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Managing Chemical Exposure. Kevin O. Rynn, PharmD, FCCP, DABAT Clinical Associate Professor Clinical Pharmacy Specialist Emergency Medicine. Awakening of America. Objectives:. Identify agents potentially used in a terrorist attack Understand the pharmacology and toxicology of these agents

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managing chemical exposure

Managing Chemical Exposure

Kevin O. Rynn, PharmD, FCCP, DABAT

Clinical Associate Professor

Clinical Pharmacy Specialist Emergency Medicine

objectives
Objectives:
  • Identify agents potentially used in a terrorist attack
  • Understand the pharmacology and toxicology of these agents
  • Understand the management of exposed patients
  • Identify unique potential threats to New Jersey residents
  • Better appreciate our role as pharmacists
introduction chemical warfare
Introduction: Chemical Warfare
  • Spartans, 429 BC
  • World War I: Germany
      • April 22nd 1915: chlorine gas against allies
        • Belgium, Hundreds killed, troops retreated
      • July 12th, 1917: Sulfur mustard
        • Injuries >>> fatalities
  • World War II: Germany
      • December 2nd 1943: Mustard bombs destroyed in Italy
  • Yemen war
      • Egypt: riot control agents, mustards, nerve agents
  • Vietnam
      • US: Tear gas and chemical herbicides
introduction chemical terrorism6
Introduction: Chemical Terrorism
  • Matsumoto: 1994
      • Sarin: residential neighborhood
      • Fatalities: 7
      • Hospital visits: 500
  • Tokyo: 1995
      • Sarin, subway system during

rush hour

      • Fatalities: 12
      • Hospital visits: > 5,000

Subway riders injured in Aum Shinrikyo

sarin gas attack, Tokyo, March 20, 1995.

(AP Photo/Chikumo Chiaki )

signs symptoms of 111 moderately or severely injured patients on admission
Eye

Miosis 99%

Eye pain 45%

Blurred vision 40%

Dim vision 38%

Tearing 9 %

Chest

Dyspnea 63%

Cough 34%

Wheezing 6%

Tachypnea 32%

ENT

Runny nose 25%

Sneezing 9%

GI

Nausea 60%

Vomiting 37%

Diarrhea 5%

Neurologic

Headache 75%

Weakness 37%

Fasciculations 23%

Numbness 19%

Decreased LOC 17%

Vertigo/dizziness 8%

Seizures 3%

Psychologic

Agitation 33%

Signs & Symptoms of 111 Moderately or Severely Injured Patients on Admission

Okumura T, et al Ann Emerg Med 1996;28(2):129-35

nerve agents
Nerve Agents
  • Physical characteristics and toxicity
  • Mechanism:
    • Cholinesterase inhibitors, excess buildup of Acetycholine (Ach)
  • Muscarinic effects
    • Postganglionic parasympathic
  • Nicotinic effects
    • Autonomic ganglia
      • Preganglionic sympathetic & parasympathetic
    • Neuromuscular junction
  • Excess Ach in CNS
results of cholinesterase inhibition
Muscarinic

Diarrhea Salivation

Urination Lacrimation

Miosis**Urination

Bradycardia Defecation

Bronchorrhea GI symptoms

Bronchospasm Emesis

Emesis

Lacrimation

Nicotinic

Tachycardia

Hypertension

Mydriasis

Neuromuscular junction**

Fasciculation

Weakness

paralysis

CNS

Anxiety, confusion, ataxia, dysarthria

Coma, Seizures**, Resp depression**

Results of Cholinesterase Inhibition

** Most important after nerve agent

rbc plasma cholinesterase levels
RBC & Plasma Cholinesterase Levels
  • Clinical utility limited
    • Related to clinical effect, but not consistently
    • Normal value range
    • Workplace usage
  • Do not wait on these for treatment!
cholinesterase levels
RBC

Difficult assay

inhibited preferentially by VX and sarin

2-PAM: regenerates levels

Regeneration rate: 1% per day (erythrocyte production)

Plasma

Easier assay

An acute phase reactant (liver protein)

Affected by low protein conditions

Declines faster acutely and regenerates faster

Cholinesterase Levels
treatment decontamination
Treatment: Decontamination
  • Selective protective measures
    • Lipophyllic agents can penetrate latex and vinyl
      • Nitrile, neoprene, butyl rubber gloves
    • Leather
    • Shared Breathing air
  • Irrigation
    • Water
    • Hypochlorite solution
    • Alkaline soap
atropine
Atropine
  • Competitive MUSCARINIC antagonist
  • Peripheral > central
    • Blood brain barrier
  • Dosing- IV or IM
    • Initial Adult 2mg

Peds 0.02mg/kg (min 0.1mg)

    • Repeat Every 2 - 5 minutes
  • Endpoints
    • Reversal of muscarinic signs of toxicity

Mod. to Severe

2-3 times this

atropine17
Atropine
  • Dosing in comparison to organic phosphorus insecticide.
  • Tokyo subway sarin attack (N=111)
    • Doses > 2mg 18.9%
    • Max dose administered 9 mg
  • Adverse effects
    • Dry mouth&skin, mydriasis, paralysis of accommodation, tachycardia

Okumura T. et al Ann Emerg Med 1996;28(2):129-35

atropine alternative routes and supply sources
Aerosolized

Ophthalmic

Miosis reversal

Causes photophobia and loss of accommodation

Glycopyrolate

IV administration of

EMS sources

Opthtalmic

Veterinary

Powder preparation

Atropine: Alternative Routes and Supply Sources
rapid atropine reformulation from bulk powder
Geller RJ, Lopez G, Cutler S, Lin D, Bachman GF, Gorman SE. Ann Emerg Med 2003;41:453-6.

