Chapter LXI: Part II: , Showing Predominance of Malarial Element . . . . 617 (60)

For those who regard statistics with habitual distrust it may perhaps be well to state that the foregoing frightful picture is no exaggeration, but is less sombre than the actual truth.

Before proceeding to consider the nature of puerperal fever it is desirable to first recall the anatomical lesions with which it is associated. These, it will be found, are for the most part inflammatory processes having their starting-point in injuries of the genital passage produced by parturition, complicated in many cases by septic changes in the blood, by secondary degeneration of parenchymatous organs, and at times by phlegmonous and erysipelatous affections in remote as well as in the adjacent serous and cutaneous tissues.

MORBID ANATOMY.--The primary lesions connected with puerperal fever are so various that the student will find it convenient to classify them according as they are situated in the mucous membrane of the utero-vaginal canal, the parenchyma of the uterus, the pelvic cellular tissue, the peritoneum, the lymphatics, or the veins. Not, indeed, that such an arrangement is strictly in accordance with clinical experience--as a rule, the inflammatory processes are rarely limited to a single tissue--but because the prognosis and treatment {986} are determined in great measure by the tissue-system which is predominantly affected. The significance of puerperal inflammations, wherever seated, likewise depends upon whether they are local and circumscribed or whether they present a spreading character.

Personally, I have found the following classification of Spiegelberg[6] of great utility as a means of keeping in mind the principal points to which inquiry should be directed in estimating the significance of the febrile conditions of childbed:

1. Inflammation of the Genital Mucous Membrane.--Endocolpitis and endometritis.

_a_. Superficial.

_b_. Ulcerative (diphtheritic).

2. Inflammation of the Uterine Parenchyma, and of the Subserous and Pelvic Cellular Tissue.

_a_. Exudation circumscribed.

_b_. Phlegmonous, diffused; with lymphangitis and pyæmia (lymphatic form of peritonitis).

3. Inflammation of the Peritoneum covering the Uterus and its Appendages.--Pelvic peritonitis and diffused peritonitis.

4. Phlebitis Uterina and Para-uterina, with formation of thrombi, embolism, and pyæmia.

5. Pure Septicæmia.--Putrid absorption.

[Footnote 6: "Ueber das Wesen des Puerperalfiebers," _Volkmann's Samml. klin. Vortr._, No. 3.]

ENDOCOLPITIS AND ENDOMETRITIS.--In the superficial, catarrhal form of inflammation the mucous membrane of the vagina is swollen and hyperæmic, the papillæ are enlarged, and the discharge is profuse; in the vaginal portion of the cervix the labia uterina are oedematous and covered with granulations which bleed at the slightest touch; in the cavity of the body there are increased transudation of serum and abundant pus-formation. The deep structures of the uterus are usually not affected. Sometimes the inflammation extends to the tubes--_salpingitis_--or, passing outward through the fimbriated extremities, it may spread over the adjacent peritoneum.

The small wounds at the vaginal orifice are at times converted into ulcers with tumefied borders. These so-called puerperal ulcers are covered with a greenish-yellow layer. They are associated usually with oedematous swelling of the labia. Under favorable sanitary conditions the deposit, which consists in the main of pus-cells, clears away and the surface heals by granulation. The ulcerative form of inflammation is very rare outside of crowded hospitals.

Diphtheritic ulcers are situated with greatest frequency in the neighborhood of the posterior commissure or around the vaginal orifice. In rarer instances they are found upon the anterior wall and in the fornix of the vagina, in the cervix, and upon the site of the placenta. The borders are red and jagged; the base is covered with a yellowish-gray, shreddy membrane; the secretion is purulent, alkaline, and fetid; and the adjacent tissues are oedematous. From the vulva they may extend to the perineum or pursue a serpiginous course down the thighs. In the uterus and about the cervix they vary as regards size, and are either of a rounded shape or form narrow bands. The intervening portions of tissue which have not undergone destructive changes swell and stand out in strong {987} relief. Where the entire inner surface has become necrosed, it is often covered with a smeary, chocolate-brown mass which, when washed away with a stream of water, leaves exposed either the deepest layer of the mucous membrane or the underlying muscular structures.

The difference between the superficial ulcerations of the genital canal and the diphtheritic form involving destruction of the deeper tissues is due to the presence in the latter of minute organisms termed micrococci, the relations of which to puerperal infection will be considered in a subsequent division.

METRITIS AND PARAMETRITIS.--In ulcerative endometritis, and even in the extreme catarrhal form, the parenchyma of the uterus likewise becomes involved. The changes which are designated under the term metritis consist in the first place of oedematous infiltration of the tissues. As a consequence, the organ contracts imperfectly and becomes soft and flabby, so that sometimes, upon post-mortem examination, it bears the imprint of the intestines.

In diphtheritic endometritis the gangrenous process may attack the muscular tissue, and give rise to losses of muscular substance--a condition known as necrotic endometritis or putrescence of the uterus.

Inflammatory changes are rarely lacking in the intermuscular connective tissue, which exhibits in places serous or gelatinous infiltration, with afterward pus formation, and with here and there small abscesses. The sero-purulent infiltration of the connective tissue is specially marked beneath the peritoneal covering of the uterus either behind or along the sides at the attachment of the broad ligaments. In the same situations the lymphatics, which normally are barely perceptible to the naked eye, are sometimes enlarged to the size of a quill, and are characterized by varicose dilatations occurring singly or presenting a beaded arrangement. In the substance of the uterus the dilated vessels are liable to be mistaken for small abscesses. The pus-like substance contained in the lymphatics is composed of pus-cells and of micrococci. From the cellular tissue surrounding the vagina, or that beneath the peritoneal covering of the uterus, the inflammation may spread by contiguity of tissue between the folds of the broad ligament, and thence pass upward to the iliac fossæ. Usually the process is unilateral. After the inflammation has crossed the linea terminalis it may take a forward direction above the sheath of the ilio-psoas muscle to Poupart's ligament, or it may creep upward, following the course, according to the side affected, of the ascending or descending colon, to the region of the kidney. It is rare for inflammation of the cellular tissue to travel around the bladder to the front. In such cases it pursues its course between the walls of the bladder and the uterus, and along the round ligament to the inguinal canal. In a few cases the cellulitis mounts above Poupart's ligament, between the peritoneum and the abdominal wall.

