Emergency Carotid Artery Thrombectomy for
Postpartum Hemiplegia
JAMES T. STURM, MD, CAMILO TORO, MD,
BRUCE D. SNYDER, MD
The case of a 22.ysar-oldpatknt who sufferedfrom postpartumhsmiplagia
due to thrombosisof ttts internal carotid artary is reported.Sha was treated
aggrssshrafywith pantobarbiil coma, angiography,and thrombactomyand
rscovsradwfth minimaldeficit. (Am J Emerg Mad 1987;5:291-293)

We recently evaluated and treated a young psychiatric
patient whose initial presentation suggested either hysteria
or reaction to phenothiazine-like drugs. The case is reported
to review the clinical presentation and management of peripartum cerebral infarction.

REPORTOFACASE
A 22-year-old right-handed white woman, gravida 1, para 0,
was admitted to St. Paul-Ramsey Medical Center on July 4, 1985,
with a blood pressure of 1601110 mm Hg, vomiting, diarrhea, and
complaints of left-sided headache and visual blurring. The patient
had a long history of major schizo-affective disorder treated with
antipsychotic and antidepressant medications and was a documented emergency department abuser. She was admitted to the
obstetrical service where 2 to 3 + proteinuria was noted and magnesium sulfate therapy was begun. Despite sedation, blood pressure remained high and a diagnosis of pre-eclampsia was made.
After an initially stable period, her blood pressures rose as high
as 174/136 mm Hg on July 7, and intravenous hydralazine was
used to control it. Because of the inability to control her severe
pre-eclampsia, an emergency cesarean section was performed and
a low-birth-weight female infant was delivered. The patient developed bacteremia secondary to endometritis, which was treated
with ampicillin and gentamicin. She defervesced, and her blood
pressure gradually responded to oral alpha methyldopa.
From the Departments of Emergency Medicine and Neurology, St.
Paul-Ramsey Medical Center, St. Paul, Minnesota.
Manuscript received June 20, 1986; revision accepted November 25,
1986.
This study was supported in part by the St. Paul-Ramsey Foundation
and the Ramsey Clinic.
Address reprint requests to Dr. Sturm: Department of Emergency
Medicine, St. Paul-Ramsey Medical Center, 640 Jackson Street, St.
Paul, MN 55101.
Key Words: Carotid artery, hemiplegia, hypercoagulability, stroke,
thrombectomy.
0735-6757187 $0.00 + .25

The patient remained uncooperative and irritable throughout her
course, and on July 14 again reported headache over her left orbit.
She had been mentioning multiple somatic symptoms. On July 16,
she reported clumsiness of her right hand, depression, agitation,
numbness, and weakness. It was believed these symptoms had a
functional basis. Perphenazine was begun, outpatient psychiatric
follow-up was arranged, and the patient was discharged.
She awoke that night at 2:00 AM with difficulty speaking and
flaccid paralysis of her right upper extremity. Evaluation in the
emergency department revealed a labile, frustrated but conscious
woman. Hysteria was suspected. The blood pressure was 136170
mm Hg, the pulse 76 bpm, and respirations 20 breaths/min. The
general physical examination was normal. Neurologic examination
showed an alert, oriented, frightened, and uncooperative patient
with a nonfluent aphasia, severe anomia but reasonably good comprehension. A right central facial paresis and right hemiparesis,
maximal in the upper extremity, was present with a right Babinski
response and right hyporeflexia. A dystonic reaction to phenothiazine-like drugs was ruled out by administration of 2 mg benztropine intravenously. There was no evidence of peripheral embolization. There were no vascular bruits and the cardiac examination
was normal. An emergency computed tomography scan showed
subtle effacement of parietal cortical sulci and indistinctness of
the gray-white interface, suggesting early infarction. The patient
was given heparin and admitted to the neurology intensive care
unit.
Admission laboratory data revealed a hemoglobin of 10.5 grams,
and a total white count of 15,600 mm3 with a shift to the left.
Coagulation parameters included a prothrombin time of 13 seconds, an activated partial thromboplastin time of 25.4 seconds,
and a thrombin time of 16.7 seconds. Serum was negative for
fibrin split products, but the fibrinogen level was 420 mg/dl (norma1, 200 to 400 mgldl) . Factor V level was 2 16% (normal, 70 to
150%). The admission platelet count was 435.000 mm’.
A pentobarbital coma was instituted with a loading dose of 20
mg/kg intravenously and a maintenance infusion of 1 mglkglhr.
The patient was placed on a ventilator and angiography performed,
which revealed near-total occlusion of the left internal carotid
artery with a tail of thrombus extending distally in the vessel (Fig.
1). A branch of the left middle cerebral artery was missing. Approximately 17 hours following onset of symptoms, the patient
underwent a left carotid thrombectomy. A jelly-like thrombus,
loosely adherent to an otherwise normal vessel wall, was removed.
Postoperatively, pentobarbital was discontinued, and the patient
gradually improved over the next 36 hours. Heparin was continued.
Postoperative carotid ultrasound studies revealed no thrombosis.
Cardiologic evaluation and echocardiography were entirely normal, Serologic screening for collagen vascular disease was negative .

