Difference between revisions of "Chemical weapons"

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'''Chemical agents''' can be released via unintended means such as a spill from a damaged railroad tank car or industrial explosion as well as by intentional means as chemical weapons.  If concern for chemical exposure exists, appropriate personal protective equipment (PPE) should be worn by first responders and everyone involved to prevent further casualties.
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==Background==
Initial management of a patient with a chemical exposure includes decontamination as it prevents further damage from the exposure as well as protects others from contamination. Aggressive management of the airway, breathing, and circulation (ABCs) should be undertaken in all cases of critically ill chemical exposure.
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*Can be released via unintended means such as a spill from a damaged railroad tank car or industrial explosion as well as by intentional means as chemical weapons.   
  
== Blister Agents (Vesicants) ==
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===Pediatric considerations===
*Lewisite (L), sulfur mustard (H), phosgene oxide (CX)
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*Higher metabolic rate and faster basal respiratory rate, causing more rapid and larger exposures
*Highly persistent
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*Skin is thinner and more permeable
*Skin primary route of exposure when in liquid form; pulmonary and GI tracts as routes in vapor form
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*Agents heavier than air have increased concentrations closer to the ground exposing children > adults
 
 
''Lewisite''
 
*Arsenic-containing compound
 
*Odor of geraniums
 
*Pain with immediate contact
 
*May turn skin grayish color around vesicles
 
 
 
''Sulfur mustard''
 
*2,2,-dichlordiethyl sulfide
 
*Odor of garlic, onion, or horseradish
 
*Damage begins at 1-2 minutes post-exposure with irreversible damage within 20 minutes
 
*Physical symptoms do not occur until approximately 20 minutes but may take up to 4 hours
 
*Penetrates skin, rubber gloves, clothing
 
*Mustard vapor exposure greater medical concern than liquid form
 
 
 
=== Pathophysiology ===
 
*Alkylation of DNA, RNA, and protein causing cell death
 
*Depletes glutathione causing cellular membrane breakdown
 
 
 
=== Symptoms ===
 
*Skin – Initially pruritus and stinging pain, superficial bullae appear over 24 hours. Blisters do not contain toxin
 
*GI – abdominal pain, nausea, vomiting, diarrhea, and weight loss
 
*Respiratory –
 
**Usually only upper respiratory tract affected
 
**Sinus congestion, sore throat, hoarseness.  Rarely pulmonary edema
 
**Epithelial sloughing and pseudomembranes causing inability to clear pathogens and dead tissue.
 
*Mucous membranes and actively reproducing cells most vulnerable to severe damage
 
*Ocular damage – occurs within 4-8 hours
 
**conjunctivitis, chemosis, blepharospasm, and corneal perforation at even low level exposures
 
*Bone Marrow – Leukopenia first (3-5 days), followed by anemia and thrombocytopenia
 
 
 
=== Treatment ===
 
*Immediate decontamination, 0.5% hypochlorite solution will inactivate sulfur mustard but not appropriate for pediatric patients
 
*Supportive care, ABCs
 
*Thermal burn-type care
 
*Fluid losses less than with thermal burns
 
*No antidotes for mustard agents
 
*N-acetylcysteine, glutathione
 
*G-CSF for patients with bone marrow suppression
 
*British antilewisite (BAL) – chelating agent to reduce systemic effects from lewisite exposure.
 
**Won’t alter the blistering effects on skin or airway.
 
**Only used for patients with shock or severe pulmonary injury given BAL side effect
 
**Relative contraindications to BAL: Renal disease, pregnancy
 
 
 
 
 
== Choking/Pulmonary Agents ==
 
*Ammonia, methyl isocyanate, methyl bromide, hydrochloric acid and chlorine, phosgene
 
*Common toxic industrial chemicals, transported widely across country
 
*Can affect central or peripheral airways
 
**burning and irritation to epithelial lining causing airway edema or pulmonary edema, hypoxia, and hypotension
 
 
 
''Chlorine''
 
*Smells of a swimming pool or bleach
 
*Most common exposure is secondary to mixing household cleaners
 
*Irritation of conjunctivae, nose, pharynx, larynx, trachea, and bronchi
 
*Individuals with gas exposure may not need decon, if skin symptoms absent
 
*Rare ocular injury as tears protect mucous membranes from direct damage
 
 
 
''Phosgene''
 
*Smell of freshly cut hay or grass
 
*Not to be confused with phosgene oxide (vesicant)
 
*Denser than air, settles in low-lying places – trenches/basements
 
*Rapid olfactory fatigue can occur leading to prolonged exposure
 
*Exposure may be secondary to fire at textile factory/house, metalwork, or burning Freon
 