The course of the inflammation is not simply fortuitous, but follows prearranged pathways in the connective tissue. König[7] and Schlesinger[8] have shown that when air, water, or liquefied glue is forced into the cellular tissue between the broad ligaments the injected mass has a tendency to invade the iliac fossæ. In Schlesinger's experiments, if the canula of the syringe was inserted into the anterior layer of the broad ligament, {988} the glue spread between the folds to the abdominal end of the Fallopian tube; thence, following the track of the vessels, it passed to the linea terminalis; and finally mounted upward along the colon or swept forward to Poupart's ligament until the advance was stopped at the outer border of the round ligament. If the injection was made to the side of the cervix through the posterior layer at the junction of the cervix and the body, the posterior layer gradually bulged out, the peritoneum was lifted from the side wall of the pelvis, and the glue passed beyond the vessels to reach the iliac fossa. If the injection was made to the side of the cervix through the anterior layer, the glue passed between the bladder and the uterus, and forward along the round ligament to the inguinal canal, while another portion of the fluid passed between the layers of the broad ligament, and reached the peritoneal covering of the side walls behind the round ligament. If the injection was made in the median line in a peritoneal fold of Douglas's cul-de-sac, the fluid travelled forward upon one side along the round ligament and thence to the posterior wall of the bladder.

[Footnote 7: _Arch. der Heilkunde_, 3 Jahrg., 1862.]

[Footnote 8: _Gynaekologische Studien_, No. 1.]

The term parametritis, introduced into use by Virchow, is, properly speaking, limited to inflammation of the connective tissue immediately adjacent to the uterus, the older one of pelvic cellulitis furnishing a more comprehensive designation for cases where, as a consequence of a progressive advance from the point of departure in the genital canal, the remoter regions have likewise been invaded. Connective-tissue inflammation presents, as the first essential characteristic, an acute oedema, the fluid which fills the gaps and interspaces consisting of transuded serum rendered opaque by the presence of pus-cells or possessing a gelatinous character. In the mild, uncomplicated cases the oedema disappears rapidly. Where the cell-collections are of moderate extent the entire process may vanish without leaving a trace of its existence. If the cell-elements, on the other hand, are present in great abundance, they, as a rule, first undergo fatty degeneration, and, after the absorption of the fluid portion, form a hard tumor composed of a fine granular detritus, which under favorable circumstances likewise after a few weeks becomes absorbed. In rare cases abscess-formation in the tumor results.

In the cellulitis resulting from septic infection, especially in cases complicated by diphtheritis, the tissues seem as if soaked with dirty serum, and contain scattered yellowish deposits, which soon present, even to the naked eye, the appearance of pus-collections. This sero-purulent oedema is always associated with lymphangitis, the lymphatic vessels possessing varicose dilatations and beaded arrangements similar to those already described in the uterine tissue. The foregoing changes are most distinct in the firm connective tissue adjacent to the uterus and at the hilum of the ovary, while they are less clearly traced in the looser structure of the broad ligament (Spiegelberg).

In favorable cases the inflammation is circumscribed, or at least is limited, by the nearest lymphatic glands. In cases of intense infection it spreads rapidly, and justifies the title bestowed upon it by Virchow of parametritic malignant erysipelas.

PELVIC AND DIFFUSED PERITONITIS.--Inflammation of the pelvic peritoneum may result from severe attacks of catarrhal endometritis, the inflammatory process either traversing the uterine tissue or passing {989} through the Fallopian tubes to the adjacent serous membrane; or it may proceed, secondarily, from the stretching and irritation occasioned by an associated parametritis.

As a rule, pelvic peritonitis is not attended with much exudation. The latter is situated upon the folds of the peritoneum limiting the cul-de-sac of Douglas, upon the ovaries, and upon the broad ligaments. In favorable cases it consists of fibrinous flakes and fluid pus. If the latter is abundant, it may become encysted by the formation of adhesions between the pelvic organs.

General peritonitis may result from the extension of a pelvic peritonitis, or from the transport of poison through the lymphatics into the peritoneal sac. In the first case the entire peritoneum is injected, and the contents of the abdominal cavity are loosely bound together by pseudo-membranes, composed of pus and coagulated fibrine. The intestines are at the same time distended and the diaphragm is pushed upward. In the so-called peritonitis lymphatica the inflammatory symptoms are at the outset lacking. The abdominal cavity is found filled with a thin, stinking, greenish or brownish fluid composed of serum and micrococci. The intestines are lax and oedematous, and the muscular structures are paralyzed, with resulting tympanitic distension. The peritoneal covering of the intestines is devoid of lustre, and covered with injected patches, or is stained of a dark-brown color. Death often ensues before the occurrence of exudation.

Septic forms of pelvic inflammation are often associated with oöphoritis, the dilated lymphatics either extending to the substance of the ovaries, where they may lead to the production of small abscesses, or, as a result of blood-dissolution, the organs become soft, pulpy, and infiltrated with discolored serum, and present hemorrhagic spots distributed over the surface.

PHLEBITIS AND PHLEBO-THROMBOSIS.--The formation of thrombi in the uterine and pelvic veins is sufficiently common during the puerperal period. The coagulation may result from compression or from enfeeblement of the circulation. A predisposition to its occurrence is created by relaxation of the uterine tissue. A normal thrombus is in itself harmless. In time it becomes organized, and the occluded vessel is converted into a connective-tissue cord, or a channel may form through it which permits the passage of the blood-stream. When, however, pus or septic matters obtain access to a thrombus, it undergoes rapid disintegration, and the particles get swept away into the circulation until arrested in the ramifications of the pulmonary artery. Wherever these poisoned emboli happen to lodge inflammation is set up in the adjacent tissues, and abscesses result (pyæmia multiplex). Sometimes countless collections of pus may form in the lungs. Less commonly abscesses are found in the liver or spleen, originating either from emboli which have already made the pulmonary circuit or from thrombi in the pulmonary veins.

