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A SYSTEM OF PRACTICAL MEDICINE.
BY AMERICAN AUTHORS.
EDITED BY
WILLIAM PEPPER, M.D., LL.D.,
PROVOST AND PROFESSOR OF THE THEORY AND PRACTICE OF MEDICINE AND OF
CLINICAL MEDICINE IN THE UNIVERSITY OF PENNSYLVANIA.
ASSISTED BY
LOUIS STARR, M.D.,
CLINICAL PROFESSOR OF DISEASES OF CHILDREN IN THE HOSPITAL OF THE
UNIVERSITY OF PENNSYLVANIA.
VOLUME 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.