It is not universally available, however, so the older kits still have a role. More recently, hydroxocobalamin has become available under the brand name Cyanokit, and provides a safer, faster, simpler treatment. Supportive treatment including oxygen, IV fluids, and airway protection in severe cases should also be a priority. Sodium thiosulfate is slower acting, however, as it cannot rapidly enter the mitochondria, and the sulfur donor group has to be shuttled to the mitochondrial rhodanese enzymes via the albumin-sulfane complex. In patients who have had smoke inhalation, sodium thiosulfate should be used alone, without the nitrites, because there may be concomitant carboxyhemoglobinemia. The second component of the kit is sodium thiosulfate, which acts as a sulfur donor for the enzyme rhodanese, the body’s natural mechanism for detoxifying cyanide, converting it to thiocyanate. One of the dangers of the nitrite-containing antidote is that inducing a methemoglobinemia in a critically ill patient could hasten their decline by further reducing oxygen delivery. The Fe3+ of metHb binds to cyanide ions more strongly than cytochrome oxidase does, so it draws the cyanide out of the cells to allow resumption of oxidative phosphorylation. These induce methemoglobinemia, which is hemoglobin with iron in the Fe3+ oxidation state instead of instead of Fe2+. In short, the nitrites used in antidote kits are either inhaled amyl nitrite, used typically in the pre-hospital setting or when IV access is not available, or IV sodium nitrite. The true mechanism of action is complicated. The older cyanide antidote kits consisted of nitrites and sodium thiosulfate. Among smokers who may have an innately poor ability to detoxify cyanide, a chronic, progressive visual loss can occur, termed tobacco amblyopia. Cyanide is also present in trace amounts in fruit seeds, but rarely poses a health risk. Ingestion of improperly prepared cassava, is one cause, and can lead to a demyelinating disorder called tropical ataxic neuropathy. In cases of smoke inhalation the clinical picture may be complicated by a concurrent carbon monoxide poisoning as well as any cutaneous burns or trauma. Symptoms can occur minutes to hours after ingestion or transdermal exposure, but are almost immediate after parenteral exposure. Initially they may have tachycardia, hypertension and tachypnea, followed by hemodynamic collapse, with bradycardia, hypotension and bradypnea. They may also develop renal failure, hepatic necrosis, pulmonary edema and rhabdomyolysis. Patients’ skin may appear red due to the venous hyperoxia. The symptoms of cyanide toxicity include nausea, vomiting, headaches, confusion and dyspnea ultimately leading to seizures, coma and death. This will manifest as red-appearing skin and retinal veins with cherry red venous blood, as well as a narrowed arterial-venous oxygen gradient. Since the cells experience a histotoxic hypoxia and cannot utilize oxygen, it remains in the bloodstream causing venous hyperoxia. This causes an anion-gap, lactic acidosis. Cyanide ions bind to ferric iron (Fe3+) present in mitochondrial cytochrome oxidases, arresting oxidative phosphorylation and forcing the cells into anaerobic metabolism. In water, cyanide exists primarily as HCN (hydrogen cyanide), which can rapidly cross cell membranes, but is in equilibrium with cyanide ions (CN–). It can also occur iatrogenically from prolonged nitroprusside infusion. While it is fortunately a rare cause for presentation to emergency departments, cyanide is one of the most rapidly fatal toxins known, so diagnosis and treatment must be expeditious.Ĭyanide toxicity can occur from a range of different exposures, including smoke inhalation from burning plastics in house fires, intentional ingestions in suicide attempts and industrial exposures among individuals working in the jewelry, photography, metallurgy or textile industries. Now there is a newer, safer agent that converts the mitochondrial toxin, cyanide, into the benign chemical cyanocobalamin, or vitamin B12. Cyanide toxicity can be quickly fatal, but there is a simple, safe treatment that can reverse its toxic effects.įor many years, cyanide toxicity was treated with multi-component cyanide antidote kits.
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