Delayed-onset status epilepticus without cholinergic features in organophosphate poisoning: a case report

Organophosphates (OPs) exert their toxic effects by inhibiting acetylcholinesterase in both central (CNS) and peripheral nervous systems (PNS), resulting in accumulation of acetylcholine and overstimulation of cholinergic synapses. Seizures associated with OP poisoning typically occur in the context of overt systemic cholinergic manifestations. We report a patient with OP poisoning who developed status epilepticus without developing peripheral cholinergic features.

A 40-year-old Sri Lankan man presented six hours after deliberate ingestion of 50 mL of profenofos (500 g/L emulsifiable concentrate). His past medical history was unremarkable. There was no history of substance misuse. On admission, he was conscious, haemodynamically stable, and did not have signs of cholinergic excess. Thirty-six hours post-ingestion, he developed generalized tonic-clonic seizures, which were refractory to intravenous (IV) midazolam boluses and IV levetiracetam. He was intubated and mechanically ventilated. Continuous electroencephalographic monitoring confirmed termination of seizure activity with an intravenous midazolam infusion. Atropine was administered empirically for possible central cholinergic toxicity. The patient made a full neurological recovery and was successfully extubated 72 h after ingestion. The patient remained asymptomatic in a six month follow up.

This case illustrates an uncommon presentation of OP poisoning: delayed-onset status epilepticus in the absence of peripheral cholinergic features. The high lipophilicity of profenofos may facilitate preferential accumulation in the CNS, leading to a predominantly central cholinergic syndrome. This underscores the importance of recognising atypical neurotoxic presentations of OP poisoning and the potential need for CNS-directed therapy even in the absence of classic peripheral signs.