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

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Cyanide PoisoningDose (mg/kg)16.014.012.010.08.06.04.02.00.0BSA 6 mL/m 2BSA 7 mL/m 2BSA 8 mL/m 24 mg/kg6.7 mg/kg10 mg/kg00.5 11.5 22.5 3 4 5 6 7 8 9 101112131415Age in YearsFig. 11-5. Body surface area versus weight dosing. This figuredescribes the relative dose in mg/kg when charted againstmedian weight and height for age. These data illustratewhy the authors propose that dosing children with sodiumnitrite at greater than the package insert recommended 6.6mg/kg is excessive and potentially harmful. Curves weredrawn after converting to dose per body surface area using50th percentile for weights and length/stature, based on theCenters for Disease Control and Prevention 2001 weightfor-agepercentiles, ages birth to 36 months and ages 2 to 20years. For conversion purposes, 4 mg/kg is equivalent to0.13 mL/kg of 3% solution, 6.6 mg/kg is 0.2 mg/kg of 3%solution, and 10 mg/kg is 0.33 mL/kg of 3% sodium nitritesolution. Body surface area calculated using the DuBois andDuBois formula.BSA: body surface areaChart: Courtesy of MAJ Thomas B Talbot, US Army MedicalResearch Institute of Chemical Defense, Aberdeen ProvingGround, Md.The awareness that carbon monoxide has thedominant effect on time of survival, but that bothcarbon monoxide and HCN, when present, appearto synergistically affect hypoxic fatality, guides somegeneral recommendations. Oxygen, general supportivemeasures, and burn and trauma management aregenerally indicated, with high benefit-to-risk ratios.Analysis for carboxyhemoglobin, lactic acidosis, oxygenation,and HCN levels should be accomplished atthe earliest opportunity. HCN-specific treatment maybe a reasonable option for severely affected smokeinhalation victims who have been properly stabilizedotherwise. Thiosulfate is reasonable, effective, andsafe, and appropriate for mass casualty situations. Itdoes not diminish oxygen carrying capacity and iswidely available; however, it does require a parenteralline be established. Hydroxocobalamin is alsoreasonable, effective, and safe. It is typically used withthiosulfate, and it does not diminish oxygen carryingcapacity. It does require a parenteral line. Amyl nitriteis reasonable and effective; it does not require parenteralaccess and can be given to persons on supportedventilation. It does reduce oxygen carrying capacitymodestly. Because treatment requires close monitoringfor hypotension, amyl nitrite is not the first choice ina mass casualty situation. Similarly, sodium nitrite iseffective and likely reasonably safe if a high level ofoversight is available. 190 The other antidotes describedin this chapter have demonstrated general effectivenessagainst cyanide poisoning but not necessarilyagainst fire exposures. They also require parenterallines and substantially more monitoring because oftheir side effect profiles.In summary, clinical management of cyanide intoxications,regardless of the victim’s age or sourceof intoxication, is based on early recognition, aggressivegeneral support measures, and early antidotalenhancement for severely ill persons otherwise atrisk for hypoxic injury. In the absence of history ofcyanide exposure, clinicians have to proceed withouta confirmed diagnosis, maintaining high levels ofawareness for adverse effects of therapy and changesin clinical course. Successful acute intervention mustbe followed with sustained care directed at underlyingcauses of intoxication and detection of delayedsequelae.CYANIDE-CAUSED CARDIAC TOXICITYHistopathologic ChangesCyanide is deposited heterogeneously in cardiactissue, with the ventricles heavily affected. The resultinghistological changes include cell swellingand hemorrhaging. 193 Cell swelling activates chloridemembrane currents, as part of the ionic derangement,changing the homeostasis of the tissue. Substratechanges include formation of lactic acid and secretionof catecholamines.One of the first manifestations of the changed electrophysiologyis bradycardia, which may soon changeto torsade de pointes and possibly culminate in ventricularfibrillation (Figure 11-6). Katzman and Penneyand Wexler et al provide additional details. 194,195On the cellular level, changes in the ion concentrationsbecome important, especially calcium overloadof the cell and increase in the extracellular potassiumconcentration, [K + ] o. The cell’s energy homeostasis 196is profoundly disturbed, and several compensatorymembrane currents are activated and others diminished.Three of the most important ones are the ATP-391
Medical Aspects of Chemical WarfareFig. 11-6. Electrocardiogram from a cyanide-intoxicated individual. The P-wave (the atrial depolarization) is eliminated, andST-segment deviation, usually a rise in the slope, becomes noticeable, followed by modulation of the T-wave. The changedmorphology is expressed in steepening and coalescing of the QRS and the T-waves. A J-wave becomes noticeable.Reprinted with permission from: Wexler J, Whittenberger JL, Dumke PR. The effect of cyanide on the electrocardiogram ofman. Am Heart J. 1947; 34:170.dependent I KATP, 197 the osmotic swelling-activatedI Cl,swell, and the calcium-dependent I Ca-L. The disequilibriumin the membrane currents caused by cyanidehas grave implications for the cell’s electrophysiology.Cyanide-caused cardiac toxicity shares some commonalitywith ischemia but is different in the level of acidityof the tissue and the nature of some of the activatedcurrents. A number of ancillary effects, including enhancedcatecholamine secretion where CA binds to αand β receptors that affect membrane currents, increasein free Mg 2+ , and pH changes also occur. 54,198–200Computational ModelsECGs and action potential morphologies aremarkers of the electrophysiological state of cardiactissue. High-performance computer simulations ofthe electrophysiology of the three types of cardiaccells—endocardial, midmyocardial, and epicardial—model the impact of specific changes to identified ioniccurrents on cardiac electrophysiology. 201–204 Usuallydormant currents appear to be critical to understand-Voltage (mV)40200-20-40-60-800 200 400Time (ms)Fig. 11-7. The effect of cyanide on a ventricular cell. Thered curve shows the change in the resting voltage and thedrastically shortened cycle length. The green curve is theunaffected condition; the red curve shows the affected cellvoltage.Voltage (mV)1.21.00.80.60.40.20-0.2-0.4-0.6-0.80 200 400Time (ms)Fig. 11-8. The change in the electrocardiogram (ECG) causedby the presence of cyanide in the tissue. The red curve showsthe normal ECG, with T-wave present. The blue curve showsthe effect of cyanide on the ECG. The cyanide-affected tissueshows considerable morphological changes and eliminationof the repolarization.392
