The underappreciated underactive bladder
Review Article

The underappreciated underactive bladder

Basil Razi1,2 ORCID logo, Kevin Zhuo1,2, Dane Cole-Clark2,3, Amanda Chung1,2,4,5,6,7

1Department of Urology, Royal North Shore Hospital, St Leonards, NSW, Australia; 2North Shore Urology Research Group (NSURG), St Leonards, NSW, Australia; 3Department of Urology, John Hunter Hospital, New Lambton Heights, NSW, Australia; 4Department of Urology, North Shore Private Hospital, St Leonards, NSW, Australia; 5Department of Urology, Sydney Adventist Hospital, Wahroonga, NSW, Australia; 6Department of Urology, Macquarie University Hospital, Macquarie Park, NSW, Australia; 7Department of Urology, Northern Beaches Hospital, Frenchs Forest, NSW, Australia

Contributions: (I) Conception and design: All authors; (II) Administrative support: A Chung; (III) Provision of study materials or patients: A Chung; (IV) Collection and assembly of data: None; (V) Data analysis and interpretation: None; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

Correspondence to: Basil Razi, B MedSci, B Sci (Hons), MD. Department of Urology, Royal North Shore Hospital, Reserve Road, St Leonards, 2065, NSW, Australia. Email: basil@basilrazi.anonaddy.me.

Abstract: Slow urinary flow is a common lower urinary tract symptom (LUTS) that frequently prompts men to consult their primary care physician. While bladder outlet obstruction (BOO) is well recognised, underactive bladder (UAB) remains underappreciate despite its significant impact on quality of life. This review highlights the pathophysiology, clinical features, and diagnostic challenges and approach to UAB in men. Improving recognition of UAB as a distinct condition separate from other LUTS aetiologies, it can facilitate earlier diagnosis and management. Slow urinary flow is highly prevalent, particularly in an ageing population. UAB is characterised by impaired detrusor muscle activity, leading to slow urinary flow, hesitancy, straining and incomplete bladder emptying. The overlap in symptoms with BOO often leads to misdiagnosis, delaying appropriate intervention. UAB has multiple underlying causes including, neurogenic, myogenic, iatrogenic and idiopathic factors. Diagnosis is further complicated by the limited availability of urodynamic studies, the gold standard for assessing detrusor underactivity. Current management options remain limited with no definitive treatments. Current strategies focus on behavioural modifications, pelvic floor exercises, timed voiding, sacral neuromodulation and intermittent catheterisation. Increased awareness of UAB among primary care physicians and urologists is essential for timely diagnosis and intervention. Recognition of UAB as a distinct clinical entity will lead to a reduction in potential complications and significant improvement in the quality of life of affected men.

Keywords: Dysfunctional voiding; lower urinary tract symptoms (LUTS); men; prostatomegaly; urethral stricture


Submitted Jan 22, 2025. Accepted for publication Feb 27, 2025. Published online Mar 26, 2025.

doi: 10.21037/tau-2025-61


Introduction

Lower urinary tract symptoms (LUTS) are highly prevalent among Australian men, particularly in the ageing population, affecting approximately 50% in men over 65 years old and 70% in men over 80 years old (1,2). Slow urinary flow, a common symptom of LUTS, significantly impact on quality of life and frequently prompts visits to their primary care physicians. While bladder outlet obstruction (BOO) is a well-recognised cause, underactive bladder (UAB) remains underappreciated.

UAB is a poorly understood and researched area. UAB is characterised by impaired detrusor muscle contractility and presents with symptoms such as slow stream, hesitancy, intermittency and incomplete emptying. The International Continence Society defines UAB as “a slow urinary stream, hesitancy, and straining to void with or without the feeling of incomplete bladder emptying and sometimes with storage symptoms” (3).

