Homero Bruschini

Surgical treatment of stress incontinence in men.

The committee was charged with the responsibility of reviewing and evaluating all published data relating to surgical treatment of male urinary incontinence since the previous consultation in 2004.

Long-Term Effect of Early Postoperative Pelvic Floor Biofeedback on Continence in Men Undergoing Radical Prostatectomy: A Prospective, Randomized, Controlled Trial

PURPOSEnThe impact of pelvic floor muscle training on the recovery of urinary continence after radical prostatectomy is still controversial. We tested the effectiveness of biofeedback-pelvic floor muscle training in improving urinary incontinence in the 12 months following radical prostatectomy.nnnMATERIALS AND METHODSnA total of 73 patients who underwent radical prostatectomy were randomized to a treatment group (36) receiving biofeedback-pelvic floor muscle training once a week for 3 months as well as home exercises or a control group (37). Patients were evaluated 1, 3, 6 and 12 months postoperatively. Continence was defined as the use of 1 pad or less daily and incontinence severity was measured by the 24-hour pad test. Incontinence symptoms and quality of life were assessed with the International Continence Society male Short Form questionnaire and the Incontinence Impact Questionnaire. Pelvic floor muscle strength was evaluated with the Oxford score.nnnRESULTSnA total of 54 patients (26 pelvic floor muscle training and 28 controls) completed the trial. Duration of incontinence was shorter in the treatment group. At postoperative month 12, 25 (96.15%) patients in the treatment group and 21 (75.0%) in the control group were continent (p = 0.028). The absolute risk reduction was 21.2% (95% CI 3.45-38.81) and the relative risk of recovering continence was 1.28 (95% CI 1.02-1.69). The number needed to treat was 5 (95% CI 2.6-28.6). Overall there were significant changes in both groups in terms of incontinence symptoms, lower urinary tract symptoms, quality of life and pelvic floor muscle strength (p <0.0001).nnnCONCLUSIONSnEarly biofeedback-pelvic floor muscle training not only hastens the recovery of urinary continence after radical prostatectomy but allows for significant improvements in the severity of incontinence, voiding symptoms and pelvic floor muscle strength 12 months postoperatively.

A guideline for the management of bladder dysfunction in Parkinson's disease and other gait disorders.

Parkinsons disease (PD) is a common neurodegenerative disorder, and lower urinary tract (LUT) dysfunction is one of the most common autonomic disorders with an estimated incidence rate of 27–80%. Studies have shown that bladder dysfunction significantly influences quality‐of‐life (QOL) measures, early institutionalisation, and health economics. We review the pathophysiology of bladder dysfunction in PD, lower urinary tract symptoms (LUTS), objective assessment, and treatment options. In patients with PD, disruption of the dopamine D1‐GABAergic direct pathway may lead to LUTS. Overactive bladder (OAB) is the most common LUT symptom in PD patients, and an objective assessment using urodynamics commonly shows detrusor overactivity (DO) in these patients. The post‐void residual (PVR) volume is minimal in PD, which differs significantly from multiple system atrophy (MSA) patients who have a more progressive disease that leads to urinary retention. However, subclinical detrusor weakness during voiding may also occur in PD. Regarding bladder management, there are no large, double‐blind, prospective studies in this area. It is well recognised that dopaminergic drugs can improve or worsen LUTS in PD patients. Therefore, an add‐on therapy with anticholinergics is required. Beta‐3 adrenergic agonists are a potential treatment option because there are little to no central cognitive events. Newer interventions, such as deep brain stimulation (DBS), are expected to improve bladder dysfunction in PD. Botulinum toxin injections can be used to treat intractable urinary incontinence in PD. Transurethral resection of the prostate gland (TURP) for comorbid BPH in PD is now recognised to be not contraindicated if MSA is excluded. Collaboration of urologists with neurologists is highly recommended to maximise a patients bladder‐associated QOL. Neurourol. Urodynam. 35:551–563, 2016.

Voiding dysfunction in patients with Parkinson's disease: Impact of neurological impairment and clinical parameters

We assessed the lower urinary tract symptoms (LUTS) of patients with Parkinsons disease (PD) and their association with different clinical parameters.

