Surgical treatment for difficulty emptying the bladder due to disco-ordination between bladder and sphincter muscle in adults with neurogenic bladder

Damage to the nervous system can lead to a lack of co-ordination (dyssynergia) between the bladder (detrusor) and the muscle at the exit of the bladder that allows people to control their bladder emptying (external urethral sphincter muscle). This urologic condition is called detrusor-sphincter dyssynergia (DSD) and is most frequently seen in people with spinal cord injury and multiple sclerosis. Insufficient relaxation of the sphincter during a voiding contraction prevents effective bladder emptying and can lead to high pressures in the bladder. People with increased bladder pressures are at an increased risk for bladder and kidney infections, which may lead to kidney damage and even failure.

Treatment is aimed at lowering these pressures by promoting proper bladder emptying. This can be achieved by inserting a thin tube (catheter) in the urethra (i.e. the tube connected to the bladder through which urine is released from the body) to empty the bladder on a regular basis (intermittent catheterisation), use of drugs, or surgery. The first step in treatment is usually not surgery, but surgical options should be considered if this is not possible or feasible. Different types of surgical treatment exist, but the optimal surgical treatment for this condition in adults is as yet unknown. This question is the subject of this review.

We found five trials, which included a total of 199 people (with an average age of 40 years) with a variety of causes of DSD. One trial showed that a surgical procedure in which an incision is made in the sphincter (sphincterotomy) is better in lowering bladder pressure than placing a permanent thin tube into the urethra (urethral stent), but only after two years.

Botulinum A toxin (BTX-A) is a toxin that targets the nervous system locally and interferes with the communications between nerves and muscles. Four trials used botulinum A toxin injections to weaken or paralyse the sphincter. These four trials independently showed that in some outcomes, BTX-A was more effective than placebo, lidocaine, or a treatment combined with drugs.

Compared to placebo, BTX-A was more effective in lowering pre-voiding and maximum bladder pressure after 30 days.

Comparing BTX-A to lidocaine injections, bladder emptying improved seven and 30 days after botulinum A toxin injection, however, not after one day. Botulinum A toxin injection without the addition of drugs (baclofen) was possibly more effective in increasing the ability of the bladder to stretch than botulinum A toxin injection combined with drugs. However, the quality of the trial reporting this was poor. The botulinum A toxin injection is effective for two to three months and therefore requires frequent reinjection, while the effects of sphincter incision seem to last for at least two years.

Two trials reported blood in the urine after injection as an undesired harmful effects (adverse effects) due to the injection of an agent. Also, muscle weakness was reported, which may relate to the BTX-A dose injected.

Overall, results from small studies with a high risk of bias have identified evidence of limited quality that BTX-A injection improves some outcomes relating to the dynamics of the bladder and urethra in storing and releasing urine 30 days after injection. However, this review showed that there was not enough evidence to identify the most effective surgical treatment for DSD.

Authors' conclusions: 

Results from small studies with a high risk of bias have identified evidence of limited quality that intraurethral BTX-A injections improve some urodynamic measures after 30 days in the treatment of functional bladder outlet obstruction in adults with neurogenic bladder dysfunction. The necessity of reinjection of BTX-A is a significant drawback; a sphincterotomy might therefore be a more effective treatment option for lowering bladder pressure in the long-term.

However, because of the limited availability of eligible trials, this review was unable to provide robust evidence in favour of any of the surgical treatment options. More RCTs are needed, measuring improvement on quality of life, and on other types of surgical treatment options for DSD since these are lacking. Future RCTs assessing the effectiveness of BTX-A injections also need to address the uncertainty about the optimal dose and mode of injection for this specific type of urological condition.

Read the full abstract...

The most common type of functional bladder outlet obstruction in patients with neurogenic bladder is detrusor-sphincter dyssynergia (DSD). The lack of co-ordination between the bladder and the external urethral sphincter muscle (EUS) in DSD can result in poor bladder emptying and high bladder pressures, which may eventually lead to progressive renal damage.


To assess the effectiveness of different surgical therapies for the treatment of functional bladder outlet obstruction (i.e. DSD) in adults with neurogenic bladder dysfunction.

Search strategy: 

We searched the Cochrane Incontinence Group Specialised Register, which contains trials identified from the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, MEDLINE In-Process, and handsearching of journals and conference proceedings (searched 20 February 2014), and the reference lists of relevant articles.