Inflammation of the veins (phlebitis) sometimes occurs when the vessels have to traverse tissues in or near the uterus infiltrated with purulent or septic materials. The endothelium then undergoes proliferation, and thrombosis is produced. Phlebitic thrombi do not necessarily break down, and may in that case act as a barrier to the progression of septic germs into the circulation (Spiegelberg). As a rule, however, {990} under the influence of inflammation and infection, they become converted into puriform masses.

The thrombi grow by accretion in the direction of the heart. They may extend from the uterus through the internal spermatic, or through the hypogastric and common iliac veins, to the vena cava. Sometimes the thrombus may be traced back to the placental site.

SEPTICÆMIA.--From these local conditions, sooner or later, secondary affections develop in distant organs. The general affection is, in great part at least, likewise of local origin. Sometimes, however, where the poison, which enters the system through the lymphatics and veins, is very active and abundant, death may follow from acute septicæmia before the changes in the sexual organs have had time to develop. The fatal result in these cases is probably due to paralysis of the heart. After death post-mortem decomposition rapidly sets in, the blood is sticky, and swelling is found in the various parenchymatous organs.

The secondary affections consist in the metastatic abscesses already noticed as produced by infected emboli, in circumscribed purulent collections due to the conveyance of septic materials into the blood-current through the lymphatics, in ulcerative endocarditis, in inflammations of the pleura, the pericardium, and the meninges, and in purulent inflammation of the joints.

A study of the nature of puerperal fever will best show how intimately these seemingly distinct processes are linked together.

EARLIER VIEWS CONCERNING THE NATURE OF PUERPERAL FEVER.[9]--According to the teachings of Hippocrates, Galen, and Avicenna, of Ambrose Paré, of Sydenham, and of Smellie, the fevers of puerperal women were attributable to the suppression of the lochia. For twenty centuries this doctrine was accepted almost without dispute, the best clinical observers confounding a symptom which is often lacking with the cause of the disease itself.

[Footnote 9: For data given, and for a great variety of historical information, vide Hervieux, _Traité clinique et pratique des maladies puerperales_.]

In 1686, Puzos[10] taught that milk, circulating in the blood, is attracted to the uterus during pregnancy and to the breasts after confinement, but that milk metastases may form in other parts, and produce the symptoms of malignant or intermittent fever. In 1746, A. de Jussieu, Col de Villars, and Fontaine advanced in support of this theory the fact that they had found, on opening the abdomen in women who had died from an epidemic which raged that year in Paris, a free lactescent fluid in the lower portion of the abdominal cavity and clotted milk adherent to the intestines. This doctrine, which seemed to be based upon, and to accord with, observation, found many adherents in France. It lost ground, however, when, in 1801, Bichat pointed out the true nature of the abdominal effusions of women who had died in childbed, and demonstrated that they were to be found likewise in peritoneal inflammations occurring in men and in non-puerperal women.

[Footnote 10: _Premier Mémoire sur les Dépôts lacteux_.]

While, during the second half of the eighteenth century, the doctrine of milk metastasis held full sway in France, in England and Germany the dominant leaders in medicine referred the causes of puerperal fevers to inflammations of the womb and of the peritoneum. With the advances made in pathological anatomy in the beginning of the present {991} century, France taking the lead, stress was likewise laid upon inflammations of the veins and of the lymphatics. The vitality of the doctrine of local inflammations is well shown by the records kept by the Health Board of this city, where a large proportion of the deaths returned from childbed fever are entered under the head of metritis, of peritonitis, of metro-peritonitis, and of puerperal phlebitis.

In opposition to the doctrines of the so-called localists, the theory that puerperal fever is an essential fever, and as much a distinct disease as typhus fever, typhoid fever, or relapsing fever, has been strenuously advocated by some of the most distinguished clinical teachers who have devoted their attention to obstetrical science.

Fordyce Barker, the most recent exponent of the essentiality of puerperal fever, in his classical work upon the _Puerperal Diseases_, states the arguments against the local origin of the diseases as follows: 1st, that puerperal fever has no characteristic lesions; 2d, that the lesions which do exist are often not sufficient to influence the progress of the disease or to explain the cause of death; 3d, that there may be inflammation, even to an intense degree, of any of the organs in which the principal lesions of puerperal fever are found, and yet the disease will lack some of the essential characteristics of puerperal fever; 4th, that the lesions are essentially different from spontaneous or idiopathic inflammations of the tissues where these lesions are found; 5th, that puerperal fever is often communicable from one patient to another through the medium of a third party, and that this is not the fact in regard to simple inflammations in puerperal women.

However, neither Barker, nor those who entertain views similar to his, question the local origin of many febrile affections in childbed, but claim that purely local inflammations have each their characteristic symptoms, which differ from those of true puerperal fever, that puerperal fever is a zymotic disease of unknown origin, and that local lesions, where they coexist, are not the primary source of trouble, but are secondary to changes in the blood.

In 1850, James Y. Simpson[11] published a short paper "On the Analogy between Puerperal and Surgical Fever." This article may well be regarded as the foundation of the modern doctrine concerning puerperal fever, and is well worthy of perusal at the present day; for, though in the then existing state of pathology many of the links were wanting which have since raised the argument to nearly a mathematical demonstration, the paper furnishes a brilliant example of the scientific foresight which is able to discern the truth even where the evidence lacks completeness.

[Footnote 11: _Edinburgh Medical Journal_.]

