These two findings would be present in cyanide toxicity due to the lack of aerobic respiration. It may be possible to further identify smoke inhalation victims who have cyanide toxicity by checking for an elevated lactate and low end tidal CO2 measurement. Nevertheless, we should not dismiss its potential importance for this indication, nor its clear advantages as a first-line antidote for other forms of cyanide poisoning. …While we should be cautious about embracing hydroxocobalamin too rapidly or too broadly for smoke inhalation at least pending further data. It appears reasonable to consider empiric hydroxocobalamin for victims who are comatose, in cardiac arrest, or have clear signs of cardiovascular extremis… For now, clinicians should assess patients individually and use cautious judgement. “”A call for routine empiric administration of hydroxocobalamin to smoke inhalation victims seems unwarranted until we have more data. I agree with the author of a 2007 editorial on hydroxycobalamin for smoke inhalation who concluded: Although the antidote hydroxycobalamin is safe, it is costly at $900 USD per 5 gram dose. Given that cyanide is produced as a result of domestic fires, smoke inhalation victims may have concomitant cyanide poisoning. Should cyanide antidote therapy be given to all smoke inhalation victims? The dose of sodium thiosulfate is 0.4 mg/kg IV up to a maximum of 12.5 g. The onset of action of this effect is too slow (up to 30 minutes) to rely on sodium thiosulfate alone for treatment of cyanide toxicity. This allows excess cyanide to be eliminated. To enhance elimination use sodium thiosulfate to provide sulfur donors for the liver enzyme responsible for cyanide metabolism (Rhodanese). The old cyanide antidote kit containing nitrites is no longer manufactured. This may be significant in smoke inhalation victims, as carbon monoxide poisoning and cyanide poisoning may both occur from smoke inhalation. Most significantly it will interfere with co-oximetry measurements of total hemoglobin, carboxyhemoglobin, methemoglobin, and oxyhemoglobin. Hydroxycobalamin will interfere with many lab tests. Hydroxycobalamin is relatively safe, causing rash, headache, and a temporary reddish discoloration of the skin, plasma, urine, and mucous membranes. Hydroxycobalamin is given at a dose of 5 g IV, with a half dose repeated if the clinical situation warrants it. Hydroxycobalamin combines with cyanide to form the harmless substance cyanocobalamin (vitamin B12). 50 g of AC can be given enterally as long as the patient is not at risk of aspiration. GI decontamination with activated charcoal (AC) is indicated in oral cyanide exposures based on animal studies which report decreased mortality among rats given AC after lethal potassium cyanide ingestions. This is more likely to happen if the cyanide toxicity is from a dermal exposure and remains on the patient’s clothing or skin. There is a possibility for caregivers to be contaminated with cyanide due to “off-gassing”. Decontamination and antidote strategies should be considered simultaneously with supportive care. While supportive care to treat cardiovascular and CNS depression is essential, no amount of supportive care can change the fact that the patient’s mitochondria can’t produce energy. Most symptoms are non-specific although cherry-red skin coloring is sometimes present.Ībout half of the population detects a bitter almond odor after inhaling cyanide.Īs with the treatment of any poisoning patient, the following 4 essential steps must be considered: Significant toxicity has resulted from rates higher than 2 mcg/kg/min.Ī patient with cyanide toxicity generally presents with cardiovascular and CNS depression despite normal oxygenation. Cyanide toxicity may occur in patients who receive prolonged infusions of sodium nitroprusside, have chronic renal failure, or in pediatric patients. The antihypertensive sodium nitroprusside contains cyanide. Domestic fires, industrial accidents, and sodium nitroprusside are more common possible causes of cyanide poisoning.įabrics, upholstery, and melamine (often used as a coating on shelves and cabinets) can all give off cyanide when burned.Ĭyanide is used in the extraction of gold and silver, and the production of nylon. The capacity to metabolize cyanide is limited, and just ~0.5mg/kg is enough to be fatal.Ĭyanide toxicity is relatively rare. Oxygen supply remains adequate but cells are unable to utilize the oxygen.Ĭyanide is present in low background levels in the environment and is safely metabolized to thiocyanate by the liver. It causes death within minutes to hours of exposure.Ĭyanide inhibits oxidative phosphorylation in the mitochondria, shutting down aerobic metabolism. Subscribe on iTunes, Android, or StitcherĬyanide is a rapidly lethal toxin. In this episode I’ll discuss cyanide toxicity.
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