Prevention of Puerperal Fever. GEO. M. KOBER, M. D., WASHINGTON, D. C., Professor of Hygiene, Medical Department, University of Georgetown. Reprinted from VIRGINIA MEDICAL SEMI-MONTHLY, January 22,1897, PREVENTION OF PUERPERAL FEVER.* By GEO. M. KOBER, M. D., OF WASHINGTON, D. C., Professor of Hygiene, Medical Department University of Georgetown. [.Reprinted from Virginia Medical Semi-Monthly, Jan. 22, 1 96 Puerperal fever has been defined by the Col- lege of Physicians of London,1 as “a continued fever, communicable bv contagion, occurring in connection witli child-bed and often asso- ciated with extensive local lesions, especially of the uterine system.” This definition was characterized b}r our own Dr. Fordyce Barker, who crossed the Atlantic purposely to join in the discussion, as “abso- lutely correct.” This is not surprising, when we remember that this author believed it to be a fever which is peculiar to puerperal women, that the symptoms of this disease are essential, and are not the consequence of any local lesion, and that it is as much a distinct disease as typhus fever, typhoid fever or relapsing fever. Dr. Barker also held that “any of the local inflammations may occur in the puerperal woman without puerperal fever; and on the other hand, puerperal fever may be so severe as to destroy life without sufficient local disease to account for the symptoms or explain the cause of death.”2 Before entering upon the dominant feature of this paper—viz., the prevention of puer- peral infection—it will be well to point out * Read at a meeting of the Medical and Surgical Society, of the District of Columbia, January 7, 1897. 2 briefly the recent views as to the etiology of this affection, and that the above definition re- quires some modification; and, lastly, that whilst the disease is most frequently commu- nicated by the attendants, they cannot be held responsible for every case of puerperal fever. I believe the sooner we abandon the idea that puerperal fever is a specific disease, pecu- liar to lying-in women, and adopt the view that a parturient woman is precisely in the same condition as a patient after a surgical operation, and therefore liable to all the local and general infections, the better it will be for the cause of humanity. As regards the etiology of puerperal fever, there has always been, and is even now, con- siderable difference of opinion. Some authors insist that the virus of this disease and of erysipelas, are practically the same. Gusserow,3 supported bv clinical and experimental evi- dence, denies this; whilst Winckel4 and Hart- mann5 are prepared to assert that in a large number of cases, the disease is brought about by the agency of Fehleisen’s micrococcus erysipelatos, which at least was present in all their cases of purulent peritonitis, diphtheritic endometritis, and the ulcerative lesions accom- panying puerperal fever. The evidence pre- sented by Hartmann leaves little room to doubt that these organisms not only invade the lymph-spaces and vessels of the skin, but also the mucous membrane and internal or- gans, and may enter the blood-vessels directly through the abraded surfaces of the mucous membrane of the genital organs. Whilst Hart- mann is careful not to assert that puerperal fever is invariably due to Fehleisen’s micro- coccus, he is quite positive that a large num- ber of cases are thus caused. There are also a goodly number of physicians who believe that the virus of scarlet fever and of diph- theria may induce puerperal fever, whilst others insist that it is simply due to blood- 3 poisoning from the absorption of decomposing blood or tissue either in the uterine or vaginal cavity—the absorption having been rendered possible by abrasions or lacerations occurring during delivery. As a matter of fact, this difference of opin- ion is by no means as great as would appear at first sight, and I believe the conflicting views will be fully reconciled in future. In the first place, a large number of competent bacte- riologists believe that the streptococcus pyo- genes and Fehleisen’s streptococcus erysipela- tos are identical. We also know that the streptococcus and staphylococcus are generally present in scarlet fever, diphtheria, and espe- cially in the so-called pseudo-diphtheritic affec- tions, and in septic wounds.* From this standpoint, puerperal fever, ery- sipelas, septicaemia, pyaemia, pseudo-diphtheria and certain throat complications of scarlet fever, are all caused by septic germs, chief of which are the streptococci and staphylococci. But it must be remembered that over thirty other organisms have been isolated and de- scribed in connection with the suppurative, pysemic or allied processes in man or the lower animals; and the point we wish to emphasize is, that any germ capable of producing the various manifestations of wound infections, is capable of causing puerperal infection. Puer- peral fever is, therefore, nothing more nor less than one of the many phases of septic infec- tions. In addition to the germ, we must have a suit- able soil for its proliferation and pathogenic effects; hence the condition known as predispo- * Prudden reports twenty-four cases of diphtheria, in which in all but two he demonstrated a streptococcus, probably identical with the streptococcus pyogenes and streptococcus erysipelatos; and Baginsky reports that of 154 cases of diphtheria treated under his super- vision, in thirty-six only streptococci and staphylococci could be demonstrated. These same germs are found in the septic throat affections of scarlatinous patients. 