A system of practical medicine. By American authors. Vol. 1
by unknown · English · Gutenberg #39157 · 3,637,378 chars · public domain (US)
The Project Gutenberg eBook of A system of practical medicine. By American authors. Vol. 1
This eBook is for the use of anyone anywhere in the United States and
most other parts of the world at no cost and with almost no restrictions
whatsoever. You may copy it, give it away or re-use it under the terms
of the Project Gutenberg License included with this eBook or online
at www.gutenberg.org. If you are not located in the United States,
you will have to check the laws of the country where you are located
before using this eBook.
Title: A system of practical medicine. By American authors. Vol. 1
Pathology and general diseases
Editor: William Pepper
Louis Starr
Release date: March 15, 2012 [eBook #39157]
Language: English
Other information and formats: www.gutenberg.org/ebooks/39157
Credits: Produced by Ron Swanson (This file was produced from images
generously made available by The Internet Archive/Canadian
Libraries)
*** START OF THE PROJECT GUTENBERG EBOOK A SYSTEM OF PRACTICAL MEDICINE. BY AMERICAN AUTHORS. VOL. 1 ***
Produced by Ron Swanson (This file was produced from images
generously made available by The Internet Archive/Canadian
Libraries)
A SYSTEM OF PRACTICAL MEDICINE.
BY AMERICAN AUTHORS.
EDITED BY
WILLIAM PEPPER, M.D., LL.D.,
PROVOST AND PROFESSOR OF THE THEORY AND PRACTICE OF MEDICINE AND OF
CLINICAL MEDICINE IN THE UNIVERSITY OF PENNSYLVANIA.
ASSISTED BY
LOUIS STARR, M.D.,
CLINICAL PROFESSOR OF DISEASES OF CHILDREN IN THE HOSPITAL OF THE
UNIVERSITY OF PENNSYLVANIA.
VOLUME I. PATHOLOGY AND GENERAL DISEASES.
PHILADELPHIA:
LEA BROTHERS & CO.
1885.
Entered according to Act of Congress, in the year 1885, by LEA
BROTHERS & CO., in the Office of the Librarian of Congress. All rights
reserved.
WESTCOTT & THOMSON, _Stereotypers and Electrotypers, Philada._
WILLIAM J. DORNAN, _Printer, Philada._
PREFACE.
The present work has been undertaken in the belief that by obtaining
the co-operation of a considerable number of physicians of
acknowledged authority, who should treat subjects selected by
themselves, there could be secured an amount of practical information
and teaching not otherwise accessible. It was determined to restrict
the selection of authors to those of this country--including
Canada--not from any want of recognition of the importance of the
studies of certain special subjects by European investigators, but
because it was felt that the proper time had arrived for the
presentation of the whole field of medicine as it is actually taught
and practised by its best representatives in America.
It is a matter of importance also that a comprehensive study shall be
made of the various forms of disease as occurring among our highly
composite population and under our varied and peculiar climatic
influences. Of course, in the present work comparative studies of this
kind must occupy a subordinate position; yet it cannot fail to enhance
both its interest and its value to have the various forms of disease
as they occur in this country discussed by those among us who are
confessedly the most competent and experienced.
The force of these observations must have been felt by the
distinguished men to whom I made application, for with scarcely an
exception they joined cordially in the laborious undertaking. I take
the greatest pleasure in testifying to the courtesy which has marked
all our relations, and which has lessened materially the labor and
strain inevitable in the production of such a work.
To ensure greater accuracy in the revision of the large amount of
proof-sheets, as well as to relieve me of some of the details
connected with the editorial work, I associated with myself Dr. THOMAS
HOLMES CATHCART, and, after sudden illness had cut short his very
promising career, I was fortunate in securing the assistance of Dr.
LOUIS STARR for the same purpose.
In order to render the work as valuable as possible to the general
practitioner, its scope has been made as comprehensive as could be
done without exceeding the limits prescribed by the nature of the
undertaking. This will be particularly noted in the section on
Gynæcology, where is presented a series of articles by eminent
specialists upon the subjects of chief importance to the general
practitioner, written with special reference to their constitutional
relations and their bearings on associated morbid conditions, while,
among the general diseases, a full article on puerperal fever has
properly been included. Important articles will also be found on
Tracheotomy, the Diseases of the Rectum and the Anus, and those of the
Bladder and the male sexual organs. Comprehensive sections have
further been provided, from the pens of distinguished specialists,
upon medical ophthalmology, medical otology, and on skin diseases,
presenting these large and complicated subjects in a clear and
practical light and with special reference to their relations to
general medical practice. In the presentation of such subjects as
hydrophobia, glanders, and anthrax care has been taken to ensure the
full discussion of these affections, not only as occurring in man, but
also in the lower animals, since it is highly important to provide the
physician with authoritative information on at least such points of
Veterinary Science as have a direct practical bearing on morbid
processes in man.
In view of the intimate relations of all questions of hygiene to the
causation and prevention of disease, in regard to which medical men
are constantly consulted, and are, indeed, often obliged to assume
weighty responsibilities, interesting articles on Drainage and Hygiene
have been provided.
In order to avoid repetition and confusion, and at the same time to
secure a comprehensive presentation of the subjects of General
Pathology and of General Etiology, Symptomatology, and Diagnosis,
considerable space has been devoted to their full discussion. The
chapter on General Morbid Processes will be found to convey distinct
and conservative teaching on all points included under that
comprehensive title, and will thus supply a solid basis for the
subsequent discussions of special morbid conditions. In any work on
General Medicine at the present day frequent allusion must be made to
the relations of various low organisms to morbid processes. This
question--or rather the series of questions which arise in connection
with this subject, and which at present form the most fruitful topic
of discussion and of investigation--will be found treated by different
authors in various places and from various standpoints. No attempt has
been made to secure uniformity of views upon a matter which is still
_sub judice_, and which demands much more skilful and critical
investigation before its true scientific position has been finally
determined. It has even been felt to be desirable to allow a certain
amount of repetition, which has naturally resulted from the
introduction of this discussion, not only in the chapter on General
Etiology, but in connection with the causation of scarlatina,
diphtheria, hydrophobia, pyæmia, puerperal fever, and phthisis.
Throughout the work the chief purpose of the editor and of his
collaborators, to furnish a concise and thoroughly practical system of
medicine, has compelled the omission of bibliographical lists, of
numerous references, and of extended discussions of theoretical views
or of controverted questions, in order that more space might be
devoted to clear descriptions of disease and to a full presentation of
the subjects of diagnosis and treatment. If it should seem, in
consequence, that inadequate recognition has been made of the labors
of others, it must be borne in mind that ample quotations and numerous
references were inadmissible in such a work as the present.
* * * * *
The classification and nomenclature which have been adopted are those
recommended by the Royal College of Physicians of England and by the
American Medical Association. Charts and tables have been inserted
wherever they were needed to elucidate the text, but after mature
reflection it was felt necessary to omit all illustrations that were
not imperatively required, although many original drawings and
paintings of high value were offered with the articles.
THE EDITOR.
OCTOBER, 1884.
CONTENTS OF VOL. I.
PAGE
PREFACE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
GENERAL PATHOLOGY AND SANITARY SCIENCE.
GENERAL MORBID PROCESSES. By REGINALD H. FITZ, M.D. . . . . . . . 35
GENERAL ETIOLOGY, MEDICAL DIAGNOSIS, AND PROGNOSIS. By HENRY
HARTSHORNE, M.D., LL.D. . . . . . . . . . . . . . . . . . . . . 125
HYGIENE. By JOHN S. BILLINGS, A.M., M.D., LL.D. (Edin.) . . . . . 173
DRAINAGE AND SEWERAGE IN THEIR HYGIENIC RELATIONS. By GEORGE E.
WARING, JR., M. Inst. C.E. . . . . . . . . . . . . . . . . . . 213
GENERAL DISEASES.
SIMPLE CONTINUED FEVER. By JAMES H. HUTCHINSON, M.D. . . . . . . 231
TYPHOID FEVER. By JAMES H. HUTCHINSON, M.D. . . . . . . . . . . . 237
TYPHUS FEVER. By JAMES H. HUTCHINSON, M.D. . . . . . . . . . . . 338
RELAPSING FEVER. By WILLIAM PEPPER, M.D., LL.D. . . . . . . . . . 369
VARIOLA. By JAMES NEVINS HYDE, M.D. . . . . . . . . . . . . . . . 434
VACCINIA. By FRANK P. FOSTER, M.D. . . . . . . . . . . . . . . . 455
VARICELLA. By JAMES NEVINS HYDE, M.D. . . . . . . . . . . . . . . 481
SCARLET FEVER. By J. LEWIS SMITH, M.D. . . . . . . . . . . . . . 486
RUBEOLA. By W. A. HARDAWAY, A.M., M.D. . . . . . . . . . . . . . 557
RÖTHELN. By W. A. HARDAWAY, A.M., M.D. . . . . . . . . . . . . . 582
MALARIAL FEVERS. By SAMUEL M. BEMISS, M.D. . . . . . . . . . . . 589
PAROTITIS. By JOHN M. KEATING, M.D. . . . . . . . . . . . . . . . 620
ERYSIPELAS. By JAMES NEVINS HYDE, M.D. . . . . . . . . . . . . . 629
YELLOW FEVER. By SAMUEL M. BEMISS, M.D. . . . . . . . . . . . . . 640
DIPHTHERIA. By ABRAHAM JACOBI, M.D. . . . . . . . . . . . . . . . 656
CHOLERA. By ALFRED STILLÉ, M.D., LL.D. . . . . . . . . . . . . . 715
PLAGUE. By JAMES C. WILSON, A.M., M.D. . . . . . . . . . . . . . 771
LEPROSY. By JAMES C. WHITE, M.D. . . . . . . . . . . . . . . . . 785
EPIDEMIC CEREBRO-SPINAL MENINGITIS. By A. STILLÉ, M.D., LL.D. . . 795
PERTUSSIS. By JOHN M. KEATING, M.D. . . . . . . . . . . . . . . . 836
INFLUENZA. By JAMES C. WILSON, A.M., M.D. . . . . . . . . . . . . 851
DENGUE. By H. D. SCHMIDT, M.D. . . . . . . . . . . . . . . . . . 879
RABIES AND HYDROPHOBIA. By JAMES LAW, F.R.C.V.S. . . . . . . . . 886
GLANDERS AND FARCY. By JAMES LAW, F.R.C.V.S. . . . . . . . . . . 909
ANTHRAX (MALIGNANT PUSTULE). By JAMES LAW, F.R.C.V.S. . . . . . . 926
PYÆMIA AND SEPTICÆMIA. By B. A. WATSON, A.M., M.D. . . . . . . . 945
PUERPERAL FEVER. By WILLIAM T. LUSK, M.D. . . . . . . . . . . . . 984
BERIBERI. By DUANE B. SIMMONS, M.D. . . . . . . . . . . . . . . . 1038
INDEX . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1045
CONTRIBUTORS TO VOL. I.
BEMISS, SAMUEL M., M.D.,
Professor of Theory and Practice of Medicine and Clinical Medicine
in the University of Louisiana, New Orleans.
BILLINGS, JOHN S., A.M., M.D., LL.D. (Edin.),
Surgeon U.S. Army, Washington.
FITZ, REGINALD H., M.D.,
Shattuck Professor of Pathological Anatomy in Harvard University,
Boston.
FOSTER, FRANK P., M.D.,
New York.
HARDAWAY, W. A., A.M., M.D.,
Professor of Diseases of the Skin in the St. Louis Post-Graduate
School of Medicine and in the Missouri Medical College, St.
Louis; President of the American Dermatological Association.
HARTSHORNE, HENRY, M.D., LL.D.,
Late Professor of Hygiene in the University of Pennsylvania,
Philadelphia.
HUTCHINSON, JAMES H., M.D.,
Physician to the Pennsylvania Hospital and to the Children's
Hospital, Philadelphia.
HYDE, JAMES NEVINS, M.D.,
Professor of Skin and Venereal Diseases in the Rush Medical
College, Chicago.
JACOBI, ABRAHAM, M.D.,
Clinical Professor of Diseases of Children in the College of
Physicians and Surgeons, New York, etc.
KEATING, JOHN M., M.D.,
Visiting Obstetrician and Lecturer on Diseases of Women and
Children to the Philadelphia (Blockley) Hospital; Surgeon to the
Maternity Hospital; Physician to St. Joseph's Hospital,
Philadelphia.
LAW, JAMES, F.R.C.V.S.,
Professor of Veterinary Science in Cornell University, Ithaca,
N.Y.
LUSK, WILLIAM T., M.D.,
Professor of Obstetrics and Diseases of Women and Children in the
Bellevue Hospital Medical College, New York.
PEPPER, WILLIAM, M.D., LL.D.,
Provost and Professor of the Theory and Practice of Medicine and
of Clinical Medicine in the University of Pennsylvania,
Philadelphia.
SCHMIDT, H. D., M.D.,
Pathologist to the Charity Hospital, New Orleans.
SIMMONS, DUANE B., M.D., Yokohama, Japan,
Late Director, Physician, and Surgeon-in-Chief of the Government
Hospital, also Consulting Surgeon to Prison and Police Hospitals
at Yokohama, Japan.
SMITH, J. LEWIS, M.D.,
Clinical Professor of Diseases of Children in the Bellevue
Hospital Medical College, New York.
STILLÉ, ALFRED, M.D., LL.D.,
Emeritus Professor of Theory and Practice of Medicine in the
University of Pennsylvania, Philadelphia.
WARING, GEORGE E., JR., M. Inst. C.E.,
Engineer of Sanitary Drainage, Newport, R.I.
WATSON, B. A., A.M., M.D.,
Surgeon to the Jersey City Charity, St. Francis, and Christ
Hospitals, Jersey City, N.J.
WHITE, JAMES C., M.D.,
Professor of Dermatology in Harvard University, Boston.
WILSON, JAMES C., A.M., M.D.,
Physician to the Jefferson Medical College Hospital and to the
Philadelphia Hospital, Philadelphia.
ILLUSTRATIONS.
FIGURE PAGE
1. MICROCOCCI . . . . . . . . . . . . . . . . . . . . . . . . . 142
2. BACTERIA . . . . . . . . . . . . . . . . . . . . . . . . . . 142
3. BACILLUS MALARIÆ . . . . . . . . . . . . . . . . . . . . . . 143
4. BACTERIA FROM GELATIN SOLUTION . . . . . . . . . . . . . . . 143
5. VIBRIOS IN GELATIN CULTURE-FLUID . . . . . . . . . . . . . . 144
6. PROTOCOCCUS FROM SLIDES EXPOSED OVER SWAMP-MUD . . . . . . . 144
7. BACILLI FROM SWAMP-MUD . . . . . . . . . . . . . . . . . . . 145
8. BACILLI FROM SEPTICÆMIC RABBIT . . . . . . . . . . . . . . . 145
9. BACILLI FROM HUMAN SALIVA . . . . . . . . . . . . . . . . . . 146
10. BACILLUS ANTHRACIS . . . . . . . . . . . . . . . . . . . . . 146
11. BACILLUS TUBERCULOSIS . . . . . . . . . . . . . . . . . . . . 147
12. CHART OF TYPICAL RANGE OF TEMPERATURE IN TYPHOID FEVER, AFTER
WUNDERLICH . . . . . . . . . . . . . . . . . . . . . . . . 282
13. CHART SHOWING RECRUDESCENCE OF FEVER FROM INDISCRETION OF
DIET. . . . . . . . . . . . . . . . . . . . . . . . . . . . 283
14. CHART SHOWING FALL OF TEMPERATURE FROM INTESTINAL HEMORRHAGE
IN TYPHOID FEVER . . . . . . . . . . . . . . . . . . . . . 284
15. PULSE-TRACING IN RELAPSES OF TYPHOID FEVER . . . . . . . . . 304
16. CHART OF TEMPERATURE IN TYPHOID FEVER WITH RELAPSE.--ORIGINAL
ATTACK . . . . . . . . . . . . . . . . . . . . . . . . . . 306
17. CHART OF TEMPERATURE IN TYPHOID FEVER WITH RELAPSE.--RELAPSE 306
18. TEMPERATURE CHART OF TYPHOID FEVER.--ABORTIVE ATTACK,
FOLLOWED BY TYPICAL ATTACK . . . . . . . . . . . . . . . . 308
19. SPIRILLUM FROM THE BLOOD IN A CASE OF RELAPSING FEVER . . . . 374
20. TEMPERATURE CHART OF TYPICAL CASE OF RELAPSING FEVER, WITH
THREE RELAPSES TERMINATING IN RECOVERY . . . . . . . . . . 379
21. TEMPERATURE CHART OF TYPICAL CASE OF RELAPSING FEVER,
TERMINATING IN RECOVERY . . . . . . . . . . . . . . . . . . 380
22. TEMPERATURE CHART FROM A CASE OF THE BILIOUS TYPHOID OR GRAVE
SUBINTRANT FORM OF RELAPSING FEVER . . . . . . . . . . . . 397
23. TEMPERATURE CHART SHOWING THE LAPSE OF A REMITTENT FEVER INTO
AN INTERMITTENT . . . . . . . . . . . . . . . . . . . . . . 600
24. CHARTS SHOWING THE TEMPERATURE CURVE IN TYPHO-MALARIAL FEVER:
PART I., SHOWING PREDOMINANCE OF TYPHOIDAL ELEMENT;
PART II., SHOWING PREDOMINANCE OF MALARIAL ELEMENT . . . . 617
GENERAL PATHOLOGY.
GENERAL MORBID PROCESSES.
GENERAL ETIOLOGY.
HYGIENE AND QUARANTINE.
DRAINAGE AND SEWERAGE IN RELATION TO THE PREVENTION OF DISEASE.
{35}
GENERAL MORBID PROCESSES.[1]
INFLAMMATION; THROMBOSIS AND EMBOLISM; EFFUSIONS; DEGENERATIONS;
TUBERCULOSIS; MORBID GROWTHS.
BY REGINALD H. FITZ, M.D.
[Footnote 1: In the preparation of this subject full and free use has
been made of the following works: _Die Cellular Pathologie_, Virchow,
4te Auflage, Berlin, 1871; _Handbuch der Allgemeinen Pathologie_, Uhle
und Wagner, 7te Auflage, Leipzig, 1876; _Handbuch der Allgemeinen
Pathologie als Pathologische Physiologie_, Samuel, Stuttgart, 1879;
_Vorlesungen über Allgemeine Pathologie_, Cohnheim, 2te Auflage,
Berlin, 1882; _Lehrbuch der Pathologischen Anatomie_,
Birch-Hirschfeld, 2te Auflage, 1er Band, Leipzig, 1882; _Lehrbuch der
Allgemeinen und Speciellen Pathologischen Anatomie_, Ziegler, 1er und
2er Theil, Jena, 1882 and 1883.]
GENERAL MORBID PROCESSES.
Disease is to be regarded as representing the result of a series of
processes called morbid or pathological, from the fact that they are
manifested by disturbances in the organism.
The processes concerned are the same in kind as those essential to
health, but they are modified in time, place, or quantity.
Morbid processes, therefore, are to be considered as modified
physiological processes tending to cause disease.
All physiological processes are subject to certain variations which
tend to produce disturbances in the functions of the body. In the
healthy organism this tendency is checked by the automatic regulators
of the functional activity of the various organs, to the importance of
which Virchow[2] long ago called attention. By their action the
influence of external agents is controlled within certain limits. The
lids close and prevent injury to the eye. Sneezing, coughing, and
vomiting bring about the expulsion of noxious irritants. Sweating aids
in neutralizing the injurious effects of exposure to high
temperatures. Rapid respiration permits a sufficient cleansing of the
blood in rarefied atmospheres. When the limits, within which the
regulation of physiological processes is possible, are exceeded, such
processes become pathological and disease begins. A morbid process,
therefore, is usually incapable of recognition till disease is
present. It may exist and disease be unsuspected and denied. A
diminished blood-supply may be one link in the process which
eventually leads to the production of disturbances. {36} Another link
is to be found in the fatty degeneration resulting from this lack of
blood.
[Footnote 2: _Handbuch der Speciellen Pathologie und Therapie_,
Virchow, 1er Band, p. 15, Erlangen, 1854.]
Such a degeneration may have long existed in the walls of a
blood-vessel, and yet the individual appear in the best of health. The
sudden rupture of the weakened wall results in death or disease. With
the manifestation of the disturbances which render the condition of
the vessel obvious the individual is said to be diseased.
