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Abstract
Carbon monoxide (CO) poisoning is common and frequently unrecognized since the signs and symptoms are relatively nonspecific. CO poisoning causes tissue hypoxia. Additionally, various animal studies have demonstrated that CO interferes with myoglobin, P450, and other enzyme function; causes lipid peroxidation through neutrophil activation; produces oxidative stress manifested by peroxynitrate deposition in endothelium; binds to cytochrome aa3, disrupting intracellular oxygen utilization; can cause neuroexcitotoxicity; and contributes to hippocampal cellular death through apoptosis. Emergency treatment for CO poisoning is 100% oxygen. Hyperbaric oxygen therapy (HBO2) is accepted in CO poisoning, although data from randomized clinical trials regarding the efficacy of HBO2 in CO poisoning is conflicting. CO poisoning, even when treated with supplemental oxygen can leave the patient with permanent neurocognitive or affective problems. Unfortunately, there appears to be no marker or constellation of signs or symptoms at presentation that predicts long-term outcome following CO poisoning. Given the neurocognitive sequelae following CO poisoning, increased awareness and prevention of CO poisoning is imperative.
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