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

Abstract

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.

Fig. 1

Patient flowchart.

Fig. 2

The raw EEG and the density spectral array during surgery. The raw EEG (top) and the density spectral array (DSA) (bottom) during anaesthesia before (a), during (b) and after burst suppression coma (c). (a) EEG under general anaesthesia before initiating burst suppression coma, showing alpha and delta waves. In the density spectral arrays (DSA) a clearly defined alpha and delta band, which is typical for propofol anaesthesia is visible. (b) EEG during burst suppression coma induced by increase in propofol. The DSA shows a preserved delta band and disappearance of the alpha band during burst suppression. (c) EEG after termination of the burst suppression at the end of surgery showing the recurrence of alpha and delta waves. The DSA shows the reappearance of the alpha band.

Fig. 3

Pooled mean arterial blood pressure. Pooled mean arterial blood pressure (MAP) data of the study participants divided into the control group (black) and dexmedetomidine group (yellow). The blood pressure values before surgery were compared with the blood pressure values up to the start of surgery (Panel a). The ratio between the same MAP values from both groups shows that the MAPs of the control group tend to decrease between induction of anaesthesia and start surgery and those of the dexmedetomidine group roughly correspond to the preoperative values (Panel b).

Fig. 4

Blood pressure as mean arterial pressure (MAP) during different stages of the procedure for both groups. All MAP values measured at the four different timepoints were pooled and are illustrated in the graph: control group (black) and dexmedetomidine group (yellow). Individual patients are shown as solid lines; summary measures (median and interquartile range) are shown for each timepoint. The first stage is defined as the time from induction of anaesthesia until start of the procedure, the second from start of the procedure until cross-clamping of the internal carotid artery (ICA), the third from beginning to end of the cross-clamping of the ICA and the fourth from unclamping the ICA until the end of the operation. At none of the four stages was there a significant difference in the median MAP shown between the two groups. The elevation at the third stage reflects our haemodynamic protocol, which included an increase in MAP by 20 mmHg from the baseline blood pressure: mostly this was achieved by the continuous use of vasopressors. A decrease of systolic arterial blood pressure is shown at the fourth stage, to achieve a target systolic blood pressure between 140 and 100 mmHg.