Presentation on theme: "Emergency Management of Nerve Agent Casualties"— Presentation transcript:
1Emergency Management of Nerve Agent Casualties THIS PRESENTATION WAS COMBINED USING SLIDES FROM TWO PRESENTATIONS CREATED BY SBCCOM -- EMS Management of Chemical Agent Casualties AND Hospital Provider Management of Nerve Agent Casualties.NOTE: Greet the class and introduce yourself. Describe a few basic concepts to be covered in this module (such as the nature of chemical agents and hazards they present).Your knowledge base can be increased by referring to the references for this module prior to lecturing.
2Hospital Provider Management of Chemical Agent Casualties MODULE 3: HOSPITAL MANAGEMENT OF CHEMICAL CASUALTIESHospitals represent a vital disaster resource to local communities. After a terrorist attack, victims - either on their own or by emergency vehicles - will go to emergency departments regardless of the level of preparedness of the medical facility. It is essential that hospitals develop an awareness and operational level of understanding regarding the consequences of a terrorist attack.This module of instruction should enable students to describe types of chemical warfare agents, recognize signs and symptoms of exposure, and describe how to manage the victims of a chemical agent attack.NOTE: Greet the class and introduce yourself. Describe a few basic concepts to be covered in this module (such as the nature of chemical agents and hazards they present).Your knowledge base can be increased by referring to the references for this module prior to lecturing.
3EMS Management of Chemical Agent Casualties MODULE 4: EMS MANAGEMENT OF CHEMICAL AGENT CASUALTIESEmergency medical service systems represent a vital disaster resource to local communities. After a chemical terrorist attack, victims and bystanders will call for field medical assistance, and their lives (as well as the well-being of EMS responders themselves) will depend on rapid and correct emergency medical response. It is essential that EMS personnel develop a working comprehension of the consequences of a chemical terrorist attack.This module of instruction should enable students to describe types of chemical warfare agents, recognize signs and symptoms of exposure, and describe how to manage the victims of a chemical agent attack.NOTE: Greet the class and introduce yourself. Describe a few basic concepts to be covered in this module (such as the nature of chemical agents and hazards they present). Hereafter, the term “chemical agents” in this lecture will refer to chemical warfare agents, except as noted with industrial chemicals.Your knowledge base can be increased by referring to the references for this module prior to lecturing.
4Objectives Describe physiological actions of nerve agents Recognize signs and symptoms of nerve agent exposureDescribe emergency management of nerve agent victimsUpon completion of this module of instruction, students will be able to accomplish these three components of the terminal learning objective.NOTE: Do not dwell on background information or industrial chemicals. Blister and nerve agents should be the main focus of this presentation.
5Nerve Agents Tabun (GA), Sarin (GB), Soman (GD), VX Most toxic of the chemical agentsPenetrate skin, eyes, lungsLoss of consciousness, seizures, apnea, death after large amountDiagnosis made clinically; confirmed in laboratory (cholinesterase)NERVE AGENTSThe nerve agents are tabun (GA), sarin (GB), soman (GD), VX as well as organophosphate pesticides. 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.
6ACh 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.AChNOTE: 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.
7ACh 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.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.
8Normal 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.AChNOTE: 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.
9AChE GB ACh How Nerve Agents Work 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).AChGBNOTE: 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.
10Effects of Nerve Agents Two types of cholinergic receptors:MuscarinicSmooth musclesExocrine glandsCranial nerves (vagus)NicotinicSkeletal musclesGangliaEFFECTS OF NERVE AGENTSThe 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.
11Signs and Symptoms of Nerve Agents Mnemonic SLUDGE-MSalivationLacrimationUrinationDefecationGI upset – nausea/vomiting, cramps, diarrheaEmesisMuscle twitching
12Signs and Symptoms of Nerve Agents Newer Mnemonic DUMBELSDiarrheaUrinationMiosisBradycardia, Bronchorrhea, BronchospasmEmesisLacrimationSalivation, Sweating
13Signs and Symptoms of Nerve Agents Muscarinic Sites Increased secretionsSalivaTearsRunny noseSecretions in airwaysSecretions in gastrointestinal tractSweatingNERVE AGENT SIGNS AND SYMPTOMS - MUSCARINIC SITESOver-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.
14Signs and Symptoms of Nerve Agents Muscarinic Sites Smooth muscle contractionEyes: miosisAirways: 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), and may also cause involuntary urination.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.