In most instances, however, the morbid process makes itself early
apparent. Disturbances of nutrition, formation, or function soon
become sufficient in quantity to attract attention from the resulting
discomfort, and the presence of disease is then recognized. The latter
is thus essentially a conventional term, and begins when the morbid
processes occasion a sufficient degree of inconvenience.
The process is never at a standstill. It either tends toward a return
to the physiological conditions, or its course is in the direction of
their destruction. As physiological processes are absolutely dependent
upon the vitality of the elements of the tissues, so those which have
become pathological cease to exist with the death of such elements. In
the dead body there is no disease, although its results remain, and
furnish the most efficient means of identifying the processes which
occasioned them.
In the study of morbid processes, therefore, one must appreciate the
normal conditions and manifestations of life in the individual.
Physiological laws govern pathological phenomena, and the latter must
always be submitted to the tests furnished by the former.
Just as little, however, as the study of anatomy familiarizes the
student with the anatomical changes resulting from diseased processes,
does the study of physiology accustom the student to the features of
disease. Pathological processes must be studied by themselves and for
themselves, although the means which are employed may be the same as
those used in physiological research.
It is evident that the exactness of method which is the demand of the
physiological investigator cannot be secured by the pathologist. The
material of the latter lies farther, beyond his control. Nevertheless,
much of the ground to be gone over is common, and the object sought
for is essentially the same--the knowledge of the conditions necessary
to maintain life.
In an introduction to the study of disease there are certain processes
which deserve early recognition. They are both the cause and the
result of disease, and may occur in various diseases, either limited
to one organ or present in a series of organs. Their treatment at
present obviates the necessity of repetition, and prepares the reader
for the special consideration of their occurrence in the various
structures and systems of the body.
These processes are named in virtue of some prominent characteristic,
and each is made up of a complex series of conditions and
disturbances. In part, they represent modifications in the circulation
of blood and lymph; in part, they consist of nutritive derangements,
whose consequences appear as the various degenerations, or as the
additions to the body, the new formations.
The processes and groups of processes in question are those included
under the following heads: inflammation; thrombosis and embolism;
effusions; degenerations; tuberculosis; and morbid growths.
{37} Inflammation.
Inflammation is characterized now, as in the time of Galen, by the
presence of redness, heat, swelling, and pain. The disturbance of
function, added to modern definitions, is to be regarded either as a
result or a cause, or both, of the variously modified physiological
processes whose sum is the inflammation.
The redness of inflammation is obviously dependent upon the presence
of an increased quantity of blood. This is readily apparent in the
direct observation of the blood-vessels of an inflamed, transparent
part of the body, as the mesentery of the frog or rabbit, or the
tongue and webbed foot of the former animal. The redness of
inflammation consequently demands the presence of blood-vessels in the
affected region, and becomes all the greater the more vascular the
part--_i.e._ the richer it is in such vessels.
Redness does not suffice for the existence of inflammation, for it may
be found in the absence of other evidence of the latter. The diffused
redness, often extensive, of birth-marks, that from venous obstruction
or temporary congestions, from vaso-motor disturbances--the section of
the sympathetic furnishing a well-known instance--are examples of
non-inflammatory redness. Inflammation may even be present without
redness, as may be constantly observed in the occurrence of
parenchymatous inflammation and of the chronic interstitial varieties.
The heat of inflammation is one of the most important clinical
features, yet not indispensable, as appears from its absence in
chronic interstitial forms of inflammation. In the acute varieties of
inflammation an elevated temperature is constant, and its observation
and record furnish a most valuable means of determining the beginning
and progress of an inflammation, which, for a time, may furnish but
little additional evidence.
The heat of inflammation is the prominent characteristic of
inflammatory fever, and it is the study of this variety of fever of
late years which has resulted in an intelligible and relatively
satisfactory theory concerning fevers in general. Information of much
value is to be found in the recent work of Wood,[3] which contains
abundant historical information, as well as extensive original
observations and conclusions.
[Footnote 3: _Fever: A Study in Morbid and Normal Physiology_, H. C.
Wood, A.M., M.D., Philadelphia, 1880. (Reprint from the _Smithsonian
Contributions to Knowledge_, No. 357.)]
Inflammatory fevers are distinguished from idiopathic forms. The
latter variety includes the occurrence of fever as an attribute of the
disease concerned, the more characteristic symptoms of which follow
the febrile outbreak. Local inflammatory processes may take place
during the progress of the disease with its fever, but such processes
are co-effects of the cause of the latter, rather than its cause. Most
of those diseases in which fever occurs as one of the joint effects of
the cause of the disease, are included among the infective or zymotic
classes.
The inflammatory fevers are those attending an acute inflammatory
process, and are secondary to, and occasioned by, the latter. The type
of this variety is seen in the fever occurring during the progress of
a wound, whether its course is toward healing or extension. Such {38}
traumatic fevers are characterized as septic or aseptic; the former
including the conditions of septicæmia and pyæmia. The aseptic
traumatic fevers, as described by Volkmann,[4] are those which pursue
their course with an elevated temperature, but without most of the
other febrile phenomena.
[Footnote 4: _Beiträge zur Chirurgie_, Leipzig, 1875, p. 24; _Sammlung
Klinischer Vorträge_, No. 121, Genzmer und Volkmann.]
Fever in general is characterized by a combination of disturbances in
the physiological processes of the body. Such processes are those
concerned in the production and dissipation of heat, in respiration
and circulation, digestion and secretion, and in mental, motor, and
other sensorial action. Such disturbances are manifested by a
persistent elevation of temperature, an increased destruction of
tissue, a quickened and modified pulse, accelerated breathing,
increased thirst, diminished appetite, and diminished quantity and
altered quality of the secretions. The sensorial disturbances include
wakefulness and stupor, headache, delirium, twitchings, cramps, and
other symptoms indicative of functional impairment of the nervous
system.
Of all these manifold evidences of fever, the elevation of temperature
is the one whose cause, range, and results have been most carefully
and critically investigated. No record of a case in which fever is
present is regarded as complete without the chart of the daily
variations in temperature, respiration, and circulation. The practical
value of such records is thus admitted, and in the experiments
relating to the origin of animal heat the observations of temperature
are as essential as the chemical analyses, each of which supplements
the other.
The more accurate determination of the heat produced in the body is
obtained either by the use of the calorimeter (an apparatus for
measuring the collected heat liberated from the body) or by estimating
the quantity of heat produced in the destruction of the constituents
of the body from quantitative analyses of the discharged carbonic acid
and urea. The results of such investigations are regarded by
Rosenthal[5] as possessing only a relative value, but justify the
conclusion that most of the heat produced in the organism results from
the oxidation of its constituents.
[Footnote 5: _Hermann's Handbuch der Physiologie_, Leipzig, 1882, iv.
2, 375.]
For the preservation of health it is essential that this heat should
be removed from the body in such quantity that the temperature of the
latter shall not vary to any considerable extent, for any considerable
time, from 37.2° C. (98.4° F.). The removal of the heat is mainly
accomplished by its radiation or conduction into a surrounding cooler
medium, and by the evaporation of moisture from the surface of the
body. Too great a removal of heat results in death from freezing,
while too great an accumulation of heat terminates fatally from the
effects of an unduly elevated temperature. To ensure the normal range
of temperature, constantly changing relations must exist between the
production of heat and its dissipation. The cooler the surroundings,
the more must heat be produced, or the less must heat be evolved from
the body.
An increased production of heat is obvious under conditions of climate
demanding prolonged exposure to low temperature. An abundantly fatty
diet promotes the formation of heat, while suitable clothing checks
its dissipation. Although it is claimed by Liebermeister that sudden
exposure to cold stimulates heat-production, Rosenthal[6] disputes
this {39} statement, and maintains that it is still to be regarded as
doubtful whether the production of heat can be varied to suit the
demands of sudden and temporary changes of temperature. With the
admission of this doubt, the regulation of the temperature of the
body, under the circumstances just referred to, is mainly accomplished
through the influence of agencies favoring or checking the loss of
heat. Since heat is largely brought to the surfaces of the body by the
circulating blood, modifications in the fulness and rapidity of this
superficial current produce corresponding differences in the amount of
heat and moisture presented. Such variations are considered to be
accomplished through the action of the vaso-motor nervous system,
whose differing effects are apparent in the pale, cool skin and the
flushed, warm surface.
[Footnote 6: _Op. cit._, 413.]
The search for the regulation of such vaso-motor action has led to the
view that the production of heat, as well as its dissipation, may be
influenced from a nervous centre. Wood[7] claims that the result of
experiments made by him proves the existence of such a heat-centre in
or above the pons. Although admitting the possibility of its being a
muscular vaso-motor centre, he regards it rather as an inhibitory
heat-centre, which acts, as suggested by Tscheschichin, by repressing
the chemical changes in the constituents of the body through which
heat is produced.
[Footnote 7: _Op. cit._, 254.]
This view is objected to by Rosenthal,[8] on the ground that the facts
are not universally agreed upon, and their interpretation is somewhat
vague. Even the increased production of heat as determined by Wood, if
admitted, may be regarded as the result of a modified circulation.
[Footnote 8: _Op. cit._, 442.]
The preservation of a normal range of temperature in general is to be
recognized as the result of variations in the relation of
heat-production to heat-dissipation. The causes which influence this
relation may act from without or from within, and are regarded as
producing their effect by means of the vaso-motor nervous system. The
causes which act from within are those concerned in the febrile
elevation of temperature. Whether the latter is associated with, or
independent of, inflammatory processes, the question of first
importance relates to the modification of physiological conditions.
The causes of the physiological production of heat and its dissipation
have already been referred to, and the same elements demand
consideration in the pathological range of temperature so striking in
fever.
Relatively accurate inductions with regard to the origin of febrile
heat were first rendered possible by the experiments of Billroth and
Weber. These observers found that the introduction of putrid material
into the circulation of animals produced fever. It was afterward shown
that various substances, not necessarily of a putrid character, might
produce the same result.
From measurements with the calorimeter of the heat produced, it was
concluded by Wood[9] that in the fever of pyæmic dogs more heat was
produced than in healthy, fasting dogs, although less than in
high-fed, healthy dogs. An increased production of heat in the fevered
animal is thus obvious, as his capacity to receive and assimilate food
is considerably less than that of a high-fed, healthy dog. The
calculations of Sanderson, referred to by Wood,[10] based upon the
analyses of eliminated carbonic {40} acid and urea, show that the
febrile human subject produces very much more heat than the fasting,
though less than the fully-fed, healthy, man.
[Footnote 9: _Op. cit._, 236.]
[Footnote 10: _Op. cit._, 239.]
An increased production of heat in fever is generally admitted,
although it alone is not to be regarded as the essential feature in
the elevated range of the temperature. The fasting man or animal under
ordinary circumstances is not febrile, and an increased production of
heat from full feeding in health, equal to that observed in fever, not
being associated with fever, it is apparent that the retention of the
produced heat is of importance for the existence of fever. Although it
has been shown by various observers that more heat is dissipated
during fever than in health, this increased loss is not in proportion
to the increased production of heat. A persistent elevation of
temperature is the necessary result. This elevation is subject to
daily and hourly differences, as is the temperature of the healthy
individual. These variations in the range of the febrile temperature
are apparently due to an agency like that which dominates the course
of normal temperatures--viz. a varying action of the vaso-motor
nervous apparatus, as well as of that controlling the secretion of
sweat, now permitting, now checking, the dissipation of the produced
heat.
For the existence of the elevated temperature of fever, therefore,
there is demanded the presence of an agent within the body which, as
stated by Wood,[11] shall act "upon the nervous system which regulates
the production and dissipation of animal heat--a system composed of
diverse parts so accustomed to act continually in unison in health
that they become, as it were, one system and suffer in disease
together." It may be that there exists, as claimed by Wood and
Tscheschichin, a heat-centre independent of the vaso-motor and other
centres, through which heat is dissipated, or it may be, as maintained
by Rosenthal, that the vaso-motor system alone is concerned in the
regulation of temperature. Such action may be inhibitory or excitant,
according to the views of the one or the other author, without
affecting the main question as above stated.
[Footnote 11: _Op. cit._, 255.]
The elevation of temperature suffices to explain for the most part
certain of the other phenomena of fever, as thirst, digestive
disturbances, increased respiration, and emaciation. A coincident
affection of various cerebro-spinal centres is demanded to explain the
altered action of the heart and the numerous nervous symptoms which
are to be found in fever. The agent producing such manifold effects is
obviously no unit. It may be introduced from without or it may arise
within the body, and its transfer to the nervous centres is
undoubtedly accomplished through the circulation.
Among those agents which act from without are to be included the
specific causes of infective diseases. It is probable that these
produce the fever, as they occasion other symptoms of the disease, and
their action may be regarded as direct, or indirect through the
secondary products of their own vital changes. In the light of the
existing facts the products of minute organisms developed outside the
human body may give rise to fever when introduced, without the
organism, into the body. The history of septicæmia contains numerous
illustrations of the pyrogenetic properties of material produced in
connection with wounded surfaces of the body exposed to the action of
minute organisms. The introduction of blood of the same, or of a
different animal, into the {41} circulation of a given animal is
followed by fever, as is the injection of considerable quantities of
water into the blood-vessels. The same is true of various chemical
substances.
It is further obvious that the agents producing fever may arise within
the body. The fever resulting from the deprivation of water, and from
the destruction of tissues, are instances of the probable origin of
pyrogenetic substances from the rapid metamorphosis of tissues.
It is suggested by Samuel[12] that under given circumstances the fever
may be sanatory. This view is based upon the probability that certain
parasitic organisms are destroyed at such temperatures as may be
produced within the body. The growth of the bacillus of malignant
pustule takes place most vigorously at a temperature of 30.5° C. (95°
F.), while its development is feeble at 40° C. (104° F.). The bacillus
of tuberculosis, as shown by Koch, thrives at temperatures between 37°
C. (98.6° F.) and 38° C. (100.4° F.), but its growth ceases at
temperatures above 41° C. (105.8° F.). The spiral fibre of relapsing
fever, which is present in the blood in great abundance at the
beginning of the febrile onset, disappears at the close, the
temperature being 42° C. (107.6° F.). It is not to be found in the
intervals between the febrile paroxysms, but reappears a few hours
before the recurrence of the fever. The history of intermittent fever
suggests a similar relation between its cause and the febrile periods.
[Footnote 12: _Op. cit._, 155.]
The value of pain as evidence of inflammation is merely relative. Its
existence depends upon the presence of sensitive nerves, and those
inflammations are the least painful which occur in parts where such
nerves are fewest.
The pain of inflammation is attributable to the pressure upon the
nerves of that product of the inflammation known as the exudation.
This pressure becomes all the greater the more abundant the exudation,
or the greater the obstruction offered to its diffusion throughout the
inflamed part. The intense pain resulting from inflammation of the
fascia or of the periosteum is thus explained, while an inflammation
of the loose connective tissue may be diffused over a wide area with
little or no pain. In the chronic varieties of inflammation, where the
exudation is but scanty, and its accumulation extended over a long
period of time, there may be no pain during the entire course of the
inflammation.
Swelling remains for consideration as the most important of the four
cardinal symptoms. Like the others, its presence is not absolutely
essential. It may exist at one time in the course of the inflammation,
and may be absent at another. Even a diminution in the size of an
organ may suggest the existence of an inflammation, for the yellow and
cirrhotic atrophies of the liver give evidence, respectively, of an
acute and chronic inflammation of this organ.
The swelling of an inflamed part is due to the presence of an
increased quantity of blood, and lymph, and to the exudation. These
constituents of the swelling are not of equal importance. Although the
quantity of blood in the part is increased, no considerable swelling
is produced, provided the flow of blood and lymph from the part be
unobstructed. The current of lymph through the larger lymphatics may
be greatly increased, yet a decided swelling be absent, unless there
is an obstruction to the passage of lymph from the inflamed region.
{42} The exudation is the most essential element of the swelling, and
our knowledge of its origin and fate includes the most important
features of the general pathology of the processes concerned.
The inflammatory exudation is represented by the accumulation, outside
the blood-vessels, of material previously within them. The prevailing
views concerning the manner of origin of this exudation, and its
relation to inflammatory processes, are essentially due to the
rediscovery by Cohnheim of the forgotten observation of Addison, that
white blood-corpuscles pass through the apparently intact walls of the
blood-vessels.
In the observation of the mesentery or other transparent part of a
suitable animal, the changes taking place in inflammation are, at the
outset, limited to the blood-vessels and their immediate vicinity. The
vessels become dilated and the rapidity of the flow within them is
soon diminished. In the veins particularly the white blood-corpuscles
separate in considerable numbers from the general current and line the
wall in constantly-increasing numbers, while the red corpuscles are
borne along the middle of the stream. The white corpuscles stagnate,
stick to the wall for a longer or shorter time, and often change their
place, while the red corpuscles are in constant and progressive
motion. In the capillaries a considerable number of white corpuscles
are found in contact with the wall, but numbers of red corpuscles are
associated with them. The formation of the exudation now begins by the
passage of white corpuscles through the apparently intact wall of the
veins and capillaries, especially of the former. Limited numbers,
under ordinary circumstances, of red corpuscles also make their way
through the walls of the capillaries. This is the phenomenon of
emigration, and is associated with the amoeboid movements of the white
corpuscles.
With the passage outward of the white and red corpuscles there is also
the effusion of liquid material. Both the liquid and solid
constituents continually escape and spread in all directions beyond
the wall, following the course of the least resistance. It is probable
that this course is defined by the pre-existing spaces within the
tissues of the part, the lymph-spaces. The exudation is more abundant
in parts richly provided with blood-vessels and in those containing
the larger spaces; it is diminished where the vessels are less
numerous or the surrounding parts more resistant, with smaller and
fewer lymph-spaces. The resulting swelling is the less when ready
opportunities for the diffusion and removal of the exudation by
lymphatics and veins are presented, and when the material appears upon
surfaces over which it may flow away.
The liquid portion of the exudation represents something more than the
transuded blood-serum, and a certain practical importance results from
the distinction drawn between an exudation and a transudation. Such a
distinction is especially called for when the inflammatory or
non-inflammatory origin of considerable quantities of fluid in the
larger cavities of the body is concerned. From a recent contribution
to our knowledge of this subject by Reuss[13] the following
information is derived: The percentage of albumen is always greater in
exudations than in transudations, and is more constant in the former
than in the latter. It increases with the severity of the
inflammation, being highest in the ichorous forms, less in the
purulent, and least in the serous exudations. When an {43}
inflammatory exudation is found to contain less albumen than usual,
the existence of a transudation with secondary inflammation is
suggested, or the exudation may have taken place in a hydræmic
individual. A sufficient number of exceptions are met with, however,
to interfere with the absolute nature of this test.
[Footnote 13: _Deutsches Archiv für Klinische Medicin_, 1879, xxiv.
583.]
The coagulation of an inflammatory exudation apparently depends upon
the contained white blood-corpuscles; the more numerous (within
certain limits) these are in a serous exudation, the more abundant is
the formation of fibrin. The cellular element likewise is that which
in abundant liquid exudations characterizes them as purulent. Although
it is generally agreed that most of the corpuscles of pus are
emigrated white blood-corpuscles, it is not necessary to admit that
all are of this nature. The cells present in an inflamed part include
those pre-existing, as well as those which escape from the vessels.
The former are the wandering cells of the connective tissues, as well
as the fixed variety, the epithelial cells of the surface of a mucous
membrane in addition to the subjacent connective-tissue cells.
Amoeboid cells outside the blood-vessels have been seen to divide, and
it is possible that such duplication may serve as the method of
formation of a certain number of pus-corpuscles. The statements
concerning the proliferation of the fixed connective-tissue cells and
of epithelium are derived from appearances, and are interpretations of
these appearances, not observations of a process.
The changes taking place along the walls of the blood-vessels being
the feature of prime importance in the observation of the progress of
an inflammation, numerous investigators have directed their attention
to the determination of the nature of the changes in the vessel wall
by means of which the escape of the corpuscles is permitted. Arnold
represents the most strenuous advocates of the stomata theory,
according to which the leucocytes pass through canals normally
existing in the wall. By means of the silver method of staining, and
by injections of various insoluble pigments into the blood-current,
certain results are met with, which give color to the view that pores
and canals are present upon and in the walls of the vessels, analogous
to those found in the diaphragm. As the latter have been shown to be
in direct communication with the lymphatic system of tubes and spaces,
so the walls of the blood-vessels have been assumed to present similar
channels of communication.
