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Transcript
WEAPONS OF MASS
DESTRUCTION
The Health Care Professional’s Role
in
Preparation & Response
Course Objectives
• At the conclusion of this program, participants will be able to:
• Define the term weapons of mass destruction (WMD) and categorize the
types of WMD most likely to be used in acts of terrorism;
• Discuss how acts of terrorism involving WMD have impacted the public
health system and the practice of medicine;
• Recognize the signs and symptoms of exposures to WMD; Utilize current
treatment modalities for patients exposed to WMD;
• Explain the health care practitioner’s role in syndromic surveillance and
reporting; and use the Health Alert Network as an informational
resource.
• Identify personal protective equipment needed by health care practitioners
when treating patients exposed to WMD;
• Explain the procedures necessary to decontaminate a casualty.
Weapons of Mass Destruction
The Threat
Weapons of Mass Destruction
The Threat
U.S. Threat increasing:
 Accessibility to these materials by an increasing number of
potential adversaries:
 International instability
 Terrorist networks
 Strength and perceived invulnerability of the United States’
homeland and military.
 Changing dynamics of non-state violence.
Why Use WMD Agents?
• Four dangerous characteristics
• Lethality
• Small quantities = devastating effects
• Portability
• Not easily detected
• Accessibility
• State sponsored terrorism
• Black market sales
• Easy to produce
• Commercially available products
Consequences:
• Potential for massive casualties
• Panic
• Fear of the unknown:
In the Tokyo subway attack out of the 5,510
individuals seeking medical attention. 4,073
were not exposed.
• Contamination
• Economic damage
• Loss of strategic position
• Social-psychological damage & political
change
Role of Healthcare Providers
• Education
For ourselves
For our patients
• Recognition
When an incident occurs
What is the cause
When to report
• Treatment
Supportive care
Pharmacotherapy
Decontamination
Medical Aspects
of
Nuclear
and
Radiological Agents
Ionizing Radiation Basics
Alpha Particle
• Heaviest and most highly charged
• Least penetrating
• Travel 4-7 inches in air
• Stopped by an ordinary sheet of paper
• External exposure not a serious hazard
• Internal exposure can be the most damaging source of radiation exposure
Beta Particle
• Smaller and travel much faster than
alpha particles
• Penetrate further into any material
or tissue
• Can travel several millimeters
through tissue but generally not
far enough to tissue, reach vital
organs
• May be a major hazard when
internal
Gamma Ray
• Similar to medical x-rays
• Are a type of electromagnetic radiation
• The most hazardous type of radiation
from sources outside the body
• Greatest distances and penetration
Penetrating Power
Ionizing Radiation Basics
Sources of Ionizing Radiation
• Hospital radiation therapy
Cobalt-60, Cesium-137
• Nuclear power fuel rods
Uranium-235. Plutonium
• Universities, laboratories, radiography and gauging
Cobalt-60, Cesium-137, Iridium-192, Radium-226
Measurement
• Rad (R): Traditional unit
(Radiation Absorbed Dose)
• Gray (Gy): Sl unit
1 Gy=100 rad=100 cGy (=1 J/Kg)
• Rem (R): Traditional unit
• Effective dose (Rad x weighting factor)
• Sievert (Sv): Sl unit
• 1 Sv=100 rem=100 cSv
Dose in Perspective (mrem)
• Chest x-ray
• US average/year
• Occupational annual limit
• Detectable physical effect
• Physical symptoms
• Death possible
• LD50
20
360
5 000
20,000
100,000
250,000
450,000
Measurement
and
Dose
Perspective
of
Ionizing
Radiation
Radiation Exposure
Nuclear
• Nuclear threat unlikely
• Expensive
• Logistically intensive
• Technologically difficult
• Attacks against nuclear storage facilities, power plants or transportation
systems possible
Radiation Dispersion Devices
• RDD’s or “Dirty Bombs”
• Combines conventional explosives with a radioactive source
(ionizing radiation)
• First seen in 1995 (Chechen rebels)
• Not a “fission” or “fusion” process
• Tool of fear
• Most probable sources would not cause severe illness from radiation
• May prevent the use of an area for prolonged periods
Clinical Effects
• Radiation interacts with atoms, depositing energy and resulting in
ionization
• Ionization can damage critical molecules or structures in a cell
• Directly hits a particularly sensitive atom or molecule in the cell
• Irreparable; the cell either dies or malfunctions
• Indirectly by interacting with water molecules
• Deposited energy leads to the creation of unstable, toxic
hyperoxide molecules
Clinical Effects
Acute Radiation Sickness
A combination of clinical
syndromes occurring:
In stages (prodromal, latent,
manifest illness)
During a period of hours to
weeks after exposure, as injury
to various tissues and organs is
expressed.