In 1847, Semmelweis, who was at that time clinical assistant to the Lying-in Hospital at Vienna, made the startling assertion that "puerperal patients were chiefly attacked with puerperal fever when they had been examined by the physicians who were fresh from contact with the poisons engendered by cadaveric decay; that fever ensued in the practice of those who after post-mortem examination washed their hands in the usual manner, whereas no fever or but few cases of disease followed when the examiner had previously washed his hands in a solution of chloride of lime." In the face of insult, ridicule, and abuse Semmelweis {992} maintained this position for years, almost unaided, with fanatical persistency. It was easy for his opponents, for the most part managers of the great lying-in asylums, to show from clinical experiences the weakness of so one-sided a theory. But the employment of the equivocal demonstration _falsus in uno, falsus in omnibus_, served only as a temporary defence against the laxity which prevailed in hospital management only a quarter of a century ago. Though Semmelweis died with no other reward than the scorn of his contemporaries, it is impossible at the present day to so much as contemplate the abuses he attacked without a shudder.

In 1860, Semmelweis published the result of his ripened experience in a treatise entitled _Die Aetiologie der Begriff und die Prophylaxis des Kindbett fiebers_, in which, abandoning his earlier exclusive position, he maintained that puerperal fever arises from the absorption of putrid animal substances, which produce first alterations in the blood, and secondly exudations. He distinguished between cases in which the infection was introduced from some external source, and which he believed to be the most frequent variety, and those where the poison was generated in the system. The sources from which the infection is derived he believed to be--1st, from the dead body, regardless of age, sex, or disease, no matter whether the latter is of puerperal or non-puerperal origin, the virulence depending upon the stage of decomposition; 2d, diseased persons, whose malady is associated with decomposition of animal tissue, no matter whether the affected person suffers from childbed fever or not, the decomposing matter alone furnishing the product from which infection is derived; 3d, physiological animal substances in the process of decomposition. As carriers of infection he regarded the fingers and hands of the physician, midwife, or nurse, sponges, instruments, soiled clothing, the atmosphere, and, in brief, anything which, after being defiled with decomposing animal matter, was brought into contact with the genitals of a woman during or subsequent to parturition. Absorption takes place from the inner surface of the uterus or from traumata in the genital canal. Infection seldom occurs in pregnancy, because of the closure of the os internum, the absence of wounded surfaces, and because of the rarity with which examinations are made; during dilatation infection is common, but exceptional during the period of expulsion, because the inner uterine surface is at that time rendered inaccessible by the advance of the child; in the placental and puerperal period infection occurs from utensils and instruments, but chiefly through the access of atmospheric air when the latter is loaded with decomposing organic matter. In rare instances auto-infection may result from spontaneous decomposition of the lochia, of bits of decidua, of coagula of blood, of necrosed tissue, or in consequence of severe instrumental labors. In a word, puerperal fever was according to Semmelweis no new specific disease, but a variety of pyæmia.

I have been thus particular in giving prominence to the labors of Semmelweis partly from justice to a man who was hated and despised in his lifetime, and partly because I believe that few outside of Germany are really cognizant of the immense service he rendered to humanity, or that to him is really due a large part of what is now current doctrine concerning the nature and prophylaxis of puerperal fever.

THE NATURE OF PUERPERAL FEVER AS REGARDED FROM THE {993} STANDPOINT OF MODERN INVESTIGATION.--The older beliefs in the suppression of the lochia and the metastases of milk have long since been relegated to the domain of old nurses' lore, and do not call for serious discussion. The localist theory, that puerperal fever is a metritis, a peritonitis, a phlebitis, or an inflammation of the lymphatics, is, as mortuary records show, still adhered to by many practitioners, and, as we have seen, is justified by the fact that puerperal fever is, with rare exceptions, associated at some period of its progress with certain inflammatory processes which have their starting-point in the generative apparatus. But the localist theory leaves out of view the existence of blood-poisoning, and yet the coexistence of a blood-poison with the local lesions is an essential feature of puerperal fever. It was this defect which gave to the advocates of the specificity of puerperal fever their real importance. The outcome of modern investigation tends, however, to prove that the puerperal poison is of a septic nature, and that the usual points of introduction of the poison are the lesions of the parturient canal. This does not, indeed, exclude other points of entry, for clinical experience renders it probable that, under certain conditions, the poison may be primarily introduced into the blood through the respiratory and digestive organs. Puerperal fever is really a surgical fever, modified, however, by the peculiar physiological conditions which belong to the puerperal state. The argument against its septic origin is based chiefly upon mistaken ideas concerning the nature of septicæmia. So long as the symptoms of the latter were derived for the most part from the effects observed as a consequence of injecting putrid materials into the veins of dogs, a confusion arose from the fact that the results obtained were commonly those of putrid intoxication, and not those of true septicæmia. Under such circumstances it was not difficult to formulate definitions of septicæmia which could be shown to be at variance with the phenomena which ordinarily exist in puerperal fever.

The argument that the infectious diseases of childbed are of a septic nature can best be understood by presenting the proofs in their orderly sequence.

1st. _It is demonstrable that septic poisons are capable of producing the lesions ordinarily associated with puerperal fever._ Thus, it is a matter of ordinary experience that the retention of a small bit of the membranes within the uterus will produce fetid lochia, and, as the result of infection, a febrile condition, which, as a rule, subsides with the expulsion of the offending body and the use of disinfectant washes. A virulent form of fever is not unfrequently occasioned by retained coagula or placental débris which have undergone decomposition. I was once sent for to see a puerperal patient suffering from fever on the fourth day following her confinement. On entering the room I found the stench intolerable; turning down the sheets, I discovered that the patient was lying in a decomposing mass, and learned that her doctor had forbidden, after the birth of her child, the removal of the soiled linen and blankets. The patient died in the third week from pyæmia multiplex.

