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. What kind of gas was released? …
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
Some add so-called blood agents (e.g. cyanide, CO) to this list. Will not discuss - Herbicides, napalm, PCBs, obstructive smoke, masking agents etc.

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
1 Sealed hood with view port
2  Respirator mask and structural helmet
3  Pressure Bleed Valve
4  Valve
5  Integral gloves
6  Sealed zipper
7  Standard Firefighting boots. This particular suit has integral booties which fit inside the boots, which attach above the leggings seen overlapping the boots.
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.
Some suggest shower
Casualty Care research Center, Uniformed Services University, Bethesda, MD

11. In cases of ingestion, do not induce emesis.
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.
CDC Protocol

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
(Note: A contaminated patient may present at an emergency room without prior warning.)

16. General measures ABCs Skin Exposure Eye 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 Inhalation 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
Why no charcoal?

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

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
: 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
BMJ
In fact they are organophosphates but unlike OP pesticides they are more potent, with faster onset,

21. Nerve Agents The V-series: The G-series: VX 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
Thus V-series can be used to slime
10-15 mg of VX on skin can kill a man

22. Mechanism of action
Normal Neurotransmission

23. Mechanism of action
Nerve agent effects

24. Cholinergic hyperstimulation Cholinergic toxidrome
Signs and Symptoms
AChE inhibition
Cholinergic hyperstimulation
Cholinergic toxidrome

25. Seconds to minutes after exposure
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. 10 minutes to 18 hours after exposure
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. Previously described vapour and liquid effects plus …
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
Atropine for intubation

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
What else is nicotinic?
Mechanism of /Side effects of Pralidoxime?
Spontaneous dealkylation

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) Moderate Sx
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
No Rx and observe for 1 hour
United States Army Medical Research Institute of Chemical Defense (USAMRICD) Medical Management of Chemical Casualties Handbook-2000 Chapter 5, Nerve agents, FR Sidell

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
Gall, D., "The Use of Therapeutic Mixtures in the Treatment of Cholinesterase Inhibition," Fundam Appl Toxicol, 1, 1981, pp
Volume 2:  A Review of the Scientific Literature As It Pertains to Gulf War Illnesses; Pyridostigmine Bromide, Beatrice Alexandra Golomb, MR-1018/2-OSDA, 1999
- FDA Waiver
- Not useful in sarin because takes long time to age

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
Do we have this? Maisonneuve Rosemont
Normal values…There is a lack of standardization in laboratory determination of AChE activity. For example, there is no standard for the collection and processing of blood samples. Even when conditions specified by the manufacturer are adhered to, it has been shown that results sometimes underestimate AChE activity by > 30%. It is difficult if not impossible to compare enzyme activities performed by different methods when conversion factors have not been developed. Therefore, samples tested for AChE activity by different methodologies may not be useful for comparison purposes. As the Vendors performing clinical services change, it is likely that cholinesterase activity will not be comparable from year to year, requiring that new baseline levels be established – a circumstance which is both time consuming and expensive, considering that baselines require the average of two different samples.
Even if different laboratories use the same assay, normal ranges reported may be variable, further eliminating the hope that values can be comparable.
N=3-8uM/ml/min

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.
ASTDR

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
Not used in warfare since 1918
Three deaths reference Eli’s article
Bruce Bairnsfather ( )

40. Chlorine Largest cause of major toxic release incidents worldwide
Between , 27,788 exposures to chlorine in US
Attractive as chemical weapon because of ease of availability
American Association of Poison Controls Centers' National Data Collection System

41. Chlorine Description Routes of exposure
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
Because of these reactions, water substantially enhances chlorine’s oxidizing and corrosive effects

42. 2 HCl (hydrochoric acid) HOCl (hypochlorous acid)
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. May occur minutes to 24 hours after exposure
Clinical effects
Skin
- Irritation, frostbite
Eyes
- Irritation, ocular burns
Upper airway
Chlorine
- Nasal,pharynx, tracheal inflammation
- Laryngospasm
Lower airway
LD50 = 430 ppm
Acids formed by the chlorine gas reaction with the conjunctival mucous membranes are buffered, in part, by the tear film and the proteins present in tears thus acid burns to the eye typically cause epithelial and basement membrane damage but rarely damage deep endothelial cells. Acid burns to the periphery of the , cornea and conjunctiva often heal uneventfully, while burns to the center of the cornea may lead to corneal ulcer formation and subsequent scarring.
- 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
Thus SCBA and chemical protective clothing
Decon: Wash skin and hair, flush eyes with saline (unless frostbite), Rx frostbite

