Volume 1 — GENERAL DISEASES. (continued 27)

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.

⁹ For data given, and for a great variety of historical information, vide Hervieux, Traité clinique et pratique des maladies puerperales.

In 1686, Puzos¹⁰ 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.

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 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. 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

¹² "Entstehung der übertragbaren Krankheiten des Wochenbettes," Beitr. zur Geburtsk. und Gynaek., Bd. iii. Heft 3, p. 345.

¹³ Contribution à l'étude de la septicémie puerpérale, Paris, 1873, p. 28.

¹⁴ Ibid., p. 394.

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

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 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.

¹⁷ Loc. cit., p. 349.

¹⁸ "Traube und Gescheidlen, Versüche über Faülniss und den Widerstand des lebender Organismus," Schles. Ges. f. vaterländische Cultur, Feb. 13, 1874.

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.

²⁰ In filtration through porous earthenware cylinders the filtrate possesses no phlogogenic properties.

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 infection. Some earlier experiments of Tiegel and Klebs²² 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.

²² Archiv für exp. Pathologie und Pharmakologie, "Beiträge zur Kenntniss der Pathogenen Schistomyceten," Band iv. Heft 3, S. 241 und ff.; Tiegel, loc. cit.

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.

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.

²⁵ "Exp. Beiträge zum Studium der septischen Infection," Deutsche Zeitschrift für Chirurgie, Bd. vi. S. 162.

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.

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 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. Tiegel²⁸ has endeavored to show that round bacteria are found normally in the internal organs of the body; but Koch²⁹ 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.

²⁸ Arch. f. Path. Anat. u. Physiol. u. f. klin. Med., vol. lx. p. 453.

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.

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 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 Doléris³¹ assures us that in puerperal fever by repeated trials, especially after a chill, he has never failed to demonstrate their presence.

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 Recklinghausen³⁵ 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 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.

³² "Ueber das Verkommen von Bacterien bei der diphtheritischen Form des puerperal Fiebers," Archiv für Gynaekologie, vol. iii. p. 293.

³³ "Untersuchungen über puerperal Fieber," Virchow's Archiv, vol. lviii. p. 437.

³⁴ Die puerperalen und pyæmischen Processe, Leipzig, 1873.

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.

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.

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 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 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.

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.

In puerperal fever it is rare to find either round bacteria or bacilli acting singly as the agent of infection. As a rule, both forms exist together in varying proportions, the predominant form, however, determining in general the character of the symptoms.

Thrombosis of the veins may be a physiological phenomenon, or may be due to an alteration of the blood, to weakness of the heart, or to local influences. So long as the clot remains firm its influence is limited to disturbances of the circulation. The pyæmic symptoms—viz. suppuration of the coagulum, the separation of emboli, and the formation of metastatic abscesses—are always dependent upon the presence of round bacteria. In phlebitis the latter are found in the endothelium and in the sheaths of the veins. The inflammation of the veins is followed by thrombosis. According to Doléris, micrococci derived from the blood are deposited upon the central extremities of the clots; beyond these dépôts a fresh inflammation is set up, followed by fibrinous coagulation. Thus the micrococci become imprisoned between two plugs. The same process may be repeated until a series of abscesses are formed. For a time no mischief may ensue. Finally, however, the resistance of the outworks is overcome, an embolus becomes detached, and an infectious abscess is opened into the blood—an event which is announced by an intense chill and the familiar systemic derangement.

In septic diseases death takes place from apnoea, partly from the inability of the blood-corpuscles to carry oxygen to the tissues, and partly from paralysis of the nerve-centres.³⁹

³⁹ Schüller, "Exp. Beiträge zur Studium der Septischen Infection," Deutsche Zeitschr. f. Chir., vol. vi. p. 149 et seq.

In hospital epidemics of puerperal fever diphtheritic patches situated upon the lesions of the vulva and in the course of the utero-vaginal canal are sometimes observed. Steurer found these patches were always associated with loss of substance, and were composed of disintegrated fibrin, white and red blood-globules, and colonies of round bacteria in great abundance. Morphologically, these so-called diphtheritic patches are identical with those which appear in the throat. Pallen⁴⁰ has reported an instance of the simultaneous occurrence of puerperal diphtheritis in the mother and throat diphtheritis in the two-weeks' old child. In lying-in hospitals it is the genital organs, as the locus resistentiæ minoris, and not the throat, which are the usual points of attack.

⁴⁰ Trans. N.Y. Obst. Soc., 1876-78, p. 78.

The question as to the extent to which erysipelas and puerperal fever are cognate diseases is in a fair way to be solved by recent investigation. Orth took the contents of a vesicle from an erysipelatous patient which contained bacteria in great abundance, and employed the same for injections under the skin of rabbits. In this way he succeeded in producing in these animals a species of erysipelas malignum. In the subcutaneous oedema and affected portions of the skin he found enormous masses of bacteria, so far exceeding in quantity the amount introduced as to prove an abundant new production.⁴¹ Samuel produced similar results by the injection of ordinary putrid fluids containing round bacteria. An affection resembling simple erysipelas he obtained most frequently by the application of fluid to a wound torn open after the second or third day.⁴² Lukomski found that erysipelas could be produced by fluid containing micrococci even when putrefaction did not exist. The contents of erysipelatous vesicles containing no micrococci excited no morbid manifestations. Where the erysipelatous process was fresh and progressing micrococci were found in great abundance in the lymphatics and canalicular spaces. Where the process was retrogressive, there were no micrococci to be found, even in cases in which inflammation existed to an intense degree.⁴³ Doléris submitted to the culture-process of Pasteur fluid obtained from vesicles which developed in the course of facial erysipelas in a man of forty years. Micrococci in chains were found in the liquids employed identical with those he had discovered in puerperal fever. In many cases I have seen an erysipelatous inflammation start from a puerperal diphtheritic ulcer upon the introitus vaginæ, and extend outward over the buttocks, the thighs, and the lower portion of the abdomen.

⁴¹ "Untersuchungen über Erysipel.," Arch. für exp. Pathol. und Pharmakol., Bd. i. S. 81.

⁴² Arch. für exp. Path. und Pharmak., Bd. i. S. 335, u. ff.

⁴³ "Untersuchungen über Erysipel.," Virchow's Archiv, Bd. lx. S. 430.

