gms | German Medical Science

Introduction: We know that the pelvic floor muscle (PF) pre-contracts before the intraabdominal pressure (IAP) increases during coughing e.g. We also know that incontinent women may have lost this PF precontraction (PFpreC). Furthermore, it is established that both maximal urethral closure pressure (UCP) and bladder neck (BN) stiffness are important factors that maintain continence. However, these continence mechanisms have not been assessed concurrently in standing women at the time of leakage.

The aim of this study was to assess which known continence mechanisms fail during provoked stress urinary incontinence (SUI).

Methods: We recruited 35 consecutive women with demonstrable SUI aged 31-77 years (median 49) and 18 healthy continent women as controls aged 21-52 years (median 34; p<.001). Parity ranged from 0-3 in healthy women (median 2) and from 0-4 in incontinent women (median 2; p=.339). All women completed a validated PF Questionnaire and underwent POPQ-staging. Women with previous PF surgery and those with prolapse beyond the hymen were excluded.

Surface EMG-electrodes were placed medial to the anterior superior iliac spine to examine the abdominal muscles. One electrode attached to a small soaked sponge was placed intravaginally at the level of the puborectalis muscle (PR). Microtip transducers were inserted urethrally to measure urethral and vesical pressures/IAP. Perineal ultrasound (PUS) was performed to assess BN and PR movements. Ventrocranial changes in position were labeled as a positive vector, dorsocaudal displacements as negative. Height of BN and PR were measured from a horizontal line with the dorsal edge of the pubic symphysis as the reference point. Stiffness of the BN and the PR was calculated by dividing the increase in vesical pressure by the descent of BN and PR during coughing. Pressure transmission ratio (PTR) was calculated by dividing the urethral pressure increase by the increase in vesical pressure.

All measurements were taken with a comfortably full bladder beyond the first desire to void at maximal 300 ml and assembled on one screen with one timeline (Noraxon TeleMyo software). EMG signals were band pass filtered between 30-1000 Hz. Continence mechanisms were assessed concurrently at the time of leakage in the standing position. Women were asked to cough three times and if no visible leakage occurred on PUS they coughed 10 times.

For pre-contraction measurements, the beginning of the increase of the IAP was marked. Raw EMG signals were amplified, the moment of increase in PF-EMG activity determined and the length of time measured until the increase in IAP started.

Results: The BN position at rest was lower in incontinent women compared with controls (18 mm vs 25 mm, p=0.001). During a cough without leakage this position further descended to 22 mm and 15 mm, respectively (p=0.045) and in coughs with leakage to 9 mm (p=0.005).

Women with SUI had a lower UCP at rest (56 cmH2O, R 18-142) compared with controls (92 cmH2O, R 26-153; p=0.025). Four incontinent women had a low pressure urethra (MUCP <20 cmH2O). During coughing, the UCP increased by 100 cmH2O (R 54-182) in controls in contrast to 74 cmH2O (R -37 -184) in incontinent women.

PF-EMG activity increased with coughing in all women. However, a PFpreC demonstrated only 26/35 (74%) incontinent but all controls.

BN descent during coughing was significantly greater in incontinent women (9mm vs 4mm). When no-leak-coughs were compared with leak-coughs, BN and PR descent were greater with the latter whereas PTRs were lower (Table 1). Stiffness of the BN was significantly lower in incontinent women.

BN funneling occurred in 27/35 women with the funnel length ranging from 4-17 mm (median 11).

Conclusion: At the time of stress urinary leakage, different continence mechanisms may fail: loss of PF precontraction, reduced BN and PR stiffness as well as BN funneling due to decreased PF support and reduced PTR due to decreased UCP.

Adequate support of the BN seems paramount. The PF and the connective tissue provide a layer against which the urethra is compressed. However, PF activity can only partially compensate lack of connective tissue BN support. Also, with a low urethral closure pressure, the situation deteriorates.