Voiding dysfunction due to detrusor underactivity: an overview

Abstract

Detrusor underactivity (DUA) is defined as a voiding contraction of reduced strength and/or duration, which prolongs urination and/or prevents complete emptying of the bladder within a 'normal' period of time. This issue is associated with voiding and postmicturition urinary symptoms, and can predispose to urinary infections and acute urinary retention. The aetiology of DUA is influenced by multiple factors, including ageing, bladder outlet obstruction, neurological disease, and autonomic denervation. The true prevalence of this condition remains unknown, as most data come from referral populations. Urodynamic testing is used to diagnose the condition, either by assessing the relationship between bladder pressures and urinary flow, or by interrupting voiding to measure detrusor pressure change under isovolumetric conditions. Current treatments for DUA have poor efficacy and tolerability, and often fail to improve quality of life; muscarinic receptor agonists, in particular, have limited efficacy and frequent adverse effects. Bladder emptying might be achieved through Valsalva straining, and intermittent or indwelling catheterization, although sacral nerve stimulation can reduce dependency on catheterization. Novel stem-cell-based therapies have been attempted; however, new drugs that increase contractility are currently largely conceptual, and the complex pathophysiology of DUA, difficulty achieving organ specificity of treatment, the limited availability of animal models, and the subjective nature of current outcome measures must be addressed to facilitate the development of such agents.

Underactive bladder in women

“…Therefore, a significant minority of women may have arrived at detrusor underactivity or clinical UAB following a period of prolonged BOO or may be chronic valsalva voiders in whom BOO (e.g., Fowler's syndrome, cystocele, and iatrogenic) represents the primary disorder for impaired emptying [19,21–23]. This clinical scenario can undoubtedly present a diagnostic and therapeutic dilemma.…”

“…To summarize, no gold standard for measuring detrusor underactivity exists, as existing diagnostic methods and indices remain limited by: complexity (e.g., Watts factor), impracticality or patient discomfort (e.g., occlusion testing), inability to account for presence of both detrusor underactivity and BOO and/or relative lack of applicability to women (e.g., BOO index), or lack of consensus on normal values (e.g., P det at Q max and Q max , voiding efficiency) [7 ■ ,21]. However, all of these measures may be more relevant to research than clinical practice, where numbers matter less than overall clinical impression.…”

Enhanced production of nitric oxide may contribute to the induction of detrusor underactivity in sucrose fed rats

“…Boone and Munoz daily self-catheterization [1,4]. Different transmitters released from urothelial cells and bladder nerves activate either relaxation or contraction pathways for proper urination [5].…”

“…For instance, detrusor overactivity, bladder outlet obstruction or painful bladder syndrome usually show alterations in the normal levels for ATP, nerve growth factor or NO [7][8][9][10]. Although DU can be observed in disorders where either the efferent or the afferent branches of the micturition reflex have been impaired [11], other potential changes in sensory transmitters are poorly understood [2].…”

“…The quality of life for patients suffering lower urinary tract symptoms (LUTS) is decreased by either overactivity or bladder underactivity (UAB), where the latter is a less understood disorder [1], besides detrusor underactivity (DU) remaining a well-defined problem of cystometric voiding performance [2]. Independently of the bladder dysfunction, the micturition reflex involves the coordinated activity of afferent and efferent neural pathways to induce relaxation of the urethral sphincter and simultaneous contraction of the detrusor to expel urine from the bladder [3].…”