Chemical Agents Chapter 6 Important Points:.

Chemical Agents Chapter 6 Important Points:

Overview History of chemical disasters / terrorism
D-I-S-A-S-T-E-R Paradigm for chemical agents Specific Agents Nerve agents Choking / Irritant Gases Cyanide Blister / Vesicants Agents Incapacitating agents Important Points:This presentation is designed to cover some of the more important aspects of chemical agents. Disasters that occur from chemical agents can be far reaching in their effect on society and may be of intentional design such as an act of terrorism or may be an accident. It is not possible to have a completely comprehensive lecture on chemical agents in a one hour time frame therefore, this lecture will attempt to hit on the highlights of the more concerning potential chemical agents and a brief overview of their treatment.

Potential Chemical Agents
Nerve Agents Tabun, Sarin, Soman, VX Blood Agents (cyanide) Hydrogen Cyanide, Cyanogen Chloride Irritant Agents Phosgene, chlorine, ammonia, mace, pepper spray Incapacitating agents BZ Vessicants Mustard, Lewisite, Phosgene oxime This lecture will cover the following groups; nerve agents, blood agents such as cyanide, irritant agents, incapacitating agents and vesicants. A complete discussion of all chemical agents is not possible in the scope if this lecture. Point out that mace and pepper spray are not included in detail in this presentation, but that they have potential for use by terrorist. They typically represent a nuisance threat.

History: World War I First large-scale use Ypres, Belgium April 1915
Chlorine, 168 tons 5,000 deaths 5 mile front The first large-scale use of chemical warfare agents was of chlorine in Ypres, Belgium in April of This was a very successful attack and resulted in about 5,000 deaths along a 5 mile front. Wind direction in speed, however, was extremely important with the timing of this attack. The shift of winds in attacks like this often resulted in contamination and exposure of unintended targets.

Chemical Casualties in WWI
Country Non-fatal Deaths Britain 180,597 8,109 France 182,000 8,000 Russia 419,340 56,000 Italy 55,373 4,627 U.S. 71,345 1,462 Austria-Hungary 97,000 3,000 Germany 191,000 9,000 It’s extremely important to point out that chemical weapons have the potential to cause widespread casualties. Of note, is the large number of non-fatal injures and fatalities on Russian troops during WWI with 56,000 deaths attributed to chemical warfare.

Terrorist Attacks Matsumoto, June 1994 Tokyo, March 1995 280 injured
7 dead Tokyo, March 1995 Terrorists have recently, of course, also used chemical warfare agents on civilian populations. In somewhat of a landmark example, such as this, was Aum Shinryhyo cult’s use of sarin in the attack in Matsumoto, Japan in June of This resulted in approximately 280 injured and 7 deaths in what is considered by most to be the trial attack for what would occur later in March 1995 in a more large-scale attack in the Tokyo subway.

Tokyo: Hospital Response
5,500 victims 11 Dead 641- St. Luke’s International Hospital No decon No EMS involvement for most In the March of 1995 Tokyo sarin subway attack, this was successful in causing 5,500 victims; 641 of these reported to St. Luke’s hospital. Sarin (30% concentration) was concealed in lunch boxes and soft-drink containers and placed on subway train floors. It was released as terrorists punctured the containers with umbrellas before leaving the trains. The incident was timed to coincide with rush hour, when trains were packed with commuters. Over 5,500 were injured in the attack. A subway station close to SLIH was one of several sites hit simultaneously in the attack; therefore, many of the victims were sent to SLIH. As the perpetrators left the trains they used umbrellas to puncture the bags. The sarin ran out onto the floor, evaporated and resulted in the illness and injuries. The majority of deaths that occurred in this incident where people who attempted to clean up the sarin. Unfortunately, the responders and hospital personnel at the time did not realize that this was a chemical event and therefore no decontamination was performed on these patients. It is important to note on this slide that the doctors are examining a patient who is fully clothed and therefore had not been decontaminated. There were several healthcare workers that became ill while caring for others as the patients were off-gassing sarin that was trapped in their clothing. Over 23% of hospital staff who treated victims had symptoms that included ocular pain, headache, sore throat, dyspnea, nausea, dizziness, and nose pain, but none was seriously affected . 1,364 EMS providers responded and 135 were exposed and developed symptoms. If the patients had merely been undressed outside in what is called “dry decontamination”, this would probably been sufficient to prevent all of these healthcare workers from becoming effected even if they did not use an personal protective equipment. Dry decontamination involves simply undressing the patient to release any trapped vapor or liquid sources that may be on the patient’s clothing. Other lessons that can be learned from the Tokyo sarin subway attack is that EMS does not transport the majority of these patients and that approximately 4 out of 5 will self transport to the hospital. The idea that all patients will be decontaminated on the scene is not a realistic one as is well demonstrated by this event. Of the 641 patients seen at SLIH on the day of the disaster, five were in critical condition. Three patients had cardiopulmonary arrest (CPA) and two were unconscious and had respiratory arrest soon after arrival (Table 2). Of these five critically ill patients, three were successfully resuscitated and able to leave on hospital day 6. One CPA patient did not respond to cardiopulmonary resuscitation (CPR) and died with findings of conspicuous miosis that continued even at the time of her death. A second patient with CPA was resuscitated but died on hospital day 28 due to irreversible brain damage.

Tokyo, Japan 1995 Although the video quality is not high, there are several important things which can be noted in this short vide clip. This first is the chaotic nature of the scene. Secondly a brief view of a patient who has arms extended stiff to provide a good example of the physical findings of nerve agent exposure. Third, there is a picture of a healthcare worker who is wiping away the excessive secretions characteristic of nerve agent exposure.

Bhopal India 1984 40 Tons of Methyl Isocyanate Population of 900,000
Estimates of affected 6,000-10,000 ? Affected ~ 400,000 Lack of safety devices Manuals in English “Mini-Bhopals in US?” In what is considered by most to be the worst industrial accident in the history of mankind, the Union Carbide plant in Bhopal India released approximately 40 tons of methyl isocyanate. In a population of approximately 900,000 people were down wind. Although, the name of the chemical released is methyl isocyanate leading one to believe that this would be a cyanide compound, in reality methyl isocyanate’s primary effect is that of an irritant gas. This incident demonstrates the ability of an irritant gas to effect large numbers of populations. It is estimated that somewhere between 6,000 and 10,000 people were immediately effected, however, there are estimated to date with long term health consequences from the exposure that may range as high as 400,000. There are many lessons that can be learned from the Bhopal India incident. In particular examples in Bhopal included a lack of safety devices and even things as simple as the fact that the safety manuals and operating manuals for the plant were written in English despite the staff being non- English speaking. Hopefully, because of regulatory agencies in the United States, we will never see anything near the effect of the incident in Bhopal however what is more likely is several mini Bhopals in the United States.

