Abstract

Delayed neurologic deterioration from vasospasm remains the greatest cause of death and major disability following subarachnoid hemorrhage. The authors assess the incidence and clinical course of symptomatic vasospasm following aneurysmal subarachnoid hemorrhage using a uniform management. One hundred seventy two consecutive patients were admitted to the neurosurgery service within 2 weeks of subarachnoid hemorrhage not attributed to vascular malformation, tumor or head injury. Four vessels study was performed in 155 patients (149 patients had aneurysms). Hypervolemic hemodilution therapy was instituted at the first sign of clinical vasospasm. Sixty nine patients (40.1%) developed characteristic signs and symptoms of clinical vasospasm with angiographic verification of spasm in all cases. All patients with clinical vasospasm received hypervolemic hemodilution therapy aiming for a hematocrit of 30-35%, pulmonary wedge pressure of 12-18 mmHg (or a central venous pressure 7-10 mmHg), and systolic pressure of 160-200 mmHg for clipped aneurysm (120-150 mmHg for unclipped aneurysm) for the duration of clinical vasospasm. Neurologic grades of 69 patients on admission: 7 patients were Hunt & Kosnik grade I, 25 were grade II, 32 were grade III, 6 were grade IV, and 1 was grade V. At the onset of clinical vasospasm, 3 were grade II, 58 were grade III, 6 were grade IV, 2 were grade V.At the end of hypervolemic hemodilution therapy, thirty one patients (44.9%) had become neurologically normal, eighteen patients (26.1%) had mild or moderate disability, and twenty patients (29.0%) had severe disability or death. There were 3 instances of pulmonary edema, and all were resolved with appropriate diuresis. Four patients rebled and died while on hypervolemic hemodilution therapy. Death or severe disability from clinical vasospasm occurred in 7.5% of all patients with subarachnoid hemorrhage. This compares favorably with the mortality and morbidity attributed to vasospasm in recent reports. Similar results have been reported for patients treated with hypervolemic hemodilution and arterial hypertension. The authors conclude that early surgery and aggressive managements of clinical vasospasm with volume expansion therapy can be accomplished with minimal morbidity.

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