Cyanide toxicity

☠️ Key Point: Cyanide poisoning is rapidly lethal — most deaths occur before hospital arrival. Survival to admission usually carries a good prognosis with prompt recognition and antidote therapy. Hydrogen cyanide is colourless with a faint bitter-almond odour (not detectable to all individuals).

🧪 About

• Highly toxic: Cyanide blocks cellular respiration within seconds to minutes, causing histotoxic hypoxia despite adequate oxygenation.
• Common sources: Smoke inhalation in house fires (especially from burning plastics, foam, wool, silk, polyurethane).
• Medicinal exposure: Prolonged or high-dose sodium nitroprusside infusion can liberate cyanide ions.
• Industrial sources: Electroplating, metal refining, jewellery manufacture, photographic and mining industries.
• Historical note: Used in execution gas chambers and as a wartime chemical weapon, illustrating its extreme lethality.

⚛️ Chemistry & Mechanism

• Form: Exists as gas (hydrogen cyanide, HCN) or salt (potassium or sodium cyanide).
• Mechanism: Cyanide binds ferric (Fe³⁺) ion of cytochrome oxidase (a₃) in mitochondria → inhibition of oxidative phosphorylation → cellular asphyxia.
• Cells switch to anaerobic metabolism → massive lactate accumulation → severe metabolic acidosis.
• Tissues remain oxygen-saturated → characteristic “cherry-red” skin and blood due to failure of oxygen extraction.

📊 Epidemiology

• Accidental: Chemical or laboratory exposure, household fires.
• Intentional: Suicide or homicide (ingestion of cyanide salts, contaminated pills, or inhalation).
• Drug-related: Prolonged IV nitroprusside infusion, amygdalin (“laetrile”) ingestion.

🩺 Clinical Features

• Early / mild: Anxiety, confusion, dizziness, tachycardia, flushing, headache, nausea, vomiting, throat or eye irritation.
• Progressive: Dyspnoea, hypotension, bradycardia, seizures, metabolic acidosis, arrhythmias, pulmonary oedema.
• Severe: Rapid collapse, deep coma, fixed dilated pupils, respiratory failure, and cardiac arrest.
• Key clues: Cherry-red skin, bitter-almond odour, soot around mouth/nose (in fire victims), elevated lactate.

🧪 Investigations

• ABG: Profound metabolic acidosis with raised anion gap.
• Lactate: Markedly raised (>8–10 mmol/L strongly suggests cyanide).
• Serum cyanide: Diagnostic but rarely available acutely — do not delay treatment.
• Co-oximetry: May show high venous O₂ saturation (“arterialised venous blood”).
• ECG: Monitor for arrhythmias secondary to hypoxia.

🧭 Management Overview

⚠️ Immediate actions: Resuscitate first — give 100% oxygen, remove exposure source, secure airway, and treat empirically if suspected (do not wait for lab confirmation).

🧍‍♂️ Additional Management Notes

• Decontamination: Remove contaminated clothing; irrigate exposed skin with copious water.
• Airway protection: Early intubation if GCS < 8.
• Monitoring: Continuous ECG, pulse oximetry, and frequent ABG/lactate reassessment.
• Fire victims: Often have combined carbon monoxide + cyanide toxicity → both require high-flow oxygen ± hydroxocobalamin.
• Consult the National Poisons Information Service (NPIS / Toxbase) urgently for dosing advice.

📈 Prognosis

• Rapid recognition and antidote administration are life-saving; recovery can be complete if treated before cardiovascular collapse.
• Neurological sequelae (ataxia, cognitive impairment, Parkinsonism) may occur after delayed or partial recovery.

📚 References

• ToxBase: Cyanide – Management
• CDC Emergency Response: Cyanide Facts
• StatPearls: Cyanide Toxicity
• Vetter J. Toxicology of cyanides. Food Chem Toxicol 2015;80:140-150.

Summary: Cyanide blocks oxidative phosphorylation, causing sudden cellular hypoxia and lactic acidosis. Hydroxycobalamin is the current antidote of choice in the UK. In any smoke-inhalation victim with unexplained acidosis or rapid collapse, suspect cyanide and treat empirically — time is life.