D: Detection I: Incident Command S: Safety & Security
A: Assess Hazards S: Support T: Triage & Treatment E: Evacuation R: Recovery This is what each letter stands for. Each action/stage is expanded upon in the following slides. This is not necessarily the order in which these actions would be taken.

D: Detection I: Incident Command S: Safety & Security
A: Assess Hazards S: Support T: Triage & Treatment E: Evacuation R: Recovery

Detection Rapid onset Common symptoms Low lying clouds or vapors
little or no warning Common symptoms Low lying clouds or vapors Dying animals or insects Unexplained odors Concentrations of Dead, dying, or sick people at the scene The detection of a chemical event may be from a variety of different mechanisms. There are commercial sensors that are available that will alarm in an industrial setting if a particular agent is detected. Unfortunately because of the expense of these devices, as well as our inability to just deploy them at random locations these devices are not likely to be useful in the event of a terrorist release of the chemical agent or a release at a site other than that of an industrial plant. The Department of Homeland Security has initiated a program to place sensors capable of detecting chemical presence in the subways of some large cities, making early detection and identification of the agent possible in these select locations. This may occur during a terrorist event or also from a transportation accident. It’s more likely, therefore, that the detection of chemical event for healthcare providers must be based on the symptomatology and circumstances surrounding the incident. One should think of a potential of a chemical event etiology for your patients illness when there is a rapid onset of the event for a large number of people with little or no warning. One would expect that the victims would all have common symptoms. Numbers of dying animals or insects at the scene or unexplained odors, low-lying clouds or vapors may also be an indication. Obviously, concentrations of dead, dying or sick people at the scene of an incident would be an indication of a potential chemical event. This would differ from a biological agent where we would expect that multiple patients would become ill but may have dispersed by the time that this becomes apparent due to the incubation period or a lag would occur and patients would have a more gradual onset of symptoms.

Detection Likely based on symptoms DUMBELS – Nerve Agent
Respiratory symptoms – irritant gases Skin symptoms – vesicants Altered mental status and anti-cholinergic syndrome – BZ Therefore, it’s important for us to remember particular groups of symptoms or toxidroms that occur with exposure to different chemical agents. These will be explained further later however, when caring for a patient or patients that are exhibiting a “dumbbells” toxidrome consisting of diarrhea, urination, meiosis, brochorrhea, broncho-constriction, bradycardia, emesis, lacrimation, salivation secretions and spreading, one should consider that a nerve agent is the potential agent. If patients are presenting primarily with respiratory symptoms but none of the other is mentioned then on should consider that an irritant gas may be involved. For patients presenting with mostly skin symptoms such as blistering and redness of the skin, one should consider vesicants. And for patients presenting with altered mental status and anti-cholinergic syndrome, one should consider an incapacitating agent such as BZ.

I: Incident Command D: Detection S: Safety & Security

Incident Command Must supply the following information:
number and type of casualties substances involved estimated time of arrival to hospital time of the incident and incident site method of contamination (vapor or liquid) necessary decontamination hazards to health care providers role of the health care facility in the incident updated information Incident command is extremely important during chemical events. It is important that the incident command location be up-wind and either level with the release sight or uphill or downhill from the release sight based on whether the suspected agent is heaver or lighter than air. The incident command center must communicate effectively with other responders as well as the healthcare facilities that will be receiving the pts.

S: Safety & Security D: Detection I: Incident Command

Scene Security It’s important to note that scene security is extremely important during a chemical event. This picture from the 1995 sarin subway attack in Tokyo shows a prime example of the lack of scene security. On this slide is a picture of a woman who is walking down the subway as if absolutely nothing is wrong while having to step over victims in order to make her way further into the subway. This slide illustrates that a chemical event may also be somewhat insidious and without obvious detection, some people may not remove themselves from the scene.

Scene Security Scene must be secured to prevent more casualties
Most (4/5) victims will go to the hospital by private/ public transportation vehicle!!! PREVENT THE HOSPITAL FROM BECOMING CONTAMINATED all personnel involved in decontamination must wear PPE The scene must be secured to prevent more casualties and also those in an outdoor release that may be down-wind must either be sheltered in place or evacuated from the area. It’s important, also, to keep in mind that ambulatory victims should be kept on the scene to prevent the local hospitals from becoming overwhelmed and contaminated. In prior disasters it has been established that approximately 4 out of 5 victims will self transport to the hospital and therefore if allowed to leave the scene are likely to overwhelm the hospital’s decontamination ability and ability to care for these patients. All personnel involved in decontamination as well as those who may be guarding entrances to the hospital must wear personal protective equip. The hospital must be secured to prevent the unauthorized entry of contaminated victims via alternate routes. Hospital plans should include the ability to “lock down” the facility within minutes to prevent any unauthorized entry and any personnel or employees of the hospital should have an ability to be identified after hours by name badge or some other mechanism. Personnel providing security at designated hospital entrances must have appropriate PPE.

Scene Security WARM ZONE 300 ft 60 ft 6,000 ft HOT ZONE
Casualty Collection Point WARM ZONE 60 ft RS 6,000 ft HOT ZONE 300 ft WIND DIRECTION RS= Release Site Minimum Site Boundaries Open Area Chemical Release Adapted from Illinois Emergency Management Agency Chem-Bio Handbook. April 2000 COLD ZONE Uphill if agent heavier than air, downhill or level if lighter than air Figure 5 CCP For an outdoor release of a chemical agent, hot, warm and cold zones must be established. The initial areas to be established are300 feet immediately up-wind from the release site as well as 6000 feet down-wind are considered to be in the hot zone of the scene. In addition, at the extent of that 6000 feet down-wind, 6000 feet across must also be established as a hot zone. This should be the initial guidlelines for establishing the scene. If winds are variable this area must extended. The contamination reduction zone or warm zone should consist of at least 60 feet in width around the boarders of the warm zone. It is also important to note that the casualty collection point (ccp) and command post exhibited on this diagram by the green star should be located up-wind. Consideration for the agent being heavier or lighter than air should also be taken into account. For agents that are heavier than air, if there are negligible winds, it is possible for those to progress toward the casualty collection point and command post if they are located down the hill from the release sight. Examples of agents that would be heavier than air include the nerve agents as well as cyanogen chloride.