4 sition plays an important role; this we find in the average civilized woman, by a lowered vitality,, the result, perhaps, of long suffering from head- aches, neuralgia and indigestion during preg- nancy, and not infrequently an abnormal loss of blood, great fatigue or exhaustion during labor. Moreover, we have a local predisposition in weak sexual and pelvic organs, and possibly in injuries, in the form slight tears and abrasions. After infection has taken place, no organ affords a better cultivating chamber than the uterus filled with a suitable medium like the lochia of a parturient woman. The blood, too, owing to an excess of waste products, the result of great muscular exertion and the return of the womb to its non-pregnant state, affords the best possible papulum for disease germs. While in the majority of cases the germs are introduced into the vagina or uterus by the hands, or in- struments of the attendants, still we shall presently allude to evidence tending to show that a puerperal woman may be infected with germs which were in her genital organs before delivery. In any event, it is reasonable to as- sume that the germs, however introduced, re- main for a time at least at the point of inva- sion and vicinity; here they grow, and as they grow they evolve the so-called ptomaines, some of which are so deadly that even small quanti- ties may prove fatal, whilst many of them act as irritants and cause an inflammation; this, as in the case of erysipelas, may go on withont suppuration. Other bacterial forms cause the white blood cells to gather about the parts; and as they proliferate in overwhelming numbers the leucocytes die, and we have inflammation with suppuration, as in purulent metritis, sal- pingitis or peritonitis; whilst still others cause inflammation with necrosis, as seen in the in- stances of diphtheritic endometritis and the ulcerative lesions. An exact classification would be premature at this time. The most we can say is, that the 5 effects of these septic germs may be local and constitutional, but always the result of absorp- tion of their toxic products. Take, for exam- ple, a case which begins within twenty-four hours after delivery with an intense and long chill, but with little or no pain in the abdomen; the face is anxious, skin pale or purplish, tongue dry or brown, pulse rapid and extremely weak, features pinched, the temperature may be high, or even subnormal, there may be vomiting, but more frequently involunthry evacuations, with delirium, suppressed or scant urine, and the patient dies within twenty-four or thirty-six hours. If these symptoms, which are also seen in other cases of acute septicaemia, are not the result of a ptomaine intoxication, it will be diffi- cult to account for them in any other manner. We need not be surprised if in just such in- stances we fail to find any great pathological changes, for the simple reason that the prolif- eration of the germs has gone on with such a rapidity as to overpower the system before marked lesions could be produced. A similar condition is observed in some malignant forms •of scarlet fever and diphtheria, but just as we see various shades and gradations in all infec- tious diseases, so we may expect to observe differences in degree in puerperal infections, conditioned upon the amount of the poison, the power of resistance of the patient, and the character and seat of the resulting pathological lesions. We have already pointed out how different forms of bacteria may cause different types of inflammatory lesions, and we can readily sur- mise how the seat of these lesions may be in- fluenced by the channels of infection. In some cases, the invaders may not be carried beyond the next lymphatic glands, there to be arrested or disposed of by the vis medicatrix nature; in other cases, the same class of germs may find their way through the lymphatics into tne ab- dominal cavity, and from there invade the 6 pleura or pericardium; in some patients, the ravages of the microbe may be confined to the vagina, uterus or appendages, resulting in chronic lesions; while in still others, they may be carried in a detached piece of a uterine thrombus to the heart and through the pulmo- nary artery and cause infarctions and abscesses in the lungs, from whence again infection may spread to other parts or organs of the body, as the