*Symptoms dependent on concentration
 
**Low: mild cough, chest tightness, shortness of breath
 
**Moderate: Lacrimation
 
**High: Non-cardiogenic pulmonary edema within 2 to 6 hours after exposure with death within 24-48 hours
 
*Symptoms may take 2-24 hours to develop
 
 
 
=== Pathophysiology ===
 
*Choking agents combine with water in respiratory tract to form acids
 
*Both chlorine and phosgene react with water in respiratory tract to form hydrochloric acid
 
 
 
=== Symptoms ===
 
Symptoms dependent on the water solubility of the chemical
 
*Highly water-soluble
 
**Anhydrous, ammonia, Hydrogen chloride, Sulfur dioxide, Formaldehyde
 
**Rapidly react with water causing damage to upper airway to vocal cords
 
**Direct tissue damage causing edema/airway obstruction and laryngospasm
 
*Moderately water-soluble
 
**Damage to moderate-sized airways (bronchioles)
 
**Bronchospasm and wheezing
 
*Poorly water-soluble
 
**Phosgene, Nitrogen dioxide
 
**Inhaled deeply into alveoli
 
**Lack of irritation of mucous membranes can cause them to go undetected
 
 
 
=== Treatment ===
 
*Liquid phosgene can cause off-gassing with release of toxin from clothes post-exposure
 
*Do not allow patient to be active as it worsens condition
 
*Diuretics and corticosteroids not shown to be effective
 
*Inhaled beta agonists for bronchoconstriction
 
  
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==Types==
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{{Chemical weapon DDX}}
  
== Cyanide Agents (CN) ==
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==[[Cyanide]] Agents (CN)==
 
*AKA Hydrocyanic acid, Formonitrile, Prussic acid
 
*AKA Hydrocyanic acid, Formonitrile, Prussic acid
 
*Mimics carbon monoxide poisoning
 
*Mimics carbon monoxide poisoning
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*Can penetrate rubber and barrier fabrics
 
*Can penetrate rubber and barrier fabrics
  
=== Pathophysiology ===
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===Pathophysiology===
 
*Cyanide inhibits cytochrome oxidase on mitochondria
 
*Cyanide inhibits cytochrome oxidase on mitochondria
 
*Cells unable to use oxygen in bloodstream
 
*Cells unable to use oxygen in bloodstream
 
*Cellular asphyxiation
 
*Cellular asphyxiation
  
=== Symptoms ===
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===Symptoms===
 
*Symptoms can be delayed up to 60 minutes
 
*Symptoms can be delayed up to 60 minutes
 
*Symptoms dependent on concentration, form of cyanide, and route of exposure
 
*Symptoms dependent on concentration, form of cyanide, and route of exposure
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*Anxiety, dizziness, headache, apnea, seizures, and coma  
 
*Anxiety, dizziness, headache, apnea, seizures, and coma  
  
=== Treatment ===
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===Management===
 
*100% oxygen and antidote therapy
 
*100% oxygen and antidote therapy
 
*Sodium nitrite (IV) or amyl nitrite (inhaled) to displace cyanide from cytochrome oxidase
 
*Sodium nitrite (IV) or amyl nitrite (inhaled) to displace cyanide from cytochrome oxidase
 
*Sodium thiosulfate: For conversion of cyanide to excretable thiosulfate
 
*Sodium thiosulfate: For conversion of cyanide to excretable thiosulfate
 
*Repeat sodium nitrite and sodium thiosulfate in 30min at half initial dose if needed
 
*Repeat sodium nitrite and sodium thiosulfate in 30min at half initial dose if needed
*Hydroxocobalamin (Vit B12a): makes CN water soluble and non-toxic
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*[[Hydroxocobalamin]] (Vit B12a): makes CN water soluble and non-toxic
 
*Cyanide Antidote Kit: Amyl nitrite pearls, sodium nitrite (IV), sodium thiosulfate (IV)
 
*Cyanide Antidote Kit: Amyl nitrite pearls, sodium nitrite (IV), sodium thiosulfate (IV)
 
*Cyanokit: Less toxic than cyanide antidote kit and shown effective in cardiac arrest
 
*Cyanokit: Less toxic than cyanide antidote kit and shown effective in cardiac arrest
  
 
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==[[Nerve Agents]]==
== Nerve Agents ==
 
 
*Acetylcholinesterase inhibitors
 
*Acetylcholinesterase inhibitors
 
*Includes household and commercial pesticides (diazinon and parathion)
 
*Includes household and commercial pesticides (diazinon and parathion)
 
*G-series (sarin, tabun, soman) and V-series (VX)
 
*G-series (sarin, tabun, soman) and V-series (VX)
*Rapidly absorbed through skin
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**G-series are volatile non-persistent agents that evaporate quickly
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**V-series high viscosity with oily consistency
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*Rapidly absorbed through skin, symptoms generally develop within 1 hour
 
*Vapors are heavier than air and tend to sink into low places
 
*Vapors are heavier than air and tend to sink into low places
*G-series are volatile non-persistent agents that evaporate quickly
 
*V-series high viscosity with oily consistency
 
*Exposure to volatile agent, symptoms can develop within 1 hour
 
 
*Sarin used in Tokyo subway attack in 1995; 5,000 sought medical attention with 12 deaths.
 
