Urge Incontinence (Overactive Bladder)

Introduction

Urge incontinence, also known as overactive bladder (OAB), results from a sudden involuntary contraction (overactivity) of the bladder detrusor muscles, creating a sudden and unstoppable need to urinate (urinary urgency), even though the bladder may contain only a small amount of urine.

According to the International Continence Society (ICS), OAB is defined as urinary urgency, usually with frequency and nocturia, in the absence of causative infection or pathological conditions.¹Hussain AN, Vincent MT, Khan NH, Cheung WW. Overactive Bladder – Treatment. Available at http://emedicine.medscape.com/article/459340-overview. Accessed on Nov 10, 2010.   Urinary frequency is defined as eight or more micturitions per day, and nocturia refers to waking up at night one or more times to pass urine.²Abrams P, Cardozo L. Fall M, et al. The standardization of terminology of lower urinary tract function: Report from the Standardization Sub-Committee of the International Continence Society. Neurourology and Urodynamics, 2002; 21(2):167-178.  

People can be afflicted by OAB at any age, though elderly people are more prone. However, it should not be considered a normal part of aging.³Nabili S. Overactive bladder. Available at http://www.medicinenet.com/overactive_bladder/article.htm. Accessed on Nov 10, 2010.  

Pathophysiology of OAB¹Hussain AN, Vincent MT, Khan NH, Cheung WW. Overactive Bladder – Treatment. Available at http://emedicine.medscape.com/article/459340-overview. Accessed on Nov 10, 2010.  

Functioning of a normal bladder requires a complex coordination of musculoskeletal, neurologic and psychological functions that govern the filling and voiding of the bladder contents. The main mechanism involved in continence is the synergic relaxation of detrusor muscles and contraction of bladder neck and pelvic floor muscles.

In bladder filling, sympathetic nerve fibers that originate from the T₁₁ to L₂ segments of the spinal cord cause contraction of the smooth-muscle fibers around the bladder neck and proximal urethra, enabling the bladder to fill. As the bladder fills, sensory stretch receptors in the bladder wall trigger a CNS response. The parasympathetic nervous system (PNS) causes contraction of the detrusor, and relaxation of the muscles of the pelvic floor and external sphincter. The PNS fibers, as well as those responsible for somatic (voluntary) control of micturition, originate from the S₂ to S₄ segment of the spinal cord in the sacral plexus. The somatic fibers innervate the external sphincter and are responsible for the voluntary control of continence in the face of a pressing desire to void. Fig. 1 illustrates the nerve supply of the bladder.

The normal adult bladder accommodates 300-600 mL of urine. When this amount reaches 400 mL, it triggers a CNS response. Cortical suppression of the PNS or voluntary contraction of the external sphincter can prevent micturition.

Any disruption in the integration of musculoskeletal and neurologic responses can lead to loss of control of normal bladder function and to urge incontinence. In addition, physiologic changes associated with aging, such as decreased bladder capacity and changes in muscle tone, further add to the development of OAB in the presence of precipitating factors. In postmenopausal women, many of these changes are related to estrogen deficiency. Perhaps the most important age-related change in bladder function that leads to incontinence is the increased number of involuntary bladder contractions (detrusor instability).

Etiology

OAB is a multifactorial disorder in both etiology and pathophysiology. Strictly speaking, no underlying condition or infection should be present. However, many different conditions can cause OAB symptoms. Depending on the etiology, these conditions are potentially treatable. Common etiologies of OAB symptoms are shown in Table 1.⁴Ellsworth PI, Brunton SA, Wein AJ, Rovner ES. Frequently asked questions in the evaluation and management of overactive bladder. J Fam Pract. 2009;58(10 Suppl):S1-11.  

Evaluation of OA B⁵Ellsworth P, Kirshenbaum E. Update on the Pharmacologic Management of Overactive Bladder: The Present and the Future. Urol Nurs. 2010;30(1):29-39.  

Initial evaluation of lower urinary tract symptoms suggestive of OAB should consist of a good history, thorough physical examination, urinalysis, and bladder diary (Table 2). The purpose of this evaluation is to rule out medical and non-medical etiologies for OAB, such as functional impairments, medication side-effects, urinary tract infections, bladder outlet obstruction, bladder tumors, or neurologic etiologies, such as stroke or multiple sclerosis. In most cases, this approach can enable a diagnosis of OAB to be made, facilitating early initiation of treatment.

Treatment⁶McDonagh MS, Selover D, Santa J, Lopez S. Drug Class Review on Agents for Overactive Bladder Final Report December 2005. Oregon Evidence-based Practice Center, Oregon Health & Science University. Available at http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=bladder. Accessed on Nov 10, 2010.  

Treatment of overactive bladder first requires a clear diagnosis of the type of incontinence associated with OAB. If multiple forms are present, it is important to determine which form is dominant. Most cases of OAB can be cured or managed using a combination of the currently available treatments, as listed below.

Surgical treatment

• Augmentation cystoplasty – bladder volume is increased by attaching a segment of the bowel

In general, the least invasive or dangerous therapeutic option should be tried first, which is typically behavioral therapy. If it fails to provide adequate relief, pharmacologic therapy can be added. Surgery is rarely required and is reserved for patients who are severely debilitated and who have an unstable bladder.

References

1. Hussain AN, Vincent MT, Khan NH, Cheung WW. Overactive Bladder – Treatment. Available at http://emedicine.medscape.com/article/459340-overview. Accessed on Nov 10, 2010.
2. Abrams P, Cardozo L. Fall M, et al. The standardization of terminology of lower urinary tract function: Report from the Standardization Sub-Committee of the International Continence Society. Neurourology and Urodynamics, 2002; 21(2):167-178.
3. Nabili S. Overactive bladder. Available at http://www.medicinenet.com/overactive_bladder/article.htm. Accessed on Nov 10, 2010.
4. Ellsworth PI, Brunton SA, Wein AJ, Rovner ES. Frequently asked questions in the evaluation and management of overactive bladder. J Fam Pract. 2009;58(10 Suppl):S1-11.
5. Ellsworth P, Kirshenbaum E. Update on the Pharmacologic Management of Overactive Bladder: The Present and the Future. Urol Nurs. 2010;30(1):29-39.
6. McDonagh MS, Selover D, Santa J, Lopez S. Drug Class Review on Agents for Overactive Bladder Final Report December 2005. Oregon Evidence-based Practice Center, Oregon Health & Science University. Available at http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=bladder. Accessed on Nov 10, 2010.