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State Of Maine Nerve Agent Antidote Kit Training Module

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State Of Maine Nerve Agent Antidote Kit Training Module

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    1. State Of Maine Nerve Agent Antidote Kit Training Module Brian Langerman, CCEMT-P, I/C EMS Coordinator – City Of Saco Kevin Bachi – NREMT-P, BS Kennebunk Fire Department

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    3. The Threat of Terrorism

    4. Potential Probability vs. Impact

    5. 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 Iraq, Matsumoto and Tokyo, Japan CHEMICAL WARFARE AGENTS - HISTORICAL PERSPECTIVE Chemical warfare agents are hazardous chemicals that have been designed for use by the military to irritate, incapacitate, injure, or kill. Some have local effects on the eyes, skin, or airways (ex. riot control agents, chlorine), and some also have systemic effects (ex. nerve agents and vesicants). Germany first utilized chemical warfare agents during World War I at Ypres, Belgium, in the late afternoon of April 22, 1915. In that attack, the Germans released 168 tons of chlorine. The allies claimed 20,000 casualties and 5,000 deaths. In July 1917, the Germans first used sulfur mustard, again in Ypres. Overall, chemical agents caused large numbers of casualties in WW I, but killed fewer than 5 percent of these casualties, excluding those from Russia (who reportedly may have had insufficient and ineffective protective masks). During World War II, Germany developed several chemical agents, including nerve agents, but did not use them in battle for reasons that are still unclear. After the Second World War, Egypt allegedly used chemicals in Yemen, and Iraq used them against Iran and the Iraqi Kurds. On June 27, 1994, the Aum Shinrikyo, a well-funded Japanese religious cult, initiated the use of chemical warfare agent terrorism in Japan. The nerve agent GB, or sarin, was manufactured in a secret facility in Japan and was first released in Matsumoto, Japan with approximately 280 casualties and 7 deaths. Nine months later, on March 20, 1995, sarin was released in five separate subway cars in downtown Tokyo. There were 12 deaths, hundreds injured (a few dozen seriously), and thousands who sought medical care. Some of the first responders were contaminated, and a few of the hospital staff suffered exposure to the chemical, possibly due to vapor off-gassing from clothing. Some of the responders required admission to hospitals.CHEMICAL WARFARE AGENTS - HISTORICAL PERSPECTIVE Chemical warfare agents are hazardous chemicals that have been designed for use by the military to irritate, incapacitate, injure, or kill. Some have local effects on the eyes, skin, or airways (ex. riot control agents, chlorine), and some also have systemic effects (ex. nerve agents and vesicants). Germany first utilized chemical warfare agents during World War I at Ypres, Belgium, in the late afternoon of April 22, 1915. In that attack, the Germans released 168 tons of chlorine. The allies claimed 20,000 casualties and 5,000 deaths. In July 1917, the Germans first used sulfur mustard, again in Ypres. Overall, chemical agents caused large numbers of casualties in WW I, but killed fewer than 5 percent of these casualties, excluding those from Russia (who reportedly may have had insufficient and ineffective protective masks). During World War II, Germany developed several chemical agents, including nerve agents, but did not use them in battle for reasons that are still unclear. After the Second World War, Egypt allegedly used chemicals in Yemen, and Iraq used them against Iran and the Iraqi Kurds. On June 27, 1994, the Aum Shinrikyo, a well-funded Japanese religious cult, initiated the use of chemical warfare agent terrorism in Japan. The nerve agent GB, or sarin, was manufactured in a secret facility in Japan and was first released in Matsumoto, Japan with approximately 280 casualties and 7 deaths. Nine months later, on March 20, 1995, sarin was released in five separate subway cars in downtown Tokyo. There were 12 deaths, hundreds injured (a few dozen seriously), and thousands who sought medical care. Some of the first responders were contaminated, and a few of the hospital staff suffered exposure to the chemical, possibly due to vapor off-gassing from clothing. Some of the responders required admission to hospitals.

    6. 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 AGENT TERRORIST ATTACKS The sarin nerve agent attack in Matsumoto, by the Aum Shinrikyo (June 27, 1994), was a haphazardly planned assassination attempt against three judges who were expected to rule against the Aum in their attempt to purchase real-estate. To prevent this ruling, the sect’s leader, Shako Asahara, ordered a sarin attack on the judges, according to confessions made later by senior Aum officials. Asahara believed that if the judges were killed they could not return a decision against the sect. The Aum converted a 2-ton, white refrigerator truck which contained three tanks to hold the liquid sarin, a heater to vaporize the chemical, and a fan to disperse the agent. The plan was to park the truck right in front of the district courthouse (pictured above) and spray the sarin through the front doors to the rooms inside. This was to occur during broad daylight, potentially exposing large numbers of innocent people to the deadly vapor. The attackers, however, arrived late at the courthouse after the judges had already left for the day. Instead of delaying the attack to the next day, the six-man team decided to release the sarin at the judges’ apartment building later that evening. CHEMICAL AGENT TERRORIST ATTACKS The sarin nerve agent attack in Matsumoto, by the Aum Shinrikyo (June 27, 1994), was a haphazardly planned assassination attempt against three judges who were expected to rule against the Aum in their attempt to purchase real-estate. To prevent this ruling, the sect’s leader, Shako Asahara, ordered a sarin attack on the judges, according to confessions made later by senior Aum officials. Asahara believed that if the judges were killed they could not return a decision against the sect. The Aum converted a 2-ton, white refrigerator truck which contained three tanks to hold the liquid sarin, a heater to vaporize the chemical, and a fan to disperse the agent. The plan was to park the truck right in front of the district courthouse (pictured above) and spray the sarin through the front doors to the rooms inside. This was to occur during broad daylight, potentially exposing large numbers of innocent people to the deadly vapor. The attackers, however, arrived late at the courthouse after the judges had already left for the day. Instead of delaying the attack to the next day, the six-man team decided to release the sarin at the judges’ apartment building later that evening.

    7. Tabun, Sarin, Soman, VX Mustard, Lewisite Phosgene, Chlorine, Ammonia, Cyanide Mace®, Pepper Spray Nerve Agents Vesicants (Blister) Industrial Chemicals Riot Control Agents Chemical Warfare Agents CHEMICAL WARFARE AGENTS The types of chemical warfare agents listed on this slide are the ones we will focus on during this module. Some of the chemical warfare agents are said to have characteristic odors, such as a horseradish or mustard smell for mustard agent, Lewisite’s aroma of geraniums, or the freshly-mown hay smell of Phosgene. However, these are not adequate warning properties for the purpose of protecting yourself against adverse health effects associated with exposure. CHEMICAL WARFARE AGENTS The types of chemical warfare agents listed on this slide are the ones we will focus on during this module. Some of the chemical warfare agents are said to have characteristic odors, such as a horseradish or mustard smell for mustard agent, Lewisite’s aroma of geraniums, or the freshly-mown hay smell of Phosgene. However, these are not adequate warning properties for the purpose of protecting yourself against adverse health effects associated with exposure.

    9. Traits of a Terrorist Terrorism IS: Politically motivated violence deliberately targeted at civilians Instruments of social and political change Terrorism seeks to break peoples will so they surrender principle to save themselves Terrorism is NOT: Senseless or random One persons terrorist is NOT another’s Freedom fighter A viable negotiating technique One to seek compromise

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    12. Terrorist Weapon Choice Depends on: Affordability of the weapon Ability to move the weapon Level of technology (usually low) Ability to deny the results if intended objective was not achieved

    13. How Nerve Agents Work

    14. Normal Nerve Function NORMAL NERVE FUNCTION Nerves communicate with muscles, organs, and other nerves by releasing chemicals or neurotransmitters at their connection site (synapse). One of the most common neurotransmitters is acetylcholine (ACh), which is released and collects at the receptor site stimulating the end organ to respond and produce a variety of effects: muscle contractions, gland secretion, and nerve-to-nerve conduction. NORMAL NERVE FUNCTION Nerves communicate with muscles, organs, and other nerves by releasing chemicals or neurotransmitters at their connection site (synapse). One of the most common neurotransmitters is acetylcholine (ACh), which is released and collects at the receptor site stimulating the end organ to respond and produce a variety of effects: muscle contractions, gland secretion, and nerve-to-nerve conduction.

