uterine and pelvic veins is sufficiently common during the puerperal
period. The coagulation may result from compression or from
enfeeblement of the circulation. A predisposition to its occurrence is
created by relaxation of the uterine tissue. A normal thrombus is in
itself harmless. In time it becomes organized, and the occluded vessel
is converted into a connective-tissue cord, or a channel may form
through it which permits the passage of the blood-stream. When,
however, pus or septic matters obtain access to a thrombus, it
undergoes rapid disintegration, and the particles get swept away into
the circulation until arrested in the ramifications of the pulmonary
artery. Wherever these poisoned emboli happen to lodge inflammation is
set up in the adjacent tissues, and abscesses result (pyæmia
multiplex). Sometimes countless collections of pus may form in the
lungs. Less commonly abscesses are found in the liver or spleen,
originating either from emboli which have already made the pulmonary
circuit or from thrombi in the pulmonary veins.
Inflammation of the veins (phlebitis) sometimes occurs when the
vessels have to traverse tissues in or near the uterus infiltrated
with purulent or septic materials. The endothelium then undergoes
proliferation, and thrombosis is produced. Phlebitic thrombi do not
necessarily break down, and may in that case act as a barrier to the
progression of septic germs into the circulation (Spiegelberg). As a
rule, however, {990} under the influence of inflammation and
infection, they become converted into puriform masses.
The thrombi grow by accretion in the direction of the heart. They may
extend from the uterus through the internal spermatic, or through the
hypogastric and common iliac veins, to the vena cava. Sometimes the
thrombus may be traced back to the placental site.
SEPTICÆMIA.--From these local conditions, sooner or later, secondary
affections develop in distant organs. The general affection is, in
great part at least, likewise of local origin. Sometimes, however,
where the poison, which enters the system through the lymphatics and
veins, is very active and abundant, death may follow from acute
septicæmia before the changes in the sexual organs have had time to
develop. The fatal result in these cases is probably due to paralysis
of the heart. After death post-mortem decomposition rapidly sets in,
the blood is sticky, and swelling is found in the various
parenchymatous organs.
The secondary affections consist in the metastatic abscesses already
noticed as produced by infected emboli, in circumscribed purulent
collections due to the conveyance of septic materials into the
blood-current through the lymphatics, in ulcerative endocarditis, in
inflammations of the pleura, the pericardium, and the meninges, and in
purulent inflammation of the joints.
A study of the nature of puerperal fever will best show how intimately
these seemingly distinct processes are linked together.
EARLIER VIEWS CONCERNING THE NATURE OF PUERPERAL FEVER.[9]--According
to the teachings of Hippocrates, Galen, and Avicenna, of Ambrose Paré,
of Sydenham, and of Smellie, the fevers of puerperal women were
attributable to the suppression of the lochia. For twenty centuries
this doctrine was accepted almost without dispute, the best clinical
observers confounding a symptom which is often lacking with the cause
of the disease itself.
[Footnote 9: For data given, and for a great variety of historical
information, vide Hervieux, _Traité clinique et pratique des maladies
puerperales_.]
In 1686, Puzos[10] taught that milk, circulating in the blood, is
attracted to the uterus during pregnancy and to the breasts after
confinement, but that milk metastases may form in other parts, and
produce the symptoms of malignant or intermittent fever. In 1746, A.
de Jussieu, Col de Villars, and Fontaine advanced in support of this
theory the fact that they had found, on opening the abdomen in women
who had died from an epidemic which raged that year in Paris, a free
lactescent fluid in the lower portion of the abdominal cavity and
clotted milk adherent to the intestines. This doctrine, which seemed
to be based upon, and to accord with, observation, found many
adherents in France. It lost ground, however, when, in 1801, Bichat
pointed out the true nature of the abdominal effusions of women who
had died in childbed, and demonstrated that they were to be found
likewise in peritoneal inflammations occurring in men and in
non-puerperal women.
