CBRNE - Nerve Agents, G-series - Tabun, Sarin, Soman Treatment & Management

Updated: Oct 02, 2021
  • Author: Kermit D Huebner, MD, FACEP; Chief Editor: Duane C Caneva, MD, MSc  more...
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Approach Considerations

Atropine and pralidoxime chloride (2-PAM Cl) are antidotes for nerve agent toxicity; however, pralidoxime must be administered within minutes to a few hours following exposure (depending on the specific agent) to be effective. Treatment consists of supportive measures and repeated administration of antidotes. [4]

Toxic effects of GB usually peak within minutes to hours and resolve within 24 hours. Thus, patients who inhale nerve agent vapor suffer peak toxic effects before arriving in the ED. Patients who present to the ED with only ocular findings following vapor exposure can be discharged home safely. Refer patients discharged home with miosis or other eye complaints to an ophthalmologist.

Onset of signs and symptoms in patients with dermal exposure to liquid GB may be delayed for as long as 18 hours. Observe these patients in the ED or hospital for at least 18 hours. As discussed in Workup, RBC or plasma cholinesterase activity alone should never determine disposition and must always be correlated with the patient's clinical status.

A variety of neurobehavioral symptoms may persist in patients exposed to nerve agents. Such patients may benefit from neurologic consultation.


Prehospital Care

Personal protective equipment

A key consideration in prehospital care is protection of emergency medical service personnel from exposure to the nerve agent until victims are decontaminated thoroughly or the need for decontamination is excluded. This involves personal protective equipment. [23]

First Responders should use a NIOSH-certified Chemical, Biological, Radiological, Nuclear (CBRN) Self Contained Breathing Apparatus (SCBA) with a Level A protective suit when entering an area with an unknown contaminant or when entering an area where the concentration of the contaminant is unknown. Level A protection should be used until monitoring results confirm the contaminant and the concentration of the contaminant. [17]


Goals of decontamination are to prevent further absorption of nerve agents by victims and to prevent the spread of nerve agents to others. If possible, decontamination should take place at the site of exposure.

Decontamination of liquid nerve agent exposure consists of removing all clothing, copiously irrigating with water to physically remove the nerve agent, and then washing the skin with an alkaline solution of soap and water or 0.5% hypochlorite solution (made by diluting household bleach 1:10) to chemically neutralize the nerve agent. Avoid hot water, strong detergents, and vigorous scrubbing, since they tend to enhance nerve agent absorption.

Skin exposure to liquid nerve agents will not necessarily result in systemic exposure if the site of exposure is decontaminated promptly. Before administering nerve agent antidotes, observe the site of exposure for localized sweating and muscular twitching. If these physical findings appear, administer antidotes; otherwise careful observation is all that is needed.

Exposure to nerve agent vapor does not require decontamination.

Often the first physical finding of minimal symptomatic exposure to nerve agent vapor is markedly constricted pupils (miosis). When exposed to liquid nerve agent, immediately flush the eyes with water for about 5 to 10 minutes by tilting the head to the side, pulling the eyelids apart with fingers, and pouring water slowly into the eyes. When exposed to nerve agent vapor, there is no need to flush the eyes. Do not cover eyes with bandages. [17]

Airway, breathing, and circulation

In cases of moderate to severe exposure, antidotes alone will not provide effective treatment, and ventilatory support is essential. Evaluate respiratory function and pulse. Ensure that the patient/victim has an unobstructed airway. Assist with ventilation as required.  Ventilatory distress is a physical finding of systemic exposure and marked resistance to ventilation is expected due to bronchial constriction and spasm. Resistance lessens after administration of atropine. Do not provide mouth-to-mouth resuscitation; contact with vapor or liquid agent may occur. If shortness of breath occurs, or breathing is difficult (dyspnea), administer oxygen. Suction secretions from the nose, mouth, and respiratory tract. [4]  


Use of nerve agent treatment autoinjectors by prehospital personnel should be guided by local policy. [23]  Administration of antidotes is a critical step in managing a patient. However, do not administer antidotes preventatively; there is no benefit to doing so. Diazepam (or other benzodiazepines) should be administered when there is evidence of seizures, usually seen in cases of moderate to severe exposure to a nerve agent. However, benbenzodiazepines do not protect against long-term adverse CNS effects. [24]  

Changes in the eye can lead to nausea and vomiting without necessarily being a sign of systemic exposure. However, if eye pain, nausea, or vomiting are seen in combination with any other physical findings of nerve agent poisoning, administer antidotes atropine and 2-PAM Cl as directed. 


Emergency Department Care

Personal protective equipment

Emergency department (ED) personnel should wear personal protective equipment similar to that worn by prehospital care personnel until adequate decontamination of victims is assured or the need for decontamination is eliminated. [23]


Goals of decontamination are to prevent further absorption of nerve agent by victims and to prevent the introduction of nerve agent into the clean ED environment.

Liquid nerve agent exposure requires formal decontamination, as outlined in Prehospital Care, before victims enter the ED. No decontamination is necessary in vapor exposure.

Previously reported terrorist episodes have demonstrated that victims who physically can flee the scene frequently bypass emergency medical services (EMS) and go directly to the nearest ED.

Airway, breathing, and circulation

The rapidity with which nerve agents act necessitates rapid medical response.

Moderately symptomatic patients require supplemental oxygen, pulse oximetry, cardiac monitoring, and early IV access.

Early endotracheal intubation and ventilatory support is paramount in treating patients with manifestations of severe toxicity.

Suction is an important adjunct to airway management, since airway secretions may be profuse in these patients.

Rapid sequence intubation may be required for airway treatment of patients with respiratory failure caused by nerve agent exposure. If rapid sequence intubation is used, avoid succinylcholine, since it is metabolized by plasma cholinesterase, leading to markedly prolonged paralysis.

Because atropine administered to hypoxic patients is associated with an increased risk of ventricular fibrillation, administer it after initial oxygenation and ventilation if possible.

Severely poisoned patients in respiratory arrest may need ventilatory assistance for several hours despite aggressive antidotal therapy. Patients in critical condition caused by complications of nerve agent poisoning, such as hypoxic brain injury, may require prolonged intensive care.

Pharmacologic treatment

Antidotes for nerve agent toxicity are atropine and pralidoxime.There is also generally no benefit in giving more than three injections of 2-PAM Cl. Atropine should be administered every 5 to 10 minutes until secretions begin to dry up. If the military Mark I kits containing autoinjectors are available, they provide the best way to administer the antidotes to healthy adults. [4] Seizures may require benzodiazepines. See Medication.





Consultation with a toxicologist via a regional poison control center may be helpful.