Notes

Outline

Training Overview

Purpose

Partnership

Background

Background

NBC “Delta”

Train-The-Trainer Courses

Leave-Behind Training Materials

Follow-On Support

Domestic Preparedness Hospital Provider Training

Overview Introduction Threat of NBC Terrorism Chemical Casualty Care Biological Casualty Care Radiological Casualty Care Special Hospital Considerations in NBC Terrorist Incidents Additional Information for Independent Reading

Course Goals Train healthcare providers to initiate the correct medical response and treatment actions in a Nuclear, Biological, or Chemical (NBC) terrorist incident, including: Identifying various threat agents, and the signs and symptoms of exposure to them Selecting the proper treatment for resulting conditions Identifying special threats to healthcare providers, such as secondary contamination

Focus - NBC Delta Nuclear Materials Biological Agents Chemical Agents

Everyday HAZMAT Incident vs. NBC Terrorism Incident HMI NBCTI Deliberate attack D Greater agent toxicity D Early hazard identification x Potential for mass casualties D Need for mass decontamination D Unusual risk to   D     healthcare providers

Everyday HAZMAT Incident vs. NBC Terrorism Incident

Instructor Introductions

Slide 17

Objectives To familiarize you with Recent NBC events The potential for terrorist use of NBC agents Sources and hazards of NBC agents Targets and indicators of NBC attacks Outcomes of NBC terrorist events So that you can recognize an NBC attack and understand the potential impacts

Potential Probability vs. Impact

NBC Terrorist Incidents Since 1970

Groups That Threaten Lone individual Identified local or non-aligned terrorist groups Internationally sponsored Doomsday cults Insurgents

Why NBC Terrorism? Agents are available & relatively easy to manufacture Large amount not needed in enclosed space NBC incident difficult to recognize Easily spread over large areas Psychological impact Can overwhelm existing resources

Proliferation of Anthrax Hoaxes B’nai B’rith, Washington, D.C. April 1997 30 persons decontaminated

Limitations of NBC Agents Effective dissemination difficult Delayed effects can detract from impact Counterproductive to terrorists’ support Potentially hazardous to the terrorist Development and use require skill

NBC Agent Sources Home production Laboratory / commercial production Industrial facilities Foreign military sources Medical / university research facilities

Potential Terrorist Targets Enclosed spaces Large crowds (high profile events) Critical facilities and infrastructure Accessible facilities with significant                          hazard / damage potential (materials in transit) Facilities of interest to terrorists’ cause

The Fallacies It can’t happen to us NBC agents are so deadly the victims will all die anyway There is nothing we can do

Practical Exercise

Trainer Points Use FBI video OR additional slides; not both Update module with recent local incidents Points to emphasize Terrorist groups have means, motive, opportunity NBC agents have far-reaching effects Advantages and limitations of NBC agents Identify potential targets in your community

Hospital Provider Management of Chemical Agent Casualties

Chemical Warfare Agents Terminal Objective Describe types of chemical warfare agents Recognize signs and symptoms of exposure Describe management of chemical agent attack victims

Chemical Warfare Agents Historical Perspective Chemicals used in military operations to kill,    injure, or incapacitate Battlefield use World War I and Middle East conflicts Terrorist use Matsumoto and Tokyo, Japan

Chemical Agent Terrorist Attacks Matsumoto: Approximately                     280 injured 7 dead Tokyo 12 dead Approximately 1,000 hospitalized 5,500 sought medical care 10% of first responders injured

Chemical Warfare Agents Tabun, Sarin, Soman, VX Mustard, Lewisite Phosgene, Chlorine, Ammonia, Cyanide Mace®, Pepper Spray Nerve Agents Vesicants Industrial Chemicals Riot Control Agents

Nerve Agents Tabun (GA), Sarin (GB), Soman (GD), VX Most toxic of the chemical agents Penetrate skin, eyes, lungs Loss of consciousness, seizures, apnea,   death after large amount Diagnosis made clinically; confirmed in laboratory (cholinesterase)

Normal Nerve Function

Normal Nerve Function

Normal Nerve Function

How Nerve Agents Work

Effects of Nerve Agents Organs with cholinergic receptors Muscarinic  Smooth muscles  Glands Nicotinic  Skeletal muscles  Ganglia

Signs and Symptoms of Nerve Agents Muscarinic Sites Increased secretions Saliva Tears Runny nose Secretions in airways Secretions in gastrointestinal tract Sweating

Signs and Symptoms of Nerve Agents Muscarinic Sites Smooth muscle contraction Eyes:  miosis Airways:  bronchoconstriction (shortness of breath) Gastrointestinal:   hyperactivity (nausea, vomiting, and diarrhea)

