CBRNE - Nerve Agents, Binary - GB2, VX2 

Updated: Jan 11, 2021
Author: Larissa I Velez-Daubon, MD; Chief Editor: Duane C Caneva, MD, MSc 



In the 1950s, the US Army began to consider the development of binary nerve agent weapons to provide increased safety during storage and handling. At that time, unitary nerve agent weapons were the only ones in existence. In unitary agents, the chemicals were produced in a plant, loaded into the missile, and stored in a ready-to-use fashion. This method has several drawbacks. Because the munitions are highly toxic, storage, handling, and deployment need to be performed with extreme caution. Unitary weapons therefore pose a considerable risk to the ground crew and others who work with the chemicals. The agents in the active form are also highly corrosive; thus, extended storage times increase the risk of a leak.

Binary weapons involve nontoxic precursors that can be loaded in munitions. Once deployed, the precursors mix and develop the nerve agent. Binary agents are not only safer to handle and store, but they are also harder to detect using NATO chemical detection equipment (and therefore easier to transport and conceal); can more easily defeat NATO protective gear; and are potentially able to circumvent the Chemical Weapons Convention list of banned agents and precursors.

Development of binary weapons began in the 1960s.  Below is a timeline (adapted from Sidell, 1997; Smart, 1996; and Organisation for the Prohibition of Chemical Weapons) that highlights important dates in the development of binary technology:

  • 1960s: The BIGEYE, a 500-lb bomb with binary technology, is developed for the US Navy. Its production was halted in 1990.

  • September 16, 1969: A 155-mm projectile filled with sarin binary reagents is test fired at Dugway Proving Ground.

  • 1976: The US Army standardizes the M687 Binary GB2 155-mm projectile.

  • 1976: The US Congress passes the Department of Defense Appropriation Authorization Act, which restricts the development and production of binary weapons unless the President certifies to the Congress that such production is essential to the national interest.

  • 1985: Public Law 99-145 (US Congress) authorizes production of chemical weapons.

  • 1987: President Reagan certifies to US Congress the need for chemical weapons.

  • December 16, 1987: M687 binary projectile starts production at Pine Bluff.

  • June 1, 1990: The United States and the Soviet Union sign the bilateral chemical weapons destruction agreement.

  • 1991: Iraq declares to the United Nations Special Commission (UNSCOM) a different binary munition concept. The projectiles would contain only 1 canister with a single precursor. Before use, the munition would be opened, and the second precursor would be added. The chemical reaction then starts just prior to the munition release.

A binary projectile contains 2 separate, hermetically sealed, plastic-lined containers fitted, one behind the other, in the body of the projectile. In the sarin (GB) binary weapon, the forward canister contains methylphosphonic difluoride (DF). The rear canister contains an isopropyl alcohol and isopropylamine solution (OPA). Only the forward canister is in the munition prior to use. Before the weapon is fired, the rear canister is added and the fuse is placed. The force of launch causes the canisters to break, which produces GB within the projectile.

Known binary agents include the following:

  • GB binary (sarin, GB2): DF is located in 1 canister, while OPA is in a second canister. The isopropyl amine binds to the hydrogen fluoride generated during the chemical reaction. After deployment of the weapon, the 2 canisters rupture and the chemical mixture produces GB.

  • GD binary (soman, GD2): DF is located in 1 canister, while a mixture of pinacolyl alcohol and an amine is in a second canister. After deployment of the weapon, the 2 canisters rupture and the chemical mixture produces GD.

  • VX binary (VX2): O-Ethyl O-2-diisopropylaminoethyl methylphosphonite (QL) is in 1 canister. The other canister contains elemental sulfur. When the weapon is fired, the canisters rupture and the chemical mixture produces VX.

  • Novichok agent ("Newcomer"): a series of nerve agents developed by the Soviet Union in the 1970s and 1990s, all in the "third generation nerve agent" category. Five variants of these agents are thought to have been produced. Some of these agents (Novichok-5, Novichok-7) are binary agents.

