Carbon monoxide intoxication: clinical features, neuropathology and mechanisms of injury.
CO intoxication, by producing cerebral hypoxia-ischaemia, may trigger neuropathological events which result in delayed neurological relapse even in patients whose earlier clinical course has appeared deceptively benign. The physician's index of suspicion must therefore be high, and it should be remembered that, even in major CO exposures, blood COHb levels may be low if a period of several hours has elapsed since exposure. The importance of recognising occult CO exposure and of treating symptomatic patients promptly cannot be overemphasized. Immediate administration of high concentrations of inspired oxygen (including hyperbaric oxygenation, if available) is the primary therapy. Hypotension and acid-base abnormalities should be promptly reversed. Prolonged bed rest is recommended to discourage delayed relapse.
D000818:Animals; D001927:Brain Diseases / Q000139:chemically induced* / Q000473:pathology; D002248:Carbon Monoxide / Q000378:metabolism; D002249:Carbon Monoxide Poisoning / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D002263:Carboxyhemoglobin / Q000032:analysis; D006801:Humans; D000860:Hypoxia / Q000139:chemically induced / Q000473:pathology; D013997:Time Factors
D002248:Carbon Monoxide; D002263:Carboxyhemoglobin