Urological age: A man is as old as his prostate, and as his flowrate.

Rosier P1

Research Type


Abstract Category

Male Lower Urinary Tract Symptoms (LUTS) / Voiding Dysfunction

Abstract 561
E-Poster 3
Scientific Open Discussion Session 31
Friday 6th September 2019
13:50 - 13:55 (ePoster Station 1)
Exhibition Hall
Voiding Dysfunction Male Bladder Outlet Obstruction
1.University Medical Center Utrecht

Peter F W M Rosier



Hypothesis / aims of study
Men with signs and symptoms of lower urinary tract dysfunction enter the (primary) health care system when they are bothered by this and or seek alleviation of their symptoms. Based on their guidelines the primary care physician (general practitioner) initiates a form of conservative management for the dysfunction after considering the likelihood of significant (not dysfunction) abnormalities, most relevant: medication side effects, concomittant diseases, urinary tract infection and or bladder or prostate neoplasm. Life style advises are e.g. based on a bladder diary. Depending on the health care system and the threshold to refer to secondary care, a primary care physician may also add medication to reduce outflow obstruction. Many patients fare well on this regime of reassurance, explanation, lifestyle advise and or medication and do not need referral to secondary care. A proportion of patients however is referred to, or returns to, specialist care after this initial management. They are disappointed, worried and or searching for alternative management. We have investigated a consecutive group of men referred with bothersome symptoms after initial management, searching for objective assessment and diagnosis and subsequently more individualized management, better tailored to the specific dysfunction.
Study design, materials and methods
754 men with symptoms of lower urinary tract dysfunction were referred and assessed with symptom-score, transrectal ultrasound and urodynamics. Patients with urinary tract infection, erytrocyturia, prostate cancer or a history of relevant other urologic or neurological abnormality or (lower) abdominal surgery were not included in this series. Patients using 5 alfa reductase were also excluded (becasue of their prostate size reducing effect). All patients had their usual (not urological) medications during urodynamic testing. Prostate size was assessed with transrectal ultrasound, on the basis of prostate dimensions LxWxHx0.52. ICS standard cystometry was done with transurethral double lumen catheter with continuous medium saline filling until strong urge to void. Patients voided in their preferred –usually standing- position. Urodynamics was systematically quality controlled. Hitting flowmeter and other peak artefacts on the traces; unequal pressure responses on coughing and expelled catheters, and also very (patient reported) unrepresentative micturictions were not included (all features were rarely occurring <<1%). Patients unable to void (>100mL) during the test (±5%, usually <40years of age) were also excluded. Micturitions were analysed with ICS standard pressure flow plot -graphs.
Patients were between 18 and 103 years of age (mean 68,4), had an IPSS 16,6 (range 3-31) and had a prostate size of 10-200 gram (mean 41,6). Urodynamically they had an average grade of bladder outflow obstruction grade 2 (intermediate) (BOOI mean 30; URA mean 33cmH2O), and (almost) normal maximum contraction on average: (BCI 99 and WFmax 10,08W/m2).
We specifically used this dataset with two fundamental aims: How is the growing prostate affecting outflow resistance and obstruction; and how are prostate-size and outflow obstruction affecting detrusor contraction? A further more clinical aim has been to unravel whether clinical parameters, other than urodynamic pressure flow date were useful to estimate the likelihood of outflow obstruction in an individual patient.
Figure 1 demonstrates that the grade of bladder outflow obstruction increases with prostate size (shown per cohort of 10grams increasing from left to right; top left graph) and  that detrusor maximum contraction increases as well (top, right hand side graph). Maximum flow decreases and age increases (bottom) when the persons were ranked according to prostate size. Detailed evaluation shows also that the most consistent increase in BOO is seen when prostate size is increased from 20-60 gram. BOO grade seems to level off after that, however is again somewhat more increased after 100gram. The association with contraction demonstrates that contraction is able to compensate (increase) up to a prostate volume of 100gram. Flowrate is maintained around the average of 10mL/s in most patients, although a decline is observable in association with larger prostates. 
Figure 2 demonstrates that our clinical prostate score (CLIPS) of <0 almost perfectly predicts the absence of bladder outflow obstruction. Not shown on the figures: For 42% of the patients the bladder capacity was limited by (terminal) detrusor overactivity with associated imperative need to urinate (correlation with TRUS: pearson .205 sig .000) and or (in 38%) by significant PVR (correlation with TRUS: pearson .076 sig .038).
Interpretation of results
These patients were referred, bothered and symptomatic. Although prostate growth is progressive over time, associated with age increase (see fig 1) and only regressive with mediation, this is not a longitudinal analysis. Certainly it is relevant that the decision to refer is determined by the amount of bother, symptoms and doubt. Person with little bother or symptoms (not referred) may have identically large prostates with lesser grade of BOO or better detrusor compensation. This sample is representing a clinical population that is potentially not entirely representative in a bio-physiological perspective but is relevant in a pathophysiological perspective.
Based on these observations we were able to (multivariate) derive a clinical prostate score; When 3 times maximum flowrate is larger than prostate size the likelihood of BOO was almost zero, as shown on figure 2; CLIPS (prostate size – 3xQmax) versus URA.
Concluding message
Our study in 754 referred men has learned that prostate (growth and) size is the core parameter associating with bladder outflow obstruction. The analysis has also learned that the detrusor muscle is compensating for this prostate growth and BOO, and achieves to maintain maximum flowrate around at least 10mL/s. Patients however are potentially referred early enough and not when the flowrate is very much lower than this. Prostate age = size is determining abnormality of voiding however symptoms are also a sign of other, associated or concomitant lower urinary tract dysfunction as overactive detrusor and also ineffective emptying, with PVR. Decompensation of detrusor muscle seems to occur at larger (>100) prostate volumes although detrusor underactivity (and overactivity) occurs in a proportion of patients in every prostate volume cohort. Urological tools to assess prostate size and flowrate (with PVR) measurement are relevant for initial diagnosis after referral or return; they direct the need for further -invasive- assessment. A not invasive clinical prostate score; CLIPS, based on flowrate and prostate size (prostate size – 3xQmax), can easily and very reliably be applied to exclude bladder outflow obstruction in male patients.
Figure 1 Prostate size /10 gram versus bladder outlet obstruction and contraction grade, versus max. flowrate and also versus age.
Figure 2 Clinical prostate score CLIPS versus URA in this cohort predicting absence of BOO when <0.
Funding none Clinical Trial No Subjects Human Ethics not Req'd Exempted because of standard care -analysis Helsinki Yes Informed Consent No
18/02/2024 02:55:12