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

Medical Aspects of Chemical Warfarelies in halving the time to administer the two antidotescompared to the MARK 1 kit.When administered in an adequate amount, atropinereverses the effects of the nerve agent in tissuesthat have muscarinic receptor sites. It decreases secretionsand reverses the spasm or contraction of smoothmuscle. The mouth dries, secretions in the mouthand bronchi dry, bronchoconstriction decreases, andgastrointestinal musculature become less hyperactive.However, unless given in very large doses, IV or IMatropine does not reverse miosis caused by nerve agentvapor in the eyes. A casualty with miosis alone shouldnot be given atropine, and pupil size should not beused to judge the adequacy of atropine dosage.The amount of atropine to administer is a matterof judgment. In a conscious casualty with mild-tomoderateeffects who is not in severe distress, 2 mg ofatropine should be given intramuscularly at 5-minuteto 10-minute intervals until dyspnea and secretionsare minimized. Usually no more than a total dose of2 to 4 mg is needed. In an unconscious casualty, atropineshould be given until secretions are minimized(those in the mouth can be seen and those in the lungscan be heard by auscultation), and until resistance toventilatory efforts is minimized (atropine decreasesconstriction of the bronchial musculature and airwaysecretions). If the casualties are conscious, they willreport less dyspnea, and if assisted ventilation is underway,a decrease in airway resistance will be noted.Secretions alone should not be the reason for administeringmore atropine if the secretions are diminishingand are not clinically significant. Mucus blockingthe smaller airways may remain a hindrance, despiteadequate amounts of atropine. In severe casualties (unconsciousand apneic), 5 to 15 mg of atropine has beenused before spontaneous respiration resumed and thecasualty regained consciousness 30 minutes to 3 hoursafter exposure. 20,66 The authors have observed severalrecovering casualties without non-life-threatening,adverse effects (such as nausea and vomiting) 24 to 36hours after exposure for which atropine was administered.20 However, there appears to be no reason to giveatropine routinely in this period.In the only battlefield data that have been published,Syed Abbas Foroutan reported using atropine muchmore aggressively and in larger amounts. 12 After aninitial IV test dose of 4 mg atropine, he waited 1 to2 minutes. If there was no sign of atropinization, hegave another 5 mg IV over 5 minutes while checkingthe pulse. He titrated his dose to pulse rate, acceleratingif the heart rate dropped to 60 beats per minute to70 beats per minute and decreasing it for pulse ratesover 110 beats per minute. This resulted in doses ofatropine, in some cases, up to 150 mg IV in 5 minutes.US doctrine, by contrast, uses a 6-mg IM loading dosefollowed by 2-mg increments until IV access is established.Foroutan ’ s protocol may reflect the pressure ofhaving large numbers of casualties to treat, the relativelack of availability of oximes, particularly far forward,and his inability to guarantee that atropine could becontinually administered during evacuation to the nextechelon of medical care.In contrast with nerve agent treatment, much largeramounts of atropine (500–1,000 mg) have been requiredin the initial 24 hours of treatment of individuals severelypoisoned by organophosphorus pesticides. 179–181Medical care providers must recognize that the amountof atropine needed for treating insecticide poisoningis different than the amount needed for treating nerveagent poisoning. Pesticides may be sequestered in thebody because of greater fat solubility or metabolized ata slower rate than nerve agents. Whatever the reason,they continue to cause acute cholinergic crises for amuch longer period (days to weeks). This point iscrucial in training personnel who are used to seeing insecticidepoisonings to manage nerve agent casualties.Insecticide casualties may require intensive care unitbeds for days; nerve agent casualties almost never doand are usually either dead or well enough to requireminimal medication within 24 hours.There has recently been increased discussion aboutthe endpoints of atropinization and the most efficientmeans to achieve it. The textbook recommendations forearly atropinization from various authors have been assessedusing model data of atropine dose requirementsin patients severely poisoned with organophosphatepesticides. 175 These authors concluded that a dose-doublingstrategy, continued doubling of successive doses,would be the most rapid and efficient way to achieveatropinization. Likewise, the treatment regimen usedby Foroutan 12 would also result in a rapid atropinization.The endpoints of atropinization recommended byArmy Field Manual 8-285, Treatment of Chemical AgentCasualties, 182 the Medical Management of Chemical AgentCasualties Handbook, 183 Foroutan, 12 and Eddleston etal 175 are very similar: lack of bronchoconstriction, easeof respiration, drying of respiratory secretions, and aheart rate > 80 to 90 beats per minute.The goal of therapy with atropine should be tominimize the effects of the agent (ie, to remove casualtiesfrom life-threatening situations and make themcomfortable), which may not require complete reversalof all of the effects (such as miosis). However, in acasualty with severe effects, it is better to administertoo much atropine than too little. Too much atropinedoes far less harm than too much unantagonized nerveagent in a casualty suffering severe effects. However,a moderately dyspneic casualty given atropine 2 mg,184