45. ED Management Decontamination if not done previously Resp: Burns:
Fluid restriction in patients with pulmonary edema/ ARDS
Beta agonists
If intubation needed perform under direct visualization (avoid blind techniques)
Burns:
Treat as thermal
Unless frostbittenDifference between ARDS and NCPE?
- Hyperchloremic met acidoisis (insufficient evidence for HCO3 although anecdotal evidence)
Get refs for HCO3/steroids
Get refs for observation time
Surgical airway if necessary

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. British soldiers at Somme, 1915
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
British soldiers at Somme, 1915

48. Phosgene Description Routes of exposure
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
The odor threshold for phosgene is 5 times higher than the OSHA PEL. Thus, odor provides insufficient warning of hazardous
concentrations.

49. Pathophysiology Phosgene Directly reacts with amine,
sulfhydryl, and alcohol groups in cells
Hydrolyzes to HCL
Phosgene
Stimulates LT synthesis
When glutathione stores depleted phosgene binds to the cellular macromolecules, causing cell necrosis in the renal and hepatic tissues.
Combines with and depletes
glutathione stores

50. Clinical effects Phosgene Skin Eyes Upper airway
- Irritation, frostbite
Eyes
- Irritation, ocular burns
Upper airway
Phosgene
- Nasal,pharynx, tracheal inflammation
- Laryngospasm
May occur minutes to 72 hours after exposure
Lower airway
Because phosgene is not very water soluble and hydrolysis tends to be slow, victims inhaling low concentrations of the gas may experience no irritation or only mild irritation of the upper airway. Lack of irritation allows victims to inhale the gas more deeply into the lungs and for prolonged periods. ---confirm
- 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
Thus SCBA and chemical protective clothing
Decon: Wash skin and hair, flush eyes with saline (unless frostbite), Rx frostbite

52. ED Management Decontamination if not done previously Resp: Burns:
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
Unless frostbitten
Steroids recommended (emed, CDC)
Solumedrol Day 1: 1000 mg IV Days 2-3: 800 mg IV Days 4-5: 700 mg IV Day 6: Reduce dose quickly if chest x-ray remains clear
Flovent: 10 puffs immediately followed by 5 puffs qh for 10 h; then 1 puff qh for at least 5 d
Surgical airway if necessary

53. Animal studies have shown some benefit with N-Acetylcystine
LT antagonists (monteleukast, zafirleukast)
NSAIDs
Aminophylline
NAC: inhibits LT release, maintains glutathione levels
Aminophylline: decreases tracheal pressures, PAP
NSAIDS: reducing pulm edema
? Methemoglobinemia level? Methylene chloride exp
osure
See e-med for w/u studies

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 Routes of exposure
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
Today, the maximum safe dose for mustard vapor is 5 mg/min/m3 for skin exposure and 2 mg/min/m3 for eye exposure. The threshold for olfactory detection of HD appears to be in the concentration range of 2-10 mg/m3

60. Cholinergic stimulation
Pathophysiology
Alkylating effect leads to cross-linking and degradation of DNA, protein, other molecules
Thus high turnover cell
lines most affected
Mustard
In the presence of a polar solvent (eg, water), the 2 side chains of HD cyclize and become biologically active. These 2 chains can attach to 2 other molecules and specifically bind to the guanine nitrogen in DNA strands, causing cross-linking and, eventually, cellular death. As expected, with the effect on DNA, cell lines with rapid turnover (eg, those in the bone marrow and gastrointestinal tract) are affected most by systemic uptake of mustard
Cholinergic stimulation

61. Clinical effects
Distinguished by relative lack of symptoms immediately after exposure
Variable latent period depending upon severity, route of exposure
The LD50 for ingestion of mustard is estimated as 0.7 mg/kg.
Skin exposure lethal dose to 50% of the exposed population (LD50) is approximately 100 mg/kg, or approximately 7 g for a person weighing 70 kg. This is approximately teaspoons of liquid

62. Clinical effects Tissue Severity Clinical Effects Time Eyes Mild
Tearing, itching, burning
4 –12 h
Mod
Erythema, lid edema, pain
3 – 6 h
Severe
Corneal damage
1 – 2 h
Airways
Rhinorrhea, epistaxis hoarseness,cough
6 – 24 h
SOB, productive cough
2 – 6 h
Skin
Erythema
2 – 24 h
Vesication

