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 photophobia dysphagia dysarthria

Botulism - Diagnosis and Treatment Clinical diagnosis - bulbar palsy with descending paralysis Mouse neutralization assay can confirm diagnosis Treatment is supportive Long-term mechanical ventilation Antitoxins are available; must be administered early CDC vaccine protective for A and B toxins

Ricin - Characteristics Toxic by multiple routes of exposure Can be dispersed as an aerosol Effective orally, by injection, or inhalation

Ricin - Pathogenesis

Ricin - Signs & Symptoms Fever, chest tightness, cough, SOB, nausea, and joint pain 4 to 8 hours after inhalation Airway necrosis and edema leads to death in 36 to         72 hours Ingestion causes N,V, severe diarrhea, GI hemorrhage, and necrosis of the liver, spleen, and kidneys - shock and death within 3 days Injection causes marked necrosis of muscles and lymph nodes with multiple organ failure leading to death

Ricin - Diagnosis & Treatment     DIAGNOSIS Difficult Routine labs are         nonspecific ELISA of blood Immunohistochemical tests may confirm

Teaching Points BW EXPOSURE: WET OR DRY AGENT AEROSOLS BACTERIAL AGENTS LETHAL:  Anthrax, Tularemia, Plague NON-LETHAL:  Q Fever VIRAL AGENTS LETHAL:  Smallpox / Monkeypox, Viral Hemorrhagic Fevers NON-LETHAL: Venezuelan Equine Encephalitis TOXINS LETHAL:  Ricin, Botulinum Toxin A NON-LETHAL:  Staphyloccal Enterotoxin B SECONDARY INFECTION IS POSSIBLE WITH Plague, Smallpox/Monkeypox, and VHF

Biological Agents Case Study Emergency departments always seem busier during a full moon despite evidence to the contrary.  Tonight was no exception.  Over a 6-hour period, it seemed that almost half of the patients presented with similar complaints of high fever, cough, shortness of breath, and generalized ill feeling.  Five young, previously healthy individuals required intubation and mechanical ventilation for severe respiratory distress.  Strangely, most of the patients knew each other from work and none of their family members were suffering similar symptoms.  At 11 p.m., the only other community hospital in the area went on diversion because all of their intensive care unit (ICU) beds were full and their need for mechanical ventilators was at a critical level.  The public health officer on call was not aware of any recent infectious outbreak.

Biological Agents What might the causative agent be? How could you identify common factors which might relate the patients to each other? How long ago might the attack have occurred? If you are suspicious that patient illnesses could be the result of a biological attack,   whom should you notify? What precautions should you and other healthcare providers take?

Hospital Management of Nuclear Casualties

Terminal Objective Be able to describe the various types of radiological hazards. Become familiar with the acute health effects from radiation contamination and exposure. Become familiar with the principles of diagnosis, treatment and management of radiation casualties.

Radiological and Nuclear Devices Simple radiological device Radiological dispersal device Reactor Improvised nuclear device Nuclear weapon

The Basics of Radiation Ionizing radiation is electromagnetic energy or energetic particles emitted from a source. Ionizing radiation is able to strip electrons from atoms causing chemical changes in molecules.

The Basics of Radiation

Ionizing Radiation - Alpha 2 neutrons and 2 protons Highly ionizing Travels several centimeters in air and a few microns in tissue Component of nuclear fallout Stopped by a thin paper or clothing Threat is inhalation or absorption of alpha emitter in wounds

Ionizing Radiation - Beta High energy “electron” emitted from nucleus Can have wide range of energies depending upon the particular radionuclide Moderately penetrating Up to a few meters in air Millimeters in tissue

Gamma or X-Ray (Photons) High energy rays Very penetrating Difficult to shield Can be produced from radioactive decay and a nuclear weapon explosion or reactor accident

Ionizing Radiation - Neutrons Neutral particle emitted from the nucleus Can be very penetrating Requires special consideration for shielding

Examples of Radioactive Materials

Radiation Half-Life Time required for a radioactive substance to lose half of its radioactivity Each radionuclide has a unique half-life Half-lives range from extremely short (fraction of a second) to millions of years Examples: Tc-99m 6.0 hrs I-131 8.05 days Co-60 5.26 yrs Sr-90 28.1 yrs Pu-239 24,400 yrs U-238 4,150,000,000 yrs

Radiation - Units of Measure rad - basic unit for measuring radiation rem - quantifies the amount of damage that is suspected from a particular type of radiation dose

