Pulmonary edema in severe preeclampsia-eclampsia: Analysis

of thirty-seven consecutive cases

Baha M. Sibai, M.D., Bill C. Mabie, M.D., Carol J. Harvey, R.N., and
Antonio R. Gonzalez, M.D.
Memphis, Tennessee

During approximately a 9-year period, 37 severe preeclamptic-eclamptic patients had pulmonary edema for
an incidence of 2.9%. The incidence was significantly higher in older patients (p < 0.0001) and in
multigravid patients (p < 0.05). Eleven (30%) had antepartum edema with 10 (90%) of the 11 having
preexisting chronic hypertension. Twenty-six (70%) had postpartum edema with an average onset of 71
hours post partum. The majority of these patients had excessive colloid and crystalloid infusions for
various medical, surgical, and obstetric complications. There were four maternal deaths and morbidity was
significant. Eighteen patients had disseminated intravascular coagulopathy, 17 had sepsis, 12 had abruptio
placentae, 10 had acute renal failure, six had hypertensive crisis, five had cardiopulmonary arrest, two had
rupture of the liver, and two had ischemic cerebral damage. The overall perinatal mortality was 530/1000
and neonatal morbidity was significant. Pulmonary edema is infrequent in severe preeclampsia-eclampsia
without associated medical, surgical and obstetric complications. The occurrence of pulmonary edema in
such patients is associated with high maternal and perinatal mortality and morbidity. (AM J OaSTEl
GVNECOL 1987;156:1174-9.)

Key words: Preeclampsia-eclampsia, pulmonary edema, pregnancy outcome

Pulmonary edema is a rare complication of Material and methods

preeclampsia-eclampsia and its development classifies
the patients as having severe disease. The occurrence
of pulmonary edema is usually associated with in-
creased maternal-perinatal mortality and morbidity.l.3
The pathogenesis of pulmonary edema continues to be
the subject of extensive investigation and several patho-
logic mechanisms have been implicated as possible eti-
ologic factors.'·lo Several reports have recently de-
scribed the cardiovascular and hemodynamic findings
associated with pulmonary edema in such patients. The
authors of these reports'·9 suggested that invasive he-
modynamic monitoring with the Swan-Ganz catheter is
clinically indicated in the diagnosis and management
of these patients.
We report here our observations from 37 recently
managed cases of severe preeclampsia-eclampsia com-
plicated by pulmonary edema. The purposes of this
clinical report are: (1) to determine the influence of
preexisting medical complications, associated obstetric
complications, and therapeutic interventions on the in-
cidence of pulmonary edema and (2) to report the
maternal-perinatal outcome and subsequent pregnancy
outcome in such patients.
From the Division of Maternal/Fetal Medicine, Department of Ob-
stetrics and Gynecology, University of Tennessee, Memphis.
Received for publication June 30,1986; revised September 22,1986;
accepted December 24, 1986.
Reprint requests: Baha M. Sibai. M.D., Department of Obstetrics and
Gynecology, Division of Maternal/Fetal Medicine, University of
Tennessee, 800 Madison Ave., Memphis, TN 38163.
The E. H. Crump Women's Hospital and Perinatal
Center in Memphis serves as a tertiary referral center
for hospitals with approximately 30,000 deliveries an-
nually in the Mid-South. From August 1977 to April
1986, 1290 of the pregnancies managed at this center
were complicated by severe preeclampsia-eclampsia.
Severe preeclampsia was defined as the presence of se-
vere hypertension (blood pressure> 1601110 mm Hg)
accompanied by significant proteinuria and/or gener-
alized edema. All patients except the one with anuria
had proteinuria (",,3 + on dipstick). In all patients with
a documented history of chronic hypertension before
pregnancy and persistent elevation of blood pressure
(at least 140/90 mm Hg on two occasions) before the
twentieth week of gestation, chronic hypertension was
diagnosed. In such patients, superimposed severe pre-
eclampsia was diagnosed in the presence of exacerba-
tion of hypertension to the above-stated levels plus sig-
nificant proteinuria during the second or last part of
gestation. The diagnosis of pulmonary edema was doc-
umented in 37 of the patients for an incidence of 2.9%.
The chart of each patient was studied to delineate
any antecedent prenatal, intrapartum, or postpartum
event leading to the development of pulmonary edema.
The information was collected at the time of diagnosis
of pulmonary edema or when the patient was admitted
to the Perinatal Center. The analysis focused on the
influence of maternal age, race, parity, presence of
preexisting medical problems, associated obstetric com-

