[Effects of anesthetic agents on intracranial pressure]

Abstract

Barbiturates, etomidate and propofol decrease cerebral blood flow (CBF), mediated by a decrease in cerebral metabolism, thus decreasing intracranial pressure (ICP). As the reduction in CBF is secondary to a decrease in cerebral metabolism, these agents will have little effect on CBF or ICP in patients without active cerebral metabolic activity. Ketamine is usually not administered for the anaesthetic management of patients at risk of intracranial hypertension because of the reported increases in cerebral metabolism, CBF and ICP. The increase in CBF, however, may be partly mediated by a sympathetically induced increase in blood pressure and partly by a simultaneous increase in PaCO2 in spontaneously breathing patients. More recent studies report no increase in ICP or flow when ventilation is controlled or when other agents are associated. There is renewed interest in ketamine because it blocks excitatory amino acid receptors in the brain. Synthetic opioids including fentanyl, sufentanil, and alfentanil have been reported to cause an increase in ICP in patients with various intracranial lesions. When blood pressure was supported, no clinically relevant increase in ICP or flow velocity with alfentanil or sufentanil was observed. Thus, the increase in ICP reported with these agents may be related to the compensatory autoregulation-mediated vasodilation, underscoring the importance of administering these agents carefully to avoid systemic hypotension. Halothane consistently increases CBF and should not be used in patients with increased ICP. In contrast, isoflurane does not cause increase in CBF at concentrations below 1 to 1.5 MAC, although the effects on cerebral blood volume are less clear. Desflurane and sevoflurane have similar effects. CO2 reactivity is preserved with all inhaled agents. In patients with increased ICP however, it would be preferable to avoid these agents or to administer very low doses.