Signs and Symptoms of Nerve Agents Nicotinic Sites Skeletal muscles Fasciculations Twitching Weakness Flaccid paralysis Other (ganglionic) Tachycardia Hypertension

Nerve Agents Other Signs and Symptoms Cardiovascular Tachycardia, bradycardia Heart block, ventricular arrhythmias Central Nervous System Acute Loss of consciousness Seizures Apnea Prolonged (4-6 weeks) Psychological effects

Signs and Symptoms of Nerve Agents Vapor Exposure Mild exposure Miosis (dim vision, eye pain), rhinorrhea, dyspnea Moderate exposure Pronounced dyspnea, nausea, vomiting, diarrhea, weakness Severe exposure Immediate loss of consciousness, seizures, apnea, and   flaccid paralysis Vapor effects occur within seconds, peak within minutes; no late onset

Signs and Symptoms of Nerve Agents Liquid Exposure Mild exposure (to 18 hours) Localized sweating Fasciculations No miosis Moderate exposure (<LD50) (to 18 hours) Gastrointestinal effects Miosis uncommon Severe exposure (LD50) (<30 minutes) Sudden loss of consciousness Seizures Apnea Flaccid paralysis Death

Diagnosis of Nerve Agent Exposure Symptomatic May be systemic or organ-specific Combination of symptoms is more definitive Situational Multiple casualties with similar symptoms Time or location factors in common

Nerve Agent Treatment Airway/ventilation High resistance Antidotes Atropine 2-PAMCl Diazepam

Nerve Agent Treatment Atropine Antagonizes muscarinic effects Dries secretions; relaxes smooth muscles Given IV, IM, ET No effect on pupils No effect on skeletal muscles IV in hypoxic patient  Ù ventricular fibrillation

Nerve Agent Treatment Starting dose - 2 mg Maximum cumulative dose - 20 mg Total dose calculated over time; but enough must be administered to abate severe symptoms if casualty               is to survive Insecticide poisoning requires much more Side effects in normal people Mydriasis Blurred vision Tachycardia Decreased secretions and sweating

Nerve Agent Treatment Atropine - How much to give? Until secretions are drying or dry Until ventilation is “easy” If conscious or casualty is comfortable Do not rely on heart rate/pupil size

Nerve Agent Treatment Pralidoxime Chloride (2PAM-Cl) Remove nerve agent from AChE in absence of aging 1 gram slowly (20-30 minutes) in IV infusion Hypertension with                                                         rapid infusion No effects at muscarinic sites Helps at nicotinic sites

Nerve Agent Treatment - Autoinjectors

MARK I Injection vs. IM or IV

MARK I Injections - Dispersal

Nerve Agent Treatment Diazepam Decreases seizure activity Reduces seizure-induced brain injury Give to severely-intoxicated casualties whether convulsing or not

Nerve Agent Treatment   Treatment regimen No signs/symptoms Reassure Observe Vapor:  1 hour Liquid:  Up to 18 hours

Nerve Agent Treatment Mild vapor exposure Miosis, rhinorrhea - observation only Increasing SOB - treat Mild liquid exposure Localized fasiculations & sweating - treat One MARK I kit (2 mg atropine/ 600 mg 2 -PAMCl) OR 1 gram 2-PAMCl IV 2 mg atropine, IM or IV Parenteral atropine will not reverse miosis

Nerve Agent Treatment Moderate vapor or liquid exposure One or two MARK I kits Or give IV: 2 to 4 mg atropine 1gm 2-PAMCl (infusion)

Nerve Agent Treatment Severe - vapor or liquid Give 3 MARK I kits or 6 mg atropine and 1 gram of 2-PAMCl as soon as possible Airway Ventilation/O2 Consider diazepam 10 mg IM (2 to 5 mg IV) Repeat atropine every 5 to10 minutes as needed Repeat 2-PAMCl in one hour

Nerve Agent Age-Related Treatment Atropine Infant (0 to 2) 0.5 mg IM IV for infants and children 0.02 mg/kg Child (2 to 10) 1.0 mg IM Adolescent (> 10) 2.0 mg Elderly 1.0 mg IM

Nerve Agent Age-Related Treatment 2-PAMCl < 20 kg 15 mg/kg IV > 20 kg 600-mg IM autoinjector Elderly 1/2 adult dose (7.5 mg/kg IV) 2 PAMCl-induced hypertension Phentolamine Adult 5 mg IV Child 1 mg IV

Nerve Agent Age-Related Treatment

Nerve Agent Summary Vapor exposure Symptoms develop suddenly Most ambulatory victims require minimal intervention Risk of secondary contamination, which is minimized by removing the victim’s clothing Requires immediate access to antidotes

