Zeleke Sinen, Watson Victoria L, Adams Catherine, Al-Ourani Mohammed
Internal Medicine, Marshall University Joan C. Edwards School of Medicine, Huntington, USA.
Pulmonary and Critical Care Medicine, Marshall University Joan C. Edwards School of Medicine, Huntington, USA.
Cureus. 2024 Dec 31;16(12):e76686. doi: 10.7759/cureus.76686. eCollection 2024 Dec.
Malignant hyperthermia is a pharmacogenetic disorder that manifests clinically as a hypermetabolic crisis when a patient with a mutation in the ryanodine or dihydropyridine receptor genes is exposed to neuromuscular blocking agents. Depolarizing neuromuscular agents are known to cause malignant hyperthermia, but cases caused by nondepolarizing agents are rarely reported. We present a case consistent with malignant hyperthermia after receipt of cisatracurium, a nondepolarizing anesthetic agent. A 57-year-old male patient presented with shortness of breath and increased edema of the lower extremities, found to be clinically volume overloaded. Respiratory status did not improve with diuresis and non-invasive ventilation. He developed severe acute respiratory distress syndrome necessitating endotracheal intubation and ventilation. The patient was beginning to clinically recover when he went into several instances of cardiopulmonary arrest with the eventual return of circulation. An intravenous infusion of cisatracurium was initiated to improve ventilation, and the patient's core temperature rose to 109 degrees F shortly thereafter. Dantrolene was given with an improvement in temperature just before the patient's family opted for comfort measures. Based on our analysis using the Naranjo score for adverse drug reactions, cisatracurium was the probable culprit for the development of malignant hyperthermia. The development of malignant hyperthermia in response to non-depolarizing neuromuscular blockers is a very rare phenomenon but should remain on the list of differential diagnoses in the setting of rapid rise in temperature so that dantrolene may be administered as quickly as possible.
恶性高热是一种药物遗传紊乱疾病,当兰尼碱或二氢吡啶受体基因发生突变的患者接触神经肌肉阻滞剂时,临床上会表现为高代谢危机。已知去极化神经肌肉阻滞剂可导致恶性高热,但由非去极化剂引起的病例报道很少。我们报告一例在接受顺式阿曲库铵(一种非去极化麻醉剂)后符合恶性高热的病例。一名57岁男性患者出现呼吸急促和下肢水肿加重,临床检查发现容量超负荷。利尿和无创通气后呼吸状况未改善。他发展为严重急性呼吸窘迫综合征,需要气管插管和机械通气。患者开始临床恢复时,出现了几次心脏骤停,最终恢复了循环。为改善通气开始静脉输注顺式阿曲库铵,此后不久患者的核心体温升至109华氏度。在患者家属选择姑息治疗之前,给予丹曲林后体温有所改善。根据我们使用纳伦霍药物不良反应评分法的分析,顺式阿曲库铵可能是恶性高热发生的罪魁祸首。对非去极化神经肌肉阻滞剂产生恶性高热是一种非常罕见的现象,但在体温迅速升高的情况下,仍应列入鉴别诊断清单,以便尽快给予丹曲林。