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PubMed2006

Incomplete emptying and urinary retention in multiple-system atrophy: when does it occur and how do we manage it?

Neurogenic urinary retention can be a major cause of morbidity in multiple-system atrophy (MSA). However, the timing of its appearance has not been entirely clear, and neither have the medical and surgical modalities for managing patients. We present the data obtained from our uroneurological assessment and therapeutic interventions at various stages of MSA. We recruited 245 patients with probable MSA. We measured postvoid residuals (PVR) and performed EMG cystometry in all patients. The grand average volume of PVR was 140 mL (range, 0-760) in our patients. The average PVR volume was 71 mL in the first year, increasing to 129 mL in the second year and 170 mL by the fifth year. The percentages of patients with complete urinary retention, acontractile detrusor, and detrusor-sphincter dyssynergia (DSD) also increased. The increase in PVR resulted in a decrease in functional bladder capacity, together with an increase in detrusor overactivity and neurogenic sphincter EMG. Clean intermittent self-catheterization (CISC) was introduced in most patients. Bladder-oriented therapy (cholinergic agents) had a limited value, whereas urethra-oriented therapy benefited patients with DSD (surgery) for up to 2 years, but syncope occurred in a subset of patients (alpha-blockers). MSA patients present with large PVR by the second year of illness, and that large PVR secondarily causes urinary frequency. CISC is the recommended treatment for most patients. Urethra-oriented medication and surgery benefit patients who would have difficulty performing CISC, although careful consideration of the short-term efficacy and potential adverse effects of these alternatives is mandatory.

Adrenergic alpha-Antagonists↗

PubMed2005

Therapy Insight: bladder dysfunction associated with multiple sclerosis.

Bladder dysfunction is a common problem for patients with multiple sclerosis. The severity of symptoms often correlate with the degree of spinal cord involvement and, hence, the patient's general level of disability. The emphasis of management is now mainly medical and is increasingly offered by nonurologists. Treatments can be highly effective, relieving patients of what are otherwise very troublesome symptoms that would compound their neurological disability. This article gives an overview of the neural control of the bladder, followed by an explanation of the pathophysiology of detrusor overactivity secondary to neurological disease. A review of methods available for treating bladder dysfunction in multiple sclerosis then follows. The treatment options for this disorder are largely medical and include established first-line measures such as anticholinergics, clean intermittent self-catheterization and the use of desmopressin, as well as potential second-line agents, such as cannabinoids, intravesical vanilloids and intradetrusor botulinum neurotoxin type A. The diminishing role of surgical intervention is also discussed.

Algorithms↗

PubMed2006

Botulinum toxin: a potential alternative to current treatment of neurogenic and idiopathic urinary incontinence due to detrusor overactivity.

OBJECTIVE: To analyze and report the current data on the treatment of both neurogenic and idiopathic detrusor overactivity with Botulinum toxin. METHODS: Literature review using Pub-Med and Medline from 1990 until June 30, 2006. RESULTS: Case series of patients with neurogenic detrusor dysfunction (NDD) and idiopathic detrusor overactivity (IDO) range from 15 to 200 patients with follow up from 12 to 36 weeks post-treatment. Significant improvements in cystometric bladder capacity, reflex volume at first urge to void, and bladder compliance are seen in nearly all patients. Approximately 50% of NDD patients achieved urinary continence and almost all had improvement in bladder control up to 36 weeks following treatment. Patients with IDO with urgency alone or with incontinence also had urodynamic as well as symptom improvement. Approximately 75% of patients with IDO and incontinence are dry at 12 weeks post-treatment. Urgency disappears on average in two thirds of patients. Quality of life scores also shows significant improvement for all groups. CONCLUSION: Botulinum toxin-A has emerged as a promising option for the treatment of neurogenic and refractory idiopathic detrusor overactivity. Studies to date have shown that not only is this treatment effective at decreasing urinary symptoms and incontinence, as well as improving potentially dangerous urodynamic measures, but it is also minimally invasive, reversible and safe. Questions over proper dosing and dilution, number of injection sites, and re-injection rates remain to be answered.