Vesicants (Blister Agents)

Mustard

Mustard Effects Quickly cyclizes in tissue Alkylates cell components, including DNA DNA damage, cell death

Mustard Effects Eye Injury Mild conjunctivitis Moderate/severe conjunctivitis, lid inflammation and edema, blepharospasm, and corneal roughening Corneal opacification, ulceration, and/or perforation Well over 95% had only mild to moderate conjunctivitis Under 1% had permanent damage to cornea

Mustard Effects Eye Injury

Mustard Effects Skin Injury Erythema Small vesicles; later coalesce Blisters/bulla Possible coagulation necrosis with liquid

Mustard Effects Airway Injury Upper:  nose sinuses, pharynx (epistaxis, sore throat, hacking cough) Mid:  Larynx (hoarseness) Lower:  Bronchioles (dyspnea, productive cough) Pulmonary edema is rare

Mustard Effects GI Injury Gastrointestinal Within 24 hours Nausea and vomiting Cholinergic effects After 3 to 5 days Tissue destruction

Mustard Effects Bone Marrow Damage Damages stem cells Decreased WBC, RBC, platelets after 3 - 5 days Survival rare if WBC < 200

Skin Treatment Decontamination must be done within minutes to reduce damage Delays in decontamination will not prevent illness, but will prevent cross-contamination Supportive care - soothing lotions, frequent irrigation, topical antibiotics, pain medication Do NOT overhydrate; not a thermal burn

Eye Treatment Topical mydriatics Topical antibiotics Vaseline on lid edges Topical steroids (only in the first 24 hrs)

Airway Treatment Cool mist, cough suppressants for mild symptoms Oxygen Assisted ventilation Early intubation Bronchodilators (steroids) Antibiotics AFTER organism identified

Lewisite Effects Causes severe irritation to eyes, skin, and airways IMMEDIATELY on exposure (no delay) Tissue necrosis, pseudomembranes Increased capillary permeability No bone marrow effects

Lewisite - Treatment Immediate decontamination British anti-Lewisite (BAL) for systemic effects Supportive Care Oxygen

Vesicant Agent Summary Agents damage eyes, skin, respiratory system; cause additional systemic effects Mustard Fast acting; symptoms delayed, no specific antidote Lewisite Fast acting, symptoms immediate, BAL antidote available Decontamination is best initial treatment

Phosgene At high concentrations: Irritates eyes, nose, upper airways; possible laryngospasm Toxic to lungs by inhalation Carbonyl group damages alveolar-capillary membrane Non-cardiac pulmonary edema: onset 2 to 12 hours Dyspnea, cough with sputum Management of non-cardiac pulmonary edema Hypoxia, fluid loss; requires pulmonary care, careful fluid replacement ABSOLUTE REST POST-EXPOSURE

Chlorine High concentration or prolonged exposure Pulmonary edema, sudden death Eye irritation, cough, dyspnea More severe airway and lung damage with high concentration Management Remove from exposure; manage airway Oxygen, ventilation, PEEP Intubation, bronchodilators

Ammonia Anhydrous Ammonia pH>12; (household ammonia pH < 12) Wide industrial use Plastics, fertilizer,  explosives Irritating, corrosive; causes necrosis, severe pain Serious injury to eyes, lungs, skin, GI tract Management Remove from exposure, decontaminate Symptomatic; maintain airway

Riot Control Agents Irritating agents, lacrimators,    “tear gas” Cause reaction in Eyes:  burning, tearing, eyelid spasm, redness Airways:  burning, coughing, dyspnea Skin:  burning, erythema Eye irrigation and supportive care

Chemical Agent Summary Vapor exposure Nerve agent symptoms develop suddenly, mustard and phosgene symptoms are delayed Most ambulatory victims require minimal intervention Risk of secondary contamination Requires airway management; antidotes for nerve agents and Lewisite

Chemical Agent Summary Liquid exposure Symptoms delayed minutes to hours  Greater need for decontamination Risk of secondary contamination, victims require clothing removal & decontamination Requires immediate access to antidotes

Hospital Management of  Biological Casualties

Biological Warfare Agents Terminal Objective Be able to describe the various types of biological warfare agents and recognize the signs and symptoms of exposure. Be able to describe how to properly manage and treat infectious victims Know which agents are a risk for secondary transmission and how to protect against this spread using personal protective equipment (PPE) and isolation measures.

