The incomplete evacuation of the bladder leads to the presence in the bladder of post-void residual urine (PVR). PVR is defined as the volume (ml) of urine left in the bladder at the end of micturition [1]. PVR is very frequently the consequence of lower urinary tract (LUT) dysfunction, with benign prostatic obstruction and underactive detrusor as its most prevalent causes in men. Threshold values delineating what constitutes an abnormal PVR are poorly defined and the impact of detrusor underactivity, in comparison to obstruction, on PVR is also non completely understood [1]. The aim of this retrospective study was to investigate the relationships of PVR with the presence of both benign prostatic obstruction and detrusor underactivity.

All male patients evaluated in three centres with invasive urodynamic evaluation (cystometry followed by pressure/flow study, performed according to the ICS standards [2]) for LUTS were included in this study. Data form files and traces in the databases were evaluated. Patients who underwent a previous surgery for BPO and presenting significant comorbidities (including neurogenic pathologies or suspected/diagnosed LUT pathologies other than BPO) were excluded. Patients taking drugs active on the LUT were included to give a more realistic picture of the patients usually seen in our labs; data of these patients were analysed separately to assess possible biases due to the treatment.
PVR obtained after the pressure/flow study was recorded and possible relationships between PVR and detrusor contractility (explored using the Bladder Contractility Index -BCI: pdetQmax +5Qmax) and bladder outlet obstruction (explored using the Bladder Outlet Obstruction Index -BOOI: pdetQmax -2Qmax) [3]. In particular, relationships between PVR and different urodynamics findings were investigated: 1. Normal voiding (N) (BCI≥100, BOOI≤40); 2. Benign Outlet Obstruction (BOO) (BCI≥100, BOOI>40); Detrusor Underactivity (DU) (BCI<100, BOOI≤40); BOO+DU (BCI<100, BOOI>40). Kruskall Wallis test was used to differentiate PVR in different groups of patients (e.g. BCI≥100 vs. BCI<100; BOOI ≤40 vs. >40). ROC curves were used to evaluate the PVR cut-off value able to better differentiate patients with BCI≥100 vs. BCI<100 and BOOI ≤40 vs. >40. 2-tailed Fisher’s exact test was used to evaluate how many patients in the different groups had PVR volume >/< the established cut-off value.

Data came from the years 2001-2018, 2015-2018 and 2017-2018 in the three databases respectively. Patients with incomplete data were excluded. Data of 407 patients were included in the evaluation. Patients were categorized as N (106, 26%), BOO (142, 34,9%), DU (128, 31,4%) and BOO+DU (31, 7,6%). A positive correlation was found between both BCI<100 (p<0.001) and BOOI>40 (p=0,007) and an increased PVR volume. Using a linear regression of logarithmic data, beta standardised showed a higher impact of BCI on PVR volume, in comparison with BOOI.
Area under the curve for ROC curve to discriminate DU with PVR was 0.61 (CI 95% 0.56-0.66) (Fig. 1). Nevertheless, using a cut-off value of 100 ml (<100 vs ≥100 ml), it was possible to find interesting findings. Only 13.3% of patients were classified as N in the group of patients with PVR ≥100 ml, vs. 29.7% in the group with PVR <100 ml (p=0.0016). On the other hand, around 52,2% of patients were classified as DU in the group of patients with PVR ≥100 ml, vs. 35.3% in the group with PVR <100 ml (p=0.0048). The number of BOO patients in the group with PVR ≥100 ml was not significantly different, in comparison to the group with PVR<100 ml. No cut-off value was able to differentiate adequately patients with BOOI ≤40 vs. >40. Patients taking drugs did not behave differently in comparison to the other patients.

According to our data, the presence of PVR seems to be more related to detrusor underactivity than to BOO. Thus, a relevant PVR should be considered the consequence of a weak detrusor more than of BOO itself. Threshold values delineating what constitutes an abnormal PVR are poorly defined. In this retrospective study we were able to show that a cut-off value of 100 ml is able to differentiate significantly the presence of patients voiding normally, in comparison to patients showing pathologic findings during the voiding phase. In particular, only 13.3% of patients who presented a PVR ≥100 ml showed a normal urodynamic pattern, in comparison to around 30% in the group with PVR <100 ml. The presence of detrusor underactivity was also significantly higher in patients with PVR ≥100 ml. Interestingly, no cut-off values of PVR were able to differentiate adequately patients with or without BOO.

According to this study, detrusor underactivity seems to impact significantly on PVR, whilst BOO does not. A cut-off value of 100 ml for PVR is able to differentiate significantly the prevalence of patients voiding normally and of patients showing detrusor underactivity. This volume could be considered a urodynamically relevant cut-off for PVR: over this cut-off value, the presence of detrusor underactivity seems significantly higher. Thus, patients with a PVR ≥100 ml should be carefully evaluated with invasive tests whenever to confirm or rule out the presence of detrusor underactivity is considered relevant.

Asimakopoulos A. D., De Nunzio C., Kocjancic E., Measurement of post-void residual urine. Neurourology and urodynamics, 35(1), 55-57, 2016
Rosier P. F., Schaefer W., Lose G., International continence society good urodynamic practices and terms 2016: urodynamics, uroflowmetry, cystometry, and pressure-flow study, Neurourology and urodynamics, 36(5), 1243-1260, 2017
Abrams P., Bladder outlet obstruction index, bladder contractility index, and bladder voiding efficiency: three simple indices to define bladder voiding function, BJU Int., 84, 14-15, 1999