THE CAUSES OF SUDDEN DEATH OF PUERPERAL WOMEN. 
AN ADDRESS 
IN 
OBSTETRICS AND DISEASES OF WOMEN 
AND CHILDREN, 
DELIVERED BEFORE THE 
AMERICAN MEDICAL ASSOCIATION, JUNE 5, 1878. 
BY 1/ 
EDWARD W. JENKS, M.D., 
DETROIT, MICH. 
CHAIRMAN OF THE SECTION ON OBSTETRICS AND DISEASES OF WOMEN AND CHILDREN; PROF. 
OF MEDICAL AND SURGICAL DISEASES OF WOMEN AND OBSTETRICS, DETROIT MEDICAL 
college; gynecologist to st. mary's and st.luke's hospitals, Detroit; 
FELLOW OF THE OBSTETRICAL SOCIETY OF LONDON, AND OF THE 
AMERICAN GYNECOLOGICAL SOCIETY; HONORARY MEMBER 
OF THE CINCINNATI OBSTETRICAL SOCIETY, OF THE 
MAINE MEDICAL ASSOCIATION, AND OF THE 
STATE MEDICAL SOCIETY OF 
OHIO, ETC. 
EXTRACTED FROM THE 
TRANSACTIONS OF THE AMERICAN MEDICAL ASSOCIATION. 
PHILADELPHIA: 
COLLINS, PRINTER, 705 JAYNE STREET. 
1878. THE CAUSES OF SUDDEN DEATH OF PUERPERAL WOMEN. 
AN ADDRESS 
IN 
OBSTETRICS AND DISEASES OF WOMEN 
AND CHILDREN, 
DELIVERED BEFORE THE 
AMERICAN MEDICAL ASSOCIATION, JUNE 5, 1878. 
B¥/z 
EDWARD W. JENKS, M.D., 
DETROIT, MICH. 
CHAIRMAN OF THE SECTION ON OBSTETRICS AND DISEASES OF WOMEN AND CHILDREN; PROF. 
OF MEDICAL AND SURGICAL DISEASES OF WOMEN AND OBSTETRICS, DETROIT MEDICAL 
college; gynaecologist to st. mary's and st. luke's hospitals, Detroit; 
FELLOW OF THE OBSTETRICAL SOCIETY OF LONDON, AND OF THE 
AMERICAN GYNAECOLOGICAL SOCIETY; HONORARY MEMBER 
OF THE CINCINNATI OBSTETRICAL SOCIETY, OF THE 
MAINE MEDICAL ASSOCIATION, AND OF THE 
STATE MEDICAL SOCIETY OF 
OHIO, ETC. 
EXTRACTED FROM THE 
TRANSACTIONS OF THE AMERICAN MEDICAL ASSOCIATION. 
PHILADELPHIA: 
COLLINS, PRINTER, 705 JAYNE STREET. 
1878. THE CAUSES OF SUDDEN DEATH OF PUERPERAL 
WOMEN. 
The rule of the Association concerning one of the duties of 
Chairmen of Sections is, that they " shall prepare and read in the 
general session of the Association, papers on the advances and 
discoveries of the past year in the branches of science included 
in their respective Sections." The strictest rendering of this law 
gives the Chairman of a Section limited power of electing a sub- 
ject for his address. As in this instance I have deviated some- 
what from the letter of the law, I deem it proper that T should 
mention as my chief reason for it that the American Journal of 
Obstetrics, for several years past, and but a short time prior to 
our annual meetings, has published an excellent and exhaustive 
annual resume of the latest views and more recent discoveries 
pertaining to obstetrics and gynaecology obtained from all parts 
of the civilized world. I was assured that it was the intention 
of the editor of that Journal to do this year as in preceding 
years. 
I have, then, for very obvious reasons, chosen not to go over 
the entire field of obstetrics and gynaecology for the composition 
of this paper, and yet, adhering to the spirit of the law, I have 
selected as my topic one which has of late elicited the deepest 
interest of obstetricians and obstetrical writers. The subject of 
this paper is "The Causes of Sudden Death of Puerperal Women." 
Were I to limit my paper simply to a review of all that has 
been published upon this subject within the last twelve months 
alone, I could dismiss it with but a few remarks. Indeed, the 
literature of the past which bears upon my theme, contains amid 
a mass of theories and reports of many cases, very little from 4 
ADDRESS IN OBSTETRICS 
which one can deduce positive knowledge, as close analysis shows 
that there has been a paucity of facts. 
The systematic works upon midwifery and puerperal diseases, 
many of which allude to the importance of the subject, contain 
only meagre chapters or brief allusions to the causes of sudden 
death of puerperal women. 
Unexpected or sudden death after gestation was alluded to and 
the histories of cases given by the older obstetrical and medical 
writers, among whom were Mauriceau,1 Peu,2 Morgagni,3 De La 
Motte,4 and Madame Lachapelle.5 
In 1814 Ramsbotham6 attributed sudden death above all other 
causes to moral emotions. 
Our distinguished countryman, the late Prof. Charles D. Meigs,7 
published in 1849 a memoir upon the sudden death of lying-in 
women from heart-clot. He was one of the first to direct atten- 
tion to the possibility of spontaneous coagulation of the blood in 
the right side of the heart and pulmonary arteries as a cause of 
death in the puerperal state. 
Paget had taken a similar view concerning a case of sudden 
death in 1845, although none of his cases happened after delivery. 
