Hypothesis / aims of study
Risk factors for urinary tract infection (UTI) has been extensively studied in patients with neurogenic lower urinary tract dysfunction (NLUTD), children and women. Although the prevalence of UTI in adult men is less frequent than in these populations, it has been noted that adult male patients with UTI show high occurrences of predisposing factors (1). Urodynamic dysfunctions are an important risk factor for UTI in NLUTD, children and women. In women, abdominal straining during voiding has been demonstrated to be a risk factor for recurrent urinary tract infections (2). However, studies on urodynamic risk factors for UTI in adult men are scarce. Our hypothesis is that urodynamic dysfunctions are also an important risk factor in men. Consequently, the objective of the present study is to assess if there is any relationship between UTI and urodynamic findings in men.
Study design, materials and methods
Study design
case-control study
Materials and methods
We carried out a case-control study. Cases were men with UTI. UTI was defined as the presence of lower urinary tract symptoms (LUTS) associated to positive urine culture (>105 colony forming units per millilitre). Controls were men with LUTS and negative urine culture. Inclusion criteria were male 18 years old or over. Exclusion criteria were neurogenic lower urinary tract dysfunction, urinary catheterization, antibiotic treatment, anatomical abnormalities of the urinary tract, urolithiasis and genitourinary neoplasms. We reviewed the most recent urodynamic studies of these patients. The mean interval between the last urodynamic study and urine culture was 12 months. Urodynamic studies were performed according ICS specifications and guidelines of Good Urodynamic practices. Detrusor contractility was calculated using the Bladder Contractility Index (BCI) (PdetQmax + 5. Qmax), and urethral resistance using the Bladder Outlet Obstruction Index (BOOI) (PdetQmax – 2. Qmax). Because of no definition of abdominal activity during voiding has been made by ICS, we measured this parameter by multiplying de abdominal pressure increment (defined as the difference between maximum abdominal pressure during voiding minus baseline abdominal pressure in cm H2O) by the time of abdominal contraction (in seconds).
The study integrated a sample of 32 cases and 95 controls. Sample size was calculated based on data published by Yang and Huang (3). Assuming that the prevalence of abdominal straining in patients with UTI is 50 % and the prevalence in the control group is 20%, an alpha level of 5%, a statistical power of 80%, and a case/ control ratio of 1 to 3, thus, the minimum sample size should be 30 patients in the case group, and 90 patients in the control group.
Qualitative variables were analysed by the Fisher exact, parametric variables by Student’s t test, and non-parametric quantitative data by Mann-Whitney’s U. Quantitative data were tested for normal distribution using the Kolmogorov-Smirnov test. A stepwise logistic regression analysis was performed to identify variables that were independently associated with UTI. Statistical significance was set at p < 0.05 bilaterally.
Interpretation of results
It is widely accepted that some urodynamic dysfunctions like post void residual urine and detrusor overactivity are related to bacteriuria, (defined as positive culture urine without considering the presence of LUTS). It has been demonstrated that residual urine increases the bladder microorganism concentration. Detrusor overactivity can alter the shape of bladder and consequently it can retain bacteria. However, the influence of these factors on UTI remain controversial. Bacteriuria does not always lead to UTI because for ITU, bacteria must enter the urinary tract. This depends on virulence of germ and on host factors. It is well known that an intact urinary tract is important for resistance against infection. One of the protective mechanisms is the glycosaminoglycan layer. This layer can be disrupted by increasing intravesical pressure. Intravesical pressure can be increased during voiding phase because of bladder outlet obstruction or abdominal strength. Our study validates this hypothesis because both conditions were related to UTI.
On the other hand, our results also confirm that other urodynamic dysfunctions like post void residual urine, detrusor overactivity or detrusor underactivity did not have influence on UTI presence. Studies that state the influence of these factors on UTI should take into consideration the presence of an increased BOOI or abdominal straining, because of the possible relationship between those factors and BOOI or abdominal straining.