*Sarin used in Tokyo subway attack in 1995; 5,000 sought medical attention with 12 deaths.
  
=== Pathophysiology ===
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===Pathophysiology===
*Acetylcholinesterase inhibitors causing excess acetylcholine at nicotinic and muscarinic receptors
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*Inhibits acetylcholinesterase → excess acetylcholine at both nicotinic and muscarinic receptors
  
=== Symptoms ===
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===Symptoms===
*DUMBELLS  
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*DUMBELLS
 
**D-Diarrhea, U-Urination, M-Miosis, B-Bronchorrhea/Bradycardia, E-Emesis, L-Lacrimation, S-Salivation/Seizures
 
**D-Diarrhea, U-Urination, M-Miosis, B-Bronchorrhea/Bradycardia, E-Emesis, L-Lacrimation, S-Salivation/Seizures
 
*Cholinergic toxidrome [[Toxidromes]]
 
*Cholinergic toxidrome [[Toxidromes]]
  
=== Treatment ===
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===Management===
 
*Nerve agents prolong succinylcholine's paralytic effect
 
*Nerve agents prolong succinylcholine's paralytic effect
*Atropine for bronchorrhea and bronchoconstriction, no max dose
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*Atropine for bronchorrhea and bronchoconstriction
*Pralidoxime to restore function of acetylcholinesterase (given over approx 30 minutes; rapid infusion can cause HTN)
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**Start at 2-6mg, double the dose q5-30min until control of secretions (no max dose)
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*Pralidoxime to restore function of acetylcholinesterase (given over approximately 30 minutes; rapid infusion can cause hypertension)
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**Give as soon as possible - must be given before "aging" occurs to be effective
 
*Benzodiazepines for seizures (standard AEDs may be ineffective)
 
*Benzodiazepines for seizures (standard AEDs may be ineffective)
 
*Mark 1 Nerve Agent antidote Kit (NAAK): 2 autoinjectors:   
 
*Mark 1 Nerve Agent antidote Kit (NAAK): 2 autoinjectors:   
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**600mg pralidoxime
 
**600mg pralidoxime
 
*DuoDote Autoinjector: 2.1mg atropine, 600mg pralidoxime in one autoinjector
 
*DuoDote Autoinjector: 2.1mg atropine, 600mg pralidoxime in one autoinjector
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*Prophylaxis in the military, high risk setting with [[pyridostigmine]]
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**Reversibly bind acetylcholinesterase before exposure to nerve agents
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**[[Pyridostigmine]] 30 mg PO q8<ref>Dunn MA, Sidell FR. Progress in medical defense against nerve agents. JAMA. 1989;262:649–652.</ref>
  
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==Differential Diagnosis==
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{{MCI types}}
  
== Pediatric considerations ==
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==Management==
*Higher metabolic rate and faster basal respiratory rate, causing more rapid and larger exposures
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*Depends on specific agent used
*Skin is thinner and more permeable
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*Regardless of agent, Decontamination and ABCs are of primary importance
*Agents heavier than air have increased concentrations closer to the ground exposing children > adults
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**Use appropriate personal protective equipment (PPE)
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**Decontamination (should take place pre-hospital or otherwise prior to entering the ED)
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***Remove all patient clothing
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***Brush off dry agent (e.g. powders), copiously irrigate skin of any liquid contaminant
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==See Also==
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*[[Toxicology (Main)]]
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*[[Weapon of mass destruction]]
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*[[Hazmat exposure]]
  
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==References==
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<references/>
  
== References ==
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[[Category:Toxicology]]
#’’Basic Disaster Life Support V.3.0 Course Manual.’’ N.p.: American Medical Association, 2012. Print.
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[[Category:EMS]]
#’’Campbell, John E. Tactical Medicine Essentials.’’ Sudbury, MA: Jones & Bartlett Learning, 2012. Print
 
#Schultz, Carl, and Kristi Koenig. “Weapons of Mass Destruction.” ‘’Rosen's Emergency Medicine Concepts and Clinical Practice.’’ By John A. Marx, Robert S. Hockberger, Ron M. Walls, James Adams, and Peter Rosen. 8th ed. Philadelphia: Mosby/Elsevier, 2013. N. pag. Print.
 