110 6mg syringes ~ 60 minutes

8 week testing

5˚C: USP standards + 5%

Pyrogen free

4 week testing

Room Temp: USP standards + 5%

Kozak RJ, Siegel S, Kuzma J. Ann Emerg Med 2003;41:685-8.

100 6mg syringes ~ 30 minutes

3 week testing

USP standards + 5%

microbiologic sterility testing

Cost Advantage

$11 vs $5,000

Rapid Atropine Reformulation From Bulk Powder
pralidoxime protopam 2 pam
Pralidoxime:Protopam®(2-PAM)
  • Cholinesterase reactivator
  • Dosing: IM or IV
    • Adult: 1-2 gms over 15-20 minutes then q6h for 24 hrs
    • Peds: 25mg/kg to max 1gm
    • C.I.: Adult 500mg/hr, peds 25mg/kg/hr
  • Improves all cholinergic symptoms
  • Aging
    • Covalent bond between nerve agent and enzyme
    • Irreversible dealkylation
treatment continued
Treatment: Continued
  • Mark 1 Kits
  • CANA
    • Convulsion antidote for nerve agents
    • Diazepam
  • NAPS
    • Nerve agent pre-treatment tablets
    • Pyridostigmine
treatment
Decontamination

Water, hypochlorite solutions

Avoid scrubbing and hot water

Topical

Calamine/other soothing lotions

Antibiotics

Systemic analgesia

Ocular injures

Irrigation

Mydriatics: homatropine or other anticholinergics

Anesthetics

Ophthalmic ointments

Constant reassurance

Respiratory

Antitussives:

Bronchodilators/mucolytics

Antibiotics

Intubation

Treatment
treatment bal
Treatment: BAL
  • British Anti-Lewisite: Dimercaprol
    • Metal chelating agent
    • BAL combined with lewisite forms stable 5 member ring
    • Dosing
      • 3 -5 mg q4hr x 4 doses
    • Adverse effects
      • GI, Hypertension, tachycardia
      • Peanut allergy
blood agents cyanides
Blood Agents: Cyanides
  • Antiquated term
    • Carried via blood to exert it’s effect
  • French
    • Franco-Prussian war: Napoleon III first to use
  • WWI: French and British
    • Hydrogen cyanide and cyanogen chloride used on battlefields
  • WWII:
    • German genocidal agent
  • Iran-Iraq war and Iraq’s suppression of Kurds
    • Apparent use with mass casualties reported
cyanide tampering
Cyanide: Tampering
  • 1982: Chicago Tylenol
    • 7 deaths
  • 1988: Yogurt
  • 1989: Dept of Agriculture
    • Cyanide traces on fruit from Chile, possible terrorist threat
cyanide
Cyanide
  • Routes
    • Inhalation, ingestion, topical
  • Primary site of action
    • Cells rather than blood
  • Interruption of cellular respiration in mitochondria
cyanide mechanism of toxicity
Cyanide: Mechanism of Toxicity
  • Binding of CN- to cytochrome a3 in mitochondria
    • Stable but not irreversible
    • CN- has higher affinity for the Fe3+ in methemoglobin
  • Interruption of oxidative phosphorylation
    • Decreased aerobic energy production(ATP)
  • Final results: cellular hypoxia
cyanide35
Cyanide
  • Homicidal and suicidal use
  • Judicial execution
  • Combustion of plastics, cigarettes, vehicle exhaust
  • Household products
    • Silver polish, acetonitriles
  • Industry: chemical syntheses
  • Hospital
    • Sodium nitroprusside
cyanide treatment
Cyanide: Treatment
  • Healthcare worker protection
  • Supportive therapy
  • Antidotal therapy
    • Displace CN- from cytochrome A3
      • Nitrite therapy
    • Enzymatic conversion of CN- to thiocyanate
      • Thiosulfate therapy
sodium nitrite
Sodium Nitrite
  • Converts Hb(Fe2+ ) to MetHb (Fe3+)
  • Preferential binding of CN-
  • Goal MetHb = 20 - 30%
  • Adverse effects
    • Excessive methemoglobin production
    • Vasodilatation: hypotension
sodium thiosulfate
Sodium Thiosulfate
  • Enzymatic (rhodanese) reaction with CN-
    • Formation of thiocyanate (SCN-)
  • Irreversible reaction
  • Renal elimination
  • Adverse effects - minimal
    • N/V
    • Arthralgias
pulmonary agents chlorine and phosgene
Pulmonary Agents: Chlorine and Phosgene
  • Increased permeability
    • Delayed pulmonary edema
  • WWI: Primary chemical agents
  • Chlorine: yellow-green cloud, pungent
  • Phosgene: colorless, fresh hay
pulmonary agents phosgene
Pulmonary agents- Phosgene
  • Low-solubility = deeper lung penetration
  • Symptoms within 4 hrs
    • Worse prognosis
    • ICU admission
  • No chest x-ray changes within 8 hours
    • Acute lung injury unlikely
  • Delayed serious symptoms
    • 15 -18 hours
pulmonary agents treatment
Pulmonary Agents: Treatment
  • Decontamination
  • Irrigation of eyes and skin
  • Oxygen
  • Endotracheal Intubation
    • Hoarseness, stridor, upper-airway burns, wheezing, altered mental status
  • Bronchodilators
  • Nebulized sodium bicarbonate
    • Neutralize chlorine derivatives
      • Efficacy data lacking
pulmonary agents treatment45
Pulmonary Agents: Treatment
  • Bed rest
    • Physical exertion exacerbates lung inflammation
  • Corticosteroids
    • Moderate to severe exposures
  • Positive End Expiratory Pressure (PEEP)
  • Antibiotic prophylactic use
    • Not recommended
riot control agents
Riot Control Agents
  • Tear gas or lacrimators
  • Aerosolized solids
  • Intense immediate self-limiting symptoms
  • Prolonged exposure with underlying lung disease
    • Bronchospasm and acute lung injury
riot control agents47
Riot Control Agents
  • Chloroacetophenone - CN
  • o-chlorobenzilidene malononitrile - CS
  • Symptoms
    • Lacrimation, photophobia, blepharospasm
    • Chest tightness, wheezing, coughing, secretions
    • Dermal burning, erythema, vesiculation
  • Recovery: 15 - 30 minutes post removal
riot control agents treatment
Riot Control Agents: Treatment
  • Removal from exposure
  • Remove clothing and placed in airtight bags
  • Irrigation
  • Symptomatic treatment
    • Ophthalmic anesthetics, bronchodilators, antihistamines
  • Capsaicin-induced dermatitis
    • Oil immersion
prevalent new jersey hazmat threats
Prevalent New Jersey HazMat Threats
  • Terrorist attack likely to involve conventional explosives & hazardous materials
  • New Jersey likely target
    • Densely populated state
    • Many companies/manufacturers
  • Most New Jerseyans live/work within short distances to chemical plants

