姚晨玲－急性一氧化碳中毒.ppt

Toxicity, Carbon Monoxide 中山医院急诊科 姚晨玲 Background Carbon monoxide (CO) is a colorless, odorless gas produced by incomplete combustion of carbonaceous material CO is formed as a by-product of burning organic compounds Pathophysiology CO toxicity causes impaired oxygen delivery and utilization CO reversibly binds hemoglobin, resulting in relative anemia. CO binds hemoglobin 230-260 times more avidly than oxygen. dissociation of CO from HbCO is slow than that of O2 from HbO2 (1/3600) Pathophysiology Resulting a leftward shift in the oxyhemoglobin dissociation curve binds to cardiac myoglobin , resulting myocardial depression and hypotension CO binds to cytochromes c and P450, impaired oxygen utilization at the cellular level. Clinical Acute carbon monoxide poisoning Mild poisoning COHb level :10%-20%. Headache, nausea, vomiting, fatigue. Moderate poisoning COHb level :30%-40%. Confusion, Agitation, Hallucination, Visual disturbance, syncope, seizure Skin: Classic cherry red skin is rare (ie, “When youre cherry red, youre dead”); pallor is present more often. Severe poisoning COHb level :40%-60%. Noncardiogenic pulmonary edema, arrhythmia, Papilledema Clinical delayed neuropsychiatric symptoms Long-term exposures or severe acute exposures frequently result in long-term neuropsychiatric sequelae. Additionally, some individuals develop delayed neuropsychiatric symptoms, often after severe intoxications associated with coma (about 3%-10% of all patients) After 2-60days “normal period”, chronic headaches, memory problems, and parkinsonian-type tremor, re-occur . delayed neuropsychiatric symptoms [病例介绍] 年近半百的李某，湖南常宁市人，在新疆打工。2002年11月27日晚，李某和另外2人睡在生火炉的房内，次日被人发现因煤气中毒昏迷，生命垂危。患者立即被送入医院进行高压氧治疗1次后，均神志清楚。李某于11月29日自行乘火车返回湖南常宁，回家后生活尚能自理就未再进行其他治疗。约20天后，李某开始出现少气懒言、情感淡漠、反应迟钝等症状，而且外出后不知道回家。家人以为他中了“邪”，先后请巫婆念咒“安神”、“驱鬼”，患者不仅不见好转，反而四肢瘫软，卧床不起，大小便失禁，完全失语……本月上旬，患者被送入湘雅医院，诊断为急性一氧化碳中毒迟发性脑病。给予高压氧及细胞活化剂治疗目前患者病情已有好转。 Lab Studies HbCO analysis Elevated levels are significant; h