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

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Vesicantsdirectly by the alkylating properties of HD or secondarilyby released cellular proteases or by chemical mediatorsof the accompanying inflammatory responseare bullous pemphigoid antigen, α-6 integrins, andlaminin-5 (nicein). 80,85 Bullous pemphigoid antigenand α-6 integrins are recognized integral proteins ofthe hemidesmosome with complex molecular attachmentsto heads of anchoring filaments. Laminin-5 ornicein is the resident protein of anchoring filaments.Loss of immunospecificity of these proteins wouldindicate a pathogenesis associated with the disablingof anchoring filaments within the lamina lucida, aprocess (vida supra) documented by ultrastructuralstudy of HD toxicity.Histopathological and ultrastructural presentationsof sulfur-mustard–induced toxicity—apparentlyirrespective of the model—demonstrate that epidermal/epithelialbasal cells of the stratum germinativumlayer are targeted early during the pathology to theexclusion of other epidermal/epithelial cells. Injuredbasal cells appearing approximately 4 to 6 hours afterexposure present progressive signs of apoptosis andirreversible necrotic cell injury and death. Associatedwith basal cell injury is the apparent disabling of anchoringfilaments of hemidesmosomes that leads todetachments within the subadjacent lamina lucida ofthe epidermal/epithelial basement membrane zone.Superimposed upon this cellular response is the effecton selected basement membrane adherent proteinsthat lose their immunospecificity to specific antiseraabEpiEpiDeDecdMvEpiMvEpiDeMvDeMvFig. 8-11. ApopTag (Millipore Corp, Billerica, Mass) staining of paraffin-embedded skin sections demonstrating temporalprogression of basal cell apoptotic profiles. (a) At 3 hr postexposure, no apoptotic basal cells were observed; only inflammatorycell infiltration was noted in papillary dermis (arrows). (b) At 6 hr postexposure, the occurrence of apoptotic basalcells is evident. ApopTag-positive cells exhibit typical characteristics of apoptosis, nuclear condensation, and margination(arrows). (c) At 12 hr postexposure, basal cells exhibiting apoptosis significantly increased at areas of microvesication (arrows).(d) At 24 hr postexposure, basal cell apoptosis progressed to necrosis, making identification of individual apoptoticcells among cellular debris difficult. Original magnification × 66.Epi: epidermisDe: dermisMv: microvesicationReproduced with permission from: Kan RK, Pleva CM, Hamilton TA, Anderson DR, Petrali JP. Sulfur mustard-induced apoptosisin hairless guinea pig skin. Toxicol Pathol. 2003;31(2): 185–190. Photographs: Courtesy of Stephanie R Froberg, GraphicsDepartment, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Md.273
Medical Aspects of Chemical Warfareand are predictive of attachment failures. Finally, theinflammatory response appears to exacerbate lesions,contributing to the formation of pervasive microvesiclesthat eventually cleave the epidermis/epitheliumfrom their supporting, underlying structures, leadingto epithelial/epidermal sloughing and denudation ofbasement membranes.EyeThe eye is the external organ most sensitive tomustard. The latent period for eye damage is shorterthan that for skin damage. Generally, the asymptomaticperiod varies with the concentration of mustardvapor and individual sensitivity. Eye irritation withinminutes after exposure has been reported. 17,86 After alow Ct exposure, a slight irritation with reddening ofthe eye may be all that occurs (Figure 8-12). As the Ctincreases, the spectrum of injury is characterized byprogressively more severe conjunctivitis, blepharospasm,pain, and corneal damage. 31,66 Photophobia willappear, and even with mild exposures, may linger forweeks.Corneal damage consists of edema with clouding,swelling, and infiltration of polymorphonuclear cells.Clinical improvement occurs after approximately 7days, with subsiding edema. Corneal vascularization(pannus) with secondary edema may last for weeks.Vision will be lost if the pannus covers the visualaxis. Severe effects from mustard exposure may beFig. 8-12. An eye injury of lesser severity in an Iraniancasualty (shown 7 d after exposure) caused by exposure tomustard. The characteristic findings were edema of the lidand conjunctival injection. Corneal ulcerations were foundwith more severe exposure.Reproduced with permission from: Willems JL. Clinicalmanagement of mustard gas casualties. Ann Med Milit Belg.1989;3S:12.followed by scarring between the iris and the lens,which restricts pupillary movements and predisposesthe individual to glaucoma. 31,87The most severe eye damage is caused by liquidmustard, which may be delivered by an airbornedroplet or by self-contamination. 61 Symptoms maybecome evident within minutes after exposure. 66 Severecorneal damage with possible perforation of thecornea can occur after extensive eye exposure to liquidmustard. The patient may lose vision, or even the eye,from panophthalmitis, particularly if drainage of theinfection is blocked, such as by adherent lids. 66 Miosissometimes occurs, probably due to the cholinergicactivity of mustard.During World War I, mild conjunctivitis accountedfor 75% of the eye injuries; complete recovery took 1to 2 weeks. Severe conjunctivitis with minimal cornealinvolvement, blepharospasm, edema of the lidsand conjunctivae, and orange-peel roughening of thecornea accounted for 15% of the cases; recovery fromthis condition occurred in 2 to 5 weeks. Mild cornealinvolvement with areas of corneal erosion, superficialcorneal scarring, vascularization, and iritis accountedfor 10% of the cases; convalescence took 2 to 3 monthsin these cases. Lastly, severe corneal involvement withischemic necrosis of the conjunctivae, dense cornealopacification with deep ulceration, and vascularizationaccounted for about 0.1% of the injuries; convalescencefrom this condition lasted more than 3 months. Onlyone person out of 1,016 mustard casualties surveyedafter World War I received disability payments fordefective vision. 