Haussmann[12] reported a case of auto-infection in the rabbit which terminated fatally. A portion of the membrane, retained in the left cornu, {994} led to diphtheritic losses of substance in the lower portion of the vagina, to hemorrhagic enteritis, and to peritonitis. The same author produced death from septicæmia by injecting into the gravid uterus of one rabbit serum from the abdomen of another which had died from infection. The post-mortem examination showed the muscles filled with granules and the peritoneum injected, but no fibrino-purulent exudation. Injections into the uterus of pus from the abdomen of a woman who had died from infectious puerperal disease produced no effect upon rabbits two weeks gravid, while in the second half of pregnancy premature delivery and death occurred, in one case in one and a half, in another in two and a half, days. In the animal which died in thirty-six hours there was commencing perimetritis and peritonitis, while in the one that died after the lapse of sixty hours the abdomen was found to contain fibrine and pus.[13] D'Espine injected into the uterus of a rabbit which had just produced her young pus from the abdomen of a woman who had died from puerperal disease two days before. This was subsequently followed by other injections of fetid fluids during the four days following. On the twelfth day the animal died. The autopsy revealed peritonitis, most marked in the pelvic cavity, inflammatory alterations in the vagina, uterus, and tubes, small abscesses in the body of the uterus, softened clots in the veins of the broad ligaments, and infarctions of the liver.[14] Schüller found that subcutaneous injections of septic material in female animals during pregnancy produced a diphtheritic ulcerative process on the uterine surface, which determined the separation of the placenta; diphtheritic patches, likewise, were found in the cornua of the uterus.[15]

[Footnote 12: "Entstehung der übertragbaren Krankheiten des Wochenbettes," _Beitr. zur Geburtsk. und Gynaek._, Bd. iii. Heft 3, p. 345.]

[Footnote 13: _Contribution à l'étude de la septicémie puerpérale_, Paris, 1873, p. 28.]

[Footnote 14: _Ibid._, p. 394.]

[Footnote 15: "Experimentelle Beiträge zum Studium der septischen Infection," _Deutsch. Zeitschr. für Chir._, Bd. vi. p. 141.]

Thus we find that in the human subject and in experiments made upon animals septic poisons introduced into the system following or near delivery produce lesions similar to those found in puerperal fever. As a further coincidence, we notice that, as in puerperal fever, the lesions from direct septic poisoning have nothing characteristic about them, producing in one case pyæmia, in another partial peritonitis, in another general peritonitis, in another diphtheritis, while in others the lesions are comparatively trivial, these differences being due to variable facta, such as the qualities of the septic poisons, the points of entry into the organism, and the resistance offered by the invaded tissues.

2d. _Septicæmia is a disease characterized by the invariable presence in the organism infected of minute bodies generally termed bacteria._[16]

[Footnote 16: In 1865, Mayrhofer (_Mon. Schr. f. Geburtsk._, vol. xxv., p. 112, 1865), at that time clinical assistant to the Lying-in Service of Braun in Vienna, stimulated by the researches of Pasteur, maintained that septic endometritis was the result of putrid fermentation within the uterine cavity, and drew attention to the vibrios--a term which he applied to the round as well as to the rod-like bacteria--as the source, and not the product, of putrefaction. He claimed that while in puerperal processes vibrios are always present, in healthy women they never occur before the second, third, or fourth day, and not always even then. The chief progress that has been made as regards our knowledge of puerperal fever in the last ten years has been in the direction of strengthening Mayrhofer's argument by careful experiment, and by defining the action of microscopic fungi in the production of septic morbid processes.]

Until very recently the whole subject of septicæmia has been in a state of wellnigh hopeless confusion. From Gaspard and Panum, through a long list of experimenters, hardly any two arrived at precisely similar {995} results. Something like an approach to order has, however, been produced since it has begun to be understood that the effects produced by septic fluids vary with the quality of the poison and the method of experimentation, and that to obtain identity in the result there must be identity in all the conditions. Thus, Samuel has shown that the same organic substance produces different effects at different stages of decomposition; again, that the enteritis which is commonly quoted as characteristic of septic poisoning occurs, as a rule, in animals when the septic fluid is injected directly into the blood, and is rare when it finds its way into the circulation through the lymphatics, as is the case usually in clinical experiences.[17] There is one experimental point of extreme practical importance too in connection with puerperal septicæmia--viz. that if the injection of a septic fluid be made directly into a vessel, toxic effects speedily follow, but are transitory, unless the amount of the fluid be large, or its virulence exceptional, or the animal very young;[18] whereas very small amounts injected subcutaneously, by developing rapidly-spreading phlegmonous inflammation, resembling malignant erysipelas in man, are capable, after a period of incubation, of producing fatal results; or they may, if injected into a shut cavity or underneath a fascia, lead to the development of an inflammation of an ichorous character. In other words, the eliminating organs suffice, under ordinary conditions, to remove from the blood the same amount of septic fluid which would prove fatal if injected into the tissues.[19] To produce similar results the injections into the blood need to be repeated at intervals. This experience leads us to the conclusion that in the tissues septic poison possesses the capacity of self-multiplication, and that in the local inflammation set up a reservoir is formed from which poison is continuously poured into the circulation.

[Footnote 17: _Loc. cit._, p. 349.]

[Footnote 18: "Traube und Gescheidlen, Versüche über Faülniss und den Widerstand des lebender Organismus," _Schles. Ges. f. vaterländische Cultur_, Feb. 13, 1874.]

[Footnote 19: In some instances in which absorption from the tissues is very rapid the effects of subcutaneous injections may be similar to those produced by injections made directly into the circulation, and the local lesion be insignificant.]

This capacity of self-multiplication which septic fluids possess has recently been found to be coincident with the presence of certain parasitic bodies, generically termed bacteria. All carefully-made experiments serve to show that if a septic fluid be deprived of these organic bodies by boiling or filtration while it continues capable of producing inflammation, the inflammation is usually of diminished intensity and remains local in its character;[20] whereas the bacteria retained upon the filter possess all the virulent properties of the original fluid.[21] This does not alone necessarily prove that the virus resides in the bacteria, for it does not exclude the possibility that both the virus and the bacteria remain upon the filter.

[Footnote 20: In filtration through porous earthenware cylinders the filtrate possesses no phlogogenic properties.]

[Footnote 21: Tiegel, _Correspondenzblatt für Schweizer Aertze_, 1871, S. 1275; Klebs, _Archiv für exp. Pathol. und Pharmakol._, Bd. i. Heft. 1, S. 35.]

