Institutional members access full text with Ovid®

Brain Tissue Oxygenation During Dexmedetomidine Administration in Surgical Patients With Neurovascular Injuries

Drummond, John Cornell MD, FRCPC* †; Sturaitis, Mary K. MD

Journal of Neurosurgical Anesthesiology: October 2010 - Volume 22 - Issue 4 - pp 336-341
doi: 10.1097/ANA.0b013e3181e4b7e3
Clinical Reports

Investigations in dogs have shown substantial dexmedetomidine (Dex)-induced reductions in cerebral blood flow (CBF) unaccompanied by reductions in cerebral metabolic rate (CMR). If this effect were to occur in humans in areas of injured brain in which CBF is already low, oxygen delivery might be critically impaired. The institutional use of brain PO2 monitoring during neurovascular surgery and the use of Dex as a component of the anesthetic allowed insight into this issue. Data from 5 neurovascular surgery patients, 2 for excision of arteriovenous malformations (AVMs), and 3 for intracranial aneurysm clipping were reviewed retrospectively. All had acute, lesion-related neurologic deficits. During general anesthesia with sufentanil and sevoflurane, with or without N2O, a parenchymal brain tissue PO2 (PbrO2) electrode was placed directly in the territory at risk from the pending neurosurgical intervention. After a stable PbrO2 value was achieved, Dex was administered by bolus (1 μg/kg over 10 min) and infusion (0.5 to 0.7 μg/kg/min). Mean arterial pressure (MAP), heart rate (HR), and PbrO2 were observed continuously for at least 25 minutes. Baseline PbrO2 values were relatively low (≤16 mm Hg) in 4 of the 5 patients, a pattern consistent with antecedent neurologic insult. In the 15 minutes after initiation of Dex administration, the pattern was one of a modest increase in Pbr02 (maximum 11.1%; P=0.0147) occurring roughly in parallel with a modest increase in MAP [maximum 3.5 mm Hg (4.5%); P=0.041]. HR did not change. Clinically significant reduction of PbrO2 did not occur before neurosurgical interventions. These observations provide no support for a direct cerebral vasoconstrictive effect of Dex in humans that is independent of any vasoconstriction that may occur as a consequence of Dex-induced reduction in CMR. At a minimum, any such effect was insufficient to have an adverse effect on oxygen delivery to brain parenchyma.

*Department of Anesthesiology, University of California

Anesthesia Service, VA Medical Center, San Diego CA

Department of Anesthesiology and Neurosurgery, Rush University Medical Center, Chicago IL

Financial Support: Department of Anesthesiology, Rush University Medical Center.

Reprints: Dr. John Cornell Drummond, MD, FRCPC, VA Medical Center-125, 3350 La Village Drive, San Diego CA 92161 (e-mail: jdrummond@ucsd.edu).

Received for publication March 30, 2010; accepted April 26, 2010

Disclosures/Conflict of Interest: There are no current (most recent 12 mo) relationships. In past, Dr. Drummond has received lecture honoraria from Hospira, and Dr. Sturaitis has received research grant support and lecture honoraria from Hospira.

Presented in part at the Annual Meeting of the IARS, Tampa FL, March 27, 2004.

© 2010 Lippincott Williams & Wilkins, Inc.