Radiation Doses in Perspective Natural background and manmade radiation       360 mrem / yr Diagnostic chest x-ray                                                    10 mrem Flight from LA to Paris                               4.8 mrem Barium enema                              800 mrem Smoking 1.5 ppd                    16,000 mrem / yr Heart catheterization     45,000 mrem Mild acute radiation sickness                   200,000 mrem LD50 for irradiation                                 450,000 mrem

Types of Radiation Exposure External irradiation - whole-body or partial-body Contamination by radioactive materials - external (deposited on the skin) or internal (inhaled, swallowed, absorbed through skin, or introduced through wounds) Incorporation of radioactive materials - uptake by body cells, tissues, or organs (bone, liver, kidney, etc) Combined radiation injury - combination of the above complicated by trauma.

Radiation Injury - External Irradiation

Radiation Injury - Contamination

Radiation Injury - Incorporation

Radiation - LD50 We know what radiations are produced We know how to measure them But the body senses cannot detect radiation.  Therefore, how can we measure the biological damage? LD50/30 Animals LD50/60 Human

Examples of LD50 for Given Species Species          Dose (rads) Guinea Pigs 250          LD 50/30 Goat 350       LD 50/30 Man 250-450   (LD 50/60) Mouse 570           LD 50/30 Rat 550-800    LD 50/30 Frog 700        LD 50/30 Snail 8,000-20,000    LD 50/30

Severity of Injury The higher the dose, the more severe the early effects and the greater the possibility of delayed effects

Acute Radiation Syndrome (ARS) Group of symptoms that develop after total body irradiation (> 100 rads) May occur from either internal or external radiation Four important factors are: High Dose High Dose Rate Whole Body Exposure Penetrating Radiation

ARS - Phases Prodromal Phase - occurs in the first 48 to 72 fours post-exposure and is characterized by nausea, vomiting, and anorexia.  At doses below about 500 rads last 2 to 4 days. Latent Phase - follows the prodromal phase and lasts for approximately 2 to 2 1/2 weeks.  During this time, critical cell populations (leukocytes, platelets) are decreasing as a result of bone marrow insult.  The time interval decreases as the dose increases. Illness Phase - period when overt illness develops Recovery or Death Phase - may take weeks or months

ARS - Hematopoitic System Blood Count

ARS - Hematopoietic Syndrome

ARS - Gastrointestinal Syndrome Radiation > 600 rads Damages intestinal lining Nausea and vomiting within the first 2 - 4 hours May develop diarrhea Associated with sepsis and opportunistic infections At 10 days could develop bloody diarrhea resulting in death

ARS - Central Nervous System Seen with radiation dose > 1,000 rads Microvascular leaks Õ edema Elevated intracranial pressure Death within hours

ARS - Skin

ARS & Trauma Radiation and Trauma   =   á Mortality Trauma is the first priority

Treatment Wound and burn care, surgery, and orthopedic repair should be done in the first 48 hours or delayed for 2 to 3 months

Survival Time

Classification, Treatment & Disposition Patients are classified in three categories based on signs and symptoms: Survival probable < 100 rads Survival possible 200 - 800 rads Survival improbable > 800 rads

Classification, Treatment & Disposition Incorporation / Internal Contamination Various medications can be used to limit uptake or facilitate removal of radioactive material Numerous medications are approved by the FDA.  Certain drugs are investigational and can be used in an emergency (i.e. Radiogardase [Prussian Blue] and DTPA) NCRP 65

Radiation Protection Principles Time Distance Shielding

Key Points No antidote for radiation exposure - treatment is primarily supportive Minimal risk to responding personnel from radiation contaminated patients Early symptoms are an indication of the severity of the radiation dose Consult with specialists for “survivable groups” Treat life-threatening injuries first

Special Hospital Considerations in NBC Mass Casualty Incidents

Special Considerations Terminal Objectives Describe the unique principles of triage, agent detection and decontamination in an NBC mass casualty incident (MCI) List factors to be considered in planning emergency response to a terrorist attack involving weapons of mass destruction

Medical Disaster A medical disaster occurs when the destructive effects of natural or manmade forces overwhelm a community’s ability to properly allocate existing resources Terrorism’s impact on the medical infrastructure World Trade Center Bombing - 6 dead; 1000 injured Oklahoma City Bombing - 168 dead; 759 injured Tokyo Subway Attack - 12 dead; 5500 injured

MCI - Disaster Planning Lessons Learned Hospitals provide most of the initial care High risk of secondary contamination Personal protective equipment is required Disaster planning must address NBC Maximize use of existing resources