11Studies conducted on rabbit eyes indicate thatmustard injury to the cornea is characterized by initialdegeneration of the epithelial cells, with changes rangingfrom nuclear swelling and nuclear vacuolization,to pyknosis and nuclear fragmentation. Epithelialloosening and sloughing occurs either by separationof the basal cells from the basement membrane, or byshearing of the cell just above its attachment to thebasement membrane. 88,89Mustard initially causes vasodilation and increasedvascular permeability in the conjunctiva, which lead toprogressive edema. Secretion of mucus occurs withinminutes of exposure. Pyknosis of epithelial cells beginsconcurrently with or shortly after these changes,leading to desquamation of the epithelium. In the laterstages, inflammatory infiltration of connective tissueand exudation are present. 88,89 Medical personnel havereported seeing delayed keratitis in humans from 8months to 20 years after mustard exposure. 29,90 Thisdelayed keratitis, in addition to the chronic inflammation,can lead to erosions and frank ulcerations.Within approximately 5 minutes, liquid mustard274
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The Coat of Arms1818Medical Departm
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Textbooks of Military MedicinePubli
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MEDICAL ASPECTS o fCHEMICAL WARFARE
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ContentsContributorsForeword by The
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ContributorsMICHAEL ADLER, PhDResea
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DONALD M. MAXWELL, MSResearch Chemi
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ForewordThe US military has been co
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PrefaceA significant concern for th
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PrologueThe original edition of Med
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xxii
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Medical Aspects of Chemical Warfare
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Nerve AgentsChapter 5NERVE AGENTSFR
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Nerve AgentsAbout 10,000 to 30,000
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Nerve Agentsphorofluoridate (DFP) w
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Nerve AgentsFig. 5-2. This schemati
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Nerve AgentsExhibit 5-1 continuedis
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Nerve Agentsactivity but only 15% t
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Nerve AgentsTABLE 5-3CHEMICAL, PHYS
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Nerve AgentsTABLE 5-4EFFECTS OF EXP
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Nerve Agentsaffecting the other eye
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Nerve Agentsmay cause severe rhinor
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Nerve Agentsof jerks and tremor.Cen
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Nerve Agentsand they were decreased
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Nerve Agentsnerve agent toxicity on
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Nerve Agentspatient. Decontaminatio
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Nerve AgentsFig. 5-5. The Mark I ki
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Nerve Agentsadministered intramuscu
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Nerve Agentsthat hydroxamine reacti
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Nerve AgentsOral administration may
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Nerve AgentsTABLE 5-7RECOMMENDED TH
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Nerve Agentsimpairment such as whee
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Nerve Agentssuboptimal, manner. The
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Nerve Agentsthan those who did not.
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Nerve Agentssible for binding nerve
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Nerve Agentsfor comparison was not
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Nerve AgentsTABLE 5-11EFFECTS OF PY
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Nerve Agentstivity of smooth muscle
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Nerve Agents38. Grob D, Lilienthal
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Nerve Agents77. McDonough JH, Shih
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Nerve Agents117. McLeod CG Jr, Sing
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Nerve Agents154. Tryphonas l, Veino
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Nerve Agents193. Funckes AJ. Treatm
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Nerve Agents235. Suzuki T, Morita H
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Nerve Agents274. Pellegrini JE, Bak
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PROCESSMedical Aspects of Chemical
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Triage of Chemical CasualtiesChapte
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Triage of Chemical Casualtiesreceiv
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Triage of Chemical Casualtiesentran
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Triage of Chemical Casualtiescatego
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Triage of Chemical CasualtiesIn a f
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Triage of Chemical Casualtiesnose)
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Triage of Chemical CasualtiesWith n
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Triage of Chemical Casualties14. Sa
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Decontamination of Chemical Casualt
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• Analyze using GC-MS with methan
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Abbreviations and AcronymsAbBreviat
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Abbreviations and AcronymsPADPRP: p
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Medical Aspects of Chemical Warfare (2008) - The Black Vault

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