Stroke, Vol 18, 365-372, Copyright © 1987 by American Heart Association
IA Awad, LP Carter, RF Spetzler, M Medina and FC Williams Jr
Delayed neurologic deterioration from vasospasm remains the greatest cause
of morbidity and mortality following subarachnoid hemorrhage. The authors
assess the incidence and clinical course of symptomatic vasospasm following
subarachnoid hemorrhage using a uniform management protocol over a 24-month
period. One hundred eighteen consecutive patients were admitted to the
neurovascular surgery service within 2 weeks of subarachnoid hemorrhage not
attributed to trauma, tumor, or vascular malformation (113 patients had
aneurysms). Early surgery was performed whenever possible, and hypertensive
hypervolemic hemodilution therapy was instituted at the first sign of
clinical vasospasm. Forty- two patients (35.6%) developed characteristic
signs and symptoms of clinical vasospasm with angiographic verification of
spasm in 39 cases. All patients with clinical vasospasm received
hypervolemic hemodilution therapy aiming for a hematocrit of 33-38%, a
central venous pressure of 10-12 mm Hg (or a pulmonary wedge pressure of
15-18 mm Hg), and a systolic arterial pressure of 160-200 mm Hg (120-150 mm
Hg for unclipped aneurysms) for the duration of clinical vasospasm. Over
the course of treatment, 60% of patients with clinical vasospasm had
sustained improvement by at least 1 neurologic grade, 24% maintained a
stable neurologic status, and 16% continued to worsen. At the end of
hypervolemic hemodilution therapy, 47.6% had become neurologically normal,
33.3% had a minor neurologic deficit, and 19% had a major neurologic
deficit or were dead. There were 3 instances of cardiopulmonary
deterioration (7%), all of which were in patients without Swan-Ganz
catheters, and all resolved with appropriate diuresis. One patient rebled
and died while on hypervolemic hemodilution therapy.(ABSTRACT TRUNCATED AT
250 WORDS)
ARTICLES
Clinical vasospasm after subarachnoid hemorrhage: response to hypervolemic hemodilution and arterial hypertension
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