    15. Normal Nerve Function When a nerve impulse reaches the synapse, ACh is released from the nerve ending and diffuses across the synaptic cleft to combine with receptor sites on the next nerve, and the electrical message continues. When a nerve impulse reaches the synapse, ACh is released from the nerve ending and diffuses across the synaptic cleft to combine with receptor sites on the next nerve, and the electrical message continues.

    16. Normal Nerve Function To stop further stimulation of the nerve, ACh is rapidly broken down by acetylcholinesterase (AChE), producing choline, acetic acid, and the regenerated enzyme. Thus, a “check and balance” system prevents the accumulation of ACh and the resultant over-stimulation of nerves, muscles, and glands. To stop further stimulation of the nerve, ACh is rapidly broken down by acetylcholinesterase (AChE), producing choline, acetic acid, and the regenerated enzyme. Thus, a “check and balance” system prevents the accumulation of ACh and the resultant over-stimulation of nerves, muscles, and glands.

    17. Nerve Agents inhibit AChE HOW NERVE AGENTS WORK The term “nerve agents” refers to chemicals that produce biological effects by inhibiting the enzyme AChE, thus allowing the neurotransmitter ACh to accumulate. Included among the “nerve agents” are some drugs (such as physostigmine and pyridostigmine) and some insecticides (Sevin®, malathion, and related insecticides). These compounds cause the same biological effects as the nerve agents developed for military use, but the latter are more than a hundred-fold more potent. As a result of inhibition of AChE, the neurotransmitter ACh accumulates to over-stimulate the organs it normally stimulates in the portion of the nervous system. This causes hyperactivity in these organs. These are all innervated by the cholinergic portion of the nervous system and have muscarinic receptors, nicotinic receptors, or a combination (central nervous system and cardiovascular system). HOW NERVE AGENTS WORK The term “nerve agents” refers to chemicals that produce biological effects by inhibiting the enzyme AChE, thus allowing the neurotransmitter ACh to accumulate. Included among the “nerve agents” are some drugs (such as physostigmine and pyridostigmine) and some insecticides (Sevin®, malathion, and related insecticides). These compounds cause the same biological effects as the nerve agents developed for military use, but the latter are more than a hundred-fold more potent. As a result of inhibition of AChE, the neurotransmitter ACh accumulates to over-stimulate the organs it normally stimulates in the portion of the nervous system. This causes hyperactivity in these organs. These are all innervated by the cholinergic portion of the nervous system and have muscarinic receptors, nicotinic receptors, or a combination (central nervous system and cardiovascular system).

    18. Nerve Agents Tabun (GA), Sarin (GB), Soman (GD),VX Nerve Agents are the 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 (Nerve agents inhibit cholinesterase) NERVE AGENTS The nerve agents are Tabun (GA), Sarin (GB), Soman (GD), and VX. Nerve agents are the most toxic of all the weaponized military agents. These agents can cause sudden loss of consciousness, seizures, apnea, and death. GB, or Sarin, is one of the more commonly stockpiled nerve agents, and it may be inhaled as a vapor, or cause toxic effects by contact with the skin in the liquid form. VX is mainly a liquid skin hazard at normal ambient temperatures. These chemicals are easily absorbed through the skin, eyes, or lungs. The diagnosis of a nerve agent poisoned Responder must be made clinically. There usually is not time for laboratory confirmation. Nerve agents (and similar substances) inhibit cholinesterase, an enzyme present in tissues and blood; there is a laboratory test to determine its activity in blood. Nerve agents are organophosphates (pesticides) that were developed by the Germans (G-agents) in the 1930s and the British (V-agents) in the 1950s during their research into finding more toxic insecticides. .NERVE AGENTS The nerve agents are Tabun (GA), Sarin (GB), Soman (GD), and VX. Nerve agents are the most toxic of all the weaponized military agents. These agents can cause sudden loss of consciousness, seizures, apnea, and death. GB, or Sarin, is one of the more commonly stockpiled nerve agents, and it may be inhaled as a vapor, or cause toxic effects by contact with the skin in the liquid form. VX is mainly a liquid skin hazard at normal ambient temperatures. These chemicals are easily absorbed through the skin, eyes, or lungs. The diagnosis of a nerve agent poisoned Responder must be made clinically. There usually is not time for laboratory confirmation. Nerve agents (and similar substances) inhibit cholinesterase, an enzyme present in tissues and blood; there is a laboratory test to determine its activity in blood. Nerve agents are organophosphates (pesticides) that were developed by the Germans (G-agents) in the 1930s and the British (V-agents) in the 1950s during their research into finding more toxic insecticides. .

    19. ROUTES OF EXPOSURE Direct Contact Inhalation Ingestion

    20. DIRECT CONTACT Skin or eyes are touched with agent vapor or liquid Nerve agents absorbed through skin VX remains on skin and absorbed more completely GB evaporates quickly, but still a threat Scrapes, cuts or other skin damage offer direct entry points freshly shaven skin, sunburn, insect bites, rashes Eyes most sensitive organ for nerve agent vapor effects

    21. Nerve agents enter through respiratory system Rapidly and effectively enter into blood stream INHALATION

    22. INGESTION Ingestion of contaminated food or drink, incidental hand to mouth or eye contact, smoking Unlikely that agent will contaminate food or drink

    23. Potential Exposure No signs or symptoms Reassure Segregate in cold zone Observe Arrange transport to ED by bus or vans Potential exposure. Asymptomatic Responders who present at the scene alleging exposure to nerve agents should be considered potentially exposed, triaged for other injuries, and segregated in an observation area in the cold zone. They may be transported to definitive care facilities by bus or vans. Potential exposure. Asymptomatic Responders who present at the scene alleging exposure to nerve agents should be considered potentially exposed, triaged for other injuries, and segregated in an observation area in the cold zone. They may be transported to definitive care facilities by bus or vans.

    24. Mild Exposure Miosis, rhinorrhea - observation only IV or IM atropine will not reverse miosis Localized fasciculations and sweating Exclusion (Hot) Zone: No immediate treatment Contamination Reduction (Warm) Zone: One MARK I Kit Atropine 2 mg IM 2-PAM 600 mg IM (Adult only) If there are mild effects from liquid exposure (localized sweating and fasciculations at the site of liquid contact), give one MARK I kit (atropine IV/IM with 2-PAM). If there are mild effects from liquid exposure (localized sweating and fasciculations at the site of liquid contact), give one MARK I kit (atropine IV/IM with 2-PAM).

    25. Moderate Exposure Miosis, rhinorrhea, SOB, wheezing, secretions, muscle weakness, GI effects Exclusion (Hot) Zone: No immediate treatment Contamination Reduction (Warm) Zone: One to two MARK I kits (repeat every 5-10 min) Atropine 2-4 mg IM (repeat every 5-10 min) 2-PAM 600-1200 mg IM Moderate systemic effects. Be more aggressive with moderate vapor exposures. Symptoms will include those for mild exposures with more severe respiratory distress, and may be accompanied by muscular weakness, and possibly GI effects (vomiting and diarrhea). Initial dose for these patients is 1 or 2 MARK I kits.Moderate systemic effects. Be more aggressive with moderate vapor exposures. Symptoms will include those for mild exposures with more severe respiratory distress, and may be accompanied by muscular weakness, and possibly GI effects (vomiting and diarrhea). Initial dose for these patients is 1 or 2 MARK I kits.

