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Nerve Gases

General Characteristics

  • Nerve gases include GA (Tabun), GB (Sarin), GD (Soman), VX, and GF
  • Nerve gases are potent organophosphate compounds that inhibit acetylcholinesterease, causing a cholinergic crisis
  • Many countries and terrorist groups have the capability to manufacture these or similar agents

Victim Triage

  • Since all nerve agents are heavier than air they will sink:
    • The triage point should be upwind and uphill of the center of the event
    • Paramedics entering the zone of contamination must wear level A personal protective gear
  • Victims must be hosed off with copious amounts of water
  • Once decontaminated, victims should be medically evaluated for symptoms and the need to administer antidotes


  • Nerve agents bind to acetylcholinesterase in a two-stage process:
    • The first stage is reversible with treatment pralidoxime
    • The second stage, or "aging," is irreversible
  • Acetylcholinesterase breaks down the neurotransmitter acetylcholine:
    • Acetylcholine remains at its post-synaptic receptor sites causing excessive cholinergic stimulation
  • Muscarinic stimulation produces the DUMBELS syndrome:
    • Diarrhea, urination, miosis, bradycardia and bronchorrhea, emesis, lacrimation, salivation
  • Nicotinic receptor stimulation produces the MTWHF syndrome:
    • Muscle pain, tremors, weakness, hypertension, fasciculation
    • Symptoms can range from muscle weakness to profound paralysis
  • Central nervous system effects:
    • Nerve agents freely cross the blood-brain barrier
    • Confusion, altered consciousness, seizures, and coma are possible symptoms


  • Counteract the cholinergic excess at all three receptor sites:
    • Atropine counteracts only muscarinic effects
    • Pralidoxime (protopam) counteracts the nicotinic effects
    • Benzodiazepines counteracts the CNS effects
  • Muscarinic symptoms:
    • Localized ocular symptoms may be treated with anticholinergic eye drops (scopolamine or homatropine)
    • Isolated bronchospasm can be treated with ipratropium bromide
    • Hypersalivation, bronchial secretions, or bradycardia can be treated with large doses of intravenous atropine, titrated to clearing of the excess secretions (not bradycardia or pupil size)
  • Nicotinic symptoms:
    • Pralidoxime (2-PAM) reactivates the enzyme acetylcholinesterase at the neuromuscular junction
    • It can only reactivate the enzyme if the aging process has not occurred, which varies from 5 minutes to 24 hours, depending upon the nerve agent
    • The recommended initial dose of 2-PAM is 1 to 2 grams I.V. slowly over 10 to 30 minutes
  • Central nervous system symptoms:
    • Any of the intravenous benzodiazepines can be used to treat seizures
    • Phenytoin and fosphenytoin are not effective
  • Patient monitoring:
    • Those with only minor symptoms, such as eye findings, may be watched for 6 to 8 hours and released if no further symptoms occur
    • Any patient who received 2-PAM should be hospitalized in an ICU
    • Any patient with neuromuscular weakness may require intubation and mechanical ventilation

Delayed Syndromes

  • Intermediate syndrome:
    • Can occur within a few days of exposure, usually after some recovery has manifested itself
    • Symptoms include a new onset of descending paralysis, clinically similar botulism, and may require re-intubation and mechanical ventilation
  • OPIND (organophosphate induced delayed neuropathy):
    • Caused by a slow inhibition of a second enzyme, NTE, up to a month after the initial exposure
    • Can lead to a sensory and motor distal neuropathy similar to Guillian-Barré syndrome
    • Recovery can be slow and incomplete
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