1/12/2024 0 Comments Cyanide antidote![]() The standard dose is 5 grams intravenously over 15 minutes. It is well tolerated but may cause a headache, gastrointestinal distress, allergic reactions, and hypertension. The other antidotes impair oxygen-carrying capacity which worsens cellular hypoxia and acidosis. Hydroxycobalamin is the antidote of choice for acute cyanide poisoning, especially if there is concomitant carbon monoxide poisoning. Cyanide poisoning victims do not show such improvement. It is important to recall that patients with carbon monoxide poisoning get better when removed from the source of the poisoning. ECG may show shortening of the ST segments. ![]() However, their levels will not be as high as in victims of cyanide poisoning. Patients with carbon monoxide toxicity may have elevated lactate levels if they have had a loss of consciousness or prolonged exposure. Patients presenting with an anion gap are also likely to have cyanide poisoning. Cyanide does not cause cyanosis and in fact, may cause a cherry red color due to the excess oxygen in the bloodstream that is unable to be used by the mitochondria for cellular respiration.Ī patient who has high levels of plasma lactate (greater than 8 mmol/L) is 94% sensitive and 70% specific for significant cyanide toxicity. Cyanide poisoning often causes prolonged unconsciousness and the need for endotracheal intubation for airway protection. Patients who remain obtunded likely have concomitant cyanide poisoning. Patients with pure carbon monoxide poisoning improve when they are removed from the smokey environment and are placed on 100% oxygen. Take note of the pupils as well.Ĭyanide poisoning causes pupillary dilationĬarbon monoxide does not affect the pupils. Suspect cyanide poisoning in patients who have soot or carbonaceous material in the nose or around the mouth or in the oropharynx. They are relatively rare in carbon monoxide poisoning. Seizures are also common in cyanide poisoning. Hypotension and bradycardia are pathognomonic for cyanide poisoning Severe poisoning will lead to the development of bradycardia, hypotension, and cardiac arrest. ![]() Patients with cyanide toxicity will present initially with tachycardia and hypertension. Organs which have low concentrations of rhodanese are more prone to damage. The thiocyanate is then excreted via the kidneys. Rhodanese is located in the mitochondria in the liver, kidneys, and skeletal muscle. This reaction allows the thiosulfate ions to react with cyanide ions to form sulfite and thiocyanate. Endogenous detoxification of cyanide occurs via the rhodanese reaction. Hydroxocobalamin binds to cyanide, forming cyanocobalamine (vitamin B-12), which is no longer toxic and is excreted by the kidneys. The one that is utilized the most is Hydroxycobalamin which is given intravenously to the poisoning victim. There are several commercial antidotes available for cyanide poisoning. It is theorized that HBO2 causes changes in the whole blood cyanide level by hyperoxygenation competing with the cyanide and forcing it out of the cells. HBO2 has been recommended for cyanide poisoning as well. Hyperbaric oxygen (HBO2) is a mainstay of treatment for carbon monoxide poisoning. ![]() Unlike carbon monoxide, which can be quantified by measuring carboxyhemoglobin level, there is no way to quantify cyanide poisoning. This activity describes the pathophysiology of cyanide poisoning and highlights the role of the interprofessional team in the management of these patients. Hydrogen cyanide has also been used in chemical warfare (gas chambers in German concentration camps in World War II) because inhalation leads quickly to death. Other sources include workplace exposure, prolonged administration of sodium nitroprusside, insecticides, metalworking, bitter almonds, and the seeds of some fruits such as apricots. Patients presenting from structure fires with carbon monoxide poisoning should be assumed to have been exposed to toxic levels of cyanide as well since most modern buildings contain these materials. Cyanide forms as a result of incomplete combustion of materials containing nitrogen (plastics, vinyl, acrylics, nylon, neoprene, rubber, insulation). Cyanide toxicity occurs commonly in patients with smoke inhalation who have been removed from burning structures.
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