chemical terrorism
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Chemical Terrorism
Amita Shroff, MD
June 10, 2010
Chemical Terrorism - Background
Dates back many years First use: World War I Modern use of chemical terrorism
Cyanide: Chicago, Illinois – 1984 Sarin :Tokyo, Japan-1995 Carbamate Insecticide: Fresno, California – 1999 Nicotine: Grand Rapids, Michigan – 2002
QUESTION 1
Reports of an unknown Chemical Substance have been released during an outdoor family concert. Participants arrive to the ED with C/O copious oral/nasal secretions, labored breathing, and muscle fasciculation. What othre PE finding should you expect? A. Dry Skin B. Miosis C. Normal Mental Status D. Constipation E. Hypotension
QUESTION 2
Group of boy scouts present to ED. They were hiking and encountered an oily, dark brown liquid with a mustard odor. They had erythema and blisters of the leg. Some have eye irritation and SOB. Which would be helpful in treating these patients A. Supportive care only B. Atropine and 2-PAM C. Sodium Nitrite D. Midazolam E. Ciprofloxacin
QUESTION 3
Terrorist release a chemical in a school with an odor of newly mown hay. Few hrs later, students start complaining of ocular and nasal irritation followed by DIB and cough. Those seen in ED have CXR with pulmonary edema. Most likely chemical of use is: A. Phosgene B. Sarin C. Cyanide D. Lewisite E.Mase
QUESTION 4
A foreign diplomat’s 12 yr son presents to the ED with C/O headache and nausea. He soon develops severe dyspnea and cyanosis. As he is moved into the trauma bay, he starts to seize. You suspect he has been exposed to: A. Soman B. Cyanide C. Sulfur Mustard D. Phosgene E. 1-Chloroacetophenone
QUESTION 5
Terrorist have released a chemical in a school bus full of children across the street from the hospital. In preparation for decon, HOSPITAL PERSONNEL should don what type of PPE? A. Self –containing breathing apparatus (SCBA), fully
encapsulating chemical protective suit B. SCBA, chemical resistant clothing C. Full face air purifying respirator, chemical resistant clothing D. Coveralls and safety shoes/boots E. Gown and gloves
Chemical Terrorism - Background
Apocalyptic groups Aum Shinrikyo, Japan (1995) Restoration of the 10 Commandments, Uganda
(2000) Political groups
Hamas/Hizbollah, Middle East (2000-present) Western Group of Federal Forces, Chechnya
(2000) Revolutionary Armed Forces of Colombia (2001) Al Qa’ida (2001-present)
1995: Nerve gas attack on Tokyo subway
1995: Nerve gas attack on Tokyo subway
Aum Shinrikyo converge at Kasumigaseki subway station
Release lethal sarin gas Terrorists take sarin antidote and escaped Commuters, blinded and gasping for air, rushed to the
exits Twelve people died, over 5,000 were treated in hospitals
(many comatose state) Japanese police raided Aum Shinrikyo headquarters Arrested hundreds of members, including: Master Shoko
Asahara.
