The diagnosis of voiding dysfunction in women is very challenging, not only due of the narrow difference of pressures to differentiate bladder outlet obstruction (BOO) from detrusor underactivity (DU), but also because straining to void can increase urinary flow. Some attention has been given to the participation of abdominal muscles during voiding but almost nothing has been said about abdominal pressure decrease, which doesn’t modify intravesical pressure but increases the calculated detrusor pressure artificially. The aim of this study was to describe the changes of abdominal pressure during voiding in women, to evaluate if the correction of the abdominal pressure decrease can modify the urodynamic diagnosis and to study if there is an association between the symptom “strain to void” and abdominal muscle participation during voiding. To our knowledge this is the first study to investigate this.

In a three year period, 565 consecutive women underwent conventional cystometry following "good urodynamic practices". At the time of examination, voiding symptoms (slow stream, straining to void, intermittent stream and feeling of incomplete emptying) were obtained by a directed anamnesis as being either present or absent without any stratification for severity. Bladder outlet obstruction (BOO) was defined using the cutoff criteria of pdetQmax ≥ 25 cm H2O + Qmax ≤ 12 mL/s (1), and detrusor underactivity (DU) was defined as a projected isovolumetric pressure 1 (PIP1 = pdetQmax + Qmax) less than 30 (2). Detrusor contraction was defined as an increase of detrusor pressure at maximum flow rate ≥ 10 cm H2O over baseline and abdominal contraction as an increase of abdominal pressure at maximum flow rate ≥ 10 cm H2O over baseline. The change of abdominal pressure during voiding was defined by the following formula: abdominal pressure at maximum flow rate minus pre-voiding abdominal pressure. Patients with pelvic organ prolapse > stage II, pelvic radiotherapy, medications active on the lower urinary tract, bladder pain syndrome/interstitial cystitis, insulin-dependent diabetes mellitus and neurological diseases were excluded (n=184). Additional patients were excluded due to technical problems (n=21). We compared age, parity, history of forceps delivery, of hysterectomy, of anti-incontinence surgery, of anorectal surgery, presence of any voiding symptom and strain to void in women with or without abdominal pressure decrease ≥ 5 cm H2O and ≥ 10 cm H2O, respectively. In women with ≥ 5 cm H2O abdominal pressure decrease during voiding, pdetQmax was corrected subtracting this negative pressure value, which was used to diagnose BOO and DU again. Wilcoxon rank-sum test was used to compare the numerical variables and chi-square test or Fisher’s exact test was used to compare the categorical variables. The information was processed with the Stata 15.1 program (StataCorp, 2017), and statistical significance was defined as P < 0.05.

Three hundred sixty women age 58.4 ± 13.2 (range 18 – 89) years formed the study group. Table 1 shows some of their clinical characteristics and urodynamic diagnosis and Table 2 shows the changes of abdominal pressure during voiding. Parity was significantly lower in patients with abdominal pressure decrease ≥ 10 cm H2O (1.74 ± 1.48 versus 2.56 ± 1.43, p=0.013) but not with abdominal pressure decrease ≥ 5 cm H2O (p=0.134), and history of anti-incontinence surgery was significantly higher in patients with abdominal pressure decrease ≥ 5 cm H2O (38.1% versus 24.6%, p=0.016) but not with abdominal pressure decrease ≥ 10 cm H2O (p=0.349). One hundred patients (27,8%) had ≥ 5 cm H2O decrease in abdominal pressure during voiding. When using the corrected pdetQmax, 2 patients lost diagnosis of BOO and 7 patients gain diagnosis of DU (9/360, 2.5% diagnostic modification). There was no association between the symptom “strain to void” and abdominal contraction during voiding (p=0.691).

In women, abdominal pressure decrease during voiding is frequent: more than a quarter of them had ≥ 5 cm H2O decrease. Because a limited number of factors were studied, those related to abdominal pressure decrease (parity and history of anti-incontinence surgery) look conflicting. Accurate knowledge of posterior compartment prolapse and anal sphincter function might have delivered additional information. Abdominal pressure increase during voiding is related to abdominal muscles participation, increasing not only intravesical pressure but also urinary flow. This explains the special attention it receives in studies that attempted to define BOO and DU in women (1, 2). As abdominal pressure decrease doesn’t modify intravesical pressure but increases the calculated detrusor pressure artificially, its correction would seem justified. The correction of pdetQmax in patients with ≥ 5 cm H2O abdominal pressure decrease during voiding led to a 2.5% diagnostic modification, which although infrequent, it can be very important for the patients involved. The symptom “strain to void” can’t be used to select women who don’t use abdominal muscles to urinate.

A high proportion of women had abdominal pressure decrease during voiding. In women with ≥ 5 cm H2O abdominal pressure decrease during voiding, pdetQmax correction led to 2.5% diagnostic modification. There was no association between the symptom “strain to void” and abdominal contraction during voiding.

Defreitas GA et al. Refining diagnosis of anatomic female bladder outlet obstruction: comparison of pressure-flow study parameters in clinically obstructed women with those of normal controls. Urology 2004; 64: 675
Tan TL et al. Stop test or pressure-flow study? Measuring detrusor contractility in older females. Neurourol Urodyn 2004; 23: 184