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抗精神病药恶性综合征的检测与管理。

Detection and management of the neuroleptic malignant syndrome.

作者信息

Bond W S

出版信息

Clin Pharm. 1984 May-Jun;3(3):302-7.

PMID:6145537
Abstract

Two patients who developed the neuroleptic malignant syndrome (NMS) are described, and pertinent literature is reviewed. A 30-year-old man developed NMS, apparently as a result of haloperidol treatment of chronic undifferentiated schizophrenia. Treatment with cooling blankets, acetaminophen, dantrolene sodium, and bromocriptine mesylate decreased abnormal vital signs, but catatonia continued. After 30 treatments with electroconvulsive therapy over a one-month period, the patient's catatonia was resolved, and he was discharged on no medication with the schizophrenia in remission. The second patient was a 22-year-old woman who developed NMS after five weeks of therapy with haloperidol and thiothixene for an acute episode of abnormal behavior. She did not respond to therapy with cooling blankets, acetaminophen, antibiotics, and amobarbital sodium. Dantrolene sodium therapy produced no improvement except for some relief of muscular rigidity. Electroconvulsive therapy (22 treatments over one month) successfully decreased the patient's elevated liver enzymes and leukocyte count, but periodic temperature elevations and catatonia continued. Prompt diagnosis and treatment of NMS are essential, as the mortality rate is 20%. Acute lethal catatonia and malignant hyperthermia are considered in differential diagnosis. Both central and peripheral pathophysiologic mechanisms are probably involved in NMS, and most cases are seen in patients with psychiatric illness. Onset of NMS does not seem related to duration of neuroleptic therapy and, in susceptible persons, additional factors may be required to trigger onset of NMS. Symptoms, including diffuse muscular rigidity, akinesia, and fever, develop within 24-72 hours. Neurologic symptoms may develop or worsen, and leukocytosis and elevated levels of liver enzymes occur. Death can result from respiratory or cardiovascular failure, and rhabdomyolysis can lead to acute renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本文描述了两名发生神经阻滞剂恶性综合征(NMS)的患者,并对相关文献进行了综述。一名30岁男性患上NMS,显然是由于使用氟哌啶醇治疗慢性未分化型精神分裂症所致。使用降温毯、对乙酰氨基酚、丹曲林钠和甲磺酸溴隐亭进行治疗后,异常生命体征有所下降,但紧张症仍持续存在。在一个月内进行了30次电休克治疗后,患者的紧张症得到缓解,且在未服用药物的情况下出院,精神分裂症已缓解。第二名患者是一名22岁女性,在使用氟哌啶醇和硫利达嗪治疗异常行为急性发作五周后患上NMS。她对使用降温毯、对乙酰氨基酚、抗生素和异戊巴比妥钠的治疗无反应。丹曲林钠治疗除了使肌肉僵硬稍有缓解外,并无改善。电休克治疗(一个月内进行22次)成功降低了患者升高的肝酶和白细胞计数,但体温仍有周期性升高,紧张症也持续存在。NMS的及时诊断和治疗至关重要,因为其死亡率为20%。鉴别诊断时需考虑急性致死性紧张症和恶性高热。NMS可能涉及中枢和外周病理生理机制,大多数病例见于患有精神疾病的患者。NMS的发作似乎与神经阻滞剂治疗的持续时间无关,在易感人群中,可能需要其他因素来触发NMS的发作。症状包括弥漫性肌肉僵硬、运动不能和发热,在24 - 72小时内出现。神经系统症状可能会出现或加重,还会出现白细胞增多和肝酶水平升高。死亡可能由呼吸或心血管衰竭导致,横纹肌溶解可导致急性肾衰竭。(摘要截选至250字)

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