Suspected Pseudocholinesterase Deficiency During Left Thyroid Lobectomy and Isthmusectomy: A Case Report.

Q4 Medicine
Jennifer Boleyn, Madison McLaury, Stephanie Wieman
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Abstract

Background: Pseudocholinesterase (butyrylcholinesterase) deficiency is an acquired or inherited condition in which decreased plasma levels of the pseudocholinesterase enzyme lead to an inability to metabolize the neuromuscular blocking agents succinylcholine and mivacurium, prolonging their paralytic effects. This often results in delayed extubation and additional intensive care requirements in the postoperative period.

Case description: We describe a case of suspected pseudocholinesterase deficiency in a previously healthy 59-year-old female who underwent a left thyroid lobectomy and isthmusectomy. The patient received 120 mg of succinylcholine chloride before intubation. The patient did not meet extubation criteria following the completion of the procedure approximately two hours after receiving succinylcholine chloride. The patient was transferred to the ICU for respiratory support and for the medication to clear from the patient's system. The patient regained muscle control approximately four hours after receiving succinylcholine chloride and was extubated without complication. The patient shared post-extubation that she had a blood relative with the diagnosis of pseudocholinesterase deficiency.

Conclusion: Pseudocholinesterase deficiency is rare but can result in potentially serious complications following the administration of succinylcholine chloride, mivacurium, or ester local anesthetics due to reduced metabolism and subsequently increased pharmacodynamic effects. Given the widespread use of succinylcholine chloride as a neuromuscular blocking agent, such as in this case, providers must be aware of the presentation, pathophysiology, diagnosis, and management. Additionally, this case demonstrates the importance of thoroughly inquiring about any personal or family history of anesthetic complications during a preoperative assessment.

左侧甲状腺叶切除术和峡部切除术期间疑似假胆碱酯酶缺乏症:病例报告。
背景:假胆碱酯酶(丁酰胆碱酯酶)缺乏症是一种获得性或遗传性疾病,血浆中假胆碱酯酶水平降低会导致无法代谢神经肌肉阻断剂琥珀胆碱和米伐库铵,从而延长其麻痹作用。这通常会导致术后延迟拔管和需要额外的重症监护:我们描述了一例疑似假性胆碱酯酶缺乏症的病例,患者是一名先前健康的 59 岁女性,接受了左甲状腺叶切除术和峡部切除术。患者在插管前服用了120毫克氯化琥珀胆碱。患者在接受氯化琥珀胆碱约两小时后完成手术,但未达到拔管标准。患者被转入重症监护室接受呼吸支持,并等待药物从患者体内排出。患者在接受氯化琥珀胆碱治疗约四小时后恢复了肌肉控制,并在无并发症的情况下拔管。患者在拔管后表示,她有一位亲属被诊断患有假性胆碱酯酶缺乏症:假性胆碱酯酶缺乏症非常罕见,但在使用氯化琥珀胆碱、米伐库铵或酯类局麻药后,由于新陈代谢降低,药效作用增强,可能导致严重并发症。鉴于氯化琥珀胆碱作为神经肌肉阻滞剂的广泛使用,例如在本病例中,医护人员必须了解其表现、病理生理学、诊断和处理方法。此外,本病例还说明了在术前评估时彻底询问任何个人或家族麻醉并发症病史的重要性。
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CiteScore
0.50
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62
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