Post on 06-Oct-2021
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Slide 1JSOMTC, SWMG(A)
NBC ‐ FIELD TREATMENT OF THE CHEMICAL CASUALTY
PFN: SOMEML14
Hours: 3.0
Slide 2JSOMTC, SWMG(A)
NBC ‐ FIELD TREATMENT OF THE CHEMICAL CASUALTY
Action: Recognize and manage a chemical agent casualty
Condition: Given a real or simulated patient or patient care scenario
Standard: In accordance with the lecture, student handouts, cited references and accepted standards of care without causing further patient harm
Slide 3JSOMTC, SWMG(A)
References:
Medical Management of Chemical Casualties ‐U.S. Army Medical Research Institute of Chemical Defense
Operational Medicine Subjects, April 2004
NBC ‐ FIELD TREATMENT OF THE CHEMICAL CASUALTY
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Slide 4JSOMTC, SWMG(A)
REASON
“Whether or not gas will be employed in future wars is a matter of conjecture, but …. we can never afford to neglect the question.”
General John J. Pershing, 1919
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Slide 6JSOMTC, SWMG(A)
AGENDA
Define a chemical agent. Communicate the descriptions and identifiers of chemical agents.
Communicate the types of detectors for chemical agents.
Understand the management and treatment of chemical exposure.
Communicate the signs and symptoms, physical exam findings, and treatment for nerve agents.
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Slide 7JSOMTC, SWMG(A)
Communicate the signs and symptoms, physical exam findings, and management of cyanide poisoning.
Communicate the signs and symptoms, physical exam findings, and management of pulmonary irritants.
Communicate the signs and symptoms, physical exam findings, and management of vesicants.
Communicate the signs and symptoms, physical exam findings, and management of incapacitating agents.
AGENDA
Slide 8JSOMTC, SWMG(A)
Define a Chemical AgentCommunicate the Descriptions and
Identifiers of Chemical Agents
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CHEMICAL AGENT WARFARE DEFINED
“A chemical substance intended for use in military operations to kill, seriously injure
or incapacitate.”
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Slide 10JSOMTC, SWMG(A)
CLASSES OF CHEMICAL WARFARE (CW) AGENTS
NERVE AGENTS
CYANIDE (BLOOD AGENTS)
PULMONARY IRRITANTS
Toxic Industrial Chemicals/Materials (TIC’s/TIM’s)
VESICANTS (BLISTER AGENTS)
INCAPACITATING AGENTS
NON TRADITIONAL AGENTS (NTA’s)
Slide 11JSOMTC, SWMG(A)
CW AGENTS: PHYSICAL STATE
The state will affect dissemination, clinical presentation and prognosis
States include:
Solid
Liquid
Gas
Vapor
Aerosol
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PERSISTENCE
Dependent on Several Factors:
Agent Volatility
Temperature
Wind
Agent‐Surface Interactions
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ROUTES OF ABSORPTION
Inhalational
Ocular
Percutaneous
Enteral
Parenteral (e.g. contaminated wounds)
IM
IV
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TOXICITY
Liquid
ID50
• Incapacitating dose for 50% of exposed population
LD50
• Lethal dose for 50% of exposed population
Vapor
Ct
• Concentration x time
Slide 15JSOMTC, SWMG(A)
COMPARATIVE TOXICITY OF AGENTS
0
1000
2000
3000
4000
5000
6000
CL CG AC H GB VXAGENT
Ct50(mg-min/m3)
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ANY QUESTIONS?
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Communicate the Types of Detectors for Chemical Agents
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DETECTORS
M8 Paper ‐ Detects liquid presence/type
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DETECTORS
M9 Paper ‐ Detects liquid presence only
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Lightweight Chemical Detector (LCD) 3.3
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LCD cont...
Detects and Identifies
Detects up to 10 different Toxic Industrial Chemicals (TIC’s)
Identifies Chemical Warfare Agents (CWAs)
CWA’s Identified
Nerve Agents
• GA (Tabun)
• GB (Sarin)
• GD (Soman)
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Slide 22JSOMTC, SWMG(A)
LCD cont...
Nerve Agents cont…
• VX
Blister Agents
• HD (Sulfur Mustard)
• L (Lewisite)
Blood Agents
• AC (Hydrogen Cyanide)
• CK (Phosgene Oxime)
Choking Agents
• CG (Phosgene)
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ANY QUESTIONS?
