Urinary incontinence in women

Abstract

Urinary incontinence symptoms are highly prevalent among women, have a substantial effect on health-related quality of life and are associated with considerable personal and societal expenditure. Two main types are described: stress urinary incontinence, in which urine leaks in association with physical exertion, and urgency urinary incontinence, in which urine leaks in association with a sudden compelling desire to void. Women who experience both symptoms are considered as having mixed urinary incontinence. Research has revealed overlapping potential causes of incontinence, including dysfunction of the detrusor muscle or muscles of the pelvic floor, dysfunction of the neural controls of storage and voiding, and perturbation of the local environment within the bladder. A full diagnostic evaluation of urinary incontinence requires a medical history, physical examination, urinalysis, assessment of quality of life and, when initial treatments fail, invasive urodynamics. Interventions can include non-surgical options (such as lifestyle modifications, pelvic floor muscle training and drugs) and surgical options to support the urethra or increase bladder capacity. Future directions in research may increasingly target primary prevention through understanding of environmental and genetic risks for incontinence.

Figure 1. Prevalence of stress, urgency and mixed incontinence stratified by age

The prevalence of stress incontinence peaks in the fifth decade and then declines, whereas the prevalence of both mixed and urgency incontinence continues to increase with age. Observational data are from France, Germany, Spain and the United Kingdom. Median prevalence data from a review of epidemiological studies from around the world have shown similar trends. Reproduced with permission from REF., Wiley.

Figure 2. Anatomy and histology of the female bladder

The bladder lies immediately behind the pubic bones. When empty, the bladder has a pyramidal shape. As it fills and distends, the bladder balloons up above the pubic bones in an ovoid shape. The muscle of the bladder wall (the detrusor) consists of interdigitating fibres of smooth muscle, arranged in circular and longitudinal layers. These can stretch up to four times their resting length, so there is no increase in linear tension (or pressure) during normal bladder filling. The bladder and the ureters are both lined by a transitional epithelium, the urothelium. It contains flattened (‘umbrella’) cells and cuboidal cells, which also enable stretch as the bladder fills. The base of the bladder is a triagonal area, called the trigone. The ureters enter at the two superior corners of this triangle and the bladder neck lies at the inferior corner. The bladder neck is in continuity with the urethra, which, in women, is 2.5–4 cm long. The internal sphincter is formed of rings of smooth muscle at the bladder neck, whereas the external sphincter is formed by the muscles of the pelvic floor. Both sphincters help to close off the urethra to maintain continence.

Figure 3. Neurological control of the urinary bladder

a | The sympathetic system predominates during the storage phase and maintains continence through the paravertebral ganglia and the hypogastric nerves and plexus. b | The parasympathetic system coordinates the voiding phase, through the sacral plexus and pelvic nerves (S2–S4). Afferent signals come from the urothelium and the bladder wall, through the pelvic nerves, and then go to the dorsal root ganglia and are projected to the periaqueductal grey, then to the posterior cingulate cortex (PCC). c | The main circuits for regulating desire to void include the insula and the lateral and medial prefrontal cortices, which feed back to the periaqueductal grey^,. The periaqueductal grey serves as a relay station for bladder information and activates the pontine micturition centre, which contracts the bladder and relaxes the urethral sphincter mechanism during voiding. d | The neurotransmitters responsible for the execution of these commands are acetylcholine and noradrenaline.

Figure 4. Urethral support

The posterior urethra lies on a supportive tissue layer composed of the anterior vaginal wall (part a) and the endopelvic fascia (part b). These structures are suspended from the arcus tendineus and in combination with a functional levator ani, create a ‘hammock’ that results in compression of the urethra with increased intra-abdominal pressure, preventing urinary leakage.

Figure 5. Uroepithelial sensory web

In the urotheliogenic hypothesis of overactive bladder syndrome (BOX 1), urothelial cells are targets for neurotransmitters released from nerves, are targets for signals from other cell types and can be activated by autocrine or paracrine mechanisms. The signalling cascades between bladder nerves, urothelial cells, smooth muscle cells, interstitial cells and blood vessels are mediated by noradrenaline and adrenaline (via the β₃-adrenergic receptors), acetylcholine (via the muscarinic M₃ receptors), Ca²⁺ (via the activity of transient receptor potential cation channel subfamily A member 1 (TRPA1) and transient receptor potential cation channel subfamily V (TRPV) channels) and ATP (via the purinoceptors P2X and the purinergic G protein-coupled receptors P2Y). Ins(1,4,5)P₃, inositol 1,4,5-trisphosphate; PKA, protein kinase A; PKC, protein kinase C; PKG, protein kinase G; NO•, nitric oxide; NOS, NO synthase. Adapted with permission from REF , American Physiological Society.

Figure 6. Diagnostic work-up of women with urinary incontinence

The initial management of urinary incontinence includes a detailed history and physical examination to identify potential reversible causes of symptoms, followed by urinalysis with microscopy, voiding diary, assessment of post-void residual volume and cough stress test to assist with diagnosis and initial management. In cases of advanced pelvic organ prolapse, prior pelvic surgery, haematuria or urinary retention, patients may be referred to a urologist or urogynaecologist. UTI, urinary tract infection.

Figure 7. Multichannel urodynamic testing

Invasive (catheterized) pressure measurements during urodynamic studies include intravesical pressure (using a probe in the bladder) and abdominal pressure (using a probe in the rectum as shown or in the vagina (not shown)). In addition, electromyography (EMG) can be used to evaluate the activity of the muscles of the pelvic floor. During the test, the bladder is filled and then the patient is asked to void, with continuous pressure monitoring during filling and emptying. In women with urgency incontinence, findings can include uninhibited contraction of the detrusor muscle during filling (detrusor overactivity) or a gradual uncomfortable rise in pressure during filling (low compliance). A formal diagnosis of stress incontinence is made by observation of leakage with coughing or exertion in the absence of detrusor contraction.

Figure 8. Surgical treatment for urinary incontinence

Surgical correction of urethral hypermobility, which results from loss of support of the bladder neck and proximal urethra such that they move during peaks of abdominal pressure, can involve the use of a synthetic mesh, suture or autologous tissue. A synthetic mesh is placed inside the vagina at the level of the mid-urethra and is passed either retropubically (part a) or via the transobturator approach (part b). Sutures are not used in either of these ‘tension-free’ procedures; the body tissues and fibrosis hold the mesh in place. Conversely, retropubic urethropexy (part c) involves the placement of permanent sutures in the anterior vaginal wall at the level of the bladder neck and proximal urethra. Finally, autologous fascial sling placement (part d) involves harvesting a strip of rectus fascia that is placed beneath the proximal urethra through a vaginal incision; the two ends of the sling are passed behind the pubic bone and are secured with permanent sutures either to each other or to the rectus fascia. Part a and part b are reproduced with permission from REF , Macmillan Publishers Limited.