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Carbon monoxide poisoning
POISONOUS SUBSTANCES
Carbon monoxide poisoning
Key points C
Carbon monoxide (CO) binds haemoglobin, thereby preventing oxygen binding and reducing the oxygen-carrying capacity of blood
C
Severe poisoning, which can lead to coma and death, is usually associated with carboxyhaemoglobin (COHb) concentration >30%
C
Features of less severe poisoning can be non-specific, e.g. headache, gastrointestinal upset, dizziness and weakness
C
The only specific treatment is to give high-flow oxygen, which greatly reduces COHb half-life
Aravindan Veiraiah
Abstract Carbon monoxide (CO) poisoning is diagnosed in 1 in 100,000 people per year in the UK, more commonly in winter and in more deprived areas. Toxicity occurs mainly through the formation of carboxyhaemoglobin (COHb), causing ischaemia of vital organs. Features are nonspecific and include headache, gastrointestinal upset, dizziness, weakness, convulsions, coma, chest pain and dyspnoea. Neuropsychiatric features can appear up to 40 days after the initial exposure. The diagnosis can be missed unless a history of exposure to sources of CO is elicited or a CO alarm triggered. There may be a history of others (including pets) with a similar illness in a particular location (e.g. home, office) and an improvement in symptoms when away from that location. A COHb concentration >5% in non-smokers, and >10% in smokers, indicates CO poisoning. COHb concentration >30% indicates severe poisoning, although lower concentrations do not rule out severe CO poisoning. Patients should be treated with high-flow oxygen, which usually results in rapid improvement. Complications, including myocardial infarction and stroke-like features, should be managed conventionally. The source of CO should be identified and eliminated. Patients and families should be educated to prevent CO poisoning in the community.
Clinical features
Carbon monoxide (CO) is a colourless and odourless gas produced by the incomplete combustion of carbon fuels. CO poisoning is diagnosed as the cause of hospital admission in 1 per 100,000 people per year in the UK. Admissions are more common in winter and in more deprived areas.1 The incidence is similar in other European Union countries.
Acute features include headache, gastrointestinal upset, dizziness, weakness, convulsions and coma. Chest pain, arrhythmias, myocardial infarction and cardiogenic shock can occur in patients with or without prior coronary artery disease. Cherry red skin, caused by very high concentrations of COHb, is rarely seen in clinical practice. Chronic poisoning can present with headache, lethargy, nausea, memory problems and flu-like symptoms. Features are non-specific, and the diagnosis can be missed if the patient or witness is not directly questioned about a history of exposure to fire or other source of CO (e.g. indoor barbecue or generator, shisha/hooka, vehicle exhaust), unless a CO alarm has been triggered. There may be a history of others (including pets) with a similar illness in a particular location (e.g. home, office) and an improvement in symptoms when away from that location. Features improve rapidly after oxygen therapy. Neuropsychiatric features can appear up to 40 days after acute exposure. These include memory impairment, disorientation, apathy, mutism, irritability, inability to concentrate, personality change, emotional lability, neuropathy, incontinence, chorea, apraxia, psychosis, dementia and parkinsonism.
Pathology and pathogenesis
Investigations
CO binds haemoglobin with a much greater affinity than oxygen and forms carboxyhaemoglobin (COHb). This reduces oxygen carriage and causes ischaemia of vital tissues, including the extrapyramidal system, cerebral cortex and myocardium. CO binds with other intracellular oxygen-carrying proteins (e.g. cytochromes), but the relevance to CO poisoning is unclear. Coronary thrombosis can occur from a prothrombotic effect of CO.2
Perform arterial or venous blood gas testing when CO poisoning is suspected. Concentrations >5% in non-smokers, and >10% in smokers, indicate possible poisoning. However, concentrations up to 14% are normal in some smokers.3 The COHb concentration is usually >30% at the time of severe poisoning, but can be lower by the time of measurement. Co-oximeters and CO breath tests can be used to detect CO exposure or poisoning, but can produce false-positive or falsenegative results. A 12-lead electrocardiogram and troponin test should be performed in all individuals with cardiac symptoms. Brain imaging should be performed in all those with neurological features.
Keywords Carbon monoxide; carboxyhaemoglobin (COHb); highflow oxygen; MRCP; poisoning; prevention
Definition and incidence
Aravindan Veiraiah MB BS MRCP is a Clinical Toxicologist with the National Poisons Information Service, and an Acute Physician at the Royal Infirmary of Edinburgh, UK. Competing interests: none declared.
MEDICINE xxx:xxx
1
Ó 2019 Published by Elsevier Ltd.
