Cerebral hypoxia after etomidate administration and temporary cerebral artery occlusion

Neurovascular surgical procedures often require temporary cerebral arterial occlusion. Although clinical validation is lacking, etomidate has often been used to attenuate the effects of cerebral ischemia in this setting. The purpose of this study was to evaluate the effects of etomidate and temporary cerebral arterial occlusion on human brain tissue oxygen pressure (PO2), carbon dioxide pressure (PCO2), and pH during intracranial aneurysm surgery. We studied nine patients presenting for cerebral aneurysm surgery. A Paratrend probe was used to determine brain tissue pH and gas tensions. Etomidate was administered to produce electroencephalographic burst suppression before temporary cerebral arterial occlusion. After etomidate administration in nine patients, brain tissue PO2 decreased 30% compared with baseline (P < 0.05). During temporary brain artery occlusion in 8 patients, tissue PO2 decreased 32% below preclip values (P < 0.05) in conjunction with a tissue PCO2 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 clipping, tissue pH decreased, compared with patients in whom PO2 remained 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 increases in inspired oxygen concentration. Low tissue PO2 during temporary clipping significantly increases the risk of tissue acidosis.

Etomidate administration alone resulted in cerebral deoxygenation. Subsequent temporary cerebral artery occlusion resulted in additional tissue deoxygenation and acidosis. These results suggest that etomidate enhances hypoxic risk in the setting of cerebral ischemia.