Detrusor underactivity (DU) is a urodynamic diagnosis (4) that can be a feature of UAB clinical syndrome. Urodynamic studies (UDS) is an invasive investigation to assess bladder function by measuring pressures (using sensors in the bladder and rectum) and uroflowmetry, which can help differentiate between DU and BOO. DU is defined as a weak or absent detrusor contraction with a slow urine flow rate resulting in incomplete bladder or prolonged emptying. BOO on the other hand is a slow urine flow rate and/or incomplete emptying in the presence of normal detrusor contractions (4,5). Despite this, DU lacks clear diagnostic criteria and unfortunately UDS is costly and not widely available, limiting its routine use. As there is no universally accepted definition of UAB, it hinders epidemiological studies, limiting the understanding of its incidence, prevalence and risk factors. Symptom overlap between UAB/DU and BOO further complicates clinical differentiation.

This article aims to provide primary care physicians and urologists with practical insights into UAB’s pathophysiology, clinical features, and diagnostic approach. Recognising UAB as a distinct cause of LUTS can enable more accurate diagnoses and improve patient outcomes.


Epidemiology

LUTS is a major global health issue with a significant economic burden, with an estimated $1.9 billion cost for just the treatment of men with LUTS (6). There have been no focused epidemiological studies to explore the contribution of UAB/DU to the development of LUTS. Early initial American population studies demonstrated a significant correlation between frequency of UAB symptoms and reported bladder concerns, catheterisation and urology visits (7). Osman et al.’s systematic review demonstrated DU rates ranging from 9–28% in men aged 18–50 years old, increasing to 48% above 70 years old (4,8). Furthermore, Singh et al.’s systematic review found a pooled prevalence of UDS proven DU in 24% in men aged 18–50 years old (9). The increase in prevalence with age reflects the age-related impairment in detrusor muscle contractility.


Clinical features

UAB lacks pathognomonic symptoms and shares significant overlap with other causes of LUTS. While primarily a voiding dysfunction, UAB may also present with storage symptoms such as urgency and frequency, often secondary to large post-void residual (PVR) volumes. Common voiding symptoms include a slow or intermittent flow, hesitancy, straining, and incomplete emptying. Chronic retention can lead to overflow incontinence (4,8).

A large cohort study comparing UAB and BOO found that UAB patients had higher rates of stress incontinence, enuresis, reduced sensation, straining, prior BOO surgeries, urinary retention, and urinary tract infections (UTIs) (10). Symptom patterns can vary with bladder sensation, patients with poor sensation often report infrequent voiding and reduced urgency, while those with preserved sensation experience frequency and urgency.


Aetiology

Voiding is a coordinated process of the bladder and bladder outlet which are controlled by a complex nervous system. UAB can arise from abnormalities affecting any part of this network which are categorised as neurogenic, myogenic, idiopathic, iatrogenic, but patients could also have more than one contributing cause (Table 1) (11).

Table 1

Aetiology of underactive bladder

Aetiology Examples
Idiopathic Ageing/physiological decline
Iatrogenic Medications, pelvic surgery, radiotherapy
Neurogenic Cerebrovascular accidents, Charcot-Marie-Tooth disease, diabetes mellitus, Friedreich’s ataxia, Guillain-Barré syndrome, Parkinson’s disease, multiple sclerosis, multiple system atrophy, spinal cord injury, spinocerebellar ataxia, traumatic brain injury
Myogenic Bladder outlet obstruction, diabetes

Neurogenic UAB occurs due to injury or disease of the micturition reflex—affecting afferent or efferent nerves, the spinal cord or the brain. Common aetiologies include cerebrovascular accidents, spinal cord injury, multiple sclerosis, Parkinson’s disease and diabetes. Urinary retention was found in 47% of stroke patients likely secondary to detrusor areflexia (12). Iatrogenic injury to pelvic nerves, spinal cord/nerve roots will also result in DU. This has been demonstrated in animal models where nerve injury caused increase PVR and reduced voiding efficiency (13).

