Editors view affiliations Michael B. Chancellor Ananias C. Front Matter Pages i-xvii. Epidemiology and Demographics of Underactive Bladder.
Underactive bladder - Understanding Continence Promotion
Pages Evaluation and Diagnosis of Underactive Bladder. Urodynamics Evaluation of Underactive Bladder. Pathophysiology and Animal Modeling of Underactive Bladder. Nonsurgical Therapy; Catheters; Devices. Current Drug Therapy for Underactive Bladder. Novel Drugs for Underactive Bladder. Neuromodulation Treatment of Underactive Bladder. Intradetrusor injections of ADMC were performed in a year-old patient with underactive bladder resulting in a decrease in maximum bladder volume and improved voiding at 1 year [ 44 ]. However, he still required occasional self-catheterization but reported no side effects such as hematuria, urgency, frequency nor infection related to the injections.
While this is a promising first case of injection of ADMC in the treatment of DUA, increasing detrusor contractility will not affect the bladder outlet relaxation. Ideally, coordinated outlet relaxation should occur with bladder contractions to allow efficient emptying. Injection of myoblasts, transformed by viral vectors, has been shown as a potential method for gene transfer to deliver therapeutic proteins into muscle in diseases such as Duchenne muscular dystrophy [ 45 ]. This method could be used to deliver genes that promote contractility of detrusor smooth muscles. Comparisons of efficiency of gene delivery between tissue injection, adenoviral infection and adenoviral transduced myoblast injection revealed that the myoblast injection was the most effective method of delivering the gene to the tissue [ 46 ].
Other forms of gene delivery involve using herpes simplex virus to delivery gene to the dorsal root ganglia which is part of the sensory afferent pathway. This method has been used to transfect the nerve growth factor NGF gene to the sensory ganglia cells innervating the bladder as a treatment of diabetic cystopathy when NGF is diminished in the DRG [ 47 ].
This same approach can be contemplated in DUA where augmented sensory input into the sensory limb of the micturition reflex can result in increased bladder contractility. Pelvic physiotherapy is usually a first line for dysfunctional voiding but little is known about the effectiveness of pelvic physiotherapy in treating DUA.
Small randomized clinical trials have shown that transcutaneous stimulation benefitted DUA in children [ 48 ]. The symptom bother perceived by these children were not described. Though the investigators stated that urodynamics were performed in all subjects confirming DUA, there were no urodynamics data presented. The investigators found that after pelvic transcutaneous stimulation, voiding frequency increased, bladder capacity decreased, voiding time decreased, and PVR also decreased.
In a rat model, direct stimulation of the pudendal nerve resulted in increased voiding efficiency in a diabetic DUA model [ 49 ]. A meta-analysis showed that sacral neuromodulation works in patients with nonobstructive urinary retention [ 50 ]. However, in many of these trials the main outcome is postvoid residual PVR volume or number of self-catheterization episodes in a day.
Sacral neuromodulation has also been shown to improve the impaired contractility in patients with detrusor hyperreflexia impaired contractility [ 51 ]. More studies are needed to further identify patients who will have successful resolution of their symptoms after implantation of a permanent neuromodulation device [ 52 ]. The future for neuromodulation might include direct stimulation of different brain areas that are involved in voiding.
Male mice void based on social rank with the male dominant mouse voiding frequently and the nondominant mice voiding much less frequently as if they had detrusor underactivity or DUA [ 53 , 54 ]. The DUA voiding behavior of the nondominant male mouse could be altered by triggering areas of the brain to make these nondominant mouse void as if it were a dominant mouse [ 55 ]. These data suggest that stimulation of certain loci in brain can lead to augmented voiding behavior.
Transcranial stimulation, whether with magnetic or other electrical energy, has been used to treat a variety of functional disorders such as depression, anxiety, tinnitus, poststroke aphasia, movement disorders, and even addiction. It is conceivable that transcranial stimulation may be used to induce voiding or increase bladder contractility during voiding.