Botulinum Toxins↗

PubMed2001

Loss of purinergic P2X(3) and P2X(5) receptor innervation in human detrusor from adults with urge incontinence.

Activation of purinergic P2X receptors associated with the parasympathetic nerves that supply the human bladder smooth muscle (detrusor) is implicated in control of detrusor contractility. The relative abundance of all seven subtypes colocalized with synaptic vesicles on parasympathetic nerves was examined in specimens from normal adult bladder, infants, and in adults with overactive detrusor contractility and a diagnosis of idiopathic detrusor instability (IDI) to determine whether receptor distribution varied with age or in patients with incontinence. Alteration in control of detrusor innervation was examined with P2X subtype-specific antibodies and an antibody against synaptic vesicles, using immunofluorescence and confocal microscopy. Detrusor samples were taken from: controls, at cystectomy for cancer or cystoscopic biopsy for hematuria (n = 22; age 33-88), child bladder, at surgical correction of vesico-ureteric reflux (n = 21; age 4 months to 2 years), and adults with detrusor instability at cystoscopy-cystodistension (n = 18; age 30-81). Adult specimens contained muscle with large varicosities (1.2 microm) along parasympathetic nerves with colocalized patches of all P2X(1-7) subtypes. Infant bladder revealed little evidence of P2X at age <9 months but approached adult levels at 2 years. Detrusor from IDI patients revealed selective absence of P2X(3) and P2X(5) beneath all the varicosities. This specific lack of P2X(3) and P2X(5) may impair control of detrusor contractility and contribute to the pathophysiology of urge incontinence.

Adult↗

PubMed2006

Detrusor underactivity: Clinical features and pathogenesis of an underdiagnosed geriatric condition.

Urinary incontinence and other lower urinary tract symptoms exert a major influence on the health and independence of frail older people. Detrusor underactivity (DU) is defined as a contraction of reduced strength and/or duration, resulting in prolonged bladder emptying and/or a failure to achieve complete bladder emptying within a normal time span. DU may influence the clinical presentation and impede the therapy of disorders as common and as disparate as detrusor overactivity, urinary retention, and benign prostatic hyperplasia. Urodynamically, nearly two-thirds of incontinent nursing home residents exhibit DU. The clinical diagnosis of DU when present alone or in association with other bladder conditions such as detrusor overactivity (detrusor hyperactivity with impaired contractility (DHIC)) is challenging, because symptoms lack adequate precision. A catheterized and increasingly noninvasive ultrasound-based postvoid residual assessment allows a bedside diagnosis of retention and may suggest the presence of DU in individuals (mostly women) with a low likelihood of bladder outlet obstruction (BOO). Nevertheless, it cannot differentiate primary DU from retention secondary to BOO. The management of individuals with DHIC remains unsatisfactory, because antispasmodic anticholinergic medications may worsen retention, whereas bethanechol does not improve bladder emptying. Human detrusor biopsies reveal axonal degeneration, muscle loss, and fibrosis in DU. Animal studies suggest that multiple risk factors, including retention itself, lack of estrogen, infection, inflammation, and aging, may contribute to DU. Priority areas for future research include efforts to facilitate clinical nonurodynamic diagnosis of probable DU plus translational research designed to address the pathogenesis of this complex multifactorial geriatric syndrome.

Aged↗

PubMed2006

Persistence of therapeutic effect after repeated injections of botulinum toxin type A to treat incontinence due to neurogenic detrusor overactivity.

