European journal of anaesthesiology · 2024
Co-administration of dexmedetomidine with total intravenous anaesthesia in carotid endarterectomy reduces requirements for propofol and improves haemodynamic stability: A single-centre, prospective, randomised controlled trial.
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Vetter Christian, Meyer Eva R, Seidel Kathleen, Bervini David, Huber Markus, Krejci Vladimir
Аннотация
BACKGROUND: Total intravenous anaesthesia guided by electroencephalography and neurophysiological monitoring may be used for carotid endarterectomy. Reduction of brain metabolic demand during cross-clamping of the internal carotid artery with propofol titrated to burst suppression requires effect-site concentrations that may delay emergence and interfere with intraoperative neurophysiological monitoring.
OBJECTIVE: To test the hypothesis that dexmedetomidine decreases the effect-site concentration of propofol required for burst-suppression in patients undergoing carotid endarterectomy.
DESIGN: Randomised controlled trial.
PARTICIPANTS: Patients undergoing carotid endarterectomy.
SETTING: University Hospital of Berne, Switzerland, from October 2018 to September 2024.
INTERVENTIONS: Patients were randomised into a control ( n = 23) and a dexmedetomidine groups ( n = 22). Total intravenous anaesthesia was administered to both groups. Patients in the dexmedetomidine group received an intravenous bolus of dexmedetomidine (0.4 μg kg -1 over 10 min) before induction, followed by a continuous intravenous infusion (0.4 μg kg -1 h -1 ). The effect-site concentrations of propofol were titrated against frontal electroencephalography parameters. Burst suppression was induced with propofol during cross-clamping of the internal carotid artery.
OUTCOME MEASURES: The primary outcome was the effect-site concentration of propofol required for burst-suppression. The secondary outcomes were the requirement for vasoactive substances, neurophysiological monitoring parameters, and postoperative delirium.
RESULTS: The effect-site concentration of propofol required for burst suppression was 4.0 μg ml -1 [3.50 to 4.90] (median [interquartile range]) in the dexmedetomidine group compared with 6.0 μg ml -1 [5.5 to 7.3] in the control group ( P < 0.001). Less norepinephrine was required in the dexmedetomidine group (total 454 μg [246 to 818] compared with 1000 μg [444 to 1326] ( P = 0.015) in the control group). Dexmedetomidine did not affect intraoperative neurophysiological monitoring.
CONCLUSION: Co-administration of dexmedetomidine to total intravenous anaesthesia for carotid endarterectomy decreased the effect-site concentrations of propofol required for burst suppression by 33%. The propofol-sparing effect and peripheral alpha-agonism of dexmedetomidine may explain the reduced requirement for vasopressors.
TRIAL REGISTRATION: Clinicaltrials.gov identifier: NCT04662177.
OBJECTIVE: To test the hypothesis that dexmedetomidine decreases the effect-site concentration of propofol required for burst-suppression in patients undergoing carotid endarterectomy.
DESIGN: Randomised controlled trial.
PARTICIPANTS: Patients undergoing carotid endarterectomy.
SETTING: University Hospital of Berne, Switzerland, from October 2018 to September 2024.
INTERVENTIONS: Patients were randomised into a control ( n = 23) and a dexmedetomidine groups ( n = 22). Total intravenous anaesthesia was administered to both groups. Patients in the dexmedetomidine group received an intravenous bolus of dexmedetomidine (0.4 μg kg -1 over 10 min) before induction, followed by a continuous intravenous infusion (0.4 μg kg -1 h -1 ). The effect-site concentrations of propofol were titrated against frontal electroencephalography parameters. Burst suppression was induced with propofol during cross-clamping of the internal carotid artery.
OUTCOME MEASURES: The primary outcome was the effect-site concentration of propofol required for burst-suppression. The secondary outcomes were the requirement for vasoactive substances, neurophysiological monitoring parameters, and postoperative delirium.
RESULTS: The effect-site concentration of propofol required for burst suppression was 4.0 μg ml -1 [3.50 to 4.90] (median [interquartile range]) in the dexmedetomidine group compared with 6.0 μg ml -1 [5.5 to 7.3] in the control group ( P < 0.001). Less norepinephrine was required in the dexmedetomidine group (total 454 μg [246 to 818] compared with 1000 μg [444 to 1326] ( P = 0.015) in the control group). Dexmedetomidine did not affect intraoperative neurophysiological monitoring.
CONCLUSION: Co-administration of dexmedetomidine to total intravenous anaesthesia for carotid endarterectomy decreased the effect-site concentrations of propofol required for burst suppression by 33%. The propofol-sparing effect and peripheral alpha-agonism of dexmedetomidine may explain the reduced requirement for vasopressors.
TRIAL REGISTRATION: Clinicaltrials.gov identifier: NCT04662177.