The prevailing views at the present time are in favor of the
artificial nature of the stomata and pores in the walls of the
blood-vessels. An increased porosity of the vascular wall in
inflammation is necessary for the occurrence of the exudation, but
such porosity is regarded rather as a physical condition permitting an
observable filtration, and a filtration of solids as well as liquids.
In this connection reference should be made to the observation of
Winiwarter, who has demonstrated that colloid material, a solution of
gelatin, passes through the vascular wall in inflammation more
readily--_i.e._ under less pressure--than through the normal wall of
the blood-vessel.
The causes of inflammation are to be regarded as those which produce
an increased porosity of the vessel wall without causing its death,
for no exudation escapes from a dead vessel, its contents becoming
clotted.
These causes may act from without or from within, primarily affecting
{44} the tissues outside the vessels, or exerting their action, at the
outset, upon the wall itself. The usual histological relation of
vessels and surrounding tissues is such that both are simultaneously
affected. The occurrence of an inflammation in non-vascular parts,
however, as the cornea, from irritation of its centre, the part
farthest removed from the surrounding blood-vessels, shows that the
affection of the vessels may be indirect as well as direct. This
indirect action is to be regarded as taking place through the agency
of nerves or through that of the nutritive currents. That nervous
influence alone does not suffice to transmit the effect of an applied
cause is apparent from the absence of inflammation of the cornea which
has become anæsthetized by section of the trigeminus nerve. With the
protection of the cornea from external irritation there is an absence
of inflammation.
The consideration of the final symptom of inflammation, the
disturbance of function, which has been added in recent times, belongs
to special rather than general pathology. It varies according to the
seat of the inflammation, the disturbed function of the brain or heart
differing from that of the liver or kidney. The clinical importance of
this symptom of inflammation is greater than of all the rest, as it is
the one whose presence is constant and indispensable.
An inflammation may exist, as already stated, without heat, redness,
or pain. The swelling may escape observation from the limited quantity
of the exudation and other causative agents, or from the
inaccessibility of the inflamed part to physical examination. The
disturbance of function, however, becomes early apparent, and is
present throughout the course of the inflammation. A knowledge of its
nature enables the seat of the latter to be recognized, and its
variations furnish a desired test of the efficiency of therapeutic
agents.
* * * * *
The causes of inflammation may be divided into the traumatic, toxic,
parasitic, infectious, dyscrasic or constitutional, and trophic.
The traumatic causes are those which act mechanically, producing an
injury to tissues by pressure, crushing, tearing, stretching, and the
like. Others represent modifications in temperature, thermic agencies,
and include extremes of cold as well as of heat. The chemicals whose
action is direct, as caustic, include a third variety of the traumatic
causes. Such chemicals are applied to surfaces, cutaneous or mucous,
and comprise the active element producing the perforating ulcer of the
stomach and duodenum, as well as such substances as potash or
sulphuric acid which may have been swallowed intentionally or
accidentally.
The toxic group of causes is closely allied to the chemical variety of
the traumatic agencies. It includes chemicals whose action is
indirect, through absorption in a diluted form rather than from direct
application in a concentrated condition. Such chemicals are derived
from without, as arsenic, phosphorus, and antimony; or may be formed
within the body, and the latter include the chemical products of
putrefactive changes--in the urine, for instance--and, with
considerable probability, certain of the active agents of
blood-poisoning in septic diseases. It is not unlikely that some of
the inflammatory affections met with among the so-called
constitutional diseases, as rheumatism and gout, may owe their origin
to the production of chemical substances within the body, excessive in
quantity if not changed in quality.
{45} The parasitic causes of inflammation are both animal and
vegetable, and act upon the surfaces of the body or within its
deeply-seated parts. Some of the animal parasites act locally at their
place of entrance, while others produce but slight disturbances in
this region, their effects usually resulting from the transfer of
their offspring to remote parts of the body. The vegetable parasites
are for the most part the various fungi, which act locally upon the
skin or on those transitional surfaces lying between skin and mucous
membrane. The resulting parasitic inflammations are known as favus,
sycosis, ringworm, thrush, etc. The border-line between such parasitic
diseases and those included among the infective diseases is somewhat
arbitrarily drawn. Parasites in the limited sense act chiefly as
foreign bodies, while the effect of minute vegetable organisms is
rather that of ferments, in virtue of their products. Such a
distinction is of relative value merely, as the micrococci and
bacteria are capable of acting in other ways than by the production of
septic material.
The infectious causes of inflammation are for the most part parasitic
in their nature, although the discovery and identification of the
parasite are in most of these inflammations assumed rather than
demonstrated. The relation of the anthrax bacillus to malignant
pustule no longer admits of a doubt, mainly in consequence of the
researches of Koch. This investigator has been enabled to establish a
definite etiological relation between the septicæmia of certain
animals and accompanying minute vegetable organisms. His recent
discovery of the bacillus of tuberculosis definitely removes the
tubercular process from the group of dyscrasic or constitutional
affections to that of the infective diseases. The constant presence of
minute organisms in relapsing fever, leprosy, malaria, typhoid fever,
diphtheria, erysipelas, and numerous other affections associated with,
if not characterized by, inflammatory conditions, renders extremely
probable the closest pathological relation between such diseases and a
microscopic organism. That an inflammatory process may be regarded of
infectious origin, it is necessary, according to Koch,[14] that a
characteristic organism should be found in all cases of the disease,
and in such numbers and distribution as to account for all the
phenomena of the disease in question.
[Footnote 14: _Untersuchungen über die Aetiologie der
Wundinfectionskrankheiten_, 1878, 27.]
These organisms may act in virtue of their growth and the consequent
demand for oxygen, as seems probable in certain cases of malignant
pustule, where the affected individual dies with symptoms of asphyxia.
Their operation may also be like that of ferments, which produce
chemical material whose effect may be remote from the immediate
presence of the minute organism. They may likewise, in connection with
their colonization in various parts of the body, act more immediately
upon the walls of the blood-vessels, and produce that increased
porosity which is so essential a factor in inflammation.
The discovery of the immediate cause of the various infective
diseases, as measles, scarlatina, variola, cholera, dysentery, mumps,
whooping cough, cerebro-spinal meningitis, and numerous other epidemic
and endemic affections, still remains a question for the future. The
constant association of microbia with any or all of such diseases is
but one fact in connection with them, and such a discovery is to be
regarded merely as a step forward, to be followed by others, each of
which represents not only an advance, but confirms the position
attained.
{46} The dyscrasic or constitutional causes of inflammation are those
which, though long established, appear less demanded as our knowledge
advances. Regarded as the result of an alteration in the composition
of the blood, it is obvious that such changes may arise from the
introduction, from without, of wholly foreign material. The dyscrasia
may also represent modifications in the relative proportion of the
normal constituents of the blood. In the former series are included
what, for the most part, have already been referred to under the toxic
and infectious causes of inflammation. The dyscrasiæ from lead,
alcohol, and the like belong to this series. Still more important are
the poisons, the virus of tuberculosis and scrofula, of leprosy and
syphilis. The dyscrasiæ known as anæmia, leucæmia, uræmia, icterus,
and diabetes are to be regarded less as inflammatory causes than as
predisposing conditions which favor the action of other groups of
causes.
The trophic causes of inflammation are those whose action is supposed
to take place through the influence of nerves. Although, as has
already been stated, a faulty innervation of tissues is an important
element in favoring the action of various inflammatory causes, there
remain certain forms of inflammation where the disturbance of nervous
action seems to be the essential feature. The occurrence of an acute
peripheral gangrene soon after certain traumatic or inflammatory
lesions of the brain or spinal cord, of articular inflammation
following chronic affections of the cerebro-spinal axis, are instances
in point. The origin and distribution of herpes zoster, the occurrence
of sympathetic ophthalmia and symmetrical gangrene, suggest a
predominant disturbance of innervation as the exciting cause. At the
same time, it is desirable to call attention to the recent
observations of MacGillavray, Leber, and others,[15] which suggest
that a sympathetic ophthalmia is due to the extension of a septic
choroiditis along the lymph-spaces of the optic nerve. It is further
apparent that in certain so-called trophic inflammations, as the
pneumonia after section of the pneumogastric, and the inflammation of
the eye following paralysis of the trigeminus, the paralysis of the
nerve is a remote, rather than an immediate cause, of the
inflammation. There still remain, however, a number of localized
inflammations whose origin is so intimately connected with nervous
disturbances as to demand, for the present at least, a corresponding
classification.
[Footnote 15: Wadsworth's "Report of Recent Progress in
Ophthalmology," _Boston Medical and Surgical Journal_, 1882, cvi.
517.]
The course of an inflammation is often indicated by the predominance
of certain symptoms, which, for the most part, indicate a condition of
the individual acted upon rather than a peculiarity of the cause. The
sthenic inflammations take place in robust individuals with powerful
hearts and an abundant supply of blood. In such persons a strong
pulse, high fever, and an injection of the superficial blood-vessels
suggested, in former times, the necessity of bloodletting as the
essential therapeutic agent. The sthenic form of inflammation was most
commonly associated with pneumonia, where the obstruction to the
passage of blood through the lungs was an important cause of the
superficial injection of the blood-vessels.
The asthenic inflammations, on the contrary, are those occurring in
feeble individuals, debilitated in consequence of pre-existing
disease, exposure, or habits. A weak heart, low febrile temperature,
and {47} superficial pallor, characterize the asthenic inflammations,
which show a frequent tendency to become localized in the more
dependent parts of the body, the force of the circulation being too
feeble to overcome the effect of gravitation.
In the typhoidal inflammations are associated those symptoms which are
so prominent in the severe varieties of typhoid fever. These are the
predominant symptoms: hebetude or low, muttering delirium, picking at
the bed-clothes, involuntary evacuations, stertor, and the like. The
nervous disturbances are associated with a feeble pulse and a dusky
hue of the skin.
The constituents of an inflammatory exudation are frequently used as a
basis of classification, and characterize the inflammation from the
anatomical point of view. As the exudation is complex in its
composition, the predominant element is made use of to designate the
variety, and in doubtful cases a combined adjective indicates the
presence of the two most abundant constituents. As the exudation is
directly derived from the blood and contains serum in addition to
white and red corpuscles, the serous, purulent, and hemorrhagic
varieties of exudation naturally arise. The fibrinous and diphtheritic
inflammations relate to the presence of membranes or false membranes.
Finally, there are the productive inflammations, resulting in the new
formation of tissue, and the destructive inflammations, where losses
of substance occur.
Serous inflammations are most frequent in those parts of the body
where the structure contains the largest lymph-spaces. The so-called
serous cavities of the body offer the most favorable opportunities for
the accumulation, as well as for the exudation, of the inflammatory
product; then follow the regions of the larger lymph-spaces, according
to the size and number of the latter.
The serous inflammations may also arise from the epithelial coverings
of the body, as the cutaneous, alimentary, and respiratory surfaces.
The serous exudations of the skin are those present in vesicles,
blisters, or bullæ, which owe their limitation to the resistance
offered to the spreading of the liquid inflammatory product by the
coherent epidermis. Serous inflammations of the alimentary canal may
assume a vesicular character, although, from the structure of its
mucous membrane and the macerating influence of its contents, the
vesicles are apt to be of an extremely transitory character.
The more important serous inflammations of the intestines are those
manifested by profuse watery evacuations, the extreme form of which is
to be found in cholera.
Serous inflammation of the lungs accompanies the more severe forms,
and usually represents but a limited and circumscribed affection,
associated with more abundant cellular and fibrinous products.
Serous inflammations of the peritoneum, pleura, pericardium, tunica
vaginalis, and central ventricles often give rise to the presence of
enormous quantities of fluid, whose partial removal from many of the
cavities concerned by operative measures frequently represents a most
beneficial result of treatment.
The smaller lymph-spaces of the connective tissue in various parts of
the body are the frequent seat of the inflammatory oedema, so called,
whose presence is an important indication of the direction assumed by
a {48} spreading inflammation, as well as a suggestion of the frequent
virulence of its cause.
In general, the serous inflammations are to be regarded as less severe
than other varieties, or as representing an early stage of what later
may be otherwise characterized by a change in the nature of the
products.
The purulent variety of inflammation is present when the exudation is
abundantly cellular. As has already been stated, such cells are, for
the most part, white blood-corpuscles. The purulent exudation, like
the serous variety, may appear either on surfaces, when the term
secretion is applied, or within the lymph-spaces of the connective
tissue over a considerable space, when the pus is said to be
infiltrated. When the infiltration is more circumscribed and the walls
of the affected lymph-spaces are destroyed, so that adjoining cavities
are thrown into larger holes, an abscess is present, from whose wall
pus is constantly derived, while the inflammation is progressive.
The attention of the surgeon, in particular, has been directed to the
isolation of the immediate cause of suppurative inflammation, and the
modern, antiseptic, treatment of wounds is essentially based upon the
view of the infectious origin of pus. The frequent presence of
microbia in purulent exudation where no precautions are taken to
exclude their admission, and their frequent absence or presence in
minute quantities where such precautions are taken, have suggested
that through their influence an inflammatory exudation is likely, if
not actually compelled, to become purulent.
Whether the microbia or their products are the cause of most
suppurative inflammations may be regarded as an open question. It is
generally admitted, however, that, as a rule, an inflammation becomes
purulent in consequence of the presence of an infective agent; in
other words, that most pus is of an infectious origin and possesses
infectious attributes. The labors of Lister in insisting upon the
exclusion of all possible putrefactive agencies in the treatment of
wounds have met with universal approval, and the basis of his
treatment remains fixed, although different methods have been devised
for its enforcement. His researches, and those stimulated by his work,
have resulted in the establishment of principles which affect the
whole field of theoretical as well as practical medicine.
Although most pus may be considered as due to the action of a virus
introduced from without, and capable of indefinite progressive
increase within the body, all pus is not to be regarded as of
infectious origin. There are pyrogenetic agencies, like petroleum,
turpentine, and croton oil, which, introduced into the body, produce
suppurative inflammation without the association of microbia.
A bland pus is usually in a state of beginning putrescence, so that it
is only relatively bland, and acquires extreme virulence when long
exposed to putrefactive agencies. It is possible that those agencies
producing an ichorous pus are the same or different from those present
in bland pus. The ichorous exudation contains less corpuscles than
bland pus, is more fluid, less opaque, strongly alkaline, of a
greenish color, and of offensive odor.
In hemorrhagic inflammation the exudation contains large numbers of
red blood-corpuscles. The occurrence of this form is sometimes
associated {49} with peculiarities of the cause, as is obvious from
the epidemics of hemorrhagic small-pox, measles, scarlatina, and
cerebro-spinal meningitis. It is also associated with peculiarities of
the individual, as in such epidemics all cases are not equally
hemorrhagic, and in scurvy the hemorrhages are attributable to the
abnormal conditions to which the sufferers are exposed. Hemorrhagic
exudations are also met with in those inflammations of serous surfaces
accompanying the outcropping of tubercular and cancerous or
sarcomatous growths. In all cases a hemorrhagic exudation represents a
grave complication, and when found in serous cavities has a certain
diagnostic, as well as prognostic, importance.
Fibrinous inflammations are characterized by the presence in the
exudation of considerable quantities of fibrin. As the prevailing
theory of the formation of fibrin demands fibrino-plastic as well as
fibrinogenous material, both are to be sought for in the exudation.
The latter is present in the liquid portion of the exudation; the
existence of the former, as well as that of the ferment, is dependent
upon the presence of the white blood-corpuscles. The more numerous
these, within certain limits, the more abundant the formation of
fibrin. As their death appears essential for the fibrinous
coagulation, the latter is most constantly met with in those parts of
the body where the white blood-corpuscles are quickest separated from
influences favoring their life. The farther removed they are from the
blood-vessels, the more likely is their early death. Fibrinous
exudations are therefore frequent and abundant in cellular and serous
(sero-cellular) inflammation of the great serous cavities of the body.
The clotted fibrin appears as false membrane lying upon the serous
surface, either smooth or rough, tripe-like, or as villosities
projecting above the surface, and again as bands, fibrinous adhesions,
stretching across the cavity and uniting opposed surfaces.
The frequent occurrence of fibrinous exudations on the mucous
membranes of the larynx and trachea, accompanied by the suffocative
symptoms known as croup, has led to the use of the term croupous
inflammation as synonymous with fibrinous inflammation, and its
application to various parts of the body where croupous--_i.e._
suffocative--symptoms are not in question. Croupous inflammation, when
used, is to be considered as an anatomical term, indicating merely the
production of fibrin, and, for the avoidance of confusion, it is
preferable to substitute fibrinous for croupous when such
inflammations are described.
The disease, croup, it is well known, may exist without a
croupous--that is, fibrinous--inflammation, as is familiarly
recognized in the constant use of the terms spasmodic, membranous, and
diphtheritic croup.
Fibrinous inflammation of the mucous membrane of the larger
air-passages is much more frequently met with than that of mucous
membranes elsewhere, as of the intestines, uterus, and bladder. The
pseudo-membranous inflammations of the latter tracts are more commonly
the result of the catarrhal and diphtheritic varieties than of the
fibrinous form. Fibrinous exudations on mucous surfaces, according to
Weigert, can only take place when the epithelium is destroyed. Hence
those causes which give rise to the destruction or detachment of the
epithelium are alone capable of producing a fibrinous inflammation of
mucous membranes, and a fibrinous laryngitis, trachitis, and
bronchitis may result from {50} the local application of such
irritants as steam or ammonia, as well as occur in the diseases croup
and diphtheria.
Fibrinous exudations may also be present within tissues, especially in
those whose meshes are wide, provided the essential elements of
coagulation are present. The coagulative necrosis of various organs,
to be more fully mentioned hereafter, is closely allied to fibrinous
clotting, the fibrino-plastic element being derived from the death of
the parenchymatous cells of the part.
In the existence of a fibrinous pneumonia the conditions are somewhat
analogous to those present in the fibrinous inflammation of serous
surfaces and of the areolar connective tissue. There is present an
abundantly cellular exudation, held in the place of its origin, the
cells undergoing rapid death and surrounded by a wall whose
superficial cells resemble in structure, if not in origin, the
endothelial cells lining the smaller lymph-spaces of connective
tissue, as well as the larger cavities within the same, known as
serous cavities.
The diphtheritic inflammation is no more to be confounded with the
disease diphtheria than is the fibrinous inflammation with the disease
croup. Although diphtheria owes its name to the frequent presence of
an apparent membrane, it may be said that the latter is not essential
to the existence of the former. Diphtheria, like croup, is an
affection in which various exudations may be present, and the
anatomical product alone does not suffice in all instances for the
recognition of the disease. In croup there may be a swollen mucous
membrane, with a slight superficial mucous exudation, or a more
abundant exudation of desquamated epithelium and mucus, as well as a
fibrinous false membrane. In diphtheria the same varieties of
exudation may occur, and in addition the diphtheritic exudation may
also be present. The latter, however, is not limited to the disease
diphtheria, for its presence is apparent in other mucous membranes
than that of the air-passages, and in the pharyngeal mucous membrane
in other diseases than diphtheria. A diphtheritic conjunctivitis,
enteritis, cystitis, and endometritis are recognized. The cutaneous
surfaces of the body may also furnish a diphtheritic exudation. The
diphtheritic inflammations of wounds and of variolous eruptions are
instances in point.
The characteristics of a diphtheritic inflammation are the presence
within the tissues of a clotted exudation, which is associated with a
defined swelling and death of the part. The exudation contains not
only dead leucocytes and interlacing fibres, but is also provided with
abundant granular material, much of which presents the well-known
peculiarities of microscopic organisms. The apparent false membrane is
thus dead, infiltrated tissue, which may be torn away from the
continuous unaffected tissue, leaving a raw, rough surface, but not
peeled from a comparatively smooth surface, as in other forms of
pseudo-membranous inflammation.
The frequent association of a superficial false membrane,
corresponding in area with that of the deeper-seated changes, in which
cells and fibres may be present, is to be recognized. The diphtheritic
process, however, is localized within, and not upon, the tissues
affected. The diphtheritic exudation represents a local death, a
necrosis, of the part concerned, and the result has frequently been
compared with the death consequent upon the action of a caustic.
