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血清素中毒:诊断与治疗的实用方法。

Serotonin toxicity: a practical approach to diagnosis and treatment.

作者信息

Isbister Geoffrey K, Buckley Nicholas A, Whyte Ian M

机构信息

Tropical Toxinology Unit, Menzies School of Health Research, Charles Darwin University, Darwin, NT, Australia.

出版信息

Med J Aust. 2007 Sep 17;187(6):361-5. doi: 10.5694/j.1326-5377.2007.tb01282.x.

DOI:10.5694/j.1326-5377.2007.tb01282.x
PMID:17874986
Abstract

Excess serotonin in the central nervous system leads to a condition commonly referred to as the serotonin syndrome, but better described as a spectrum of toxicity - serotonin toxicity. Serotonin toxicity is characterised by neuromuscular excitation (clonus, hyperreflexia, myoclonus, rigidity), autonomic stimulation (hyperthermia, tachycardia, diaphoresis, tremor, flushing) and changed mental state (anxiety, agitation, confusion). Serotonin toxicity can be: mild (serotonergic features that may or may not concern the patient); moderate (toxicity which causes significant distress and deserves treatment, but is not life-threatening); or severe (a medical emergency characterised by rapid onset of severe hyperthermia, muscle rigidity and multiple organ failure). Diagnosis of serotonin toxicity is often made on the basis of the presence of at least three of Sternbach's 10 clinical features. However, these features have very low specificity. The Hunter Serotonin Toxicity Criteria use a smaller, more specific set of clinical features for diagnosis, including clonus, which has been found to be more specific to serotonin toxicity. There are several drug mechanisms that cause excess serotonin, but severe serotonin toxicity only occurs with combinations of drugs acting at different sites, most commonly including a monoamine oxidase inhibitor and a serotonin reuptake inhibitor. Less severe toxicity occurs with other combinations, overdoses and even single-drug therapy in susceptible individuals. Treatment should focus on cessation of the serotonergic medication and supportive care. Some antiserotonergic agents have been used in clinical practice, but the preferred agent, dose and indications are not well defined.

摘要

中枢神经系统中血清素过量会导致一种通常被称为血清素综合征的病症,但更确切地说是一种毒性谱——血清素毒性。血清素毒性的特征包括神经肌肉兴奋(阵挛、反射亢进、肌阵挛、僵硬)、自主神经刺激(高热、心动过速、多汗、震颤、潮红)以及精神状态改变(焦虑、激动、意识模糊)。血清素毒性可分为:轻度(可能使患者担忧或不担忧的血清素能特征);中度(导致明显痛苦且值得治疗但不危及生命的毒性);或重度(一种以严重高热、肌肉僵硬和多器官功能衰竭迅速出现为特征的医疗紧急情况)。血清素毒性的诊断通常基于至少具备斯特恩巴赫10项临床特征中的三项。然而,这些特征的特异性非常低。亨特血清素毒性标准使用一组更小、更具特异性的临床特征进行诊断,包括阵挛,已发现其对血清素毒性更具特异性。有几种药物机制会导致血清素过量,但严重的血清素毒性仅在作用于不同部位的药物联合使用时发生,最常见的是包括单胺氧化酶抑制剂和血清素再摄取抑制剂。在其他联合用药、过量用药甚至易感个体的单药治疗中会出现不太严重的毒性。治疗应侧重于停用血清素能药物并给予支持性护理。一些抗血清素药物已在临床实践中使用,但首选药物、剂量和适应症尚未明确界定。

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