Overactive Bladder Syndrome

This article is currently under review and may not be up to date. Please come back soon to see the finished work! (9/08/2021)

Original Editor - Laura Ritchie, posting on behalf of Julia Wiebe, MPT Class of 2022 at Western University, project for PT9581.

Top Contributors - Laura Ritchie

Introduction[edit | edit source]

Overactive bladder (OAB) has been defined by the International Continence Society (ICS) as “urinary urgency, usually accompanied by frequency and nocturia, with or without urgency urinary incontinence (UUI), in the absence of a urinary tract infection (UTI) or other obvious pathology.” Urgency is a hallmark characteristic of OAB and involves the sudden, compelling desire to urinate, which is often difficult to defer.[1] Typically, OAB is not considered life threatening; however, the array of associated symptoms can negatively impact one’s quality of life, but also represent a significant burden to the public health system.[2]

Relevant Anatomy and Physiology[edit | edit source]

The pelvic floor musculature (PFM) acts as a hammock to support the pelvic viscera, which includes the bladder, rectum, and reproductive organs. Within this musculature are openings for the urethra, vagina and rectum. Normally the PFM are contracted to tighten these passages but relax when the bladder and rectum are full to release urine or faeces.

The bladder is the main organ involved in micturition (i.e. the process of urination). While the mechanism behind micturition involves a complex interplay between the urinary tract and nervous system, there are two main phases to micturition; 1) urine storage and 2) voiding, with the bladder and PFM acting in an antagonist relationship to control this process. During storage, the bladder muscle is relaxed while the urinary sphincters are contracted. Conversely, when the bladder is full, the bladder muscle contracts while the urinary sphincter is relaxed so urine can be expelled from the body. However, in OAB, the reflex that controls these muscles is disrupted causing the bladder muscles to contract involuntarily, even when the bladder is not full. Consequently, this results in a false sense to void and/or loss of voluntary control of urination (urinary incontinence).

Etiology and Pathophysiology[edit | edit source]

The etiology behind OAB is not fully understood and still under investigation. However, research into understanding the pathogenesis of OAB is limited by the fact that it is a symptom-based diagnosis.[3] As such there are three main hypotheses that have been proposed. However, micturition is a complex mechanism therefore it is likely that the pathophysiology behind OAB is multi-factorial, involving a combination of each hypothesis.

  1. Urotheliogenic theory suggests that urgency is initiated by abnormal activity or signaling in the bladder urothelium.
  1. Myogenic theory suggests that muscarinic receptors within the detrusor become more sensitive to cholinergic stimulation, which leads to increased spontaneous activity.
  1. Neurogenic theory suggests that there is damage/disruption to the central inhibitory pathways and/or sensitization of peripheral nerves within the detrusor that trigger the micturition reflex.

Epidemiology[edit | edit source]

OAB can affect both men and women, with prevalence increasing with age.[4] Estimates of OAB prevalence and social burden vary greatly. However, it is important to note that there is a disparity between those reported to be affected with OAB and those who actually seek and receive treatment. The reasons for this so-called “iceberg phenomenon” have been reported as either the patient did not think it was important enough, they were never asked about it by their healthcare provider, believed that OAB symptoms were normal and something they just had to live with, were too embarrassed or reluctant to discuss it, or they were unaware it could be dealt with. Regardless of these factors, the driving force for many to seek treatment was due to increased symptom severity or bother.[2]

Clinical Presentation/Symptoms[5][edit | edit source]

While OAB is common, especially in older adults, it is not considered a normal part of aging.  Common symptoms associated with OAB may include:

  • The sudden urge to urinate that is difficult to control
  • Leaking or unintentional loss of urine, sometimes immediately after an urgent need to urinate (urgency incontinence)
  • Frequent urination, usually eight or more times in 24 hours
  • Waking up more than two times in the night to urinate (nocturia)

However, it should be noted that OAB cannot be diagnosed by these symptoms alone because these symptoms can occur in many other disorders.[6] A thorough workup should therefore be conducted that includes the patient’s voiding history, a medical evaluation, physical exam and the appropriate tests to rule out urinary tract infections, neurological conditions or other pathologies.[7] A bladder diary may also be recommended to help understand the nature and severity of the condition.[8]

Management and Treatment[edit | edit source]

Conservative treatment is recommended by the ICS as the first line treatment for OAB symptoms.[1] Conservative treatment is tailored to the individual and their symptom characteristics but often consists of lifestyle modifications, bladder training and pelvic floor muscle training. A combination of conservative treatments has been found to be most effective. Oral medications are considered second-line treatment. However, improved outcomes have been observed when combined with conservative options.[9] When conservative options have failed, a referral to a urologist or urogynecologist with specialization in UI is necessary for consideration of surgical treatment.[10]

