Mitterschiffthaler G, Hackl J M, Neumann R
Klinik für Anaesthesie und Allgemeine Intensivmedizin, Universität Innsbruck.
Anaesthesist. 1989 Apr;38(4):210-3.
We report on a patient with neuroleptic malignant syndrome (NMS) caused by a therapy for endogenous depression. The symptoms were hyperpyrexia (39.2 degrees C), rigidity, elevated creatine kinase (CK: 594 U/l) and coma. After transfer from an outside hospital, he was treated, at first without effect with dantrolene p.o. (80 mg q.i.d.) and i.v. (1 mg/kg-1/h-1). Clinical improvement and temperature reduction were noted when the levels of neuroleptic drugs fell during unspecific intensive care with mechanical ventilation, sedation (flunitrazepam, barbiturates), relaxation (pancuronium), and hydration. After uncomplicated weaning from the ventilator the patient became more cooperative and was returned to the psychiatric ward. Further treatment took the form of combined drug therapy with biperiden and flunitrazepam and in addition a series of 12 electroconvulsive therapies (ECT). The elevated CK levels initially decreased, serum potassium levels were found to be within normal limits, and myoglobinuria was not detected during the further course. Trigger agents for NMS are antipsychotic drugs such as thioxanthenes, phenothiazines and butyrophenones. Because the signs and symptoms are so similar to those of malignant hyperthermia (MH), it has been suggested that NMS and MH are related diseases. The postulated mechanisms of NMS become apparent in the CNS, whereas those of MH affect the muscle cell itself. An abnormal in vitro contraction test after NMS should suggest to triggering of MH crisis after succinylcholine administration in anaesthesia for ECT.(ABSTRACT TRUNCATED AT 250 WORDS)
我们报告一例因内源性抑郁症治疗引发神经阻滞剂恶性综合征(NMS)的患者。症状包括高热(39.2摄氏度)、强直、肌酸激酶升高(CK:594 U/l)以及昏迷。从外院转来后,起初口服(80毫克,每日四次)和静脉注射(1毫克/千克/小时)丹曲林治疗无效。在进行机械通气、镇静(氟硝西泮、巴比妥类药物)、松弛(泮库溴铵)和补液的非特异性重症监护期间,当神经阻滞剂药物水平下降时,临床症状改善且体温降低。在顺利脱机后,患者变得更加配合,随后转回精神科病房。进一步治疗采用了比哌立登和氟硝西泮联合药物治疗,此外还进行了12次电休克治疗(ECT)。最初升高的CK水平有所下降,血清钾水平在正常范围内,后续病程中未检测到肌红蛋白尿。NMS的触发因素是抗精神病药物,如噻吨类、吩噻嗪类和丁酰苯类。由于其体征和症状与恶性高热(MH)非常相似,有人提出NMS和MH是相关疾病。NMS的假定机制在中枢神经系统中较为明显,而MH的机制则影响肌肉细胞本身。NMS后异常的体外收缩试验应提示在ECT麻醉中使用琥珀酰胆碱后引发MH危机。(摘要截短至250字)