In 1850 McCormac8 attributed the sudden death of puerperal 
women to the entrance of air into the circulation by the uterine 
veins. 
McClintock admitted and afterwards rejected this hypothesis 
as a cause of sudden death, in an excellent paper written in 1852.9 
Hecker10 in 1855 was of the opinion that unexpected or sudden 
death occurred most frequently as the result of obliteration of 
the pulmonary artery, an embolism proper. 
Moynier11 and Mordret12 each in 1858 wrote upon this subject. 
In 1863 Olhausen13 wrote upon the introduction of air by the 
uterine veins as a cause of sudden death. 
1 Traite des mal. des femmes et de celles qui sont accouchSes, Paris, 1668-94. 
2 La Pratique des accoucliemens, Paris, 1694. 
3 De sedibus et causes morborutn, Loud. 1763. 
4 Traite des accouch. naturels, non naturels et contre nature, Paris, 1715. 
6 Pratique des accouch., Paris, 1825. 
6 London Medical Repository, 1814. 
7 Philadelphia Medical Examiner, 1849. 
8 Provincial Medical and Surgical Journal, 1850. 
9 Dublin Medical Press, 1852. 
10 Deutsche Klinik, 1855. 
11 Mem. Acad, de Med., Paris, tome xxii. 
12 De la mort subite dans l'6tat puerperale, Thdse, Paris, 1858. 
13 Monatsch. fur Gebur., tome xxviii. AND DISEASES OF WOMEN AND CHILDREN. 
5 
Hcrvieux, who already in 1861 and 1868 had published two 
articles upon sudden death after accouchement, devoted a long 
chapter to the subject in his voluminous work upon puerperal 
diseases in 1870.1 He attributes sudden death of puerperal women 
to lesions either of the circulatory, respiratory, or nervous systems, 
but gives the greatest prominence to puerperal poisoning. 
The same year M. Challier de Grand Champ,2 in a thesis an- 
nounced that sudden death after gestation was most often due to 
pre-existing causes, the principal one being an alteration of the 
blood. 
In 1873, M. Lamy3 wrote upon sudden deaths of puerperal 
women, which he believed most frequently due to an alteration 
of the blood, or to an organic affection itself aggravated by par- 
turition, or to nervous susceptibility. 
Coste,4 in his memoir, in 1876, upon puerperal myocarditis, 
announces in the most emphatic manner that this disease is the 
principal cause of sudden death of puerperal women-" que la 
mort subite aprbs V accouchement est presque toujours le resultat d' 
une myocardite." 
Sir James Simpson and our distinguished countryman, Prof. 
Fordyce Barker, in his excellent work upon the subject,5 have 
each added valuable contributions to the literature of the subject. 
Winckel6 also devotes a short chapter to it. 
Through the Transactions of the Obstetrical Society of London 
are scattered papers upon the causes of sudden death of puerperal 
women. 
In the medical journals of late years under various titles are 
many cases noticed of sudden death of puerperal women, with 
different theories given as to the causes of death. Many of these 
contain no pathological facts, and are not deserving of any spe- 
cial notice. The most noticeable and worthy articles of which I 
have any knowledge, that have not been alluded to, will be men- 
tioned later in this paper. 
1 Traite clin. et prat, des inalad. puerp. suites de couches, Paris, 1870. 
2 These, Paris, 1870. 
3 De la mort subite, des femmes eu couches. Thdse, Paris, 1873. 
4 De la myocardite puerperale, Paris, 1876. 
5 Puerperal Diseases. By Fordyce Barker, Clinical Prof, of Midwifery in the 
Bellevue Hospital Medical College, etc. etc. New York, 1878. 
6 The Pathology and Treatment of Childbed. By F. Winckel, Prof, in Univ, 
of Rostock. Translated by James R. Chadwick, M.D., of Boston. Philadelphia, 
1876. 6 
ADDRESS IN OBSTETRICS 
DISEASES OF THE CIRCULATORY SYSTEM AS A CAUSE OF SUDDEN- 
DEATH IN A PUERPERAL STATE. 
Among the causes of sudden death of puerperal women, will 
be considered, diseases of the circulatory system. 
Of the valvular lesions of the heart, mitral insufficiency seems 
to imperil the puerperal woman least, and mitral stenosis most. 
McDonald1 has collected eight puerperal cases complicated with 
mitral insufficiency. In these cases there were three deaths, and 
five recoveries. Only two of the deaths could be called sudden, 
or 25 per cent. The same author, has collected twelve cases of 
chronic cardiac disease, in which mitral stenosis was the leading 
heart lesion. 
A brief abstract of these cases will better enable us to estimate 
the relation of this lesion to sudden death in puerperal women. 
Case I. Mitral stenosis, haemoptysic, palpitation, dyspnoea, at 
end of sixth month of first pregnancy; pulmonary and general 
oedema in the second pregnancy; labor supervening spontane- 
ously about the end of eighth month ; death sudden on sixth day 
after delivery. 
Case II. Mitral and tricuspid stenosis, with insufficiency ; 
dropsical symptoms in 1873, a month after confinement ; embol- 
ism of branch of left middle cerebral artery, with hemiplegia 
of the right side three months afterwards; recovery. Pregnancy 
again in 1878, with great aggravation of previous symptoms of 
dropsy and dyspnoea. Labor premature at beginning of ninth 
month ; easv. Death from exhaustion ; contraction of both auri- 
cular-ventricular orifices; enlargement of both ventricles; atro- 
phy of posterior half of left corpus striatum. 
