Hypothesis / aims of study
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.
Study design, materials and methods
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.
Interpretation of results
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.