Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
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