Carbon Monoxide Poisoning

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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.

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.

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. The value of hyperbaric oxygen is, however, unclear.

Carbon monoxide poisoning kills 50 people and seriously injures nearly 200 in the UK each year, but the overwhelming majority of cases go unrecognised, unreported, and untreated. A study in the USA in 2007 found an emergency department attendance rate of 50,000 annually, a significant increase on previous estimates.[1]

Risk factors[2]

  • Inadequately serviced fires - there is an increased risk in winter and a greater risk in the households which use solid fuel. 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.

Low-level poisoning[3]

Early features
The physical symptoms of carbon monoxide poisoning are subtle and low-level exposure may produce no abnormal physical signs.[4]

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.[3]

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.

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.[5]

Chronic poisoning[6]
This is often unsuspected and unrecognised and features may appear nonspecific - eg, headache, nausea and flu-like symptoms. They are most common in winter, as that is when fires are used and ventilation is restricted.

Carbon monoxide poisoning 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. Symptoms may include:

  • Headache.
  • Nausea and vomiting.
  • Vertigo.
  • Alteration in consciousness.
  • A subjective feeling of weakness.

High-level poisoning[3]

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

  • Personality change.
  • Poor performance on the mini mental state examination.
  • Tachycardia and tachypnoea.
  • Dizziness and 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 kidney injury, 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 at post-mortem.
  • Referral 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 U&Es 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, obtain a CXR, 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.

Because of the nonspecific features of carbon monoxide poisoning, there is often a wide range of differential diagnoses to consider. For example:

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 Public Health England.
  • 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 Public Health England.

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.[7]
  • The evidence concerning the use of hyperbaric oxygen is controversial.[7]
  • Metabolic acidosis should be corrected by increasing oxygen delivery to the tissues. Sodium bicarbonate is contra-indicated.
  • Give mannitol 1 g/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 CNS 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 following few weeks and if the patient is a smoker, he/she should stop smoking.
  • Blood gases must be monitored with use of oxygen in chronic obstructive pulmonary disease.
  • Prognosis may be unpredictable.
  • Many cases recover spontaneously but there are no currently effective treatments for long-term sequelae.
  • Most people with mild, accidental poisoning are able to return to their former job within a month.[8]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.
  • In patients with encephalopathy which eventually improves, MRI scan abnormalities can be seen to resolve in correlation with clinical features.[9]
  • 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.[10]

Even very low levels of carbon monoxide can produce a significant reduction in cognitive functioning. 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. 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.[11]

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.[12]

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Further reading and references

  1. Hampson NB, Weaver LK; Carbon monoxide poisoning: a new incidence for an old disease. Undersea Hyperb Med. 2007 May-Jun34(3):163-8.

  2. Whincup P, Papacosta O, Lennon L, et al; Carboxyhaemoglobin levels and their determinants in older British men. BMC Public Health. 2006 Jul 186:189.

  3. Carbon monoxide poisoning; NICE CKS, April 2009

  4. Quinn DK, McGahee SM, Politte LC, et al; Complications of carbon monoxide poisoning: a case discussion and review of the literature. Prim Care Companion J Clin Psychiatry. 200911(2):74-9.

  5. Song IU, Chung SW; Chorea as the first neurological symptom of delayed encephalopathy after carbon Intern Med. 201049(11):1037-9. Epub 2010 Jun 1.

  6. Sharma S, Gupta R, Paul BS, et al; Accidental carbon monoxide poisoning in our homes. Indian J Crit Care Med. 2009 Jul-Sep13(3):169-70.

  7. Guzman JA; Carbon monoxide poisoning. Crit Care Clin. 2012 Oct28(4):537-48. doi: 10.1016/j.ccc.2012.07.007.

  8. Prockop LD, Chichkova RI; Carbon monoxide intoxication: an updated review. J Neurol Sci. 2007 Nov 15262(1-2):122-30. Epub 2007 Aug 27.

  9. 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 Jun13(2):64-70.

  10. Hampson NB, Rudd RA, Hauff NM; Increased long-term mortality among survivors of acute carbon monoxide poisoning. Crit Care Med. 2009 Jun37(6):1941-7.

  11. Schwartz L, Martinez L, Louie J, et al; An evaluation of a carbon monoxide poisoning education program. Health Promot Pract. 2010 May11(3):320-4. Epub 2009 Jan 14.

  12. Carbon monoxide; Public Health England