Urodynamic Changes Following a Staged Trial of Sacral Neuromodulation in Patients With Detrusor Underactivity.

Abstract

Objective: Sacral neuromodulation (SNM) is an established treatment for detrusor underactivity (DU) and nonobstructive urinary retention. The mechanism of action for SNM in DU, however, remains poorly understood. The objective of this study was to investigate the urodynamic study (UDS) changes in DU patients during the trial period following first stage tined-lead placement (FSTLP).

Materials and methods: Retrospective chart review was performed to identify patients diagnosed with DU on initial UDS, who had repeat UDS during the 2-week trial period following FSTLP by a single clinician. Urodynamic parameters including maximum flow rate (Qmax), detrusor pressure at maximum flow (PdetQmax), post-void residual (PVR), voiding efficiency (VE), and detrusor contractility index (DCI) were collected. Using the definition of improvement in baseline VE of ≥ 50% post-FSTLP or improvement in DCI of ≥ 50% in complete voiders, patients were divided into "responders" and "nonresponders." Pre- and post-FSTLP urodynamic findings were compared using Wilcoxon signed-rank tests.

Results: A total of 17 patients were identified who met the inclusion criteria. Repeat UDS were done on account of inability or unwillingness to perform clean intermittent catheterization and thus inability to chart an accurate bladder diary. There were 9 female and 8 male patients. Four patients (23.5%) had pure DU while the other 13 (76.5%) had concurrent detrusor overactivity (DO-DU). Among all patients, there was a statistically significant improvement in PdetQmax (14 vs. 29 cmH₂O, p < 0.01) and DCI (62 vs. 92, p < 0.01). Six patients (35.3%) responded to the trial of SNM for DU. Among responders, statistically significant improvements in Qmax (5 vs. 15.5 mL/s, p = 0.03), PVR (215 vs. 80 mLs, p = 0.04), VE (22.9% vs. 82.5%, p = 0.04), and DCI (29 vs. 97.5, p = 0.03) were observed. Nonresponders had improvement in PdetQmax (14 vs. 29 cmH₂O, p = 0.02), but not in Qmax (9 vs. 10 mL/s, p = 0.89).

Conclusions: Among all patients, an improvement in PdetQmax and DCI was observed. Responders exhibited improvement in Qmax, PVR, VE, and DCI without statistically significant improvement in PdetQmax. Nonresponders had statistically significant improvement in PdetQmax, but not in Qmax. Possible mechanisms of action of SNM in DU patients based on our data are inhibition of the guarding reflex/relaxation of the urethra (shown by improvement in Qmax in responders only) and direct strengthening of bladder contractility (shown by improvement in PdetQmax in all patients). Improvement in Qmax was observed exclusively in responders suggesting the former mechanism is the predominant one. Further larger prospective studies are required to confirm these findings.