Carbon Monoxide Poisoning
Carbon Monoxide Poisoning
Description, Causes and Risk Factors:
Carbon monoxide (CO) is a highly poisonous substance produced by the incomplete burning of gas and Liquid Petroleum Gas (LPG).
Carbon monoxide 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.
Carbon monoxide poisoning is caused by inhaling combustion fumes. When there's too much carbon monoxide in the air, your body replaces the oxygen in the hemoglobin of your red blood cells with carbon monoxide. This keeps life-sustaining oxygen from reaching your tissues and organs.
Various appliances fueled by wood or gas produce carbon monoxide, including:
Car and truck engines.
Fuel-burning space heaters.
Normally the amount of carbon monoxide produced by these sources isn't cause for concern. But if appliances aren't kept in good working order or if they're used in a closed or partially closed space — such as using a charcoal grill indoors or running your car in a closed garage — the carbon monoxide can build to dangerous levels.
Smoke inhalation during a fire also can cause carbon monoxide poisoning.
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. 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.
Symptoms tend to correlate well with the patient's peak blood carboxyhemoglobin levels. Many symptoms are nonspecific.
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%.
Headache and nausea can begin when levels are 10 to 20%.
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, which may increase risk of respiratory failure.
Because symptoms can be vague, nonspecific, and variable, the diagnosis 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 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. 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. Hyperbaric O2 therapy typically should be considered for patients who have any of the following:
Ongoing chest pain.
Loss of consciousness (no matter how brief).
A carboxyhemoglobin level > 25%.
Life-threatening cardiopulmonary complications.
Hyperbaric O2 therapy should also be considered for pregnant patients.
Patients are placed in a chamber at 2 to 3 atmospheres of O2. 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, and evidence for the efficacy of hyperbaric O2 therapy is somewhat inconclusive.
NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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