Clinical vasospasm after subarachnoid hemorrhage: Response to hypervolemic hemodilution and arterial hypertension

Abstract

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 hypervolemk 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 undipped 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. Death or major neurologic deficit from clinical vasospasm occurred in <7% of all patients with subarachnoid hemorrhage. This compares favorably with the morbidity and mortality attributed to vasospasm in recent reports. The authors conclude that early surgery and aggressive management of clinical vasospasm with hypervolemic hemodilution therapy can be accomplished with minimal morbidity. This management strategy may lower the incidence of death and disability from vasospasm after subarachnoid hemorrhage. © 1987 American Heart Association, Inc.