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有机磷杀虫剂中毒后中间综合征

Intermediate syndrome following organophosphate insecticide poisoning.

作者信息

Yang Chen-Chang, Deng Jou-Fang

机构信息

Department of Environmental and Occupational Medicine, National Yang-Ming University School of Medicine, Taipei, Taiwan, ROC.

出版信息

J Chin Med Assoc. 2007 Nov;70(11):467-72. doi: 10.1016/S1726-4901(08)70043-1.

Abstract

Acute organophosphate insecticide poisoning can manifest 3 different phases of toxic effects, namely, acute cholinergic crisis, intermediate syndrome (IMS), and delayed neuropathy. Among them, IMS has been considered as a major contributing factor of organophosphate-related morbidity and mortality because of its frequent occurrence and probable consequence of respiratory failure. Despite a high incidence, the pathophysiology that underlies IMS remains unclear. Previously proposed mechanisms of IMS include different susceptibility of various cholinergic receptors, muscle necrosis, prolonged acetylcholinesterase inhibition, inadequate oxime therapy, downregulation or desensitization of postsynaptic acetylcholine receptors, failure of postsynaptic acetylcholine release, and oxidative stress-related myopathy. The clinical manifestations of IMS typically occur within 24 to 96 hours, affecting conscious patients without cholinergic signs, and involve the muscles of respiration, proximal limb muscles, neck flexors, and muscles innervated by motor cranial nerves. With appropriate therapy that commonly includes artificial respiration, complete recovery develops 5-18 days later. Patients with atypical manifestations of IMS, especially a relapse or a continuum of acute cholinergic crisis, however, were frequently reported in clinical studies of IMS. The treatment of IMS is mainly supportive. Nevertheless, because IMS generally concurs with severe organophosphate toxicity and persistent inhibition of acetylcholinesterase, early aggressive decontamination, appropriate antidotal therapy, and prompt institution of ventilatory support should be helpful in ameliorating the magnitude and/or the incidence of IMS. Although IMS is well recognized as a disorder of neuromuscular junctions, its exact etiology, incidence, and risk factors are not clearly defined because existing studies are largely small-scale case series and do not employ a consistent and rigorous definition of IMS. Without a clear understanding of the pathophysiology of IMS, specific therapy is not available. The prognosis of IMS, however, is likely to be favorable if respiratory failure can be promptly recognized and treated accordingly.

摘要

急性有机磷杀虫剂中毒可表现出3个不同阶段的毒性作用,即急性胆碱能危象、中间综合征(IMS)和迟发性神经病。其中,IMS因其频繁发生及可能导致呼吸衰竭的后果,被认为是有机磷相关发病和死亡的主要促成因素。尽管发病率很高,但IMS的病理生理学仍不清楚。先前提出的IMS机制包括各种胆碱能受体的不同易感性、肌肉坏死、乙酰胆碱酯酶抑制时间延长、肟治疗不足、突触后乙酰胆碱受体下调或脱敏、突触后乙酰胆碱释放失败以及氧化应激相关的肌病。IMS的临床表现通常在24至96小时内出现,影响无胆碱能体征的清醒患者,累及呼吸肌、近端肢体肌肉、颈部屈肌以及由运动性颅神经支配的肌肉。通过通常包括人工呼吸的适当治疗,5 - 18天后可完全康复。然而,在IMS的临床研究中,经常报告有IMS非典型表现的患者,尤其是复发或急性胆碱能危象的持续状态。IMS的治疗主要是支持性的。然而,由于IMS通常与严重的有机磷毒性和乙酰胆碱酯酶的持续抑制同时发生,早期积极的去污、适当的解毒治疗以及及时给予通气支持应有助于减轻IMS的严重程度和/或发病率。尽管IMS被公认为是一种神经肌肉接头疾病,但其确切病因、发病率和危险因素尚未明确界定,因为现有研究大多是小规模病例系列,且未采用一致且严格的IMS定义。由于对IMS的病理生理学缺乏清晰的认识,尚无特异性治疗方法。然而,如果能及时识别并相应治疗呼吸衰竭,IMS的预后可能良好。

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