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Chemical Weapon Exposures

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Handbook on medical aspects of NBC defensive operations (1996) Overview ... Chest radiography, pulse oximetry, ABG if inhalation exposure. Nerve Agents. Nerve Agents ... – PowerPoint PPT presentation

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Title: 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 Moscows 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 its
    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-contained breathing apparatus (SCBA) should
    be used in all response situations.
  • Skin Protection Chemical-protective clothing
    should be worn when 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 eye irritation 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 their own decontamination.
  • Remove and double-bag contaminated clothing 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 to 5 minutes.
  • Flush exposed or irritated eyes with plain water
    or saline for at least 5 minutes.
  • Remove contact lenses if present and easily
    removable without additional trauma to the eye.
  • In cases of ingestion, do not induce emesis.
  • Administer 4 to 8 ounces 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 undergone decontamination or who
    have been exposed only to gas or vapour and who
    have no evidence of skin or eye irritation
    generally pose no serious risks of secondary
    contamination.
  • Personnel require no specialized protective gear.

13
ED Management Principles
  • Emergency Room Procedures in Chemical Hazard
    Emergencies 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.
  • Test visual 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 of water do not give activated
    charcoal. Consider endoscopy
  • If a large dose has been ingested and the
    patients condition is evaluated within 30
    minutes after ingestion, consider gastric lavage.
  • 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
Nerve Agents
  • The V-series
  • VX
  • The G-series
  • Taban (GA)
  • Sarin (GB)
  • Soman (GD)
  • 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
Management
  • General management
  • Specific antidotes
  • Atropine
  • Pralidoxime Chloride
  • Diazepam
  • Pre -treatment

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
  • RBCAChE
  • 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 miosis and/or mild rhinorrhea when they
    reach the medical facility do not need to be
    admitted.
  • All other patients who have had exposure 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 a
    pungent irritating odour.
  • Only slightly soluble in water, but on contact
    with moisture it forms hypochlorous acid (HClO)
    and hydrochloric acid (HCl). HClO readily
    decomposes, forming oxygen 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 than
    permissible exposure level
  • i.e. Odour provides insufficient warning of toxic
    levels
  • Prolonged severe exposure more likely than with
    Cl2
  • At lt 8 degrees C, colorless fuming liquid
  • Combustion product of many household 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
51
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
  • Keep warm and quiet any activity subsequent to
    exposure may increase likelihood of death

52
ED Management
  • Decontamination if not done previously
  • Resp
  • Fluid restriction in patients with pulmonary
    edema/ ARDS
  • Beta agonists
  • High dose inhaled/IV steroids for severe
    inflammation or known severe exposure
  • PEEP
  • If intubation needed perform under direct
    visualization (avoid blind techniques)
  • Burns
  • Treat as thermal

53
  • Animal studies have shown some benefit with
  • N-Acetylcystine
  • LT antagonists (monteleukast, zafirleukast)
  • NSAIDs
  • Aminophylline

54
Disposition
  • All patients should be hospitalized for 48 hours
    for observation
  • Respiratory symptoms warrant ICU admission
  • Survival to 48 hours predicts likely recovery

55
Vesicants
56
Introduction
  • A group of chemical agents that burn and blister
    tissue with which they come into contact

Mustard gases
Lewisite
Sulfur mustard
Halogenated oximes
Phosgene Oxime
57
Mustard gases
  • A group of sulphur-, nitrogen-, and oxygen-based
    vesicant compounds with similar chemical and
    biological effects
  • First used by Germany at Ypres, Belgium in 1917

Gassed John Singer Sargent, 1918
58
  • Since then has been used extensively in numerous
    conflicts, including by Iraq in the 1980s
  • Stored at 7 sites in the U.S.

59
Sulfur Mustard
  • Description
  • Typically a yellow to brown oily substance with a
    slight garlic or mustard odor.
  • Individual odor threshold variability
  • Because of stable liquid form can be used coat
    (slime) surfaces
  • Routes of exposure
  • Inhalation
  • Skin/Eye contact
  • Ingestion

60
Pathophysiology
Alkylating effect leads to cross-linking and
degradation of DNA, protein, other molecules
Thus high turnover cell lines most affected
Mustard
Cholinergic stimulation
61
Clinical effects
  • Distinguished by relative lack of symptoms
    immediately after exposure
  • Variable latent period depending upon severity,
    route of exposure

62
Clinical effects
63
Delayed clinical effects
  • Leukopenia /- pancytopenia can occur 3-5 days
    post-exposure

64
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
  • Decontaminate all casualties!

