Updated: 3/28/2019

Cyanide Poisoning

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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
  • Etiology
    • cyanide poisoning can occur from many exposures, including inhalation, ingestion, or direct contact
      • fires
        • especially with burning carpets and textiles
      • occupational
        • plastic and rubber industry, rodent pesticides, etc.
      • medical
        • sodium nitroprusside, which contains 5 cyanide groups per molecule
          • add sodium thiosulfate to nitroprusside solution to prevent cyanide poisoning
      • diet
        • stone fruits (apricots, plums, peaches, etc.) and apples contain cyanide compounds in their stones/seeds
      • ingestion of cyanide salts
        • suicidal or homicidal acts
  • 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
Treatment
  • Management approach
    • supplemental oxygen is not useful in this case
    • all contaminated clothes should be removed
    • all wounds from cyanide exposure should be cleaned
  • Medical
    • hydroxocobalamin
      • first-line
        • mechanism
          • hydroxocobalamin combines with cyanide to form cyanocobalamin, which is renally excreted
    • sodium thiosulfate
      • first-line
        • mechanism
          • thiosulfates convert cyanide to thiocyanide, which can be renally excreted
    • nitrates
      • second-line
        • mechanism
          • nitrates convert hemoglobin to methemoglobin, which will bind to cyanide
        • contraindicated
          • concomitant carbon monoxide toxicity
    • activated charcoal
      • indication
        • if cyanide is ingested
Complications
  • Parkinsonism
    • basal ganglia is susceptible to cyanide toxicity via hypoxic effects or direct cellular injury
 

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