Propofol

Sedative drugs that decrease ICP via an effect on cerebral metabolism and CBF include most of the intravenous anesthetic agents except keta-mine. All have a depressant effect on the central nervous system, resulting in a dose-related decrease in level of consciousness and metabolic rate. Propofol has a similar metabolic and vascular profile to barbiturates, causing a dose-related decrease in cerebral metabolic rate and coupled decrease in CBF, resulting in a reduction in ICP in patients with cerebral metabolic activity. However, in some studies the decrease in CBF exceeded the concomitant decrease in metabolic rate. Its pharmacokinetic profile, with a short half-life, makes it a particularly suitable sedative agent in neurosurgical patients, allowing prompt neurological assessment within 2-3 hours of discontinuation of the infusion in usual doses (50-150 ^g/kg/min). In a multicenter trial, propofol was efficacious in reducing ICP although the study failed to show an improvement in neurological outcome. In high doses (>300 ^g/kg/min), it can be used to induce pharmacological coma with burst-suppression on electroencephalogram to achieve maximal metabolic suppression for control of ICP. In children, when used as a continuous infusion for a prolonged period, propofol has been reported to be associated with the development of a metabolic syndrome that is characterized by acidosis, rhabdomyolysis, cardiac failure and a high mortality rate [7]. More recently, a similar syndrome has also been reported to occur in head-injured adults treated with propofol >5 mg/kg/h [8]. In both children and

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