(SANITIZED)UNCLASSIFIED ARTICLES ON OBSTETRICS AND GYNECOLOGY, 1955(SANITIZED)

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• Document Creation Date: December 27, 2016
• Document Release Date: June 18, 2014
• Sequence Number: 5
• Publication Date: October 5, 1956
• Content Type: REPORT

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EXPERIENCES WITH ACTII AND
EOSINOPHIL COUNTS IN NORMAL
PREGNANCY AND TOXEMIA
JAMES HENRY FERGUSON, M.D.
New Orleans, La.
From the Department of Obstetrics and Gyne-
cology. Tulane University of Louisiana and
the Charity Hospital of Louisiana at
New Orleans
Reprinted from
AMERICAN JOURNAL OF OBSTETRICS
AND GYNECOLOGY
St. Louis
Vol. 61, No. 3, Pages (303-608, March, 1951
( Printed In the I S. A.
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EXPERIENCES WITH ACTH AND EOSINOPHIL COUNTS IN
NORMAL PREGNANCY AND TOXEMIA*
JAMES HENRY FERGUSON, 31.D., NEW ORLEANS, LA.
(From the Department of Obstetrics and Gynecology, Tulane University of Louisiana and
the Charity Hospital of Louisiana at New Orleans)
WITH the surprising and increasing range of usefulness of ACTH and
cortisone it is natural that the effect of these drugs should be investi-
gated in pre-eclampsia. Cases of normal pregnancy, pre-eclampsia, and
chronic hypertensive disease with superimposed pre-eclampsia have been
treated with ACTH and the results will be recorded here. The recognition
of the value of counts of circulating eosinophils, and alterations caused by
various agents, as an index of pituitary-adrenocortical function, provides a
new tool for the study of normal pregnancy and pre-eclampsia. Observations
on eosinophil counts in nonpregnant, normal pregnant, and toxemic women
will be recorded.
The adrenal cortex is increased in size in pregnancy. It has long been
suspected of playing some role in pre-eclampsia. Extensive changes have
been found in the gland after deaths from eclampsia. Selye' and others2. 3
have suggested eclampsia may belong in the group called diseases of adaption.
This would be characterized in part by hyperactivity of the pituitary and
adrenal cortex. Hofbauer4 emphasized the importance of a disturbed hor-
monal balance in the etiology of toxemia, in particular an increased activity
of the pituitary, adrenal cortex, and accessory adrenal medullary tissue in
the cervical ganglions. Sodium and chloride retention, increased urinary 17-
ketosteroids and uric acid excretion, and a supposed pronounced eosinopenia
were cited as evidence of activation of the pituitary adrenocorticotropic secre-
tion The positive water and sodium balance of pre-eclampsia points to the
adrenal cortex with its important regulatory action.
I. Eosinophil Counts
Eosinophil counts were made as described by Hoche� and associates with
the use of a wet technique with a mouitication of Randolph's eosinophil stain.�
A white cell pipette and special counting chamber were used. Counts are
expressed in number of cells per cubic millimeter. The average eosinophil
count in the peripheral blood is in the order of 150 to 200 with a wide normal
range. Coppinger and Goldner found counts in preoperative patients ran
from 11 to 718. Rath and associates� reported eosinophil counts in preg-
nancy ranged from 6 to 545. The mean counts by month were from 126 to 167.
Patients tested in this investigation were usually in hospital at bed rest
and fasting. The mean counts in 13 nonpregnant control women, 41 women
with normal pregnancies, 20 with pre-eclifinpsia, and 8 women with chronic
'This work was supported by a grant from Ell Lilly & Company.
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hypertensive disease and superimposed pre-eclampsia are shim n in Table I
The means in this group, and in all other groups studied here, were analyzed
by Student's t test. There was no significant difference in any of this group.
There was a greater variability in the pre-eclamptic patients. Fourteen
normal and 10 pre-eclamptic postpartum women tested on usually the first or
second postpartum day were essentially alike.
TABLE I. EOSINOPHIL COUNTS IN NONPREGNANT, PREGNANT, AND TOXEMIC WOMEN
NO PATIENTS
MEAN
STANDARD
DEVIATION
Nonpregnant control
13
147.1
+ 69.0
Normal pregnancy
41
113.1
� 77.0
Pre-eclampsia
20
129.0
+144.0
Pre-eclampsia and chronic hypertension
8
151.9
+ 91.9
Postpartum normal
14
125.3
+109.4
Postpartum pre-eclampsia
10
173.9
�168.1
Four-Hour Epinephrine Test �Under the influence of certain stimuli
(stress, operations, labor. epinephrine) the anterior pituitary causes the
adrenal cortex to produce more of its hormones. With this adrenocortical
activity there appears a significant percentage decrease in circulating eosino-
phils. In the presence of a deranged or damaged anterior pituitary-adreno-
cortical system this fall in eosinophils will not occur. Isolated eosinophil
counts are of little value because of the wide range in the counts in normal
persons: the decrease, or absence of decrease, following attempt to stimulate
the adreral cortex is the important observation. The work of Long and
others�, " demonstrated that epinephrine could stimulate an intact pituitary-
adrenocortical system and established the value of the four-hour test, counts
before stimulation and four hours later, in testing for dysfunction in this
system. A fall of greater than 50 per cent is expected in a normal person.
By-passing the pituitary, the adrenocorticotropic hormone (ACTII) can be
given and in the presence of a normally functioning adrenal cortex the stone
change in eosinophils occurs.
Twelve nonpregnant, 12 normal pregnant, and 10 pre-eclamptic women
were giwn subcutaneous injections of 0.3 mg, of epinephr;ne, with eosinophil
counts taken before injection and four hours later. The patients W ere in hos-
pital at hed rest and an interval of over three hours without food preceded
the second count. There were no significant differences in the mean per-
centage changes in the three groups (Table II) Again there was a greater
variability in the pre-eclampties. Thirteen normal and 9 pre-eclamptic post-
partum patients were tested and there was a diminished response in both
classes
TABLE 11. EPINEI MUNE R TEST
-
NO. PATIENTS
MEAN
PERCENTAGE
CHANGE
F:OSINOPIIILS
STANDARD
DEVIATION
Nonpregnant control
Normal pregnancy
Pre-eclampsia
12
12
10
-54.2%
-58.2%
-56.6%
�18.5
�18.6
�36.4
Postpartum normal
Postpartum pre-eclampsia
13
9
-20.;'%
-37.79k
-159.2
�29.7
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Eclampsia.�It has been reported that eosinophils disappear from the
peripheral circulation in eclampsia 12 One eclamptic patient, incidentally
with quintuplets, tested three hours after convulsion, had a level of 213 eosino-
phils per cubic millimeter Eighteen hours later it was 481 and a week later
it was 131. This patient had no allergic disease. A second eclamptic patient.
tested seven hours after a convulsion, was found to have a count of 0; 30
hours after the convulsion it was 75. A third eclamptic patient had a level
of 25 when tested twenty-four hours after a convulsion. A fourth was tested
41/2 hours after convulsion and the count was 0. Furthermore, 5 women with
what would often be termed "severe pre-eclampsia" were tested and no re-
markable counts resulted. Two of these women were later tested in labor
and showed the reduction in count reported elsewhere, and observed by the
author, in normal women in labor.
No unusual counts were noted in cord blcod specimens or in the presence
of hyperemesis gravidarum, diabetes, or a dead fetus. One pre-eclamptic pa-
tient with abruptio showed a near absence of eosinophils, 6, but another
woman with the same diagnosis had 63. The result in an epinephrine test
on a case of hyperemesis was �79 per cent.
The four-hour ACTH test (25 mg.) was used on 4 pre-eelamptic patients.
1 normal pregnant woman, and 2 postpartum pre-eclampties. The response
was in general subnormal in all groups. This can be explored further when
ACTH is cheaper
II. ACTH
At the time of this Is riting no reports are available on the use of pituitary
adrenocorticotropic hormone ( Arl'H) in pregnancy or its complications. The
use of ACTH seems illogical because of its occasional exhibition of sodium-
retaining properties. However, because of its diverse pharmacological and
physiological actions and its unanticipated usefulness in many disease syn-
dromes it certainly deserves a trial in pre-eclampsia. If toxemia of late preg-
nancy is a disease in which hyperactivity of the pituitary-adrenocortical sys-
tem is a prominent feature. as mentioned earlier in reports, ACTH would be
expected to make this complication worse.
The effect of ACTH and cortisone in certain other conditions are of in-
terest. Forsham and associates" reported considerable fluid retention when
normal patients received 10 mg of ACTII every six hours for a period of four
to six days. In nephrosis ACTH has had a variable effect. Diuresis and xater
retention have both been observed in different patients during therapy as well
as a diuresis following cessation of therapy. Rapid decrease in albuminuria
and improved kidney function have been noted." This variability in response
is not unexpected as cortical steroids have been known to cause either water
retention or loss. The complex picture of adrenal cortex and water metab-
olism has been thoroughly reviewed by Gaunt and co-workers." ACTH and
cortisone have caused both edema and diuresis in arthritics." In glomerulo-
nephritis, cortisone caused water retention, followed by a saline diuresis."
Clinical Trial.�Nine women in the latter weeks of pregnancy were treated
with A('TII (Armour) All were hospital patients and generally at bed rest
Intake and output were accurately measured before, during, and for several
days after therapy. Weights were recorded at the same time each day. Each
patient had a daily fasting blood chemistry performed for glucose, uric acid,
and total serum proteins; in some cases chlorides and blood urea nitrogen
were also measured. This blood was utilized for a daily eosinophil count.
This collection was made one to three hours after the last injection of ACTH.
Regular observations of blood pressure were made. There were daily hemato-
erits and tests for glycosuria. Some patients were on a regular hospital diet
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and received no medication. Others were on the toxemia regimen of sedation,
ammonium chloride, and low salt diet. All patients received fluids ad lib.
Brief abstracts of case histories in the order in which they were treated
follow:
CASE 1.�L. T. Normal primipara. 38 weeks' gestation. 10 mg. ACTH every 6
hours for 7 days. No other medication Regular diet. No evidence water retention
Gain V. pound in the 7 treatment days.
CASE 2.�G. K. Chronic hypertension. Acutely superimposed pre eelainpsia at term.
Controlled and lost 5 pounds on 2 days of toxemia regimen. Then AoTH 10 mg. every 6
hours added. Loss 41/2 pounds in 3 days and went into spontaneous labor.
CASE 3.�D. H. Severe pre-eclampsia at 36 weeks. No improvement on first hospital
day. Then ACTH 10 mg. every 6 hours ad led to toxemia treatment. Albuminuria cleared
on third day but blood pressure and ode' la improved only slightly. Output over 2,000
c.c. every 24 hours. Normal spontaneous labor on seventh hospital day.
CASE 4.�L. W. Normal multipara at 39 weeks. 10 mg. ACTH every 6 hours for 10
days. Loss (3 pounds while receiving ACTH.
CASE 5.�M. B. 37 year-old multipara. Chronic hypertensiv� disease with acute
pre-eclampsia. After 7 days with improvement, ACTH 10 nig. every 6 hours added to
toxemia regimen and continued for 9 days. Loss 7 pounds during ACTH therapy and
output over 4,000 c.c. each day.
CASE 6.�E L. Chronic hypertension with pre eclampsia. Improved on 2 days'
toxemia treatment to which was ther added 10 mg. ACME every 6 hours. In three days
of treatment continued to improve losing 4 pounds with an output over 4,000 c.c every
24 hours.
CASE 7 �I'. A. Pre-eclanipsia. Primipara at 32 weeks. Improved on toxemia regi-
men. Third hospital day, ACTH 20 mg, every 6 hours and toxemia regimen discontinued.
Received 720 mg. over 9 days. Loss only 2 pounds while on ACTH and edema remained
urchanged. Output ()ter 4,000 e.e. daily.
