Pediatric emergency medicine trisk 4567 4567
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to cause systemic effects, whereas a fatal dose (still smaller than a pinhead) may
lead to sudden collapse, convulsions, paralysis, apnea, and death after a latent
period of only 10 to 30 minutes. Because absorption from inhalation is fast and
complete, patients who have inhaled nerve-agent vapor typically do not
deteriorate once they are removed from exposure. However, the latency conferred
by the time needed for the nerve agent to traverse the epidermis means that
symptoms may arise (gradually or, with a high dose, suddenly) and progress
minutes to hours after exposure and even after successful decontamination of the
surface of the skin. Vapor-exposed patients typically exhibit either gradual or
sudden-onset local effects such as miosis, lacrimation, rhinorrhea,
hypersalivation, bronchoconstriction, and bronchorrhea followed or accompanied
by, if the dose or duration of exposure is high enough, systemic effects involving
the GI tract, skeletal muscles, and the CNS. Patients exposed via the skin may
also exhibit local effects (diaphoresis and fasciculations) and then systemic
effects either gradually or all at once, but after a delay. With high doses, collapse,
apnea, and death from bolus delivery to the circulation may be so rapid that
miosis and other peripheral muscarinic effects may not have time to develop.
Management. The diagnosis of traditional nerve-agent poisoning is primarily by
clinical recognition of acute signs and symptoms and by observing the response
to antidotal therapy. Routine toxicologic studies do not identify OP compounds or
their metabolites in blood or urine, and the ability to measure acetylcholinesterase
is not widely available. Although presumptive antidotal therapy for symptomatic
patients is indicated, treatment is not needed for exposed asymptomatic patients.
These patients, however, should be carefully observed if there is any possibility
of concomitant exposure to liquid nerve agent. As discussed previously, in this
setting immediate decontamination is an urgent medical intervention, since it can
decrease the internal dose of the agent. The drugs of choice to treat nerve-agent
toxicity are atropine for its antimuscarinic effects and pralidoxime (also called 2PAM), which serves to reactivate acetylcholinesterase. Atropine treats
bronchospasm and increased bronchial secretions, bradycardia, and GI effects and
may lessen seizure activity. However, atropine will not improve skeletal muscle
paralysis. Atropine is dosed initially at 0.05 mg/kg, with a minimum dose of 0.1
mg and a maximum of 5 mg ( Table 132.4 ). It should be given in repeat doses
until secretions decrease and airway resistance lessens; a typical total dose of
atropine for an adult nerve-agent victim is 20 to 30 mg, as opposed to over 20,000
mg that may be needed in an adult exposed to an OP pesticide (there is at least
one known case of a pediatric pesticide poisoning that required a total of 5,000
