are 
finally transformed into a smeary or putty-like substance. This con- 
sists of chalky salts, fat, and cholesterin, and only a few of the hook- 
lets of the echinococcus remain to betray the origin of the mass. JBudd 
compares these hooks to the bones and teeth remaining- after the decay 
of larger animals. 
In other cases the echinococcus sac gradually distends till it finally ECHIXOCOCCI OF THE LIVER. 
671 
bursts. If the distended and tliinned peritoneal covering ruptures at 
the same time, the contents of the sac enter the peritoneal cavity, and 
there is severe peritonitis. In the same way, if the sac has become 
adherent to the neighboring parts, it may be evacuated into the stom- 
ach, intestines, gall-ducts, neighboring blood-vessels; or, when the dia- 
phragm has been gradually thinned, and finally perforated by the 
pressure, the sac may empty into the pleural cavity or into the lung 
adherent to the pleura. In still other cases, the hydatid excites in- 
tense inflammation in its vicinity, particularly in the fibrous envelope be- 
longing to the liver. This appears to occur particularly in those cases 
where the sac bursts inside of the liver, and its contents come in direct 
contact with its parenchyma. In such cases, besides shreds of the 
mother vesicle, and sometimes single, still perfect daughter vesicles, the 
cyst contains purulent masses tinged with bile. These cases are evi- 
dently not due to inflammation of the mother vesicle, but the pus has 
entered the sac from without. The abscesses of the liver, thus induced, 
may have any of the terminations described in Chapter II. If it per- 
forates externally, rudiments of the echinococcus vesicle are mingled 
with the pus that escapes. 
Symptoms axd Course.—As a rule, echinococci inhabit the liver 
for years before they attract attention, or the disease is suspected. The 
gradual growth sufficiently explains the absence of inconvenience, or 
its tardy appearance. In most cases where the disease is recognized, 
its discovery is not brought about by the subjective symptoms, but by 
the patient himself, or the physician accidentally noticing that the right 
hypochondrium is prominent, and contains a tumor. If the hydatid, 
and with it the liver itself, attain a considerable size, the feelings of 
pressure and tension in the right side, so often mentioned, are occasion- 
ally induced. The diaphragm, pressed upward, may have its action 
interfered with. The compression of the lower lobe of the right 
lung and the collateral hyperaemia in the non-compressed portions of 
lung may induce dyspnoea and broncliial catarrh. In the same way, 
ascites and icterus of variable amount may result from compression 
of the branches or trunk of the portal vein of the small ducts, or 
the excretory duct of the bile; but all these symptoms are excep- 
tional. 
Physical examination is the most important, and in the majority of 
cases is the sole means of diagnosis. Like large and numerous carci- 
nomatous tumors, large and numerous hydatids in the liver are also 
often evident on inspection. In these cases also there is a prominence 
in the right hypochondrium, extending below the navel, and into the 
left hypochondrium; and, while the shape of the swelling reminds us 
of the liver, we notice on it slight elevations of different sizes. At the 672 
DISEASES OF THE LIVER. 
same time, the right half of the thorax may be dilated, the lower ribs 
being moved irpward and outward. On palpation we may still more 
distinctly recognize the enlargement of the liver, and the inequality of 
its surface. The protuberances appear more yielding than those due 
to the softest forms of cancer. Occasionally there is distinct fluctua- 
tion. The percussion-sound is absolutely dull all over the enlarged 
liver. On percussing over the hydatid itself, in some cases we notice 
a peculiar thrill (Piorry's Fr6missement liydatique), similar to that 
obtained by striking on tolerably stiff glue. 
Among the symptoms of the termination of the disease, those of 
the gradual atrophy of the sac cannot be given, as this termination 
only occurs in small hydatids which cannot be diagnosed. If the 
hydatid burst into the peritoneal sac, we have the same symptoms 
as in perforation of ulcers of the the stomach. If the hydatids 
were not previously diagnosed, we cannot tell what substance 
has entered the peritonaeum. The patients die in a few days of the 
rapidly-fatal peritonitis. We can only recognize perforation into the 
stomach, intestines, or lung, when portions of the hydatid are vomited, 
evacuated at stool, or coughed up. If the echinococcus vesicle excite 
inflammation in its vicinity, the enlargement of the liver, previously 
free from pain, now becomes very painful, and is especially very sen- 
sitive to pressure. There are chills and high fever, and we have the 
picture of suppurative hepatitis, and its results, which were described 
in Chapter II. If the abscess of the liver perforate externally, we 
may occasionally find traces of the peculiar laminated membrane, or 
some of the hooks of the hydatid in the pus. 
Treatment.—Fomentations of strong solutions of common salt 
over the region of the liver have been recommended for hydatids of 
that organ, and JBudd says that, from the peculiar attraction and affin- 
ity of the hydatid cyst for salt, it is possible that the collection of the 
latter in the fluid thus effected may prevent the further development 
of the echinococcus, or destroy it altogether. Others recommend prep- 
arations of iodine and mercurials, on account of their known “ anti- 
parasitic” effect, and anthelmintics are used for the same reason. 
These remedies deserve little confidence, as they have been advised on 
theoretical grounds, and not from actual experience. If we conclude 
to use them, we should at least choose those least injurious to the 
organism. In Iceland they appear to open hydatids boldly; in this 
country very bad results have occurred from opening them without 
precaution; and, when we decide on puncturing them, the same rules 
are necessary as in opening abscesses of the liver. # MULTILOCULAR HYDATIDS. 
673 
CHAPTER XI. 
MULTILOCULAR HYDATIDS. 
Etiology.—Recently, on post-mortem examination, large portions 
of the liver have been found transformed into a peculiar mass, which 
consisted of a connective-tissue stroma, and numerous large and small 
cells filled with a gelatinous substance. The first observers considered 
these growths as alveolar carcinoma; but careful microscopical exam- 
ination showed that the gelatinous contents of the cells consisted of 
the tissue peculiar to the echinococcus, and hence placed it beyond 
doubt that the affection was due to a brood of hydatids. 
It is difficult to determine the mode of origin of these tumors, 
which, according to Virchow are designated multilocular echinococcous 
tumors; but it is most probable that this is not a peculiar species of 
parasite, but only that there is a peculiarity about the migration, 
seat, and growth. Virchow believes that this form of the disease 
results from the echinococcus embryo entering the lymphatics of the 
liver, and their sacs developing there: JLeukart locates these pro- 
cesses in the blood-vessels; Friedreich, who, in one case found the 
hepatic duct plugged with echinococci, locates them in the gall-ducts. 
I am indebted to a letter from Kttchenmeister for the following simple 
explanation, which I believe to be the correct one : “ After the emi- 
gration of an echinococcus embryo, instead of the usual form of the dis- 
ease, we have a multilocular hydatid cyst, if no connective-tissue sac 
form around the embryo, or if this sac be ruptured by the parasite 
before it has become hard and resisting. When the echinococcus has 
no firm envelope, it can grow freely in all directions, and spreads par- 
ticularly in the directions where it finds least resistance. If in its 
wanderings it has entered one of the many channels that traverse the 
liver, or if it has subsequently broken through the wall of one of these 
canals, it advances along it, and may finally fill the entire canal sys- 
tem thus affected. As Virchow, Leukart, and Friedreich, who are 
certainly trustworthy observers, reached different results, as each of 
these observers found different canal systems of the liver filled with 
echinococci, we are justified in supposing that the emigrations and 
perforation of the parasites may occur into the lymphatic, or blood- 
vessels, or into the bile-ducts, but that each of these canal systems may 
remain free from them. 
Anatomical Appearances.—Multilocular hydatids almost always 
occur in the right Jobe of the liver; in only one of the three cases that 
I have seen was the left lobe affected. They may reach the size of a 674 
DISEASES OF TIIE LIVER. 
child’s head or become even larger. The connective-tissue stroma is 
generally far advanced in fatty metamorphosis. The cells opened by 
an incision strongly remind us of the holes on the cut surface of a 
piece of well-baked black bread. On microscopic examination of the 
gelatinous substance contained in them, we immediately recognize the 
characteristic membrane of the echinococcus, which is strewn with 
numerous chalk concrements. On the other hand, it usually requires 
a long search to discover a circlet of hooks or single members from it, 
and we rarely find perfect scoleces. In a single one of my cases, at 
the periphery of the tumor there were vesicles as large as a cherry, 
whose inner wall was thickly covered with a colony of well-preserved 
scoleces. In all reported cases, except my last one, the centre of the 
mass had suppurated; the cavity resulting from the suppuration con- 
tained a dirty brownish-gray fluid, which consisted mostly of detritus 
masses, chalky concrements, fat globules, and cholesterin crystals. 
The wall, rendered uneven by numerous small fossae (opened alveoli), 
had in many places an ochre-colored coating in which beautiful haema- 
toidin crystals could be seen microscopically. 
Symptoms and Course.—Of course the symptoms of multilocular 
hydatids must vary with the canal system of the liver, which is filled 
and obstructed with the echinococcous masses. This explains the 
remarkable fact that the somewhat hasty description of the symptoma- 
tology given by Friedreich of the multilocular hydatid cyst so ex- 
actly suits some cases, that the disease has been repeatedly diagnos- 
ticated from that description; wThile in other cases even the most 
prominent points of his description have been wanting. I shall try 
to avoid Ft'iedreic/i’s errors in the following description, which is 
taken partly from my own comparatively numerous observations, partly 
from a careful analysis of the reported cases of other observers, which 
are not very numerous : 
The disease is almost always latent at the commencement; as a 
rule, the first symptoms appear after it has made considerable progress. 
Some patients have their attention called to the disease by a feeling 
of pressure and fulness in the right hypochondrium, or by the acci- 
dental discovery that they have a tumor in the abdomen. They have 
nothing else to complain of; the appetite and digestion are good; the 
strength and nutritive condition leave nothing to desire; there is no 
jaundice or symptoms of obstruction in the roots of the portal vein. 
On examining the abdomen, we find in the right hypochondrium a 
tumor, which unmistakably belongs to the liver; the liver may either 
retain its normal shape, or there may be slight elevations on its surface, 
such as occur in carcinomatous and syphilitic diseases. Even where 
there is extensive central suppuration, the resistance of the liver tumor MULTILOCULAR HYDATIDS. 
675 
is usually very decided; fluctuation was only noticed in one of tlie cases 
observed by Griesinger. 
When the disease commences and runs its course with the above 
symptoms, it can never be recognized with certainty, or absolutely dis- 
tinguished from other diseases of the liver, particularly carcinomatous 
or syphilitic. In the first case I saw, death was caused by apoplexy; 
the preparation was presented to me as an immense suppurating cancer 
of the liver. The attending physician had not made out the nature of 
the nodular, stony tumor of the liver, whose gradual growth he had 
watcl ed for years. The patient had no icterus during the latter years 
of his life; he only had a slight jaundice, of short duration, about ten 
years before his death. In a second case, carefully observed for several 
months, at my clinic, besides the above, symptoms, there were albumi- 
nuria and general dropsy; the case was diagnosed as syphiloma of the 
liver and amyloid degeneration of the kidneys. Only the second half 
of the diagnosis was confirmed by the autopsy. Instead of a syphi- 
loma, the liver contained a multilocular hydatid tumor, as large as the 
head. This patient was never jaundiced. In both patients the pas- 
sages and excretory bile-ducts were entirely pervious. 
These observations not only disprove Friedreich's assertion, that 
marked icterus is among the most constant symptoms of multilocular 
hydatid, but they also prove that, in cases where there is no obstruction 
of the bile-ducts by echinococci, and, consequently, where there is no 
obstruction and reabsorption of bile, the patient’s state may long re- 
main as endurable as in the ordinary form of hydatid. After a long 
time, the advancing suppuration of the tumor and the fever accompa- 
nying it appear to impair the nutrition, and to develop a cachexia, 
which finally carries off the patient, if he does not die of some inter- 
current disease. In my second case, death was hastened by the second- 
ary disease of the kidneys (whose occurrence, in multilocular hydatids, 
Friedreich expressly denies). 
The symptoms and course of the disease are entirely different when 
the bile-ducts are obstructed by echinococci locating in them, or break- 
ing into them from without. In these cases, at least in their later 
stages, the disease is not unfrequently so characteristic that an approxi- 
mate, or even an absolute, diagnosis may be made. The series of 
symptoms is opened by an apparently inoffensive icterus, but this 
steadily increases; all remedies used for it prove unavailing, and it 
gradually becomes excessive. The faeces usually soon lose their color, 
a proof that all the gall-ducts or the excretory ducts are closed. As 
there are no dyspeptic symptoms, and as the occurrence of the icterus 
is preceded by no severe paroxysms of pain, Ave may, with great proba- 
bility, exclude catarrh of the excretory bile-ducts and their obstruction 676 
DISEASES OF THE LIVER. 
by calculi; but the true ground of the obstruction is at first entirely 
obscure. In one patient, where there was finally no doubt about the 
diagnosis, at the first consultation, I was obliged to limit myself to 
saying, “ There is an obstruction of the excretory bile-ducts, from some 
cause unknown to me.” Early in the disease, on examining the abdo 
men, we find the liver enlarged; but even this symptom does not 
enable us to make a diagnosis until the enlargement has become very 
marked, or the resistance of the liver has greatly increased, and while 
its surface remains smooth. Where the faeces are discolored and the 
icterus excessive, we are most apt to ascribe the enlargement of the 
liver also to biliary obstruction. On the other hand, if, while there is 
excessive and obstinate icterus, and complete discoloration of the faeces, 
we find enlargement of the liver, but not of the gall-bladder, we should 
suspect multilocular hydatids. Under such circumstances, the obstruc- 
tion is, most probably, not in the ductus choledochus, but in the ductus 
hepaticus, for when the former is obstructed, the gall-bladder also is 
usually distended by the obstructed bile. Obstruction of the hepatic 
duct is rare, but probably its most frequent cause is multilocular hy- 
datids, and hence, when we think we have found it obstructed, we 
should suspect this disease. The suspicion that there is a multilocular 
hydatid cyst in the liver increases, and may become a certainty, if, be- 
sides the above symptoms, the liver becomes uneven and nodular as 
the disease progresses. From that time swelling of the liver, from 
simple biliary obstruction, may be excluded; the case can only belong 
to one of the varieties of liver-disease where the form of the organ is 
thus changed—that is, it must be cirrhosis, syphilitic, or carcinomatous 
disease, or hydatids. The rest of these diseases are hardly ever accom- 
panied by complete discoloration of the feces, and excessive and obsti- 
nate biliary obstruction, in which the gall-bladder does not participate, 
while these are very frequent accompaniments of multilocular hydatids. 
Hence, if we find a hard nodular enlargement of the liver with those 
symptoms, we are justified in diagnosing a multilocular hydatid. 
In many cases, in the course of the disease, there are ascites, enlarge- 
ment of the spleen, gastric and intestinal haemorrhage, occasionally 
also haemorrhage from other mucous membranes, and effusion of blood 
into the cutaneous tissue. But none of these symptoms are pathogno- 
monic of multilocular hydatid; they result from the great biliary ob- 
struction and reabsorption of bile, and, as we shall show in the next 
chapter, occur just as often in other forms of obstinate obstruction and 
reabsorption of bile. 
Treatment.—Treatment can accomplish nothing in multilocular 
hydatids; occasionally the inefficiency of the remedies used for the 
icterus strengthens the diagnosis. Of course, there is no way of re- jaundice. 
677 
ducing the size of the tumor, or of improving the jaundice and incon- 
veniences dependent on it, or of permanently maintaining the strength 
and nutrition of the patient. Nor does the attempt at tapping, made 
in Griesinger’s case, encourage imitation. 
CHAPTER XII. 
BILIAKY OBSTRUCTION IN THE LITER, AND CONSEQUENT ICTERUS 
HEPATOGENOUS ICTERUS [JAUNDICE]. 
Etiology.—The gall-ducts have no contractile elements to urge 
their contents onward. Hence we are led to the conclusion that the 
bile in the biliary passages is pressed forward by the same force that 
caused it to enter the ducts, the secretory pressure. The compression 
to which the liver is subjected, from the descent of the diaphragm 
during inspiration, assists the evacuation of the bile-ducts, it is true, 
but we should not over-value this force, for the gall-bladder, on which 
the pressure must be greater than on the firm liver, may be greatly 
distended with bile, while the movements of respiration go on unin- 
terruptedly. At all events, the forces that pass the bile along its ducts 
are so weak that they cannot readily overcome even the slightest ob- 
stacle, and a very inconsiderable obstruction to the evacuation of the 
bile suffices to cause it to collect in the liver—that is, to induce reten- 
tion of bile. 
If the bile-ducts and the liver-cells become very full, and the lateral 
pressure in them attains a certain height, a large part of their contents 
enters (filters into) the blood-vessels and lymphatics. This is the most 
frequent cause of jaundice. Recent investigations have placed it be- 
yond a doubt that, in the icterus due to obstruction and reabsorption 
of bile (also called resorption jaundice or hepatogenous jaundice, in 
contradistinction to hcematogenous, which will be described hereafter), 
not only the coloring matter of the bile, but its other constituents, 
particularly the acids, are taken into the blood. As has been proved 
by numerous experiments, these acids possess to a peculiar degree 
the property of dissolving the red-blood corpuscles. By injecting 
weak solutions of them into the blood of animals, we may artificially 
induce the so-called hsematogenous icterus, as the liberated coloring 
matter of the blood is transformed into biliary coloring matter. As it 
is firmly established, both that in biliary obstruction the bile-acids 
enter the blood, and that the absorption of these acids into the blood 
sets free the coloring matter of the latter and transforms it into biliary 
coloring matter, we may correctly say that every hepatogenous icterus 
is accompanied by a hiematogenous, or, more accurately, every hepa- 
togenous induces a haematogenous icterus. 678 
DISEASES OF THE LIVER. 
Of the diseases of the liver that have already been described, some, 
such as fatty and lardaceous liver, never induce icterus, as they never 
cause compression of the bile-ducts; others, such as cirrhosis, cancer, 
and hydatids, sometimes induce biliary obstruction, sometimes they do 
not. Where the bile-ducts are compressed, if the retention of bile be 
only partial, its rcabsorption and the icterus do not become excessive; 
the unimpeded flow of bile from the bile-ducts, which are not obstruct- 
ed, gives some color to the feces. The case is different when the 
ductus hepaticus or choledochus is compressed by tumors of the liver 
or plugged up by hydatids; then the biliary obstruction becomes ab- 
solute, the icterus very marked, and the feces totally discolored. 
Total retention of bile, with its results, is much more frequently 
caused by disease or compression of the excretory bile-ducts than by 
disease of the liver. This condition will occupy us in the next sec- 
tion ; in this chapter we shall only speak of the changes induced in 
the liver by biliary obstruction, and of its results. 
Anatomical Appearances.—The size of the liver may be in- 
creased by general excessive biliary obstruction, just as by decided 
congestion of the blood; but the swelling rapidly subsides as soon as 
the obstruction to the flow of bile is removed. The form of the liver 
is not altered by the enlargement. In high grades of the affection, 
the larger as well as the smaller bile-ducts appear dilated and dis- 
tended with bile. The color of the liver is deep yellow, and, in the 
highest grades, olive green; it is not usually regular, but mottled. 
