Nerve Agent Antidote Kit Training Objectives:

Nerve Agent Antidote Kit Training Objectives:
Types of CBRNE Incidents Signs & Symptoms of Nerve Agent Exposure NAAKs Escape Hoods Protocols for NAAK Usage Practice Test

The Threat of NBC Terrorism

Potential Probability vs. Impact
NUCLEAR WEAPON BIOLOGICAL AGENT IMPROVISED NUCLEAR DEVICE POTENTIAL IMPACT CHEMICAL AGENT OR TOXIC INDUSTRIAL CHEMICAL RADIOACTIVE MATERIAL PROBABILITY/LIKELIHOOD

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 (riot control agents, chlorine), and some also have systemic effects (nerve agents and vesicants). Germany first utilized chemical warfare agents during World War I at Ypres, Belgium, in the late afternoon of April 22, 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 Agent Terrorist Attacks
Matsumoto: Approximately 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 Warfare Agents
Nerve Agents Vesicants (Blister) Industrial Chemicals Riot Control Agents Tabun, Sarin, Soman, VX Mustard, Lewisite Phosgene, Chlorine, Ammonia, Cyanide Mace®, Pepper Spray 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. NOTE: Students might be interested to know that mustard agent got its name from its mustard or horseradish-like odor. The sense of smell is, in any case, a poor detector for chemical warfare-type agents, because a detectable odor would likely mean that a serious exposure has already occurred. An important point for hospital care providers, however, is that conscious patients may be able to provide agent odor information which might aid in diagnosis and treatment. Information on the common industrial chemical cyanide is provided in the Additional Reading section at the end of this book.

Nerve Agents Tabun(GA), Sarin(GB), Soman(GD),VX
Most toxic of the chemical agents Penetrate skin, eyes, lungs Loss of consciousness, seizures, apnea, death after large amount Diagnosis made clinically; confirmed in laboratory (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 casualty 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. . INSTRUCTOR NOTE: To reinforce the fact that nerve agents, while being a weapon of mass destruction, are nevertheless similar in some ways to common pesticides, students might be asked if they have ever used Malathion, Diazinon, or some other common domestic insecticides. Point out that such common substances which are of organophosphate composition are, in fact, household “nerve agents” for insects.

Normal Nerve Function ACh Nerve, gland or muscle 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. ACh Ach=Acetylcholine stimulates muscle contraction, gland secretion & nerve to nerve conduction NOTE: In this graphic, the receptor target to the right of the synapse could be the continuing nerve, a gland, or a muscle. NOTE: At instructor’s discretion, an optional video describing nerve agent physiological effects may be used.

Normal Nerve Function ACh 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. NOTE: Emphasize that the effect of unwanted electrical message propagation depends on the receiving end organ. A gland will continue to secrete, a muscle will continue to contract, a nerve will continue to generate additional electrical impulses. Electrical Message continues…

Normal Nerve Function AChE ACh
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. ACh NOTE: This slide is an artist’s depiction of AChE metabolism of the neurotransmitter. The actual location of AChE is on the post-synaptic membrane, not in the synaptic cleft. Consider re-emphasizing that inhibition of the AChE allows accumulated ACh to continue stimulating muscle contraction, gland secretion, and nerve propagation of unwanted impulses. This mechanism relates directly to the signs and symptoms resulting from nerve agent exposure, and relating this process of effects to patients with apparently bizarre and varied symptoms could be extremely important in making a correct diagnosis in the aftermath of a terrorist attack. To stop further stimulation Ach is broken down by AChE ,preventing overstimulation

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). ACh GB Ach accumulates and causes over-stimulation of nerves, muscles and glands

Nicotinic & Muscarinic

Ach & Glandular Response

Ach on Skeletal Muscle

Ach on Smooth Muscle

Atropine Working

Atropine on Gland

Atropine on Smooth Muscle

AchE and how Oxime works

NA at Nerve Synapse

NA on Gland

NA on Skeletal Muscle

NA on Smooth Muscle

Normal AchE Response

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. NOTE: The distinction between muscarinic and nicotinic receptor sites in the body is extremely significant, because atropine, the major antidote to nerve agent poisoning, has its primary effect on organs with muscarinic receptor sites. Atropine is relatively ineffective on organs with nicotinic receptor sites.