1174
Volume 156
Number 5
Table I. Clinical characteristics
Mean age (yr)*
<25 yr (No.)t
Mean gravidity:j:
Gravida 1 (No.)
Average mean arterial pressure (mm Hg)
Chronic hypertension (No.)§
*p = 0.004.
tp = 0.02; odds ratio 10: 1.
:j:p = 0.004; odds ratio 16: 1.
§p = 0.04.
plications, type of anesthesia and mode of delivery,
therapeutic measures used, and laboratory findings.
Additional data included time of onset of edema in
relation to delivery, medications, and procedures used,
maternal-perinatal outcome, and subsequent preg-
nancy outcomes.
The diagnosis of pulmonary edema was made on the
basis of clinical and arterial blood gas findings that were
confirmed by chest x-ray film. Laboratory evaluation
included serial determination of coagulation profile,
liver function tests, and remil function tests. Dissemi-
nated intravascular coagulopathy is defined as the pres-
ence of thrombocytopenia « 100 x 10 3/mm 3), low fi-
brinogen «300 fLg/di), positive fibrin split products
(>40 fLg/dl), and prolonged prothrombin and partial
thromboplastin times. Hemolysis and elevated liver en-
zymes are defined as described in a recent report. II
Oliguria was defined as urine output of <400 ml in 24-
hour period. Serum and urine osmolality, urine soc
dium, and urine creatinine were measured in patients
with oliguria. Fractional excretion of sodium was also
calculated. These findings were used to determine the
etiology of the oliguria (renal or prerenal).
Management of these patients included oxygen sup-
plementation, furosemide, antihypertensive medica-
tions, and digitalis as indicated on the basis of the un-
derlying cause. Central hemodynamic monitoring was
performed in 18 patients (11 patients had Swan-Ganz
catheter insertion and seven had central venous pres-
sure monitoring only).
Infant clinical data included gestational age, birth
weight, Apgar scores, and perinatal outcome. In ad-
dition, subsequent pregnancy outcome was analyzed
when available.
Results were analyzed by Student's t test for com-
parison of means and X2 or Fisher's exact test for com-
parison of frequencies.
Results
During the study period there were 1089 patients
with severe preeclampsia and 201 patients with eclamp-
Pulmonary edema in severe preeclampsia-eclampsia 1175
Antepartum Postpartum Total
(n = 11) (n = 26) (n = 37)
31.l ± 6.1 4.4 ± 5.5 26.8 ± 6.3
1 13 14
3.6 ± 2.4 2.3 ± 1.5 2.7 ± 1.9
4 10 14
147 ± 29 139 ± 19 142 ± 23
10 10 20
sia. The incidence of pulmonary edema in this group
of patients was 2.9%. A total of 1008 patients had pure
preeclampsia-eclampsia while 282 patients had chronic
hypertension. The incidence of pulmonary edema in
patients with superimposed disease was 7.1 % while it
was 1.7% III patients with pure preeclampsia
(p < 0.0001, odds ratio 4.5: 1). Thirteen patients (35%)
were admitted with pulmonary edema while 24 (65%)
developed pulmonary edema during the course of their
management.
The onset of pulmonary ed~ma was before delivery
in 11 patients (30%) ~nd after delivery in 26 (70%).
Table I summarizes the clinical characteristics in these
patients. Twenty-one patients (51 %) had either poor
or no prenatal care. Twenty-nine patients (78.4%) were
black and 8 (21.6%) were white. This finding is similar
to the respective frequency in the group without pul-
monary edema. The average maternal age of
26.8 ± 6.3 years in this group of patients is significantly
higher (p < 0.0001) than the average maternal age
(20.7 ± 4.9 years) in the patients who did not have
pulmonary edema. Moreover, within the group having
pulmonary edema, patients having antepartum onset
of edema had significantly higher mean age (p < 0.005)
and higher mean gravidity (p < 0.05) than patients
having postpartum onset of edema. In addition, 10 of
the 11 with antepartum pulmonary edema had preex-
isting chronic hypertension. Three of the 14 nullipa-
rous patients had chronic hypertension and one had
cardiac disease (tricuspid atresia). The other 10 pa-
tients had pure preeclampsia. All 10 cases were asso-
ciated with one or more of the following complica-
tions: massive transfusions, surgical procedures, sepSIS,
anemIa.
Table II summarizes the laboratory findings at the
time of development of pulmonary edema in all pa-
tients. There were no differences in laboratory findings
except for albumin (p = 0.02) between patients having
antepartum edema (3.0 ± 0.36 gm/dl) and those hav-
ing postpartum edema (2.56 ± 0.46 gm/dl). These dif-
ferences reflect delayed fluid mobilization in the post-
1176 Sibai et al.
Table II. Laboratory findings
Test Mean ± SEM
Platelet count x 10'/mm' 147 ± 22
<100 x 10' (No.) 19 (51%)
Creatinine (mg/dl) 2.5 ± 0.45
> 1.2 mg/dl (No.) 18 (49%)
Uric acid (mg/dl) 8.6 ± 0.45
>6 mg/dl (No.) 35 (95%)
Albumin (gm/dl) 2.7 ± 0.1
~2.7 gm/dl (No.) 29 (54%)
Serum glutamic oxaloacetic 558 ± 178
transaminase (U/L)
>70 UlL (No.) 16 (43%)
Bilirubin (mg/dl) 3.1 ± 0.9
> 1.2 mg/dl (No.) 17 (46%)
partum group. Eighteen patients (48.6%) had dissem-
inated intravascular coagulopathy and 16 (43.2%) had
hemolysis, elevated liver enzymes, and low platelets.
The majority of these complications were associated
with abruptio placentae and/or fetal death. The aver-
age creatinine clearance was 61 ± 40 mllinin (range 0
to 161). Ten patients had acute renal failure with a