According to Frerichs, on microscopical examination, we sometimes 
find the entire contents of the liver-cells pale yellow, sometimes there 
is a deposit of fine granular pigment, particularly in the vicinity of the 
nuclei. After the disease has lasted some time, the liver-cells contain 
firm collections of pigment in the form of yellow, reddish-brown, or 
green rods, spheres, or angular fragments. The cells containing pig- 
ment lie chiefly in the vicinity of the central veins. 
Even when the obstruction to the excretion of bile is not removed, 
the previously-enlarged liver may become smaller, and may even be 
reduced below its normal size; at the same time it acquires a dark- 
green or even black color, and loses its consistence, becoming soft and 
capot. In such cases the nutrition of the liver-cells has been impaired 
by compression of the afferent blood-vessels, and by pressure, from the 
distended bile-ducts, perhaps also from the pressure of the bile collect- 
ed in the cells. On microscopical examination, we find most of the 
cells broken down into a fine granular detritus, while some still con- 
tain pigment. 
On autopsy of jaundiced bodies, collections of bile-pigment may be 
found in almost all the organs and fluids. Besides the characteristic JAUNDICE. 
679 
color of the skin, conjunctiva, and urine (of which we shall speak more 
particularly when describing the objective symptoms of the disease), 
as soon as the body is opened we notice the lemon-color of the fat in 
the subcutaneous tissue, mesentery, pericardium, and elsewhere. The 
fibrinous coagula in the heart and blood-vessels, the fluid in the peri- 
cardium, and any pathological transudations or exudations of the peri- 
cardium, pleura, and peritonaeum, have a distinctly jaundiced appear- 
ance. The less red the normal color of the different tissues is, the 
more marked is the pathological yellow color; hence it is more evident 
in the serous and fibrous membranes, the walls of the vessels, the 
bones, cartilages, etc., than in the muscles, spleen, etc. Only the brain, 
spinal marrow, and nerves form an exception, as only a slight color 
can be seen in them. Frerichs supports the previous observations, 
according to which the secretions proper, the saliva, tears, and mucus, 
contained no bile-pigment, while the albuminous and fibrinous exuda- 
tions are rich in it. The changes in the kidneys, which were first fully 
described by the above observer, are very interesting. In old and in- 
tense cases of icterus he found the kidneys of an olive-green color, and 
some of the uriniferous tubules filled with a brown or black deposit. 
On more careful examination, in the pale uriniferous tubules, he saw 
the epithelial cells, which were really perfect, colored brown by pig- 
ment : the dark uriniferous tubules were filled with a coal-black, hard, 
brittle mass. The pigmentation of the epithelium began in the Mal- 
pighian capsule, increased in the convoluted tubuli uriniferi, while 
the black, coal-like masses were chiefly found in the straight tubules. 
Symptoms and Course.—Premonitory symptoms almost always 
precede the characteristic signs of biliary obstruction. These consist 
of the symptoms of the disease that lead to contraction and closure 
of the bile-ducts; and, as this is most usually catarrh of the duode- 
num, they are most frequently those of gastro-duodenal catarrh. If 
these have existed for a longer or shorter time, the passage of the 
catarrh to the ductus choledochus, or the closure of the bile-ducts in 
any way, is almost always first shown by the peculiar dark color of the 
urine, and the light color of the faeces. But generally it is not these 
symptoms, but it is yellowness of the skin and eyes, that induces the 
patient to seek medical aid. Sometimes the skin is only slightly yel- 
low, sometimes it is an intense saffron color; later, and in the higher 
grades, called melan-icterus, it may be greenish or even mahogany 
color. At those parts of the body where the epidermis is thin, so that 
the deeper layers of the rete Malpighii, where the pigment is located, 
shine through, the color is most intense, as on the forehead, aloe nasi, 
elbows, breast, etc. The yellow hue of the sclerotic, which may also 
be quite dark, is very characteristic of icterus, and is important in the 680 
DISEASES OF THE LIVER. 
diagnosis between jaundice and other discolorations. The yellow tint 
of the skin and sclera completely disappears by artificial light, so that 
we cannot recognize jaundice at night. We may see that the exter- 
nal mucous membranes are also yellow, by pressing the blood from the 
lips or gums of a patient with jaundice; when the finger is removed, 
the spot left will not be white, but yellow. Sometimes the urine is 
light brown, like thin beer, sometimes dark, like porter; after stand- 
ing in the air, it almost always becomes greenish. If we agitate the 
discolored urine, its froth is distinctly yellow, and a strip of linen or 
white paper dipped in it becomes yellow, and this often suffices to dis- 
tinguish between the coloring matter of the bile and other coloring 
matter in the urine. The test with nitric acid containing some nitrous 
acid is more certain. On adding this, the brown of the bile-coloring 
matter successively becomes green, blue, violet, red, and finally pale 
yellow. To note the changes well, we should carefully let some of 
the acid run down the inside of a champagne or test glass, containing 
the urine to be tested, so that it will reach the bottom, and there will 
be only a gradual admixture of the acid with the urine. If there be 
any bile-coloring matter present, and we let the urine stand a while, 
the various layers immediately above the nitric acid show different 
colors, and the above series of colors may be perfectly or partly dis- 
tinguished from above downward. The reaction may be incomplete, 
or may fail entirely, if the urine has stood exposed to the air for some 
time, and already has a greenish color. According to Frerichs, the 
opposite occurs occasionally; the reaction does not take place till the 
urine has stood in the air for some time; until quite recently the oc- 
currence of the bile-acids in the urine during icterus has been denied 
by celebrated authorities. There are certain difficulties in their detec- 
tion in jaundiced urine by Pettenkofer’s test, which shows very small 
quantities of the bile-acids by inducing a purplish-red color, when to 
the solution containing them we add a small amount of sugar, and 
then gradually add concentrated sulphuric acid. This reaction cannot 
be directly used when the fluid to be examined, as the urine, also con- 
tains substances which are directly colored by the addition of sulphuric 
acid. Hoppe-Seyler deserves the credit of having disproved the erro- 
neous belief that in jaundice the urine contained only the coloring 
matter of the bile, and not the bile-acids, and of having proved the 
presence of the latter in the jaundiced urine by a complicated but per- 
fectly reliable process. 
Bile-pigment constantly occurs in the sweat also, so that the linen 
is colored yellow, particularly at those parts where the patients sweat 
much. The milk of nursing-women has also been found colored yellow. 
The most noticeable change in the faeces, from obstruction to the JAUNDICE. 
681 
flow of bile into the intestines, is their more or less complete discolora- 
tion. Where the excretory duct of the bile is incompletely closed, or 
the biliary obstruction partial, they have a loamy color, while they are 
clay-colored where the ductus hepaticus or choledochus is completely 
obstructed. As the amount of bile poured into the intestines during 
twenty-four hours is estimated at about two pounds, we may readily 
understand why the faeces are almost always dry. But, moreover, 
physiology teaches that, by excluding bile from the intestines, the ab- 
sorption of fat is restricted, if not arrested; this explains the long- 
known fact that the feces of jaundiced patients contain far more fat 
than do those of healthy persons. Professor Trommer, who examined 
the feces of two of my students, who ate exactly the same amount of 
bread, butter, and cold meat, but of whom one was jaundiced, the 
other perfectly healthy, found far more fat in the feces of the former 
than in those of the latter. Lastly, the putrid decomposition of the 
contents of the intestines appears to be avoided by the action of the 
bile on them; hence patients, in whom no bile is emptied into the 
bowels, usually suffer from flatulence, and the flatus passed, as well 
as the feces, have a very disagreeable odor. 
Besides the abnormal color of the skin, sclerotica, urine, sweat, milk, 
and besides the discoloration of the feces, and the difficulties connected 
with the absence of bile from the intestines, we find that almost all 
patients with jaundice due to biliary obstruction rapidly emaciate, 
and become very languid and sleepy. As both the amylacea and 
protein substances are digested while there is no bile-in the intestines, 
if there be no coincident gastric and intestinal catarrh, the emaciation 
can only be ascribed to the change in the absorption of fat. As has 
been previously stated, JSischoJf has experimentally shown that a 
plentiful supply of fat may cause less consumption of the tissues of 
the body. It is very probable that the withdrawal of fat may have 
the opposite effect, and induce an increased use of the fat collected in 
the body. Even the exceptions, where jaundiced patients remain well 
nourished, although no bile reaches their intestines, do not disprove 
this explanation. For it has been observed that, while most dogs with 
artificial biliary fistula emaciate greatly, some remain well nourished, 
and it is particularly those that eat a great deal. In the same way, 
it has been observed that it is just those persons that have an excellent 
appetite and good digestion during their jaundice, who do not emaciate. 
Hence we may assume that failure of the supply of fat can be re- 
placed by increased supply of hydrocarbons, and protein substances. 
The discovery, that in icterus the bile-acids are reabsorbed, and that 
their presence in the blood induces the disintegration of the red-blood 
corpuscles, shows another cause for the poverty of the blood, the emaci 682 
DISEASES OF THE LIVER. 
ation and the cachexia, which often become very marked in protracted 
icterus. The languor, also, and the great inclination to sleep appear to 
depend not only on the bad nutrition, but to be greatly due to the 
toxic influence of the bile-acids on the nerves and muscles. 
The slow pulse of patients with jaundice appeared to be intimately 
associated with the emaciation and loss of strength. It was not con- 
sidered necessary to refer this symptom to the entrance of the constit- 
uents of the bile into the blood, and to compare their action to that of 
digitalis, for the retardation of the pulse was observed in the so-called 
hunger-cure, and in the convalescence from severe illness after the 
fever had stopped; but the useful experiments of llohrig have shown 
that, in patients with icterus, the slow pulse mostly depends on the 
presence of bile-acids in the blood. 
The same is true of the itching which annoys many patients with 
icterus. This has been referred to the dry, scaly state of the patients’ 
skin, as it was also seen in senile marasmus. But its proportionate 
frequency in icterus, and its rare occurrence in marasmic conditions, 
render it probable that it is due to an irritation of the cutaneous 
nerves by the constituents of the bile deposited in the rete Malpighii. 
It is true, the itching is often absent in the highest grades of icterus, 
while in moderate grades it is very troublesome; and it is almost 
always periodical—peculiarities difficult to explain if the symptom be 
due to irritation from the acids or coloring matter of the bile. 
Yellow vision—Xanthopsia—very rarely occurs in icterus. It is 
doubtful whether this be due to the yellow hue of the transparent 
media of the eye, or whether it depends on abnormal innervation, 
and is one of the first symptoms of acholia, of which we shall pres- 
ently speak. 
The course and termination of the disease depend chiefly on 
whether the obstruction to the evacuation of the bile can be removed 
soon, late, or not at all. In the first case, when the obstruction is over- 
come, the symptoms of retention of bile disappear quite rapidly, and 
the disease ends in recovery. At first, the faeces resume their normal 
hue, and the dark color of the urine and the symptoms due to satura- 
tion of the tissues, with pigmented nutritive fluid, soon pass off. The 
discoloration of the skin disappears last, particularly when the epider- 
mis is thick. If enlargement of the liver has been observed while the 
flow of bile was obstructed, this also subsides when the flow becomes 
free. The strength and nutrition also improve rapidly. 
Since, in icterus dependent on obstruction of the excretory gall- 
ducts, the return of the normal color to the faeces is almost always the 
first sign of improvement, the physician, and often also the patients, 
usually await its occurrence with great anxiety. Sometimes, how- JAUNDICE. 
683 
ever, the faeces acquire a weak, bilious color, without the bile-ducts 
having become pervious. This depends on their admixture with jaun- 
diced blood-serum, or jaundiced inflammatory products. (Even in high 
grades of icterus the intestinal mucus contains no bile-coloring mat- 
ter, otherwise the faeces would never lose their color.) Small haemor- 
rhages into the intestines, such as quite frequently occur during con- 
tinued obstruction of the excretory bile-ducts, most commonly lead to 
error; they do so the more readily, as a very slight admixture of blood 
with the faeces does not induce any characteristic color, particularly when 
the blood-serum is jaundiced. 
If the biliary obstruction continue for some time, or if it depend on 
causes that cannot be removed, the jaundice attains the highest grade, 
and the nutrition may suffer so much that the patient will finally die 
of marasmus or dropsy. 
In rare cases the final result is hastened by the occurrence of gastric 
or intestinal haemorrhage. These result from the same causes as in 
cirrhosis and pylephlebitis. The escape of blood from the vessels of the 
gastric and intestinal mucous membrane is just as much obstructed in 
the former case by the compression of the capillaries of the liver from 
the distended gall-ducts, as it is in the latter by the compression of the 
hepatic vessels from the contracting connective tissue, or by the ob- 
struction of the portal vein. But in explaining these haemorrhages, 
besides the mechanical obstruction to the flow of blood, we must also 
take into consideration the disturbed nutrition of the gastric and in- 
testinal capillaries, especially as, in the course of icterus, haemorrhages 
also occur in other parts, particularly in the skin, as petechiae. We 
have repeatedly said that the inclination to bleeding, the so-called 
haemorrhagic diathesis, can only be explained by disturbed nutrition 
of the walls of the vessels, and that the latter very frequently occurs in 
advanced anaemia and cachexia. 
The occurrence of severe disturbances in the nervous system during 
an attack of jaundice is far more dangerous. These rarely begin with 
delirium or convulsions; they are rather apt to commence with para- 
lytic symptoms. The patients are insuperably sleepy, finally become 
soporose, and die in tjiis state. Henoch calls attention to the fact that 
Hippocrates had recognized the bad prognostic indication of this sign, 
for he says, Ex morbo regio fatuitas aut stupiditas mala est. The 
most varied hypotheses have been started about the occurrence of these 
brain and nervous symptoms. Recently the inclination has been 
mostly toward the view that these symptoms depend on poisoning by 
the bile-acids, for, on injecting these into the blood of animals, we ob- 
serve symptoms of poisoning indicative of paralysis of the nervous 
system. To this it is objected that the bile-acids exist in the blood in 684 
DISEASES OF THE LIVER. 
every case of icterus, while these severe nervous affections are very 
rare. Leyden attempts to meet this objection by calling attention to 
the fact that the severest symptoms are avoided by the continued 
excretion of the bile-acids through the kidneys, which prevents their 
excessive collection in the blood. The correctness of this explanation 
appears to be supported by the fact that a remarkable fatigue is 
scarcely ever absent, no matter how slight the jaundice, as well as the 
fact that a diminution of the secretion of urine has been always con- 
sidered as having a bad effect on the course of jaundice. On the 
other hand, it is opposed by the fact that, in haematogenous icterus, in 
which, as Leyden very particularly notices, no bile-acids can be discov- 
ered in the urine, the same severe nervous difficulties are observed 
even more frequently than in hepatogenous icterus. I do not consider 
the question as settled. The proportionately frequent occurrence of 
severe disturbances of innervation in cases where there is only a slight 
amount of icterus, but a severe and extensive degeneration of the liver, 
may be far more readily explained by the hypothesis of Frerichs, 
already alluded to, than by the equally hypothetical poisoning by the 
bile-acids. Moreover, the assertion, that the excessive collection of bile- 
acids in the blood and in the tissues is avoided by their continued ex- 
cretion through the kidneys, is opposed by the fact that the excessive 
collection of the bile-pigment is not prevented by its continued and 
plentiful excretion through those organs. If the affair were as simple 
as Leyden suggests, the frequency of the occurrence of symptoms of 
poisoning -would still be in some proportion to the intensity of the 
icterus, which is not the case, as is well known. 
In slight grades of biliary obstruction, physical examination does 
not show any enlargement of the liver. In higher grades, on the 
contrary, such as those due to complete closure of the ductus liepaticus 
or clioledochus, we may often recognize very decided enlargement of 
the liver by palpation and percussion. • Its surface appears smooth, 
and as the consistence is increased the lower border is very distinct. 
If the ductus clioledochus be closed, we may generally feel the dis- 
tended gall-bladder as well as the liver-tumor. If the liver-dulness 
diminish without decrease of the icterus, it is a bad sign, for it indi- 
cates consecutive atrophy of the liver. 
Treatment.—We can only treat those cases of biliary obstruction 
successfully where we are in a position to fulfil the causal indications. 
Hence we are powerless against the cases caused by most hepatic dis- 
eases, such as echinococcus, carcinoma, or cirrhosis, while we are some- 
times successful in treating those cases due to obstructions in the bile- 
ducts. The remedies vaunted as specifics in icterus are such as have a 
favorable effect on the diseases of the bile-ducts; we shall speak of them JAUNDICE. 
685 
in the next section. This is particularly true of the Karlsbad springs, 
which have a world-wide reputation for their efficacy in jaundice. 
Many patients, who have gone to Karlsbad with the most intense 
jaundice, return cured in a few weeks; but these are only persons 
whose icterus depended on catarrh of the bile-ducts, or on their ob- 
struction by gall-stones. If jaundiced patients, with an incurable ob- 
struction of the bile-ducts, go to Karlsbad, their jaundice is not im- 
proved by the use of the waters; blit they die sooner than they other- 
wise would, because the symptoms of congestion are increased, and 
the destruction of the liver-cells is hastened by the augmented secre- 
tion. This assertion is well supported by cases. The internal use of 
nitrate of potash, calomel, of the bitter and soluble extracts, of emetics 
and purgatives, does just as little good as the Karlsbad waters in 
icterus, unless it fulfil the causal indications. 
When we succeed in removing the obstacle to the excretion of bile, 
the indications from the disease do not require any thing further; 
when we cannot succeed, they cannot be fulfilled. 
The symptomatic indications require, first of all, an improvement of 
the depressed state of the patient by a proper diet. We should order 
meats, particularly cold meats and strong soups ; but as fat is not ab- 
sorbed when the bile does not enter the intestines, and consequently 
is not well borne, the use of gravies, butter, etc., should be just as 
strictly forbidden, while the patients remain at home, as when they go 
to Karlsbad, where, according to the diet list, the use of these articles 
is very reprehensible. In the next place, we should particularly attend 
to the constipation, from which most patients with jaundice suffer, and 
which depends partly on dryness of the fasces, partly on absence of 
irritation of the intestinal mucous membrane from the bile; but we 
should avoid saline laxatives, using instead slight drastics, such as in- 
fusion of senna, lenitive electuary, and rhubarb and aloes. As quan- 
tities of bile-pigment are evacuated with the urine, we may attempt to 
hasten the disappearance of the icterus by prescribing diuretics, such 
as bitartrate of potash, soluble cream of tartar, acetate and carbonate 
of potash. These are urgently indicated when the amount of urine 
is diminished, as the obstruction of the uriniferous tubules, to which 
Frerichs has called attention, may cause a retention of the con- 
stituents of the urine, and it is possible that the obstructions may be 
washed away by an increased secretion of urine. When the biliary 
obstruction has been removed, we may advise lukewarm baths, steam, 
soap-and-potash baths, to cause a more rapid removal of the epidermis, 
and thus relieve, as quickly as possible, the annoying itching and the 
jaundiced color. 686 
DISEASES OF THE LIVER 
CHAPTER XIII. 
ICTERUS WITHOUT REABSORPTION OF BILE—HEMATOGENOUS ICTERUS. 
Etiology.—Physicians have long observed that there are cases of 
jaundice that cannot be referred to retention and reabsorption of bile. 
The supposition, that in severe and extensive degenerations of the 
liver the constituents of the bile collect in the blood, because they are 
not excreted by the affected organ, is completely refuted by the reli- 
able observation that the bile and its constituents are not formed in 
the blood and simply excreted by the liver, but that the bile is first 
formed by the liver. 