A: Assess Hazards I: Incident Command S: Safety & Security S: Support
D: Detection I: Incident Command S: Safety & Security A: Assess Hazards S: Support T: Triage & Treatment E: Evacuation R: Recovery

Assess Hazards Ongoing threat of contamination to other individuals
contamination control must be continually assessed and enforced by safety officer badges must be given to hospital personnel guards must wear PPE at ingress points law enforcement assist with crowds, traffic, and casualty flow Secondary devices? A continuous and on going assessment of the threats or hazards that may be present on the scene must occur. One must always consider the potential use of a secondary device in any terrorist event. Falling debris, head strike hazards, potential explosions, gas leaks, traffic and crowd control as well as the more obvious threats of secondary devices must be considered.

S: Support D: Detection I: Incident Command S: Safety & Security

Support Public health organizations DMAT’s State Disaster Teams
Poison control centers Health care providers Medical research centers Medical examiners Emergency response units and first responder organizations DMAT’s State Disaster Teams Safety and medical equipment manufacturers Federal agencies FBI Hazardous Materials Response Unit Local law enforcement The release of any chemical agent is likely to require support from multiple organizations. Early during the disaster, one should consider what support will be needed in the form of transportation, state disaster teams or resources, or whether or not federal resources such as disaster medical assistance teams (DMAT) will be required or needed to participate. A stress on HazMat and decontamination resources will also be stressed during a chemical disasters. In addition, healthcare facilities must be notified early during the disaster and in large scale disasters one should consider the use of secondary treatment facilities such as nursing homes or clinics that may be converted into acute treatment centers for those that are less injured.

Support: Health care providers
Use primary care clinics and urgent care centers Volunteers All individuals should be oriented to the disaster plan Communication systems often become overwhelmed during disasters and therefore, plans should be in place for personnel to report if they are unable to communicate whether or not they are needed. Some personnel should be designated or sent to secondary treatment facilities if they are to be used. A personnel pool will allow the assignment of personnel where they are most needed.

Support: Supplies / Pharmaceuticals
Vendor Agreements ventilators other equipment Essential pharmaceuticals Atropine can be stockpiled powder form Vendor agreements should be in place to rapidly procure ventilators and other equipment that may be necessary in the treatment of chemical casualties. In particular, the irritant gases and or nerve agents may result in large numbers of victims witch may require ventilators for care. In addition, essential pharmaceuticals such as atropine and pralidoxime (2-PAM) must be stockpiled at the local facilities or regions. Although ventilators and antidotes are contained in the strategic national stockpile (SNS), because of logistical, bureaucratic and distribution delays of the SNS it is not safe to assume that these will be available for the acute care of these pts. Therefore local, regional and state resources must be made available in the event that the SNS can not be received and distributed in a sufficiently rapid fashion. The problem with stockpiling of atropine can be mitigated by using the powdered form which has an extended shelf life.

T: Triage &Treatment D: Detection I: Incident Command
S: Safety & Security A: Assess Hazards S: Support T: Triage &Treatment E: Evacuation R: Recovery

E: Evacuation D: Detection I: Incident Command S: Safety & Security
A: Assess Hazards S: Support T: Triage &Treatment E: Evacuation R: Recovery

Evacuation Most victims will self transport
Consider school buses for minimal pts Caution Contaminated pts Off-gassing Open windows Use vents As stated previously, most victims will self transport to the hospital, however, the distribution of these patients to local healthcare facilities can be better managed by arranging for transport of these victims. For any minimal patients, one should consider the use of public transportation or school buses, however, one should use caution to make sure that any contaminated patients are not placed on these vehicles as well as opening the windows and using vents to prevent any off-gasing from affecting others on the bus.

R: Recovery D: Detection I: Incident Command S: Safety & Security

Recovery Most difficult aspect of a chemical event
All areas of the hospital, buses, ambulances, equipment checked for persistence of chemicals Law enforcement investigate human remains for evidence Psychological sequelae The picture in this slide is of the workers cleaning the subway cars from the Tokyo sarin subway attack. The recovery from a disaster should begin early for a chemical event in particular, large numbers of worry well would be expected and therefore the psychological sequelae from the event may be the most difficult to mitigate. All equipment must be cleaned and decontaminated or disposed of which may represent huge logistical problems.

Nerve Agents A structural representation of Sarin.

Nerve Agents Organophosphates Are similar to insecticides: Sarin VX
Malathion Diazinon Chlorpyrifos Sarin Demonstrated on the slide are the chemical structure of the more common nerve agents, those being sarin, soman, tabun and vx. The nerve agents are all organophosphates and are similar to the insecticides. VX Soman Tabun

Nerve Agents Nerve agents VX G-agents liquids ambient temperatures
Vapor heavier than air VX Nonvolatile Persistent liquid threat G-agents Volatile Nonpersistent vapor and liquid threat The nerve agents are all liquids at room temperature and are divided into two major categories. Those that are volatile and nonpersistent are the G-agents. Those that are nonvolatile and persistent - being VX. The G-agents, being volatile, represent more of a vapor threat but also a liquid threat. If left over time they will eventually evaporate and dissipate in an open environment and therefore are considered nonpersisent. VX, on the other hand, is more the consistency of cooking oil and is nonvolatile. It does represent a vapor threat but represents a significant liquid threat. The risk of secondary contamination exists with G and VX agents but more so with VX. Both of these agents will produce vapor that is heavier than air and therefore should be taken into account when at a scene to insure that there are not populations in danger in down-hill areas

Nerve Agent Properties
Tabun (GA) Sarin (GB) Soman (GD) VX LCt50 Mg(min)/m3 400 100 50 10 Vapor Density (air = 1) 5.63 4.86 6.33 9.20 Topical LD50 mg 1000 1700 Aging half-life 14 hours 5 hours 2-6 minutes 48 hours This table is meant to represent the concentration and lethality of the different nerve agents. Of note is that the topical, lethal dose 50 of VX is 1/10 of that of Tabun as well as the significant differences in the lethal concentration or LCT50 that are demonstrated there. You can also note that the vapor density of VX is much heavier than that of sarin, which is the lightest of the nerve agents. One important point to note on this slide is the aging half life. This is the time that transpires between exposure to the agent and the bond between the nerve agent and acetylcholinesterase becoming permanent. Once aging occurs the administration of pralidoxime is not beneficial and the acetylcholinesterase will remain inactivated. More acetylcholine must be produced to replace the inactivated forms bound to the nerve agent. VX has an aging half life of nearly 48 hours as compared to that of 2-6 minutes for Soman.

