Chemical Weapon Exposures
Management in the ED
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
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? …
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)
Overview
General Management Principles
Nerve Agents
Pulmonary Agents
Vesicants
Incapacitating Agents
Pre-Hospital Care
Managing Hazardous Material Incidents.
Agency for Toxic Substances and Disease Registry, Center for
Disease Control, 2001
Decontamination Zones

Hot Zone
– Respiratory Protection:
Pressure-demand, selfcontained breathing
apparatus (SCBA) should
be used in all response
situations.
– Skin Protection: Chemicalprotective clothing should
be worn when local and
systemic effects are
unknown.
– Basic ABCs
HAZMAT Suit
Clara Ca, Fire Dept.
Santa

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
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


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.

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.
ED Management Principles
Emergency Room Procedures in Chemical Hazard
Emergencies: CDC National Centre for Environmental Health,
November 2002
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.
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

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.

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 patient’s condition
is evaluated within 30 minutes after ingestion, consider
gastric lavage.

Inhalation Exposure
– Supplemental oxygen
– Bronchodilators if bronchospastic
Investigations



CBC, glucose, and electrolytes, renal, LFTs
ECG, cardiac monitoring
Chest radiography, pulse oximetry, ABG if inhalation
exposure
Nerve Agents
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
Nerve Agents

The G-series:
Taban (GA)

The V-series:
VX
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
Mechanism of action
Normal Neurotransmission
Mechanism of action
Nerve agent effects
Signs and Symptoms
AChE inhibition
Cholinergic hyperstimulation
Cholinergic toxidrome
Signs and Symptoms
Eyes
Miosis, eye pain,
headache,injection,
lacrimation
Vapour Exposure
Seconds to minutes
after exposure
Nose
Rhinorrhea
Oral
Salivation
Airways
Bronchoconstriction,
bronchorrhea
Signs and Symptoms
Skin
Localized sweating,
fasciculations
Liquid Exposure
10 minutes to 18
hours after exposure
GI
Diarrhea, nausea,
vomiting
Cardiac
Brady, heart
block
Signs and Symptoms
Severe exposure
Previously
described vapour
and liquid effects
plus …
CNS
LOC, seizures,
fasciculations
Weakness, paralysis
Resp
Apnea
GI/GU
Bowel/bladder
incontinence
Seconds to minutes (vapour)
Minutes to hours (liquid)
Management

General management
 Specific antidotes
–
–
–
–
Atropine
Pralidoxime Chloride
Diazepam
Pre -treatment
Antidotes
Atropine
 2 mg IV/IM q5- 15 min to
effect
 Muscarinic action
-smooth muscle
-glandular epithelium
-cardiac muscle
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
Antidotes
Diazepam
 Seizure prophylaxis and
treatment
 10 mg IV at onset of severe
symptoms regardless of
seizure activity
MARK I kit
Atropine 2 mg
 Pralidoxime Cl 600 mg
 Issued to military personnel

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
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
Mechanism of action
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
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.
Pulmonary Agents
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)
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
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
Pathophysiology
Cl2 + H2O
2 HCl (hydrochoric acid)
+
[O-]
HCl
+
HOCl (hypochlorous acid)
Cellular injury via
oxidation of
functional groups in
cell components
HCl + [O-]
Clinical effects
Skin
- Irritation, frostbite
Eyes
- Irritation, ocular burns
Upper airway
- Nasal,pharynx, tracheal
inflammation
Chlorine
- Laryngospasm
Lower airway
May occur minutes to
24 hours after
exposure
- Inflammation and
loss of pulmonary
capillary integrity
Pulmonary edema,
hypoxia
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
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
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.
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
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 < 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
Pathophysiology
Directly reacts with amine,
sulfhydryl, and alcohol groups in
cells
Hydrolyzes to HCL
Phosgene
Stimulates LT synthesis
Combines with and depletes
glutathione stores
Clinical effects
Skin
- Irritation, frostbite
Eyes
- Irritation, ocular burns
Upper airway
Phosgene
May occur minutes to
72 hours after
exposure
Precipitated by
exertion
- Nasal,pharynx, tracheal
inflammation
- Laryngospasm
Lower airway
- Inflammation and
loss of pulmonary
capillary integrity
Pulmonary edema,
hypoxia
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
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

Animal studies have shown some benefit with
–
–
–
–
N-Acetylcystine
LT antagonists (monteleukast, zafirleukast)
NSAIDs
Aminophylline
Disposition

All patients should be hospitalized for
48 hours for observation
– Respiratory symptoms warrant ICU admission

Survival to 48 hours predicts likely
recovery
Vesicants
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
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

Since then has been used extensively in
numerous conflicts, including by Iraq in the
1980s
 Stored at 7 sites in the U.S.
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
Pathophysiology
Alkylating effect leads to crosslinking and degradation of DNA,
protein, other molecules
Thus high turnover cell
lines most affected
Mustard
Cholinergic stimulation
Clinical effects

Distinguished by relative lack of symptoms
immediately after exposure

Variable latent period depending upon
severity, route of exposure
Clinical effects
Tissue
Severity Clinical Effects
Time
Eyes
Mild
Tearing, itching, burning
4 –12 h
Mod
Erythema, lid edema, pain
3–6h
Severe
Corneal damage
1–2h
6 – 24 h
Severe
Rhinorrhea, epistaxis
hoarseness,cough
SOB, productive cough
Mild
Erythema
2 – 24 h
Severe
Vesication
2 – 24 h
Airways Mild
Skin
2–6h
Delayed clinical effects

Leukopenia +/- pancytopenia can occur 3-5
days post-exposure
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
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
Additional tests

Urine thiodiglycol
Disposition

Observation for 12 hours
 If asymptomatic or mild Sx can discharge with
close follow-up
Lewisite

An arsenical vesicant, first synthesized in
1918
 No confirmed use in warfare, although
stockpiled by several nations
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
Pathophysiology
Lewisite
Exact mechanism of cell damage
not known. Inhibits enzymes
with thiol groups (e.g. alcohol
dehydrogenase)
Clinical effects

Absorbed 10 times faster than mustards
 Immediate clinical effects
 More toxic than mustard
– 14 ug of Lewisite can cause vesication
Clinical effects
Skin
-Immediate pain
-Erythema within 30 min
-Vesication within a few hours
Lewisite
Eyes
- Irritation, severe
ocular burns
GI
-Severe abdo pain, n,
hematochezia if
ingested
- Hepatic necrosis
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
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
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
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

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.
Additional tests

Urinary arsenic excretion
Disposition

Observation for 18-24 hours
 If asymptomatic or mild Sx can discharge with
close follow-up
Riot control agents
Riot control agents

Irritants
 Hallucinogens (e.g. BZ)
 Vomiting agents (e.g. Adamsite)
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

Description
– All are solids and
require dispersion
device to aerosolize
particles

Routes of exposure
– Inhalation
– Skin/Eye contact
– Ingestion
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

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
Clinical effects
Skin
-Pain, burning, erythema
Eyes
-Lacrimation, blepharospasm,
injection
Irritants
ENT
-Sneezing, salivation
Resp
-Cough, broncorrhea,
subjective sensation of
breathing difficulty
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
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
Useful References
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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
Jul;21 (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
Online Resources

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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