Review of underactive bladder

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Journal of the Formosan Medical Association (2017) xx, 1e7

Available online at www.sciencedirect.com

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Review Article

Review of underactive bladder Yi-Huei Chang a, Justin Ji-Yuen Siu a, Po-Jen Hsiao a, Chao-Hsiang Chang a,b, Eric Chieh-Lung Chou a,b,* a b

Department of Urology, China Medical University Hospital, Taichung 40447, Taiwan School of Medicine, College of Chinese Medicine, China Medical University, Taichung 40402, Taiwan

Received 11 May 2017; received in revised form 29 August 2017; accepted 7 September 2017

Abstract In clinical practice, many patients cannot empty their bladders within an acceptable duration. Common complaints include weak urinary stream and incomplete emptying, which may affect quality of life. Bladder emptying requires sufficient detrusor contractile power, velocity, and durability. The urodynamic term for inadequate detrusor contraction is detrusor underactivity (DU). Although this definition was provided by the ICS, it may not be clinically practical. Analogous to the relationship between overactive bladder (OAB) and detrusor overactivity (DO), the symptom complex caused by DU is termed underactive bladder (UAB). Many conditions lead to UAB, such as advanced age, neurogenic bladder and BOO, but the definite pathophysiology directly leading to UAB is still being widely studied without a widely-accepted consensus. The preferred mainstream treatment for increased residual urine volume caused by UAB is intermittent catheterization, while pharmacotherapy is still disappointing after decades of development. There are no studies on surgical treatment for UAB with an acceptable level of evidence. We reviewed the recent literature on UAB and DU to provide a comprehensive discussion of the related presentation, etiology, diagnosis and management. Copyright ª 2017, Formosan Medical Association. Published by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/bync-nd/4.0/).

Definition Underactive bladder (UAB) as an entity has been gaining attention in recent years. UAB could be seen as a clinical complex, this could not be defined only by clinical symptoms and urodynamic study is the most important diagnostic tool.

* Corresponding author. 2 Yude Road, Taichung, 40447, Taiwan. Fax: þ886 4 22060619. E-mail address: [email protected] (E.C.-L. Chou).

Back in 2002, International Continence Society has already defined detrusor underactivity as a contraction of reduced strength and/or duration, resulting a failure to achieve complete bladder emptying within a normal time span, this definition is not always clinically practical.1 Recently, experts’ consensus had definition for underactive bladder: “a symptom complex suggestive of detrusor underactivity and is usually characterized by prolonged urination time with or without a sensation of incomplete bladder emptying, usually with hesitancy, reduced sensation on filling, and a slow stream”.2

https://doi.org/10.1016/j.jfma.2017.09.006 0929-6646/Copyright ª 2017, Formosan Medical Association. Published by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Please cite this article in press as: Chang Y-H, et al., Review of underactive bladder, Journal of the Formosan Medical Association (2017), https://doi.org/10.1016/j.jfma.2017.09.006

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Y.-H. Chang et al.

Abbreviation DU OAB DO UAB BOO LUTS DUA BCI Pdet Qmax Vdet

detrusor underactivity overactive bladder detrusor overactivity underactive bladder bladder outlet obstruction lower urinary tract symptoms Detrusor underactivity Bladder contractility index detrusor pressure maximum urinary flow rate detrusor contraction velocity

Prevalence Underactive bladder is an aging disorder, the incidence increased with age and this condition is usually concomitant with BOO and/or OAB. Because of inconsistency of definition, the incidence of UAB is variation. In Resnick et al.,3 patient younger than 50 years old had 9e28% incidence of detrusor underactivity and 48% in those over 70 years. In the largest clinical urodynamic series of 1179 patients older than 65 years of South Korea,4 46.5% of men and 72.6% of women were diagnosed with detrusor under activity and usually coexisted with BOO and/or OAB.

