Emergency War Surgery NATO Handbook: Part I: Types of Wounds and Injuries: Chapter VI: Chemical Injury
United States Department of Defense
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Hydrogen cyanide (AC) and certain of its congeners form highly stable complexes with metalloporphyrins such as cytochrome oxidase. Aerobic cellular metabolism comes to a virtual halt. Venous blood remains as oxygen rich as arterial blood, accounting for the "cherry red" postmortem appearance of cyanide victims. Death is due to cytotoxic hypoxia.
High volatility and relatively low toxicity (50-100 times less than those of nerve agents) limits its operational utility in open spaces. Potassium cyanide poisoning of water and food supplies is an old terrorist tactic that one should be aware of.
Diagnosis: The diagnosis of hydrogen cyanide inhalation is difficult to make without a history. Cyanogen chloride (CK) is more readily recognized because its irritant properties cause tearing and coughing in sublethal does.
Treatment: Immediate removal of casualties from the contaminated atmosphere prevents further inhalation. Nitrites are effective antidotes. They form methemoglobin, to which the cyanide ion binds preferentially; however, overly enthusiastic methemoglobin conversion reduces available hemoglobin, imperiling intravascular oxygen transport. Sodium nitrite for intravenous use (10 ml of 3% solution) is stocked in forward field medical facilities. (The amyl nitrite "pearl" for inhalation has been removed from issue.) Sodium thiosulfate (50 ml of 25% solution, IV) provides free sulfur to convert toxic cyanide to a far less toxic thiocyanate ion.
Manual or mechanical ventilation is central to resuscitation of apneic casualties. Those in respiratory distress will be aided by oxygen inhalation.
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