mean creatinine clearance of 9.9 ± 6.7 mUmin (range
o to 20) and a mean serum creatinine level of 6.1 ± 2.1
mg/dl (range 2.3 to 9.3). The etiology of oliguria was
renal in nine cases (fractional excretion of sodium> I,
urine sodium> 40 mEq/L, urine/plasma osmolal-
ity < 1.2) and prerenal in one patient (fractional ex-
cretion of sodium < I, urine sodium < 10 mEq/L, and
urine/plasma osmolality> 1.2). Four of the 10 patients
required dialysis.
Management and pregnancy outcome. Thirteen
patients were admitted with pulmonary edema. Two
of these patients had cesarean section elsewhere and
were then referred with acute renal failure and dis-
seminated intravascular coagulopathy complicating the
edema. One other patient presented with pulmo-
nary edema following delivery of twins at 20 weeks'
gestation (one of the twins was delivered in a local
clinic prior to referral). This patient was not treated
with [3-sympathomimetics. An additional patient with
eclampsia and oliguria developed pulmonary edema
after mannitol treatment elsewhere. The remaining pa-
tients had pulmonary edema complicating a long-
standing chronic hypertensive disease.
Fifteen patients had general anesthesia, seven had
epidural anesthesia, and the remainder received nar-
cotic analgesia during labor and local anesthesia for
delivery. Of the seven women given epidural anes-
thetics, two patients presented with antepartum pul-
monary edema and five developed postpartum edema
(in two cases edema developed within 24 hours and in
three it was seen >72 hours post partum). The use of
concomitant "fluid loading" was not a factor in the etiol-
ogy of pulmonary edema in any of these seven patients.
Nineteen patients (51%) had cesarean sections and 18
(49%) were delivered vaginally. Three patients had lap-
May 1987
Am.J Obstet Gynecol
Table III. Associated maternal complications*
Complication n I %
Metritis-sepsis 17 45.9
Abruptio placentaet 12 32.4
Disseminated intravascular coagulopathyt 18 48.6
Acute renal failuret 10 27.0
Cardiopulmonary arrest 5 13.5
Aspiration 3 8.1
Ascitest 8 21.6
Pulmonary embolism 2 5.4
Ruptured livert 2 5.4
Hypertensive crisist 6 16.2
Cerebral damaget 2 5.4
Tricuspid atresia 1 2.7
*All patients except three had associated complications.
tManifestation of severe preeclampsia-eclampsia.
arotomy after delivery (two because of ruptured liver
hematomas and one because of a diagnosis of liver fail-
ure). All three patients developed postpartum edema
secondary to massive blood transfusions.
Twenty-six patients had postpartum pulmonary
edema. The average time to onset of edema was 71
hours (range 2 to 360 hours). Sixteen (61.5%) devel-
oped edema more than 48 hours post partum. The
majority of these patients had multiple obstetric, med-
ical, and surgical complications requiring various ther-
apeutic interventions.
Table III summarizes the maternal complications in
these patients. Disseminated intravascular coagulopa-
thy and sepsis were the most frequent complications.
In addition, most of the patients had more than one
complication. All three patients with aspiration had car-
diogenic pulmonary edema. Nine of the 10 patients
with acute renal failure had acute tubular necrosis; the
other had cortical necrosis eventually requiring a kid-
ney transplant. Four of the ten required dialysis and in
six cases there were complications (abruptio placentae,
stillbirth, and disseminated intravascular coagulopa-
thy). The duration of dialysis ranged between 5 days
and 2 weeks in three patients. The other patient re-
quired dialysis until the transplant was performed.
Twenty-one patients (57%) received excessive crys-
talloid or colloid therapy for various reasons. Two of
these patients received such therapy to treat oliguria
associated with severe preeclampsia, with the remain-
der receiving this therapy for associated multiple com-
plications. Three patients in this group received epi-
dural analgesics. All three received a prehydration load
of 500 ml of crystalloids. All 21 received blood (average
of 7 units per patient, range 2 to 18). Sixteen of the 21
received fresh-frozen plasma and 12 received platelets.
In addition, almost all of the patients received >4000
ml of crystalloids during a 24-hour period.
All patients received intravenous magnesium sulfate
and 30 received intravenous hydralazine. Nine patients
required nitroprusside infusions for control of hyper-
Volume 156
Number 5
tension, while four patients required dopamine infu-
sion for cardiovascular support.
The 37 pregnancies resulted in 39 births (two sets of
twins). There were 12 stillbirths and six neonatal deaths
for a perinatal mortality rate of 53011 000. Eleven (61 %)
of the perinatal deaths were related to abruptio pla-
centae, two were related to ruptured liver hematomas,
and one was due to trisomy 18.
The mean birth weight was 1775 ± 183 gm (range
235 to 4015). The mean gestational age was 32.4 ± 0.9
weeks (range 20 to 40). Thirteen infants (33.3%) were
~30 weeks, 14 (35.9%) were between 31 and 36 weeks,
and 12 (30.8%) were >36 weeks' gestation. The Apgar
score was ~4 at 1 minute in 14 (51.8%) live-born infants
and <7 at 5 minutes in 10 (37%).
Maternal outcome. There were four maternal
deaths. Two of the deaths were related to cerebral dam-
age with both patients having flat electroencephalo-
