NBC ‐FIELD TREATMENT OF THE CHEMICAL CASUALTY PFN: SOMEML14

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Slide 1JSOMTC, SWMG(A)

NBC ‐ FIELD TREATMENT OF THE CHEMICAL CASUALTY

PFN: SOMEML14

Hours: 3.0



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


References:

Medical Management of Chemical Casualties ‐U.S. Army Medical Research Institute of Chemical Defense

Operational Medicine Subjects, April 2004


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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



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


Define a Chemical AgentCommunicate the Descriptions and

Identifiers of Chemical Agents


CHEMICAL AGENT WARFARE DEFINED

“A chemical substance intended for use in military operations to kill, seriously injure

or incapacitate.”

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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)


CW AGENTS: PHYSICAL STATE

The state will affect dissemination, clinical presentation and prognosis

States include:

Solid

Liquid

Gas

Vapor

Aerosol


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


TOXICITY

Liquid

ID50

• Incapacitating dose for 50% of exposed population

LD50

• Lethal dose for 50% of exposed population

Vapor

Ct

• Concentration x time


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?


Communicate the Types of Detectors for Chemical Agents


DETECTORS

M8 Paper ‐ Detects liquid presence/type

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DETECTORS

M9 Paper ‐ Detects liquid presence only


Lightweight Chemical Detector (LCD) 3.3


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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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)


ANY QUESTIONS?


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


NERVE AGENTS

Substances that cause biological effects by inhibiting the enzyme acetylcholinesterase (AChE).


SPECIFIC AGENTS

GA (Tabun)

GB (Sarin)

GD (Soman)

GF

VX

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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


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


NERVE TRANSMISSION:NERVE TO NERVE

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NERVE TRANSMISSION:NERVE TO TARGET ORGAN


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


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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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


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)


EFFECTS ON SMOOTH AND CARDIAC MUSCLE

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EFFECTS ON EXOCRINE GLANDS


NICOTINIC EFECTS

Skeletal muscles

Fasciculations

Fatigue

Flaccid paralysis

Preganglionic nerves

Tachycardia

Hypertension


EFFECTS ON STRIATED (SKELETAL) MUSCLE

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HEART RATE VARIABLE

Muscarinic (vagal) decreases )

Nicotinic (ganglionic) increases )

Hypoxia: decrease oxygen )

May be high, low, normal )


CNS EFFECTS

Acute, large exposure to nerve agent

Loss of consciousness

Seizures

Apnea

Death


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


MANAGEMENT MARCHE (2)

Massive hemorrhage/Mask Check

Airway/Antidotes

Respirations/ Spot decontamination

Circulation/ Countermeasures

Hypothermia /Head wounds

Evacuation

Supportive Care


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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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


Antidote Treatment Nerve Agent Auto‐Injector (ATNAA)


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


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


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


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


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?


Communicate the Signs and Symptoms, Physical Exam Findings,

and Management of Cyanide Poisoning


CYANIDEA naturally occurring, rapidly acting

poison found in many plant sources

(also known as blood agents)

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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


NONMILITARY USES

Poisonings

Terrorists, executions, homicides, suicides

Industry

Electroplating

Plastics processing

Gold and silver extraction

Fumigation

Photography

Metallurgy


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


SITE OF ACTION

Primary site of action: Cells rather than blood

Organelles affected: Mitochondria


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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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


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


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


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


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


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-


ANY QUESTIONS?

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Communicate the Signs and Symptoms, Physical Exam Findings, and Management of Pulmonary

Irritants


PULMONARY IRRITANTS

Compounds that result in varying degrees

of pulmonary edema, usually after a

symptom‐free period.


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


SPECIFIC AGENTS

PFIB’s (Perfluoroisobutylene’s) ‐given off when teflon burns‐lines the interior of many armored vehicles


SPECIFIC AGENTS

Oxides of Nitrogen ‐products of burning gunpowder which can build to toxic levels with repetitive firing of artillery

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ANATOMY

Upper Airway

Naso/oropharynx to larynx

Central Airways

conducting

larynx to terminal bronchiole

Peripheral Airways

gas exchange

respiratory bronchiole to alveoli


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)


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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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


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


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


CHLORINE ‐ TISSUE EFFECTS

Effects are Local Not Systemic

In Central Airways ‐ from HCl

necrosis, sloughing

In Peripheral Airways

damage alveolar‐capillary membrane


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


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


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


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


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


ANY QUESTIONS?


Communicate the Signs and Symptoms, Physical Exam Findings, and Management of Vesicants

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VESICANTS

Also known as blister agents


SPECIFIC AGENTS

Sulfur Mustard (H,HD)

Nitrogen Mustard (HN1, HN2, HN3)

Lewisite = chlorovinyldichloroarsine (L)

Mustard / Lewisite Mixtures (HL,HT,TL)

Phosgene Oxime (CX)


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)


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


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


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


SKIN EFFECTS

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VESICANT EFFECTS


BLIND LEADING THE BLIND


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


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


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


MUSTARD: LONG TERM

Carcinogen/Mutagen

No evidence of human reproductive toxicity

Chronic Exposure

Respiratory cancer

Unclear: chronic bronchitis, emphysema


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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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


Vesicant Comparison


PHOSGENE OXIME

Urticant, not vesicant

Rapid onset

Corrosive to all tissues (skin, eyes, lungs)

Management same as mustard

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ANY QUESTIONS?


Communicate the Signs and Symptoms, Physical Exam Findings, and Management of Incapacitating

Agents


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)


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


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


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


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


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


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


ANY QUESTIONS?


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


DECONTAMINATION

Early decon protects casualty

within minutes

Late decon protects medical personnel and facility


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


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


PHYSICAL REMOVAL

M295 Individual Equipment Decontamination Kit

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PHYSICAL REMOVAL

Reactive Skin Decontamination Lotion (RSDL)


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


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


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)


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.


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.


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


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


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

51


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


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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NBC ‐FIELD TREATMENT OF THE CHEMICAL CASUALTY PFN: SOMEML14

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