Case III. Mitral stenosis; hemiplegia, with a certain degree 
of aphasia; labor premature in consequence of accidental hemor- 
rhage on 21st of February, 1877, being about three weeks too 
early. Urgent symptoms during delivery, which was ended by 
forceps. Recovery. 
Case IV. Mitral stenosis; labor at full term; threatened symp- 
toms of weakness and iregularity of the pulse during the second 
stage. Delivery by forceps. Recovery. 
Case V. Mitral stenosis; miscarriage about fifth month, and 
death thirty-six hours afterwards. 
Case VI. Mitral stenosis; breathlessness from the age of 
i Obstet. Journ. Great Britain and Ireland, 1877. AND DISEASES OF WOMEN AND CHILDREN. 
7 
fifteen; symptoms much worse after marriage. Miscarriage 
about fourth month of pregnancy, and sudden death immediately 
after. Post-mortem revealed great mitral contractions. Both 
auricles and right ventricle dilated and hypertrophied. 
Case VII. Extreme stenosis of mitral valve; violent palpita- 
tion and severe breathlessness for three or four years; sudden 
death from pulmonary engorgement, immediately after the pa- 
tient's fourth labor. Post-morte.m examination revealed the lungs 
healthy, but engorged with blood. Mitral valve only admitted 
tip of little finger. 
Case VIII. Stenosis of the left mitral of moderate amount. 
Severe chest symptoms (oedema and congestion of the lungs) 
during the later months of second pregnancy. Premature labor 
suggested, but came on spontaneously before arrangements could 
be completed, and patient died during confinement of suffocative 
oedema of lungs. Postmortem proved internally oedematous. 
Heart ordinary size. Aorta strikingly small; pulmonary artery 
dilated; mitral valve contracted. This case is one of Hecken's, 
and was one of the first well-described cases directing the atten- 
tion of obstetricians to this important subject. 
Case IX. Mitral stenosis, with insufficiency ; dilatation of the 
right side of the heart. Severe chest symptoms from oedema of 
the lungs. Symptoms during labor very critical; venesection. 
Liquor amnii excessive. Recovery. 
Case X. Mitral stenosis with insufficiency ; no special trouble 
before the sixth month ; then breathlessness, palpitation, cough, 
expectoration of rusty sputum, and occasionally blood. Labor 
premature during seventh month, with unconsciousness and ex- 
tremely alarming symptoms. After this, remission of urgent 
symptoms. Death nine months afterwards with Bright's disease. 
Post-mortem examination revealed a pericardium distended with 
fluid; heart twice the ordinary size; both auricles and right 
ventricle greatly dilated ; left ventricle natural size; left auri- 
culo-ventricular opening admitted only one finger. Lungs partly 
collapsed, partly emphysematous and oedematous. 
Case XI. Mitral stenosis; slight attack of acute rheumatism 
after second confinement, followed by severe illness involving 
heart and kidneys. Admitted to the hospital in seventh month 
of third pregnancy, with symptoms referable to mitral stenosis, 
with dilatation and venous congestion. Induction of premature 
delivery thought of toward end of eighth month, but labor super- 8 
ADDRESS IX OBSTETRICS 
vened spontaneously, patient being in a state of unconsciousness. 
Death three months afterwards. Post-mortem examination showed 
great dilatation of right heart and left auricle ; slight enlargement 
of left ventricle. Mitral opening too small to allow a finger to 
pass; valves thickened, evidences of pulmonary infarction recent, 
and of old-standing hydrothorax. 
Case XII. Mitral stenosis and insufficiency, with aortic insuf- 
ficiency ; enlargement of left side of heart, consequent upon an 
acute attack following the tenth pregnancy, which was a pla- 
centa praevia. Aggravation of symptoms during the latter half 
of the eleventh pregnancy. Spontaneous premature labor in the 
eighth month whilst patient was in a state of unconsciousness. 
Cardiac symptoms much aggravated therewith, and death forty- 
eight hours afterwards. Post-mortem examination showed en- 
largement of left heart. Left auriculo-ventricular valve thickened 
and nodulated. Mitral opening allowed.one finger to pass. The 
right heart only moderately dilated. 
Of these twelve cases nine were fatal, and six of them during 
abortion or delivery, or within a few hours afterwards. In other 
words, seventy-five per cent, of the cases were fatal and fifty per 
cent, suddenly fatal. 
Four of the cases were primipar ; and of these three died, 
and two very suddenly. 
Three were pregnant for a second time; of these two died very 
suddenly. The other five cases, at the time they were under 
observation, were respectively confined for the third, fourth, sixth, 
tenth, and twelfth time; all died but the last, and two very sud- 
denly. 
In no case was death caused by embolism, but rather by suf- 
focative oedema of the lungs, congestive bronchitis with or with- 
out actual pulmonary hemorrhage, extreme dyspnoea, and cardiac 
irregularity, culminating in abortion and death, either during or 
shortly after delivery. 
From these facts we are bound to expect the above circle of 
phenomena to occur in a pregnancy complicated with a badly 
compensated mitral stenosis. 
Dr. MacDonald, in the article quoted from, records five cases 
of aortic incompetency, of which the following is a brief abstract: 
Case I. Aortic insufficiency, with mitral obstruction; pulse 
extremely irregular during labor; great tendency to faint. De- 
livery by forceps. Recovery. AND DISEASES OF WOMEN AND CHILDREN. 
