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. Simpson11 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.
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 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 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.
Haussmann12 reported a case of auto-infection in the rabbit which terminated fatally. A portion of the membrane, retained in the left cornu, 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