OBJECTIVES: To study the effect of repeated botulinum toxin type A injections into the detrusor in patients with neurogenic detrusor overactivity and incontinence to determine the safety of repeated injections, the persistence of the clinical and urodynamic treatment efficacy, and potential changes in bladder compliance. METHODS: Seventeen patients with neurogenic detrusor overactivity who had received three or more botulinum toxin type A injections into the detrusor were studied. The clinical and urodynamic data were analyzed at baseline (before the first injection), after the first injection, and after the last repeated injection. RESULTS: No systemic side effects were observed for the total of 91 injections. The mean number of injections per patient was 5.4 (range 3 to 9). The mean number of incontinence episodes per day decreased from 2.6 at baseline to 0 after the first injection, and remained at 0 after the last injection. The maximal cystometric bladder capacity and reflex volume increased significantly after the first and last injection compared with at baseline. The maximal detrusor pressure decreased significantly after the first and last injection compared with at baseline. No difference in compliance was found from baseline to the first or last injection. CONCLUSIONS: Repeated injections of botulinum toxin A into the detrusor muscle are a safe and valuable treatment option for neurogenic detrusor overactivity. After repeated injections, the effect on the clinical and urodynamic parameters remained constant. Also, repeated injections did not decrease bladder compliance.

Botulinum Toxins, Type A↗

PubMed2005

[Subjective patient satisfaction after injection of botulinum-a toxin in detrusor overactivity].

PURPOSE: The established treatment for overactive detrusor function consists of anticholinergic drugs. But this treatment can fail or produce intolerable side effects. We therefore investigated the effect of botulinum-A toxin in treating overactive detrusor function in patients with neurogenic and nonneurogenic bladder dysfunction. We were particularly interested in patient satisfaction with this therapy. MATERIAL AND METHODS: The subjects were 38 patients who had overactive detrusor function of different origins and in whom therapy with anticholinergic drugs had failed. To measure results, we used urodynamic studies and a questionnaire that consisted of 27 validated questions ("Urogenital Distress Inventory UDI-6", "Symptom Severity Index" and "Symptom Impact Index") as well as a satisfaction questionnaire. We injected 200 - 300 U of botulinum-A toxin (Botox) cystoscopically. RESULTS: At least 4 weeks after injection, 90 % of the patients reported clear improvement of their voiding situation and 93 % stated that they would undergo this procedure again. The frequency of micturition decreased by 29 % in average, and the increased postvoid residual volume was clinically irrelevant. Patients reported side effects or complications in 6.7 % of cases. The satisfaction scale (0 - 10) averaged 6.9. Urodynamically, reflex volume increased by 85 %, maximal bladder capacity increased by 47 %, and bladder pressure decreased by 33 %. CONCLUSIONS: Botulinum-A toxin injection into the overactive detrusor muscle seems to be very effective. The effect is not only reflected in urodynamic studies but also in the subjective patient satisfaction.

Adult↗

PubMed2003

A review of the L-arginine - nitric oxide - guanylate cyclase pathway as a mediator of lower urinary tract physiology and symptoms.

Lower urinary tract symptoms (LUTS) are common and costly conditions that affect millions of men and women worldwide. A focal area of research into the cause and potential treatment of LUTS is the nitric oxide pathway, which is involved in nerve-induced relaxation in the lower urinary tract. Isoforms of NOS, including nNOS, eNOS, and iNOS, have been identified in the lower urinary tract of both animals and humans. Nerves that are immunoreactive to nitric oxide synthase (NOS) mainly serve the bladder outlet region, but some serve the detrusor. Pathology of the l-arginine-nitric oxide-cGMP pathway involving nNOS and eNOS may lead to impaired relaxation of the urethral outlet, increased bladder afferent activity, and detrusor smooth muscle overactivity. Such pathology has been implicated in the conditions of detrusor instability, urinary incontinence and outlet obstruction. iNOS may play an important role in inflammatory and infectious conditions of the bladder. Strategic manipulation of nitric oxide (NO), or interventions that address its mechanisms of action, possibly by pharmacological means or with gene therapy, may restore function or produce desired functional effects in the lower urinary tract.

Arginine↗

PubMed2004

P2X3-immunoreactive nerve fibres in neurogenic detrusor overactivity and the effect of intravesical resiniferatoxin.