{51} The immediate cause of a diphtheritic inflammation is now
generally attributed to the action of microbia which enter the tissue
from without, and in their growth beneath the surface produce not only
the local, but also the remote, constitutional disturbances which are
associated with a diphtheritic inflammation. The investigations of
Wood and Formad[16] point to ordinary putrefactive organisms as a
sufficient cause for the diphtheritic inflammation of diphtheria,
while other observers demand a specific organism as the exciting
cause. The occurrence of diphtheritic inflammations in various parts
of the body, in regions, as the intestine, where putrefactive
processes are constantly present, and in the bladder and uterus, where
the phenomena of putrefaction are often associated with diphtheritic
inflammation, suggest the efficacy of ordinary putrefactive agencies
in producing the latter. As all microbia found in putrefaction are not
alike, and as the properties of certain, differ from those of others,
and as our knowledge of the effects of all is but fragmentary, the
characteristics of specific germs for a diphtheritic inflammation of
one part of the body, or of all parts of the same, must still be
regarded as not proven.
[Footnote 16: _Research on Diphtheria for the National Board of
Health_, 1880, Supplement No. 7.]
Productive inflammations are those which result in the new formation
of tissues. One of the frequent products of inflammation is fibrous
tissue, which, at first abundantly cellular, later becomes more
vascular, and is finally transformed into a tissue whose fibres
predominate over its cells. This formation of a cicatricial tissue
demands further recognition when the termination of inflammation is
considered.
In a more limited sense certain inflammations are called productive
when multiple circumscribed new formations, as cancer, sarcoma,
tubercle, and the like, arise in connection with the ordinary products
of inflammation. Such new formations are of frequent occurrence in
serous membranes, and a tuberculous pericarditis or a cancerous
peritonitis, indicates that a growth of tubercles or cancerous nodules
has taken place, in addition to a more or less abundant exudation with
various proportions of serum fibrin and cells. This association of
ordinary and transitory inflammatory products with the formation of
more permanent tissues may be found within organs as well as upon
surfaces. A tubercular arachnitis or lepto-meningitis presents the
various products of an inflammation of the pia mater with an abundant
formation of tubercles. In like manner, a tubercular pneumonia, or a
tubercular nephritis suggests an association of neoplastic growth and
inflammation, in the lung and kidney. Such a relation offers a basis
for the theory in favor of the inflammatory origin of tumors, and is,
in part at least, a cause for the frequent consideration of tubercles
as mere inflammatory products, wholly cellular or cellular and
fibrous, subject to the same modifications as take place during the
course of ordinary inflammations.
Even if tuberculous and scrofulous inflammations are regarded as
inflammatory processes, modified by a specific cause and by
peculiarities of the individual, the cancerous and sarcomatous
inflammations are still to be considered as representing an
association of inflammatory disturbances and specific new formations,
the cause of the latter not being the cause of the former. As ordinary
inflammations of the regions concerned may take place in the absence
of the neoplasms, so may the {52} specific growth appear in the same
regions without anatomical or clinical evidence of inflammation.
The classification of inflammation as to its products is supplemented
by distinctions drawn with reference to the seat. The exudations may
be superficial or deep-seated; they may lie within the cells,
parenchyma, of an organ, or within the interstitial tissue of the
same.
The product of superficial inflammations may lie on the surface, as in
the case of inflamed mucous membranes, or immediately below the
surface, as in numerous cutaneous inflammations, of which erysipelas
may serve as the type. The term catarrhal, applied to superficial
inflammations, carries with it the idea of displacement, flowing, of
the exudation. The product of a catarrhal inflammation must be largely
liquid, that such a displacement may readily take place, and the
catarrhal exudation is chiefly composed of an excess of those elements
which are present in the normal, physiological secretion from the
membrane concerned. Mucus therefore represents a frequent constituent
of the catarrhal exudation, and mucous as well as muco-purulent
catarrhs of the gastro-intestinal, bronchial, genito-urinary, and
other mucous membranes are recognized. The catarrhal inflammation of
the respective membranes usually represents the mildest form, as it
demands an intact epithelium, and a ready removal of the inflammatory
product.
As the cause of a catarrhal inflammation may occasion a destruction of
the epithelium or a necrosis of the mucous membrane, the frequent
association of catarrhal with fibrinous or diphtheritic inflammations
is obvious. In such cases the clinical importance of the latter
varieties gives them the precedence in the designation of the
inflammation. The retention of the catarrhal products is the frequent
cause of permanent disturbances of a more or less serious nature.
These result in part from the mechanical obstruction offered to the
function of parts beyond the seat of obstruction, as pulmonary
atelectasis; and in part from the changes taking place in the retained
product. Purulent otitis media with its dangerous or fatal results,
and gangrene of the lung terminating in septic pleurisy, are not
infrequent instances of severe disturbances from putrefaction of the
retained products of a primarily catarrhal inflammation. A cheesy
degeneration of the catarrhal cells leads to a surrounding fibrous, or
destructive, inflammation, with a corresponding diminution in the
function of the organ affected.
Of the deep-seated varieties of inflammation, that requiring special
mention is the phlegmonous form. This runs its course within the less
dense fibrous tissue known as the areolar or cellular tissue. The term
cellulitis is usually employed by English writers to indicate the seat
and nature of the process, and although the use of the term cellular
tissue is rapidly becoming obsolete, the convenience of cellulitis
favors the retention of the latter name.
The exudation lies within the larger lymph-spaces, and is therefore
sometimes designated as the result of a lymphangitis, the deep-seated,
wider lymph-spaces being concerned rather than those more superficial.
Certain forms of phlegmonous inflammation are of decidedly infectious
origin, and, when seated subcutaneously, are known as phlegmonous
erysipelas, being thus distinguished from the simple erysipelas, whose
seat is defined by the small superficial lymph-spaces of the skin.
{53} Infective forms of cellulitis are also frequently met with in the
loose, sub-peritoneal tissue of the pelvis. The infectious element
usually proceeds from the uterus, and excites the malignant oedema of
the broad ligament, the septic parametritis, or the pelvic cellulitis,
according as the lymph-spaces inflamed lie nearer the fundus or
cervix, and as the direction of the current is upward toward the
spine, or outward toward the sub-peritoneal lymphatics of the pelvic
wall.
Parenchymatous inflammation is present when the exudation is taken
into the cells of an organ, or when the changes dependent upon
inflammation of an organ take place within its functionally important
cells. Virchow originally used the term parenchymatous inflammation in
contradistinction to secretory inflammation, the changes in the former
occurring within the elements of the tissues, while in the latter the
exudation made its appearance on the surface of the organ.
Parenchymatous inflammation is manifested by a degeneration of the
cells affected. This may terminate in their destruction through the
conversion of their protoplasm into fat-drops, fatty degeneration;
although more frequently a simple accumulation of albuminoid granules
(granular degeneration) occurs. The latter represents a transitory
condition, from which a return to the normal state readily takes
place. This form of inflammation is met with in those organs which
present a sharply-defined contrast between the functionally important
cells and the connective tissue which surrounds them. The liver,
kidneys, heart, spleen, pancreas, and glands in general, are
consequently the most frequent seat of parenchymatous inflammation.
Opposed to this variety is the interstitial inflammation. The
exudation of the latter remains within the connective-tissue framework
of the organ. It is essentially cellular in character, and the number
of cells is comparatively small. With their presence and the
possibility of their nutrition a permanent increase in the quantity of
the fibrous tissue of the organ is permitted. This becomes relatively
greater in the course of time, and the parenchymatous cells become
degenerated and absorbed. Interstitial inflammations are likely to
become chronic in character, and, from the outset, are usually
associated with parenchymatous changes.
An important clinical distinction is drawn with reference to the
duration of an inflammation. Acute inflammations are those whose
course is rapid, whose progress is associated with graver disturbances
of function, and with a greater prominence of the cardinal symptoms.
The chronic forms occupy more time in their progress, the functional
disturbances, though severe, are injurious more from their protracted
persistence, than their temporary violence, while redness, swelling,
heat, and pain are symptoms of trifling prominence.
The exudation in acute inflammation, if recovery takes place, is
rapidly removed from the place of its origin, while in the chronic
variety it tends to become a part of the region in which it lies, or,
if removed, slowly disappears, and may be constantly replaced. Acute
inflammations may become chronic, and the chronic variety is liable to
acute exacerbations.
The distinction between acute and chronic inflammations is essentially
one of convenience, and, when considered from the anatomical point of
view, relates rather to the persistence of the results. These may be
{54} present as a variously modified exudation or as a degenerated
condition of the parenchyma of the organ or tissue affected.
Inflammation terminates in resolution, production, or destruction.
For resolution to occur it is necessary that the causes of
inflammation cease to act, either by their removal or their isolation,
and that their results be removed. With the removal of the results
there is often associated the removal of the cause. That such may take
place it is necessary that the function of the vessel walls be so
restored that the exudation ceases to escape. Inflammatory products
already outside the vessels, if present on surfaces with external
outlets, are carried along in the course of the excretions. If they
lie within the cavities of the body not opening externally, their
removal is accomplished through the medium of the circulating lymph
and blood, by absorption. The liquid portion of the exudation becomes
a part of the circulating fluids of the body. The fibrin is converted
into a granular detritus, which eventually disappears from the place
of its formation. The leucocytes may return to the blood-vessels or
enter the lymphatics; the latter course probably being the one taken
by the larger number of the corpuscles. Many undergo a fatty
degeneration, and as they lie in lymph-spaces their conversion into an
emulsion permits a removal of the mechanical obstruction to the flow
of lymph through the spaces in which they were accumulated. The red
blood-corpuscles are destroyed, their pigment being dissolved by the
surrounding fluid and removed in the course of the circulation and
excretions, or it becomes transformed into granules or crystals, which
may remain in the place of their formation, or be transferred, within
amoeboid cells, to remote parts of the body.
When the exudation is abundant, as in the great lymph-sacs of the
body--the several serous cavities--and especially when the openings in
the walls of these sacs are obstructed or the currents within them are
feeble, absorption takes place with great difficulty, and demands a
long interval of time. The fibrinous and cellular portion of such an
exudation frequently becomes converted into a caseous mass, from a
partial fatty degeneration and inspissation. This mass becomes
isolated from the cavity in which it lies, usually at the most
dependent portion, by the formation of a capsule of connective tissue.
It may subsequently become infiltrated with lime salts, calcified, and
thus remain comparatively inert throughout the life of the individual.
The productive termination of inflammation is manifested by the new
formation of connective tissue. This tissue is variously designated,
as the inflammatory process is limited to the surfaces of the body
exposed to the air, or the surfaces of cavities and organs, or as it
lies within organs or the deep-seated parts of the body. In numerous
instances it becomes a permanent constituent of the body, and, as time
is usually essential for its formation, its occurrence is indicative
of a chronic, rather than an acute inflammation. Certain chronic
inflammations are progressive in character, the production of
connective tissue being continuous, with perhaps occasional
intermissions, as in the chronic interstitial inflammations of organs
and tissues. The new-formed tissue, which at the outset is rich in
cells, becomes in time more fibrous, and associated with this change
in structure is a physical modification, manifested by its shrinkage.
This new formation may fill a gap resulting from the destruction of
tissue in {55} the progress of an inflammation, when it is present as
cicatricial tissue--the scar which is usually met with upon the
surfaces of the body or of certain of its organs. When opposed
surfaces are united by the new-formed tissue, the term adhesion is
applied; the adhesions being present as fibrous bands, cords, or
membranes. The pericardial milk-spots and thickenings, the tendinous
or semi-cartilaginous, indurated patches of serous membranes and of
the intima of arteries, are all regarded as manifestations of a
chronic inflammation of these tissues. With the localization of the
inflammation in the outer walls of the bronchi and blood-vessels a
thickening of the external sheath results, called a peri-bronchitis,
arteritis, or phlebitis, as the case may be.
The new formation of blood-vessels is essential for the production and
preservation of this connective tissue, and both arise from
pre-existing tissues. Pus-corpuscles represent the simple cellular
product of an inflammation, and their existence is but transitory.
With the new formation of blood-vessels imbedded in abundant cells
there exists a granulation-tissue, likewise transitory, but out of
which arises the permanent fibrous tissue. The question is still
mooted as to the part played by exuded white blood-corpuscles in the
production of the permanent results of inflammation. It is generally
conceded, especially since the observations of Ziegler, that they are
capable of transformation into lasting constituents of tissue, into
blood-vessels as well as into cells and fibres. Whether all the
resulting permanent products of inflammation are dependent upon their
activity, or whether the pre-existing fixed elements participate, is
still to be considered undecided.
What, at present, appears most probable is, that from exuded
leucocytes there arise, in the course of several days, larger
cells--epithelioid or endothelioid--which are eventually associated
with still larger cells, more irregular in shape, and provided with
projecting filaments, giant-cells. Both varieties may result from the
enlargement of leucocytes by fusion or by the assimilation of
nutriment. The epithelioid cells eventually become fusiform or
stellate, and their projections, as well as those of many of the
giant-cells, become fibrillated. The fibrils of adjoining cells,
becoming united, are thus transformed into a meshwork of fibrous
bundles enclosing irregular spaces, while the nuclei of the cells,
with the immediately surrounding protoplasm, remain upon these bundles
as the permanent cells of the new-formed tissue. The blood-vessels
arise from pre-existing vessels, chiefly capillaries, and probably are
also formed from the cells present in the exudation. The former method
is indicated by the projection of solid sprouts from the wall of a
capillary, which may unite, forming arches, and communicate with
sprouts from neighboring capillaries, thus forming bridges. Both
arches and bridges then become hollowed and admit the circulating
blood. Ziegler maintains that the projections of the larger
epithelioid cells and giant-cells become elongated, and eventually
fused with capillaries, or the projections from capillaries. When this
fusion is accomplished the cells become hollowed, their cavities
communicating with those of the blood-vessels. These epithelioid
cells, whose formation and transformation are of such importance in
the history of productive inflammation, are designated by Ziegler as
formative cells, and are frequently derived from the exuded white
blood-corpuscles, though not identical with them.
{56} The inflammations not terminating in resolution or production,
end in the destruction of the part. This result occurs when the
nutrition of the inflamed territory is so diminished, by the changes
in and around the vessels, as to become insufficient for its
preservation. As the nutriment is derived through the blood-vessels,
the more complete and the more permanent the stagnation in them the
more likely is death to result. This event also depends upon the
quantity and quality of the exudation. The more abundantly cellular
the latter, the more likely is an abscess or ulcer to result.
As most abundantly cellular exudations are considered to be dependent
upon the presence of putrefactive agencies, those inflammations of a
predominant putrid character (gangrenous inflammations) are those
terminating in destruction. The dead product is present as a slough or
sequestrum, when dead soft or hard tissues are detached, entire or in
part, from the living; or as a granular detritus contained in a more
or less abundant liquid. The inflammatory process producing the slough
and sequestrum is characterized as a gangrenous inflammation of soft
parts or a caries of bone, while the process resulting in the
formation of the granular detritus, and which has no necessary
connection with putrefactive agencies, is called a softening, from the
physical condition of its result.
Thrombosis and Embolism.
A blood-clot formed within a blood-vessel during life is called a
thrombus. The entire process of which the thrombus is the essential
element is designated thrombosis.
These terms were introduced by Virchow[17] to avoid the confusion
which resulted from regarding the process and result as synonymous
with inflammation of the vessel. All writers, even at present, do not
adhere to this strictness of meaning. For a thrombus of the vulva
indicates a clot of extravasated blood within the connective tissue of
the labium; in like manner, a vaginal thrombus is the effused and
clotted blood in the loose connective tissue surrounding the vagina.
These exceptions are gradually disappearing, and the word hæmatoma,
tumor composed of clotted blood, is being substituted in both
instances. A cancerous thrombus represents a mass of cancerous tissue
whose growth is extended along the course of a vessel, its wall having
been penetrated. In general, however, the term thrombus, unless
otherwise qualified, is used as first stated.
[Footnote 17: _Handbuch der Speciellen Pathologie und Therapie_,
Erlangen, 1854, i. 159.]
Although thrombosis is commonly a morbid process, it is not uniformly
so. Its physiological significance is illustrated by the part it takes
in the closure of the umbilical and uterine vessels, after childbirth.
The surgeon makes use of it in his efforts to overcome certain of the
ill effects of amputation, and to accomplish a cure of such local
diseases as aneurism, where it is deemed important to diminish the
supply of blood.
The thrombus being a blood-clot, it is composed, like the latter, of
fibrin and blood-corpuscles. It is presumable that the fibrinous part
of a thrombus owes its origin to the same conditions which determine
the presence of fibrin in blood removed from the vessels during life
or in that within the vessels after death.
{57} According to A. Schmidt,[18] the blood and other fluids, in which
clotted fibrin makes its appearance, contain two generators, called
fibrino-plastic and fibrinogenous. The former is considered to be
paraglobulin, a substance contained mainly in the white
blood-corpuscles, while the fibrinogenous generator is held in
solution in the plasma of the blood. When these materials are acted
upon by a third, the fibrin ferment, clotting takes place and fibrin
is formed. It is thought that the ferment is intimately connected with
the white blood-corpuscles, for with the microscope coagulation is
seen to advance as these become destroyed, and where the leucocytes
are most abundant, there coagulation advances most rapidly. The
elements of clotted fibrin are always present in circulating blood,
but Brücke has shown that blood remains fluid, under ordinary
circumstances, because of its constant contact with the normal
vascular wall.
[Footnote 18: Rollett, _Hermann's Handbuch der Physiologie_, Leipzig,
1880, iv. 1, 114.]
The general causes of thrombosis are those which produce an abnormal
condition of the endothelium, a rapid destruction of the white
blood-corpuscles, or a stagnation of the blood. With the presence of
one of these causes there is often conjoined another, and the
conditions under which they are present are conveniently used in the
classification of thrombi.
Although stagnation of the blood is often an important immediate cause
of its coagulation, it is apparent, from the investigations of
Durante[19] and others, that stagnant blood clots in the living
vessels only when their endothelium is in an abnormal condition. With
the co-existence of abnormal endothelium and stagnant blood, thrombi
form with greater frequency and become more voluminous in a given
interval of time.
[Footnote 19: _Wiener Medizinische Jahrbucher_, 1871, 321.]
The importance of the death of white blood-corpuscles in the formation
of thrombi is generally admitted, and is especially insisted upon by
Weigert. According to the observations of Zahn, the nucleus of certain
thrombi is the result of the death of these leucocytes and their
accumulation upon an altered intima. The experiments of Naunyn,
Köhler, and others show that a thrombus may be rapidly produced by the
injection into the blood of fibrino-plastic substances, and of those
through which free hæmoglobin is admitted into the circulation. The
former may be expressed from a fresh blood-clot; the latter may be
obtained by thawing frozen blood, or by injecting such material
(bile-acids, for instance) into the circulating blood as rapidly
destroys the red blood-corpuscles. Although Weigert lays special
stress upon the destruction of white blood-corpuscles in the formation
of the thrombus, it appears, from the experiments above referred to,
that indirectly the destruction of the red corpuscles is also of
importance.
Although largely made up of fibrin, a thrombus also contains
blood-corpuscles, both red and white, and the appearance of the mass
is modified according to the variations in the relative proportions of
these constituents.
Zahn[20] divides thrombi, according to their color, into red, white or
colorless, and mixed varieties. The red owes its color to a large
number of red blood-corpuscles, while the white and mixed forms
contain various proportions of white blood-corpuscles and fibrin and a
diminished number {58} of red corpuscles. The cause of this difference
in the color of thrombi is to be sought for in their method of origin.
When blood clots slowly in a dish, the heavier red corpuscles settle
to the bottom, and the lighter white corpuscles form a superficial
layer. Stagnant blood clotting rapidly furnishes a uniformly red mass.
The red thrombus, like the red clot, is the result of the rapid
coagulation of stagnant blood. The white thrombus, on the contrary,
largely composed of white blood-corpuscles, represents a constantly
increasing deposition of these from flowing blood. The mixed thrombi
arise from a combination of both conditions, and are usually white at
the outset. Thrombi formed in the heart and larger arteries are
usually white, those in the auricular appendages and on venous valves
are mixed, while red thrombi are more common in arteries and veins,
since the conditions favoring their origin are more frequently met in
such vessels.
[Footnote 20: _Virchow's Archiv_, 1875, lxxii. 85.]
Thrombi are frequently stratified, in consequence of the successive
deposition of new layers of blood-corpuscles and fibrin upon a
pre-existing thrombus. Circulating blood is therefore necessary for
the stratification, and such thrombi are likely to be mixed in color.
Unstratified thrombi are usually white or red, the former largely
composed of agglomerated white blood-corpuscles so moulded and
situated as to prevent a stagnation of blood in their vicinity, while
the red thrombus is rarely stratified, since its formation demands a
stoppage of the blood-current. Stratification is intimately connected
with the enlargement or growth of the thrombus, which takes place from
the surface exposed to the flowing blood, and which is greater or less
according to the seat of the thrombus.
