MSP6 Hargreaves Olson

Slide1: 

Chemical Terrorism – Core Concepts Presented by James Hargreaves, DO Linda Olson, EdD November 18, 2004 Sponsored by BORDERS Alert and Ready UND School of Medicine and Health Sciences

Overview: 

Overview Introduction Chemical Agent Characteristics Major Chemical Weapons Nerve Agents Vesicants Cyanide Pulmonary Toxic Agents Riot Agents Decontamination Triage Summary

Chemical Warfare Agents: 

Chemical Warfare Agents

Chemical Warfare Agents -History: 

Chemical Warfare Agents -History Chemicals used in military operations to kill, injure, or incapacitate Battlefield use World War I and Middle East conflicts

History of Chemical Warfare Agents: 

History of Chemical Warfare Agents Sarin (GB) manufactured in Iraq

Use of Chemical Warfare Agents: 

Use of Chemical Warfare Agents US has munitions with sarin and VX in land mines, projectiles, bombs

Terrorist Use: 

Terrorist Use

Chemical Agent Characteristics: 

Chemical Agent Characteristics Most are liquids, may produce vapor less volatile Phosgene Mustard Cyanide VX Vapors tend to be heavier than air --- Direction and wind speed --- Persistence

Chemical Agents - Persistence: 

Chemical Agents - Persistence Chemical agents are affected by the environment The colder it is, the more persistent the agent

Introduction to Nerve Agents: 

Introduction to Nerve Agents Organophosphates Inhibit enzyme acetylcholinesterase Are extremely dangerous and can enter the body through the air or on contact with the skin Insecticides are similar Can be released using bombs, missiles, spray tanks, rockets and land mines

Nerve Agents: 

Nerve Agents Principle agents Tabun (GA) Sarin (GB) Soman (GD) VX Penetrate skin, eyes, lungs Diagnosis made clinically; confirmed in laboratory (cholinesterase)

Method of Action : 

Method of Action Acetylcholine is a common neurotransmitter found in the central and peripheral nervous system Acetylcholine is released from an axon terminal, moves across the synaptic cleft to bind to a receptor on the other side of the synapse (post-synaptic membrane) The action of acetylcholine is stopped by an enzyme called “acetylcholinesterase” (AChE).

Clinical Effects of Nerve Agents: 

Clinical Effects of Nerve Agents Route of exposure Vapor vs liquid Dose of exposure Duration of exposure Health status

Case Study: 

Case Study Dr. Frederick Sidell, an expert in chemical munitions, US Army Medical Research Institute of Chemical Defense will present a case history of nerve agent poisoning.

Signs and Symptoms of Nerve Agent Poisoning: 

Signs and Symptoms of Nerve Agent Poisoning Muscarinic Diarrhea Urination Miosis Bradycardia, bronchorrhea, bronchospasm Emesis Lacrimation Salivation, secretion, sweating Nicotinic Mydriasis Tachycardia Weakness Hypertension, Hyperglycemia Fasciculations Cholinergic Nervous System Central Nervous System Confusion Coma Convulsion

Eye Effects: 

Eye Effects Pictures courtesy of – United States Army Medical Research Institute of Chemical Defense Chemical Casualty Care Division

Treatment: 

Treatment Personal Protection Decontamination Antidotes Atropine– reverse bronchorrhea & bronchoconstriction Pralidoxime chloride Diazepam Ventilate Apneic Bag-valve-mask Suction secretions

Vesicants (Blister Agents): 

Vesicants (Blister Agents) Vesicants Sulfur mustard Lewisite Phosgene Oxime

Vesicants: 

Vesicants Three types of Vesicants Sulfur mustard Lewisite Phosgene oxime Characteristic signs Erythema Vesicles

Vesicants: 

Vesicants Properties Persistent Oily Liquid Biochemical Damage DNA alkalization Rapid onset - seconds to minutes Clinical Damage Delayed – hours No Pain or Redness Immediately

Mustard Clinical Effect: 

Mustard Clinical Effect Redness and blistering skin Irritation and damage to eyes Damage to lining of airways May cause laryngeal edema GI effects Vomiting Diarrhea Bone marrow suppression

Mustard Effects - Eye Injury: 

Mustard Effects - Eye Injury

PK Carlton video clip on Decon: 

PK Carlton video clip on Decon Paul K. Carlton, Jr., M.D. Lt. General, USAF (Ret) Director, Homeland Security The Texas A&M University System Health Science Center

Sulfur Mustard - Treatment: 

Sulfur Mustard - Treatment Decontaminate Protect self Observe patient at least 8 hours Skin care Airways Hematological Infection

Mustard Long-term Effects: 

Mustard Long-term Effects Tracheobronchial tree stenosis Hypo-hyper pigmentation Visual impairment

Lewisite : 

Lewisite Similar to mustard Damages skin, eyes, airways Differs from mustard Clinical effects within seconds of exposure Antidote dimercaprol (BAL)

Phosgene Oxime: 

Phosgene Oxime Phosgene Oxime Urticarial Corrosive Rapid onset No antidote

Cyanide : 

Cyanide Cytochrome oxidase Inhibited by cyanate No energy production anaerobic metabolism (acidosis)

Clinical Effects ofLarge Amount of Cyanide Inhalation: 

Clinical Effects of Large Amount of Cyanide Inhalation Rapid onset and death transient, rapid and deep breathing Loss of consciousness and convulsions Breathing stops Heart stops