Hematopoietic Syndrome
• Dose range: > 0.7 Gy
• Effects: stem cells of all marrow cell lines
• Prodromal Period
Nausea, vomiting, anorexia, possible
diarrhea
Onset at 3-24 hours, duration <48 hours
Severity = increases with dose
• Latent Period
Mostly asymptomatic, except mild
weakness 3-4 weeks
Hair loss/weight loss, about day 14
Manifest Illness
Onset 3-5 weeks
Bone marrow atrophy
hemorrhage and infection
Clinical Effects
Gastrointestinal Syndrome
• Dose range: >6 Gy
• Effects: Gl stem cells and small vessels
Prodromal Period
Severe N/V diarrhea fever in 1-4 hours
• Latent Period
5 – 7 days
Manifest Illness
Paralytic ileus, bloody diarrhea, severe
vomiting, shock, sepsis
Cardiovascular / CNS Syndrome
• Dose: >20 Gy
• Effects: small blood vessels, especially in brain
• Cerebral edema, death 2-3 days
Clinical Actions
Triage
• By conventional injuries
• Trauma
• Burns
• By radiation injury
• Prodromal symptoms
• N/V < / > 4 hours is the yardstick
• Hematologic picture
Treatment
• Standard emergency medical procedures
• Decontaminate AFTER stabilized
• Radiation injury NOT acutely life
threatening
• Supportive Care
• Clean environment
• Vascular integrity: IV fluids, blood
products,
stop losses
• Prophylactic antibiotics
• Definitive Treatments
• Cytokines
Clinical Actions
Internal Contamination
• Reduce intake and deposition
• Increase elimination
• Blocking and Diluting Agents
• Kl, calcium, aluminum, barium, strontium salts
• Chelating Agents
• EDTA, DTPA, Deferoxamine, Penicillamine, Prussian Blue
Dosimetry
• Initially
• RADIACs
• Nasal swabs (~5% of lung deposition)
• Skin appearance
• CBC q 4-6 h
• Later
• Nuclear medicine equipment
• Bioassay: Excretion Sampling
• Baseline and 24-hour urine/stool collections
(according to nuclide)
Medical Aspects
of
Chemical Agents
Medical Aspects
Chemical Agent Hazards
• The ability to present a health hazard is
dependent upon:
• The composition of the material
• Volatility or persistency
• Route of exposure
• Amount of exposure
Composition
• Aerosol – a collection of very small solid particles or liquid
droplets suspended in a gas
• Vapor – the gaseous form of a substance at a temperature
lower than the boiling point of that substance at a given
pressure
Key Point:
Aerosols settle faster than vapors
Volatility / Persistency
Volatility – the degree to which a
substance will spontaneously evaporate
• Dependent upon:
• Chemical composition
• Ambient temperature and air pressure
• Wind speed
• Surface contact
Persistency – the degree to which a
substance resists evaporation and poses a
liquid hazard.
Key Point:
Volatile chemicals are a vapor hazard
Persistent chemicals are a contact hazard.