1995: Nerve gas attack on Tokyo subway
Master Shoko Asahara (Cult Leader)
Chemical Terrorism - Effects
Toxic effects: Topical injury
Skin Eyes Mucous membranes of respiratory tract
Systemic absorption Dermal Respiratory
Chemical Terrorism - Treatment
General treatment of contaminated victims: Triage Emergent resuscitation Decontamination if needed Airway / cardiopulmonary support Emergent antidotal therapy
Decontamination
Chemical Terrorism - Decontamination
Decontamination Appropriate level PPE required (hot zone) Field / Special designated area outside the ED
Simple disrobement: removes ≥ 80-90% Irrigation with soap and tepid water 0.5% sodium hypochlorite (adults) Pediatrics Considerations:
Warmer water (>37.8C) Low pressure systems
Chemical Terrorism - Decontamination
Vapor exposure: clothing removal and hair-washing (sufficient)
Liquid dermal exposure: thorough decontamination necessary
Ocular exposure: copious irrigation
Chemical Terrorism - PPE Level A
Highest level of protection Highly contaminated area (hot zone) Self contained breathing apparatus (SCBA) Fully encapsulated suit
Slightly pressurized Chemical resistant gloves
Hot, bulky and clumsy
Chemical Terrorism - PPE
Level B Lower level than A Respiratory protection, less skin protection Outside hot zone / partially decontaminated pts SCBA Non-pressurized suit Butyl rubber gloves/boots Hot, bulky and clumsy
Chemical Terrorism - PPE
Level C Lower than Levels A & B Contaminants have been identified (low [ ]) Air-purifying respirator: sufficient Some protection against skin contact Equipment: easier to work with
Chemical Terrorism - Agents
Nerve agents Vesicants Pulmonary agents (irritant gases) Riot control agents Incapacitating agents Cyanide
Nerve Agents
Highly toxic Organophosphate insecticides (signs and
symptoms) Powerful inhibitors of acetylcholinesterase
(AChE) Acetylcholine accumulation → abnormal
neurotransmission
Nerve Agents
AchE inhibited by nerve agent →Acetylcholine accumulation → Abnl neurotransmission
Breakdown of Acetylcholine
Acetylcholine accumulation
Nerve Agents – Clinical Sx’s
Central Altered mental status → lethargy → coma, ataxia, convulsions and respiratory depression
Nicotinic
Neuromuscular junction
Sympathetic ganglion
Muscle fasciculation and twitching → weakness → flaccid paralysis
Tachycardia, hypertension and metabolic abnormalities (↑ glucose, ↓ K+, and acidosis)
Cholinergic Syndrome
Nerve Agents – Clinical Sx’s
Muscarinic (parasympathetic)
Smooth muscle
Exocrine gland
Ocular: miosis, visual blurring, and lacrimation
Respiratory: rhinorrhea, bronchospasm and ↑ bronchial secretions (cough, wheezing, and dyspnea)
CV: bradycardia, hypotension and AV block
Dermal: flushing + sweating
GI: salivation, N/V, diarrhea and abdominal cramps
GU: frequency, urgency and incontinence
Cholinergic Syndrome
Nerve Agents
Onset and type of symptoms depends: Concentration Route of exposure
Vital sign abnormalities: Sympathetic ganglia Parasympathetic ganglia
Nerve Agents - Exposure
Low doses: Miosis Cojunctival injection Pain Rhinorrhea
High doses: Respiratory effects
Severe exposure: Neurologic findings
Death: Respiratory depression and apnea
Nerve Agents - Exposure
Vapor exposure (triad): Ocular Nasal Respiratory
Dermal exposure (progression): Localized sweating and fasciculations → nausea,
vomiting , diarrhea and fatigue Severe exposure → respiratory and neurologic
symptoms
Nerve Agents
Children: Less likely: miosis and peripheral
parasympathetic effects More likely: CNS depression, hypotonia,
weakness and seizures Animal studies: children only need 10-33% of
lethal dose on an equivalent mg/kg basis
Nerve Agents - Examples
Agent Odor
Sarin (most volatile) Odorless
Venom X [VX] (most potent / persistent)
Odorless
Tabun Fruity
Soman Fruity/Camphorous
1995: Sarin episode in Tokyo
Nerve Agents - Management
Self protection / PPE (contamination HIGH) Agents readily absorbed Patient decontamination:
Warm water / soap ? Diluted bleach solution (adults)
Nerve Agents - Management
Restoring ventilation and oxygenation Aggressive use of antidotes Cardiac monitoring: dysrhythmias (torsades) Benzodiazepines – neuroprotective Close observation
Nerve Agents - Antidote
Atropine .05 -.10 mg/kg IV or IM Min 0.1mg, max 5mg Repeat Q 2-5 min for secretions Pralidoxime (2-PAM) 25-50 mg/kg IV or IM Max 1 gm Repeat Q 30-60 min (persistent
weakness)
Nerve Agents - Antidote
Atropine •Reverses parasympathetic findings
•Blocks muscarinic receptors
• No effect on motor endplates
• Lacrimation
• Salivation
• Vomiting+diarrhea
• Urination
• Bronchorrhea
• Bronchospasm
• Bradycardia
2-PAM • Reactivates AChE (nucleophilic attack on agent)
• Reverses nicotinic, muscarinic and CNS effects
• Weakness
• Fasciculations
Nerve Agents - Antidote
Military Mark I autoinjector kits: 2 mg of atropine 600 mg of 2-PAM