    26. Severe Exposure Unconscious, seizing, flaccid, apnea Exclusion (Hot) Zone: 3 MARK I kits IM as soon as possible Contamination Reduction (Warm) Zone: 3 MARK I kits IM as soon as possible Atropine 2-6 mg IM 2PAM 600-1800 mg IM Severe systemic effects. The antidotes should be administered as early as possible because airway management will not be possible until atropine reduces the bronchoconstriction. Intubate, ventilate and oxygenate the patient, and give three MARK I kits until the patient is oyygenated. Oxygenate the patient and suction secretions. Initially, ventilation may be difficult due to increased resistance, but the early administration of atropine will reduce this. Initial treatment should consist of three MARK I kits. After hypoxia is reversed, additional 2 mg doses of atropine IV may be given at 3- to 5-minute intervals PRN until secretions diminish or until airway resistance is within normal limits. Severely intoxicated patients may require up to 15 to 20 mg of atropine over the first 3 hours of treatment If inadequate supplies of antidotes are available, then they must be rationed accordingly.Severe systemic effects. The antidotes should be administered as early as possible because airway management will not be possible until atropine reduces the bronchoconstriction. Intubate, ventilate and oxygenate the patient, and give three MARK I kits until the patient is oyygenated. Oxygenate the patient and suction secretions. Initially, ventilation may be difficult due to increased resistance, but the early administration of atropine will reduce this. Initial treatment should consist of three MARK I kits. After hypoxia is reversed, additional 2 mg doses of atropine IV may be given at 3- to 5-minute intervals PRN until secretions diminish or until airway resistance is within normal limits. Severely intoxicated patients may require up to 15 to 20 mg of atropine over the first 3 hours of treatment If inadequate supplies of antidotes are available, then they must be rationed accordingly.

    27. Severe Exposure (cont.) For seizures: Paramedics may administer Midazolam (Versed) IM Adult: 5 mg IM IM midazolam is used for seizures. IM midazolam is used for seizures.

    28. SLUDGEM / DUMBELS Salivation Lacrimation (Tears) Urination Defecation GI Upset Emesis (Vomiting) Miosis (Pinpoint pupils) Diarrhea Urination Miosis Bronchospasm/bradycardia Emesis Lacrimation Salivation Sludgem is the old acronym for Nerve agent exposure and has been replaced with Dumbels. Sludgem is the old acronym for Nerve agent exposure and has been replaced with Dumbels.

    29. Effects of Nerve Agents Organs with cholinergic receptors Muscarinic (Atropine works) Smooth muscles Exocrine glands Nicotinic (Atropine ineffective) Skeletal muscles Ganglia (Sympathetic/Parasympathetic) EFFECTS OF NERVE AGENTS The clinical effects of nerve agents are in organs that have cholinergic receptors. These are divided into muscarinic sites and nicotinic sites. Organs with muscarinic receptors include smooth muscles and exocrine glands (post-ganglionic parasympathetic fibers); those with nicotinic sites are skeletal muscles and pre-ganglionic (sympathetic and parasympathetic) fibers. EFFECTS OF NERVE AGENTS The clinical effects of nerve agents are in organs that have cholinergic receptors. These are divided into muscarinic sites and nicotinic sites. Organs with muscarinic receptors include smooth muscles and exocrine glands (post-ganglionic parasympathetic fibers); those with nicotinic sites are skeletal muscles and pre-ganglionic (sympathetic and parasympathetic) fibers.

    30. Signs and Symptoms of Nerve Agents Muscarinic Sites Increased secretions Saliva Tears Runny nose Secretions in airways Secretions in gastrointestinal tract Sweating NERVE AGENT SIGNS AND SYMPTOMS - MUSCARINIC SITES Over-stimulation at muscarinic sites will increase secretions. The victim may experience increased saliva, tearing, runny nose, phlegm in the airways, sweating, and copious secretions in the respiratory and gastrointestinal tracts. NERVE AGENT SIGNS AND SYMPTOMS - MUSCARINIC SITES Over-stimulation at muscarinic sites will increase secretions. The victim may experience increased saliva, tearing, runny nose, phlegm in the airways, sweating, and copious secretions in the respiratory and gastrointestinal tracts.

    31. Signs and Symptoms of Nerve Agents Muscarinic Sites Smooth muscle contraction Eyes: miosis Airways: bronchoconstriction (shortness of breath) Gastrointestinal: hyperactivity (nausea, vomiting, and diarrhea) The accumulated ACh also causes pinpoint pupils (miosis), bronchoconstriction (shortness of breath), and hyperactivity of the gastrointestinal tract (nausea, vomiting, and diarrhea). This man was accidentally exposed to an unknown amount of nerve agent vapor. The series of photographs shows his eyes gradually recovering their ability to dilate. All photographs were taken with an electronic flash (which blinks too quickly for the pupil to react to) after the subject had been sitting in a totally dark room for 2 minutes. These photographs were taken (from top to bottom) at 3, 6, 13, 20, 41, and 62 days after the exposure. The accumulated ACh also causes pinpoint pupils (miosis), bronchoconstriction (shortness of breath), and hyperactivity of the gastrointestinal tract (nausea, vomiting, and diarrhea). This man was accidentally exposed to an unknown amount of nerve agent vapor. The series of photographs shows his eyes gradually recovering their ability to dilate. All photographs were taken with an electronic flash (which blinks too quickly for the pupil to react to) after the subject had been sitting in a totally dark room for 2 minutes. These photographs were taken (from top to bottom) at 3, 6, 13, 20, 41, and 62 days after the exposure.

    32. Signs and Symptoms of Nerve Agents Nicotinic Sites (Over-stimulation of Ach) Skeletal muscles Fasciculations Twitching Weakness Flaccid paralysis Other (ganglionic) Tachycardia Hypertension NERVE AGENT SIGNS AND SYMPTOMS - NICOTINIC SITES There are also nicotinic receptors which are stimulated by ACh. Over-stimulation causes skeletal muscle fasciculations, twitching, cramping, weakness, and finally paralysis. There is also stimulation of the pre-ganglionic fibers which may contribute to hypertension and tachycardia. The combination of pinpoint pupils and muscle fasciculations is the most reliable clinical evidence of organophospate (nerve agent) poisoning. NERVE AGENT SIGNS AND SYMPTOMS - NICOTINIC SITES There are also nicotinic receptors which are stimulated by ACh. Over-stimulation causes skeletal muscle fasciculations, twitching, cramping, weakness, and finally paralysis. There is also stimulation of the pre-ganglionic fibers which may contribute to hypertension and tachycardia. The combination of pinpoint pupils and muscle fasciculations is the most reliable clinical evidence of organophospate (nerve agent) poisoning.

    33. Nerve Agents Other Signs and Symptoms Cardiovascular Tachycardia, bradycardia Heart block, ventricular arrhythmias *Most disappear once antidote is given Central Nervous System Acute Loss of consciousness Seizures Apnea Prolonged (4-6 weeks) Psychological effects OTHER SIGNS AND SYMPTOMS OF NERVE AGENTS Cardiovascular. Bradyarrhythmias, heart block, tachyarrhythmias (sinus tachycardia), and ventricular arrhythmias (ventricular tachycardia and ventricular fibrillation) may occur, but most disappear once the antidote is given. Central nervous system. Acute severe effects include loss of consciousness, seizures, and apnea. Effects from a mild exposure include nervousness, fatigue, minor memory disturbances, irritability, and other minor psychological symptoms. The latter, whether caused by a severe or mild exposure, might linger for 4 to 6 weeks after exposure before resolving. OTHER SIGNS AND SYMPTOMS OF NERVE AGENTS Cardiovascular. Bradyarrhythmias, heart block, tachyarrhythmias (sinus tachycardia), and ventricular arrhythmias (ventricular tachycardia and ventricular fibrillation) may occur, but most disappear once the antidote is given. Central nervous system. Acute severe effects include loss of consciousness, seizures, and apnea. Effects from a mild exposure include nervousness, fatigue, minor memory disturbances, irritability, and other minor psychological symptoms. The latter, whether caused by a severe or mild exposure, might linger for 4 to 6 weeks after exposure before resolving.