Clinical symptoms The clinical manifestations of UAB include straining to void, voiding difficulty with sensation of incomplete emptying, increased post-void residual urine volume and chronic urinary retention. Some patients with UAB may complain of infrequent voiding, decreased desire to void, or even overflow incontinence. If a patient presents with increased post-void residual urine volume, but complains of decreased voiding frequency instead of urinary frequency, the clinician should be wary of possible UAB. The main problem is overlapping of symptoms between UAB and BOO. These two situations share many symptoms such as straining, hesitancy, intermittency and weak stream, which also present in patients with UAB, and increase the difficulty in differentiating between pure UAB and concomitant UAB and BOO.4 Interestingly, when the severity of voiding LUTS increases, the occurrence of storage LUTS such as urgency, frequency and nocturia may also increase.5 Furthermore, patients with UAB-related chronic urinary retention may gradually develop complications such as overflow incontinence, nocturnal enuresis or infrequent voiding. Some patients may develop bladder urolithiasis, recurrent UTIs or even renal failure.1

Etiology The urinary bladder functions as a reservoir and pump. The detrusor underactive could be category to different site dysfunction, including pre-vesicle, vesicular, and post-

vesicle category. Pre-vesicle site are usually neurogenic, originating from the central neuron control, peripheral motor and sensory neurons and synapses.6 Vesicular site may arise from the detrusor muscle, interstitial tissue or diverticula.7 Post-vesicle site likes bladder outlet obstruction may cause decompensated bladder contractility.8 Chronic BOO may decrease the contractility of the detrusor muscle, but this phenomenon occurs more often in males. The prerequisite for smooth micturition are low bladder outlet resistance, good bladder contractility and intact reflex pathways. If any of these goes wrong, voiding dysfunction may occur. Bladder contractile dysfunction (including contractile strength, velocity and duration) causes annoying LUTS. Detrusor underactivity (DUA) is usually a progressive disease and some situation contributes mixed site dysfunction. Age itself is a marker for organ aging and may cause nerve control, detrusor degeneration and bladder outlet obstruction related situation. Diabetes mellitus is a systemic disease, and its end organ damage includes that of the bladder. Besides motor and sensory neuropathies, chronic elevated blood sugar levels and the presence of free radicals will induce collagen deposition in the detrusor muscle and extracellular matrix, leading to altered bladder function.9,10 Neural injury of disease is another cause of detrusor underactive, including cerebral stroke,11 Parkinson’s disease,12 multiple sclerosis13 or peripheral neuropathy. A minor proportion of DUA are iatrogenic, such as pelvic surgery related nerve injury14,15 or drug-related bladder contractile dysfunction.12 These situations are usually caused by specific events, and often presents with a definite time of onset of voiding dysfunction. In short, DUA may be classified into neurogenic, myogenic and mixed types. The specific cause of DUA should be determined, or the case may otherwise be classified as idiopathic.

Evaluation and diagnosis The initial evaluation of a patient complaining of UAB symptoms is identical to general LUTS evaluation, including taking a history of present illness (LUTS and bowel habit), past history (medical, surgery and trauma), medications (paying attention to any drugs that may exacerbate voiding symptoms, such as antimuscarinic agents, antihistamines or alpha-agonists). A detailed bladder diary of at least 3 days is highly recommended because it can provide invaluable information which may be hard to conceptualize through routine history taking.16 Physical examination should be comprehensive, and should at least include digital rectal examination (prostate palpation, anal tone and bulbocavernosus reflex) and neurological examination (identify dermatomes where sensory impairment may be present). Pelvic floor examination is also important in women, BOO related to high grade pelvic organ prolapse must be considered in the differential diagnosis of female patients with UAB. If neurological deficits are present, neurological consultation and MRI of the spine should be considered. First line tests include urinalysis and post-voiding residual urine volume. Uroflowmetry, pressure-flow studies,

