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Carbon Monoxide Poisoning

This PatientPlus article is written for healthcare professionals so the language may be more technical than the condition leaflets. You may find the abbreviations list helpful.

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 30-90 minutes and 100% oxygen at hyperbaric pressure of 2.5 atmospheres reduces it to 15-23 minutes.2 The value of hyperbaric oxygen is, however, unclear (see below).

Epidemiology

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 study in the USA in 2007 found an emergency department attendance rate of 50,000 annually, a significant increase on previous estimates.4

Risk factors2,5

  • 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 nonspecific and so a high level of suspicion is required.
  • The fetus is more vulnerable to carbon monoxide 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 10-15% 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

Presentation

Low-level poisoning1,8

Early features

Low-level exposure may produce no abnormal physical signs. Symptoms are likely to be mild and may include nausea, subjective weakness, headache and poor concentration/memory. Carbon monoxide poisoning is likely to be suspected in circumstances where exposure to a source has taken place and symptoms improve when the patient has been removed from the source.

Late features

Some patients develop later symptoms perhaps after several weeks of apparent recovery from the incident. This late stage is more common in those aged over 40.2,8

Neurological or neuropsychiatric features including disorientation, apathy, mutism, irritability, inability to concentrate, personality change, Parkinsonism and parietal lobe lesions.9 Memory loss is thought to be a late feature, but the link with carbon monoxide poisoning has been challenged.10

Encephalopathy develops 2-6 weeks after the initial acute intoxication. Urinary incontinence and/or faecal incontinence and disturbance of gait are common.Rarely, chorea may be the presenting feature.11

Chronic poisoning12

This is often unsuspected and unrecognised and features may appear nonspecific, e.g. 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%.

High-level poisoning

The above symptoms may be more severe. In addition there may be:

Investigations1,2

  • The GP will need to refer the patient to hospital for investigation and management if applicable.
  • Direct spectrophotometric measurement of HbCO in a blood gas analyser is the gold standard, although the initial level may not correlate with severity. A bedside HbCO oximeter is now available (this is not to be confused with an oximeter which measures blood levels). Symptoms such as headaches start around 10% whilst at 50-70% seizure, coma and death may occur.
  • Arterial blood gases may show a metabolic acidosis and possible methaemoglobinaemia.
  • 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, lactate dehydrogenase (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.
  • Haematological investigations may be needed to exclude disseminated intravascular coagulation (DIC) and thrombotic thrombocytopenic purpura (TTP).
  • Check human chorionic gonadotrophin (hCG) if pregnancy is a possibility.
  • If symptoms are severe, get a chest X-ray, as pulmonary oedema may develop.
  • MRI scan may show cerebral abnormalities.
  • Neuropsychological testing, involving assessment of concentration, fine movements and problem solving may be useful in providing diagnostic and prognostic information.

Differential diagnosis2

Management1,2,8

What GPs should do

If low-level exposure is suspected

  • Remove the person (and others) from the source and advise them to stay away from the area until it has been ventilated.
  • If a woman is pregnant arrange for urgent assessment by an obstetrician.
  • Check an HbCO level to establish the diagnosis or monitor exhaled carbon monoxide level (a suitable meter may be available from a smoking cessation clinic).
  • Contact the local Health Protection Unit (HPU) to arrange environmental testing and management. Contact details available from the Health Protection website - www.hpa.org.uk.
  • Seek specialist advice if in any doubt:
    • UK National Poisons Information Service (NPIS) 0844 892 0111
    • UK Teratology Information Service (UKTIS) 0844 892 0909 for advice about pregnant women (out of hours, telephone NPIS).

If a high level of CO poisoning is suspected:

  • Arrange for the removal of the person (and others) from the source of the exposure.
  • Check and manage airways, breathing and circulation.
  • Give oxygen at up to 100% (most GPs may not have this available).
  • Arrange for urgent hospital transfer.
  • Check blood glucose whilst waiting for the ambulance to exclude hypoglycaemia that may need to be treated urgently.
  • Contact the local HPU - contact details available from the Health Protection website - www.hpa.org.uk.

What hospital doctors should do

  • Give oxygen at 100% concentration. Expert evidence suggests that this reduces the half-life of HbCO . It may be required for 24 hours.
  • The evidence concerning the use of hyperbaric oxygen is controversial and there is no international consensus. Although in widespread use in other countries (notably the USA), UK recommendations are that it should not be employed, as the evidence base does not support its superiority over 100% oxygen in terms of long-term clinical outcomes.
  • Metabolic acidosis should be corrected by increasing oxygen delivery to the tissues. Sodium bicarbonate is contra-indicated.
  • Give mannitol 1g/kg intravenously over 20 minutes if cerebral oedema is suspected.
  • Monitor the heart rhythm for 4-6 hours.
  • Measure the HbCO 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.
  • 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 if the patient is a smoker, stop smoking.
  • Blood gases must be monitored with use of oxygen in chronic obstructive pulmonary disease.

