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A CF  J ! # @$ % @ ' @( ) @* +,- . / 0 1 82 M3 O4 Q5 S6 U7 W8Y9 [: ]; _< a= c g&i'k. m o s u x  JIFJ J 5#J J_$.$.$.$.$.$.$.$.$.2$>/`|St .$.$.$.$.$.$.$.$.$.$.b$;TԔp=K_͹[&. `1?P3@8{| g4IdId~0 Vppp <4ddpjFg4%d%d~0 p@ pp<4!d!dpj( ?  O =<}: VESICANTS  OBJECTIVESEKnow the mechanism of action (pathophysiology) Identify signs and symptoms for all routes of exposure and the clinical time course Know specific pre and post exposure treatment regimens Understand the specific pharmacology of each treatment regimen Understand the prognosis and triage for mild, moderate, and severe exposure FPPFMILITARY VESICANTSGMustards Sulfur (agent) Nitrogen (chemotherapy) Lewisite Phosgene oximeB n'nn ('$(MUSTARD HISTORY1822: First synthesized (Despretz) Mid-1800s: Synthesized again (Niemann, Guthrie) 1880s: Manufacturing process (Meyer) 1917: First battlefield use (Germany)<$1FM$<WORLD WAR I CW CASUALTIES CW Casualties %Fatal Germany 200,000 4.5 France 190,000 4.2 Britain 189,000 4.2 U.S. 73,000 2.0 Russia 475,000 11.8 Kurds 5,000 100?x333 3 36 WW I USEXCaused more than 70% of chemical casualties Lethality low; under 5% Long convalescence= WORLD WAR II*The Bari mustard disaster 02 December 1943+P+ POST-WORLD WAR IaItaly against Ethiopia Japan against China Iraq against Iran, Kurds Alleged: Egypt against Yemenbb MUSTARDYHS: Hun Stoff H: Impure HD: Distilled, pure HL: Mustard/Lewisite HT: Mustard/agent TZZ SULFUR MUSTARD CH2 - CH2 - Cl Mustard S CH2 - CH2 - Cl CH2 - CH2 - OH Thiodiglycol S CH2 - CH2 - OHZ  *    -   MUSTARDOily liquid Light yellow to brown Vapor heavier than air Liquid heavier than water Low volatility; persistent Freezes/melts at 58Fn MUSTARD DETECTION*Liquid: M8, M9 papers Vapor: M256A1; CAM++ MUSTARD PENETRATIONThrough skin surfaces in 2 minutes 80% on skin evaporates Part is  fixed in skin, rest circulatesdc( MUSTARDrQuickly cyclizes in tissue Alkylates cell components (DNA, proteins) DNA damage leads to: cell death mutation`n ,P(FF_$  MUSTARD TOXICITYVapor unprotected (mg" min/m3) Eye 10 to 50 Airways 100 to 500 Skin 200 to 1,000 Death 1,500Djx$3$3$3L$>MUSTARD TOXICITYMUSTARD: DAMAGESHSkin Eyes Airways Systemic: Bone marrow GI tract CNS Lymphoid tissue(Z-Z-CMUSTARD CASUALTIES FROM WWI Eyes& & & & & & & & & ...85% Respiratory Tract& ...75% Scrotum & & & & & & .....42% Face & & & & & & .& & & ..27% Anus & & & & & & & & & .24% Legs& & & & & & ...& & & .11% Buttocks & & & & & & .....10% Hands & & & & & ...& & & ..4% Feet& & & & & & ...& & & 1.5%Z        MUSTARD: ONSETiCellular interaction: 1 to 2 minutes Clinical effects: 2 to 48 hours Usually 4 to 8 hours>&P!F"Fj(MUSTARD: SKINjErythema Small vesicles; later coalesce Blisters/bulla Possible coagulation necrosis with liquid exposure.73FkFMUSTARD: ONSETChemical cell damage: 1 to 2 minutes Clinical effects: 2 to 48 hours Usually 4 to 8 hours MUSTARD: EYEMild: conjunctivitis, blepharospasm Moderate: lid inflammation and edema, blepharospasm, corneal roughening Severe: Corneal opacification, ulceration, and/or perforationJ%IF(?F$u8 MUSTARD: EYE^75% only mild conjunctivitis Return to duty in 2 weeks 15% moderate conjunctivitis Return to duty 4-6 weeks 10% severe; under 1% with residual damage 0.1%  legal blindnessdxxxxBxBMUSTARD: ACUTE EFFECTS7Upper airway Hemorrhage Pain Larynx Hoarseness StridorP  w9MUSTARD: ACUTE EFFECTSkTrachea/bronchi bronchospasm pseudomembranes Small airway and alveoli (massive exposure) hemorrhagic edemaP-$ -$ MUSTARD: DEATHKUsually pulmonary: Damaged airways Infection Depressed immune system Sepsis,x9x(9$MUSTARD: MARROWjDamaged stem cells Decreased WBC, RBC, platelets (Day 7 to day 14) Survival rare if WBC <200 (Iran / Iraq)k@Ak$ MUSTARD: GIhEarly (< 24 hours): transient symptoms cholinergic effect Late (>3 days): severe damage cytotoxic effectXn&nnn$& $ SEVERE MUSTARD EXPOSURESCNS Apathy, lethargy Euphoria Convulsions, only with massive exposure! Coma DeathHP$)   MUSTARDeRadiomimetic (DNA) epithelial cells (eye, pulmonary, skin, GI) hematopoetic damages many tissues BR$R $MUSTARD: SYMPTOMSVSymptoms within 4 hours = severe injury Airway symptoms within 6 hours is often fatal8(Z.PV$DIFFERENTIAL DIAGNOSISIsolated cases: plant, animal, other chemicals Many cases: Latent effects: Mustard Immediate effects: Lewisite, Phosgene Oxime\0(  ->GMUSTARD: DIAGNOSTICSNon-specific CBC Early chemical pneumonitis: fever, WBC, chest x-ray Pneumonia: sputum exam / culture Urinary thiodiglycol: DA TB Med 2962PFF6PPFGPFF MUSTARD: MANAGEMENT Protect Self!!!!DECONTAMINATION`Early decon protects casualty within minutes Late decon protects medical personnel and facilityD3 3"MANAGEMENT: SKINSoothing cream/lotion Unroof large blisters Debridement of burns Frequent irrigation Antibiotics: Topical / Systemic (cellulitis) Systemic analgesics Appropriate IV fluids and electrolytes#MANAGEMENT: EYESSoothing eye drops Topical mydriatics Topical antibiotics Vaseline on lid edges Avoid topical analgesics Topical steroids - ?? Sunglasses$MANAGEMENT: AIRWAYSSteam, cough suppressants Oxygen Bronchodilators, steroids Early intubation Assisted ventilation Antibiotics AFTER organism identified% MANAGEMENT: GI:Atropine Antiemetics Fluid therapy Electrolyte replacement;;$&!MANAGEMENT: MARROWeBlood component replacement RBC, WBC, Platelets Marrow transplants Hormonal therapy Reverse isolationBxx6x$ 6$)$MUSTARD: LONG TERMCarcinogen / mutagen No evidence of human reproductive toxicity Chronic exposure Respiratory cancer Unclear: chronic bronchitis, emphysema(S:S:*%MUSTARD: LONG TERMmNo evidence of cancer after one or two exposures Chronic eye problems / damage may follow severe eye exposuren@dn+&LEWISITEZWorld War I origin; not used Possible use by Japan vs China No other known use Sparse data[[$,'LEWISITEaOily, amber to brown liquid Freezing point ~ 0F Heavier than air, water Persistent Geranium odorbb-(LEWISITE: TOXICITYVapor Eyes Effects 2 mg-min/m3 Vesication 1,500 mg-min/m3 Death 1,500 mg-min/m3 Liquid Blister 14 mg Death 2.8 gvK3K3 .)LEWISITE: MECHANISMeContains arsenic carcinogen ?? Reacts with many constituents: cellular necrosis Mechanism unknowndPP22ZE/*LEWISITE: DAMAGESEyes Skin Airways Capillaries$0+LEWISITE: TIME OF ONSET:Pain, irritation within 1 min Tissue necrosis within 5 min;:(1,LEWISITE: SKIN5Progresses to blister More necrosis than from mustard65$2-LEWISITE: EYESxPain, blepharospasm on contact Rapid edema of conjunctiva, lids Eyes swollen shut in an hour Damage to iris and cornear<!PPA$ $3.LEWISITE: AIRWAYSSevere irritation Bronchial epithelial necrosis, similar to mustard More prone to pseudomembranes, pulmonary edema than mustardH2P2<F4/LEWISITE SHOCKIncreased capillary permeability Plasma volume decreased Hemoconcentration Hypotension Pulmonary edema Circulatory failure Death(!a!$a 61LEWISITE: MANAGEMENTvImmediate decontamination Treat as mustard lesion British Anti-lewisite (BAL) Dimercaprol Systemic Topical Ophthalmic 6ZZ72LEWISITE: TREATMENTHospital care - severe exposure IM injection of BAL (10% in oil) Initial dose: 0.5cc per 25 lbs (up to 4cc total) May be given at 4, 8, 12 hours after initial dose(!!83BAL SIDE EFFECTSxLacrimation Constriction of throat GI cramps, vomiting, nausea Anxiety, myalgias Hypertension May last up to 30 minutes yny94PHOSGENE OXIME (CX)uRapid onset Toxic, irritating, corrosive Urticant, not vesicant Sparse data Never used in combat Stockpiled by USSR :5PHOSGENE OXIME (CX)Phosgene oxime corrosive to all tissues (skin, lungs, eyes) Pulmonary edema Phosgene oxime manufactured from Phosgene Phosgene (CG) - lung agent only p<ZZ*!<<O<7PHOSGENE OXIME: MANAGEMENT$4Management: Symptomatic Supportive Same as mustard4'$& ;SUMMARY ANY QUESTIONS?F, /8P  ` ̙33` ` ff3333f` 333MMM` f` f` 3>?" dd@(?" dd@   " @ ` l2 n?" dd@   @@``@n?" dd@  @@``PT    @ ` ` p>>  +(  `|   6$ @jP  T Click to edit Master title style! !  0 j  RClick to edit Master text styles Second level Third level Fourth level Fifth level!     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