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Underactive bladder cystometry and video-assisted urodynamic studies may be ordered for further investigations in pre-operative scenarios or for complicated patients. UAB and BOO may coexist with overlapping symptoms. If there is obvious voiding difficulty with evidence of BOO, treatment should be first directed towards relieving BOO. After initial treatment of BOO, the voiding function should be re-assessed. If improvement is suboptimal, UAB or other cause of BOO may be present. At this stage, urodynamic study or even cystoscopy is indicated. Urodynamic study may provide information on whether the patient has DSD, dysfunctional voiding or DU. Cystoscopy may reveal urethral stricture, bladder diverticulum or other bladder outlet abnormalities. Positive cystoscopic findings aforementioned are usually treatable. The only clinically available tool to assess UAB is invasive UDS, which may unmask DU, but there are no universally acceptable diagnostic criteria for DU.1 There are many ways to evaluate detrusor muscle function: - Bladder contractility index (BCI) Z Pdet@Qmax þ 5Qmax.17 - Schafer pressure/flow nomogram, which simultaneously evaluates detrusor function and BOO.18 - Watts factor, which evaluates the detrusor contractile strength and speed. - Bladder contractile speed and durability - Bladder sensation BCI is a simpler formula to quickly evaluate detrusor contractile function, and is clinically more practical. However, when BOO is present it cannot differentiate between BOO and DU. BCI >150 suggests detrusor overactivity. BCI 100e150 is considered normal, and BCI <100 suggests detrusor underactivity.17 Theoretically, the detrusor pressure (Pdet@Qmax) at the time of Qmax can be used to assess whether the patient has DU when voiding stops, the isovolumetric Pdet may represent bladder contractility.19 Some scholars propose that a patient should be diagnosed of DU during PFS if Bladder contractility index <100 (men) and Qmax 12 mL/s and Pdet@Qmax 10 cm H2O (women).4 We can use this simple method as a quick screening test for DU. Previous studies suggested that the evaluation of detrusor muscle function, albeit more complicated, could be used as a confirmatory test for DU. The Schafer pressure/flow nomogram is primarily used to differentiate between patients with BOO or genuine DU.18,20 The X-axis represents Pdet and the Y-axis represents Qmax. The line between specific points on the two axes represents urethral resistance. According to different levels of obstruction, the nomogram is classified into seven zones that represent seven grades of urinary obstruction. Grades 0-I suggest that the patient has no obstruction; grade II suggests mild or equivocal obstruction, grades IIIeVI suggests increasing severity of obstruction. The Schafer nomogram can more comprehensively delineate the clinical picture in regard to the patient, detrusor function and BOO. A point in the lower left corner signifies DU without BOO; while the lower middle area signifies BOO and DU. A point in the right lower corner can be interpreted

3 as BOO with compensatory detrusor contraction that results in overall lower Qmax. Watts factor is computed from a mathematical formula that assesses the work done per unit of surface area of the bladder.21 It is a complicated formula because it is corrected for the muscle power required for contraction without any change in length or without any load. The major parameters include Pdet and Vdet, i.e. the detrusor pressure and contractile velocity, respectively. Watts factor Z [(Pdetþ a) (Vdet þ b)  ab]/2p, a and b are constants (a Z 25 cm H20, b Z 6 mm/s) generated from previous studies. During voiding, these two parameters change, therefore WF changes as well. Some scholars suggest that WF > 7 W/m2 signifies DU.22 Table 1 compares Schafer nomogram, Watts factor and BCI as tools for diagnosing DU. Among these three tools, Schafer nomogram is the only one that evaluates BOO, but it does not include Vdet. Only WF includes Vdet. BCI is easier to use, but does not include Vdet and cannot evaluate for the presence of BOO. We can conclude that all the above methods have different strengths and drawbacks, and currently there is no perfect and simple evaluation method (Table 1).

Detrusor contraction speed and duration Although it is not widely discussed, it is logical to assume that detrusor contraction speed is related to DU.23 Studies have suggested that when detrusor contraction slows down or is not synchronized, detrusor contraction speed may decrease. This may be related to connexin 43 proteins, which is a specialized proteins expressed between the membranes of connected detrusor muscle and function as s propagation of electrical responses.24

Bladder sensation The assessment of bladder afferent nerve function is important in the evaluation of DU. It affects the initiation and maintenance of detrusor contraction. This is usually assessed by the “first sensation”, “first desire”, “strong desire” and “capacity” components of the UDS .. This is after all an invasive procedure that may make the patient uneasy and hence void “unnaturally”. Some studies advocate using intravesical electrodes to test bladder sensation. Despite being more quantitative and objective, it is unvalidated and invasive. Further research is required to provide more information on this concept.25

Table 1 The comparison of formula to measure detrusor function.

Schafer nomogram Watts factor BCI

Pdet

Qmax

Vdet

BOO

þ þ þ

þ þ

þ -

þ -

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Management Conservative management Conservative management includes behavior modification therapy. Patients with impaired bladder afferent nerves may use timed voiding to avoid bladder distention. Double voiding may also be used to relieve incomplete emptying leading to uncontrolled frequency. If DU presents, patients void with exerting manual pressure on the abdomen at the location of the bladder (Crede maneuver) may promote bladder emptying; however, vesicoureteral reflux of urine may occur, therefore only patients without BOO may be suitable candidates for this method. In case of dysfunctional voiding, because the urethro-vesicle reflex is impaired, DU may be present. Pelvic floor physiotherapy and biofeedback may be used to provide conditioning, although the success rate varies.26

Intermittent/continual catheterization If the post-voiding residual urine volume is significant, clean intermittent urethral catheterization should be considered. Intermittent urethral catheterization could be performed by himself or caregiver with sterilized and performed after voiding at regular intervals. In case when then patient cannot perform intermittent catheterization, suprapubic catheterization may be considered if continual catheterization is required.

