Cyanide Poisoning

Background

• MOA: inhibition of cytochrome oxidase a3 in the mitochondria, leading to disruption of the electron transport chain and aerobic metabolism
• Via ingestion or inhalation, absorbed readily and quick onset of action
  • inhalation exposure is common in house fires - burning vinyl produces aerosilized cyanide
  • common co-exposure with CO
  • prolonger nitroprusside infusions
• clinical signs of hypoxia despite normal oxyhemoglobin concentration and pulmonary oxygen diffusion:
  • headache/anxiety
  • nausea/vomiting
  • metallic/bitter almond taste and odor
  • coma/seizures
  • liver/kidney failure
  • ischemic pain
  • rhabdomyolysis
  • death
• a normal lactate essentially rules out this diagnosis!

Management

• early recognition of cyanide toxicity
• elimination of ongoing exposure (contaminated clothing, etc) --> probably should call Ontario Poison Control as well, and gather effective collateral if possible
• neutralization or competitive binding of cyanide to target mitochondrial dysfunction:
  • hydroxycobalamin avidly binds cyanide to produce cyanocobalamin (soluble, nontoxic, and excreted easily). Dose is 5 grams for adults. This is the preferred treatment.
  • induction of methemoglobinemia with nitrites (avoid in coHb toxicity)
  • sodium thiosulfate which donates sulfur to cyanide to produce thiocyanate (harmless)

References

1. MKSAP - Pulm/Crit Care