Chemical Weapon Exposures

1. Chemical Weapon Exposures Management in the ED Suj Sivaraman R3 Emergency Medicine McGill University

2. October 23, 2002 50 Chechen rebels, storm Moscow’s House of Culture Theatre during a performance of Nord-Ost, taking 700 hostages. The rebels demand Russian withdrawal from Chechnya, and threaten to kill the hostages if demands are not met. TV footage from inside the shows that the rebels have explosives strapped to their bodies as well as throughout the theatre

3. October 26, 2002 After three days of fruitless negotiations an unknown gas, meant to incapacitate the rebels, is released in the theatre. Most of the rebels and 116 hostages die. What kind of gas was released? …

4. Chemical Weapon “A chemical substance which is intended for use in military operations to kill, seriously injure or incapacitate people because of it’s physiologic effects” NATO. Handbook on medical aspects of NBC defensive operations (1996)

5. Overview General Management Principles Nerve Agents Pulmonary Agents Vesicants Incapacitating Agents

6. Pre-Hospital Care Managing Hazardous Material Incidents. Agency for Toxic Substances and Disease Registry, Center for Disease Control, 2001

7. Decontamination Zones

8. Hot Zone • Respiratory Protection: Pressure-demand, self-containedbreathing apparatus (SCBA) should be used in all responsesituations. • Skin Protection: Chemical-protective clothing should be wornwhen local and systemic effects are unknown. • Basic ABCs HAZMAT Suit Santa Clara Ca, Fire Dept.

9. Warm Zone (decontamination) • Victims exposed only to gas or vapours who have no skin or eyeirritation may be transferred immediately to the Support Zone. • All others undergo basic decontamination Emergency Response Decon Unit Union County, NJ

10. Decontamination • Patients who are able and cooperative may assist with theirown decontamination. • Remove and double-bag contaminatedclothing and personal belongings. Casualty Care research Center, Uniformed Services University, Bethesda, MD

11. Flush exposed or irritated skin and hair with plain water,mild soap, for 3 to5 minutes. • Flush exposed or irritated eyes with plain water or saline for atleast 5 minutes. • Remove contact lenses if present and easilyremovable without additional trauma to the eye. • In cases of ingestion, do not induceemesis. • Administer4 to 8ounces of water to dilute stomach contents if the patient is alert. HAZMAT Shower Emergency Medical Products Inc.

12. Cold (support) zone • Be certain that victims have been decontaminated properly • Victims who have undergonedecontamination or who have been exposed only to gas orvapour and who have no evidence of skin or eye irritationgenerally pose no serious risks of secondary contamination. • Personnel require no specializedprotective gear.

13. ED Management Principles Emergency Room Procedures in Chemical HazardEmergencies: CDC National Centre for Environmental Health, November 2002

14. Preparation • 1.  Try to determine agent identity. • 2.  Break out personal protection equipment, decon supplies, antidotes, etc. • 3.  Don personal protective equipment, set up hotline. • 4.  Clear and secure all areas which could become contaminated. • 5.  Prepare to or secure hospital entrances and grounds. • 6.  Notify local emergency management authorities if needed. • 7. If an organophosphate is involved, notify hospital pharmacy that large amounts of atropine and 2-PAM may be needed.

15. When the victim arrives … • 8. Does chemical hazard exist? • Known release/exposure (including late notification) • Liquid on victim's skin or clothing • Symptoms in victim, EMTs, others • Odour (H, L, phosgene, chlorine)          • 9. Hold victim outside until preparations are completed • 10. If patient is grossly contaminated OR if there is any suspicion of contamination, decontaminate patient before entry into building in isolated decontamination area

16. General measures • ABCs • Skin Exposure • If chemical burns are present, treat as thermal burns. • Eye Exposure • Ensure that adequate eye irrigation has been completed. • Testvisual acuity. • Slit lamp • Fluorescein stain. • Ophthalmology for patients who have severe corneal injuries.

17. Ingestion Exposure • Do not induce emesis. If alert administer activated charcoal. • If a corrosive material is suspected, administer 4 to 8 ounces ofwater do not giveactivated charcoal. Considerendoscopy • If a large dose has been ingested and the patient’s condition isevaluated within 30 minutes after ingestion, consider gastriclavage. • Inhalation Exposure • Supplemental oxygen • Bronchodilators if bronchospastic

18. Investigations • CBC, glucose, and electrolytes, renal, LFTs • ECG,cardiac monitoring • Chest radiography, pulse oximetry, ABG if inhalation exposure

19. Nerve Agents

20. Nerve Agents • Organophosphate compounds discovered in 1936 by Gerhard Schrader (IG Farben, Germany) while researching organophosphate pesticides • Never used in WWII, but after the war the Soviets, U.K., and U.S. began pursuing nerve agent research • 1980-88: During Iran-Iraq War, Iraq thought to have used nerve agents against Iran and Iraqi Kurds • March 1995: Japanese Aum Shinrykio cult used Sarin gas in Tokyo underground resulting in 5,500 casualties and killing 12

21. The G-series: Taban (GA) Sarin (GB) Soman (GD) The V-series: VX Nerve Agents • At room temp amber to colourless liquid state • Weak fruity (G) to fishy (VX) smell • G-series more volatile (sarin) than V-series • V-series more toxic

22. Mechanism of action Normal Neurotransmission

23. Mechanism of action Nerve agent effects

24. Signs and Symptoms AChE inhibition Cholinergic hyperstimulation Cholinergic toxidrome

25. Signs and Symptoms Eyes Miosis, eye pain, headache,injection, lacrimation Nose Vapour Exposure Rhinorrhea Seconds to minutes after exposure Oral Salivation Airways Bronchoconstriction, bronchorrhea