Virchow⁴⁴ has so far given in his adhesion to the new school as to say: "Especially in this connection are to be mentioned the diphtheritic process and the erysipelatous, especially erysipelas malignum. The granular deposit in diphtheritically affected tissues, of which I formerly spoke, has more and more proven to be of a parasitic character. What we formerly regarded as simple, organic granules, as infiltration or exudation, has since proven to be a dense aggregation of micro-organisms which penetrate into the tissues and cells to compass their destruction."

⁴⁴ Die Fortschritte der Krieg's Heilkunde, Berlin, 1874.

Thus we find in surgical fever, in puerperal fever, in diphtheria, and in erysipelas the presence of a common element which links them together, and which establishes the relationship which has long been recognized as existing between these various processes.

4th. The differences between surgical and puerperal septicæmia are due to differences partly structural and partly physiological in the wounded surfaces exposed to septic contamination.

A certain amount of misapprehension has arisen from the circumstance that along with many coincidences in the symptoms of puerperal and surgical fever there are observable differences which, from a purely clinical point of view, would justify a separate classification of the two affections. It will not do, however, to ignore the fact that the conditions which prevail in the parturient canal subsequent to labor have no strict analogue in the lesions which the surgeon is called upon to treat, and that therefore a complete identity as to all the clinical features of puerperal and surgical fever would hardly be within the range of possibility.

In the puerperal state it is necessary to take into account the blood-changes induced by pregnancy, the effects of shock and exhaustion in protracted labors, the frequency of hemorrhage, the deep situation of puerperal wounds, the presence of clots, decidua, and dead tissue in a state of disintegration or decomposition, the ease with which deleterious matters are absorbed by the wide lymphatic interspaces, the serous infiltration of the pelvic tissues, the exaggerated size of the lymphatics and veins, and the proximity of the peritoneal cavity.

Samuel,⁴⁵ in speaking of the immunities and dispositions to septic poisoning, says: "The statistical frequency of septic puerperal disease is due to the length of the parturient canal, to the fact that through this long passage there must pass all the pathological and physiological excretions, and to the soiling of these parts with fingers, instruments, and secretions which have become the bearers of sepsis." He found, on the other hand, that it was extremely difficult to produce a progressive ichorous condition by daily painting an open stump with a septic fluid,⁴⁶ though the same was readily obtained when an infinitesimal quantity of septic fluid was injected underneath a fascia.

⁴⁵ "Ueber die Wirkung des Faülniss Process auf den lebenden Organismus," Arch. f. exp. Pathologie, vol. i. p. 343.

⁴⁶ Loc. cit., p. 339.

5th. In the present state of our scientific knowledge it is necessary to admit that there is a limited number of febrile and inflammatory disturbances occurring in puerperal women, the bacterial origin of which may be fairly questioned. As illustrations of this class may be mentioned: 1. Cases of catarrhal endometritis due to errors of diet and exposure. Indeed, I have frequently, in hospital practice, been able to trace severe cases of cellulitis, pelvic peritonitis, and general peritonitis occurring in the winter season to the patient getting out of bed dripping with perspiration, and clad only in a night-dress, and going thus barefooted over a cold, uncarpeted floor to the water-closet. 2. Cases of puerperal disorders proceeding from emotional causes, the nervous system furnishing the first impulse to the disturbed action. 3. Cases of excessive vulnerability in non-pregnant women; individuals are sometimes found so susceptible that a parametritis follows a simple application of the tincture of iodine to the cervix. 4. Cases of pelvic peritonitis starting from old intra-peritoneal adhesions. 5. Cases of peritonitis and retro-peritoneal inflammations secondary to ulcerative processes in the cæcum or the descending colon. This condition is apt to be masked during pregnancy, but starts into activity during childbed as a consequence of fecal accumulation or of excessive purgation.

It is by no means easy to decide as to the precise nature of local inflammations following lacerations of the cervix and the bruising or crushing of the soft parts in long or instrumental labors. The marvellous absence of heat, pain, redness, and swelling in wounds treated in strict accordance with the principles of Lister, the very slight reaction when the atmosphere is pure, and the severity of these symptoms in overcrowded hospitals, tend indeed to strengthen the belief that even the simplest inflammations proceeding from wounds owe their origin in great part to septic germs. But, on the other hand, in hospital practice it is not uncommon to observe puerperal inflammations and febrile conditions which possess this distinctive peculiarity—that they in no wise visibly affect the health of puerperal patients in their vicinity. The symptoms of blood-poisoning too are either absent or present to a subordinate extent. Probably the difficulty is best solved by assuming with Genzmer and Volkmann⁴⁷ that there is such a thing as an aseptic surgical fever due to the absorption of the products of physiological tissue-changes at the seat of injury. In surgical cases, even where the precautions of Listerism have been faultlessly observed, febrile movements of considerable intensity, but of no prognostic signification, are of frequent occurrence. While in puerperal women we can never exclude the possibility of the septic infection of puerperal wounds, it is in accordance with clinical experience to assume that a high fever belonging to the aseptic class may coincide with a septic process of insignificant proportions.

⁴⁷ Genzmer and Volkmann, "Ueber septisches und aseptisches Wundfieber," Samml. klin. Vorträge, No. 121.

GENERAL SYMPTOMS.—As in other infectious diseases, there is, from the time of the entry of the poison into the system up to the outbreak of fever, a distinct period of incubation. The first febrile symptoms usually occur within three days of the birth of the child. An attack coming on a few hours after childbirth is indicative of infection during or previous to labor. The third day is the one upon which ordinarily the beginning of the fever is to be anticipated. After the fifth day an attack is rare, and at the end of a week patients may be regarded as having reached the point of safety. Apparent exceptions to this rule are probably referable to cases of mild parametritis, in which the initial fever and the pain were insufficient to attract attention to the existence of local inflammation.

The symptoms of puerperal fever vary with the character of the local affections and with the extent to which the general system participates in the disturbed action. The different groups of puerperal processes possess the following pathognomonic symptoms—viz. increased temperature, enlargement of the spleen, disturbed involution, and sensitiveness of the uterus upon pressure (Braun).

In most cases the fever is ushered in by chilly sensations or by a well-defined chill. This symptom, however, does not possess much prognostic importance. A chill is significant of a sudden change between the temperature of the skin and that of the surrounding medium. It may, therefore, be absent in pernicious forms of fever, provided only that the temperature changes are inaugurated slowly, whereas it may follow a trifling increase of the body-heat if, as sometimes happens in sleep, the moist skin is exposed to cool currents of air. Repeated chills indicate phlebitis and pyæmia.

