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  • Carbon monoxide (CO) poisoning is commonly due to smoke inhalation, but also results from exposure to malfunctioning of or improperly vented heating and cooking appliances, automobile exhaust fumes, and methylene chloride, a component of paint strippers.
  • The toxic effects of CO poisoning result from tissue hypoxia and reperfusion injury in the brain.
  • Clinical signs and symptoms of CO poisoning are notoriously nonspecific and correlate only roughly with the COHb concentration.
  • Any illness affecting more than one member of a family or group from a common environment requires that CO poisoning be ruled out.
  • The half-life of COHb is decreased to 90 minutes with an Fio2 of 100%, and 23 minutes with hyperbaric oxygen (HBO) therapy.

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Carbon monoxide (CO) has historically been the most common etiology of poison-related deaths. Three thousand to four thousand cases of CO-related deaths occur yearly in the United States. According to poison center data, in 2006 there were roughly 16 000 reported cases of CO toxicity, with approximately 25% attributed to victims younger than 19 years; there were 1829 cases in children younger than 6 years.1 Overall, CO was responsible for 46 deaths.1 While mortality secondary to CO is significant, morbidity from delayed cognitive sequelae is a significant problem, especially in the unintentionally poisoned patient.

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Carbon monoxide is an insidious poison because it is colorless, odorless, tasteless, and nonirritating. CO is formed as a by-product of the incomplete combustion of fossil fuels or materials such as wood or charcoal. Children and family members are commonly exposed to CO from malfunctioning furnaces, generators, or charcoal grills. Motor exhaust from automobiles and houseboats are also sources of significant exposure. Methylene chloride, a hydrocarbon commonly found in paint stripping chemicals, is metabolized to CO by the liver, and can result in delayed CO poisoning after respiratory, dermal, or gastrointestinal exposure.2

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One effect of CO poisoning is the production of a functional anemia. CO binds to hemoglobin with 240 times the affinity of oxygen, displacing oxygen from its normal binding site. In doing so, the hemoglobin molecule is altered, resulting in increased affinity for any oxygen already bound. The oxyhemoglobin dissociation curve is therefore shifted to the left, resulting in tissue hypoxia.

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Carbon monoxide also binds to metalloproteins such as myoglobin and cytochromes C oxidase, and P-450 oxidase. Cytochrome inhibition results in disruption of electron transport and interference with cellular respiration. Myocardial myoglobin can be affected, resulting in reduction of contractility and cardiac output, further reducing tissue oxygen delivery.

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Ischemic–reperfusion injury to the brain after CO poisoning is an area of great interest and ongoing research. Interaction with the free radical nitric oxide results in a cascade of events including endothelial injury and leukocyte adherence. Activated lymphocytes may cause the conversion of xanthine dehydrogenase to xanthine oxidase, which promotes the formation of oxygen free radicals. The final common pathway is the development of delayed lipid peroxidation and ...

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