Carbon Monoxide Poisoning
Carbon monoxide (CO) poisoning causes acute symptoms such as headache, nausea, weakness, angina, dyspnea, loss of consciousness, seizures, and coma. Neuropsychiatric symptoms may develop weeks later. Diagnosis is by carboxyhemoglobin levels and ABGs, including measured O2 saturation. Treatment is with supplemental O2. Prevention is often possible with household CO detectors.
CO poisoning, one of the most common fatal poisonings, occurs by inhalation. CO is a colorless, odorless gas that results from incomplete combustion of hydrocarbons. Common sources of CO in poisonings include house fires and improperly vented automobiles, gas heaters, furnaces, hot water heaters, wood- or charcoal-burning stoves, and kerosene heaters. CO is produced when natural gas (methane or propane) burns. Inhaling tobacco smoke results in CO in the blood but not enough to cause poisoning.
The elimination half-life of CO is about 4.5 h with inhalation of room air, 1.5 h with 100% O2, and 20 min with 3 atmospheres (pressure) of O2 (as in a hyperbaric chamber—see Recompression Therapy).
Mechanisms of CO toxicity are not completely understood. They appear to involve
Displacement of O2 from Hb (because CO has greater affinity for Hb than does O2)
Shifting of the O2-Hb dissociation curve to the left (decreasing release of O2 from Hb to tissues—see Figure: Oxyhemoglobin dissociation curve.)
Inhibition of mitochondrial respiration
Possibly direct toxic effects on brain tissue
CO poisoning symptoms tend to correlate well with the patient’s peak blood carboxyhemoglobin levels. Many symptoms are nonspecific.
Headache and nausea can begin when levels are 10 to 20%.
Levels > 20% commonly cause vague dizziness, generalized weakness, difficulty concentrating, and impaired judgment.
Levels > 30% commonly cause dyspnea during exertion, chest pain (in patients with coronary artery disease), and confusion.
Higher levels can cause syncope, seizures, and obtundation.
Hypotension, coma, respiratory failure, and death may occur, usually when levels are > 60%.
Patients may also have many other symptoms, including visual deficits, abdominal pain, and focal neurologic deficits. If poisoning is severe, neuropsychiatric symptoms and signs (eg, dementia, psychosis, parkinsonism, chorea, amnestic syndromes) can develop days to weeks after exposure and become permanent. Because CO poisoning often results from house fires, patients may have concomitant airway injuries (see Burns : Smoke inhalation), which may increase risk of respiratory failure.
Because symptoms can be vague, nonspecific, and variable, the diagnosis of CO poisoning is easily missed. Many cases of mild poisoning with nonspecific symptoms are mistaken for viral syndromes. Physicians must maintain a high level of suspicion. If people from the same dwelling, particularly a heated dwelling, experience nonspecific flu-like symptoms, CO exposure should be considered.
If CO poisoning is suspected, the carboxyhemoglobin level is measured with a CO-oximeter; venous samples can be used because arteriovenous differences are trivial. ABGs are not measured routinely. ABGs and pulse oximetry, alone or combined, are inadequate for diagnosis of CO poisoning because O2 saturation reported in ABGs represents dissolved O2 and is thus unaffected by carboxyhemoglobin concentration; furthermore, the pulse oximeter cannot differentiate normal Hb from carboxyhemoglobin and thus provides a falsely elevated oxyhemoglobin reading. Noninvasive CO detectors have not been shown to be accurate or useful in the diagnosis of CO exposure or toxicity.
Although elevated carboxyhemoglobin levels are clear evidence of poisoning, levels may be falsely low because they decrease rapidly after CO exposure ends, particularly in patients treated with supplemental O2 (eg, in an ambulance). Metabolic acidosis can be a clue to the diagnosis. Other tests may help evaluate specific symptoms (eg, ECG for chest pain, CT for neurologic symptoms).
Patients should be removed from the source of CO and stabilized as necessary. They are given 100% O2 (by nonrebreather mask) and treated supportively. Although its use is becoming increasingly controversial, hyperbaric O2 therapy (in a chamber at 2 to 3 atmospheres of 100% O2) typically should be considered for patients who have any of the following:
Hyperbaric O2 therapy should also be considered for pregnant patients, possibly at lower serum CO levels than in nonpregnant patients.
Hyperbaric O2 therapy may decrease the incidence of delayed neuropsychiatric symptoms. However, this therapy may cause barotrauma and, because therapy is not available at most hospitals, may require transfer of patients, who may not be stable; also, a chamber may not be available locally. Evidence for the efficacy of hyperbaric O2 therapy is becoming more controversial, with some studies suggesting harm. In cases where hyperbaric O2 therapy is considered, consultation with a poison control center or hyperbaric expert is strongly recommended.
Prevention involves checking sources of indoor combustion to make sure they are correctly installed and vented to the outdoors. Exhaust pipes should be inspected periodically for leaks. Cars should never be left running in an enclosed garage. CO detectors should be installed because they provide early warning that CO is free in a dwelling’s atmosphere. If CO is suspected in a dwelling, windows should be opened, and the dwelling should be evacuated and evaluated for the source of CO.
CO poisoning (eg, caused by house fires, improperly vented automobiles, gas heaters, furnaces, hot water heaters, wood- or charcoal-burning stoves, or kerosene heaters) is one of the most common fatal poisonings.
Consider toxicity is patients with nonspecific symptoms (eg, flu-like symptoms in winter) or unexplained metabolic acidosis.
Measure CO level with a CO-oximeter.
Do not rule out toxicity based on a normal CO level because levels can decrease rapidly, particularly after treatment with supplemental O2.
Treat with 100% O2.
For severe poisoning, consult an expert or poison control center to discuss treatment with hyperbaric O2.