The final product of the weapon is of the same chemical structure as the original nerve agent. The term binary refers only to the storage and deployment method used, not to the chemical structure of the substance. This article discusses management of chemical nerve agents in general; the reader can also refer to CBRNE - Nerve Agents, G-series - Tabun, Sarin, Soman and CBRNE - Nerve Agents, V-series - Ve, Vg, Vm, Vx for more detailed information on each particular agent.


Nerve agents comprise various compounds that have the capacity to inactivate the enzyme acetylcholinesterase (AChE). They are generally divided into 2 families, the G agents and the V agents (VX is the prototype of V agents). The Germans developed the G agents (ie, tabun [GA], sarin [GB], soman [GD]) during World War II. The G agents are highly volatile liquids that pose mainly an inhalation hazard. The V agents were developed later in the United Kingdom. They are approximately 10 times more toxic than GB. The V agents are less volatile and have an oily consistency; thus, they mainly pose a contact hazard. They are considered "persistent agents," which means that they can remain viable on surfaces for long periods of time. The Novichok agents have a much lesser known profile, but some are said to be 5-8 times more potent than VX, and others more than 10 times more potent than soman (GD).

Nerve agents bind to AChE much more potently than organophosphate and carbamate insecticides do. AChE is the enzyme that mediates the degradation of acetylcholine (ACh). ACh is an important neurotransmitter of the peripheral and central nervous systems. Acetylcholine activates 2 types of receptors, muscarinic and nicotinic. Nicotinic ACh receptors are found at the skeletal muscle and at the autonomic ganglia. The muscarinic receptors are found mainly in the postganglionic parasympathetic fibers and the brain. Therefore, nerve agent toxicity is manifested as excessive cholinergic transmission at both types of receptor sites.

ACh is released when an electrical impulse reaches the presynaptic neuron. The neurotransmitter travels across the synaptic cleft and reaches the postsynaptic membrane. There, it binds to its receptor (muscarinic or nicotinic). This interaction leads to activation of the ACh receptor and signal transmission in the postsynaptic side of the cleft. Normally, after this interaction between ACh and its receptor, ACh is rapidly degraded (hydrolyzed) into choline and acetic acid by AChE. This renders the ACh receptor active again. Choline undergoes reuptake into the presynaptic cell and is used to regenerate ACh.

Nerve agents act by inhibiting the hydrolysis of ACh by AChE. They bind to the active site of AChE, rendering it incapable of deactivating ACh. Any ACh that is not hydrolyzed can continue to interact with the postsynaptic receptor, which results in persistent and uncontrolled stimulation of that receptor. After persistent activation of the receptor, fatigue results. This is the same principle exhibited by the depolarizing neuromuscular blocker succinylcholine. The clinical effects of nerve agents are the result of this persistent stimulation and subsequent fatigue at the ACh receptor.

In an initial step, the enzyme becomes inactivated, but not permanently. Some degree of reactivation of the AChE enzyme occurs in this initial phase, but the process is slow. An additional reaction between AChE and the nerve agent makes their interaction irreversible, a phenomenon known as "aging." For the clinical effect to be reversed after aging occurs, new AChE enzyme must be produced. This irreversible bond is one difference between organophosphate compounds (including nerve agents) and carbamates, which bind reversibly to AChE. This concept is also used for pretreatment of military personnel with the carbamate pyridostigmine.

The typical aging half-lives for the different nerve agents are listed as follows:

  • GA (tabun) - 14 hours

  • GB (sarin) - 5 hours

  • GD (soman) - 2-6 minutes

  • VX - 48 hours

  • Novichok agents - unknown aging time



United States

No instances of binary nerve agent use or intentional release have been reported in the United States.


Although G agents were synthesized during World War II, no evidence exists that they ever were used in actual combat. Evidence is available that they were tested in concentration camps, however. The only known instance in which nerve agents were used in combat was during the Iran/Iraq war. The Iraqis also allegedly used them against the Kurds, most infamously at the town of Halabja in 1987. GB was used in Matsumoto, Japan, in 1994, and in the Tokyo subway attack in 1995, in the only two reported terrorist uses of sarin.