Immediate IM use in the field Stockpile (civilian first responder) Not approved in pediatrics Pediatric auto-injector recently approved
Nerve Agents - Aging
Aging: permanent inhibition of AChE activity (irreversible covalent binding)
Need early 2-PAM therapy prior to aging
Nerve Agents
Difference from organophosphate pesticide poisoning: Continuous infusions usually not necessary
(atropine or 2-PAM) Delayed peripheral neuropathies not seen
Life support + antidotal therapy →prognosis good
Potential advances in treatment: More effective oximes: HI-6 Fetal bovine serum acetylcholinesterase
Vesicants
Vesicants: agents that produce blistering Severe dermal manifestation in children Released as an aerosol 3 primary vesicants:
Sulfur mustard (H and HD)
Lewisite (L)
Phosgene oxime (CX)
Vesicants - Sulfur Mustard (SM)
Vesicants - Sulfur Mustard (SM)
Most viable threat ( ≥ 12 countries have SM in their arsenals)
Easiest to synthesize WWI: more casualties then all chemical
agents combined 1980’s: >45,000 casualties in Iran-Iraq war
Alkylating agent, highly reactive and electrophilic
Oily liquid with odor of garlic, mustard or horseradish
LD 50 is approximately 1.5 teaspoons Clinical effects: dose dependent Symptoms usually delayed for 4-8 hours
Vesicants - Sulfur Mustard (SM)
Symptoms: Low doses: vessication Higher doses: vessication and systemic toxicity
Skin: erythema → blister formation Ocular: edema, conjunctival injection, corneal
ulceration Respiratory: cough/hoarseness, tachypnea,
bronchospasm, pulmonary edema
Vesicants - Sulfur Mustard (SM)
Systemic absorption involves: Hematopoietic GI CNS
Expected mortality = 3% for those reaching medical facility
Children: More rapid onset Worse dermal reactions
Vesicants - Sulfur Mustard (SM)
Vesicants – Lewisite (L)
Vesicants – Lewisite (L)
Potency similar to sulfur mustard Oily, colorless liquid with geranium odor Released by Japan during wartime Known stockpiles in Russia Active ingredient: trivalent arsenic Inhibits various enzymes and glycolysis Skin irritation and pain present within 15-30
minutes, blister formation by 2 hours
Vesicants – Lewisite (L)
Skin lesions: less erythema more tissue destruction then sulfur mustard
lesions Ocular pain and irritation within minutes Central airway inflammation and upper
airway irritation Edema in severe cases Hypotension and hemolytic anemia rare
Vesicants – Lewisite (L)
BAL (British anti-Lewisite) or dimercaprol: Arsenic chelator Prevents / decreases severity of skin and eye
lesions if applied within minutes of exposure Topical form not widely available IM BAL reduces mortality from systemic effects of
lewisite
Vesicants – Phosgene Oxime (CX)
Extensive tissue damage Instantaneous pain and irritation of the skin,
eye and airways Skin → blanches → turns gray → urticarial,
erythematous and edematous → necrosis / eschar formation
True vesicle formation DOES NOT occur
Vesicants – Phosgene Oxime (CX)
Ocular findings similar to lewisite Pulmonary edema is common and may see
bronchiolitis
Vesicants Vesicant toxicity: clinical diagnosis Urinary thiodiglycol metabolites will confirm
sulfur mustard exposure Death most frequently occurs 5-10 days after
exposure (pulmonary insufficiency / infection) Long-term hospitalization expected
Vesicants - Treatments
PPE for healthcare workers Immediate decontamination (water and soap) Only water for phosgene oxime exposure Dilute hypochlorite solution (adults) – for
water insoluble mustards and lewisites
Vesicants - Treatments
No antidote Aggressive airway, fluid, electrolyte and pain
management ? GCSF - mustard induced leukopenia Infection prevention with antibiotics Burn center referral
Pulmonary Agents (Irritant Gases)
Pulmonary agents classified according to anatomical infliction
Affect central or peripheral pulmonary system Central: Upper airways (cough or stridor) Peripheral: lower airways (pulmonary edema)
Pulmonary Agents (Irritant Gases)
Phosgene (CG, carbonyl chloride, D-Stoff, or green cross)
Chlorine
Nitrogen oxides
Ammonia
Pulmonary Agent - Phosgene
Pulmonary Agents - Phosgene
Gas with a density 4X that of air Found in plastics, pharmaceutical and textile
industries When released:
forms a white cloud odor of newly mown hay
Water insoluble
Pulmonary Agents - Phosgene
Initially asymptomatic with perception of odor Mild exposure:
Eyes, nose, throat and upper airway irritation Major toxicity:
Acid burn to lower airways Diffuse capillary leak Pulmonary edema
Pulmonary edema: delay 4-6 hrs (as late as 24 hrs)
Pulmonary Agents – Phosgene
Management Primarily supportive care Decontamination: removal of victim to fresh air Respiratory:
Pulmonary secretions Bronchospasm Pulmonary edema
Aggressive treatment of secondary bacterial infections
Pulmonary Agents - Phosgene
Management: Steroids: ?severe bronchospasm Anti-inflammatory agents (NAC/ibuprofen): ?
