CEREBRAL HYPOXIA AFTER ETOMIDATE ADMINISTRATION AND TEMPORARY CEREBRAL-ARTERY OCCLUSION

Neurovascular surgical procedures often require temporary cerebral art erial occlusion. Although clinical validation is lacking, etomidate ha s often been used to attenuate the effects of cerebral ischemia in thi s setting. The purpose of this study was to evaluate the effects of et omidate and temporary cerebral arterial occlusion on human brain tissu e oxygen pressure (Po,), carbon dioxide pressure (PCO2), and pH during intracranial aneurysm surgery. We studied nine patients presenting fo r cerebral aneurysm surgery. A Paratrend(R) probe was used to determin e brain tissue pH and gas tensions. Etomidate was administered to prod uce electroencephalographic burst suppression before temporary cerebra l arterial occlusion. After etomidate administration in nine patients, brain tissue PO2 decreased 30% compared with baseline (P < 0.05). Dur ing temporary brain artery occlusion in 8 patients, tissue PO2 decreas ed 32% below preclip values (P < 0.05) in conjunction with a tissue PC O2 increase of 23% (P < 0.05) and a 0.1-unit decrease in pH (P < 0.05) . In patients in whom PO2 decreased below 10 mm Hg during temporary cl ipping, tissue pH decreased, compared with patients in whom PO2 remain ed above 10 mm Hg (P < 0.05). These results demonstrate that etomidate administration during cerebral aneurysm surgery decreases tissue PO2 and that in these patients, tissue PO2 does not increase with increase s in inspired oxygen concentration. Low tissue PO2 during temporary cl ipping significantly increases the risk of tissue acidosis. Implicatio ns: Etomidate administration alone resulted in cerebral deoxygenation. Subsequent temporary cerebral artery occlusion resulted in additional tissue deoxygenation and acidosis. These results suggest that etomida te enhances hypoxic risk in the setting of cerebral ischemia.