In order to grasp the many symptoms of puerperal fever, it is necessary to keep separately in mind the clinical features of each of the local processes, although in fact the latter rarely occur singly, but to a greater or less extent in combination with others.

The symptoms of ENDOMETRITIS AND ENDOCOLPITIS.—The uncomplicated catarrhal inflammation of the uterus and vagina is the most frequent and the mildest of the diseases of childbed. In endometritis the uterus is large, flabby, and sensitive upon pressure; the after-pains are often unusually severe, involution is retarded, and the lochia become fetid, remain sanguinolent for a longer period than usual, and at the outset may be temporarily suspended. Sometimes the large intestine is distended with flatus. In endocolpitis the vaginal discharge is thin and purulent, the patient experiences pain and burning in the acts of defecation and urination, and, where the wounds of the vulva and vagina assume an ulcerative character, there is often found at the same time inflammatory oedema of the labia.

The fever in these cases is ushered in frequently, but not always, by chilly feelings, and the temperature reaches its height usually upon the evening of the third or fourth day, is remittent, almost intermittent in character, and rarely exceeds 102° to 103° F. In mild forms the occurrence of the fever is often overlooked or is referred to disturbance produced by the secretion of the milk. In severer attacks the febrile symptoms may continue from three to seven days. At the end of a week the swelling of the labia subsides, the discharge becomes thick, and ulcers, if present, begin to assume a healthy granulating appearance.

In diphtheritic ulcerations, and in endometritis due to decomposing remains of the ovum, the load condition is often complicated by the invasion of the neighboring tissues.

The symptoms of PARAMETRITIS and PERIMETRITIS (Pelvic peritonitis⁴⁸).—The symptoms of these two affections, as would be naturally expected from the proximity of the peritoneum to the pelvic connective tissue, for the most part overlap. It must be very rare for one form to occur entirely independent of the other. For this reason it will be found convenient to consider first the symptoms common to both morbid processes, and subsequently to direct attention to what are believed to be points of distinction between them.

⁴⁸ The following clinical history, together with the statistical details, is borrowed in great part from the description of Olshausen ("Ueber puerperale Parametritis und Perimetritis," Volkmann's Samml. klin. Vortr., No. 28), the exactitude of which I have had abundant opportunity to verify.

During the period of incubation there are usually no prodromic symptoms. Elevations of temperature in the course of the first twelve hours following labor are equally frequent under perfectly normal conditions. Suspicious symptoms are disturbed sleep, excessively painful after-pains, and a pulse of 80 to 90.

The beginning of the fever occurs in 90 per cent. within the first four days of childbed; most frequently upon the second or third day, and taking place upon the fourth day in scarcely 12 to 15 per cent. of the cases. If five days have elapsed without fever, the period of danger, with very rare exceptions, may be regarded as having passed.

At the outset the fever, especially in perimetritis, is ushered in by chilly sensations or by an intense chill. The temperature rises rapidly, though the highest point is usually not reached before the second, and in rare cases not before the third, day. In most cases the heat in the axilla exceeds 103°, and may even mount up to 105°. The decline occurs gradually, the fever ending in 70 per cent. in the course of a week, in 20 per cent. in two weeks, and only in 10 per cent. extending beyond that period. Protracted cases indicate abscess formation.

The fever does not, however, always pursue a regular course. In place of progressively declining until the termination is reached, the high temperature of the second day may be attained upon one or more occasions. The morning remissions are at first slight, but become marked as the disease approaches its close. In cases of long duration the morning hours are often free from fever, a circumstance calculated to mislead a physician who sees his patient but once a day. A pulse of 80 to 90 beats, a disturbed sleep, lack of appetite, and sensitiveness to pressure upon the sides of the uterus are, however, symptoms which should serve as a warning of some disturbing cause, and should lead the physician to renew his visit in the latter part of the day.

If, from a mistaken notion that the morbid process has come to an end, the patient is allowed prematurely to resume her household duties, the pains across the abdomen and along the hip and thigh return, and an examination reveals the existence of exudation in the pelvic cavity or upon an iliac fossa.

Errors of this kind are most frequent in cases of parametritis associated with slight peritoneal inflammation, as the local pain is then insignificant, and the initial chill, happening on the third or fourth day, is apt to be ascribed to engorgement of the breasts.

Relapses after the complete disappearance of febrile disturbance occur in 15 to 20 per cent. They are usually shorter, but sometimes more obstinate, than the original attack. As a rare exception may be mentioned cases with evening remissions and morning exacerbations.

In circumscribed pelvic inflammations the pulse rarely exceeds 120 beats to the minute. A pulse of 140, of more than half a day's duration, betokens severe septic complications, and is therefore of evil omen. In some cases the slow pulse observed after labor makes its influence felt in the first day or two of the fever, so that the curious phenomenon may be witnessed of a temperature of 104° coinciding for a time with a pulse ranging between 50 and 70 beats to the minute.

As regards other symptoms, headache and sleeplessness are rarely absent. Profuse sweating follows the first febrile attack, and frequently recurs during the course of the disease.

Pain is present at the onset in the majority of cases, and is then usually most violent. The spontaneous pain, which is due to the affection of the peritoneum, subsides in great part in the course of one or two days, but the sides of the uterus remain sensitive to pressure. In the rare cases of pure parametritis, however, this symptom may be absent altogether. The pain, like that from the inflammation of serous membranes, is of a lancinating character. Sometimes it is associated only with the contractions of the uterus. After-pains occurring under unusual circumstances, as in primiparæ or after the third day, are to be regarded with suspicion.

Vomiting occurs occasionally, but is comparatively rare unless the peritonitis becomes diffused and spreads to the region of the stomach. The appetite is lost, and only returns, as a rule, with the departure of the fever. The tongue is coated and moist, and constipation is common. In other cases there is diarrhoea with rumbling in the bowels, but without pain or tenesmus. The urinary secretion is rarely interfered with, and when this is the case it indicates the extension of the inflammation to the peritoneum covering the bladder.

Most cases of perimetritis and parametritis terminate in five or ten days, the fever and other symptoms gradually subsiding. When, as may happen in exceptional instances, the temperature falls suddenly from a high degree to one below the normal level, the body grows icy cold, the pulse becomes small and irregular, and symptoms of collapse develop. But in twelve to twenty-four hours the symptoms of collapse subside, and the disease reaches its end with a disappearance of the alarming manifestations.