Thrombi are usually divided into those from compression, dilatation,
traumatism, and marasmus; in all of which groups an abnormal condition
of the endothelium is to be met with.
Thrombi from compression are frequently formed in veins, in the
vicinity of growing tumors. Their presence is most constant when the
vein is compressed between a resistant surface, especially bone, and
the tumor. A compression of the smaller blood-vessels within an organ,
as the liver or kidney, may take place in consequence of chronic
interstitial inflammation, or the growth of cancerous or other
malignant tumors in such organs. The production of this form of
thrombus is sought for in the treatment of certain aneurisms by direct
pressure, the resulting stagnation of blood being followed by a
coagulation within the aneurismal sac.
Thrombi from dilatation are met with both in dilated arteries and
veins. In aneurism and varix a slowing of the blood-current is
present, and the intima of the diseased region is frequently in such
an abnormal condition that a clotting of the blood readily takes
place. The shape and situation of the dilatation are of importance in
promoting the formation of the thrombus; the more pedunculate and the
more voluminous the sac the more certain is the thrombosis.
Traumatic thrombi result from a direct injury to the vessel. This may
be mechanical, as in the application of ligatures for the obliteration
of vessels, the tearing of the veins during childbirth, and the
infliction of wounds of every variety. The injury may likewise be
chemical, from the action of caustics; somewhat analogous to which,
are the effects of heat and cold. Allied to the traumatic thrombi are
those which arise {59} from acute inflammation of the intima extending
from wounds or inflammatory processes in the vicinity of
blood-vessels.
Marantic thrombi are those whose origin is attributable to that
enfeebled condition of the body known as marasmus. This represents a
weakening of the several functions, especially the circulation,
respiration, and locomotion. Such may take place in disease or old
age; and it is important to bear in mind those diseases in which
marasmus is likely to arise, as thrombosis often proves a complication
of such affections. Protracted fevers, as typhus and typhoid,
puerperal diseases, the disturbances following surgical operations,
chronic wasting diseases, as the tuberculous and scrofulous
affections, are all likely to be accompanied by thrombosis. Stagnation
of the blood, as well as alterations of the intima, is an important
local condition in this variety of thrombosis, which is usually
valvular or parietal at the outset, and may be both arterial and
venous. Such thrombi are likely to become continued and to serve as a
frequent source of embolism.
Thrombi are also divided into primitive, or autochthonous, and
secondary varieties. The primitive thrombus is one which owes its
local origin to conditions existing at the place of its formation and
attachment. The secondary variety demands for its existence a
primitive thrombus, whose place of development is remote in time and
seat, and from which a part has been transferred to serve as the
nucleus for the secondary formation.
The continued thrombus is often confounded with the secondary variety.
Continuance is rather a quality of all thrombi, and is essentially
growth, whether by lamellation or agglomeration. Such continued
thrombi are extended in the course of the circulation, usually by a
conical end, which is pointed toward the heart in the case of venous
thrombi, but away from this organ when the thrombi are arterial.
Parietal and obstructing thrombi form another subdivision. The former
arise from a limited part of the wall of the heart or blood-vessel,
and project into its cavity. They are always in contact with flowing
blood, and are white or mixed in color and primitive. They may attain
a considerable size, and may eventually become obstructing thrombi.
The latter are so called when they are of sufficient size to cause a
considerable or total obstruction to the current of blood. In the last
case the vascular canal is wholly filled by the thrombus. The shape of
the older parietal forms is usually globular or pedunculate, owing to
the growth in all directions except at the place of attachment; the
obstructing thrombi are elongated.
Thrombi are also characterized by consistency and relative absence of
moisture. A thrombus is brittle and dry as compared with a clot. In
distinguishing between the two, difficulty arises only in the case of
a thrombus which may have formed within a few hours before death.
Post-mortem clots are moist, elastic, readily withdrawn from
blood-vessels, and have a smooth and lustrous surface. Their color is
either red, gray, grayish-yellow, or yellow, and is very often mixed.
The lighter colors are due to causes which favor the precipitation of
red blood-corpuscles before actual clotting takes place, or which
occasion an increase of the white blood-corpuscles in fibrin. The
thrombus becomes adherent to the vessel wall within a few hours, after
its formation, in the case of the red thrombus, and at once, in the
case of the white variety. A clot is never adherent, although it may
seem so from its entanglement between the trabeculæ and {60} tendons
of the heart and the cavernous framework of venous sinuses. Such
apparent adhesions are easily recognized by the smooth, shining,
intact intima which is disclosed after the removal of a clot.
The thrombus not only tends to become enlarged by further depositions
of material from the blood, but it also tends to become diminished in
size from the contractile properties of its fibrinous constituent.
Moisture is forced from the thrombus in consequence of this shrinkage,
and its dryness is increased by subsequent absorption through the wall
to which it adheres.
The changes eventually taking place in the thrombus are known as
organization, calcification, and softening.
Organization is the transformation of the thrombus into a mass of
fibrous tissue. This is accomplished, according to the researches of
Baumgarten,[21] by an outgrowth of endothelium from the intima of the
vessel, the thrombus being absorbed as the growth of tissue advances.
In the case of a thrombus due to the ligation of a vessel, a
granulation-tissue also makes its way into the thrombus between the
ruptured coats, and the new-formed fibrous tissue which replaces the
thrombus becomes vascularized through this granulation-tissue. The
vascularization of thrombi surrounded by unbroken walls is most likely
to result from the extension into the thickened intima of new-formed
branches of the vasa vasorum. Cohnheim claims that the organization of
the thrombus may take place solely through the entrance of migratory
cells, without any active participation of elements of the vascular
wall. The canal is thus obstructed or obliterated by a fibrous tissue,
which is pigmented or not, as the pre-existing thrombus contained red
blood-corpuscles or not. These, when present, become transformed into
granular or crystalline hæmatoidin, which may remain as a permanent
constituent of the new-formed tissue.
[Footnote 21: _Die sogenannte Organisation der Thrombus_, Leipzig,
1877.]
Even when the thrombus is completely obstructing at the outset, it is
not necessary that a total obliteration of the vessel should result
from its organization. It not rarely happens, either before or after
the thrombus has yielded to the fibrous growth, in consequence of the
shrinkage of the fibrin of the thrombus or of the contraction of the
fibrous tissue replacing it, that gaps arise which become
communicating canals. Through these the blood flows, and the vessel
thus becomes only obstructed, not obliterated. The sieve-like tissue
thus formed is spoken of as the result of a cavernous or sinus-like
transformation of the thrombus. The length of time necessary for the
removal of the thrombus and its replacement by fibrous tissue varies
considerably. A vascularized granulation-tissue may be present within
a week, and in the course of a month the thrombus may have been wholly
removed, or a period of months may elapse and the thrombus and
granulation-tissue still be present side by side.
The calcification of a thrombus takes place when the latter becomes
impregnated with salts of calcium and magnesium. The condition may be
present in thrombi which are exposed to a rapidly-flowing arterial
stream, as well as in those which lie in venous pockets outside the
course of the direct current of blood. The well-known phlebolites are
examples of the latter variety. A calcified thrombus may be intimately
united to the vascular wall, the results of calcification and
organization being associated. Calcification and, in particular,
organization represent favorable {61} events in the history of
thrombosis, as through their occurrence the process comes to an end,
and disturbances, either local or remote, are prevented.
The softening of the thrombus, on the contrary, is always a source of
danger. This is partly due to the nature of the products of the
softening, whether bland or septic, and partly to the mechanical
disturbances produced by the transfer of portions of the softened
thrombus to remote parts of the body. All thrombi may become softened.
When the process of organization advances normally, the softened parts
are absorbed as rapidly as the formation of vascularized fibrous
tissue progresses. If this formation is checked or stopped, the
process of disintegration still continues. White corpuscles undergo
fatty degeneration; red corpuscles give up their coloring matter and
become converted, like the fibrin, into granules, and there results a
granular detritus. This is present as a viscid, semi-fluid material,
either red, gray, or yellow, according to the color of the thrombus.
This simple softening is to be regarded as essentially chemical in
character, and begins at the oldest portion of the thrombus and
advances toward the periphery. Its products are capable of absorption
without the production of serious disturbances, and are usually
prevented from direct entrance into the blood-vessel containing the
thrombus by the continuation of the latter from new coagulation or
deposition upon its surface. The thrombus is thus extended as the
softening progresses.
When the thrombus is comparatively free from red blood-corpuscles, the
softened product, in consequence of its yellowish color, opacity, and
viscidity, resembles pus. The so-called encysted abscesses projecting
into the cavity of the heart, from its wall, are parietal and globular
thrombi, in the interior of which softening has occurred. This form of
softening is called simple or bland, as it is free from any evidence
of local suppuration, inflammation, or general constitutional
disturbance attributable to an absorption of poisonous material.
Septic softening is accompanied by general evidences of a
blood-poisoning, and by the local phenomena of purulent inflammation.
A suppurative thrombo-phlebitis or arteritis, occurs; that is, an
acute inflammation of the wall of the vessel, corresponding in its
origin to the seat of the thrombus, and characterized by the formation
of pus. In the earliest stage the softened thrombus need not present
products differing in appearance from those occurring in simple
softening, but their effect is manifested by a rapidly-advancing
inflammation of the vascular wall and by the evidence of septicæmia.
Inoculation with such material produces a group of symptoms classified
under the head of blood-poisoning.
Cohnheim lays special stress upon the presence of micrococci in the
softened material, and it is generally agreed that the virulence of
septic softening is connected with, if not due to, the presence of
microbia. A septic softening may be induced by besmearing, with septic
material, the outside of a blood-vessel containing a thrombus, and
this form of softening is usually associated with those conditions
favoring this relation. Such are the gangrenous wounds following
surgical operations, the putrid inflammatory processes affecting the
uterine wall after childbirth, the offensive inflammations of the
middle ear, and the like. It is possible for a septic softening to
occur independently of such contiguous or continuous relations with
the surfaces of the body. It is considered, {62} however, that the
micrococci present in a softened thrombus must have obtained admission
from without through one of the surfaces of the body, mucous or
cutaneous, or through undiscovered abrasions of even intact surfaces
of peculiar structure, as the alveolar wall or the intestinal mucous
membrane. The thrombus is regarded as affording a favorable soil for
the growth and activity of the organism.
The mechanical effect of a thrombus varies according to the venous or
arterial seat of the same. Venous thrombi, as they are continued
toward the heart, tend to become completely obstructing thrombi. In
most parts of the body the venous anastomoses are so numerous that the
obstruction of a vein is readily compensated for through the
collateral venous circulation. When such a compensation is prevented
by an extension of the thrombus from branch to branch, and finally to
the trunk, an accumulation of blood in the peripheral veins must
result. The remote parts become swollen, from the distension of the
vessels with blood and the transudation of liquid, and eventually
solid material from the blood. Venous thrombosis thus leads to oedema,
and even hemorrhage. The more rapidly the obstructing thrombus
extends, the earlier and more extreme is the oedema likely to become,
while the slower the advance of the thrombus, the more favorable is
the opportunity for an enlargement of the collateral vessels through
which a sufficient flow of blood is permitted to check oedema and
preserve nutrition.
Local mechanical disturbances from arterial thrombi are scarcely
perceptible till obstruction is produced, and the results of arterial
obstruction will be mentioned in detail in connection with the
phenomena of embolism. Cardiac thrombi may occasion local disturbances
from interfering with the action of the valves of the heart. Those
thrombi which are attached to the valves, especially when calcified,
may produce inflammation and aneurism of the opposed wall of the
heart, by friction. The most frequent mechanical disturbance from the
non-obstructing parietal thrombi of the heart and arteries results
from the detachment of fragments and their transfer as emboli to
remote parts of the body.
An embolus is a foreign body in a blood-vessel, usually too large to
pass through the smallest capillaries, and the disturbances resulting
from its presence are included under the term embolism. Although most
emboli are detached portions of thrombi, any foreign body of suitable
size may become an embolus. Such are tissues, as the pulmonary elastic
fibres, fragments of diseased valves of the heart and of the intima of
arteries, or portions of tumors growing into vascular canals. Others
are globules of oil entering the torn veins when fat-tissue becomes
crushed, or air-bubbles admitted through veins either wounded by
instruments or opened after parturition by the dislodgment of their
obstructing thrombi. Still others are granules of pigment derived from
the coloring-matter of the blood, as in melanæmia, or introduced from
without, as india-ink and cinnabar. The echinococcus has been found as
an embolus, and it is highly probable that the cysticercus, the
trichina, and other animal parasites may be disseminated as emboli
over the body.
Vegetable parasites, like the bacterium and aspergillus, have also
been included in the list, although the disturbances resulting from
their presence are less due to mechanical obstruction than to
colonization and growth. The experimenter uses the most various
objects as emboli--bits {63} of wood, rubber, and glass, globules of
mercury, fragments of tissue, etc. Emboli are to be regarded as of
arterial or venous origin. The arterial emboli are carried toward the
capillaries, while venous emboli are carried toward the heart. The
effect of both is partly or wholly mechanical, and partly due to the
specific properties of the constituents.
The mechanical effect of an embolus is manifested by the obstruction
it offers to the circulation, and the degree of the obstruction
depends upon the size, shape, and density of the embolus and the
nature and size of the vessel obstructed. An embolus may be so large
as to be unable to pass through the valvular orifices of the heart. A
long and narrow embolus might pass through a vessel which would not
admit one which was short and thick. A jagged and dense embolus, by
repeated blows or prolonged and forcible contact, might cause a
weakening or rupture of the wall of a vessel, and thus produce an
aneurism. Certain vessels (the terminal arteries of Cohnheim) furnish
the sole supply of arterial blood to a district, and when they are
obstructed, the results, to be mentioned later, differ widely from
those taking place where free vascular anastomoses exist. When a trunk
bifurcates, the larger branch usually receives the embolus.
Venous emboli are those which approach the heart by the peripheral
veins of the body or the pulmonary veins, and the liver by the
radicles of the portal vein. Emboli from the veins of the body are
carried through the right side of the heart, if not so large as to be
stopped at the tricuspid or pulmonary opening. As they enter the
latter, they are carried along its course under the influence of
gravity and the direction and force of the current, which are
determined by the direction and relative size of the bifurcations of
the artery, the right primary branch being larger than the left.
Eventually, a point of the artery is reached whose diameter is less
than that of the embolus, and the latter is stopped. This point
usually corresponds with a place of bifurcation, and the embolus
frequently rides the wall separating the branches.
Emboli from the radicles of the portal vein owe their most frequent
origin to thrombi associated with inflammatory processes in the
intestine, especially of the cæcum and vermiform appendage, to
inflammatory processes in the spleen and obstruction to the flow of
blood through the splenic artery, or to inflammatory changes
proceeding from the kidneys. Such venous emboli are carried toward the
heart, but are stopped on the way by the intrahepatic branches of the
portal vein.
Arterial emboli are those which enter the left side of the heart from
the lungs, which arise in the left ventricle or auricle, which may
pass through an open foramen ovale from the right auricle, or which
arise from the arterial wall. They are carried along the course of the
arterial circulation, and are distributed over the different regions
and organs of the body. Usually following the more direct course of
the circulation, they are more likely to enter the abdominal aorta
than to be carried toward the brain or upper extremities. Embolism of
the carotids, especially of the left carotid, is more likely to ensue
than embolism of the subclavians. Embolism of the coronary arteries is
rare, while embolism of the splenic artery, the left renal and left
iliac arteries, is comparatively common, and in the order mentioned.
When an embolus is found, or embolism suspected, the source is always
{64} to be searched for in those regions from which the affected part
receives its blood. The source of arterial and portal emboli is
usually found with ease, while the pulmonary embolus may come from so
wide a region, the body-veins, that much time may be spent before its
place of origin is discovered. An appreciation of the laws of the
transfer of emboli renders such a discovery almost certain.
When the embolus reaches a point beyond which it cannot pass, the
resulting disturbance depends essentially, as shown by Cohnheim, upon
the presence or absence of arterial anastomoses beyond the place of
obstruction. He gives the name terminal arteries to those which have
no anastomosing arterial branches. These are met with in the spleen,
kidneys, lungs, brain, and retina. If the obstructed artery is not
terminal, the embolus may produce no further disturbance, the
collateral supply of blood through the anastomoses sufficing for the
nutrition and function of the part. If, however, the vessel is a
terminal artery, and the embolus is completely obstructing, the supply
of arterial blood must be wholly cut off from the region beyond the
seat of obstruction.
If the embolus does not completely obstruct at once, it soon becomes
sufficiently large for this result to ensue in consequence of a
secondary coagulation. The rider assumes legs extending into the
arterial branches beyond the place of obstruction, and a body which
extends backward in the course of the circulation to the nearest
branch. The result of the total obstruction of the vessel is to cut
off the admission of arterial blood, producing a local anæmia. The
contraction of the elastic tissues of the part propels toward the
capillaries a certain quantity of the blood in the vessels beyond the
point of obstruction, till this force becomes neutralized by the
blood-pressure in the vessels surrounding the obstructed region. The
anæmic part may subsequently become engorged with blood; it may die, a
region of anæmic necrosis resulting, or the dead portion may become
softened.
The engorgement of the obstructed territory has received the name of
hemorrhagic infarction. A solid, wedge-shaped mass of a reddish-brown
color is present, whose shape is due to the arborescent branching of
the terminal arteries. According to Cohnheim, the engorgement of the
region with blood takes place from venous regurgitation into the
obstructed part, till the intravenous pressure is overcome by the
resistance of the tissues in the region affected. The capillaries and
larger vessels thus become distended, and an escape of liquid and
solid constituents of the blood takes place. If the veins are provided
with valves, or the venous regurgitant current is opposed by gravity,
the hemorrhagic infarction is prevented or greatly impeded.
Litten,[22] on the contrary, who has furnished a recent contribution
to this subject, claims that the hemorrhagic results of embolism are
not accomplished through venous regurgitation, unless increased venous
tension is produced by coughing, vomiting, and like efforts. His
experiments lead him to maintain that arterial blood from surrounding
tissues is supplied to the obstructed region through the anastomosing
capillaries. The force is not sufficient to drive the blood through
the capillaries into the veins beyond, but an accumulation takes place
in the capillaries, which become dilated and distended. The escape of
blood-corpuscles and {65} serum then takes place, the more freely, as
Weigert[23] suggests, the larger and more numerous are the
pre-existing spaces in the organ. Hence the infarction becomes the
most characteristically developed in such organs as the lungs and
spleen. Causes which obstruct the venous flow, as well as those which
increase the arterial tension, promote the hemorrhagic infarction.
[Footnote 22: _Untersuchungen über den hemorrhagischen Infarct.,
etc._, Berlin, 1879.]
[Footnote 23: _Virchow's Archiv_, 1878, lxxii. 250.]
A necrosis of the part whose direct arterial supply is cut off takes
place when the structure of the organ affected is such that the
admission of arterial blood is wholly interfered with. This is the
case in the heart and kidneys, and to a less extent in the spleen. The
opportunity is presented for the diffusion of a fibrinogenous fluid,
lymph or blood-serum, through the cells of the organ which contains
the other essentials for coagulation, and the dead part presents the
characteristics attributed by Weigert[24] to death from clotting of
the protoplasm, coagulative or ischæmic necrosis.
[Footnote 24: _Ibid._, 1880, lxxix. 87.]
Embolism of the cerebral arteries produces softening of the brain, not
a hemorrhagic infarction or a yellowish necrosis. Weigert attributes
this result, on the one hand, to the absence in the brain of abundant
cells from which are to be had the ferment and fibrino-plastic
material necessary for coagulation, and, on the other, to the closure
of the spaces into which blood might collect by the rapid swelling of
the tissues from the exuded lymph.
The hemorrhagic results of embolism are also met with in obstruction
of branches of the mesenteric artery, which is considered by Litten,
at least from its function and in connection with its sluggish
current, to correspond with a terminal artery.
If the patient outlives these more mechanical results of embolism, the
local changes taking place are those tending to remove the
extravasated blood or the dead tissues. The embolus has become an
obstructing thrombus, and its removal is accomplished in the manner
already stated in connection with the subject of thrombosis. The
wedge-shaped nodule of hemorrhagic infarction becomes decolorized
through the absorption, in part, of the blood-pigment. That portion
which is not absorbed remains at the site of the original lesion as
granular or crystalline blood-pigment. A granulation-tissue is formed
at the periphery, which extends into the infarcted region, very much
as the endothelial and vascularized growth extends into a thrombus.