Nerve Agent Pathophysiology
Acetylcholine Neurotransmitter parasympathetic nervous system neuromuscular endplate Ganglia Sympathetic parasympathetic Acetylcholine serves as the primary neurotransmitter at numerous sites in the body.

Cholinergic Nerve Function
AChE This slide illustrates how acetylcholine leaves the end of one nerve and crosses the synaptic cleft to bind with receptors on either the muscle or nerve to be effected. ACh

Cholinergic Nerve Function
AChE ACh GB When this happens the nerve or muscle being effected is made to depolarize and exert whatever the function of that nerve or muscle is. During normal functioning, the acetylcholine shortly after bonding to the site is deactivated by an enzyme called acetylcholinesterase. When acetylcholinesterase breaks up acetylcholine into 2 parts, it no longer exerts its function on the muscle or nerve being stimulated, and is returned to the nerve and the plate for regeneration

Acetycholine Metabolism
This slide illustrates diagrammatically the hydrolysis of acetylcholine into choline and acetic acid by the enzyme acetylcholenestrace.

Acetylcholinesterase Inhibition
This slide demonstrates diagrammatically the bond that is formed between the nerve agents or other organophosphates on the enzyme cholinesterase. Of importance is to note that once the chemical transformation has occurred in the bond between the organophosphate and the cholinesterase enzyme is considered “aged” as is shown in part C of the slide, the administration of 2-Pam on the aged bond is ineffective at breaking it.

Nerve Agent Symptoms (dumbells) Diarrhea Urination Miosis
Bradycardia, Bronchoconstriction, Bronchorrhea Emesis Lacrimation Salivations, Secretions, Sweating Because of the stimulation at all of the sites at which acetylcholine is used as a neurotransmitter, a variety of symptoms are seen on organophosphate in nerve agent exposure. However, most commonly these pts will exhibit a toxidrome of symptoms referred to as dumbells. This neumonic stands for diarrhea, urination, miosis, bradycardia, bronchoconstriction, bronchorrhea, emesis, lacrimation, salivations, secretions, and sweating. It is important to note however, that miosis may not be seen in skin insposures only and bradycardia is rarely seen. (dumbells)

Nerve Agent Symptoms: Nicotinic
Mnemonic for the days of the week M: mydriasis (pupil dilation) T: tachycardia W: weakness tH: hypertension F: fasciculations Because of the characteristics of the sites that are stimulated by the persistent acetylcholine, the variety of other symptoms may also be seen in nerve agent exposure. The nicotinic sites that are stimulated may cause mydriasis or pupil dilation, tachycardia, weakness, hypertension and fasciculations. These symptoms may or may not be seen or may be seen with rapid variation between nicotinic and muscarinic symptoms as described earlier with the dumbells mnemonic period. For example, a patient may rapidly alternate between bradycardia and tachycardia. Fasciculations are commonly seen with skin exposures to nerve agents.

Nerve agent exposure - Vapor
Low exposure Meiosis (dim vision, eye pain) Rhinorrhea Dyspnea High exposure Immediate loss of consciousness Seizures Apnea Flaccid paralysis Vapor effects occur within second, peak within minutes: no late onset These symptoms can be confusing depending on the route of exposure as well as the degree of exposure. It is therefore more useful to break nerve agent exposures into those which occur as primarily vapor and those which are primarily skin or liquid exposures. Patients with vapor exposures that are low level may exhibit meiosis which is exhibited by the patient with a complaint of eye pain and dimmed vision, a runny nose and some difficulty breathing. Patients which have a high concentration exposure to nerve agents will have an immediate loss of consciousness, seizures, apnea and flaccid paralysis. It is important to note that any vapor exposures occur within seconds of exposure, peak within minutes, and never have a delay to onset of symptoms. The picture included on slide 33 is that of a patient with an accidental laboratory exposure to soman vapor. The picture was taken in complete dark with a flash and therefore the patient’s eyes should be fully dilated. The picture at the top was taken one day after exposure to the soman and the picture at the bottom was taken 62 days later. As you can see, the pupil constriction or meiosis took an extended period of time to resolve.

Nerve Agents: Liquid Large amount (LD50) (<30 minutes)
Small amount (up to 18 hrs) Localized sweating Fasiculations No miosis Moderate amount (<LD50) (18 hrs) GI effects Miosis uncommon Large amount (LD50) (<30 minutes) Sudden loss of consciousness Seizures Apnea Flaccid paralysis Death Liquid exposures, unlike vapor exposures, may have a delayed onset of symptoms. Very small amount of concentrations may have a delayed onset of symptoms up to 18 hours, however it is important to note that pictured on the slide is a lethal dose of VX on a penny. Another way of visualizing the amount of VX that is lethal is to imagine a packet of artificial sweetener containing 1000 grains of the sweetener. If a single grain out of the packet were to come in contact with your skin, and it were VX, then it would be lethal. Therefore, the term “small exposure” must be taken in context. Patients with very small exposures may just have localized sweating in the area of skin contamination, some fasiculations but typically do not exhibit any meiosis. Patients with less than the LD50, but significant exposures, may have GI effects predominating with meiosis still being uncommon. Patients with large skin exposures, that being >LD50, have a fairly rapid (defined as less than 30 minutes) sudden onset of loss of consciousness, seizure, followed by apnea, flaccid paralysis and death.

Nerve Agent-Triage Tokyo Sarin Consider cardiac arrest as immediate?
3/6 victims in cardiac arrest resuscitated Majority were worried well Consider cardiac arrest as immediate?

Nerve Agents: Treatment
ABC’s, supportive care Antidotes Atropine 2 mg IV/IM/ET Repeat doses as necessary End point is dry secretions, easier ventilation 2-PAMCl 1 gram slow IV or Mark I kit IM (600 mg) Benzodiazepines, PRN for seizures The treatment of nerve agents is not only supportive in nature as is the case with all chemical agent exposures but also consists of the administration of atropine to counteract the muscarenic side effects of the nerve agents and also the administration of 2-PAMCl or pralidoxime to regenerate the acetycholinesterase enzyme. Atropine with a starting dose of 2 mg should be administered either IV via intramuscular injection by auto injector or otherwise, or via endotracheal tube if no IV access in obtainable. The patient may require multiple doses of atropine with the end point of atropine administration being the drying of secretions or easier ventilation if the patient is being ventilated by bag-valve-mask. Bradycardia and pupil size should not be used as end points for atropine administration. If the patient is cardiac arrest, then the atropine must be administered IV. 2-PAMCl is administered as 1gm slow IV over several minutes or via Mark I auto injector. The auto injector dose is 600mg IM. 2-PAMCl serves to regenerate and break the bond between the organophosphate nerve agent and acetylcholinerase. Seizures should be treated with benzodiazepines such as, ativan or valium. The benzodiazepines may be administered IV, IM or by PR.