    34. 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 5 minutes; if no effects within 20 minutes probably safe to assume there has not been an exposure. VAPOR EXPOSURE SIGNS AND SYMPTOMS After a mild exposure to vapor of a volatile nerve agent like GB, the most common effects are miosis (often with pain in the eye or head, complaints of dim or blurred vision, or possibly nausea and vomiting), conjunctival injection, rhinorrhea, and some degree of bronchoconstriction and bronchosecretions (with associated complaints of “a tight chest” or “shortness of breath”). A moderate exposure to the agent may bring on additional systemic symptoms, such as nausea, vomiting and diarrhea. Increased respiratory difficulty would also occur, and the patient could be expected to experience a sensation of general muscle weakness. After a severe exposure to vapor, the casualty will almost immediately lose consciousness, and seizures will begin within 1 to 2 minutes. After several minutes of seizing, apnea and flaccid paralysis will occur. If the exposure has been small and a victim is removed from the area of the exposure, shortness of breath may improve. In this situation, the removal of clothing is often adequate decontamination. Effects begin within a minute or so after vapor exposure and generally do not worsen significantly once the casualty is out of the contamination. Peak effects usually occur within the first 5 minutes following exposure. VAPOR EXPOSURE SIGNS AND SYMPTOMS After a mild exposure to vapor of a volatile nerve agent like GB, the most common effects are miosis (often with pain in the eye or head, complaints of dim or blurred vision, or possibly nausea and vomiting), conjunctival injection, rhinorrhea, and some degree of bronchoconstriction and bronchosecretions (with associated complaints of “a tight chest” or “shortness of breath”). A moderate exposure to the agent may bring on additional systemic symptoms, such as nausea, vomiting and diarrhea. Increased respiratory difficulty would also occur, and the patient could be expected to experience a sensation of general muscle weakness. After a severe exposure to vapor, the casualty will almost immediately lose consciousness, and seizures will begin within 1 to 2 minutes. After several minutes of seizing, apnea and flaccid paralysis will occur. If the exposure has been small and a victim is removed from the area of the exposure, shortness of breath may improve. In this situation, the removal of clothing is often adequate decontamination. Effects begin within a minute or so after vapor exposure and generally do not worsen significantly once the casualty is out of the contamination. Peak effects usually occur within the first 5 minutes following exposure.

    35. 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 LIQUID EXPOSURE SIGNS AND SYMPTOMS Persistent agents like VX present more of a liquid contact hazard. The onset of effects following exposure can be delayed from 10 minutes to 18 hours after contact with the agent, depending on the dose. A mild exposure could present as small fasciculations and diaphoresis on the skin at the site of the droplet. Moderate exposure effects might be gastrointestinal (GI), including nausea, vomiting, and diarrhea. A droplet the size of a Lethal Dose for 50 percent of the exposed population (LD50) (10 mg for VX as shown on this penny) on the skin could cause severe exposure symptoms, such as sudden loss of consciousness, seizures, flaccid paralysis, and apnea will occur within minutes. LIQUID EXPOSURE SIGNS AND SYMPTOMS Persistent agents like VX present more of a liquid contact hazard. The onset of effects following exposure can be delayed from 10 minutes to 18 hours after contact with the agent, depending on the dose. A mild exposure could present as small fasciculations and diaphoresis on the skin at the site of the droplet. Moderate exposure effects might be gastrointestinal (GI), including nausea, vomiting, and diarrhea. A droplet the size of a Lethal Dose for 50 percent of the exposed population (LD50) (10 mg for VX as shown on this penny) on the skin could cause severe exposure symptoms, such as sudden loss of consciousness, seizures, flaccid paralysis, and apnea will occur within minutes.

    36. 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 DIAGNOSIS OF NERVE AGENT EXPOSURE Diagnosis of casualties exposed to nerve agent will be based primarily on observations of symptoms. Casualties may exhibit indications of exposure to a specific organ system, such as miosis, or may be suffering from systemic effects such as vomiting or seizures. Any combination of nerve agent symptoms without a definite alternative cause should generate a high index of suspicion that organophosphate poisoning has occurred. The combination of pinpoint pupils and muscle fasciculations is the most reliable clinical evidence of organophospate poisoning. Suspicion that the poisoning could be a terrorist attack involving nerve agents (rather than accidental) should be triggered by the occurrence of several or many casualties with similar nerve agent-like symptoms, particularly if the casualties arrive within a short time period, or all developed symptoms while at the same location or event. While chemical agent detection and identification may eventually confirm a suspicion that a nerve agent attack has taken place, the results of chemical monitoring will probably not be available soon enough to be useful in the initial diagnosis of exposed victims. DIAGNOSIS OF NERVE AGENT EXPOSURE Diagnosis of casualties exposed to nerve agent will be based primarily on observations of symptoms. Casualties may exhibit indications of exposure to a specific organ system, such as miosis, or may be suffering from systemic effects such as vomiting or seizures. Any combination of nerve agent symptoms without a definite alternative cause should generate a high index of suspicion that organophosphate poisoning has occurred. The combination of pinpoint pupils and muscle fasciculations is the most reliable clinical evidence of organophospate poisoning. Suspicion that the poisoning could be a terrorist attack involving nerve agents (rather than accidental) should be triggered by the occurrence of several or many casualties with similar nerve agent-like symptoms, particularly if the casualties arrive within a short time period, or all developed symptoms while at the same location or event. While chemical agent detection and identification may eventually confirm a suspicion that a nerve agent attack has taken place, the results of chemical monitoring will probably not be available soon enough to be useful in the initial diagnosis of exposed victims.

    37. Treatment Self-protection Decontamination Self-protection. The process of treating nerve agent casualties may be divided into several components. The first and most important concept is to protect yourself. Don’t rush in! Assess the situation and the information you have been given as to the types of casualties before you do anything. Always stay upwind when you are unprotected. Be wary that there may be secondary devices and perpetrators among your victims. In situations where the signs and symptoms suggest nerve agent casualties, assume the presence of liquid contamination until proven otherwise. Whenever possible, make sure that the victims’ clothing is removed and any areas of liquid exposure have been decontaminated prior to handling patients, if you do not have personal protective equipment (PPE). Decontamination. If you do become contaminated, remember the four steps you learned in awareness training; blot off the agent, strip off all your clothing, flush the affected areas with large amounts of water, and cover the affected area. Make sure that patients exposed to nerve agents have had their clothing removed prior to transporting them to the hospital. Liquid-exposed casualties should be decontaminated (for example, with soap and water or bleach) prior to being handled or loaded into the ambulance. Verification of decontamination must be done by visual observation of the decontamination process.Self-protection. The process of treating nerve agent casualties may be divided into several components. The first and most important concept is to protect yourself. Don’t rush in! Assess the situation and the information you have been given as to the types of casualties before you do anything. Always stay upwind when you are unprotected. Be wary that there may be secondary devices and perpetrators among your victims. In situations where the signs and symptoms suggest nerve agent casualties, assume the presence of liquid contamination until proven otherwise. Whenever possible, make sure that the victims’ clothing is removed and any areas of liquid exposure have been decontaminated prior to handling patients, if you do not have personal protective equipment (PPE). Decontamination. If you do become contaminated, remember the four steps you learned in awareness training; blot off the agent, strip off all your clothing, flush the affected areas with large amounts of water, and cover the affected area. Make sure that patients exposed to nerve agents have had their clothing removed prior to transporting them to the hospital. Liquid-exposed casualties should be decontaminated (for example, with soap and water or bleach) prior to being handled or loaded into the ambulance. Verification of decontamination must be done by visual observation of the decontamination process.

