Carbon Monoxide Poisoning
Carbon monoxide (CO) is a colourless, odourless, tasteless gas produced by incomplete combustion of organic material.
Exposure to carbon monoxide may occur:
- When fuel burning appliances are poorly installed, faulty, not maintained or used inappropriately, for example:
- Chimneys or flues are blocked
- There is a lack of ventilation in the room
- Gas ovens are used inappropriately for heating
- Barbeques are used inside homes, caravans or tents for cooking or heating
- Shisha pipes are used in poorly ventilated rooms
- When petrol or diesel engine exhaust gases are retained in an enclosed space
- From smoke in burning buildings
- From paint remover or aerosol propellants
Pathophysiology
Exposure to carbon monoxide causes tissue hypoxia because:
- Carbon monoxide has a much higher affinity for haemoglobin than oxygen (240 times greater). This displaces oxygen from the haemoglobin molecule which preferentially binds carbon monoxide forming carboxyhaemoglobin.
- The oxyhaemoglobin dissociation curve is shifted 'to the left' thus decreasing the amount of oxygen available to cells at a given oxygen pressure.
- Once formed, carboxyhaemoglobin takes several hours to dissociate, resulting in a prolonged reduction in the oxygen-carrying capacity of the blood.
- Within cells carbon monoxide binds to intracellular myoglobin and mitochondrial cytochrome enzymes resulting in a prolonged reduction in the capacity for cellular respiration.
The severity of carbon monoxide poisoning is largely related to the amount of carbon monoxide inhaled. As exposure to a constant concentration of carbon monoxide is maintained, the carboxyhaemoglobin level increases until an equilibrium is reached with the ambient air. This level is dependent on the duration of exposure, the concentration of carbon monoxide, and breathing volumes relating to respiratory rate and depth.
Risk factors
Those most at risk of harm from carbon monoxide poisoning include:
- Older people
- Children
- Pregnant women
- People with respiratory disease, cardiovascular disease or anaemia
Clinical features
Ask people with possible symptoms about:
- C: Cohabitees and co-occupants: Is anyone else in the house affected?
- O: Outdoors: Do symptoms improve when they are out of the building?
- M: Maintenance: Are their fuel burning appliances and vents properly maintained?
- A: Alarm: Do they have a carbon monoxide alarm?
Always consider carbon monoxide poisoning as a cause of symptoms, particularly if more than one member of a household (including pets) is affected and if symptoms improve on leaving the property.
- Exposure to low levels of carbon monoxide may cause:
- Nausea or vomiting
- Headache
- Blurred vision
- Dizziness
- Flushing
- Weakness
- Exposure to higher levels of carbon monoxide may cause:
- Cardiovascular features
- Tachycardia and hypotension
- Myocardial ischaemia or infarction
- Cardiac arrhythmias
- Pulmonary oedema
- Neurological features
- Confusion
- Personality change
- Dizziness and ataxia
- Impaired consciousness
- Seizures
- Focal neurological deficit
Investigations
Diagnosis is based on a clinical triad: history of CO exposure, elevated carboxyhaemoglobin levels, and symptoms consistent with CO poisoning. Measure exhaled carbon monoxide levels using a breath test if it is available — this must be done as soon as poisoning is suspected, as levels of carbon monoxide decline once the person is away from the source.
- Carboxyhaemoglobin (CO-Hb) level
- Normal levels are 1-3% and up to 10% in smokers
- Toxic effects may appear at levels of 15 - 20%
- A level of 30% indicates severe exposure
- Arterial blood gas
- Metabolic acidosis (tissue hypoxia)
- Raised lactate (tissue hypoxia)
- PaO2 should be normal
- Serum lactate
- May be raised in severe poisoning (could also indicate cyanide toxicity)
- ECG and cardiac monitoring
- May show tachycardia, cardiac ischaemia, arrhythmias or prolonged QT interval
- Troponin
- May be raised in cardiac ischaemia
- Creatine kinase
- May be raised in skeletal muscle damage
- Chest x-ray
- To screen for non-cardiogenic pulmonary oedema
- CT head
- May be indicated in patients presenting with acute neurological symptoms; may see focal lesions and/or cerebral oedema
Management
- The elimination half-life of carbon monoxide decreases as the inspired fraction of oxygen increases. The elimination half-life of carbon monoxide at sea-level is about 4 - 6 hours in room air, 76 minutes on 100% oxygen and 20 minutes on oxygen at 2.5 atmospheres pressure.
- Give 100% oxygen using a tight fitting reservoir mask with an inflated seal. Where available, consider the use of nasal high flow cannulae to deliver oxygen at up to 60 L/min. This should be continued until the person is asymptomatic and carboxyhaemoglobin levels are 3% or less in non-smokers, and 10% or less in smokers (usually about 6 hours). All patients who require assessment should be observed for at least 4 hours after exposure. Asymptomatic patients can then be considered for discharge with advice to return if symptoms develop.
- Evidence for the use of hyperbaric oxygen therapy in CO poisoning remains uncertain. NPIS does not currently recommend hyperbaric oxygen therapy.
- Those at highest risk for death are patients with severe metabolic acidosis (low pH on blood gas), those with very high CO-Hb levels (>25-30%), fire as a source of CO exposure, loss of consciousness or need for mechanical ventilation.
Complications
- The majority of people exposed to carbon monoxide recover, however some people develop neuropsychiatric features; this is more likely in people who have been seriously poisoned or who become unconscious during the poisoning episode.
- The onset of complications may be delayed, by up to 40 days, and is more common in people aged over 40 years.
- Features may include: apathy, apraxia, chorea, dementia and Parkinsonism, disorientation, emotional lability, neuropathy, inability to concentrate, incontinence, memory impairment, mutism, personality change, psychosis.