If the fever subsides within a week exudation is somewhat rare. Its continuance beyond that date should lead to a careful exploration of the pelvic organs. The exudation is usually demonstrable in the course of the second week or at the beginning of the third week. It is recognized, according to its location, by external or by internal examination, or, where the deposit is considerable, by both methods. In most cases the deposit is extra-peritoneal, and is situated between the folds of the broad ligament, above and to the sides of the vaginal cul-de-sac. It has generally a rounded form, though with less convexity than fibrous and ovarian tumors. Sometimes, however, the tumor is flat below, like a board. It seldom exceeds in size that of a large apple. In fresh exudations the sensation produced is often that of a hard tumor surrounded by a softer layer, due to continued succulence of the soft parts. In a few weeks they may reach or exceed the hardness of a fibroid tumor. The older the tumor, unless suppuration sets in, the less sensitive it becomes. Often the exudation extends to the pelvic walls. The uterus, as a rule, is fixed, and in cases of large tumors becomes pushed toward the opposite side, while as a consequence of later shrinkage the fundus may be drawn permanently toward the affected side.

The cul-de-sac of the vagina is rendered broader and flatter by the pressure of the deposit, or, when the tumor is deep enough, the vaginal surface may be rendered convex. Behind the uterus the exudation is as it were flattened antero-posteriorly, and in some cases it may be felt in the form of rigid bands between the posterior ligaments which enclose the cul-de-sac of Douglas. The ante-uterine tumors have a spherical shape and depress the vagina anteriorly.

Tumors situated in the iliac fossa have a more or less convex form, and may be of such considerable size that the swelling may be recognized by the eye through the abdominal walls. As the exudation between the broad ligaments may in these cases have been slight from the beginning, or may have subsequently disappeared by absorption, the iliac tumors have often apparently a spontaneous origin.

Sometimes the uterus is surrounded by exudation, and the entire pelvis appears as though it were a mould filled with a solid mass. The fornix is then often pressed downward, and irregular rounded masses are to be felt through the vaginal walls.

The recognition of parametritic tumors through the abdominal coverings is possible when they are situated above Poupart's ligament, in the upper portion of the broad ligaments, and in the iliac fossæ.

The pain and the functional disturbances in the pelvic organs depend upon the size and situation of these inflammatory deposits. Of the functional troubles may be mentioned frequent and painful micturition, obstinate constipation and difficult defecation, contractures of the ilio-psoas muscles when the exudation is seated beneath the sheath or between the muscle and the pelvic bones, disturbances of motility in the abductor muscles, paresis of the lower extremities, and radiating pains in the upper portion of the thigh and in the renal and lumbar regions, produced by pressure upon the obturator, the crural, the cutaneous, and the sciatic nerves.

So long as fever is present the exudation rarely diminishes. If absorption takes place in one point, growth almost certainly follows in some other direction. When, however, the apyretic period is reached, the exudation, as a rule, disappears rapidly, so that often in the course of six weeks no trace of its existence remains. In a smaller number the solid mass may persist for months or even years.

After the fever has departed the patient usually feels well. The sleep and appetite return, the night-sweats disappear, the pulse often falls to 50 or 60 beats, and the temperature is in many cases for a time subnormal in character.

Where the fever persists for from five to six weeks there is always a suspicion of abscess formation. With the exception of afternoon fever and night-sweats the patient may feel very comfortable. Then the exudation becomes sensitive, the spontaneous pains recur, sleep is lost, and locomotion, defecation, and urination occasion acute suffering. The fever becomes violent, chills announce the presence of pus, and finally, about the seventieth or eightieth day, perforation of the abscess takes place. The usual seat at which the pus is discharged is just above Poupart's ligament; next in frequency perforation takes place into the colon, and in rare instances into the bladder, the uterus, and vagina. Fortunately, of very rare occurrence is the discharge of pus into the peritoneal cavity, which is naturally followed by acute peritonitis. Another likewise unfrequent but most dangerous accident is the septic infection of the abscess—an occurrence referred to by Olshausen to the diffusion of intestinal gases through the walls of the tumor.

In suppuration of parametritic exudations the pus commonly forms in small scattered collections, and rarely gives rise to large abscesses.

Although parametritis and perimetritis are usually found associated together, there are always cases in which the one form of inflammation so far predominates over the other as to justify an attempt to establish a clinical distinction between them.

In the beginning of the attack, sharp pain, high fever, and tympanitic distension of the lower abdomen are symptomatic of inflammation in the pelvic peritoneum. Whether the cellular tissue is simultaneously implicated can only be determined by a digital examination after the abdominal sensitiveness has subsided. The absence of the objective signs of cellulitis would then contribute to prove that the case had been one in which the peritoneum had been in the main affected. On the other hand, moderate fever, pain elicited only on pressure, and tympanitic distension confined to the colon, coinciding with exudation between the folds of the broad ligament, would be indicative of a nearly pure cellulitis.

A palpable exudation is by no means the necessary product of peritoneal inflammation. Indeed, in many cases, the distinctive symptoms of the latter may be present for from four to eight days, and may then subside without leaving a trace of its existence at the pelvic brim.

The demonstration of a fluid effusion by noting the change of level upon shifting the position of the patient is rarely possible, either because the quantity is too small or because it quickly becomes confined by pseudo-membranous adhesions between the intestines.

Bandl⁴⁹ mentions as a sign of local peritonitis, sometimes noticeable, a number of resistant points or tumors near the pelvic brim or above one of the iliac fossæ, due to a matting together of the intestines or to their adhesion to the uterine appendages. They are distinguished from solid tumors by their emitting a tympanitic sound upon percussion and by their changing position in consequence of an accumulation of urine in the bladder or of feces or gases in the bowels. Again, all tumors may be reckoned as intra-peritoneal which very rapidly form behind or to the side of the uterus from enclosed exudation-products, and which at the same time rise far above the level of the pelvic brim. If, however, they start from the cul-de-sac of Douglas, and do not much exceed the linea terminalis, or if they occupy an iliac fossa, it becomes very difficult to decide whether they are of intra- or extra-peritoneal origin. The peritoneal exudation, however, long remains soft and fluctuating. It arises, as a rule, behind the uterus, and does not exhibit a tendency to spread to the sides or to the anterior or posterior pelvic walls.

