Part 151

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.--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.

In 1686, Puzos 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.

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 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.

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 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. 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. 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.

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.

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. 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; 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. 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.

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; whereas the bacteria retained upon the filter possess all the virulent properties of the original fluid. 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.

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 were attended with positive results, and more recently confirmatory evidence has been furnished by Pasteur and Doléris. Hiller, rarely quoted now, arrived at different conclusions. He found that bacteria washed in pure water were innocuous. 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. 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, "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. 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.