Urinary incontinence is defined as the condition in which there is involuntary loss of urine, which can be objectively demonstrated and which is a social or hygienic problem. It should be noted that the volume of urine lost is not a feature of the definition, but the ability of an independent person to confirm that there is urine loss is essential.

Urinary incontinence is an important condition because it causes significant distress. It is generally accepted that around 15% of the adult female population have a significant problem with urinary incontinence, for which they are getting treatment or would like treatment if it is available. Urinary incontinence is a major quality-of-life (QOL) issue. Patients can become reclusive, unwilling to go out and feel a burden to their loved ones. Incontinence increases in age with the incidence of an overactive bladder as high as 50% or more in institutionalized elderly females.

The commonest types of urinary incontinence in women are:

 stress urinary incontinence (SUI)

 overactive bladder (OAB)

 mixed incontinence (SUI and OAB)

 retention with overflow

 fistula.

Stress urinary incontinence (SUI) is the commonest cause of urinary incontinence in adult women, accounting for 40% of cases. SUI is a sign or a symptom, but if this is proven at urodynamic testing, then it is called ‘urodynamic stress incontinence’ (USI). This has replaced the old term ‘genuine stress incontinence’. SUI is leakage that occurs when there is a rise in intra-abdominal pressure without a detrusor contraction; women therefore notice leakage on coughing, laughing, sneezing, etc. and, in severe cases, even on walking or on rising from a sitting position.

An overactive bladder (OAB; previously called detrusor instability, detrusor overactivity or detrusor hyperreflexia), occurs when a woman is incontinent in response to an involuntary detrusor contraction. This accounts for about 25% of cases of incontinence in adult women as a sole diagnosis. The woman will experience urgency, and if she cannot reach the toilet and the bladder contraction persists, she will be incontinent. As the problem tends to happen both day and night, she will usually also complain of urinary frequency and nocturia, and, in severe cases, enuresis (bed wetting).

Increasingly, women have a pattern of mixed incontinence (having both SUI and OAB) and this now accounts for around 30% of cases.

Retention with overflow is only common in elderly female patients or in those with a neurological problem. The denervated bladder continues to fill until it simply spills over, resulting in leakage.

A fistula is an abnormal communication between two epithelial surfaces and, in the UK, usually results as a complication of surgery. In less affluent countries, obstructed labour is a common cause. Any communication between the lower urinary tract (ureter, bladder or urethra) and the genital tract (uterus and vagina) will result in continuous dribbling incontinence. Fistulae account for only 1 in 1000 cases of incontinence in women in the UK.

It is important to be aware that any incontinent woman may have more than one type of coexisting incontinence. As stated, SUI and OAB commonly coexist, and voiding difficulty or retention can accompany either or both of these.

The mechanism of continence must be understood if the pathophysiology of incontinence is to be understood. In the normal woman, continence is maintained at the level of the bladder neck. If, for instance, a radio-opaque medium was to be placed in the bladder of a normal, continent woman and that woman was asked to stand, an X-ray would demonstrate that urine does not flow into the urethra. The concept therefore arose of a so-called proximal urethral sphincter, a mechanism present in the region of the bladder neck and proximal urethra, which maintains continence. It was originally considered that this was an arrangement of smooth muscle in the proximal urethra. However, no such sphincter mechanism based upon muscle, exists. There is smooth muscle in the proximal urethra but it generally runs in a longitudinal rather than a circular direction and as such, could not maintain continence.

It is now considered that the so-called proximal urethral sphincter mechanism is a water-tight seal, which maintains the pressure in the urethra greater than the pressure in the bladder. The anatomical basis of that seal is considered to be a series of arteriovenous anastomoses within the wall of the proximal urethra. These can be demonstrated on histological examination. They allow some degree of turgor pressure to be exerted circumferentially around the urethra, which results in the formation of a hermetic seal by keeping the urethra occluded. The effect of any pressure exerted around the periphery of a hollow tube is to occlude that tube. If the pressure is exerted in numerous places around the circumference of the tube, then the tube will simply close. Such is the proximal urethral sphincter.