Special Considerations - Overview Preparedness for an MCI Training Command, control, communication PPE Decontamination Detection Triage Staff preparedness Logistics / supplies Hospital space utilization Evidence preservation Exercising “ the plan”

NBC “Delta” Planning Considerations Planning similar to other disasters Unique characteristics of an NBC terrorist attack must be considered Pro-active and integrated planning, coordination, and training is essential Must be familiar with local incident management system “All hazards approach” to disaster planning

Current Preparedness Must improve state of readiness Training and equipment lacking Agent recognition Patient management Patient decontamination Patient transport Supplies and equipment Antidote PPE Decontamination

NBC “Delta” Planning Readiness Phase Take a genuine inventory of current capabilities and rectify any deficiencies Instruct personnel about the disaster plan using realistic scenarios Ensure plan addresses triage, decontamination, and treatment

NBC “Delta” Planning Planning Phase Develop strategies to overcome resistance to preparedness Incorporate responsible people in the planning process Keep the plan cost effective Plan for problems that may occur Communication and sharing of information Security, traffic control, hospital access Staff identification, triage, decontamination, information management

NBC “Delta” Planning Planning Phase Participate in joint planning Work together with EMS, law enforcement, fire, LEPC Integrate plan into community- wide disaster plan Develop mutual aid agreements Develop policies and procedures

NBC “Delta” Planning Planning Phase Acquire necessary equipment Purchase PPE and decontamination equipment and provide training Stockpile antidotes & other medications Make sure facility remains open and viable

NBC “Delta” Planning Recovery Phase Focus shifts from acute injury and illness to the everyday needs of the population May have increased need for medications, shelter, food, water, clothing, and emotional support Hospital staff emotional needs and fatigue

Training Hospitals must first prepare to treat the everyday HAZMAT contaminated patient Once established, HAZMAT training should be  supplemented to include NBC Training must be facility-wide and tailored to the needs of the hospital staff Train using realistic scenarios Equipment training available from commercial sources Public education should also be considered

Command, Control & Communications Community orchestrated and coordinated response based on the incident command model At the incident scene At the healthcare facility

Command, Control & Communications Accurate, timely notifications Disaster scene to hospital Hospital to disaster scene Communications Community to disaster scene Disaster scene to hospital Hospital to disaster scene Within the hospital

Command, Control & Communications Media Coordination Accurate communications At the disaster scene At the hospital Provide the media Dedicated space Timely and accurate updates Public relations

Personal Protective Equipment (PPE) Equipment and training mandated OSHA (29 CFR 1910.120                                                    and 1910.134) NIOSH EPA JCAHO

Levels of PPE Level A - IDLH environments, fully encapsulated, requires SCBA Level B - Chemicals or substances with inhalation hazard, requires SCBA or SAR Level C - Known contaminants, requires air-purifying respirator

PPE PPE for decontamination personnel PPE for healthcare providers Limitations of PPE Staff rotation

PPE - Biological Self-Protection Treat every patient with respiratory complaints and open wounds as an “infectious source” Normal standard universal precautions for most BW agents HEPA filter mask upgrade for pneumonic          plague / smallpox / VHF Special protective garments usually not necessary Precaution upgrades in areas of the hospital where aerosols could be generated:  lab centrifuges, autopsy facilities, etc.

PPE - Radiological Self-Protection Respiratory - Particulate mask (level C minimum) Shielding Dosimeter

Decontamination Decontamination removes harmful substances Hospital preparedness for decontamination Decon of casualties                                                  arriving at the                                                  healthcare facility Vapor exposure Liquid exposure Mass casualty incident

Decontamination Vapor verses liquid exposure Mass casualty incidents Ambulatory vs. non-ambulatory Decon methods Water vs. bleach Location of decon area

Decontamination Decon of casualties arriving at the hospital Already decontaminated Not decontaminated Decon of healthcare providers Decon Team Members Treating personnel

NBC Agent Detection

Biological Agent Detection Many biological agents can be identified by standard hospital laboratory techniques Standard laboratory procedures may require 12 to 48 hours to yield results Treatment should be based on index of suspicion; should not await test results

Radiation Detection Instrumentation G.M. Survey Meter Dose Rate Meter - Ionization                                 Chamber Alpha Meter Neutron Meter Personal Dosimeters Film Badge Thermoluminescent Dosimeter Quartz Fiber Dosimeter Electronic Instantaneous Read Out Dosimeter