⁴⁹ Handbuch der Frauenkrankheiten, red. Von Billroth, 5te Abschnitt, p. —.

Still more difficult is it to decide as to the seat of exudations met with beneath the abdominal walls. When diffused and continuous with a pelvic deposit the diagnosis is uncertain. It is only safe to assume the peritoneal origin of extravasations of a rounded form, of a fluctuating consistence, and when they are situated high up and are disconnected from exudation at the pelvic brim. An opening of the abscess through the navel would indicate a peritoneal source, while the discharge through the abdominal parietes would point to a seat in the connective tissue.

After the perforation of an abscess the fever and pain subside; the wound, if external, either closes in the course of one or two weeks, or fistulas form which become the source of protracted suppuration.

In psoas abscesses the exudation extends beneath the sheath of the muscle or between the iliacus and the bone. In puerperal patients they proceed from an inflammation originating in the broad ligament. They are situated too deep to be easily palpated. The pains they occasion are referred rather to the hip or knee than to the abdomen. The contracture of the psoas muscle furnishes a diagnostic sign which distinguishes this form from the superficial abscesses of the iliac fossæ. The pus eventually is discharged beneath Poupart's ligament, in the lower portion of the inguinal fossa, at some point upon the crest of the ilium, or exceptionally along the thigh. Often the discharge is maintained for months.

The symptoms of GENERAL PERITONITIS.—This form generally begins with the usual symptoms of pelvic inflammation, but the tenderness, which at first was limited to the side of the uterus, gradually spreads over the entire abdomen. The abdominal pain is of a tearing, lancinating, sometimes colicky character. It is increased by the slightest bodily movement, by jarring of the bed, or even by the weight of the bed-clothes.

As a consequence of the peritoneal inflammation and of the accompanying exudation, the muscular walls of the bowels become paralyzed, and tympanitic distension results from the accumulation of gases. In the dependent portions of the peritoneal cavity it is often possible to demonstrate by percussion the presence of fluid exudation, though distinct fluctuation is rarely to be made out. The size of the abdomen is due much more to the tympanites than to the amount of effusion. Sometimes the liver, with the diaphragm, is pushed by the swollen bowels to the level of the fourth or third rib, and exercises such a degree of compression upon the posterior portion of the lungs as to place the patient in danger of suffocation. The respirations are jerky and attended with a moaning sound.

The loss of muscular power in the intestines permits the contents of the middle portion to pass unchecked toward the duodenum, and thence, upon accidental contractions of the abdomen, they may pass to the stomach and be ejected by vomiting. The first vomited matter has a dark-green color, and that ejected afterward presents the color of intestinal matter. Constipation at the outset may be subsequently followed by colliquative diarrhoea.

The fever begins, as a rule, though not always, with an intense chill, the temperature rises to 104°, and the pulse becomes small, hard, and resistant. Its frequency rapidly increases, varying from 120 to 160 beats to the minute. The skin is sometimes dry, sometimes dripping with perspiration. In fatal cases, as the end approaches, the temperature frequently falls, while the pulse becomes more rapid, the face assumes a pinched, anxious expression, sweat gathers upon the forehead, the extremities grow icy cold, and the patient dies in collapse. The duration of peritonitis averages not more than from four to six days.

In cases of recovery the pulse improves, the vomiting ceases, and the tympanites disappears. The diffuse exudation then becomes converted into circumscribed tumors, which on palpation are felt on the side of the pelvis and extending upward to the level of the umbilicus. Upon internal examination the uterus is often found depressed by the weight of the fluid, which likewise may bulge the cul-de-sac of Douglas into the pelvic cavity. Sometimes the exudation may become encysted above the pelvis and leave the contents of the latter free. In still other cases the uterus may become attached high up to the abdominal walls, so that the vaginal portion disappears and the os is reached with difficulty.

The peritoneal exudation may, as in pelvic inflammations, become absorbed and disappear. When, however, it is surrounded by loops of intestines it is apt to undergo purulent and septic changes, and the abscesses may then become discolored and filled with stinking gases. The patient, whose previous improvement has been watched with delight, now loses appetite, the pulse becomes frequent, the strength fails, and death may follow from septic fever or from rupture of abscess into the abdominal cavity.

In the pyæmic form—a still more deadly variety of peritonitis—the symptoms differ materially from those which have been recounted. As, however, it constitutes only a single one of the pathological changes connected with the poisoning of the blood through the lymphatic system, its consideration belongs properly to the study of the septic infection.

The symptoms of SEPTICÆMIA LYMPHATICA.—The symptoms of blood-poisoning in the infectious diseases of childbed vary to a considerable extent according to the channel through which the septic germs enter the general circulation. In the murderous epidemics which prevail in lying-in hospitals the lymphatics are, as a rule, the vessels primarily invaded. It is to this form that the cases already described belong, where, with diphtheritic patches upon the utero-vaginal canal and sero-purulent oedema of the parametrium, there are associated pyæmic peritonitis and deformation of the blood-corpuscles; or where, following the migrations of the round bacteria, the serous cavities become successively involved, septic vegetations gather upon the heart, and the glomeruli of the kidneys become choked with micrococci. The lymphatic form of septicæmia develops soon after labor, and is always ushered in by a chill. The temperature rises to 104° or even higher, and the pulse is thin and frequent. The abdomen swells rapidly, without being especially painful. Indeed, painless distension of the intestines is one of the characteristics of an acute invasion of the lymphatics. Peritoneal effusion is absent in cases which run a rapid course, and is distinctly recognizable only in a peritonitis of long continuance. The effusion is not so much due to exudation as to a transudation of serum with which micrococci are commingled. At the same time the tongue is moist, but slightly coated, and at times quite clean. Sometimes there is diarrhoea due to catarrh or to a diphtheritic affection of the colon. When the bowels have been constipated the administration of a purgative may provoke discharges which it may be found difficult to arrest. The skin is bathed in perspiration. At the beginning and during the course of the disease bleeding at the nose is of not infrequent occurrence.

Toward the end the pulse runs up to 140 to 160 beats, while in many cases the temperature falls. Immediately after death the heat of the body may for a short time exceed the highest point reached during life. The respirations are superficial and jerky. In many instances the face, the neck, and the fingers are blue from defective oxygenation of the blood. At the same time the skin becomes clammy and the extremities cold.