Nerve agent: Treatment
Atropine Starting dose - 2 mg Maximum cumulative dose - 20 mg Insecticide poisoning requires much more Side effects in normal people Mydriasis Blurred vision Tachycardia Decreased secretions and sweating It is important to note that the starting dose for atropine administration is 2mg however, patients may require large doses particularly in pesticide poisonings. The maximum cumulative dose in nerve agent exposure should probably not exceed 20mg per patient. It’s also important to note that atropine administration in normal, healthy people will cause significant side effects that may be misinterpreted as symptoms of nerve agent exposure. If this occurs and people mistake these symptoms as the need for more atropine, the results may be fatal. Therefore, it is important to keep in mind that the end point for atropine administration is the drying of secretions and/or ease of ventilation of the patient.

Nerve Agent Treatment Atropine – How much to give?
Until secretions are drying or dry Until ventilation is easy If conscious or the patient is comfortable Do not rely on heart rate or pupil size

Nerve Agents: Treatment 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 Liquid exposure Symptoms delayed minutes to hours Greater need for decontamination High risk of secondary contamination; victims require decontamination (clothing removal & washdown) Requires immediate access to antidotes In summary for the nerve agents, patients with vapor exposure will develop symptoms suddenly and require immediate access to antidotes. These patients may receive dry decontamination just by removing their clothing if they do not have any liquid or skin contamination. Most ambulatory patients in this setting will require minimal intervention in that if they are not already effected severely by the vapor exposure they are unlikely to require much in the way of intervention. Patients with liquid exposures may have symptoms delayed from minutes to hours and are in need of water decontamination. There is a high risk of secondary contamination to healthcare providers and therefore these patients must have all clothing removed and adequate decontamination performed. These patients also have significant exposures and because of the delay of symptoms, they may require observation and frequent re-assessment to determine the need for antidote therapy.

Irritant Gases (Choking Agents)

Irritant Agents Irritate respiratory tract or damage lung tissue
Combine with moisture to form acids or bases Three groups based on water solubility Highly water soluble Moderately water soluble Low water solubility Examples: Ammonia, chlorine, phosgene Irritant gases are defined as gases that combine with moisture in the tissue of the airway to damage the respiratory tract or lung tissue. Examples of irritant gases include ammonia, chlorine, phosgene or a multitude of other gases. One can predict the symptoms caused by an irritant gas based on the water solubility which is generally broken down into low, moderate and high water solubility. When these agents combine with the moisture in the airway they generally convert into either an acid or a base and damage the tissues.

Irritant Gas Symptoms Highly water soluble - ammonia
Moderately water soluble - chlorine When highly water soluble agents such as ammonia enter the airway their ability to combine with the moisture in the airway rapidly, causes them to primarily involve the mucosa of the upper airway. Even when inhaled in large quantities the irritation is rapid and extreme to the point that it causes laryngospasm and prohibits the entry of the ammonia into the moderate sized and lower airways. This irritation of the mucosa may be of a sufficient amount to cause extreme swelling and occlusion of the airway. Most deaths from high water solubility agent exposures occur from airway obstruction. Moderately water soluble such as chlorine are slower to combine with the moisture in the airway and therefore are inhaled deeper into the airways before exerting their effects. Therefore a patient with moderately water soluble agent exposure may have some burning of the mucous membranes but not as severe as those with high water soluble agent exposures such as ammonia will have. The damage to the moderately water soluble airways will be exhibited as bronchospasm and wheezing primarily. In extremely large or high concentration inhalations the patient may have entire involvement of the respiratory system. Patients with poorly water soluble agent inhalations generally do not exhibit much in the way of symptoms early during the exposure because of the slow nature with which the poorly water soluble agent combines with the moisture in the airway. The prototypical poorly water soluble irritant gas is phosgene or nitrogen dioxide. These agents are inhaled all the way into the alveoli of the lung where they combine with the water there to form hydrochloric acid or nitric acid. The patient then develops pulmonary edema several hours later. Poorly water soluble - phosgene

Irritant Gas - Symptoms
Mucous membrane irritation and excess mucous production Conjunctivitis Coughing Dysphonia (hoarseness) Stridor and aphonia Bronchospasm Shortness of breath Non- cardiogenic pulmonary edema As described previously, patients with irritant gas symptoms will exhibit degrees of involvement of their airway based on water solubility. However, all patients with irritant gas exposures may have bronchospasm, shortness of breath, non-cardiogenic pulmonary edema, coughing, conjunctivitis, as well as the various sets of symptoms listed on this slide. Again, the predominance of the symptoms may predict the agent which caused the injury, keeping in mind that there will be some crossing over of symptoms.

Highly Water Soluble Irritant Gases
Ammonia Formaldehyde Hydrogen Chloride Sulfur Dioxide Mostly upper airway to vocal cords laryngospasm As described previously ammonia, formaldehyde, hydrogen chloride, and sulfur dioxide are highly water soluble irritant gases. In patients exposed to these, severe burns of the upper airway may occur as well as laryngospasm may prevent inhalation of the agent into other parts of the airway. These patients are in need of aggressive airway management as any hint of airway compromise exhibited by stridor may be an indication of impending airway obstruction.

Moderately Water Soluble Irritant Gases
Chlorine Hydrochloric acid Hypochlorus acid Greenish-yellow gas Slightly slower to combine with water Affects upper airway Affects lower airways Chlorine is the prototypical moderately water soluble irritant gas. When inhaled into the moderately sized airways it combines with the water there to form hydrochloric and hypochlorus acid. The patients, therefore, will have some upper airway involvement but will also have significant wheezing and bronchospasm due to the moderate sized airway involvement.

Poorly Water Soluble Irritant Gases
Phosgene (COCl2) Forms hydrochloric acid Nitrogen dioxide (NO2) Forms nitric acid Inhaled into alveoli before combining with water Results in pulmonary edema (20 min to 24 hrs) As described previously, phosgene, when inhaled into the lower airway forms hydrochloric acid while nitrogen dioxide combines with the water in the alveoli to form nitric acid. Acid in the alveoli results in noncardiogenic pulmonary edema. The symptoms may be delayed 20 minutes or so, or may be delayed up to 24 hours.

