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

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

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<strong>Medical</strong> <strong>Aspects</strong> <strong>of</strong> <strong>Chemical</strong> <strong>Warfare</strong>buddy system was used because any soldier able toself-administer diazepam does not need it. Medics andunit lifesavers were issued additional diazepam autoinjectorsand could administer two additional 10 mgdoses at 10-minute intervals to a convulsing casualty.Current policy states that diazepam is given followingthe third Mark I or ATNAAs when the condition<strong>of</strong> the casualty warrants the administration <strong>of</strong> threeMark I kits or ATNAAs. <strong>The</strong> United Kingdom usesa drug similar to diazepam known as Avizafone. 132Avizafone is a water-soluble, prodrug formulation <strong>of</strong>diazepam that is bioconverted to diazepam followinginjection.If a convulsing or seizing casualty is being treatedin a medical treatment facility, research has shown thatother anticonvulsant benzodiazepines (eg, lorazepam[Ativan, Wyeth, Madison, New Jersey]), midazolam[Versed, Roche, Basel, Switzerland]) are just as effectivein stopping nerve-agent–induced seizure as diazepam.138 Experimental work has also shown that midazolamis twice as potent and twice as rapid in stoppingnerve-agent–induced seizures compared to diazepamwhen the drugs are administered IM, the route <strong>of</strong>administration for immediate field treatment. 107,211For these reasons, efforts are currently underway forFDA approval <strong>of</strong> midazolam as treatment <strong>of</strong> nerveagent–inducedseizures and the eventual replacement<strong>of</strong> diazepam by midazolam in the convulsive antidotenerve agent injectors.<strong>The</strong>rapy for Cardiac ArrhythmiasTransient arrhythmias occur after nerve agent intoxicationand after atropine administration in a normalindividual. <strong>The</strong> irregularities generally terminateafter the onset <strong>of</strong> atropine-induced sinus tachycardia(see discussion <strong>of</strong> cardiac effects above).Experimental studies 156,215 have shown that whenanimals are poisoned with ChE inhibitors and thenallowed to become cyanotic, rapid IV administration <strong>of</strong>atropine will cause ventricular fibrillation. This effecthas not been reported in humans.After severe intoxication from exposure to an organophosphateinsecticide, a 20-year-old patient wasstabilized with atropine and ventilatory support, buther ECG showed depression <strong>of</strong> the ST segment and flattening<strong>of</strong> the T wave, presumably because <strong>of</strong> persistentsinus tachycardia secondary to large doses <strong>of</strong> atropine(287 mg in 4 days; total <strong>of</strong> 830 mg). She was givena β-adrenergic blocking agent (propranolol), whichslowed the heart rate to 107 beats per minute, normalizingthe ST-T changes. <strong>The</strong> normal ECG pattern andheart rate <strong>of</strong> 107 beats per minute persisted, despiterepeated doses <strong>of</strong> atropine. In effect, this produced apharmacologically isolated heart, with both cholinergicand adrenergic blockade. <strong>The</strong> authors reporting on thecase suggested that propranolol might be <strong>of</strong> value inprotecting against the effects <strong>of</strong> atropine and organophosphorusintoxication. 216SPECIFIC TREATMENT BY EXPOSURE CATEGORY<strong>The</strong> goals <strong>of</strong> medical therapy <strong>of</strong> any poisoningare, in most cases, straightforward: to minimize thepatient ’ s discomfort, to relieve distress, and to stopor reverse the abnormal process. <strong>The</strong>se goals are thesame in the treatment <strong>of</strong> a patient with nerve agentintoxication.<strong>The</strong>rapy should be titrated against the complaints <strong>of</strong>dyspnea and objective manifestations, such as retching;administration <strong>of</strong> the contents <strong>of</strong> Mark I kits (or atropinealone) should be continued at intervals until reliefis obtained. Seldom are more than two to three MarkI kits required to provide relief. Topical application <strong>of</strong>atropine or homatropine can effectively relieve eye orhead pain not relieved by Mark I injections.<strong>The</strong> signs <strong>of</strong> severe distress in a fellow soldier, suchas twitching, convulsions, gasping for breath, andapnea, can be recognized by an untrained observer.A casualty ’ s buddy will usually act appropriately, butbecause a buddy ’ s resources are few, the level <strong>of</strong> assistanceis limited: a buddy can administer three MarkI kits and diazepam and then seek medical assistance.In a more sophisticated setting, adequate ventilationis the highest priority, but even the best ventilatorsprovide little improvement in the presence <strong>of</strong> copioussecretions and high airway resistance. Atropinemust be given until secretions (nose, mouth, airways)are decreased and resistance to assisted ventilation isminimal.<strong>The</strong> goals <strong>of</strong> therapy must be realistic. Current medicationswill not immediately restore consciousnessor respiration or completely reverse skeletal muscleabnormalities, nor will IM or IV drug therapy reversemiosis. Muscular fasciculations and small amounts<strong>of</strong> twitching may continue in a conscious patient longafter adequate ventilation is restored and the patientis walking and talking.Although in practice exposure categories are neverclear-cut, different therapeutic measures are recommendedfor treating nerve agent casualties at differentdegrees <strong>of</strong> exposure severity. Treatment is based onthe signs and symptoms caused by the particular exposure(Table 5-7). <strong>The</strong> following suggested exposurecategories are based on the casualty presenting signsand symptoms.190

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