The attempt also to refer some cases of jaundice to spasm of the 
excretory bile-duct, because no obstruction to the excretion of the bile 
could be found on autopsy, may be regarded as a failure. As the ex- 
cretory bile-ducts contain muscular elements, it is of course possible 
that they may be temporarily closed by spasmodic contraction, but it 
is excessively improbable that such a spasm would continue so long, 
as physiological experiments prove is necessary, as to induce the grade 
of biliary obstruction requisite for the passage of bile from the bile- 
ducts into the blood-vessels and lymphatics, and the production of 
icterus. The occurrence of icterus spasticus is more than doubtful. 
Lastly, it is also very improbable that, under certain circumstances, 
more bile is prepared than the bile-ducts can accommodate, and that 
icterus is induced because part of the excess of bile enters the blood- 
vessels and lymphatics. 
Frerichs has advanced a new hypothesis for the explanation of this 
form of jaundice: he considers it probable that a filtration of bile from 
the bile-ducts into the blood-vessels results not only from an overfill- 
ing of the bile-ducts, but from too little fulness of the blood-vessels. 
The icterus not unfrequently seen with thrombus of the portal vein is 
explained thus: blood is supplied to the liver only by the hepatic 
artery, and thus the hepatic vein and capillaries are not so well filled; 
some cases of icterus neonatorum are explained by the sudden cessa- 
tion of the supply of blood to the liver through the umbilical vein, and 
the icterus in yellow fever because the roots of the portal vein are 
emptied by the large intestinal hemorrhages. 
The views regarding the occurrence of jaundice without retention 
and reabsorption of bile have totally changed since the observations of 
Virchow, Kuline, and Iloppe-Seyler have shown that bile-coloring 
matter may be formed from the free coloring matter of the blood with- 
out the action of the liver; and wTe may induce artificial jaundice in 
animals, by injecting substances that dissolve the blood-corpuscles. ICTERUS WITHOUT RE ABSORPTION OF BILE. 
687 
There is now no doubt that some of the formerly enigmatical forms 
of icterus are due to the disintegration of blood-corpuscles, and the 
transformation of the freed coloring matter circulating in the blood 
into bile-coloring matter. This is particularly true of those cases of 
icterus occasionally caused by poisoning from chloroform or ether; for, 
as experiment proves, these substances possess the power of dissolving 
blood-corpuscles. The slight icterus in excessive hydrsemia also 
doubtless depends on the fact that blood-corpuscles are destroyed by 
a large amount of water in the blood. 
This mode of origin is very probable, although not absolutely 
proved for other varieties of jaundice—as in that occurring after snake- 
bites, in that observed constantly in yellow fever, quite often in recur- 
rent fever, septicaemia, and puerperal fever, and more rarely in other 
infectious and acute febrile diseases. It is a very interesting fact that 
in the latter diseases even the older physicians suspected a dissolutio 
sanguinis when they ran a pernicious course, when the fever was very 
high, when there was great prostration, and when severe nervous 
symptoms, jaundice of the skin and conjunctiva, appeared. We will 
not discuss the question as to whether the disintegration of the blood- 
corpuscles in the above diseases is the result of the high temperature, 
or whether in high fever products form from the excessive transforma- 
tion of tissue which dissolves the blood-corpuscles, but I must repeat 
my former assertion that every hepatogenous icterus leads to a hema- 
togenous one through absorption of the biliary acids. 
The jaundice in pylephlebitis also, and even some of the cases 
where it occurs with abscess of the liver, belong to the hsematogenous 
form. A short time since I had the opportunity of observing a patient 
with a large abscess of the liver, who suffered from symptoms of jaun- 
dice as long as an intense fever, with very typical intermittent course 
and severe chills, lasted. When the fever ceased, the bile-coloring 
matter, and the albumen that had occurred coincidently in the urine 
disappeared, and the jaundiced hue of the skin and conjunctiva were 
soon lost. The jaundice which, as previously stated, occasionally oc- 
curs with ulcerative endo-carditis appears also to be hsematogenous, but 
I doubt if icterus neonatorum ever belongs here. 
Lastly, I must repeat my former opinion that every hepatogenous 
icterus, resulting from reabsorption of the bile acids, leads to a luema- 
togenous icterus. 
Anatomical Appearances.—Jaundice that is not due to reten- 
tion and reabsorption of bile rarely reaches a high grade; on autopsy 
we usually tind only a faint yellow color of the outer coat of fat and 
of the other tissues. A more important point in the post-mortem 688 
DISEASES OF TIIE LIVER. 
diagnosis of liaematogenous icterus, and for distinguishing it from the 
hepatogenous, is the circumstance that in the former the liver is not 
strongly jaundiced, while in the latter the signs in the liver of reab- 
sorption of bile are always the most prominent. The normal color of 
the contents of the intestines, particularly the greenish hue of the con- 
tents of the duodenum, as well as the positive observation that the 
bile-ducts and excretory passages are quite pervious, leaves no doubt 
that it is a case of liaematogenous icterus. But, in judging of the per- 
viousness of the bile-ducts, we must guard against mistakes. The fact, 
that by pressing on the gall-bladder we may press a few drops of bile 
from the ductus choledochus into the duodenum, does not at all prove 
that during life this passage was perfectly free; on the contrary, this 
may be done where, from the presence of a gray plug of mucus and 
epithelium, in the intestinal portion of the ductus choledochus, we may 
be quite certain that there was catarrh of the duct, and a hepatogenous 
icterus. Buhl and Liebermeister have the credit of first calling- 
attention to the changes found in the liver and other organs in haema- 
togenous icterus. According to Liebermeister, the changes in the 
liver-cells and in the epithelium of the uriniferous tubules consist 
“ in an excessive collection of small and fine fat globules, or else only 
of cloudy, probably albuminous substance in them; ” in other cases, 
“ the cells have fallen into detritus and numerous fat globules have 
appeared; analogous changes also occur in the substance of the heart.” 
These parenchymatous degenerations (Liebermeister) of the liver, 
kidneys, and heart, show that, under the influence of the same injurious 
causes that induce a disintegration of the blood-corpuscles (that is, a 
parenchymatous degeneration of the blood), the firm tissues of the 
body may be affected in the same way. 
Symptoms and Couese.—As we have already shown, liaemato- 
genous icterus is only one symptom of extended disturbances. Hence 
we cannot well give an exact description of its symptoms and course, 
and wTe must confine ourselves to calling attention to those points 
which, occurring in icterus, show that it is not due to reabsorption of 
retained bile, but to a transformation of the coloring matter of the 
blood into that of the bile in the circulation. 
Attention to the etiology aids us greatly. If icterus occurs after 
the action of the injurious influences mentioned in the first part of this 
chapter, or in the course of some of the diseases there mentioned, the 
presumption is that the case is one of liaematogenous icterus. This 
supposition is strongly supported if the faeces appear of a normal or 
very dark color. If, with the commencement of the symptoms of jaun- 
dice, the beat of the heart and pulse become irregular and intermittent; 
if, along with the coloring matter of the bile, albumen appear in the ACUTE YELLOW ATROPHY OF THE LIVER. 
689 
urine ; and if, besides these symptoms, we have severe disturbances of 
the nervous system, I consider the diagnosis of hhematogenous icterus 
as quite certain. leyden also reckons among its criteria the discolora- 
tion of the urine, which is very slight in proportion to that of the skin, 
and particularly the absence of bile-acids from the urine. If it were 
proved that, even in moderate grades of hepatogenous icterus, the bile- 
acids could be constantly and certainly found, their absence from the 
urine -would, indeed, be a certain criterion of lihematogenous icterus. 
Treatment.—Hhematogenous icterus does not require any par- 
ticular treatment; it disappears as soon as we can remove the original 
disease. But, unfortunately, we are rather powerless in this respect; 
still, in those cases occurring during very intense fever, we may expect 
most from an antipyretic course of treatment. 
CHAPTER XIV. 
Etiology.—In acute yellow atrophy of the liver—a very obscure 
disease, for which we find no analogy—in a short time the liver becomes 
smaller, soft, and pulpy, and, on microscopical examination of the atro- 
phied and softened organ, we find that the liver-cells are mostly de- 
stroyed. 
From the fact that the liver, which has been swollen by continued 
biliary obstruction, occasionally becomes smaller, and softens, and that, 
in this form of atrophy, the liver-cells are also found disintegrated, 
acute yellow atrophy has been referred to obstruction of the bile in 
the finer bile-ducts. But this supposition is opposed, on the one hand, 
by the circumstance that, in acute yellow atrophy of the liver, the gall- 
ducts are found empty, or filled with mucus; and, secondly, that no 
obstruction to the flow of bile can be found in them. 
Other observers take the view that the destruction of the liver-cells 
is, it is true, the result of pressure on them, or on the vessels nourish- 
ing them, and that this pressure is exercised by the distended bile- 
ducts, but that the over-filling and distention of the bile-ducts do not 
depend on stasis of their contents, but on excessive formation of bile, 
on polycholia. But since, neither at the commencement of acute 
yellow atrophy of the liver, nor during its first stages, are there signs 
of increased flow of bile into the intestine, the supposition of excessive 
formation of bile, as the cause of this disease, appears neither proved 
nor probable. 
Most recent pathologists consider acute yellow atrophy of the liver 
as the result of a peculiar form of hepatitis; and, indeed, its acute 
ACUTE YELLOW ATROPHY OP THE LIVER. 690 
DISEASES OF TIIE LIVER. 
course, and the rapid and extensive destruction of the liver-cells, would 
indicate an inflammatory process. Moreover, Frerichs claims to have 
found a free exudation surrounding the lobuli of the liver, in some 
parts of the organ, where the process was not yet far advanced. Leav- 
ing out of the question this interstitial exudation, which is probably 
not constant, acute yellow atrophy of the liver would appear to belong 
to the parenchymatous inflammations, i. e., to those forms of inflam- 
mation where there is no free exudation between the elements of the 
tissue, but where the elements of the parenchyma themselves swell by 
taking up an albuminous substance, and subsequently undergo a com- 
bined molecular and fatty degeneration. Against this view, which was 
advanced by liebermeister, or, at least, first precisely stated by him, 
the most we can say is, that the course of inflammations in other organs, 
particularly in the kidneys, is entirely different, and that there is no 
parenchymatous inflammation in which, in a very short time, while the 
affected organ rapidly becomes smaller and softer, the tissue elements 
are destroyed, as they are in acute yellow atrophy of the liver. 
Whether the destruction of the parenchyma-cells of the liver, in 
acute yellow atrophy, be of inflammatory origin or not, this disease is 
apparently not primary and idiopathic, but the result of a severe con- 
stitutional affection. The supposition that this constitutional disease 
is due to the action of a poisonous, miasmatic substance taken into the 
blood, to an infection, cannot at present be proved, although the occa- 
sional epidemic occurrence of the disease is favorable to such a view. 
The popular comparison of acute yellow atrophy of the liver with the 
fatty liver seen after poisoning by phosphorus, is unsound, and has 
caused many mistakes. In phosphorus-poisoning we have a fatty in- 
filtration / in acute yellow atrophy there is a fatty degeneration of 
the liver-cells: these are decidedly different forms of disease. I con- 
sider the attempt to refer acute yellow atrophy of the liver to poison- 
ing by the bile-acids as a failure. Even the slight grade of the icterus 
existing in most cases refutes the correctness of this hypothesis. It 
must be acknowdedged that the greater or less intensity of the jaundice 
gives the best means of judging whether much or little bile has been 
reabsorbed; for, although we can only determine from this the amount 
of bila-coloring matter that has been reabsorbed, still this gives the 
means for deciding the amount of bile-acids absorbed. It is true, 
Leyden has attempted to explain the frequent absence of symptoms of 
poisoning by the bile-acids in excessive and protracted icterus, by say- 
ing that, in most cases, their collection in the blood is avoided by their 
elimination through the kidneys. But this explanation is very doubtful. 
Daily experience teaches that, in closure of the excretory bile-ducts, in 
spite of large quantities of bile-pigment being steadily thrown out by ACUTE YELLOW ATROPHY OF THE LIVER. 
691 
the kidneys, the icterus increases regularly as long as the bile-ducts 
remain closed. What right have we to suppose that absorption of the 
bile acids into the blood is compensated for by their excretion through 
the kidneys, when it is so evident that this does not occur in the case 
of the coloring matter ? 
The disease is very rare; it never occurs in childhood. It is met 
with more frequently in women than in men, and most frequently 
during pregnancy. It is interesting to note that pregnancy, which 
greatly favors the occurrence of parenchymatous inflammation of the 
kidneys, is undoubtedly accompanied by a predisposition to analogous 
disease of the liver. 
Anatomical Appearances.—In high grades of acute yellow 
atrophy of the liver, the organ is much diminished in bulk,, occasionally 
being less than half its normal size. Its thickness is particularly di- 
minished, so that it appears flattened. Its serous covering is loose, 
often even in folds. The parenchyma is relaxed and flabby, and the 
liver is sunk in against the posterior wall of the abdomen. The organ 
is dull yellow, its consistence diminished, and its acini irrecognizable. 
On microscopical examination, instead of the normal liver-cells, we 
only find detritus masses, fat globules, and pigment granules. In the 
right lobe, where the changes were less advanced, Frcricks found 
“ between the lobules, surrounded by hyperaemic vessels, a dirty gray- 
ish-yellow mass, which separated them. Farther off the hyperaemia 
of the capillaries disappeared, the lobules became smaller and yellow- 
er, and the intervening gray substance was in excess.” The gall-ducts 
and bladder usually contain a scanty mucous secretion. The faeces 
are generally only slightly colored; the contents of the intestines are 
often bloody. The spleen is enlarged in most cases. Ecchymoses 
are frequent, particularly in the peritonaeum and in the gastric and 
intestinal mucous membrane, and not very rarely in the other serous 
membranes and in the skin. In the kidneys, Frerichs not only found 
deposits of pigment in the epithelium, but also fatty degeneration and 
disintegration of the epithelial cells. The same observer found quan- 
tities of leucin in the blood, and in the urine evacuated from the blad- 
der; in the latter there were also tyrosin and a peculiar extractive 
matter. 
Symptoms and Course.—The first stage of the disease has no 
very characteristic symptoms. The patients suffer from loss of appe- 
tite, pressure and fulness in the epigastrium, and other symptoms that 
remind us of gastro-intestinal catarrh. There is also in most, but not 
in all, cases a moderate jaundice, which may excite the suspicion that 
the catarrh of the duodenum has invaded the ductus choledochus. Not 
a single symptom betrays the great danger overhanging the patient. 692 
DISEASES OF THE LIYEE. 
In the second stage the jaundice increases, the region of the liver be- 
comes sensitive to pressure, the patients complain of severe headache, 
become restless, excited, and finally delirious. Occasionally the ex- 
citement extends to the motor nerves, so that there are local or general 
muscular twitchings. But soon, and sometimes without any previous 
symptoms of irritation, the patient is seized with insuperable depres- 
sion and lassitude; he falls into a deep sleep, from which he can at 
first be aroused momentarily, particularly by pressure over the liver, 
but later cannot be awakened at all. Then the previously normal or 
even retarded pulse almost always becomes frequent. The tempera- 
ture rises very high; tongue and gums become dry and covered 
with sordes; the fasces and urine are evacuated involuntarily. The 
collapse increases, the very frequent pulse becomes smaller, there is 
copious perspiration, and, without arousing from his coma, the patient 
usually dies the second day, more rarefy the fourth or fifth day, or 
later. We might be tempted to regard the icterus in acute yellow 
atrophy of the liver as hematogenous, and to explain it by saying 
that the blood-corpuscles are destroyed in the same way as the liver- 
cells by the exciting cause of the disease. But the discoloration of 
the contents of the intestines, although incomplete, and the jaundiced 
appearance of the liver, as compared with the other organs, render the 
correctness of this explanation very questionable. The intensely 
bilious color of the liver shows that the discoloration of the contents 
of the intestines is not due to arrested production of bile, that is, to 
acholia. Nor can the icterus be referred to catarrh of the excretory 
bile-ducts, of which the first symptoms of the disease remind us, for 
neither the gall-bladder nor ducts are distended with bile. I agree 
with Buhl and Bamberger, who refer the obstruction and reabsorption 
of bile to a blocking up of the origin of the bile-ducts by fatty and 
molecular detritus of the liver-cells. It is difficult to explain the brain- 
symptoms, which are the most prominent symptoms of acute yellow 
atrophy of the liver. We have already spoken of our reasons for not 
referring them to poisoning by the bile-acids. Bamberger also says: 
“ So much is certain, the brain-symptoms cannot be regarded as cho- 
lemic, for both the grade and duration of the jaundice are too slight 
for this to be the case.” Since in acute yellow atrophy the liver-cells 
are extensively destroyed, and as in this disease abnormal products of 
destructive assimilation have been found in the urine, there is some 
ground for attributing the brain-symptoms in acholia to poisoning by 
noxious substances, which are formed instead of the normal products 
of the change of tissue. But I do not consider even this explanation 
as proved. It is possible that the same cause may induce both the 
degeneration of the liver and the brain troubles. The hemorrhages ACUTE YELLOW ATROPHY OF THE LITER. 
693 
occurring during the disease are apparently the result of disturbed 
nutrition of the capillary walls, of an acute haemorrhagic diathesis, 
which is also seen to occur in many other severe diseases that affect the 
composition of the blood. Frerichs refers the intestinal haemorrhage, 
and the enlargement of the spleen, partly to compression of the capil- 
laries of the liver. 
Physical examination gives very important results, as it shows very 
rapid decrease of the liver-dulness, the sole pathognomonic symptom 
of acute yellow atrophy of the liver. At first the percussion-sound 
becomes very full in the epigastrium, because the diminution in size be- 
gins in the left lobe of the liver; but often, even after a few days, we 
can find no trace of liver-dulness. The total disappearance of liver- 
dulness is partly due to the relaxed organ shrinking together and be- 
ing pressed against the spine by the inflated intestines. Besides the 
decrease of liver-dulness, the increase of spleen-dulness is important; 
but the enlargement of the spleen is not always so marked that it can 
be made out by physical examination, and sometimes it does not 
occur. 
Treatment.—It is evident that we can say nothing that is re- 
liable and founded on experience, concerning the treatment of a dis- 
ease of which it is doubtful whether it ever ends in recovery. If we 
could distinguish the first stage of this disease from that of catarrhal 
jaundice, we should apply leeches about the anus, cold compresses 
over the right hypochondrium, and give saline laxatives. In the 
second stage, according to all observations made, abstraction of blood 
has an injurious effect on the course of the disease. On the other 
hand, powerful drastics, aloes, extract of colocynth, croton-oil, etc., are 
recommended, particularly by English physicians. While there are 
symptoms of irritation in the nervous system, great excitement, delir- 
ium and subsultus, ice is usually applied to the head ; when paralysis 
occurs, cold douches are given; this treatment, having been found of 
occasional benefit in inflammatory brain affections, has been applied to 
the cases from poisoning. Although almost all comatose patients re- 
vive momentarily during the douche, we cannot count on a permanent 
benefit from it in acute yellow atrophy of the liver. The same is true 
of the internal and external use of irritants, which are recommended 
for the paralytic symptoms ; of the mineral acids given when petechia* 
occur, and of the ice-pills that are prescribed for the severe vomiting, 
and for the gastric and intestinal haemorrhage. SECTION II. 