The threat of the use of nerve agents in terrorism is pervasive. Countries that are in political turmoil are at a higher risk for terrorist events. An unknown number of countries and terrorist groups may possess or have the capacity to manufacture nerve agents.

In recent years, there have been instances of assasinations using nerve agents, some of them thought to have been transported and/or deployed in the binary form:

  • February 3, 2017: Kim Jong-nam, the estranged older brother of North Korea's leader, Kim Jong-un, was assasinated while at the airport in Malaysia. Two women rubbed some chemicals on his face in rapid succesion. He died soon after. VX was detected and it is thought that each women applied a precursor of this nerve agent. 
  • March 2018: Sergei Skripal and his daughter Yulia were poisoned in Salisbury, England. British authorities identified the culprit as a Novichok agent.
  • June 30, 2018: Dawn Sturgess and Charlie Rowley were poisoned by a Novichok agent in Amesbury, England. Ms. Sturgess died as a consequence. The pair had found a glass bottle with a clear liquid near the site of the Skripal's poisonings. The contents of the bottle are thought to be discarded agent from the Salisbury incident. 


Toxicity of nerve agents is measured in two forms, median lethal concentration (LCt50) and median lethal dose (LD50). The LD50 is the lethal dose to 50% of exposed population, and refers to liquid or solid exposures. LCt50 refers to the inhalational toxicity of the vapor form of a volatile agent. Ct refers to the concentration of the vapor or aerosol in the air (measured as mg/m3) multiplied by the time the individual is exposed (measured in minutes). The LCt50 thus refers to the vapor exposure necessary to cause death in 50% of an exposed population. With an LCt50 of 10 mgXmin/m3, VX is the most toxic of the nerve agents (see Table 1).

Table 1. Toxicity of Nerve Agents (Open Table in a new window)


Chemical Name

LCt50, mgXmin/m3




Ethyl N -dimethylphosphoramidocyanidate




Isopropyl methylphosphonofluoridate




Pinacolyl methylphosphonofluoridate




O-Ethyl S-2-diisopropylaminoethyl methylphosphonothioate





Sensitivity to nerve agents varies with the individual, but no studies have addressed differential susceptibility based on race.


Everyone is at risk of being a target of terrorism. Military personnel are theoretically at increased risk; however, no gender predilection exists. No studies have been performed looking at differential susceptibility to nerve agents according to gender.


Everyone is at risk of being a target of terrorism. Military personnel are theoretically at increased risk; however, no predilection based on age exists.

Some limited evidence exists that children may be more susceptible than adults to the effects of organophosphate insecticides. In animal studies, lethal doses for immature and juvenile rats were 10% and 33%, respectively, of the lethal dose for adult rats.




The onset of symptoms after an exposure to a nerve agent varies depending on the route of exposure and the nature of the specific agent.

  • After inhalation, onset is extremely rapid because of the high vascularity of the lungs. The lungs are also important primary target organs. Dim or blurry vision caused by diffusion of the nerve agent through the cornea and subsequent interaction with the pupillary muscle is extremely common after a vapor exposure.

  • After dermal exposure to the G (volatile) agents, systemic effects may be delayed for minutes. In the case of VX, systemic effects may not appear until several hours after dermal exposure. The symptoms tend to be localized at first, with sweating and fasciculations, and may thus be overlooked by the patient. The onset of symptoms also depends on the area of skin that is exposed, and on the presence of sweat and ambient temperature. The rate of penetration is greatest in the thinner areas of the skin.

  • In many patients, history of exposure to a nerve agent is absent. In case of a terrorist attack, suspect the diagnosis when several patients present with symptoms of cholinergic excess. Occupational history may also aid in making the diagnosis. Military personnel and laboratory personnel are at a higher risk for exposures to the nerve agents.