Marcus, S, Ruck B. New Jersey Medicine 2004;101(9):34-43.

new jersey department of environmental protection dep
New Jersey Department of Environmental Protection (DEP)
  • New Jersey Toxic Catastrophe Prevention Act (TCPE)
    • > 100 companies
    • Implement risk management plan (RMPs)
  • NJ DEP list chemicals and threshold quantities

http://www.nj.gov/dep/rpp/tcpa/

new jersey s top 10 list
Ammonia

Chlorine

Difluoroethane

Hydrogen chloride

Hydrogen fluoride

Hydrogen sulfide

Ozone

Pentane

Toluene diisocyanate

Vinyl Acetate monomer

New Jersey’s Top 10 List
ammonia
Ammonia
  • Background
    • Refrigerant, fertilizer, explosives, synthetic fiber, petroleum industry, manufacture of chemicals including methamphetamine
  • Signs and Symptoms
    • Ocular and respiratory
  • Treatment
    • Supportive
    • Copious amounts of water
chlorine
Chlorine
  • Background
    • Bleaching fabrics, rubber and plastic manufacturing, production of chemicals, meds, and pesticides, water purification, sanitizing
    • Reacts with water to form HCl and hypochlorous acid
  • Signs & Symptoms
    • Ocular and respiratory
  • Treatment
    • Supportive
    • Cautious supplemental O2
hydrogen fluoride
Hydrogen Fluoride
  • Background
    • Electronic circuits and plastics production
    • Glass, metal, stone, porcelain etching
    • Cleaning products
    • Fluoride ion responsible for tissue damage
    • Readily penetrates and causes deep tissue destruction/burns
    • Hypocalcemia
  • Signs & Symptoms
    • Derm: Burns, erythemia, pain
    • GI: N/V abdominal pain
hydrogen fluoride treatment
Hydrogen Fluoride: Treatment
  • Assess electrolyte and cardiac status
  • Irrigation
  • Calcium gluconate
    • Forms insoluble precipitate of calcium fluoride, preventing absorption of F ion
    • Alleviate pain and prevent extension
    • Topical, intra-dermal, intra-arterial
    • Inhalation
new jersey conclusions
New Jersey Conclusions
  • Many Locations that house chemicals
    • Risks to citizens working in or living near
  • Health care works prepare to manage these exposures
  • Protocols should be available
conclusions
Conclusions
  • Hospital roles
  • Pharmacist roles
  • Poison center roles