姚晨玲－急性一氧化碳中毒

nullToxicity, Carbon Monoxide Toxicity, Carbon Monoxide 中山医院急诊科 姚晨玲BackgroundBackgroundCarbon 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 PathophysiologyPathophysiologyCO 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) PathophysiologyPathophysiologyResulting 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. nullClinicalClinicalAcute 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 you're cherry red, you're dead”); pallor is present more often. Severe poisoning COHb level :40%-60%. Noncardiogenic pulmonary edema, arrhythmia, Papilledema ClinicalClinicaldelayed 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 symptomsdelayed 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 StudiesLab StudiesHbCO analysis Elevated levels are significant; however, low levels do not rule out exposure, especially if the patient already has received 100% oxygen or if significant time (8h) has elapsed since exposureLab StudiesLab StudiesArterial blood gas PaO2 levels should remain normal. Oxygen saturation is accurate only if directly measured but not if calculated from PaO2, which is common in many blood gas analyzers. PCO2 levels is normal or mildly decreased Lab StudiesLab StudiesEEG CT scan DiagnosisDiagnosisHistory Clincal Lab studies DifferentialsDifferentialsToxicity, Sedative-Hypnotics Stroke Diabetic Ketoacidosis Neoplasms, BrainTreatmentTreatmentPrehospital Care: Promptly remove from continued exposure TreatmentTreatmentEmergency Department Care Continue 100% oxygen therapy until patient is asymptomatic and HbCO levels are below 10%. Perform intubation for the comatose patient or, if necessary, for airway protection Early blood samples may provide much more accurate correlation between HbCO and clinical status; however, do not delay oxygen administration to acquire them. cardiac monitoring TreatmentTreatmentHyperbaric oxygen therapy (HBO) nullThe rationale for the use of HBOHBO produces a more rapid reduction in COHb levels. The half-life of COHb is 4-5 hours in a person at rest breathing room air. 80 minutes by administration of 100% oxygen at sea level 22-23 minutes by treatment with hyperbaric oxygen (HBO) at 3 atmospheres absolute (ATA) ii) HBO induces cerebral vasoconstriction, which may reduce intracranial pressure and cerebral edema, iii) HBO result in more rapid dissociation of CO from respiratory cytochromes iv) HBO may antagonize the oxidative injury that occurs after CO poisoning. TreatmentTreatmentprevent and cure the cerebral edema recovery of cerebral function PrognosisPrognosisprevent