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

Medical Aspects of Chemical Warfarehypercontraction and hyperextension of sarcomeres,focal myocytolysis, and the development of contractionbands that are the result of the breakdown ofmarkedly hypercontracted myofibril bundles. This isfollowed by an inflammatory response (24 hours orless), which begins with edema and neutrophil infiltrationand ends with mononuclear cell infiltration andscavenging of necrotic sarcoplasm by macrophages.This is followed by a stage of repair (72 hours or less),which begins with a proliferation of fibroblasts andends with myofiber loss and replacement fibrosis.Some studies have shown a relationship betweenthe development of seizures following nerve agentexposure and the occurrence and severity of cardiaclesions. 131Ventricular fibrillation, a potentially fatal arrhythmia,has been seen after administration of a ChEinhibitor and atropine. It can be precipitated by theIV administration of atropine to an animal that hasbeen rendered hypoxic by administration of a ChEinhibitor. 155,156 Although this complication has notbeen reported in humans, atropine should not begiven intravenously until the hypoxia has been at leastpartially corrected.Because of the well-recognized possibility that ventricularfibrillation can occur in a hypoxic heart givenatropine, many intensive care unit physicians andnurses are reluctant to give the large amounts of atropinethat may be required to treat acute nerve agentpoisoning. The authors have observed that this issuehas come up in several training exercises. Althoughdata are fragmentary, the literature suggests that thechance of death from acute nerve agent poisoningis greater than the chance of ventricular fibrillationfrom atropine on a hypoxic heart, at least in initialfield management. Once the patient has reached ahospital setting where proper monitoring is possible,it should be less problematic to administer atropinesafely in the amounts required while giving oxygenas necessary.Heart RateAlthough it is frequently stated that a patient intoxicatedwith a nerve agent will have bradycardia,this is not proven by clinical data. In a review of therecords of 199 patients seen at the Edgewood ArsenalToxic Exposure Aid Station for mild-to-moderatenerve agent exposure (one or more definite signs orsymptoms of nerve agent intoxication, such as miosisor a combination of miosis with dim vision or a tightchest), 13 presented with heart rates less than 64 beatsper minute. There were 13 patients with heart rates of64 to 69 beats per minute, 63 with heart rates of 70 to 80beats per minute, 41 with heart rates of 81 to 89 beatsper minute, 38 with heart rates of 90 to 99 beats perminute, and 31 with heart rates higher than 100 beatsper minute. A heart rate of 64 to 80 beats per minute isconsidered normal in adults. 157 Thus, 13 patients (6.5%)had low heart rates, and 110 patients (55%) had highheart rates (69 of these patients [35%] had heart rates> 90 beats per min).Reports of the heart rates of patients severely intoxicatedby insecticides vary. In a report 158 describing 10patients (9 of whose consciousness was moderatelyto-severelyimpaired), 7 presented with heart ratesover 100 beats per minute, and the other 3 had heartrates over 90 beats per minute (5 had a systolic bloodpressure of 140 mm Hg or higher, a diastolic bloodpressure of 90 mm Hg or higher, or both). In anotherreport, 159 the heart rates of three unconscious patientswere slow (one had cardiac arrest). Two acutely ill, unconsciouspatients were described in a comprehensivereview of organophosphorus poisoning 54 ; one had aheart rate of 108 beats per minute, the other 80 beatsper minute. The authors of the study pointed out thatcardiovascular function is usually maintained untilthe terminal stage and that blood pressure and heartrate increase in the acute stage but may decline later.Heart rate was not listed in their tabulation of signsand symptoms.GENERAL TREATMENT PRINCIPLESThe principles of treatment of nerve agent poisoningare the same as they are for any toxic substanceexposure: namely, terminate the exposure; establishor maintain ventilation; administer an antidote if oneis available; and correct cardiovascular abnormalities.Most importantly, medical care providers or rescuersmust protect themselves from contamination. If thecaregiver becomes contaminated, there will be one morecasualty and one fewer rescuer. Protection of the rescuercan be achieved by physical means, such as masks,gloves, and aprons, or by ensuring that the casualtyhas been thoroughly decontaminated. The importanceof casualty decontamination should be obvious, but itis often forgotten or overlooked.This section discusses the general principles of treatingnerve agent poisoning. The specific treatment ofcasualties in the six exposure categories (suspected,minimal, mild, moderate, moderately severe, andsevere) is addressed in the next section.Terminating the ExposureThe first and perhaps most important aspect of treatingacute nerve agent poisoning is decontaminating the180