grams. One maternal death occurred in a patient with
eclampsia at term who suffered mutliple convulsions
during transport and had cardiac arrest at the time of
arrival to the perinatal center. She was comatose and
remained so until death 9 weeks post partum. Her
course was complicated by cerebral damage, dissemi-
nated intravascular coagulopathy, and prolonged adult
respiratory distress syndrome with pulmonary fibrosis.
The second patient had cardiac arrest from severe hy-
poxia secondary to esophageal intubation. She had
decerebrate rigidity and a flat electroencephalogram
immediately post partum. She died 5 days later. A third
patient had tricuspid atresia. Her hospital course was
complicated by cardiac arrest, disseminated intravas-
cular coagulopathy, and oliguria. She was discharged
home 15 days later. She was readmitted twice to another
hospital. She developed massive pulmonary embolism
during her subsequent admission with sudden death
about 8 weeks post partum. The other patient had hy-
pertensive cardiomyopathy and was admitted with an-
tepartum pulmonary edema, which was controlled. She
then developed postpartum pulmonary edema. She was
discharged home after 1 week. A postpartum check-
up 1 week later was unremarkable. She was readmitted
5 days later with pulmonary edema and pleural effu-
sions. Sudden death due to massive embolism occurred
5 days later (4 weeks post partum). Both patients had
autopsy findings revealing massive pulmonary emboli.
Thirty-one of the 33 surviving patients had follow-
up data ranging from 3 months to 8 years. Both patients
that were lost to follow-up had preexisting chronic hy-
pertension. Of the 31 patients that were followed up,
18 had chronic hypertension while 13 were normoten-
sive on follow-up. Thirteen of the 31 patients were
nulliparous. Three had preexisting chronic hyperten-
sion and two of the remaining 10 developed hyperten-
sion on follow-up.
Eighteen patients had subsequent deliveries. Ten of
Pulmonary edema in severe preeclampsia-eclampsia 1177
the 18 were normotensive; four pregnancies were com-
plicated by chronic hypertension and four by pre-
eclampsia. Three of the latter four pregnancies were
complicated by abruptio placentae and stillbirth (one
with pulmonary edema).
Comment
Pregnancies complicated by severe preeclampsia-
eclampsia are characterized by functional derangement
of multiple organ systems such as the cardiovascular,
renal, hepatic, hematologic, and central nervous sys-
tems. The patients usually have generalized arterial
vasospasm resulting in increased systemic vascular re-
sistance (increased afterload), reduced plasma volume
(decreased preload), and increased left ventricular
stroke work index (hyperdynamic heart." 1 In addition,
renal function is impaired, serum albumin is reduced,
and capillary permeability is increased due to endo-
thelial cell injury. Consequently, the above changes will
predispose these patients to an increased risk of pul-
monary edema.' However, pulmonary edema is infre-
quently encountered in well-managed cases of pure
preclampsia. This results from the fact that most pa-
tients are young and in good heatlh, which allows for
compensatory mechanisms that ensure adequate tissue
perfusion in spite of the above functional derange-
ments. These compensatory mechanisms vary consid-
erably from patient to patient, depending on factors
that might complicate severe preeclampsia-eclampsia.
The incidence of pulmonary edema in this study was
2.9%. The high incidence of pulmonary edema en-
countered in this report emphasizes the seriousness of
severe preeclampsia-eclampsia as a major cause of ma-
ternal mortality and morbidity. In addition, it under-
scores the importance of close observation of such pa-
tients with severe complications throughout labor and
delivery and for a minimum of 72 hours post partum.
The incidence was significantly higher in older patients,
in multigravid patients, and in those with preexisting
chronic hypertension. In fact, 54% of the patients with
pulmonary edema had chronic hypertension with su-
perimposed preeclampsia-eclampsia. It is of interest to
note that 90% of patients developing antepartum pul-
monary edema had preexisting chronic hypertension.
In addition, the acute onset of hypertensive crisis was
responsible for the development of pulmonary edema
in six of the patients. Furthermore, most of the patients
with abruptio placentae and disseminated intravascular
coagulopathy had chronic hypertension with super-
imposed preeclampsia-eclampsia. These findings tend
to emphasize the importance of hypertensive cardio-
vascular disease as an etiologic factor in pulmonary
edema. The present results confirm to a large extent
most of the conclusions of Cunningham et al. 11 regard-
ing this subject.
The majority of patients in this study had marked
1178 Sibai et al.
abnormalities of the hepatic, renal, and hematologic
systems. Eighteen patients had disseminated intravas-
cular coagulopathy as described previously, 18 had
significant renal impairment (serum creatinine> 1.2
mg/dl), and 20 (54%) had reduced serum albumin
levels «2.7. gm/dl). Several of these patients required
massive colloid and crystalloid infusions to correct these
abnormalities. These findings tend to emphasize the
