Management of cyanide poisoning from smoke inhalation

This is combined cyanide and carbon monoxide poisoning with an inhalation airway injury. The lactate of 14 mmol per litre is the bedside surrogate for cyanide and is the trigger for empirical antidote; the carboxyhaemoglobin of 22 per cent confirms the partner toxin. Do not wait for a blood cyanide level — it is rarely available in time to guide the first dose.^[1]

Resuscitate in parallel. Airway — the hoarseness, the soot in the mouth and the singed nasal hair are inhalation-injury signs and the respiratory rate of 8 with a GCS of 6 mandates rapid sequence intubation now, before oedema closes the airway. Breathing — 100 per cent oxygen via the ventilator from the moment of intubation; this treats both toxins, because it is synergistic with the cyanide antidote and shortens the carbon monoxide half-life from about five hours on room air to about one hour.^[4] Circulation — cardiac monitoring, two large-bore cannulae, a balanced crystalloid bolus for the hypotension, and an early vasopressor (noradrenaline) if shock persists, recognising that the myocardium is failing.^[3]

The antidote is hydroxocobalamin 5 g intravenously (70 mg per kilogram) over 15 minutes. It binds cyanide directly and stoichiometrically to form cyanocobalamin (vitamin B12), which is excreted in the urine; the reaction is immediate and enzyme-independent.^[2] Sodium thiosulfate 12.5 g intravenously (50 mL of the 25 per cent solution — the adult dose in the NITHIODOTE label) is given in combination for the severe poisoning — it provides the rate-limiting sulfur donor for the rhodanese pathway that converts cyanide to thiocyanate.^[3]

Justification of the antidote choice. Hydroxocobalamin is preferred over the alternatives because it causes neither hypotension nor methaemoglobinaemia. The sodium and amyl nitrite kit works by inducing methaemoglobinaemia to "pull" cyanide off cytochrome oxidase; methaemoglobin cannot carry oxygen, and the label warns that sodium nitrite should be used with caution in smoke inhalation or carbon monoxide poisoning because of the potential for worsening hypoxia — so the nitrite kit is avoided in smoke inhalation. Dicobalt edetate chelates cyanide directly, but its use in the absence of cyanide leads to serious cobalt toxicity — the IPCS antidote monograph records anaphylactic shock, hypotension and ventricular arrhythmias among its serious effects — so it is reserved for the confirmed pure-cyanide case and has no place when the diagnosis is presumptive.^[3]

After the antidote, continue 100 per cent oxygen, reassess the lactate and the gas, treat the carbon monoxide (discuss with the on-call hyperbaric unit given the loss of consciousness and the neurological involvement), and admit to intensive care. Liaise with the burns centre for the inhalation injury. Warn staff that hydroxocobalamin turns the skin and urine red for several days — an expected and harmless effect to be distinguished from haematuria and rhabdomyolysis.^[2]