DISEASES OF TIIE GALE-DUCTS. 
CHAPTER I. 
CATARRH OF THE GALL-DUCTS—ICTERUS CATARRHALIS. 
Etiology.—The larger bile-ducts of the liver, the ductus hepati- 
eus, cysticus, choledochus, and the gall-bladder, are lined with a mucous 
membrane, having cylindrical epithelium and racemose glands. This, 
like other mucous membranes of similar texture, is quite often the seat 
of catarrhal inflammation. The small calibre of the gall-ducts and excre- 
tory passages gives peculiar importance to this otherwise mild disease. 
The narrow canals are easily obstructed by the swelling of their mucous 
membrane, and by collections of mucus, and these are the most frequent 
causes of obstruction and reabsorption of bile. 
In some cases catarrh of the bile-ducts results from excessive liyper- 
Eemia of the liver, in which the mucous membrane of the bile-ducts par- 
ticipates. Thus hypermmia of the parenchyma of the liver and of the 
gall-ducts accompanies the development of cancer of the liver. If this 
reach a high grade, it may lead to catarrh of the bile-ducts, and thus 
to icterus. Too little attention has hitherto been paid to this mode 
of origin of icterus in carcinoma of the liver. Cases of carcinoma of 
the liver occur in which there is not the slightest doubt that the icterus 
depends on this catarrh of the bile-ducts. If the jaundice be only tem- 
porary, and the feces are more or less discolored as long as the jaun- 
dice lasts, and are again normally colored when it disappears, we can- 
not refer the jaundice to compression of the bile-ducts or excretory 
passages by a cancerous tumor, but must refer it to a cause that comes 
and goes, or at least increases and diminishes. We have such a cause 
in the liyperaemia which is present in all organs in the vicinity of new 
formations, particularly of carcinoma, and which occasionally becomes 
excessive, and at other times diminishes. The same is true of the 
temporary icterus in multilocular echinococci, and in many of the cases CATARRH OF THE GALL-DUCTS—ICTERUS CATARRIIALIS. 
695 
accompanying heart-disease, emphysema of the lungs, and other dis- 
eases which impede the escape of blood from the liver. We shall 
speak in a separate chapter of the intense catarrh caused by gall- 
stones, as they readily induce ulceration, and then lead to severe and 
peculiar symptoms. Lastly, perhaps the irritation from abnormal bile 
may induce catarrh of the bile-ducts; but this has never been proved, 
and is very problematical. 
By far the most frequent cause of catarrh of the bile-passages is 
the propagation of the catarrhal inflammation about the opening of 
the ductus clioledochus into the duodenum. This duodenal catarrh is 
almost always accompanied by gastric catarrh, and hence the jaundice 
caused by it is usually called gastro-duodenal jaundice, or icterus sim- 
plex, on account of its frequency, freedom from danger, and its mild 
course. The gastric and duodenal catarrh which extends to the gall- 
ducts may arise from the most various causes, and for the etiology of 
gastro-duodenal jaundice we refer to what has been said of the etiology 
of gastric and intestinal catarrh. 
Anatomical Appearances.—In acute catarrhal inflammation the 
mucous membrane of the gall-ducts is reddened, relaxed, and swollen. 
Its surface is covered with mucous and epithelial masses. If the swell- 
ing of the mucous membrane be considerable, the ductus choledochus 
becomes impassable, particularly that part which traverses the wall of 
the duodenum transversely, running for some lines between the layers 
of the wall (the “ portio intestinalis ”), while the bile-ducts in the liver 
are dilated, and filled with bile containing more or less mucus. The 
parenchyma of the liver also shows the previously-described characters 
of moderate biliary obstruction. After the catarrh has lasted some 
time, the redness of the mucous membrane subsides, but its swelling 
and hypertrophy, together with a plug of mucus and epithelium, form 
an insuperable obstacle to the flow of bile. In such cases the bile- 
ducts are often enormously dilated, and the enlarged liver shows the 
signs of great biliary obstruction. The dilatation and distention with 
bile often commence in the ductus choledochus immediately above the 
obstructed portio intestinalis. (For the state of the gall-bladder in 
contraction or closure of the excretory bile-ducts, see Chapter III.) 
Symptoms and Course.—In most cases catarrh of the bile-ducts is 
readily recognized by the symptoms of obstruction and reabsorption 
of bile. When these appear gradually, and increase slowly, our sus- 
picions should first be directed toward catarrh of the bile-ducts, be- 
cause catarrhal jaundice is so frequent, as compared with other forms 
of the disease. But this is scarcely ever a primary affection ; it almost 
always accompanies catarrh of the gastric and intestinal mucous mem- 
brane ; hence it is almost characteristic of catarrh of the bile-ducts, 696 
DISEASES OF THE GALL-DUCTS. 
that symptoms of gastric and intestinal catarrh precede the jaundice 
for days, or even weeks, and continue while the disease lasts. In this 
sense, we may consider the coated tongue, bad taste, eructations, and 
other dyspeptic symptoms, as among the premonitions and symptoms 
of catarrhal jaundice. The longer the catarrh of the bile-ducts con- 
tinues, and the more completely the excretory duct is closed by it, the 
greater will be the discoloration of the feces, and the more intense the 
jaundiced color of the skin and urine, and the more the general health 
and nutrition of the patient will suffer. The liver appears distinctly 
swollen in many cases, and in some of them it is considerably en- 
larged. 
If the disease run a favorable course, the improvement shows itself 
in a week or two, by a return of appetite, by the tongue cleaning off, 
and by decrease of the dyspeptic symptoms. Then we may hope that 
the catarrh of the bile-ducts will subside with the gastro-duodenal 
catarrh, and in fact, after a few days, the returning color of the feces 
shows that the ductus choledochus is open, and the clearer color of the 
urine indicates that the biliary obstruction is less, and that less bile is 
reabsorbed. The bile-pigment deposited in the rete Malpighii disap- 
pears more slowly. After the feces are strongly colored with bile, 
and the urine has regained its normal tint, the skin remains jaundiced 
for a time, and finally this last symptom of the disease disappears. In 
other cases the catarrh of the bile-ducts, as well as that of the stomach 
and duodenum, becomes chronic. The disease drags on for weeks or 
months, the jaundice becomes excessive, the patients emaciate de- 
cidedly, and the liver enlarges considerably. But these cases also 
almost always terminate in recovery, particularly under proper and 
energetic treatment; and the biliary obstruction caused by catarrh of 
the ducts very rarely runs an unfavorable course with the symptoms 
before described. 
Treatment.—Experience teaches that catarrh of the bile-ducts 
rapidly disappears when the catarrh of the intestinal mucous mem- 
brane, which has attacked the gall-ducts, subsides. Hence the causal 
indications require the same measures that we have recommended in 
the treatment of gastric and intestinal catarrh. Under the circum- 
stances there mentioned, an emetic may be indicated; in other cases 
diaphoretics, in still others, careful regulation of the diet suffices. We 
shall not repeat in detail what we have previously said, but only call 
attention again to the excellent effect in gastric and intestinal catarrh 
of the carbonates of the alkalies, particularly as existing in the Karls- 
bad and Marienbad waters. While we have denied all direct influence 
of the Karlsbad waters on biliary obstruction and jaundice, still there 
is no better treatment for most patients than the use of these waters. CROUPOUS AND DIPHTHERITIC INFLAMMATION. 
697 
because in the majority of cases none better fulfils the causal indica- 
tions. If the circumstances of the patient do not allow of his being 
sent to a watering-place, we may let him use the “ Karlsbad diet ” at 
home, and order soda-water or artificial Marienbad or Karlsbad water. 
From this treatment alone we shall see the most favorable and speedy 
results in catarrhal jaundice. 
In some cases the indications from the disease may be fulfilled by 
the administration of an emetic. During the act of vomiting, the bile 
is forced out of the gall-ducts and bladder, toward the mouth of the 
ductus choledochus, and an obstructing plug of mucus may thus be 
pressed out of the latter. We might give emetics far more frequently, 
if the obstruction of the ductus choledochus were not more frequently 
caused by the swelling of the mucous membrane than by mucous 
plugs, and if we did not fear that the untimely use of an emetic 
might render worse the gastro-intestinal catarrh. Nitro-muriatic acid 
has a great reputation in the treatment of catarrhal jaundice; it is 
used externally, in the form of foot-baths ( § ss—j. to a foot-bath) and 
as fomentations over the liver, or internally ( 3 ss—j. to 3 vj. of muci- 
lage, a tablespoonful every two hours). The internal administration 
might possibly have a favorable influence on the intestinal catarrh; 
perhaps it might also excite contractions in the excretory bile-ducts, 
and thus cause the expulsion of obstructing coagula. The external 
use of aqua regia would scarcely be of any benefit. The action of the 
drastics is explained by the effect they have of increasing the peristaltic 
action of the intestines, which extends to the ductus choledochus. 
But generally these have no favorable influence on the catarrhal jaun- 
dice, for which they are given so much. The exhibition of calomel 
(gr. j every evening), and of the Vienna decoction (two tablespoon- 
fuls every morning), according to the so-called English method, is ob- 
jectionable, although many patients with catarrhal jaundice recover 
in spite of this treatment. Slight laxatives are only advisable when 
there is obstinate constipation. Then we may use some one of the 
tartrates, particularly tartrate of potash, or a decoction of tamarinds 
( 3 j—ij to § vj—viij) with acid, tartar. (3 j— 3 ss.) and syrup, sennce c. 
mannae; or we may prescribe infusum sennas compositum or lenitive 
electuary. 
CHAPTER II. 
CROUPOUS AND DIPHTHERITIC INFLAMMATION OF THIS GALL-DUCTS. 
Inflammations of the gall-ducts with fibrinous exudations are ex 
ceedingly rare, and when they do occur it is only in the course of 
severe diseases, such as protracted typhus, septicaemia, cholera, etc. 698 
DISEASES OF THE GALL-DUCTS. 
In croupous inflammation, we find the mucous membrane of the gall- 
bladder covered with a more or less firm false membrane, and in the 
ducts we find tubular coagulations, enclosing inspissated bile, and caus- 
ing biliary obstruction. In diphtheritic inflammation, the tissue of the 
mucous membrane is infiltrated at certain places with a fibrinous exuda- 
tion, which causes sloughing of the mucous membrane, and from sepa- 
ration of the slough deep losses of substance occur. These processes 
cannot be recognized during life. Even an intense icterus occurring 
during typhus, septicaemia, cholera, etc., cannot be referred to a 
croupous or diphtheritic inflammation of the bile-ducts, as it far more 
frequently occurs without any perceptible change in them. 
CHAPTER III. 
OBSTRUCTION AND CLOSURE OF THE EXCRETORY GALL-DUCT AND CON- 
SECUTIVE DILATATION OF THE BILE-DUCTS. 
Etiology.—The excretory gall-ducts are most frequently con- 
tracted and closed by catarrhal swelling of their mucous membrane 
and by collection of mucus. Among the further causes of this contrac- 
tion and closure, and of consecutive dilatation of the bile-ducts above 
the contraction, are: 1. Tumors pressing on the excretory ducts, or 
growing into them. Sometimes they are caused by carcinoma of the 
liver, pancreas, stomach, or duodenum; sometimes by caseous or other 
degeneration of the lymphatic glands ; sometimes by abscesses; rarely 
by hydatid cysts, aneurisms, or collections of hard faeces in the colon ; 
and lastly, in a few cases, by multilocular echinococci, that have wan- 
dered into the gall-ducts or broken through into them, and have thence 
reached the ductus hepaticus. 2. Occasionally there is a more or less 
complete closure of the ductus choledochus, hepaticus, or cysticus, from 
cicatricial contractions, which remain in the excretory bile-ducts, or in 
the duodenum after ulcers have healed, or the thickening and consecu- 
tive atrophy of the peritonaeum after peritonitis, particularly when the 
excretory bile-ducts are at the same time distorted or bent. 3. Lastly, 
foreign bodies, particularly stony concretions, obstruct or close the 
excretory bile-ducts. 
When the ductus hepaticus is constricted or closed, the consecutive 
dilatation of the gall-passages is limited to the bile-ducts of the liver. 
But if the ductus choledochus becomes impervious, the ductus hepati- 
cus, cysticus, and the gall-bladder, are all dilated. Finally, if the duc- 
tus cysticus alone be closed, no bile can enter the gall-bladder, it is 
true, but its mucous membrane continues to secrete mucus, and the DILATATION OF THE BILE-DUCTS. 
699 
gall-bladder becomes more 'and more distended by tlie secretion. This 
state is called hydrops vesica} fellece. 
Anatomical Appearances.—According as one or other of the 
above causes prevails, the anatomical appearances vary so greatly, 
except in the general effect of the constriction or closure of the excre- 
tory bile-ducts, that we shall refrain from giving a detailed description 
of them. If its mouth be entirely closed, the ductus choledochus may 
attain the size of the small intestine, and the dilatation extends through 
the ductus hepaticus and its branches to the capillary gall-ducts. The 
gall-bladder is also dilated, but its dilatation is not in proportion to 
that of the gall-ducts, because, from the acute angle at which it opens, 
it is compressed by the dilating ductus choledochus. The liver shows 
the changes that we have described as characteristic of the highest 
grade of biliary obstruction; it is at first enlarged, and on section the 
dilated gall-ducts look like large cysts filled with bile; subsequently, 
they may become smaller, from atrophy of the liver. In hydrops 
vesicce fellece, the gall-bladder becomes a translucent, tense cyst, as 
large as a fist, or a child’s head even, which contains a serous fluid, re- 
sembling synovia. Its muscular filaments are separated and atrophied, 
the mucous membrane has lost its structure, and has acquired the look 
of a serous membrane. In some cases closure of the cystic duct leads 
to atrophy of the gall-bladder; its mucous and bilious contents become 
inspissated, and changed to a chalky mass, while the walls are thick- 
ened and atrophied by chronic inflammation. Finally, there remains 
only a hard tumor, as large as a pigeon’s egg, filled with a chalky pulp. 
Symptoms and Course.—Contraction and closure of the ductus 
hepaticus and choledochus are characterized by the symptoms of exces- 
sive biliary obstruction, uncomplicated by those of gastro-duodenal 
catarrh, but occasionally accompanied by those of neoplasia or other 
growths in the abdomen, or of chronic peritonitis, or of gall-stones, 
etc. The icterus is more decided, and the faeces more discolored than 
in any other form of biliary obstruction. We usually find the liver 
enlarged, and if the ductus choledochus be closed we also feel the full 
and distended gall-bladder. Later the consecutive dilatation of the 
liver may also be observed. If we find cancerous tumors in the abdo- 
men, if there has been colic from gall-stones, or if any other symptoms 
indicate the variety of the closure, the diagnosis becomes more certain. 
In most cases it is only possible to recognize the closure, without being 
able to make out its cause. 
Hydrops vesicce fellece is readily diagnosed, if it be simple and not 
complicated with obstruction and closure of the ductus hepaticus or 
choledochus. If we find a pear-shaped, movable, occasionally fluctuat- 
ing tumor starting from the incisura vesicas felleae, in a patient who is 700 
DISEASES OF TIIE GALL-DUCTS. 
not jaundiced, we may diagnose closure of’ the cystic duct and disten- 
tion of the gall-bladder by mucous secretion, or hydrops vesicas felleae. 
As it is almost always impossible to remove the cause of the con- 
traction or closure of the bile-ducts, it is impossible to treat them suc- 
cessfully. 
CHAPTER IY. 
GALL-STONES AND TIIEIR CONSEQUENCES CHOLELITHIASIS. 
Etiology.—In spite of numerous works on tliis subject, the origin 
of gall-stones is very obscure. Particles of mucus, or (far more rarely) 
foreign bodies in the gall-passages, appear to play an important part 
in the formation of gall-stones, for they form the nucleus in almost all 
cases, and they at least form the point on which the solid constituents 
of the bile may be deposited. It cannot be decided whether such 
deposits occur when the bile is normal, or only when it is somewhat 
concentrated, or when of abnormal composition. As a combination 
of chalk with bile-pigment is almost always deposited immediately 
around the above-mentioned nucleus, and as this combination almost 
always occurs in greater or less quantities, it is thought that excess 
of chalk in the bile, from drinking lime-water, has something to do 
with the formation of gall-stones. But, besides this, it is probable that 
the bile from which gall-stones, rich in cholesterin, are formed, has only 
a slight solvent power over cholesterin; and as it has been found that 
both cholesterin and biliary coloring matter with lime are dissolved by 
tauro-cliolic acid and tauro-cholate of soda, it was very natural to con- 
sider a lack of tauro-cliolic acid in the bile, or a decomposition of the 
tauro-cholic acid in the gall-bladder, as the possible cause of gall-stones. 
Gall-stones occur more frequently in women than in men, far more 
frequently in old than in young persons; and, without our being able 
to explain why, they are particularly frequent in patients with carci- 
noma of the stomach or liver. Perhaps this is somewhat due to the 
catarrh of the bile-passages, which, as we said in Chapter I., often ac- 
companies carcinoma of the liver. 
Anatomical Appearances.—The size of gall-stones varies from 
that of a hemp-seed to that of a hen’s egg. The smallest concrements 
are distinguished from gall-stones proper by the name of “ biliary sedi- 
ment.” Most frequently there is only one calculus, in other cases 
there are a great number of them. Solitary stones are usually round 
or egg-shaped, or they have exactly the shape of the gall-bladder. 
Their surface is sometimes smooth, sometimes more rough and glandu- 
lar. If there are several stones, they have almost always become 
smoothed on the sides that touch, and have a polyhedral form, with GALL-STONES AND THEIR CONSEQUENCES—CHOLELITHIASIS. 
701 
edges, corners, and smooth surfaces, or they have convex and concave 
facettes, which give them a peculiar appearance. Biliary calculi have 
a low specific gravity; when recently removed, they may be mashed 
by the fingers; when dried, they usually split, and finally break down 
into dust. Biliary calculi vary greatly in color; some are whitish, or 
pale yellow, from slight imbibition of bile, others are dark brown, 
and others still are greenish or blackish. They often consist of va- 
rious layers, and light-colored strata may alternate with dark ones. 
Calculi, consisting chiefly of cholesterin, have a marked, striated crys- 
talline structure, while those that contain chiefly biliary coloring mat- 
ter with lime have an earthy fracture. Most biliary calculi are chemi- 
cally composed of cholesterin, and have a small amount of biliverdine 
only about their nucleus; others consist of a mixture of cholesterin 
and biliverdine; the latter is sometimes distributed regularly through 
the mass, sometimes there are alternate layers of cholesterin and of 
the coloring matter of the bile with lime. We rarely meet calculi con- 
taining no cholesterin, but composed of bile-pigment and lime, or of 
carbonate and phosphate of lime (Lehmann). 
In most cases no structural changes can be discovered in the coats 
of the gall-bladder, even when it contains numerous calculi with sharp 
edges. But occasionally, particularly in the fundus of the bladder, 
we find a considerable injection and puffing of the mucous membrane, 
or there is an ulcerative loss of substance of variable size and depth. 
