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Case Reports
. 2024 Oct 4;24(1):213.
doi: 10.1186/s12894-024-01600-x.

Sacral neuromodulation for Organophosphate-induced delayed neuropathy neurogenic lower urinary tract dysfunction: a case report

Affiliations
Case Reports

Sacral neuromodulation for Organophosphate-induced delayed neuropathy neurogenic lower urinary tract dysfunction: a case report

Junjie Han et al. BMC Urol. .

Abstract

Background: Organophosphate-Induced Delayed Neuropathy (OPIDN) is a rare neurological disorder triggered by exposure to organophosphorus compounds. These compounds exert their neurotoxic effects by impacting the nervous system, leading to systemic manifestations. Urinary system symptoms are infrequently observed in clinical settings. Currently, effective therapeutic interventions for OPIDN-related urinary symptoms are lacking. Sacral nerve modulation therapy, an FDA-approved approach for managing lower urinary tract symptoms, presents as a promising option. Herein, we present a case of OPIDN-induced lower urinary tract obstruction successfully treated with sacral nerve modulation therapy, resulting in substantial symptom relief.

Case report: A 27-year-old male patient presented with severe bilateral hydronephrosis, attributed to low bladder compliance and accompanied by a fever persisting for 6 days. The patient's medical history revealed accidental ingestion of organophosphate pesticide (Dimethoate) with no concomitant underlying diseases. In consideration of the potential for OPIDN, surgical intervention in the form of sacral neuromodulation (phase I) was undertaken. Subsequent evaluation one month post-surgery revealed notable improvements in both bladder compliance and bilateral hydronephrosis, necessitating sacral neuromodulation (phase II). Presently, following a 5-month follow-up period, the patient remains asymptomatic and in favorable health.

Conclusion: This patient achieved long-term relief using sacral neuromodulation.

Keywords: Neurogenic bladder; Organophosphate-induced delayed neuropathy (OPIDN); Organophosphorus compounds; Peripheral nerve axons; Sacral neuromodulation.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Pretreatment CT-Abdomen demonstrating hydronephrosis in both kidneys and the bilateral ureters (A) and bladder wall thickening and bladder capacity reduction(B)
Fig. 2
Fig. 2
Pre-test urodynamics showed the following: During the storage phase, the bladder’s initial sensation occurred at 36 ml, with a strong urge at 54 ml and a maximum infusion volume of 140 ml. The patient was instructed to urinate, but no urine was produced. After removing the pressure catheter, the maximum urine flow rate was 8 ml/s, with a urine volume of 50 ml. Following catheter insertion, 300 ml of urine was drained, likely due to the expansion of the ureter (A).Post-second-stage implantation, urodynamic review showed the following: During the storage phase, the bladder’s initial sensation occurred at 134 ml, with a strong urge at 269 ml and a maximum infusion volume of 316 ml. The maximum urine flow rate was 16 ml/s, with a total urine volume of 310 ml and a residual urine volume of 10 ml (B)
Fig. 3
Fig. 3
Cystography demonstrating pear bladder
Fig. 4
Fig. 4
After electrical stimulation of sacral nerve implantation
Fig. 5
Fig. 5
Posttreatment CT-Abdomen demonstrating hydronephrosis relief in both. kidneys and the bilateral ureters (A) and bladder wall thinning and bladder capacity. Expanding (B). Cystography demonstrating pear bladder disappeared (C)

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