    38. Who Can Administer Mark 1 kits In the State of Maine, an emergency responder can only administer the Mark 1 kits to themselves, or another emergency responder If you and your partner have an exposure, and your partner becomes symptomatic, treat yourself first and then treat your partner

    39. Nerve Agent Treatment Escape the Area* / Notify Dispatch Decontaminate (strip down / H2O) DO NOT ENTER ONCE SUSPICION EXISTS IF Symptomatic use the NAAK Kits: Atropine 2-PAMCl TREATMENT OF NERVE AGENT EXPOSURE - AIRWAY AND VENTILATION Establishment of a patent airway is essential for the survival of the severely exposed patient. Severely intoxicated patients will die if aggressive airway management is not quickly available. With large numbers of victims, rapid scene and resource assessment will influence triage decisions regarding interventional therapy. Because of the intense bronchoconstriction and secretions associated with nerve agent exposure, effective ventilation may not be initially possible due to high airway resistance (50 to 70 cm H2O). Adequate atropinization will reverse these muscarininc effects; therefore, atropine should be administered before other measures are attempted. Endotracheal intubation, followed by positive pressure ventilation with a bag-valve mask, should be performed as quickly as possible. Periodic suctioning of secretions will help to improve ventilation and air exchange. Patients with seizures and respiratory failure can be saved with immediate and adequate intervention. Antidote administration. Three medications are used to treat the signs and symptoms of nerve agent intoxication: atropine sulfate, pralidoxime chloride, and diazepam. The general indications for use of these antidotes will be presented first, followed by a discussion of their use in the treatment of mild, moderate, or severe nerve agent intoxication. TREATMENT OF NERVE AGENT EXPOSURE - AIRWAY AND VENTILATION Establishment of a patent airway is essential for the survival of the severely exposed patient. Severely intoxicated patients will die if aggressive airway management is not quickly available. With large numbers of victims, rapid scene and resource assessment will influence triage decisions regarding interventional therapy. Because of the intense bronchoconstriction and secretions associated with nerve agent exposure, effective ventilation may not be initially possible due to high airway resistance (50 to 70 cm H2O). Adequate atropinization will reverse these muscarininc effects; therefore, atropine should be administered before other measures are attempted. Endotracheal intubation, followed by positive pressure ventilation with a bag-valve mask, should be performed as quickly as possible. Periodic suctioning of secretions will help to improve ventilation and air exchange. Patients with seizures and respiratory failure can be saved with immediate and adequate intervention. Antidote administration. Three medications are used to treat the signs and symptoms of nerve agent intoxication: atropine sulfate, pralidoxime chloride, and diazepam. The general indications for use of these antidotes will be presented first, followed by a discussion of their use in the treatment of mild, moderate, or severe nerve agent intoxication.

    40. Nerve Agent Treatment Atropine Side effects in normal people Mydriasis (Pupil Dilation) Blurred vision Tachycardia Decreased secretions and sweating The initial parenteral dose of atropine is 2 to 6 mg in the adult, with subsequent doses titrated to the severity of the nerve agent signs and symptoms. Treatment for chemical nerve agent exposure might require up to 10 to 20 mg of atropine, or more if required to abate severe symptoms. Severely symptomatic casualties who receive inadequate atropine will be difficult to ventilate effectively, and will therefore have a poorer prognosis than those treated with sufficient medication to abate the most serious airway symptoms. (In patients poisoned with insecticides, over 2,000 to 3,000 mg of atropine might be necessary.) When atropine therapy exceeds the amount necessary to reverse the effect of the cholinergic hyperstimulation, it may cause toxicity manifested by dry mouth, flushing, and diminished sweating, but this would be extremely unlikely in a patient poisoned by an organophosphate (OP) compound. Side effects in unexposed people (not poisoned by OP compounds) include mydriasis, blurred vision, tachycardia, and diminished secretions. The latter (i.e., loss of sweating) may be of concern in a hot environment.The initial parenteral dose of atropine is 2 to 6 mg in the adult, with subsequent doses titrated to the severity of the nerve agent signs and symptoms. Treatment for chemical nerve agent exposure might require up to 10 to 20 mg of atropine, or more if required to abate severe symptoms. Severely symptomatic casualties who receive inadequate atropine will be difficult to ventilate effectively, and will therefore have a poorer prognosis than those treated with sufficient medication to abate the most serious airway symptoms. (In patients poisoned with insecticides, over 2,000 to 3,000 mg of atropine might be necessary.) When atropine therapy exceeds the amount necessary to reverse the effect of the cholinergic hyperstimulation, it may cause toxicity manifested by dry mouth, flushing, and diminished sweating, but this would be extremely unlikely in a patient poisoned by an organophosphate (OP) compound. Side effects in unexposed people (not poisoned by OP compounds) include mydriasis, blurred vision, tachycardia, and diminished secretions. The latter (i.e., loss of sweating) may be of concern in a hot environment.

    41. Nerve Agent Treatment Pralidoxime Chloride (2PAM-Cl) Remove nerve agent from AChE in absence of aging (ie enzyme and agent can become bound irreversibly- has to be given in 4-6 hrs (Sarin) 60hrs (VX) and 2 min for Soman 200 mg in each autoinjector No effects at muscarinic sites Helps at nicotinic sites TREATMENT - PRALIDOXIME CHLORIDE (2PAMCl) This is an antidote that can specifically break the bond between the nerve agent and the enzyme AChE and remove the agent. This will free the enzyme, making it once again available to break down ACh. Clinically, this will decrease muscle twitching, improve muscle strength, and allow the patient to breathe better; however, it has little effect on the muscarinic effects described previously. The bond between the enzyme and the nerve agent can age, a process by which the enzyme and agent become irreversibly bound. The half time for aging of sarin is 4 to 5 hours; this means that half of the bound sarin-enzyme complex can be reactivated 4-5 hours after sarin exposure by administration of the antidote. For VX exposure, the half time for aging of the VX-enzyme complex is 60 hours. The complete time for aging of sarin is about 10 times the half time (40-50 hours), and at this point the bond becomes permanent. Usually, there is plenty of time to treat patients with 2-PAMCl after exposure to nerve agents with the exception of GD. The soman-enzyme complex ages in about 2 minutes. TREATMENT - PRALIDOXIME CHLORIDE (2PAMCl) This is an antidote that can specifically break the bond between the nerve agent and the enzyme AChE and remove the agent. This will free the enzyme, making it once again available to break down ACh. Clinically, this will decrease muscle twitching, improve muscle strength, and allow the patient to breathe better; however, it has little effect on the muscarinic effects described previously. The bond between the enzyme and the nerve agent can age, a process by which the enzyme and agent become irreversibly bound. The half time for aging of sarin is 4 to 5 hours; this means that half of the bound sarin-enzyme complex can be reactivated 4-5 hours after sarin exposure by administration of the antidote. For VX exposure, the half time for aging of the VX-enzyme complex is 60 hours. The complete time for aging of sarin is about 10 times the half time (40-50 hours), and at this point the bond becomes permanent. Usually, there is plenty of time to treat patients with 2-PAMCl after exposure to nerve agents with the exception of GD. The soman-enzyme complex ages in about 2 minutes.

    42. MARK I Injections - Dispersal EFFECTIVENESS OF DISPERSION INTO TISSUE Rapid absorption of antidote following automatic injection is enhanced by the degree of tissue dispersion achieved by the autoinjector. The radiograph shows IM autoinjector doses (Lagre Picture) compared to standard syringe IM doses (Small Picture). The autoinjector medication is obviously more efficiently diffused into surrounding muscle due to the force with which it is expelled from the injector (as seen in photo.)EFFECTIVENESS OF DISPERSION INTO TISSUE Rapid absorption of antidote following automatic injection is enhanced by the degree of tissue dispersion achieved by the autoinjector. The radiograph shows IM autoinjector doses (Lagre Picture) compared to standard syringe IM doses (Small Picture). The autoinjector medication is obviously more efficiently diffused into surrounding muscle due to the force with which it is expelled from the injector (as seen in photo.)

    43. Nerve Agent Treatment Treatment regimen No signs/symptoms Reassure Observe Vapor: 1 hour Liquid: Up to 18 hours TREATMENT REGIMEN - LATENT EFFECTS Asymptomatic responders who present alleging exposure to nerve agents should be considered potentially exposed, triaged for other injuries, and observed for up to 1 hour if a vapor exposure is alleged, or up to 18 hours if a liquid exposure is possible (or if the exposure history is uncertain). TREATMENT REGIMEN - LATENT EFFECTS Asymptomatic responders who present alleging exposure to nerve agents should be considered potentially exposed, triaged for other injuries, and observed for up to 1 hour if a vapor exposure is alleged, or up to 18 hours if a liquid exposure is possible (or if the exposure history is uncertain).