Prognosis2,8

  • Prognosis may be unpredictable.
  • Many cases recover spontaneously but there are no currently effective treatments for long-term sequelae.9
  • Most people with mild, accidental poisoning are able to return to their former job within a month.13,14 Early diagnosis and effective treatment reduce short- and long-term effects.
  • Neuropsychiatric testing may provide prognostic information in determining delayed sequelae.
  • Persistent neurological impairment may be associated with abnormal findings on CT scan.
  • Parkinsonism may develop after poisoning. If so, it usually starts within a month.15
  • In patients with encephalopathy which eventually improves, MRI scan abnormalities can be seen to resolve in correlation with clinical features.16
  • A poor outcome is associated with cardiac arrest, coma, metabolic acidosis, and high HbCO levels.
  • An American study found that people treated for acute carbon monoxide poisoning had an increased risk of long-term mortality, principally associated with psychiatric disorders, injuries and violence.17

Prevention1,2,8

Even very low levels of carbon monoxide can produce a significant reduction in cognitive functioning.18 Avoidance of poisoning requires gas fires to be fitted by an appropriately registered engineer 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.19 They should be compliant with European Standard EN 50291 and show a British Standards Kitemark or Loss Prevention Certification Board logo. One American study reported a successful outcome from public educational sessions which included distribution of free alarms.20

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.21

History

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.22 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.

Document references

  1. Blumenthal I; Carbon monoxide poisoning. J R Soc Med. 2001 Jun;94(6):270-2.
  2. Shochat G; Toxicity, Carbon Monoxide, eMedicine, Apr 2010
  3. Walker E, Hay A; Carbon monoxide poisoning. BMJ. 1999 Oct 23;319(7217):1082-3.
  4. Hampson NB, Weaver LK; Carbon monoxide poisoning: a new incidence for an old disease. Undersea Hyperb Med. 2007 May-Jun;34(3):163-8. [abstract]
  5. Whincup P, Papacosta O, Lennon L, et al; Carboxyhaemoglobin levels and their determinants in older British men. BMC Public Health. 2006 Jul 18;6:189. [abstract]
  6. CMO Update 35; A communication to all doctors from the Chief Medical Officer, Dept of Health, January 2003.
  7. Ghim M, Severance HW; Ice storm-related carbon monoxide poisonings in North Carolina: a reminder. South Med J. 2004 Nov;97(11):1060-5. [abstract]
  8. Carbon monoxide poisoning, Clinical Knowledge Summaries (April 2009)
  9. Choi IS; Parkinsonism after carbon monoxide poisoning. Eur Neurol. 2002;48(1):30-3. [abstract]
  10. Deschamps D, Geraud C, Julien H, et al; Memory one month after acute carbon monoxide intoxication: a prospective study. Occup Environ Med. 2003 Mar;60(3):212-6. [abstract]
  11. Song IU, Chung SW; Chorea as the first neurological symptom of delayed encephalopathy after carbon Intern Med. 2010;49(11):1037-9. Epub 2010 Jun 1. [abstract]
  12. Harper A, Croft-Baker J; Carbon monoxide poisoning: undetected by both patients and their doctors. Age Ageing. 2004 Mar;33(2):105-9. [abstract]
  13. Annane D, Chevret S, Jars-Guincestre C, et al; Prognostic factors in unintentional mild carbon monoxide poisoning. Intensive Care Med. 2001 Nov;27(11):1776-81. Epub 2001 Oct 16. [abstract]
  14. Prockop LD, Chichkova RI; Carbon monoxide intoxication: an updated review. J Neurol Sci. 2007 Nov 15;262(1-2):122-30. Epub 2007 Aug 27. [abstract]
  15. Piantadosi CA; Diagnosis and treatment of carbon monoxide poisoning. Respir Care Clin N Am. 1999 Jun;5(2):183-202. [abstract]
  16. Hsiao CL, Kuo HC, Huang CC; Delayed encephalopathy after carbon monoxide intoxication--long-term prognosis and correlation of clinical manifestations and neuroimages. Acta Neurol Taiwan. 2004 Jun;13(2):64-70. [abstract]
  17. Hampson NB, Rudd RA, Hauff NM; Increased long-term mortality among survivors of acute carbon monoxide poisoning. Crit Care Med. 2009 Jun;37(6):1941-7. [abstract]
  18. Amitai Y, Zlotogorski Z, Golan-Katzav V, et al; Neuropsychological impairment from acute low-level exposure to carbon monoxide. Arch Neurol. 1998 Jun;55(6):845-8. [abstract]
  19. Krenzelok EP, Roth R, Full R; Carbon monoxide ... the silent killer with an audible solution. Am J Emerg Med. 1996 Sep;14(5):484-6. [abstract]
  20. Schwartz L, Martinez L, Louie J, et al; An evaluation of a carbon monoxide poisoning education program. Health Promot Pract. 2010 May;11(3):320-4. Epub 2009 Jan 14. [abstract]
  21. Carbon monoxide, Health Protection Agency
  22. Gas Historical Network

Internet and further reading

Acknowledgements

EMIS is grateful to Dr Laurence Knott for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2010.
Document ID: 1904
Document Version: 21
Document Reference: bgp1387
Last Updated: 11 Aug 2010
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