Cyanide poisoning

Cyanide may be used in insecticides, photograph development and the production of certain metals. Toxicity results from reversible inhibition of cellular oxidising enzymes (cytochrome system), affinity for Fe3+, reduced aerobic respirationHydrogen Cyanide (HCN) and carbon monoxide (CO) are the 2 major products of combustion in closed spaces.

Presentation

• 'classical' features: brick-red skin, smell of bitter almonds
• acute: hypoxia, hypotension, headache, confusion
• chronic: ataxia, peripheral neuropathy, dermatitis

Mild - Dizziness, anxiety, tachycardia, nausea, drowsiness/ confusion

Moderate - Vomiting, reduced consciousness, convulsions, cyanosis

Severe - Deep coma, fixed unreactive pupils, cardiorespiratory failure, arrththmias, pulm: oedema

Management

• supportive measures (mild): 100% oxygen, GI decontamination if early/ acute
• definitive (moderate/ severe): hydroxocobalamin (intravenously) 5g over 15min repeated once if required, also combination of amyl nitrite (inhaled), sodium nitrite (intravenously), and sodium thiosulfate (intravenously) or dicobalt edetate 300mg IV over 1min, then 50mL 50% glucose IV (repeat once if no response after a minute)

Basics:

• Cobalt ion in Hydroxycobalamin (B12) binds to intracellular cyanide ions => cyanocobalamin --> excretes in the urine
• Sodium Thiosulfate serves as sulfur donor to promote hepatic rhodanese-mediated conversion of cyanide to thiocynate => excretes in the urine
• Sodium Nitrite (an oxidant) pick up electrons from Ferrous (Fe2+) ion of Hb and convert it into Ferric (Fe3+), thereby purposely creating Methemoglobin which in turn can sequester cyanide as cyanomethemoglobin