Myogenic UAB relates to detrusor muscle cell dysfunction and structural extracellular matrix changes. Patients with UAB/DU often exhibit higher amount of abnormal detrusor cell ultrastructure (14,15). Chronic ischemia, diabetes mellitus and BOO are well-recognised causes. Elevated PVR increases the intravesicular pressure leading to detrusor hypertrophy and hyperplasia. Chronic retention will result in an oxidative stress, inflammation and ischaemia causing fibrosis and extracellular matrix remodelling, impairing the bladder’s ability to generate sufficient pressure for emptying (16).

Diabetes has been implicated in the development of UAB (and LUTS) through both neurogenic and myogenic pathways. Poorly controlled diabetes results in autonomic neuropathy, down regulation of proteins essential for smooth muscle contraction, bladder fibrosis and apoptosis secondary to oxidative stress, all resulting in eventual DU (11,12).

Idiopathic causes of UAB are poorly understood but may result from ageing or metabolic effects on the lower urinary tract (11). Age-related changes include detrusor ultrastructure changes (15), reduced bladder sensation, impaired emptying, and elevated PVR (17). However, it is important to note, not every elderly person will develop UAB, suggesting the presence of other undiscovered underlying mechanisms. Additionally, there are younger patients who suffer from UAB/DU without any evidence of neurological disorder or BOO (11).


Diagnosis

The evaluation of UAB requires a thorough assessment of the patient’s LUTS. Validated symptom questionnaires, such as the International Prostate Symptom Score (18) or the International Consultation on Incontinence Questionnaire for Male LUTS (ICIQ-MLUTS) (19), provide an excellent baseline for symptoms and facilitate post-treatment comparisons, rather than differentiating between diagnoses. Additionally, a detailed history focusing on potential causes (Table 1), other co-morbidities, medications, lifestyle and psychosocial factors is essential.

Bladder diaries with frequency/volume chart are underutilised but provides valuable insight into the patient’s voiding patterns (20). Physical examination should focus on the suprapubic region, external genitalia and perineum to exclude cancers, structural causes or infections. Bladder PVR scans and uroflowmetry should supplement the physical examination. A normal PVR is generally considered less than 100 mL, while greater than 300 mL is elevated (21). However, PVR values should be interpreted in the clinical context. Routine investigations should include urinalysis and urine microscopy, culture, and sensitivity and common blood tests to assess renal function. Prostate specific antigen testing should only be considered when prostate cancer is a concern and with appropriate counselling.

Uroflowmetry offers valuable information into urinary flow and can be readily performed in a clinic or consultation rooms. The flowmeter calculates and graphs the voiding phase from which the voiding volume and total time, maximal flow rate (Qmax) as time to reach Qmax can be ascertained. A normal Qmax is considered to be >15 mL/s in males and >20 mL/s in females (22). Accurate readings require a voided volume of at least 100 mL.

UDS is the gold standard for diagnosing DU and only method to assess the contractility of the detrusor (Figure 1). Unfortunately, there is no standardisation for the diagnosis criteria for DU. There are various validated indexes which can be determined as part of UDS, including bladder contractility index (BCI, Pdet@Qmax + 5Qmax), BOO index (BOOI, Pdet@Qmax − 2Qmax), bladder voiding efficiency (BVE, voided volume/bladder capacity) and projected isovolumetric pressure (11). A BCI <100 with no evidence of BOO (i.e., low BOOI) and low flow would be indicative of DU. It is important to note these indices are only validated in men (23). Urodynamics is thus crucial to distinguish UAB/DU from BOO.

Figure 1 Example of a urodynamics study demonstrating underactive bladder. The patient was filled to a capacity of 480 mL during which there was normal bladder compliance and no evidence of detrusor overactivity. During the voiding phase the patient voided 341 mL, with a pDet of 30 cmH2O at a Qmax and a Qmax of 9.9 mL/s. The bladder contractility index is 80, with no evidence of bladder outlet obstruction.