liver, spleen, kidneys and brain, and cause metastatic abscesses, and perhaps various de- rangements of the nervous system, such as puerperal mania, convulsions, delirium, in- somnia, or paralysis. While it is possible that some of these affections may develop simul- taneously in the puerperal state, in the majority of instances they are the result of septic infec- tion, not suspected until the autopsy reveals a thrombosis of the veins of the brain, or puru- lent meningitis. It is generally held that the lochia of a healthy woman, after confinement, contains no micro-organisms, and that the vaginse of women, who have never used injections, or been subjected to digital examinations, is free from pyogenic organisms. Crede,6 therefore, claims that every case of puerperal fever is the result of an infection from without, while others jump to the conclusion that the germs are invariably introduced by the physician or nurse. While it is true that no puerperal infection can take place without the entrance of germs, it has been shown by Velits,7 and the expe- rience of nearly every accoucheur, that infec- tion has taken place without a digital exami- nation having been made; and we also know that many of the pathogenic germs may be present in the vagina or exposed surfaces of the body, as the skin and mucous membranes of perfectly healthy individuals. Steffeck8 (1892) examined the vaginal secre- tions of twenty-nine pregnant females, and 7 found staphylococcus pyogenes albus in nine, staphylococcus pyogenes aureus in three, and streptococcus pyogenes in one. This, however, affords no argument to the opponents of the “germ theory,” for it simply shows that disease-germs may exist within the bod}T and the disorder they give rise to may be absent; and we maintain that an infectious disease does not exist merely because some noxious micro-organisms have taken their abode in the system, but because the host has furnished a suitable soil for their proliferation, and functional and structural changes have been brought about by the agency of bacterial products. The question of soil also explains why a woman may b<- infected with septic germs which were in her vagina long before delivery, but remained dormant or harmless until the blood and other conditions offered a suitable environment for their proliferation, and why some women, with a decomposing foetus or placenta, do not infect themselves, and yet are the cause of a profound septicaemia in others. In the majority of cases, however, the dis- ease is communicated by the attendants, and in order to point out briefly the various sources of the poison and the manner in which it is conveyed, and also for the purpose of illustra- ting the identity of puerperal and wound or septic infection, we adduce the following data; Semmelweis9 was the first to point out that the poison could be brought on the hands of students going from the dissecting-room to the lying-in ward and examining the women in labor. In 1841, an epidemic of puerperal fever occurred in the Maternity of the General Hos- pital of Vienna and lasted for twenty months. Of 5,000 parturient women, about 800, or 10 per cent., died. From 1841 to 1846, the Mater- nity was divided into two departments—one for students and the other for midwives ; the patients were sent to each of the two divisions 8 on alternate days. The fatality in the stu- dents’ wards of 20,042 patients was 1,989 deaths, or 9.92 per cent., and in the midwives’, it was only 3.38 per cent., or 691 deaths in 17,791 deliveries. Whilst Semmelweis was en- deavoring to solve this mystery, he became convinced, by the death of a friend who fell a victim' to phlebitis and secondary abscess after an operation wound, that the pathological lesions in this case were exactly what he had so often noticed in fatal puerperal cases, and he reasoned that the cause in both were blood- poisoning by decomposed particles of a dead body. He therefore ordered every student, be- fore examining a pregnant woman, to wash his hands with chlorinated lime water. At this time, in the middle of 1847, the percentage of mortality was about 12 per cent.; six months later, it was reduced to 3 per cent., and in 1848, the second year of this precautionary measure, the death-rate fell to 1.27 per cent. Semmelweis,10 in 1847, also called attention to the fact that puerperal infection may arise from suppuration; and Sir Spencer Wells re- fers to the fact that the death of several women has been distinctly traced to midwives, who have inoculated the germs of purulent ophthal- mia with a fatal result to one woman, and who have carried the poison and fever to a success- ion of other parturient women who afterwards died of puerperal peritonitis—both streptococci and staphylococci having been found in the pus. Such cases, of which the medical annals sup- ply a large number, will serve to explain the mystery of occurrences like that of Dr. Rutter, of Philadelphia, who had, in 1842, a large num- ber