#http://www.ncbi.nlm.nih.gov/pubmed/15094583
 

Latest revision as of 18:20, 14 May 2018

Background

  • Can be released via unintended means such as a spill from a damaged railroad tank car or industrial explosion as well as by intentional means as chemical weapons.

Pediatric considerations

  • Higher metabolic rate and faster basal respiratory rate, causing more rapid and larger exposures
  • Skin is thinner and more permeable
  • Agents heavier than air have increased concentrations closer to the ground exposing children > adults

Types

Chemical weapons

Cyanide Agents (CN)

  • AKA Hydrocyanic acid, Formonitrile, Prussic acid
  • Mimics carbon monoxide poisoning
  • Smell of bitter almonds but not all people can smell cyanide
  • Absorbed through skin, inhaled or ingested
  • Can affect individuals near fire with synthetic materials or plastics
  • Can penetrate rubber and barrier fabrics

Pathophysiology

  • Cyanide inhibits cytochrome oxidase on mitochondria
  • Cells unable to use oxygen in bloodstream
  • Cellular asphyxiation

Symptoms

  • Symptoms can be delayed up to 60 minutes
  • Symptoms dependent on concentration, form of cyanide, and route of exposure
  • CNS and cardiovascular system most susceptible
  • Initially hypertension and tachycardia progressing to bradycardia, hypotension, and arrhythmias late
  • Anxiety, dizziness, headache, apnea, seizures, and coma

Management

  • 100% oxygen and antidote therapy
  • Sodium nitrite (IV) or amyl nitrite (inhaled) to displace cyanide from cytochrome oxidase
  • Sodium thiosulfate: For conversion of cyanide to excretable thiosulfate
  • Repeat sodium nitrite and sodium thiosulfate in 30min at half initial dose if needed
  • Hydroxocobalamin (Vit B12a): makes CN water soluble and non-toxic
  • Cyanide Antidote Kit: Amyl nitrite pearls, sodium nitrite (IV), sodium thiosulfate (IV)
  • Cyanokit: Less toxic than cyanide antidote kit and shown effective in cardiac arrest

Nerve Agents

  • Acetylcholinesterase inhibitors
  • Includes household and commercial pesticides (diazinon and parathion)
  • G-series (sarin, tabun, soman) and V-series (VX)
    • G-series are volatile non-persistent agents that evaporate quickly
    • V-series high viscosity with oily consistency
  • Rapidly absorbed through skin, symptoms generally develop within 1 hour
  • Vapors are heavier than air and tend to sink into low places
  • Sarin used in Tokyo subway attack in 1995; 5,000 sought medical attention with 12 deaths.

Pathophysiology

  • Inhibits acetylcholinesterase → excess acetylcholine at both nicotinic and muscarinic receptors

Symptoms

  • DUMBELLS
    • D-Diarrhea, U-Urination, M-Miosis, B-Bronchorrhea/Bradycardia, E-Emesis, L-Lacrimation, S-Salivation/Seizures
  • Cholinergic toxidrome Toxidromes

Management

  • Nerve agents prolong succinylcholine's paralytic effect
  • Atropine for bronchorrhea and bronchoconstriction
    • Start at 2-6mg, double the dose q5-30min until control of secretions (no max dose)
  • Pralidoxime to restore function of acetylcholinesterase (given over approximately 30 minutes; rapid infusion can cause hypertension)
    • Give as soon as possible - must be given before "aging" occurs to be effective
  • Benzodiazepines for seizures (standard AEDs may be ineffective)
  • Mark 1 Nerve Agent antidote Kit (NAAK): 2 autoinjectors:
    • 2mg atropine
    • 600mg pralidoxime
  • DuoDote Autoinjector: 2.1mg atropine, 600mg pralidoxime in one autoinjector
  • Prophylaxis in the military, high risk setting with pyridostigmine
    • Reversibly bind acetylcholinesterase before exposure to nerve agents
    • Pyridostigmine 30 mg PO q8[1]

Differential Diagnosis

Mass casualty incident

Management

  • Depends on specific agent used
  • Regardless of agent, Decontamination and ABCs are of primary importance
    • Use appropriate personal protective equipment (PPE)
    • Decontamination (should take place pre-hospital or otherwise prior to entering the ED)
      • Remove all patient clothing
      • Brush off dry agent (e.g. powders), copiously irrigate skin of any liquid contaminant

See Also

References

  1. Dunn MA, Sidell FR. Progress in medical defense against nerve agents. JAMA. 1989;262:649–652.