Selection criteria: 

Randomised controlled trials (RCTs) or quasi-RCTs comparing a surgical treatment of DSD in adults suffering from neurogenic bladder dysfunction, with no treatment, placebo, non-surgical treatment, or other surgical treatment, alone or in combination.

Data collection and analysis: 

Two review authors independently assessed trial quality and extracted data.

Main results: 

We included five trials (total of 199 participants, average age of 40 years). The neurological diseases causing DSD were traumatic spinal cord injury (SCI), multiple sclerosis (MS), or congenital malformations.

One trial compared placement of sphincteric stent prosthesis with sphincterotomy. For urodynamic measurements, results for postvoid residual urine volume (PVR) and cystometric bladder capacity were inconclusive and consistent with benefit of either sphincteric stent prosthesis or sphincterotomy at three, six, 12, and 24 months. Results for maximum detrusor pressure (Pdet.max) were also inconclusive at three, six, and 12 months; however, after two years, the Pdet.max after sphincterotomy was lower than after stent placement (mean difference (MD) -30 cmH2O, 95% confidence interval (CI) 8.99 to 51.01).

Four trials considered botulinum A toxin (BTX-A) injection in the EUS, either alone or in combination with other treatments. The comparators included oral baclofen, oral alpha blocker, lidocaine, and placebo. The BTX-A trials all differed in protocols, and therefore we did not undertake meta-analysis. A single 100 units transperineal BTX-A injection (Botox®) in patients with MS resulted in higher voided urine volumes (MD 69 mL, 95% CI 11.87 to 126.13), lower pre-micturition detrusor pressure (MD -10 cmH2O, 95% CI -17.62 to -2.38), and lower Pdet.max (MD -14 cmH2O, 95% CI -25.32 to -2.68) after 30 days, compared to placebo injection. Results for PVR using catheterisation, basal detrusor pressure, maximal bladder capacity, maximal urinary flow, bladder compliance at functional bladder capacity, maximal urethral pressure, and closure urethral pressure at 30 days were inconclusive and consistent with benefit of either BTX-A injection or placebo injections. In participants with SCI, treatment with 200 units of Chinese manufactured BTX-A injected at eight different sites resulted in better bladder compliance (MD 7.5 mL/cmH2O, 95% CI -10.74 to -4.26) than participants who received the same injections with the addition of oral baclofen. Results for maximum uroflow rate, maximal cystometric capacity, and volume per voiding were inconclusive and consistent with benefit of either BTX-A injection or BTX-A injection with the addition of oral baclofen. However, the poor quality of reporting in this trial caused us to question the relevance of bladder compliance as an adequate outcome measure.

In participants with DSD due to traumatic SCI, MS, or congenital malformation, the results for PVRs after one day were inconclusive and consistent with benefit of either a single 100 units transperineal BTX-A (Botox®) injection or lidocaine injection. However, after seven and 30 days of BTX-A injection, PVRs were lower (MD -163 and -158 mL, 95% CI -308.65 to -17.35 and 95% CI -277.57 to -39.03, respectively) compared to participants who received lidocaine injections. Results at one month for Pdet.max on voiding, EUS activity in electromyography, and maximal urethral pressure were inconclusive and consistent with benefit of either BTX-A or lidocaine injections.

Finally, one small trial consisting of five men with SCI compared weekly BTX-A injections with normal saline as placebo. The placebo had no effect on DSD in the two participants allocated to the placebo treatment. Their urodynamic parameters were unchanged from baseline values until subsequent injections with BTX-A once a week for three weeks. These subsequent injections resulted in similar responses to those of the three participants who were allocated to the BTX-A treatment. Unfortunately, the report presented no data on placebo treatment.

Only the trial that compared sphincterotomy with stent placement reported outcome measures renal function and urologic complications related to DSD. Results for renal function at 12 and 24 months, and urologic complications related to DSD at three, six, 12, and 24 months were inconclusive and consistent with benefit of either sphincteric stent prosthesis or sphincterotomy.

Adverse effects reported were haematuria due to the cystoscopic injection and muscle weakness, of which the latter may be related to the BTX-A dose used.

All trials had some methodological shortcomings, so insufficient information was available to permit judgement of risk of bias. At least half of the trials had an unclear risk of selection bias and reporting bias. One trial had a high risk of attrition bias, and another trial had a high risk of reporting bias.