Aetiology

Inhalation of carbon monoxide is the main route of poisoning; exposure may be accidental or intentional.[1]

Intentional carbon monoxide poisoning as an act of self-harm may be due to exposure to car exhaust fumes in a closed garage.

Accidental poisoning can occur as a result of exposure to carbon monoxide from internal combustion engines (vehicle or generator), building fires, and indoor sources such as improperly vented stoves or heaters. Faulty boilers are a common cause, and account for approximately 27% of accidental exposures to carbon monoxide.[7]​ Accidental poisoning is more common during the winter months when heating systems are in use and windows are kept closed.

Other sources of carbon monoxide exposure include combustion of carbonaceous fuels (petrol, natural gas, kerosene, oil, boat exhaust fumes, gas-powered stoves in outdoor areas, pick-up truck exhaust fumes), and paint removers and aerosol propellants.[1][5][12][13][14][15][16]​​​

Pathophysiology

Carbon monoxide has 230 to 300 times the affinity for haemoglobin compared with oxygen.[2][17]​​ As a result, carbon monoxide preferentially binds to haemoglobin, which displaces oxygen and leads to the formation of carboxyhaemoglobin.[1][2]​ This shifts the oxyhaemoglobin dissociation curve to the left, thereby decreasing the amount of oxygen available to cells.[17]​ Therefore, high-flow oxygen is administered to treat carbon monoxide poisoning because increasing the concentration of oxygen decreases the half-life of carbon monoxide binding to haemoglobin.[2]

Carbon monoxide also binds to cytochromes and guanylyl cyclase, and has increased affinity with myoglobin. This leads to its cardiovascular effects such as hypotension, ischaemia, dysrhythmias, and myocardial impairment. Other effects of carbon monoxide exposure include generation of free oxygen radicals and inactivation of mitochondrial enzymes, resulting in impaired cellular function.

More recent research has shown that nitric oxide levels are increased in carbon monoxide poisoning, resulting in vasodilation, which further causes hypotension, syncope, and cerebral lesions. It has been hypothesised that nitric oxide is also responsible for cumulative damage to the brain, which results in the delayed neurological sequelae.

Studies also report biochemical and antigenic changes in major basic protein. This, in combination with products of lipid peroxidation, may lead to immunological cascade activation. This results in cell damage. Other suggested mechanisms of cell injury and death include glutamate-mediated neuronal injury, atherogenesis, cytochrome P-450 involvement, and apoptosis.[15]

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