Thiocyanate methemoglobin

The administration of sodium thiosulfate (12.5 grams a 25 percent solution administered intravenously at a flow rate of 2.5-5mL/min over a 10-minute period of time) will result in the conversion of the much more toxic cyanide to its less toxic thiocyanate form. This treatment of cyanide poisoning with sodium thiosulfate should follow the use of sodium nitrite. The administration of both the sodium nitrite and sodium thiosulfate is dependent upon the hemoglobin of the patient. The Fe2+ form of hemoglobin will also be oxidized by the sodium thiosulfate and sodium nitrite to the Fe3+ form (methemoglobin). This oxidized form binds cyanide readily to form a stable complex which can be metabolized. See ASIDEon CYANIDE. 

The cyanide antidote kit contains amyl nitrate, sodium nitrate, and sodium thiosulfate. Nitrates convert hemoglobin to methemoglobin, which in turn competes for cyanide with the mitochondrial oxidase complex. Amyl nitrate pearls, administered by inhalation, can be utilized as a first aid measure when intravenous (IV) access is impossible or will be delayed. If IV access is available, IV sodium nitrate is preferred, followed by sodium thiosulfate. Sodium thiosulfate reacts with cyanide to form nontoxic thiocyanate, which is then excreted into the urine. 

After the initial therapy of methemoglobin inducers, the cyanide has to be converted to thiocyanate which is eliminated in urine. This enzymatic detoxification of cyanide is facilitated by a sulfur donor like sodium thiosulfate. The mechanism of this reaction was discussed earlier under elimination of cyanide. High tissue oxygen markedly potentiates the effects of this reaction. In cases where methemoglobin formation is not desirable, sodium thiosulfate together with oxygen alone is sufficient. The utility of... 

Tominaga MY, Midio AF. Modified method for the determination of thiocyanate in urine by ion-exchange chromatography and spectrophotometry. Rev Farm Bioquim Univ Sao Paulo, 1991 27 100-105. Tomoda A, Hashimoto K. The determination of cyanide in water and biological tissues by methemoglobin. 

Sodium nitrite or amyl nitrite can be used in cyanide poisoning. They promote formation of methemoglobin, which binds CN" ions, forming cyanomethemoglobin. This prevents the inhibitory action of CN on complex IV of the electron transport chain. Cyanomethemoglobin is then reconverted to methemoglobin by treatment with sodium thiosulfate, forming the less toxic thiocyanate ion (SCN ). 

The cyanide antidote kit contains amyl nitrite, sodium nitrite, and sodium thiosulfate. The nitrites convert hemoglobin to methemoglobin, which has a higher affinity for the cyanide ion (forming cyanmethemoglobin) than cjTochrome oxidase. Subsequent treatment with sodium thiosulfate results in the formation of methemoglobin and thiocyanate ions. 

A. Specific ieveis. Cyanide ieveis may be obtained but are not usually available rapidly enough to guide treatment when cyanide poisoning is suspected. Cyanide levels may not accurately reflect toxicity because of simultaneous production of methemoglobin, which binds some of the cyanide. Cyanide levels greater than 1 mg/L usually produce a demonstrable lactic acidosis. Thiocyanate levels higher than 50-100 mg/L may cause delirium and somnolence. 

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