Pediatric emergency medicine trisk 4573 4573
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miosis in 43% of children exposed to OP pesticides, isolated CNS effects (stupor
and coma) in the absence of peripheral muscarinic effects, incidences of seizures
varying from 8% to 22%, and weakness and hypotonia (seen in 70% to 100% of
victims) often in the absence of glandular secretions. The clinician should be
prepared for subtle and sometimes significant differences in children from the
classic cholinergic toxidrome seen in adults.
Disposition and Prognosis. The disposition of exposed patients depends on
severity of symptoms and route of exposure. Most patients presenting after vapor
exposure manifest peak toxicity by the time of hospital arrival with only miosis,
which may persist for up to 6 weeks. These children may be discharged. After
dermal exposure, symptom onset may lag up to 18 hours, even after thorough
skin decontamination, and most experts recommend a 24-hour observation period
even for initially asymptomatic victims.
The prognosis for full recovery from even severe nerve-agent poisoning
appears to be good with timely life-support interventions and adequate antidotal
therapy. Apneic patients have recovered ventilatory function within 3 hours, and
once consciousness was regained, muscle weakness and obtundation have
resolved over a few days, whereas miosis and subtle mental status effects have
persisted for several weeks. Significant histologically demonstrable
neuropathologic changes in brain tissue persisting after acute exposures are
typically seen only in exposed individuals who exhibited seizure activity during
the acute cholinergic crisis. Nerve agents appear not to cause intermediate
syndrome (IMS), a syndrome of weakness, especially of cranial nerve–innervated
muscles (neck flexors and respiratory muscles) and limb muscles seen in
survivors of Sri Lankan suicide attempts involving OP insecticides. Two acutely
poisoned Japanese nerve-agent casualties, one from the Tokyo attack and one
from an earlier attack in Matsumoto, developed organophosphate-induced
delayed neurotoxicity, or OPIDN (also called organophosphate-induced delayed
polyneuropathy, or OPIDP), a delayed polyneuropathy resulting in long-term and
in some cases permanent upper motor neuron lesions with spasticity and
hyperreflexia. However, these are the only known cases associated with nerveagent exposure, and it is likely that extremely high exposures are necessary to
cause this delayed neuropathy. Exposure or suspected exposure to nerve agents
has also been associated with a syndrome that has been called chronic
organophosphate-induced neuropsychiatric disorders (COPIND) and, more
recently, organophosphorus ester–induced chronic neuropathy (OPICN), a
constellation of neurobehavioral and neurologic effects including defective
