What’s known on the subject? and What does the study add?
Based on the observation of bladder mass increase in BOO animal models, it has been suggested that it could be possible to determine the presence of male bladder outlet obstruction (BOO) by ultrasound estimated bladder weight (UEBW). In the present study, we tried to reproduce the results correlating UEBW and BOO without success. Furthermore, we could not find any correlation of UEBW and IPSS.
Despite some studies emphasizing the value of UEBW as an efficient non-invasive method to evaluate lower urinary tract obstruction, our data demonstrate that UEBW did not present any individual correlation with clinical and urodynamic BOO.
• To evaluate the correlation between ultrasound-estimated bladder weight (UEBW) in patients with different degrees of bladder outlet obstruction (BOO).
• We evaluated 50 consecutive non-neurogenic male patients with lower urinary tract symptoms (LUTS) referred to urodynamic study (UDS). All patients self-answered the International Prostate Score Symptoms (IPSS) questionnaire. After the UDS, the bladder was filled with 150 mL to determine UEBW.
• Patients with a bladder capacity under 150 mL, a previous history of prostate surgery or pelvic irradiation, an IPSS score <8, a bladder stone or urinary tract infection were excluded.
• After a pressure–flow study, the Schafer linear passive urethral resistance relation nomogram was plotted to determine the grade of obstruction: Grades I–II/VI were defined as mild obstruction, Grades III–IV/VI as moderate obstruction, and Grades V–VI/VI as severe obstruction.
• The UEBW was 51.7 ± 26.9, 54.1 ± 30.0 and 54.8 ± 28.2 in patients with mild, moderate and severe BOO, respectively (P= 0.130). The UEBW allowed us to define four groups: (i) UEBW <35 g; (ii) 35 g ≤ UEBW < 50 g; (iii) 50 g ≤ UEBW < 70 g; and (4) UEBW ≥ 70 g.
• We did not find any differences in age, prostate weight, IPSS, PVR, cystometric bladder capacity, presence of detrusor overactive and degree of obstruction in the aforementioned groups.
• Despite the fact that some studies have emphasized the value of UEBW as an efficient non-invasive method for evaluating lower urinary tract obstruction, our study suggests that UEBW does not present any individual correlation with LUTS or objective measurements of BOO.
BPH is a highly prevalent disease. The main consequence of BPH is BOO, which becomes clinically evident as the patient develops lower urinary tract voiding symptoms (LUTS). The diagnosis of BOO can be non-invasively recognized based on voiding symptoms, uroflow and post-voiding residual (PVR). However, voiding symptoms are not exclusive to BOO. They may be associated with bladder underactivity, which can be an important confounding variable generating low urinary flow and high PVR. Thus, the definitive diagnosis is determined by pressure–flow studies during invasive urodynamic evaluation. The pressure–flow study also allows determination of BOO degree, which may be very useful in therapeutic decisions.
It has been extensively demonstrated that BOO produces significant macro- and microscopic modifications in animal bladders, depending on the duration and degree of obstruction [1,2]. Bladder components such as smooth muscles and extra-cellular matrix show the potential to respond to mechanical stress, increasing their mass by means of hyperplasia and hypertrophy . Furthermore, it has been shown that BOO can determine the hypertrophy of detrusor muscular fibres, an increase in collagen deposition and changes in post-ganglionar cholinergic fibres . It could increase bladder weight by three- to six-fold after partial ligation of the urethra .
Based on bladder behaviour after BOO in animal models, the ultrasound-estimated bladder weight (UEBW) has been investigated in men with BOO . Because the BOO seems to increase the bladder weight, it has been suggested that it might be possible to determine the presence of BOO by detecting an increase in bladder weight . This view is not, however, unanimous. Recently, the bladder wall thickness (BWT) was evaluated for different voiding dysfunctions and presented no significant difference among patients with normal urodynamics, BOO or an overactive bladder .
In the present study, we compare the UEBW with clinical and urodynamic parameters for voiding symptoms to determine if it is possible to use UEBW as a non-invasive way to identify or at least be employed for BOO screening in male patients.
