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.

[PREFACE]

GENERAL PATHOLOGY AND SANITARY SCIENCE.

[GENERAL MORBID PROCESSES]. By REGINALD H. FITZ, M.D.

[GENERAL ETIOLOGY, MEDICAL DIAGNOSIS, AND PROGNOSIS]. By HENRY HARTSHORNE, M.D., LL.D.

[HYGIENE]. By JOHN S. BILLINGS, A.M., M.D., LL.D. (Edin.)

[DRAINAGE AND SEWERAGE IN THEIR HYGIENIC RELATIONS]. By GEORGE E. WARING, JR., M. Inst. C.E.

GENERAL DISEASES.

[SIMPLE CONTINUED FEVER]. By JAMES H. HUTCHINSON, M.D.

[TYPHOID FEVER]. By JAMES H. HUTCHINSON, M.D.

[TYPHUS FEVER]. By JAMES H. HUTCHINSON, M.D.

[RELAPSING FEVER]. By WILLIAM PEPPER, M.D., LL.D.

[VARIOLA]. By JAMES NEVINS HYDE, M.D.

[VACCINIA]. By FRANK P. FOSTER, M.D.

[VARICELLA]. By JAMES NEVINS HYDE, M.D.

[SCARLET FEVER]. By J. LEWIS SMITH, M.D.

[RUBEOLA]. By W. A. HARDAWAY, A.M., M.D.

[RÖTHELN]. By W. A. HARDAWAY, A.M., M.D.

[MALARIAL FEVERS]. By SAMUEL M. BEMISS, M.D.

[PAROTITIS]. By JOHN M. KEATING, M.D.

[ERYSIPELAS]. By JAMES NEVINS HYDE, M.D.

[YELLOW FEVER]. By SAMUEL M. BEMISS, M.D.

[DIPHTHERIA]. By ABRAHAM JACOBI, M.D.

[CHOLERA]. By ALFRED STILLÉ, M.D., LL.D.

[PLAGUE]. By JAMES C. WILSON, A.M., M.D.

[LEPROSY]. By JAMES C. WHITE, M.D.

[EPIDEMIC CEREBRO-SPINAL MENINGITIS]. By A. STILLÉ, M.D., LL.D.

[PERTUSSIS]. By JOHN M. KEATING, M.D.

[INFLUENZA]. By JAMES C. WILSON, A.M., M.D.

[DENGUE]. By H. D. SCHMIDT, M.D.

[RABIES AND HYDROPHOBIA]. By JAMES LAW, F.R.C.V.S.

[GLANDERS AND FARCY]. By JAMES LAW, F.R.C.V.S.

[ANTHRAX (MALIGNANT PUSTULE)]. By JAMES LAW, F.R.C.V.S.

[PYÆMIA AND SEPTICÆMIA]. By B. A. WATSON, A.M., M.D.

[PUERPERAL FEVER]. By WILLIAM T. LUSK, M.D.

[BERIBERI]. By DUANE B. SIMMONS, M.D.

[INDEX]

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.

GENERAL PATHOLOGY.

GENERAL MORBID PROCESSES.

GENERAL ETIOLOGY.

HYGIENE AND QUARANTINE.

DRAINAGE AND SEWERAGE IN RELATION TO THE PREVENTION OF DISEASE.

GENERAL MORBID PROCESSES.¹

INFLAMMATION; THROMBOSIS AND EMBOLISM; EFFUSIONS; DEGENERATIONS; TUBERCULOSIS; MORBID GROWTHS.
BY REGINALD H. FITZ, M.D.

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 Virchow² 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. Another link is to be found in the fatty degeneration resulting from this lack of blood.

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.

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.

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 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.

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 Rosenthal⁵ 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.

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, Rosenthal⁶ disputes this 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.

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. Wood⁷ 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.

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.

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 Wood⁹ 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 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.

⁹ Op. cit., 236.

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.

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 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 Samuel¹² 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.

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.

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 Reuss¹³ 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 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.

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 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.

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.

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.

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.

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 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 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 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 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.

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 Formad¹⁶ 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.

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 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.

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 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 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.

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 Virchow¹⁷ 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.

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.

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.

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 Durante¹⁹ 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.

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.

Zahn²⁰ 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 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.

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 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 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.

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 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.