Decontamination within 1 to 2 minutes is the
only way to prevent tissue damage
65
ED Management
  • Decontamination if not done previously
  • Shower, mild soap, Na hypochlorite solution
  • Resp
  • Beta agonists prn
  • If intubation needed perform under direct
    visualization (avoid blind techniques)
  • Skin
  • Blisters
  • Drain large, tense blisters
  • Blister fluid is not vesicant
  • Eythema
  • Topical analgesia

66
Additional tests
  • Urine thiodiglycol

67
Disposition
  • Observation for 12 hours
  • If asymptomatic or mild Sx can discharge with
    close follow-up

68
Lewisite
  • An arsenical vesicant, first synthesized in 1918
  • No confirmed use in warfare, although stockpiled
    by several nations

69
Lewisite
  • Description
  • Pure Lewisite is an oily, colourless liquid,
    while impure Lewisite is amber to black with
    odour of geraniums.
  • Routes of exposure
  • Inhalation
  • Skin/Eye contact
  • Ingestion

70
Pathophysiology
Exact mechanism of cell damage not known.
Inhibits enzymes with thiol groups (e.g. alcohol
dehydrogenase)
Lewisite
71
Clinical effects
  • Absorbed 10 times faster than mustards
  • Immediate clinical effects
  • More toxic than mustard
  • 14 ug of Lewisite can cause vesication

72
Clinical effects
Skin
  • Immediate pain
  • Erythema within 30 min
  • Vesication within a few hours

Eyes
Lewisite
- Irritation, severe ocular burns
GI
  • Severe abdo pain, n, hematochezia if ingested
  • Hepatic necrosis

73
Clinical effects
Upper airway
- Nasal,pharyngeal, tracheal inflammation -
Laryngospasm
Lower airway
Lewisite
- Inflammation and loss of pulmonary capillary
integrity Pulmonary edema, hypoxia
Cardiovascular
- Lewisite shock
74
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
  • Decontaminate all casualties

75
ED Management
  • Decontamination if not done previously
  • Shower, mild soap, Na hypochlorite solution
  • Resp
  • Beta agonists prn
  • If intubation needed perform under direct
    visualization (avoid blind techniques)
  • Skin
  • Blisters
  • Drain large, tense blisters
  • Blister fluid is not vesicant
  • Eythema
  • Topical analgesia

76
Antidotes
British Anti-Lewisite (BAL)
  • 3-5 mg/kg IM q4h x 4 doses
  • If severe exposure additional doses 2 mg/kg qd x
    3-4 d
  • No effect on the local lesions of the skin, eyes
  • Binds to arsenic moiety of L and
    prevents/reverses binding to enzymes
  • Severe toxicity thus use only if shock or severe
    pulmonary injury

77
  • Alkalization of the urine stabilizes the
    Dimercaprol-metal complex and has been proposed
    to protect the kidneys during chelation therapy.
  • If acute renal insufficiency develops,
    hemodialysis should be considered to remove the
    Dimercaprol-arsenic complex.

78
Additional tests
  • Urinary arsenic excretion

79
Disposition
  • Observation for 18-24 hours
  • If asymptomatic or mild Sx can discharge with
    close follow-up

80
Riot control agents
81
Riot control agents
  • Irritants
  • Hallucinogens (e.g. BZ)
  • Vomiting agents (e.g. Adamsite)

82
Irritants
  • CN (Chloroacetophenone,Mace)
  • First RCA
  • CS (orthochlorobenzalomalonitrile)
  • More effective and less toxic than CN
  • OC (oloresin capiscum, pepper spray)
  • Currently used by most law enforcement agencies

83
  • Description
  • All are solids and require dispersion device to
    aerosolize particles
  • Routes of exposure
  • Inhalation
  • Skin/Eye contact
  • Ingestion

84
Clinical effects
  • Prolonged conjunctivitis, corneal opacities and
    iritis associated with CN
  • CS exposure under high humidity and temperature
    can lead to skin vesication
  • Reports of permanent eye damage due to blast
    force from dispenser

