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Updated: Mar 28 2019

Cyanide Poisoning

  • Snapshot
    • A 45-year-old woman presents to the emergency room after ingesting an unknown substance in a suicide attempt. She is confused and reports having a headache, nausea, and vomiting. Beside her was a bottle of powder labeled “potassium sodium cyanide.” On physical exam, she is hypoxic and tachycardic. She has a unique almond-odor and her cheeks are flushed. She is given activated charcoal and a toxicology panel is sent to the laboratory. Oxygen supplementation does not improve her hypoxia and she is started empirically on nitrate and thiosulfate for cyanide poisoning, as this hospital does not carry hydroxocobalamin.
  • Introduction
    • Clinical definition
      • cyanide is a lethal poison that can act rapidly and fatally
    • Pathogenesis
      • mechanism of cyanide poisoning
        • cyanide binds ferric ion (Fe3+) in the mitochondrial cytochrome complex IV, which inhibits oxidative phosphorylation
        • this causes the cell to convert to anaerobic metabolism, causing accumulation of lactic acid and a metabolic acidosis
        • results in functional hypoxia, as cells, cannot use oxygen
    • Prognosis
      • can be rapidly fatal if untreated
  • Presentation
    • Symptoms
      • hypoxia not responsive to supplemental O2
      • central nervous system
        • headaches
        • confusion
        • vertigo
    • Physical exam
      • cardiovascular
        • initially tachycardic and hypertensive
        • then bradycardic and hypotensive
      • almond breath odor
      • pulmonary edema
      • flushing “cherry-red” skin
        • due to high venous oxyhemoglobin concentration
      • cyanosis
      • irritant dermatitis if skin is exposed to cyanide
      • nausea and vomiting if cyanide is ingested
  • Studies
    • Labs
      • ↑ lactic acid
      • arterial blood gas
        • metabolic acidosis with anion gap
      • carboxyhemoglobin and methemoglobin
        • if concern for concomitant carbon monoxide poisoning
      • cyanide concentration
        • results are typically not available in time
    • Making the diagnosis
      • most cases are clinically diagnosed
  • Differential
    • Carbon monoxide poisoning
      • distinguishing factor
        • often presents with cyanide poisoning
        • improvement with 100% oxygen
  • Complications
    • Parkinsonism
      • basal ganglia is susceptible to cyanide toxicity via hypoxic effects or direct cellular injury
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