Hypothesis / aims of study
The natural history of bladder function in young women with idiopathic detrusor overactivity (DO) is not well established.
It is accepted that bladder outlet obstruction can result in bladder and renal deterioration. The accepted sequalae of overloaded smooth muscle is hypertrophy and bladder compensation. This is due to the increased amount of smooth muscle cells which leads to hypoxia and oxidative stress, increasing the production of free radicals. The rise in number of free radicals leads to inflammatory changes, increasing the amount of collagen compared to smooth muscle. As a result, bladder compliance is decreased and voiding contractility impaired, known as bladder decompensation (1).
It is not well documented whether chronic idiopathic DO results in a similar bladder compensation / decompensation process. Determining the rate and type (compensation/decompensation) of bladder dysfunction in chronic idiopathic DO and whether it is associated with secondary dysfunctional voiding (DV, resulting from guarding against DO) would help to aid counselling and management.
This original retrospective study aims to assess the change in urodynamic parameters between serial tests in women with idiopathic DO and their association with BOO.
Study design, materials and methods
Our retrospective study compared initial and subsequent UDS from 11 female patients. The inclusion criteria were nulliparous females <35 years of age who demonstrated DO on initial UDS. The exclusion criteria were the presence of neuropathy, anatomical BOO, sacral neuromodulation or Botox within 12 months of their subsequent UDS study.
All urodynamic studies were conducted in accordance with the ICS Good Urodynamics Practice Document. Urodynamic parameters analysed included: maximum cystometric capacity (MCC), bladder compliance, presence of detrusor overactivity (DO), voided volume, maximum detrusor pressure during voiding (max.Pdet), detrusor pressure at maximum flow (Pdet.Qmax), maximum flow rate (Qmax) and post void residual (PVR).
We recorded whether patients had undergone either Botulinum Toxin (Botox) or sacral neuromodulation (SNM) therapy and whether patients still reported urgency and/or urge urinary incontinence (UUI) symptoms at 6 weeks for Botox and 6 months for SNM.
Results
Mean age (±SD) at initial test and interval were 15.4±5.6 and 6.2±3.4 years respectively. 8/11 patients had previously received a minimum of 100 units of Botox, with 6/8 continuing to have urgency and 4/8 having UUI symptoms at 6 weeks post-injection. 4/11 patients underwent an SNM trial, 3/4 had a successful trial with 50% improvement in symptoms. However, all 3 patients continued to report urgency symptoms at 6 months with 1 patient reporting UUI.
Figure 1 includes the UDS data from initial and subsequent visits. Mean (±SD) MCC at initial and subsequent UDS were 355±188 ml compared to 265±89 ml respectively (p = 0.14). 8/11 patients had a DOpeak ≥40 cmH2O at initial UDS compared to 9/11 at 2nd investigation. Mean (±SD) bladder compliance at initial and subsequent UDS were 60±78 and 62±86 ml/cmH2O respectively (p = 0.83). Mean (±SD) PVR at initial and subsequent UDS were 43±58 and 87±165 respectively (p = 0.63).
Mean (±SD) DO peak pressure (DOpeak) and max.Pdet during voiding at initial presentation were 78±53 cmH2O, and 55±16 cmH2O respectively, compared to 68±30 cmH2O and 52±32 cmH2O at follow up respectively (p = 0.51 and 0.83). Figure 2 demonstrates the change in DOpeak with time.
There was a strong negative correlation between the DOpeak at initial presentation and decrease in DOpeak at follow-up (r= 0.8). 5/11 initially unobstructed women were diagnosed with BOO (diagnosed using radiology and the pressure / flow relationship during the entire voiding phase) at the subsequent test.
Interpretation of results
9/11 patients demonstrated high pressure DO (DOpeak ≥40 cmH2O) during the 2nd UDS, with mean (±SD) MCC decreasing from 355±188 ml to 265±89 ml (p = 0.14). This demonstrates that idiopathic DO in young females is a complex diagnosis which can be unresolved by 1st and 2nd line treatment options.
Bladder compliance, max.Pdet during voiding and PVR do not significantly deteriorate in the time frame of this study, indicating that bladder decompensation does not overtly occur. However, ~1/2 of the cohort demonstrated DV at subsequent UDS.