Carbon monoxide (CO) is a colourless, odourless, tasteless, non-irritating gas that is produced by incomplete combustion of organic material due to insufficient oxygen. Important causes of carbon monoxide poisoning include inhalation of:

1. Smoke in burning buildings
2. Petrol or diesel engine exhaust gases retained in closed spaces
3. Burnt gases from faulty gas or solid fuel appliances used for domestic heating or cooking
4. Burnt gases from gas or solid fuel appliances intended for outdoor use only such as charcoal BBQ or camping stoves

Carbon monoxide has a much higher affinity for haemoglobin than oxygen (220 times greater). The oxyhaemoglobin dissociation curve is shifted ‘to the left’ thus decreasing the amount of oxygen available to cells at a given oxygen pressure.

CO poisoning causes platelet and neutrophil activation, free radical formation and lipid peroxidation in brain and other tissues through an immunological mechanism.

CO binds to fetal haemoglobin and shifts the already left-shifted fetal oxyhaemoglobin dissociation curve further to the left. The half-life of CO in the fetus is longer than that in the mother and is of particular concern when considering treatment options.

Cigarette smoking leads to COHb concentrations of up to about 12% in heavy smokers.

Administration of oxygen speeds the elimination of CO from the body. Without therapy, the elimination half-life of CO is 4-6 hours. Administration of high flow oxygen by a tightfitting mask at normal atmospheric pressure reduces half-life to approximately 76 mins. In hyperbaric oxygen chamber at 2.5 atmosphere absolute pressure, the elimination half-life is further decreased to 20 mins.

Clinical features:

• With lower-level or chronic CO poisoning, the person has: – headache (often tension-type) (90%), nausea & vomiting (50%), vertigo (50%), Alteration of consciousness (30%).
• With higher-level CO poisoning, the above symptoms are more severe and are associated with the following symptoms and signs: –
  • The appearance of intoxication or a personality change
  • Impaired mini mental-state examination
  • Vertigo and ataxia
  • Breathlessness and tachycardia
  • Chest pain (due to angina or myocardial infarction)
  • Loss of consciousness (with very high levels of carbon monoxide, this may be followed by death within a few minutes)
  • Seizure or multiple seizures
  • Abnormal neurological signs including blindness, deafness, and extrapyramidal effects. The onset of neurological deterioration may be delayed by several days. Memory impairment and changes in personality may persist long term
  • High risk features include chest pain, history of unconsciousness, any continuing neurological symptoms or signs (especially cerebellar features) and pregnancy due to the effects on the foetus
• The classic description of cherry pink or red complexion is very rare and associated with the most severe and fatal cases.
• Use the COMA questions to raise or lower your suspicion of carbon monoxide poisoning: –
  • C – Cohabitees/companions Is anyone else in the property affected (including pets)
  • O – Outdoors Do the symptoms improve when out of the building?
  • M – Maintenance Are any fuel-burning appliances and vents properly maintained?
  • A – Alarm Does the affected building have a carbon monoxide alarm?
• Arranging immediate hospital assessment for all pregnant women.
• Indications of severity – include one or more of the following:
  1. Any new objective acute neurological signs e.g., increased tone, upgoing planters, coma
  2. Need for ventilation
  3. ECG indication of infarction or ischaemia
  4. Clinically significant acidosis
  5. Initial carboxyhaemoglobin greater than 30%

Diagnosis & investigations: –

Diagnosis is based on a clinical triad: history of CO exposure, elevated carboxyhaemoglobin levels, and symptoms consistent with CO poisoning.

1. Measure COHb – arterial or venous – Toxic effects may appear at levels of 15 – 20%. A level of 30% indicates severe exposure
2. Lactate (a high lactate (> 10 mmol/L) ‎may suggest concurrent cyanide exposure)‎
3. Blood glucose to exclude hypoglycaemia
4. ‎12 lead ECG‎
5. Arterial blood gas will show
   • Metabolic acidosis (tissue hypoxia)‎
   • Raised lactate (tissue hypoxia)‎
   • PaO2 should be normal.

Management in the Emergency department: –

Severe cases of CO poisoning should be managed as follows in the ED:

1. Maintain clear airway and ensure adequate ventilation
2. Administer 100% oxygen ASAP, until the person is asymptomatic and CO levels are ≤ 3% in non-smokers, and ≤ 10% in smokers (usually about 6 hours).
3. ‎treat any ECG changes for example, QRS prolongation (treat with sodium ‎bicarbonate) & QT prolongation (treat with magnesium sulphate)‎
4. Hypotension – correct by raising the foot of the bed and by adequate ‎fluid resuscitation with crystalloid
5. Metabolic acidosis – if severe metabolic acidosis persists despite ‎correction of hypoxia and adequate fluid resuscitation, consider ‎correction with IV sodium bicarbonate.
6. Cyanide poisoning testing: – Indirect test: Lactic acidosis with arterialisation of venous blood (due to cessation of intracellular respiration and oxygen extraction). (See treatment in the next chapter)
7. Indications for hyperbaric oxygen therapy (HBOT) – A CO-Hb concentration of > 20% should be an indication to consider hyperbaric oxygen although the decision should be taken with other indicators listed below:
   • Loss of consciousness at any stage
   • Neurological signs other than headache
   • Myocardial ischaemia/arrhythmia diagnosed by ECG
   • The patient is pregnant (The foetal Hb has a greater affinity for CO than maternal Hb)