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Chemical Terrorism Amita Shroff, MD June 10, 2010.

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Presentation on theme: "Chemical Terrorism Amita Shroff, MD June 10, 2010."— Presentation transcript:

1 Chemical Terrorism Amita Shroff, MD June 10, 2010

2 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

3 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

4 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

5 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

6 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

7 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

8 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)

9 1995: Nerve gas attack on Tokyo subway

10 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.

11 1995: Nerve gas attack on Tokyo subway Master Shoko Asahara (Cult Leader)

12 Chemical Terrorism - Effects Toxic effects: Topical injury Skin Eyes Mucous membranes of respiratory tract Systemic absorption Dermal Respiratory

13 Chemical Terrorism - Treatment General treatment of contaminated victims: Triage Emergent resuscitation Decontamination if needed Airway / cardiopulmonary support Emergent antidotal therapy

14 Decontamination

15 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

16 Chemical Terrorism - Decontamination Vapor exposure: clothing removal and hair- washing (sufficient) Liquid dermal exposure: thorough decontamination necessary Ocular exposure: copious irrigation

17 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

18 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

19 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

20 Chemical Terrorism - Agents Nerve agents Vesicants Pulmonary agents (irritant gases) Riot control agents Incapacitating agents Cyanide

21 Nerve Agents Highly toxic Organophosphate insecticides (signs and symptoms) Powerful inhibitors of acetylcholinesterase (AChE) Acetylcholine accumulation → abnormal neurotransmission

22 Nerve Agents AchE inhibited by nerve agent →Acetylcholine accumulation → Abnl neurotransmission Breakdown of Acetylcholine Acetylcholine accumulation

23 Nerve Agents – Clinical Sx’s CentralAltered 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

24 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

25 Nerve Agents Onset and type of symptoms depends: Concentration Route of exposure Vital sign abnormalities: Sympathetic ganglia Parasympathetic ganglia

26 Nerve Agents - Exposure Low doses: Miosis Cojunctival injection Pain Rhinorrhea High doses: Respiratory effects Severe exposure: Neurologic findings Death: Respiratory depression and apnea

27 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

28 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

29 Nerve Agents - Examples AgentOdor Sarin (most volatile)Odorless Venom X [VX] (most potent / persistent) Odorless TabunFruity SomanFruity/Camphorous 1995: Sarin episode in Tokyo

30 Nerve Agents - Management Self protection / PPE (contamination HIGH) Agents readily absorbed Patient decontamination: Warm water / soap ? Diluted bleach solution (adults)

31 Nerve Agents - Management Restoring ventilation and oxygenation Aggressive use of antidotes Cardiac monitoring: dysrhythmias (torsades) Benzodiazepines – neuroprotective Close observation

32 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)

33 Nerve Agents - Antidote AtropineReverses 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

34 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

35 Nerve Agents - Aging Aging: permanent inhibition of AChE activity (irreversible covalent binding) Need early 2-PAM therapy prior to aging

36 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

37 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)

38 Vesicants - Sulfur Mustard (SM)

39 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

40 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)

41 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)

42 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)

43 Vesicants – Lewisite (L)

44 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

45 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

46 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

47 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

48 Vesicants – Phosgene Oxime (CX) Ocular findings similar to lewisite Pulmonary edema is common and may see bronchiolitis

49 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

50 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

51 Vesicants - Treatments No antidote Aggressive airway, fluid, electrolyte and pain management ? GCSF - mustard induced leukopenia Infection prevention with antibiotics Burn center referral

52 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)

53 Pulmonary Agents (Irritant Gases) Phosgene (CG, carbonyl chloride, D- Stoff, or green cross) Chlorine Nitrogen oxides Ammonia

54 Pulmonary Agent - Phosgene

55 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

56 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)

57 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

58 Pulmonary Agents - Phosgene Management: Steroids: ?severe bronchospasm Anti-inflammatory agents (NAC/ibuprofen): ? pulmonary edema 24- hour observation for all asymptomatic patients

59 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

60 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

61 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)

62 Pulmonary Agents - Chlorine Management: Supportive care Humidified oxygen Bronchodilators ? Nebulized sodium bicarbonate (3.75%) solution Skin decontamination

63 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

64 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)

65 Pulmonary Agents - Ammonia Fertilizer and industrial chemical Highly water soluble Colorless, alkaline, corrosive gas Rapidly reacts with water to form ammonium hydroxide Pungent odor

66 Pulmonary Agents - Ammonia Immediate eye, mucous membrane and throat irritation Lower airway involvement: Bronchospasm Pulmonary edema Reactive airway disease

67 Pulmonary Agents - Ammonia Treatment Supportive Humidified oxygen and bronchodilators Ocular irrigation → evaluation for corneal burns

68 Riot Control Agents

69 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

70 Riot Control Agents CS (0-chlorobenzylidene malonitrile) CN (1-chloroacetophenone) “mace” OC (capsaicin) “pepper spray”

71 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

72 Riot Control Agents Management Removal from exposure Copious ocular irrigation Skin decontamination

73 Incapacitating Agents - Military Military incapacitating agents: physiologic or mental effects Usually not lethal Recovery: several hours to days Anticholinergic deliriants (QNB, BZ)

74 Incapacitating Agents Signs and symptoms (Anticholinergic): Delirium Hallucinations Mydriasis Tachycardia Ileus Dry mucous membranes Absent axillary sweat Urinary retention Hyperthermia

75 Incapacitating Agents Treatment: Supportive care Benzodiazepines to prevent: Hyperthermia Rhabdomyolysis Physostigmine: Refractory seizures Profound tachycardia

76 Incapacitating Agents Other incapacitation agents: (besides military agents) Stimulants Potent opioids (carfentanyl, aerosol fentanyl) Hallucinogens (LSD, Cannabinoids) Vomiting Agents

77 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

78 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

79 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

80 Mild exposures: Tachypnea and hyperpnea Tachycardia Flushing Dizziness and headaches Diaphoresis Nausea and vomiting Serious exposures: Seizures, coma and apnea Cardiac arrest Cyanide

81 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

82 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

83 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 [ ]

84 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

85 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

86 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

87 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

88 New antidote under investigation: Hydroxocobalamin (vitamin B12a) Cyanide couples with cobalt → cyanocobalamin (nontoxic) No hypotensive side effects (Na nitrite) Pediatric data lacking

89 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

90 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

91 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

92 Chemical Terrorism


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