So far, attempts at isolating the microspores of septicæmia and cultivating them separately in vehicles composed of water holding in solution inorganic constituents, or sterilized fluids containing organic matters, or of the semi-solid gelatinous substances recommended by Koch, have been only partially successful in proving them to be the sole source of {996} infection. Some earlier experiments of Tiegel and Klebs[22] were attended with positive results, and more recently confirmatory evidence has been furnished by Pasteur and Doléris.[23] Hiller, rarely quoted now, arrived at different conclusions. He found that bacteria washed in pure water were innocuous.[24] But pure water had long before been proven by observers to be inimical to the well-being of the organisms in question. Schüller says that Hiller's experiments prove apparently that while a putrid fluid may be in the highest degree poisonous, its component parts--viz. either the fluid or the bacteria singly--are neither deadly nor poisonous.[25] The fact is, that isolation experiments are subject to what has hitherto been in most experiments an unavoidable source of error. As Davaine noted early in his observations, the physiological action of bacteria is very dependent on the constitution of the medium in which they are developed, which is in entire harmony with what is known of organisms much higher in the scale. "Many plants," says Burdon-Sanderson,[26] "containing active principles, become inert when transplanted from an appropriate soil." Bucholtz, in a series of experiments designed to test the influence of antiseptics upon the vitality of bacteria, found not only a difference between those taken directly from the infusion and those cultivated in artificial fluids, but between bacteria derived from the same source and cultivated in modifications of the nutrient medium.[27] Then, too, it is not always safe to transfer to the human species the results of experiments made upon the lower animals. Indeed, among animals, not only in different species, but in varieties of the same species, differences in the susceptibility to septicæmic poisons are found ranging from gradations as to the intensity of the effect produced to absolute immunity. In anthrax, a disease analogous to the one in question, the bacterial origin has been established beyond dispute by the inoculation of isolated bacilli, which multiply in the blood and permeate in enormous numbers the lungs, liver, kidneys, spleen, and glandular structures. If the same unequivocal testimony has as yet not been obtained from isolation experiments as regards septicæmia, it is reasonable to suppose that this is due to the defects in the technique, for which it is presumable the ingenuity of investigators will in future find the remedy.

[Footnote 22: _Archiv für exp. Pathologie und Pharmakologie_, "Beiträge zur Kenntniss der Pathogenen Schistomyceten," Band iv. Heft 3, S. 241 und ff.; Tiegel, _loc. cit._]

[Footnote 23: In this connection may be mentioned some very interesting experiments by Dr. George Gaffky (_Experimentellen Erzengte Septicæmie, Mittheilungen aus den Kaiserlich, Gesundh. Amte_), in which micrococci from the blood of septicæmic mice were successfully cultivated in a gelatine preparation, and produced, when inoculated in small quantities, the symptoms identical with those obtained by inoculating the blood itself.]

[Footnote 24: "Exp. Beiträge zur Lehre von der organisirte Natur der Contagion und von der Faülniss," _Archiv für klinische Chirurgie_, Bd. xvii. Heft 4, S. 669 u. ff.]

[Footnote 25: "Exp. Beiträge zum Studium der septischen Infection," _Deutsche Zeitschrift für Chirurgie_, Bd. vi. S. 162.]

[Footnote 26: "Lectures on the Relations of Bacteria to Disease," _British Med. Journal_, March 27, 1875. See also Klebs, "Beiträge zur Kenntniss der Pathogenen Schistomyceten," _Arch. für Pathol. und Pharmakol._, Bd. iii. S. 321.]

[Footnote 27: "Antiseptica und Bacterien," _Arch. f. exp. Pathol. und Pharmakol._, Bd. iv., Heft 1 und 2.]

It is, however, from the constant presence of the bacteria in infected wounds, and their distribution through the tissues, that the argument in favor of connecting septic symptoms with the bacteria has been mainly deduced. Here the ground is sufficiently solid, and, judged by ordinary laws of scientific evidence, the pathological importance of the microspores {997} may be regarded as established. To be sure, we find them in tongue-scrapings of healthy individuals, but tongue-scrapings are poisonous if injected into the tissues. That they do not ordinarily prove so in the mouth is no more singular than that woorari can be swallowed with impunity. Tiegel[28] has endeavored to show that round bacteria are found normally in the internal organs of the body; but Koch[29] states that he has on many occasions examined normal blood and normal tissues by means which prevented the possibility of overlooking bacteria, or of confounding them with granular masses of equal size, and that he has never in a single instance found organisms.

[Footnote 28: _Arch. f. Path. Anat. u. Physiol. u. f. klin. Med._, vol. lx. p. 453.]

[Footnote 29: On _Traumatic Infective Diseases_, New Sydenham Soc. publication p. 15.]

It is stated that bacteria are sometimes absent from the blood withdrawn during life in septic diseases. As, however, their constant presence has been confirmed in the vessels and glomeruli of the kidneys, it is fair to assume that those organs, acting as filters, must have received the colonies observed in them from the general circulation.

The difficulty of obtaining bacteria from the blood in many cases during life in septic diseases does not, however, as was once supposed, invalidate the theory of their pathogenic importance. Septicæmia is at present employed as a collective term for a number of processes which may occur singly or in combination with one another. When a relatively large quantity of a putrid fluid is injected into the veins of an animal, death follows from the action of a chemical poison (sepsin). The blood during life rarely displays the presence of bacteria, the latter disappearing in the circulation. In animals thus poisoned blood does not possess infectious properties. This form is termed putrid intoxication. That the poison in these cases is, however, produced by the bacteria is shown by experiments of Gutmann,[30] who demonstrated that bacteria from a drop of putrid blood cultivated in Cohn's solution developed in the fluid a poison which, when injected into the veins of dogs, occasioned death with all the symptoms of putrid intoxication. Still more conclusive were the experiments of Koch. This observer injected four drops of putrid blood beneath the skin of mice. The latter died in from four to eight hours. There were no bacteria in the blood, and the blood was not infectious. When, however, a single drop was injected, the mice often remained unaffected, but in a third of the cases they became ill after twenty-four hours, death occurring in from forty to sixty hours. The blood during life communicated the same disease to other mice, and bacilli were always present in large numbers. In these cases the dissolved poison in the fluid injected was too small in amount to destroy life, and death resulted only after a period of incubation as a consequence of the multiplication of bacilli in the blood and in the tissues.