OBJECTIVES: The ATP-gated purinergic receptor P2X3 is expressed by small diameter sensory neurons and has been identified in normal and neurogenic human bladder suburothelial fibres. Animal models have shown that ATP is released by the urothelium during bladder distension, suggesting a mechanosensory role for P2X3 receptors in normal bladder function. Successful treatment of spinal neurogenic detrusor overactivity (NDO) with intravesical resiniferatoxin (RTX), which partly acts on suburothelial C fibres, provides evidence for the emergence of a C fibre-mediated spinal reflex. The aim of this study was to investigate the possible role of P2X3-positive innervation in this pathological voiding reflex by comparing suburothelial P2X3 immunoreactivity of controls and in patients with NDO before and after intravesical RTX. METHODS: Bladder biopsies were obtained from 8 controls and 20 patients with refractory NDO enrolled in a trial of intravesical RTX. P2X3 nerve fibre density and intensity were studied in the specimens by immunohistochemistry. RESULTS: P2X3-IR nerve fibres were significantly increased in patients with NDO compared to controls (p=0.014). Thirteen patients had pre- and post-RTX biopsies available for immunohistochemistry; 5 of them responded clinically and 8 were non-responders. In the 5 patients who responded to RTX, there was a significant decrease in P2X3-positive fibres (p=0.032), whereas in non-responders, P2X3-IR nerve fibre density did not change significantly. CONCLUSIONS: In patients with NDO, the numbers of P2X3-IR nerve fibres were increased in the suburothelium. There was a significant decrease in P2X3 immunoreactivity in responders to RTX, indicating a potential pathophysiological role for the P2X3 expressing fibres.

Diterpenes↗

PubMed1998

Abolition of cystitis-induced bladder instability by local spinal cord cooling.

PURPOSE: The efficacy of lumbosacral spinal cord cooling for the suppression of reflex urinary incontinence was evaluated in a rat model of cystitis-induced bladder instability. MATERIALS AND METHODS: In female Sprague-Dawley rats, overactivity of the detrusor muscle was induced by inflammation of the urinary bladder. Isovolumetric intravesical pressure, urethral perfusion pressure and electromyographic (EMG) activity of the external urethral sphincter (EUS) were recorded simultaneously during repetitive local cooling (-2C or +15C) and rewarming (to 37C) of the dorsal L6/S1 spinal cord segments. RESULTS: Mustard oil-induced inflammation led to a marked instability of the urinary bladder without affecting urethral outlet functions. Local cooling of the dorsal lumbosacral spinal cord with temperatures of -2C as well as +15C completely abolished bladder voiding contractions in rats with an inflamed bladder as well as in non-inflamed control animals. Cooling had little effect on the EMG activity of the EUS and increased the urethral perfusion pressure. The suppression of detrusor reflex contractions was reversed within 1-7 min. after rewarming of the spinal cord. CONCLUSIONS: Cooling of the dorsal spinal cord at the origin of the parasympathetic innervation of the bladder can be used for a reversible suppression of bladder instability without affecting the urethral outlet. Thus, local spinal cord cooling may offer a suitable method to restore continence in cases of reflex incontinence.

Animals↗

PubMedDate not supplied

Effects of drugs used in the therapy of detrusor hyperactivity on the volume-induced contractions of the rat urinary bladder.

In this study we examined the effects of the drugs most commonly utilized in the therapy of overactive detrusor, on the volume-induced contractions of rat urinary bladder. Anticholinergics such as propantheline bromide and emepronium bromide, as well as oxybutynin decreased the amplitude of the voiding contractions after intravenous (i.v.) administration in a dose-dependent way. These anticholinergics, on the other hand, generally increased the frequency of the contractions. Nifedipine dose-dependently reduced the amplitude of the contractions. Flavoxate induced a dose-related decrease in the frequency without effects on the amplitude of the peaks. Its main metabolite 3-methylflavone-8-carboxylic acid (MFCA) was inactive after i.v. administration. Terodiline was active on the amplitude and apparently on the frequency of the voiding contractions. The alpha-adrenoceptor antagonist prazosin, as well as indomethacin, inhibited only the frequency of the voiding contractions. All the drugs active in reducing the frequency of the voiding contractions after i.v. administration, proved effective also after intracerebroventricular (i.c.v.) injection. The model of the volume-induced contractions of rat urinary bladder, seems to be a useful tool to evaluate in vivo the effects of a compound on the bladder, allowing the possibility of distinguishing among antimuscarinics and calcium antagonists, which peripherally decrease bladder contractility, and other drugs inducing a decrease in the frequency of the voiding reflex acting on the micturition centre(s) in the central nervous system (CNS).