The situation becomes more complex, in that if a pressure study is performed to compare the pressure in the urethra with the pressure within the bladder, then while the pressure in the proximal urethra exceeds that in the bladder, the greatest pressure difference exists at the mid-urethra. This is the so-called distal urethral sphincter mechanism. This does have an anatomical basis in muscle in that striated muscle, innervated by spinal roots S2–4, is found within the wall of the mid-urethra.

There are further features which aid the maintenance of continence, particularly the supporting tissues around the urethra, which maintain the proximal urethra in an intra-abdominal position. The importance of this position is that if the proximal urethra is intra-abdominal, then any pressure rise within the abdomen will be transmitted equally to the bladder and the proximal urethra; the pressure difference will not change and continence will therefore be maintained. Weakness or damage to the supporting tissues may predispose to SUI. The supporting tissues are characterized anatomically as the pubourethral ligaments, derived from the fascia of the pelvic floor, and, to a lesser degree, the pelvic floor musculature, namely levator ani. It has been demonstrated that vaginal delivery may denervate both the pubourethral ligaments and levator ani, the nerve damage being manifest within the pudendal nerve. Thus, vaginal delivery may predispose towards SUI.

There is also the concept of bladder stability. The bladder muscle, the detrusor, should only contract during micturition, whereas it should relax during bladder filling. Such a situation is described as a ‘stable’ bladder. In women who have an overactive bladder, the detrusor initially relaxes during filling but then contracts involuntarily. Such a situation is termed an overactive bladder (OAB). If the contraction is modest, then the woman will appreciate the contraction as urinary urgency, but if the contraction is strong enough to elevate the pressure in the bladder above that in the urethra, then there will be the symptom of urge incontinence.

SUI clearly requires some degree of weakness of both the proximal and distal urethral sphincter mechanisms. While no single aetiological factor exists in all women with SUI, there are a series of predisposing factors which often explain the condition. These include:

 pregnancy

 prolapse

 menopause

 collagen disorder

 obesity.

Vaginal delivery may cause denervation of the pudendal nerve and hence damage to the supporting tissues of the urethra. Moreover, the pudendal nerve in part supplies innervation to the distal urethral sphincter. The first vaginal delivery is more likely than a subsequent vaginal delivery to cause SUI, and this incontinence may be preventable by elective caesarean section. There is also a transient form of SUI, which occurs during pregnancy but is not present outside of pregnancy. The mechanism of this incontinence is a combination of the raised intra-abdominal pressure related to uterine contents together with the smooth-muscle-relaxant effect of progesterone. Thus, some women will describe SUI during pregnancy but not at other times.

Prolapse and SUI coexist in over 50% of cases. Only if the bladder neck/continence mechanism is prolapsing is the prolapse per se, the cause of this. The relationship otherwise relates to poor pelvic floor function secondary to pudendal nerve damage, which is the main aetiology of both conditions.

Many women date the onset of their symptoms from the menopause. There is evidence that the withdrawal of oestrogen reduces the so-called maximal urethral closure pressure; hence the pressure in the urethra is not as great as it used to be. The effect of this pressure reduction is that a smaller rise in intra-abdominal pressure will result in SUI.

Collagen is a major component of the pubourethral ligaments. There are several different types of collagen within the body and there is evidence that there are different types of collagen in varying proportions in the pubourethral ligaments of women who become incontinent compared with the pubourethral ligaments of those who do not.

In the majority of women, the aetiology of an overactive bladder is unknown. Neurological conditions, typically multiple sclerosis, stroke or cervical spine lesions, are known to be a cause of overactivity but it is very uncommon for such patients to present de novo at a urogynaecology clinic. There is also a link between psychological upset and OAB, with such patients having a higher than background incidence of anxiety and neuroses.

The aetiology of voiding difficulty in the female is the opposite of that in the male. In women, it is due to an underactive detrusor (hypotonia) in 90% of cases, and in only 10% of cases does it reflect anatomical obstruction. The aetiology of the detrusor hypotonia is usually simply ageing, with the natural reduction in muscle fibres and muscle strength being enough to bring about a clinical problem. There is some evidence that young women who put off voiding during their adult life (‘infrequent voiders’) are more prone to this problem. Women with neurological disease can have voiding difficulty due to either detrusor hypotonia or obstruction, in the latter case secondary to inappropriate contraction of the urethral sphincter.