importance of multiple organ failure as an etiologic
factor in pulmonary edema. These results are in agree-
ment with the similar findings reported by Benedetti
et al.'
Pulmonary edema developed after delivery in 26
(70%) of the patients. Almost all of these patients re-
ceived massive colloid and crystalloid therapy. This
finding is in agreement with most of the results and
interpretations of previous workers." 4. 7 The mecha-
nisms responsible for this increased incidence in the
postpartum period have recently been reviewed by Be-
nedetti et aU and Hankins et al. 12 The average time to
onset of edema in this group of patients was 71 hours
with 16 (61.5%) having the onset >48 hours post par-
tum. This finding is different from those reported by
others" 1. 7 but is in agreement with the hemodynamic
findings reported by Hankins et al. 12 The mechanism
responsible for the high incidence of late-onset post-
partum edema may be related to delayed postpartum
mobilization of extracellular fluids, as described by
Hankins et al.,12 and to the high number of associated
maternal complications. In addition, several of these
women had underlying hypertensive cardiovascular
factors that were similar to those in many of the patients
reported by Cunningham et al. 10
The patients included in this report had a high in-
cidence of associated medical, surgical, and obstetric
complications (Table III). The presence of these com-
plications increases the magnitude of derangement in
multiple organ systems by reducing the capacities of
several compensatory mechanisms resulting in subop-
timal tissue perfusion and ultimate decompensation. In
addition, the presence of many of these complications
mandates the use of large volumes of fluids and various
medications that may have contributed to the devel-
opment of edema. These findings suggest that patients
with these complications need close monitoring in an
intensive care facility. The development of pulmonary
edema was potentially preventable in some of these
patients if central hemodynamic monitoring was used.
We agree with the recommendation of previous
investigators'-9 regarding the need for using Swan-Ganz
catheter monitoring in the management of complicated
cases of severe preeclampsia-eclampsia, especially those
with persistent 0liguria,13 those requiring massive fluid
therapy, and patients requiring potent antihypertensive
medications such as sodium nitroprusside. The use of
May 1987
Am J Obstet Gynecol
nitroprusside was deemed necessary in nine of these
patients. Our experience indicates that < 1% of piltients
with severe preeclampsia-eclampsia require such a
therapy.
Ten patients in this study had acute renal failure
(nil1e had tubular necrosis and one had cortical necro-
sis), Six of them (including the one with cortical necro-
sis) were complicated by abruptio placentae, fetal death,
and disseminated intravascular coagulopathy. This
complication underscores the need of aggressive blood
replacement in the management of such patients in an
attempt to prevent the development of acute renal
failure.
Donnelly and Lock l reported on 533 patients that
died from toxemia. Pulmonary edema was considered
the cause of death in 25% of the cases. Lopez-Llera 2
reported 86 fatal cases of eclampsia. Severe respiratory
insufficiency was the cause of death in 11.6% of the
cases. The maternal death rate in this study was 10.5%.
However, two of the maternal deaths were due to mas-
sive pulmonary embolism in pa~ients with serious heart
abnormality. The other two de<l-ths were related to isch-
emic cerebral damage, one of which was due to anes-
thetic accident. The findings of this study reveal that
these pregnancies are associated with poor perinatal
outcome. The overall perinatal mortality was 530 out
of 1000. However, most of the perinatal deaths were
related to either abruptio placentae or extreme pre-
maturity.
In summary, pulmonary edema is infrequent in the
well-managed patient with severe preeclampsia-
eclampsia without associated medical, surgical, and ob-
stetric complications. The incidence is influenced by
preexisting chronic hypertension, maternal age, and
parity. The occurrence of pulmonary edema in such
patients is associated with high maternal and perinatal
mortality and morbidity.
REFERENCES
1. Donnelly JF, Lock FR. Causes of death in five hundred
thirty-three fatal cases of toxemia in pregnancy. AM J
OBSTET GYNECOL 1954;68:184.
2. Lopez-Llera M. Complicated eclampsia: fifteen years' ex-
perience in a referral medical center. AM J OBSTET Gy-
NECOL 1982;142:28.
3. Benedetti TH, Kates R, Williams V. Hemodynamic ob-
servations in severe preeclampsia complicated by pul-
monary edema. AMJ OBSTET GYNECOL 1985;152:330.
4. Phelan JP, Yurth DA. Severe preeclampsia. I. Peripartum
hemodynamic observations. AM J OBSTET GYNECOL 1982;
144:17.
5. Strauss RG, Keefer JR, J3urke T, Civetta JM. Hemo-
dynamic monitoring of cardiogenic pulmonary edema
complicating toxemia of pregnancy. Obstet Gynecol 1980;
55: 170.
6. Keefer JR, Strauss RJ, Civetta JM, Burke T. Noncardi-
ogenic pulmonary edema and invasive cardiogenic mon-
itoring. Obstet Gynecol 1981;58:46.
7. Henderson DW, Vilos GA, Milne KJ, Nichol PM. The
role of Swan-Ganz catheterization in severe pregnancy-
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Number 5

