Soriano Francisco Garcia, Vianna Elcio dos Santos Oliveira, Velasco Irineu Tadeu
Division of Clinical Emergency, Department of Medicine, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
Sao Paulo Med J. 2003 May 5;121(3):121-4. doi: 10.1590/s1516-31802003000300007. Epub 2003 Aug 8.
A case of neuroleptic malignant syndrome and acute respiratory distress syndrome is presented and discussed with emphasis on the role of muscle relaxation, creatine kinase, and respiratory function tests.
A 41-year-old man presented right otalgia and peripheral facial paralysis. A computed tomography scan of the skull showed a hyperdense area, 2 cm in diameter, in the pathway of the anterior intercommunicating cerebral artery. Preoperative examination revealed: pH 7.4, PaCO2 40 torr, PaO2 80 torr (room air), Hb 13.8 g/dl, blood urea nitrogen 3.2 mmol/l, and creatinine 90 mmol/l. The chest x-ray was normal. The patient had not eaten during the 12-hour period prior to anesthesia induction. Intravenous halothane, fentanyl 0.5 mg and droperidol 25 mg were used for anesthesia. After the first six hours, the PaO2 was 65 torr (normal PaCO2) with FiO2 50% (PaO2/FiO2 130), and remained at this level until the end of the operation 4 hours later, maintaining PaCO2 at 35 torr. A thrombosed aneurysm was detected and resected, and the ends of the artery were closed with clips. No vasospasm was present. This case illustrates that neuroleptic drugs can cause neuroleptic malignant syndrome associated with acute respiratory distress syndrome. Neuroleptic malignant syndrome is a disease that is difficult to diagnose. Acute respiratory distress syndrome is another manifestation of neuroleptic malignant syndrome that has not been recognized in previous reports: it may be produced by neuroleptic drugs independent of the manifestation of neuroleptic malignant syndrome. Some considerations regarding the cause and effect relationship between acute respiratory distress syndrome and neuroleptic drugs are discussed. Intensive care unit physicians should consider the possibility that patients receiving neuroleptic drugs could develop respiratory failure in the absence of other factors that might explain the syndrome.
本文报告并讨论了一例神经阻滞剂恶性综合征合并急性呼吸窘迫综合征的病例，重点强调了肌肉松弛、肌酸激酶及呼吸功能检查的作用。
一名41岁男性患者出现右耳痛及周围性面瘫。头颅计算机断层扫描显示在前交通动脉走行处有一个直径2 cm的高密度区。术前检查结果如下：pH 7.4，动脉血二氧化碳分压（PaCO₂）40托，动脉血氧分压（PaO₂）80托（室内空气），血红蛋白（Hb）13.8 g/dl，血尿素氮3.2 mmol/L，肌酐90 mmol/L。胸部X线检查正常。患者在麻醉诱导前12小时未进食。静脉注射氟烷、0.5 mg芬太尼及25 mg氟哌利多进行麻醉。最初6小时后，在吸入氧分数（FiO₂）为50%时，PaO₂为65托（PaCO₂正常）（PaO₂/FiO₂为130），并一直维持在此水平直至4小时后手术结束，同时PaCO₂维持在35托。检测到一个血栓形成的动脉瘤并进行了切除，动脉两端用夹子夹闭。未发现血管痉挛。该病例表明，神经阻滞剂可导致与急性呼吸窘迫综合征相关的神经阻滞剂恶性综合征。神经阻滞剂恶性综合征是一种难以诊断的疾病。急性呼吸窘迫综合征是神经阻滞剂恶性综合征的另一种表现形式，此前报告中未被认识到：它可能由神经阻滞剂药物独立产生，与神经阻滞剂恶性综合征的表现无关。本文讨论了关于急性呼吸窘迫综合征与神经阻滞剂药物之间因果关系的一些考量。重症监护病房的医生应考虑到接受神经阻滞剂药物治疗的患者在不存在其他可能解释该综合征的因素时发生呼吸衰竭的可能性。