15Signs and Symptoms of Nerve Agents Nicotinic Sites Skeletal musclesFasciculationsTwitchingWeaknessFlaccid paralysisOther (ganglionic)TachycardiaHypertensionGBAChNERVE AGENT SIGNS AND SYMPTOMS - NICOTINIC SITESThere 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 organophosphate (nerve agent) poisoning.
16Nerve Agents Other Signs and Symptoms CardiovascularTachycardia, bradycardiaHeart block, ventricular arrhythmiasCentral Nervous SystemAcuteLoss of consciousnessSeizuresApneaProlonged (4-6 weeks)Psychological effectsOTHER SIGNS AND SYMPTOMS OF NERVE AGENTSCardiovascular. 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.
17Signs and Symptoms of Nerve Agents Vapor Exposure Mild exposureMiosis (dim vision, eye pain), rhinorrhea, dyspneaModerate exposurePronounced dyspnea, nausea, vomiting, diarrhea, weaknessSevere exposureImmediate loss of consciousness, seizures, apnea, and flaccid paralysisVapor effects occur within seconds, peak within minutes; no late onsetVAPOR EXPOSURE SIGNS AND SYMPTOMSAfter 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.
18Signs and Symptoms of Nerve Agents Liquid Exposure Mild exposure (to 18 hours)Localized sweatingFasciculationsNo miosisModerate exposure (<LD50) (to 18hours)Gastrointestinal effectsMiosis uncommonSevere exposure (LD50) (<30 minutes)Sudden loss of consciousnessSeizuresApneaFlaccid paralysisDeathLIQUID EXPOSURE SIGNS AND SYMPTOMSPersistent 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.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.
19Diagnosis of Nerve Agent Exposure SymptomaticMay be systemic or organ-specificCombination of symptoms is more definitiveSituationalMultiple casualties with similar symptomsTime or location factors in commonDIAGNOSIS OF NERVE AGENT EXPOSUREDiagnosis 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.
20Nerve Agents Treatment Removal from exposureDecontaminationAirway/ventilationHigh resistanceAntidotesAtropine2-PAMClDiazepamTREATMENT OF NERVE AGENT EXPOSURE - AIRWAY AND VENTILATIONEstablishment 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.
21Nerve Agents Treatment AtropineAntagonizes muscarinic effectsDries secretions; relaxes smooth musclesGiven IV, IM, ETNo effect on pupilsNo effect on skeletal musclesIV in hypoxic patient Ù ventricular fibrillationTREATMENT - ATROPINEAtropine 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.
22Nerve Agents Treatment Starting dose - 2 mgMaximum cumulative dose - 20 mgTotal dose calculated over time; but enough must be administered to abate severe symptoms if casualty is to surviveInsecticide poisoning requires much moreSide effects in normal peopleMydriasisBlurred visionTachycardiaDecreased secretions and sweatingThe 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.Atropine is given prior to 2-PAMCl.
23Nerve Agents Treatment Atropine - How much to give?Until secretions are drying or dryUntil ventilation is “easy”If conscious or casualty is comfortableDo not rely on heart rate/pupil sizeAtropine 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 for clinical monitoring after nerve agent exposure.NOTE: While nebulized bronchodilators such as albuterol are one standard approach to relieving dyspnea due to bronchoconstriction, these medications will be less effective than atropine when treating a nerve agent casualty. The primary effect of albuterol is on beta-adrenergic receptors, while atropine has the specific anti-cholinergic action necessary to counteract the effects of bronchoconstriction and hypersecretion caused by nerve agent exposure.
24Nerve Agents Treatment Pralidoxime Chloride (2-PAMCl)Remove nerve agent from AChE in absence of aging1 gram slowly (20-30 minutes) in IV infusionHypertension with rapid infusionNo effects at muscarinic sitesHelps at nicotinic sitesTREATMENT - 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.Give 2-PAMCl after atropine.AChE2-PAMClNerve AgentNOTE: 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.
25Nerve Agents Treatment - Autoinjectors TREATMENT - AUTOINJECTORS - MARK I KITAtropine 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.