Phosgene (CG) Most dangerous of pulmonary agents Use in WWI
Developed as warfare agent, first use 1917 U.S. Produces > 1 billion pounds/yr for industrial uses Odor of New Mown Hay Poor Warning Properties odor may not be detected accumulates in low areas (trenches) Phosgene is an interesting agent in that it was developed for use in WWI as a chemical warfare agent. It was first used in 1917 with mixed results. However, it is currently manufactured in quantities greater than 1 billion pounds per year as an industrial compound and precursor for other products. Phosgene is said to have the odor of newly mown hay, although it’s warning properties are very poor. The victim may not detect the odor at all or if they smell it initially accommodation (extinguishment of the ability to smell) occurs very quickly. Phosgene is heavier than air and therefore may accumulate in low lying areas or trenches.

Phosgene (CG) Low concentrations Moderate concentrations
mild cough, chest tightness, shortness of breath Moderate concentrations lacrimation High concentrations pulmonary edema (2-6 hours) death (24-48 hours) Initial presence/absence of symptoms do not predict severity of exposure In low concentration exposures the victim, once symptoms develop, may have some mild shortness of breath and cough. In slightly higher concentrations the victim may also have some eye irritation and lacrimation. In high concentration exposures the patient may develop pulmonary edema and death may rapidly follow. It is important to note that the presence or absence of symptoms does not necessarily predict the severity of exposure to phosgene. In fact, the only predictor of survival from phosgene exposure is whether or not the victim exerts themselves after the exposure. Patients which exert themselves have a much higher instance of pulmonary edema and death than those who rest.

Irritant Gases: Triage
Majority – Worried well? Airway compromise – immediate Severe shortness of breath- immediate Mild SOB, No airway compromise – delayed Mild mucous membrane symptoms – minimal Respiratory arrest – expectant Patients with irritant gas exposure are likely to require medical attention. However, it is likely that the majority of patients which will seek care may be the worried well. Any patient exhibiting signs of airway compromise after irritant gas exposure should be considered in the immediate triage category. Likewise patients which have severe shortness of breath should also be considered immediate. Patients exhibiting mild shortness of breath and no airway compromise should be considered delayed and those complaining only of mild mucous membrane symptoms should be considered minimal. Patients who are in respiratory arrest should be considered expectant as less an airway can be obtained immediately and the patient ventilated.

Irritant Gases: Treatment
Dry decontamination usually adequate Water for mucous membrane irritation ABC’s Oxygen PRN Early airway management highly and moderately water soluble exposures Inhaled beta agonist PRN wheezing Observation and support phosgene hrs? Dry decontamination or removal of all of the clothing is usually adequate for treatment of irritant gas exposures unless the patient has mucous membrane irritation. For any patient with mucous membrane irritation water should be applied to those areas. If there is any doubt, the patient should receive full water decontamination. The treatment of irritant gas exposure is primarily supportive in nature with aggressive early airway management for patients with high and moderately water soluble exposures. Airway compromise is the most often cause of death in these patients. The patient should be treated with beta agonist as needed for swelling and for patients with phosgene exposure, they may need to be observed for at least hours to ensure that they do not develop pulmonary edema.

Irritant Gas - Summary Solubility determines physiologic effect
Dry decon is usually all that is needed Incident Command and treatment areas– upwind Treatment is supportive Early airway management critical Consider intubation for stridor Be prepared for surgical airway Transport contaminated separate from decontaminated In summary, the solubility will determine the physiologic effect of the irritant gases. The treatment is primarily supportive in nature with early aggressive airway management. Care should also be taken to not transport contaminated patients to the hospital.

Cyanide

Cyanide (AC, CK) Formerly referred to as “blood agents”
Hydrogen Cyanide AC Cyanogen Chloride CK Odor “bitter almonds”? – “musty” smell Odor not a reliable indicator (genetic) Combines with Cytochrome a3 and Inhibits Oxygen Utilization (bright red venous blood) Cyanide is referred to by the nato designations of AC for hydrogen cyanide and CK for cyanogen chloride. The military designation also refers to these as blood agents as they cause a poison via the blood stream. This term, however, is somewhat being abandoned as it is a misnomer and the term asphysixant is probably a better term to use. Cyanide is said to have the odor of bitter almonds, although this has been disputed in research recently completed in Arizona. In their experience, not a single person ever exposed to low levels of cyanide determined their ability to smell it has ever described it as “a bitter almond smell”. Most people, however, describe the smell of cyanide as that of being “musty”. Odor is not a reliable indicator not only because of confusion over what it should smell like, but also because the ability to smell cyanide is genetically determined. Therefore, some people do not have the ability to smell cyanide at all. Cyanide exerts its effects on the body by combining with cytochrome oxydase and inhibiting the utilization of oxygen. This is typically taught as the patient therefore having bright red venous blood however, this has also been disputed in recent studies. The researchers and their studies have suggested that greater than 50% of patients with cyanide poisoning will indeed present with cyanosis and not the bright red blood as described previously.

O2 O2 O2 O2 CN- O2 + H+ Cyt a cyt a3 Cu Cyt c H20 ADP ATP
This slide is of the electron transport chain in the inner membrane of a mitochnodria. It is at this step in the process of producing ATP, which is the energy currency of the cell, that oxygen is used to facilitate ATP production. The slide illustrates the movement of electrons from cytocrome c through the cytocrome a complex to transform ADP into ATP in the final step of oxidation taking O2 plus hydrogen to produce water and the ATP as desired. However when cyanide binds to the cytocrome oxydase it inhibits this last very important step in the process and therefore significantly impairs the production of energy in the cell. It also inhibits the use of oxygen at this step. The oxygen, therefore, builds up hence the description of bright red venous blood. (although cyanosis may be more common).

Cyanide - Sources Pits of many plants
Cherries, peaches, almonds, lima beans Cassava plant root Combustion of carbon -> cyanide Plastics- acrylonitriles U.S. sources manufacture 300,000 tons of hydrogen cyanide annually Cyanide is found in many naturally occurring sources such as the pits of many plants. It is important, therefore, to note that the body is capable of handling small amounts of cyanide exposures, since we are exposed to them on a routine basis. It is only when the system for metabolizing cyanide is overwhelmed that we get the binding of cyanide to the mitochondrial energy producing complex. It is important to note that the United States manufactures greater that 300,000 tons of hydrogen cyanide for industrial uses annually. Therefore, one should consider that a terrorist need not have an extensive mechanism for the production of cyanide but rather just needs to derail a transport car, which is conveniently labeled with identifying plaques, in order to obtain a large quantity if cyanide or to cause its release.