Slide 24JSOMTC, SWMG(A)
FOR EACH CW AGENT:
Know the Pathophysiology
Know Physical Properties
Know Signs and Symptoms
Diagnosis (with differential diagnosis)
Management (with pre/post treatment)
Triage (prognosis)
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Communicate the Signs and Symptoms, Physical Exam Findings, and Treatment for Nerve Agents
Slide 26JSOMTC, SWMG(A)
NERVE AGENTS
Substances that cause biological effects by inhibiting the enzyme acetylcholinesterase (AChE).
Slide 27JSOMTC, SWMG(A)
SPECIFIC AGENTS
GA (Tabun)
GB (Sarin)
GD (Soman)
GF
VX
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Slide 28JSOMTC, SWMG(A)
PHYSICAL PROPERTIES
Clear, colorless liquids (when fresh), not “nerve gas”
Tasteless, most are odorless
Freeze/melt <0 degrees Celsius
Boil >150 degrees Celsius
Volatility GB>GD>GA>GF>VX
Penetrate skin, clothing
Slide 29JSOMTC, SWMG(A)
NORMAL PHYSIOLOGY
Electrical impulse travels down the nerve
Nerve impulse causes release of the neurotransmitter, acetylcholine (ACh)
ACh stimulates receptor sites on the target organ
Causes the target organ to act
ACh is destroyed by acetylcholinesterase (AChE)
No more organ activity
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NERVE TRANSMISSION:NERVE TO NERVE
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NERVE TRANSMISSION:NERVE TO TARGET ORGAN
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NERVE AGENT ALTERED PHYSIOLOGY
Enzyme (AChE) is inhibited
Does not destroy ACh
Excess ACh continues to stimulate target organ
Persistent target organ stimulation results in symptoms
Dependent upon nerve agent, signs and symptoms are irreversible due to the aging of the agent
Slide 33JSOMTC, SWMG(A)
AGING TIMES FOR NERVE AGENTS
Name Synonym “Aging”
SARIN GB About 5 hours
SOMAN GD About 2 minutes
TABUN GA Less than 14 hours
VX None About 48 hours
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Slide 34JSOMTC, SWMG(A)
SITES OF ACTION(Two Major Types of Cholinergic Receptors)
Muscarinic (DUMBELS) Smooth muscles
Exocrine glands
Vagus nerve
Nicotinic (MTWHF) Skeletal muscles
Preganglionic nerves
Both ( 3 C’s) CNS
Slide 35JSOMTC, SWMG(A)
MUSCARINIC EFFECTS
Smooth Muscles
Airways ‐ constriction
GI tract ‐ constriction
Pupils ‐ constriction
Exocrine Glands
Increased secretions from eyes, nose, mouth, airways, GI tract and skin
Vagus Nerve
Heart (bradycardia)
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EFFECTS ON SMOOTH AND CARDIAC MUSCLE
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EFFECTS ON EXOCRINE GLANDS
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NICOTINIC EFECTS
Skeletal muscles
Fasciculations
Fatigue
Flaccid paralysis
Preganglionic nerves
Tachycardia
Hypertension
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EFFECTS ON STRIATED (SKELETAL) MUSCLE
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Slide 40JSOMTC, SWMG(A)
HEART RATE VARIABLE
Muscarinic (vagal) decreases )
Nicotinic (ganglionic) increases )
Hypoxia: decrease oxygen )
May be high, low, normal )
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CNS EFFECTS
Acute, large exposure to nerve agent
Loss of consciousness
Seizures
Apnea
Death
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CNS EFFECTS
Acute, small exposure to nerve agent
Minor CNS effects
• Slowness in thinking and decision making
• Sleep disturbances
• Poor concentration
• Emotional problems
• Other minor problems
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CNS EFFECTS
Minor CNS effects
May last for 3 to 6 weeks
May follow any exposure
Not always present
Very slight, subtle
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MANAGEMENT MARCHE (2)
Massive hemorrhage/Mask Check
Airway/Antidotes
Respirations/ Spot decontamination
Circulation/ Countermeasures
Hypothermia /Head wounds
Evacuation
Supportive Care
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MANAGEMENT, cont.