We evaluated 50 consecutive non-neurogenic male patients with LUTS referred to urodynamic evaluation who fulfilled the inclusion criteria. The study was submitted and approved by an independent ethics committee, and all patients signed an informed consent. Before undergoing urodynamic study (UDS), all patients were clinically evaluated and answered the International Prostate Score Symptoms (IPSS) and a health-related quality of life (HRQL) questionnaire. Patients with a cystometric bladder capacity under 150 mL, a previous history of prostate surgery or pelvic irradiation, an IPSS score <8, a bladder stone, an indwelling catheter or urinary tract infection were excluded, along with those who did not agree to participate in the study. Patients using alfa-blockers were washed out for 8 weeks before UDS. Patients with a urinary tract infection were appropriately treated and then underwent UDS.
The UDSs were performed following the International Continence Society good urodynamic practice . Cistometry was performed in a semi-recumbent position, and the pressure–flow study was performed in a standing position. The vesical and rectal catheters were zeroed at atmospheric pressure; the transducers were allocated at the reference height at the level of the upper edge of the pubic symphysis. After positioning the intra-vesical catheters and the rectal balloon, the bladder was filled at a rate of 50 mL/s, and vesical and rectal (abdominal) pressures were recorded with a urodynamic apparatus (Aquarius 120, Laborie Medical Technologies corp., Montreal). After the pressure–flow study, the Schafer linear passive urethral resistance relation nomogram was plotted, and the following criteria were used to determine the grade of obstruction: Grades I–II/VI were defined as mild obstruction, Grades III–IV/VI as moderate obstruction, and Grades V–VI/VI as severe obstruction.
After the pressure–flow study, the bladder was filled with 150 mL to determine the UEBW. To determine the ultrasound-estimated prostate and bladder weight, the same blind physician evaluated all patients with an ultrasound apparatus (Aloka SSD-2000 Multiview) using a 7.5-MHz/60 deg/40 mm transducer. The UEBW was determined according to previously described formula [6,7]. Statistical analysis was performed according to the variable distribution. anova and Student’s t test were used for parametric distributions, and a similar credibility test and the Kruskal–Wallis test for non-parametric distributions. The sample size was determined based on a previous study that demonstrated a relationship between UEBW and BOO . It was calculated considering a probability of 90% that the study would detect a relationship between the Schaffer grade of obstruction and UEBW at a two-sided 0.05 significance level, if the true change in the UEBW is 10 g, and based on the assumption that the standard deviation of the UEBW is 11.
The UEBW allowed us to define four groups: (i) UEBW < 35 g; (ii) 35 g ≤ UEBW < 50 g; (iii) 50 g ≤ UEBW < 70 g; and (iv) UEBW ≥ 70 g. Patient characteristics are shown in Table 1. The UEBW was similar in patients with mild, moderate and severe BOO (P= 0.130). Twenty (40%) patients presented with mild obstruction (UEBW = 51.7 ± 26.9), twenty (40%) with moderate BOO (UEBW = 54.1 ± 30.0) and ten (20%) with severe BOO (UEBW = 54.8 ± 28.2). We also did not find any difference in UEBW comparing those patients presenting mild (n= 20) with those presenting moderate/severe (n= 30) BOO (UEBW = 54.3 ± 28.3). In the same way, overactive bladder was evenly distributed in the UEBW groups.
Table 1. Patient characteristics and distributions according to ultrasound estimated bladder weight (UEBW)
Group 1 UEBW < 35 g Average = 18.5 g
Group 2 35 g ≤ UEBW < 50 g Average = 35 g
Group 3 50 g ≤ UEBW < 70 g Average = 61 g
Group 4 UEBW ≥ 70 g Average = 83 g
G2, similar credibility test; H, Kruskal–Wallis test (P < 0.05). IPSS, International Prostate Score Symptoms questionnaire; HRQL, health-related quality of life; OAB, overactive bladder; PVR, post-voiding residual.
68.2 ± 7.2
70.9 ± 5.1
68.7 ± 8.4
67.3 ± 8.3
66.8 ± 7.5
Diabetic patients (n)
Mean prostate weight (g)
56.4 ± 23.4
45.5 ± 28.2
65.5 ± 35.2
57 ± 29.3
58.8 ± 39.3
27.1 ± 5.6
20.7 ± 10.6
21.2 ± 10.3
22.2 ± 8.7
22.6 ± 8.4
4.7 ± 1.1
4.1 ± 1.5
4.1 ± 2
4.6 ± 1.4
4.4 ± 1.4
95.6 ± 86.1
124.3 ± 116.3
175.8 ± 118.8
183.9 ± 240
187.2 ± 120
Schafer`s nomogram (median)
296.1 + 165.8
352.3 + 161.9
398.8 + 168
444 + 240
351.6 + 180.2
The UEBW did not show any correlation with Schafer’s classification for BOO, nor with patients’ lower urinary tract symptoms, as shown in Figs 1 and 2.
