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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