9 
Case II. Extreme aortic insufficiency, with great mitral ob- 
struction; haemoptysis; frequent cough, dyspnoea, and vomiting. 
Premature labor came on spontaneously at end of eight months. 
Dyspnoea and repeated attacks of syncope during labor. Death 
three weeks afterwards from suffocation, congestion, and oedema 
of the lungs. Post-mortem examination revealed the mitral ori- 
fice so contracted as to admit only the passage of a little finger. 
Aortic valves reduced to mere stumps; heart dilated and hyper- 
trophied ; lungs oedematous and congested. 
Case III. Aortic insufficiency,'with mitral stenosis, referable 
to an attack of rheumatic fever five years before. Suffered from 
a severe cold about the end of the third month of pregnancy. 
Severe symptoms began about the sixth month. Pain in left 
chest, palpitation, tendency to faint, haemoptysis, nephritis, con- 
vulsions, parturition; sudden death. Post-mortem examination 
revealed aortic valves much diseased and acutely inflamed, and 
the mitral much stenosed. 
Case IV. Severe case of aortic insufficiency. Violent pre- 
cordial pain and dyspnoea at about the twenty-eighth week of 
pregnancy. Improvement under treatment for a time; but a 
return of the distressing symptoms on slight exertion. Pregnancy 
interrupted by spontaneous premature labor about the thirty- 
fourth week. Labor easy, and remission of urgent symptoms 
rapid. 
Case V. Aortic insufficiency; slight case ; dyspnoea and palpi- 
tation apparent about the sixth month. Under treatment the 
patient got better, but premature labor came on in the eighth 
month, and was followed by recovery. 
Of the two suddenly fatal cases in this group, it will be ob- 
served that both were complicated with mitral stenosis, so that 
from what has been previously shown we may reasonably refer 
the fatal results mainly to the mitral obstruction. 
In the Revue des Sciences Medicates, July, 1877, is given an ex- 
haustive review of this subject, which includes Marty's table1 of 
two hundred and four puerperal cases complicated by valvular 
lesions of the heart. In sixty-five cases there was mitral insuffi- 
ciency; twenty-nine premature confinements, with frequent and 
grave complications; and three sudden maternal deaths. In 
1 Influence de la grossesse et des couches sur 1'appareil circulatoire et troubles 
gravido-cardiaques, par Porak. 10 
ADDRESS IN OBSTETRICS 
forty cases there was mitral stenosis, with twelve premature con- 
finements; and three sudden maternal deaths. In fifty one cases 
there was mitral insufficiency and stenosis, with twelve prema- 
ture confinements, and four sudden deaths. In fifteen cases there 
was aortic insufficiency, with but one complication, and no 
death. In five cases there was aortic stenosis, with two sudden 
deaths. In three cases there was aortic and mitral insufficiency, 
with one sudden death. 
This table shows also that the liability to sudden death is far 
greater in mitral stenosis than in any other form of valvular 
disease. 
ENDOCARDITIS AS A CAUSE OF SUDDEN DEATH IN THE 
PUERPERAL STATE. 
Simpson was about the first to note the influence of the puer- 
peral state upon endocarditis. This influence he supposed to be 
exerted through the presence of lactic acid in the blood of the 
pregnant woman.1 
Virchow2 regards puerperal endocarditis as a form of puer- 
peral fever to be classed with the peritoneal forms, as both affect 
a serous membrane. At the time of his report upon the subject 
he had within a year and a half eighty-three cases of sudden 
death from this cause. All the cases were remarkable by the 
absence of lesions of the genital organs or of other parts of the 
body which could account for the intensity of the fever and 
other symptoms. His observations forced him to the conclusion 
that the disease of the lining membrane of the heart was the 
origin of other pathological changes. More frequently he found 
evidences of recent endocarditis which had caused a degenera- 
tion of the mitral valves. Particles of these bioken-down valves 
had been loosened and carried into the circulation. These ob- 
structed the capillaries and produced circumscribed inflamed 
spots. 
Finally, Virchow found in the vessels supplying blood to these 
spots a plug composed of the debris of the softened valves. In 
one case death was determined by softening of the entire heart. 
In one case of Virchow's, cited by Vast, and later by Mar- 
tineau, of ulcerative puerperal endocarditis, a post-mortem exami- 
1 Obs. Memories, etc., Edin., 1856, page 69. 
2 Gynaecological Society of Berlin, March 9th, 1858. AND DISEASES OF WOMEN AND CHILDREN. 
11 
nation revealed the uterus perfectly sound, but in a great number 
of organs were found the so-called metastatic spots, viz., in the 
kidneys, spleen, liver, eyes, etc. In each of these spots was 
found an artery plugged with detritus of the broken-down endo- 
cardium. Hence in all cases of puerperal disease in which there 
exist these metastatic spots, and the condition of the abdominal 
organs does not account for the great frequency of the pulse and 
general disorder, a careful examination of the heart is advised. 
Aiilfeld1 records a case of acute endocarditis, attended with 
vegetation on mitral valves, leading to capillary cerebral embol- 
ism, convulsions, delivery by forceps, and sudden death. Post- 
mortem examination revealed vegetations of the mitral valves 
from the size of a millet-seed to that of a pea. Extravasation of 
blood under the pia mater; hundreds of capillary apoplexies in 
the gray substance of the brain, some about the size of a millet- 
seed or pea, one the size of a lentil in the pons Varolii. 
