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.

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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.