The conflicting evidence concerning the influence of high-dose steroids on intracranial pressure (ICP) and outcome following severe head injury has led to the institution of the prospective double-blind controlled trial reported here. Severely head-injured patients admitted to intensive care during a 3-year period were randomly allocated to a dexamethasone- or placebo-treated group. Adults in the steroid group received dexamethasone, 50 mg intravenously, as a bolus on admission to the neurosurgical unit, then 100 mg on Days 1, 2, and 3, 50 mg on Day 4, and 25 mg on Day 5 on continuous intravenous infusion. Children received proportionate intravenous dosages calculated on a weight basis. Severity of head injury was assessed from admission Glasgow Coma Scale (GCS) scores and the appearance of the admission computerized tomography scan. Intracranial pressure (ICP) was monitored in all patients from the surface subarachnoid space. Outcome at 6 months was assessed using the Glasgow Outcome Scale. Steroid and placebo groups were similar in terms of admission GCS score, intracranial pathology, incidence of associated injuries, and time interval from injury to admission to intensive care. The ICP generally increased during the first 48 hours of intensive therapy; there was no difference in this trend between the steroid and placebo groups. A poorer outcome was observed in patients with elevated ICP who received steroids. No increase in the incidence of pulmonary, gastrointestinal, or other extracranial complications was seen in the steroid group. The 6-month outcome did not differ between the steroid and placebo groups. No advantage of high-dose dexamethasone on ICP trends or clinical outcome in the treatment of severe head injury has emerged from this study.

Ten patients with intracranial lesions, anaesthetized with thiopentone and nitrous oxide (70%) in oxygen (30%) received etomidate 0.2 mg kg-1 i.v. Ventilation was controlled in each patient. Intracranial pressure (i.c.p.) and mean arterial pressure (m.a.p.) were recorded. I.c.p. decreased significantly in all patients (0.01 greater than P greater than 0.001). Although PaCO2 decreased during the period of measurement, the extent and time-course of this change suggested that it was not mainly responsible for changes in i.c.p. M.a.p. decreased in most patients, but the decrease was statistically significant only at 3 and 4 min after the administration of etomidate (0.05 greater than P greater than 0.02). The changes in cerebral perfusion pressure (c.p.p.) and heart rate were not clinically or statistically significant. We conclude that etomidate can be used for the induction of anaesthesia in patients with intracranial space-occupying lesions without increasing i.c.p. or seriously reducing c.p.p.

Intracranial pressure has been measured in 45 patients undergoing neurosurgery during the induction of deliberate hypotension using either sodium nitroprusside or trimetaphan. A statistically significant increase in intracranial pressure (ICP) occurred during the early stages of the infusion of nitroprusside in normocapnic patients. A non-significant increase in ICP was obtained in hypocapnic patients. The mean ICP increased from 6.3 mm Hg to 11.7 mm Hg when the arterial pressure was reduced slightly, but the response in individual patients varied widely (range -1.6 mm Hg to +20.9 mm Hg). When the arterial pressure (BP) had decreased to 70% of the value existing before infusion of nitroprusside, mean ICP returned to control values and thereafter decreased with further reductions in BP. In patients rendered hypotensive with trimetaphan, there was no change in mean ICP but two patients showed moderate increases (+9.3 mm Hg and +5.7 mm Hg). The mechanism of the increase in ICP with nitroprusside is thought to be expansion of the intracranial blood volume as a result of cerebral vasodilatation. Trimetaphan does not usually produce ICP changes except when intracranial compression is severe, for in these circumstances a small change in intracranial blood volume consequent upon autoregulation may trigger an increase in ICP.