Lebert2 reports a case of acute articular rheumatism in the 
fourth month of pregnancy; there was an abortion in the sixth 
month, followed by ulcerative endocarditis and embolism of the 
left subclavian, the abdominal aorta, and common iliac artery ; 
sudden death. Post mortem examination showed a flabby, dilated, 
large fatty heart, extensive ulceration of the mitral valves, more 
especially of the posterior cusp, which was completely destroyed. 
Emboli were found in left subclavian, abdominal aorta, and 
both iliacs. 
Of four cases recorded by Simpson,3 in which a post-mortem 
examination proved the embolism to be due to the escape of 
cardiac vegetations, one of the patients had, a year previous 
to the fatal pregnancy, suffered from rheumatic endocarditis. 
Another had an attack of acute rheumatism during the preg- 
nancy, and died a few days after delivery. A third suffered from 
endocarditis supervening only after her premature delivery. A 
fourth was due to ulcerative puerperal endocarditis. These cases 
especially illustrate with great force the risk of severe embolism 
and sudden death which cases of recent rheumatic endocarditis 
run by becoming pregnant, and so lighting up a fresh and more 
severe endocarditis. The practical deduction clearly is, that all 
1 Archiv fur Gynak., Bd. iv. S. 158. 
2 Ibid., Bd. iii. 8. 10 und foly. 
' Selected Obstet. Works, p. 525. 12 
ADDRESS IN OBSTETRICS 
women who have suffered from endocarditis should be discouraged 
from marrying or becoming pregnant, as the peculiar changes 
of the pregnant and puerperal state render it probable that an 
ulcerative endocarditis will be excited and bring with it embolism 
and sudden death. 
Fatty Heart.-That a fatty heart should be a cause of sudden 
death in puerperal women we may readily admit, since the most 
reliable observations of all deaths in persons affected with this 
disease place the sudden deaths at two-thirds of the entire number. 
But as it occurs during the latter half of life, and is one of the 
degenerative changes belonging to that period, it is obvious that 
it must be relatively infrequent in puerperal women. 
Of the positive observations I have been able to find but two 
cases in which a sudden death was due to a fatty heart. 
The first case was reported by myself.1 Patient aged thirty-six; 
had been out of health for some years. Was safely delivered of 
her third child with no particular difficulty, but died suddenly 
about three hours afterwards. Post-mortem examination revealed 
a markedly fatty heart and kidneys. Uterus was contracted and 
normal. Careful microscopic examination was made of the 
heart, demonstrating beyond a doubt its fatty degeneration. 
The other case is reported by Winckel:2 Woman, aged thirty- 
five, was delivered of her fifth child. The labor was difficult; 
the funis prolapsing, and forceps being required. Ulcers on the 
cervix uteri were the source of a parametric exudation on the 
right side as large as one's fist; there was also a continued fever. 
Patient died quite suddenly on the sixth day wi h symptoms of 
pulmonary oedema. The autopsy showed fatty degeneration of 
the heart. 
We may fairly suspect that a closer post-mortem examination 
of all the cases of sudden death in the puerperal state would 
many times reveal a fatty heart as the organ at fault. 
Coste,3 in bis monograph before mentioned, has especially em- 
phasized myocarditis as a very common cause of death in puer- 
peral women. But of the five reported cases on which he bases 
his conclusion, at least four of them seem to us more nearly to 
1 Detroit Review of Medicine and Pharmacy, vol. vi. p. 345. 
2 Winckel on Childbed, 1876, p. 221. 
3 Op. cit., p. 73. AND DISEASES OF WOMEN AND CHILDREN. 
13 
fall under the head fatty heart; and even in the remaining one, 
it is not at all dear that the sudden death was caused by myocar- 
ditis alone. As it is almost impossible to diagnosticate the dis- 
ease during life, we pass it with this brief mention as a possibly 
rare cause of sudden death in puerperal women. 
DISEASES OF THE ARTERIES AS A CAUSE OF SUDDEN DEATH IN 
PUERPERAL WOMEN. 
Local arteritis as a cause of sudden death in puerperal women 
has not been very carefully studied. All admit that it speedily 
ends in the formation of an obstructing fibrinous or sanguineous 
concretion in the tube of the inflamed artery. 
Simpson1 reports a case observed with the most scrupulous 
exactness. The patient was a primipara, and two weeks after 
delivery was brought into the hospital suffering from gangrene 
of the lower extremities. Death occurred soon. An autopsy 
revealed an entire absence of disease in the heart, its walls, 
valves, or cavities. But an inch and one-half above the bifurcation 
of the aorta was found a fibrinous plug occluding the entire artery 
and extending along the common iliac, so as to obstruct both the 
external and internal iliacs on each side. The upper part of the 
plug was flattened and closely adherent to the arterial walls. At 
the most inflamed part the calibre of the artery was contracted. 
More positive observations are needed in making autopsies of 
those suddenly dying in the puerperal state to determine the 
structure of the existing plugs and the exact condition of the 
arterial wall at the point of obstruction. 
With such observations we may more accurately estimate the 
actual importance of this cause of sudden death. 
That arteritis may produce sudden death by forming and set- 
ting free emboli, we have the most abundant evidence from the 
records of Simpson, Meigs, Playfair, Paget, Baron, Dubin, 
Richelet, and others. The special locality in which they ob- 
served the most fatal results from this source, was the pulmonary 
artery. 