The monitoring and stimulation is completely automated and constantly occurring throughout time dynamic such that the patient does not have to provide any input to the system. This closed-loop feedback system is intended to mimic normal storage and emptying of urine through modulation of both sensory and motor pathways of the micturition reflex. An animal model proof of concept was tested in which monitoring of bladder filling was measured by electrical currents triggered by bladder filling. These electric signals from bladder filling was then used to feedback to initiate pudendal nerve stimulation [ 56 ].
As discussed above, pudendal nerve stimulation can augment bladder emptying in a diabetic DUA rat model [ 49 ], but pudendal nerve stimulation at different parameters can also increase bladder storage capability [ 57 ]. The closed-loop feedback systems are designed with the neurogenic bladder in mind because, often, the neurogenic bladder has both storage and emptying problems.
However, it is quite possible to have a simpler closed-loop design for use in DUA. In , the U. The device is inserted and left indwelling in the urethra for a period up to 30 days. It is anchored in place by silicone tines that are deployed at the bladder neck during insertion. For removal, the device is pulled out with gentle outward force which collapses the silicone tines and allows the device to come out and be exchanged for a new device. The patient turns on the pump within the InFlow with a remote control when she wants to void. With the pump on, urine is pumped out of the bladder, through the InFlow and out the urethral meatus.
This creates a flow similar urinary flow as volitional voiding. There have been no published studies on the use of the InFlow. The risks would be like having an indwelling urethral catheter since both are foreign body within the lower urinary tract connected to the external environment. These risks include urinary tract infection, bladder stones, urethral erosion and development of a patulous urethra.
Long-term use of this device may also result in the rare development of squamous cell carcinoma from chronic foreign body in the lower urinary tract. Therefore, this device is likely best utilized for a short period of time until the DUA spontaneously resolves or another form of treatment is instituted. There are many potential future treatments for DUA. Drug treatments require a more granular understanding of bladder, urethral and pelvic floor neurophysiology.
A better understanding of how all the layers urothelium, lamina propria, and muscularis propria integrate with each other to provide efficient bladder emptying is needed. While stem cells and regenerative techniques appear to be the wave of the future, there need to be long-term studies to ensure that neoplasms do not form. Furthermore, increasing bladder contractions does not necessarily mean that the bladder outlet synchronously relaxes.
Gene therapy can be contemplated, though this approach appears less favorable than stem cell and regenerative therapies. Neuromodulation techniques have advanced along with technology to involve studies using closed-loop feedback systems. Noninvasive transcranial stimulation approaches, used in many functional disorders, should be studied in DUA. While an indwelling motorized urethral device can assist with bladder emptying without use of a catheter, this device should be used for short time periods due to risks of foreign body in lower urinary tract.
The future of treating DUA could involve a combination approach of all of the therapies discussed. National Center for Biotechnology Information , U.
Journal List Investig Clin Urol v. Investig Clin Urol. Published online Dec Toby C. Chai and Tambudzai Kudze. Find articles by Toby C.
Find articles by Tambudzai Kudze. Author information Article notes Copyright and License information Disclaimer. Corresponding author. Corresponding Author: Toby C. Received Jul 14; Accepted Nov This article has been cited by other articles in PMC. Abstract Underactive bladder UAB is a term used to describe a constellation of symptoms that is perceived by patients suggesting bladder hypocontractility. Keywords: Detrusor underactivity, Future treatments, Underactive bladder. GENE THERAPY Injection of myoblasts, transformed by viral vectors, has been shown as a potential method for gene transfer to deliver therapeutic proteins into muscle in diseases such as Duchenne muscular dystrophy [ 45 ].
References 1. The standardisation of terminology in lower urinary tract function: report from the standardisation sub-committee of the International Continence Society. Is the use of parasympathomimetics for treating an underactive urinary bladder evidence-based? BJU Int. Combination of a cholinergic drug and an alpha-blocker is more effective than monotherapy for the treatment of voiding difficulty in patients with underactive detrusor.
