TOXBASE Factsheet

Carbon Monoxide
Updated 1/2004*

Type of product:
A colourless, odourless gas.

Mechanism of toxicity:
Carbon monoxide combines with haemoglobin to reduce the oxygen carrying capacity of the blood. This causes the oxyhaemoglobin dissociation curve to be shifted to the left impairing oxygen delivery to tissues. Carbon monoxide may also inhibit cytochrome oxidase thereby preventing the cells from utilising the reduced amounts of oxygen they receive. Catalytic converters and the associated lower carbon monoxide emissions did not result in a reduction in numbers, rates or percentages of exhaust gas suicides in one study (Routley and Ozanne-Smith,1998). The short term exposure limit is 200 ppm (232 mg/m3).

Carbon monoxide - features and management

Updated 1/2004

Immediate Features:
Headache, nausea, irritability, weakness and tachypnoea followed by dizziness, ataxia, agitation, impairment of consciousness and respiratory failure. Cerebral oedema and metabolic acidosis may develop in serious cases. Less common features include skin blisters, rhabdomyolysis, acute renal failure, pulmonary oedema, myocardial infarction, retinal haemorrhages, cortical blindness, choreoathetosis, and mutism.

Late Features:
The majority of people exposed to carbon monoxide recover uneventfully but others develop neuropsychiatric features after periods of several weeks free of symptoms. These delayed
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features are more common in those over the age of 40 years and include memory impairment, disorientation, apathy, mutism, irritability, inability to concentrate, personality change, Parkinsonism and parietal lobe lesions. Urinary and/or faecal incontinence and gait disturbance are common. Fortunately, the great majority recover completely or to a considerable extent within a year.

Chronic poisoning:
Chronic carbon monoxide poisoning is frequently undiagnosed since the features are non specific. It is often associated with the use of faulty gas heaters in unventilated areas and therefore occurs more commonly in the winter months. Features include headache, nausea and flu-like symptoms. The diagnosis should be considered particularly if there are other members of the same house experiencing similar symptoms.

Indication of severity:
One or more of the following:
G G G G G G

Any new objective acute neurological signs e.g. increased tone, upgoing plantars Coma Need for ventilation ECG indication of infarction or ischaemia Clinically significant acidosis Initial carboxyhaemoglobin > 30%

But note that the link between carboxyhaemoglobin level and outcome is weak

Management:
1. Remove from exposure. 2. Maintain a clear airway and adequate ventilation. 3. Give oxygen in as high concentrations as possible. 4. Metabolic acidosis should be corrected by increasing oxygen delivery to the tissues. The use of intravenous sodium bicarbonate may make this more difficult and is therefore best avoided. 5. Give mannitol 1g/kg intravenously over 20 minutes if cerebral oedema is suspected.

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6. Monitor the heart rhythm. 7. Measure the carboxyhaemoglobin concentration as an emergency. A carboxyhaemoglobin percentage of 30% indicates severe exposure. However, concentrations less than this do not exclude significant poisoning and the relationship between carboxyhaemoglobin and severity of poisoning and/or clinical outcome is poor. 8. In patients who have been unconscious look for extrapyramidal features and retinal haemorrhages to assess the severity of CNS toxicity. 9. The role of hyperbaric oxygen therapy has been controversial. However, a recent large double blind trial has shown benefit in patients with loss of consciousness, CNS features of poisoning, cardiac ischaemia or metabolic acidosis (Weaver, 2002). These patients were treated with hyperbaric oxygen on 3 occasions in 24 hours, the first treatment being given on average within 5.8 hours of exposure. Patients were not entered beyond 24 hours of exposure. It is uncertain how quickly hyperbaric oxygen needs to be given in light of another study which shows lack of benefit when hyperbaric oxygen was started later than in this series (a mean of 7.3 hours after exposure). In the latter series patients received treatment daily for 3 days (Scheinkestel, 1999). Hyperbaric oxygen therapy should only be considered if there is easy and rapid access to a suitable hyperbaric chamber. The NPIS Directors do not support transfer over long distances for small clinical benefit. You should discuss the possibility of using hyperbaric oxygen with your local poisons service: in the UK NPIS 0870 600 6266, in Ireland NPIC (01) 809 2566, if your patient is severely poisoned (see above for indications).

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