Eventually, a patch of cicatricial tissue remains as the sole
indication of the previous disturbance. This termination is rather
suggested for the hemorrhagic infarctions of the lungs. The results
are more apparent and more easily demonstrated in the case of the
anæmic necroses, and the somewhat irregular depressions with
wedge-shaped scars, seen upon the surface of the spleen or kidneys,
call attention to the probable nature of the process giving rise to
these results. A source of embolism must also be associated, that
these scars may be regarded as of embolic origin. The embolic
softenings of the brain are likewise represented in after years by
losses of substance. The superficial, yellow patches or localized
oedematous blebs, with corresponding atrophy of the convolutions
beneath, call attention to a nutritive disturbance, as do cyst-like
cavities in the deeper parts of the brain. Here, too, a source of
embolism must be found, that {66} the local destruction of tissue may
be attributed to embolic obstruction of vascular territories.
When the embolus arises from a septic thrombus, the results differ
from those above described. The embolus then carries not only
mechanical possibilities, but also a virulent action. The latter is
manifested by the rapid production of local inflammatory disturbances,
as circumscribed abscesses and gangrenous destruction of tissue. Since
emboli are frequently lodged near the surfaces of organs, a septic
pleurisy, pericarditis, or peritonitis is the usual result of the
dissemination of the virus contained in the embolus. This virus is
similar in character to that found in septic softening of the
thrombus, and, like it, is intimately connected with the presence of
microbia. Whether the latter are specific in character, as maintained
by Klebs and others, or whether they are to be included among those
associated with putrefactive processes, still remains an open
question.
The symptoms of thrombosis obviously depend upon the resulting
obstruction to the circulation of blood, and in the case of primitive
thrombi are gradual in their occurrence. The degree of mechanical
obstruction is determined by the nature of the thrombus, whether
parietal or obstructing, and by that of the vessel, whether provided
with anastomoses sufficient to permit a compensatory collateral
circulation or not. In the former case, if the thrombus is small and
deep-seated, there may be no symptoms to indicate its presence. When
the collateral circulation is insufficient to remove the blood from a
region whose efferent venous trunk is completely filled with a
thrombus, the phenomena of stagnation are produced. The part becomes
oedematous, and red blood-corpuscles escape from the distended vessel.
If the obstructed vein is superficial, the seat of the thrombus is
indicated by the resistance and sensitiveness of the part.
Characteristic disturbances of function are associated with thrombosis
of the various organs of the body. If the cerebral sinuses are
affected, mental disturbances arise; if a cardiac thrombosis is
present, it is frequently accompanied by irregularity and feebleness
of the heart. When the portal and renal veins are obstructed,
functional disturbances arise in the parts from which they receive
their blood.
The symptoms of embolism, like those of arterial thrombosis, are
primarily due to anæmia. Suddenness is their characteristic in
embolism, while they are gradual and progressive in the case of
thrombosis. An embolic anæmia is complete or incomplete according to
the terminal or anastomosing character of the obstructed vessel. The
effect of the anæmia is to stop or check the function of the part, and
varies according to the size and situation of the vessel. Hemiplegia,
or perhaps aphasia or other evidence of localized disturbance, follows
central embolism; angina pectoris, with a disturbed cardiac action,
results from embolism of the coronary artery. Sudden suffocative
symptoms, with open air-passages, suggest embolism of the larger
branches of the pulmonary artery. A considerable hæmaturia often
excites suspicion of an embolism of the renal artery, the hemorrhage
coming from the vessels in the neighborhood of the obstructed region.
Embolism of a large artery of an extremity is often localized by the
sensation of a blow at the part, to be followed by absent pulsation,
pallor, and coldness of the region beyond the place of obstruction.
{67} The symptoms of the subsequent effects of thrombosis and embolism
are to be inferred from what has already been stated with regard to
the nature of the possible lesions. To enter into their detailed
consideration would demand more space than is permitted, and would
modify an established sequence or necessitate a repetition, which is
undesirable in a systematic treatise.
Effusions.
The various fluids of the body are derived from without, and admitted
into the blood-vessels. The physiological transudation through the
walls of these vessels, in the main modified serum, becomes lymph as
it appears in the several lymph-spaces. From the latter the transuded
fluid either returns through the lymph-vessels to the blood-current or
makes its appearance upon surfaces as secretions. These are variously
modified as they pass through the specific cells of glands or as they
are met with in the several closed cavities of the body.
The transudations thus occurring may vary in quantity within certain
limits, the latter being somewhat indefinite, owing to the
difficulties in the way of exactly measuring the fluid transuded. The
greater part of this transudation is represented by the quantity of
lymph flowing through the main lymph-trunk, and of the secretion from
the glandular surfaces of a given region of the body; but that
transuded fluid is not included which may return to the blood-vessels
without being carried into the general lymph-current or secreted from
a gland. Such a direct return may be considered to take place whenever
the pressure upon the outside of the vessel wall is greater than that
within the latter, or when the chemical composition of the fluids on
the two sides of the filter permits endosmosis as well as exosmosis.
This varying relation in the direction of the current through the
vessel wall is likely to be of frequent, if not constant, occurrence
in connection with the physiological processes taking place throughout
the body.
The undue accumulation of the transudation in the various closed
cavities of the body is known as dropsy, and the fluid present is
regarded as an effusion or an exudation. These terms are often applied
somewhat vaguely, now being used as synonymous, again as representing
different conditions of the transudation, which are attributed to the
varying conditions of its accumulation.
Exudation is more generally used when an inflammatory process is the
cause of the increased transudation, while effusion is more strictly
associated with causes other than inflammatory. In the present
consideration this etiological distinction will be maintained.
To appreciate the conditions under which pathological accumulations of
fluid, whether effusions or exudations, may arise, it is desirable to
bear in mind the essential conditions which prevail in the occurrence
of transudation, since the former are likewise chiefly derived from
the blood and are transuded through the walls of its vessels. These
conditions are largely dependent upon the laws governing the diffusion
of substances through an animal membrane, the vascular wall
representing the filter. As a living membrane its relation is
dependent upon vital as well as {68} physical conditions, and the
former produce certain important modifications in the physical process
of filtration.
The transudation through the vessels takes place chiefly through those
with the thinnest walls, the capillaries, although it is probable that
a certain degree of transudation may also occur through the walls of
the smallest veins. The causes which are instrumental in promoting the
circulation of the blood--viz. the contraction and dilatation of the
heart, the contraction of the arteries, the inspiratory action of the
thorax, and muscular movements throughout the body--are also essential
in producing the flow of lymph; and the existence of pressure upon the
hæmic side of the filter is the first feature of importance in
occasioning the transudation. The constant removal of the transudation
from the outer side results from the pressure being less in this
position.
At the same time, an increase in the quantity of blood in the vessels
is not necessarily productive of any considerable increase in the
fluid transuded. Cohnheim calls attention to the experiments of Worm
Müller, which show that a plethoric condition may readily be produced
by the injection of quantities of blood into the circulation of
animals, the amount of which cannot exceed twice the volume of the
animal's blood without producing death. Although a temporary increase
of the blood-pressure results, a return to the normal quickly follows.
This is permitted by the propulsion of the excess of blood into the
capillaries and veins, which become consequently distended, especially
those of the abdominal organs. There is no increased transudation
corresponding with the quantity of fluid introduced, nor is there any
considerable distension of the blood-vessels of the skin, subcutaneous
or intermuscular connective tissue. Such experiments show no permanent
increase in the blood-pressure within the large veins if there is no
obstruction to the admission of venous blood into the heart,
presumably owing to their capacity for considerable distension.
Although experiments show that a simple plethora with great distension
of the capillaries of the abdominal organs occasions no considerable
increase of transudation, a different result follows a hydræmic
plethora[25] induced by the injection of immense quantities of salt
water into the blood-current--often six times as much liquid as the
animal had blood. Here, too, the arterial blood-pressure shows no
permanent increase, nor does that within the large veins become
perceptibly increased till enormous quantities of fluid are injected.
The blood flows through the vessels with increased rapidity in
consequence of the diminished friction of the diluted blood, and an
increased transudation begins at once. The various glands, salivary
and gastro-intestinal, kidneys and liver, secrete more copiously, and
the flow of a dilute lymph from the thoracic duct becomes greatly
increased, while that from the cervical lymphatics becomes moderately
accelerated. The lymph from the extremities, however, is no greater in
quantity than that flowing from an animal in a perfectly normal
condition. The localization of the increased transudation from the
blood-vessels is further characterized by the abundant accumulation of
watery fluid in all the abdominal organs and abdominal cavity, in the
salivary glands and surrounding connective tissue, while elsewhere in
the body the organs and tissues are almost invariably in the same
condition with {69} regard to moisture as are those of a healthy
animal under normal circumstances.
[Footnote 25: Cohnheim and Lichtheim, _Virchow's Archiv_, 1877, lxix.
106.]
The importance of these experiments with reference to the causes of
the transudation of fluid from the blood is obvious. The pressure upon
the walls of the blood-vessels cannot become sufficiently increased to
be accompanied with augmented transudation until limits are reached
which are beyond the possibilities of occurrence in the human body.
When such limits are attained in animals, the increased pressure,
however great it may be, does not suffice to produce a general
transudation, but one limited to the vessels of those parts of the
body whose normal function is connected with too abundant transudation
of fluid. A simple hydræmic condition of brief duration has been
proven, by experiment, insufficient to give rise to increased
transudation, neither increased secretion nor increased flow of lymph
taking place. The inference from these experiments is that an
increased transudation is more dependent upon conditions of the filter
than upon those of blood-pressure. The absence of any observable
changes in the filter leads to the assumption of an increased
permeability, of physiological occurrence in certain parts of the
body, as the chief feature in the occurrence of increased
transudations.
Dropsy arises when the transudation is accumulated. As dropsical
accumulations are transudations from the blood, essentially
blood-serum with a diminished percentage of albumen, and as such
blood-serum is practically lymph from its presence in the
lymph-vessels, dropsical effusions are to be regarded as stagnant
lymph. Such stagnations may be present in the small lymph-spaces
within the connective tissue, or in the larger lymph-sacs, as the
peritoneal, pleural, pericardial, and scrotal cavities. In like
manner, the stagnation may take place in the cavities of joints and in
those of the brain and cord, although the latter represent functional
rather than structural lymph-canals.
The term oedema is applied to the accumulation in the
connective-tissue lymph-spaces in general, while the term anasarca is
confined to those cases where the subcutaneous lymph-spaces are
concerned. The accumulation in the great lymph-cavities is known as
ascites when peritoneal, hydrothorax when pleural, hydropericardium
when pericardial, hydrocele when in the cavity of the tunica
vaginalis, hydrocephalus if within the ventricles of the brain, and
hydromyelocele when within the central canal of the spinal cord.
The accumulation of dropsical effusions may be considered as possibly
resulting from an obstruction to the channels through which the
transudation should flow, or from insufficient force to overcome
normal obstructions, or from an abnormally increased transudation.
Lymph-channels are frequently obstructed, but no appreciable diffused
retention of lymph results unless the thoracic duct is obstructed.
This rare affection is followed by enormous distension of the thoracic
and abdominal portions of the parts beyond the stenosis. Ascites and
hydrothorax may follow, but not necessarily any considerable oedema of
the peripheral parts of the body. As a result of the distension of the
thoracic duct, rupture is not unlikely to take place, and the effused
fluid contains chyle.[26]
[Footnote 26: Quincke, _Deutsches Archiv für Klin. Med._, 1875, xvi.
121.]
{70} That the obstruction is not followed by oedema is attributable to
the innumerable anastomoses between the lymph-spaces, and also to the
probability that a part of the transuded fluid returns to the
blood-vessels when the obstruction is impassable.
The forces necessary to promote the flow of lymph have already been
mentioned, and their entire removal is inconsistent with life. A
diminution of their activity is more likely to result in a diminished
flow of lymph than its accumulation, although a slowing of the
lymph-current may represent a favoring element in the accumulation of
an increased transudation.
The occurrence of dropsy with unobstructed lymph-channels, and in the
presence of efficient agencies in promoting the flow of lymph,
indicates the importance of an increased transudation as the chief
element in the occurrence of a dropsical accumulation. An increased
transudation, with resulting oedema, is readily produced by preventing
the flow of blood from a part, and may be directly observed with the
microscope. Cohnheim states that after a sudden venous obstruction, in
case an efficient collateral circulation does not interfere, the
capillaries and small veins become distended with stagnant blood and
appear as masses of red blood-corpuscles. This distension results from
the continuance of the arterial flow into the capillaries of the
obstructed region under a pressure which is only neutralized by the
resistance of the tissues and the transudation from the capillaries.
Sotnitschewsky[27] shows that a concurrent paralysis of the vaso-motor
nerves, as claimed by Ranvier, is unnecessary. The transudation
through the capillary wall is increased, the flow of lymph from the
part is accelerated, and oedema arises when the transudation is so
much augmented that the calibre of the lymph-vessels is insufficient
for its removal; and the greater this insufficiency the greater is the
oedema. With the continuance of the arterial flow and intravenous
resistance, red blood-corpuscles are forced through the filter, and
form an important constituent of the effusion from venous stagnation.
[Footnote 27: _Virchow's Archiv_, 1879, lxxvii. 85.]
Although the existence of an increased pressure upon the capillary
wall is obvious from the experiment referred to, there is no increased
arterial pressure--rather a diminution--and the important element in
occasioning the increased permeability of the capillary wall is the
obstruction to the outflow of venous blood from the oedematous region.
In consequence of the latter the arterial flow is followed by
increased transudation.
Dropsies resulting from venous obstruction, as well as those following
an obstruction of the thoracic duct or its branches, or of the several
lymphatics of a part, are classified as mechanical dropsies. That from
venous obstruction is the most frequent, and its seat may lie in the
course of venous trunks or in the heart, lungs, or liver. The venous
obstruction must be so situated that the stagnant blood is unable to
find a ready escape through collateral branches. The more sudden and
complete it is, the more likely is the effusion to contain
considerable numbers of red blood-corpuscles.
In addition to the element of venous stagnation in producing increased
transudation, the condition of the filter is of importance. The
occurrence of oedema in chronic diseases, especially of the kidneys,
and in those attended with protracted suppuration, continued
hemorrhage, and the {71} rapid growth of tumors, has usually been
attributed to the watery condition of the blood, with a diminution of
the albumen. Cohnheim, however, suggests that the condition of the
vessel wall is of more importance than the contents as the immediate
cause of the increased transudation. The more or less protracted
action of various agents--temperature, insufficient oxygen, and
diminished albumen--is likely to so modify the condition of the
endothelium as to favor an increased permeability of the wall.
Experiments show that a simple acute hydræmia produces no increased
transudation, and that a chronic hydræmia, if connected with dropsy,
is likely to be influential by increasing the permeability of the
wall. Even in those cases where a hydræmia and an oedema co-exist, the
localization of the latter is favored by obvious disturbances of the
function of the capillary walls, as in case of the cutaneous oedema
after scarlatina. In like manner, a feeble heart, favoring venous
stagnation, and gravitation are of importance, as general causes, in
promoting dropsy in hydræmic conditions.
The possibility of the occurrence of oedema through nervous influence
is not to be denied. The localized and fleeting oedema of urticaria
and erythema, the swollen lip and tongue in connection with digestive
disturbances, are not to be explained by the two main factors of
oedema--viz. venous stagnation and increased permeability of the
vascular walls. Cohnheim refers to the rapid occurrence of oedema of
the tongue as a result of irritation of the lingual nerve, and oedema
is known to occur rapidly in cases of acute myelitis. A similar result
follows the experimental destruction of the spinal cord, although the
mechanism of its production is not apparent.
Dropsies are subdivided, as regards their distribution, into general
and local forms. The causes producing the two varieties are
essentially those already described. The causes of all local dropsies
are not always to be regarded as the same. Regions which are the seat
of mechanical dropsies are often affected by inflammation, with
abundant serous exudation--the so-called inflammatory dropsy. The
properties of the effusion and exudation are quite different, the
former having a small percentage of albumen, but few leucocytes, with
a corresponding absence of fibrin, and few or many red
blood-corpuscles. The exudation, on the contrary, is highly
albuminous, though less so than the blood-plasma; it contains numerous
leucocytes and much fibrin; under ordinary circumstances there are but
few red blood-corpuscles.
The local dropsies are often characterized by special terms. Hydrops
ex vacuo is applied to the collections of fluid found in closed
cavities with unyielding walls, as the cranium and thorax, or to the
recurrence of fluid in cavities from which the same has been rapidly
removed, in the absence of inflammatory disturbances. Collateral
oedema is usually applied to the association of oedema with
inflammatory disturbances, and represents an extension of the
inflammatory process to the region concerned. Oedema of the glottis
and circumscribed oedema of the lung are instances. The term
hypostatic oedema is often used to designate the association of oedema
and inflammation, the former caused by the latter, and to indicate the
effect of gravitation in the localization of oedema from the general
causes already mentioned.
Another localized oedema of interest, from its frequent occurrence and
{72} importance, is oedema of the lungs, often taking place toward the
end of life, at times quite suddenly. This form has usually been
attributed to increased transudation from arterial congestion or
venous stagnation. The former view is directly refuted by the
experiments of Welch,[28] who offers the explanation now accepted.
With the obliteration of three-fourths of the arterial supply to the
lungs of the animals experimented upon, no oedema resulted from the
assumed collateral fluxion into the branches of the pulmonary artery
which were left open. The obliteration of the same area of venous
distribution was necessary before the occurrence of oedema. Oedema of
the lungs was further found to result from a ligature of the aorta
near the heart. The comparative frequency of oedema of the lungs in
man, and the rarity of such extreme mechanical disturbances as those
produced experimentally, led Welch to paralyze the left ventricle. The
conditions as regards the pulmonary circulation then corresponded with
those mentioned as causes for oedema from venous obstruction. The
continued action of the right ventricle forced blood into the
pulmonary capillaries, where it was compelled to accumulate in
consequence of the inability of the left ventricle to receive and
expel it. Welch consequently regards the immediate cause of this form
of pulmonary oedema as a predominant weakness of the left ventricle. A
weak heart does not suffice for the production of the oedema, since
this condition is not found when both ventricles are alike enfeebled.
[Footnote 28: _Virchow's Archiv_, 1878, lxxii. 375.]
Degenerations.
The degenerations represent disturbances in the nutrition of the
tissues of the body, in consequence of which their functions become
impaired, if not destroyed. The latter result obviously attends the
death of cells, which may occur in the course of the degeneration. The
processes concerned are called necrobiotic by Virchow, as they
represent vital processes leading to death. Although in many of them
the cell is decaying during their continuance, its recovery is
possible with the disappearance of the conditions which have
transformed physiological into pathological processes. The
degenerations affect intercellular substance as well as cells, and are
called metamorphoses, infiltrations, or degenerations, as a
transformation of normal into abnormal material, or the addition of
extraneous substances, or the functional impairment of the part
assumes the greatest prominence.
_Cloudy Swelling, Albuminoid Infiltration, Granular Degeneration,
Parenchymatous Degeneration._
Of the various modifications in the appearance of cells under
pathological conditions, there is none, perhaps, more commonly met
with than that known by the above terms. A granular appearance may be
regarded as an essential characteristic of protoplasm, and is an
attribute of cells of epithelial origin as well as of those which
belong to other groups of tissues. The abundance of granules present
in a normal cell depends largely upon its shape, size, and situation.
These granules present various {73} relations to chemical agents, some
being soluble in alcohol and ether, others in acids and alkalies, and
many of them, especially those met with in the form of degeneration
now being considered, show from the various reactions that they are of
the nature of albumen. Since their exact composition, in all
instances, is undetermined, they are called albuminoid, and when in
excess the cell is considered to be infiltrated with these granules,
and the organ presents the appearances regarded as characteristic of
an albuminoid infiltration. A granular cell becomes much more granular
when it is thus infiltrated, and it is therefore a matter of
difficulty to recognize from the appearance of certain single cells,
as those of the liver or kidney, whether or not the number of granules
present is abnormally increased. When, however, a large number of
cells of any given organ contain more than the normal quantity of
these albuminoid granules, the appearance of the organ becomes
modified. In extreme cases the latter is swollen, doughy in
consistency, with ill-defined structural details, and in all instances
presents an opaque appearance. The term cloudy swelling is thus purely
descriptive, and was applied by Virchow to designate the optical
appearances of the condition in question. The granules, which
disappear on the addition of acids and alkalies, are apparently either
added to the cell or result from a precipitation within the same.
