Kramer Kaitlin, Payne Thomas, Brooks Mitchell, Barry Jessica, Mahajan Neha, Malcolm Samantha, Braithwaite Hannah, Wang Alex, Thompson Chris, Liyanagama Keith, Sanders Robert D
Department of Anaesthetics, Royal Prince Alfred Hospital, Sydney, NSW, Australia.
Faculty of Medicine and Health, University of Sydney, Sydney, NSW, Australia.
BJA Open. 2024 Dec 16;13:100359. doi: 10.1016/j.bjao.2024.100359. eCollection 2025 Mar.
Intraoperative awareness, without explicit recall, occurs after induction of anaesthesia in approximately 10% of persons under 40 yr of age. Most anaesthetic agents minimally suppress the noradrenergic system. We hypothesised that addition of dexmedetomidine, which suppresses noradrenergic activity, may reduce encephalographic (EEG) arousal in response to tracheal intubation; such an effect would lay the foundation for future studies of dexmedetomidine in reducing intraoperative awareness.
A single-site randomised, placebo-controlled trial with sex-based stratification was conducted. Participants, aged 18-40 yr old, undergoing intubation for general anaesthesia were eligible for recruitment and randomly allocated to receive dexmedetomidine or placebo. Dexmedetomidine (0.5 μg kg) was given as a 5-min loading dose before induction. Bispectral index (BIS) values were collected during the induction phase of anaesthesia and the isolated forearm technique was used to assess patients' responsiveness before and after tracheal intubation. The primary outcome was the effect of dexmedetomidine on changes in BIS from pre-to postintubation.
A total of 51 patients were recruited and included in the primary analysis. We did not observe an effect of dexmedetomidine on changes in BIS after tracheal intubation (mean difference -1.13, 95% confidence interval [CI] -4.87 to 2.62; =0.556). Dexmedetomidine reduced the estimated plasma propofol concentration at loss of responsiveness (difference [dexmedetomidine - placebo]: -1.06 μg ml, 95% CI -1.66 to -0.46; <0.001) and before intubation (difference [dexmedetomidine - placebo]: -1.84 μg ml, 95% CI -2.79 to -0.90; <0.001). There was one patient in the placebo group who gave positive responses in the isolated forearm test before and after tracheal intubation.
Dexmedetomidine demonstrated an anaesthetic-sparing effect at induction of anaesthesia but did not prevent EEG arousal after tracheal intubation, as defined by an increase in the BIS value.
Australia and New Zealand Clinical Trials Registry (Trial ID: ACTRN12622000754741).
在40岁以下人群中，约10%的人在麻醉诱导后会出现无明确回忆的术中知晓。大多数麻醉药物对去甲肾上腺素能系统的抑制作用较弱。我们假设，添加抑制去甲肾上腺素能活性的右美托咪定，可能会减少气管插管引起的脑电图（EEG）觉醒；这种效应将为未来右美托咪定减少术中知晓的研究奠定基础。
进行了一项基于性别的分层单中心随机安慰剂对照试验。年龄在18 - 40岁、接受全身麻醉插管的参与者符合招募条件，并被随机分配接受右美托咪定或安慰剂。右美托咪定（0.5μg/kg）在诱导前作为5分钟负荷剂量给药。在麻醉诱导期收集脑电双频指数（BIS）值，并采用孤立前臂技术评估气管插管前后患者的反应性。主要结局是右美托咪定对插管前后BIS变化的影响。
共招募了51例患者并纳入主要分析。我们未观察到右美托咪定对气管插管后BIS变化有影响（平均差值 -1.13，95%置信区间[CI] -4.87至2.62；P = 0.556）。右美托咪定降低了意识消失时的估计血浆丙泊酚浓度（差值[右美托咪定 - 安慰剂]：-1.06μg/ml，95%CI -1.66至 -0.46；P < 0.001）以及插管前的浓度（差值[右美托咪定 - 安慰剂]：-1.84μg/ml，95%CI -2.79至 -0.90；P < 0.001）。安慰剂组有1例患者在气管插管前后的孤立前臂试验中呈阳性反应。
右美托咪定在麻醉诱导时显示出节省麻醉药物的作用，但并未如BIS值增加所定义的那样预防气管插管后的EEG觉醒。
澳大利亚和新西兰临床试验注册中心（试验编号：ACTRN12