('Ass 8.�C. I'. Pre eclampsia superimposed on chronic hypertensive disease at term.
Received 30 mg. MTH every 0 hours for '!-_-te doses and went into spontaneous labor.
CAsE 9.�G. E. Normal primipara at 39 weeks. 30 nig. ACTH every 6 hours for
total 1.04 Gm. on 9 days. No other treatment. Gain 4 pounds. Output usually over 3,000
e.e. each day. No edema. Lost 2 pounds in 2 days after discontinuing treatment.
The pronounced metabolic changes reported by others were not found to
occur in pregnant women when treated with ACTH, whether pre-eelampsia
was present or not. On doses as small as 10 mg. every 6 hours water retention
and a rise in serum uric acid have been reported in normal patients. Blood
sugars have been raised and serum proteins have declined More pronounced
metabolic shifts and water retention have been noted on dosages of 25 mg.
every 6 hours. The smaller doses are effective in many conditions responsive
to ACTI I, for example, the collagen diseases. This is pointed out as explana-
tion that all patients in this study received ACTH in quantities that are in a
usually effective range.
ACTH did not alter the blood uric acid, glucose, or serum protein in any
case in the' present study. The hematocrits were unchanged. Ivo variations
in blood urea nitrogen or chlorides followed Crlyeosuria did not develop
The reduction in eosinophil counts that others have reported,". 18 often
to the point of disappearance of these cells from the peripheral blood, did not
occur here exeept in one ease (G. E.), the normal patient who received 30 mg.
every 6 hours In her ease the daily eosinophil count was lowered to 3 to
6 cells per cubic millimeter. In all other cases there was no reduction in
eosinophils.
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ACTH did not definitely affect, favorably or unfavorably, the clinical
course of pre-eclampsia. Patients made the improvement that would usually
be expected from bed rest or the toxemia regimen, if used. G. E., the patient
who received the greatest amount of the drug, showed mild water retention.
No consistent change in the blood pressure was noted except that in a
majority of cases the graded reduction that would be expected from rest in
hospital was observed. One patient (D. H.) had an inconsistent slight eleva-
tion on the hourly recording that followed administration of the drug.
Two women (M. B. and P. A.) had electrocardiograms before and at the
termination of ACTH therapy. There was no evidence of hypopotassemia.
None of the many side effects reported by others occurred. Forsham"
noted 25 mg. ef ACTII caused uterine cramps and 3 women bled who had not
menstruated for a year The ACTH may have been a factor in the cases of
the 5 women who went into labor while under treatment. At the time, most
batches of the drug were reported running 0.02 to 0.04 USP units of oxytocin
to 25 mg.
Four of the 9 patients experienced heartburn while receiving ACTH and
only then. No other reports of heartburn as a side effect of ACTH therapy
have been noted. This reaction should not be surprising in light of the ill
effects of ACTII in trials with peptic ulcer'� and the report of a perforated
ulcer during treatment of periarteritis nodosa.2� The pregnant woman has an
inclination to develop heartburn due to the horizontal positioning of the
stomach and atonicity of the gut. ACTH in these cases was apparently the
extra burden needed to produce this symptom
Comment
Th, lack of significant differences in eosinophil counts in toxemia and
normal pregnancy appears to make this procedure valueless as an indication
of the status of pregnant diabetic women as proposed by P. White." The ab-
sence of lowered eosinophil counts in toxemia casts some doubt on the pres-
ence of increased pituitary adrenocortical stimulation, at least as detectable
by this test.
The possibility of pre-eclampsia being a state of depleted adrenal reserve
seems ruled out by the normal results found in the four-hour epinephrine test.
At the same time it appears that the anterior pituitary has lost none of its
power to stimulate the production of corticosteroids. Some of the counts
and epinephrine tests were done in the most serious forms of the syndrome.
There was no apparent difference in the mild and severe forms. It has been
remarked that there was a greater variability in the results in pre-eclampsia.
No correlation in clinical course and eosinophil count or the fou--hour epi-
nephrine test could be made.
The fact that ACTII failed to produce definite increased water retention
in pregnancy and pre-eclampsia, conditions of natural water retention, is
particularly interesting. The possibility that pre-eclampsia may be influenced
by doses greater than 30 mg. every six hours should be considered. This
thought is supported by Thorn's" contention that unless a fall in eosinophils
follows ACTH therapy no conclusions can be drawn on its therapeutic efficacy.
It might be hypothesized that the ACTII administered to these pregnant
women depressed the secretion of the pituitary's adrenocortical hormone
enough to block expected physiologic reaction.
The failure of response to ACTH may mean that the adrenal gland in
pregnancy is already under the stimulation of the patient's endogenous ACTH
and not capable of responding to this dose. A concept that the adrenal cortex
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is exhaustet: seems untenable because of the normal response to epinephrine.
Daughaday and MacBryde23 suggested the possibility of an adrenocortical
salt hormone that is independent of ACTH.
The lack of water retention following ACTII therapy indicates that eL-
cessive adrenocortical stimulation is probably not the cause of positive water
balance in pregnancy or pre-eclampsia. Obviously a great deal more study
is needed to understand the relationship of the adrenal cortex to pregnancy
and toxemia.
Conclusions
There is no significant difference in the number of eosinophils in the
peripheral blood of women who are not pregnant, women who have a normal
pregnancy, and patients with pre-eclampsia. There is no evidence of altered
anterior pituitary-adrenocortical function in pre-eclampsia or normal preg-
nancy when evaluated by the four-hour epinephrine test. Disappearance of
eosinophils from the circulation occurs in eclampsia but is not a constant
phenomenon. ACTH in doses which are usually therapeutic has no definite
effect on pre-eclampsia or normal pregnancy. The pregnant woman appears
peculiarly resistant to ACTH as she fails to show expected physiological
changes.
References
1. Selye, H.: J. Clin. Endocrinol. 6:117, 1946.
2. Parviainen, S., Soiva, K., and Ehrnrooth, C. A.: Acta obst. et gynec. Scandinav 29:
186. 1949.
3. Garrr*.t, S. S.: West. J. Surg. 58: 229, 1950.
4. Hofbauer, J : OBST. & GYNEC. 59: 1383, 1950.
5. Roche, M., Thorn, G. W., and Hills, A. G.: New England J. Med. 242: 307, 1950.
6. Henneman, P. H., Wexler, H., and Westenhaver, M. M.: 3. Lab. & Clin. Med. 34:
1017, 1949.
7. Coppinger, W. R., and Goldner, M. G.: Surgery 28: 75, 1950.
8. Rath, C E., Caton, W., Reid, D. E., Finch, C. A, and Conroy, L.: Surg., Gynec. & Obst.
90: 320, 1950.
9. Vogt, M.: J. Physic)]. 104: 60, 1945.
10. Long, C. N. H.: Federation Proc. 6: 461, 1947.
11. Recant, L., Hume, D. M., Forsham, P. H., and Thorn, G. \V.: .1 Clin. Endocrinol 10:
187, 1950.
12. Davis, M. E., and Hulit, B. E.: J. Clin. Endocrinol. 9: 714, 1949.
13. Forsham, P. IL, Thorn, G. W., Prunty, F. T., and Hills, A G.: .1. (lin. Endocrinol. 8:
15, 1948.
14. Farnsworth, E. B. " Proceedings of the First Clinical Arrii Conference, 1950,"
Philadelphia, The Blakiston Company, pp. 297-317.
15. Gaunt, R., Birnie, J. H.. and Eversole, W. J.: Physiol. Rev. 29: 281, 1949.
16. Slocumb, C. H., Polley, H. F., Hench, P. S., and Kendall, E. C.: Proc Staff Meet.,
Mayo Clin. 25: 476, 1950.
17. Kieth, N. M., Power, M. H., and Daugherty, G W.: Proc Staff Meet., Mayo Clin. 25:
491, 1950.
18. Hills, A. G., Forsham, P. H., and Finch, C. A.: Blood 3: 755, 1948.
19. Spiro, H. M.: Cited by Thorn et al. � New England .T. Med. 242: 865, 1950.
20. Beck, J. C, Browne, J. S. L., Johnson, L. G., Kennedy, B J., and MacKenzie, D W :
Canad. M. A .1. 62: 413, 1950.
21. White, P. Am. .1 Med. 7: 609, 1949.
22. Thorn, G. W., Forshani, P. H , Frawley, T. F., Hill, S. R., Jr., Roche, M., Stnehelin, D.,
and Wilson, D. L.. New England J Med. 242: 783, 1950.
23. Dnughaday, W. H., and MacBryde, C. M.: .T. Clin Investigation 29: 591, 1950.
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RUPTURE OF THE MARGINA
SINUS OD' Till: PLACENTA
JAMES HENRY FERGUSON, M.D.
New Orleans, La.
From the DePartment of Obstetrics and Gyne-
cology. Tuiane University School of Medicine.
New Orleans. and the Obstetric and Gyne-
cologic Service of Charity Hospital of
Louisiana at New Orleans
Reprinted from
AMERICAN JOURNAL OF OBSTETRICS
AND GYNECOLOGY
St. Louis
Vol. 69, No. 5, Pages 995-1004, May, 1955
(Printed In the 1'. S. A.)
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RUPTURE OF THE MARGINAL SINUS OF THE PLACENTA*
JAMES HENRY FERGUSON, M.D., NEW ORLEANS, LA.
(From the Department of Obstetrics and Gynecology, Tulane University School of Medicine,
New Orleans, and the Obstetric and Gynecologio Service of Charity Hospital of Louisiana at
New Orleans)
BELIEVE rupture of the marginal sinus is a lesion that merits further
1. illumination because it is a frequent cause of maternal hemorrhage and, in
a sense, is a new complication of pregnancy. I will try to devE1 p the two
ideas that rupture of the marginal sinus is far from rare and that it has some
of the quality of newness.
I know that many have doubts that there actually exists such a thing as
a marginal sinus, let alone a rupture of the marginal sinus. It would be naive
to think that any skeptic is going to be convinced this morning but possibly
disbelievers and the hitherto disinterested will be persuaded to look for rupture
of the marginal sinus. My experience has been that if men will look for rupture
of the marginal sinus they will find it. The sinus itself has been described so
many times in the literature of anatomy I do not feel that I have to defend
its existence.
The reasons we can look upon rupture of this marginal sinus as a new
lesion are several. I have learned that in some hospitals it is so new the
diagnosis has never been made or, apparently, not even considered. From
other hospitals I have news that rupture of the marginal sinus has only
recently been sought for the first time and found. From the literature I
sense that rupture of the marginal sinus is neglected in many places.
To the best of my knowledge, and of our record librarian's, the diagnosis
of rupture of the marginal sinus never appeared on the face sheet of a patient's
chart at the Charity Hospital in New Orleans until the second half of 1951.
Prior to July, 1951, I had never diagnosed a case of rupture of the marginal
sinus nor had I ever searched for one. My attention was called in 1951 to
this example of morbid parturition by the publication of Fish and his
associates.' It seemed to me this might be an important lesion that deserved
more attention and better understanding. Therefore this study was undertaken.
Where had rupture of the marginal sinus been meanwhile? Or, better
put, where had most of us been in relation to rupture of the marginal sinus?
Possibly you have asked yourself, or will ask yourself, this question. If I ever
heard of rupture of the marginal sinus before 1951 it must have been in a most
unreceptive moment.
The diagnosis of rupture of the marginal sinus has not been acknowledged
by a listing in the Standard Nomenclature of Diseases. It can be described
� Presented at the Twenty-second Annual Meeting of the Central Association of Obstetri-
cians and Gynecologists, St. Louis, Mo., Oct. 7 to 9, 1954.