Animals↗

PubMed1994

The role of patient history in the diagnosis of urinary incontinence.

OBJECTIVE: To assess the clinical usefulness and validity of patient history in the diagnosis of genuine stress incontinence and detrusor overactivity. DATA SOURCES: A literature search was performed for publications addressing the clinical evaluation of urinary incontinence between 1975-1992. METHODS OF STUDY SELECTION: Nineteen of 29 articles during this period reported data in such a manner as to allow statistical comparison of patient history to the diagnosis based on urodynamic evaluation. DATA EXTRACTION AND SYNTHESIS: Each article was assessed for the following information: inclusion and exclusion criteria, method of obtaining patient history, clinical evaluation, and diagnostic criteria. Patients in each article were classified according to their history and urodynamic diagnosis. Sensitivity, specificity, and predictive values were calculated for each article, as well as for the combined data from all articles. Combined data from all 19 articles produced a total of 3092 and 2950 patients evaluated for genuine stress incontinence and detrusor overactivity, respectively. A clinical history consistent with stress incontinence, when compared to a urodynamically based diagnosis, showed a sensitivity of 0.906, a specificity of 0.511, a positive predictive value of 0.749, and a negative predictive value of 0.771. A comparison of clinical history suggestive of an overactive detrusor and urodynamic evidence of spontaneous bladder activity revealed a sensitivity of 0.735, specificity of 0.552, positive predictive value of 0.561, and negative predictive value of 0.728. CONCLUSION: Patient history alone is not an accurate tool in the diagnosis of genuine stress incontinence or detrusor overactivity, and should not be the sole determinant of diagnosis or treatment.

Aged↗

PubMed2004

Does magnetic stimulation of sacral nerve roots cause contraction or suppression of the bladder?

AIMS: The aim of this study was to resolve the paradox as to whether magnetic stimulation of sacral nerve roots results in contraction or suppression of the bladder, in both normal individuals and patients with spinal cord injury (SCI). MATERIALS AND METHODS: Seven males with complete SCI and neurogenic detrusor overactivity (NDO) and five normal males were investigated. Bladder capacity and maximum cystometric capacity were determined, respectively, in these groups. Magnetic stimulation was applied to sacral nerve roots using a multi-pulse magnetic stimulator and coil. Stimulation was applied at half capacity, near-full capacity, and during NDO or voiding (in normal individuals). Single and intermittent bursts of stimulation were applied. RESULTS: Neither single nor intermittent bursts of magnetic stimulation of the sacral nerve roots resulted in significant bladder pressure rises. Occasionally, following cessation of the magnetic stimulation bladder contractions were seen in patients with NDO. These contractions had an unpredictable and variable latency. As previously reported, magnetic stimulation suppressed NDO in patients with SCI, and suppressed voiding in normal individuals. CONCLUSIONS: Bladder contractions are occasionally observed in patients with NDO following withdrawal of stimulation. This phenomenon hypothetically arises as a result of removal of the bladder suppression provided by magnetic stimulation, rather than direct motor pathway stimulation (as has been reported by others). The ability of sacral magnetic stimulation to suppress detrusor contractions is reaffirmed.

Adult↗

PubMed2006

Metabolic syndrome and lower urinary tract symptoms secondary to benign prostatic hyperplasia.

