Carbon monoxide (CO) poisoning is common and frequently unrecognized since
the signs, and symptoms are relatively nonspecific. CO poisoning causes tis
sue hypoxia. Additionally, various animal studies have demonstrated-that CO
interferes with myoglobin, P450, and other enzyme function; causes lipid p
eroxidation through neutrophil activation;produces oxidative stress manifes
ted by peroxynitrate deposition in endothelium; binds to cytochrome aa3, di
srupting intracelluar oxygen utilization; tan cause neuroexcitotoxicity; an
d contributes to hippocampal cellular death through: apoptosis. Emergency t
reatment 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 HBO, in CO poisoning is conflicting. CO poisoning
, even when treated with supplemental oxygen can leave the patient with per
manent neurocognitive or affective problems. Unfortunately, there appears t
o be no marker or constellation of signs or symptoms at presentation that p
redicts longterm outcome following CO poisoning. Given the neurocognitive s
equelae following CO poisoning, increased awareness and prevention of CO po
isoning is imperative.