995
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996 FERGUSON
Obst & Gynec
May. 1955
and coded as, "Placental vessels, hemorrhage, cause undetermined" (79 x
-Y00.7), or it could be, "rupture or perforation" (Y00.3), or "rupture"
(Y00.5).
History
I have not been able yet to piece together a continuous history of this
concept of bleeding froni a ruptured marginal sinus. Actually, it is far from
being a newly recognized complication of pregnancy. It seems merely to have
been overlooked for a few recent decades. The earliest article on rupture of
this sinus that I have read is well over a century old. Jacquemier in France
wrote about it at least as early as 1839.2 He thought that rupture of a marginal
sinus was frequent in normal pregnancy, in premature separation of the
placenta, and in placenta previa. Something Jaequemier said is of interest
to us today because it describes the experience I am reporting: "While I was
at the Maternite, I examined with great care the placentas of almost all of the
women who had had a hemorrhage, either during pregnancy or in labor. I
have found in some clear proof that the loss of blood came from the circum-
ference of the placenta without this showing signs of earlier detachment."
In Edinburgh both Duncan3 and Simpson4 wrote about it in the 1870's.
They understood bleeding from the sinus at the placental margin to be one
of the major causes of antepartum hemorrhage. From Paris in 1893 Budin5
provided drawings that depict exactly what I am talking about this morning.
The prominence and the number of the corroborators that these men mention
suggest that bleeding from the marginal sinus was a widely used diagnosis.
What has happened to rupture of the marginal sinus in the intervening
years I can only guess. Possibly the men whose textbooks and schools dominated
American obstetrics in the first half of this century slighted it because they
were more intrigued by abruptio and placenta previa. Some of our textbooks
and the current literature convey the idea that the two most common causes
of bleeding in the last trimester or semester of pregnancy are placenta previa
and abruptio. We can have reason to suspect that this is entirely wrong.
They may be the most important because they are the most dangerous, but
I do not think they are the most frequent. A solid argument can be built
for the claim that there are more common varieties of bleeding in this part of
pregnancy and one of them is rupture of the marginal sinus. There is also
a substantial group in which the cause of bleeding is never accurately identified
Anatomy of the Marginal Sinus
The marginal sinus of the placenta is a system of veinlike channels of
great delicacy and thinness. These sinuses lie in the decidual tissue at the
edge of the placenta and they discontinuously encircle the placenta. The name
'circular sinus'' has also been used The lengths and diameters of the
sinuses vary The caliber is in the order of 2 to 5 mm. I have seen a sinus
filled or, better perhaps, ruptured, and replaced b a finger of clotted blood
that measured 2 cm in diameter.
With experience you can identify the marginal sinus rapidly by incising
into the placenta's margin. Perforations into the sinuses can be disclosed by
peeling back the membranes at their placental attachment and wiping clean
the edge of the placenta. I know that many have looked for the marginal sinus
and ha N e been disappointed. Sonic were mistakenly seeking an unbroken,
uniform vessel that made a circle around the placenta. Actually the sinuses
have no obvious intercommunications as viewed under the conditions imposed
upon us, i.e , inspection of the maternal surface of the placenta, out of the
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RUPTURE OF MARGINAL SINUS OF PLACENTA
997
uterus and in our hands. Another reason for failure to recognize the marginal
sinus is that when the fresh specimen is held in the hands with the maternal
surface uppermost, the blood, still liquid, escapes from the sinuses, if it has
not already done so; the walls of the sinuses collapse and their flaccidity makes
it difficult to identify them. Parts of the marginal sinus may be left behind
in the decidua at the time of the placental separation.
For class demonstration of the marginal sinus take two or three normal
placentas and let them lie overnight in a refrigerator, not a freezer. Blood
in the marginal sinuses at first is liquid and will remain in that state for some
time. The next day, in the portions where the blood has not drained away,
the sinus cavities can be identified by the casts of coagulated blood they
contain.
These sinuses contain venous maternal blood and are part of the placental-
uterine plexus that forms the maternal blood-collecting system. From these
sinuses the blood passes to other decidual vessels, to the uterine veins, and
hence into the mother's general circulation. Recent experimental work has
confirmed that the blood in the marginal sinus is maternal blood!' In 1873
Turner,7 in an exposition on the circulation of maternal blood in the placenta,
could cite a formidable list of corroborators. He named the circular sinus as
part of that circulatory system.
Observations at the Charity Hospital
My own attempt to learn something about rupture of the marginal sinus
covers three periods and two slightly different approaches. The first portion
of these observations began July 1, 1951, with the collection and examination
of as large a number of placentas as possible from the women with antepartum
hemorrhage on the obstetric unit of the Tulane Service of the Charity Hospital
at New Orleans. The study continued for one year and by a wide margin
lacked being a continuous series of cases. In that fiscal year there were 4,103
deliveries on the Tulane Service. I identified 16 cases of hemorrhage as being
due to rupture of the marginal sinus. These cases will be combined with
others in my description of the syndrome.
In the first and third quarters of this year (1954) we were successful in
gathering and categorizing by cause of bleeding the placentas from every
case with antepartum bleeding on the Tulane Obstetric Service at the same
hospital. Because there were 2,251 deliveries in those 6 months we can get
sonic notion as to the frequency of the various causes of bleeding. The use
of this number of patients might introduce some sampling errors so I do not
claim that my incidences are any more than notions. I think they do hint that
rupture of the marginal sinus is something big enough for us to give more
thought to it.
During the intervals between the studies the diagnosis of rupture of the
marginal sinus was made a number of times by the residents. These cases are
not available for inclusion in this report.
I made my criteria for the diagnosis rather severe to elicourage objectivity
and to avoid errors inherent in any effort to find a place for a new or neglected
subject. The sine qua non for diagnosis was the immediate postpartum exhibi-
tion at the margin of the placenta of a clot that was continuous with clotted
blood in the marginal sinus. This is a stringent requirement and certainly some
eases were discarded into the group in which no diagnosis could be made
because the clot at the placental margin was dislodged in passage through the
cervix, vagina, and the obstetrician's hands. The clot at the margin is usually
not large and does not give the impression that it has interposed itself between
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998
FERGUSON Am j Obst. & Gynec
May. 1955
the placenta and the uterus. I would guess that the clot at the margin
averages betv,3en 50 and 100 c.c. The clotted blood in the sinus is not difficult
to find because this cylinder of blood is usually thick, appearing to burst from
its confines. Conceivably there are cases in which the blood did not clot and
which therefore are not included.
Table I shows the causes of bleeding in the 97 cases of uterine antepartum
bleeding on the Tulane Obstetric Service of Charity Hospital in the first and
third quarters of 1954. There were 2,251 women delivered on the unit in those
six months. In that period there were 33 cases of rupture of the marginal sinus,
a ratio of one to 68 cases. There were only 6 cases of placenta previa and 13
cases of abruptio. The cause of bleeding could not be positively determined in
30 eases. Cervicitis, low-lying placenta, and a circumvallate placenta were
less frequent causes of bleeding.
TABLE I. CAUSES Or HEMORRHAGE, 97 CASES IN 2,251 DELIVERIES
Rupture of the marginal sinus 33 cases
Cause undetermined 30 cases
Abruptio 13 cases
Cervicitis 10 cases
Placenta previa 6 cases
Low-lying placenta 4 cases
Circumvallate placenta 1 case
I should define the qualifications that were needed for a case to be con-
sidered one of antepartum hemorrhage. Rather than base it on an estimation
of the amount of blood seen, on which two persons rarely agree, I have included
all cases in which there was enough blood loss that the patient's blood was
typed and cross-matched, the facilities for cesarean section alerted, and then
a vaginal examination performed. The qualification of preparedness for opera-
tion eliminates several eases of abortion, one of them a missed abortion. A
case of bleeding from condylomas in the vagina is also excluded
In each case of rupture of the marginal sinus the diagnosis of placenta
previa had been ruled out by failure to palpate a placenta on vagiial examina-
tion. Abruptio was dismissed as a diagnosis when neither the placenta nor
the clinical picture was considered diagnostic by the staff.
These inflexible criteria serve to prevent rupture of the marginal sinus
at this time from being a diagnosis of exclusion or elimination. Such a diagnosis
would be a had start for our comprehension of a lesion that may be entering
a renaissance.
Rupture of the Marginal Sinus
When you pick up the placentas and handle them to become better
acquainted with the marginal sinus you will see that its delicacy and peripheral
position make it vulnerable. It is easy to imagine that with the changes that
went on directly under it there could have been a disturbance, a tearing, that
permitted blood to escape The changes in the uterus that could effect this
were the uterine contractions, formation of the lower uterine segment, efface-
ment, and dilatation With slight traction on the membranes you can tear
open some sinuses. This can be visualized in the photograph, Fig. 1. There
is a possibility that inside the uterus the fetal surfaces make a traction in the
direction of the cervical os. To these changes and stresses it appears that the
edge of the placenta that is closest to the cervical os would be the most exposed
and some data that support this conjecture will be presented
Because that which transpired does so under cover, we will for the time
being have to assume that blood escapes from the marginal sinus, dissects
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Numbcr;
impTi la: AIA10.1N1L SINUS OF krENT k 9'19
between the membranes and the uterus. and makes its xvfi to the eer�ix I
think that we lui�e collected enough indireet Idellet� that just that happo.s.
It is not taking aii more liberties with our innonnation than %%e do %sith
abruptio We ha\ C seen the end results of abruptm but exactly how it tran-
spired is a surmise In some specimens I lia�e seen a track the blood made on
the (Amnon as it mode its way from the sinus iupture to the 1)1)(11111v in the
membranes (and the eer% teal us)
The -Pi eases of rupture of the marginal sinus that I lia�e rolleeted
hardl gi�e me the teinerit at this date to slate what the clinical picture of
the sildroine is. Not nian cases have been anal3zed in the literature. There
has been only one larger series of eases than mine and that contained but one
more case As I relate a description of iti patients and N% hat ha ppent'll to
them I unfortunatel3 see no elites to a predeli�er diagnosis of rupture of
the marginal sinus. There were no trends diseernible iii 1he age or race of
the patients. When more eases are collected this ma3 turn out to be a com-
plication of tiiuiltipartt . of the patients were pregnant for the first
tune iind :17 per cent had been pregnant ti�e or more times. The median length
of gestation for these cases was 36 weeks. All exeept 5 women were delivered
within two da .s of the onset of bleeding, so recurrent hemorrhage may not be
a prominent feature
Ent 1 I terus v. ith placenta in sitm shot% ing marginal sinus Eighth month of to egnuneY
( Courtesy 1)r Harold Cummins, 1)etia rtment of %maim's'. l'ulane 1 n 'rsit Y)
(inf.% 7. or 14 per vent, of thi.se women with rupture of the marginal sinus
had toxemia I /ft tin same '(l'\ tee it has ieet'iit k been tabulated that in a
period of um. ear 19 per cent of the patients had hi pertensi�e albummurie
disorders; of pregnant.% ' Thus at present it does not appear that rupture
the marginal sinus will be an added burden for toxemic women
In all eases the bleeding was painless Increase in uterine tone and
Ienderness to ti,iltituu iuial 'alPation were ne%ei deinonstrate41 hut it does not
seem to be he ((11(1 the realm of possibilitx that a coin (lion of elotted blood
at a placental margin and between the membranes and the un vie, will at some
tune cause pain If someone �Ntarts putting hail tug questions to these patients
we will presentl% ha t' revorded that some of these patients uu.i e 'ain oi
tenderness This tiw of iiNton taking has often led to a diagnosis of .ihruptio
where no abrupt to emsted
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1000 FERGUSON
Am J Obst & Gynec
May, 1955
In relation to labor, the bleeding appears to be anything but a late
occurrence. In 31 of these 49 eases the bleeding began either shortly before
labor, at the onset of labor, or early in the first stage of labor. Bleeding
began in the second stage of labor in only 5 cases.