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During the next few days, the patient showed progressive improvement in the use of her right arm, regaining almost full proximal strength. Her speech similarly improved such that it was
virtually normal by discharge, nine days after admission. At one
month follow-up, her aphasia had cleared completely but she had
residual clumsiness of her right hand. She has been maintained
on low-dose aspirin and was doing well at six months’ follow-up.

DISCUSSION
Multiple studies attest to the increased risk of cerebral
infarction during and immediately after pregnancy. ’ Unlike
stroke in the older individual, underlying atherosclerosis is
unusual. The mechanism appears to be spontaneous thrombus formation within the heart, extracranial carotid or vertebral arteries, the trifurcation of the middle cerebral artery,
or intracranial venous structures. Arterial occlusions tend
to occur during the second and third trimesters of pregnancy
and during the first week after delivery. Venous thrombi
usually are seen one to four weeks after childbirth. Other
rarer causes of focal central nervous system syndromes must
be considered and recently have been reviewed. ’
The experience we have reported is anecdotal. There are
no published series of young patients, without atherosclerosis, who have undergone surgical treatment of acute
thrombotic occlusion of the carotid artery. Previous reports
of acute carotid thrombectomy have described older patients
with atherosclerosis
as the precipitating
cause of acute
thrombosis. The successful outcome of this patient may have
been serendipitous.
The initial diagnostic evaluation of this patient began with
a noninvasive CT scan that showed left parietal ischemia.
The next test chosen was arteriography of the extracranial
and intracranial circulation. Arteriography is invasive, but
it is the only method of completely evaluating the entire
circulation to the cerebrum. The noninvasive Doppler examination of the carotid circulation does not provide enough
resolution to evaluate the patient for operation on the carotid
artery, and has no ability to image the intracranial circulation. The noninvasive carotid ultrasound has been used in
follow-up to ascertain that the thrombosis has not recurred.
The relatively higher risk of stroke in the pregnant woman
warrants a higher index of suspicion on the part of clinicians
evaluating a pregnant patient with neurologic symptoms.
Our higher index of suspicion in this patient was diluted
and offset by two prejudices. First, this psychiatric patient
was an abuser (two to three times weekly) of the emergency
department who was known by the treating physicians to
have exaggerated symptoms many times in the past. Secondly, the patient had been treated previously for dystonic
reactions to phenothiazine-like
drugs. The initial differential
diagnosis included hysterical paralysis and dystonic reaction
to phenothiazine-like
drugs. A detailed neurologic examination appeared to rule out hysteria, and a trial dose of 2

292

FIGURE 1. The angiogram shows a radiolucency representing thrombus
that begins at the bifurcation of the external and internal carotid arteries
(arrow) and tails distally into the internal carotid.

was given intravenously.
Only when the
benztropine failed was a genuine neurologic deficit considered.
This case is most instructive because it is a reminder that
even hypochondriacs
and emergency department abusers
can present with catastrophic illnesses. The lesson learned
here is that when a hysteric, hypochondriac, or emergency
department abuser presents for medical attention, a common
course of action is to assume that it is merely another instance of abuse. The appropriate protocol with such patients
mg benztropine