    44. 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) Parenteral atropine will not reverse miosis TREATMENT OF MILD VAPOR AND LIQUID EFFECTS Mild vapor effects: The presence of miosis and rhinorrhea requires observation only. If the victim is suffering from airway effects (shortness of breath, chest tightness, and profuse airway secretions) that are not improving, then treat with 2 mg of atropine IM or IV, or with the MARK I kit. If they are comfortable although slightly short of breath, give nothing and observe. Supplemental oxygenation will be needed only in those patients with pulmonary or cardiac disease. IM atropine dosing can be repeated at 5 to 10 minute intervals as needed. [Note: Patients with pinpoint pupils may have severe light sensitivity and pain, but only require reassurance since these symptoms will resolve. At the hospital, these patients should be given a topical atropine or homatropine only for relief of severe pain in the eye(s) or head because the drug causes blurred vision. This may be done if miosis occurs as part of moderate or severe systemic effects as well.] Mild liquid effects: If there are mild effects from liquid exposure (localized sweating and fasciculations at the site of liquid contact), give 2 mg of atropine and 600 mg 2-PAMCl IM (MARK I kit) or 1 gram (gm) 2-PAMCl IV slowly over 20 to 30 minutes. TREATMENT OF MILD VAPOR AND LIQUID EFFECTS Mild vapor effects: The presence of miosis and rhinorrhea requires observation only. If the victim is suffering from airway effects (shortness of breath, chest tightness, and profuse airway secretions) that are not improving, then treat with 2 mg of atropine IM or IV, or with the MARK I kit. If they are comfortable although slightly short of breath, give nothing and observe. Supplemental oxygenation will be needed only in those patients with pulmonary or cardiac disease. IM atropine dosing can be repeated at 5 to 10 minute intervals as needed. [Note: Patients with pinpoint pupils may have severe light sensitivity and pain, but only require reassurance since these symptoms will resolve. At the hospital, these patients should be given a topical atropine or homatropine only for relief of severe pain in the eye(s) or head because the drug causes blurred vision. This may be done if miosis occurs as part of moderate or severe systemic effects as well.] Mild liquid effects: If there are mild effects from liquid exposure (localized sweating and fasciculations at the site of liquid contact), give 2 mg of atropine and 600 mg 2-PAMCl IM (MARK I kit) or 1 gram (gm) 2-PAMCl IV slowly over 20 to 30 minutes.

    45. Nerve Agent Treatment Moderate vapor or liquid exposure One or two MARK I kits TREATMENT OF MODERATE VAPOR AND LIQUID EXPOSURE Moderate Vapor Exposure: Be more aggressive with moderate vapor exposures. Symptoms will include those for mild exposures with more severe respiratory distress and may be accompanied by muscular weakness and possibly GI effects (vomiting and diarrhea). Initial dose for these patients is 1 or 2 MARK I kits containing a total of 2 mg atropine and 600 mg 2-PAMCl. Treatment may also be given IV, with 2 to 4 mg atropine given IV push, and 1 gram of 2-PAMCl given by IV infusion slowly. This dosing can be followed by repeat doses of 2 mg of atropine at 5 to 10 minute intervals as needed, and 600 mg of 2-PAMCl for a total of 1,800 mg 2-PAMCl with the MARK I kit IM (or 1 gm 2-PAMCl IV over 20 to 30 minutes for a total of three doses at hourly intervals). Moderate Liquid Exposure: For moderate toxicity several hours after liquid exposure, 2 mg of atropine and 600 mg 2-PAMCl should be given initially. Repeated doses of atropine and 2-PAMCl may also be necessary. Oxygen may be needed in those with cardiac or pulmonary disease who have severe breathing difficulty, but generally, it is not necessary. TREATMENT OF MODERATE VAPOR AND LIQUID EXPOSURE Moderate Vapor Exposure: Be more aggressive with moderate vapor exposures. Symptoms will include those for mild exposures with more severe respiratory distress and may be accompanied by muscular weakness and possibly GI effects (vomiting and diarrhea). Initial dose for these patients is 1 or 2 MARK I kits containing a total of 2 mg atropine and 600 mg 2-PAMCl. Treatment may also be given IV, with 2 to 4 mg atropine given IV push, and 1 gram of 2-PAMCl given by IV infusion slowly. This dosing can be followed by repeat doses of 2 mg of atropine at 5 to 10 minute intervals as needed, and 600 mg of 2-PAMCl for a total of 1,800 mg 2-PAMCl with the MARK I kit IM (or 1 gm 2-PAMCl IV over 20 to 30 minutes for a total of three doses at hourly intervals). Moderate Liquid Exposure: For moderate toxicity several hours after liquid exposure, 2 mg of atropine and 600 mg 2-PAMCl should be given initially. Repeated doses of atropine and 2-PAMCl may also be necessary. Oxygen may be needed in those with cardiac or pulmonary disease who have severe breathing difficulty, but generally, it is not necessary.

    46. Nerve Agent Treatment Severe - vapor or liquid Give 3 MARK I kits Airway Ventilation/O2 Consider Midazolam 5 mg IM and repeat the atropine every 5 to10 minutes as needed Repeat 2-PAMCl TREATMENT OF SEVERE EXPOSURE The severe vapor-exposed casualty will be unconscious, possibly seizing or post-ictal, twitching or flaccid, possibly apneic or with severe dyspnea. There may be effects in two or more body systems (dyspnea, vomiting/diarrhea, severe twitching, loss of consciousness). These casualties should be given 6 mg or atropine IM immediately, and 2-PAMCl should be started. Alternatively, 3 MARK I kits should be given as quickly as possible, with diazapam considered. These patients will require assisted ventilation with oxygen. TREATMENT OF SEVERE EXPOSURE The severe vapor-exposed casualty will be unconscious, possibly seizing or post-ictal, twitching or flaccid, possibly apneic or with severe dyspnea. There may be effects in two or more body systems (dyspnea, vomiting/diarrhea, severe twitching, loss of consciousness). These casualties should be given 6 mg or atropine IM immediately, and 2-PAMCl should be started. Alternatively, 3 MARK I kits should be given as quickly as possible, with diazapam considered. These patients will require assisted ventilation with oxygen.

    47. Treatment Airway/ventilation Antidotes Atropine Pralidoxime (2-PAM) Midazolam Airway and ventilation. Establishment of a patent airway is essential for the survival of the severely exposed patient. Severely intoxicated patients will die if aggressive airway management is not quickly available. With large numbers of victims, rapid scene and resource assessment will influence triage decisions about treatment. Because of the intense bronchoconstriction and secretions associated with nerve agent exposure, effective ventilation may not be initially possible due to high airway resistance without giving antidote first (50 to 70 cm H2O). Endotracheal intubation, followed by positive pressure ventilation with a bag-valve mask, should be performed as quickly as possible. Periodic suctioning of secretions will help to improve ventilation and air exchange. Patients with seizures and respiratory failure can be saved with immediate and adequate intervention. Antidote administration. Three medications are used to treat the signs and symptoms of nerve agent intoxication: atropine sulfate, pralidoxime chloride, and midazolam. The general indications for use of these antidotes will be presented first, followed by a discussion of their use in the treatment of mild, moderate, or severe nerve agent intoxication.Airway and ventilation. Establishment of a patent airway is essential for the survival of the severely exposed patient. Severely intoxicated patients will die if aggressive airway management is not quickly available. With large numbers of victims, rapid scene and resource assessment will influence triage decisions about treatment. Because of the intense bronchoconstriction and secretions associated with nerve agent exposure, effective ventilation may not be initially possible due to high airway resistance without giving antidote first (50 to 70 cm H2O). Endotracheal intubation, followed by positive pressure ventilation with a bag-valve mask, should be performed as quickly as possible. Periodic suctioning of secretions will help to improve ventilation and air exchange. Patients with seizures and respiratory failure can be saved with immediate and adequate intervention. Antidote administration. Three medications are used to treat the signs and symptoms of nerve agent intoxication: atropine sulfate, pralidoxime chloride, and midazolam. The general indications for use of these antidotes will be presented first, followed by a discussion of their use in the treatment of mild, moderate, or severe nerve agent intoxication.