Whether death is caused through syncope, as held by Virchow, 
or through cerebral anaemia, as thought by Panum, or through 
asphyxia, as claimed by Bertin, may be still a question. It is 
1 Obstetrical Works, p. 539. 14 
ADDRESS IN' OBSTETRICS 
evident that all the results are due to the fact that the blood is 
kept from the air. 
The connection of phlebitis with sudden death in the puer- 
peral state has long been recognized, especially since the fact has 
been made clear that fragments of the plugs caused by the phle- 
bitis may be set free and form obstructions in the vessels else- 
where, particularly in the pulmonary circulation. 
Simpson1 records four cases of plugging of the pulmonary 
arteries in the puerperal state, in which death occurred with 
fearful suddenness and rapidity. In all of these instances uterine 
or cerebral phlebitis preceded the pulmonary obstruction. 
Winckel, Levy, Hecker, Makinder, Charcot, Hervieux, Steele, 
Chantreuil, and others, report similar cases, in which an early 
and sudden death followed the detachment of a portion of the 
thrombus. 
It is of interest to note that in most of these cases the cause of 
the sudden embolism is ever-exertion, such as lifting, stooping, 
rapid movements, etc. Thus a piece of the primary thrombus 
is broken off, and in a few moments carried to the pulmonary 
artery. 
The relation of hemorrhage, ante- and post partum, to sudden 
death is so fully dwelt upon in all obstetrical works, and lec- 
tures, and magazine contributions, that we pass it with a simple 
mention. 
Few obstetric practitioners are devoid of terrible experiences 
fully illustrating the relation of such hemorrhage to sudden 
puerperal deaths. 
As a cause of puerperal diseases in general, septicaemia has 
given rise to widespread and long-continued discussion and dif- 
ference of opinion. That it has been an influential cause of sud- 
den death in puerperal women there can be no doubt. As it has 
appeared in hospitals or epidemics in various places, it has pro- 
duced appalling lists of sudden death. 
You will remember that in London during the years 1760, 1768, 
and 1770, it so prevailed that in some lying-in hospitals almost every 
patient died. It is said of the Edinburgh Infirmary in 1773 that 
"almost every woman, as soon as she was delivered, was seized 
1 Obstetrical Works, p. 346. AND DISEASES OF WOMEN AND CHILDREN. 
15 
with this disorder, and all of them died." Nor did the lying-in 
establishments on the Continent fare better. Thus the J/azson 
<Z'Accouchements of Paris during a number of different years pre- 
sented a mortality of one in three or even greater. In Vienna 
during 1823, nineteen per cent, of the cases died, and in 1842 
sixteen per cent. In Berlin, in 1862, hardly a single patient 
escaped. 
Numerous other instances here and abroad will occur to you 
all and sufficiently emphasize the statement that septicaemia in its 
most malignant forms is one of the chief causes of sudden death 
in puerperal women. To illustrate this matter Prof. Barker1 
reports the following :- 
A prirnipara during the seventh month of her pregnancy began 
rapidly to fail in health, lost strength, became dull and sleepy; 
had slight fever; vomiting; offensive diarrhoea. Refusing to 
have labor brought on at once, she rapidly sank, so that in four 
days she became unconscious. Pulse rapid; skin cold. In a 
short time the membranes were ruptured; labor came on ; and 
with little trouble she was delivered of a putrid foetus. She died 
a few hours after. In this case the source of infection was the 
dead foetus. 
Equally suddenly fatal cases are on record of puerperal women 
dying from a blood poison derived from broken-down portions of 
the placenta, or gangrenous destruction of a part of the neck or 
other portion of the uterus. 
So also cases of sudden death are well authenticated from a 
poison carried to the women by a nurse or physician, or carried 
from cases of erysipelas, scarlet fever, diphtheria, etc. The 
sources of the poison are both autogenetic and heterogenetic. 
In short, it matters little whether the poison be engendered 
in some part of the generative tract of the woman or carried to it 
from without; if only she is in proper condition to be profoundly 
affected by it, sudden death is almost inevitable. 
The suddenness of the death is regulated by two factors, the 
susceptibility of the patient and the virulence of the poison. 
When both factors exist to a considerable extent, remedial agents 
are as futile as in cases struck dead by lightning, or as in cases 
overwhelmed by any other powerful poison, as morphia, atropia, 
or arsenic, etc. Apparently the human protoplasm may be de- 
1 Puerperal Diseases, p. 402. 16 
ADDRESS IN OBSTETRICS 
prived of its essential properties with great rapidity by the 
peculiar form of poison under consideration. 
The relations of septicaemia to thrombosis and embolism are 
not fully worked out. 
Recent investigations respecting the phenomena of coagulation 
of the blood seen to indicate a plausible explanation of one phase 
of this relationship. 
Many years since Prof. Schmidt demonstrated that no fibrine 
exists in the living healthy body; and that the fibrine of the blood- 
clot is derived from the union of the fibrino-plastin and fibrino- 
gen of the blood. Later he demonstrated that in order to pro- 
duce a union of these two factors a third substance was necessary. 
This third substance has been traced to the white blood-corpus- 
cles; but in order that it may act in producing fibrin it must be 
set free by the disintegration of these corpuscles. 
The reason for believing that the white blood-corpuscles con- 
tain the ferment necessary to the coagulation of blood are well 
stated by Dr. Burdon Sanderson.1 First he shows that certain 
white blood-corpuscles disintegrate from the moment that they 
leave the blood stream. The experimental proof of this is as 
follows: Blood from an artery or vein is caught in a tall jar in 
which it is rapidly cooled by a freezing mixture placed about it. 