pulmonary edema 24- hour observation for all asymptomatic patients
Pulmonary Agents - Phosgene
Poor prognosis: dyspnea or pulmonary edema within 4 hours
Patients usually survive if symptomatic after 6 hrs and ICU available
Recovery within 3-4 days
Pulmonary Agents - Chlorine Widely available Dense, green-yellow gas with pungent odor Intermediate water solubility → upper + lower
airways affected Early inflammatory injury
Formation of acids and oxidants upon contact with moist mucous membranes
Pulmonary Agents - Chlorine
Mild Exposure: Immediate ocular, nasal and upper airway
irritation Nausea and vomiting
Severe Exposure: (sx within 12-24 hrs) Coughing and hoarseness Pulmonary edema Permanent reactive airway disease (inhalation)
Pulmonary Agents - Chlorine
Management: Supportive care Humidified oxygen Bronchodilators ? Nebulized sodium bicarbonate (3.75%) solution Skin decontamination
Pulmonary Agents-Nitrogen Oxide
Silo gas: Product of fire combustion Industrial process Military blast weapons
Limited water solubility Lower airway toxicity
Nitrogen oxide converted to nitric acid → alveolar injury → pulmonary edema
Pulmonary Agents-Nitrogen Oxide
Triphasic illness: Dyspnea and flu-like symptoms Transient improvement Pulmonary edema with worsening dyspnea (24-
72 hrs) Other consequences:
Methemoglobinemia Bronchiolitis obliterans (late complication)
Pulmonary Agents - Ammonia
Fertilizer and industrial chemical Highly water soluble Colorless, alkaline, corrosive gas Rapidly reacts with water to form ammonium
hydroxide Pungent odor
Pulmonary Agents - Ammonia
Immediate eye, mucous membrane and throat irritation
Lower airway involvement: Bronchospasm Pulmonary edema Reactive airway disease
Pulmonary Agents - Ammonia
Treatment Supportive Humidified oxygen and bronchodilators Ocular irrigation → evaluation for corneal burns
Riot Control Agents
Riot Control Agents
Lacrimators or “tear gas” Significant disruption and panic in crowds Transient but intense noxious effects Symptoms resolve within a few hours Pulmonary edema with large exposure in
confined spaces
Riot Control Agents
CS (0-chlorobenzylidene malonitrile)
CN (1-chloroacetophenone) “mace”
OC (capsaicin) “pepper spray”
Riot Control Agents Symptoms
Immediate irritation of eye and respiratory tract Blepharospasm Lacrimation Coughing, sneezing and rhinorrhea Burning sensation: exposed skin and mucous
membranes Nausea, headaches and photophobia ↑ [ ], skin blistering / pulmonary involvement
Riot Control Agents
Management Removal from exposure Copious ocular irrigation Skin decontamination
Incapacitating Agents - Military
Military incapacitating agents: physiologic or mental effects
Usually not lethal Recovery: several hours to days Anticholinergic deliriants (QNB, BZ)
Incapacitating Agents Signs and symptoms (Anticholinergic):
Delirium Hallucinations Mydriasis Tachycardia Ileus Dry mucous membranes Absent axillary sweat Urinary retention Hyperthermia
Incapacitating Agents
Treatment: Supportive care Benzodiazepines to prevent:
Hyperthermia Rhabdomyolysis
Physostigmine: Refractory seizures Profound tachycardia
Incapacitating Agents Other incapacitation agents: (besides military
agents) Stimulants Potent opioids (carfentanyl, aerosol fentanyl) Hallucinogens (LSD, Cannabinoids) Vomiting Agents
Cyanide
Long term use as a toxin for sinister purposes Chemical terrorism agent: limited
volatility in open air low lethality compared to nerve gas
