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Clinical Research

Organophosphate induced delayed neuropathy after an acute cholinergic crisis in self-poisoning

, , , , &
Pages 488-492 | Received 15 Jul 2020, Accepted 29 Sep 2020, Published online: 20 Oct 2020
 

Abstract

Introduction

Despite organophosphate pesticide is the most prevalent cause of acute poisoning in low- and middle-income countries, data on organophosphate induced delayed neuropathy (OPIDN) are limited. We aimed to characterize organophosphates’ long-term effects on the peripheral nervous system after an acute cholinergic crisis in adults.

Methods

We performed a prospective observational study in an academic hospital of north India in patients aged 13–40 years with acute organophosphate ingestion. After resolving the cholinergic crisis, the patients were followed for six months with neurologic assessments, including history, neurologic examination, and nerve conduction study (NCS).

Results

Twenty-three patients were recruited to the study. All but one had normal neurological examination and NCS at discharge from hospital a median duration of six days (interquartile range, 3–10) after self-poisoning. Eight (34.8%) developed OPIDN during the six-month follow-up. Three patients had symptomatic neuropathy, and NCS detected subclinical peripheral nerve involvement in five. All cases were associated with chlorpyrifos ingestion (8/17 total chlorpyrifos cases). Two OPIDN cases had foot drop and gait ataxia at three-month which persist at six-month. One patient had distal paresthesia at three months, which improved at a six-month follow-up. NCS in OPIDN cases invariably revealed axonal degeneration, injury to motor fibers more than sensory fibers, and frequent peroneal nerve involvement. None of the baseline characteristics, including the ingested amount, predicted clinical or subclinical OPIDN in chlorpyrifos self-poisoned patients on a univariant analysis.

Conclusion

Peripheral nerve involvement is not uncommon after recovery from a cholinergic crisis in chlorpyrifos self-poisoning and debilitating in some patients. Detection of subclinical injury on NCS may provide an early window to prevent severe symptomatic neuropathy.

Acknowledgment

The authors thank Mrs. Sunaina Verma for her help with statistics.

Disclosure statement

No potential conflict of interest was reported by the author(s).

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