The sensorium, in cases which run a rapid course, is usually affected at an early period. The patients appear somnolent, are restless in bed, have light delirium, and respond only when spoken to loudly. As a rule, they make but little complaint, and, were it not for the dyspnoea, would have nothing to disturb their sense of comfort. Very few, even as death approaches, have any idea of the danger that threatens them. Now and then, in place of stupor, great restlessness, and even a maniacal condition, is developed. Albumen is usually found in the urine.

Pleurisy, so frequently associated with lymphatic septicæmia, is frequently double, more rarely single, and begins, as a rule, with sharp pain in the side and an aggravation of the previous dyspnoea. Pericarditis is less frequent, and occurs usually without symptoms toward the close of life. The joint affections are characterized by redness and swelling, and by pain, which is sometimes so great that touching the inflamed part suffices to arouse the patient from sopor. Sometimes fluctuation is felt, but death occurs before perforation and discharge of the pus.

The most frequent ending is death, which follows in from two to twenty-one days, and, as a rule, between four and seven days. Recovery is, however, possible.

The symptoms of SEPTICÆMIA VENOSA (phlebitis uterina, pyæmia metastatica).—The putrid infection of a thrombus at the placental site may take place within twenty-four to forty-eight hours after labor. Usually, however, the approach is insidious, and the disease develops from an apparently insignificant endometritis or parametritis; or the patient, with the exception perhaps of a tired feeling, of slight chilly sensations, and of profuse perspiration, may not have been conscious of any indisposition for days preceding the attack, or even until the first getting up from childbed. The initial chill in typical cases is characterized by its violence and duration. In some cases it may last for hours. It is accompanied and followed by high temperature, the febrile attack ending with profuse perspiration as in intermittent fever, with which it is apt to be confounded. The fall in temperature often assumes the form of a prolonged remission.

In many cases the pulse rises and falls with the variations in the body heat, while in others it remains permanently above the average. A frequent pulse is always a suspicious symptom in childbed, even where the other symptoms are apparently normal.

Erratic chills announce the lodgment of emboli in distant organs. With the formation of metastatic abscesses in the lungs and other parenchymatous organs the typical character of the disease changes. In place of chills occurring at irregular intervals, followed by remissions and periods of apparent improvement, the fever is continuous, the pulse becomes small and rapid, while sopor, slight delirium, a dry skin, a dry, brown, cracked tongue, and a moderately tympanitic abdomen, give the case the appearance of one of typhus fever.

Peritonitis is present in hardly one-third of the cases. The abdomen is therefore flat and soft, and often is not sensitive upon pressure. Icterus, due to disintegration of the blood-corpuscles, is an ominous symptom.

Death usually occurs in the second or third week. In the typhus-like cases, however, it may follow the first attack speedily. Recovery is possible where the organs secondarily affected are not of too great importance.

A combination of the lymphatic and venous forms of septicæmia is not uncommon in cases running a protracted course.

The symptoms of PURE SEPTICÆMIA.—Under the title of pure septicæmia should be placed cases in which the absorption of putrid materials into the blood gives rise to symptoms of intense blood-poisoning without the development of local lesions. A common example of this form is met with in the fever which results from the presence in the uterus of decomposing coagula or portions of retained ovum, the fever subsiding with the removal of the disturbing cause. In like manner we sometimes meet with cases of intense septic poisoning followed by speedy death, in which the post-mortem examination reveals only changes in the blood and softening of the parenchymatous organs. The symptoms are often similar to those produced by the injection of putrid materials containing rod-like bacteria into the vessels of animals. As the long bacteria do not possess the capacity of self-reproduction in the blood, to produce fatal results the quantity of putrid fluid injected must be large or be frequently repeated. This form is said not to be inoculable.

CAUSES.—The effects of a poisoned state of the atmosphere as a cause of puerperal fever is best observed in the so-called nosocomial malaria of hospitals. In days gone by, before I had learned by experience that the safe conduct of a lying-in service depends upon the fastidious exclusion of every source of contamination, I had frequent occasion to witness febrile outbreaks among puerperal women in the Bellevue Hospital, which were instantly arrested by the simple transfer of the inmates of the affected ward to a wholesome locality, though no changes were simultaneously made in either the personnel or the utensils of the service. In these instances it seems fair to assume that the previous unhealthy condition was not due to the direct transfer of an inoculable matter from patient to patient by the attendants, but by something residing in the air of the vacated apartment. In the inquiry as to the production of this condition it can be assumed that it is not caused by aggregation alone. The medical wards of Bellevue, always crowded, have often furnished in times of need safe receptacles for puerperal patients. It is certainly not due to the presence of the ordinary constituents of the atmosphere. We must therefore look for some additional element capable of unfavorably affecting the economy. What this element really is, is demonstrated by a familiar clinical experience. When the disturbance produced by nosocomial malaria is not at an early stage arrested by change of locality, the secretions of patients affected become inoculable. Then the epidemic spreads rapidly, and assumes continuously a more and more severe type. If during an epidemic the external genitals be carefully watched, now and then diphtheritic patches will be noticed to form upon them. At first these patches may disappear or yield readily to treatment. When an epidemic has assumed a pestilential form the patches, which may in isolated cases make their appearance at any time in a hospital, are rarely absent in fatal cases. The composition of the patches tells the tale of what it is in the atmosphere which accomplishes the charnel-house work. Favoring conditions have led to the multiplication of disease-germs in the air, and have fitted them to become the active producers of disease.

In a patient dying in the early stages of an epidemic there may be no diphtheritic manifestations, though the tissues and secretions are filled with bacteria. As, however, the epidemic gains headway, the lesions of the generative apparatus, and especially of the external organs, which are most exposed to air, become covered with patches which swarm with micrococci. Under the conditions named it is certainly more in accord with ordinary scientific reasoning to conclude that the micrococci play an important part in the production of puerperal fever than that the puerperal fever produces the micrococci.

To be sure, bacteria or their spores are always present in the air, and it may be fairly asked how patients are ever spared from their perverse industry. The answer is, that the effect produced by the atmosphere of a hospital is dependent partly upon the quantity, and partly upon the quality, of the suspended germs. Floating spores, when sparsely distributed, rarely possess the power of invading a healthy organism. In the inauguration of an epidemic the first patient severely attacked is usually one whose powers of resistance are broken down by prolonged labor, by hemorrhage, by poverty, or some other condition leading to impaired vitality.