Clinical Effectsof Smaller Amounts of Cyanide: 

Clinical Effects of Smaller Amounts of Cyanide Symptoms Anxiety Agitation Vertigo Nausea Muscular trembling Unconsciousness Apnea Cardiac arrest Antidotes are very effective } Later stage

Cyanide Treatment: 

Cyanide Treatment Protect yourself Move patient to safe area Decontaminate Administer the antidote

Cyanide Antidote Treatment: 

Cyanide Antidote Treatment Methemoglobin inducers Amyl nitrite Sodium Nitrite Sulfur donor Sodium Thiosulfate Cyanide Antidote Kit

Pulmonary Toxic Inhalants: 

Pulmonary Toxic Inhalants

Inhalent Properties: 

Inhalent Properties Gas or particulate Water soluble Reactivity Host factors

Toxic Inhalation: 

Toxic Inhalation Major Clinical Effects Asphyxiation Simple-displace oxygen e.g. closed space fire Systemic Met hemoglobin Cyanide Direct toxicity to respiratory mucosa Increased water soluble more toxic to upper airways

Toxic Inhalation: 

Toxic Inhalation Major Clinical Effects Systemic toxicity Mustard inhalation – leukopenia Allergic response

Slide37: 

CO2 O2

CLINICAL CONSIDERATIONS: 

CLINICAL CONSIDERATIONS Peripheral agents cause pulmonary edema damage alveolar-capillary membrane Latent period symptom onset may be delayed hours to days Dyspnea objective signs appear later than symptoms Crackles Hypoxia Frothy Sputum Sudden death may occur laryngeal obstruction (edema/spasm) bronchospasm

Complications of Toxic Inhalants: 

Complications of Toxic Inhalants Hypoxia Hypercarbia Pulmonary edema Infection Avoid exertion

Chlorine : 

Chlorine Pungent odor-good warning Greenish, yellow gas High density, so accumulates in low lying area Corrosive- splits hydrogen from oxygen in moist tissue resulting in hydrochloric acid

Dr. John Urbanetti: 

Dr. John Urbanetti Serves as Consultant to the Surgeon General in Toxic Inhalation and holds a staff position at Yale University. Dr. Urbanetti has had broad experience in identifying and treating unusual inhalational exposures including sulfur and nitrogen mustards, chlorine, cyanide and phosgene and will present a phosgene case history.

Phosgene (military designation CG): 

Phosgene (military designation CG) White cloud Odor of newly mown hay Slightly soluble in water Hydrolyzed to form HCL

Polymer Fume Fever: 

Polymer Fume Fever Teflon pyrolyses at 450˚C Influenzae like Onset 1-2 hr post exposure Symptoms: Malaise Chills Fever to 40˚C Sore Throat Hoarseness Chest tightness Treatment Remove patient from site of exposure Signs and symptoms gradually resolve over 24 to 48 hours

Perfluoroisobutylene (PFIB) - Clinical Effects: 

Perfluoroisobutylene (PFIB) - Clinical Effects Teflon Pyrolysis at >800° C liberates PFIB 10X more toxic than phosgene latent period of 1-4 hours followed by increasing dyspnea s/s of pulmonary edema usually recover within 72 hours, w/o sequelae

Decontamination of Chemical Agents: 

Decontamination of Chemical Agents Decontamination is the process by which a chemical agent is removed or the amount is decreased so that it no longer presents a hazard. The goals of decontamination are: To prevent further exposure to victims To prevent secondary contamination Health Care Workers medical facility Personnel MUST NOT enter a contaminated area without full personal protective equipment including respiratory protection

Chemical Agents Decontamination Chart: 

Chemical Agents Decontamination Chart Decontaminate patient Remove Clothing Bag Place outside Wash Rinse Dry Clean Clothes

Principles of Mass Casualty Triage: 

Principles of Mass Casualty Triage To do the greatest good for the greatest number of people Dynamic process Assessment Categorization Treatment Reevaluation Security

Medical Triage : 

Medical Triage Rapid categorization of victims At casualty site Most experienced Person Level of medical care needed Know consequences of injuries burn blast crush injuries chemical biological Radiological Color coding

Medical Triage Color Coding: 

Medical Triage Color Coding Red – Urgent Require immediate lifesaving interventions ABC Yellow – Delayed Do Not Require immediate lifesaving interventions Treatment can be delayed Green – Minor Minimal No medical care Black – Expectant or Deceased Not expected to survive Due to injuries & resources

Slide50: 

1 Miosis, Sweating, Fasciculations, Copious Secretions No Yes 2 H/O Chlorine Cholinesterase Poisoning Atropine, 2PAM Pulmonary Toxic Inhalation Syndrome, Bronchodilator, Oxygen 3 H/O burns within minutes of exposure No Yes Yes No 4 Thermal Burns No Yes 6 Consider Lewisite Use BAL, Vesicant Mgmt. Consider Phosgene or Hot chlorinated hydrocarbons Consider Phosgene No Yes 5 Eyes irritated or burns 2-12 hrs after expo Observe for 6 hours For onset of ARDS Mustard, Vesicant Mgmt. Protocol Alert for Pulmonary Toxic Inhalation Syndrome Vesicant Mgmt. Protocol Chemical Victims

More training available: 

More training available Part 1 – Core Concepts (web-based) Part 2 – Onsite Training (hands-on/didactic) Advanced (web-based) http:/www.bordersalertandready.com