SN7 SHORT NOTE 5M

Describe cyanide poisoning with its mechanism and treatment.

Forensic Medicine · 2nd Professional — Para-Clinical

Sources and Mechanism

Cyanide is the most rapidly acting of all common poisons. It acts by binding the ferric iron of cytochrome C oxidase, arresting the terminal step of the mitochondrial electron transport chain, so that the cell cannot use oxygen although it is fully supplied with it — the definition of histotoxic anoxia.

Sources — potassium and sodium cyanide in electroplating, gold and silver refining, and jewellery workshops, which is the usual Indian occupational and suicidal source; hydrocyanic (prussic) acid; fumigants and pesticides; combustion of polyurethane, wool, silk and plastics in fires, so that fire victims are poisoned by cyanide and carbon monoxide together; and plant sources — the kernels of bitter almond, apricot, peach and cherry, and cassava, all of which contain cyanogenic glycosides such as amygdalin
Fatal dose — about 200 to 300 mg of potassium cyanide; fatal period may be within 2 to 10 minutes for a large dose, which is why it has been used for assassination and for suicide by those wanting certainty

Feature	Description
Onset	Almost immediate with a large dose — a cry, loss of consciousness, convulsions and death in minutes; slower with smaller doses or with the ingestion of plant material, where hours may elapse
Early symptoms	A bitter acrid taste, constriction of the throat, giddiness, headache, anxiety and breathlessness
Respiration	Rapid and deep initially (from carotid body stimulation), then slow and gasping. Severe dyspnoea without cyanosis is the characteristic paradox
The paradoxical sign	The skin is pink or normal and the venous blood is bright red, because the tissues never extract the oxygen — so the venous blood looks arterial. Arterialisation of the retinal veins may be seen on fundoscopy
Metabolic	Profound high anion gap metabolic acidosis with a very high lactate, and a reduced arteriovenous oxygen difference — the most useful rapid investigations
Odour	Bitter almonds on the breath and at autopsy — but a large minority of people are genetically unable TO smell it, so its absence excludes nothing
Postmortem	Bright red or pink lividity; the bitter almond odour on opening the body and the stomach; congestion of all organs; and corrosion of the gastric mucosa where a salt was swallowed, since the salts are alkaline. Blood is preserved with NO preservative in an airtight container

CLINICAL PEARL

Cyanide is the poison in which the patient is profoundly hypoxic and pink. The tissues cannot use oxygen, so it stays in the blood — the venous blood returns bright red, the skin does not turn blue, and the retinal veins look arterial. Severe dyspnoea without cyanosis, with a huge lactate, in someone from an electroplating or jewellery workshop, is the presentation, and treatment cannot wait for confirmation.

Treatment

Speed is everything; the antidote must be given on clinical suspicion, since laboratory confirmation takes far longer than the patient has
Remove from exposure and give 100% oxygen, which is beneficial despite the mechanism being histotoxic, and decontaminate the skin and clothing
Hydroxocobalamin is the antidote of choice where available — it binds cyanide to form cyanocobalamin, which is excreted; it is safe, and can be given to a fire victim in whom carbon monoxide poisoning also exists, where nitrites would be dangerous. It turns the skin and urine red
The classical cyanide antidote kit — AMYL nitrite by inhalation, then sodium nitrite intravenously, which deliberately induce methaemoglobinaemia: methaemoglobin binds cyanide preferentially, drawing it off the cytochrome oxidase to form cyanmethaemoglobin. This is then followed by sodium thiosulphate, which supplies sulphur to the enzyme rhodanese, converting cyanide to thiocyanate, which is excreted renally
The danger of the nitrites — they reduce oxygen-carrying capacity, and are therefore hazardous in a fire victim who also has carboxyhaemoglobin and in children. Sodium thiosulphate alone is safe in that situation
Supportive care — ventilation, correction of the acidosis with bicarbonate, and treatment of convulsions

Medicolegal Aspects and Applied Aspects

Manner — suicidal, particularly among those with occupational access (electroplaters, jewellers, laboratory and photographic workers); accidental in industry and in fires; and homicidal, historically, and used for judicial execution in the gas chamber and for suicide in wartime
Treat on suspicion, not on confirmation; a patient with severe metabolic acidosis, a very high lactate and no cyanosis from a plating workshop should receive the antidote immediately
Use hydroxocobalamin in fire victims and avoid nitrites; smoke inhalation produces both cyanide and carbon monoxide, and inducing methaemoglobinaemia in that setting can be fatal
Do not exclude cyanide because nobody can smell it; the ability is genetically determined and absent in a large minority of examiners
Protect yourself and the staff; vomit and gastric contents release hydrogen cyanide, and rescuers and mortuary staff have been poisoned. Ventilate, and avoid mouth-to-mouth resuscitation
Send blood with NO preservative in a full airtight container, refrigerated, and analyse promptly; cyanide is volatile and the concentration falls with storage
Consider cassava and apricot kernels in an unexplained case; cyanogenic glycosides act more slowly and the source may not be recognised as a poison at all

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