Cyanide Poisoning

Potent rapid-onset toxin, especially with inhalation of HCN (volatile liquid).

May be absorbed through mucous membranes; CN ingestion results in slower onset.

Diffuses rapidly through body with high intracellular fixation to cytochrome aa ₃ in cellular mitochondria to paralyze aerobic metabolism.

Main target organs: CNS and heart.

Animal experiments: Apnea precedes cardiac collapse.

If CN toxicity resulted from fire or smoke exposure, consider also CO and other toxins.

One third of pts with CO toxicity exposed to domestic fires also have increased CN.

Be alert for CN poisoning in donors for organ transplantation.

Major route of CN detoxification: Conversion to thiocyanate, which requires sulfane sulfur donor (e.g., thiosulfate) and enzyme (e.g., rhodanese); without renal excretion, increase in thiocyanate can cause CNS abnormalities.

Minor route: Hydroxocobalamin (one form of vitamin B ₁₂ ) chelates CN to form cyanocobalamin.

metHb ferric ion has high affinity for CN.

Combustion product of natural and synthetic polymers

Industrial chemistry (e.g., metals and plastics preparation)

Plants: May contain cyanogenic glycosides

Na nitroprusside: Overtreatment (>0.5 mg/kg/h within 24 h)

Abuse (e.g., suicide, Chicago CN-laced-Tylenol murders [1982], terrorism, chemical warfare)