eMedicine Specialties > Urology > Neurogenic Bladder and Overactive Bladder

Overactive Bladder - Treatment

Author: Aneela Naureen Hussain, MD, FAAFM, Assistant Professor, Department of Family Medicine, State University of New York Downstate Medical Center; Consulting Staff, Department of Family Medicine, University Hospital of Brooklyn
Coauthor(s): Miriam T Vincent, MD, PhD, Professor and Chair, Department of Family Practice, State University of New York Downstate Medical Center; Nadia H Khan, MD, Clinical Assistant Instructor, Staff Physician, Department of Family Practice, SUNY- Downstate Medical Center; Wellman W Cheung, MD, FACS, Clinical Assistant Professor of Urology, Clinical Assistant Professor of Obstetrics and Gynecology, State University of New York Downstate Medical School
Contributor Information and Disclosures

Updated: Aug 18, 2009

Introduction

Background

Overactive bladder (OAB) is a condition caused by sudden involuntary contraction (overactivity) of the bladder detrusor muscles. According to the International Continence Society (ICS), OAB is characterized as urinary urgency, with or without urge incontinence, usually with frequency and nocturia, in the absence of causative infection or pathological conditions.

The term OAB has been adopted by the US Food and Drug Administration (FDA) to expand the number and types of patients eligible for clinical trials. OAB includes not only urge incontinence but also urgency, frequency, dysuria, and nocturia. Other terms used include detrusor instability and detrusor hyperreflexia.

Urge incontinence is characterized by a strong sudden need to urinate, immediately followed by bladder contraction, resulting in an involuntary loss of urine. Urge incontinence is one of the most common types of urinary incontinence.

The treatment of OAB is aimed at reducing the debilitating symptoms in order to improve the overall the quality of life in affected patients. Anticholinergic agents that target the muscarinic receptors in the bladder (antimuscarinic agents) are the treatment of choice, as they reduce the contractility of the detrusor muscle. However, the use of antimuscarinic drugs is limited by certain adverse effects, particularly dry mouth and constipation.

Various attempts have been made to improve the organ selectivity of these drugs to overcome the adverse effects. These include the development of new antimuscarinic agents with structural modifications and the use of innovative drug-delivery methods. The advancement in the drug-delivery systems extends to the long-term therapeutic efficacy, with improved tolerability and patient compliance; however, future prospective therapies are aimed at novel targets with novel mechanisms of action, including beta3-adrenoceptor agonists, K+ channel openers, 5-HT modulators, and botulinum toxin.¹ These prospective therapies are currently at different stages of clinical development.

Among other investigational therapies, neurokinin receptor antagonists, alpha-adrenoceptor antagonists, nerve growth factor inhibitors, gene therapy, and stem cell–based therapies are of considerable interest. The future development of new modalities in OAB treatment appears promising.

For additional information, see the eMedicine articles Overactive Bladder: Etiology, Diagnosis, and Impact and Overactive Bladder in Children.

Pathophysiology

A normal bladder operates through a complex coordination of musculoskeletal, neurologic, and psychological functions that allow filling and voiding of the bladder contents. The prime effector of 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 Th11 to L2 segments of the spinal cord, which innervate smooth-muscle fibers around the bladder neck and proximal urethra, cause these fibers to contract, allowing 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, while the muscles of the pelvic floor and external sphincter relax. The PNS fibers, as well as those responsible for somatic (voluntary) control of micturition (urination), 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.

The normal adult bladder accommodates 300-600 mL of urine; a CNS response is usually triggered when the volume reaches 400 mL. However, urination can be prevented by cortical suppression of the PNS or by voluntary contraction of the external sphincter.

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, favor the development of OAB when precipitating factors intervene. 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).

A preliminary diagnosis of OAB can be made based on history (see History), physical examination (see Physical), and a few simple office and laboratory tests (see Lab studies).

Frequency

United States

The US Department of Health and Human Services has reported that approximately 13 million people in the United States have OAB and other forms of incontinence. The National Overactive Bladder Evaluation (NOBLE) Program reported that the overall prevalence of OAB in the study participants was 16.5% (N=5204).²

International

The frequency data on OAB found in Europe are similar to that found in the United States.

Mortality/Morbidity

The symptoms of OAB include frequent urination, urinary urgency, and urge incontinence. OAB may cause significant social, psychological, occupational, domestic, physical, and sexual problems. These symptoms should not be considered a normal part of aging.

In 1995, the total economic cost of OAB in the United States was estimated at $26 billion. OAB has been shown to significantly impair quality of life,^3,4 increase depression scores, and reduce quality of sleep. OAB that involves urge incontinence is associated with the most severe impairment. Persons with OAB who have poor sleep quality report chronic fatigue and difficulty performing daily activities. An increased number of hip fractures due to falls in elderly persons have been attributed to OAB because of the strong nocturia component. Many such falls involve the individual tripping or losing balance while getting out of bed, resulting in injury. Individuals with OAB develop coping strategies to manage their problems (eg, modifying fluid intake, toilet mapping, reduced physical or social activity) and therefore experience an altered lifestyle that affects their quality of life.