The form in which the blood appeared was in all the forms that blood can
take. Bright red bleeding predominated. Clots and dark red blood were also
recorded. Blood in different physical forms was often seen in the same patient.
No patient showed general signs of acute blood loss. In 5 instances it was
believed the patient had lost over 500 c.c. In only 9 of the 49 women was the
estimated blood loss less than 100 c.c.
The effect of rupture of the membranes is of interest in every type of
last-trimester bleeding. I cannot say whether artificial rupture of the mem-
branes will dependably control this bleeding because it has not been tried often
enough. In 8 cases the membranes were already ruptured when the bleeding
began. The height of the placenta in the uterus would seem to make tamponade
less likely than in marginal placenta previa.
Rupture of the marginal sinus gives promise of being less hazardous for
the fetus than abruptio and placenta previa. This should not be surprising
because the blood that is lost is maternal blood, characteristically is not
great in quantity, and would not profoundly disturb the placentouterine union.
One of my babies was a 26-week stillborn but the others did not give a distinct
impression that as a group they were handicapped by the rupture of the
marginal sinus. I have data only on the immediate postnatal state of the
babies.
Thirty-six per cent of the babies in my series were premature by weight
(2,500 grams or less). As the premature rate at the Charity Hospital is about
14 per cent there may be a significant relationship between rupture of the
marginal sinus and premature birth.
I have no indication that any other pathologic condition occurs with any
frequency in association with rupture of the marginal sinus. There have been
no cases of hypofibrinogenemia. The third stage of labor appeared unaffected
At another state charity hospital two of our residents operated on a woman
because of a diagnosis of abruptio. Later they decided that the true diagnosis
was rupture of the marginal sinus. Fifty per cent of the surface of the
uterus had the discoloration typical of Couvelaire uterus.
From the data I have, let me construct a picture of the hypothetical, typical
Patient who has rupture of the marginal sinus. She is a multipara and not
yet at term. She may be of any race or age. Painless bleeding began close
to the time she thought she went into labor. The amount of bleeding was not
life-threatening When I did a vaginal examination I learned that she was
in the first stage of labor, the membranes were intact, and the placenta could
not be palpated. It did not seem to be a case of abruptio but to play it safely
I ruptured the membranes to hasten labor. Labor proceeded at a normal pace
and there was enough bleeding to be a little worrisome. The infant to my relief
did not appear to be affected by the hemorrhage. I delivered the placenta
carefully in order not to dislodge the clots. I examined the placenta immediately
and on the placental margin, at the side nearest the rent in the membranes, I
found an elongated clot. This clot w is attached to clotted blood in the
marginal sinus.
Bleeding of Undetermined Origin
In the table listing the causes of bleeding in a six-month period you may
have been surprised to see there were 30 cases in which the cause of bleeding
was unknown In the 1951-1952 series there were 30 such cases documented
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and, I am sure, many more undocumented. A digression may be in order for
a moment on this subject, which is really not remote from our attempt to
establish a place for rupture of the marginal sinus. I believe that bleeding of
undetermined origin is a comparatively frequent occurrence and that it does
not happen only at the Charity Hospital. It is an event that goes unnoted,
unremembered, unrecorded in the literature, and unmentioned in the next
clay's doctors' dressing room conversation because of a failure to provide a
dramatic quality.
When 1 read reports on the incidence and management of bleeding in the
last trimester I am surprised that in so many papers all of the cases are
neatly packaged into the various diagnoses. They are either able to make a
diagnosis in each bleeding case or are omitting cases in which the diagnosis
was uncertain. In some, if they have rupture of the marginal sinus, these
cases are being diagnosed as something else or are among the cases unmentioned.
I suspect many cases of rupture of the marginal sinus are being labeled
abruptio, low-lying placenta, or placenta previa.
This classification of bleeding of undetermined origin is slighted in many
reports because this diagnosis does not get on the face sheet, the first sheet,
of the patient's chart and is therefore uncoded. There is a code for this
diagnosis. This bleeding did not finally threaten the mother's life and did
not kill the baby so when the time came in the record library to write the
diagnosis it was forgotten. In my personal experience as a laborer in record
libraries I learned that when a woman had bled at the end of her pregnancy
and no placenta had been found over the cervical os by vaginal examination
or at cesarean section the case was often called an abruptio, possibly a "mild"
abruptio. In some medical communities "low implantation" may be popular.
Contributing to this spurious extinction of the diagnosis of bleeding of
undetermined origin is the feeling that such a diagnosis is an admission of
professional ineptitude.
Comment
Could it be possible that the placenta with the rupture of the marginal
sinus is the placenta with one edge not sufficiently low on the uterine wall to
qualify for marginal placenta or low implantation yet is low enough to have
i+- ...arginal sinus torn ny tne actions of the uterus in labor or in the prepara-
tion for labor? Some observations I have made tend to substantiate this. The
location of the laceration in the membranes often suggests that the placental
margin was not far away from the cervix. Also, if you will carefully examine
any placenta and its membranes, taking care not to extend the rent in the
membranes, you will see that this rent is usually not in the apex of the sac but
is eccentric. This year in 18 cases of rupture of the marginal sinus we noted
the relationship between the sinus rupture site and the tear in the membr&nes.
In 2 of the sacs the rent was exactly at the apex but in all of the remaining 16
specimens the sinus rupture and the rent in the sac were on the same side.
This observation seems to strengthen the concept of bleeding from the marginal
sinus.
During these months of investigation into the marginal sinus 2 normal
deliveries have occurred in which the placenta, examined immediately after
delivery, had a large clot at its margin and that clot %%as connected to clotted
blood in the marginal sinus. But there had been no bleeding at any time' In
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1002 FERGUSON
Am. J Obst. & Gynec.
May. 1955
other words it was the exact picture of rupture of the marginal sinus without
the external bleeding. At first this was rather disconcerting but have we not
always had cases of concealed hemorrhage in abruptio? So why not in rupture
of the marginal sinus? A number of reasons could be postulated why the blood
did not pry between the membranes and the uterus to the cervical os: e.g., all
of the blood promptly clotted, the blcod lacked pressure, the membranes were
too adhesive, the distance from the placental margin to the cervix was too great,
or there was not enough time. To learn if this symptomless variety of rupture
of the marginal sinus was frequent 47 placentas, taken completely at random,
were examined closely for evidence of this lesion and none was found.
It is natural that we should think of bleeding from the marginal sinus in
terms of abruptio, placenta previa, and low implantation of the placenta be-
cause they are the conditions from which it will have to be distinguished.
Jacquemier in 1839 pointedly warned against thinking that separation of the
placenta had taken place when it was only a rupture of the circular sinus. A
certain amount of blending of one of these placental complications into the
other may be inevitable.
Abruptio at times has been a diagnosis to which cases have been assigned
without sufficient justification. Abuse of the diagnosis of either abruptio or
rupture of the marginal sinus can be avoided by strict adherence to definitions.
As we collect more and more information about rupture of the marginal sinus
and it attains the secure place in our teaching and practices that it deserves,
what are we going to think about studies of abruptio that originate in institu-
tions where the diagnosis of rupture of the niarginal sinus is not made? We
are going to think that some of the abruptions were ruptures of the marginal
sinus/ When groups of cases of abruptio are reported and the cases classified
by the gravity of the condition of the mother, a large number, sometimes over
50 per cent, may be listed as "mild." Might not some of these be ruptures of
the marginal sinuses? The practical importance of this is that, when we sub-
tract these "mild" cases, abruptio becomes a more serious condition and possi-
bly the indication for radical management is augmented.
We have been thinking of abruptio in terms of reports in the journals and
in our own experience; in both of these backgrounds the cases of abruptio were
diluted with cases of rupture of the marginal sinus. Because of the grave
potentialities of abruptio it is important for us to learn more about rupture
of the marginal sinus, separate it from abruptio, and reappraise abruptio in
the light of our new information.
Is it possible that some eases of abruptio begin with rupture of the marginal
sinus? Thr, easiest way out for the blood would seem to be toward the cervical
os, drawn there by gravity, a point of lower resistance, and the myometrial
activity. Is it possible that when rupture of the marginal sinus occurs in some
selected women, for example toxemic women, the blood might dissect under
the placenta instead of between the membranes and the uterus? Could a
placenta that is altered, for example the placentas of toxemic women, be one
in which it would be easier for the blood to go under the placenta than else-
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RUPTURE OF MARGINAL SINUS OF PLACENTA
1003
where? Infarcted placentas may not be as firmly attached as others and thus
may permit blood to get under them. Only 6 placentas of abruptio have been
closely examined for details of the marginal sinus and rents in the membranrs.
For 3 of them it was simply recorded that there were clots in some portion of
the marginal sinus. In 3 more recent cases the clots in the marginal sinus
were on the same side as the rent in the membranes. These few observations
serve as nothing more than a stimulus to search further for a possible connec-
tion between abruptio and rupture of the marginal sinus.
The abnormally implanted placenta has a sinus that could be very easily
torn by the changing shape of the cervix. There is really nothing new about
this idea. It was all told in the last century. Jaequemier recognized the possi-
bility. Seventy-five years ago Duncan described bleeding from the marginal
sinus in a marginal placenta previa without detaament of the placenta. As
the marginal sinus is only a part of the uteroplacental sinus network that bleeds
in placenta previa this should not be difficult for us to accept. I have seen
placentas from cases of marginal placenta previa that were indistinguishable
from the placentas of rupture of the marginal sinus.
Summary
Rupture of the marginal sinus is found to be the most common cause of
antepartum bleeding during a six-month period that included 2,251 deliveries.
The next largest number of cases of hemorrhage was in a group in which the
cause could not be determined. Abruptio and placenta previa were less fre-
quent causes of hemorrhage. The anatomy of the marginal sinus and some
characteristics of its rupture are described. Many cases of rupture of the
marginal sinus have been misdiagnosed as abruptio, there is a need to differ-
entiate these two conditions.
References
1. Fish, J. S., Bartholomew, R. A., Colvin, E. D., and Grimes, W. it.: Ant. J OBST. & GYNEC.
61: 20, 1951.
2. Jacquemier, J. M.: Arch. gen. de med., 3rd series, 5: 330, 1839.
3. Duncan, J. M.: Contributions to the Mechanism of Natural and Morbid Parturition,
Edinburgh, 1875, A. and C. Black, p. 307.
4. Simpson, J Y.: Selected Obstetrical and Gynaecological Works, New York, 1871, D. Apple
ton and Co., p. 221.
5. Budin, P.: Bull. et mem. Soc. obst. et gynec. de Paris, p. 110, 1893.
6. Earn, A. A., an 1 Nicholson, D.: Ant. J. OBST. & GYNEC. 63: 1, 1952.
7. Turner, W.: J Anat. & Physiol. 7: 120, 1873.
8. Ferguson, J. H., and Miller, H. K.: Unpublished data.
Discussion
DR. W C. KEETTEL, Iowa City, !own.�There have been many excellent papers
written concerning placenta previa and premature separation of the placenta; unexplained
antepartum bleeding, however, although very common, has received little attention until
recently. This increased interest in placental pathology directed toward ascertaining the
cause of such bleeding is gratifying.
In die past the existence of the marginal sinus had been questioned, though now the
majority recognize the sinus as an anatomical entity. Most agree that this sinus occasionally
ruptures during pregnancy, producing varying amounts of vaginal bleeding
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1004 FERGUSON Am. J Obst &Gynec.
May, 1955
The confusing issue then is whether marginal sinus rupture is to be considered as a
new and distinct clinical entity, or should it be included as an occasional causative factor in
the bleeding of the placenta previa and premature sen .....e o' the placenta. The essayist,
along with Fish, feels that one can clearly distingu s between rupture of the marginal sinus
and premature separation of the placenta. The criteria being: (1) the presence of a clot
at the margin of the placenta that is continuous with clotted blood in the sinus, and (2)
painless bleeding at term. They mention that at times the bleeding of placenta previa and
premature separation may be caused by marginal sinus rupture.