26MARK I Injection IM vs. IV MARK I INJECTION VS. IM OR IV ROUTEUsing cardiac response as an indicator of atropine uptake over time, the above chart demonstrates the effectiveness of the MARK I injector at administering the medication. While intravenous atropine predictably has an immediate effect, it is an effect which also begins to diminish rapidly. Standard intramuscular injections of atropine may not cause peak effects for nearly an hour, whereas the autoinjector administration, due to its force of injection, causes peak reaction in half the time noted for a standard IM dose. The MARK I injection effects are also seen to be of comparatively long duration.
27MARK I Injections Dispersal EFFECTIVENESS OF DISPERSION INTO TISSUERapid 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.)
28Nerve Agents Treatment DiazepamDecreases seizure activityReduces seizure-induced brain injuryGive to severely intoxicated casualties whether convulsing or notTREATMENT - DIAZEPAMSeizures are treated with benzodiazepines such as diazepam. These medications can be used IV or via an autoinjector which contains 10 mg of diazepam. In an emergency department setting where respiratory status can be closely monitored, higher doses may be necessary; animal data shows that doses which equate to 30 or 40 mg in humans may be required to stop seizures. Some authorities recommend treating all severely exposed patients with diazepam whether they are convulsing or not. If three atropine MARK I kits are required initially because of the victim’s clinical presentation, diazepam should be administered immediately thereafter. Other benzodiazapines commonly used in hospitals may work equally well.It is important for emergency department personnel to be aware that other commonly used anticonvulsants, including phenytoin, valproic acid, phenobarbitol, and carbamazepine, are INEFFECTIVE against nerve agent-induced seizures. The pathophysiology of this state is not the same as commonly encountered status epilepticus. One class of drugs which is not commonly used in status epilepticus but which, based on animal data, is highly effective against nerve agent-induced seizures is the anticholinergic class. Trihexyphenidyl HCI and scopolamine have been shown effective in monkeys in ongoing studies.NOTE: The FDA has approved Diazepam use in nerve agent-induced seizures. The military fields this medication only for anticonvulsant use. Many emergency medical services have other benzodiazepines more readily available. Animal data indicates that the other benzodiazepines are as efficacious as diazepam, and in particular midazolam (Versed) may work faster than others in this class.
29Nerve Agents Treatment No signs/symptomsReassureObserveVapor: 1 hourLiquid: Up to 18 hoursTREATMENT REGIMEN - LATENT EFFECTSAsymptomatic 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).Whether this protracted observation takes place in a hospital, mass casualty holding area or other location will be dictated by circumstances and local protocols. Those under such observation must be watched carefully by a qualified medical care provider, because liquid agent victims may suffer a sudden onset of life-threatening difficulties.
30Nerve Agents Treatment Treat with:Mild vapor exposureMiosis, rhinorrhea - observation onlyIncreasing SOB – treatMild liquid exposureLocalized fasiculations & sweating - treatOne MARK I kit (2 mg atropine/ 600 mg 2-PAMCl)OR1 gram 2-PAMCl IV2 mg atropine, IM or IVParenteral atropine will not reverse miosisTREATMENT OF MILD VAPOR AND LIQUID EFFECTSMild 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, which requires no medical treatment beyond reassurance and observation. EMS personnel should consider this fact when assessing the possible impact of a chemical terrorism incident in their communities.
31Nerve Agents Treatment Moderate vapor or liquid exposureMore severe respiratory distressMuscular weaknessNausea, vomiting, and diarrheaTreat with:One or two MARK I kitsORIV:2 to 4 mg atropine1gm 2-PAMCl (infusion)TREATMENT OF MODERATE VAPOR AND LIQUID EXPOSUREModerate 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.
32Nerve Agents Treatment Severe vapor or liquid exposureUnconsciousSeizing or post-ictalApneic or severe dyspneaTwitching or flaccidEffects in 2 or more body system3 MARK I kits OR6 mg atropine IV and1 gram of 2-PAMCl IVAirwayVentilation/O2Consider diazepam 10 mg IM (2 to 5 mg IV)Repeat atropine every 5 to 10 minutes as neededRepeat 2-PAMCl in one hourTREATMENT OF SEVERE EXPOSUREThe 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 pressure 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; these devices would require overriding if ventilation of a nerve agent patient were to be accomplished effectively. Pediatric bag valve masks also commonly contain a pressure relief vent which would have to be occluded to ventilate effectively.
