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一氧化碳中毒:机制、表现及治疗中的争议

Carbon monoxide poisoning: mechanisms, presentation, and controversies in management.

作者信息

Olson K R

出版信息

J Emerg Med. 1984;1(3):233-43. doi: 10.1016/0736-4679(84)90078-7.

DOI:10.1016/0736-4679(84)90078-7
PMID:6491241
Abstract

Carbon monoxide (CO) remains the leading cause of death due to poisoning in the United States. CO produces toxicity by binding to hemoglobin, thereby reducing oxygen-carrying capacity, and by binding to myoglobin, which may impair cardiac output and result in cerebral ischemia. Severe CO poisoning results in coma or encephalopathy, but milder intoxication may occur with nonspecific symptoms suggestive of hysteria, hyperventilation, psychosis, or viral syndrome. Survivors of severe CO poisoning may have permanent neurologic or neuropsychiatric sequelae. Subtle memory deficits or personality changes may not be readily apparent to the examining physician. Administration of 100% oxygen at ambient pressure remains convenient, safe, and inexpensive. Hyperbaric oxygen can shorten the half-life of carboxyhemoglobin and can carry oxygen independent of hemoglobin. However, it is not known if either 100% oxygen or hyperbaric oxygen can actually alter mortality or improve neurologic outcome in survivors. Carefully controlled prospective studies should be carried out to assess the potential value of hyperbaric oxygen in CO poisoning.

摘要

在美国,一氧化碳(CO)仍然是中毒致死的首要原因。CO通过与血红蛋白结合产生毒性,从而降低携氧能力,并通过与肌红蛋白结合,这可能损害心输出量并导致脑缺血。严重的CO中毒会导致昏迷或脑病,但轻度中毒可能表现为类似癔症、换气过度、精神病或病毒综合征的非特异性症状。严重CO中毒的幸存者可能会有永久性的神经或神经精神后遗症。细微的记忆缺陷或性格变化可能不易被检查医生察觉。在常压下给予100%的氧气既方便、安全又便宜。高压氧可以缩短碳氧血红蛋白的半衰期,并且可以独立于血红蛋白携带氧气。然而,尚不清楚100%的氧气或高压氧是否真的能改变死亡率或改善幸存者的神经预后。应该进行严格控制的前瞻性研究,以评估高压氧在CO中毒中的潜在价值。

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