    48. Atropine Given IV, IM, ET Antagonizes muscarinic effects Dries secretions; relaxes smooth muscles Does not affect miosis, fasciculations, muscle strength (nicotinic) May cause cardiac arrhythmias IV in hypoxic patient (v-fib) Atropine. Atropine works to block the effect of the accumulated neurotransmitter, ACh, at muscarinic sites. The more ACh at the sites, the more atropine is required to counteract its effects. Atropine can be administered intravenously (IV), intramuscularly (IM), or endotracheally. Atropine given IV or IM will reverse the muscarinic effects such as runny nose, salivation, sweating, bronchoconstriction, bronchial secretions, nausea, vomiting, and diarrhea. Atropine will not reverse nicotinic effects such as fasciculations, twitching, or muscle weakness. When given by the IV, IM, or ET routes, atropine will not reverse the pinpoint pupils (miosis), unless given in very high doses. Although the IV route of atropine administration is preferred when treating systemic effects, this should be avoided in hypoxemic nerve agent casualties (severely exposed, apneic). Because studies have documented the occurrence of ventricular fibrillation when atropine is administered IV to hypoxemic animals, it is preferred to use atropine IM in severely exposed victims until hypoxemia is reversed. Atropine. Atropine works to block the effect of the accumulated neurotransmitter, ACh, at muscarinic sites. The more ACh at the sites, the more atropine is required to counteract its effects. Atropine can be administered intravenously (IV), intramuscularly (IM), or endotracheally. Atropine given IV or IM will reverse the muscarinic effects such as runny nose, salivation, sweating, bronchoconstriction, bronchial secretions, nausea, vomiting, and diarrhea. Atropine will not reverse nicotinic effects such as fasciculations, twitching, or muscle weakness. When given by the IV, IM, or ET routes, atropine will not reverse the pinpoint pupils (miosis), unless given in very high doses. Although the IV route of atropine administration is preferred when treating systemic effects, this should be avoided in hypoxemic nerve agent casualties (severely exposed, apneic). Because studies have documented the occurrence of ventricular fibrillation when atropine is administered IV to hypoxemic animals, it is preferred to use atropine IM in severely exposed victims until hypoxemia is reversed.

    49. Atropine Starting dose - 2 mg Maximum cumulative dose - 20 mg Side effects in normal people Dilated pupils Blurred vision Tachycardia Decreased sweating The initial parenteral dose of atropine is 2 to 6 mg in the adult, with subsequent doses titrated to the severity of the nerve agent signs and symptoms. Treatment for chemical nerve agent exposure might require up to 10 to 20 mg of atropine. (In patients poisoned with insecticides, over 2,000 to 3,000 mg of atropine might be necessary.) When atropine therapy exceeds the amount necessary to reverse the effect of the cholinergic hyperstimulation, it may cause toxicity manifested by dry mouth, flushing, and diminished sweating, but this would be extremely unlikely in a patient poisoned by an organophosphate compound. Side effects in normal people (not poisoned by an organophosphate compound) include dilated pupils, blurred vision, tachycardia, diminished secretions, and decreased sweating. The latter may be of concern for responder in PPE or in a hot environment.The initial parenteral dose of atropine is 2 to 6 mg in the adult, with subsequent doses titrated to the severity of the nerve agent signs and symptoms. Treatment for chemical nerve agent exposure might require up to 10 to 20 mg of atropine. (In patients poisoned with insecticides, over 2,000 to 3,000 mg of atropine might be necessary.) When atropine therapy exceeds the amount necessary to reverse the effect of the cholinergic hyperstimulation, it may cause toxicity manifested by dry mouth, flushing, and diminished sweating, but this would be extremely unlikely in a patient poisoned by an organophosphate compound. Side effects in normal people (not poisoned by an organophosphate compound) include dilated pupils, blurred vision, tachycardia, diminished secretions, and decreased sweating. The latter may be of concern for responder in PPE or in a hot environment.

    50. Atropine Atropine - How much to give? Until secretions are drying or dry Until ventilation is “easy” If conscious, and victim is comfortable Don’t rely on heart rate/pupil size Atropine dosing is guided by the patient’s clinical presentation and should be given until secretions are dry or drying and ventilation becomes less labored. When shortness of breath, increased airway resistance, and secretions have abated and the patient is breathing easier, he or she has received enough atropine. Heart rate and pupillary size, ordinarily accurate reflections of atropine dosing, are not useful to determine the effectiveness of antidote therapy in treating a nerve agent casualty.Atropine dosing is guided by the patient’s clinical presentation and should be given until secretions are dry or drying and ventilation becomes less labored. When shortness of breath, increased airway resistance, and secretions have abated and the patient is breathing easier, he or she has received enough atropine. Heart rate and pupillary size, ordinarily accurate reflections of atropine dosing, are not useful to determine the effectiveness of antidote therapy in treating a nerve agent casualty.

    51. Atropine Overdose If excessive atropine is administered: Signs of atropinization will become even more severe and patient may also develop blurring of vision delirium urinary retention When signs and symptoms of atropinization develop, no more atropine should be injected until atropinization subsides

    52. Pralidoxime Chloride (2-PAM) Remove nerve agent from AChE in absence of aging (2-PAM “crowbar”) Does not reverse muscarinic effects on glands and smooth muscles Helps at nicotinic sites Pralidoxime chloride (2-PAM) is an antidote that can specifically break the bond between the nerve agent and the enzyme AChE and remove the agent. Think of it as a “crowbar” -- it pries the nerve agent off the enzyme. This will free the enzyme making it once again available to break down ACh. Clinically, this will decrease muscle twitching, improve muscle strength, and allow the patient to breathe better; however, it has little effect on the muscarinic effects described above. The bond between the enzyme and the nerve agent can age, which is a process by which the enzyme and agent become irreversibly bound. This means that if the antidote is not administered within 4 to 6 hours after sarin (the aging time for the sarin-enzyme complex) or within 60 hours after VX (the aging time for the VX-enzyme complex), the bond becomes permanent. Usually, there is plenty of time to treat patients with 2-PAM after exposure to nerve agents with the exception of soman (GD). The soman-enzyme complex ages in about 2 minutes.Pralidoxime chloride (2-PAM) is an antidote that can specifically break the bond between the nerve agent and the enzyme AChE and remove the agent. Think of it as a “crowbar” -- it pries the nerve agent off the enzyme. This will free the enzyme making it once again available to break down ACh. Clinically, this will decrease muscle twitching, improve muscle strength, and allow the patient to breathe better; however, it has little effect on the muscarinic effects described above. The bond between the enzyme and the nerve agent can age, which is a process by which the enzyme and agent become irreversibly bound. This means that if the antidote is not administered within 4 to 6 hours after sarin (the aging time for the sarin-enzyme complex) or within 60 hours after VX (the aging time for the VX-enzyme complex), the bond becomes permanent. Usually, there is plenty of time to treat patients with 2-PAM after exposure to nerve agents with the exception of soman (GD). The soman-enzyme complex ages in about 2 minutes.

    53. 2-PAM may cause: blurred vision diplopia impaired accommodation headache nausea 2-PAM Adverse Reactions

    54. Midazolam Decreases seizure activity Reduces seizure-induced brain injury Must observe carefully for respiratory depression Midazolam. Seizures are treated with drugs such as midazolam (Versed). Midazolam. Seizures are treated with drugs such as midazolam (Versed).

