Treatment of ischemic deficits from cerebral vasospasm with high dose barbiturate therapy

In 12 patients with life-threatening neurological deficits from vasospasm refractory to other measures, high dose barbiturate therapy was used in an attempt to prevent permanent changes in the brain. In each case angiography was performed and intracranial pressure was measured. Dexamethasone, a low molecular weight dextran, and mannitol were administered. If intracranial pressure (ICP) was elevated, drainage of cerebrospinal fluid and hyperventilation were used. Arterial pressure was maintained at not less than 140/90 preoperatively and 180/100 postoperatively. Barbiturate therapy was continued until vasospasm decreased angiographically and ICP was normal. Eleven of the 12 patients perished. One had a fatal rebleed. One died of an iatrogenic hemothorax. Four died from uncontrollable intracranial hypertension. One improved slightly and then died from a cardiac arrhythmia. One died of increased ICP when her ventriculostomy malfunctioned. One improved and was responding purposefully to pain, only to die suddenly with a low ICP. Two patients became awake and responsive to verbal commands; 1 of these died from Klebsiella meningitis and the other died from an intracerebral hematoma. In the 3 patients in whom hypothermia was also used, profound alterations in acid-base and fluid electrolyte balance occurred. These discouraging results are most likely a reflection of the severity of the patients' condition at the beginning of therapy. There may be some benefit of barbiturates in the management of vasospasm, and the potential effectiveness of barbiturates may be more obvious if therapy is started at an earlier stage. However, until further evidence of the usefulness of this modality becomes manifest, it should be limited to patients with life-threatening impairments unresponsive to all other measures.