During 1977-1978, 127 patients with severe head injury were admitted and underwent intracranial pressure (ICP) monitoring. All patients had Glasgow Coma Scale (GCS) scores of 7 or less. All received identical initial treatment according to a standardized protocol. The patients' average age was 29 years; 60% had multiple trauma, and 35% needed emergency intracranial operations. Treatment for elevations of ICP was begun when ICP rose to 20 to 25 mm Hg, and included mannitol therapy and drainage of cerebrospinal fluid (CSF) when possible. Forty-three patients (34%) had ICP greater than or equal to 25 mm Hg; of these, 36 (84%) died. The mortality rate of the entire group was 46%. During 1979-1980, 106 patients with severe head injury were admitted and underwent ICP monitoring. Their average ager was 29 years; 51% had multiple trauma, and 31% underwent emergency intracranial surgery. All patients received the same standardized protocol as the previous series, with the exception of the treatment of ICP. In this present series: if ICP was 15 mm Hg or less (normal ICP), patients were continued on hyperventilation, steroids, and intensive care; if ICP was 16 to 24 mm Hg, mannitol was administered and CSF was drained; if ICP was 25 mm Hg or greater, the patients were randomized into a controlled barbiturate therapy study. Twenty-six patients (25%) had ICP's of 25 mm Hg or greater, compared to 34% in the previous series (p less than 0.05), and 18 of these 26 patients (69%) died. The overall mortality for this current series was 28% compared to 46% in the previous series (p less than 0.0005). This study reconfirms the high mortality rate if ICP is 25 mm Hg or greater; however, the data also document that early aggressive treatment based on ICP monitoring significantly lessens the incidence of ICP of 25 mm Hg or greater and reduces the overall mortality rate of severe head injury.

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This is a prospective randomized study of the efficacy of steroid therapy in patients with severe head injury. One hundred patients were randomized into two equal groups: the steroid group received 5 mg/kg/day of methylprednisolone, and the nonsteroid group received no drug. The groups were similar in their clinical features. All patients received a standardized therapeutic regimen. The patients were also classified as early responders or nonresponders to the overall treatment protocol without regard to steroid administration, on the basis of change in Glasgow Coma Scale score during the first 3 days of admission. There was no statistically significant difference in the outcome of the steroid and nonsteroid group at 6 months. Of the responders who were on steroids, 74% had good outcomes or were disabled, compared with 56% of the responders who did not receive steroids. In the nonresponder group, the patients on steroids were actually associated with a worse outcome than those who did not receive steroids: 75% of the nonresponders who received steroids were dead or vegetative, compared to 56% of those who were not receiving steroids. The data suggest that: 1) the effect of steroids may be different for different patient groups; 2) in order to identify these patients, a sensitive coma scale is needed; and 3) a rational approach to steroid therapy in head-injured patients may be to start all patients on steroids, but to discontinue their use in patients identified as not benefiting from steroid therapy.