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左侧甲状腺叶切除术和峡部切除术时疑似假性胆碱酯酶缺乏症:1 例报告。

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

机构信息

University of South Dakota Sanford School of Medicine, Sioux Falls, South Dakota.

Avera Sacred Heart Hospital, Yankton, South Dakota.

出版信息

S D Med. 2024 Jun;77(6):266-269.

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.

摘要

背景

假性胆碱酯酶(丁酰胆碱酯酶)缺乏症是一种获得性或遗传性疾病,其特征是血浆中假性胆碱酯酶水平降低,导致无法代谢神经肌肉阻滞剂琥珀酰胆碱和米库氯铵,从而延长其瘫痪作用。这通常会导致术后拔管延迟和需要额外的重症监护。

病例描述

我们描述了一例先前健康的 59 岁女性疑似假性胆碱酯酶缺乏症的病例,该女性接受了左侧甲状腺叶切除术和峡部切除术。患者在插管前接受了 120 毫克琥珀酰胆碱氯。大约在接受琥珀酰胆碱氯两小时后,患者在手术完成后不符合拔管标准。患者被转至 ICU 进行呼吸支持,并等待药物从患者体内清除。患者在接受琥珀酰胆碱氯约四小时后恢复肌肉控制,并在无并发症的情况下拔管。患者在拔管后分享说,她有一个血亲患有假性胆碱酯酶缺乏症。

结论

假性胆碱酯酶缺乏症很少见,但由于代谢减少,随后药效学作用增加,在给予琥珀酰胆碱氯、米库氯铵或酯类局部麻醉剂后可能导致潜在的严重并发症。鉴于琥珀酰胆碱氯作为神经肌肉阻滞剂的广泛应用,如本例中,医生必须了解其表现、病理生理学、诊断和管理。此外,该病例表明在术前评估中彻底询问任何麻醉并发症的个人或家族史的重要性。

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