    55. Autoinjectors

    56. Auto-Injectors Simple, compact injection systems Permit rapid injection of required antidotes Prevent needle from being subject to cross-contamination Enable rapid and accurate administration even if care giver or patient is in protective clothing

    57. Directions for Use

    59. 4. After auto-injector has been activated, empty container should be disposed of properly It cannot be refilled nor can the protruding needle be retracted It should be disposed of in a “sharps” container 5. Note dosage on triage tag or write on chest or forehead of patient

    60. Riot Control Agents Summary 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 RIOT CONTROL AGENTS Most people are familiar with riot control agents or “tear gas.” These agents are used by the military for training, and by law enforcement agencies to subdue crowds or individuals. Mace is sold for individual protection in small spray devices. Pepper spray, derived from the capsicum family of peppers, is relatively new, and is used by the military, law enforcement, and for personal protection. These agents produce eye, nose, mouth, skin, and respiratory tract irritation. This class of chemical agents causes involuntary eye closing due to irritation. For police, this is an effective weapon as it can disable an assailant. The deleterious effect is usually transient (about 30 minutes after exposure). Medical treatment for those exposed to riot control agents will have to deal with their effects on the eyes, respiratory tract, and skin. Eyes should be irrigated copiously with water or saline. Remove contact lenses. Utilize slit lamp exam to make certain that all solid particle foreign bodies are removed. Follow-up with an ophthalmologist is recommended. Treat wheezing with bronchodilators or steroids if standard bronchodilators fail. Provide oxygen therapy if indicated. Most symptoms should be maximal within 1 to 2 hours. Most skin exposures require little more than reassurance. With prolonged pain, decontaminate with soap and water or a solution containing a carbonate and/or a bicarbonate. Do NOT use bleach. Delayed onset dermatitis should be managed with frequent irrigation and soothing ointments or creams.RIOT CONTROL AGENTS Most people are familiar with riot control agents or “tear gas.” These agents are used by the military for training, and by law enforcement agencies to subdue crowds or individuals. Mace is sold for individual protection in small spray devices. Pepper spray, derived from the capsicum family of peppers, is relatively new, and is used by the military, law enforcement, and for personal protection. These agents produce eye, nose, mouth, skin, and respiratory tract irritation. This class of chemical agents causes involuntary eye closing due to irritation. For police, this is an effective weapon as it can disable an assailant. The deleterious effect is usually transient (about 30 minutes after exposure). Medical treatment for those exposed to riot control agents will have to deal with their effects on the eyes, respiratory tract, and skin. Eyes should be irrigated copiously with water or saline. Remove contact lenses. Utilize slit lamp exam to make certain that all solid particle foreign bodies are removed. Follow-up with an ophthalmologist is recommended. Treat wheezing with bronchodilators or steroids if standard bronchodilators fail. Provide oxygen therapy if indicated. Most symptoms should be maximal within 1 to 2 hours. Most skin exposures require little more than reassurance. With prolonged pain, decontaminate with soap and water or a solution containing a carbonate and/or a bicarbonate. Do NOT use bleach. Delayed onset dermatitis should be managed with frequent irrigation and soothing ointments or creams.

    61. 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 NERVE AGENT SUMMARY Volatile nerve agents, such as sarin, are non-persistent chemicals that pose primarily an inhalation hazard. Symptoms of exposure develop within seconds, but tend not to worsen if the victim is able to be evacuated from the area. Those individuals who either inhale a toxic dose or are unable to be evacuated from the release site, will experience the highest mortality rates. Those individuals who are able to leave the release area quickly or who are exposed to low levels of the agent will experience the least amount of symptoms and will require minimal medical intervention (the “walking wounded”). Since these agents are highly volatile, first responders and medical personnel are at risk of becoming secondarily contaminated from agent off-gassing. This occurs if the victim’s clothing is not properly handled and responders fail to wear appropriate respiratory protection. Symptomatic individuals require immediate treatment, including airway management and antidote therapy. Nerve agents such as VX are very persistent agents, do not readily vaporize, and pose primarily a liquid threat. The symptoms from such a contamination may be delayed for minutes to hours depending on the concentration, dose, and location of the contaminant on the skin (absorption occurs more readily on moist areas of the skin). Symptoms may even develop slowly in cases where liquid exposure is high. Because victims of a VX attack are contaminated with a liquid, decontamination takes on a higher priority to limit the amount of agent absorption and to minimize the risk of spreading the contamination. Decontamination should ideally be provided simultaneously with antidote administration and airway management, when necessary. NERVE AGENT SUMMARY Volatile nerve agents, such as sarin, are non-persistent chemicals that pose primarily an inhalation hazard. Symptoms of exposure develop within seconds, but tend not to worsen if the victim is able to be evacuated from the area. Those individuals who either inhale a toxic dose or are unable to be evacuated from the release site, will experience the highest mortality rates. Those individuals who are able to leave the release area quickly or who are exposed to low levels of the agent will experience the least amount of symptoms and will require minimal medical intervention (the “walking wounded”). Since these agents are highly volatile, first responders and medical personnel are at risk of becoming secondarily contaminated from agent off-gassing. This occurs if the victim’s clothing is not properly handled and responders fail to wear appropriate respiratory protection. Symptomatic individuals require immediate treatment, including airway management and antidote therapy. Nerve agents such as VX are very persistent agents, do not readily vaporize, and pose primarily a liquid threat. The symptoms from such a contamination may be delayed for minutes to hours depending on the concentration, dose, and location of the contaminant on the skin (absorption occurs more readily on moist areas of the skin). Symptoms may even develop slowly in cases where liquid exposure is high. Because victims of a VX attack are contaminated with a liquid, decontamination takes on a higher priority to limit the amount of agent absorption and to minimize the risk of spreading the contamination. Decontamination should ideally be provided simultaneously with antidote administration and airway management, when necessary.

    62. 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 Volatile nerve agents (such as sarin) are non-persistent chemicals that pose primarily an inhalation hazard. Their symptoms of exposure develop within seconds, but tend not to worsen if the victim is able to be evacuated into a fresh air environment.. Those individuals who either inhale a toxic dose, are unable to be evacuated from the release site, or have underlying lung disease, will experience the highest morbidity and mortality rates. Victims who are able to leave the release area quickly or who are exposed to low levels of the agent will typically experience the least amount of symptoms and will require minimal medical intervention (the “walking wounded”). Since these agents are highly volatile, first responders and medical personnel are at risk of becoming secondarily exposed from agent off-gassing. This occurs if the victim’s clothing is not properly handled and responders fail to wear appropriate respiratory protection. Symptomatic individuals require immediate treatment, including airway management and antidote therapy. In contrast to the nerve agents, symptoms of phosgene and mustard vapor exposure do NOT develop rapidly. Victims of vapor exposure to these agents will have no symptoms at the time of exposure, but will have serious ones later on. While there is no antidote for mustard exposure, BAL can be used in treatment of Lewisite exposure. CHEMICAL AGENT SUMMARY Volatile nerve agents (such as sarin) are non-persistent chemicals that pose primarily an inhalation hazard. Their symptoms of exposure develop within seconds, but tend not to worsen if the victim is able to be evacuated into a fresh air environment.. Those individuals who either inhale a toxic dose, are unable to be evacuated from the release site, or have underlying lung disease, will experience the highest morbidity and mortality rates. Victims who are able to leave the release area quickly or who are exposed to low levels of the agent will typically experience the least amount of symptoms and will require minimal medical intervention (the “walking wounded”). Since these agents are highly volatile, first responders and medical personnel are at risk of becoming secondarily exposed from agent off-gassing. This occurs if the victim’s clothing is not properly handled and responders fail to wear appropriate respiratory protection. Symptomatic individuals require immediate treatment, including airway management and antidote therapy. In contrast to the nerve agents, symptoms of phosgene and mustard vapor exposure do NOT develop rapidly. Victims of vapor exposure to these agents will have no symptoms at the time of exposure, but will have serious ones later on. While there is no antidote for mustard exposure, BAL can be used in treatment of Lewisite exposure.

    63. 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 VX and blistering agents are persistent chemicals that do not readily vaporize, and pose primarily a liquid threat. The symptoms from such a contamination may be delayed for several minutes to hours depending on the concentration, dose, and location of the contaminant on the skin (absorption occurs more readily on moist areas of the skin). Because victims of these types of attacks are contaminated with a liquid, decontamination takes on a higher priority to limit the amount of agent absorption and to minimize the risk of spreading the contamination. Decontamination should ideally be provided simultaneously with antidote administration and airway management, when necessary. VX and blistering agents are persistent chemicals that do not readily vaporize, and pose primarily a liquid threat. The symptoms from such a contamination may be delayed for several minutes to hours depending on the concentration, dose, and location of the contaminant on the skin (absorption occurs more readily on moist areas of the skin). Because victims of these types of attacks are contaminated with a liquid, decontamination takes on a higher priority to limit the amount of agent absorption and to minimize the risk of spreading the contamination. Decontamination should ideally be provided simultaneously with antidote administration and airway management, when necessary.

    64. ANY QUESTIONS ???

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