Hypothesis / aims of study
Pelvic organ prolapse (POP) in young women is uncommon. When bladder pain syndrome/interstitial cystitis (IC/BPS) coexists, lower urinary tract symptoms reflect a mixed mechanism: structural support failure, pelvic floor overactivity with dysfunctional voiding, and bladder pain sensitization. We aimed to describe presentation, objective voiding findings, treatment sequence, and follow-up outcomes in a case series of young women with multicompartment POP and an IC/BPS phenotype. To our knowledge, published literature largely describes (i) older cohorts where POP-related pain and urgency may mimic IC/BPS[1,3], and (ii) isolated case reports linking ligament repair and IC/BPS symptom resolution[2]. A focused case series of young women with multicompartment POP and IC/BPS managed with uterus-sparing hysteropexy followed by IC/BPS-directed therapy plus pelvic floor rehabilitation is sparsely reported.
Study design, materials and methods
Prospective observational case series of 6 women aged 31 to 33 years with POP stage II to III. All had bulge symptoms and culture -negative LUTS for about 1 year, with frequency, urgency, nocturia, and pain or burning with bladder filling. Uroflowmetry with surface EMG and post-void residual (PVR) were assessed in all; raised EMG activity during voiding was present in all cases, with prolonged flow pattern documented in cases 4 to 6. Two women had stress urinary incontinence (SUI); urge urinary incontinence (UUI) was present in cases 4 to 6. All underwent sacrospinous hysteropexy with pelvic floor reconstruction; transobturator tape was added for the two SUI cases. Intraoperative cystoscopy was performed in all. Postoperative IC/BPS care included intravesical instillation, elimination diet, and structured pelvic floor rehabilitation, voiding mechanics, bladder re-training. Follow-up was 12 to 18 months.
Results
Six women aged 31–33 years had stage II–III multicompartment POP with culture-negative LUTS and IC/BPS-type bladder filling pain. Two had stress urinary incontinence (cases 1–2); urge incontinence was present in cases 4–6. Dyspareunia was reported in five patients (cases 2–6). All demonstrated raised EMG activity during voiding; cases 4–6 also showed a prolonged flow pattern. Preoperative PVR ranged 120–170 mL (120, 130, 120, 170, 120, 150). At 12–18 months’ follow-up, overall bulge symptoms resolved in all, and no prolapse recurrence was reported. Postoperative PVR decreased to 10–30 mL (10, 20, 20, 30, 20, 30). Pain improved from VAS 6–8 to 0–3. Daytime frequency decreased from 10–15/day to 5–9/day and nocturia from 3–5/night to 0–1/night. PGI-I was 2 in cases 4–6. Nocturia reached zero in cases 3 and 5, and pain reached zero in cases 4 and 6. Additional functional outcomes: two patients conceived after uterus-sparing repair (due May 2026 and June 2026). One patient previously not sexually active for 4 years resumed intercourse post treatment; dyspareunia improvement was documented in cases 5 and 6.
Interpretation of results
In this young cohort, objective dysfunctional voiding physiology (raised EMG activity with elevated PVR and prolonged flow in half the cases) coexisted with structural prolapse and an IC/BPS phenotype. Durable improvements were observed in emptying (PVR reduction), pain, and storage symptoms alongside absence of symptomatic recurrence, supporting the clinical value of addressing both anatomy and pelvic floor and bladder pain pathways.