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

Nerve Agentsmay cause severe rhinorrhea. One exposed workercompared the nasal secretions to the flow from aleaking faucet, and another told the authors that thesecretions were much worse than those produced bya cold or hay fever.Rhinorrhea also occurs as part of an overall, markedincrease in secretions from glands (salivary, pulmonary,and gastrointestinal) that follows a severe systemicexposure from liquid on the skin and, under thiscircumstance, becomes a secondary concern to both thecasualty and the medical care provider.Pulmonary SystemThe pulmonary effects of nerve agent poisoning arecrucial, probably the most important component ofthe nerve agent poisoning toxidrome. A nerve agentdeath is almost always a pulmonary death, whetherfrom bronchoconstriction, bronchorrhoea, central apnea,paralysis of the muscles of respiration, or, in mostcases, a combination of all of these. Military medicsare trained to focus on respiratory status as the mostimportant parameter of the effectiveness of treatmentin nerve agent poisoning.After exposure to a small amount of nerve agentvapor, individuals often complain of a tight chest(difficulty breathing), which is generally attributed tospasm or constriction of the bronchiolar musculature.Secretions from the muscarinically innervated gobletand other secretory cells of the bronchi also contributeto the dyspnea. Exposure to sarin at a Ct of 5 to 10 mg/min/m 3 will produce some respiratory discomfort inmost individuals, the discomfort and severity increasingas the amount of agent increases.Several decades ago, investigators attempted tocharacterize pulmonary impairment caused by exposureto nerve agents by performing pulmonary functionstudies (such as measurements of vital capacityand maximal breathing capacity) on subjects exposedto small amounts of sarin vapor (the Ct values forsarin ranged up to 19.6 mg/min/m 3 ). 63 Some observersfound increases in airway resistance 64 and otherchanges, while other researchers did not. 65Although these studies yielded conflicting results,clinical practitioners have found that the inhalationof nerve agent vapor or aerosol causes dyspnea andpulmonary changes that are usually audible on auscultation.These changes are noticeable after low Ctexposures (5–10 mg/min/m 3 ) and intensify as theCt increases. The pulmonary effects begin withinseconds after inhalation. If the amount inhaled islarge, the effects of the agent include severe dyspneaand observable signs of difficulty with air exchange,including cyanosis. Clinically, this resembles a severeasthmatic attack.If the amount of the inhaled agent is small, a casualtymay begin to feel better within minutes after movinginto an uncontaminated atmosphere, and may feelnormal in 15 to 30 minutes. The authors observed that itwas not uncommon, for example, for individuals whohad not received atropine or other assistance to arriveat the Edgewood Arsenal Toxic Exposure Aid Stationabout 15 to 20 minutes after exposure and report thattheir initial, severe trouble in breathing had alreadydecreased markedly. If the exposure was larger, however,relief was likely to come only after therapeuticintervention, such as administration of atropine.Attempts to aid ventilation in severely poisonedcasualties can be greatly impeded by constriction ofthe bronchiolar musculature and by secretions. Onereport 66 mentions thick mucoid plugs that hamperedattempts at assisted ventilation until the plugs wereremoved by suction. Atropine may contribute to theformation of this thicker mucus because it dries outthe thinner secretions.A severely poisoned casualty becomes apneic andwill die as a result of ventilatory failure, which precedescirculatory system collapse. Three major factorscontribute to respiratory failure: obstruction of airpassages by bronchoconstriction and by respiratorysecretions; weakness followed by flaccid paralysisof the intercostal and diaphragmatic musculatureneeded for ventilation; and a partial or total cessationof stimulation to the muscles of respiration from theCNS, indicating a defect in central respiratory drive.Older data on the relative contributions of each ofthese factors in causing death were summarized in areport 67 describing original studies in nine species. Theauthors of the report concluded that central respiratoryfailure appeared to dominate in most species,but its overall importance varied with the species, theagent, and the amount of agent. For example, underthe circumstances of the studies, failure of the centralrespiratory drive appeared to be the major factor inrespiratory failure in the monkey, whereas bronchoconstrictionappeared early and was severe in the cat.The authors of another report 68 suggest that the presenceof anesthesia, which is used in studies of nerveagent intoxication in animals, and its type and depthare also factors in establishing the relative importanceof central and peripheral mechanisms.In another study, 69 bronchoconstriction seen in thedog after IV sarin administration was quite severecompared with that in the monkey. Dogs have thickairway musculature, which may explain that finding.Differences in circulatory and respiratory effectswere seen between anesthetized and unanesthetizeddogs given sarin. 70 Convulsions and their associated173