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首页> 外文期刊>Kaohsiung Journal of Medical Sciences >Human carbofuran intoxication with myocardial injury mimicking acute myocardial infarction
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Human carbofuran intoxication with myocardial injury mimicking acute myocardial infarction

机译:模仿急性心肌梗塞的人卡百呋喃中毒并伴有心肌损伤

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A 51-year-old man with a history of hypertension drank about 50 mL of pesticide, containing carbofuran, after an argument with his family. He was found drowsy, weak, and unable to talk about 15 minutes after the argument. No chest tightness, diaphoresis, dyspnea, or chest pain were noted. He was brought to the hospital immediately, presenting with tachycardia (112 beats/min), hypertension (192/96 mmHg), and tachypnea (26 breaths/min). Physical examination revealed drowsy and agitated consciousness (Glasgow coma scale of E3V2M5) and small pupil size, but no obvious airway secretion or abnormality in breath sound, heart sound or abdomen. The laboratory examination revealed decreased cholinesterase level (3.67 kU/L). Electrocardiography showed diffuse ST-T segments depression over precordial leads (Fig. 1A). Gastric lavage with activated charcoal and atropine infusion were given. He developed hypoxemic respiratory failure 2 hours later, requiring intubation for mechanical ventilation. After admission to the intensive care unit, adequate hydration and atropine infusion were prescribed for suspected carbofuran intoxication. Elevated cardiac enzyme levels (creatine phosphokinase, 242 IU/L; creatine kinase-MB, 15.7 ng/mL; and troponin-I, 2.04 ng/mL) were noted, so dual antiplatelets and heparinization were given because acute myocardial infarction (AMI) could not be excluded. However, the cardiac enzyme levels reached a peak within a few hours, and the follow-up electrocardiography showed interval disappearance of the ST-T segments depression (Fig. 1B). Bedside echocardiography showed adequate systolic function without valvular abnormality or wall motion defect. Tachyarrhythmia-related injury was less likely because tachycardia soon subsided at the emergency department. Stress cardiomyopathy was also not favored because echocardiography showed normal wall motion. Therefore, carbofuran-related cardiotoxicity, rather than AMI, tachyarrhythmia or stress cardiomyopathy, was concluded, so clopidogrel and heparin were discontinued. Cardiac catheterization was suggested but refused because of no further associated cardiac symptoms and signs. He was soon discharged uneventfully without obvious sequelae in 1 week.
机译:在与家人吵架后,一位有高血压病史的51岁男子喝了约50毫升含有呋喃丹的农药。辩论后十五分钟,他被发现昏昏欲睡,虚弱,无法说话。没有发现胸闷,发汗,呼吸困难或胸痛。他被立即送往医院,表现为心动过速(112次/分钟),高血压(192/96 mmHg)和呼吸急促(26次/分钟)。体格检查显示昏昏欲睡和神志不清(格拉斯哥昏迷评分为E3V2M5)和瞳孔小,但呼吸道,心音或腹部无明显气道分泌物或异常。实验室检查发现胆碱酯酶水平降低(3.67 kU / L)。心电图显示心前区导线上弥漫性ST-T节段压低(图1A)。给予灌胃活性炭和阿托品输注。 2小时后,他出现了低氧血症性呼吸衰竭,需要进行插管以进行机械通气。进入重症监护病房后,为疑似呋喃丹中毒开了足够的水合作用和阿托品输注。注意到心脏酶水平升高(肌酸磷酸激酶为242 IU / L;肌酸激酶-MB为15.7 ng / mL;肌钙蛋白-I为2.04 ng / mL),因此给予双重抗血小板和肝素化作用是因为急性心肌梗死(AMI)无法排除。但是,心脏酶水平在几个小时内达到峰值,随后的心电图检查显示ST-T节段下降的间隔消失(图1B)。床旁超声心动图显示出足够的收缩功能,没有瓣膜异常或壁运动缺陷。与心律失常相关的伤害可能性较小,因为心动过速很快在急诊室消退。应力性心肌病也不受欢迎,因为超声心动图显示正常的壁运动。因此,得出了与呋喃丹有关的心脏毒性,而不是AMI,心律失常或应激性心肌病,因此停用了氯吡格雷和肝素。建议进行心脏导管插入术,但由于没有进一步的相关心脏症状和体征而被拒绝。很快,他在1周内顺利出院,没有明显的后遗症。

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