[Footnote 10: _Premier Mémoire sur les Dépôts lacteux_.]
While, during the second half of the eighteenth century, the doctrine
of milk metastasis held full sway in France, in England and Germany
the dominant leaders in medicine referred the causes of puerperal
fevers to inflammations of the womb and of the peritoneum. With the
advances made in pathological anatomy in the beginning of the present
{991} century, France taking the lead, stress was likewise laid upon
inflammations of the veins and of the lymphatics. The vitality of the
doctrine of local inflammations is well shown by the records kept by
the Health Board of this city, where a large proportion of the deaths
returned from childbed fever are entered under the head of metritis,
of peritonitis, of metro-peritonitis, and of puerperal phlebitis.
In opposition to the doctrines of the so-called localists, the theory
that puerperal fever is an essential fever, and as much a distinct
disease as typhus fever, typhoid fever, or relapsing fever, has been
strenuously advocated by some of the most distinguished clinical
teachers who have devoted their attention to obstetrical science.
Fordyce Barker, the most recent exponent of the essentiality of
puerperal fever, in his classical work upon the _Puerperal Diseases_,
states the arguments against the local origin of the diseases as
follows: 1st, that puerperal fever has no characteristic lesions; 2d,
that the lesions which do exist are often not sufficient to influence
the progress of the disease or to explain the cause of death; 3d, that
there may be inflammation, even to an intense degree, of any of the
organs in which the principal lesions of puerperal fever are found,
and yet the disease will lack some of the essential characteristics of
puerperal fever; 4th, that the lesions are essentially different from
spontaneous or idiopathic inflammations of the tissues where these
lesions are found; 5th, that puerperal fever is often communicable
from one patient to another through the medium of a third party, and
that this is not the fact in regard to simple inflammations in
puerperal women.
However, neither Barker, nor those who entertain views similar to his,
question the local origin of many febrile affections in childbed, but
claim that purely local inflammations have each their characteristic
symptoms, which differ from those of true puerperal fever, that
puerperal fever is a zymotic disease of unknown origin, and that local
lesions, where they coexist, are not the primary source of trouble,
but are secondary to changes in the blood.
In 1850, James Y. Simpson[11] published a short paper "On the Analogy
between Puerperal and Surgical Fever." This article may well be
regarded as the foundation of the modern doctrine concerning puerperal
fever, and is well worthy of perusal at the present day; for, though
in the then existing state of pathology many of the links were wanting
which have since raised the argument to nearly a mathematical
demonstration, the paper furnishes a brilliant example of the
scientific foresight which is able to discern the truth even where the
evidence lacks completeness.
[Footnote 11: _Edinburgh Medical Journal_.]
In 1847, Semmelweis, who was at that time clinical assistant to the
Lying-in Hospital at Vienna, made the startling assertion that
"puerperal patients were chiefly attacked with puerperal fever when
they had been examined by the physicians who were fresh from contact
with the poisons engendered by cadaveric decay; that fever ensued in
the practice of those who after post-mortem examination washed their
hands in the usual manner, whereas no fever or but few cases of
disease followed when the examiner had previously washed his hands in
a solution of chloride of lime." In the face of insult, ridicule, and
abuse Semmelweis {992} maintained this position for years, almost
unaided, with fanatical persistency. It was easy for his opponents,
for the most part managers of the great lying-in asylums, to show from
clinical experiences the weakness of so one-sided a theory. But the
employment of the equivocal demonstration _falsus in uno, falsus in
omnibus_, served only as a temporary defence against the laxity which
prevailed in hospital management only a quarter of a century ago.
Though Semmelweis died with no other reward than the scorn of his
contemporaries, it is impossible at the present day to so much as
contemplate the abuses he attacked without a shudder.