Clinical signs and symptoms are related to excessive stimulation at the cholinergic nicotinic and muscarinic receptors both centrally and peripherally. Some central (CNS) effects may not be mediated by cholinergic receptors. In particular, some effects are suspected to occur on glutamate N -methyl-d-aspartate (NMDA) and gamma-butyric acid (GABA) receptors, which may contribute to nerve agent–mediated seizures and CNS neuropathology. See below for a summary of the clinical effects of nerve agents (adapted from Marrs, 1996).[1]

Signs and symptoms correlate with the severity of the exposure and are primarily related to excessive activation and subsequent fatigue at the cholinergic receptors. Some authors have divided exposures into minimal, moderate, and severe. Signs and symptoms associated with each level of exposure are summarized in Table 2.

Table 2. Severity of Toxicity From Liquid and Vapor Exposures (Open Table in a new window)

Severity of Exposure

Signs and Symptoms - Liquid*

Signs and Symptoms - Vapor†


Localized sweating at site

Localized fasciculations at site



Slight dyspnea


Above-mentioned symptoms and the following:

Nausea, vomiting, and diarrhea

Generalized weakness

Above-mentioned symptoms and the following:

Moderate-to-marked dyspnea

(bronchorrhea and/or bronchoconstriction)


Above-mentioned symptoms and the following:

Loss of consciousness


Generalized fasciculations

Flaccid paralysis and apnea

Above-mentioned symptoms and the following:

Loss of consciousness


Generalized fasciculations

Flaccid paralysis and apnea

* Onset possibly delayed

† Rapid onset of symptoms

Central (CNS) effects

CNS effects include the following:

  • Anxiety

  • Restlessness

  • Seizures

  • Failure to concentrate

  • Depression

Acetylcholine muscarinic (postganglionic parasympathetic)

DUMBELS is a commonly used mnemonic, as follows:

  • D - Diarrhea

  • U - Urination

  • M - Miosis

  • B - Bronchorrhea, bronchoconstriction

  • E - Emesis

  • L - Lacrimation

  • S - Salivation

Acetylcholine nicotinic (motor endplate, sympathetic and parasympathetic ganglia)

These signs and symptoms include the following:

  • Pallor

  • Tachycardia

  • Hypertension

  • Muscle weakness or paralysis

  • Fasciculations


Some of the most common effects of nerve agents are miosis and conjunctival injection. Patients may report eye pain, dim vision, and blurred vision. This most likely is due to direct contact between the agent and the pupillary muscle of the eye.

Miosis may persist for long periods and may be unilateral. Dim vision is, in part, due to the severe miosis, whereas the eye pain is directly caused by ciliary muscle spasm.

Patients exposed to VX may not experience miosis. This is probably because exposures to VX are generally dermal, and, thus, the eye is not directly exposed to the agent. However, miosis may be present as a delayed sign of VX exposure.


Rhinorrhea is common after vapor exposure, from direct exposure of the nasal mucosa to the nerve agent.

Rhinorrhea can also result as part of the systemic toxicity seen after exposures by other routes.


Shortness of breath is another common symptom after any form of exposure. It can vary from a sensation of tightness in the chest to frank respiratory distress, pulmonary edema, gasping, and apnea. This shortness of breath is caused by both the bronchoconstriction and excessive bronchial secretions that may result from muscarinic overactivity.

In severe exposures, paralysis of the respiratory muscles occurs due to respiratory muscle fatigue.

Muscarinic and nicotinic hyperactivity in the central nervous system can also produce a centrally mediated apnea.

Respiratory failure due to central apnea, bronchorrhea and bronchoconstriction, respiratory muscle paralysis, or a combination thereof is often the cause of death in nerve agent poisoning.

Skeletal muscle

Fasciculations, either localized or generalized, are observed after severe exposures. Myoclonic jerks (twitches) may also be observed.

Eventually, the muscles fatigue and a flaccid paralysis ensues.


With small liquid exposures, localized sweating and fasciculations can occur.

Generalized, profuse diaphoresis can occur with larger exposures.


Abdominal cramping can occur.

With larger exposures, nausea, vomiting, and diarrhea are more prominent.


The patient may present with either bradycardia or tachycardia. Increases in heart rate results from predominance of the adrenergic stimulation, whereas predominant parasympathetic tone results in vagal stimulation and bradycardia. Heart rate is an unreliable sign of nerve agent poisoning.