of cases of puerperal fever, whilst his brother obstetricians had none. He bathed, changed his clothes, shaved off his hair, left the city for a week, and visited his next confinement case with an entire change of clothing; still the pa- tient perished from the dreadful fever. It was not until 1875,11 that a contemporary practi- 9 tioner of Dr. Rutter mentioned as a possible explanation, the fact that his collegue was suf- fering all this time from an obstinate ozsena, acquired from a neglected pustule, following inoculation upon the index finger. Apart from digital or instrumental inocula- tion, there is no question that th 3 germs may be conveyed in the air because many of the pyogenic germs have been demonstrated in the air and dust of hospitals, and they may of course cling to the walls, floor, furniture, 'bed- ding, clothing, etc. Dr. Garrigues12 refers to the fact that whilst he was connected with the Maternity Hospital, a new building was erect- ed for the lying-in women; it had scarcely been opened before a violent epidemic of puer- peral fever broke out, compelling the evacua- tion of the building. In the opinion of one of the surgeons, this outbreak was due to guano, with which the adjacent grounds has been cov- ered as a fertilizer. The cause of another epidemic of puerperal fever in one of the New York Asylums12 was found to be a dead rat undergoing decomposi- tion in the cellar, and Fehling12 observed an outbreak of puerperal fever, diphtheria, and erysipelas, which was caused by the leakage of a waste-pipe, the drainage polluting the soil upon which the hospital was erected, and as soon as this was corrected the epidemic stop- ped. We know, from clinical experience, that just such unsanitary surroundings, as also bad food, impure air and water, absorption of pu- trid gases formed in the intestinal tract, etc., predispose to wound infection, and hence also to puerperal infection; but we cannot say whether such conditions actually increase the virulence of otherwise harmless bacteria, or simply diminish the power of resistance, or whether they operate by causing an alteration of the blood, and thus render it a suitable soil for their proliferation. There is good reason 10 for assuming that puerperal infection may- take place through the mucous membrane of the lungs. Depaul, quoted by Garrigues,12 re- ported to the French Academy, in 1858, the case of a student midwife, who nursed a very severe case of puerperal fever. While she was washing the genitals, she felt an unpleasant sensation; in the evening she was taken sick, and died on the third day “with all the symp- toms of the most characteristic puerperal fe- ver.” The post-mortem confirmed the diagnosis, and she was furthermore found to be a virgin and not in a menstrual period ; there was no evidence to show that infection had taken place through abrasions, etc. That there is a systemic infection in puerpe- ral fever is shown by the fact that Karlinsky15 demonstrated staphylococci in the milk of a woman suffering from this fever; her infant was attacked with septicremia, neonatorum in the form of gastro enteric catarrh, peritonitis,, pleuritis, double parotitis, and lobular pneu- monia; and the same bacteria were found in the blood and intestinal contents of the child as wTere present in the milk of the mother. Siredy18 reports another striking case in point. A man suffering for six months from a stercoral abscess was nursed by his two nieces. Both were pregnant, and were delivered with an interval of twro months; and, in spite of easy labors, both developed severe puerperal infection, and the child of the first had, a few days after its birth, a whitlow, a large abscess on the buttocks, and erysipelas all over the body. We have pointed out the various sources of the poison, and the possibilities of even auto- infection are frequent enough, when we recall the fact that Steffeck found pyogenic organisms in the vaginal secretions in 13 out of 29 preg- nant females examined by him. This very fact shows that it is not sufficient for us to simply 11 render our person, fingers and instruments aseptic, but that it is equally essential to re- move or destroy any germs which may be present in the vagina before delivery; for no one can know how soon the system may offer a suitable soil for their proliferation and jeop- ardize the life of the patient. The accoucheur who neglects the rules of modern midwifery certainly ignores establish- ed scientific truths; and though he may flatter himself with having had few if any cases of puerperal fever, he does not deny that many of his patients suffered from some one of the nu- merous forms of puerperal infection, which he naively calls, however, mere idiopathic affec- tions. My own experience with antiseptic midwife- ry has satisfied my conscience and professional pride, for even the old grannies of California appeared to think that I was either very lucky or painstaking in the management of my