[Footnote 30: Vide Semmer, "Putride Intoxication," etc., _Virchow's Arch._, vol. lxxxi. p. 109.]

In another class of cases Koch experimented, not with putrid blood, but with a fluid produced by macerating a piece of mouse-skin in distilled water. Of this he injected a syringeful into the back of a rabbit. The result was peritonitis, swelling of the spleen, gray wedge-shaped patches in the liver, and in the lungs were found dark-red patches the size of a pea, devoid of air--all appearances in harmony with what is designated as pyæmia. Oval micrococci were found in great numbers {998} everywhere throughout the body. But the point of special interest in the present connection is the fact that wherever these micrococci come in contact with the red blood-corpuscles the latter stick together and become arrested in the minute capillary network. The thrombi thus formed are further enlarged by the deposition of micrococci, which multiply, block up individual capillary loops, and invade contiguous tissues. In the blood-current itself, however, the micrococci do not increase in numbers, and cannot always be found in the circulation upon a single examination, but Doléris[31] assures us that in puerperal fever by repeated trials, especially after a chill, he has never failed to demonstrate their presence.

[Footnote 31: _La Fievre Puerperale, etc._, p. 120.]

As to the exact manner in which these minute bodies exercise their pernicious influence, whether they operate mechanically, or whether they produce a virus in the process of nutritive activity, or whether, as is probable, both suppositions are correct, must be decided by future investigations. It is enough for us to note that the connection between sepsis and bacteria is intimate and vital.

3d. _Pathogenic bacteria are invariably associated with puerperal fever, and to them the infectious qualities of the disease are due._ I have been explicit regarding the evidence concerning bacteria in septic diseases, because it places the question of the infectious group of puerperal fever cases in the following position: Experiences occurring clinically, as well as those produced upon animals, teach us that certain lesions and symptoms, similar to those we are accustomed to regard as characteristic of puerperal fever, results from septic poisoning. In a large class of cases, however, the connection between childbed fever and sepsis has been deduced rather from analogy than direct proof. For those who chose to regard such as due to a specific poison peculiar to the puerperal state there was really no objection. If, however, bacteria are characteristic of septic poisoning, the question presents itself in a different light, and we have to inquire whether, in the less obvious cases, bacteria are present in puerperal fever in the proportions and groupings that we find them in other diseases due to putrid infection. Now, it is precisely proof of this nature that has recently been abundantly rendered.

Waldeyer,[32] Orth,[33] Heiberg,[34] and Von Recklinghausen[35] found the tissues and lymphatics of the parametria filled with pus-like masses, which consisted, in addition to pus-cells, chiefly of bacteria. Bacteria swarmed in the fluid of the peritoneal cavity. In one case examined by Waldeyer six hours after death, while the body was still warm, the peritoneal exudation was like an emulsion, and furnished an abundant deposit which consisted almost entirely of bacteria. Orth injected ten minims of peritoneal fluid from a woman dead of puerperal fever into the abdomen of a rabbit. As the animal was dying he broke up the medulla oblongata, and found in the peritoneal fluid enormous quantities of these {999} organisms. In puerperal fever round bacteria have been likewise found, though in less quantities, in the lymphatics of the diaphragm and in the fluids of the pleura, the pericardium, and the ventricles of the brain. In post-mortem examinations of fresh subjects the serous fluids, withdrawn under proper precautions, do not contain round bacteria except in cases of septic infection.[36] Orth found in the purulent contents of the vessels of the funis, in children who died of sepsis, precisely the same formations as existed in the exudations of the mother.

[Footnote 32: "Ueber das Verkommen von Bacterien bei der diphtheritischen Form des puerperal Fiebers," _Archiv für Gynaekologie_, vol. iii. p. 293.]

[Footnote 33: "Untersuchungen über puerperal Fieber," _Virchow's Archiv_, vol. lviii. p. 437.]

[Footnote 34: _Die puerperalen und pyæmischen Processe_, Leipzig, 1873.]

[Footnote 35: For the views of Von Recklinghausen I am indebted to his pupil Steurer. Vide the writer's paper on "The Nature, Origin, and Prevention of Puerperal Fever," _Trans. of the International Med. Congress_, Phila., 1876.]

[Footnote 36: Klebs, "Beiträge zur Kenntniss der Pathogenen Schistomyceten," _Archiv für exp. Pathol. und Pharmakol._, vol. iv. p. 441 _et seq._]

Doléris, in a remarkable essay already referred to, published in 1880,[37] furnishes not only conclusive evidence of the presence of bacteria in the various tissues and serous cavities of women dying of puerperal fever, but has added the evidence of their pathogenic character by cultivating them apart in sterilized fluids, and by reproducing in animals, by means of subcutaneous injections of the isolated bacteria, the infarctions, the blood-changes, and the suppurative processes of the original disease.

[Footnote 37: _La Fievre Puerperale et les Organismes Inférieurs._]

So far, the generic term bacteria has been employed to indicate the disease-germs which are the active agents of infection in puerperal fever. It is not, however, intended to assume that the germs of septic processes are all identical, or that they all produce precisely the same pathological conditions. Koch, indeed, maintains that a distinct specific bacterial form is found in such closely-allied affections as pyæmia, septicæmia, gangrene, and erysipelas, the different forms possessing, however, this link in common--viz. that they are alike generated in putrefying media. Singularly enough, the bacterium termo and the bacterium commune--to which the fetidity of matters undergoing putrefaction is due--are in themselves harmless. They are rapidly destroyed in the circulation, and are not inoculable. Fetid discharges from wounds are not therefore necessarily dangerous. The putrid odor serves a useful purpose, as it gives warning of the existence of conditions which favor the development of life-destroying organisms; but the latter may develop without the concurrence of the forms which give rise to putrefaction--a fact of considerable importance in view of the common belief that septic infection is excluded by the absence of fetid odors.