It is hard for me to see how bleeding at the margin of the placenta, particularly where
there is an adherent clot that may depress some of the marginal placental tissue, is materially
different except in location from premature separation of the placenta. Where the mem
branes are dissected away from the decidua by bleed because this is the path of least
resistance, is this not really premature separation of the membranes and a form of placental
separation
Two years ago before this Society, Dr. Paalman discussed circumvallate placenta and
pointed out how frequently antepartum bleeding was encountered. He and others have
maintained that the bleeding with this type of placenta is due to the fragility of the decidual
covering of the marginal sinus. I wonder what Dr. Ferguson's experience has been con-
cerning this point?
In our clinic and in others the diagnosis of premature separation of the placenta
includes both the toxic and nontoxic type of separation. The diagnosis of the mild type of
separation must not be construed as a "waste basket" diagnosis as the author mentioned.
Naturally, with this broader concept, minor degrees of separation are recognized, and on
occasion even though the bleeding is painless and the uterus is nontender, if the placenta
shows significant signs of separation, they are included. Is it less exact to state that the
bleeding is from placental separation which at times is due to sinus rupture than to state
that marginal sinus rupture is a distint clinical entity',
Sexton, Hertig, Reid, and Harris have written concerning this problem and have felt
that the rupture of the marginal sinus should be included as one of the causes of nontoxic
placental separation. To me this seems more logical and will lead to far less confusion. The
treatment by necessity must be the same as that employed in the management of mild nontoxic
separation, since the diagnosis cannot be made until after the delivery of the placenta.
This presentation has been well organized and presented and I have enjoyed reading it
The paper emphasizes the following points. (1t There are many causes of antepartuni
bleeding (2) The treatment of antepartum bleeding must be individualized according to
the eausp. ( ) Abdominal delivery should never lie resorted to for the treatment of
undiagnosed antepartum bleeding (.1) Significant bleeding from the marginal sinus does
occur.
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TOXEMIA OF PREGNANCY AT THE
CHARITY HOSPITAL IN NEW ORLEANS
JAMES HENRY FERGUSON, M.D., F.A.C.S., Miami, Florida, and
HENRY K. MILLER, M.D., Baton Rouge, Louisiana
Reprint from
SURGERY, Gynecology & Obstetrics
SEPTEMBER, 1955
VOLUMh 101,257-268
Copyright, 1955, by The Franklin H. Martin Memorial Foundation
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TOXEMIA OF PREGNANCY AT THE
CHARITY HOSPITAL IN NEW ORLEANS
JAMES HENRY FERGUSON, M.D., F.A.C.S., Miami, Florida, and
HENRY K. MILLER, M.D., Baton Rouge, Louisiana
MANY NEW ORLEANIANS have been asked,
"What is toxemia of pregnancy like at the
Charity Hospital? You have more deliveries
than any other hospital in the United States
and you are reputed to have so much toxe-
mia. How much do you really have? Is
toxemia frequent because you have such a
large Negro population? Do many of these
women have chronic hypertensive disease?
Is the fetal loss from toxemia high? How
many of these patients do you section?"
The present article attempts to define the
problem of toxemia of pregnancy at the
Charity Hospital and to answer the above
questions. To accomplish this the authors
personally reviewed the hospital records of
all of the women who were delivered on the
Tulane Service of the Charity Hospital in
1 calendar year, 1950. With the use of rigid
definitions, we selected the patients who had
toxemia and grouped them according to
their type of toxemia. The hospital records
of the babies born to these mothers were
From the Department of Obstetrics and Gynecology, School of
Medicine, Tulane University, and the Charity Hospital of
Louisiana at New Orleans.
Huidols IBancroft, Ph.D., Professor of Biostatics, Tulane Uni-
versity, aided in designing and interpreting this survey.
also examined. A number of important data
on the course of pregnancy and fetal out-
come were collected and analyzed. This
afforded an opportunity to compare our ex-
perience with that of other hospitals, to
evaluate our treatment and to provide base
lines for current and contemplated research.
The investigation was started in early
1952, and the year 1950 was selected for no
other reason than that it was the most re-
cently completed calendar year which al-
lowed sufficient time to assume that hyper-
tension would persist indefinitely. There is
no reason to doubt that 1950 is a representa-
tive year.
The patients studied in this report con-
stitute a fair sample of the hospital's pa-
tients. The Tulane Service gives maternity
care to approximately 40 per cent of the pa-
tients delivered in the hospital, and there is
no bias in the selection of patients for the 3
services of the hospital.
In 1950 the number of mothers who were
delivered on the Tulane Service was 3,899.
The hospital records of 4 mothers and of 4
babies of toxemic mothers, all unrelated,
could not be found. We verified that these 4
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2 Surgery, Gynecology & Obstetrics � September 1955
mothers were discharged alive from the
hospital.
A 1 year record may introduce some
sampling error and where this is possible,
restraint will have to be used in drawing
conclusions. For example, the incidence and
outcome of comparatively unusual cases,
like abruptio placenta, may be awry in a
period of 1 year. However, a 1 year sample
would be sufficient to make valid conclu-
sions on the frequency of the various types of
toxemia, perinatal mortality, antepartum
care, age, parity, residence, and birth
weights.
BACKGROUND OF THE PATIENTS
The patients cared for at the Charity
Hospital in New Orleans are drawn from
the poorer people of the State of Louisiana.
Financial eligibility for admission is deter-
mined on an individual basis. Couples with
an expected child or 1 child must not have
an income in excess of 175 dollars a month.
In 1950, 82 per cent of all the women de-
livered on the Tulane Service were Negroes.
Approximately 65 per cent of the births at
the hospital were to moths from New
Orleans, the remainder coming 'from other
parts of the state. The percentages of white
and Negro toxemic women with residence
outside of New Orleans were 53 per cent
and 45 per cent, respectively. These figures
may indicate that there is no decided tend-
ency for women of a particular race to come
to the Charity Hospital from outside of New
Orleans because of this complication.
The diets of the women attending our
antepartum clinics have been found by Fer-
guson and Hinson to be about the poorest
recorded in the United States (13, 16). Only
4 per cent of 209 women were eating the
recommended daily allowance of 85 grams
of protein. In a random sampling of 24 hour
food consumption, 45 per cent of the women
had had no milk, 31 per cent no meat, 66
per cent no egg, and 28 per cent no vege-
table or fruit.
Attendance at clinic is not good. Nineteen
per cent of the toxemic women described in
this article had no antepartum care and 20
per cent made only 1 to 4 antepartum visits.
Thirty-three per cent of the toxemic mothers
did not return for a postpartum visit.
CLASSIFICATION OF TOXEMIA
In this report the terms "toxemia of preg-
nancy," "toxemia," and "toxemic" will
have their broadest connotation, embracing
all of the hypertensive and albuminuric dis-
orders of pregnancy. "Pre-eclampsia" and
"pre-eclamptic" will be used only in the
sense defined later. Each case of toxemia is
assigned to one of the following subgroups:
(1) pre-eclampsia; (2) eclampsia; (3) chronic
hypertensive diseaze; (4) chronic hyper-
tensive disease with superimposed pre-
eclampsia; (5) unclassified.
The reported incidence of toxemia in a
hospital depends on who writes the diagnosis
on the face sheet of the hospital chart and
what he uses as criteria of diagnosis. For this
study the following definitions were uni-
formly used by the authors for the evalua-
tion of each patient's chart and for the de-
termination of the diagnosis. The definitions
were patterned after those in the Williams-
Eastman textbook because it was used by
the Tulane medical students. The classifica-
tion adopted in 1952 by the subcommittee of
the American Committee on Mater nal Wel-
fare was not available when we started this
study.
DEFINITIONS
Hypertension. Hypertension is the observa-
tion of a systolic blood pressure of 140 milli-
meters of mercury or above, or a diastolic
blood pressure of 90 millimeters of mercury
or above. The elevation must be found on at
least 7 iccasions 24 or more hours apart.
Albuminuria. A patient has albuminuria
when there is a definite positive test for pro-
tein with a catheter specimen of urine that is
devoid of pus and blood.
Pre-eclampsia. Pre-eclampsia is defined as
hypertension or albuminuria that develops
after the twenty-fourth week of pregnancy
and disappears after delivery.
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TABLE 1 �TOXEMIA OF PREGNANCY
Diagnosis
Toxemia (all cases)
Pre-eclampsia
Eclampsia
Chronic hypertensive disease
Chronic hypertensive disease with
superimposed pre-eclampsia
Unclassified
Ferguson, Miller: TOXEMIA OF PREGNANCY 3
AT CHARITY HOSPITAL OF LOUISIANA IN NEW ORLEANS, TULANE
SERVICE, 1950
Incidence
on
No. of service
Calls Per cent
Per cent
of
toxemic
patients
Live _Stillbirths_ Neonatal Prematures
births No. Per cent deaths (live)
736
19
709
49
6.5
21
109
349
9
47.4
349
13
3.6
4
34
10
0.3
1.4
13
1
�
5
8
180
4.6
24.2
167
19
1(1.6
5
30
167
4.3
22.7
158
14
6.4
3
29
30
0.8
4.1
28
2
1
8
Chronic hypertensive disease. Patients with
chronic hypertensive disease are those in
whom hypertension appears before the
twenty-fourth week of gestation and persists
indefinitely after delivery.
Chronic hypertensive disease with superimposed
pre-eclampsia. Patients with chronic hyper-
tensive disease who have superimposed pre-
eclampsia are those who develop further
elevation of systolic blood pressure of 30 or
more millimeters of mercury, further eleva-
tion of the diastolic pressure of 15 or more
millimeters of mercury, or albuminuria.
Difficulties of classification. Many unques-
tionable cases of toxemia were difficult to
classify because of an insufficient number of
observations on the patients. This was usually
due to the patients' laxity in participating in
antepartum care and in returning for the
postpartum visit. Women referred to the
hospital were often not accompanied by a
case record. Even when the patients' records
furnished what should have been sufficient
data, classification was sometimes difficult
because the cases did not fit well into the
classification used here (nor the classifica-
tion formulated by the American Commit-
tee on Maternal Welfare). Perplexing hy-
pertension ensembles which recurred with
some regularity were: (a) hypertension that
began after the twenty-fourth week of preg-
nancy and persisted indefinitely, (b) hyper-
tension in several pregnancies, and blood
pressure normal in the 1950 pregnancy until
the end of pregnancy, when hypertension
reappeared, (c) hypertension that appeared
late in two or more pregnancies and late in
the 1950 pregnancy but was inconsistently
found in the intervals between pregnancies,
(d) hypertension at the postpartum visit and
only then, (Meyer has described the local
experience with this phenomenon and Kal-
treider and Gilbert the experience else-
where), (e) hypertension that began before
the twenty-fourth week of pregnancy and
was not present at the postpartum visit or in
a subsequent pregnancy, (f) hypertension in
2, 3, or more pregnancies and at postpartum
visits, but did not appear in the 1950 preg-
nancy. (a), (b), and (c) are considered in
this report to have chronic hypertensive dis-
ease. So frequently was it difficult to decide
which were chronic hypertensive diseases
and which was pre-eclampsia that we were
tempted to suggest that they were not two
diseases but one.
Albuminuria in labor. There was no attempt
made to separate cases in which albuminuria
was found only during labor from those in
which it was discovered at other times.
Ideally this should be done. The observation
that labor can cause transient albuminuria
without other evidence of toxemia has been
made variously. Winnifred Seegars exam-
ined catheter specimens of 50 nontoxic
women in labor at the Sara Mayo Hospital,
New Orleans, and found that 16 gave a
positive test for protein. Douglas remarked
that at the New York Lying-in Hospital pro-
tein was observed in the urine of the major-
ity of normal women at the time cf delivery.