Many disturbances in cardiac rhythm have been reported after both organophosphate and nerve agent poisonings.

Heart blocks and premature ventricular contractions can occur.

The most concerning arrhythmias reported are torsade des pointes and ventricular fibrillation.

Central nervous system

Smaller exposures to nerve agents have reportedly resulted in behavioral changes such as anxiety, psychomotor depression, intellectual impairment, and unusual dreams.

Large exposures to nerve agents result in loss of consciousness, central apnea, and seizures.


Nerve agents are not readily available. Suspect nerve agent exposures in military personnel or research laboratory workers who may have access to these substances. Also suspect nerve agent poisoning when several patients present with signs of cholinergic overstimulation. This second presentation would be typical during a terrorist attack.



Diagnostic Considerations

Toxicity due to a nerve agent is suggested when several persons present with the symptoms discussed above.

Differential diagnoses mainly include poisoning by organophosphate or carbamate insecticides. However, an exposure to hydrogen cyanide or hydrogen sulfide could also be confused with a severe nerve agent exposure, since exposure to all those agents can result in sudden cardiovascular collapse.

Differential Diagnoses



Laboratory Studies

Many studies have related symptoms to laboratory parameters in cases of nerve agent exposures. A review of those studies is beyond the scope of this article but can be found in Chemical Warfare Agents: Toxicology and Treatment by Marrs, Maynard, and Sidell.

However, laboratory tests do not aid in the immediate treatment of patients exposed to nerve agents. Laboratory studies are most useful in observing long-term exposures over time when the individual's baseline measurement is known. Never withhold treatment while waiting for laboratory results. Nevertheless, laboratory analysis may be used to help document an exposure to a nerve agent, may help quantify the exposure, and may aid in the evaluation of the patient's recovery.

Red blood cell cholinesterase (RBC-ChE) levels: RBC-ChE is believed to be the most reliable indicator of the tissue cholinesterase status. However, baseline cholinesterase values vary significantly depending on age, ethnicity, nutritional status, and other individual factors. RBC-ChE levels are altered later in the course of the acute illness or with chronic exposures.

Plasma cholinesterase (butyrylcholinesterase [BuChE]) levels: This enzyme is also termed pseudocholinesterase. With organophosphate pesticide toxicity, this is the earliest enzyme to be inhibited and the earliest to be regenerated. However, sarin and VX preferentially bind RBC-ChE; thus, for these agents, the RBC cholinesterase is a more sensitive indicator of acute nerve agent exposure.

Blood concentrations of nerve agents are not available in clinical laboratories. The US Army Medical Research Institute of Chemical Defense can process blood samples and can be used as a reference laboratory.

Order basic laboratory studies in all but minimally symptomatic patients. Electrolytes and arterial blood gases aid in the evaluation of fluid status, oxygenation, and the acid/base balance. Observe the temperature in a serial fashion because patients can become hypothermic.

Imaging Studies

See the list below:

  • Request chest radiography for any severely dyspneic or intubated patient.

Other Tests

See the list below:

  • Additional tests do not provide information that aids in the treatment of patients with nerve agent poisoning. Presently, no information supports the use of tests to predict outcome.


See the list below:

  • Endotracheal intubation and mechanical ventilation may be needed for patients with ventilatory and/or respiratory failure.



Prehospital Care

Keep in mind that rescue personnel may themselves become affected by nerve agents. The cornerstones of prehospital management are based on rapid termination of exposure (ie, evacuation and decontamination), treatment of life-threatening emergencies, and administration of antidotes, if available. Whenever possible, decontamination should take place prior to transportation of the patient to a clean area. This prevents cross-contamination and additional exposures.

  • Decontamination techniques vary according to the extent and route of exposure.[2]

    • After exposure to any toxic vapor, evacuation and provision of fresh air is the most important first step. Clothes should be removed, since they can trap enough vapor to cause secondary victims. In the Tokyo subway attack, 10% of the caregivers at the hospital developed miosis after exposure to nondecontaminated victims.