Atropine – A cholinergic blocking agent. Blocks excess acetylcholine = decreased secretions and reduced smooth muscle constriction.
Dose: 2mg in auto‐injector, but can be given until decreased secretions and breathing is easier. No effect on skeletal muscles.
Pralidoxime Chloride (e.g. 2‐PAM) ‐ Removes agent
from the enzyme. Cannot reactivate the chemical
agent but reactivates AChE. Affects nicotinic sites = increase in skeletal muscle strength. No clinical effects at muscarinic sites.
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Slide 46JSOMTC, SWMG(A)
MANAGEMENT, cont. Scopolamine‐ traditionally used as an anti‐mimetic and sedative
•FDA approved•MOA same as atropine/ anti‐secretory
•Greater CNS potency•More rapidly crosses the BBB
•Scopolamine is used after the administration of 3 ATNNA’s and 1 CANA with no resolution
Administer 0.8 mg Scopolamine via IO and flush. IM as secondary route
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Antidote Treatment Nerve Agent Auto‐Injector (ATNAA)
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Convulsion Antidote Nerve Agent(CANA)
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“3 D’s”Auto‐Injector Administration
Signs and Symptoms ATNNA (1st Dose) CANA
DIM 1 x ATNAA Not Recommended
DRENCHED 2 x ATNAA Consider for prevention of Seizures
DISABLED 3 x ATNAA Administer for Tx and prevention of seizures
Slide 50JSOMTC, SWMG(A)
MANAGEMENT, cont.
If the patient does not improve after 3 ATNAA and 1 CANA
•Administer Scopolamine bump of .8mg
• Start Atropine drip of 1mg every 3 min
Once atropinization has been achieved, restrict drip to 10‐20% of original dose. Monitor for reoccurrence .
• Administer 500mg of 2‐PAM (Bolus)
Then start a drip of 2‐PAM
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RECOVERY
Severe Casualty:
Without complications, conscious, breathing, in 2 to 3 hours
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RETURN TO DUTY
Dose‐dependent, need dependent
Could be hours with minor exposure
Many days after severe exposure
Consider:
vision
minor, subtle mental effects
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PRE‐TREATMENT WITH PYRIDOSTIGMINE
A Carbamate
Transient binding to AChE
Prevents AChE from binding permanently to the nerve
agent
Carbamylation of only a small amount of AChE needed
Helpful against GA and GD, but not against GB, GF or
VX
Pretreatment
Most effective when followed by antidote therapy
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PRE‐TREATMENT, cont.
Dose: 30mg every 8 hours
Commander starts/stops use
Safe when dosed properly
Used in clinical medicine over 50 years
• Used in TX for Myasthenia Gravis
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ANY QUESTIONS?
Slide 56JSOMTC, SWMG(A)
Communicate the Signs and Symptoms, Physical Exam Findings,
and Management of Cyanide Poisoning
Slide 57JSOMTC, SWMG(A)
CYANIDEA naturally occurring, rapidly acting
poison found in many plant sources
(also known as blood agents)
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Slide 58JSOMTC, SWMG(A)
COMMON SOURCES
Naturally occurring chemical Found in most living organisms
• Man: < 0 . 3 mcg / mL in blood
Foods and other plants Lima beans, cassava root, peach pits
Combustion Plastics, synthetic fibers
Nitriles (acrylic and nylon manufacture)
Cigarette smoke
Fumigant / pest killer
Slide 59JSOMTC, SWMG(A)
NONMILITARY USES
Poisonings
Terrorists, executions, homicides, suicides
Industry
Electroplating
Plastics processing
Gold and silver extraction
Fumigation
Photography
Metallurgy
Slide 60JSOMTC, SWMG(A)
HISTORY AND MILITARY USE Scheele: Isolated in (1782)
Napoleon: Troops dipped bayonets
WW I: French
Nazi Germany: Zyklon B
Japan: Against the Chinese in WWII
Stockpiled by U.S. in WWII
Chemical agent identification kits
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SPECIFIC AGENTS
Hydrogen Cyanide (AC)Odor of bitter almonds, peach pits, burning rope
Very volatile
Cyanogen Chloride (CK) Pungent, irritating to the eyes and respiratory tract
Very volatile
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SITE OF ACTION
Primary site of action: Cells rather than blood
Organelles affected: Mitochondria
Slide 63JSOMTC, SWMG(A)
MECHANISM OF ACTION
Cyanide has a strong affinity for metals, especially ferric iron (Fe3+)
Carried by the blood from the lungs or GI tract to the cells
Binds to cytochrome oxidase (cyt a3) in the mitochondria – cell energy producer
CN‐has higher affinity for the Fe3+ in cyt a3 than for
Fe2+ in hemoglobin
A stable but reversible binding
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Slide 64JSOMTC, SWMG(A)
MECHANISM OF ACTION
Blocks Cellular Respiration (oxidative phosphorylation)
Occurs in the mitochondria
Blocks aerobic production of ATP (energy molecule)
Histotoxic anoxia leads to cell death
Anaerobic metabolism lactic acidosis
Slide 65JSOMTC, SWMG(A)
CLASSIC SIGNS
Rapid onset of symptoms
Bright red venous blood and fundal vessels
Profound metabolic acidosis
Odor of bitter almonds
Tachypnea, hypertension and bradycardia without cyanosis
Respiratory depression without cyanosis
Slide 66JSOMTC, SWMG(A)
MANAGEMENT
Protect Self!
