Carbon Monoxide Poisoning

Carbon monoxide is a colorless, odorless gas produced by incomplete combustion, commonly from faulty heating appliances, generators, vehicle exhaust in enclosed spaces, and smoke inhalation in structural fires.

Toxicity results from its markedly higher affinity for hemoglobin than oxygen. It forms carboxyhemoglobin and shifts the oxygen dissociation curve to the left. Together these severely impair oxygen delivery to tissues despite a potentially normal or even elevated measured oxygen saturation on standard pulse oximetry, which cannot distinguish carboxyhemoglobin from oxyhemoglobin.

Carbon monoxide also has direct cellular toxic effects, including binding to cytochrome oxidase and myoglobin, contributing to injury beyond the effect on oxygen carrying capacity alone.

Symptoms are often non-specific, which is part of why the diagnosis is frequently missed, particularly in mild to moderate poisoning. It is especially easy to miss where multiple household members present with similar vague symptoms, itself a useful clue prompting consideration of a shared environmental exposure.

• Mild to moderate poisoning: headache, dizziness, nausea, fatigue, and a sensation resembling a viral illness, sometimes leading to misdiagnosis as a flu like syndrome, particularly in winter months when heating related exposure is more common.
• More severe poisoning: confusion, chest pain (from myocardial ischemia, since the heart is particularly sensitive to impaired oxygen delivery), palpitations, and, in significant poisoning, syncope, seizures, and coma.
• Classic cherry red skin discoloration is a late and unreliable sign, rarely seen in practice, and its absence should not be used to exclude the diagnosis.
• Delayed neurological sequelae can occur days to weeks after apparent recovery from acute poisoning, including cognitive impairment, personality change, and parkinsonian features. This is an important and under-recognized complication that should be discussed with patients and their families as part of counseling on prognosis and follow up.
• Pregnant patients and their fetuses are particularly vulnerable, given fetal hemoglobin's even higher affinity for carbon monoxide than adult hemoglobin, and a lower threshold for aggressive treatment is applied in this group.

• Standard pulse oximetry is unreliable and should not be used to exclude carbon monoxide poisoning, since it cannot distinguish carboxyhemoglobin from oxyhemoglobin and will often read falsely normal or reassuring.
• Carboxyhemoglobin level, measured by co-oximetry on an arterial or venous blood gas sample, is the key diagnostic test. It confirms exposure and provides a rough (though imperfect) guide to severity. The correlation between carboxyhemoglobin level and clinical severity is not absolute, and treatment decisions should be guided by clinical presentation as much as the number itself.
• ECG and troponin should be checked given the risk of myocardial ischemia, particularly in patients with significant exposure or pre-existing cardiovascular risk factors.
• Lactate is often elevated, reflecting impaired tissue oxygen delivery.
• A careful exposure history, including checking for other affected household members or pets, and assessment of the source appliance or environment, both supports diagnosis and is essential for preventing re-exposure after discharge.

Differentials include other causes of headache, nausea, and non-specific malaise (viral illness, migraine). Where cyanide co-exposure is possible (as in smoke inhalation from structural fires, where both gases are commonly generated together), cyanide toxicity should be specifically considered and treated where clinically suspected. It has its own distinct and equally urgent antidote requirements.

• Immediate removal from the source of exposure and administration of high flow, 100% oxygen via a non-rebreather mask (or via an endotracheal tube if intubated) is the first and most important treatment step. This substantially accelerates the dissociation of carbon monoxide from hemoglobin and reduces the carboxyhemoglobin half life considerably compared to breathing room air.
• Oxygen therapy is continued until the patient is asymptomatic and the carboxyhemoglobin level has normalized, generally for a minimum period regardless of how quickly symptoms appear to resolve.
• Hyperbaric oxygen therapy further accelerates carbon monoxide elimination and may reduce the risk of delayed neurological sequelae. It is considered for patients with severe poisoning, loss of consciousness, significant neurological or cardiac symptoms, pregnancy with significant exposure, or a very high carboxyhemoglobin level, where availability and transfer logistics allow.
• Supportive care addresses any associated complications, including management of seizures, arrhythmia, or myocardial ischemia should they occur.
• Before discharge, arrangements should be made to address the source of exposure (appliance inspection or repair, carbon monoxide detector installation) to prevent recurrence. Safety netting advice should be given regarding the possibility of delayed neurological symptoms, with a route for follow up assessment if these develop.

Referral: poison control or toxicology service for guidance on severity assessment and hyperbaric oxygen candidacy; hyperbaric medicine service where indicated and available; cardiology for significant myocardial injury.