INCIDENCE OF TOXEMIA
Seven hundred and thirty-six mothers on
the Tulane Obstetric Service had toxemia of
pregnancy in 1950. This is an incidence of
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4 Surgery, Gynecoloo & Obsteirics � September 1955
19 per cent. A separation of thew! cases into
the various subgroups of toxemia is given in
Table I and the subgroups are individually
considered later in this paper. There was 1
maternal death.
It is impossible to z-o.-npare accurately our
incidence of toxemia with those of other hos-
pitals because of the differences in definitions
and methods of reporting. Compar;sons of
the frequency of toxemia in the local popu-
lations are even less reliable because of dis-
similarities in the service that each report-
ing hospital performs in its community, the
differing eligibility of patients for hospital
admittance, varying regional dependence as
a referral point for seriously ill patients, and
other selective factors that would not be
recognized by the casual reader. These
shortcomings should be kept in mind as we
examine the frequency with which some
hospitals have recently been seeing toxemia.
By any standard the Charity Hospital pa-
tients have a good deal of toxemia. The
figure of 25.2 per cent for nonconvulsive
toxemia at the "University of Tennessee-
Gaston, 1946-1949" (given by Dieckmann)
is the only higher incidence we can find.
Wellen (28) reported an incidence of 5.17
per cent of hypertensive conditions in preg-
nancy at the Bellevue Hospital in a 15 year
period ending in 1950. Lundgren reported
that the incidence of toxemia in 1950 at fhe
Margaret Hague Maternity Hospital was
11.9 per cent. From the ward service of the
Sloane Hospital for Women, 1931 to 1950,
the toxemia rate was 12.2 per cent. In 1947
to 1949, 3.1 per cent of the parturients were
toxic at the Royal Victoria Montreal
Maternity Hospital.
The high rate of toxemia at the Charity
Hospital is probably not because of its large
colored census. In 1950, 18 per cent of the
women delivered on the Tulane Service
were of the white race and 17 per cent of
the toxemic mothers were white. The pro-
portion of the women in the pre-eclampsia-
eclampsia groups that were white was 21
per cent; 12 per cent of the chronic hyper-
tensive women were white.
This investigation provided a unique op-
portunity to measure the incidence of toxe-
mia, and each of its components, in a popu-
lation. In 1950, 89 per cent of all the Negro
babies born in New Orleans to mothers with
residences in New Orleans were born at
Charity Hospital. This is a relatively high
proportion of all the Negro babies born in
New Orleans. It has previously been stated
that the mothers on the Tulane Service are
an unbiased sample of the mothers delivered
at the hospital and should be considered
adequate for the estimation of the frequency
of toxemia in the Negro population. The
residence and race of each mother w-re
recorded in this survey and from these data
it is estimated that approximately 19 per
cent of the Ne Orleans Negro mothers
must have toxe.nia.
PRE-ECLAMPSIA
The number of mothers who had pre-
eclampsia was 349. They represented 9 per
cent of the entire service and 47 per cent of
the toxemic patients. Forty-seven per cent
of these pre-eclamptics were primigravidas
and 32 per cent were 19 years old or younger.
The incidence of pre-eclampsia among all
the Negro women on the service was 8.6 per
cent.
This incidence of pre-eclampsia would
have been much higher if, instead of the
requirement that hypertension be observed
on 2 occasions 24 or more hours apart, we
had used the American Committee on
Maternal Welfare's classification, which
utilizes a 6 hour interval. If that commit-
tee's criteria of edema and weight gain had
been used to diagnose pre-eclampsia, a very
much greater number of women would have
to be considered pre-eclamptic. Our insist-
ence that albuminuria be claimed only on a
catheter specimen devoid of pus and blood
reduced the number of patients diagnosed as
pre-eclamptic. The diagnosis was based on
albuminuria alone in 5 cases.
To make certain that our collection of
pre-eclamptics was not heavily weighted
with women who had minor hypertension
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those women who had minimal blood pres-
sure elevation were sorted. There were 61
women, 17 per cent of all the pre-eclampti-s,
whose systolic blood pressure was always
recorded as below 146 millimeters of mer-
cury and whose diastolic blood pressure was
always below 96 millimeters of mercury.
These women had no perinatal fetal deaths.
Some of our eclampsia appears in women
with these false security engendering levels
of hypertension; we will have to continue
treating with vigor these "mild" cases.
When we compared the monthly inci-
dences of pre-eclampsia in 1950 we saw no
seasonal trend except for an unremarkable
tendency to be more frequent in January
through May. The monthly rate ranged
from a low of 4.3 per cent in November (the
month in which most eclampsia appeared!)
to 12.2 per cent in March.
"Severe" pre-eclampsia is frequently de-
fined as pre-eclampsia marked by a systolic
blood pressure of 160 millimeters of mercury
or over, or a diastolic blood pressure of 110
millimeters of mercury or over. The same
definition will be used in this essay. One
hundred and seventy-three women, which
was 50 per cent of our pre-eclamptics, quali-
fied for this category. They provided 10 of
the 13 stillborn babies that the pre-eclamp-
tic women had.
It has been said that modern antepartum
care has not reduced the frequency of pre-
eclampsia but it has curbed severe pre-
eclampsia and eclampsia. This has also been
our impression. Wellen claimed that at the
Bellevue Hospital antepartum care did not
influence the incidence of severe pre-eclamp-
sia (27). For each toxemic woman in this
Charity Hospital study, the week she began
antepartum care and the number of her
visits were recorded. Similar data are not
available from any large group of normal
patients at this hospital for comparison. An
attempt was made with this information to
show that early institution of antepartum
care and a greater number of visits increased
the likelihood of the mild form of this com-
plication rather than the severe form. The
Ferguson, Miller: TOXEMIA OF PREGNANCY 5
week in which antepartum care began was
plotted against the number of isits and
many comparisons made between the pa-
tients with mild pre-eclampsia and those
with severe pre-eclampsia. As far as these
dati could demonstrate there were no dif-
ferences between the mild and the severe
pre-eclamptics that were statistically signi-
ficant. Because of the numerous variables
involved we do not believe that these obser-
vations disprove that good antepartum care
prevents severe pre-eclampsia.
Seventy-six of the women with pre-
eclampsia were hospitalized before labor for
a total of 410 hospital days, an average of
5.4 days per hospitalized pre-eclamptii pa-
tient.
Fifteen of the pre-eclamp tic women (4 per
cent) were delivered by cesarean section,
only 4 of those because of the pre-eclampsia.
These pre-eclamptic mothers had only 13
stillbirths (3.6 per cent) and 4 babies that
expired in the neonatal period. This is a
perinatal death rate of 4.8 per cent, or 49
per thousand live births.
In 1950 our management of pre-eclampsia
and other forms of toxemia was generally
conservative. The low section rate speaks for
itself. Immediate hospitalization Jn the ap-
pearance of pre-eclampsia was desired but
was an ideal frequently unattained. In the
hospital bedrest and sedation were the main-
stays of therapy; phenobarbital was the drug
used most often, while morphine or meperi-
dine were used when greater sedation was
indicated. Ammonium chloride and 10 per
cent dextrose infusions were close to routine
measures. Mercurial diuretics were used in-
frequently then and on an experimental
basis. Hypotensor drugs were untried.
The choice of induction of labor was in-
fluenced by response to treatment, severity
of the pre-eclampsia, week of gestation, size
of the fetus, distance from home to hospital,
tractability of the patient and favorableness
of the cervix. Seven per cent of the pre-
eclamptics had induced labors that could be
recognized by reading their charts and the
most frequent method was pitocin infusion.
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6 Surgery, Gynecology & Obstetrics � September 1955
Stimulation of the uterus by "stripping" of
the membranes during vaginal examination
was widely practiced. Local anesthesia for
delivery was frequently used and general
anesthesia comparatively little.
ECLAMPSIA
There were 10 cases of eclampsia on the
TulaLie Service, in 1950. These patients
formed 0.26 per cent of all the patients de-
livered on the service and 1.4 per cent of the
toxemic patients. Two of these patients had
no antepartum care and 1 had been attended
by an outside practitioner. Only 1 eclamptic
had made more than 1 antepartum visit.
Half of the eclamptics lived outside of New
Orleans.
Youth predominated in this group. Only
1 was over 30 years of age. All were Negroes.
Seven were primigravidas. Our convulsive
toxemia showed some tendency to be grouped
together by month. Four cases appeared in
November, 2 in September, and 2 in March.
One patient was delivered by cesarean
section. There was only 1 stillborn and that
infant was born at home without an attend-
ant. The patient was transferred to the hos-
pital after delivery and had a postpartum
convulsion. She had had no antepartum
care. One mother had twins that survived
and another had quintuplets that all died in
the neonatal period. There were 3 prema-
ture babies among the single births and all
survived; 1 was of less than 28 weeks' gesta-
tion.
The treatment of eclampsia followed
closely that of pre-eclampsia. No unusual
techniques were used until tracheotomy was
introduced in November 1950, for the
eclamptic with respiratory embarrassment.
It was used in one of these patients and has
been increasingly used since.
CHRONIC HYPERTENSIVE DISEASE
There were 347 women with chronic
hypertensive disease delivered on the Tulane
Service in 1950. This number constituted 47
per cent of the toxemic patients and 9 per
cent of all the patients delivered in that year.
Thus the Tulane experience was compost..!
of almost exactly the same number of women
with chronic hypertensive disease as with
pre-eclampsia. Eighty-eight per cent of the
women with this persistent hypertension
were Negroes and they formed 9.5 per cent
of all the Negro women delivered on the
service. Of the 347 women with chronic
hypertensive disease, 167 (48 per cent) had
superimposed pre-eclampsia as described in
"Definitions." The women with and those
without superimposed pre-eclampsia are
discussed jointly in this section and will
be considered separately in the two succeed-
ing subsections.
As anticipated, these women were older
parturients. Forty-six per cent were 30 years
of age or over and 7 per cent were 40 years
or over. Nevertheless, chronic hypertensive
disease proved to be a disease not exclusively
of older nor of multiparous women. Forty-
eight women were pregnant for the first time
and 29 were less than 20 years of age.
The women with a chronic hypertension
background provided a formidable portion
of the stillbirths born to toxemic mothers,
specifically 33 stillbirths or 70 per cent of all
the dead born babies. However, the effect of
a chronic hypertensive condition on our
prospects of a Jive baby were not as pessi-
mistic as others have found nor was the still-
birth rate adversely affected by the super-
imposition of pre-eclampsia.
Due to their small number these cases
cannot validly be used to test the thesis that
it is better, from the viewpoint of fetal sal-
vage, to induce labor rather than to wait for
a spcntaneous onset. It is impossible to learn
from the patients' records how many had
their date of delivery advanced by vigorous
loosenings of the membranes during vaginal
examinations. Furthermore, as would be
expected, the patients with the greatest
hypertension, the most intractable albumi-
nuria, and the poorest fetal survival record
were in general the ones selected for induc-
tion. Thirty-six patients with chronic hyper-
tensive disease (17 of them with superim-
posed pre-eclampsia) were induced by one
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of the more overt methods and they deliv-
ered 7 stillborns. The mothers of 6 of these 7
stillborns also had abruptio, so possibly the
abruptio was the indication for induction
rather than the hypertensive disease.
Conservatism ruled in the management of
chronic hypertensive disease. Only 1.7 per
cent of all the chronic hypertensive women
had cesarean section primarily because of
the hypertension. The Negro chronic hyper-
tensives who availed themselves of ante-
partum care were seen in a special toxemia
clinic because of the unwieldiness of the
large regular clinics. The conduct of this
clinic has been described by one of us (10).
