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Carbon monoxide is a colorless, odorless, nonirritating gas that displaces oxygen from hemoglobin, resulting in early tissue hypoxia and delayed neurologic damage. Sources of exposure to carbon monoxide include the incomplete combustion of any carbonaceous fuel (eg, gasoline, kerosene, natural gas, and charcoal) or the metabolism of inhaled methylene chloride (paint stripper).
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A history of exposure to gas heat or smoke inhalation, or multiple victims with altered mental status, acidosis, or coma should alert one to the possibility of carbon monoxide poisoning. The clinical features of carbon monoxide poisoning are highly variable and primarily relate to hypoxic effects on the cardiovascular and neurologic systems (Table 127-1). Symptoms range from from “flu-like” symptoms, such as headache, dizziness, nausea, and vomiting, to coma. The “classic finding” of cherry red lips is rarely seen in living patients. Patients with significant poisoning may experience long-term neurological and cognitive problems.
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A venous, or arterial, blood sample for cooximetry is the most reliable test to diagnose carbon monoxide poisoning. Although carboxyhemoglobin (COHb) levels confirm exposure, they do not necessarily correlate with symptoms or prognosis. Baseline COHb may be as high as 3% in nonsmokers and 10% in smokers. Higher levels are suggestive of CO exposure. The use of bedside pulse cooximetry in the ED to screen for CO exposure is still under investigation.
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Standard pulse oximetry is unreliable in the presence of increasing COHb as oxygen saturation readings will be artificially high. Additional laboratory and imaging abnormalities seen in symptomatic patients may include elevated anion gap metabolic acidosis, elevated lactate, elevate creatine phosphokinase, elevated troponin, ECG changes consistent with ischemia, and bilateral globus pallidus lesions on MRI.
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The differential diagnosis is wide due to the nonspecific nature of the symptoms and includes flu-like illness, gastroenteritis, exposure to other toxins, and infectious causes of mental status changes. Cardiovascular compromise after poisoning may represent a concomitant myocardial infarction.
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Remove patients from the source of exposure and address airway, breathing, and circulation.
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Begin treatment in all patients suspected of CO poisoning with the highest concentration of supplemental oxygen available (eg, 100% oxygen via facemask with reservoir) and continue until the patient is asymptomatic. Provide continuous monitoring of vital signs, heart rate, and rhythm. Establish IV access.
Guidelines for hyperbaric oxygen therapy (HBO) in patients with severe poisoning are listed in Table 127-2. Indications for pediatric and adult HBO are similar. The threshold COHb for initiating HBO in pregnant patients is lower because of concerns for the fetus. Consult with a hyperbaric specialist. Patients must have a secure airway and stable hemodynamics before ...