The standard treatment for overactive bladder starts with patient education and behavior therapies, followed by antimuscarinic agents. For patients with urgency urinary incontinence refractory to antimuscarinic therapy, currently both American Urological Association (AUA) and European Association of Urology (EAU) guidelines suggested that intravesical injection of botulinum toxin A should be offered. The mechanism of botulinum toxin A includes inhibition of vesicular release of neurotransmitters and the axonal expression of capsaicin and purinergic receptors in the suburothelium, as well as attenuation of central sensitization. Multiple randomized, placebo-controlled trials demonstrated that botulinum toxin A to be an effective treatment for patients with refractory idiopathic or neurogenic detrusor overactivity. The urinary incontinence episodes, maximum cystometric capacity, and maximum detrusor pressure were improved greater by botulinum toxin A compared to placebo. The adverse effects of botulinum toxin A, such as urinary retention and urinary tract infection, were primarily localized to the lower urinary tract. Therefore, botulinum toxin A offers an effective treatment option for patients with refractory overactive bladder.

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.

Overactive bladder (OAB) is defined as urgency, usually with frequency, nocturia, and incontinence. Patients with liver cirrhosis often present with urinary complaints. The possible reason for this is fluid redistribution, which may induce OAB resulting from portal hypertension and ascites. We conducted this study to investigate predictors of OAB in cirrhotic patients. A total of 164 patients with chronic viral hepatitis-related liver cirrhosis were enrolled and 158 (96.3%) completed the Overactive Bladder Symptoms Score (OABSS) questionnaire. Age, severity of liver cirrhosis, comorbidities, serum sodium level, use of diuretics, body mass index and renal function were also recorded. In the study cohort, the prevalence of OAB was 31.01% and the prevalence of urge incontinence (OAB wet) was 18.3%. Patients with an urgency score ≥2 in OABSS had a significantly lower platelet level (p = 0.025) regardless of the use of diuretics. In addition, 98 patients (62%) with nocturia and 29 patients (18%) with urge incontinence had significantly lower levels of serum albumin (p = 0.028 and 0.044, respectively). In conclusion, patients with liver cirrhosis have a high prevalence of overactive bladder. A low platelet and low serum albumin level in these patients may be predictors for overactive bladder. And longer PT-INR is also a possible biomarker for nocturia.