Toxicity, Carbon Monoxide

1. Toxicity, Carbon Monoxide 中山医院急诊科 姚晨玲

2. 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

3. 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)

4. 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.

6. 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 you're cherry red, you're dead”); pallor is present more often. • Severe poisoning • COHb level :40%-60%. • Noncardiogenic pulmonary edema, arrhythmia, Papilledema

7. 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 .

8. 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。

9. Lab Studies • HbCO 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 exposure

10. Lab Studies • Arterial 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

11. Lab Studies • EEG • CT scan

12. Diagnosis • History • Clincal • Lab studies

13. Differentials • Toxicity, Sedative-Hypnotics • Stroke • Diabetic Ketoacidosis • Neoplasms, Brain

14. Treatment • Prehospital Care: • Promptly remove from continued exposure

15. Treatment • Emergency 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

16. Treatment • Hyperbaric oxygen therapy (HBO)

17. The rationale for the use of HBO • HBO 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.

18. Treatment • prevent and cure the cerebral edema • recovery of cerebral function

19. Prognosis prevent