Carbon Monoxide Poisoning

Carbon monoxide is produced by the incomplete combustion of carbon or carbon-containing compounds in an inadequate supply of oxygen. Carbon monoxide competes with oxygen to form carboxyhaemoglobin (HbCO) instead of oxyhaemoglobin but it has 210 times the affinity for haemoglobin. In an atmosphere of 21% oxygen and 0.1% carbon monoxide, therefore, the blood will leave the lungs about 50% saturated with oxyhaemoglobin and 50% saturated with carboxyhaemoglobin.¹ An ambient carbon monoxide level of 100 parts per million (ppm) produces 16% HbCO at equilibrium, which is sufficient to produce clinical symptoms. It also binds to intracellular carriers of oxygen, causing tissue asphyxiation. Carbon monoxide binds even more avidly to cardiac myoglobin than to haemoglobin.²

Carbon monoxide may result from the combustion of wood or fossil fuels such as gas, oil and coal with inadequate oxygen supply. It is present in a car exhaust if oxygen is limited as in a garage or with the choke engaged. In someone who has escaped from a fire, both smoke inhalation and carbon monoxide poisoning must be considered, as must hydrogen sulphide poisoning. Tobacco smoke also contains carbon monoxide. It is a colourless, odourless gas and so cannot be detected by the normal senses.

Carbon monoxide is excreted through the lungs. The half-life in a normal atmosphere is 3 to 4 hours. 100% oxygen reduces this to 30 to 90 minutes and 100% oxygen at hyperbaric pressure of 2.5 atmospheres reduces it to 15 to 23 minutes.² The value of hyperbaric oxygen is however unclear (see below).

Carbon monoxide poisoning kills 50 people and seriously injures nearly 200 in the United Kingdom each year, but the overwhelming majority of cases go unrecognised, unreported, and untreated.³ A recent study in America found an emergency department attendance rate of 50,000 annually, a significant increase on previous estimates.⁴

Risk factors^2,5

• Inadequately serviced fires - there is an increased risk in winter, and whilst 20 million households in the UK use gas fires, there is a greater risk in the 2 million households which use solid fuel (statistics quoted in the Chief Medical Officer's letter, 2003).⁶ Any carbon-based fuel can be hazardous, including oil.
• Running a petrol or diesel engine in a confined space increases the risk. Simply having the windows and doors of a garage open is not enough.
• Proximity to a conflagration such as a house fire - during the assessment and management of burns, do not forget the possibility of carbon monoxide poisoning and smoke inhalation too.
• Acute toxicity results from a single exposure but chronic carbon monoxide poisoning also needs to be recognised. The latter often results from a poorly serviced gas fire and the elderly are most at risk. Clinical features are non-specific and so a high level of suspicion is required.
• The fetus is more vulnerable to CO toxicity because of the natural leftward shift of the dissociation curve of fetal haemoglobin, a lower baseline PaO2, and levels of HbCO at equilibration that are 10 to 15% higher than maternal levels. The neonate also has high levels of fetal haemoglobin.
• In the USA outbreaks of carbon monoxide poisoning occur when there are ice storms that cause loss of electric power and, in the extreme cold, people turn to alternative sources of heat.⁷

Early features¹

• These include headache, nausea, irritability, weakness and tachypnoea.
• This may be followed by dizziness, ataxia, angina, hypotension, arrhythmias, agitation, seizures, impairment of consciousness and respiratory failure.
• Cerebral oedema and metabolic acidosis may develop.
• Less common features include skin blisters, rhabdomyolysis, acute renal failure, pulmonary oedema, myocardial infarction, retinal haemorrhages, cortical blindness and choreoathetosis.
• The classical cherry red coloration is rarely seen in life although it may be seen on the post mortem slab.

Late features^2,8

• Most people make an uneventful recovery but some develop later symptoms perhaps after several weeks of apparent recovery from the incident. This late stage is more common in those over 40.
• Neurological or neuropsychiatric features including disorientation, apathy, mutism, irritability, inability to concentrate, personality change, Parkinsonism and parietal lobe lesions. Memory loss is thought to be a late feature, but the link with carbon monoxide poisoning has been challenged.⁹ Encephalopathy develops 2-6 weeks after the initial acute intoxication.¹⁰
• Urinary incontinence and/or faecal incontinence and disturbance of gait are common.
• Most patients recover fully or considerably within a year.

Chronic poisoning¹¹

This is often unsuspected and unrecognised and features may appear non-specific. Headache, nausea and flu-like symptoms. They are most common in winter as that is when fires are used and ventilation is restricted. It should be suspected if more than one person in a household has such symptoms that do not appear to be due to a viral infection. There may be black, sooty marks near a fire.