85
  • Reports of death in literature
  • Associated with CN
  • Agent used in excess, and exposed refused to exit
    confined space
  • 1977 case report of 11 year old boy,
  • Exposed to OC, initially asymptomatic for four
    hours, then upper airway obstruction and
    respiratory arrest
  • 1994 review by International Association of
    Police Chiefs concluded that OC was not a factor
    in any reviewed deaths
  • 18 of 22 associated with positional asphyxia
    exacerbated by drugs or underlying disease

86
Clinical effects
Skin
  • Pain, burning, erythema

Eyes
  • Lacrimation, blepharospasm, injection

Irritants
ENT
  • Sneezing, salivation

Resp
  • Cough, broncorrhea, subjective sensation of
    breathing difficulty

87
Management
  • Decontamination
  • Wash exposed skin with mild soap, water /- 6 Na
    bicarbonate solution
  • Na hypochlorite solution can exacerbate skin
    lesions
  • Saline irrigation of exposed eyes
  • Supportive management
  • Effects generally self-limiting
  • Most patients can be discharged, further
    inpatient monitoring and care if respiratory or
    severe symptoms

88
For the prize
  • For a charm of powerful trouble,
  • Like a hell broth boil and bubble
  • Double, double, toil and trouble
  • Fire burn and cauldron bubble

Macbeth, Act IV, Scene I William Shakespeare,
1623
89
Useful References
  • Brennan RJ, Waeckerle JF et al. Chemical warfare
    agents emergency medical and emergency public
    health issues. Ann Emerg Med. 1999 Aug 34 (2)
    191-204
  • Britten S. Chemical weapons. Lancet. 1985 May 25
    1 (8349) 1220.
  • Evison D, Hinsley P, Rice P. Chemical weapons.
    BMJ. 2002 Feb 9 324. 332-5
  • Greenfield RA, Baron BR et al. Microbiological,
    biological, and chemical weapons of warfare and
    terrorism. Am J Med Sci 2002 Jun 323(6) 326-40
  • Gunderson CH, Lehmann CR et al. Nerve agents a
    review. Neurology 1992 May 42 (5) 946-50
  • Heck JJ, Geiling JA et al. Chemical weapons
    History, Identification, and Management. Critical
    Decisions in Emergency Medicine. 1999 Aug. 13
    (12) 1-7.
  • Janowsky DS. Central anticholinergics to treat
    nerve agent poisoning. Lancet. 2002 Jan 19 359
    (9302) 256-6.
  • Karalliedde L, Gauci CA, Carter M. Chemical
    waepons. BMJ. 1991 Feb 23 302 (6774) 474.
  • Lockwood AH. Chemical and biological weapons.
    JAMA. 1991 Aug 7 266 (5) 652
  • Murray VS, Volans GN. Management of injuries due
    to chemical weapons. BMJ. 1991 Jan 19 302
    (6769) 129-30
  • Sidell FR, Borak J. Chemical warfare agents II.
    Nerve agents. Ann emerg Med. 1992 Jul21
    (7)865-71.
  • Stone A. Chemical weapons. U.S. research on
    sedatives in combat sets off alarms. Science.
    2002 Aug 2 297 (5582) 764
  • Waeckerle JF. Domestic preparedness for events
    involving weapons of mass destruction. JAMA.
    2000 Jan 12 283 (2) 252-4
  • Wright P. Injuries due to chemical weapons. BMJ.
    1991 Jan 26 302 (6770) 239

90
Online Resources
  • Agency for Toxic Substances and Disease Registry
    (ATSDR) Managing Hazardous Materials Series
    http//www.atsdr.cdc.gov
  • A Review of the Scientific Literature as it
    Pertains to Gulf War Illnesses --Volume 5
    Chemical and Biological Warfare Agents Wililliam
    S. Augerson. Review for US Department of Defense
    http//www.rand.org/publications/MR/MR1018.5/index
    .html
  • American Academy of Clinical Toxicology
    http//www.clintox.org/
  • CDC National Center for Environmental Health
    http//www.cdc.gov/nceh/
  • The Chemical Weapons Convention (1997)
    Organisation for the Prohibition of Chemical
    Weapons http//www.opcw.org/
  • U.S. Army Medical Institute of Chemical Defense.
    Management of Chemical Casualties Handbook 1999
    http//ccc.apgea.army.mil/
  • Warfare - Chemical, Biological, Radiological,
    Nuclear And Explosives http//www.emedicine.com
  • World Health Organization. Chemical Incidents and
    Emergencies http//www.who.int/pcs/chem_incid_main
    .html
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