First-line Treatment: Conservative Options[10][edit | edit source]

  • Lifestyle changes: dietary modifications (e.g. limiting fluid intake, reducing/eliminating consumption of caffeine, carbonated beverages, and alcohol, decreasing fluid intake before bedtime), weight loss
  • Bladder training: modifying voiding habits by incrementally delaying urination for longer periods
  • Pelvic floor muscle training (PFMT): exercises taught by a physical therapist that help strengthen the pelvic floor muscles. May enhance the inhibitory effect of the pelvic floor muscle contractions on the detrusor.

Second-line treatment: Oral medications[edit | edit source]

  • Antimuscarinics: These are the mainstay pharmacological treatment for OAB. However, they are frequently discontinued due to bothersome side-effects. Mechanism of action involves blocking the muscarinic receptors on the detrusor muscle, which are responsible for bladder contraction, thereby decreasing its ability to contract. This class of drugs work mainly during the storage phase.[10] [11]
    • Common antimuscarinics: oxybutynin, tolterodine, darifenacin, fesoterodine, trospium
  • Beta-3 adrenoreceptor agonists (e.g. mirabegron): Relatively newer class of drugs to treat OAB. Mechanism of action works by relaxing the bladder detrusor muscle. Fewer side-effects compared to antimuscarinics. However, further clinical studies are required to assess long term effectiveness and patient tolerance.[10]

Third-line Treatment: Surgical Options[10][edit | edit source]

  • Botox: Recommended for patients with refractory OAB or for those where oral medications are contraindicated or intolerable. Procedure involves Botox being injected into the detrusor muscle. Involves risk of urinary retention leading to potential need for catheterization
  • Sacral neuromodulation: Only recommended for those with refractory UUI, severe refractory OAB symptoms or those unwilling to risk the complications associated with Botox (i.e. urinary retention leading to potential need for catheterization). Procedure involves insertion of an electrode into the S3 foramen which stimulates the nerves to the bladder and perineum. Adverse effects include pain, lead migration infection and electric shock.
  • Posterior tibial nerve stimulation: Procedure involves the insertion of a small needle into the posterior tibial nerve which modulates the S2-S4 nerves of the sacral plexus. Only recommended for those who are not suitable candidates for Botox or sacral neuromodulation.

References[edit | edit source]

  1. 1.0 1.1 Haylen BT, De Ridder D, Freeman RM, Swift SE, Berghmans B, Lee J, et al. An International Urogynecological Association / International Continence Society joint report on the terminology for female pelvic floor dysfunction. Neurourol Urodyn. 2010;29:4–20.
  2. 2.0 2.1 Reynolds WS, Fowke J, Dmochowski R. The burden of overactive bladder on US public health. Curr Bladder Dysfunct Rep. 2016;11(1):8-13.
  3. Andersson KE, Michel MC. Urinary Tract. 1st Ed. Springer Berlin Heidelberg; 2011.
  4. Eapen RS, Radomski SB. Review of the epidemiology of overactive bladder. Res Rep Urol. 2016;8:71–76.
  5. Mayo Clinic Staff. “Overactive Bladder.” Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/overactive-bladder/symptoms-causes/syc-20355715. Published March 20, 2020. Accessed June 29, 2021.
  6. Wyndaele JJ. Overactive bladder, differential diagnosis, and clinical utility of fesoterodine. Int J Gen Med. 2012;5:943-951.
  7. Palmer CJ, Choi JM. Pathophysiology of overactive bladder: current understanding. Curr Bladder Dysfunct Rep. 2017; 12:74–79.
  8. Leron E, Weintraub AY, Mastrolia SA, Schwarzman P. Overactive bladder syndrome: evaluation and management. Curr Urol. 2018;11(3):117-125.
  9. Gormley EA, Lightner DJ, Burgio KL, et al. Diagnosis and treatment of overactive bladder (non-neurogenic) in adults: AUA/SUFU guideline. J Urol. 2012;188(6 Suppl):2455-2463.
  10. 10.0 10.1 10.2 10.3 10.4 Brown ET, Martin L, Dmochowski RR. New evidence in the treatment of overactive bladder. Curr Opin Obstet Gynecol. 2015 Oct;27(5):366-72.
  11. Andersson KE, Chapple CR, Cardozo L, Cruz, et al. Pharmacological treatment of overactive bladder: report from the International Consultation on Incontinence. Curr Op in Urol. July 2009;19(4): 380-394.