• R E Carlin, D J McGraw, J R Calimlim, and M F Mascia.
• Department of Anesthesiology, State University of New York Health Science Center at Syracuse 13210, USA.
• J Clin Anesth. 1998 Mar 1;10(2):109-13.

Study ObjectiveTo determine the utility of cerebral oximetry for monitoring the adequacy of cerebral blood flow (CBF) during carotid cross-clamp.DesignProspective study.SettingUniversity hospital.Patients16 consecutive ASA physical status III (or higher) patients for awake carotid endarterectomy (CEA).InterventionsRegional cerebral oxygen saturation (SaO2) was monitored continuously during CEA, which was performed by the same surgeon, and with standard regional anesthetic, sedation, monitoring, and operative techniques. Data were recorded and analyzed using repeated measures analysis of variance (ANOVA).Measurements And Main Results14 hemodynamically stable patients demonstrated significant decreases in cerebral SaO2 from baseline: 69 + 1.8% to 64 + 1.2% at carotid cross-clamp (p < 0.001). After 5, 10, and 15-minute cross-clamp time, cerebral SaO2 was 63 + 1.4%, 64 + 1.5%, and 63 + 1.4%, respectively (p < 0.001, vs. baseline). On cross-clamp removal, cerebral SaO2 rose significantly: 67 + 1.6% (p < 0.01 vs. 5, 10, and 15 min). Two hypotensive patients (mean arterial pressures of 40 and 43 mmHg) developed signs and symptoms of global cerebral ischemia, with a concomitant decrease in cerebral oximetry (40% and 48%, respectively). These changes resolved with correction of hypotension.ConclusionCerebral SaO2 decreased significantly on carotid cross-clamp in patients undergoing awake CEA. Hemodynamically stable patients demonstrated no evidence of regional brain failure when SaO2 decreased to 63% (mean decrease of 7.2%). Two hemodynamically unstable patients had evidence of global brain failure when SaO2 was less than 48% (mean decrease of 36%). Our findings suggest that cerebral oximetry reflects CBF, and it may be an effective, noninvasive method of monitoring regional cerebral oxygenation changes during CEA. Significant reductions in regional SaO2 may be tolerated without evidence of brain failure. Further studies are needed to define an SaO2 threshold that reflects regional brain failure.

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