The Dept of Anaesthesia & Intensive Care, CUHK thanks

for an unrestricted education grant
BASIC instructor/provider course, Hong Kong, July 2nd-4th
Other upcoming courses
Home Feedback Contents

Cyanide

Up Beta blocker Carbon monoxide Cyanide Dextropropoxyphene Digoxin Ethylene glycol Gamma hydroxybutyrate Isopropanolol Lithium Methaemoglobinaemia Methanol Paracetamol Paraquat Pesticides Recreational drugs Salicylate Theophylline Tricyclic anti-depressants


Charles Gomersall & Carolyne Chau

Mode of poisoning

  • inhalation of hydrogen cyanide gas
    • combustion product of cyanide containing products
      • plastics
      • glue removers
      • wool, silk, nylon
      • various seeds and plants
    • chemical weapon
  • sodium nitroprusside infusion
  • absorption of cyanide-containing solutions or gas through skin

Mechanism of toxicity

  • binds to cellular cytochrome oxidase and interferes with cellular respiration

Pharmacology

  • metabolized to less toxic metabolite thiocyanate (renally excreted)
  • small proportion chelated by hydroxycobalamin

Clinical features

  • onset of cell toxicity very rapid
  • early manifestations:
    • anxiety, confusion
    • dyspnoea
    • headache
    • tachycardia
    • hypertension
  • rapidly progresses to:
    • stupor, coma
    • fits
    • fixed, dilated pupils
    • hypoventilation
    • hypotension, cardiovascular collapse
    • bradycardia, heart block, ventricular arrhythmias
  • odour of bitter almonds. However ability to detect this is genetically determined and therefore sign is unreliable
  • venous blood looks the colour of arterial blood
  • hallmarks of severe cyanide toxicity are persistent hypotension and academia despite adequate arterial oxygenation

Investigations

  • severe lactic acidosis
  • high mixed venous saturation

Treatment

  • 100% O2 but mainstay of treatment is early use of antidotes
  • amyl nitrite
    • induces formation of methaemoglobin. Cyanide has high affinity for ferric iron in methaemoglobin and as a result methaemoglobin is an effective scavenger of unbound cyanide
    • administration by inhalation of crushable pearls: inhale for 15-30 sec with rest of 30 sec between inhalations. One pearl lasts ~2-3 mins. Aim for methaemoglobin of ~5%
  • sodium nitrite 300mg over 10 mins to provoke formation of methaemoglobinaemia (scavenger for hydrogen cyanide )
  • sodium thiosulphate 150 mg/kg IV followed by infusion of 30-60 mg/kg/h to convert cyanide to thiocyanate. Risk of thiocyanate toxicity, particularly in the presence of renal insufficiency. Thiocyanate readily dialyzable.
  • cobalt ethylenediaminetetraacetic acid 600 mg IV over 1 min, accompanied by glucose 50% 25 ml, followed by another 300 mg if there is no response. Chelates cyanide. 
  • hydroxycobalamin 4-5 g IV. Not approved for use in cyanide toxicity in USA
  • gastric lavage followed by activated charcoal
  • induced emesis not recommended
  • for cyanide poisoning due to smoke inhalation, most authorities recommend use of thiosulfate, oxygen, and supportive measures and recommend reserving nitrites for patients who are hypotensive, acidemic, or comatose
  • sodium bicarbonate for metabolic acidosis
  • attendant staff must not undertake expired air resuscitation

Further reading

Mokhlesi B. Adult toxicology in critical care. Part II: specific poisonings. Chest 2003; 123:897-922

 © Charles Gomersall & Carolyne Chau March 2005

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
Copyright policy    Contributors