33Nerve Agents Age-Related Treatment AtropineInfant (0 to 2) mg IMChild (2 to 10) mg IMAdolescent (> 10) mg IMElderly mg IMIV for infants and children mg/kgSPECIAL AGE-RELATED ANTIDOTE DOSING CONSIDERATIONSAtropine: Certain members of the population may be more sensitive to atropine. These include infants, young children, and the elderly. Pediatric experts have divided the age groups for IM administration of atropine. These doses may be repeated as clinically indicated.If atropine is to be given IV, then the dose is 0.02 mg/kilogram (kg) for infants up through young adults.If only standard MARK I kits are available, the use of a 2 mg atropine autoinjector can be used, but infants and small children are at risk of being injured by the autoinjector needle. The most significant adverse effect of high dose atropine in the younger patient is the inhibition of sweating.Elderly: In the frail or medically compromised adult, use a 1 mg dose and repeat as necessary.CategoryInfantChildAdolescentDose0.5 mg single dose1.0 mg single dose2.0 mg single doseAge0 to 2 years2 to 10 yearsYoung adultNOTE: Advise students that the proper antidote dose varies with age group, and that the dosing information is included in their course materials. This will prevent expending an extended period of time covering information they can refer to directly later.
34Nerve Agents Age-Related Treatment 2-PAMCl< 20 kg 15 mg/kg IV> 20 kg 600-mg IM autoinjectorElderly 1/2 adult dose (7.5 mg/kg IV)2-PAMCl-induced hypertensionPhentolamine Adult - 5 mg IVChild - 1 mg IVSPECIAL AGE - RELATED ANTIDOTE DOSING CONSIDERATIONS (continued)Pralidoxime chloride: No data are available for 2-PAMCl use in nerve agent exposed children. The standard IV dose for a patient from an infant to a 70-kg person is 15 mg/kg, with the dose repeated twice at hourly intervals. Above 70 kg, the dose should be a total of 1 gm, repeated twice at hourly intervals as necessary. For IM use, the doses should be :These may be adjusted according to subsequent clinical presentation.Elderly: If frail, hypertensive, or with renal disease, use one-half the usual adult dose of 2-PAMCl (7.5 mg/kg IV).If hypertension becomes significant during the administration of the 2-PAMCl, treat with IV phentolamine as follows:Adult: 5 mg IVChild: 1 mg IVWeight< 20 kg> 20 kgDose15 mg/kg600 mg autoinjectorNOTE: Advise students that the proper antidote dose varies with age group, and that the dosing information is included in their course materials.
35Nerve Agents Age-Related Treatment Diazepam- Infants > 30 days old mg/kg IVto 5 years q 2 to 5 min(max 5 mg)- Children > 5 years mg IVq 2 to 5 min(max 10 mg)SPECIAL AGE - RELATED ANTIDOTE DOSING CONSIDERATIONS (continued)Diazepam: Recommended pediatric doses:Infants > 30 days to age 50.2 to 0.5 mg/kg IV slowly every 2 to 5 minutes to maximum dose of 5 mg1 mg IV every 2 to 5 minutes to maximum dose of 10 mgChildren > 5 yearsNOTE: Advise students that the proper antidote dose varies with age group, and that the dosing information is included in their course materials.
36Nerve Agents Summary Liquid exposure Vapor exposure Symptoms develop suddenlyMost ambulatory victims require minimal interventionRisk of secondary contamination, which is minimized by removing the victim’s clothingRequires immediate access to antidotesLiquid exposureSymptoms delayed minutes to hoursGreater need for decontaminationHigh risk of secondary contamination; victims require decontamination (clothing removal & washdown)Requires immediate access to antidotesNERVE AGENT SUMMARYVolatile 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.
37Reference DOMESTIC PREPAREDNESS TRAINING TEAM HELPLINE: (800) FAX: (410)U.S. ARMY SBCCOMATTN: AMSSB-RDP5183 BLACKHAWK ROADABERDEEN PROVING GROUNDMARYLANDU.S. Solder and Biological and Chemical Command (SBCCOM)TRAINING OVERVIEWThe Domestic Preparedness program was established in The program’s primary proponent agency is the United States Army Soldier and Biological Chemical Command (SBCCOM), headquartered at the Edgewood Area of Aberdeen Proving Ground, Maryland.NOTE: CBDCOM re-organized and merged with another U. S. Army command in The new organization is known as SBCCOM, the Soldier and Biological Chemical Command.iii