Terminate exposure ‐ “move, mask, decon”
MARCH (2)
Observe 24 to 48 hours
Correct metabolic acidosis
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MANAGEMENT, cont.
Administer Antidotes
Sodium Nitrite • Forms methemoglobin (Fe3+) – displaces cyanide from cytochrome oxidase
• 10ml of 3% solution IV over five to fifteen minutes
• Monitor blood pressure ‐ STOP if systolic BP drops below 80
• Give one‐half original dose if signs recur
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MANAGEMENT, cont. Sodium Thiosulfate
• A sulfur donor – cyanide converted to thiocyanate in the liver which is eliminated from the body through the kidneys
• 12.5gm in 50cc ampule IV over 10 minutes immediately following sodium nitrite
• If sodium nitrite is repeated, repeat at one‐half of the original dose
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ANTIDOTE THERAPY
Cyanide Antidote Kit
Methemoglobin Formers
• Amyl Nitrite
• Sodium Nitrite
Sulfur Donor• Sodium Thiosulfate
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ANTIDOTE THERAPY
Cyanokit
Hydroxocobalamin
• It is a vitamin B12 that is found in food.
• It has a property that binds to an ion in cyanide. Turns it into cyanocobalamin
• Excreted in urine
• Easier to use because it’s one drug as opposed to two
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SUMMARY
Killed millions throughout history. Top terroristconsideration
Battlefield or terrorist use probably as a vapor (enclosedarea)
Variable potency (LCt50) because of body’s natural metabolism, but rapidly acting in high concentrations
Cellular poison, NOT a “blood” agent
Nitrites generate metHb, which “pulls” cyanide from cyt a3 temporarily
Thiosulfate provides sulfides to help liver enzyme rhodanese form thiocyanate which is excreted in the urine
CN-
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ANY QUESTIONS?
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Communicate the Signs and Symptoms, Physical Exam Findings, and Management of Pulmonary
Irritants
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PULMONARY IRRITANTS
Compounds that result in varying degrees
of pulmonary edema, usually after a
symptom‐free period.