26. Signs and Symptoms Skin Localized sweating, fasciculations Liquid Exposure GI 10 minutes to 18 hours after exposure Diarrhea, nausea, vomiting Cardiac Brady, heart block

27. Signs and Symptoms CNS Severe exposure LOC, seizures, fasciculations Weakness, paralysis Previously described vapour and liquid effects plus … Resp Apnea GI/GU Bowel/bladder incontinence Seconds to minutes (vapour) Minutes to hours (liquid)

28. General management Specific antidotes Atropine Pralidoxime Chloride Diazepam Pre -treatment Management

29. Antidotes Atropine • 2 mg IV/IM q5- 15 min to effect • Muscarinic action • -smooth muscle • -glandular epithelium • -cardiac muscle

30. Antidotes Pralidoxime Chloride • 1 g IV over 15-30 min q 1 hr to effect • Nicotinic action • -skeletal muscle • Aging: Irreversible binding of nerve agent to AChE Soman: 2 minutes VX: 48 hours

31. Antidotes Diazepam • Seizure prophylaxis and treatment • 10 mg IV at onset of severe symptoms regardless of seizure activity

32. MARK I kit • Atropine 2 mg • Pralidoxime Cl 600 mg • Issued to military personnel

33. Initial dosing • Mild Sx (i.e. miosis and mild rhinorrhea) • 1 MARK I kit or equivalent OR • No Rx and observe for 1 hr if vapour exposure and mild symptoms • Moderate Sx • 1-2 MARK I kits or equivalent • Severe Sx • 3 MARK I kits or equivalent • Diazepam auto-injector or equivalent

34. Pre-Treatment Pyridostigmine • In animal studies shown to be effective, particularly against rapidly aging nerve agents (e.g. Soman) • No human evidence • FDA waiver for use by military during Gulf War but not currently approved for civilian use in Canada or U.S. • 30 mg po q8h • ? association with Gulf War Syndrome

35. Mechanism of action

36. Additional tests • RBC–AChE • Decreased in nerve agent poisonings (cholinesterase inhibition) • Systemic effects correlate with decrease of 20-25% in levels • Significant variability so treat the patient not the value • Useful for documenting exposure and monitoring recovery

37. Disposition • Patients exposed to nerve agent vapour who have only miosisand/or mild rhinorrhea when they reach the medical facility donot need to be admitted. • All other patients who have hadexposure to nerve agent should be hospitalized for observation.

38. Pulmonary Agents

39. Chlorine • First used as a chemical weapon in 1915 by Germany at Ypres, Belgium • Released 160 tons of Cl2 when wind was favourable, resulting in 5,000 dead and 10,000 wounded Bruce Bairnsfather (1888-1959)

40. Chlorine • Largest cause of major toxic release incidents worldwide • Between 1988-1992, 27,788 exposures to chlorine in US • Attractive as chemical weapon because of ease of availability

41. Chlorine • Description • At room temperature, yellow-green gas with apungent irritating odour. • Only slightly soluble in water, but on contact withmoisture it forms hypochlorous acid (HClO) and hydrochloricacid (HCl). HClO readily decomposes, formingoxygen free radicals. • Not explosive but reacts or forms explosive compounds with other substances (e.g. NH3, acetylene) • Routes of exposure • Inhalation • Skin/Eye contact

42. Pathophysiology 2 HCl (hydrochoric acid) + [O-] Cl2 + H2O HCl + HOCl (hypochlorous acid) Cellular injury via oxidation of functional groups in cell components HCl+ [O-]

43. Clinical effects Skin - Irritation, frostbite Eyes - Irritation, ocular burns Upper airway Chlorine - Nasal,pharynx, tracheal inflammation - Laryngospasm Lower airway - Inflammation and loss of pulmonary capillary integrity Pulmonary edema, hypoxia May occur minutes to 24 hours after exposure

44. Pre-hospital management • General measures • Low risk of secondary contamination from victims who have been exposed to gas, however liquid soaked skin or clothing may cause off-gassing • No need for decontamination if no skin or eye irritation

45. ED Management • Decontamination if not done previously • Resp: • Fluid restriction in patients with pulmonary edema/ ARDS • Beta agonists • If intubation needed perform under direct visualization (avoid blind techniques) • Burns: • Treat as thermal

46. Disposition • 6 to 24 hours observation • Asymptomatic patients or minor Sx (eyes, cough) may be released with close follow-up and advice to return if respiratory symptoms recur • Hospitalization if: • Symptoms persist after 6 hours. • Patient was severely exposed. • Child was exposed. • Patient has a history of underlying respiratory or cardiovascular disease.

47. Phosgene • First synthesized in 1812 • First used in 1915 by Germany at Ypres, Belgium • Attractive as chemical weapon because of ease of availability British soldiers at Somme, 1915

48. Phosgene • Description • At room temperature, colourless, nonflammable gas with a suffocating odour like new mown hay. • Odour threshold is five times higher thanpermissible exposure level • i.e. Odour provides insufficient warning of toxic levels • Prolonged severe exposure more likely than with Cl2 • At < 8 degrees C, colorless fuming liquid • Combustion product of manyhousehold products that contain volatile organochlorine compounds. (household solvents, paint removers) • Routes of exposure • Inhalation • Skin/Eye contact

49. Pathophysiology Directly reacts with amine, sulfhydryl, and alcohol groups in cells Hydrolyzes to HCL Phosgene Stimulates LT synthesis Combines with and depletes glutathione stores

50. Clinical effects Skin - Irritation, frostbite Eyes - Irritation, ocular burns Upper airway Phosgene - Nasal,pharynx, tracheal inflammation - Laryngospasm May occur minutes to 72 hours after exposure Lower airway - Inflammation and loss of pulmonary capillary integrity Pulmonary edema, hypoxia Precipitated by exertion