STURM ET AL n EMERGENCY CAROTID ARTERY THROMBECTOMY

should be to systematically disprove the possibility of serious illness and to document the disproof in the record.
The value of barbiturate coma is not proven by this case.
We will discuss how barbiturate coma might have helped
this patient. Animal studies have documented improved outcome in models of focal cerebral ischemia using barbiturate
coma therapy.2-5 Reduced size of infarction and reduced
clinical deficits in animal models have been documented.
Progress in this area has been slow because of the extreme
difficulty in producing a standard set of clinical conditions
under which to test this approach in human beings. The
clinical trials by Slogoff and Nussmeier6.7 seem to have
identified a group in which this could be tested (patients
undergoing open heart surgery or cardiopulmonary bypass)
and have found convincing evidence, in a well-designed
trial, that barbiturate anesthesias seem to prevent effectively
the development of fixed focal deficits.
Prior to the Nussmeier study, small series and anecdotal
cases supporting the use of barbiturate therapy for anticipated or actual focal cerebral ischemia had appeared in the
literature.8~‘1Some anecdotal negative experiences also have
been reported. 12.13Based on current information, the effective use of barbiturate coma in circumstances of anticipated
or actual focal cerebral ischemia should attempt to follow
these guidelines: 1) Barbiturate coma should be induced
either prior to the episode of ischemia or preferably within
one hour of its onset. Note that this actually may be within
an hour of progression of a preexisting minor deficit and,
therefore, the clinical monitoring of stroke patients for progression must be quite close. 2) Barbiturate anesthesia is
contraindicated in patients with massive, fixed deficits or
indications of extensive hemispheric infarction on CT scan.
3) Barbiturate coma may be contraindicated in patients who
have a fixed obstruction of a major intracranial vessel (e.g.,
middle cerebral artery) unless plans for revascularization
(bypass or embolectomy) are made.

CONCLUSION
Cerebral ischemia is a rare but potentially fatal complication of pregnancy. Symptoms suggesting cerebral ischemia during pregnancy and the peripartum period should
be investigated thoroughly.
REFERENCES
1. Donaldson JO: Neurology of Pregnancy. Philadelphia, WB
Saunders, 1978, pp 115-l 56
2. Smith AL, Hoff FT, Nielson SL, et al: Barbiturate protection in
acute focal cerebral ischemia. Stroke 1974;5:127
3. Michenfelder JD, Milde JH: Influence of anesthetics on metabolic, functional, and pathological responses to regional cerebral ischemia. Stroke 1975;6:405-410
4. Mosely JI, Laurent JP, Molinari GF: Barbiturate attention of the
clinical course and pathologic lesions in a primate stroke model.
Neurology (Minneap) 1982;25:870-874
5. Michenfelder JD: Barbiturates for brain resuscitation: Yes and
no. Anesthesiology 1982;57:74-75
6. Slogoff S, Girgis KZ, Keats AS: Etiologic factors in neuropsychiatric complications associated with cardiopulmonary bypass. Anesth Analg 1982;61:903-911
7. Nussmeier NA, Ralund C, Slogogg S: Neuropsychiatric complications after cardiopulmonary bypass: Cerebral protection by
a barbiturate. Anesthesiology 1986;64:165-170
8. McMeniman WJ, Fletcher JP, Little JM: Experience with barbiturate therapy for cerebral protection during carotid endarterectomy. Ann R Coll Surg Engl 1984;66:361-364
9. Gross Cl, Adams HP, Sokoll MD, et al: Use of anticoagulants,
electroencephalographic monitoring, and barbiturate cerebral
protection in carotid endarterectomy. Neurosurgery 1981;9:1-5
10. Astrup J: Barbiturate protection in focal cerebral ischemia. Stand
J Clin Lab Invest 1980;40:201-203
11. Steen PA: Barbiturate protection against ischemic brain damage.
Stand J Clin Lab Invest 1980;40:205-207
12. Lawner PM, Sineone FA: Treatment of intraoperative middle
cerebral artery occlusion with pentobarbital and extracraniallintracranial bypass. J Neurosurg 1979;51:71 O-712
13. Rockoff MA, Marshall LF, Shapiro HM: High dose barbiturate
therapy in humans; clinical review of 60 patients. Ann Neurol
1979;6:494-499

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