The ulceration may lead to perforation of the gall-bladder. If this 
occurs before the wall has become adherent to neighboring parts, the 
contents enter the peritonaeum and cause general peritonitis. If, on 
the other hand, the gall-bladder be perforated after it has formed firm 
adhesions with neighboring parts, there may be communication with 
the intestines or perforation outwardly. In some cases the inflamma- 
tion induced by gall-stones is less destructive. The walls of the blad- 
der are thickened, and, after a while, undergo cicatricial retraction; 
the contents become dry and chalky. And, finally, in such cases we 
find the biliary calculi embedded in a chalky mass, and firmly enclosed 
by the shrunken and atrophied gall-bladder. 
In the gall-ducts of the liver, biliary calculi may excite suppurative 
hepatitis. In the excretory ducts, large calculi either cause ulceration 
and perforation or complete closure of the duct, so that the states de- 
scribed in Chapter III., excessive biliary congestion, or, if the cystic- 
duct be closed, hydrops vesicte felleas result. In some cases the bile- 
ducts are so dilated, by the pressure of the bile from behind, that the 
latter squeezes past the calculi, or that even comparatively large cal- 
culi are forced into the duodenum. 
Symptoms and Course.—On autopsy, large calculi or numerous 702 
DISEASES OF THE GALL-DDCTS. 
small concrements are often found in the gall-bladder, which apparent- 
ly had no effect on the health of the patient during life. We may 
even say that it is exceptional for calculi in the gall-bladder to cause 
trouble, or betray themselves by any definite symptoms. Calculi of 
small size may even pass through the ductus cysticus or choledochus 
without exciting pain or any other symptom. The experiences at 
bathing-places, such as Karlsbad, where the stools are carefully ex- 
amined for gall-stones, afford numerous examples of this. 
Among the morbid processes which gall-stones induce, as above 
stated, we have already described suppurative hepatitis and obstruc- 
tion of the excretory bile-ducts, so that we may here limit ourselves 
to describing the symptoms that arise during the passage of large gall- 
stones through the excretory passages, and, during their impaction 
there, the so-called gall-stone colic, as well as the symptoms of inflam- 
mation and ulceration of the gall-bladder and excretory ducts, which 
are excited by gall-stones in some few cases. 
Gall-stone colic begins unexpectedly and suddenly at the moment 
a concrement passes from the gall-bladder to the ductus cysticus and 
becomes impacted there. The patient is seized with a piercing or 
griping, insupportable pain, which starts from the right hypochondrium 
and spreads over the whole abdomen, often also to the right side of 
the thorax, and even to the right shoulder. The abdominal muscles 
are cramped and very sensitive to pressure; the patients sigh and 
moan, double up, and roll about on the bed or floor. During all this 
there is no fever, but there are a number of other symptoms. The 
pulse becomes small, the skin cool, the face pale and distorted; occa- 
sionally the patient actually faints. In some cases the patients are 
affected with spasmodic trembling or chills; in other cases there are 
convulsions either general or limited to the right half of the body. 
There is most frequently obstinate sympathetic vomiting. After a 
few hours, or in severe cases not till next day, the sufferings of the 
patient are usually moderated, and the general disturbance quieted. 
This remission, during which, however, the patient still suffers severe- 
ly, and still has a small pulse, and pale, cool skin, appears to corre- 
spond to the passage of the concrement from the cystic duct into the 
ductus choledochus, which, except the portio intestinalis, is a somewhat 
wider canal. The symptoms do not change very much till the concre- 
ment has passed the ductus choledochus and entered the duodenum. 
Then the patient is entirely free from pain and uneasiness; the pulse 
rises, the warmth of the skin returns, and the distortion of the counte- 
nance disappears. This passage, from great agony to complete ease, 
often occurs in a very short time, and then the contrast is very strik- 
ing. In other cases the pain does not cease suddenly, but subsides GALLSTONES AND THEIR CONSEQUENCES—CHOLELITHIASIS. 
703 
gradually; this is probably because the irritated nerves of the gall- 
ducts are only gradually quieted, just as, when the eye is irritated by 
a foreign body, it remains irritable for a time after the body has been 
removed. Very rarely gall-stone colic terminates fatally with the 
symptoms of excessive faintness, passing into true palsy. Somewhat 
more frequently it is followed by the symptoms of permanent closure, 
or of inflammation and ulceration of the excretory bile-ducts. 
Jaundice is not by any means a constant symptom of gall-stone 
colic. There can be no obstruction and reabsorption of bile from im- 
paction of the calculus in the cystic duct; and, as we have before 
stated, even a temporary closure of the ductus choledochus does not 
result in icterus. Usually, after the symptoms of impaction have sub- 
sided, there is a slight jaundice, which is very temporary if the impac- 
tion in the ductus choledochus has not continued longf. After reaching 
the duodenum, the calculi are rarely vomited; far more frequently they 
are passed at stool, and this passage is only exceptionally accompanied 
by abdominal pain or muco-bloody diarrhoea. It is almost always 
unnoticed, so that the calculus is only discovered on careful examina- 
tion of the faeces. After the attack has passed, we are often unable 
to find any calculus, even if we place the faeces on a sieve and wash 
them through it. In such cases the probabilities are that the impact- 
ed concrements have gone back from the cystic duct into the gall- 
bladder. 
There are still some dark points in our knowledge of gall-stone 
colic. It is remarkable and unexplained that, in some persons, gall- 
stones do not show any inclination to leave their place in the gall- 
bladder, while in others they very frequently pass through the ducts. 
We are not even clear as to how the calculi are pressed from the gall- 
bladder into the cystic duct, although it is most probable that they are 
floated onward, as it were, by the bile which is driven forward by the 
contractions of the gall-bladder. This view is supported, among other 
things, by the fact that gall-stone colic is particularly liable to occur 
during digestion. Lastly, we would suppose that, during a gall-stone 
colic, we might, from a variation in the intensity of the symptoms, dis- 
tinguish three periods, the first corresponding to the impaction of the 
calculus in the very narrow cystic duct, the second to its passage into 
the somewhat wider ductus choledochus, the third to its impaction 
again in the very narrow portio intestinalis of the ductus choledochus; 
but we usually observe nothing that can be referred to these phases. 
The inflammations and ulcerations caused by gall-stones do not in- 
duce any uneasiness till the peritonseum participates in the inflamma- 
tion ; then we have the above-described symptoms of partial chronic, 
and, occasionally, of acute peritonitis. The seat of the pain over the 704 
DISEASES OF THE GALL-DUCTS. 
gall-bladder, as well as attacks of gall-stone colic that have preceded 
the pain, and, in rare cases, the discovery of a distention and fulness 
of the gall-bladder by calculi (Oppolzer), may excite the suspicion that 
the walls of the gall-bladder are inflamed and ulcerated on account of 
the concrements in it. If the gall-bladder be perforated before it has 
become adherent to the surroundings, we have the symptoms so often 
described, which are almost pathognomonic of the entrance of foreign 
bodies into the peritonaeum, and, in a few days, the patient dies of 
diffuse peritonitis. If the neighboring organs have become adherent 
to the gall-bladder, when this is perforated, the pain is limited to the 
region of the gall-bladder; besides the above symptoms, there is dis- 
turbance of the functions of the bowels, and the symptoms of the dis- 
ease often remain obscure till they are explained by the passage of a 
calculus, which is so large that it could not possibly have passed the 
ductus choledochus. Concrements entering the intestines through an 
abnormal communication between them and the gall-bladder may be 
so large as to pass through the bowels with difficulty, and may give 
rise to the symptoms of obstruction of the intestines. I have a choles- 
terin calculus larger than a pigeon’s egg, which was given to me as an 
intestinal calculus, and which was passed with great pain by a lady, 
“ after repeated attacks of hepatitis.” If the inflamed bladder adhere 
to the anterior wall of the abdomen, we may occasionally feel it as a 
hard circumscribed tumor; subsequently the abdominal walls them- 
selves become inflamed, an abscess forms in them, from which pus, bile, 
and often a great number of gall-stones, may be evacuated. The ab- 
scess does not always open at the part of the wall lying over the gall- 
bladder, but occasionally opens at a distance, after fistulous passages 
have formed in the walls. The fistula rarely closes after one or a few 
concrements have been evacuated; it more frequently lasts for a long 
while or always, constantly or at intervals pouring out bile, and, if 
the cystic duct be closed, a limpid fluid. 
Inflammation and ulceration of the excretory bile-ducts, caused by 
calculi, are preceded by the symptoms of gall-stone colic; but this, 
instead of terminating, as it might, in complete recovery, leaves pain 
in the region of the liver, and great sensitiveness to pressure. When 
the impaction of the calculus, and the consequent inflammation, has 
affected the ductus choledochus, there is also intense icterus, and other 
symptoms of excessive biliary obstruction. Far more rarely, from its 
angular form, the calculus closes the excretory duct incompletely, so 
that small quantities of bile continue to reach the intestine. In such 
cases the fasces are not entirely discolored, and the icterus does not 
become so intense. In this case, also, there may finally be perforation, 
and consequent peritonitis (Andral). But more frequently, the pa- GALL-STONES AND THEIR CONSEQUENCES—CHOLELITHIASIS. 
705 
tients die of the results of biliary obstruction, with the symptoms of 
marasmus, or of acholia. 
Treatment.—We should try to preserve patients, who have had 
one or more attacks of gall-stone colic, from new attacks, and from the 
other consequences of biliary calculi. The more frequently the attacks 
have been repeated, and the more the surfaces, angles, and facettes of 
the calculi passed induce the belief that there are others remaining in 
the gall-bladder, the more imperative are the rules for insuring protec- 
tion. Experience shows that, under the use of the Karlsbad waters, 
immense quantities of gall-stones are evacuated, with proportionately 
little difficulty. The same is true of the use of other alkaline mineral 
waters, of the waters of Vichy, Marienbad, Kissengen, etc. We can- 
not explain this fact. We do not know whether their efficacy depends 
solely on the rich formation of a thin, fluid bile, by which the gall- 
stones are readily washed downward, or whether the bile is rendered 
so strongly alkaline by the use of these waters as to dissolve the color- 
ing matter and lime, or the cholesterin; but we should not delay pre- 
scribing the treatment till its mode of action can be explained. In the 
treatment of the states induced by gall-stones, Durande’s remedy also 
enjoys a great reputation; this consists of ether 3 iij, and oil of tur- 
pentine 3 ij. According to the original prescription, half a drachm of 
this is to be given in the morning, and the dose is gradually increased 
until about a pound of the mixture has been taken. The fact that 
ether and oil of turpentine dissolve biliary calculi placed in them does 
not justify the hope that they will dissolve any concrements in the 
gall-bladder, if they are introduced into the stomach. Hence, if Du- 
randds remedy has a favorable influence on the conditions induced by 
gall-stones, as we must suppose it has, from the recommendations of 
numerous and good observers, this can only take place in some other 
way, which is entirely unknown to us. Recently various substitutes 
for Durande’s remedy, and variations from the original dose, have been 
proposed. There is a popular mixture of oil of turpentine, Sij, with 
spirits of ether, 3 j, which is prescribed, in drop-doses, by lladem,acker 
and his followers, not only for gall-stones, but for all possible liver- 
diseases, whether we know what they are or not. 
In the treatment of gall-stone colic, the bold employment of opium 
deserves the most reliance. We may give twelve drops of laudanum 
or a quarter of a grain of acetate of morphia at a dose, and repeat it 
every hour or two till there is slight narcotism. If the patients vomit, 
so that they cannot retain medicines given by the stomach, we may 
give subcutaneous injections of a strong solution of morphia, or ene- 
mata of laudanum, or let the patient carefully inhale chloroform. Warm 
baths, also, as well as warm narcotic compresses over the liver occa- 706 
DISEASES OF THE GALL-DUCTS. 
sionally, appear to moderate the pain and shorten the attack. If this 
be, nevertheless, protracted, and the region of the liver become very 
sensitive to pressure, we should apply a number of leeches to the right 
hypochondrium; in such cases they appear to have a favorable effect, 
although we cannot understand why. The patient not unfrequently 
becomes so collapsed that, besides the above-mentioned remedies, we 
are obliged to give analeptics. Pieces of ice are most efficacious for 
the severe, and occasionally very obstinate, vomiting. Emetics and 
laxatives, given during the attacks, increase the pain, and, moreover, 
they may prove dangerous. On the contrary, after the attack, we 
should administer mild laxatives for a while, so that any concrements 
in the intestines may be evacuated as soon as possible. 
In inflammations and ulcerations of the bile-passages caused by 
gall-stones, we must limit ourselves to the treatment of symptoms, as 
we are unable to remove the exciting cause. Fluctuating abscesses in 
the abdominal walls should be opened early; any remaining fistuke 
should be treated according to the rules of surgery. Obstructions of 
the intestinal canal by large gall-stones are to be treated as previously 
advised; severe and distressing pain should be relieved by narcotics. DISEASES OF TIIE SPLEEN’. 
CHAPTER I. 
HTPEEJaCA OF THE SPLEEN. 
Etiology.—The variations in the amount of blood in an organ 
may be the more decided, the more yielding its parenchyma and en- 
velope, and the more numerous its vessels, and the thinner their walls. 
The spleen has a very yielding capsule, its numerous vessels have very 
thin walls, and appear to communicate with large cavities within. This 
explains how the spleen may be enormously distended by injections 
of water, or by blowing up, as well as the fact that, during life, the 
amount of blood in it may be very much increased, and it may, conse- 
quently, be very decidedly enlarged. 
The slighter the elasticity of the envelope, and of the walls of the 
vessels of an organ, the slower the disappearance of distention induoed 
by any temporary cause. If we imagine an organ where the envelope 
and the walls of the vessels have no elasticity, it would remain perma- 
nently enlarged, if once distended by a momentary increase of the 
blood flowing in, or by a momentary obstruction to that flowing out; 
just as a wax-tube, that has a fluid passing through it, remains perma- 
nently dilated if we momentarily increase the pressure on its inner 
wall. As the capsule, trabeculae, and walls of the splenic vessels offer 
but little opposition to its enlargement, so also, from their slight elas- 
ticity, they can only slowly remove any enlargement of the organ. If 
the spleen be swollen during a paroxysm of intermittent fever, after 
the subsidence of the paroxysm, it remains enlarged longer than other 
organs that were enlarged at the same time, but which were richer in 
elastic elements, and particularly such as had vessels with more elas- 
ticity than the vessels and cavities of the spleen. We shall hereafter 
show that the decrease of swelling of the spleen is probably caused 
by its contractile elements. 
In the spleen as in other organs we must distinguish two forms of 
hypersemia, fluxion and obstructive engorgement. 708 
DISEASES OF THE SFLEEX. 
Fluxion causes.—1. Splenic enlargements in the acute infectious 
diseases / the enlargement in typhus and intermittent fevers, in the 
acute exanthemata, puerperal fever, septicaemia, etc. We do not know 
whether the increased flow of blood into the spleen in these diseases 
be due to a relaxation of the already yielding tissue of the spleen, or 
to a paralysis of the muscular elements of the walls of the vessels, and 
of the trabeculae. {Jaschkowitz observed that, after dividing the 
branches of the sympathetic going to the spleen, it became very large 
and excessively vascular. If he only divided some of the nerves, the 
hyperaemia was limited to the parts of the spleen supplied by the 
divided nerves.) The manner in which the infected blood may alter 
the elasticity of the tissue of the spleen, or the contractility of its 
muscular elements, is just as obscure. The swelling of the spleen in 
intermittent fever has been explained by saying that, during the chill, 
the circulation on the surface of the body is decidedly disturbed, and, 
on account of the ischaemia of the skin, the internal organs, and among 
these the spleen particularly, are overloaded with blood. But these 
conditions are of only secondary importance, as is proved by the fact 
that the amount of splenic enlargement is not at all in proportion to 
the severity of the chill, that the spleen also enlarges during the hot 
stage, and finally, because enlargement of the spleen occurs from mala- 
rial infection when there is no fever. 2. Fluxion to the spleen occurs 
in anomalies of menstruation ; we might repeat of this form all that 
was said of the occurrence of hyperasmia and hmmorrhage from the 
gastric mucous membrane arising from the same cause. 3. Injuries, 
inflammations, and neoplasia; in the spleen induce fluxions. We may 
best observe this form of hyperaemia in haemorrhagic infarction of the 
spleen (see Chapter IV.). 
There is a physiological engorgement of the spleen a few hours 
after every meal, that is, at the time when the lateral pressure in the 
portal vein is greater from the increased supply of blood coming from 
the filled intestinal veins, and when the flow of blood from the splenic 
vein is obstructed. Abnormal congestion is induced by obstruction 
and closure of the portal vein, such as occur in numerous diseases of 
the liver, as cirrhosis, pylephlebitis, and others. Since most of these 
last a long while, besides the hyperaemia of the spleen, we usually find 
its results which will be spoken of in the next chapter. Engorgement 
of the spleen is far less constant and excessive in heart and lung dis- 
eases, where the Aoav of blood from the vena cava is obstructed, and 
this obstruction extends through the vessels of the liver to those of 
the spleen. It is difficult to explain why, in spite of excessive cyano- 
sis and general dropsy, the spleen often remains of normal size, and 
not very vascular in heart and lung disease. It is even more remark- HYPERAEMIA OF THE SPLEEN. 
709 
able that, in atrophic nutmeg-liver, hyperaemia of the spleen is even 
absent as a rule. 
Anatomical Appearances.—Except in cases where the capsule 
of the spleen is thickened and unyielding, we find the hypertrophied 
organ larger and heavier than a healthy spleen. The increase in size 
and weight may be so great that the organ will have from four to six 
times its normal weight. The normal spleen of a healthy adult is four 
to five inches long, three to four inches wide, and one to one and a half 
inches thick; its weight is about eight ounces. The spleen enlarged 
by hyperaemia maintains its form, its capsule usually appears tense and 
smooth, and where the swelling has somewhat subsided, it is occasion- 
ally relaxed and wrinkled. The consistence of the spleen is dimin- 
ished. This is also true of the enlargement of the spleen occurring in 
malarial diseases, as long as it is recent, and as long as other changes, 
that will be spoken of hereafter, have not occurred. The enlarged 
spleen, found in patients who have died of typhus, puerperal fever, 
septicaemia, etc., is often so soft that, when cut through, the paren- 
chyma flows off like pulp. In judging of the consistence of this tumor, 
we must, however, remember the early decomposition of the bodies. 
The color of the spleen is darker in proportion as the hyperaemia is 
recent and excessive. In the most recent cases and in high grades of 
hyperaemia, the parenchyma often looks like a blackish red-blood 
coagulum, later it appears lighter colored, or from admixture of pig- 
ment is somewhat gray. 
On microscopical examination, we find no foreign elements with 
the normal cells of the spleen pulp, and numerous blood-corpuscles, 
so that we have no right to refer this enlargement of the spleen to a 
process of inflammation and exudation. Acute splenic enlargement 
appears to depend either solely on increase of the blood contained in 
it, and serous infiltration of the tissue, or on a coincident temporary 
increase of the substance of the spleen. 
When the hyperaemia has existed a long time, the increase of the 
pulp of the spleen is unmistakable; it greatly changes the appearance 
and consistence of the organ; the spleen remains permanently en- 
larged, and we have the state called “ chronic spleen tumor ” or hyper- 
trophy of the spleen, which we shall describe in the next chapter. 
