Neurosurgery
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We have divided head injury into three categories based on the Glasgow Coma Scale (GCS) (severe, 3-8; moderate, 9-12; and minor, 13-15). In a previous report, we described significant disability after minor head injury. The present report describes 199 patients with moderate head injury, 159 of whom underwent follow-up examinations at 3 months. ⋯ The major predictors of unemployment after minor head injury were premorbid characteristics (age, education, and socio-economic status). In contrast, all predictors in moderate head injury were measures of the severity of injury (length of coma, CT diagnosis, GCS on discharge). We conclude that: (a) moderate head injury, not described previously in the literature, results in mortality and substantial morbidity intermediate between those of severe and minor head injury; (b) unlike minor head injury, the principal predictors of outcome after moderate head injury are measures of the severity of injury; and (c) more attention should be directed to patients with moderate head injury than to those with the most severe injuries, in whom brain damage is probably irreversible and all forms of management have demonstrated little success.
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In 58 patients with progressive neurological deterioration from angiographically confirmed cerebral vasospasm after spontaneous subarachnoid hemorrhage, arterial hypertension was induced in an attempt to improve their deficits. The most effective regimen consisted of intravascular volume expansion, blockade of the vagal depressor response, and the administration of antidiuretics and vasopressor agents. With this protocol, arterial blood pressure could be sustained at high levels for prolonged periods. ⋯ Elevating systemic arterial pressure in states of cerebrovascular insufficiency resulting from vasospasm is safe if meticulous attention is paid to physiological, biochemical, and hematological parameters, with the exception that it may be hazardous in the presence of an untreated ruptured or intact aneurysm. Intravascular volume expansion and induced hypertension are effective in reversing ischemic deficits from vasospasm provided that treatment commences before cerebral infarction and that adequate pressures are maintained for a sufficient period. The production of a hypervolemic state by the use of colloid and crystalloid infusion accompanied by atropine blockade of the vagal depressor response and blunting of the diuresis with vasopressin enables arterial pressure to be elevated for longer than 1 week.