Int J Urol. The effect of age on the autonomic innervation of the urinary bladder. Br J Urol. Urothelial barrier deficits, suburothelial inflammation and altered sensory protein expression in detrusor underactivity. J Urol. Detrusor underactivity: clinical features and pathogenesis of an underdiagnosed geriatric condition.
J Am Geriatr Soc. Management of detrusor dysfunction in the elderly: changes in acetylcholine and adenosine triphosphate release during aging. It must also be noted that if DU and BOO co-exist, diagnosis can be difficult as both conditions impact on the PdetQmax, an essential component of diagnostic formulas. Abrams et al. CUR is classified as low pressure or high pressure 6. These patients typically have voiding symptoms of hesitancy, slow stream and sensation of incomplete emptying. Half of high pressure CUR patients develop upper tract dilatation and altered renal function.
The outcome of men with CUR has been reported. Bates et al. The authors concluded that complications are uncommon and patients can be conservatively managed but outpatient review is prudent. Ghalayini et al. They were reviewed at 3 and 6 months. However, neither of these studies distinguished between high pressure and low pressure CUR patients.
What is Neurogenic Bladder?
It is likely that most of the treatment benefit was seen in high pressure CUR patients. To answer this question, we must look at the natural history of untreated DU, then examine the short term and long term outcomes of TURP in these patients. Thomas et al. The mean age of the men was No identifiable causes were found for the AUR.
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Potts et al. They defined success as no future retention, need for catheterizations or surgery. All these parameters showed statistically significant improvement. A possible mechanism for short term symptomatic improvement in men with DU treated with TURP, is that the surgery reduces the bladder outlet resistance and allows easier abdominal straining and hence improved bladder emptying.
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The long term results in these men seem to show a reversal of symptoms back to pre-op baseline. Symptoms were unchanged from pre-TURP baseline. Urodynamic studies showed no change in detrusor contractility and there was still small but significant improvement in PdetQmax and BOOI bladder outlet obstruction index. This confirms that the benefit of TURP in reducing outlet resistance is maintained for a long time.
The detrusor contractility had not worsened, yet the symptoms had reverted back to baseline. A possible explanation is that the efficiency of abdominal straining worsens as these men age and the symptoms return over time. This data suggests that DU is not a contraindication for TURP; in fact most patients will get short term improvement in their symptoms likely due to the decrease in outlet resistance, but this improvement tends not to be sustained over a longer time. The surgical reduction of bladder capacity is an uncommonly performed procedure. Thorner et al. Three patients underwent synchronous bladder diverticulectomy and three underwent suprapubic prostatectomy in addition to cystoplasty.
The authors stated that the ideal patient was one who had a large bladder capacity but still retained some detrusor contractility on urodynamics, and had no urethral obstruction. An acquired bladder diverticulum is usually as a result of chronic BOO or neurogenic voiding dysfunction. As the diverticulum is lacking detrusor muscle, it may contribute to poor detrusor contraction, chronic retention of urine, recurrent UTI, haematuria, abdominal pain and is at risk of malignant transformation.
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However, most bladder diverticula are typically asymptomatic and found during cystoscopy investigating other lower urinary tract symptoms. If the diverticulum is considered a source of the symptom the patient should undergo video urodynamics. This will provide information about location, size, reflux, and emptying of the diverticulum upon voiding. In addition, upper tract imaging with ultrasound, should be performed to rule out hydronephrosis or ureteral obstruction. Asymptomatic patients may be monitored with urine cultures and endoscopic surveillance.
Recent advances in the understanding and management of underactive bladder
Surgical management of the bladder diverticula is only necessary when the patient is symptomatic or has a recurrent infection, stones, urinary obstruction and vesicoureteral reflux. The data reporting on the effect of diverticulectomy on chronic urinary retention is limited to small studies and case reports only 15 - Adot Zurbano et al.
They found that the duration of detrusor contraction was the only pre-operative parameter significantly altered by the presence of a bladder diverticulum.