The present study evaluates the possibility of determining BOO using UEBW. We evaluated 50 consecutive men with symptomatic BOO (average IPSS score of 22), the majority of them with moderate/severe urodynamic-demonstrated BOO (60% of patients). Based on previous published studies that have determined a correlation between UEBW and BOO , Schaffer’s nomogram was used to determine BOO and its correlation with different bladder-weight groups (35 g or greater). Despite the findings of recent studies that have emphasized the value of UEBW as an efficient non-invasive method with which to evaluate lower urinary tract obstruction, we could not find any correlation of IPSS, PVR and pressure–flow with UEBW.
Animal studies have extensively demonstrated that BOO produces significant macro- and microscopic alterations in animal bladder, which depend on the time of expression and degree of obstruction [1,2,5]. Furthermore, it has been shown that BOO can determine the hypertrophy of detrusor muscular fibres, increase collagen deposition and cause changes in post-ganglionar cholinergic fibres . Based on the observation of bladder mass increase in BOO animal models, it has been suggested that it might be possible to determine the presence of BOO by identifying an increase in bladder weight in men [6,7]. Thus, the ultrasound evaluation of the bladder wall thickness, internal and external circumference at a fixed bladder filling, has been suggested as an alternative to determine UEBW and BOO [6,7].
Recently, bladder wall thickness (BWT) was evaluated in 180 patients with LUTS to determine if this measure could be used as a non-invasive test to determine BOO and other non-neurogenic voiding dysfunctions. The authors concluded that BWT does not provide an alternative to urodynamics for diagnosing voiding dysfunction . In the present study, we tried to reproduce the results correlating UEBW with BOO, but without success. Furthermore, we could not find any correlation of UEBW with IPSS. We observed that several patients with UEBW under 30 g had a severe obstruction (Schafer’s score >IV) and several patients with UEBW over 50 g had a mild obstruction (Schafer’s score ≤II).
Bladder components such as smooth muscles and extra-cellular matrix show the potential to respond to mechanical stress, increasing their mass by means of hyperplasia and hypertrophy . A noticeable feature of bladder response to experimentally induced partial outlet obstruction in all animal models is the speed and magnitude with which the organ increases in mass. Within 2 weeks, rabbits’ bladder mass can increase five- to six-fold . In rats, bladder mass can increase three- to five-fold within 2 weeks [11–13]. However, it seems that the bladder size and weight are more related to bladder decompensation than with BOO. Bladder weight seems to increase proportionally with time as the bladder enters a decompensated status. Weights of rabbit bladders that remain compensated increase slowly; weights of bladders that enter and progress through decompensation, however, increase at a significantly higher rate. Thus, bladder mass may be more strongly correlated wtih bladder decompensation than with BOO .
It would be expected that the responses of patients with BOO would be similar to those in the animal models. However, there are several differences between human and animals that could interfere with bladder behaviour. In animal models [11–13], BOO is an acute event that does not allow bladder adaptation to the new condition and rapidly progresses to a decompensated status. On the other hand, men with BPH and BOO have a gradual and progressive obstruction. In addition, individual characteristics, such as aging, intrinsic genetic characteristics, degree of bladder vascularization, neurological problems, body weight, diabetes and other co-morbidities, may play an important role in bladder decompensation in response to an increase in outlet resistance.
Bladder mass will be related to the duration and degree of BOO associated with individual intrinsic characteristics. Our data show that there are patients with a similar degree of BOO but a significant difference in UEBW. This may be the result of BOO duration and individual intrinsic bladder responses to BOO. Further studies are necessary to determine the real value of UEBW and its correlation with BOO.
Despite the findings of some studies that emphasize the value of UEBW as an efficient non-invasive method with which to evaluate lower urinary tract obstruction, our data suggest that UEBW does not present any individual correlation with clinical and urodynamic BOO.