George Braitberg, in Critical Care Nephrology (Third Edition), 2019 TreatmentĬyanide poisoning is treated differently in different parts of the world. In treatment of H 2S toxicity, there is no role for thiosulfate. Similarly to cyanide toxicity treatment, administration of nitrites relieves the toxicity of H 2S by formation of methemoglobin followed by sulfmethemoglobin, which is chemically analogous to cyanomethemoglobin. Hydrosulfide anion (HS −) derived from hydrogen sulfide (H 2S) also inhibits cytochrome oxidase by binding to ferric heme. The cyanide bound to metHb is always in equilibrium with free CN −, and this uncomplexed cyanide is converted to thiocyanate (SCN − nontoxic) by administration of thiosulfate ( Chapter 6). CyanmetHb is no more toxic than metHb, and cells containing it can be eliminated by normal body processes. Once metHb is formed, CN − can replace OH − at position 6 of the iron, since it has a higher affinity for Fe 3+ than OH −. First, some of the normal hemoglobin is converted to methemoglobin by intravenous infusion of a solution of NaNO 2 or by inhalation of amyl nitrite. Treatment of cyanide poisoning consists of diverting the cyanide into the production of cyanmetHb. Cyanide poisoning is detected by the characteristic odor of HCN gas (odor of bitter almonds) on the breath and by laboratory tests (absorption spectra, tests for CN −). It does produce cytotoxic anoxia by inhibiting cytochrome oxidase, thereby preventing utilization of O 2 by tissues ( Chapter 13).

Bhagavan, Chung-Eun Ha, in Essentials of Medical Biochemistry (Second Edition), 2015 CyanmethemoglobinĬyanide poisoning does not cause production of cyanohemoglobinemia or cyanosis.

Cyanide antidote kit contains