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SPECIFIC AGENTS
Chlorine ‐ first chemical warfare agent of significance. Used in modern industry and transported on highways and railroads
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SPECIFIC AGENTS
Phosgene ‐ industrial
chemical commonly manufactured, stored and transported
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SPECIFIC AGENTS
PFIB’s (Perfluoroisobutylene’s) ‐given off when teflon burns‐lines the interior of many armored vehicles
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SPECIFIC AGENTS
Oxides of Nitrogen ‐products of burning gunpowder which can build to toxic levels with repetitive firing of artillery
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Slide 79JSOMTC, SWMG(A)
ANATOMY
Upper Airway
Naso/oropharynx to larynx
Central Airways
conducting
larynx to terminal bronchiole
Peripheral Airways
gas exchange
respiratory bronchiole to alveoli
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PHYSICAL/CHEMICAL PROPERTIES
Irritants
Centrally Acting
•high solubility (ammonia, HCl)
•high reactivity (mustard, Lewisite)
Intermediate (chlorine)
Peripherally Acting
• low solubility/reactivity (phosgene, PFIB, NO2, HC)
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MECHANISM OF ACTION
Chlorine and Phosgene Classic Examples
Gases at STP
Mechanism: peripheral agents cause pulmonary edema
•damage alveolar‐capillary membrane
Adult Respiratory Distress Syndrome (ARDS)
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Slide 82JSOMTC, SWMG(A)
CLINICAL CONSIDERATIONS
Latent Period
Symptom onset may be delayed hours to days
• Dyspnea
Objective signs appear later than symptoms
• crackles
• hypoxemia
• frothy sputum
Sudden Death May Occur
laryngeal obstruction (edema/spasm)
bronchospasm
Slide 83JSOMTC, SWMG(A)
CLINICAL CONSIDERATIONS
Infectious Bronchitis / Pneumonitis Common
3‐6 days post‐exposure
fever, WBC, infiltrates NOT always infection
prophylactic antibiotics NOT indicated
Effects Exacerbated by Exertion
compensatory mechanisms overwhelmed
strict rest, even if asymptomatic
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SIGNS AND SYMPTOMS
Early Symptoms
Eye and airway irritation
Dyspnea, cough
Substernal pressure
Late symptoms
Crackles at lung bases
Watery secretions
Hypoxemia, hypovolemia, death
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CHLORINE ‐ PHYSICAL PROPERTIES
2.5 times heavier than air
Green‐yellow color
Acrid, pungent odor
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CHLORINE ‐ TISSUE EFFECTS
Effects are Local Not Systemic
In Central Airways ‐ from HCl
necrosis, sloughing
In Peripheral Airways
damage alveolar‐capillary membrane
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CHLORINE ‐ CLINICAL EFFECTS
Mild Exposure suffocation, choking sensation
ocular, nasal irritation
chest tightness, cough
exertional dyspnea
Moderate Exposure above symptoms + hoarseness, stridor
pulmonary edema within 2‐4 hours
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CHLORINE ‐ CLINICAL EFFECTS
Severe Exposure
severe dyspnea at rest
may cause pulmonary edema within 30‐60 min
copious upper airway secretions
sudden death may occur from laryngospasm
Slide 89JSOMTC, SWMG(A)
CHLORINE EXPOSURE
36 y/o female
2 hrs post exposure
Resting dyspnea
Diffuse crackles
PaO2 32 torr (room air)
CXR:
diffuse edema
w/o cardiomegaly
Slide 90JSOMTC, SWMG(A)
PHOSGENE ‐ CLINICAL EFFECTS
Mild Exposure
mild cough
dyspnea
chest tightness
Moderate Exposure
above symptoms plus
ocular irritation, lacrimation
smoking tobacco produces bad taste
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PHOSGENE ‐ CLINICAL EFFECTS
Severe Exposure
Severe cough, dyspnea
Onset of pulmonary edema within 4 hours
May produce laryngospasm
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PHOSGENE EXPOSURE
42 y/o female
2 hrs post exposure
Rapidly increased dyspnea
PaO2 40 torr (room air)
CXR: infiltrates ‐ perihilar
fluffy
diffuse interstitial
Death 6 hrs post exposure
Slide 93JSOMTC, SWMG(A)
MANAGEMENT Terminate exposure!
ABC’s (intubate if stridor present)
Enforce rest!
Manage airway secretions
Prevent/treat bronchospasm ‐ “asthma therapy”
Treat hypoxemia with oxygen, PPV with PEEP
Treat hypotension with IV fluids
Re‐evaluate and monitor for 24 to 48 hours
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SUMMARY
Inhaled Toxic Agent Effects May Be:
Central, peripheral, or combined
Latent Period ‐ “dose” dependent
Onset of Effect
Symptoms occur before signs
< 4 hours ‐ severe, often lethal exposure
> 4 hours ‐ lethality less likely
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ANY QUESTIONS?
