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

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.