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Carbon monoxide is the commonest agent used in completed suicides by poisoning in Australia and the United Kingdom.
Carbon monoxide is produced by incomplete combustion and is found in car exhaust, faulty heaters, fires and in industrial settings.
Carbon monoxide poisoning may result in significant long-term neuropsychological sequelae.
Oxygen increases the elimination of carbon monoxide, and the extent of increase is proportional to the inspired oxygen pressure.
The optimal mode of oxygen delivery to improve clinical outcomes remains controversial.
Carbon monoxide (CO) poisoning is an important cause of mortality and morbidity from poisoning. Immediate resuscitation including 100% oxygen therapy is essential and the long-term results of most patients will be good with this simple intervention. It is unclear whether any additional intervention will reduce the low but important risk of serious long-term neurological damage.
Carbon monoxide is a colourless, odourless, tasteless and non-irritant gas produced by incomplete combustion of hydrocarbons. Small amounts are also produced endogenously by normal metabolic processes. The most common sources of significant exposure are car exhausts, cigarette smoke, fires and faulty home heaters and barbecues. Catalytic converters reduce the production of CO and are in all cars manufactured in the last decade or two. Carboxyhaemoglobin (COHb) concentrations in cigarette smokers range as high as 10%.
The pathophysiology of CO exposure is complex and incompletely understood. Upon exposure, CO binds to haemoglobin with an affinity 210 times that of oxygen, thereby decreasing the oxygen-carrying capacity of blood. CO can also produce injury by several other mechanisms, including direct disruption of cellular oxidative processes, binding to myoglobin and cytochrome oxidases and causing peroxidation of brain lipids. However, the end result in any case is tissue hypoxia, leading to varying degrees of end-organ damage and eventually death. The severity of poisoning is a function of the duration of exposure, the ambient concentration of CO and the underlying health status of the exposed individual. Although it is useful for diagnosis when detected, the COHb level on arrival correlates poorly with outcome.
Poisoning with CO is an important cause of unintentional and intentional injury worldwide. In the United States alone, an estimated 1000 to 2000 accidental deaths due to CO exposure occur each year, resulting from an estimated 40,000 exposures. In Australia and the United Kingdom, it is the most common agent in completed suicide by poisoning. In East Asia, there is a recent epidemic of self-poisonings due to the burning of charcoal.
Prevention of environmental or occupational exposure is possible with CO air monitors. The threshold CO concentration of concern is reduced if exposed people are exercising or at high altitudes (increased breathing rate and pulmonary blood flow), as these increase uptake.
The introduction of catalytic converters has reduced CO production in vehicle exhaust; this may have contributed to fewer fatal suicidal poisonings in some countries.
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