Hypothesis / aims of study
Primary bladder neck obstruction (PBNO) is thought to account for ~50% of bladder outlet obstruction (BOO) diagnoses in men under 50 years of age(1).
The three possible interventions for PBNO include: watchful waiting (till patient completes family) +/- pharmacotherapy or surgical intervention. Pharmacotherapy through the use of α – blockers only reports variable success. The most effective treatment for PBNO is surgical intervention through bladder neck incision (BNI). Retrograde ejaculation, which occurs in 10-50% of BNI cases, deters many patents till they have completed their family.
Bladder outlet obstruction can cause tissue changes in the bladder wall through increased oxidative stresses and smooth muscle hypertrophy, resulting in bladder dysfunction (BD)(2). The natural history of PBNO is not well characterised, therefore clinicians aren’t able to confidently counsel a patient on how untreated BOO may result in BD and ultimately renal impairment.
The aim of our study is to retrospectively analyse and compare bladder parameters for patients diagnosed with PBNO who have undergone two urodynamic (UDS) investigations following a decision of ‘watchful waiting’; to see if we can evaluate the presence and progression of BD.
Study design, materials and methods
We compared initial and subsequent UDS data from 12 male patients diagnosed with PBNO using video urodynamics. These patients underwent a period of ‘watchful waiting’, aged 13-47 years at initial UDS (median 34 years). The number of days between the UDS investigations ranged from 111-2653 (mean 1140 days).
All urodynamic studies were performed in accordance with the ICS ‘Good Urodynamics Practice’ standard. Urodynamic parameters analysed included the presence of detrusor over activity (DO), bladder compliance, cystometric capacity, bladder outlet obstruction index (BOOI), and the presence of vesico-ureteric reflux (VUR).
Interpretation of results
Bladder dysfunction progresses in three consecutive stages: hypertrophy, compensation and decompensation. 8 of the 12 patients had demonstrated DO during their initial UDS investigation, indicating they were already in the compensatory stage.
Bladder compliance decreased in 67% of patients, indicating an increase in collagen deposition (a result of smooth muscle hypertrophy). Three patients had a bladder compliance < 40 ml/cmH2O at initial UDS compared to seven at subsequent UDS. Reduced bladder compliance can create unsafe storage pressures, resulting in VUR and subsequent impaired renal function. Increased collagen deposition in the bladder wall would also be expected to decrease detrusor contractility during voiding. An increasing collagen to smooth muscle ratio is characteristic of the transition between bladder compensation to decompensation.
One patient had an initial bladder compliance of 30 ml/cmH2O. After an interval of 2653 days there was an artefactual increase in bladder compliance, as grade IV VUR was observed in the 2nd UDS investigation. VUR dampens Pdet whilst making cystometric capacity an overestimate, resulting in a bladder compliance which appears normal. Fluoroscopic video is required to diagnose unsafe bladders in this scenario.
Independently, time does not appear to be an indicator of bladder dysfunction progression in this cohort. Confounding factors include: age, severity of obstruction and the stage of obstruction when the patients initially presents.