Slide 96JSOMTC, SWMG(A)
Communicate the Signs and Symptoms, Physical Exam Findings, and Management of Vesicants
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VESICANTS
Also known as blister agents
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SPECIFIC AGENTS
Sulfur Mustard (H,HD)
Nitrogen Mustard (HN1, HN2, HN3)
Lewisite = chlorovinyldichloroarsine (L)
Mustard / Lewisite Mixtures (HL,HT,TL)
Phosgene Oxime (CX)
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MUSTARD
Physical Properties
Oily light yellow to brown liquid
Odor of garlic, onion or mustard
Vapor heavier than air
Liquid heavier than water
Freezes/melts at 57 degrees Fahrenheit
Pathophysiology
Quickly cyclizes in tissue
Alkylates cell components (DNA, proteins)
DNA damage leads to cell mutation and death
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MUSTARD TOXICITY
Liquid
Blister 10ug
Death 100 mg/kg
7 gm/70 kg (on skin surface)
(350 mg absorbed)
Slide 101JSOMTC, SWMG(A)
MUSTARD
Target Organs
Skin
Eyes
Airways
Systemic ‐ bone marrow, GI tract, CNS, lymphoid tissue
Signs and Symptoms
Skin ‐ erythema, vesicles, blisters, necrosis
Eyes ‐ conjunctivitis, lid inflammation, blepharospasm, corneal opacification, ulceration and/or perforation
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MUSTARD
Airways – soreness, hoarseness, non‐productive cough, hemorrhage, pain, hoarseness, stridor
GI‐nausea, vomiting
Systemic ‐ damage to bone marrow stem cells, CNS symptoms seen in severe exposure (convulsions, coma, death)
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SKIN EFFECTS
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Skin Sensitivity to Vesicants Skin Region:
Palms of hands and soles of feet
Palmar surface of fingers; back of hands and fingers
Lateral surface of fingers and general skin of the body
Genitalia
Moisture in skin
Cold dry skin
Hot dry skin
Cold moist skin
Normal (temperature) dry skin
Normal (temperature) moist skin
Hot moist skin
LOW
HIGH
LOW
HIGH
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SKIN EFFECTS
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VESICANT EFFECTS
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BLIND LEADING THE BLIND
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EYE EFFECTS
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MANAGEMENT: EYES
Tetracaine Eye Drops for pain
20 min NaCl flush with Morgan’s Lens ( LR is appropriate for Acids)
Neomycin Eye Drops Prevent Eyelids sticking shut
Allow eyes to drain
Avoid tight bandaging
Slide 110JSOMTC, SWMG(A)
MANAGEMENT: SKIN
Immediate Decontamination!
General Supportive Care
Debridement of Burns
Frequent Irrigation
Antibiotics: Topical/Systemic (cellulitis)
Systemic Analgesics
Appropriate IV Fluids and Electrolytes
Burn Unit in Severe Cases
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MANAGEMENT: AIRWAYS
Steam, cough suppressants
Oxygen
Bronchodilators, steroids
Early intubation
Assisted ventilation
Antibiotics AFTER organism identified
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MANAGEMENT: MARROW
Reverse Isolation
Blood Component Replacement
RBC, WBC, platelets
Granulocyte Colony Stimulating Factor
Marrow Transplants
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MUSTARD: LONG TERM
Carcinogen/Mutagen
No evidence of human reproductive toxicity
Chronic Exposure
Respiratory cancer
Unclear: chronic bronchitis, emphysema
Slide 114JSOMTC, SWMG(A)
LEWISITE
Physical Properties oily, colorless liquid
heavier than air and water
more volatile than mustard
geranium odor
freezes/melts at about 0 degrees Fahrenheit
Signs and Symptoms skin ‐ blisters, necrosis
eyes ‐ pain, blepharospasm, edema of lids/conjunctiva, corneal damage\
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Slide 115JSOMTC, SWMG(A)
LEWISITE, cont.
Airways ‐ severe irritation
Management
immediate decontamination
treat as mustard lesion
Equally damaging breakdown products found in blister fluid
Treatment
British Anti‐Lewisite (BAL); Dimercaprol
Slide 116JSOMTC, SWMG(A)
Vesicant Comparison
Slide 117JSOMTC, SWMG(A)
PHOSGENE OXIME
Urticant, not vesicant
Rapid onset
Corrosive to all tissues (skin, eyes, lungs)
Management same as mustard
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Slide 118JSOMTC, SWMG(A)
ANY QUESTIONS?
