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Diagnosis And Management Of Carbon Monoxide Poisoning In The Emergency Department

February 2011

Abstract

Carbon monoxide (CO) poisoning has a case-fatality rate as high as 30%. CO impairs oxygen delivery and peripheral utilization causing cellular hypoxia secondary to its 200-fold affinity for hemoglobin compared with oxygen. The acute neurologic effects of CO poisoning are the result of cellular hypoxia. Up to half of patients with CO exposure develop delayed neuropsychological sequelae. Headache is the most common presenting complaint, although severely poisoned patients may develop acute neuropsychological symptoms such as ataxia and cognitive disturbances. Standard pulse oximetry is incapable of distinguishing between carboxyhemoglobin (COHb) and oxyhemoglobin. Non-invasive pulse co-oximetry, which uses multiple wavelengths of light specifically absorbed by oxyhemoglobin, deoxyhemoglobin, COHb, and methemoglobin, can be useful at triage to rapidly identify patients with significant exposure. All patients with suspected CO exposure should undergo COHb-level testing in addition to an ECG and cardiac monitoring due to potential for myocardial ischemia or dysrhythmias. There is no clinically relevant difference between arterial and venous COHb samples. The mainstay of treatment in CO poisoning is oxygen therapy as it competitively displaces CO from hemoglobin. Use of hyperbaric oxygen (HBO) therapy in CO poisoning remains controversial. A systematic review of the literature did not find sufficient evidence that HBO reduces the incidence of delayed neurological sequelae.

Keywords: carbon monoxide, CO, poisoning, treatment, carboxyhemoglobin, hyperbaric oxygen, hyperbaric oxygen therapy, HBO, NBO, co-oximetry

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