Please cite this article as: Veiraiah A, Carbon monoxide poisoning, Medicine, https://doi.org/10.1016/j.mpmed.2019.12.013
POISONOUS SUBSTANCES
Where appropriate, the source of CO should be identified and eliminated. This can require the help of a gas engineer (e.g. to identify a faulty flue) or the local public health team. Patient and public education (e.g. about maintenance of appliances, installing CO monitors, fire safety) is crucial to prevent CO poisoning in the community. A
Differential diagnosis Acute poisoning Infections with non-specific features Cyanide poisoning (house fire) Chemical incident from other noxious gas Chronic poisoning Various chronic illness with fatigue neuropsychiatric features
KEY REFERENCES 1 Ghosh RE, Close R, McCann LJ, et al. Analysis of hospital admissions due to accidental non-fire-related carbon monoxide poisoning in England, between 2001 and 2010. J Public Health (Oxf) 2016; 38: 78e81. 2 Caron-Cantin M, Abbott M, Brooks-Lim E, Adeagbo B. Intracoronary thrombus formation following carbon monoxide poisoning. J Forensic Sci 2018; 63: 1573e6. 3 Wald NJ, Idle M, Boreham J, Bailey A. Carbon monoxide in breath in relation to smoking and carboxyhaemoglobin levels. Thorax 1981; 36: 367. 4 Ozturan IU, Yaka E, Suner S, et al. Determination of carboxyhemoglobin half-life in patients with carbon monoxide toxicity treated with high flow nasal cannula oxygen therapy. Clin Toxicol (Phila) 2019; 57: 617e23. 5 Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJ. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev 2011; 4: CD002041.
Management High-flow oxygen via face mask reduces the half-life of COHb from 320 minutes to 80 minutes. Giving up to 60 litres/minute of oxygen using high-flow nasal cannulae can further reduce the half-life to <40 minutes.4 Hyperbaric oxygen has been shown to reduce the half-life of COHb to similar levels, but its cost and associated practical challenges are considerable, and more evidence from randomized controlled trials is needed.5 Complications (e.g. cardiovascular, neurological) should be treated and followed up conventionally. Patients who have been asymptomatic since exposure should be reassured that they are unlikely to develop complications. Individuals who were symptomatic at admission should be informed that there is a small risk they may develop neuropsychiatric problems up to 6 weeks after CO exposure.
MEDICINE xxx:xxx
2
Ó 2019 Published by Elsevier Ltd.
Please cite this article as: Veiraiah A, Carbon monoxide poisoning, Medicine, https://doi.org/10.1016/j.mpmed.2019.12.013
Carbon monoxide poisoning
Key points C
Carbon monoxide (CO) binds haemoglobin, thereby preventing oxygen binding and reducing the oxygen-carrying capacity of blood
C
Severe poisoning, which can lead to coma and death, is usually associated with carboxyhaemoglobin (COHb) concentration >30%
C
Features of less severe poisoning can be non-specific, e.g. headache, gastrointestinal upset, dizziness and weakness
C
The only specific treatment is to give high-flow oxygen, which greatly reduces COHb half-life
Aravindan Veiraiah
Abstract Carbon monoxide (CO) poisoning is diagnosed in 1 in 100,000 people per year in the UK, more commonly in winter and in more deprived areas. Toxicity occurs mainly through the formation of carboxyhaemoglobin (COHb), causing ischaemia of vital organs. Features are nonspecific and include headache, gastrointestinal upset, dizziness, weakness, convulsions, coma, chest pain and dyspnoea. Neuropsychiatric features can appear up to 40 days after the initial exposure. The diagnosis can be missed unless a history of exposure to sources of CO is elicited or a CO alarm triggered. There may be a history of others (including pets) with a similar illness in a particular location (e.g. home, office) and an improvement in symptoms when away from that location. A COHb concentration >5% in non-smokers, and >10% in smokers, indicates CO poisoning. COHb concentration >30% indicates severe poisoning, although lower concentrations do not rule out severe CO poisoning. Patients should be treated with high-flow oxygen, which usually results in rapid improvement. Complications, including myocardial infarction and stroke-like features, should be managed conventionally. The source of CO should be identified and eliminated. Patients and families should be educated to prevent CO poisoning in the community.
Clinical features
Carbon monoxide (CO) is a colourless and odourless gas produced by the incomplete combustion of carbon fuels. CO poisoning is diagnosed as the cause of hospital admission in 1 per 100,000 people per year in the UK. Admissions are more common in winter and in more deprived areas.1 The incidence is similar in other European Union countries.