Puerperal-fever epidemics due to contamination of the atmosphere, and not to direct contagion, do not at once reach the maximum of intensity. At first the temperature tables indicate the prevalence of milk fever; next follow cases closely resembling those of mild paludal poisoning; and, finally, if these warnings are unheeded and reliance is placed upon antiperiodic remedies rather than upon prompt closure of the threatened ward, the pestilence develops. In the conduct of lying-in hospitals it should never be forgotten that with the multiplication of the septic germs the danger increases.

At the same time, the quality of the agents which pervade the air where hospital patients are confined is an important element in the genesis of febrile outbreaks. The bacterium termo, which causes putrefaction, is not in itself, as we have already mentioned, a source of danger. A stinking odor is not necessarily incompatible with a low mortality-rate. The importance of the common forms of bacteria, according to Pasteur, results from the fact that by their power to consume oxygen they pave the way for the active development of the pernicious germs, nearly all of which thrive only in media in which that element has been materially diminished. Again, there is reason to believe that the same germs are not⁵⁰ always equally active for evil. Gravitz claims that the ordinary varieties of aspergillus and penicillium found everywhere on the surface of the ground, on moistened walls, on food of every variety, on decaying leaves and fruit, and whose spores are universally present in the purest air, can by a succession of cultures be gradually brought to flourish in a warm alkaline fluid, and that they then acquire the capacity to penetrate living tissues, to proliferate in them, to excite local necroses, and to cause death in the course of three days. The resistance of micrococci to carbolic and salicylic acids is found experimentally to depend in a measure upon the nature of the vehicle in which they are cultivated (Buchholz). The action of septic fluids varies too with the age of the infusions, with the materials employed, and with the conditions under which the poison-germs are generated.

⁵⁰ Gravitz, "Ueber Schimmel vegetationen im thierischen organismus," Virch. Arch., vol. lxxxi, p. 355.

Micrococci multiply in hospitals when organic materials favorable to their growth are present in sufficient quantities. Perrin, Quenquand and others have shown that the hospital wards in Paris, especially those upon the surgical and maternity divisions, contain an infinite number of vibrios, bacteria, and all the coccus forms (Charpentier). Robin⁵¹ has demonstrated the existence of albuminoid matters in water condensed upon vessels containing freezing mixtures and placed in overcrowded wards of hospitals. When the results of crowding become manifest, these albuminoid matters not only impart a fetid odor and putrefy with great rapidity, but rapidly impart putrefaction to healthy muscle and normal blood with which they are brought into contact. Pasteur was able by the microscopic examination of the lochia from patients in the services of Hervieux and Lucas-Champonnière to predict, from the character of the contained organisms, an impending attack of fever in advance of the slightest symptom betokening danger.

⁵¹ Leçons sur les Humeurs, Paris, 1867, p. 195.

It is unquestionably the lochial discharge which makes it such a difficult task to keep a maternity ward in a healthful condition. Putrid blood has been found to be the most favorable material for septic experiments. It was noticeable in Bellevue Hospital that febrile outbreaks always arose in, and were usually confined to, the ward in the hospital which, by a bad arrangement, was assigned to patients for the first four or five days following confinement—i.e. during the period of the lochia cruenta. As puerperal fever is rare after the fifth day, this at first sight would seem natural. But if a patient was transferred directly after confinement, during one of these unhealthy periods, to the ward containing the patients who had passed the first five days, but had not completed the ten days, she would escape the fever. It was always the same ward that required to be disinfected. In a communicating apartment all the confinements took place, and at all times, therefore, the conditions were present for loading the atmosphere with the products of decomposing blood. In the summer months, so long as the windows were open and the air was diluted by the continuous passage of fresh currents, the patients enjoyed immunity from nosocomial malaria. In the autumn, so soon as it became necessary to close the windows partially on account of the cool nights, it was not uncommon for the more trivial disturbances, such as so-called milk fever, the hospital pulse, and catarrhal affections of the genitalia, to manifest themselves. Through the months of February, March, and April the mortality was usually greatest. During the winter months there was, as a rule, crowding of patients, insufficient ventilation, stagnation of the air, and the rapid accumulation of disease-germs. That the later winter months should prove the most perilous is in accordance not only with the theory of continuous accumulation, but with the experimental fact that weeks sometimes elapse before a decomposing substance acquires the highest degree of virulence.

Apart from the nosocomial malaria of hospitals, there is reason to believe in the influence at times of certain general widespread atmospheric states which affect the entire community. In the year 1871 the mortality from childbed in New York was 399; in 1872, 503; in 1873, 431; in 1874, 439; and in 1875, 420. Now, the excess in the deaths for 1872 was due wholly to an increase in the cases of metria, those from ordinary accidents remaining nearly the same as in the preceding years. The disease certainly did not extend into the city from the hospitals serving as foci, for the mortality at Bellevue Hospital was hardly more than half the usual average. There was no especial mortality that year from either diphtheria, erysipelas, or scarlatina, but the aggregate mortality was the largest known in the history of the city. There are no positive data connecting the civil deaths from puerperal fever in 1872 with parasiticism, but the prevalence of epizoötics, of epidemic catarrhal affections, of peculiarly fatal forms of pneumonia and other diseases which are now attributed to the presence of minute organisms in the atmosphere, renders such a source highly probable.

It is proper to say here that, though the argument is very strong in favor of regarding the genitalia of puerperal women as the exclusive point of entry of infectious materials into the system, it seems impossible at the present time to make all the facts coincide with such a theory. I have the records of a number of cases occurring during an epidemic of puerperal fever in which patients were either attacked with fever previous to parturition, or in whose cases the unusual length of labor, the frequency of post-partum hemorrhage, and the imperfect contraction of the uterus immediately after confinement were signs of some abnormal influence exercised upon the economy at an early period of labor previous to the existence of traumatism. That deleterious materials may find other channels for entering the system than a wounded surface is evidenced by the cachectic condition not unfrequently produced in physicians by too assiduous attendance in dissecting-rooms and places in which post-mortem examinations are conducted. One severe and rapidly fatal case of puerperal fever which occurred in Bellevue Hospital I find it impossible to attribute to any other cause than that the woman for five months previous to her confinement served as a helper in a lying-in ward. The post-mortem examination disclosed no special local lesions, but her symptoms were those of intense septicæmia. French writers report instances of toxæmic conditions developing in young midwives during puerperal-fever epidemics. While we are not prepared to go as far as Tarnier, who says, "It is probable that the lungs, by their extent and activity, offer conditions most favorable to absorption, and that often, if not always, it is by them that poisoning occurs," it does not yet seem time to give up the idea that under exceptional circumstances the respiratory and the digestive tracts may allow the passage of materials of a septic character.