Parasympathomimetics The human bladder has five types of muscarinic receptors. The most common type is M2, but the major receptor involved with detrusor contraction is M3. Parasympathomimetics directly stimulate muscarinic receptors or inhibit anticholinesterase to increase the acetylcholine concentration between the synapses, which increases bladder contraction. The commonly used bethanechol is a non-selective muscarinic agonist, but because it is not subtype specific, its effects are not limited to the bladder.27 The clinician may consider parasympathomimetics when the detrusor muscle and bladder sensation are both intact. If a patient has normal bladder sensation, meaning those who still complain of urgency or does not have infrequent voiding, the effects of bethanechol may be better. If the patient has infrequent voiding, the effects of drugs may be limited, and intermittent catheterization can be considered.28 Because of the adverse effects, such as gastrointestinal upset (polysialia, nausea, diarrhea), blurred vision, bronchospasm, and life-threatening cardio-inhibitory effects and unclear therapeutic benefits, most urological guidelines do not recommend parasympathomimetics as an answer to UAB.

a-Adrenoceptor antagonists Alpha blockers can decrease urethral muscle tone, effectively reducing UAB related to BOO.29 In a model using mice with lumbar canal stenosis, the combination of a1 antagonist and cholinesterase inhibitor

Y.-H. Chang et al. significantly reduced residual urine, but also reduced maximum cystometric capacity. Yamanishi et al., suggested a combination of a-blocker and muscarinic agents even in patients without BOO, and their study found that the combination therapy lead to improved IPSS, especially the voiding-related components.30 Furthermore, the flow rate improved and the post-void residual urine volume decreased. In the study of 119 patients, 36 had lumbar disease, 39 had peripheral neuropathy, and the remaining 44 patients had idiopathic DU. In the combination arm, voiding scores of female patients improved from 9.31  5.93 to 7.00  6.15 (P Z 0.0120). Voiding scores of males improved from 12.53  4.14 to 6.93  4.80 (P Z 0.0001). The parameters improved more obviously after therapy in the combination arm when compared to monotherapy arms of cholinergic or alpha-blockers.

Future prospects in pharmacotherapy In the future, super-selective muscarinic agonists may be developed to increase efficacy and decrease unwanted side effects. Alternative manipulation of muscarinic receptors, such as presynaptic M2-receptor antagonist or postsynaptic allosteric receptor enhancement is also being developed. Intravesical prostanoid administration may reduce postoperative urinary retention. Risk Ratio 3.07 (95% CI 1.22 to 7.72).31 Prostanoids such as PGE1 and PGE2 are signal transducers of the micturition reflex. PGE1 and PGE2 increases detrusor contraction and causes non-striated sphincter relaxation, therefore is also a promising direction for drug development.32 Compounds that enhance impaired bladder afferent neural function has drawn less attention, but this may be another promising direction.

Electrical stimulation More than three decades ago, anterior sacral root stimulation has been proven to improve voiding function in patients with completer spinal cord injury.33 Electrical stimulation is more intense and is usually used as a short-term treatment with quicker treatment response; electrical modulation is of a lower voltage and is usually applied over multiple sessions over a longer period of time with more gradual benefits. Electrical stimulation to the anterior sacral root may also affect the external striated sphincter and cause contraction. This unwanted effect may be countered by the difference in contractile duration of non-striated and striated muscle after stimulation, but some patients would inevitably demonstrate interrupted voiding. Intravesical electrotherapy was proposed by Katona et al.,34 A catheter tipped with an electrode was inserted into the bladder. The other end of the circuit was closed by an electrode placed on an area of skin with normal sensation. Electrostimulation was done for an hour daily for around 10e15 days. Animal experiments have proven that IVE works by activating mechanosensitive bladder afferent nerves.35 Continuous stimulation may normalize bladder sensation and motor pathways, thus improving voiding function. As