The role of membranous urethral afferent autonomic innervation in the continence mechanism after nerve sparing radical prostatectomy: a clinical and prospective study

PURPOSEnWe evaluated the somatic and autonomic innervation of the pelvic floor and rhabdosphincter before and after nerve sparing radical retropubic prostatectomy using neurophysiological tests and correlated findings with clinical parameters and urinary continence.nnnMATERIALS AND METHODSnFrom February 2003 to October 2005, 46 patients with prostate cancer were enrolled in a controlled, prospective study. Patients were evaluated before and 6 months after nerve sparing radical retropubic prostatectomy using the UCLA-PCI urinary function domain and neurophysiological tests, including somatosensory evoked potential, and the pudendo-urethral, pudendo-anal and urethro-anal reflexes. Clinical parameters and urinary continence were correlated with afferent and efferent innervation of the membranous urethra and pelvic floor. We used strict criteria to define urinary continence as complete dryness with no leakage at all, not requiring any pads or diapers and with a UCLA-PCI score of 500. Patients with a sporadic drop of leakage, requiring up to 1 pad daily, were defined as having occasional urinary leakage.nnnRESULTSnTwo patients were excluded from study due to urethral stricture postoperatively. We evaluated 44 patients within 6 months after surgery. The pudendo-anal and pudendo-urethral reflexes were unchanged postoperatively (p = 0.93 and 0.09, respectively), demonstrating that afferent and efferent pudendal innervation to this pelvic region was not affected by the surgery. Autonomic afferent denervation of the membranous urethral mucosa was found in 34 patients (77.3%), as demonstrated by a postoperative increase in the urethro-anal reflex sensory threshold and urethro-anal reflex latency (p <0.001 and 0.0007, respectively). Six of the 44 patients used pads. One patient with more severe leakage required 3 pads daily and 23 showed urinary leakage, including 5 who needed 1 pad per day and 18 who did not wear pads. Afferent autonomic denervation at the membranous urethral mucosa was found in 91.7% of patients with urinary leakage. Of 10 patients with preserved urethro-anal reflex latency 80% were continent.nnnCONCLUSIONSnSensory and motor pudendal innervation to this specific pelvic region did not change after nerve sparing radical retropubic prostatectomy. Significant autonomic afferent denervation of the membranous urethral mucosa was present in most patients postoperatively. Impaired membranous urethral sensitivity seemed to be associated with urinary incontinence, particularly in patients with occasional urinary leakage. Damage to the afferent autonomic innervation may have a role in the continence mechanism after nerve sparing radical retropubic prostatectomy.

Urine is Necessary to Provoke Bladder Inflammation in Protamine Sulfate Induced Urothelial Injury

PURPOSEnThe bladder is normally impermeable to possible hostile environmental factors and toxic urinary wastes. Any disruption of the permeability barrier would permit the leakage of urine constituents into the underlying cells layers and subsequent inflammation. Protamine sulfate, which increases urothelial permeability, is used in experimental models of cystitis. We examined whether protamine sulfate alone could cause bladder inflammation or if the association of protamine sulfate and urine is needed for this condition.nnnMATERIALS AND METHODSnFemale Wistar rats (Center for the Development of Experimental Models for Medicine and Biology, Federal University of São Paulo, São Paulo, Brazil) had the bladder catheterized and instilled with protamine sulfate (10 mg) or sterile saline for 30 minutes. To exclude urine other groups of rats underwent bilateral nephrectomy and the same procedure was used. One day after instillation the bladders were removed for histopathology. Edema and vascular congestion were graded from 0-none to 3-severe. Polymorphonuclear and mast cells were counted. The Kruskal-Wallis test was performed for statistical analysis.nnnRESULTSnIntravesical instillation of protamine sulfate in nonnephrectomized rats led to inflammation, in contrast to findings in rats instilled with saline. On the other hand, nephrectomized rats showed no inflammatory changes following the instillation of protamine sulfate or saline. The mast cell count was similar in all groups.nnnCONCLUSIONSnBladder inflammation in this experimental model of urothelial injury was not due to protamine sulfate alone. The association of protamine sulfate and urine was necessary to trigger the inflammatory cascade. Thus, urine indeed has an important role in the development of bladder inflammation in an environment of higher urothelial permeability.