In puerperal fever Doléris found the prevailing pathogenic organisms consisted of bacilli or rods, and micrococci or round bacteria in the varieties of micrococci, simple points; diplococci, double points; and chains or wreaths. The bacilli he regarded as the source of acute, rapid septicæmia, while pus-production was associated with the multiplication of the round bacteria, and especially of the diplococci.

4th. _The presence of germs in puerperal fever serves not only to fix cases hitherto doubtful in the category of septic diseases, but affords the most satisfactory explanation of the protean phenomena of puerperal fever itself._

We have seen, from both Koch's and Gutmann's experiments upon animals, that death may occur independently of bacteria by the rapid absorption of a chemical poison developed in a putrefying fluid. Clinical experiences, such as the speedy death sometimes observed when retained coagula or portions of placenta undergo decomposition within the uterine cavity, renders it probable that similar cases of putrid intoxication are {1000} not unknown in puerperal women, though, so far, the anatomical demonstration of the fact has not been furnished.

In cases, however, where puerperal fever has a distinct period of incubation, and progresses step by step to the fatal ending, bacteria are always found invading the tissues of the genital canal. In rare cases they pass by the Fallopian tube to the peritoneal cavity and excite salpingitis and peritonitis. More commonly from local lesions they enter the canalicular spaces of the connective tissue forming the framework of the genital canal, which is continuous with the subperitoneal connective tissue of the pelvis. From the canalicular space they enter the lymphatics. Cellulitis is excited by their presence, and the lymphatic glands become inflamed and enlarged. In pernicious forms they produce a sero-purulent oedema, which spreads rapidly with a wave-like progress after the manner of erysipelas; or in milder cases the progress of the disease-germs is arrested by the lymphatic glands or the resistance offered by the tissues themselves, and the ordinary circumscribed phlegmon is produced. By the lymphatics which accompany the vessels of the Fallopian tubes they reach the ovaries (puerperal ovaritis), and by the broad ligaments they pass to subperitoneal tissues of the iliac and lumbar regions. Through the same system they are conveyed to the great serous cavities of the body. In the peritoneum they give rise, unless death occurs too speedily, to pyæmic peritonitis, which, unlike the traumatic form, is attended with but little pain, and for which the claim has been set up that it is peculiar to puerperal fever. The wide stomata upon the abdominal surface of the diaphragm allows the facile entrance of the organisms into its lymphatics. Waldeyer found in diaphragmitis the lymphatics of the diaphragm filled with bacteria. And thus, following the lymphatic system, if we only admit that bacteria are the active agents of sepsis, the frequency, in severe types of puerperal fever, of inflammation of the serous membranes of the peritoneum, the pleuræ, the pericardium, the meninges, and the joints finds an easy explanation. Nor is it altogether accident which determines in different cases the precise serous membranes which are affected. The widespread ramifications of the lymphatic system would naturally give rise to eccentric inflammations in place of those following the apparent continuity of tissues.

The ductus thoracicus is the principal channel through which the bacteria enter the blood. It is possible that they may further obtain access into the circulation through the radicles which furnish the communications between the capillaries and the lymphatics. We have seen that bacteria are found with difficulty in the blood during life. A few hours after death they swarm in that fluid. That they do, however, enter the general circulation during life is incontestable. Steurer writes: "As the kidneys are the great filters of the human system, I never neglected to examine them, and almost invariably found micrococci filling the arterioles and glomeruli." This is in correspondence with what occurs in other septic diseases, and accounts for the albuminuria and interstitial nephritis which often supervene in the advanced stages.

The action of the bacilli upon the blood differs materially from that of the round bacteria. So soon as the latter come in contact with the red corpuscles, the corpuscles stick together and form larger or smaller clots in the blood. They then are no longer able to pass through the minute {1001} capillary networks, but are arrested in the larger or smaller vessels (Koch). The micrococci in the resulting infarctions multiply, and migrate into the vessels and cellular tissue of the neighborhood. Thus fresh foci of infection are formed. Or by their destructive action they may, when situated near the serous surfaces, penetrate into the serous cavities, and in this way indirectly occasion peritonitis, pleurisy, meningitis, and purulent inflammations of the joints. When the micrococci enter directly into the circulation, they sometimes, in passing through the heart, adhere to the endocardium and the valves, where they cause exudation and ulceration, and give rise to the so-called endocarditis ulcerosa puerperalis.[38] The red globules of the blood undergo changes of shape, assume a stellate aspect, and rapidly disappear. The white globules are greatly increased in numbers, and the blood itself becomes nearly colorless. A certain amount of light is thrown upon these blood-changes by Doléris, who added micrococci to the fresh blood of a frog and watched the ensuing changes under the microscope. The micrococci could be seen in the act of penetrating the red globules, which thereupon lost their color and became shrunken, and, following the discharge of the organisms, which meantime had multiplied in an astonishing manner, little or nothing of the original globules remained.

[Footnote 38: Heiberg, _Die puerperalen und pyæmischen Processe_, Leipzig, 1873, pp. 22 and 34, with references to cases reported by Wiege and Eberth.]

In the bacillar form of septicæmia the blood is dark and has a semi-gelatinous appearance, compared by French writers to partially-cooked gooseberry jelly. The red globules, though they exhibit the various stages of deformation, are not diminished in number. The disease is further characterized by ecchymoses and minute apoplectic effusions, and by the absence of pus-formation. In the artificial septicæmia produced by Koch in mice by means of bacilli the rod-like organisms were found to enter the white corpuscles and to compass their destruction. They did not cause the red globules to adhere together, and there was no clogging of the capillary circulation. All the principal structures of the animals subjected to experiment were infiltrated with bacilli. The distribution of the latter was apparently accomplished by the blood-vessels, and not by the lymphatics, the bacilli probably effecting their entrance into the vessels by virtue of their penetrative power, in place of traversing preformed pathways. Possibly it is this action of the bacilli which causes the weakening of the vessel-walls, as evidenced by the large number of red corpuscles which pass out from them.