Increasing evidence recently has pointed toward a relationship between lower urinary tract symptoms (LUTS) and the presence of metabolic syndrome. This relationship has been supported by recent epidemiologic findings. Possible pathophysiologic links also have been proposed to explain the relationship between these two syndromes. The increasing prevalence of obesity in the United States makes this an increasingly relevant problem. Animal studies support a link between autonomic nervous system (ANS) overactivity and the development of urinary symptoms, low bladder compliance, compensatory prostatic hyperplasia, and blockage of the same using alpha-blockade. There appears to be a significant link between ANS overactivity as part of the metabolic syndrome and LUTS secondary to benign prostatic hyperplasia (BPH). However, it is unlikely that ANS overactivity could be responsible for the development of LUTS. Rather, ANS overactivity plays a key role in increasing the severity of LUTS above an intrinsic basal intensity that is determined by the genitourinary anatomic/pathophysiologic characteristics of each BPH patient. This paper defines metabolic syndrome as a collection of abnormalities, including being overweight (visceral abdominal fat distribution), dyslipidemia, hypertension, impaired glucose metabolism, elevated C-reactive protein (chronic inflammation), and autonomic-sympathetic overactivity, with insulin resistance as the hypothesized underlying pathogenic mechanisms.

Animals↗

PubMed2006

Bladder sensation in peripheral nerve lesions.

OBJECTIVE: To present bladder sensory data of three common peripheral nerve lesions (e.g., distal, intermediate/focal, and proximal). METHODS: We measured first sensation (FS) and bladder capacity (BC) (not exceeding 600 ml) in 71 patients with peripheral nerve lesions: 35 diabetic neuropathy (D group), 6 post-pelvic surgery (S), and 27 cauda equina syndrome due to lumbar spondylosis (L). We excluded those with detrusor overactivity or low compliance that might affect bladder sensation. RESULTS: The mean FS was 301.7 ml (D), 271.3 ml (S), and 189.4 ml (L), with the largest being in the D group (P < 0.05); the mean BC was 495.2, 475.4, and 391.4 ml, with the largest being in the D group (P < 0.05); who commonly had less frequent toileting. The mean post-void residual volume was 106.5, 29.0, and 42.0 ml; the values tended to increase along with BC. In the D group, the mean FS in patients with skin hypoalgesia as detected by pin prick and in those without it was 407.8 and 210.0 ml. The percentage of patients with FS < 100 ml was 5.7%, 0%, and 7.4%, respectively, who commonly had urinary urgency and frequency. CONCLUSIONS: Bladder sensation is affected in diabetic neuropathy more severely than in intermediate/proximal lesions, together with somatic sensory disturbance. Bladder sensory disturbance leads to less frequent toileting, resulting in bladder over-distension and large post-void residuals. A small proportion of patients with peripheral nerve lesions develop urinary urgency, presumably reflecting irritation of the afferent nerve fibers or the urothelium.

Aged↗

PubMed1998

Effects of verapamil on bladder instability induced by partial outflow obstruction in rat.

BACKGROUND: Overactivity of the detrusor due to benign prostatic hyperplasia may be induced by hyperpermeability of the smooth muscle cell membrane to calcium. We investigated the effect of verapamil, a calcium channel blocker, on detrusor function in outflow obstructed and control rat bladders. METHODS: Verapamil was injected intravenously via a catheter inserted into the internal jugular vein in doses of 0.5, 1.0, 2.0, 4.0, and 10.0 mg/kg in rat bladders with and without partial outflow obstruction under urethane anaesthesia. The intravesical pressure was monitored continuously. We measured the tidal voided urine volume, the voiding pressure, the pressure at which micturition was induced, and the end-point pressure of micturition. RESULTS: The tidal voided urine volume was significantly decreased in the obstructed bladders before administration of verapamil. Verapamil had similar effects in cystometric parameters in obstructed and control bladders. Verapamil increased the tidal voided urine volume, the pressure at which micturition was induced, and the end-point pressure of micturition, and reduced the voiding in obstructed and control bladders. Verapamil at doses of 4.0 mg/kg or higher induced significant arrhythmia. CONCLUSIONS: Verapamil reduced the contractile force of the bladder and increased the capacity and residual urine volume in both normal and obstructed bladders. Thus, although calcium channel blockers such as verapamil may be effective in treating a hyperactive bladder, they may have adverse cardiovascular effects.