Bladder Compliance What Does it Represent: Can We Measure it, and is it Clinically Relevant?

To report the conclusion of the Think Thank 8 on Compliance Discussions during the second ICI‐RS meeting in 2010.

Cranberries and lower urinary tract infection prevention

Lower urinary tract infections are very common diseases. Recurrent urinary tract infections remain challenging to treat because the main treatment option is long-term antibiotic prophylaxis; however, this poses a risk for the emergence of bacterial resistance. Some options to avoid this risk are available, including the use of cranberry products. This article reviews the key methods in using cranberries as a preventive measure for lower urinary tract infections, including in vitro studies and clinical trials.

Urinary glycosaminoglycans excretion and the effect of dimethyl sulfoxide in an experimental model of non-bacterial cystitis

PURPOSEnWe reproduced a non-bacterial experimental model to assess bladder inflammation and urinary glycosaminoglycans (GAG) excretion and examined the effect of dimethyl sulfoxide (DMSO).nnnMATERIALS AND METHODSnFemale rats were instilled with either protamine sulfate (PS groups) or sterile saline (control groups). At different days after the procedure, 24 h urine and bladder samples were obtained. Urinary levels of hyaluronic acid (HA) and sulfated glycosaminoglycans (S-GAG) were determined. Also to evaluate the effect of DMSO animals were instilled with either 50% DMSO or saline 6 hours after PS instillation. To evaluate the effect of DMSO in healthy bladders, rats were instilled with 50% DMSO and controls with saline.nnnRESULTSnIn the PS groups, bladder inflammation was observed, with polymorphonuclear cells during the first days and lymphomononuclear in the last days. HA and S-GAG had 2 peaks of urinary excretion, at the 1st and 7th day after PS injection. DMSO significantly reduced bladder inflammation. In contrast, in healthy bladders, DMSO produced mild inflammation and an increase in urinary HA levels after 1 and 7 days and an increase of S-GAG level in 7 days. Animals instilled with PS and treated with DMSO had significantly reduced levels of urinary HA only at the 1st day. Urinary S-GAG/Cr levels were similar in all groups.nnnCONCLUSIONSnIncreased urinary levels of GAG were associated with bladder inflammation in a PS-induced cystitis model. DMSO significantly reduced the inflammatory process after urothelial injury. Conversely, this drug provoked mild inflammation in normal mucosa. DMSO treatment was shown to influence urinary HA excretion.

Urinary Glycosaminoglycans as Biomarker for Urothelial Injury: Is It Possible to Discriminate Damage From Recovery?

OBJECTIVESnThe glycosaminoglycan (GAG) layer is referred to as a bladder protective factor. We reproduced an experimental model of urothelial damage to assess GAG metabolism in the process of injury and recovery of the urothelium.nnnMETHODSnWistar female rats were bladder catheterized and instilled with either protamine sulfate (PS groups) or sterile saline (control groups). At different days after the procedure, 24-hour urine samples were obtained. The urinary levels of hyaluronic acid (HA) and sulfated glycosaminoglycan were determined in all groups and in nonmanipulated rats (day 0). Additionally, sulfated-GAG synthesis was assessed by the incorporation of [(35)S]-inorganic sulfate. The bladders were analyzed by histochemical staining for HA and immunofluorescence for heparin sulfate and syndecan-4.nnnRESULTSnUrinary HA and sulfated-GAG were elevated after PS injection (P <0.05). A greater concentration of [(35)S]-labeled GAG in the PS group animals on the fifth day and, especially, on the seventh day represented increased GAG synthesis at these periods (P <0.05). Bladder sections from the PS group animals on day 1 showed a greater amount of HA in the urothelium. PS instillation damaged the urothelium layer of heparin sulfate and syndecan-4 seen in the control animals. On day 5, patchy areas of a restored layer were seen, and, on day 7, this layer had completely regenerated.nnnCONCLUSIONSnUrinary GAG cannot differentiate urothelial damage from recovery. Elevated levels of urinary GAG can result from either desquamation of the surface cell GAG layer or increased GAG synthesis to regenerate the damaged urothelium.