Race

OAB affects millions of people worldwide, regardless of race.

Sex

The overall prevalence of OAB is similar among men (16%) and women (16.9%). However, OAB with urge incontinence is more prevalent in women then in men (7.6% and 2.6%, respectively). OAB in men is often related to obstruction; therefore, it may be important to differentiate between obstruction and irritative symptoms prior to the initiation of treatment.

Age

The prevalence of OAB increases with age. However, OAB should not be considered a normal part of aging. Twenty percent of the population aged 70 years or older report symptoms of OAB; 30% of those aged 75 years or older report symptoms.

Clinical

History

The history to evaluate urinary incontinence should be based on key questions. These questions are focused on urgency, nocturia (>3 times per night), frequency (>8 times per day), and urinary incontinence. If the patient answers affirmatively to the screening questions, a 24-hour bladder diary should be given to the patient to complete and reviewed during a subsequent visit. Sample questions can include the following:

• Do you ever leak urine when you have a strong urge on the way to the bathroom? How often?
• How frequently do you empty your bladder during the day?
• How many times do you get up to urinate after going to sleep? Is it the urge to urinate that wakes you?
• How many pads a day do you wear for protection?
• Does this problem inhibit any activity or prevent you from doing things you like to do?

Physical

A comprehensive physical examination can help to determine the nature, severity, and impact of the patient's symptoms.

• Abdominal examination: This is used to rule out diastasis recti, masses, ascites, and organomegaly, which can influence intra-abdominal pressure and urinary tract function. A palpable bladder may imply overflow incontinence or an obstructive problem.
• Pulmonary and cardiovascular evaluation: This may be indicated to assess control of cough or the need for medications such as diuretics.
• Neurological examination: This involves an assessment of the lumbosacral nerve roots and should include deep-tendon reflexes, lower-extremity strength, sharp/dull sensation, and the bulbocavernosus and clitoral sacral reflexes. Abnormal findings such as deep tendon hyperreflexia or an absence of the bulbocavernosus reflex should alert the physician to possible underlying neurologic lesions contributing to urinary incontinence.
• Pelvic examination
  • A pelvic examination is used to evaluate for inflammation, infection, and atrophy. Such conditions can increase afferent sensation, leading to urinary urgency, frequency, dysuria, and overactive bladder (OAB).
  • Because the urethra and trigone are estrogen-dependent tissues, estrogen deficiency can contribute to urinary incontinence and urinary dysfunction. The most common signs of inadequate estrogen levels include thinning and paleness of the vaginal epithelium, loss of rugae, disappearance of the labia minora, and presence of a urethral caruncle.
  • In females, the levator ani muscle function can be evaluated by asking the patient to tighten her vaginal muscles and to hold the contraction as long as possible. Normally, a woman can hold such a contraction for 5-10 seconds. Voluntary levator ani muscle contractions that are very weak or absent are an indication that biofeedback training sessions with a pelvic floor physical therapist may be necessary (see Further Outpatient Care).
  • The bimanual examination should also include a rectal examination to check anal sphincter tone and, for fecal impaction, the presence of occult blood or rectal lesions. In males, the rectal examination should also be focused on the prostate to rule out benign prostate hypertrophy (BPH).

Causes

OAB is primarily a neuromuscular problem in which the detrusor muscle contracts inappropriately. These contractions often occur regardless of the amount of urine in the bladder. OAB may result from any of the following etiologies:

• Neurologic injuries
  • Spinal cord injury
  • Stroke
• Neurologic diseases
  • Multiple sclerosis
  • Dementia
  • Parkinson disease
  • Medullary lesions
  • Diabetic neuropathy
• Nonneurogenic causes: Detrusor hyperactivity can also occur in the absence of a neurogenic etiology. Contractions can be spontaneous or induced by rapid filling of the bladder, postural changes, or even walking or coughing. Because these causes are nonneurogenic in nature, the pressing need to urinate can be contained for a few minutes from when it is first sensed. Nonneurogenic origins of detrusor hyperactivity include local genitourinary conditions such as infection, bladder cancer, bladder stones, bladder inflammation, or bladder outlet obstruction.
• Medications: Diuretics can cause symptoms of urge incontinence because of increased bladder filling, stimulating the detrusor. Bethanecol can also cause urge incontinence through its stimulation of bladder smooth-muscle contraction.
• Idiopathic: A specific cause cannot be identified in only rare cases.
• Cardiologic: Heart failure or peripheral venous and vascular disease can also contribute to OAB. During the day, such individuals have excess fluid collect in dependent positions (feet and ankles). When they recline to go to sleep, much of this fluid becomes mobilized and increases renal output, thereby increasing urine output. Many of these patients describe increased nocturia that manifests as OAB.

• Search for CME/CE on This Topic »

• Overactive Bladder and Continence Guidelines: Implementation, Inaction or Frustration?