No therapeutic abortion could be found in
the records. Hospitalization was the rule
when pre-eclampsia appeared and the hos-
pital management was as described under
"Pre-eclampsia."
Without superimposed pre-eclampsia. There
were 180 women who had chronic hyper-
tensive disease and who avoided the super-
imposition of pre-eclampsia. This was 24
per cent of all the toxemic mothers and 52
per cent of the chronically hypertensive
women.
To learn if these 180 patients included
many with a minimal blood pressure eleva-
tion we separated all women whose systolic
blood pressure throughout this pregnancy
was below 146 millimeters of mercury and
the diastolic pressure below 96 millimeters
of mercury. There were 30 such cases. It is
worth noting that in this group of 30 women
with "mild" hypertension there were 5 pe-
rinatal fetal deaths.
Many of the women in this category had
had toxemia of pregnancy before: 27 once
before, 27 twice, 14 thrice, and 9 had it 4 or
more times. With complete records of the
patients' past experiences these figures would
be higher. Many had been attended previ-
ously by midwives and their blood pressures
had been observed only recently in life.
Needless to say, no meaningful observations
could be made on the frequency of the
various types of toxemia that they had had
in earlier pregnancies.
Ferguson, Miller: TOXEMIA OF PREGNANCY 7
Eleven of these women were delivered by
cesarean section, only 2 of them directly be-
cause of the hypertension.
This group provided 19 dead born in-
fants, an incidence of 11 per cent; 11 of
these infants weighed 2,500 grams or less.
There were 22 liveborn premature infants,
4 of whom had neonatal deaths; 3 of the
survivors weighed less than 1,000 grams at
birth. One mature baby died in the neo-
natal period.
With superimposed pre-eclampsia. There were
167 women with chronic hypertensive dis-
ease and superimposed pre-eclampsia. Thus
48 per cent of the women with chronic
hypertensive disease had this augmentation
of their difficulties. Our patients with chronic
hypertensive disease had a chance of devel-
oping pre-eclampsia which was not quite 5
times greater than that of our normott�isive
women in 1950. Jones reported from the
Providence Lying-in Hospital that patients
with essential hypertension had 14 times the
usual expectancy of eclampsia. At the Mar-
garet Hague Maternity Hospital Lundgren,
McCaw, and Burnett and their associates
found that 24 per cent of the chronic hyper-
tensive women had pre-eclampsia in 1950,
while one-third and one-fifth of them had it
in 1949 and 1948.
Sixty-six of the women in tit :2 group had
been hospitalized before labor because of
their pre-eclampsia for a total of 608 days,
an average of 9.2 days per patient.
Using the previously cited qualifications,
the condition of only 26 of these women
(16 per cent) could escape being called
"severe."
As in the other group of women with
chronic hypertensive disease, documented
pr vious episodes of toxemia were common
despite incomplete past histories. Thirty-one
women were known to have had toxemia
once before, 20 twice 15 thrice, and 10 had
it A or more times.
hese patients showed no distinctive
monthly trend in the onset of pre-eclampsia.
The blood pressure standard for this diag-
nosis could 1,3e more sharply defined. In its
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8 Surgery, Gynecology & Obstetrics � September 1955
present form it allows considerable latitude
on the part of the man who determines the
diagnosis in each case. In this survey any
further elevation or the prescribed magnitude
(30 systolic or 15 diastolic) that occurred
in the latter weeks of pregnancy satisfied
the blood pressure qualification. This highest
blood pressure was compared to the highest
obtained earlier in this pregnancy. The
physiologic lowering of the blood pressure in
mid-pregnancy served to confuse. Fifty-nine
of these 167 women had albuminuria and
allowed no equivocation. Because the sepa-
ration of chronic hypertensive disease and
that disease with superimposed pre-eclamp-
sia was difficult in so many instances we
were made freshly aware that the borderline
between chronic hypertensive disease and
pre-eclampsia was indistinct enough to chal-
lenge its existence.
The patients with chronic hypertensive
disease and those with chronic hypertensive
disease plus pre-eclampsia were compared to
see if any prophylactic effect of antepartum
care could be observed. The contrast was
made by means of data on the week of gesta-
tion that antepartum care was started and on
the numbei of visits, exactly as was done in
the analysis of mild pre-eclampsia and severe
pre-eclampsia. These aspects of antepartum
care could not be demonstrated to have in-
fluenced whether or not a patient with
chronic hypertensive disease acquired pre-
eclampsia. Again, the variables involved are
numerous, and we do not claim that ante-
partum care is unimportant in the worsening
of this hypertensive syndrome.
Two select groups of women with chronic
hypertensive disease at the Charity Hospital
clinics are available for comparison with the
1950 patients. Twenty-eight women who as
controls received a placebo in a clinical ex-
periment began antepartum care by at least
the twentieth week of pregnancy and were
usually seen weekly in a special clinic. They
had a 37 per cent incidence of superimposed
pre-eclampsia (9). A similar control group of
139 cnronic hypertensive women who re-
ceived unusually close attention had 27 per
cent of its members develop a superimposi-
tion of pre-eclampsia (12). The lower inci-
dence of pre-eclampsia in these groups sug-
gests that careful antepartum treatment is
an important factor in curbing this com-
plication.
Thirteen women had 'cesarean section, 4 of
them primarily because of toxemia.
There were 14 stillbirths, an 8 per cent
incidence in the subgroup, of which 2 were
plural births and 3 were premature. In this
classification of toxemia our fetal survival
record continues to compare favorably with
that reported elsewhere. In the Margaret
Hague Maternity Hospital the superimposi-
tion of this acute illness on chronic hyper-
tensive disease raised the fetal loss from 18.5
per cent to 50 per cent, according to Cos-
grove and Chesley. Contrary to the usual
experience, our stillbirth and perinatal death
rates were slightly less in the chronic hyper-
tensive women who had superimposition of
pre-eclampsia. Why this should be so can
only be guessed. Possibly the appearance of
pre-eclampsia spurred the decision to ter-
minate pregnancy rather than to allow it to
go through the perilous later weeks of a hy-
pertensive pregnancy. The slightly higher
percentage of cesarean section, induced la-
bors, and premature babies in the super-
imposed pre-eclampsia group suggests this is
what happened.
UNCLASSIFIED
Thirty women are placed in an unclassi-
fied group because they uadoubtedly had
toxemia, and we cannot accurately cata-
logue them at this time. The inability to
classify the cases is usually due to nonap-
pearance except for delivery, desertion, or
referral without a case history. No woman
included here, or elsewhere in this report,
had the symptom complex frequently termed
"chronic nephritis." There were no cases of
glomerulonephritis. Section was performed
in 3 cases, in 1 of them for toxemia. The
only noteworthy observation on the babies is
that there were 2 stillborns, 10 premature
births, and 1 neonatal death.
t
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FETAL OUTCOME
These 736 toxemic mothers had 709 live
born babies of which 45 were plural births.
Not distinguishing live born and dead born,
there were 22 sets of twins and 1 set of quin-
tuplets.
There were 49 stillbirths including plural
births and babies of all weights. This is 6.5
per cent of all the babies delivered of toxemic
mothers and a stillbirth rate of 69.1 per
thousand live births. This is almost treble
that of the hospital rate. In all of our figures
on fetal outcome embellishing corrections
are not made for any factor. All infants born
in the delivery unit or en route to it are in-
cluded. It will be noted simply that these 49
stillbirths included 29 premature, 4 plural
births, and 7 infants of less than 28 weeks'
gestation. Patients of 20 weeks' gestation or
over are admitted to the delivery unit; the re-
mainder of the pregnant women go to a
gynecology ward. The stillbirth rates for the
service or the hospital in 1950 are not avail-
able for comparison. The most pertinent
figure that has been computed is the still-
birth rate of 27.7 per thousand live births at
the Charity Hospital for the year ending
June 30, 1953.
The analysis of fetal survival in each of the
subgroups is given in the paragraphs dealing
with them and in Table I. Chronic hyper-
tensive disease was more lethal for the fetus
than the acute forms of toxemia. The mothers
with pre-eclampsia-eclampsia had 23 peri-
natal fetal deaths, an incidence of 6 per cent.
The mothers with chronic hypertensive dis-
ease, both with and without superimposed
pre-eclampsia, had 44 perinatal fetal deaths,
or 13 per cent. The probability of this differ-
ence occurring by chance is less than 1 in
1,000. To test further the peril to the fetus
from chronic hypertensive disease, the peri-
natal fetal mortality of pre-eclampsia-
eclampsia can be compared to the 15 per cent
perinatal mortality rate of chronic hy-
pertensive disease without superimposed pre-
eclampsia. Again, the probability of this
difference occurring by chance is less than
1 in 1,000.
Ferguson, Miller: TOXEMIA OF PREGNANCY 9
Our stillbirth rate of 6.5 per cent and peri-
natal rate of 9.2 per cent compare well with
figures published from other hospitals. Keep-
ing in mind the lack of uniform standards, we
can note that Cosgrove and Chesley an-
nounced an infant death rate of about 50 per
cent in superimposed pre-eclampsia (ours,
8.2 per cent). At the Margaret Hague Ma-
ternity Hospital in 1950 the stillbirth rate for
toxemia was 15 per cent. Wellen (27) re-
ported an infant mortality of 12.4 per cent in
specific hypertensive disease and 15.3 per
cent in essential hypertension at the Bellevue
Hospital. Jones recorded that at the Provi-
dence Lying-in Hospital mild hypertensive
disease with superimposed pre-eclampsia
had a perinatal mortality of 21.9 per cent.
From the Liverpool Maternity Hospital,
Hamilton and his associates quoted a peri-
natal mortality rate of 19.7 per cent for pre-
eclampsia. Agilero reported from Caracas a
death rate of 20 per cent, 4 times that of the
hospital. At the Royal Victoria Montreal
Maternity Hospital, Hendelman and Phil-
pott had an uncorrected fetal mortality of 43
per cent in severe pre-eclampsia and 5.3 per
cent in mild pre-eclampsia. The total fetal
loss with nonconvulsive toxemia at the Chi-
cago Lying-in Hospital (1940-1950) was re-
ported by Dieckmann as 7 per cent (7). A
more complete record of the fate of the fetus
in toxemia can be found in a paper of Taylor
and associates; we appear to have better re-
sults than are generally being reported.
Prematurity. A premature infant is defined
here as one with a birth weight of 2,500
grams or less. These 736 toxemic mothers had
109 live prematures. This is an incidence of
prematurity, as usually computed, of 15 per
cent. There were also 29 dead born prema-
ture babies. The incidence of prematurity
among all the mothers on the Tulane Service
or in the entire hospital in that year is not
available for comparison. The most germane
figure at hand is the 14 per cent incidence of
prematurity for the hospital in 1952 to 1953.
These two 12 month spans should be com-
parable. Thus it seems that toxemia cannot
account for the high incidence of prematurity.
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10 Surgery, Gynecology d..7 Obstetrics � September 1955
The number of premature babies produced
in each classification of toxemia is given in
Table I. The chronically hypertensive moth-
ers had 59 premature babies and the almost
equal size pre-eclampsia-eclampsia group
had 42 premature babies.
Six of these premature infants resulted
from cesarean sections done because of tox-
emia and 18 prematures were born following
induced labors. The inability to say exactly
how many had induced labors has already
been explained. Twenty-one of the babies
born alive weighed 1,500 grams or less and
13 weighed 1,000 grams or less. Among the
total of 70 stillborns and neonatal deaths
there were 44 prematures.
.Neonatal deaths. All infants dying within 30
days of birth are here considered neonatal
deaths. There were 21 neonatal deaths of
infants born to these toxemic mothers. This is
a neonatal death rate of 29.6 per thousand
live births. The only figure at hand for com-
parison is the hospital rate of 23.4 per thou-
sand live births in 1952 to 1953. Fifteen of the
1950 deaths occurred in premature infants, 5
of whom were under 1,000 grams at birth.