Frequently associated with these albuminoid granules are others,
distinctly recognizable as globules of fat. An apparent increase of
nuclei is often observed, and in certain organs, as the kidneys, the
cells seem less coherent than is normally the case. The study of this
condition in the kidneys is further of interest as indicating that the
border-line between a parenchymatous degeneration and a parenchymatous
inflammation is purely arbitrary. From similar exciting causes there
may be associated, with the described alterations of the epithelial
lining of the tubes, the exudation of albumen, the formation of casts,
the desquamation of epithelium, and the presence of leucocytes within
the tubules.
When the macroscopic changes are of moderate degree, and the
disturbance of function relatively slight, while the concurrent
alterations elsewhere, from the simultaneous action of the same cause,
are predominant and characteristic of the disease, the condition is
conveniently regarded as a degeneration occurring in the course of the
latter, rather than an inflammation. The latter term, on the contrary,
is to be applied when the granular infiltration of the cells is
associated with other evidences of an inflammatory exudation, and when
the pathological disturbances are to be directly attributed to the
parenchymatous changes.
It is customary to speak of cloudy swelling as a nutritive change, and
the condition may be induced by those causes which interfere with the
nutrition of parts or of the whole of an organ. Many authorities
regard this granular or parenchymatous degeneration as closely allied
to fatty degeneration, since many of the causes which produce the one
occasion the other. The former is often spoken of as an earlier stage
of the latter, from the frequent association of the albuminoid
granules with numerous globules of fat as a result of the more
prolonged or more intense action of a given cause.
Organs which give evidence of a granular degeneration contain, as a
rule, a diminished quantity of blood. This feature is usually
attributed to the pressure of the swollen cells upon capillary
blood-vessels. The {74} anæmic organ obviously becomes still more
cloudy, gray, and opaque in appearance from the diminished quantity or
impoverished quality of the blood.
The granular degenerations of the heart, liver, and kidneys, as a
whole, usually occur simultaneously, and afford a most important means
for the post-mortem recognition of the infective diseases. The
condition is therefore to be looked for in the exanthemata, especially
in small-pox and scarlet fever, also in erysipelas, septicæmia in its
manifold forms, diphtheria, typhoid and typhus fevers, cerebro-spinal
meningitis, etc. A common feature in all these cases is the occurrence
of fever, and it has been claimed that this element is the cause of
the degeneration. In opposition to this view is the well-known fact of
its presence in afebrile cases of poisoning from carbonic oxide, and
its absence in certain cases of pneumonia and exposure to high
temperatures.
The universal occurrence of cloudy swelling in fatal cases of the
affections above mentioned leads to the inference of its presence in
those instances terminating in recovery without obvious permanent
impairment of the organs and tissues concerned. It is therefore agreed
that the process may terminate in resolution--_i.e._ in a
disappearance of the excess of granular material. On the other hand,
its association, under circumstances, with fatty degeneration suggests
as extremely probable that the latter condition may represent a result
of the albuminoid infiltration. Even if this more serious issue
exists, the possibilities are still at hand for an absorption of the
degenerated material and a restitution of the destroyed protoplasm.
The effect upon the individual is evidently determined by the
persistence and dissemination of the condition, which, in turn, are
controlled by the immediate cause and the peculiarities of the
individual acted upon.
_Fatty Metamorphosis, Fatty Degeneration, and Fatty Infiltration._
The fat which is present within the body under physiological
conditions owes its origin primarily to the food taken. A diet which
is abundantly fatty furnishes a direct source for much of the fat
which appears accumulated in the various organs and tissues. Although
it may now appear that such a statement needs but little confirmation,
it is not long since the opinion prevailed that nearly all the fat in
the body came from the hydrocarbons of the food. This seemed all the
more plausible as the herbivora readily accumulated fat, although
their diet might contain this element in very small quantities.
Hofmann[29] made a decisive experiment with reference to the origin of
fat from fatty food by feeding a dog, made lean by starvation, with
bacon in abundance, but with little meat. In the course of a few days
the greater part of the fat introduced was deposited within the
tissues of the animal. Other experimenters have arrived at a similar
result, and it can no longer be questioned that fat, accumulated
within the body, owes its origin chiefly to the absorption of fat from
the food taken.
[Footnote 29: _Zeitschrift für Biologie_, 1872, viii. 153.]
Another source for the fat of the body has long been
suggested--namely, the albuminates of the food. In the admirable
article on the formation of fat by Voit,[30] from which most of the
information herein {75} presented is derived, it is claimed that he
and Pettenkofer were the first to prove the origin of fat in the body,
under normal conditions, from albumen. This proof was an inference,
however, although presenting a high degree of probability. Valuable
evidence in the same direction was furnished by Kemmerich, who found
that the milk of a cow during a certain period held more fat than was
contained in the food; Subbotin and Voit have shown that more milk is
secreted the richer the diet in albumen. Still other observers have
furnished more decisive proof that fat is formed from albuminates.
[Footnote 30: _Hermann's Handbuch der Physiologie_, 1881, vi. 1, 235.]
Two sources for fat in the body under physiological conditions are
thus recognized: 1, the free fat in the food; 2, the fat derived from
the decomposition of the albuminates of the food.
Voit admits the possibility of the hydrocarbons serving as a third
source, although this possibility is unnecessary in most cases. Should
instances arise, however, where other sources for fat are found
insufficient, the hydrocarbons must be regarded as filling the gap.
Fat which is taken into the body is considered to be either consumed
or stored. That which is stored is chiefly accumulated in the great
reservoirs--viz. the subcutaneous and perinephritic fat tissue, the
mesentery, omentum, and bone-marrow--although it may be found
elsewhere, in the fluids and tissues of the body. This accumulation
serves as a source to be drawn from in case of need, and is called
upon where the easily-decomposed soluble albumen is disposed of by the
functional activity of the cells. An acting muscle demands food for
its work, and consumes first the soluble albumen, then the fat. An
excessive waste of fat is delayed by the decomposition of
hydrocarbons, but the demands may become so great that albumen, fat,
and hydrocarbons are consumed more rapidly and constantly than they
can be supplied. It being, therefore, admitted that fat is formed from
the albuminates, as well as from the fat of the food, the question
readily presents itself whether fat may not be formed from the fixed
albuminates of the body, especially from those contained within its
cells.
It is well known that in the secretion of sebum the superficial cells
of the sebaceous follicles contain fat in great quantity, while the
deeper layers are comparatively free from any appearances indicative
of the presence of fat. It is further admitted that when pus is
retained for a time the individual corpuscles contain fat-drops in
quantity and become transformed into fatty granular corpuscles.
Eventually, the pus is transformed into a detritus in which fat-drops
are found in great number.
Similar appearances may be present in the protoplasm of muscular
tissue, the cells of the liver, kidneys, and gastric glands, when
poisonous doses of phosphorus or arsenic are given. The occurrence of
an acute fatty metamorphosis of the cells of various organs in
new-born children has repeatedly been observed. The presence of fat in
various organs of the body in pernicious anæmia, and in the heart in
connection with stenosis of the coronary artery, is universally
recognized. The abuse of alcohol, long-continued obstruction to the
flow of venous blood, exposure to high temperatures, are all known to
be conditions in connection with which fat-drops are found in the
various cells of the body. The effects of poisoning with phosphorus
and arsenic are of special importance, as showing that the abundance
of fat present in the cells represents a result of the degeneration of
these cells, {76} since it takes place when the animal is deprived of
food. Although there is an evident destruction of albumen, there is
also a diminished elimination of carbonic acid and admission of
oxygen. These facts are explicable on the ground that the fat present
is not consumed, and the accumulation in the cells is evidence of this
lack of consumption. The fat is not simply stored, as none is taken
in, nor is any food received from which fat might be formed. Its
presence, therefore, must be regarded as due to degeneration.
Since fat may be formed in the body as a result of the metamorphosis
of cell-protoplasm, it is desirable to ascertain whether there are any
means by which stored fat may be distinguished from that present as
the result of a degeneration of the cell. The term fatty infiltration
has been used to indicate the presence of stored fat, the latter being
regarded as simply taken into the cell and retained for a longer or
shorter time, without any necessary interference with other functions
possessed by the cell.
In fatty degeneration, on the contrary, it is considered that the
quantity of fat present indicates a corresponding diminution in the
albuminates of the cell, and is connected with a diminution in the
function of the latter, all the greater the more abundant the fat.
It is found that in fatty infiltration, as a rule, the fat is present
in large drops, the size of the cell being increased in proportion to
the quantity of fat present. Although there may be several drops
present, they tend to run together, as is suggested by their different
size, varying proximity, and the constant presence of a considerable
quantity of protoplasm. In organs, on the contrary, whose function is
seriously, even fatally, impaired, the fat, as a rule, assumes rather
a granular form. Many minute fat-drops are present, and the cell is
not particularly, if at all, increased in size. The more abundant the
fat the less the protoplasm. Appearances are met with indicating a
transition between cells with few fat-granules and those with many.
If the morphological appearances of fatty infiltration and of fatty
degeneration were constant, there would obviously be little or no
difficulty in determining the nature of the process manifested by the
presence of fat. The exceptions occur both in fatty infiltration and
fatty degeneration. In the cells of the liver of an animal poisoned
with phosphorus fat makes its appearance in large drops, while in the
heart and kidneys of the same animal the fat is present in a granular
form.
During absorption from the intestine in the process of digestion fat
is present in the epithelium in a finely granular form. When digestion
is completed fat is no longer met with in these cells. The presence of
large or small drops, therefore, cannot be regarded as a sufficient
test of the origin of the fat. It is of equal, if not greater,
importance to bear in mind the organ concerned.
In the heart, liver, kidneys, and gastric glands, as well as
elsewhere, with the exception, perhaps, of the mammary gland, the
presence of many small fat-drops in the cells indicates a degeneration
of its protoplasm. The presence of large fat-drops, on the contrary,
in the organs and tissues, with the exception of the liver, indicates
an infiltration. Large fat-drops, then, may be present in the cells of
the liver as the result of an infiltration or of a degeneration. In
order to form a satisfactory opinion of the {77} nature of the
appearances in the liver in doubtful cases, it is important to note
the condition of those organs which may be simultaneously in a state
of fatty degeneration.
The accumulation of fat under physiological conditions is obviously
brought about, on the one hand, by those causes which permit a free
introduction, absorption, and deposition, and, on the other, by those
which check its oxidation or elimination with the secretions of the
body, as the bile, in which it may be present to a considerable
extent. A diet rich in fat, or in albuminates readily converted into
fat, offers a favorable element for the absorption of fat by the
healthy individual. If the organism demands but little of this fat for
oxidation, as in the case of the sedentary person, an accumulation is
likely to occur. This may become so considerable that obesity results.
Tissues in which normally but little fat is accumulated may become
infiltrated to a large extent. The intermuscular fibrous tissue thus
becomes loaded, and the activity, as well as the nutrition, of the
muscles is impaired. This accumulation may be manifested not only in
the voluntary muscles, but in the heart as well, which may present
abundant sub-pericardial and sub-endocardial fat, the myocardium also
being interlarded with streaks of fat, the so-called fatty
infiltration of the heart. The abdominal walls may become thickened to
the extent of a couple of inches, and the mesentery, omentum,
perinephritic tissue, and liver may become enormously increased in
weight from the mass of accumulated fat.
This infiltration of fat may take place under pathological as well as
physiological conditions. It is apparent that those causes which check
oxidation are likely also to prevent the consumption of fat, and it is
well known that the destructive processes in the lung, grouped under
the term pulmonary consumption, accomplish this result. Something
more, however, is necessary than the obliteration of pulmonary
blood-vessels and the destruction of an aërating surface. There may
be, as in emphysema of the lung, a diminished respiratory and vascular
surface, yet evidences of fatty infiltration, particularly of the
liver, are wanting. It seems probable that the constant anæmia, with
the loss of the blood-corpuscles, of pulmonary phthisis is an
important additional factor in checking oxidation in this disease.
This factor, it is needless to say, is not a necessary occurrence in
pulmonary emphysema.
Litten[31] has shown that when certain animals are exposed to high
temperatures the appearances of fatty infiltration and degeneration
are present in various organs of the body. He attributes the fatty
degeneration to a direct poisoning of the red blood-corpuscles and a
resulting diminution of the oxidizing processes.
[Footnote 31: _Virchow's Archiv_, 1877, lxx. 10.]
It is universally admitted that in chronic alcoholism a fatty liver is
frequently met with, even in the absence of those chronic interstitial
tissue-changes usually characterized under the name cirrhosis. Alcohol
is known to check the reception of oxygen and the elimination of
carbonic acid, and, whatever other disturbance of cell-activity it may
produce, its effect in favoring the accumulation of fat is directly
attributable, in part at least, to this disturbance of oxidation.
In those conditions known as cachexiæ, the constant accompaniment of
progressive and wasting diseases, as cancer, leucæmia, chronic
dysentery, {78} etc., a fatty infiltration, particularly of the liver,
is a frequent accompaniment. A cachexia is dependent upon a complex
series of processes, many of which tend to check oxidation, and in
this respect is to be grouped with the conditions previously
mentioned. That the associated fatty infiltration is intimately
connected with the deficient oxidation is not to be doubted, although
the agents producing this deficiency may vary in detail.
The causes which favor fatty degeneration are numerous, and the result
represents one of the most serious conditions which can affect an
organ. As oxidation represents the chief means of normally disposing
of fat, so, pathologically, deficient oxidation favors the retention
of fat due to degeneration. Were a constant renewal of protoplasm to
take place, the degenerated fat might be displaced into the
circulation or retained within the cell. If the latter event should
occur, the result would be apparent as an infiltration, owing to the
increased size of the cell, although the condition giving rise to the
presence of the fat is a degenerative process. The importance of
impairment of nutrition as the chief cause for fatty degeneration is
thus obvious. It may readily be produced, experimentally, by measures
which check the flow of blood to a part. The same measures necessarily
prevent the presence of abundant oxygen, as fewer red blood-corpuscles
are presented.
Fatty degeneration resulting from impaired nutrition is apparent in
the heart in consequence of stenosis of its coronary arteries, in the
kidneys as a result of interstitial processes obstructing the
capillary circulation, in the brain from obliterative processes in the
arteries at the base or within the organ, and in blood-vessels from
the effect of age.
The cause of fatty degeneration may be general as well as local. In
poisoning from phosphorus and arsenic the appearances in most of the
organs indicate an actual destruction of protoplasm. Analysis of the
secretions confirms this inference, as the production of urea is
largely increased. Furthermore, there is less oxygen taken in and less
carbonic acid eliminated. As has been previously stated, these
conditions may be present in the starving animal. The fatty
degeneration is thus easily explained as a metamorphosis of
cell-protoplasm, and the deficient oxidation of the fat calls direct
attention to its accumulation rather than elimination.
In acute yellow atrophy of the liver and in cases of severe jaundice
fatty degenerations are constantly met with. That the origin and
accumulation of fat in these affections is also due to rapid
tissue-metamorphosis and checked oxidation is highly probable.
Although the elimination of urea diminishes rather than increases, as
shown by Schultzen and Riess, there are other links in the chain of
retrograde changes, as the appearance of leucin and tyrosin,
indicative of the extensive destruction of albuminates.
It is unnecessary in a work of the present character to call attention
to all the possible circumstances under which fat is present in the
body as the result of degeneration. Mention may be made of the acute
parenchymatous (fatty) degeneration of new-born children, of the
results of excessive bleeding, and of pernicious anæmia otherwise
occasioned. The fatty degeneration of the uterus after parturition, of
paralyzed muscles, and of tumors, the atrophic fatty degeneration of
the liver in chronic {79} passive congestion (nutmeg liver), are all
well-known examples. To these may be added the fatty degenerations
associated with amyloid and interstitial processes. It is apparent
that in most of these instances the common features of rapid
tissue-metamorphosis and deficient oxidation are present, and, being
present, offer a ready explanation for the appearance of the fat.
The clinical importance of fatty metamorphosis requires consideration
in connection with the description of the diseases in which its
occurrence is a constant feature. As the presence of fat in cells is
not necessarily pathological, so an interference with the function of
the cell is not invariably implied by its presence. When its existence
is suggestive of a local destruction of albuminates, a diminution of
cell-activity is a necessary consequence. Such diminished activity
must produce different results as the cells are those of muscles, of
vessels, or of glandular organs.
Even if fat is found in cells under conditions favoring such a
suggestion, it does not follow that the destruction of the cell must
result. Not only is it possible that the fat may be reserved for
eventual oxidation, and its place in the protoplasm be filled by
normal constituents, but it is also possible that the fat may be
eliminated, as such, from the body. The latter event is made apparent
by the experiments of numerous observers referred to by Cohnheim, who
have found free fat in the urine after its introduction into the
venous current.
_Cheesy Metamorphosis, Cheesy Degeneration, Caseation._
Virchow introduced the term cheesy metamorphosis, tyrosis, to
designate the process resulting in the incomplete absorption of pus
and the production of apparently similar changes in certain other
occasional constituents of the body. The characteristic cheesy
appearances were regarded as due to the inspissation of the material
concerned, in consequence of the absorption of its fluid. With this
inspissation there was frequently associated a partial fatty
degeneration, and the cheesy matter represented dead material, which
might undergo further changes, of which softening and calcification
were the more important.
Inflammatory products, as pus and fibrin, were especially prone to
become thus transformed, as well as other relatively transitory
materials of new formation--viz. tubercle and parts of various tumors.
The type of the cheesy metamorphosis was found in the enlarged
lymphatic glands, commonly called scrofulous.
The importance of a clear understanding of the cheesy metamorphosis is
now a matter of history. It is merely necessary to allude to the fact
that these cheesy products were formerly regarded as indicative of the
presence of tubercle, and were the tubercles. Tuberculization and the
cheesy condition were synonymous terms, and their indiscriminate use
led to much confusion with reference to the nature of tubercle.
Quite recently Weigert[32] has called attention to the conditions
present in necrosis resulting from the intermediate stoppage of the
blood-current in a part. The effect is manifested, under favoring
circumstances, by a cheesy appearance of the affected region, to which
the terms decolorized hemorrhagic infarction, anæmic or ischæmic
necrosis, have been applied. {80} Weigert lays stress upon the
existence of a coagulation of the protoplasm of the cells, with an
early disappearance of the nuclei, as the essential feature of this
form of necrosis, the conditions present being regarded as analogous
to those met with in the coagulation of the blood. The term
coagulative necrosis has consequently been introduced by Cohnheim to
represent the process first fully described in detail by Weigert. The
optical and physical properties of the ischæmic or coagulative
necroses of tissue are often manifested as cheesy appearances,
although the term coagulative necrosis includes conditions which do
not present a suggestion of cheese. It is thus apparent that cheesy
appearances may result in two ways: 1, by the inspissation of material
in a state of partial fatty degeneration; 2, by a coagulation of the
constituents of cells whose blood-supply is suddenly and completely
cut off. In the more restricted sense these caseous appearances are
regarded as indicative of a cheesy metamorphosis which arises by the
former of these methods. Cheesy appearances, on the contrary,
dependent upon the sudden death of a part, indicate an ischæmic or
coagulative necrosis.
[Footnote 32: _Virchow's Archiv_, 1880, lxxix. 87.]
Whatever may be the origin of the cheesy condition, the material
presenting this appearance is liable to further changes, known as
softening and calcification. The former event results from the soaking
of the dead part with liquid, in consequence of which a detritus
results. The softening usually begins at the oldest part of the cheesy
mass, and advances toward the periphery. The sanatory evacuation of
the emulsive detritus is permitted when a surface continuous with that
of the external surface of the body is reached, as instanced by the
escape of softened cheesy material from the lungs through a bronchus.
The possibility of the complete removal of the dead mass is thus at
hand, and an eventual obliteration of the resulting cavity may take
place by an adhesive inflammation of its walls.
The complete absorption of the cheesy material of an ischæmic necrosis
may occur by the extension into the latter of a granulation-tissue
from the periphery. Whenever cheesy appearances are found on surfaces,
as the degenerated tubercles of mucous membranes or the circumscribed
necroses in diphtheritic inflammation or in typhoid fever, healing may
be accomplished by their detachment as sloughs, a clean ulcer being
left. Cheesy material is frequently encapsulated--_i.e._ imbedded in a
layer of dense connective tissue, a condition which indicates a local
cessation of the process through which the cheesy appearances arose.