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!
DN induce emesis. If within 30 min of exposure consider OG lavage. No evidence for charcoal
Decontamination within 1 to 2 minutes
is the only way to prevent tissue damage

65. ED Management Decontamination if not done previously Resp: Skin:
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
Expansive

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 Routes of exposure
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 Lewisite
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 Lewisite Skin Eyes GI 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 Lewisite Upper airway Lower airway Cardiovascular
- Nasal,pharyngeal, tracheal inflammation
- Laryngospasm
Lower airway
Lewisite
- Inflammation and loss of pulmonary capillary integrity
Pulmonary edema, hypoxia
High-dose exposure to Lewisite may cause “Lewisite shock,” a
condition resulting from increased capillary permeability and
subsequent intravascular fluid loss, hypovolemia, and organ
congestion.
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
Thus SCBA and chemical protective clothing
Decon: Wash skin and hair, flush eyes with saline. Can use NaHClO.
DN induce emesis. No evidence for charcoal

75. ED Management Decontamination if not done previously Resp: Skin:
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
Do not replace fluids as per burn formulas

76. British Anti-Lewisite (BAL)
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
Systemic effects, no topical version available (CDEM)
Effective when given within 2 hours of exposure (CDEM)
14% chance of adverse reaction; reactions can include nausea, vomiting, burning sensation of mouth and eyes, lacrimation, rhinorrhea, salivation, burning of the extremities, dental pain, chest pain, anxiety, agitation, hypertension, and tachycardia;
Contraindictions include pre-existing renal disease, pregnancy (except in life threatening circumstances) and concurrent use of medicinal iron.

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.
CDEM says dialysis may be harmful…?

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
Get chemical structures!

83. Description Routes of exposure
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
Check reference for case report

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 Irritants Skin Eyes ENT Resp Pain, burning, erythema
Lacrimation, blepharospasm, injection
Irritants
ENT
Sneezing, salivation
Resp
PFTs done immediately after exposure in mixed populations have shown minimal alterations
GI: lethal dose in animals 200 mg/kg (14 g/kg in humans) developed erosions. Rx with ? Cathartics, antacids, surgical observation
Cough, broncorrhea, subjective sensation of breathing difficulty

87. Management Decontamination Supportive management
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 Aug; 34 (2):
Britten S. Chemical weapons. Lancet May 25; 1 (8349): 1220.
Evison D, Hinsley P, Rice P. Chemical weapons. BMJ Feb 9;
Greenfield RA, Baron BR et al. Microbiological, biological, and chemical weapons of warfare and terrorism. Am J Med Sci 2002 Jun; 323(6):
Gunderson CH, Lehmann CR et al. Nerve agents: a review. Neurology 1992 May; 42 (5):
Heck JJ, Geiling JA et al. Chemical weapons: History, Identification, and Management. Critical Decisions in Emergency Medicine Aug. 13 (12): 1-7.
Janowsky DS. Central anticholinergics to treat nerve agent poisoning. Lancet Jan 19; 359 (9302):
Karalliedde L, Gauci CA, Carter M. Chemical waepons. BMJ Feb 23; 302 (6774): 474.
Lockwood AH. Chemical and biological weapons. JAMA Aug 7; 266 (5): 652
Murray VS, Volans GN. Management of injuries due to chemical weapons. BMJ Jan 19; 302 (6769):
Sidell FR, Borak J. Chemical warfare agents: II. Nerve agents. Ann emerg Med Jul;21 (7):
Stone A. Chemical weapons. U.S. research on sedatives in combat sets off alarms. Science Aug 2; 297 (5582): 764
Waeckerle JF. Domestic preparedness for events involving weapons of mass destruction. JAMA Jan 12; 283 (2): 252-4
Wright P. Injuries due to chemical weapons. BMJ Jan 26; 302 (6770): 239

90. Online Resources
Agency for Toxic Substances and Disease Registry (ATSDR) Managing Hazardous Materials Series
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
American Academy of Clinical Toxicology
CDC National Center for Environmental Health
The Chemical Weapons Convention (1997) & Organisation for the Prohibition of Chemical Weapons
U.S. Army Medical Institute of Chemical Defense. Management of Chemical Casualties Handbook
Warfare - Chemical, Biological, Radiological, Nuclear And Explosives
World Health Organization. Chemical Incidents and Emergencies