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The Coat of Arms1818Medical Departm
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Textbooks of Military MedicinePubli
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MEDICAL ASPECTS o fCHEMICAL WARFARE
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ContentsContributorsForeword by The
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ContributorsMICHAEL ADLER, PhDResea
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DONALD M. MAXWELL, MSResearch Chemi
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ForewordThe US military has been co
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PrefaceA significant concern for th
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PrologueThe original edition of Med
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xxii
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Medical Aspects of Chemical Warfare
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Nerve AgentsChapter 5NERVE AGENTSFR
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Nerve AgentsAbout 10,000 to 30,000
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Nerve Agentsphorofluoridate (DFP) w
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Nerve AgentsFig. 5-2. This schemati
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Nerve AgentsExhibit 5-1 continuedis
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Nerve Agentsactivity but only 15% t
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Nerve AgentsTABLE 5-3CHEMICAL, PHYS
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Nerve AgentsTABLE 5-4EFFECTS OF EXP
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Nerve Agentsaffecting the other eye
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Nerve Agentsmay cause severe rhinor
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Nerve Agentsof jerks and tremor.Cen
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Nerve Agentsand they were decreased
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Nerve Agentsnerve agent toxicity on
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Nerve Agentspatient. Decontaminatio
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Nerve AgentsFig. 5-5. The Mark I ki
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Nerve Agentsadministered intramuscu
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Nerve Agentsthat hydroxamine reacti
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Nerve AgentsOral administration may
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Nerve AgentsTABLE 5-7RECOMMENDED TH
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Nerve Agentsimpairment such as whee
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Nerve Agentssuboptimal, manner. The
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Nerve Agentsthan those who did not.
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Nerve Agentssible for binding nerve
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Nerve Agentsfor comparison was not
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Nerve AgentsTABLE 5-11EFFECTS OF PY
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Nerve Agentstivity of smooth muscle
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Nerve Agents38. Grob D, Lilienthal
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Nerve Agents77. McDonough JH, Shih
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Nerve Agents117. McLeod CG Jr, Sing
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Nerve Agents154. Tryphonas l, Veino
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Nerve Agents193. Funckes AJ. Treatm
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Nerve Agents235. Suzuki T, Morita H
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Nerve Agents274. Pellegrini JE, Bak
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Page 363 and 364: Medical Aspects of Chemical Warfare
Page 375 and 376: PROCESSMedical Aspects of Chemical
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Triage of Chemical CasualtiesChapte
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Triage of Chemical Casualtiesreceiv
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Triage of Chemical Casualtiesentran
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Triage of Chemical Casualtiescatego
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Triage of Chemical CasualtiesIn a f
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Triage of Chemical Casualtiesnose)
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Triage of Chemical CasualtiesWith n
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Triage of Chemical Casualties14. Sa
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Decontamination of Chemical Casualt
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• Analyze using GC-MS with methan
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Abbreviations and AcronymsAbBreviat
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Abbreviations and AcronymsPADPRP: p
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Medical Aspects of Chemical Warfare (2008) - The Black Vault

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