In 1860, Semmelweis published the result of his ripened experience in
a treatise entitled _Die Aetiologie der Begriff und die Prophylaxis
des Kindbett fiebers_, in which, abandoning his earlier exclusive
position, he maintained that puerperal fever arises from the
absorption of putrid animal substances, which produce first
alterations in the blood, and secondly exudations. He distinguished
between cases in which the infection was introduced from some external
source, and which he believed to be the most frequent variety, and
those where the poison was generated in the system. The sources from
which the infection is derived he believed to be--1st, from the dead
body, regardless of age, sex, or disease, no matter whether the latter
is of puerperal or non-puerperal origin, the virulence depending upon
the stage of decomposition; 2d, diseased persons, whose malady is
associated with decomposition of animal tissue, no matter whether the
affected person suffers from childbed fever or not, the decomposing
matter alone furnishing the product from which infection is derived;
3d, physiological animal substances in the process of decomposition.
As carriers of infection he regarded the fingers and hands of the
physician, midwife, or nurse, sponges, instruments, soiled clothing,
the atmosphere, and, in brief, anything which, after being defiled
with decomposing animal matter, was brought into contact with the
genitals of a woman during or subsequent to parturition. Absorption
takes place from the inner surface of the uterus or from traumata in
the genital canal. Infection seldom occurs in pregnancy, because of
the closure of the os internum, the absence of wounded surfaces, and
because of the rarity with which examinations are made; during
dilatation infection is common, but exceptional during the period of
expulsion, because the inner uterine surface is at that time rendered
inaccessible by the advance of the child; in the placental and
puerperal period infection occurs from utensils and instruments, but
chiefly through the access of atmospheric air when the latter is
loaded with decomposing organic matter. In rare instances
auto-infection may result from spontaneous decomposition of the
lochia, of bits of decidua, of coagula of blood, of necrosed tissue,
or in consequence of severe instrumental labors. In a word, puerperal
fever was according to Semmelweis no new specific disease, but a
variety of pyæmia.
I have been thus particular in giving prominence to the labors of
Semmelweis partly from justice to a man who was hated and despised in
his lifetime, and partly because I believe that few outside of Germany
are really cognizant of the immense service he rendered to humanity,
or that to him is really due a large part of what is now current
doctrine concerning the nature and prophylaxis of puerperal fever.
THE NATURE OF PUERPERAL FEVER AS REGARDED FROM THE {993} STANDPOINT OF
MODERN INVESTIGATION.--The older beliefs in the suppression of the
lochia and the metastases of milk have long since been relegated to
the domain of old nurses' lore, and do not call for serious
discussion. The localist theory, that puerperal fever is a metritis, a
peritonitis, a phlebitis, or an inflammation of the lymphatics, is, as
mortuary records show, still adhered to by many practitioners, and, as
we have seen, is justified by the fact that puerperal fever is, with
rare exceptions, associated at some period of its progress with
certain inflammatory processes which have their starting-point in the
generative apparatus. But the localist theory leaves out of view the
existence of blood-poisoning, and yet the coexistence of a
blood-poison with the local lesions is an essential feature of
puerperal fever. It was this defect which gave to the advocates of the
specificity of puerperal fever their real importance. The outcome of
modern investigation tends, however, to prove that the puerperal
poison is of a septic nature, and that the usual points of
introduction of the poison are the lesions of the parturient canal.
This does not, indeed, exclude other points of entry, for clinical
experience renders it probable that, under certain conditions, the
poison may be primarily introduced into the blood through the
respiratory and digestive organs. Puerperal fever is really a surgical
fever, modified, however, by the peculiar physiological conditions
which belong to the puerperal state. The argument against its septic
origin is based chiefly upon mistaken ideas concerning the nature of
septicæmia. So long as the symptoms of the latter were derived for the
most part from the effects observed as a consequence of injecting
putrid materials into the veins of dogs, a confusion arose from the
fact that the results obtained were commonly those of putrid
intoxication, and not those of true septicæmia. Under such
circumstances it was not difficult to formulate definitions of
septicæmia which could be shown to be at variance with the phenomena
which ordinarily exist in puerperal fever.