Thus treated, the blood remains uncoagulated, the red blood disks 
sink to the bottom, the white ones rise to the top, and serum 
separates the two. If under a microscope we examine almost 
immediately the top layer, we shall find countless white blood- 
corpuscles. But if a few moments have elapsed a certain number 
of these corpuscleswill be observed in all stages of disintegration. 
In the process of disintegration the corpuscles first break up 
into granules, but eventually disappear. From these granules 
the first formed filaments of fibrine are seen to take their origin. 
Further, if the white blood-corpuscles be withdrawn, coagulation 
is arrested. Proof of this statement is rendered possible by the 
fact that leucocytes at the temperature of freezing acquire such 
firmness and consistence, that they are held back by the ordinary 
methods of filtration. 
Thus by appropriate apparatus, uncoagulated blood can be 
freed from its white blood-corpusles. The filtrate thus obtained 
is absolutely transparent and deprived of its power of coagu- 
1 British Medical Journal, Jan. 12, 1878. AND DISEASES OF WOMEN AND CHILDREN. 
17 
lation. If the white blood-corpuscles on the filter be washed 
and added to the decorpusculated plasma, the latter is restored 
to its original coagulability. 
With these facts before us, and those cases in which cerebral, 
pulmonary, and other embolisms occur to cause sudden death in 
the puerperal state, we get an intelligent suggestion as to the 
mechanism by which the fatal result is brought about. 
The uterine sinuses and the internal surface of the uterus are 
loaded with breaking-down blood-corpuscles, white and red. 
Usually the balance of nutritive forces is such that all the effete 
materials are carried out of the uterus, and discharged from the 
body as lochia. In certain exceptional cases this balance is lost, 
and more or less of the effete material is carried into the venous 
circulation. This material, by its contact with the fibrinogen 
and fibrino-plastin of the blood, is able to produce blood-clots, 
and so emboli more or less numerous, according to the circum- 
stances of the case. We have no doubt that very many cases of 
embolism have this direct origin. 
Meantime other elements of the effete material are producing 
their depressing and disorganizing effects upon other protoplas- 
mic elements of the body. For one purpose it matters not 
whether we regard the poison of puerperal fever as one sui gen- 
eris or not. Under definite circumstances we very certainlv ob- 
serve but one result, viz., sudden death. As we have indicated, 
this may be brought about,by the formation of emboli in the 
blood, through the action of the disintegrated white blood-corpus- 
cles; secondly, by the paralyzing influence of other poisonous ele- 
ments upon other protoplasmic structures essential to life; and 
thirdly, by the simultaneous formation of emboli and genera] 
poisoning. 
If we accept the view that broken-down white blood-corpuscles 
circulating in the blood may determine the formation of blood- 
clots, we can readily understand how a ferment derived from the 
uterine sinuses may pass through the capillaries of the lungs, 
and afterwards produce an embolus in the cerebral arteries, or 
capillaries, or in the liver, kidneys, or any part of the general 
capillary or arterial systems. 
We look for researches which will render equally clear the con- 
stitutional effects produced by the other elements of puerperal 
poisoning, which are doubtless more far reaching in their effects 
and equally as fatal. 
2 18 
ADDRESS IN OBSTETRICS 
The introduction of air into the uterine veins is an occasional 
cause of sudden death in puerperal women. McClintock cites 
six examples which were probably due to this cause. Lacha- 
pelle1 relates two; Baudelocque2 two ; Simpson, Lionel, and Her- 
vieux, each one; Bussy3 of Birming am, in fifty cases of sudden 
death in the puerperal state, found air in the heart and uterine 
veins. Smith4 reports one case; Leven5 reports three cases of 
similar nature. In most of these cases a careful post-mortem ex- 
amination confirmed the diagnosis. 
The chief symptoms produced by this accident are due to the 
more or less complete stoppage of blood in the pulmonary capil- 
laries. Unquestionably after delivery the uterine sinuses are 
nearly as well adapted as the veins of the neck to facilitate the 
entrance of air. 
If in any manner air enters the uterus it is easy to understand 
how the alternate contraction and relaxation of the uterus would 
open the mouths of the sinuses and force air into the veins. 
Doubtless the entrance of air is facilitated by an exhausting 
hemorrhage, such as would temporarily lower the venous blood- 
pressure. 
Dr. Graily Hewitt6 refers to a case in which sudden death 
occurred shortly after the removal of an adherent placenta, and 
under symptoms that rendered it certain that the cause was the 
entrance of air into the veins. The introduction of the hand 
into the uterus for turning or other intra-uterine operations is 
occasionally the cause of sudden death by facilitating the intro- 
duction of air into the veins. 
Tetanus is an occasional cause of sudden death in the puerperal 
state. Simpson7 has collected twenty-five cases. Of the nature 
of the disease it cannot be said to differ at all from that which 
ocurs in the ordinary surgical practice. Here as elsewhere, three 
conditions seem essential to determine its occurrence: first, a 
wound; second, an undetermined sensitive condition of the nervous 
system; and third, a peculiar state of the atmosphere. There is 
good evidence for believing that a neuritis is originated in 
the sensitive nerves at the point of the wound, and that this 
1 Op. citat., p. 76. 
3 Arch, fiir Gynaec., Bd. iii. 
5 British Med. Journal, 1857. 
7 Obstet. work, p. 510. 
2 Op. citat., p. 16. 
4 British Med. Journal, 1856. 
6 Lond. Obstet. Trans., vol. x. p. 28. AND DISEASES OF WOMEN AND CHILDREN. 
19 
extends upward to the motor tract of the spinal cord, producing 
in the latter a hypersensitive condition. Be this as it may, the 
fact remains undoubted that tetanus may cause sudden death in 
the puerperal state. 
