A patient exposed to some organophosphates may develop additional symptoms within a few days after the acute intoxication phase. This is "intermediate" between the acute and late neurotoxic changes.
Onset: 1 to 4 days after the acute exposure
Mechanism: prolonged acetylcholinesterase inhibition, resulting in impaired presynaptic and postsynaptic neuromuscular transmission. Excessive calcium ion entry into muscle cells can result in muscle necrosis.
Agents implicated: fenthion, dimethiate
Clinical features
(1) absence of muscle fasciculations
(2) acute respiratory paresis which can result in acute respiratory failure
(3) weakness in muscles supplied by the cranial nerves
(4) weakness in neck flexors
(5) weakness in proximal limb muscles
(6) decreased deep tendon reflexes
(7) no response to oximes (cholinesterase reactivators) or atropine
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