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

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Nerve Agentsadministered intramuscularly, will report improvementwithin 5 minutes. A caregiver should resist thetemptation to give too much atropine to a walking,talking casualty with dyspnea. In general, the correctdose <strong>of</strong> atropine for an individual exposed to a nerveagent is determined by the casualty’s signs and symptoms,the route <strong>of</strong> exposure (vapor or liquid), and theamount <strong>of</strong> time elapsed since exposure.Atropine <strong>The</strong>rapy after Inhalational Exposure toVaporAfter vapor exposure, the effects <strong>of</strong> nerve agentsappear very quickly and reach their maximum activitywithin seconds or minutes after the casualty isremoved from or protected against the vapor. In whatwere apparently high concentrations <strong>of</strong> nerve agentvapor, two individuals collapsed (one at EdgewoodArsenal, Maryland, in 1969 and one at Dugway ProvingGround, Utah, in 1952), unconscious, almost immediatelyafter taking one or two breaths, and 4 to 5minutes later they were flaccid and apneic. 20,66 Even atvery low concentrations, maximal effects occur withinminutes <strong>of</strong> exposure termination. Because effectsdevelop so rapidly, antidotal therapy should be morevigorous for a casualty seen during or immediatelyafter exposure than for a casualty seen 15 to 30 minuteslater. For example, if a soldier ’ s buddy in the field or acoworker in a laboratory suddenly complains <strong>of</strong> dimvision in an environment suspected <strong>of</strong> containing nerveagent vapor, the buddy or worker should immediatelyadminister the contents <strong>of</strong> one Mark I antidote kit orATNAA. <strong>The</strong>re may be continuing exposure beforethe casualty can exit the environment or don a mask,or the effects from the exposure already absorbed maycontinue to develop for several minutes. On the otherhand, if the casualty is seen at the medical aid station(installation or field) 15 to 30 minutes after the vaporexposure has terminated, an antidote is not needed ifmiosis is the only sign (atropine given intramuscularlyhas very little effect on miosis). Effects caused by nerveagent vapor will not progress after this time.If a casualty is seen immediately after exposure fromvapor only, the contents <strong>of</strong> one Mark I kit or ATNAAshould be given if miosis is the only sign, the contents<strong>of</strong> two kits or injectors should be administered immediatelyif there is any dyspnea, and the contents <strong>of</strong>three kits should be given for severe dyspnea or anymore severe signs or symptoms. When seen 15 to 30minutes after an exposure to vapor alone, the casualtyshould receive no antidote if miosis is the only sign,the contents <strong>of</strong> one Mark I kit or ATNAA for mild ormoderate dyspnea, the contents <strong>of</strong> two kits or injectorsfor severe dyspnea (obvious gasping), and the contents<strong>of</strong> three kits or injectors and diazepam (with additionalatropine, but no more oxime) if there are more serioussigns (such as collapse or loss <strong>of</strong> consciousness). If dyspneais the most severe symptom, relief should beginwithin 5 minutes, and the drugs should not be repeateduntil this interval has passed. <strong>The</strong> aggressive therapygiven immediately after the onset <strong>of</strong> effects is not forthose early effects per se (eg, atropine is relatively ineffectiveagainst miosis), but is in anticipation <strong>of</strong> moresevere effects within the following minutes.Atropine <strong>The</strong>rapy after Dermal Exposure to Liquid<strong>The</strong> therapy for an individual whose skin has beenexposed to nerve agent is less clear. <strong>The</strong> onset <strong>of</strong> effectsis rarely immediate; they may begin within minutes<strong>of</strong> exposure or as long as 18 hours later. Generally,the greater the exposure, the sooner the onset; andthe longer the interval between exposure and onset<strong>of</strong> effects, the less severe the eventual effects will be.Effects can begin hours after thorough decontamination;the time <strong>of</strong> onset may be related to the duration<strong>of</strong> time the agent was in contact with the skin beforedecontamination.<strong>The</strong> problem with treating dermal exposure is notso much how to treat a symptomatic casualty as it isdeciding to treat an asymptomatic person who hashad agent on the skin. <strong>Medical</strong> personnel usually havelittle or no information about the exposure incident,because the casualty <strong>of</strong>ten does not know the durationor amount <strong>of</strong> exposure.Unlike, for example, lewisite exposure, nerve agentdoes not irritate the skin. <strong>The</strong> first effects <strong>of</strong> agent onthe skin are localized sweating and fasciculations <strong>of</strong>underlying musculature (rippling), which usually arenot observed. If these effects are noted, however, thecasualty should immediately self-administer or begiven the contents <strong>of</strong> one Mark I kit or ATNAA. <strong>The</strong>sesigns indicate that the chemical agent has penetratedthe skin layers.In general, an asymptomatic person who has hadskin contact with a nerve agent should be kept undermedical observation because effects may begin precipitatelyhours later. Caregivers should not administer thecontents <strong>of</strong> a Mark I kit or ATNAA to an asymptomaticperson, but should wait for evidence <strong>of</strong> agent absorption.However, if an individual is seen minutes aftera definite exposure to a large amount <strong>of</strong> nerve agenton the skin (“large” is relative; the LD 50for skin exposureto VX is only 6–10 mg, which is equivalent to asingle drop 2–3 mm in diameter), there may be somebenefit in administering antidotes before the onset <strong>of</strong>effects. When the occurrence <strong>of</strong> exposure is uncertain,the possible benefits <strong>of</strong> treatment must be weighed185

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