Methemoglobin cyanide poisoning treatment

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. 

Patients who are critical and do not satisfactorily respond to supportive therapy should be administered specific cyanide antidotes as outlined in Table 19.5. Cyanide antidotes have been classified into three main groups based on their mechanism of action (1) methemoglobin inducers, (2) sulfur donors, and (3) cobalt compounds. The definitive treatment of cyanide poisoning differs in various countries due to different medical practices and guidelines. The safety... 

B. Treatment. Successful treatment for acute cyanide poisoning depends upon rapid fixation of the cyanide ion, either by methemoglobin (metHB) formation or by fixation with cobalt compounds. Drug treatments include, compounds producing Methemoglobin, Hydroxyocobalamin, and Dicobalt edetate. Any casualty who is fully conscious and breathing... 

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 ). 

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. 

Ten Eyck RP, Schaerdel AD, Ottinger WE. 1986. Comparison of nitrate treatment and stroma-free methemoglobin solution as antidotes for cyanide poisoning in a rat model. Journal of Toxicology and Clinical Toxicology 23 477-487. 

Poison Treatment As discussed previously, methemoglobin binds well and competes with cytochrome oxidase for cyanide ions. Consequently, the antidote developed for cyanide poisoning involves increasing the formation of methemoglobin in the blood, by inhalation of amyl nitrate vapor (Chen 1952). Antidote kits contain amyl nitrate ampoules. To administer the antidote, the ampoule is broken in a cloth such as a handkerchief and held close to the victim s nose while artificial respiration is being conducted. Resuscitation by mouth is not recommended a mechanical resuscitator should be used instead. If the victim does not respond to the amyl nitrate treatment, a medical professional would then increase the methemoglobin production by intravenous injection of sodium nitrate followed by administration of thiosulfate to increase the activity of the rhodanese enzyme. 

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