Case Presentation: 39-year-old female presented 1 hour after ingesting 50-60 mL of phenthoate 50% emulsified concentrate, an Organophosphate (OP) compound, with salivation, lacrimation, vomiting, diarrhea, and respiratory distress with bilateral wheeze and crepitations. Serum cholinesterase (SChE) was markedly reduced (2680 U/L), while other investigations were normal. She was treated with gastric lavage, atropine, oxime therapy, and early intubation. After 10 days of mechanical ventilation, she improved and was discharged on day 15 with full recovery.5 days later, she returned with new-onset bilateral lower-limb weakness. On readmission, our first concern was repeat OP compound consumption which may have caused cholinergic crisis or Intermediate Syndrome (IMS); but ruled out by normal SChE levels and the absence of muscarinic or nicotinic signs. Over 48–72 hours, weakness progressed to the upper limbs with dysarthria and dysphagia. She remained fully conscious; examination revealed LMN bulbar palsy, hypotonia, generalized areflexia, grade 2/5 limb power, preserved sensation, and flexor plantars.Given her OP exposure 20 days earlier, OP-induced delayed neuropathy (OPIDN) was considered, along with differentials for acute flaccid paralysis such as botulism, porphyria, poliomyelitis, critical illness neuropathy, myasthenic crisis, electrolyte disturbances, HIV-associated neuropathy, and acute myelopathy. Electrolytes, organ function tests, and MRI spine were normal. Nerve conduction studies revealed a pure motor axonal polyradiculoneuropathy consistent with the AMAN variant of GBS. CSF showed albuminocytologic dissociation (7 cells/mm³, protein 312 mg%). With no recent history of infection or vaccination, OP exposure was the likely trigger.Her respiratory weakness worsened, requiring re-intubation. She received five cycles of plasmapheresis with gradual bulbar and respiratory improvement. She was extubated by day 11 and discharged on day 16 with limb strength improved to grade 4/5. At 6 month follow-up, she had regained full muscle strength.
Discussion: Organophosphate poisoning causes acute cholinergic toxicity and, less commonly, IMS or OPIDN. GBS following OP exposure is exceptionally rare and often difficult to recognize because its early features can resemble OP-related neuromuscular syndromes. In our patient, the onset of ascending paralysis shortly after recovery from OP poisoning, normal SChE levels and absence of cholinergic features excluded recurrent toxicity and IMS.Although OPIDN was considered, the rapid ascending paralysis, bulbar involvement, areflexia, and preserved sensation favored an alternative diagnosis. Electrophysiology showing pure motor axonal involvement and CSF albuminocytologic dissociation confirmed the AMAN variant of GBS. With no preceding infection or vaccination, recent OP exposure was the most reasonable cause.This case highlights the need to consider GBS in patients presenting with delayed weakness after OP poisoning. Early recognition and immunomodulatory treatment are essential, as demonstrated by this patient’s excellent recovery following plasmapheresis.
Conclusions: This case illustrates a rare case of GBS triggered by OP poisoning. Clinicians must consider GBS in addition to OPIDN and IMS, in patients with delayed neuromuscular weakness after OP exposure. Early differentiation through careful examination and electrophysiologic/CSF studies enables timely treatment and can significantly improve outcomes.