Postpartum cerebral vasospasm treated with
hypervolemic therapy
Paul T. Akins, MD, PhD, Kirk J. Levy, MD, Anne H. Cross, MD, Mark P. Goldberg, MD, and
Marc H. Schieber, MD, PhD
St. Louis, Missouri
In a 23-year-old woman, gravida 1, para 1-0-0-1, headaches and seizures developed 1 week after an
uncomplicated delivery. Cerebral angiography revealed severe, diffuse cerebral vasospasm, Her
symptoms resolved with hyperosmolar, hypervolemic therapy and nimodipine. Magnetic resonance
angiography on postpartum day 23 confirmed persistent, severe vasospasm, and repeat magnetic
resonance angiography on postpartum day 33 demonstrated interval improvement. This report
documents the time course of a case of postpartum vasospasm and its response to hypervolemic,
hyperosmolar therapy and nimodipine. (Am J Obstet Gynecol 1996;175:1386-8.)
Key words: Cerebral vasospasm, angiography (magnetic resonance), eclampsia, puerperium

Late postpartum eclampsia is an u n c o m m o n neurologic complication of pregnancy. In a small subset of
patients cerebral angiography has demonstrated severe
narrowing of cerebral blood vessels consistent with vasospasm? ~ We describe the time course of a complicated
case diagnosed and monitored by serial neurologic imaging and the response to hyperosmolar, hypervolemic
therapy and nimodipine, a widely used treatment for
vasospasm caused by subarachnoid hemorrhage.
Case report

A 23-year-old woman, gravida 1, para 1-0-0-1, had
throbbing headaches and two generalized seizures on
postpartum day 7 and was admitted to an outside hospital. She had an uncomplicated term pregnancy and spontaneous vaginal delivery without epidural anesthesia, and
she did not receive bromocriptine. Results of medical,
pelvic, and neurologic examinations were normal. On
admission, the blood pressure was 140/92 mm Hg but
elevated to 190/120 on postpartum day 10. Findings of
routine laboratory studies and cerebrospinal fluid examination were normal except for a uric acid level of 6.5
mg/dl. A magnetic resonance imaging scan of the brain
was normal. Electroencephalography performed while
the patient was awake demonstrated sharp activity in the
left temporal region, and acyclovir was administered for
possible encephalitis. O n postpartum day 10 she was discharged on a regimen of phenytoin and acyclovir.
From the Department of Neurology, Washington University School of
Medicine.
Receivedfor publication November 6, 1995; revisedFebruary 15, 1996;
acceptedFebruary 28, 1996.
Reprint requests: Paul T. Akins, MD, PhD, Department of Neurology,
Washington University Schoolof Medicine, Box 8111, 660 South Euclid
Ave., St. Louis, MO 63110.
Copyright © 1996 by Mosby-YearBook, Inc.
0002-9378/96 (~5.00+ 0 6/1/73370
1386

O n postpartum day 11 the patient became unable to
walk and asked the same questions repetitively. She was
seen at Barnes Hospital on postpartum day 12. Blood pressure was 122/70 mm Hg. Neurologic examination revealed a normal mental status except for a delayed response to commands, a narrow, shuffling, apractic gait,
and brisk deep tendon reflexes that were more pronounced in the legs than arms. Cerebral angiography on
postpartum day 12 revealed diffuse, severe narrowing of
arteries (Fig. 1, A and B) with patent cerebral veins and
sinuses and no aneurysms. Repeat laboratory analysis was
remarkable for a creatinine level of 1.6 m g / d l and clear
cerebrospinal fluid with an opening pressure of 12 cm, 7
white blood cells/mm 3 (6 mononuclear leukocytes, I polymorphonuclear leukocyte), 161 red blood cells/mm 3, a
glucose value of 47 m g / d l (serum 86 mg/dl), and a pr Otein level of 67 mg/dl. There were no elevations in urine
protein, antinuclear antibody, or anticardiolipin antibody
levels or in VDRL (Venereal Disease Research Laboratory)
test results. Erythrocyte sedimentation rate was 19 mm/hr.
The patient was treated with volume expansion with 5%
dextrose in normal saline solution at 400 m l / h r and 12.5
gm of albumin infused every 6 hours. The blood pressure
rose to 1,60/100 mm Hg, and the symptoms resolved. She
was weaned from therapy over postpartum days 14 to 17.
The blood pressure declined to 126/92 mm Hg. A headache developed on postpartum day 15, and she fell as a
result of the recurrence of the gait disorder on postpartum
day 18. Hypervolemic therapy was reinstated, and nimodipine (60 mg orally every 4 hours) was added. Blood pressure increased to 180/100 mm Hg, the headache resolved,
and gait returned to normal. Despite a normal appearance of the magnetic resonance imaging scan, three-dimensional time-of flight magnetic resonance angiography (Siemens, Germany; 1.5 T) on postpartum day 23
demonstrated persistent, severe arterial narrowing (Fig. 1,
Cand D), and repeat magnetic resonance angiography on
postpartum day 33 (Fig. 1, E a n d F) indicated partial reso-

Volume 175, Number 5
Am] Obstet Gynecol

Akins et al.