    • In dermal exposures, the patient should be undressed. Any visible droplets should be blotted away. Abrasion of the skin by vigorous scrubbing increases absorption of the agent and should be avoided. Nerve agents can be neutralized with alkaline solutions such as soap and water or 0.5% hypochlorite solution (which releases chlorine), followed by a water rinse.[3] However, decontamination should not be delayed to seek hypochlorite or other special solutions; copious water is generally good enough for decontamination.

  • The military has autoinjector kits (MARK 1) that contain 2 antidotes, an oxime (AChE reactivator) and atropine.[4] Some ambulance systems and hazardous materials (HAZMAT) teams also have these kits available for use in the prehospital setting.

  • During a mass casualty incident, most patients arrive to the emergency department without the benefit of prior emergency medical services (EMS) or HAZMAT intervention. According to the 1998 report by Okumura et al, in the Tokyo subway sarin attack, 85% of patients arrived to the ED by private car.[5] This means that the emergency department must be prepared to treat potentially large numbers of contaminated individuals.

Emergency Department Care

If decontamination has not occurred, the emergency department should be able to provide this service prior to the patient's entrance to the hospital. If weather permits, decontamination stations can be set up outside. All hospital personnel in contact with contaminated individuals must wear full protective gowns (eg, rubber apron, rubber gloves, protective mask). Medical management is discussed in Medication.


Contact the regional poison center (1-800-222-1222) whenever nerve agent poisoning is suspected. In case of a multiple casualty incident, activate the hospital emergency plan and notify local authorities for advice and support.



Medication Summary

Table 3 summarizes the different agents used to treat patients with nerve agent poisoning. Table 4 provides some general treatment guidelines.

All but the mildest exposures cause some degree of respiratory compromise. For this reason, oxygen should be readily available. Most of these symptoms are the result of bronchorrhea and bronchoconstriction and improve after appropriate administration of antidotes. Ventilatory support may be needed for severely poisoned patients because of respiratory muscle paralysis. Oxygen is supplied via nasal cannula, face mask, or nonrebreather mask. Remember that inspired oxygen concentrations of 50-100% carry a substantial risk of lung damage when used for more than a few hours.

Table 3. Drugs Used to Treat Patients With Nerve Agent Poisoning* (Open Table in a new window)


Dose (Adult)





2 mg q5-10min prn

Note: The MARK 1 kit contains 2 mg of atropine.


Excessive muscarinic symptoms

Relative: IV route in hypoxia has been associated with ventricular fibrillation.

Pralidoxime chloride (Protopam, 2-PAM)

15-25 mg/kg over 20 min; can be repeated after 1 h

Note: The MARK 1 kit contains 600 mg of pralidoxime.


Symptomatic nerve agent poisoning

Rapid infusion may result in hypertension; may worsen symptoms in carbamate poisoning

Diazepam (Valium)

2-5 mg IV

10 mg IM


Moderate or severe signs of poisoning, seizures


*Adapted from Sidell, 1992.[6]

Table 4. Summary of Treatment Modalities According to Severity of Exposure* (Open Table in a new window)

Severity/Route of Exposure

Atropine (Adult Dose)








Decontamination and 18-h observation for liquid exposures


2 mg for severe

rhinorrhea or

dyspnea; may be


Administer if dyspnea

is not improving

or if GI

symptoms occur


Decontamination and 18-h observation for liquid exposures; oxygen


6 mg; may need to repeat

Administer with atropine

Administer even in absence of seizures

Decontamination; oxygen


Start with 6 mg; may need to repeat

Administer with atropine; should repeat once or twice

Administer even in absence of seizures

Airway, breathing, and circulation; decontamination

*Adapted from Sidell, 1992.[6]

Anticholinergic agents

Class Summary

These agents antagonize ACh at the muscarinic receptor.

Atropine IV/IM (Isopto, Atropair, Atropisol)

Antagonizes ACh at muscarinic receptor, leaving nicotinic receptors unaffected. In contrast to organophosphate insecticides, nerve agents rarely require >20 mg. Continue administration until excess muscarinic symptoms improve, which can be gauged by increased ease of breathing in the conscious patient or improvement in ease of ventilation in the intubated patient.