The argument that the infectious diseases of childbed are of a septic
nature can best be understood by presenting the proofs in their
orderly sequence.
1st. _It is demonstrable that septic poisons are capable of producing
the lesions ordinarily associated with puerperal fever._ Thus, it is a
matter of ordinary experience that the retention of a small bit of the
membranes within the uterus will produce fetid lochia, and, as the
result of infection, a febrile condition, which, as a rule, subsides
with the expulsion of the offending body and the use of disinfectant
washes. A virulent form of fever is not unfrequently occasioned by
retained coagula or placental débris which have undergone
decomposition. I was once sent for to see a puerperal patient
suffering from fever on the fourth day following her confinement. On
entering the room I found the stench intolerable; turning down the
sheets, I discovered that the patient was lying in a decomposing mass,
and learned that her doctor had forbidden, after the birth of her
child, the removal of the soiled linen and blankets. The patient died
in the third week from pyæmia multiplex.
Haussmann[12] reported a case of auto-infection in the rabbit which
terminated fatally. A portion of the membrane, retained in the left
cornu, {994} led to diphtheritic losses of substance in the lower
portion of the vagina, to hemorrhagic enteritis, and to peritonitis.
The same author produced death from septicæmia by injecting into the
gravid uterus of one rabbit serum from the abdomen of another which
had died from infection. The post-mortem examination showed the
muscles filled with granules and the peritoneum injected, but no
fibrino-purulent exudation. Injections into the uterus of pus from the
abdomen of a woman who had died from infectious puerperal disease
produced no effect upon rabbits two weeks gravid, while in the second
half of pregnancy premature delivery and death occurred, in one case
in one and a half, in another in two and a half, days. In the animal
which died in thirty-six hours there was commencing perimetritis and
peritonitis, while in the one that died after the lapse of sixty hours
the abdomen was found to contain fibrine and pus.[13] D'Espine
injected into the uterus of a rabbit which had just produced her young
pus from the abdomen of a woman who had died from puerperal disease
two days before. This was subsequently followed by other injections of
fetid fluids during the four days following. On the twelfth day the
animal died. The autopsy revealed peritonitis, most marked in the
pelvic cavity, inflammatory alterations in the vagina, uterus, and
tubes, small abscesses in the body of the uterus, softened clots in
the veins of the broad ligaments, and infarctions of the liver.[14]
Schüller found that subcutaneous injections of septic material in
female animals during pregnancy produced a diphtheritic ulcerative
process on the uterine surface, which determined the separation of the
placenta; diphtheritic patches, likewise, were found in the cornua of
the uterus.[15]
[Footnote 12: "Entstehung der übertragbaren Krankheiten des
Wochenbettes," _Beitr. zur Geburtsk. und Gynaek._, Bd. iii. Heft 3, p.
345.]
[Footnote 13: _Contribution à l'étude de la septicémie puerpérale_,
Paris, 1873, p. 28.]
[Footnote 14: _Ibid._, p. 394.]
[Footnote 15: "Experimentelle Beiträge zum Studium der septischen
Infection," _Deutsch. Zeitschr. für Chir._, Bd. vi. p. 141.]
Thus we find that in the human subject and in experiments made upon
animals septic poisons introduced into the system following or near
delivery produce lesions similar to those found in puerperal fever. As
a further coincidence, we notice that, as in puerperal fever, the
lesions from direct septic poisoning have nothing characteristic about
them, producing in one case pyæmia, in another partial peritonitis, in
another general peritonitis, in another diphtheritis, while in others
the lesions are comparatively trivial, these differences being due to
variable facta, such as the qualities of the septic poisons, the
points of entry into the organism, and the resistance offered by the
invaded tissues.