Fig. 1. Postpartum vasospasm was monitored with serial neuroimaging. A and B, Cerebral angiography
on postpartum day 12 revealed severe arterial narrowing after right carotid (A, lateral view) and left
verebral artery (B, anteroposterior view) injections. C and D, Magnetic resonance angiography on
postpartum day 23 showed persistent arterial narrowing. E and F, Repeat study on postpartmn day 33
revealed interval improvement. Collapsed axial images of circle of Willis and proximal cerebral vessels
were viewed in a dorsal-ventral orientation (C and E). Posterior circulation was imaged in an anteroposterior (D and F) projection. Narrowing was present in anterior (open arrows) and middle (solid arrows)
cerebral arteries (A, C, and E) and in basilar artery (solid arrows, B, D, and F).

1387

1388 Akins et al.

lution. She was weaned off hypervolentic therapy over
postpartum days 33 to 40. Nimodipine was administered
for a total of 21 days, and phenytoin was discontinued 1
month after discharge. In follow-up at 6 months she had
returned to work, results of examination were normal except for a persistently brisk right patellar reflex, and blood
pressure was 116/84 m m Hg.
Comment

Cerebral vasospasm as a complication of pregnancy is
rare. It was first recognized in the European literature. 2
Other terms have been applied to it, such as postpartum
angiopathy (vasculopathy or arteriopathy) or isolated angiitis. The pathogenesis is poorly understood. Although
some cases have been viewed as isolated central nervous
system vasculitis and treated with immunosuppressant
agents, pathologic documentation was not available. In
the single reported autopsy study3 the cerebral blood
vessels had slight intimal thickening without perivascular
inflammation. We favor vasospasm as the explanation for
the angiographic findings. The pathologic characteristics
of eclampsia suggest that vasospasm may affect other
organs such as the liver.
We identified 20 patients described in the English literature with angiographically documented vasospasm in
the peripartum period. Most patients had a severe prodromal headache. Some patients had fluctuating focal
deficits. Visual field deficits, dysphasia, dyscalculia, and
coma were also reported. The condition is not benign.
Five patients had strokes, and one died? Patients with
pregnancy-associated vasospasm were first seen from the
day of delivery to 3 weeks post partum. The duration of
this condition is variable. Clinically, symptoms resolved in
many patients within a week, whereas others had prolonged courses lasting several weeks and complicated by
strokes.
We treated our patient with hypervolemic therapy and
nimodipine because of the success of this treatment for
cerebral vasospasm caused by subarachnoid hemorrhage.
The patient had a well-defined clinical response to the
initiation of treatment. A relapse occurred when hypervolemic therapy was tapered off, and improvement occurred when it was reinstated. Hypertensive agents such
as phenylephrine were not used and, in theory, could

Novmeber 1996
AmJ ObstetGynecol

exacerbate the condition. Other reported treatments for
postpartum cerebral vasospasm have included intravenous magnesium sulfate, antihypertensive agents, nimo-'
dipine, and steroids. There was no clear correlation between treatment modality and stroke, although the only
patient who received verapamil (240 mg/day) died?
In contrast to our patient's normal magnetic resonance
imaging scan, it is more common in eclampsia to find
increased T2-weighted signal intensity at the junction of
cortex and white matter, particularly in the parietooccipital regions. The preferential involvement of the occipital
lobes may be the source of the visual symptoms reported
by patients with eclampsia. Only a minority of patients
with these findings will have vasospasm demonstrated by
angiography. If the edema represents disruption of the
blood-brain barrier, hyperosmolar, hypervolemic therapy
may be detrimental in eclamptic patients with increased
T2-weighted signal intensity.
This case report provides some useful observations.
Cerebral angiography was necessary to diagnose postpartum vasospasm and exclude aneurysms and sagittal sinus
thrombosis. Magnetic resonance angiography provided a
noninvasive method to follow its course. Hypertension
associated with postpartum cerebral vasospasm may be
beneficial to maintain perfusion to ischemic brain, and
antihypertensive agents in such patients with known vasospasm should be avoided. In patients with symptoms of
postpartum cerebral vasospasm, hypervolemic therapy
and nimodipine may alleviate cerebral ischemia while
spontaneous resolution of this condition is awaited.
We thank D.T. Cross III, MD, and Mark Bahn, MD
(neuroradiologists), and Todd Williams and Kenneth
Hirstein (radiology technicians) for their assistance.
REFERENCES

t. Raps EC, Galetta SL, Broderick M, Atlas SW. Delayed periparturn vasculopathy: cerebral eclampsia revisited. Ann Neurol
1993;33:222-5.
2. Rascol A, Guiraud B, Manelfe C, Clanet M. Accidents vasculaires cerebraux de la grossesse et du post partum. In: Deuxieme Conference de la Salpetriere sur les MaladiesVasculaires
Cerebrales. Paris: Baillere, 1980:84.
3. Geraghty JJ, Hoch DB, Robert ME, Vinters HV. Fatal puerperal cerebral vasospasm and stroke in a young women. Neurology 1991;41:1145-7.