The ICS defines dysfunctional voiding (DV) in females as ‘an intermittent and/or fluctuating flow rate due to involuntary intermittent contractions of the peri-urethral striated or levator muscles during voiding in neurologically normal women’. DV can result in complete retention or low flowrate with either high or reduced voiding pressure. High-pressure, low-flow (HP-LF) voiding can result in bladder and renal dysfunction, with the accepted natural progression of bladder outlet obstruction being smooth muscle hypertrophy, compensation and finally decompensation.

SNM is a widely used therapy in women diagnosed with DV. Women with HP-LF voiding are likely at greater risk of bladder and renal deterioration post-SNM therapy compared to women who present with acontractile bladder at baseline UDS.

Unlike anatomical bladder outlet obstruction (BOO), functional BOO (fBOO) typically results in peaks and troughs in both flowrate and detrusor pressures, potentially invalidating the use of Pdet.Qmax and Qmax to fully describe the voiding phase. The area under the pressure-flow curve (AUC) represents the cumulative detrusor pressure during the entire void and is likely a more reliable parameter of risk of secondary bladder and renal dysfunction. 

The aim of this original study is to assess if the pressure-flow AUC changes following long-term SNM in women who present with functional HP-LF voiding.

We compared the urodynamic data of 7 female patients’ pre- and post- long-term SNM therapy. The inclusion criteria were women who demonstrated irregular flowrate pattern and raised Pdet (Avg Pdet>30cmH2O) with a change in mid-urethral calibre observed radiographically during voiding (anatomical BOO excluded via flexible cystoscopy). Exclusion criteria included known neuropathies (abnormal brain and spine MRI/neurological examination) or previous history of pelvic radiation therapy. 

All patients underwent a 2-stage sacral neuromodulation procedure, with a 1st stage tined lead, following a standardised technique. Programs are chosen with the active cathode being the electrode which had the best on-table response and results in mid-line sensation such as urethra, vagina, perineum or anus at the lowest stimulation amplitude. Pulse width and frequency parameters were 210 µs and 14 Hz respectively. 
Successful outcomes were defined by a minimum of 50% improvement in lower urinary tract symptoms (LUTS) and function (parameters include voided volumes, post void residuals, self-catheterisation frequency, urinary frequency, urgency, urge urinary incontinence or nocturia symptoms). Patients have 4 follow up appointments within the 1st year following their 2nd stage procedure continued with annual appointments. 

All urodynamic studies were conducted in accordance with the ICS good Urodynamics Practice Document. We compared the AUC (AUC=∫Pdet.dt, illustrated in figure 1) and AUC/VV (normalised to voided volume) at initial presentation and following long-term SNM using paired t-tests. Other UDS parameters analysed included the presence of detrusor over activity (DO), the peak pressure of DO (DO PP),  bladder compliance, maximum cystometric capacity (MCC), voided volume, maximum detrusor pressure during voiding (max.Pdet), maximum flow rate (Qmax) and post void residual (PVR).
The Patients Global Impression of Change (PGIC) scale assessed the patient’s subjective interpretation of SNM therapy.

The initial presentation age and the static maximum mid-urethral pressure ranged from 21-49 years (median 42) and 112-183 cmH2O (median 144) respectively. The number of days between 2nd stage SNM and subsequent UDS ranged from 161-1234 (median 986) days. Latest PGIC score ranged from 4-7 (median 6).  

Figure 2 contains the UDS parameters pre and post long-term SNM therapy. The mean (±SD) change in AUC and AUC/VV between baseline presentation and following long term SNM were -1747 (±3194) cm.H2O.s (p= 0.198) and -68.7(±168.9) cm.H2O.s.ml^(-1) (p=0.323) respectively. 

The mean change in Qmax and post void residuals (PVRs) following long term SNM were +3.3(±4.2) ml/s (p=0.01) and -21.0(±44.6) ml (p=0.26) respectively. There was a mean change in max.Pdet of -6.7(±6.4) cm.H2O (p=0.03). There was no statistically significant change in UDS storage parameters, with a mean change of +3.8(±160.5) ml (p=0.95) and +48.4(±95.1) cm.H_2 O.ml^(-1) (p=0.32) for cystometric capacity and compliance respectively. DO was demonstrated by two patients at initial and subsequent investigation.

Our results did not demonstrate a statistically significant nor a notable trend change in AUC or AUC/VV post long-term SNM therapy, comparable to previous studies which compared UDS parameters pre and post short term SNM therapy (1, 2, 3). This indicates that female patients with HP-LF voiding are at risk of further bladder and renal deterioration. There was not an overt deterioration of urodynamic filling phase parameters or renal function indicating that bladder and renal deterioration is not likely to occur in the time frame of this study.

Women with HP-LF voiding secondary to DV who undergo long-term SNM therapy don’t demonstrate a reduction in detrusor pressure during the entire voiding phase. This relatively long-term and novel data indicates this cohort should be monitored for deterioration in bladder/renal function.

Everaert K, Plancke H, Lefevere F, Oosterlinck W. The urodynamic evaluation of neuromodulation in patients with voiding dysfunction. Br J Urol. 1997;79(5):702-707. doi:10.1046/J.1464-410X.1997.00145.X
DasGupta R, Fowler CJ. Urodynamic Study of Women in Urinary Retention Treated With Sacral Neuromodulation. J Urol. 2004;171(3):1161-1164. doi:10.1097/01.JU.0000113201.26176.8F
Drossaerts J, Rademakers KLJ, Rahnama’I SM, Marcelissen T, van Kerrebroeck P, van Koeveringe G. The Value of Ambulatory Urodynamics in the Evaluation of Treatment Effect of Sacral Neuromodulation. Urol Int. 2019;102(3):299-305. doi:10.1159/000493988

Continence 7S1 (2023) 100932
DOI: 10.1016/j.cont.2023.100932