Another and frequent source of puerperal fever is by direct inoculation. Any material of a septic character, introduced into the genital passages of a woman during or after confinement, may produce a general infection of the system. But the point upon which I wish especially to dwell is that it is possible to trace epidemics of puerperal fever directly to the carrying of puerperal poison from patient to patient through the medium of attendants. In such cases changes in wards and the most rigid sanitary precautions avail but little, so long as the affected personnel is continued in charge. Unless this fact is fully recognized, all the cleverest devices in hospital construction will fail to prevent the occurrence of disasters. In theory, the doctrine of the contagiousness of puerperal fever has ceased to be the subject of dispute; and yet no longer than thirty years ago it was combated as a pernicious heresy by both Meigs and Hodge of Philadelphia, at that time regarded as the best authorities upon obstetrical questions in this country. Hodge, addressing his students, said: "The result of the whole discussion will, I trust, serve not only to exalt your views of the value and dignity of our profession, but to divest your minds of the overpowering dread that you can ever become, especially in women under the extremely interesting circumstances of gestation and parturition, the ministers of evil—that you can ever convey, in any possible manner, a horrible virus so destructive in its effects and so mysterious in its operations as that attributed to puerperal fever;" and Meigs, in his letters to students, writes: "I prefer to attribute them to accident or to Providence, of which I can form a conception, rather than to a contagion of which I cannot form any clear idea, at least as to this particular malady." Contrasted with these rhetorical utterances, in an essay published in 1843 by Prof. Oliver Wendell Holmes, entitled Puerperal Fever as a Private Pestilence, the opposing testimony in favor of contagion was presented with equal literary and scientific skill. The evidence was complete and conclusive, and has exercised a most beneficial influence upon the practice of midwifery in America. With his many claims to our admiration and esteem there is probably no title which Prof. Holmes wears with greater pride than that of pioneer in a movement that has done so much to prevent the slaughter of innocent women and the wrecking of happy homes.

Thanks to changed theoretical views, physicians seem now rarely to be the carriers of contagion. At least, in studying the records of New York City for nine years, I find that the occurrence of two deaths from puerperal disease, following one another so closely as to lead to the suspicion of inoculation, occurred to thirty physicians; a sequence of three cases occurred in the practice of three physicians: one physician lost three cases, and afterward two, in succession; one physician had once two deaths, once three deaths, and twice four deaths, following one another; finally, a physician reported once a loss of two cases near together, then of six patients in six months and then of six patients in six weeks. Thus in the practice of more than twelve hundred physicians in nine years I find, excluding cases occurring in hospitals, that the experience of thirty-six only lends color to the idea that puerperal fever is due to criminal neglect on the part of the medical profession. Undoubtedly in many of these cases, too, the responsibility is only apparent, as when a practitioner has, for example, had the misfortune to lose in one week a woman from puerperal convulsions, and another in the following week from placental hemorrhage. Singularly enough, not one of the sequences mentioned occurred in the practice of a physician connected with a lying-in hospital. In face of the charge that the physicians holding obstetrical appointments in public institutions are active disseminators of puerperal fever through populous communities, I find that the total loss from all puerperal causes, occurring in the private practice of ten physicians intimately associated with such institutions, numbered during the nine years but twenty-one cases. Of these, thirteen were the result of ordinary accidents, and only eight cases of metria proper, of which one was developed before the physician was called in attendance; whereas a single physician, holding no hospital appointment, lost during the same time twenty-seven cases, of which twenty-one were cases of metria.

There is, however, a survival of the older ideas, chiefly to be seen among the laity, in propositions to secure absolute immunity from puerperal fever in hospital patients by confining them in wooden structures or by conducting births under carbolic acid spray.

I have been interested in endeavoring to ascertain how far experience corresponds with Semmelweis's original theory that puerperal fever owes its origin to poisonous materials obtained from dissecting-rooms and introduced into the genital canal by the hands of physicians attending cases of labor. With this view I have made personal application to a number of gentlemen who have engaged in midwifery practice while performing the functions of demonstrators of anatomy in our medical schools. H. B. Sands, of the College of Physicians and Surgeons, reports that in the five years during which he held the office of demonstrator he attended about sixty cases of labor. All did well. He lost his first patient, from childbed, a short time after he had resigned his position in the dissecting-room. J. W. Wright, the present professor of surgery in the Medical Department of the New York University, who held for one year the position of demonstrator in the Woman's College, writes me that "during the year I attended one hundred and four cases, including twenty-two forceps cases, two of craniotomy, two of podalic version, and four of breech presentation. Of this number I lost two cases, one from phlegmasia dolens complicating uræmia, from both of which troubles the patient had suffered during her previous labor, and one from double pneumonia, the result of unusual exposure following confinement. Out of these one hundred and four cases I can recall but three or four cases of metritis, and those of a mild character; I have never thought they had any special connection with my duties in the dissecting-room. I may add that for ten years I have attended a pretty large number of confinements each year, and that during the whole of this time I have been in the habit of making autopsies as occasion has offered, and of handling and examining pathological specimens both in and out of the dissecting-room, notwithstanding which my death-record among this class of cases has been unusually low." Samuel B. Ward, formerly demonstrator at the Woman's College, at present professor of surgery in the Medical School at Albany, writes: "While I was daily in the dissecting-room during the winter sessions of the school from 1868 to 1872, I attended thirty-two confinements, of which I have notes. All of the patients recovered, nor did any of them suffer from any complication that could be traced to infection." It is familiarly known that after Semmelweis had introduced the practice, among the physicians attending patients at the large lying-in hospital in Vienna, of washing the hands in a solution of chloride of lime, there was a great diminution in the mortality which prevailed, notwithstanding which G. Braun reports, however, that in 1857, in the month of July, in two hundred and forty-five deliveries there were seventeen deaths. The following month Klein gave orders to suspend the use of disinfectants. By chance, in August there were only six deaths out of two hundred and fifty confinements, and in September, of two hundred and seventy-five patients, none died. From 1857 to 1860 the mortality was slight, though disinfectants were not used, while during the three following years, in spite of the systematic and persistent employment of these agents, the death-rate once more assumed formidable proportions.⁵²