Symptoms and Course.—Hyperaemic swelling of the spleen al- 
most always develops without the patient complaining of pain; usually 
he is only sensitive on deep pressure in the left hypochondrium. This 
observation corresponds to the general experience that tension of tis- 
sues which are very expansible causes little pain, while tension of 
membranes, ligaments, etc., which are stretched with difficulty, excites 
severe pain. If, during an intermittent, a typhus or similar state, the 710 
DISEASES OF THE SPLEEN. 
patients of their own accord complain of pain in the region of the 
spleen, it may either be because the capsule of the spleen has become 
thickened and unyielding from former disease, or from the occur- 
rence in the spleen or its capsule of inflammatory processes, which may 
also occur during these affections. 
In most cases there are no other subjective symptoms either, at 
least such as can be certainly referred to hyperaemia of the spleen, and 
not to the original disease. Hence the splenic affection would almost 
always be overlooked if the physician did not know that it very con- 
stantly occurred in certain diseases, and if he did not examine each 
case by palpation and percussion, to find whether any enlargement of 
the organ existed. I will call attention to one symptom of excessive 
hyperaemia of the spleen, which I think can be readily explained, and 
referred to mechanical causes. Experience shows that some patients 
with intermittent fever are very pale and anaemic after a very few 
paroxysms, and that the pallidity of the skin and mucous mem- 
branes disappears in a few days when a few doses of quinine have ar- 
rested the paroxysms. This symptom cannot depend on the rapid con- 
sumption of the blood and its speedy restoration. Although the tem- 
perature rises very high during the paroxysm of the intermittent, and 
we know that high fever is accompanied by decided and rapid con- 
sumption of the blood, still in no other disease where the temperature 
reach'es the same height, and remains there even longer than in inter- 
mittent, does the patient become anaemic in so short a time. On the 
other hand, if a continued and high fever has caused poverty of the 
blood, the symptoms disappear far more slowly than does the paleness 
resulting from a few paroxysms of intermittent fever. My observa- 
tions and those of others, particularly of Griesinger, show that the 
rapidity with which the symptoms of anaemia develop and the grade 
that they attain are in direct proportion to the rapidity with which the 
spleen enlarges, and to the grade that this enlargement reaches; that, 
particularly in children, in whom the spleen usually acquires a propor- 
tionally large size after very few paroxysms, threatening symptoms of 
excessive hyperaemia develop early, but disappear very quickly after 
the arrest of the paroxysms and the subsidence of the tumor. Hence 
it can hardly be doubted that the appearance and disappearance of 
these anaemic symptoms are associated with the occurrence and subsi- 
dence of the hyperaemia of the spleen. It is not probable that the 
excessive anaemia, which develops in a few days in intermittent fever, 
depends on disturbance of the spleen, caused by the hyperaemia, al- 
though, in severe disease of the spleen, the blood is gradually impov- 
erished, apparently from disturbance of the influence of that organ on 
the formation of the blood. On the other hand, although not posi- HYPEROEMIA OF THE SPLEEN. 
711 
tively certain, it is very probable, from what was said above, that the 
overloading of the spleen with blood induces anaemia in the rest of the 
body, and consequently that the pallor of the patient depends less on 
impairment of the quality of the blood than on its abnormal distribu- 
tion. We may compare the effect that overloading of the spleen with 
blood has on the rest of the body, to that induced by a large aneurism 
tilled with blood, or by the overloading of one of the lower extremities 
with blood from the application of Junod's boot. If, after the cessa- 
tion of the intermittent paroxysms, or after the administration of 
quinine, the spleen regains its normal size from its elasticity, or from 
the contraction of the irritable elements of the tissue, the anomalous 
distribution of the blood will cease. This explains how the redness of 
the skin and lips, which has been lost during the intermittent fever, 
may return in a few days. 
The hypenemia of the spleen that occurs in the course of typhus 
and similar diseases usually subsides when they have run their course, 
without leaving any structural change. The case is different where the 
enlargement depends on intermittent or other fluxionary or obstruct- 
ive hypenemia, if it continues for a long time, on account of continued 
action of the exciting cause. In the next chapter we shall attempt to 
prove that so-called hypertrophy of the spleen is a necessary result of 
long-continued hypenemia. In very rare cases hypenemia of the spleen 
proves fatal, from rupture of the distended organ. Tins termination 
has been seen both in paroxysms of intermittent fever, and in typhus 
and cholera. Death results with the symptoms of internal haemor- 
rhage either immediately after the rupture of the spleen, or else not 
for several hours or days. 
Physical examination furnishes the most important, and often the 
sole means, of diagnosis of hypenemia of the spleen. While speaking 
here of the physical signs that occur in hypercemic swelling of the 
spleen, we shall say a few words concerning the physical diagnosis of 
diseases of the spleen in general. 
The upper part of the spleen lies in the hollow of the diaphragm, 
and is covered by the lower border of the left lung; its lower part lies 
in immediate apposition with the wall of the thorax, and normally 
does not quite reach to the angle of the ribs. Percussion is frequently 
the sole means of recognizing an enlargement of the spleen, as that 
organ frequently does not reach below the margin of the ribs even 
when decidedly enlarged. The normal dulness of tne spleen extends 
from the upper margin of the eleventh rib to the ninth rib; anteriorly 
it is bounded by a line drawn from the anterior end of the eleventh 
rib to the nipple; posteriorly the spleen-dulness cannot be defined 
from that of the left kidney. Its greatest thickness is about two 712 
DISEASES OF THE SPLEEN. 
inches. If the spleen enlarges, its dulness partly extends forward and 
downward, and partly, by pushing the diaphragm before it, upward, but 
rarely higher than the fifth rib. If the intestines be distended by gas, 
and the abdominal walls be tense, the dulness extends more upward; 
if the intestines be empty, and the abdominal walls relaxed, it extends 
more anteriorly and downward. The spleen-dulness changes its place 
during respiration, being about an inch lower on deep inspiration, and 
about an inch higher on full expiration. When the patient lies on the 
right side, the spleen-dulness is less ; hence it is well to examine the 
patient in different positions, and, if we wish to determine whether 
the extent of dulness varies from time to time, we should carefully 
note in what position of the patient the previous examination was 
made. 
If tumors of the spleen project below the ribs, and be not too soft, 
we may readily recognize them, and distinguish them from other 
tumors by palpation. While they have only a moderate extent, they 
can often only be felt when the patient inspires deeply ; on expiration, 
they disappear beneath the ribs. When the growth is considerable, 
the swelling gradually extends from the left hypochondrium, obliquely, 
toward the navel. It almost always maintains the characteristic form 
of the spleen, particularly the shallow excavation in the anterior 
rounded edge. The tumor follows the movements of the diaphragm, 
can be readily moved, and changes its position with the position of the 
body. When the spleen is very large, instead of taking an oblique 
direction, it often passes directly dowmward into the pelvis, and, be- 
coming less movable, no longer follows the motions of the diaphragm. 
The spleen-dulness may disappear from the thorax, as a result of 
elongation of the ligament attaching the spleen to the diaphragm, from 
the wTeight and size of the enlarged organ. 
In some cases even inspection shows the enlargement of the spleen 
by a prominence of the left hypochondrium and left half of the abdo- 
men, in which the contours of the spleen are occasionally noticed. 
The spleen enlarged by liyperaemia does not by any means always 
extend below the ribs, and, even when it does, may escape detection 
by palpation if it be very soft. 
If hypernemia of the spleen accompany abdominal typhus, on per- 
cussion we usually find the dulness extending more backward, on ac- 
count of the meteorism of the intestines; if, on the other hand, it ac- 
company an intermittent, the dulness rather extends toward the axilla, 
and occupies the left hypochondrium. 
Treatment.—In accordance with what we have said of its course, 
liyperaemia of the spleen is rarely the object of treatment. If we can 
remove the original disease, it almost always disappears in a short HYPERTROPHY OF THE SPLEEN. 
713 
time without our interference. For those forms that do not sub- 
side spontaneously, particularly for those caused by malaria, we have 
a very effective remedy. If we avoid all exaggeration, and rely on 
trustworthy observations, it still appears probable that, in the whole 
materia medica, there are very few remedies that act certainly 
against any diseases as quinine and the preparations of Peruvian bark 
do in the hyperaemia of the spleen resulting from malaria. We do not 
know whether quinine acts by directly inducing contraction of the 
muscular elements of the spleen, or whether it acts as an antidote to 
the malaria, and, by destroying the cause, arrests its results, or whether 
it removes the hyperaemia of the spleen in some other way; but we 
do know that, if, after the attacks have ceased, the spleen remains en- 
larged or decreases in size very slowly, the disappearance of the swell- 
ing is caused or hastened by giving large doses of quinine. It is cer- 
tain that the effect of quinine on hyperaemia of the spleen cannot be 
solely due to its arresting the fever. 
According to Fleury's observations, the enlarged spleen is reduced 
several centimetres during the application of the cold douche. Fleury 
refers to the observations of Andral and Piorry in support of his as- 
sertions. This procedure deserves attention in treating hyperaemia of 
the spleen, if circumstances permit it. 
CHAPTER II. 
HYPERTROPHY OF THE SPLEEN CHRONIC ENLARGEMENT OF THE 
SPLEEN ANiEMIA ET CACHEXIA SPLENICA. 
Etiology.—I consider the name of hypertrophy of the spleen as 
best suited for that form of enlargement of the organ, where its size 
and weight are increased, without any change in its texture being ob- 
servable. But in the form of enlargement of the spleen under consid- 
eration, the increase of the trabecular tissue is unimportant, as com- 
pared with the far greater increase of the pulp, and the latter forms 
the most important factor in the enlargement. 
With our present knowledge, in most cases we cannot fully an- 
swer the question as to whether the increase of the pulp of the spleen 
be due to excessive formation, a “ hyperplasia” of its cellular ele- 
ments, or to their abnormal accumulation as a result of obstruction 
to their escape. It is almost universally believed that the spaces 
between the trabeculae of the spleen, which contain the pulp, in 
some way communicate with the vessels. If this view is the true one, 
that is, if the blood flows through those spaces, and constantly car- 
ries cellular elements out of them, just as the lymph flowing through 714 
DISEASES OF THE SPLEEN. 
the cells in the lymphatic glands carries cellular elements from them 
into the lymph, it is most probable that, if the stream of blood in the 
spleen is much retarded, the pulp of the spleen must increase, be- 
cause less of its cells are carried into the blood. The increased size 
of the current due to distention of the vessels, and still more to disten- 
tion of the intertrabecular spaces from the hyperaemic swelling, very 
decidedly retards the current of blood in the spleen; and, since long- 
continued hyperaemia of the organ constantly induces hypertrophy, it 
is very probable that this form of hypertrophy of the spleen, at least, 
is due to accumulation of the pulp, and not to its excessive formation. 
When speaking of leucinemia (see appendix to this chapter), 
we shall mention a degeneration of the spleen which cannot be ana- 
tomically distinguished from the one under consideration, but which 
must be separately considered, because the changes it induces in the 
composition of the blood are so peculiar that we must suspect a de- 
cided functional difference. We shall show that in leuchaemia the en- 
largement of the spleen is not due to retention of the cellular ele- 
ments, but to their multiplication. 
Among the different forms of fluxionary hypenemia, those caused 
by malaria most frequently induce hypertrophy of the spleen; and we 
find chronic enlargement of that organ, not only when the malarial in- 
fection assumes the form of an intermittent fever, but also when it 
induces remittent fever, or a chronic disease, without paroxysms. 
Where malaria is endemic, numbers of persons have immense spleens, 
and it even appears as if the largest tumors are found in persons who 
escape regularly recurring paroxysms of fever. 
Among the congestive hypersemias, those caused by cirrhosis of 
the liver and obliteration of the portal vein most frequently result in 
hypertrophy of the spleen, and this is the strongest proof of the cor- 
rectness of the hypothesis that this form of spleen-disease is caused in 
a purely mechanical way, by accumulation of cellular elements, as a 
result of obstructed escape of the blood. 
Recently a number of cases of decided hypertrophy of the spleen, 
occurring without any perceptible cause, have been observed and de- 
scribed. As the anatomical appearances of these “idiopathic” en- 
largements of the spleen appeared to correspond entirely with those of 
leuchaemic spleens, of which we shall hereafter speak, and as the 
symptoms observed during life (except the increase of the colorless 
corpuscles of the blood) were very similar to those of leuchaemia, the 
name of pseudo-leucluemia has been proposed for this disease, while 
other observers designate it as anaemia or cachexia splenica. In the 
so-called pseudo-leucliaemia, besides the affection of the spleen, there is 
almost always an analogous affection of the lymphatic glands, that is, HYPERTROPHY OF THE SPLEEN. 
715 
their decided enlargement depending on simple increase of the normal 
elements. In some cases the spleen is most affected (splenic form), 
in others the lymphatic glands (lymphatic forms). 
Anatomical Appearances.—As a result of hypertrophy, the 
spleen may become so enormous as to measure one foot to a foot and 
a half long, over six inches wide, and oyer four thick. It may attain 
a weight of twelve pounds or more. The form of the enlarged organ 
is not changed; its resistance is increased, so that it occasionally be- 
comes as hard as a board. In recent cases, the color of the paren- 
chyma is dark-brownish red, in older ones it is usually the color of the 
muscles or pale red. If the hypertrophy has resulted from malarial 
affection, the pale, homogeneous, and dry cut surface usually has a 
gray tinge, or we find dark spots in it. In the appendix to this sec- 
tion, when speaking of melanaemia, we shall more particularly describe 
the extensive deposits of pigment which occasionally remain in the 
spleen after pernicious intermittent fever. The capsule of the hyper- 
trophied spleen is usually thickened, cloudy, and not unfrequently ad- 
herent to its surroundings. The thickened and rigid trabecula? of the 
spleen appear as white striae on the cut surface. 
Besides the closely-packed normal elements of the pulp of the spleen 
and interspersed pigment, microscopical examination does not show 
any foreign formations. In the idiopathic as well as in the leuchaemic 
enlargements of the spleen, we not unfrequently find wedge-shaped 
masses similar to the haemorrhagic infarctions to be described in Chap- 
ter IV. 
Symptoms and Course.—While examining a previously healthy 
and fresh-looking person for an acute disease, we not unfrequently find 
a great enlargement of the spleen. Such cases prove either that a 
morbidly-enlarged spleen can fulfil its functions, or that other organs 
may act vicariously for it. In favor of the latter supposition is the 
well-known fact that dogs, from which the spleen has been removed, 
may live a long while, be well nourished, propagate the species, etc. 
The relative or even perfect good health, often found in persons 
with old enlargement of the spleen, is very analogous to the perfect 
health and blooming looks of persons who, for years, have had enlarged 
lymphatic glands in the neck or elsewhere. If we carefully examine 
the history we shall find that when the enlargement of the spleen or 
the swelling of the glands occurred, the patient’s state was not by any 
means so fair as at the time of examination, but that there were at 
that time more or less decided signs of anaemia and cachexia. This 
appearance of anaemic symptoms, at the time of the occurrence of the 
enlargement of the spleen and lymphatic glands in question, and the 
subsequent disappearance of the anaemia, in spite of the continuance of 716 
DISEASES OF THE SPLEEN. 
the tumors, are perfectly in accordance with the doctrine that the spleen 
and lymphatic glands are the places where the blood-corpuscles are 
formed. Apparently the state of affairs is as follows: When the cells 
formed in the intertrabecular spaces of the spleen, or in the cells of 
the lymphatic glands, are retained in any wray, and are not normally 
borne along by the blood and lymph, they accumulate in these places; 
the spleen or the lymphatic glands, as the case may be, swell up and the 
blood becomes poor, as the used-up blood-corpuscles are not replaced 
by others. If the obstruction to the passage of the young cells into 
the circulation be removed, the growth of the spleen and lymphatic 
glands ceases, and the blood is gradually improved by a sufficient sup- 
ply of young cells, even if the enlarged spleen or lymphatic glands do 
not decrease in size. 
If the spleen continues to enlarge for a long time, there is great 
impoverishment of the blood. The patients become excessively dull 
and feeble; their skin grows waxy, and brunettes acquire a clayey look 
(“ splenetic ”). The lips and visible mucous membranes also appear 
very pale and bloodless. Since the number of blood-corpuscles aerated 
in the lungs is diminished, the usual number of inspirations no longer 
suffices to supply the blood with oxygen, and to remove the carbonic 
acid. Hence the patients are short-breathed, and, where bodily ex- 
ertion and similar causes increase the demands for oxygen, they suffer 
from dyspnoea. The nutrition of the walls of the capillaries also 
suffers from the impoverishment of the blood, and they become morbid- 
ly fragile, causing a haemorrhagic diathesis. Capillary haemorrhages 
occur without perceptible cause, apparently spontaneously, particularly 
epistaxis, and we have petechiae from haemorrhages in the tissue of the 
skin. The common assertion, that in disease of the spleen the bleed- 
ing usually proceeds from the left nostril, is false. If the disease con- 
tinues to progress, the anaemia, or more properly the liydraemia, finally 
increases to a so-called dropsical crasis; there is usually oedema of the 
lower extremities, and in severe cases there is gneeral dropsy. 
If the above symptoms be observed in a patient who has enlarge- 
ment of the spleen, as a result of malarial infection, or as a complica- 
tion of cirrhosis of the liver, it may be difficult to decide what part of 
the symptoms is due to the disease of the spleen, and what to the 
original disease; nevertheless, the fact that the grade of the hydrremia, 
both in the malarial infection and in the cirrhosis, has a certain relation 
to the amount of enlargement of the spleen, justifies us in not rating too 
tow the effect of the spleen-disease on the impoverishment of the blood 
even in such cases. This influence is far more striking in cases where 
the enlargement of the spleen is independent of other diseases, and 
occurs as a primary and idiopathic affection. HYPERTROPHY OF THE SPLEEN". 
717 
I would find it difficult to make a distinction between the so-called 
pseudoleucliaemia (a very unsuitable name) and the chronic spleen-dis- 
ease which has been recognized for ages and has frequently been care- 
fully described. Steadily increasing impoverishment of the blood, 
great paleness of the skin and visible mucous membranes, haemorrha- 
gic diathesis, and in severe cases dropsical symptoms, together with 
the enlargement of the spleen which is often decided, form the symp- 
toms of the pretended new disease. These symptoms, which are often 
considered as pathognomonic of spleen-disease, reach a very high grade, 
and finally cause death in idiopathic enlargement of that organ: first, 
because we cannot arrest the enlargement; secondly, because in many 
cases the affection of the spleen is accompanied by a similar disease of 
the lymphatic glands. In most of seven cases of idiopathic enlargement 
of the spleen that have come under my own observation, and have 
been reported by my assistant, Dr. Matter, in the “ Berliner klinischen 
Wochenschrift,” besides the enlargement of the spleen, there was de- 
cided swelling of numerous lymphatic glands. After what we have pre- 
viously said, it cannot appear strange that the simultaneous disease of 
the spleen and of the lymphatic glands, which also participate in the 
formation of the blood-corpuscles, is a very dangerous complication, and 
that it should induce the highest grade of impoverishment of the blood. 
As hypertrophy most frequently causes very great enlargement of 
the spleen, the enlargement may be recognized, on physical examina- 
tion, both by inspection and palpation as well as by percussion. The 
tumor preserves the characteristic form of the sjfleen; its resistance is 
increased, although not so much so as lardaceous spleen, which we 
shall describe in the next chapter. 
Treatment.—Recent hypertrophy of the spleen, resulting from 
malarial infection, calls for the same treatment that was recommended 
in chronic hyperoemia of that organ. Change of residence and the use 
of the preparations of Peruvian bark, particularly of quinine, are exceed- 
ingly useful; but the patient should not return to the malarial region 
too soon, and should perseveringly use the quinine for a long time. 