SLUDGEM Salivation Lacrimation (Tears) Urination Defecation GI Upset
Emesis (Vomiting) Miosis (Pinpoint pupils)

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.

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. NOTE: Pupil size of the above patient at 3 days post-exposure was approximately 2 mm, and at 62 days was approximately 8 mm. This test was developed to identify minute deficiencies in pupil response due to the effects of nerve agent exposure. Under normal indoor lighting conditions, the pupils of a nerve agent casualty might appear normal within approximately 7 days, but testing an exposure victim in complete darkness emphasizes the fact that pupil response does not completely return to normal for many weeks. *Dark room for 2 min 3,6,13,20,41, and 62days after exposure

Signs and Symptoms of Nerve Agents Nicotinic Sites (Over-stimulation of Ach)
Skeletal muscles Fasciculations Twitching Weakness Flaccid paralysis Other (ganglionic) Tachycardia Hypertension GB ACh 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. *Myosis and fasciculations is the most reliable evidence of OPP*

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. NOTE: An optional sequence from the Chemical Stockpile Emergency Preparedness Project (CSEPP) video showing the effects of ACh and AChE may be shown.

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. NOTE: Emphasize that the effects of vapor exposure appear almost immediately. An emergency department patient who has exhibited no effects within 20 minutes after a possible vapor exposure most likely did not suffer a (vapor) exposure.

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. 10mg of VX LD50=lethal dose for 50% of the exposed population while the other 50% would suffer lesser effects NOTE: The droplet on the penny is a simulant used for demonstration purposes, and is not actually VX, which is nearly colorless. One example to help explain the effects of an LD50 of VX would be to explain that if a drop of the size depicted above were put on the skin of 100 people, 50 of those people would die from the agent’s effects, with the remainder suffering lesser signs and symptoms. While this could occur in minutes in some victims, it could take hours in others, because a number of factors effect the rate at which the body absorbs liquid agent. A patient potentially exposed to liquid nerve agent should be kept under medical observation for 18 hours to guard against potentially serious delayed effects.

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.

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 * Use Escape Hood if needed 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. NOTE: It is important to stress that attempts to ventilate the rigid airways of a nerve agent patient before treatment with atropine will be very difficult or totally unsuccessful.

Nerve Agent Treatment Atropine Dose
Antagonizes muscarinic effects (Blocks the effect of Ach) Dries secretions; relaxes smooth muscles Dose 2 mg in each autoinjector TREATMENT - 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 (ET). Parenteral atropine will reverse the muscarinic effects such as rhinorrhea, salivation, sweating, bronchoconstriction, bronchorrhea, nausea, vomiting, and diarrhea. Atropine will not reverse nicotinic effects such as fasciculations, twitching, or muscle weakness. Nor are miosis or ciliary body spasm reversed by parenteral atropine; relief of intractable pain in or around the eye requires the instilling of 1 percent homatropine or atropine topically. Although the IV route of atropine administration is preferred when treating system effects, this should be avoided in hypoxic nerve agent casualties. Because studies have documented the occurrence of ventricular fibrillation when atropine is administered IV to hypoxic animals, atropine should be administered IM in these patients. NOTE: Atropine is, of course, a common medication in ambulances as well as healthcare facilities. Care should be taken in planning for response to nerve agent exposure, however, because the quantity of atropine needed to treat organophosphate exposure is far in excess of that which is typically used to care for a cardiac patient. Counting on cardiac dosages of the medication to deal with the effects of a nerve agent attack could lead to complete depletion of a hospital’s stock of atropine.

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.

