Pediatric emergency medicine trisk 4565 4565
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The clinical presentation of severe nerve-agent poisoning overlaps with
that of severe cyanide poisoning, though nerve agents may produce
cholinergic effects and are more likely to produce cyanosis.
Hemodynamic effects may be either excitatory or inhibitory, depending
on balance between sympathomimetic and muscarinic effects.
Nerve-agent poisonings generally require atropine to counter the
cholinergic effects, as well as pralidoxime to counter the neuromuscular
effects.
Prophylactic treatment with benzodiazepines to prevent seizures is
indicated in large exposures.
Nerve agents (including the compounds sarin, soman, tabun, and VX) are
organophosphorus esters and, like the less potent “organophosphate” (OP)
insecticides, are potent and essentially irreversible inhibitors of
acetylcholinesterase (see Chapter 102 Toxicologic Emergencies ). Certain oximes
can dissociate bound nerve agents from acetylcholinesterase but only initially;
after a variable period a portion of an alkyl group is nonenzymatically lost from
the enzyme in a process called aging, and the resulting nerve agent—
cholinesterase complex becomes refractory to oxime action. The time required for
these agents to undergo aging varies from a few minutes for soman to 48 hours
for VX. Nerve-agent vapors are heavier than air and would thus affect persons
closer to the ground (e.g., young children) disproportionately.
Toxicology. Nerve agent–induced inhibition of acetylcholinesterase causes the
neurotransmitter acetylcholine to accumulate in cholinergic synapses and in
neuromuscular and neuroglandular junctions; this excess of acetylcholine initially
causes end-organ stimulation that may then lead to end-organ failure. Cholinergic
sites are found in the central nervous system (CNS), in the neuromuscular
junctions of somatic nerves, in parasympathetic nerve endings, in some
sympathetic nerve endings (e.g., sweat glands), and in both parasympathetic and
sympathetic ganglia.
The cholinergic syndrome thus produced is classically divided into CNS
effects, nicotinic effects (at neuromuscular junctions and sympathetic ganglia),
and muscarinic effects (in smooth muscles and exocrine glands). CNS effects
include altered mental status progressing through lethargy to coma, ataxia,
convulsions, and respiratory depression (central apnea). Nicotinic effects include
muscle fasciculations (including tics) and twitching, and then weakness