• Headache occurs in 90%
• Nausea and vomiting occurs in 50%
• Vertigo occurs in 50%
• Alteration in consciousness occurs in 30%
• A subjective feeling of weakness occurs in 20%

Severe poisoning^12,2

One or more of the following suggest a severe condition:

• Neurological signs such as increased muscle tone and extensor plantar response
• Coma
• Need for ventilation
• ECG suggests ischaemia or infarction
• Metabolic acidosis
• HbCO >30% but the link between HbCO and outcome is weak

• The GP will need to refer the patient to hospital for investigation and management if applicable.
• Arterial blood gases may show a metabolic acidosis and possible methaemoglobinaemia.
• HbCO can be measured, although the initial level may not correlate with severity. Symptoms such as headaches start around 10% whilst at 50 to 70% seizure, coma and death may occur.
• ECG may show myocardial ischaemia or infarction and creatine kinase or troponin levels may indicate myocardial damage.
• In severe cases other investigations may include urea and electrolytes because of metabolic acidosis, LDH for tissue damage and in chronic severe cases urinalysis may show both albumin and glucose.
• If there is an unexplained metabolic acidosis after an industrial fire, consider cyanide toxicity.
• Check hCG if pregnancy is a possibility.
• If symptoms are severe get chest Xray as pulmonary oedema may develop and it should also be done if hyperbaric oxygen is considered.
• MRI may show cerebral abnormalities.

• Acute respiratory distress syndrome
• Alcohol toxicity
• Altitude illness
• Cluster headache
• Cyanide poisoning
• Depression
• Diabetic ketoacidosis
• Encephalitis
• Gastroenteritis
• Hypoglycaemia
• Hypothyroidism
• Labyrinthitis
• Lactic acidosis
• Meningitis
• Methaemoglobinaemia
• Migraine
• Smoke inhalation
• Tension headache
• Alcohol toxicity
• Narcotic toxicity

• Remove from the source of exposure.
• Maintain a clear airway and adequate ventilation.
• Give oxygen in as high concentrations as possible. It may be required for 24 hours.
• Metabolic acidosis should be corrected by increasing oxygen delivery to the tissues. Sodium bicarbonate is contraindicated.
• Give mannitol 1g/kg intravenously over 20 minutes if cerebral oedema is suspected.
• Monitor the heart rhythm for 4 to 6 hours.
• Measure the carboxyhaemoglobin concentration as an emergency. HbCO of 30% indicates severe exposure but much lower concentrations do not exclude significant poisoning and the relationship between HbCO and severity of poisoning and clinical outcome is poor.
• If the patient is unconscious, look for extrapyramidal features and retinal haemorrhages to assess the severity of central nervous system toxicity.
• As mentioned above, hyperbaric oxygen reduces the elimination times for carbon monoxide and hence would seem a promising therapy for severe cases in an attempt to reduce the incidence of neurological complications. However, a systematic review found that the actual benefits were small if any and this is in keeping with other reviews.¹³ A Cochrane review found that more evidence is required from a large multi-centre trial.¹⁴ A systematic review on the use of hyperbaric oxygen in this and other conditions is, at the time of writing, being carried out by NHS Quality Improvement Scotland, and is due to report in April 2008.¹⁵ Thereafter, NICE may consider including it in their work program.¹⁶ A pragmatic approach is to consider hyperbaric oxygen if a chamber is available within 6 hours and HbCO>25% or if the patient is pregnant or has significant neurological symptoms.
• Asymptomatic patients with HbCO below 10% may be discharged although if the patient is pregnant there is concern for the fetus.
• Limit exertion for the next few weeks and stop smoking.
• Blood gases must be monitored with use of oxygen in COPD.

Neurological and neuropsychiatric complications often resolve but may take a year to do so. Parkinsonism may develop after poisoning. If so it usually starts within a month. Many cases recover spontaneously but there are no currently effective treatments for long-term sequelae.¹⁷ Most people with mild, accidental poisoning are able to return to their former job within a month.^18,19 Early diagnosis and effective treatment reduce short and long term effects.²⁰ In patients with encephalopathy which eventually improves, MRI scan abnormalities can be seen to resolve in correlation with clinical features.¹⁰

Even very low levels of carbon monoxide can produce a significant reduction in cognitive functioning.²¹ Avoidance of poisoning requires gas fires to be fitted by competent people and to be adequately serviced. Soot by the flue suggests problems. Oil and coal burners also need servicing. Open fires that let smoke back into a room need the chimney to be swept. Never leave a car engine running in the garage as the passive ventilation of an open garage door is inadequate. Portable oil fires and paraffin stoves are a potential problem. Be aware of the problem, especially in the elderly. Carbon monoxide detectors with alarms are available and reduce morbidity.²² In the event of exposure, a rapid and organised response by healthcare personnel and the emergency services helps to reduce mortality and morbidity. The Health Protection Agency has produced some Incident Management guidelines to facilitate this.²³

Domestic gas used to be produced from coal. This gas was produced by passing a limited amount of air and steam over hot coke to produce hydrogen and carbon monoxide. C + O2 = CO2. C + CO2 = 2CO. This was an exothermic reaction that was alternated with the reaction with steam that was endothermic. C + H2O = H2 + CO. Hence unburned domestic gas contained a large amount of carbon monoxide. Natural gas is mostly methane and North Sea Gas has replaced coal gas as domestic fuel since the 1960s.²⁴ This has brought about a substantial reduction in poisoning from carbon monoxide, both accidental and intentional. It is because of the risk of carbon monoxide poisoning, as well as the risk of explosion, that the smell was artificially introduced to domestic gas supplies.