cases, and, as a result, my obstetric practice in- creased. I mention this, not as a matter of egotismr but to impress the importance of preventive measures so aften deprecated by older men. Apart from adhering strictly to the rules of antiseptic midwifery, I have endeavored to place my patients, when engaged sufficiently early, in the best possible condition as regards the general health, before delivery. Most of the lying-in hospitals have adopted strict rules for the management of cases of la- bor, whereby all students or physicians are ex- cluded from attending a case of labor, if they have come in contact within the last thirty-six hours with septic germs, whether in the dis- secting-room or in the treatment of septic wounds or erysipelatous and diphtheritic pa- tients. In some of the University Hospitals,, the attendants are required to register in the “control book,” for the purpose of tracing the source of infection, but no enlightened medi- 12 cal man or student would wish to attend a la- bor case, under the circumstances mentioned, without taking a full bath with 2 drachms of bichloride of mercury, and devote special at- tention to the disinfection of his hair, beard, hands, and finger-nails. As soon as labor sets in, the patient receives a full bath with warm water and soap, and is dressed in clean clothes and placed in a clean bed; a rubber sheet, previously disinfected with a solution of bichloride of mercury (1:1000), is put under the sheet; she then receives an ene- ma of soap suds, and the abdomen, thighs, buttocks, and especially the hair and folds of the skin, are carefully disinfected with solution of bichloride of mercury (1:2000), whilst the vagina is douched either with 2 quarts of this solution, or with a 2 per cent, solution of creo- line. The attendants should be surgically clean— this involves a careful toilet of the hands, and arms, and especially of the finger-nails with brush, soap, and water, after which the hands should he rinsed in water, and immersed in a bichloride of mercury solution (1:2000) for at least three minutes. The vaginal exploration should be as delicate as possible, and not ex- tend, unless necessary, beyond the external os uteri, and of course should not be unnecessa- rily repeated, and never without previous dis- infection of the hand in the bichloride solu- tion. Lint, cotton, or napkins should likewise be wrung out in a warm bichloride solution before application to the vulva, whilst instru- ments had better be disinfected by immersion in a 5 per cent, solution of carbolic acid. The best lubricant is glycerine with 3 per cent, of carbolic acid or mollin, with 5 per cent, of the same. In tedious labor, the vaginal antiseptic douches are repeated every three hours, and when the presenting part appears at the vulva Garrigues recommends the application of a piece of lint wrung out in the bichloride solu- 13 tion, which serves other useful purposes besides presenting a too free access of air to the vagina as the foetus moves to and fro. In every case where the uterus has been in- vaded by the hand or instruments of the ac- coucheur, or after still births with evidence of decomposition, intrauterine injections are call- ed lor. About 1 quart of a bichloride of mer- cury solution (1:4000) or preferably a 2 per cent, solution of creoline of a temperature be- tween 110°-115° F., should be cautiously in- jected whilst the patient lies on her back ; the porcelain jar should not be held more than a foot above the fundus uteri. After the injec- tion, the fluid should be squeezed out from tho womb, and permitted to escape from the vagi- na by placing the patient on her side. In any case, after the removal of the after- birth, the patient is again washed with the bichloride solution (1:2000), employing absorb- ent cotton for the vulva and clean muslin rags for the skin; especial attention should be paid to the removal of the blood-clots from the hairy parts, which is often most quickly accomplish- ed by cutting part of them off. In the Mater- nity Hospital of New York, it is the rule to compress the womb with the hand for half an hour before the binder is put on, and to the latter is fastened an antiseptic occlusive dress- ing, recommended and described by Dr. Gar- rigues12 to obstetric practice, and consisting, according to his directions,’of—(1) a piece of lint, 12x8 inches, folded twice lengthwise, so as to he 3 inches wide; (2) a piece of oiled mus- lin, 4x9 inches; (3) a large pad of cotton bat- ting, and (4) a piece of muslin half a yard square. The lint is wrung out of the solution of bichloride (1:2000), and carefully applied over the'vulva and anus. The oiled muslin is washed with the same solution and placed over the lint, turning the edges forward against the inside of the thighs. These two constitute the antiseptic part of the dressing. The pad of 14 cotton outside serves only to keep the compress in opposition to the entrance of the genital ca- nal, and