Route to Exposure
• Persistent agents exert toxic effects primarily by direct exposure
• Systemic absorption may occur with large exposures
• Non-persistent agents are primarily a respiratory hazard
• Vapor may effect the eyes and skin
Amount of Exposure
• Effects are proportional to the amount of exposure
• For liquid exposure:
• ED50 is the amount of agent that will cause effects in 50% of those exposed
• LD50 is the amount that will result in death in 50% of those exposed
For vapor exposure:
• Concentration time product (Ct) is used
• Calculated based on agent concentration
62g and duration of exposure
• Concentration expressed as mg/m³
• Time expressed in minutes
• Does not take into account rate and depth
of respiration
Example
Exposure to 4 mg/m³ of a
given agent for 10 minutes =
Ct of 40-mg m/m3
Exposure to 10 mg/m³ of a
given agent for 4 minutes =
Ct of 40-mg m/m3
Classification & Characteristics
Nerve
Tabun
Sarin
Soman
Vesicarts
Mustard
Lewisite
CyanideBlood
Pulmonary
Hydrogen Cyanide
Phosegene
Cyanogen Chloride
Chlorine
Phosgene Oxima
VX
Generally liquid at room temperature
• Disseminated as vapor or aerosols
• Time of onset is seconds to hours
Riot Control
Maze
Tear Gas
Pepper Spray
Nerve Agents
AGENT
Tabun
Sarin
Soman
VX
AGENT
SYMBOL
GA
GB
GD
VX
ODOR
None or
fruity
None or fruity
None
None or
Sulfur
RATE OF
ACTION
INHALATION: Very fast
Skin penetration: seconds to minutes
PERSISTENCY
Non-persistent
Persistent
Nerve Agents
Mechanism of Action
• A substance that causes effects by inhibiting
acetylcholinesterase ( AChE)
• The enzyme that breaks down acetylcholine (Ach)
Normal Physiology
Electrical impulse goes down nerve
Impulse causes release of ACh, carrying impulse across synapse
ACh Stimulates receptor site on organ & causes organ to act
ACh is destroyed by AChE
Organ activity ceases
Exposure to Nerve Agent
Impaired Physiology
AChE is inhibited and does not destroy Ach, which continues to stimulate organ and
causes overstimulation
Toxicity
GA
GB
GD
VX
LCt
mg-min/m³
400
100
70
10
LD
mg/70kg
1,000
1,700
50
10
Nerve Agent Clinical Effects
Effects of exposure depend on dose and route
• Small amounts of vapor first affect sensitive organs of the face, eye,
airway
• Small amounts of liquid on the skin causes localized affects at the
point of contact
• Lethal amounts cause rapid cascade of events
Eye
• Miosis is a characteristic sign of
exposure
• Complaints of
Pain
Dim vision
Blurred vision
Conjunctival injection
Respiratory
• Rhinorrhea (dose dependent)
• Bronchoconstriction and increased
secretions
• Respiratory arrest (CNS mediated)
• Complaints of
• Tight chest
• Severe breathing difficulty
• Gasping, irregular breathing
Nerve Agent Clinical Effects
Gastrointestinal / Genitourinary
• Nausea, vomiting
• Pain in abdomen
•Diarrhea involuntary defecation or urination
Central Nervous System
• Large amounts
• Loss of consciousness
• Seizure activity
• Apnea
• Begins in minutes after large exposure
• Asymptomatic period of 1 to 30 minutes
after skin contact with a liquid agent
Glands
• Increase in secretions
Lacrimal
Nasal
Salivary
Bronchial
Skeletal Muscle
• Fasciculation and twitching
• Large amount
• Fatigue
• Muscular flaccidly
SLUDGE
S - Salivation
L - Lacrimation
U - Urination
D - Defecation
G - Gastric distress
E - Emesis
Laboratory Findings
• Decreased RBC-ChE activity
• Poor correlation between degree of enzyme inhibition and amount of
exposure or physical signs
• Severe systemic effects generally indicate inhibition of 70 – 80%
• Wide inter- and intrapersonal variability
• Other laboratory findings will relate to complications
Medical Management
Management of a casualty with nerve agent intoxication consists of
decontamination, ventilation, administration of antidotes, and supportive
therapy. The condition of the patient dictates the need for each of these and
the order in which they are instituted.
Ventilation
• Requirement may last from 0.5 to 3 hours
• Airway resistance is high (50-70cm of water)
• Bronchoconstriction and secretions require vigorous pulmonary toilet
Antidotes
• Atropine
• Pralidoxime chloride
•Benzodiazepenes
Atropine
• Anticholinergic drug
• Blocks excess acetylcholine
• Clinical effects at muscarinic sites
• Dries secretions & relaxes smooth
muscle
• Dose
• 2mg every 15 minutes
• Can require 15 to 20 mg
• Therapy endpoints
