Medical Aspects of Chemical Warfare (2008) - The Black Vault

Medical Aspects of Chemical WarfareExhibit 11-1PROCEDURES FOR COLLECTING AND STORING BLOOD SAMPLES FOR DELAYED CYANIDEANALYSISProcedure 1Step 1. Collect a blood sample in a blood collection tube containing an anticoagulant (eg, EDTA, heparin, sodiumcitrate).Step 2. Add 0.05 mL of 0.05 mol/L sodium nitrite per 1 mL of blood, cover, and let stand for 2 minutes.Step 3. Store at -20 °C until analysis can be performed. 1Procedure 2Step 1. Prepare blood collection tubes containing the anticoagulant sodium citrate (~ 17 mg). Add 20 μL of 50%aqueous solution of sodium nitrite (~10 mg), and dry in vacuo over anhydrous calcium chloride.Step 2. Collect a 5-mL blood sample.Step 3. Store at 5°C. 2Procedure 3Step 1. Collect a blood sample in a blood collection tube containing an anticoagulant (EDTA or heparin). Ensurethat the top is not made of rubber.Step 2. Add 1 mL of whole blood to 10 mL of the acid silver sulfate reagent (20 mmol in 0.5 mmol H 2SO 4).Step 3. Store at -20°C until analysis can be performed. 3(1) Lundquist P, Sörbo B. Rapid determination of toxic cyanide concentrations in blood. Clin Chem. 1989;35:617–619. (2) Vesey CJ,Langford RM. Stabilization of blood cyanide. J Anal Toxicol. 1998; 22:176–178. (3) Lundquist P, Rosling H, Sorbo B. Determination ofcyanide in whole blood, erythrocytes and plasma. Clin Chem. 1985;31:591–595.glucoseTCAcycle—+—+NAD2e -ATP—+Fig. 11-2. Cyanide binds the terminal enzyme of the cytochromeoxidase enzyme system. The enzyme system islocated within the inner lamina of the mitochondria. Theblockade interrupts the electron flow through the cytochromeoxidase system, thereby disrupting ATP production and bothmitochondrial and cytoplasmic ionic balance.ATP: adenosine triphosphateHCN: cyanideNADH: nicotinamide adenine dinucleotideTCA: tricarboxylic acid cycle2e - : two electronsATPATPHCNO 2H 2 OCytochromeoxidaseand support during recovery. Often, but not always,recovery is complete. In addition to medical therapeutics,it may be necessary for rescuers and providers toprotect themselves from cyanide in the environment,on the casualty, or in exhaled air and vomitus. Oncesuccessful medical care begins, providers will needto support the casualty through neurological crisisincluding coma, seizures, and respiratory failure. Theywill need to manage cardiorespiratory crisis, includingpulmonary edema, and they may need to manage otherorgan effects, such as toxic hepatitis and renal failure.After acute recovery, they need to prepare for psychiatriccare and possible delayed neuropathology.Cyanide is known to inhibit some 40 enzymes,including several metalloenzymes containing iron,copper, or molybdenum. 125 These reactions may wellcontribute to cyanide toxicity. The dominant effectsof acute, high-dose exposure, however, result fromcyanide’s primary effect of inhibiting cytochromec oxidase. This action impairs oxygen uptake andutilization, resulting over time in partial or completecessation of oxidative metabolism, termed histotoxicanoxia. In massive cyanide poisoning, the mechanismsof toxicity appear to be more complex. In particular,382