The number of babies born to the mothers
with each toxemia diagnosis were: pre-
eclampsia, 4; eclampsia, 5 (quintuplets);
chronic hypertensive disease, 8; chronic hy-
pertensive disease with superimposed pre-
eclampsia, 3; unclassified, 1.
As in other hospitals our follow-up on neo-
natal survival is not complete. Healthy
mothers and babies are usually discharged
on the second or third postpartum day. A
good number of the babies are brought back
to this hospital for subsequent care for the
same reasons that brought the mother to the
hospital so surveillance during the neonatal
time is reasonably good.
Malformations. Among the 740 live and
dead born babies there were 13 considered
to have major anomalies, an :ncidence of 1.7
per cent. There was no remarkable distribu-
tion of the cases among the various types
of toxemia. Although we do not have a
figure for the general incidence of anomalies
in the hospital, our percentage for babies of
toxemic mothers does not seen. to support
the concern of de Watteville and others over
a meaningful concurrence of fetal malforma-
tion and toxemia.
One baby had congenital syphilis. The
diagnosis of retrolental fibroplasia was not
made on any baby.
MISCELLANEOUS
Abruptio. There were 24 cases of abruptio,
3 per cent of the toxemia cases. They were
distributed as follows: pre-eclampsia, 5;
eclampsia, 0; chronic hypertensive disease,
12; chronic hypertensive disease with super-
imposed pre-eclampsia, 5; unclassified, 2.
Six of the cases were terminated by cesarean
section with 7 perinatal deaths (twins) and
18 ended in vaginal delivery with 10 peri-
natal deaths.
Bieber reported that in 1942 to 1952 the
incidence of abruptio at the Charity Hospital
was 0.44 per cent. On the Louisiana State
University Services at the Charity Hospitals
in New Orleans and Lafayette, Tatum found
an abruptio occurrence of 0.5 per cent. It is
important to realize that until 1951 the diag-
nosis of rupture of the marginal sinus was
not recorded at the Charity Hospital; figures
on abruptio under these conditions may be
open to some adjustment (11).
Anemia. Practically every woman had a
hemoglobin or hematocrit determination on
admission. In this report hemoglobins of less
than 10 grams per 100 milliliters or hemato-
crits of less than 30 per cent are considered
evidence of anemia. When there was dis-
agreement in the two tests a mean corpuscu-
lar hemoglobin concentration of less than 30
is used for the criterion of anemia. There
were 43 women (6 per cent) with anemia.
The distribution of anemia was pre-eclamp-
sia, 20 cases; eclampsia, 2; chronic hyper-
tensive disease, 8; chronic hypertensive dis-
ease with superimposed pre-eclampsia, 12;
unclassified, 1.
Diabetes. Five mothers were diabetic. Each
had a live baby that survived. One had a
cesarean section because of the diabetes and
the remainder had spontaneous labors and
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deliveries. In 1950 early delivery of diabetics
was not practiced as frequently as now.
Pyelonephritis. Twenty women (3 per cent)
were treated in the hospital for pyelonephri-
tis. Undoubtedly there were others treated
on an outpatient basis.
Heart disease. Ten women were recognized
as having heart disease that antedated the
1950 pregnancy. Five were clearly due to
rheumatic fever. This group does not include
women with long standing hypertensive car-
diovascular disease and minor depletions of
cardiac reserve.
Cesarean section. Forty-one patients (6 per
cent) had cesarean sections. The primary in-
dications were listed as: toxemia 12, dispro-
portion 10, previous section 9, abruptio 5,
faulty presentation 3, placenta previa 1, and
diabetes 1.
Eye grounds. One hundred and thirty-five
women had ophthalmoscopic examinations
and 80 (59 per cent) were considered ab-
normal. The group with chronic hyperten-
sive disease and superimposed pre-eclampsia
had the greatest number examined and
greatest percentage with abnormal fundi.
Electrocardiograms. Significant electrocar-
diographic changes were found in 36 (18
Fr cent) of the 205 women tested.
Chest roentgenograms. One hundred and
forty-nine patients had x-ray films of the
chest during hospitalization and 36 were
abnormal. The most common abnormality
was some degree of cardiac enlargement.
Other studies. Two hundred and fifteen pa-
tients had blood chemistry tests done at
least once and 145 patients had at least 1
renal function test but the interpretation of
these tests is beyond the scope of this paper.
Urinary suppression. No toxemic woman in
1950 had lower nephron nephrosis. One pa-
tient (with chronic hypertensive disease) is
considered as having anuria, if we define
anuria as no excretion of urine in a 12 hour
period; this patient subsequently improved.
Oliguria we define as the excretion of less
than 600 milliliters of urine in any 24 hours.
There were 12 patients with oliguria, 5 of
whom had eclampsia.
Ferguson, Miller: TOXEMIA OF PREGNANCY 11
Maternal death. There was 1 death among
the toxemic women on the service in 1950.
This patient had chronic hypertensive dis-
ease and died of pulmonary embolism after
a cesarean hysterectomy.
The patient was a 38 year old colored para
9, gravida 11. She was known to have had
hypertension for 17 years. Near term a cesar-
ean section was performed because of 2
previous sections. The first section was done
because of a large baby (15,Iq pounds). The
operation was started under local anesthesia
and finished under ethylene and ether. After
delivery of twins a subtotal hysterectomy
and bilateral salpingo-oophorectomy was
done. One ovary contained a 7 centimeter
dermoid cyst. The lower extremities were
examined daily and there was no muscle
tenderness or Homans' sign. The postopera-
tive course was febrile due to pneumonitis
but she was discharged well on the twelfth
postoperative day. The day after discharge
she collapsed at home and died suddenly.
The coroner's diagnosis was pulmonary
embolism.
Induction of labor. Labor was induced in 65
women. Pitocin infusion was the most popu-
lar form of induction and was used in 38
instances. We have no hesitancy in the em-
ployment of this method of induction in
toxemia. Our use of pitocin infusion has in-
creased since 1950. No considerable dele-
terious effect on toxemia has been observed
(23).
SUMMARY
The problem of toxemia of pregnancy at
the Charity Hospital in New Orleans was
audited by means of a careful study of the
hospital records of all of the patients deliv-
ered on the Tulane Service in 1950. The
patients were from the low income group of
the state and 82 per cent were Negroes. The
patients with toxemia were designated by
scrupulous adherence to definitions and were
divided into groups with pre-eclampsia,
eclampsia, chronic hypertensive disease with-
out superimposed pre-eclampsia, and chronic
hypertensive disease with superimposed pre-
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12 Surgery, Gynecology & Obstetrics � ,:eptember 1955
eclampsia; there was a small unclassified
group. Three thousand eight hundred and
ninety-nine patients were delivered on the
service in 1950 and 736, or 19 per cent, had
toxemia. Forty-seven per cent of the patients
had pre-eclampsia, and 47 per cent had
chronic hypertensive disease. Forty-eight per
cent of the patients with chronic hypertensive
disease had pre-eclampsia superimposed on
that illness. There were 10 eclamptics. The
large Negro census did not seem to be the
cause of the high rate of toxemia. There was
1 maternal death. The stillbirth rate of 6.5 per
cent compared very favorably with the rates
reported elsewhere. The cesarean section
rate was 6 per cent and the primary indica-
tion for the operation in the majority of these
women was not the toxemia.
REFERENCES
1. ADDER�, 0 El fcto in las toxemias del cmbarazo
(The fetus in the toxemias of pregnancy) Acta
med., Venezolana, 1954, 2. 62.
2. BIEBER, G. F. Review of 353 cases of premature
separation of the placenta. Am. J. 01,st. Gyn., 1953,
65: 257.
3. BURNETT, L. F, and HAMEL, J. I Toxemia report
for 1948. Bull. Margaret Hague Mat. Hosp., 1949,
2: 118.
4. COSGROVE, S. A., and CHESLEY, L. C. The clinical
management of the late toxernias of pregnancy.
Obst. Gyn. Survey, 1948, 3: 769.
5. DE WATTEVILLE, H. Toxaemias of Pregnancy.
Human and Veterinary. A Ciba Foundation Sym-
posium. Pp. 202-203. Philadelphia: The Blakiston
Co., 1950.
6. DIECKMANN, W. J. The Tnxemias of Pregnancy. 2nd
ed. P. 46. St. Louis: C. V. Mosby Co., 1952.
7. Ibid., p. 623.
8. DOUGLAS, R. G. 155th Annual Report of the Society
of the Lying-in Hospital of the City of New York.
P. 14. 1953.
9. FERGUSON, J. H. Effect of stilbestrol on pregnancy
compared to the effect of a placebo. Am. J. Obst.
Gyn., 1953, 65: 592.
10. Idem. El funcionamiento de una clinica de toxemia
para pacientes ambulatorios (The conduct of a
toxemia clinic for ambulatory patients) Rev obst
gin., Caracas, 1953, 13: 196.
11 Idem. Rupture of the marginal sinus of tile pla-
centa. Am. J Obst. Gyn., in press.
12. Idem. The effect of a supplement of methionine and
vitamin B on pregnancy and prematurity Obst
Gyn., in press.
13. FERGUSON, J. H., and HINSON, M L Importance of
protein in maternal diets. and a Charity Hospital
survey. J. Louisiana M. Soc., 1953, 105 18
14. HAMILTON, J., JETTCOATE, T. N. A., and LISTER, U
M. Foetal mortality in toxaemia of late pregnancy
according to mode of delivery. J. Obst. Gyn Brit
Empire, 1949, 56: 413.
15. HENDELMAN, M., and PHILPOTT, N W. A clinical
report on the toxemias of pregnancy. Am. J Obst
Gyn., 1952, 63: 72.
16 HiNsoN, M. L., and FERGUSON, J H. Food habits of
pregnant women in Charity Hospital clinics. Bull.
Tulane M. Fac., 1951, 10 138.
17 Jotas, W. S. Essential hypertension with superim-
posed pre-eclampsia. Am. J. Obst. Gyn., 1951, 62
387.
18. KALTREIDER, D. F, and GILBERT, C. R. Unexpect-
ed hypertension in the early and late puerperium
Am. J. Obst. Gyn., 1951, 61 � 161.
19. LUNDGREN, L. E., and McDANIEL, G. C. Toxemia
report for 1950 Bull. Margaret Hague Mat. Hosp.,
1952, 5. 16.
20. McCAw, W H., and PARSONS, R. M. Toxemia
report for 1949 Bull. Margaret Hague Maternity
Hosp., 1951, 4 52.
21 MEYER, H. Hypertension following a normal preg-
nancy. Am. J. Obst. Gyn, 1938, 35 150.
22. MEYER, H., and NADLER, S. B. Unexpected post-
partum hypertension. Am. J Obst Gyn, 1941, 41.
231.
23. SCHNEIDER, G. T., FERGUSON, J. H, and MILLER,
H. K. Intravenous administration of dilute pitocin
in obstetrics. N. Orleans M. & S. J , 1951, 104 139.
24. SEEGARS, W. Unpublished data.
25. TATUM, H. J Placental abruption. Obst. Gyn.
1953, 2: 447.
26. TAN LOR, H. C., JR., TILLMAN, A. J. B., and BLANCH-
ARD, J. Fetal losses in hypertension and pre-
eclampsia-I, an analysis of 4432 cases. Surg. Obst.,
1954, 3. 225.
27 WELLEN, I. Specific hypertensive disease of preg-
nancy, factors affecting infant mortality. Am. J.
Obst. Gyn., 1952, 64: 271.
28. Mem. The infant mortality in specific hypertensive
disease of pregnancy and in essential hypertension.
Am. J. Obst. Gyn., 1953, 66: 36.
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