Nerve Agent Treatment Pralidoxime Chloride (2PAM-Cl) Nerve Agent
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 AChE 2-PAMCl Nerve Agent 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. This antidote breaks the bond between the nerve Agent and AChE and removes the agent NOTE: The speed with which Soman ages probably will not be significant from the immediate medical treatment standpoint for two reasons: 1. The exact identity of the chemical agent (Soman vs. other nerve agents) probably will not be immediately known after an attack. 2. The amount of 2-PAMCl used will not harm the patient. Administration of the 2-PAMCl should be by slow IV infusion, over 20 to 30 minutes. Rapid IV infusion will produce hypertension. The oxime can also be given IM, 1 gram in 3.3 ml in divided doses, as in the MARK I autoinjector.

Nerve Agent Treatment - Autoinjectors
TREATMENT - AUTOINJECTORS - MARK I KIT Atropine and pralidoxime chloride (2-PAMCl), are used by the military in autoinjectors which together are called the MARK I kit. The atropine autoinjector contains 2 milligrams (mg) of atropine and is administered IM by pressing the end of the device onto the thigh. A spring pushes the needle into the muscle and causes the atropine to be injected. This device causes atropine to be absorbed more rapidly than when administered by a conventional needle and syringe. The other autoinjector contains 600 mg of 2-PAMCl. The Food and Drug Administration (FDA) has approved the autoinjectors, but local protocols will determine their use in the field.

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 (on left) compared to standard syringe IM doses (on right). 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 inset photo.)

Nerve Agent Treatment Treatment regimen No signs/symptoms Reassure
Observe Vapor: 1 hour Liquid: Up to 18 hours TREATMENT REGIMEN - LATENT EFFECTS Asymptomatic victims who present to the ED 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).

Parenteral atropine will not reverse miosis
Nerve Agent Treatment One MARK I kit (2 mg atropine/ 600 mg 2 -PAMCl) Parenteral atropine will not reverse miosis Mild vapor exposure Miosis, rhinorrhea - observation only Increasing SOB – treat Mild liquid exposure Localized fasiculations & sweating - treat 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. NOTE: After the 1995 Tokyo subway nerve agent attack, 95 percent of symptomatic casualties suffered only from miosis.

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.

Nerve Agent Treatment Severe - vapor or liquid Give 3 MARK I kits
Airway Ventilation/O2 Consider diazepam 10 mg IM (2 to 5 mg IV) Repeat atropine every 5 to10 minutes as needed Repeat 2-PAMCl in one hour 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. NOTE: It should be emphasized that antidote administration must be the top priority in treating a severely exposed nerve agent casualty. Maintaining the airway and providing ventilatory support will be vital, but these measures are unlikely to be effective if atropine has not been administered. Airway constriction and hypersecretion can require positive pressure ventilation at 70 cm/H20 or higher pressures prior to treatment with atropine. This is particularly significant in light of the fact that some bag valve mask ventilators have pressure relief valves preset to 45 cm/H20.

Nerve Agent Summary Vapor exposure Liquid 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 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.

Riot Control Agents Irritating agents, lacrimators, “tear gas”
Cause reaction in Eyes: burning, tearing, eyelid spasm, redness Airways: burning, coughing, dyspnea Skin: burning, erythema Eye irrigation and supportive care 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. NOTE: Though the signs and symptoms related to riot control agents are generally temporary, exposure to high levels of the chemicals can result in more serious illness. This is especially true in the elderly, children, and individuals with underlying pulmonary disease such as asthma and COPD.

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
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.

Escape Hood Video

Nerve Agent Antidote Kit Training Objectives:

Similar presentations

Presentation on theme: "Nerve Agent Antidote Kit Training Objectives:"— Presentation transcript:

Similar presentations

About project

Feedback

Log in

Auth with social network:

Nerve Agent Antidote Kit Training Objectives:

Similar presentations

Presentation on theme: "Nerve Agent Antidote Kit Training Objectives:"— Presentation transcript:

Similar presentations

About project

Feedback