The same may be said of the infiltration of the cheesy mass with
earthy salts--calcification--an event which will again be referred to
in connection with the consideration of the general subject.
_Hyaline Degeneration, Fibrinous Degeneration, Croupous
Metamorphosis._
Certain of the conditions now regarded as indicative of a coagulative
necrosis or a hyaline degeneration were previously described by Wagner
as the result of a croupous or fibrinous metamorphosis. According to
this observer, the cell-contents were transformed, under certain
circumstances, into a substance resembling externally clotted fibrin.
The formation of croupous and diphtheritic membranes, especially of
the larynx, pharynx, and trachea, was thus explained, also the hyaline
casts of the kidney.
{81} The results of this metamorphosis presented a hyaline appearance
under the microscope, and the term hyaline degeneration is now applied
more especially to indicate the production of microscopic changes,
while the hyaline appearances visible to the eye are rather included
under mucous, colloid, or amyloid metamorphoses.
The limitations in the use of the term hyaline degeneration are but
ill defined. On the one hand, there is included the transformation of
muscular tissue, first discovered by Zenker; on the other, the various
changes described by Recklinghausen and others, among which are
embraced the results of Wagner's croupous metamorphosis. As the
hyaline appearances are a frequent result of coagulative necrosis,
these terms are frequently used to indicate the same condition,
according as the optical or etiological features are uppermost in the
mind of the observer.
The hyaline or waxy degeneration of muscular fibre described by Zenker
represents a metamorphosis of the protoplasm of striated muscle in
particular, although the fusiform cells of the muscular coat of the
stomach and intestine may present a similar transformation.
The microscopic appearances are more characteristic than those visible
to the naked eye. To the latter the muscle appears paler, more
translucent, and homogeneous, and proves to be more brittle than
normal. The muscular fibres are found with the microscope to be
swollen, irregular in outline, the myosin transformed into flaky,
glistening masses, without evidence of the normal transverse
striation. These appearances have given rise to the term waxy
degeneration, which suggests a possibility of confusion with the
earlier recognized waxy degeneration of organs, due to the presence of
amyloid material. The waxy transformation of muscular fibre, however,
does not present the reaction with iodine characteristic of amyloid
substance. The degeneration of the muscle is usually regarded as the
result of a coagulation of the myosin, and it is claimed by Cohnheim
that the latter takes place only in dead muscle, either during the
life of the individual or as a post-mortem appearance.
The hyaline degeneration of muscular fibre is found in certain febrile
diseases, as typhoid and typhus fevers, scarlatina, variola, and
cerebro-spinal meningitis. It may also be met with when a muscle has
been exposed to violence, as in the insane who have been placed under
mechanical restraint. It has further been found in the vicinity of
tumors, especially where muscles have been invaded by their growth.
Cohnheim and Weil describe a similar condition in the tongue of frogs
after ligature of the lingual artery.
The pathological importance of the above-mentioned degeneration of
muscle is most prominent in cases of typhoid fever. The occurrence in
this disease of the hæmatoma or blood-tumor of the rectus abdominis is
thus explained, the degenerated muscle and its contained blood-vessels
being ruptured. The muscles of the thigh and the diaphragm frequently
undergo this degeneration; the change is more rarely met with in other
muscles of the body.
Recklinghausen regards a hyaline substance, hyalin, as a normal
constituent of cell-protoplasm which escapes in drops when the cell
dies. Its presence indicates a diminution in the vitality of the cell
from various causes. Under the microscope it appears as a sharply
defined, highly refractive meshwork, enclosing spaces of irregular
shape and size, in {82} which are frequently found nuclei, more rarely
cells or granules. Langhans has described this appearance as
channelled fibrin. It has been met with in the placenta, diphtheritic
membranes, blood-vessels, tubercles, and gummata.
The latest contribution to the history and nature of this form of
degeneration has been furnished by Vallat,[33] from whose article many
of the above data have been obtained.
[Footnote 33: _Virchow's Archiv_, 1882, lxxxix. 193.]
_Mucous Degeneration, Mucous Metamorphosis, Mucous Softening._
Of the various degenerations presenting a colloid--_i.e._
gelatinous--condition, the mucous variety is one of the most striking.
Its gross appearances may not differ materially from those to be
described under the head of colloid degeneration, but the diagnostic
characteristic of the change is to be found in the presence of mucin.
The presence of this substance is readily detected by the addition of
acetic acid to mucus, the effect being a fibrillated appearance of the
latter, the fibres presenting a more or less parallel distribution.
This fibrillation of mucus is regarded as the result of a coagulation
of its mucin, previously held in solution by an alkali. Mucin is thus
present in the body as a normal constituent, and, in the secretions
from mucous membranes, owes its origin to the existence of epithelial
cells, whether these represent gland-cells, as in the case of the
muciparous glands of the bronchial mucous membranes, or whether they
are superficial cells, as those of the gastric and intestinal mucous
membranes.
In the origin of mucus as a secretion from glands Heidenhain[34]
claims that a destruction of gland-cells accompanies the continuance
of the secretion. At the outset, however, the mucin escapes from the
cells, the latter remaining relatively intact. With the persistence of
the secretion there results a destruction and a new formation of the
muciparous cells. In the pathological production of mucus from mucous
membranes, as in catarrh, there is no reason to doubt that the
persistence of an irritation is the cause of abundant mucus, and that
the latter is dependent upon the rapid formation and destruction of
epithelial cells.
[Footnote 34: _Hermann's Handbuch der Physiologie_, 1880, v. 64.]
The origin of mucus from epithelial cells under physiological and
pathological conditions being apparent, it readily follows that the
epithelioid cells of tumors might be supposed to be liable to a
similar metamorphosis. It is well known that cancerous tumors,
especially those of the stomach and large intestine, are frequently
met with, which present an abundant gelatinous material, more or less
completely filling the spongy, fibrous meshwork. These are the
alveolar, gelatinous, or colloid cancers.
The gelatinous or colloid material often gives the reaction of mucin,
and the microscopic appearances of the tumor show that the jelly-like
substance lies in that part of the tumor which corresponds with the
position of the epithelioid cells. The latter are found in various
stages of degeneration, the appearances being similar to those
observed in the mucous degeneration of true epithelium.
The prevailing theory of the origin of cancer from epithelial
structures {83} readily suggests an explanation for the frequency of
the mucous variety of cancer in connection with those parts from which
mucus normally arises from the degeneration of the epithelium.
The mucous metamorphosis affects connective tissues as well as
epithelium. The Whartonian jelly of the umbilical cord and the
vitreous humor of the eye are known, through the investigations of
Virchow, to owe their gelatinous condition to the presence of mucin.
The latter lies in the intercellular substance; that is, between the
cells. The appearance of these indicates no degenerative process, but
the presence of mucin is obviously an essential constituent of the
tissue. Whether this mucin represents a transformation of the gelatin
of the intercellular substance, or a secretion from the fixed cells,
or a metamorphosis of the migratory cells of the tissue, is not known.
In mucous tissue, however, there is present mucin, wholly independent
of any epithelial degeneration. Mucous tissue is present in the eye as
a normal constituent of the adult, and in the umbilical cord as a
normal constituent of the infant at full term. It is also abundantly
met with in the subcutaneous and intermuscular tissues of the foetus.
Its pathological occurrence in the adult as a circumscribed tumor, the
myxoma, may also be mentioned.
A gelatinous substance containing mucin is found in the adult
independent of the mucous tissue, but obviously arising from a
transformation of intercellular substance. The most striking example
of this occurrence is the cystoid softening of cartilage, especially
of the costal cartilages of old people, the basis substance being
transformed into a fluid containing mucin. A similar metamorphosis is
of frequent occurrence in the intervertebral disks and in the
destruction of cartilage in acute and chronic inflammations of the
joints. The intercellular substance of cartilaginous tumors also
becomes softened and converted into a liquid containing mucin.
In osteomalacia and in the absorption of bone the mucous degeneration
of the bone-cartilage plays an important part. The lime salts are
first set free, and the cartilage then undergoes a mucous
degeneration; the product is either absorbed or remains as a liquid
within cavities of large or small size. The mucous metamorphoses of
fibrous and fat-tissues, likewise of bone-marrow, are well recognized
instances of the occurrence of a mucous transformation of the
intercellular substance of connective tissues. Finally, clotted
fibrin, so often met with as the product of the inflammation of serous
surfaces, may undergo a mucous metamorphosis, and, thus transformed,
offer a suitable material for absorption.
_Colloid Degeneration, Colloid Metamorphosis._
Laennec used the term colloid in a descriptive sense to indicate a
gelatinous appearance, and for a long time its use was thus
restricted. As the colloid appearances were found to differ in their
chemical reaction, their distribution, and their pathological
importance, and as the term was further extended to include
appearances seen with the microscope, it obviously became necessary to
subdivide the colloid series of changes according to the observed
differences. Its use is now limited to those gelatinous conditions or
appearances due to the presence of a fixed albuminate, homogeneous or
finely granular, translucent, colorless or pale {84} yellow, of
varying consistency, which does not become fibrillated on the addition
of acetic acid, and which does not change in color when acted upon by
iodine. This albuminate is considered in most instances to represent
the result of a transformation, a metamorphosis of cells, and is
associated with an impairment of their function--a degeneration which
is progressive, and leads, sometimes, to the destruction of the organ,
as occurs in certain instances of colloid degeneration of the thyroid
body. Usually, the process is limited, affecting particular parts
rather than the whole of an organ. The reaction presented by a
solution of sodium albuminate in the presence of neutral salts leads
to the view that colloid material may represent a coagulation of an
albuminous substance or substances under favoring conditions. The
presence of colloid masses in the kidney thus meets with a plausible
explanation.
The place of its typical occurrence is the thyroid body in certain
cases of goitre, and it is early met with as a homogeneous substance
replacing the granular cell-protoplasm. With its increase the latter
disappears, and the entire cell is transformed into a homogeneous
sphere. At times the colloid substance may be seen to project from the
surface of the cell as a pale rounded clump. The aggregation of these
clumps results in the presence of masses of various size, in which may
be found granules of fat or pigment and crystals of cholesterin, which
are accidental, not essential. Colloid masses are sometimes met
with--in lymphatic glands, for instance--as concretions, mulberry-like
aggregations of stratified colloid bodies, which may be infiltrated
with earthy salts. Colloid material may eventually become liquefied,
transformed into a sodium albuminate; and the presence of cysts in
certain varieties of goitre is thus explained. The coexistence in the
kidney of colloid accumulations and watery cysts has led to the view
that the latter may, under certain circumstances, result from the
former through the liquefaction of the colloid material. The same view
is held with regard to the origin of cysts frequently met with in the
choroid plexuses.
The colloid metamorphosis of cells is also to be found in the
epithelium of mucous membranes and their glands, in the prostate,
suprarenal capsule, sebaceous glands of the skin, and in the cells of
certain tumors.
_Amyloid Degeneration, Amyloid Infiltration, Waxy Degeneration,
Lardaceous Degeneration._
The colloid appearances due to the amyloid degeneration of cells are
of the greatest clinical importance from their frequent occurrence and
the gravity of the symptoms connected with their presence. In amyloid
degeneration there is the transformation of the cell-protoplasm into
an albuminous material different from other albuminates found in the
body. This transformation is at the expense of the functional activity
of the cell, and the latter becomes inert. Amyloid degeneration
represents no mere substitution, but an addition, since the affected
tissue is increased in volume. The albuminate was called amyloid by
Virchow in consequence of its color-reaction with iodine. Its method
of origin is wholly unknown, never being found in the circulating
fluids nor in articles of food. It is met with chiefly in the cell,
although its presence in the intercellular substance of old people is
recognized, and its occurrence in {85} the midst of the thrombotic
deposition on inflamed valves and in the results of inflammatory
processes is also recorded.
At present the question is under discussion whether the amyloid
degeneration may affect cells of the most varied character, or whether
it is limited to those of connective tissues. Eberth[35] maintains
that in all cases the amyloid disturbance is seated in the connective
tissue. Kyber,[36] the latest investigator, in opposition to this view
maintains that this affection is not limited to the connective tissue,
but may also be seated in the parenchymatous cells of organs. Whether
the one of these views is to exclude the other, or whether both are
not correct, remains for future investigation to decide.
[Footnote 35: _Virchow's Archiv_, 1880, lxxx. 138; 1881, lxxxiv.]
[Footnote 36: _Ibid._, 1880, lxxxi. 7, 111.]
Wherever the amyloid material may be situated, the result is a
transformation of the cells into a homogeneous, glistening, colorless
material, which occupies more space than the original cell, and, when
abundant, is accompanied with a loss of the primitive details of the
cell-structure. This material is recognized by the color it presents
when acted upon by iodine alone, by iodine and sulphuric acid, or by
methyl-aniline. The first produces a reddish-brown color, the second a
blue, and the last a violet or purple color. These reactions are all
characteristic, and the first is of special value in the macroscopic
recognition of the process, while the last two are of special
importance in the microscopic recognition of the earlier stages of the
affection.
With the advance of the degeneration and its dissemination, the organ
affected presents, in the diseased portions, pale-gray, glistening,
translucent patches, and becomes increased in size and density in
proportion to the quantity of amyloid material present. The change
appears primarily in the vessel wall or outside the same, and there
results a diminution in the calibre of the vessels, with a lessened
quantity of blood in the organ.
From the homogeneous and translucent appearance of the surface and the
increased density of the tissues the resemblance to bacon or wax is
suggested, and the terms lardaceous, bacony, or waxy degeneration have
been applied. Notable differences in degree and seat occur in
connection with the organs diseased. In the spleen, for example, the
change may be limited to the arteries of the Malpighian bodies and
their immediate surroundings. To this condition the term sago spleen
is applied, the enlarged, rounded, translucent, and projecting bodies
suggesting granules of boiled sago. The appearances of the diseased
part are further affected by the association of other conditions, as
the presence of fat or pigment. When fat is present, it is often to be
regarded as a result of the gradual and progressive increase in the
obstruction to the circulation of blood in the organ.
Although so little is known of the immediate cause of amyloid
degeneration, its distribution in the various organs of the body is
fully ascertained, as well as certain of the conditions which are
likely to be followed by its presence. It is known to occur as a
localized process in cartilage, in the conjunctiva, in certain tumors,
cardiac thrombi, scars, retained inflammatory products, and renal
casts. The causes of this localized appearance are wholly obscure, and
little or no general inconvenience results. Its presence, however, on
a large scale and in various parts of {86} the body at the same time,
is met with under such circumstances as indicate a distinct
etiological relation. An appreciation of these circumstances is of
importance, since their existence demands an investigation as to the
probable presence of the degeneration. The organs thus affected are
the spleen, liver, kidneys, and intestine. It is to their disturbance
of function that the pathological importance of amyloid degeneration
is to be especially attributed.
Other organs which may sometimes be affected are the lymphatic glands,
pancreas, suprarenal capsules, omentum, uterus, bladder, prostate
gland, heart, and thyroid body. In the case of a general diffused
infiltration these organs are variously degenerated, now some, and
again others, showing a more extensive alteration, while few or many
may be simultaneously diseased. The longer the process has continued,
the greater the degree of the disturbance and the larger the number of
the organs infiltrated. Although, in general, a period of months and
years may be demanded for these extensive changes, very serious
disturbances may arise within a short time, and Cohnheim[37] records
several cases which suggest that widely diffused amyloid degeneration
may occur within a few months--in one instance in less than four
months.
[Footnote 37: _Virchow's Archiv_, 1872, liv. 271.]
All that is at present known with regard to the etiology of this
process applies to certain general diseases with which in the course
of time it is likely to be associated. These have one element in
common, that of chronicity, and are likewise the occasion of a
progressive wasting of the body. Of these affections, that which holds
the first place is chronic pulmonary consumption, especially that form
in which extensive destruction of the lungs and ulcers of the
intestine are present. Another disease whose effects are in like
manner to be regarded as general is syphilis, and in the later stages
of this disease amyloid degeneration is likely to occur, and often to
represent by its resulting disturbances the immediate cause of death.
Again, chronic suppurative processes, especially those due to disease
of the bones and joints, are a frequent antecedent of amyloid
degeneration. Finally, the process has been found in connection with
leucæmia, chronic intermittent fever, rickets, gout, and certain
malignant tumors. This last group, however, is one in whose sequence
the degeneration is to be regarded as exceptional.
The clinical importance of this process is due to the resulting
disturbances in the function of such important organs as the liver and
intestines, the spleen and lymphatic glands, and the kidneys. The
nature of these disturbances obviously demands detailed consideration
in connection with the description of the diseases of the respective
organs. It may be mentioned here that the infiltration of the walls
leads to a narrowing of the calibre of blood-vessels, and thus a
diminution in the supply of blood to the part or organ. The resulting
impairment of nutrition becomes enhanced from the condition of the
blood, which is impoverished from the simultaneous infiltration of the
blood-making organs. The nutrition of the individual thus suffers as
well as that of the immediately diseased organ. Fatty degeneration and
atrophy of the parenchymatous cells of organs like the liver and
kidneys is the constant result of long-continued and extensive
infiltration of these glands.
Mention is intentionally omitted of the so-called amyloid bodies, {87}
corpora amylacea, considered in connection with amyloid degeneration
in most text-books on pathology and pathological anatomy. They usually
present a different reaction with iodine, their origin has but little
in common, their distribution is for the most part unlike, and little
or no clinical importance is to be attached to their presence.
_Calcification, Ossification, Petrifaction._
When salts previously held in solution are precipitated under abnormal
circumstances in the tissues of the body, the part is said to be
calcified, ossified, or petrified. Although these terms are often used
as equivalent, the last is to be regarded as more general than its
predecessors, since it includes the deposition of other than the
calcareous salts.
In the pathological ossification, as well as its physiological
prototype, the carbonates and phosphates of calcium and magnesium are
present in a specially formed tissue of the nature of bone-cartilage,
whereas calcification occurs independently of such a new-formed
tissue. The deposition of the calcareous salts takes place either in
the cells or intercellular substance of living or dead tissues, when
the terms calcification or ossification are applied, or as
accumulations of various size in tissues or canals, which are known as
concretions and calculi.
The immediate causes of the physiological deposition in the formation
of bone are so obscure that only more or less probable explanatory
theories are advanced, to all of which obvious objections arise. The
causes of a pathological precipitation may be regarded as equally
hidden. It is apparent, however, that old age usually furnishes the
necessary factors. This in part may be due to the feeble nutrition
associated with impairment of function in advancing years. In part it
may be the result of the numerous opportunities offered in a long life
for the occurrence of inflammation, the products of which are
frequently infiltrated with calcareous salts. The latter are
apparently kept in solution by the action of living cells, for, though
presented to all in the fluids of the body, they are precipitated most
constantly in dead parts or in the vicinity of those cells whose
function is presumably lessened from disease or age. The solvent
action of living cells is further demonstrated by the effect of the
giant-cells in removing calcium salts from living or dead bone.
The causes of calcification are therefore to be regarded as local,
depending upon a destruction or weakening of the cells of a
part--conditions which are directly attributable to an interference
with nutrition. The deposition of calcium salts thus represents a
disorder of nutrition, and may be experimentally produced by agencies
which occasion a necrosis of tissues.
Although the immediate causes of the precipitation of the calcium
salts must be expressed somewhat vaguely, the places and effects of
their accumulation are sufficiently well known, as are the resulting
appearances. The presence of these salts in sufficient quantity
produces a homogeneous, granular, strongly refractive appearance of
the cell or intercellular substance, in addition to a greatly
increased resistance to pressure. When muriatic acid is added to the
affected part, the salts are dissolved, with the escape of abundant
bubbles of gas when a carbonate is present, and with a rapid fading of
the glistening appearance, without effervescence, {88} when the salt
is a phosphate. After the removal, the cell or intercellular substance
is readily recognized, with such modifications in its appearance as
may be due to the action of the strong acid. The parts in which this
deposition or infiltration has taken place are either relatively
normal in appearance or variously altered from disease, and the
calcium salts are to be regarded as absorbed from the constituents of
the food and deposited, or as taken up and transferred from the bones
of the body. That both sources are drawn upon is obvious from the
abnormal presence of calcareous material in the soft parts, in
connection with increased density of the bones, as well as with a
diminution in the density of the latter. The term calcification is
more correctly applied to the presence of the salts in normal tissues
other than bone, or in the products of disease not simulating
bone-cartilage in structure. A pathological ossification is to be
considered pre
Showing first 200,000 characters. Full text: gutenberg.org/ebooks/39157