Carbon Monoxide and Smoke Inhalation

Cause
This is seen most commonly in the non-diving population but can also occur in diving due to breathing gas contamination. It is a common mode of attempted suicide and accidental cases occur due to faulty or incorrectly ventilated gas appliances in the home. Vehicle exhaust fumes are a frequent source of both accidental and non-accidental poisoning.

Prevention (for divers)

• Always ensure that the air intakes of air compressors are upwind of and well away from any exhaust fumes. Also ensure that the compressor is well maintained as combustion of lubricant within the compressors cylinders, even those of an electric compressor, may contaminate the compressed air
• If possible, avoid air intakes drawing air from inside compartments; intakes should be sited outside in the open
• Breathing gas must be obtained from authorised, reputable source

Symptoms and Signs
Clinical features depend on duration and severity of exposure. Headache, nausea, dizziness and non-specific malaise are early symptoms; nausea and vomiting is commonly misdiagnosed as gastroenteritis, especially if several members of a family are affected. With increasing severity of intoxication motor disturbances such as weakness and ataxia appear; sensory features such as tinnitus and deafness appear to be centrally mediated. Progressive stupor and unconsciousness occur with severe poisoning and are commonly complicated by vomiting and aspiration of stomach contents. Evidence of cardiac ischaemia such as chest tightness/pain, ECG abnormalities and dysrhythmias are most often seen in patients with pre-existing coronary disease. Significant myocardial dysfunction may occur without specific ECG evidence of ischaemia.

Note

In divers, the symptoms of carbon monoxide poisoning may be masked at depth by the raised partial pressure of oxygen (PO2). Therefore, although the rate at which carbon monoxide is absorbed increases with depth, the symptoms are likely to become more severe during the ascent phase of a dive as the PO2 decreases.

Management
The diagnosis is established by measuring blood carboxyhaemoglobin (COHb) level. The upper limit of normal is approximately 5% in non-smokers and 10% in smokers. Carboxyhaemoglobin levels do NOT correlate with severity of poisoning and should not be used to decide whether hyperbaric oxygen therapy is indicated.

See the treatment summary initial management algorithm for the A & E management of acute carbon monoxide poisoning.

Indications for emergency HBO treatment following carbon monoxide exposure are:

1. Neurological deficit (hearing and gait assessment is important)
2. Cognitive impairment (especially arithmetic skills, memory), personality change
3. Clinical evidence of myocardial involvement (chest pain, ECG abnormalities, elevated cardiac enzymes)
4. Pregnancy (the foetus is especially vulnerable to the effects of CO poisoning)
5. History of sustained loss of consciousness (i.e. unconscious on arrival at hospital)
6. Inability to assess adequately (e.g. concurrent drug overdose)

Royal Navy Therapeutic Table 60 is used for initial treatment, with Royal Navy Therapeutic Table 66 used for re-treatments. It is likely that severely poisoned patients (i.e. those that are transferred unconscious and intubated) benefit from at least one re-treatment (see ITU management algorithm). Further HBO treatments in this group and in less severely affected patients (see non-ITU management algorithm) should be guided by clinical evidence of persisting neurological abnormality.

Adequate resuscitation prior to commencement of HBO treatment is important. The possibility of concomitant self-poisoning with drugs such as salicylates, paracetamol, tricyclic antidepressants and ethylene glycol should be considered. Rhabdomyolysis from sustained immobility on a hard surface is not uncommon and may precipitate acute renal failure.

The role of HBO therapy in the management of patients with no persisting neurological abnormalities is unclear. A minority of those with a history of loss of consciousness develop a delayed neurological syndrome with prominent behavioural or frankly neuropsychiatric features that may appear up to three weeks following exposure. The risk increases with advancing age and duration of coma. The syndrome may respond to HBO treatment even after a delay of several weeks.

Note
In cases of suspected carbon monoxide poisoning in divers the source of breathing gas should be isolated, and samples sent for analysis as soon as possible.

Useful References

1. Broome JR, Skrine H, Pearson RR. Carbon monoxide poisoning: forgotten not gone! British Journal of Hospital Medicine 1988; 39(4): 298-300, 302, 304-5.
2. Ducassé JL, Celsis P, Marc-Vergnes JP. Non-comatose patients with acute carbon monoxide poisoning: hyperbaric or normobaric oxygenation? Undersea Hyperbar Med 1995; 22(1): 9-15.
3. Gorman DF, Clayton D, Gilligan JE, Webb RK. A longitudinal study of 100 consecutive admissions for carbon monoxide poisoning to the Royal Adelaide Hospital. Anaesth Intens Care 1992; 20(3): 311-316.
4. Mathieu D, Nolf M, Durocher A, Saulnier F, Frimat P, Furon D, et al. Acute carbon monoxide poisoning. Risk of late sequelae and treatment by hyperbaric oxygen. Journal of Toxicology - Clinical Toxicology 1985; 23(4-6): 315-324.
5. Norkool DM, Kirkpatrick JN. Treatment of acute carbon monoxide poisoning with hyperbaric oxygen: a review of 115 cases. Ann Emerg Med 1985; 14(12): 1168-1171.

The Undersea Medicine Division works to a protocol developed specifically for the United Kingdom in terms of the types of carbon monoxide poisonings most commonly seen and the health economics involved in a country where hyperbaric therapy is only available at a limited number of centres. The algorithms used are based on evidence from the available scientific literature. They are in the process of being ratified by the British Hyperbaric Association.

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