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

Medical Aspects of Chemical Warfare• Pulmonary edema, usually very marked,occurred. The pleural cavities generally containedan excess of fluid.• The lungs, upon removal from the thorax,were voluminous, heavy, and bluish-red incolor; occasionally, petechial hemorrhagesand alternating patches of emphysema andcollapsed lung tissue were noted.• Section of lungs showed an exudation offrothy fluid from the cut surface.• Irregular, alternating areas of edema and acuteemphysema were noted.• The trachea, bronchi, and bronchiole weregenerally filled with thin, yellowish, serosanguineousfluid.• There was little or no inflammatory change inthe larynx, trachea, and bronchi.• The veins were engorged.• The heart, especially on the right side, wasdilated.• Petechial hemorrhages were often found beneaththe endocardium.• The pericardial fluid increased in amount.• The abdominal viscera showed the presenceof generalized venous engorgement andcongestion.• The meninges of the brain were congested.Methyl IsocyanateIn December 1984, in Bhopal, India, a massive leakof methyl isocyanate resulted from operational andequipment malfunctions in a pesticide plant. Manythousands of residents of the city, most in proximityto the plant, suffered sublethal and lethal respiratoryinjuries, the expected consequences of high-level exposureto this type of potent irritant chemical vapor.Animal toxicological information was limited priorto the accident, but has since confirmed that the lungis the major target of these lethal injuries, invariablywith pulmonary edema. Early concerns about acutecyanide intoxication were not supported by subsequentscientific inquiry. Superficial corneal erosionsdid not result in permanent eye injury. The primaryunresolved (and perhaps irresolvable) medical issueis the incidence and determinants of long-termrespiratory injury in the survivors. Limited availableevidence suggests that chronic damage, when present,is or resembles fibrosing bronchiolitis obliterans,the expected consequence when permanent injuryresults from acute, high-level irritant gas exposure.Definition of the follow-up population is uncertain,and exposure information is lacking. Dose-responserelationships are not likely to emerge from follow-upstudies. 168PerfluoroisobutylenePFIB primarily affects the peripheral compartment ofthe pulmonary system. Although animal studies occasionallyreport disseminated intravascular coagulationand other organ involvement, these effects only occurwith substantial pulmonary injury to the peripheralcompartment of the pulmonary system, suggesting thatsystemic hypoxia is a major factor. 169 No human studieshave reported organ involvement other than the respiratorysystem. Pathological data on acute human exposureto PFIB are not available; however, pathological data onanimals show both histological and ultramicroscopicchanges occurring within 5 minutes of exposure. 170Interstitial edema with alveolar fibrin depositionprogresses rapidly over 24 hours, and then graduallysubsides until the patient is fully recovered. At 72 hours,a type II pneumocyte hyperplasia is seen (interpretedas consistent with known reparative processes). Somelong-term pathological changes in animals have beennoted but most animal studies do not identify suchlong-term effects. 171 Human long-term pathological dataare available for only one reported case: a 50-year-oldwoman who experienced approximately 40 episodes ofpolymer fume fever—typically occurring from smokingcontaminated cigarettes. Eighteen months after her lastepisode, progressive exercise dyspnea was noted. A cardiopulmonaryphysical examination, chest radiograph,and arterial blood gas were all normal. Pulmonaryfunction testing supported a provisional diagnosis ofalveolar capillary block syndrome (decreased diffusioncapacity of carbon monoxide, increased exercisealveolar-arterial oxygen gradient, and minimal airwaydisease). Death occurred from an unrelated cause. Theautopsy provided histological evidence of moderateinterstitial fibrosis with minimal chronic inflammatorycell infiltrate. 172 Only two human deaths from pyrolysisproducts of polymerized organofluorides have beenreported. 173,174Oxides of NitrogenInhalation of nitric oxide causes the formation ofmethemoglobin. Inhalation of nitrogen dioxide resultsin the formation of nitrite, which leads to a fall in bloodpressure, production of methemoglobin, and cellularhypoxia, which causes rapid onset pulmonary edema.The clinical response to oxides of nitrogen exposureis essentially triphasic. In phase 1, symptoms appearmore or less quickly, depending on the intensity ofexposure. With a low dose, initial eye irritation, throattightness, chest tightness, cough, and mild nausea mayappear. Once the casualty is removed from the sourceof exposure, these symptoms disappear spontaneouslyover the next 24 hours. However, at 24 to 36 hours326