Slide 119JSOMTC, SWMG(A)
Communicate the Signs and Symptoms, Physical Exam Findings, and Management of Incapacitating
Agents
Slide 120JSOMTC, SWMG(A)
INCAPACITATING AGENTS
Agents designed not to injure or kill, but
to induce disorientation or other temporary
effects leading to impaired performance
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CLASSES
Irritants ‐ riot control agents
CS
CN (Mace)
DM (Adamsite ‐ vomiting agent)
Pepper sprays
CNS Stimulants
CNS Depressants
Psychedelics
Deliriants ‐ mainly anticholinergics (BZ, agent 15)
Slide 122JSOMTC, SWMG(A)
BZ
Characteristics
Stable crystalline solid
An anticholinergic
Odorless
Half‐life of 3‐4 weeks in moist air
Usually dispersed as an aerosol
Absorbed through inhalation, but can be ingested and absorbed through the skin
Cannot be detected at present time
Slide 123JSOMTC, SWMG(A)
BZ
Mechanism of Action Onset ‐ 0.5‐4 hours (inhalation or ingestion), 36 hours following skin exposure
Blocks acetylcholine (opposite effects from nerve agent)
Muscarinic effects ‐ understimulation of smooth muscle and exocrine glands – may last up to 96 hours
• Ocular ‐ mydriasis, paralysis of accomodation (“blind as a bat”)
Oral ‐ dry mouth, thirst (“dry as a bone”)
• Cardiac ‐ labile heart rate
• GI ‐ decreased motility and secretions
• GU ‐ urinary retention, bladder distension
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BZ
• Skin ‐ decreased sweating, flushing, (“red as a beet”)hyperthermia (“hot as a hare”)
• Neuromuscular ‐ incoordination, ataxia
• CNS ‐ decreased level of consciousness, illusions, visual hallucinations, disturbances in judgment and insight, short term memory loss, easy distractibility, slurred, senseless speech, disorientation to time and place, behavioral lability, paranoia
No direct nicotinic effects ‐ skeletal muscle
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BZ Management
Protect Self!
Decontaminate with soap and water
Observe and/or restrain
Early evac
Antidote: Physostigmine ‐ Anticholinesterase (elevates levels of acetylcholine)• IM – Adults 45 mcg/kg Children 20 mcg/kg
• By mouth (mix with juice) – 60 mcg/kg if patient cooperates –bitter taste
• IV (least preferred) – 30 mcg/kg (titrate slowly 1 mg/min or less) – continuous monitoring needed
• Treat dosing to patient’s mental status – repeat over 4 to 5 days
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ANY QUESTIONS?
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NON TRADITIONAL AGENTS
A chemical or biochemical material that is not categorized as a chemical warfare agent as defined by the Chemical Weapons Convention
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NON TRADITIONAL AGENTS
Novichok Agents Stable, less volatile, deliverable by solid, difficult to detect
4th Generation Agents Evolved agents that would be stronger than the original agents that came out during World War I
More damaging
Harder to treat
Pharmaceutical Based Agents (PBA) World wide availability
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PBA Fentanyl
Inhalation: 1‐3 min
Ingestion: 60‐ 150 min
Acts primarily through opioid receptors in the brain, spinal cord, smooth muscle
100x more potent than morphine
Fentanyl vs Carfentanil
100x more potent than fentanyl
3‐5 min after exposure: active/alert
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PBA
Fentanyl vs Carfentanyl cont…
5‐7 min: increasingly lethargic, muscular rigidity, tremors
6‐9 min: unresponsive, respiratory distress
10‐30 min: Convulsions, apnea and death
Renarcotization likely to occur 15‐50 min after tx
Large amounts of Nalaxone will be needed
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ANY QUESTIONS?
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Understand the Management and Treatment of Chemical Exposure
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DECONTAMINATION
Decon ASAP!