Biological Warfare (BW) Agents - History Oldest of the NBC triad of agents Used for > 2,000 years Sieges of middle ages Smallpox blankets given to Native Americans Germany in World War I Japan in World War II

Aerosol / Infectivity Relationship

BW - Epidemiologic Clues Large epidemic with high illness and death rate HIV(+) individuals may have first susceptibility Respiratory symptoms predominate Infection non-endemic for region Multiple, simultaneous outbreaks Multi-drug-resistant pathogens Sick or dead animals Delivery vehicle or intelligence information

BW - Epidemiological Information Travel history Infectious contacts Employment history Activities over the preceding 3 to 5 days

Biological Agents - Types and Characteristics Bacteria Viruses Toxins

Bacteria as Biological Agents Bacteria Single celled microorganism Invade tissue; cause inflammatory reaction or produce toxins May form spores Anthrax Plague Tularemia Q Fever

Anthrax - Microbiology Bacillus anthracis - gram +, spore-forming bacillus Endemic infection in animals Humans develop infection naturally from handling contaminated fluids or hides (“Woolsorters Disease”)

Anthrax - Pathogenesis Inoculation, ingestion, or inhalation of spores which may travel to the regional lymph nodes Vegetative bacteria produce edema factor and lethal factor (toxins) Inhalation route has highest mortality and is most likely route to be used by terrorists Inhaled anthrax causes a mediastinitis rather than a pneumonia Untreated skin infection - 21% mortality if septicemia develops (treated 1%)

Cutaneous Anthrax

Gastrointestinal Anthrax

Inhalational Anthrax 2 to 6-day incubation period followed by fever, myalgias, cough, and fatigue Initial improvement followed by abrupt onset of respiratory distress, shock, and death in 24 to 36 hours Physical findings are nonspecific, pneumonia is rare Chest x-ray - may show widened mediastinum with or without a bloody pleural effusion 50 % of cases have associated hemorrhagic meningitis

Prevention of Secondary Anthrax Transmission No documented cases of person-to-person transmission of inhalational anthrax has ever occurred Cutaneous transmissions are possible Universal precautions required

Anthrax - Soviet Incident An accident at a Soviet military compound in Sverdlovsk (microbiology facility) in 1979 resulted in an estimated 66 deaths downwind.

Inhalational Anthrax - Sverdlovsk

Inhalational Anthrax Post Mortem - Sverdlovsk

BW Anthrax - Diagnosis Clinical picture of sudden onset of respiratory distress with mediastinal widening on x-ray A small number of patients may present with GI or cutaneous anthrax Gram stain of blood and blood cultures - but these may be late findings in the course of the illness ELISA and immunohistology testing may confirm diagnosis but samples must go to reference laboratory

Anthrax - Treatment Acute Treatment Usually futile in severe mediastinitis patients who inhaled or ingested spores Ciprofloxacin - 400 mg IV q 8 to 12 hr Doxycycline - 100 mg IV      q 12 hr X 4 wks Vaccination begins at the start of drug therapy

Anthrax - Pediatric Treatment Prophylaxis Penicillin Doxycycline IV Therapy Penicillin Doxycycline

Anthrax Disease Complex Summary

Plague - Microbiology Yersinia pestis - gram(-), non-motile, non-spore forming bacillus Fleas living on infected rodents spread infection to humans Recovery offers temporary immunity

Plague - Pathogenesis Produces disease by being consumed by macrophages and transported to regional lymph nodes, causing regional adenitis Bacteremia - spread to other organs (lungs, spleen, liver, and brain)

Plague Transmission

Pneumonic Plague Prevention of Secondary Infection Secondary transmission is possible and likely

Plague Endemic Counties

Inhalational (Pneumonic) Plague                         Signs and Symptoms 2 to 3 day incubation period followed by high fever, myalgias, chills, HA, and cough with bloody sputum In contrast to anthrax, pneumonia and sepsis develop acutely and may be fulminant with patients developing dyspnea, stridor, cyanosis, and circulatory collapse Patchy infiltrates or consolidation seen on chest x-ray

Bubonic Plague Signs and Symptoms Erythema, fever, rigors Bubo formation in regional lymph nodes Bubo aspiration and gram stain is diagnostic Differentiate from Tularemia Cat-scratch fever Staph-strep lymphadenitis

Acral Gangrene

Plague - Acral Gangrene

Plague - Diagnosis Gram stain and culture of lymph node aspirates, sputum, or CSF samples Bipolar staining “Safety Pin” may be present Immunoassays are also available

Plague - Treatment Care is otherwise supportive Vaccine effective only for bubonic plague Prophylaxis - tetracycline or doxycycline Antibiotics must be started within 24 hours of symptoms to impact survival Streptomycin (30 mg/kg/day IM divided BID for 10 days) Doxycycline (100 mg IV BID for 10 days) Chloramphenicol for plague meningitis