Hospital Triage Use a triage system in an MCI that parallels normal routine Practice regularly to ensure familiarity Triage is a continual process Re-triage all victims transported by EMS Set up triage area near the ED entrance Shielded and secure Readily accessible

Triage “Greatest good for the greatest number of casualties” Psychological impact Classification: Red Yellow Green Black Limitations: Time consuming User variability Lack of familiarity

START Triage TRIAGE CRITERIA: Respiratory status Perfusion and pulse Neurological status TRIAGE CATEGORIES: Walking wounded - “Green” or minimal  (relocate when told) Normal findings - “Yellow” or delayed  (unable to relocated) Abnormal - “Red” or immediate Non-salvageable - “Black” or expectant

START - Respiratory Status

START - Perfusion

START - Neurological Status

Nerve Agent Triage - “Immediate” Unconsciousness or convulsions Two or more body systems involved

Nerve Agent Triage - “Delayed” Initial symptoms are improving (miosis still present) Recovering well from pre-hospital antidote therapy

Nerve Agent Triage - “Minimal” & “Expectant” Minimal Walking and talking which indicates intact breathing and circulation

Mustard Triage Delayed 2 to 50% BSA burns by liquid Eye involvement Minimal < 2% BSA burns by liquid in non-critical areas

Triage of Biological Casualties Triage of biological agent casualties is different Symptoms are delayed Initial cases may go unrecognized More difficult to detect Epidemiological information becomes critical

Radiological Triage Triage: Stabilize the patient first and only when this is done does one consider irradiation and contamination. Ensure ABCs

Triage - Psychological Casualties Disasters produce tremendous emotional and psychological stress, with large numbers of psychogenic casualties Presenting signs could be confused with organic disease Use of START triage system maintains focus on objective signs of disease & minimizes impact of subjective complaints on the triage process Psychological casualties are usually triaged as “minimal”

Triage - Hospital Arrivals Casualty arrival is uncoordinated Arrival times vary Closest hospital is typically overwhelmed Medical needs of unaffected community continue

Triage - Contaminated Human Remains Problems are agent-specific Decontamination Containment Refrigeration until definitive disposal Follow local coroner and medical examiner protocols Establish cooperative agreements for fatality management Secure personal effects Not all can be decontaminated

Staff Preparedness Plan for the needs of the unaffected population Prepare to receive large numbers of casualties Prepare to receive large numbers of dead Rotate staff to avoid   congestion and fatigue, especially  personnel in PPE

Logistics / Supplies Highest priority:  getting the right resources to the right place at the right time Personal protective equipment and dosimetry Medications / antidotes / vaccines Mechanical ventilators Isolation rooms remote from other patients Identify current inventory and augment as necessary Develop a procedure to access external assets

Maximal Utilization of Hospital Space Identify alternative medical treatment areas Planning for use of available space Open areas Isolated areas Temporary morgue

Handling of Evidence Maintaining evidence is critical for an investigation Clothing Embedded foreign bodies Decontamination runoff Chain of Evidence must be maintained

Exercising the Plan Start small - few casualties Be realistic Coordinate with other agencies / hospitals Exercise frequently DON’T WAIT FOR A DISASTER TO HAPPEN

Teaching Points Hospitals must expand their emergency planning and scope of services to include NBC care Concentrate on the disaster planning process Develop policies & procedures Train frequently using realistic scenarios

Scenario A national basketball championship was what the city needed to boost its national reputation, and tonight was the night.  Every hotel within 30 miles was booked with fans eagerly awaiting the game. After the national anthem was played the crowd began to loudly chant their team’s respective fight song.  The sounds within the stadium were deafening.

Scenario Just as the game was ready to begin fans from section “A” started to run from their seats.  Total chaos ensues.  In a rampage fans were pushing and shoving trying to get out through the exit doors.  Many were being trampled upon during the exodus.  Most were coughing, rubbing their eyes, and many appeared to be choking. 911 was called and the closest hospital, two blocks away, was also notified.

Scenario Assume you are working in the emergency department, please answer the following: After notification, what would you do? Where would you set up triage? Who would function as the triage officer? Where would you set up & perform decon?

Scenario Within 15 minutes of the incident 100 victims arrive at your hospital without the assistance of EMS How will you control access into your hospital? What level of protective gear should be worn? Should these victims be decontaminated? How will you decontaminate these victims? Where will you treat the first wave of victims?

Scenario Victims are complaining of shortness of breath, cough, eye & throat irritation, and burning skin. What chemical were they exposed to? What clues would you look for to help you identify the agent? Lacking positive agent identification, how would you begin treatment? What medications/antidotes are necessary?