Even in old cases of hypertrophy we should try the effect of these 
remedies. Of the numerous derivatives recommended for the treatment 
of chronic enlargement of the spleen, the cold douche alone appears 
serviceable, while blistering-plaster, issues, the actual cautery, etc., 
over the spleen, promise but little benefit. The preparations of iron 
are very extensively and very properly used in the treatment of this 
affection; among these, muriate and iodide of iron are particularly 
celebrated. We will not undertake to say whether they have any in- 
fluence in decreasing the size of the spleen, or whether their beneficial 
effect is due to the improvement of the quality of the blood. The effect 718 
DISEASES OF TIIE SPLEEN. 
is best when we combine the preparations of iron with quinine, or if 
we order the use of chalybeate mineral waters in some mountainous 
region, and at the same time let the patient take quinine continually. 
Treatment does no good in hypertrophy of the spleen due to cirrhosis, 
pylephlebitis, etc. 
CHAPTER III. 
LARDACEOUS SPLEEN AMYLOID DEGENERATION OP TIIE SPLEEN. 
Etiology.—In lardaceous spleen the walls of the vessels and the 
cellular elements of the pulp degenerate just as the liver-cells do in 
lardaceous liver. More rarely, in the so-called sago-spleen, the pulp is 
unaffected, the cells and nuclei only undergoing the lardaceous or amy- 
loid degeneration. 
Regarding the etiology of lardaceous spleen, we may refer to what 
was said of the analogous disease of the liver. The dyscrasi® there 
mentioned, scrofula, rachitis, tertiary syphilis, and mercurialism, also 
induce amyloid degeneration of the spleen. Lardaceous spleen only 
exceptionally complicates tuberculosis; on the other hand, it occurs 
quite frequently in malarial diseases, although far more rarely than 
simple hypertrophy. 
Anatomical Appearances.—Amyloid degeneration may cause as 
great enlargement of the spleen as results from the hypertrophy men 
tioned in the last chapter. The lardaceous spleen is very heavy, and 
excessively hard; if we attempt to bend it, we find that, besides being 
hard, it is very friable. The color is usually a pale violet *red; the 
little blood contained in it is watery ; the cut surface is homogeneous, 
smooth, dry, and has a lardaceous, waxy lustre. On microscopical ex- 
amination, we find the cellular elements of the pulp enlarged, of a dull 
color, with pale, homogeneous contents. On adding a solution of 
iodine, the preparation becomes yellowish red, and on a further ad- 
dition of sulphuric acid it becomes violet and blue. 
If the degeneration be limited to the Malpighian bodies, the organ 
is not usually so much enlarged. On incising the spleen, we find 
roundish, gelatinous granulations, resembling swollen sago, scattered 
through the moderately firm parenchyma. Microscopical examination 
show’s that the cells and nuclei of the Malpighian bodies are changed 
in the manner above described for the spleen-pulp. 
Symptoms and Course.—In lardaceous degeneration of the spleen 
also, the patients are very amende and cachectic. Epistaxis, petechias, 
and dropsy, are more frequent than in simple hypertrophy. And in 
this form of enlargement of the spleen it is even more difficult than in 
the preceding ones, to say how far these symptoms depend on the ILEMORRIIAGIC INFARCTION OF THE SPLEEN. 
719 
Driginal disease, and how far on the degeneration of the spleen. More- 
over, besides the lardaceous degeneration of the spleen, there is usuallv 
an analogous affection of the liver and kidneys, which increases the im- 
poverishment of the blood. Physical examination often shows enor- 
mous enlargement of the organ. 
In spite of the similarity of the symptoms, the diagnosis between 
the two forms of chronic enlargement of the spleen is usually easy. 
The occurrence of enlargement of the spleen in the course of one of 
the above-mentioned diseases, coincident disease of the liver and kid- 
neys, steady growth of the tumor, which never recedes, and its un- 
common firmness, speak in favor of lardaceous spleen, and against 
simple hypertrophy. 
Treatment.—Treatment is useless in lardaceous spleen. It is 
true, iodide of iron has a certain reputation, and it is possible that the 
impoverishment of the blood, and the dyscrasia causing the splenic 
disease, may be improved by its use; but, even if this happens, it is 
not probable that the size of the spleen will decrease, or that its struc- 
ture will again become normal. 
CHAPTER IY. 
HAEMORRHAGIC INFARCTION AND INFLAMMATION OF THE SPLEEN— 
SPLENITIS. 
Etiology.—In no organ is haemorrhagic infarction more frequent 
than in the spleen, and in most cases it undoubtedly proceeds from ob- 
struction of a small artery by an embolus. The size of the splenic 
artery and the rapidity with which the blood flows through it (a 
necessary result of the slight obstruction the blood meets in the 
spleen) explain why emboli from the aorta most readily enter the 
splenic artery. The emboli usually originate in the left heart, and 
are fibrinous coagula that have been deposited on rough places on 
the valves, in endocarditis and valvular disease, and have subsequently 
been washed off by the blood. When autopsy reveals extensive 
valvular disease, with roughness or rupture of the valves and chorda1 
tendineae, it is almost a. rarity not to find old or recent infarctions in 
the spleen. Far more rarely the emboli come from necrosed spots in 
the lungs, and have passed through the pulmonary vein and left heart, 
before entering the aorta and splenic artery. 
Haemorrhagic infarctions of the spleen also exceptionally occur in 
those diseases which usually induce only excessive hyperaemia of that 
organ. We find it as well in malarial infection as in typhus, septi- 
caemia, and the acute exanthemata. Jaschkowitz found that, when he 
had divided some of the nerves of the spleen, the pathological changes 720 
DISEASES OF THE SPLEEN". 
usually called haemorrhagic infarctions sometimes occurred in the parts 
of the spleen supplied by the nerves that had been divided. 
As it is doubtful whether the parenchyma of the spleen be nor- 
mally separated from the current of blood by the walls of the vessels, 
it becomes a question whether haemorrhagic infarction be due to an 
escape of blood from the vessels, or whether it be not rather owing to 
a coagulation of the blood in the vessels and in the intertrabecular 
spaces. In the latter case haemorrhagic infarction would represent 
thrombus of those spaces, as it were, and, like other thrombi, would 
be the result of a retardation of the current of blood. 
Primary inflammation of the spleen is an exceedingly rare disease. 
Even injuries are more apt to cause rupture than inflammation of that 
organ. Consecutive inflammation and suppuration of the spleen are 
more frequently induced by haemorrhagic infarctions, particularly by 
those occurring during infectious diseases. If the infarction be a 
primary coagulation in the vessels and in the intertrabecular spaces 
(which is at least as probable as the opposite view), then the splenitis 
would hold the same relation to the infarction that phlebitis does to 
thrombus of the veins. 
Anatomical Appearances.—Haemorrhagic infarctions of the 
spleen are roundish, or more frequently wedge-shaped collections (with 
the bases outwardly) of the size of a pea or a hen’s egg. At first they 
are dark brown, or brownish red, and quite hard. The entire spleen is 
enlarged by fluxionary hyperaemia, the peritonaeum over the infarction 
is freshly inflamed. Later the collections become of a dirty-yellow color, 
starting from the centre. The final result varies: either fatty degen- 
eration occurs, and the mass is reabsorbed, and in place of the infarc- 
tion we have a retracted, callous cicatrix, or else a yellow, cheesy 
mass, which may become calcareous, remains; or, lastly, the infarction 
softens, and there is an abscess filled with detritus, in which pus-cor- 
puscles also appear after a time. The latter course chiefly is taken by 
those cases where small but numerous infarctions occur in typhus and 
similar diseases. 
We know nothing about the anatomical changes in primary splenitis 
before it has induced abscess. Occasionally we find the abscess in- 
capsulated in a proliferation of connective tissue; in other cases it is 
surrounded by disintegrated connective tissue, or the entire spleen, 
except its capsule, has become disintegrated, so that the latter forms a 
large sac, which is filled with pus. Finally the capsule of the spleen 
is perforated, and the contents of the abscess either enter the abdo- 
men, or, if the capsule has previously become adherent to the parts 
around, it enters some neighboring organ. Cases have been reported 
where the pus, from an abscess of the spleen, has entered the stomach, HEMORRHAGIC, infarction of the spleen. 
721 
or colon, or, passing through the diaphragm, has reached the pleural 
sac, or has perforated outwardly, through the abdominal walls. It is 
only in very rare cases that an abscess of the spleen dries up, its con- 
tents becoming inspissated and calcareous, or breaking through the 
capsule, and being evacuated. 
Symptoms and Course.—Where haemorrhagic infarction occurs in 
the course of an infectious disease, it is almost always first recognized 
at the autopsy. On the other hand, where it accompanies heart-disease 
it can often be recognized during life. If endocarditis or valvular dis- 
ease has been diagnosed in a patient, and he complains of pain in the 
left hypochondrium, which is increased by pressure; if there be vomit- 
ing also, and physical examination shows enlargement of the spleen, 
which did not exist a few days previously, we may decide that there is 
haemorrhagic infarction of that organ. The pain is due to the partial 
peritonitis which almost always accompanies the infarction. The vom- 
iting is a sympathetic symptom. And, lastly, the enlargement of the 
spleen is the result of fluxionary hyperaemia. In almost all the cases 
I have seen, the above combination of symptoms commenced with a 
chill, and was accompanied by repeated chills. We have already said 
that these do not justify us in deciding on a septicmmic affection. 
Most cases of abscess of the spleen that have been described have 
been latent, and were not recognized during life. Chills, hectic fever, 
cachectic appearance, rapid emaciation, and dropsical symptoms showed 
that there was some severe disease, but its nature was not discovered. 
If, besides these symptoms, there was pain in the left hypochondrium, 
and enlargement of the spleen could be detected, it was occasionally 
possible to form a probable diagnosis. Distinct fluctuation was very 
rarely found. 
If the abscess perforate the capsule of the spleen, and its contents 
be emptied into the abdomen, we have the symptoms of diffuse peri- 
tonitis ; or, if they have entered a capsulated space, those of a cir- 
cumscribed peritonitis. If its contents enter the stomach or colon, 
mixed blood and pus are vomited or passed at stool. If the perfora- 
tion take place into the pleura, into the lungs, or outwardly, the symp- 
toms are similar to those described for perforation of abscesses of the 
liver in these directions. 
Treatment.—In haemorrhagic infarction, as in suppurative spleni- 
tis, treatment is of no avail. We can only give palliatives for the 
most urgent symptoms. Where the pain is severe, we should order 
local abstraction of blood and cataplasms ; for the sympathetic vomit- 
ing carbonates and bicarbonates of the alkalies, or, if it be very obsti- 
nate, we may give narcotics; fluctuating abscesses should be opened 
early, and with the same precautions as in abscesses of the liver. 722 
DISEASES OF THE SPLEEN. 
CHAPTER V. 
TUBERCULOSIS, CARCINOMA, HYDATIDS OF TIIE SPLEEN. 
Tuberculosis of the spleen occurs, sometimes, under the form of 
numerous gray miliary tubercles, as one part of miliary tuberculosis; 
sometimes it complicates tuberculosis of the intestines and mesenteric 
glands, under the form of yellow, cheesy conglomerations of tubercle, 
which rarely attain the size of a hazel-nut, and only exceptionally 
break down and form vomicae. Tuberculosis of the spleen cannot be 
recognized during life, and hence there can be no question about its 
treatment. 
Carcinoma also is rarely observed in the spleen. Medullary car- 
cinoma is the only one of the various forms that ever occurs here. In 
almost all the cases on record, the disease did not affect the spleen 
primarily, but accompanied carcinoma of the stomach, liver, or retro- 
peritoneal glands. The spleen may acquire an uneven, nodular ap- 
pearance from large cancerous tumors. From the great rarity of car- 
cinoma of the spleen, it should be the last disease thought of when we 
are trying to determine the nature of an enlargement of that organ; 
we should only make the diagnosis of carcinoma of the spleen when 
the enlargement no longer retains the characteristic form of the spleen, 
but has an irregular, nodulated surface, and when there is at the same 
time carcinoma of the stomach or liver. 
Hydatids of various size and number are also seen rarely in the 
spleen, and almost exclusively in cases where they also occur in the 
liver. During life they can only be recognized when hemispherical pro- 
tuberances, with the previously-described peculiarities of hydatid cysts, 
can be felt on the enlarged spleen. APPENDIX TO THE DISEASES OF THE SPLEEN. 
We do not propose to treat of leuchaemia and melanaemia, in the 
second volume, among ‘diseases of the blood, but to class them among 
diseases of the spleen, as they generally depend on affections of that 
organ. But, as there are also cases of leuchaemia, and even some of 
melanaemia, where the blood-affection cannot be referred to disease of 
the spleen, these affections must be described in an appendix. 
CHAPTER I. 
leuchaemia (leucocytiiaEmia—Bennett). 
Etiology.—A temporary increase of the colorless corpuscles of 
the blood takes place in a number of physiological and pathological 
conditions, as, during pregnancy, inflammatory diseases, or after great 
loss of blood. This variation of the blood, from its normal state, is no 
more an independent disease than hyperinosis and hypnosis, anaemia, 
or liydraemia, but it is the result of various states. 
The case is different with leuchaemia. This very interesting dis- 
ease is defined by Virchow as a “ change in the constitution of the 
tissue of the blood,” the blood being classed among the tissues; in it 
white corpuscles are to a great extent formed instead of red ones, so 
that the number of the former increases, while that of the latter dimin- 
ishes. We found our description on the classical work of Virchow, 
who has shown that leuchaemia may depend either on disease of the 
spleen, or of the lymphatic glands, and that there are two forms of 
leuchaemia, the splenic and lymphatic. The changes of the spleen in 
the former, and of the lymphatic glands in the latter, consist chiefly in 
an increase of the cellular elements composing the pulp of the spleen, 
or filling the cells of the lymphatic glands. 
Since in leuchaemia we find the blood loaded with the elements, 
whose accumulation in the spleen and lymphatic glands causes the 
swelling of these organs, it would appear that the leuchasmic tumors 724 
APPENDIX TO THE DISEASES OF THE SPLEEN. 
are due to an increased formation of cellular elements, and not to their 
retention, as we thought was probable in the other forms of enlarged 
spleen and lymph glands. It is a question whether the cells, so plen- 
tifully formed in the spleen and lymphatic glands during leuchoemia, 
differ in any way from those formed under normal circumstances. If 
we could suppose that only the white corpuscles of the blood origi- 
nated from the colorless cells of the lymph and spleen pulp, leuchacmia 
might be regarded as a simple hyperplasia. Although the transfor- 
mation has not been directly observed, still it cannot be doubted that, 
under normal circumstances, the red corpuscles also originate from the 
colorless lymph-corpuscles, and from colorless cells of the spleen-pulp; 
hence, in explaining leuchaemia, where this transformation is much 
limited, we must suppose that the numerously-formed cells do not 
possess the power of becoming red blood-corpuscles. 
In certain cases of this disease, described by Virchow, Friedreich, 
and Bottcher, other oigans also, as the liver, kidneys, intestinal mu- 
cous membrane, and pleura, produced lymphatic elements at circum- 
scribed spots ; so that, as Vircliow says, in these cases there was not 
only a lymphatic dyscrasia, but at the same time a lymphatic dia- 
thesis. 
The etiology of leuchasmia is entirely obscure. The disease is met 
with in both sexes, but more frequently in males than in females; it is 
very rare in childhood. Most cases recorded have affected persons of 
middle age. No connection has been proved between this disease 
and malarial infection, or scrofula. In a few cases the disease ap- 
peared to have a certain relation to menstruation and to the puerperal 
state. 
Anatomical Appearances.—While, in normal blood, there are 
about three hundred and fifty red blood-corpuscles to one white one, 
in leuchaemia the number of white corpuscles may become so much in- 
creased, and that of the red ones so much diminished, that the former 
will become a sixth or even half as many as the latter. In the splenic 
form of the disease the white blood-corpuscles are not distinguishable 
from those of normal blood; they are distinct, -well-developed cells. 
In the lymphatic form, on the other hand, Virclioxo and other observ- 
ers found numerous free nuclei and small cells, both of which corre- 
sponded exactly with the elements found in the lymphatic glands. If 
the spleen and lymphatic glands were diseased at the same time, if 
the spleen-disease prevailed, there were more of the larger, cellular ele- 
ments in the blood; on the other hand, the more extensive the dis- 
ease of the glands, the more numerous were the small lymphatic ele- 
ments. Examinations of leuchaemic blood have shown that its specific 
gravity is much less than that of normal blood: while the latter may be LEU CII /EM 1A—LE UCO C YTILE MIA 
725 
considered as 1055, tliat of leuchcemic blood was found to be from 1036 to 
1049. The diminution of the specific gravity of the serum of the blood 
was slighter and less constant. In the leuch acinic blood the proportion 
of water had increased, while, in spite of the increase of the white 
corpuscles, that of the solid constituents was decreased, as a result of 
the excessive diminution of the red corpuscles. This, together with 
the low specific gravity of the white blood-corpuscles, explains the 
diminution of the specific gravity of the blood as a whole. The albu- 
men, fibrin, and salts of the blood show no decided or constant anom- 
aly The diminution in the amount of iron, which is considerable, is 
explained by the deficiency in red blood-corpuscles. And lastly, in 
leuchacmic blood, Scherer found certain constituents of the splenic 
fluid, such as hypoxanthin, lactic, formic, and acetic acids, and a body 
whose reactions corresponded with those of glutin; however, other con- 
stituents that Scherer has found in the spleen-fluid, particularly uric 
acid, leucin, etc., have not been found in leuchaemic blood. 
On autopsy of persons who have died of leuchaemia in the heart, 
particularly the right one, and in the large blood-vessels, we often find 
yellow or yellowish-green, soft, smeary coagula, like thickened pus. 
In the smaller branches of the pulmonary artery, also, and in the veins 
of the heart and cerebral membranes, discolored puruloid contents have 
occasionally been found. The proportion of white blood-corpuscles 
varies in blood taken from different parts of the body. In that from 
the right heart, vena cava, and pulmonary artery, it is greater than in 
that from the left heart, and, in a case observed by De JPury, it was 
twice as great in the splenic as in the jugular vein. 
In most of the cases of leuchaemia that have been published, the 
spleen was found greatly enlarged; its weight not unfrequently reached 
five to seven pounds, or more. In some cases the resistance of the 
enlarged spleen was increased but little, or not at all; in others (ap- 
parently older cases) it was decidedly greater. There was always 
plenty of spleen-pulp present; the thickened trabeculae formed white 
striae through it. Microscopic examination showed “ the normal ele- 
ments, only they were more closely packed together ” ( Virchow), just 
as in the above-described hypertrophic enlargement of the spleen, with 
which the leuchaemic also agrees in its general appearance. In most 
cases the capsule of the spleen was thickened, and was often adherent 
to the parts around. In many cases, besides the hypertrophy, there 
were recent or old haemorrhagic infarctions in the spleen. 
