![]() ![]() in patients without severe burns, this corresponds to a cyanide level of > 40 micromol/L.smell of bitter almonds may be present (not everyone can detect or recognise this smell!)Ĭonsider cyanide toxicity as the diagnosis in patients who collapse with a raised lactate level.may appear ‘pink’ due to high SvO2 following oxygen administration.hypotension, bradycardia, reduced GCS and respiratory depression, cardiovascular collapse.Progressive features will result from end-organ damage secondary to anaerobic respiration and histotoxic hypoxia.nausea, vomiting, headache, dyspnoea, increased respiratory rate, hypertension, tachycardia, altered level of consciousness and seizures.Milder exposures result in non-specific features including: onset of symptoms over ~30 minutes with ingestion (depending on the dose). ![]() rapid loss of consciousness and seizures with inhalation.The elimination half-life of cyanide is 2-3 hours.The body’s supply of thiosulfate is limited so it is the rate limiting step in cyanide metabolism.Thiocyanate is non-toxic (unless it accumulates with high levels) and is excreted in the urine.Rhodanese catalyses the reaction of CN + thiosulfate to form thiocyanate and sulphite.Cyanide is metabolised via the liver enzyme rhodanese (named before international enzyme nomenclature was standardised, hence -ese not -ase!).Cyanide is rapidly absorbed and taken up into cells.Sodium nitroprusside, metabolised to cyanide and may accumulate with prolonged high dose infusions.Amygdalin is hydrolysed by two enzymes (amygdalin hydrolase and prunasin hydrolase) most effectively in crushed, moistened kernels, resulting in the formation of HCN and glucose.Acetonitrile is slowly metabolised by the liver and may lead to cyanide toxicity over 24 hours.stimulates neurotransmitter release, such as N-methyl-D-aspartate (NMDA), causing neurotoxicity and seizures.stimulates biogenic amine release causing pulmonary and coronary vasoconstriction, which results in pulmonary edema and heart failure.binds the ferric (Fe3+) ion of cytochrome oxidase causing ‘histotoxic hypoxia’ and lactic acidosis.Fumigant in airplanes, buildings, ships.deliberate contamination of medications and food) Chemical warfare and acts of terrorism (e.g.acetonitrile (industrial solvent used as cosmetic remover and in laboratories).cyanide salts used in metal extraction and refining, electroplating, photography and fumigation) almonds, apricot kernels and other Prunus species such as peach, apple, cherry and plum) Cyanogenic glycosides such as amygdalin (e.g.Smoke inhalation (fires burning plastics, wools, silk and other natural and synthetic polymers).this corresponds to about 1 teaspoonful of a 2% solution of hydrocyanic acid and to about 200 mg of potassium cyanide.Average lethal dose of prussic acid (hydrogen cyanide, HCN) taken by mouth between 60 and 90 mg (adult).First discovered in 1786 by Scheele, who extracted it from the dye Prussian blue – and promptly died from exposure to the vapours.Cyanide is a potentially lethal toxic agent that can be found in liquid and gaseous form. ![]()
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