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Nerve Agents: Tabun (GA), Sarin (GB), Soman (GD), and VX

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Routes Of Exposure
  • Inhalation
  • Skin or eye contact
  • Ingestion
 
Clinical Health Effects
      Acute Exposure
  • Nerve agents alter cholinergic synaptic transmission at neuroeffector junctions at skeletal myoneural junctions and autonomic ganglia (nicotinic effects), and in the CNS. Initial symptoms depend on the dose and route of exposure.
  • Muscarinic effects include pinpoint pupils; blurred or dim vision; conjunctivitis; eye and head pain; hypersecretion by salivary, lacrimal, sweat, and bronchial glands; narrowing of the bronchi; nausea, vomiting, diarrhea, and crampy abdominal pains; urinary and fecal incontinence; and slow heart rate.
  • Nicotinic effects include skeletal muscle twitching, cramping, and weakness. 
  • Relatively small to moderate vapor exposure causes pinpoint pupils, rhinorrhea, bronchoconstriction, excessive bronchial secretions, and slight to moderate dyspnea.

 

      Central Nervous System (CNS)
  • Nerve agents cause behavioral and psychological changes in humans. CNS effects include irritability, nervousness, fatigue, insomnia, memory loss, impaired judgment, slurred speech, and depression. High exposures may produce loss of consciousness, seizures, and apnea.

 

      Respiratory
  • Inhalation of nerve agent vapors causes respiratory tract effects within seconds to minutes. Symptoms include excessive rhinorrhea and bronchial secretions, chest tightness, and difficulty breathing due to constriction of bronchial muscles and mucous secretions. Respiratory failure may occur due to CNS depression.

 

      Cardiovascular
  • Vagal stimulation may produce bradycardia, but pulse rate may be increased due to ganglionic stimulation, and the effects of hypoxia. Bradyarrhythmias and hypertension may occur.

 

      Gastrointestinal
  • Abdominal pain, nausea and vomiting are common manifestations of exposure by any route but may be the first systemic effects from liquid exposure on skin. If these symptoms occur within an hour of dermal exposure, severe intoxication is indicated. Diarrhea and fecal incontinence may also occur.

 

      Skeletal muscles
  • Nerve agents stimulate skeletal muscle producing fasciculations and twitching leading to fatigue and flaccid paralysis. Muscle twitching/fasciculations are clinical identifiers that indicate possible nerve agent exposure.

 

      Metabolic
  • Profuse sweating may occur.

 

      Ocular
  • Symptoms may occur from local effects of vapor exposure and from systemic absorption. Pinpoint pupils and spasm of the muscle of visual accommodation (i.e., ciliary muscle) leading to blurred and dim vision, aching pain in the eye, and conjunctivitis are typical effects.

 

      Potential Sequelae
  • CNS effects such as fatigue, irritability, nervousness and impairment of memory may persist for as long as 6 weeks after recovery from acute effects.

 

Laboratory Tests
  • Routine laboratory studies for all admitted patients include CBC, glucose, and serum electrolyte determinations.
  • Chest X-ray and pulse oximetry (or ABG measurements) are recommended for severe exposures.
  • Symptomatic and asymptomatic patients suspected of significant exposure should have determinations of red blood cell (RBC) cholinesterase activity, the most useful test for nerve agent poisoning.

 

Exposure/Contamination
  • Persons whose skin or clothing is contaminated with nerve agent can contaminate rescuers by direct contact or through off-gassing vapor.
  • Persons whose skin is exposed only to nerve agent vapor pose no risk of secondary contamination; however, clothing can trap vapor.

 

Treatment
  • Acute Exposure – When possible, atropine and 2-PAM Cl should be given under medical supervision to symptomatic patients who have known or strongly suspected nerve agent toxicity. Patients who are comatose, hypotensive, or seizing or have cardiac dysrhythmias should be treated according to advanced life support (ALS) protocols.
  • Eye – Severity of miosis cannot be used as an indicator of the amount of exposure or effectiveness of the antidotes. Maximum miosis may not occur until an hour or more after exposure.  If severe eye pain or nausea and vomiting occur, consider topical administration of atropine or homatropine.
  • Skin – Skin must be decontaminated within minutes following exposure to nerve agent. Because of the high toxicity, rapid absorption, and volatility, it is unlikely that a patient brought to a medical facility will have nerve agent on the skin. However, some nerve agent may remain in the hair or clothing and should be decontaminated if not previously done.
  • Inhalation – Ventilatory support is essential. Suction secretions from the nose, mouth, and respiratory tract.  Resistance to ventilation is expected due to bronchial constriction and spasm; lessens after administration of atropine.
  • Ingestion – Do not induce emesis because of the risk of pulmonary aspiration of gastric contents which may result from abrupt respiratory arrest, seizures, or vomiting.If the patient is alert and charcoal has not been given previously, administer slurry of activated charcoal. If the patient's condition is evaluated within 30 minutes after ingestion, consider gastric lavage.

 

Disposition/Followup
  • Patients exposed to nerve agent vapor that have only miosis and/or mild rhinorrhea when they reach the medical facility do not need to be admitted. All other patients who have had exposure to nerve agent should be hospitalized and observed closely.
  • Patients who have severe exposure should be evaluated for persistent CNS sequelae.
  • Patients should be advised to avoid organophosphate insecticide exposure until sequential RBC cholinesterase activity (measured at weekly to monthly intervals) has stabilized in the normal range.
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