Management

Currently there are no definitive treatment to cure UAB or significantly improve quality of life (Figure 2). The watchful waiting approach involves regular screening of upper tracts, PVR and renal function. Conservative treatment options include deprescription of parasympathomimetic and anticholinergic medications, behavioural modifications such as adjustment to medication/diuretic and fluid intake schedules. Cholinergic agonists, such as bethanechol, have been used for urinary retention, however the American Urological Association (AUA) does not recommend its use due to its significant side effect profile and marginal improvement in PVR (21). Techniques such as pelvic floor relaxation and double voiding can be beneficial, other techniques include triggered reflex voiding such as Crede or Valsalva manoeuvres. Triggered voiding techniques may potentially contribute to vesico-ureteric reflex and increased upper tract pressures. However, there is no strong evidence supporting their effectiveness or demonstrating harm (4).

Figure 2 Algorithm for evaluation of male LUTS with a focus on UAB. BOO, bladder outlet obstruction; BCI, bladder contractility index; BOOI, bladder outlet obstruction index; CISC, clean intermittent self-catheterisation; EUC, electrolytes, urea & creatinine; IDC, indwelling urethral catheter; LUTS, lower urinary tract symptoms; PVR, post void residual; SPC, suprapubic catheter; UAB, underactive bladder; US, ultrasound.

Pharmacotherapy for UAB is an evolving area with several proposed treatments currently under investigation. Parasympathomimetic drugs such as ASP8302 (positive allosteric modulator of the muscarinic M3 receptor) (24) and Acotiamide (selective inhibitor of acetylcholinesterase) (25) have shown potential in early clinical trials. These medications have been found to improve urinary flow rate, bladder contractility and reduce PVR. TAC-302, a novel drug which promotes neuronal growth has demonstrated an increase BCI and BVE in both men and women (26).

Sacral neuromodulation is an established treatment for either nonobstructive urinary retention and UAB with a reported success rate of approximately 80% (11,27-29). A tined lead is placed in the S3 foramen stimulating S3 nerve root, thereby modulating the afferent and efferent signals of the bladder (30,31). Other methods of electrical stimulation techniques include percutaneous tibial nerve stimulation and experimental intravesical electrical stimulation, however these are not included in either the EAU or AUA guidelines (11).

Patients who are unable to completely or safely empty their bladder should be taught intermittent self-catheterisation, typically recommended 4–6 times a day. Whilst effective, it does carry risks, including potential for UTIs, strictures, haematuria and false passages. Alternatively some patients (e.g., frail, high risk anaesthetic or comorbid patients) may be better suited to long term urethral or suprapubic catheterisation (32), suprapubic are preferred due to risk of traumatic urethral erosion.


Conclusions

Recognising UAB is challenging due to symptom overlap with other LUTS aetiologies. It should be considered in older patients or those with a history of neurological conditions, diabetes, or chronic retention. Referral to a urologist is warranted for patients with recurrent UTIs, elevated PVR, or persistent symptoms despite initial interventions, including pharmacological treatments or BOO surgery. As a frequently underdiagnosed condition, UAB has a substantial impact on men’s quality of life, highlighting the importance of timely diagnosis and management.


Acknowledgments

None.


Footnote

Peer Review File: Available at https://tau.amegroups.com/article/view/10.21037/tau-2025-61/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tau.amegroups.com/article/view/10.21037/tau-2025-61/coif). A.C. reports proctor for artificial urinary sphincter, male sling, inflatable penile prosthesis (IPP) from Boston Scientific; proctor for inflatable penile prosthesis (IPP) from Coloplast; support from Medtronic to attend advanced SNM course; as an advisory board member for Coloplast. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. Informed consent was obtained from the patients to include their urodynamic result.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.


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Cite this article as: Razi B, Zhuo K, Cole-Clark D, Chung A. The underappreciated underactive bladder. Transl Androl Urol 2025;14(3):841-847. doi: 10.21037/tau-2025-61

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