is itself held by the muslin kerchief, which is folded like a cravat and fastened to the binder with four pins in front and two be- hind. A good binder should go down beyond the trochanters, and a A-shaped opening left at the genitals, which is closed by the pad just described. This dressing is changed every six hours, or oftener, if the patient has a move- ment or passes her urine in the meantime. Before the fresh dressing is applied, the geni- tals and nearest parts are irrigated with the bichloride solution (1:2000), the patient lying on a bed-pan. No injection is given ; nay, the genitals are not touched.” The cost of these dressings averages about one dollar for the whole lying in period, but it has paid me in more than one respect to adopt these precau- tions. The results of strict antisepsis, of which Dr. Garrigues’ method is of course the type of per- fection, have been most beneficial. We have already learned what Semmelweis accomplish- ed by compulsory disinfection of the hands in the Vienna Maternity; the results have been more striking since we have correct ideas of germicides. Whilst a century ago the mortal- ity at the Lying-in Department of the Hotel Dieu amounted to 10 per cent., it has been re- duced since 1881 to 1.1 per cent. In Berne,14 it has been reduced from 4.5 per cent, to 0.83 per cent., and at Basle,15 the mortality in 1872 still reached 3.33 per cent., whilst in 1886 it was reduced to 0.98 per cent. Of 29,098 de- liveries by prominent obstetricians in Great Britain and Ireland,16 there were 251 deaths, or 0.86 per cent. The statistics of the Maternity at Lyons before and after the introduction of antiseptics, furnished by Dr. Vincent, are ex- tremely suggestive. In the 8 years before 1878 the deaths varied from 79 to 21 per 1,000, or 7.9 to 2.1 per cent. In the following 6 years to 15 1883, when carbolic acid was used as an anti- septic, the mortality fell to 9 per 1,000, or 0.90 per cent.; and after 1884, when the bichloride was introduced, the mortality has gradually fallen until it is less than 1 in 1,000; in 1887, but one death occurred among 1,231 births. Dr. Vincent informed Sir Spencer Wells that the bichloride solution of the strength only of 1 to 2 to 4,000, no harm has in any case been traced to the mercury. The average mortality in the Maternity Hospital of New York, between 1875 and 1883—i. e., prior to the introduction of strict antisepsis with bichloride of mercury, was 4.7 per cent., or 146 deaths in 3,504 deliv- eries; from 1884 to 1888 inclusive, there were 2,271 deliveries with 24 deaths—a total mortal- ity of 1.06 per cent., and that from sepsis was only 0.27 per cent., and Dr. Garrigues,12 who deserves special credit for his devotion to anti- septic midwifery, informs us that the change in regard to morbidity is no less remarkable; whilst formerly nearly 1 out of 4 women de- livered was seriously sick, and 1 in 5 from pu- erperal inflammations; since the change there have been very few sick puerperal, and, with few exceptions, the cases have been very mild, and he says: “We have every year had cases, which, from all symptoms, such as pain, tender- ness, and swelling, had to be diagnosticated as cellulitis, and still the thermometer showed no rise in temperature, a phenomenon which I can only account for by supposing that the inflam- mation was of purely traumatic origin, due to the bruising of the genital canal by the pas- sage of the child, and that the aseptic way in which labor is conducted, as well as the pre- cautions we take during the lying-in period, excludes all infectious germs, which develop so easily in bruised tissues.”12 1819 Q Street N. IV. 16 Bibliogkaphy. 1 Sir Spencer Wells. The Prevention of Preventable Disease.—Glasgow Med. Journal. 1893. 4 Series 40. Pp. 1-17. 2 Fordyce Barker. The Puerperal Diseases. 4th Edi- tion. 1878. Pp. 476. 3 Gusserow. Archiv. Gyncikologie. 1885. XXV. Pp. 169. 4 Winckel. Verhandl. der deuts. Gesellshaft f. Gynii- kologie. 1st Congr. Pp. 78. 5 Hartmann. Archiv. of Hygiene. VII. Pp. 83. 6 Cred6. Gesunde und Kranke Wochnerinnen Leipzig. 1886. 7 Velits. K. Gesellschaft der Aerzte in Pest-Sitzung M'arz 24, 1884. 8 Sternberg. Immunity and Serum Therapy. 1895. P. 13. 9 Semmel weis. Die iEtiologie. der Begriff. u. die Proph- ylaxis des Kindbettfiebers Wien 1861. Pp. 61-63. 10 Wiener Zeitschrift, December, 1847 ; Schmidt Jahrbucher. 1848. Vol. LVIII. P. 196. 11 Amer. Jour. Med. Sciences. April, 1875. P. 474. 12 Garrigues Henry. Puerperal Infection. American System of Obstetrics. Vol. II. Pp. 302-339-351. 13 Karlinsky. Wiener Med. Wochenschrift. 1888. No. 28. 14 Goldberg H. Zur Mortalitat statistik der Entbin- dungs Anstaldt in Bern. 15 Handschin W. Ueber Mortalitat u. Morbiditiit des Puerperal fiebers Basel. Diss. 1888. 16 Matthews Duncan. Mortality of Childbed and Ma- ternity Hosp., Edinburgh. 1871. Pp. 22-23. 17 Sir6dey. Les Maladies Puerperales. Paris. 1884. P. 112. 18 Garrigues. Med. Record. December 29, 1883.