Terrorist Use of Cyanide
Tylenol – 1982 – Killed 7 Rev Jim Jones – 1978 – Killed 900 1995 Aum Shinrikyo Several subway restrooms after attack Found acid and cyanide salt cyanide salt + acid cyanide gas Terrorists have used cyanide on multiple occasions as noted on slide 55,terrorist use of cyanide. Most notably, in 1995 the Aum Shinrikyo cult who carried out the sarin Tokyo subway attack also had designed a cyanide release in several of the subway restrooms. This consisted of cyanide salts that were designed to be dropped into acid and therefore producing hydrogen cyanide gas. It is unknown whether this was designed as a secondary device and was discovered before it was enacted or if the device failed and therefore did not produce any casualties.

Cyanide Triage M-A-S-S Triage Likely few critical victims
Most either dead Others with minor exposure Good supportive care may save many in absence of antidote Cyanide exposures, in particular, deserve a discussion of triage in that because of the body’s ability to metabolize cyanide and the fact that it is very lethal in high concentrations it is unlikely that we will see a large number of critical victims from a cyanide release. Most victims will be dead on the scene before EMS is able to assist them and others with very minor exposures that are able to remove themselves from the environment will likely have very minor symptoms and will be able to metabolize the cyanide without assistance. In either case, good supportive care of patients may save many in the absence of antidote.

Cyanide Treatment Remove to Fresh Air Oxygen, supportive care
Pasadena Kit (Was Lilly Kit) Of course, therefore the treatment for cyanide is to remove the victim to fresh air to cease the exposure. Oxygen and supportive care are paramount. The cyanide antidote kit, formally referred to as the Lilly Kit, is now referred to as the Pasadena Kit.

Cyanide Treatment Step 1 Step 2 Step 3 amyl nitrite Sodium nitrite
inhale 30 sec/min until IV) Step 2 Sodium nitrite 10 ml of 3% IV over 5-10 minutes Step 3 Sodium thiosulfate 50ml of 25% IV over 20 minutes Cyanide treatment consists of 3 steps. The first is to induce methemoglobinemia. This is done by having the patient inhale amyl nitrite and also by administering sodium nitrite IV, once an IV is established. The goal of inducing methemoglobinemia is to cause the cyanide to leave the cytrochrome oxidase on the mitochondria and bind to the red blood cell where the iron has been transformed into the Fe3+ of methemoglobin. This occurs because the cyanide has a greater affinity for the iron of methemoglobin than it does for the cytrochrome oxidase. Because the cyanide victim requires very rapid treatment in significant exposures, this is done first by amyl nitrite. Amyl nitrite perles are crushed in a gauze and held over the victim’s mouth and nose for 30 seconds out of each minute. This should be done until the IV is established in the ability to give sodium nitrite. If the patient is being ventilated via a bag valve mask or bag valve endotracheal tube, the amyl nitrite should be held over the intake of the bag valve mask. Once an IV is established, the patient is given sodium nitrite 10 ml of 3% solution IV over 5-10 minutes. Once this has begun, the inhalation of amyl nitrite is no longer necessary. The third step in cyanide treatment is to administer sodium thiosulfate. As mentioned previously, the body is able to metabolize cyanide, however the weight limiting step in this process is the availability of sulfur to assist in the conversion of cyanide into thiocyanate. Thiocyanate is a water soluble non-toxic substance that can then be excreted from the body.

CN- CN- rbc Fe2+-Hb Cyt a3 Amyl nitrite Sodium nitrite Fe3+-Hb Fe3+-Hb
MetHb CN- This slide is a graphic representation of the treatment of cyanide poisoning. In the upper right hand corner of the screen is a red blood cell in it’s normal state. The iron in normal hemoglobin is of the Fe2+ or ferrous variety. Once amyl nitrite and sodium nitrite are administered the Fe2+ is oxidized into Fe3+ which is known as methemoglobin. The administration of sodium nitrite results in the production of more methemoglobin. The cyanide previously bound to the cytochrome oxidase has a greater affinity for the Fe3+ molecule of the methemoglobin and therefore, leaves the cytochrome oxidase to bind to the methemoglobin iron molecules. The administration of sodium thiosulfate provides the necessary sulfur donor for the enzyme rhodanase to metabolize the cyanide into thiocyanate which is a harmless material and may be excreted in the urine. Sodium thiosulfate thiocyanate Excreted in urine

Cyanide Treatment Summary
Induce methemoglobinemia Amyl nitrite, Sodium nitrite Create thiocyante Sodium thiosulfate Good supportive care even in absence of antidote Therefore, in summary and to review, the treatment of cyanide consists of the inducement of methemoglobinemia with amyl nitrite and sodium nitrite and the administration of sodium thiosulfate to aid in the conversion into thiocyanate and excretion. It is also important to re-emphasize that good supportive care in the absence of antidote may save many patients.

Blister Agents/Vesicants
Sulfur mustard Phosgene Oxime CX Nitrogen mustard Lewisite L Blister agents and vesicants are chemicals which when exposed to human skin result in significant damage, blistering, and drying out of the skin and mucous membranes. Examples of vesicants include sulfur mustard, nitrogen mustard, phosgene oxime, and lewisite. It is important to note that phosgene oxime is a vesicant and is not the same as the phosgene gas that was described earlier.

Mustard Physical Characteristics
Oily liquid so poorly volatile Light Yellow in Color Garlic odor Freezes at 57 F Penetrates rubber gloves Mustard is the prototypical blister agent, therefore, it will be covered in the most detail. It is an oily liquid and is very poorly volatile, is said to be light yellow in color and have the odor of garlic. It freezes at 57 degrees F and therefore cannot be used in a cold environment. It is important to know that mustard can penetrate rubber gloves and this needs to be taken into account when selecting personal protective equipment.

Lewisite Characteristics
Organic arsenical with vesicant properties Colorless, oily liquid Odor of geraniums Lewisite is also a vesicant and is colorless and also an oily liquid like that of mustard. Lewisite is said to have the odor of geraniums. All of the vesicants act to rapidly penetrate cells and generate a toxic intermediate. The result is that DNA damage and protein damage occur within minutes causing cell death. Cells which are rapidly dividing, such as the skin, are the most susceptible.