2d. _Septicæmia is a disease characterized by the invariable presence
in the organism infected of minute bodies generally termed
bacteria._[16]
[Footnote 16: In 1865, Mayrhofer (_Mon. Schr. f. Geburtsk._, vol.
xxv., p. 112, 1865), at that time clinical assistant to the Lying-in
Service of Braun in Vienna, stimulated by the researches of Pasteur,
maintained that septic endometritis was the result of putrid
fermentation within the uterine cavity, and drew attention to the
vibrios--a term which he applied to the round as well as to the
rod-like bacteria--as the source, and not the product, of
putrefaction. He claimed that while in puerperal processes vibrios are
always present, in healthy women they never occur before the second,
third, or fourth day, and not always even then. The chief progress
that has been made as regards our knowledge of puerperal fever in the
last ten years has been in the direction of strengthening Mayrhofer's
argument by careful experiment, and by defining the action of
microscopic fungi in the production of septic morbid processes.]
Until very recently the whole subject of septicæmia has been in a
state of wellnigh hopeless confusion. From Gaspard and Panum, through
a long list of experimenters, hardly any two arrived at precisely
similar {995} results. Something like an approach to order has,
however, been produced since it has begun to be understood that the
effects produced by septic fluids vary with the quality of the poison
and the method of experimentation, and that to obtain identity in the
result there must be identity in all the conditions. Thus, Samuel has
shown that the same organic substance produces different effects at
different stages of decomposition; again, that the enteritis which is
commonly quoted as characteristic of septic poisoning occurs, as a
rule, in animals when the septic fluid is injected directly into the
blood, and is rare when it finds its way into the circulation through
the lymphatics, as is the case usually in clinical experiences.[17]
There is one experimental point of extreme practical importance too in
connection with puerperal septicæmia--viz. that if the injection of a
septic fluid be made directly into a vessel, toxic effects speedily
follow, but are transitory, unless the amount of the fluid be large,
or its virulence exceptional, or the animal very young;[18] whereas
very small amounts injected subcutaneously, by developing
rapidly-spreading phlegmonous inflammation, resembling malignant
erysipelas in man, are capable, after a period of incubation, of
producing fatal results; or they may, if injected into a shut cavity
or underneath a fascia, lead to the development of an inflammation of
an ichorous character. In other words, the eliminating organs suffice,
under ordinary conditions, to remove from the blood the same amount of
septic fluid which would prove fatal if injected into the tissues.[19]
To produce similar results the injections into the blood need to be
repeated at intervals. This experience leads us to the conclusion that
in the tissues septic poison possesses the capacity of
self-multiplication, and that in the local inflammation set up a
reservoir is formed from which poison is continuously poured into the
circulation.
[Footnote 17: _Loc. cit._, p. 349.]
[Footnote 18: "Traube und Gescheidlen, Versüche über Faülniss und den
Widerstand des lebender Organismus," _Schles. Ges. f. vaterländische
Cultur_, Feb. 13, 1874.]
[Footnote 19: In some instances in which absorption from the tissues
is very rapid the effects of subcutaneous injections may be similar to
those produced by injections made directly into the circulation, and
the local lesion be insignificant.]
This capacity of self-multiplication which septic fluids possess has
recently been found to be coincident with the presence of certain
parasitic bodies, generically termed bacteria. All carefully-made
experiments serve to show that if a septic fluid be deprived of these
organic bodies by boiling or filtration while it continues capable of
producing inflammation, the inflammation is usually of diminished
intensity and remains local in its character;[20] whereas the bacteria
retained upon the filter possess all the virulent properties of the
original fluid.[21] This does not alone necessarily prove that the
virus resides in the bacteria, for it does not exclude the possibility
that both the virus and the bacteria remain upon the filter.
[Footnote 20: In filtration through porous earthenware cylinders the
filtrate possesses no phlogogenic properties.]
[Footnote 21: Tiegel, _Correspondenzblatt für Schweizer Aertze_, 1871,
S. 1275; Klebs, _Archiv für exp. Pathol. und Pharmakol._, Bd. i. Heft.
1, S. 35.]