induced hypertension. AM ] OBSTET GYNECOL 1984; preeclampsia-eclampsia. AM ] OBSTET GYNECOL 1986;

148:570.
8. Cotton DB, Gonik B, Dorman K, Harris R. Cardiovascular
alterations in severe pregnancy-induced hypertension:
relationship of central venous pressure to pulmonary
capillary wedge pressure. AM] OBSTET GYNECOL 1985;
151:762.
9. Cotton DB, Jones MM, Longmire S, et al. Role of
intravenous nitroglycerin in the treatment of severe
pregnancy-induced hypertension complicated by pul-
monary edema. AM] OBSTET GYNECOL 1986;154:91.
10. Sibai BM, Taslimi MM, El-Nazer A, et al. Maternal-
perinatal outcome associated with the syndrome of he-
molysis, elevated liver enzymes, and low platelets in severe
155:501.
11. Cunningham FG, Pritchard]A, Hankins GDV, et al. Peri-
partum heart failure: idiopathic cardiomyopathy or com-
pounding cardiovascular events? Obstet GynecoI1986;67:
157.
12. Hankins GDV, Wendel GD, Cunningham FG, et al. Lon-
gitudinal evaluation of hemodynamic changes in eclamp-
sia. AM] OBSTET GYNECOL 1984;150:506.
13. Clark SL, Greenspoon ]S, Aldahl D, Phelan ]P. Severe
preeclampsia with persistent oliguria: management of he-
modynamic subsets. AM] OBSTET GYNECOL 1986;154:
490.