Vesicant Mechanism RAPIDLY penetrates cells and generates toxic intermediate Alkylates DNA, RNA, protein-->disrupts cell function-->cell death Rapidly dividing cells most susceptible

Vesicant Symptoms Binds Irreversibly within minutes “Fixing”.
Onset of symptoms 4-8 hours Tissue Damage Within Minutes Without Symptoms for Hours Topical – Eyes, Airway, Skin Systemic – Bone Marrow, GI, CNS Vesicants bind irreversibly within minutes of exposure, referred to as “Fixing”. Therefore, in order to prevent symptoms decontamination must occur within a matter of a few minutes. The patient will not have symptoms immediately except in very large exposures and will begin to exhibit symptoms 4-8 hours after exposure despite the fact that damage is occurring within minutes. The topical symptoms include the eyes, the airway and the skin, being most effected. The eyes are the most sensitive resulting in chemosis conjunctivitis. Systemic effects can also be seen with bone marrow suppression and nausea and vomiting. In very large exposures CNS depression may also be seen.

Small vesicles may coalesce to form bullae
Mustard - Skin Erythema 2-24 hours Small vesicles may coalesce to form bullae High dose exposure – central zone of coagulation necrosis The erythema from mustard or other vesicant exposures begins within 2-24 hours. This initially starts off as very small vesicles that may come together to form bullae. Patients with very high dose exposures may develop a central zone of coagulation necrosis in the exposed area.

Vesicant Treatment Immediate decontamination (2 minutes)
Victim may not undergo decontamination since symptoms delayed Remove clothes and wash skin with soap and water Avoid overhydration; fluid losses less than with thermal burns To prevent symptoms, the patient must undergo decontamination within 2 minutes of exposure. All patients should undergo immediate decontamination that is very thorough. Secondary contamination from mustard is a serious problem. This was exhibited in a case in France where children playing with an unexploded chemical ordinance that detonated and were sprayed in mustard. They did not inform their parents of what had happened and when they later developed a mysterious skin rash were taken to the local hospital. The children were admitted to the hospital and were successful in exposing a large number of the hospital staff before the cause was determined. Therefore, it should be kept in mind that any patient with mustard exposure should be thoroughly decontaminated to prevent secondary contamination of healthcare providers.

Lewisite Treatment British Anti-Lewisite (BAL) chelating agent
only administer to victims with shock or severe pulmonary injury in consultation with the poison center 3-5 mg/kg IM every 4 hours x 4 doses Side effects: nausea/vomiting, headache, burning sensation of lips, chest pain, anxiety For patients exposed to lewisite, a treatment in the form of British Anti-Lewisite agent or BAL may be administered. It is a chelating agent that should only be administered to patients with shock or severe pulmonary injury. This is done so as a dose of 3-5 mg/kg IM every 4 hours x 4 doses. This treatment is not without significant side effects namely in the form of significant nausea and vomiting and characteristic burning sensation of the lips as well as chest pain.

Incapacitating Agents
Not meant to be lethal “inability to perform one’s mission” Incapacitating agents are designed to do exactly as their name implies, incapacitate the victim, not to kill them. This is useful from a chemical warfare standpoint in that incapacitated combatants require greater resources on the part of the enemy in order to care for those who have been effected. These agents may also be used by tactical units in order to incapacitate a victim. The prototypical incapacitating agent is BZ or BZ 3 Quinuclidinyl Benzilate which is a potent anti cholinergic agent 25 times more potent than atropine. One can then predict the symptoms that you would see with a BZ exposure as being similar to that of atropine only much greater.

Incapacitating Agents: BZ
BZ--3-quinuclidinyl benzilate Anticholinergic Agent 25-times more potent than atropine

BZ: Symptoms “Mad as a Hatter” “Dry as a Bone” “Blind as a Bat”
“Hot as a Hare” “Red as a Beet” Patients with BZ exposure will exhibit a typical anti cholinergic toxidrome of “mad as a hatter, dry as a bone, blind as a bat, hot as a hare, red as a beet”. Mad as a hatter refers to the altered mental status and bizzare behavior that these patients often exhibit. Dry as a bone refers to the fact that these patients will have dry skin, dry mucous membranes and complain of thirst. The phrase blind as a bat refers to the mydriasis that occurs with anti cholinergic administration causing blurry vision. Hot as a hare refers to the fact that the patients will complain of being hot and have hot, dry skin. Red as a beet refers to the red skin that occurs with anti cholinergic exposure.

BZ: Treatment Control patient KEEP VICTIM COOL Physostigmine 1-2 mg IV
atropine at bedside seizures and cardiac arrhythmias rare Patients may be sedated with benzodiazepines. The mainstay of BZ treatment is the administration of physostigmine 1-2 mg IV. This should be done with caution however and atropine should be at the bedside as cardiac arryhythmias may occur but are rare. The patient may also exhibit seizures with the administration of physostigmine. The victim may also be hyperthermic and with an altered mental status and therefore cooling measures as well as control of the patient to keep them safe should be performed.

BZ: Summary Sx: Not all chemical exposures are nerve agents
Red, Hot, AMS, Tachycardia Not all chemical exposures are nerve agents Supportive care / cooling Physostigmine In summary, BZ as an incapacitating agent will leave the patient with an altered mental status and confused, therefore unable to complete their mission. It is also important to point out that not all chemical exposures are nerve agents and that the administration of atropine to a patient with BZ exposure could be lethal. Therefore, one should use caution when evaluating these patients to ensure that they are able to distinguish between an anti cholinergic and a cholinergic crisis. The treatment of BZ is supportive in nature as well as the as the administration of physostigmine.

Summary: Chemical Agents
ABC’s & supportive Decontamination Nerve Agents DUMBELS Treatment: atropine/ 2PAM Irritant Gases Sx’s based on water solubility Aggressive airway management Cyanide Amyl nitrite/ sodium nitrite Sodium thiosulfate Vessicants Decon a must Supportive care BAL for lewisite BZ AMS, red and hot Physostigmine In summary, the treatment of chemical agent exposures are good A,B,C’s and supportive care. Decontamination is a must for these patients except for the irritant gases unless they have skin or mucous membrane involvement. Patients with nerve agent exposures will exhibit typical toxidromes remembered by the mnemonic dumbells. The treatment of nerve agent exposures includes the atropine and 2-PAM. Irritant gas symptoms can be predicted based on the water solubility of agent and aggressive airway management and good supportive care is the mainstay of treatment. Cyanide treatment consists of 3 stages; the administration of amyl nitrite inhaled, the administration of sodium nitrite both of which induce methemaglobinemia, which is followed by the administration of sodium thiosulfate to convert cyanide into thiocyanate. Vesicants were discussed as well, as well as the importance of decontamination and good supportive care. Patients with exposure to lewisite may also be given BAL. And, the incapacitating agent of BZ results in an altered mental status and a red, hot, dry patient. This is treated with good supportive care, cooling and the administration of physostigmine.

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Chemical Agents Chapter 6 Important Points:.

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