In the lymphatic form, the lymph-glands often formed immense 
tumors. Of the glands situated within the body, chiefly the mesen- 
teric, lumbar, and epigastric have been found enlarged; of the periph- 
eral, the cervical, axillary, and inguinal glands. Usually, the spleen 726 
APPENDIX TO THE DISEASES OF THE SPLEEX. 
was also diseased, but Virchow saw one case where the spleen was of 
normal size. I myself have seen a case on which there was no au- 
topsy, but in which no decided enlargement of the spleen could be 
observed during life, while the lymphatic glands were enormously en- 
larged. In all the cases the enlarged lymphatic glands were quite 
soft and pale, their surface smooth and watery-looking, the cortical 
substance was particularly swollen, in some cases to the thickness of 
one-half to three-fourths of an inch ; it had a homogeneous, almost me- 
dullary, appearance, and, on pressure, evacuated a turbid, watery fluid. 
Microscopic examination showed that the enlargement was entirely due 
to an excessive formation of cells, nuclei, and granules, similar to those 
occurring in normal glands. In most cases of this disease, the liver 
was found enlarged; it was occasionally soft, but usually hard and 
dense. 
An exceedingly interesting pathological new formation of lymphatic 
elements, outside of the lymph-glands, has been observed in some cases 
of leuchsemia. In two cases, in the parenchyma of the liver, and in 
one case in the kidneys also, Virchow found small white spots, from 
which, on pressure, there was evacuated a whitish fluid, consisting only 
of closely-packed free nuclei, and some small cells, which were almost 
filled by their nuclei. The new formation was enclosed by a fine mem- 
brane, could be quite readily freed from the surrounding parenchyma, 
and appeared to come from the walls of the blood-vessels and bile- 
ducts. Bottcher observed a similar case. And, in one case of leuchae- 
mia, Friedreich found extensive proliferation of nuclei and small cells, 
not only in the liver and kidneys, but also at circumscribed spots in 
the pleura, and in the gastric and intestinal mucous membrane, which 
caused partial thickenings of the pleura, and numerous elevations, of 
varied extent and prominence, in the stomach, small intestines, and 
rectum. Friedreich also succeeded in proving that the leuchacmic 
tumors of the pleura and intestinal mucous membrane originated from 
the connective-tissue corpuscles of those membranes. 
Symptoms and Course.—Usually the first symptoms of leuchremia 
are swelling of the abdomen, a feeling of pressure and fulness in the 
left hypochondrium, and other signs of enlargement of the spleen. 
The enlargement has either come on without pain or fever, so that the 
time of its occurrence could not be dated, or it has taken place at in- 
tervals, during which there was pain in the region of the spleen, and 
the patient was feverish. And in the lymphatic form, also, the en- 
largement of the glands in the neck, axilla, etc., which has taken place 
slowly, or at intervals, first calls attention to the disease. In a few 
well-observed cases, which throw a very clear light on the dependence 
of the dyscrasia on the disease of the spleen and lymphatic glands, it LEUCHAEMIA—LEUCOCYTILEMIA. 
727 
ivas found that the enlargement of the spleen and glands existed for 
months and years before the disorder of the blood showed itself. 
As the blood becomes impoverished in red corpuscles, the patient 
becomes pale and cachectic; and as the corpuscles not unfrequently 
become fewer in leuchaemia than in the highest grades of chlorosis, 
the patients have a waxy appearance in typical cases. There are also 
almost always complaints of want of breath and hastened respiration, 
for which symptoms no sufficient explanation can be found in the respi 
ratory organs, and which appear due to decrease of red blood-corpuscle 
by which the exchange of gases in the lungs is apparently effected. 
If the diaphragm be much pressed upward by the enlarged spleen, or 
if, as often happens, bronchial catarrh develop in the course of the dis- 
ease, the dyspnoea may become very great. Such a combination of 
symptoms should always excite the suspicion that the patient is suffer- 
ing from leuchaemia, and induce an examination of the blood. For 
this purpose we do not need a large venesection, and the debilitated 
and bloodless state of the patient almost always forbids this. In the 
blood that has been drawn we find at the border, between the buffy 
coat and the clot, single clumps, or a connected, loose, grayish layer, 
consisting of colorless blood-corpuscles. If, by beating, we free the 
blood that has been drawn of its fibrin, after standing for some time in 
a narrow glass, the heavy red corpuscles sink, and the lighter colorless 
ones form a whitish, purulent-looking, or milky layer in the upper part 
of the vessel. If we place a drop of the blood, recently drawn, under 
the microscope, we do not see a very few white corpuscles in the field, 
as we do in normal blood, but there are quantities of them which are 
not scattered around among the red corpuscles, but are more apt to be 
congregated in irregular clumps, as they are very adherent. 
The course of the disease varies. In some, but, by no means, in 
all cases, besides the above symptoms, there is a haemorrhagic dia- 
thesis. The patients have numerous haemorrhages, from the nose par- 
ticularly, more rarely from the intestinal canal, or into the tissue of the 
skin, sometimes into the brain. The fatal termination is hastened by 
this complication. The patients either die suddenly of apoplexy, or 
are so exhausted by repeated and abundant loss of blood that they 
soon die of exhaustion and anaemia. If a haemorrhagic diathesis does 
not develop, the disease almost always runs a tedious course, and may 
even continue for years. In such cases the enlargement of the spleen 
and lymphatic glands reaches a very high grade; the tension of the 
capsule of the spleen, and the inflammatory irritation in it, developed, 
perhaps, by the tension, or by haemorrhagic infarctions accompanying 
the hypertrophy, cause occasional pain in the region of the spleen and 
febrile symptoms. In these protracted cases the liver also is gener- 728 
APPENDIX TO THE DISEASES OF THE SPLEEN. 
ally enlarged. The patients become much emaciated, and have a very 
pale, cachectic look; the dyspnoea increases, and becomes extreme. 
Sediments of the urates, or of pure uric acid, are very frequently found 
in the urine. It is possible that their formation is partly due to the 
dyspnoea and fever; but there is also a probability that the uric acid 
is formed by the higher oxidation of the liypoxanthin that is so abun- 
dant in the blood. In many cases there is bronchial catarrh, so that 
the patients have severe cough, with mucous expectoration. Still more 
frequently there is intestinal catarrh, which leads to obstinate diarrhoea. 
Dropsy often occurs toward the end. That this does not occur sooner, 
as we should expect from the analogy with other conditions where the 
patient is pale and cachectic, is doubtless due to the fact that, in leu- 
chacmia, the decrease of the red blood-corpuscles is not accompanied 
by a corresponding decrease of the serum of the blood, as it is in other 
exhausting diseases. In the later stages of leuchacmia, the fever, which 
was at first temporary, usually becomes permanent. Tilde, who care- 
fully measured the temperature, in one case, found a constant increase 
of one to one and one-half degrees during the latter weeks of life. If 
no complication occurs, death results from gradual exhaustion; it is 
often preceded by symptoms of disturbed brain-function, delirium, or 
stupor. 
Treatment.—Up to the present time no case of recovery from 
leucliaemia is known, hence we cannot recommend any treatment that 
has actually proved successful. Quinine, iron, and iodine preparations 
have been used on account of their efficacy in some diseases of the 
spleen, and in anaemia. In the case of lymphatic leucliaemia that was 
under my observation, the enlargement of the glands temporarily sub- 
sided under the opposite mode of treatment, under the use of Zitt- 
manri’s decoction. I afterward sent the patient to a water-cure es- 
tablishment, where he improved and became healthy-looking. After a 
few months, however, the disease returned, advanced rapidly, and 
ended in death. 
CHAPTER II 
Etiology.—In melanoemia tliere is found in the blood a granular 
pigment, partly free, partly enclosed in cells, partly embedded in small 
hyaline coagula. There is no doubt that this pigment comes from the 
coloring matter of the blood, but it is a question where and under 
what circumstances it is formed. 
Almost all observers regard the spleen as the place where the pig- 
ment is formed in melanmmia. The frequent occurrence of pigmented 
MELANJEMIA. MELANAEMIA. 
729 
cells in the spleens of animals, which some observers regard as phys- 
iological, others as pathological, as well as the fact that in melaiuemia 
the pigment is almost always most abundant in the spleen, certainly 
favors the idea that the pigment is chiefly formed in the spleen, but 
does not prove that it is formed there only, and is not formed in other 
organs at the same time. Frerichs describes a case where be found 
no pigment in the spleen, while he found so much in the liver, that be 
was obliged to regard tbis organ as the place where it was formed. 
The extensive occurrence of pigment in the blood presupposes 
extensive destruction of red blood-corpuscles. Whether this takes 
place exclusively in the spleen or whether it takes place in other 
organs at the same time, all observations prove that it is due to the 
influence of malarial infection. The milder forms of simple intermit- 
tent fever do not, however, appear to cause the formation of pigment 
in the blood at all or else only moderately, and only the severe and 
obstinate forms, but particularly the pernicious intermittent, appear to 
cause the higher grades of melanremia in this country. The corre- 
sponding reports of physicians in the tropics, about the dark color of 
the different organs, particularly of the brain, in the bodies of patients 
that have had remittent fever, render it very probable that this form 
of malarial disease also constantly, or at least very frequently, causes 
melanremia. 
It is very probable that the dilatation of the blood-vessels and the 
consequent retardation of the current of blood (see page 711) become 
so great in pernicious intermittent, and in remittent marsh-fevers of 
the tropics, that the blood stagnates in the spleen. We might further 
suppose that the corpuscles in the stagnating blood are destroyed, and 
hence an altered pigment is developed from their hematin, processes 
which we often observe in stagnating extravasated blood. This ex- 
planation of the formation of pigment in a purely mechanical way is 
refuted by the fact that in intermittent fever the enlargement of the 
spleen, and consequently the retardation of the current of blood 
through it, may be very decided without the occurrence of melanasmia; 
and, on the contrary, melanaemia is found in cases where the spleen is 
only moderately enlarged. Hence we must suppose that marsh miasm 
has a pernicious influence on the red corpuscles in some other way 
that we do not yet know; and that in our country only in certain 
epidemics, but in the tropics in the endemic fevers, this influence fre- 
quently or constantly causes an extensive necrosis of the red blood- 
corpuscles, and the formation of pigment from its hematin (Grie■ 
singer). 
Virchow's labors on the subject of pathological pigments readily 
explain why the pigment found in the blood appears not only as free 730 
APPENDIX TO THE DISEASES OF THE SPLEEN. 
granules, but also as enclosed in colorless cells. This observer saw 
that, in dissolving the hematin in a drop of blood by adding water, 
the hematin became most distinct in the colorless blood-corpuscles, 
and hence it is probable that, in the extensive destruction of blood- 
cells in the spleen, the hematin enters the colorless elements of the 
spleen-pulp, and with these reaches the blood. It is more difficult to 
explain the occurrence of pigment in the blood in the form of irregular 
flakes. It is possible that these flakes consist of fibrin that has pre- 
cipitated on the angular granules; but it is more probable that the 
substance adherent to the pigment-granules, surrounding them like a 
bright border, consists of the protein substance that was combined 
with the fibrin in the blood-corpuscles that were destroyed ( Virchow). 
Anatomical Appearances.—In melamemia the pigment found in 
the blood of the heart and vessels is black ; more rarely besides the 
black we find bro\yn or yellowish-brown, rarely yellowish-red pigment. 
With acids and caustic alkalies it shows the following conditions, which 
Virchow has found peculiarly characteristic of pathological pigment: 
the more recent formations become pale and finally lose their color en- 
tirely, while the older ones resist the reaction of these reagents a long 
time (Frerichs). The small pigment-granules have an .irregularly 
roundish form. As Meckel, the first observer of pigment in the blood, 
saw, a larger or smaller number of these is almost always united, by a 
colorless substance, to roundish, spindle-shaped, or irregular flakes. 
The cells containing pigment sometimes have the size and form of the 
white corpuscles of the, blood ; sometimes they are larger, and club or 
or spindle shaped; the latter resemble the spindle-shaped cells in the 
spleen-pulp, which Folliker considers the epithelium of the splenic 
vein. Besides these forms, Frerichs observed large clumps of pig- 
ment of irregular shape, as well as cylindrical bodies that looked like 
small vessels. 
With the blood the pigment enters all the organs of the body, and, 
according to the amount collecting in the capillaries, colors them more 
or less. According to Planer and Frerichs, we almost always find 
the most pigment in the spleen, so that it appears slate-gray and often 
almost black. Next to the spleen, the greatest amount of pigment is 
found in the liver and brain, particularly in the cortical substance. 
The liver is often steel-gray or blackish; the cortical substance of the 
brain chocolate or graphite color. Not unfrequently there is also a con- 
siderable collection of pigment in the kidneys, as a result of which 
usually the cortical substance has gray points in it. In the pulmonary 
vessels, particularly in the smaller ones, there is occasionally a large 
amount of pigment. In the vessels of the other tissues and organs it 
is never accumulated to any great extent; but the skin, mucous mem* MELANAEMIA. 
731 
branes, cellular tissue, and lymphatic glands, also have a more or less 
decidedly gray color. Frerichs sums up the appearances in melanasmia 
by saying: “ In marked cases of the disease pigment is found wher- 
ever the blood goes, and is the more abundant the smaller the capilla- 
ries of the part, that is, the more readily impaction of the flakes may 
occur.” 
Symptoms and Course.—Many cases of melanaemia cause no per- 
ceptible disturbance of function, and the organs have been found over- 
loaded with pigment, on autopsy of persons who have died of the most 
varied diseases. This was true in more than one-third of the cases ob- 
served by Planer. On the other hand, patients often die quickly with 
severe brain-symptoms, and on autopsy we find the evidences of mela- 
naemia, particularly an accumulation of pigment in the vessels of the 
brain, or numerous small extravasations of blood through the brain- 
substance. Former observations of great pigmentation of the cerebral 
substance in persons who had died of comatose intermittent, as well as 
the experience of the tropics, which shows that the brain is very dark- 
colored in most persons who have died of severe remittent fever, have 
acquired greater sigtiificance, since we know that the dark color of the 
brain depends on an accumulation of pigment in its vessels, and have 
rendered it very probable that the obstruction of the cerebral ves- 
sels (with or without consecutive rupture of the walls of the capillaries) 
caused the brain-symptoms in severe malarial diseases. This view, 
advanced by Meckel, appeared to be supported by numerous observa- 
tions of Planer and Frerichs. Both of these observers described cases 
of melancemia where the patients had severe cerebral symptoms, either 
headache and dizziness, delirium or convulsions, but particularly coma. 
The cases observed by Frerichs all occurred during a malignant epi- 
demic of intermittent fever; they developed partly from simple inter- 
mittent paroxysms, had an irregular intermittent or remittent course, 
and partly yielded to quinine; they presented exactly the symptoms 
of a febris intermittens comitata, maniaca, epileptica, comitosa, apo- 
plectica. With all this there are important reasons for doubting the 
dependence, at least the constant dependence, of the cerebral symp- 
toms in pernicious malarial fever on an obstruction of the vessels of the 
brain by pigment. In opposition to the hypothesis of such a connec- 
tion, Frerichs calls attention to the fact that in many cases, even when 
the brain is very dark-colored, no decided disturbance of the circulation 
can be perceived; and further, that in spite of the dark color of the brain, 
there are often no cerebral symptoms ; and lastly, that severe cerebral 
symptoms have been observed where there was none of this pigmenta- 
tion of the brain (in twenty-eight cases of intermittens cephalica that 
Frerichs observed, the dark color of the brain was absent in six). The 732 
APPENDIX TO THE DISEASES OF THE SPLEEN. 
typical occurrence of these brain-symptoms, as well as the occasionally 
successful treatment of them by quinine, appears to me just as weighty 
an argument against their dependence on obstruction of the cerebral 
vessels by pigment. For it is impossible to see how the obstruction 
should exist during the paroxysm and disappear during the apyrexia, 
and there is just as little probability that the exhibition of quinine 
could have a favorable effect on obstruction of the cerebral vessels. 
According to what has been said, with our present knowledge, we 
can affirm nothing certainly of the connection between melanemia and 
the disturbance of the brain function. It is certainly possible that the 
poisoning of the blood by marsh miasm, in malignant intermittent 
fever, may excite other cerebral disturbances besides accumulation of 
pigment in the cerebral vessels, and independently of that. 
In another series of cases, Planer and Frerichs found anomalies of 
the renal functions in melanaemia. Occasionally the secretion of urine 
was entirely arrested; in other cases there was albuminuria; in still 
others, haematuria. The same objections urged against the dependence 
of the brain-symptoms on obstruction of the cerebral vessels must be 
equally valid against the dependence, at least the constant depend- 
ence, of functional disturbance of the kidneys on obstruction of the 
renal vessels. Among others, Frerichs saw albuminuria occur with- 
out pigmentation of the kidneys ; and, on the other hand, albuminuria 
was absent in five cases where there was pigment in the kidneys. 
But, if there was albuminuria, this observer found that the amount 
of albumen in the urine was decidedly increased during the paroxysm, 
and decreased or disappeared during the interval. From analogy with 
other miasmatic affections, it certainly cannot be denied that the infec- 
tion of the blood with marsh miasm may disturb the nutrition and 
functions of the kidneys, even without obstruction of the vessels. 
Lastly, in melanaemia Frerichs observed exhausting intestinal 
haemorrhage, profuse diarrhoea, acute serous effusions into the peritoneal 
sac, and bloody suffusion of the serous coat of the intestines. It ap- 
pears improper to refer this symptom also to obstruction of the ves- 
sels of the liver, and to congestion in the roots of the portal veins; 
for, although in all the cases observed by Frerichs, next to the spleen, 
the liver appeared to contain the most pigment, the symptoms that 
apparently indicated disturbance of the circulation in the roots of the 
portal veins were not by any means constant, and were not nearly so 
frequent as the cerebral symptoms. Moreover, the intestinal hemor- 
rhages observed by Frerichs in three cases had distinct intermissions ; 
and, while they resisted treatment directed against the hemorrhage di- 
rectly, they yielded to large doses of quinine. Frerichs even refers 
the fatal result in one of these three cases to neglect in the adminis- MEL AX.-EM I A. 
733 
tration of quinine. In these cases, also, it would be difficult to believe 
in an intermittent obstruction of the blood-vessels. 
It may be offered as an objection to referring the above symptoms 
to melanaemia, that there are but few symptoms that we certainly 
know belong to that disease itself, and are not the immediate effects 
of malarial poisoning. Among these are the dark color of the skin, 
which is caused by the quantity of pigment in the blood-vessels of the 
skin, and the microscopical observation of pigment in the blood. In 
mild cases the skin is of an ashy-gray color, in severe ones it is yel- 
lowish brown. If we find this color in a person who has had an ob- 
stinate and severe intermittent fever for some time, or if it appears 
that this intermittent belonged to a malignant epidemic, and had the 
symptoms of a febris comitata, we should strongly suspect melanasmia, 
and make a microscopical examination of the blood. 
Treatment.—Prophylaxis and the causal indications demand the 
same general rules as we shall give, in the second volume, for the 
treatment of pernicious intermittent fever. We cannot fulfil the indi- 
cation from the disease, as we know tio remedy that will remove the 
pigment from the blood. In recent -cases the symptomatic indications 
may require the administration of iron, and a nourishing diet; for, as 
Frerichs justly says, the excessive loss of red corpuscles causes chloro- 
sis, as well as melanasmia. Later the former often disappears, while 
the latter continues. In one case that I saw, several months passed 
before the patient recovered under the use of iron; subsequently he 
was equal to the hardest work, and presented no anomaly except the 
color of his skin. When he died, several years afterward, of pneumo- 
nia, the autopsy still showed distinctly the signs of melanasmia. 
END OP VOL. I.