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首页> 外文期刊>The Internet Journal of Toxicology >A Fatal Case Of Methomyl Poisoning Leading To Fulminant Hepatic Failure
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A Fatal Case Of Methomyl Poisoning Leading To Fulminant Hepatic Failure

机译：导致甲基化性肝功能衰竭的致命毒死例

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Methomyl is highly toxic carbamate poison which can cause muscarinic, nicotinic and central nervous system side-effects. It has also been associated with acute pancreatitis, as well as hepatic and renal dysfunction. Here we attempt to describe a case of 24-year-old male with suicidal ingestion of methomyl poisoning who developed fulminant hepatic failure in the absence of any evidence for acute viral or ischemic hepatitis, which later proved to be fatal. To-date this is the first reported case of methomyl associated fulminant hepatotoxicity. However further studies are warranted to closely study the association of liver failure with methomyl toxicity. Case Report A 25 year old married male was presented in the emergency room in an unconscious state. The family gives a history that the patient was completely with no documented past medical history, when he was seen to drink a half a cup full of whitish powder mixed with juice and about 30 minutes later started to complain of abdominal pain, became drowsy and then unresponsive. He was brought to the emergency room within about 30 minutes of becoming unconscious. His Glasgow coma scale (GCS) of 4/15 on presentation with constricted pupils with normal pulse and blood pressure while examination for other systemic signs was negative. He was immediately intubated and shifted to intensive care unit on mechanical ventilation with 70% FiO2. The same night the family brought the near empty wrapper of the powder sache and it was found to be a locally manufactured carbamate poison with 90% methomyl inside. The patient’s toxicology screen was negative for ethanol, benzodiazepines, barbiturates, cocaine metabolites, cannabinoids, opiates and amphetamine like compounds. He had metabolic acidosis with pH of 7.25 and bicarbonate of 17 which was treated with bicarbonate infusion. The facility for serum levels for methomyl were not available but as per the witnessed history and partially emptied wrapper of the sache of poison was confirmed to be Methomyl. The patient was started on 2 mg atropine every 15-20 minutes and received about 62 mg of atropine which was titrated to achieve atropinization while keeping in mind pulmonary secretions and by the second day the patient was opening eyes spontaneously and alert, oriented to person but difficult to arouse. He did not require any ionotropic support nor had any hypotension spells and his ECG remained normal. He was not put on any antibiotics. His chest x-ray showed no abnormality and CT brain was normal (see figure 1A).
机译：灭虫灵是剧毒的氨基甲酸酯类毒物，可引起毒蕈碱，烟碱和中枢神经系统副作用。它也与急性胰腺炎以及肝和肾功能障碍有关。在这里，我们尝试描述一例自杀性摄入甲基苯甲基中毒的24岁男性，在没有任何急性病毒性或缺血性肝炎证据的情况下发生暴发性肝衰竭，后来证明是致命的。迄今为止，这是报道的第一个与灭多威相关的暴发性肝毒性病例。但是，有必要进行进一步的研究来密切研究肝功能衰竭与灭多威毒性之间的关系。病例报告一名25岁已婚男性在昏迷状态下出现在急诊室。一家人的病史是，患者完全没有病史，当时他被喝了半杯混合了果汁的发白粉末，大约30分钟后开始抱怨腹痛，嗜睡，然后没有反应。他昏迷约30分钟后被带到急诊室。他的格拉斯哥昏迷量表（GCS）为4/15，表现为脉搏和血压正常的收缩瞳孔，而其他全身性体征的检查均为阴性。他立即被插管，并转入重症监护病房接受70％FiO2的机械通气。同一天晚上，一家人把粉袋里的空包装纸带了过来，发现它是一种本地制造的氨基甲酸酯毒物，里面有90％的甲hom基。患者的毒理学筛查结果显示乙醇，苯并二氮杂卓，巴比妥酸盐，可卡因代谢产物，大麻素，阿片类药物和苯丙胺类化合物为阴性。他患有代谢性酸中毒，pH为7.25，碳酸氢盐为17，接受碳酸氢盐输注治疗。尚无用于测定灭多威血清水平的设施，但根据目击历史，已确认部分毒化的毒药包装纸为甲基灭多威。患者每15-20分钟开始服用2毫克阿托品，并接受约62毫克阿托品的滴定，以实现Atropinization，同时牢记肺部分泌物;到第二天，患者自发睁开眼睛并保持警觉，以人为本很难引起。他不需要任何离子支持，也没有低血压发作，他的心电图保持正常。他没有服用任何抗生素。他的胸部X光片未见异常，CT脑正常（见图1A）。

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