一例丁酰胆碱酯酶活性显著降低的儿童因米库氯铵阻滞延长导致苏醒延迟：病例报告

文献信息

中文摘要

背景： 儿童全身麻醉后苏醒延迟并不常见，需要及时评估药理学、代谢及神经系统方面的原因。残余神经肌肉阻滞仍是一个重要的可逆性原因，尤其是在使用依赖血浆胆碱酯酶代谢的短效神经肌肉阻滞剂时。
病例报告： 我们报告一例既往健康的三岁男孩，在芬太尼、丙泊酚、七氟烷和米库氯铵全身麻醉下接受择期腺样体切除术、扁桃体部分切除术和鼓膜置管术。手术后，患者未能恢复自主呼吸、有目的的动作或对疼痛刺激的反应。对此，给予新斯的明以逆转可能的残余神经肌肉阻滞；然而，未观察到立即的临床改善，并继续机械通气。无法进行定量神经肌肉监测。因此，无法客观评估残余阻滞，给予新斯的明时的阻滞深度仍不清楚。患者被转至三级儿科中心进一步评估。数小时后，自主呼吸和运动活动恢复，患者成功拔管。回顾性家族史显示，患者的祖父在麻醉后恢复时间延长。随后的实验室检测显示血浆丁酰胆碱酯酶活性显著降低（2493 U/L；参考范围7000-19,000 U/L），强烈提示遗传性丁酰胆碱酯酶缺乏症。
结论： 本病例强调了在儿童麻醉后苏醒延迟时考虑残余神经肌肉阻滞、维持气道保护以及获取相关家族史以指导未来管理的重要性。

英文摘要

Background: Delayed emergence after general anesthesia in pediatric patients is uncommon and requires prompt evaluation of pharmacological, metabolic, and neurological causes. Residual neuromuscular blockade remains an important reversible cause, particularly when short acting neuromuscular blocking agents dependent on plasma cholinesterase metabolism are used. Case report: We report the case of a previously healthy three-year-old boy who underwent elective adenoidectomy, tonsillotomy, and tympanostomy under general anesthesia with fentanyl, propofol, sevoflurane, and mivacurium. Following the procedure, the patient failed to regain spontaneous breathing, purposeful movements, or response to painful stimuli. In response, neostigmine was administered to reverse possible residual neuromuscular blockade; however, no immediate clinical improvement was observed, and mechanical ventilation was continued. Quantitative neuromuscular monitoring was unavailable. Therefore, residual blockade could not be objectively assessed, and the depth of blockade at the time of neostigmine administration remained unknown. The patient was transferred to a tertiary pediatric center for further evaluation. Several hours later, spontaneous breathing and motor activity recovered, and the patient was successfully extubated. Retrospective family history revealed prolonged recovery after anesthesia in the patient's grandfather. Subsequent laboratory testing demonstrated markedly reduced plasma butyrylcholinesterase activity (2493 U/L; reference range 7000-19,000 U/L), raising a strong suspicion of inherited butyrylcholinesterase deficiency. Conclusions: This case highlights the importance of considering residual neuromuscular blockade in delayed emergence after pediatric anesthesia, maintaining airway protection, and obtaining relevant family history to guide future management.