Self decontaminate in <1‐2 minutes
Decontaminate for liquids is a higher priority over vapor. Decon for vapor may not be necessary
80‐90% of contaminants are removed with the rapid removal of contaminated clothing
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DECONTAMINATION
Early decon protects casualty
within minutes
Late decon protects medical personnel and facility
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DECONTAMINATION PRINCIPLES
Decon as far forward possible
Decon only what is necessary
Decon by priority
Decon as soon as possible
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CHEMICAL DECONTAMINATION
Soap and water (fresh or salt)
Removal is via hydrolysis
Hypochlorite (bleach)
Oxidative chlorination
0.5% for skin
5.0% for equipment
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PHYSICAL REMOVAL
Flushing with water (fresh or salt)
Water and soap is one of the best deconmethods for all CWA’s even if it
doesn’t neutralize the agent
Absorbent materials:M291 Skin Decontamination Kit
•Mixture of dry resin
• 6 individual packets in a wallet sized pouch
• Absorbs and neutralizes liquid agents on skin
• Do not apply to open wounds
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PHYSICAL REMOVAL
M295 Individual Equipment Decontamination Kit
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PHYSICAL REMOVAL
Reactive Skin Decontamination Lotion (RSDL)
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PHYSICAL REMOVAL
RSDL cont: FDA approved skin decontaminant
Viscous yellow lotion impregnated into a polymer sponge
Ph 10.5
Water soluble for ease of removal post decon application
5 year shelf life‐temperature dependent
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PHYSICAL REMOVAL RSDL cont: Removes and neutralizes many chemical agents such as Tabun, Sarin, Soman, Vx, Mustard, NTA’s and certain TICs
NEEDS TO BE ON SKIN FOR AT LEAST TWO MINUTES IN ORDER TO NEUTRALIZE
May lead to future cancer risks
If left on the skin for more than 6hrs = itchy and a possible rash
If used with Sulfur Mustard and Chlorine, it is important to know that it can be flammable
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PHYSICAL REMOVAL
Absorbable material: should only be used on dry decontamination of the skin and equipment
• Fuller’s earth
• Clean Sand
• Flour
• Baby wipes
Used when ambient temperature is freezing and/or other decon equipment is not available
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WOUND DECONTAMINATION
First, Protect Self!Nerve and vesicant wounds could be hazardous• Look for contaminated material
Vapor hazard from wounds is miniscule
Double latex gloves or one pair of butyl rubber gloves, extra gloves and continual change out is a must
Hypochlorite 0.5% for 5 minutes into contaminated wounds (not for eyes, CNS, open chest or abdominal wounds)
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ANY FINAL QUESTIONS?
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TERMINAL LEARNING OBJECTIVE
ACTION: Recognize and manage a chemical agent casualty.
CONDITIONS: Given a real or simulated patient or patient care scenario.
STANDARD: In accordance with the lecture, student handouts, cited references and accepted standards of care without causing further patient harm.
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AGENDA
Define a chemical agent. Communicate the descriptions and identifiers of chemical agents.
Communicate the types of detectors for chemical agents.
Understand the management and treatment of chemical exposure.
Communicate the signs and symptoms, physical exam findings, and treatment for nerve agents.
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Communicate the signs and symptoms, physical exam findings, and management of cyanide poisoning.
Communicate the signs and symptoms, physical exam findings, and management of pulmonary irritants.
Communicate the signs and symptoms, physical exam findings, and management of vesicants.
Communicate the signs and symptoms, physical exam findings, and management of incapacitating agents.
AGENDA
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REVIEW
Name three routes that chemical agents may use to enter the body.
INHALATIONAL, OCULAR, PERCUTANEOUS
A detector used by soldiers to detect both the presence and type of a liquid chemical agent.
M8 PAPER
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REVIEW
Name two steps that should be taken when decontaminating a wound suspected of being contaminated by a chemical agent.
1. Protect self
2.Flush with 0.5% hypochlorite solution for 5 minutes
Agents that inhibit acetylcholinesterase are called:
Nerve agents
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REVIEW
Sodium nitrite and sodium thiosulfate are used to treat exposure to this agent.
CYANIDE
This agent is a dense, acrid, pungent, greenish‐yellow gas that is easily recognized by both color and odor.
CHLORINE
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REVIEW
An oily, odorous liquid that is generally regarded as persistent because of its low volatility.
MUSTARD
Which of the following is a specific antidote for an anticholinergic incapacitating agent? Physostigmine, pyridostigmine, neostigmine
PHYSOSTIGMINE
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REASON
“Whether or not gas will be employed in future wars is a matter of conjecture, but …. we can never afford to neglect the question.”
General John J. Pershing, 1919
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