This is a colourless, odourless, tasteless, nonirritating gas formed on incomplete combustion of organic fuels. Exposure to CO is frequently due to defective gas, oil or solid-fuel heating appliances. CO is a component of car exhaust fumes and deliberate exposure to these is a common method of suicide. Victims of ﬁres often suﬀer from CO poisoning. CO combines reversibly with oxygen-carrying sites of HAEMOGLOBIN (Hb) molecules with an aﬃnity 200 to 300 times greater than oxygen itself. The carboxyhaemoglobin (COHb) formed becomes unavailable for oxygen transportation. In addition the partial saturation of the Hb molecule results in tighter oxygen binding, impairing delivery to the tissues. CO also binds to MYOGLOBIN and respiratory cytochrome enzymes. Exposure to CO at levels of 500 parts per million (ppm) would be expected to cause mild symptoms only and exposure to levels of 4,000 ppm would be rapidly fatal.
Each year around 50 people in the United Kingdom are reported as dying from carbon monoxide poisoning, and experts have suggested that as many as 25,000 people a year are exposed to its eﬀects within the home, but most cases are unrecognised, unreported and untreated, even though victims may suﬀer from long-term eﬀects. This is regrettable, given that Napoleon’s surgeon, Larrey, recognised in the 18th century that soldiers were being poisoned by carbon monoxide when billeted in huts heated by woodburning stoves. In the USA it is estimated that 40,000 people a year attend emergency departments suﬀering from carbon monoxide poisoning. So prevention is clearly an important element in dealing with what is sometimes termed the ‘silent killer’. Safer designs of houses and heating systems, as well as wider public education on the dangers of carbon monoxide and its sources, are important.
Clinical eﬀects of acute exposure resemble those of atmospheric HYPOXIA. Tissues and organs with high oxygen consumption are aﬀected to a great extent. Common eﬀects include headaches, weakness, fatigue, ﬂushing, nausea, vomiting, irritability, dizziness, drowsiness, disorientation, incoordination, visual disturbances, TACHYCARDIA and HYPERVENTILATION. In severe cases drowsiness may progress rapidly to COMA. There may also be metabolic ACIDOSIS, HYPOKALAEMIA, CONVULSIONS, HYPOTENSION, respiratory depression, ECG changes and cardiovascular collapse. Cerebral OEDEMA is common and will lead to severe brain damage and focal neurological signs. Signiﬁcant abnormalities on physical examination include impaired short-term memory, abnormal Rhomberg’s test (standing unsupported with eyes closed) and unsteadiness of gait including heel-toe walking. Any one of these signs would classify the episode as severe. Victims’ skin may be coloured pink, though this is very rarely seen even in severe incidents. The venous blood may look ‘arterial’. Patients recovering from acute CO poisoning may suﬀer neurological sequelae including TREMOR, personality changes, memory impairment, visual loss, inability to concentrate and PARKINSONISM. Chronic low-level exposures may result in nausea, fatigue, headache, confusion, VOMITING, DIARRHOEA, abdominal pain and general malaise. They are often misdiagnosed as inﬂuenza or food poisoning.
First-aid treatment is to remove the victim from the source of exposure, ensure an eﬀective airway and give 100-per-cent oxygen by tight-ﬁtting mask. In hospital, management is largely suppportive, with oxygen administration. A blood sample for COHb level determination should be taken as soon as practicable and, if possible, before oxygen is given. Ideally, oxygen therapy should continue until the COHb level falls below 5 per cent. Patients with any history of unconsciousness, a COHb level greater than 20 per cent on arrival, any neurological signs, any cardiac arrhythmias or anyone who is pregnant should be referred for an expert opinion about possible treatment with hyperbaric oxygen, though this remains a controversial therapy. Hyperbaric oxygen therapy shortens the half-life of COHb, increases plasma oxygen transport and reverses the clinical eﬀects resulting from acute exposures. Carbon monoxide is also an environmental poison and a component of cigarette smoke. Normal body COHb levels due to ENDOGENOUS CO production are 0.4 to
0.7 per cent. Non-smokers in urban areas may have level of 1–2 per cent as a result of environmental exposure. Smokers may have a COHb level of 5 to 6 per cent.