Definition and symptoms of underactive bladder.

Underactive bladder (UAB) is a symptom syndrome reflecting the urodynamic observation of detrusor underactivity (DU), a voiding contraction of reduced strength and/or duration, leading to prolonged or incomplete bladder emptying. An International Continence Society Working Group has described UAB as characterised by a slow urinary stream, hesitancy and straining to void, with or without a feeling of incomplete bladder emptying and dribbling, often with storage symptoms. Since DU often coexists with bladder outlet obstruction, or storage dysfunction (detrusor overactivity or incontinence), the exact contribution of the DU to the presenting complaints can be difficult to establish. The presence of voiding and post voiding lower urinary tract symptoms (LUTS) is implicitly expected in UAB, but a reduced sensation of fullness is reported by some patients, and storage LUTS are also an important factor in many affected patients. These may result from a postvoid residual, but often they do not. The storage LUTS are often the key driver in leading the patient to seek healthcare input. Nocturia is particularly common and bothersome, but what the role of DU is in all the range of influences on nocturia has not been established. Qualitative research has established a broad impact on everyday life as a result of these symptoms. In general, people appear to manage the voiding LUTS relatively well, but the storage LUTS may be problematic.

Current pharmacological and surgical treatment of underactive bladder.

Generally accepted guidelines are not yet available on the management of underactive bladder (UAB). Although the natural history of UAB is still not fully understood, observation may be an acceptable management option in patients with tolerable lower urinary tract symptoms and little risk of upper urinary tract damage. If needed, scheduled and double voiding may be recommended as an effective and safe add-on therapy. Parasympathomimetics have been widely used for the management of UAB, but the evidence does not support clinical benefit. The efficacy of alpha-blockers has also not yet been clearly demonstrated. However, selective alpha-blockers may help to enhance voiding efficiency and to decrease possible upper tract damage. Sacral neuromodulation is a surgical option for nonobstructive UAB approved by the Food and Drug Administration. However, the response rate of test stimulation is not high and the efficacy of permanent implants does not always coincide with that of test stimulation. Although surgery to reduce outlet resistance may be a viable option in UAB with presumed obstruction, surgery seems to have little role in those without obstruction. Latissimus dorsi detrusor myoplasty has shown promising results in restoring voluntary voiding in selected patients. The procedure requires a multidisciplinary team approach of urologists and plastic reconstructive experts. In summary, current treatments of UAB remain unsatisfactory. The multifactorial nature of UAB pathogenesis complicates the appropriate management for each patient. Future research to establish a more clinically relevant definition of UAB will be required to open new era of UAB management.