Animals↗

PubMed2003

Pressure-flow variables in patients treated with tolterodine for detrusor overactivity.

OBJECTIVE: To test the hypothesis that drug treatment which modifies detrusor function (tolterodine) may influence the higher detrusor pressure at urethral opening and closure recorded in patients with detrusor overactivity than in those with stable bladders. PATIENTS AND METHODS: All patients treated with tolterodine in the treatment arm of a phase III, randomized, placebo-controlled trial of tolterodine were eligible for the study. Patients underwent urodynamics before and immediately after 4 weeks of therapy. The detrusor pressure at urethral opening, at maximum flow and at urethral closure, and the maximum bladder capacity and postvoid residual urine volume were recorded from matched urodynamic studies in the trial. Patients with a reduction in urinary frequency of more than two voids per 24 h were defined as responders to treatment and urodynamic data were dichotomised accordingly to allow comparison. RESULTS: There were no between-group differences in either the detrusor pressure at opening or closure when responders were compared with non-responders. Successful treatment was associated with a statistically significant change in bladder capacity and postvoid residual volume, although the change in residual volume was not clinically significant. Values of detrusor pressure at opening before treatment were greater in non-responders. CONCLUSION: The absence of changes in the pressure-flow plot variables is in keeping with previous studies reporting the search for a urodynamic variable which might be used to predict a favourable outcome after drug treatment.

Benzhydryl Compounds↗

PubMed2006

Tension-free vaginal tape sling procedure for the treatment of stress urinary incontinence in Hong Kong women with and without pelvic organ prolapse: 1-year outcome study.

OBJECTIVE: To assess the outcome of patients who underwent a tension-free vaginal tape sling procedure alone versus patients who underwent concomitant pelvic floor surgery. DESIGN: Retrospective cohort study. SETTING: Urogynaecology unit of a university teaching hospital, Hong Kong. PATIENTS: Patients diagnosed with moderate-to-severe urodynamic stress incontinence and underwent a tension-free vaginal tape sling procedure from September 1999 to August 2004. MAIN OUTCOME MEASURES: Objective cure rate of stress urinary incontinence 1 year following tension-free vaginal tape sling procedure was assessed. Patients were considered objectively cured if no stress urinary incontinence was evident on urodynamic studies at 1-year follow-up. Subjective cure rates at 4 months and 1 year after tension-free vaginal tape sling procedure were also assessed. Other outcome measures included intra-operative and perioperative complication rates, and the rate of de-novo detrusor overactivity at 1 year. RESULTS: Of 302 patients recruited, 250 (82.8%) completed 1-year follow-up. There were 157 (62.8%) patients who had a tension-free vaginal tape sling alone, and 93 (37.2%) had tension-free vaginal tape sling and concomitant pelvic floor surgery for pelvic organ prolapse. All patients had urodynamic studies before and 1 year following surgery. The objective cure rate was 87.3% for patients with tension-free vaginal tape sling alone, and 80.6% for tension-free vaginal tape sling with concomitant procedures (Chi squared test, P>0.05). The subjective cure rates for tension-free vaginal tape sling alone and tension-free vaginal tape sling plus concomitant procedures were 89.2% and 86.0% at 4 months, and 93.0% and 94.6% at 1 year, respectively (Chi squared test, P>0.05). The most common complication was postoperative urinary retention (15.2%), followed by de-novo detrusor overactivity at 1 year (10%), and bladder perforation (8%). CONCLUSION: The tension-free vaginal tape sling procedure alone or in combination with pelvic floor surgery are equally effective for the treatment of female stress urinary incontinence.

Aged↗