Updated: 3/27/2019

Cyanide Poisoning

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Snapshot
  • A 60-year-old man presents to the emergency room after being caught in a fire. He woke up in the middle of the night to sirens blaring and discovered smoke from the neighboring apartment. He, along with other residents, was brought to the hospital for further evaluation. He reports having some dizziness and headaches. On exam, his lungs are clear to auscultation and there is no erythema in his throat. His cheeks are cherry-red in color and his lips are cyanotic. His oxygen level is 85% and does not improve with oxygen supplementation. He is started on hydroxocobalamin and thiosulfate for cyanide poisoning. He is also continued on 100% oxygen for carbon monoxide poisoning as well.
Introduction
  • Clinical definition
    • cyanide is a lethal poison that can act rapidly and fatally
  • Epidemiology
    • incidence
      • rare
  • 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
  • Diagnostic testing
    • ↑ 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
  • Salicylate poisoning
    • distinguishing factor
      • causes early respiratory alkalosis and transitions to mixed metabolic acidosis and respiratory alkalosis
      • may cause tinnitus
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
    • antidotes bind to cyanide, induce methemoglobinemia (which provides an alternative binding site for cyanide), or act as sulfur donors (which detoxifies cyanide and transforms it to thiocyanate)
  • First-line
    • hydroxocobalamin, a precursor to vitamin B12
      • combines with cyanide to form cyanocobalamin, which is renally excreted
    • thiosulfate
      • thiosulfates convert cyanide to thiocyanide, which can be renally excreted
  • Second-line
    • nitrates
      • nitrates convert hemoglobin to methemoglobin, which will bind to cyanide
      • contraindicated in those with concomitant carbon monoxide toxicity
  • Other treatments
    • 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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