Class Summary

These reactivators of AChE enzyme are generally divided into 2 groups, monopyridinium and bispyridinium types. Pralidoxime belongs to the monopyridinium group and is the oxime used in the United States. Oximes should be administered concomitantly with atropine. After aging occurs, the usefulness of pralidoxime is minimal. VX has a slow aging process (estimated at 48 h); thus, delayed treatment with oximes may be beneficial. In contrast, aging half-life for GD is only 2-6 min, which makes pralidoxime impractical in this type of exposure.

A subset of the bispyridinium oximes termed H oximes (H for Hagedorn) contains variations of conventional extant oximes. These include agents such as HI-6, HGG-12, and HGG-42. They have been studied in the military setting but are not available for use in the United States. H oximes have shown promise in reactivating aged enzyme after GD exposure. The bispyridinium oxime termed obidoxime (Toxogonin) has been successfully tested for GB and GA intoxication. Pralidoxime is ineffective in GA.

In most cases, the specific agent involved is unknown. Do not delay or withhold antidote use while awaiting agent identification. The empiric use of pralidoxime is encouraged to prevent aging of the nerve agent with the AChE.

Pralidoxime (Protopam)

Oximes are reactivators of AChE. Can be used IM (as with military autoinjectors) or IV. The IV route is more likely to be practical in ED setting. The half-life of pralidoxime is 1 h, and it is renally excreted.


Class Summary

Seizures can be observed in severe nerve agent poisoning. For this reason, treatment with benzodiazepines has been advocated as part of the antidotal armamentarium. Experts advocate use of benzodiazepines prophylactically in patients with moderate-to-severe poisoning as well as with patients who are actively seizing. Dose should be 2-5 mg IV or 10 mg IM. With active seizures, diazepam should be titrated to effect.

Diazepam (Valium, Diazemuls, Diastat)

Belongs to benzodiazepine family, members of which act by stimulating GABA (the main inhibitory neurotransmitter in CNS) receptors, resulting in sedation and increased seizure threshold.

Midazolam (Versed)

Used as alternative in termination of refractory status epilepticus. Because midazolam is water soluble, it takes approximately 3 times longer than diazepam to reach peak EEG effects. Wait 2-3 min to fully evaluate sedative effects before initiating procedure or repeating dose.



Further Outpatient Care

See the list below:

  • Patients who are discharged from the hospital do not usually require further instructions or care. Nerve agents have not been associated with organophosphate-induced delayed neuropathy. Advise patients with miosis not to drive at night until their visual deficit resolves, which may take several weeks.

  • Posttraumatic stress disorder is common after terrorist events; patients may need a psychiatric evaluation or referral.

Further Inpatient Care

See the list below:

  • Admit all patients with liquid exposures for observation, even if initially asymptomatic. Onset of symptoms with these exposures may be delayed as long as 18 hours.

  • After a vapor exposure with only minimal symptoms, the patient can usually be discharged home.

  • Admit patients who have more than simple miosis for observation and further inpatient care.

Inpatient & Outpatient Medications

See the list below:

  • The cornerstone of management is the early use of antidotes (atropine and pralidoxime). No evidence supports the use of long-term therapy after the acute phase is over.


See the list below:

  • Prompt delivery of antidotes is of foremost importance in these patients. Transfer to a higher level of care facility may be arranged after decontamination, antidote administration, and stabilization of the patient.


See the list below:

  • Patients with status epilepticus or hypoxemia may experience anoxic brain injury.

  • Delayed or insufficient use of pralidoxime can lead to protracted muscle weakness.


See the list below:

  • If patients recover from the acute effects of the exposure, chronic effects are generally not expected. Subtle behavioral and cognitive changes have been noted to persist for days to weeks after the initial exposure. Patients may have permanent sequelae if they experienced anoxia during the acute phase of the poisoning.

Patient Education

See the list below:

  • For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education articles Chemical Warfare and Personal Protective Equipment.