Plague - Pediatric Treatment Prophylaxis Doxycycline Trimethoprim/Sulfamethoxazole IV Therapy Streptomycin (over 1 year of age) Gentamicin Chloramphenicol

Plague Disease Complex

Viruses as Biological Agents Smallpox Viral Hemorrhagic Fevers (VHF) Venezuelan Equine Encephalitis (VEE)

Viruses - General Characteristics RNA or DNA within a protein coat Require a host to function and survive Many viruses attack a specific type of cell causing disease or cancer

Viruses - General Characteristics May cause disease through direct cytopathic effect, immune complex deposition and other effects May result in end-organ system failure, vascular damage Few antiviral medications available Vaccination is the most effective means of preventing infection

Smallpox - Microbiology Variola (Var-ï-óla) virus, an Orthopox virus, both minor and major forms of smallpox exist Structure is a large DNA virus Declared eradicated in 1980 and the U.S. stopped its civilian vaccination in 1981, U.S. military stopped in 1985

Smallpox - Pathogenesis

Smallpox - Case Study In 1963, en route by air from Australia to Sweden, a seaman stops in Djakarta, Singapore, Rangoon, Calcutta, Karachi, Teheran, Damascus, and Zurich Fifteen days later he develops a fever and rash Diagnosed with smallpox; 19 cases identified More than 300,000 vaccinated worldwide

Smallpox - Diagnosis & Treatment     DIAGNOSIS Clinical presentation Demonstrate virus from vesicular sampling via electron microscopy Confirmation by tissue culture

Smallpox - Prevention of Secondary Infection Contagious All contacts are quarantined for at least 17 days Infectious until all scabs are healed over

Monkeypox Virus

Smallpox / Monkeypox - Clinical Course Summary

Viral Hemorrhagic Fevers (VHF) - Microbiology RNA viruses causing high fevers and generalized vascular damage Human infections by insect bites or by contact with blood and body fluids

VHF Pathogenesis Fever, myalgias, prostration Cases evolve into shock and generalized mucous membrane hemorrhage Conjunctival injection, petechial hemorrhage, and hypotension Abnormal renal and LFT - poor prognosis Mortality varies; 50 - 80% Ebola Zaire Disease severity and survival depends on various host factors; target organ is the vascular bed.

VHF Treatment Hemodynamic resuscitation and monitoring Invasive Swan Gantz catheter as feasible Careful fluid management use of colloid Vasopressors and cardiotonic drugs Cautious sedation and analgesia No anti-platelet drugs or IM injections Coagulation studies and replacement of clotting factors / platelet transfusions

Prevention of Secondary VHF Transmission No vaccine is available at this time Single room w/ adjoining anteroom as only entrance handwashing facility with decontamination solution Negative air pressure if possible Strict barrier precautions gloves, gown, mask. shoe covers, protective eyeware/faceshield consider HEPA respirator for prominent hemorrhage, vomiting, diarrhea, cough

Prevention of Secondary VHF Transmission Chemical toilet All body fluids disinfected Disposable equipment/sharps into rigid containers and autoclaved/incinerated Double-bag refuse-outside bag disinfected Electronic/mechanical equipment can be paraformaldehyde disinfected

Prevention of Secondary VHF Transmission Wash / irrigate wound site immediately Mucous membranes (eye, mouth, nose) Continuous irrigation with rapidly flowing water or sterile saline for >15 minutes Skin Scrub for >15 minutes while copiously soaking the wound with detergent solution Germicidal solution (Dilute 1 part laundry bleach with 9 parts tap water)

The VHF RNA Viruses

Ebola Case Study April 5, 1995 -  Zaire laboratory worker - fever and bloody diarrhea May 17 - 93 cases - 92% fatality - most cases were in health care providers June 25 - 296 cases

Toxins as Biological Agents Botulinum Ricin Staphylococcal Enterotoxin B (SEB)

Toxins General Characteristics Naturally produced poisons More toxic per weight than manmade chemical agents Non-volatile Minimal absorption in intact skin Not prone to person-to-person transmission

Botulinum Toxin - Characteristics Neurotoxin produced by Clostridium botulinum - Botulism Most lethal compound per weight (15,000 times more toxic than the nerve agent VX) Different toxicity if inhaled or ingested

Botulism - Pathogenesis Blocks the release of ACh at 3 places in the presynaptic terminal of the neuromuscular junction and autonomic nervous system Bulbar palsies and skeletal muscle weakness

Botulism - Signs & Symptoms Descending paralysis Bulbar palsies blurred vision mydriasis diplopia ptosis