Dexmedetomidine does not increase the incidence of intracarotid shunting in patients undergoing awake carotid endarterectomy.

Systemic administration of dexmedetomidine (DEX) decreases cerebral bloodflow (CBF) via direct alpha-2-mediated constriction of cerebral blood vessels and indirectly via its effect on the intrinsic neural pathway modulating vascular smooth muscle. Reduction in CBF without a concomitant decrease in cerebral metabolic rate has raised concerns that DEX may limit adequate cerebral oxygenation of brain tissue in patients with already compromised cerebral circulation (e.g., carotid endarterectomy [CEA]). In this study, we established the incidence of intraarterial shunting used as a sign of inadequate oxygen delivery in a consecutive series of 123 awake CEA performed in our institution using DEX as a primary sedative. Data were prospectively recorded in 151 patients who underwent CEA during the study period. Eighteen patients were sedated with midazolam and fentanyl (M/F) for medical or logistical reasons. Patients thought to be at risk of an intraoperative stroke were treated with a prophylactic intraarterial shunt. These patients, as well as those who required general anesthesia, were excluded from the final analysis. Five patients (4.3%) in the DEX group required intraarterial shunts. The incidence of shunting in patient undergoing awake CEA in our institution is 10% (historical control). No patients developed a stroke or other serious complications. It appears that the use of DEX as a primary sedative drug for CEA does not increase the incidence of intraarterial shunts.