Carbon Monoxide Poisoning

Last Updated on by FRCEM Intermediate

Overview

  • Carbon monoxide (CO) is a colorless, odorless gas produced by incomplete combustion of carbonaceous material
  • A high index of suspicion is required accidental exposures from incomplete combustion in charcoal burners, faulty heaters, house fires, and industrial accidents

Pathophysiology

  • Carbon monoxide has a higher affinity for hemoglobin than oxygen. Shifting the oxygen-hemoglobin curve to the left.

Investigation

  • ABG
    • Carboxyhemoglobin HbCO (elevated levels are significant, but low levels do not rule out exposure)
    • lactate (tissue hypoxia -also in the context of combustion, high lactate (>10 mmol/L) may suggest concurrent cyanide exposure )
    • MetHb (exclude)
  • ECG: sinus tachycardia, ischemia
  • Pulse oximetry measurements unreliable in the context of CO poisoning
  • urinalysis (bHCG for pregnancy)

Severity based on Carboxyhemoglobin level

Non- smokers <3%
Heavy smokers <12%
Severe symptoms 10-30%
Coma 50-70%

Elevated levels are significant, but low levels do not rule out exposure

Tobacco smokers have higher baseline concentrations of COHb (3 to 10%) and therefore will reach toxic concentrations earlier in any exposure

Clinical Features

Mild toxicity: Nausea, headache, poor memory
Moderate toxicity: Hypotension, tachycardia, ataxia, confusion
Severe toxicity: Metabolic acidosis, coma, and death

Other Signs
Non-cardiogenic pulmonary edema
Lactic acidosis
Rhabdomyolysis
Hyperglycaemia
Disseminated intravascular coagulation
Bullae
Alopecia
Sweat gland necrosis

Indications of severity include one or more of the following:

  • Any new objective acute neurological signs e.g increased tone, upgoing plantars, coma
  • Need for ventilation
  • ECG indication of infarction or ischemia
  • Clinically significant acidosis
  • Initial carboxyhemoglobin greater than 30%

Management

  • High flow O2 via non-rebreather mask until asymptomatic
    • The biological half-life of CO in a sedentary healthy adult is 4–5 hours
    • This half-life decreases with oxygen administration
      • ~ 40–80 minutes with the administration of 100% oxygen
      • ~ 20 minutes with hyperbaric oxygen (2 atmospheres)
  • Early intubation in the comatose patient / inhalational injury from smoke
  • Treat coexistent cyanide toxicity if suspected (e.g. house fire) (Elevated anion gap acidosis, Lactate more than 7 mmol/L) Give antidote if suspected toxicity: Sodium thiosulphate/Hydroxocobalamin as Cyanokit/Dicobalt edetate/Sodium nitrate + sodium thiosulphate
  • consider for hyperbaric oxygen in
    • All pregnant patients
    • Significant LOC
    • Signs of ischemia
    • Significant neurological deficit
    • Metabolic acidosis

 

Pregnancy

  • 24 hours of high flow if pregnant
  • Consider hyperbaric oxygen
  • Consider Foetal monitoring in the form of a CTG +/- an obstetric consultation.

Significant CO poisoning in the mother often results in foetal death or neurological damage
The foetus is thought to be especially susceptible to CO poisoning due to:

  • low oxygen pressures
  • the high affinity of foetal hemoglobin for CO
  • much longer half-life of CO in the foetal circulation

There may be an added benefit from HBO in this setting

  • HBO shortens the half-life of CO
  • allows delivery of oxygen to the tissues independent of hemoglobin
  • HBO appears to be safe in pregnancy

 

Reading:

Carbon Monoxide Poisoning

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