Devastating effects in a crowded, closed room
Cyanide
Toxicity: Interference with normal mitochondrial oxidation → lactic acidosis
High affinity for ferric iron (Fe3+) Brain and heart targeted because most
dependent on oxidative phosphorylation
Cyanide
Clinical presentation: route and dose of exposure
Inhalation of gas: LOC within seconds Oral exposure: symptoms from 30 min up to
several hours “Bitter almond” smell
Mild exposures: Tachypnea and hyperpnea Tachycardia Flushing Dizziness and headaches Diaphoresis Nausea and vomiting
Serious exposures: Seizures, coma and apnea Cardiac arrest
Cyanide
Cyanide
Laboratory findings: Cyanide levels (levels > 1.0 mg/L produce
acidosis) Large anion gap (lactic acidosis) Venous blood gas: diminished arterial-venous o2
(Ao2-Vo2) difference EKG changes
Management: Removal of victim to fresh air Removal of any wet clothing and skin decon Intensive supportive care
100% oxygen Mechanical ventilation Circulatory support (crystalloids and vasopressors) Correction of metabolic acidosis (IV NaHCO3) Benzodiazepines for seizure control
Antidotes: Sodium nitrite and sodium thiosulfate
Cyanide
Cyanide - Antidote Stage I – Sodium Nitrite:
Methemoglobin-forming agent (high affinity for cyanide)
Antidote should be infused slowly over 5-10 minutes
Nitrite induced hypotension Pediatric dosing based on weight and hgb [ ]
Cyanide
Stage I – Sodium Nitrite: Methemoglobin levels should be monitored Levels peak at 35-70 minutes
10-15% (therapeutic level) Levels of 20-30%: headaches and nausea Levels of 30-50%: weakness, dyspnea and
tachycardia Levels of 50-70%: dysrhythmias, CNS depression and
seizures Level of 70%: death
Cyanide
Stage I – Sodium Nitrite: Amyl nitrite perles: administered first Perles crushed in gauze and held near nose and
mouth for 30 seconds Produces a methemoglobin level of 3-7 % Once IV line established, sodium nitrite can be
administered Little utility in severely toxic patient
Cyanide
Stage II – Sodium thiosulfate: Provision of a sulfur donor Conversion of cyanide → thiocyanate
Less toxic Renally excreted
Treatment: Efficacious and benign Used alone for mild to moderate cases
Taylor Cyanide Antidote Kit:
• Amyl Nitrite (inhaled) + Sodium nitrite (IV): formation of methemoglobin which combines with cyanide (high affinity)
• Sodium thiosulfate (IV) – produces thiocyanate, excreted in urine
Cyanide
Cyanide
New antidote under investigation: Hydroxocobalamin (vitamin B12a)
Cyanide couples with cobalt → cyanocobalamin (nontoxic)
No hypotensive side effects (Na nitrite) Pediatric data lacking
Summary/Take Home Points
Decontamination Appropriate PPE Disrobing, Water/soap Peds considerations
Nerve Agents (Sarin) Acetylcholinesterase inhibitors → cholinergic
syndrome (SLUDGE) (3 B’s) NMJ: muscle fasciculation and twitching Respiratory/neurological symptoms Antidote: Atropine/ 2-PAM
Summary/Take Home Points
Vessicants Derm/ocular manifestations Severe: respiratory
Sulfur mustard: garlic/mustard odor Lewisite: geranium odor / antidote: BAL Phosgene oxime: no vesicle formation
Pulmonary agents Severe respiratory symptoms/pulmonary edema
Phosgene: newly mown hay smell
Summary/Take Home Points
Cyanide Lactate acidosis Bitter almond smell Seizures/coma Antidote: Sodium nitrite and sodium thiosulfate
Monitor methemoglobin levels
Other agents: Riot control agents Incapacitating agents
Chemical Terrorism
THANKS!!
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