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:
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- 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
Pathophysiology
- Nerve agents bind to acetylcholinesterase in a two-stage process:
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- The first stage is reversible with treatment pralidoxime
- The second stage, or "aging," is irreversible
- Acetylcholinesterase breaks down the neurotransmitter acetylcholine:
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- Acetylcholine remains at its post-synaptic receptor sites causing excessive cholinergic stimulation
- Muscarinic stimulation produces the DUMBELS syndrome:
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- Diarrhea, urination, miosis, bradycardia and bronchorrhea, emesis, lacrimation, salivation
- Nicotinic receptor stimulation produces the MTWHF syndrome:
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- Muscle pain, tremors, weakness, hypertension, fasciculation
- Symptoms can range from muscle weakness to profound paralysis
- Central nervous system effects:
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- Nerve agents freely cross the blood-brain barrier
- Confusion, altered consciousness, seizures, and coma are possible symptoms
Treatment
- Counteract the cholinergic excess at all three receptor sites:
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- Atropine counteracts only muscarinic effects
- Pralidoxime (protopam) counteracts the nicotinic effects
- Benzodiazepines counteracts the CNS effects
- Muscarinic symptoms:
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- 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:
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- 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:
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- Any of the intravenous benzodiazepines can be used to treat seizures
- Phenytoin and fosphenytoin are not effective
- Patient monitoring:
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- 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:
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- 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):
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- 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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