Pregnancy after trans catheter embolization of a uterine

arteriovenous malformation
W. Poppe, M.D., F. A. Van Assche, M.D., Ph.D., G. Wilms, M.D., A. Favril, M.D., and
A. Baert, M.D., Ph.D.
Leuven, Belgium

A 25-year-old woman with a congenital uterine arteriovenous malformation had a long history of repeated
excessive vaginal bleeding. She was successfully treated with transarterial embolization. She had normal
menstrual periods for 6 months and subsequently conceived. She was delivered of a normally grown baby
at 35 weeks. To the best of our knowledge, this is the third pregnancy described after successful
embolization of an arteriovenous malformation. (AM J OSSTET GYNECOL 1987;156:1179-80.)

Key words: Uterine arteriovenous malformation, transarterial embolization

Uterine arteriovenous malformations are very un-
common, and successful conservative treatment is sel-
dom reported." 2 In our case reported here, in order
to preserve reproductive capability, we used transcath-
eter embolization to stop the periods of heavy vaginal
bleeding. Pregnancy was advocated after 6 months!
Case report
A 25-year-old woman, gravida 1, para 0, was admit-
ted to the hospital because of recurrent heavy vaginal
bleeding. In her history we noted that 3 months after
a curettage for a missed abortion, she had recurrent
episodes of extensive vaginal bleeding that necessitated
several blood transfusions. Before that pregnancy she
had a normal menstrual pattern.
Hysterosalpingography, hysteroscopy, and curettage
initially revealed no abnormal signs. During curettage
From the Department of Obstetrics and Gynecology and the Depart-
ment of Radiology, University K.U. Leuven.
Received for publication September 25, 1986; accepted November 17,
1986.
Reprint requests: Dr. W. Poppe, Department of Obstetrics and Gy-
necology, U. Z. Gasthuisberg, Herestraat, 49, B-3000 Leuven,
Belgium.
bleeding again started and was controlled by a utero-
cervicovaginal tamponade. The titer of the l3-subunit
of human chorionic gonadotropin was normal and
blood coagulation tests were normal. Neither histo-
pathologic examination of the curettements nor cer-
vical cytologic test results showed any abnormality.
A few months later the patient was admitted again
because of a new episode of heavy vaginal bleeding in
combination with severe low abdominal pain. The con-
centration of the l3-subunit of human chorionic gonad-
otropin was negative. Vaginal examination showed no
uterine enlargement and no adnexal mass. The bleed-
ing was controlled with hemostatic doses of conjugated
estrogens. Ultrasound showed no abnormal images.
Hysterosalpingography was repeated and at maximal
filling a large draining vein at the left ventrolateral
aspect of the uterus was seen. Furthermore some in-
trauterine adhesions were visualized.
Percutaneous transfemoral angiography showed bi-
lateral hypertrophy of the uterine arteries ending in a
tortuous hypertrophic arterial mass especially on the
left side of the uterus with massive filling of early drain-
ing hypertrophic veins. A hypervascular nodule was
seen in the uterine wall. Computerized tomographic
scan confirmed the vascular nature of the lesion. A

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