• Atropine eyedrops
Nerve Agent Actions
Benzodiazepenes
• Diazepam / Lorazapem
• Decrease seizure activity
• Administered to patient with severe
symptoms regardless if seizure
activity is present
• Further doses titrated to seizure
activity
Pralidoxime Chloride
• Attaches to the nerve agent and breaks
the agent-enzyme bond
• Clinical effects at nicotinic sites
• Stops muscle fasiculations
• Dose
• Should be initiated concurrently with atropine
• 1 gram IV over 20min
• Repeated q1h for two or three additional doses
Nerve Agent Actions
Triage Immediate
• Unconscious
• Convulsing
• Postictal
• Apneic
Delayed
• Liquid – contamination without symptoms
• Recovering after antidotal therapy
Minimal
• Walking and talking after exposure
Vesicants
AGENT
Mustard
Lewisite
Phosgen Oxime
AGENT SYMBOL
H
K
CX
ODOR
Garlic
Geraniums
Irritating
RATE OF
ACTION
No immediate
symptoms
absorption in
seconds
Immediate Pain
Immediate
symptoms can get
worse every time
PERSISTENCY
Persistent
Persistent
Non-persistent
Mechanism of Action
• Cause of death by interfering with DNA
and cellular function (radiomimetic)
• Primarily a liquid threat may become vapor
at higher temperatures
• Agents
– Mustard (H, HD)
– Lewisite (L)
Toxicity
• Through skin surfaces within 2 minutes
– Cellular interaction: 1 to 2 minutes
– Clinical effects: 2 to 48 hours (avg. 4-8)
• Penetration is enhanced by moisture, heat, and
thin skin
Liquid
• Blister 10μg
• Death 100 mg/kg 7 gm/70 kg
Clinical Effects of Nerve Agents
• Have local and systemic effects
• Effects dependent on:
– Ambient temperature and humidity
– Site exposed
Clinical Effects of Nerve Agents
Skin
•
•
•
•
Erythema (appears 2 – 48hrs)
Small vesicles; later coalesce
Blisters (12 – 24hrs)
Blister fluid is clear, and does not contain
mustard
• Weeks to months for complete healing
Clinical Effects of Nerve Agents
Airway
• Upper Airway
– Burning & irritation of nose, sinuses & pharynx;
laryngitis and nonproductive cough
– Damage to the trachea and upper bronchi lead to
productive cough
• Lower Airway
– Increasingly severe productive cough
– Distal airways & alveoli only affected in terminal
event: pulmonary edema not usually seen
• Death by respiratory failure
– Mechanical obstruction & laryngospasm
– Secondary pneumonia
Clinical Effects of Nerve Agents
Eye
• Very sensitive to mustard vapor
• Short latent period
• Mild
– Conjunctivitis
– Blepharospasm
• Moderate
– Lid inflammation, edema
• Severe
– Corneal opacification, ulceration, perforation
Clinical Effects of Nerve Agents
GI
• Primarily through ingestion
• Early (<24 hours)
– Transient symptoms
– Cholinergic effect
• Late (>3 days)
– Severe damage
– Cytotoxic effect
Clinical Effects of Nerve Agents
CNS
• CNS effects remain poorly defined
• Animal work demonstrates mustards are
convulsants
• Several human case reports describe
neurological effects with large amounts
Clinical Effects of Nerve Agents
Hematopoetic
• Bone marrow depression
– Severe cases of skin and inhalation exposure
– Usually irreversible
Diagnostic Studies
• Differential diagnosis includes contact
dermatitis, drug eruption, or severe
sunburn
• CBC
- Early leukocytosis followed by leukopenia
• Early chemical pneumonitis
– Fever, WBC, chest x- ray
• Pneumonia: sputum exam / culture
Medical Management: Skin
• Soothing cream/lotion (0.25% camphor
and menthol, calamine)
• Small blisters (under 1-2cm) left intact
• Systemic analgesics
• Appropriate IV fluids and electrolytes
Medical Management: Eyes
• Irrigation
• Artificial tears
• Topical mydriatics
• Topical antibiotics
• Vaseline on lid edges
• Topical analgesics (nsaid drops)
• Avoid topical anesthetics
• Sunglasses
Medical Management: Airway
•
•
•
•
•
Steam, cough suppressants
Oxygen
Bronchodilators, steroids
Early intubation
Assisted ventilation, early use of PEEP or
CPAP
• Bronchoscopy
• Antibiotics AFTER organism identified
Medical Management: GI
• Antiemetics
• Fluid therapy
• Electrolyte replacement
Antidotes
• British Anti-lewisite (BAL)
– Initial dose: 0.5cc per 25 lbs IM (up to 4cc)
– May be repeated at 4, 8, 12 hours after initial
dose
• Must consider toxicity of treatment
– Hypertension
– Nausea/vomiting
Triage
• Immediate
• Airway effects
• within the first
several hours after
exposure
Delayed
• Most patients
• 5% to 50% BSA
• Moderate lung
effects
• Ocular injuries