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Underactive bladder with other treatment modalities that act on neural transmission, the treatment effects of IVE may be reduced if there is complete bladder denervation or bladder fibrosis. IVE did not bring significant complications, except for a few cases of UTI. Sacral nerve modulation mainly targets patients with non-obstructive urinary retention and DUA.36 In patients with pelvic floor or sphincter dysfunction, when afferent signals of the urethral sphincter fail to transmit properly, bladder afferent signals may be inhibited at the level of the sacral spinal cord, which may lead to impaired bladder contractions. SNM may be applied to inhibit abnormal urethral afferents to regain bladder function.37

Botulinum toxin When DU originates from functional bladder outlet obstruction, botulinum toxin may be injected to the external sphincter to cause relaxation, and reduce bladder outlet resistance. The weakened detrusor may benefit greatly from reduced urethral resistance to produce a greater flow rate. Botulinum toxin is FDA-approved to be used for detrusor injections. However, currently there is inadequate evidence to support injections to the external sphincter.38,39 There is also no consensus of a standard dosage; therefore, despite the plethora of clinical studies, it is currently an off-label regimen. Further studies must be done before a conclusion can be drawn on the definite benefits of this treatment.

Surgery Bladder outlet surgery DU may be caused by anatomical BOO, or may present concomitantly with BOO. Whether relieving BOO surgically is beneficial to this type of patient has been a matter of debate. Advocates believe that after relieving BOO, detrusor rehabilitation may be attempted. The clinician must differentiate between patients complaining of voiding difficulty but do not have significant post-void residual urine volume, and those with significant RU that require catheterization. In patients with insignificant RU, the BOO is usually less significant even if present because of the lower detrusor pressure when compared to those that require catheterization. Thomas et al., 2004 proposed that in such cases bladder outlet surgery usually did not produce satisfactory results. His study was limited by the small number of subjects (22 men were treated with TURP to improve the voiding LUTS caused by DU).40 Prognostic factors for poor results after bladder outlet surgery include low Pdet, old age and significant RU.41,42 However, there are still some patients in the above subgroup that may void only after bladder outlet surgery. Such patients are usually younger; for patients who do not want to be catheterized, surgery may be attempted as a desperate measure. For female patients with BOO, most commonly urethral or bladder neck stricture, urethral sounding is an option. Successful long term outcome of transurethral incision of bladder neck for women with underactive bladder had

5 reported,43 especially higher vesicle pressure had better surgical outcomes. However, we should pay attention to incontinence and stricture problem after bladder neck incision in female patients.

Urinary diversion Urinary diversion with bowel segments is a relatively major operation for a functional problem. Methods include ileal conduit, continent pouch, or orthotropic neobladder. Most patients can accept intermittent catheterization, and it is also a safer and simpler option, therefore it is uncommon for a patient to undergo urinary diversion for the sole indication of DU. When a patient cannot perform intermittent catheterization, but is also unwilling to be catheterized, a continent pouch may answer the problem. A neobladder may be considered in patients with adequate fitness and renal function. Studies have shown that the contraction strength of a neobladder approaches that of the native bladder.44

Reconstructive surgery When a bladder diverticulum is large enough, a significant portion of the bladder capacity lacks contractile potential, which leads to chronic urinary retention. Partial cystectomy should be done to remove the diverticulum. Stenzl and colleagues (1998) proposed transferring a latissimus dorsi flap and wrapping it around the bladder, and then attaching it to the pelvic fascia and ligaments.45 The patient must learn to control the bladder by contracting the latissimus dorsi flap. After long term follow-up, of the 24 patients who originally relied of catheterization, 17 patients could void spontaneously with minor PVR, and their BCI remarkably increased to normal ranges. Perioperative complications, such as pelvic abscesses, wound infections and deep vein thrombosis were reported, yet no long-term complications occurred. However, scarce followup studies were found in the literature.

Conclusion An underactive bladder patient may concomitantly present with pre-vesicle and post-vesicle problems, so the clinician must identify the most likely origin of UAB. If a treatable problem is identified, treatment should be offered. Unfortunately, in clinical practice a definite origin of UAB may often be absent, or multiple problems may present together. The clinician should adopt multi-modality or even multi-disciplinary therapy to provide an individualized treatment plan to the patient.

Disclosure statement The authors declare no conflict of interest.

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Please cite this article in press as: Chang Y-H, et al., Review of underactive bladder, Journal of the Formosan Medical Association (2017), https://doi.org/10.1016/j.jfma.2017.09.006