Acute features include headache, gastrointestinal upset, dizziness, weakness, convulsions and coma. Chest pain, arrhythmias, myocardial infarction and cardiogenic shock can occur in patients with or without prior coronary artery disease. Cherry red skin, caused by very high concentrations of COHb, is rarely seen in clinical practice. Chronic poisoning can present with headache, lethargy, nausea, memory problems and flu-like symptoms. Features are non-specific, and the diagnosis can be missed if the patient or witness is not directly questioned about a history of exposure to fire or other source of CO (e.g. indoor barbecue or generator, shisha/hooka, vehicle exhaust), unless a CO alarm has been triggered. There may be a history of others (including pets) with a similar illness in a particular location (e.g. home, office) and an improvement in symptoms when away from that location. Features improve rapidly after oxygen therapy. Neuropsychiatric features can appear up to 40 days after acute exposure. These include memory impairment, disorientation, apathy, mutism, irritability, inability to concentrate, personality change, emotional lability, neuropathy, incontinence, chorea, apraxia, psychosis, dementia and parkinsonism.
Pathology and pathogenesis
Investigations
CO binds haemoglobin with a much greater affinity than oxygen and forms carboxyhaemoglobin (COHb). This reduces oxygen carriage and causes ischaemia of vital tissues, including the extrapyramidal system, cerebral cortex and myocardium. CO binds with other intracellular oxygen-carrying proteins (e.g. cytochromes), but the relevance to CO poisoning is unclear. Coronary thrombosis can occur from a prothrombotic effect of CO.2
Perform arterial or venous blood gas testing when CO poisoning is suspected. Concentrations >5% in non-smokers, and >10% in smokers, indicate possible poisoning. However, concentrations up to 14% are normal in some smokers.3 The COHb concentration is usually >30% at the time of severe poisoning, but can be lower by the time of measurement. Co-oximeters and CO breath tests can be used to detect CO exposure or poisoning, but can produce false-positive or falsenegative results. A 12-lead electrocardiogram and troponin test should be performed in all individuals with cardiac symptoms. Brain imaging should be performed in all those with neurological features.
Keywords Carbon monoxide; carboxyhaemoglobin (COHb); highflow oxygen; MRCP; poisoning; prevention
Definition and incidence
Aravindan Veiraiah MB BS MRCP is a Clinical Toxicologist with the National Poisons Information Service, and an Acute Physician at the Royal Infirmary of Edinburgh, UK. Competing interests: none declared.
MEDICINE xxx:xxx
1
Ó 2019 Published by Elsevier Ltd.
Please cite this article as: Veiraiah A, Carbon monoxide poisoning, Medicine, https://doi.org/10.1016/j.mpmed.2019.12.013
POISONOUS SUBSTANCES
Where appropriate, the source of CO should be identified and eliminated. This can require the help of a gas engineer (e.g. to identify a faulty flue) or the local public health team. Patient and public education (e.g. about maintenance of appliances, installing CO monitors, fire safety) is crucial to prevent CO poisoning in the community. A
Differential diagnosis Acute poisoning Infections with non-specific features Cyanide poisoning (house fire) Chemical incident from other noxious gas Chronic poisoning Various chronic illness with fatigue neuropsychiatric features
KEY REFERENCES 1 Ghosh RE, Close R, McCann LJ, et al. Analysis of hospital admissions due to accidental non-fire-related carbon monoxide poisoning in England, between 2001 and 2010. J Public Health (Oxf) 2016; 38: 78e81. 2 Caron-Cantin M, Abbott M, Brooks-Lim E, Adeagbo B. Intracoronary thrombus formation following carbon monoxide poisoning. J Forensic Sci 2018; 63: 1573e6. 3 Wald NJ, Idle M, Boreham J, Bailey A. Carbon monoxide in breath in relation to smoking and carboxyhaemoglobin levels. Thorax 1981; 36: 367. 4 Ozturan IU, Yaka E, Suner S, et al. Determination of carboxyhemoglobin half-life in patients with carbon monoxide toxicity treated with high flow nasal cannula oxygen therapy. Clin Toxicol (Phila) 2019; 57: 617e23. 5 Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJ. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev 2011; 4: CD002041.
Management High-flow oxygen via face mask reduces the half-life of COHb from 320 minutes to 80 minutes. Giving up to 60 litres/minute of oxygen using high-flow nasal cannulae can further reduce the half-life to <40 minutes.4 Hyperbaric oxygen has been shown to reduce the half-life of COHb to similar levels, but its cost and associated practical challenges are considerable, and more evidence from randomized controlled trials is needed.5 Complications (e.g. cardiovascular, neurological) should be treated and followed up conventionally. Patients who have been asymptomatic since exposure should be reassured that they are unlikely to develop complications. Individuals who were symptomatic at admission should be informed that there is a small risk they may develop neuropsychiatric problems up to 6 weeks after CO exposure.
MEDICINE xxx:xxx
2
Ó 2019 Published by Elsevier Ltd.
Please cite this article as: Veiraiah A, Carbon monoxide poisoning, Medicine, https://doi.org/10.1016/j.mpmed.2019.12.013