• Minimal
– Skin lesions covering <5% BSA
Cyanides / Blood Agents
AGENT
Hydrogen Cyanide Cyanogen chloride
AGENT SYMBOL
CX
ODOR
Bitter almonds
CK
RATE OF ACTION Immediate, Seconds
PERSISTENCY
Non-persistent
Cyanides / Blood Agents
• Route of exposure is inhalation
• Body can detoxify a limited amount
– Binds to sulfur molecule, converting to
thiocyanate
• Primary site of action at cellular level
• Interruption of cellular respiration in
mitochondria by binding to cytochrome a3
– Result is anaerobic metabolism lactic to
acidosis
Clinical Effects
• Lower concentrations
– Hyperpnea
– Feelings of anxiety apprehension
– Weakness
– Nausea
– Muscular trembling
• The “classical” cherry red skin, and smell
of bitter almonds are seldom seen
Clinical Effects
• Higher concentrations
• Effects manifest primarily in the CNS
• Transient hyperpnea followed by
convulsions ~ 15 seconds after
exposure
• Respiratory activity ceases 2 – 3 minutes
• Cardiac activity ceases within 6 – 8
minutes
Diagnostic Studies
• Blood cyanide levels
• Mild effects at 0.5 mcg/ml – 1.0 mcg/ml
• Coma, convulsions and death at greater
than 2.5 mcg/ml
• Anion gap acidosis
• Venous blood gas analysis
• Higher than normal venous
oxygen content
Medical Management
• General supportive therapy
• Ventilatory support
• Circulatory support (crystalloids/vasopressors)
• Treat metabolic acidosis (hyperventilation and
bicardbonate administration)
• Specific antidotal therapy
• Cleaves cyanide-cytochrome a3 bond
• Sulfur donor
Antidotal Therapy
• Amyl nitrite
• Given by inhalation by crushing vials
• 15 minutes on; 15 minutes off
• Converts Hb02 (Fe2+) to metHb (Fe3+), but inhalation
leads to variable metHb levels
• Sodium nitrite
• Converts Hb02 (Fe2+) to metHb (Fe3+)
• 300 mg IV of a 3% soln (30 mg/mL) = 10 mL
• Sodium thiosulfate
• Sulfur donor
• 12.5 g IV of a 25% soln (250 mg/mL) = 50mL
Experience with Antidotes
“The combination of sodium nitrite and sodium
thiosulfate is the best therapy against cyanide and
hydrocyanic acid poisoning. The two
substances intravenously injected, one after the
other, namely the nitrite followed by the thiosulfate,
are capable of detoxifying approximately twenty
lethal doses of sodium cyanide in dogs and are
effective even after
respiration has stopped. As long as the heart is still
beating, the chances of recovery by utilizing this
method are very good.”
-Chen et al.
Pulmonary Agents
AGENT
Phosgene
Chlorine
AGENT SYMBOL
CG
CL
ODOR
Newly mown
grass or hay
Swimming pool
RATE OF ACTION Immediate symptoms can get worse
over time
PERSISTENCY
Non-persistent
Triage
• Immediate
• Presents within
minutes with
apnea or seizure
Delayed
• Mild effects
• Successfully
treated
Minimal
• Asymptomatic 5 minutes after removal
from exposure
Toxicity
• Absorbed almost exclusively by inhalation
• Penetrates down to bronchioles & alveoli
• Consumed at the alveolar capillary
alveolar-membrane
– No significant systemic distribution
• Membrane injury results in fluid
extravasation and pulmonary edema
Clinical Effects
• Pulmonary symptoms develop following a latent
period that is dependent on dose and physical
activity post-exposure
• Airway
Eye
• Mild cough
• Ocular irritation
• Dyspnea
• Lacrimation
• Chest tightness
• Corneal
• Rales
opacities
• Laryngospasm
• Corneal
perforation
Diagnostic Studies
• Differential Diagnosis
• Other chemical agent exposures
• Other causes of pulmonary edema
• No commonly available laboratory tests
• Increased hematocrit may reflect
hemoconcentration
• Arterial blood gases may show a low PaO2
• Decreased peak expiratory flow rates
• Early findings on chest x-ray are hyperinflation,
followed by pulmonary edema
Medical Management
• Supportive care
• Strict bed rest
• O2, PPV with PEEP / CPAP to maintain
PaO2
• Bronchodilators for bronchospasm
• IV fluids for hypotension (3rd spacing)
• Surveillance cultures
• Antibiotics when indicated
Triage
Immediate
• Pulmonary edema
anytime after
exposure
Delayed
• Dyspnea with no
objective findings
• Re-triage q1h
• Observe 24h
Minimal
• Asymptomatic with known exposure
• Mild eye or upper airway irritation
• Re-triage q2h, Discharge in 12h
Summary
Weapons of Mass Destruction can include:
• Nuclear and Radiologic Agents
• Chemical Agents
• Nerve Agents
• Pulmonary Agents
Triage and Treatments
• Vary by type of agent and exposure