![]() House fires, wood-burning stoves/gas heaters, furnaces in enclosed and poorly ventilated spaces.Toxic coingestions: If intentional poisoning is suspected, screen for other substances: e.g., acetaminophen, salicylates, alcohol (see acetaminophen toxicity and salicylate toxicity).The globus pallidus is commonly affecte d (unspecific findings, usually bilateral ).Retinal hemorrhage (good indicator of CNS toxicity).Signs of extrapyramidal syndrome (e.g., rigidity). ![]() Symptomatic patients (e.g., altered mental status).Findings may include increased troponin and/or cardiac hypomotility.Select patients : cardiac enzymes and echocardiography.Findings may include signs of myocardial ischemia and/or arrhythmias.All patients: ECG and cardiac monitor for 4–6 hours.Inhalation injury: airway examination (e.g., direct laryngoscopy).Screen for affected organs and toxic coingestions. Other routine laboratory studies: serum lactate, BMP, pregnancy test.pH: Tissue hypoxia may lead to high anion-gap metabolic acidosis.The COHb level is used to guide therapeutic decisions.Start 100% oxygen immediately if clinical suspicion for CO poisoning is high! Diagnostic workup should not delay oxygen administration (see treatment). Abnormal COHb level on venous/arterial CO oximetry.Any symptoms of CO poisoning (see “Clinical features”).Ideally, all three criteria should be present to confirm acute poisoning, but symptoms vary widely and the history of exposure is not always evident. SpO 2 is not useful when screening for CO poisoning! Oximeters cannot distinguish between COHb and oxyhemoglobin. Portable pulse CO oximetry may show abnormal COHb Ĭlinical features do not correlate well with the COHb level.Standard pulse oximetry: normal-appearing or ↑ SpO 2 (as pulse oximeters cannot distinguish between COHb and oxyhemoglobin). ![]() Symptoms of concurrent cyanide poisoning : See cyanide.Fundoscopic findings: bright red retinal vessels, retinal hemorrhages, papilledema (indicative of cerebral edema).Cherry-red skin with bullous skin lesions: after exposure to high levels (rare and usually seen postmortem).Inhalation injury : associated with fire-related exposures.Altered mental status (e.g., agitation, confusion, somnolence, memory loss).The correlation between feature severity and COHb level is poor. Chronic CO poisoning may also occur when individuals are chronically exposed to low levels of CO symptoms are nonspecific and treatment consists of eliminating the source of CO exposure. In addition, supportive care should be provided with a focus on airway management and oxygenation. ![]() Management consists of 100% supplemental oxygen and possibly hyperbaric oxygen. CO toxicity should be suspected in any individual with a history of exposure and symptoms consistent with CO toxicity, and the diagnosis can be confirmed by an elevated COHb level on CO oximetry. Importantly, pulse oximetry will often show a normal waveform because standard pulse oximeters are unable to differentiate between oxyhemoglobin and carboxyhemoglobin ( COHb). Symptoms are variable and nonspecific and include nausea, headache, and fatigue. Carbon monoxide (CO) toxicity causes tissue hypoxia via multiple mechanisms and is most commonly due to exposure to house fires, wood-burning stoves, or motor vehicle exhaust fumes.
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