Another cause of sudden death of lying-in women is puerperal 
convulsions. The older obstetrical teachers were accustomed to 
say that one-half of the patients attacked with this disease died. 
Barker, from statistics of published cases collected in 1855, showed 
that thirty-two per cent, of all cases occurring before and during 
labor, and twenty two per cent, of those after delivery ended 
fatally. From his own practice and in consultation, Dr. Barker 
has seen since 1855 sixty-five cases of puerperal convulsions, 
with a mortality of nine cases, or about fourteen per cent. Of 
course these cases had the advantage of the most recent and skil- 
ful modes of treatment, so that we may not expect to find better 
results elsewhere. No doubt the increased frequency with which 
chloroform and chloral have been used has greatly diminished 
the death rate. 
For our purpose it is needless to discuss the causes of puer- 
peral convulsions. Obstetrical literature is largely occupied with 
such diseases. 
Other infrequent causes of sudden death in the puerperal state, 
which lack of time forbids our dwelling upon at length, are : 
Rupture of the heart; rupture of the uterus; apoplexy ; profound 
moral emotion, and mental excitement; shock, and traumatism. 
To conclude, we may remark (1) The causes of sudden death 
fall naturally under four heads: (a) Lesions of the circulatory 
system; (Z>) Lesions of the respiratory system; (c) Lesions of 
the nervous system ; and (cZ) Puerperal septicaemia. 
(2) In its wide-reaching relations to the other causes of sudden 
death, puerperal septicaemia stands pre-eminent, as very many 
lesions of the circulatory, respiratory, and nervous systems are 
the direct or indirect results of blood poisoning. 
(3) It is more than probable that small and large emboli may 
be formed in any part of the circulatory system by the action of 
disintegrated blood-corpuscles upon the fibrinogen and fibrino- 
1 Puerperal Diseases, p. 125. 20 
ADDRESS IN OBSTETRICS 
plastin. The minuteness of the particles of white blood-corpus- 
cles enables them to pass with the greatest freedom through 
capillaries of the smallest diameter and afterwards by their fer- 
ment acting upon other elements to produce concretions in the 
vessels. Obviously the plain duty of every obstetrician is to 
prevent the absorption of any decomposing materials from the 
uterus. Emphatic as was this statement of old, it gathers new 
meaning and greater force from the new researches respecting 
the agency of decomposing white blood-corpuscles in producing 
blood coagulation. 
(4) Of the various valvular lesions mitral stenosis is clearly the 
most dangerous to the pregnant or puerperal woman. In fact 
the liability to sudden death of those affected with this heart 
lesion is frightful. 
(5) The usual mode of sudden death in puerperal women 
affected with valvular lesions is by the damming back of blood 
upon the lungs, causing pulmonary oedema, etc. 
(6) Endocarditis, old or recent, if existing in a woman at the 
beginning of pregnancy, is extremely liable to be re-kindled by 
the changed blood of the pregnant woman, and to run the course 
of ulcerative endocarditis. Thus material for countless emboli 
is furnished, and the woman's life placed in imminent peril. 
(7) Endocarditis may result as one of the forms of the so-called 
puerperal fever, just as the peritoneum may become involved in 
the same diseased process by the same blood poisoning. 
(8) Arterial degeneration may produce death in two ways: (a) 
The white blood-globules caught on the roughened surface of 
the vessels may be broken in pieces, and the ferment set free, 
which unites in a blood clot the fibrinogen and fibrino-plastin ; (&) 
An increase of the arterial pressure may rupture the diseased 
vessel, and so cause sudden death. 
(9) Arteritis is a very rare occasion of sudden death. 
(10) Phlebitis, on the other hand, is a very frequent source of 
the gravest complication of the puerperal state, viz., sudden 
death. 
(11) No more certain cause of sudden death exists than the intro- 
duction of large quantities of air into the uterine sinuses. The 
anatomical relation of the mouths of the uterine sinuses are such 
that the relaxation of the uterus leaves them more or less open. 
If air be present in the uterus it will fill the partially open 
sinuses, and by the next uterine contraction be forced into the AND DISEASES OF WOMEN AND CHILDREN. 
21 
venous circulation, and so to the right side of the heart and pul- 
monary capillaries. 
Relatively, however, the entrance of air into the veins is a 
very infrequent cause of sudden death in the puerperal state. 
(12) Of the causes of sudden death to puerperal women ope- 
rating mainly through the nervous system, puerperal eclampsia 
is the most conspicuous. But its nature, its origin, and its treat- 
ment have been so unfolded during the last twenty years, that 
its death-rate has been vastly diminished. 
(13) Finally, every physician should feel himself bound by a 
professional obligation to investigate with the most painstaking 
minuteness the pathological anatomy of every case of sudden 
puerperal death that falls under his observation. With a broader 
scope of reliable data, the conditions underlying each cause of 
sudden death may be so thoroughly made known that most sud- 
den deaths may be prevented. 
As already stated, the mortality of puerperal convulsions dur- 
ing the last twenty years has been reduced from thirty-two to 
fourteen per cent. This is but one illustration of what has been 
done by our science and art in the past, but it is a significant 
prophecy of what we may expect in the future.