Urinary incontinence (UI) is a common problem affecting up to two thirds of all women. Its prevalence is easily underestimated in the clinical setting, since patients will often fail to bring the condition to the attention of their physician. It is estimated that only one in four symptomatic women seek help for this problem.1

Prevalence and impact
The prevalence of UI increases with age. Stress incontinence tends to be more common in younger and middle aged women and mixed incontinence is more common in the older age group. Overall, stress incontinence is more common (49%) followed by mixed incontinence (29%) and pure urge incontinence (21%).2

The Leicester MR incontinence study3 of individuals older than 40 years found that 33.6% of the population reported significant urinary symptoms but only 3.8% felt the need for help with their symptoms. A study looking at the incidence and prevalence of over active bladder symptoms in the UK, using data collected from the General Practice Research Database (GPRD), reported the overall prevalence of OAB-related symptoms was 3.87 per 1000 persons with an incidence of 2.79 per 1000 person years.4

UI is not associated with mortality, but it has significant impact on morbidity and quality of life affecting older person’s emotional wellbeing, social function and general health. UI can also cause cellulites, pressure ulcer, urinary tract infections, social withdrawal, depression and sexual dysfunction. 

Care worker burden is higher with incontinent older persons, which can contribute to decisions to institutionalise. It was estimated in the USA, the total direct and indirect cost for UI in the year 2000 was approximately $19.5 billion.5

The overall cost of incontinence to the NHS is difficult to calculate. The Continence Foundation calculated the figure of £354 million in 1998 and this figure does not take into account nursing home, residential care and long-term hospital patients who are getting managed for incontinence.6 Turner et al in 2004 estimated the annual NHS cost of treating clinically significant storage symptoms in women to be £233 million.7 UI has a larger economic impact than many other chronic conditions and diseases. The aim of this article is to give an overview of the current understanding of pathophysiology, evaluation and its relevance to clinical management.

Recent developments
UI in women is not a recent medical and social phenomenon, but its importance as a medical problem is increasing. Several factors are responsible for the increased attention, such as:8

  • Women are more willing to talk openly about this disorder and in most cases it is a treatable condition, consequently less embarrassment and fewer social stigmas are associated with the diagnosis9
  • As the population ages, increased attention is getting paid to incontinence as it is often the chief reason for institutionalisation of elderly people
  • The general public is becoming more aware about the problem and the treatment options that are available and are getting better access to information about incontinence products and about specialists who have interest and expertise in these disorders
  • Academic interest in UI disorders is increasing among basic scientists, clinical researchers and clinicians and therefore the sub-specialities such as uro-gynaecology and female urology are expanding 
  • Better understanding of functional anatomy of the pelvic floor due to increased research and study in this field in the last decade has had a significant role in the development and refinement of urodynamics and the techniques of dynamic imaging of the pelvic floor and lower urinary tract, along with electrophysiological testing which helps in accurate diagnosis and management.

Disorders of UI have been in medical literature since antiquity. Lesions such as genito-urinary fistula have been uncovered in the mummified remains of corpses dating back to 2000 BC.8 In the 1830s and 40s, John Peter Mettauer first reported on the successful closure of vesico-vaginal fistula, which was causing debilitating UI.8

In the early 1900s Howard A Kelly did much work in female incontinence and he is credited with the first significant surgical procedure for stress incontinence, now referred as the Kelly Plication.8,10 Since Kelly’s time literally hundreds of procedures for the treatment of female incontinence have been devised, but only a few have stood the test of time. New procedures and modifications of the older ones continue to be developed. More recently procedures stressing minimally invasive surgical access have come to the forefront.8,11

Mechanism of continence in women
The main factors that contribute to continence are bladder compliance and efficient urethral sphincter mechanism.12 Bladder filling and urine storage require accommodation of increasing volumes of urine at a low intravesical pressure and with appropriate sensation (normal compliance), a bladder outlet that is closed at rest and remains so during increase in intra-abdominal pressure and absence of involuntary bladder contractions (detrusor overactivity).

Bladder emptying requires coordinated contraction of the bladder smooth muscle in an adequate magnitude and duration with concomitant lowering of resistance at the level of the smooth and striated sphincter and absence of anatomic obstruction. The principles underlying the function of a sphincter are watertight apposition of the urethral lumen, compression of the wall around the lumen, structural support to keep the proximal urethra from moving during increase in pressure and a means of compensating for abdominal pressure changes (pressure transmission) and neural control.

The urethra consists largely of a rich vascular sponge lined by moist mucosal layer and surrounded by a coat of smooth muscle, fibro-elastic tissue and striated muscle. The mucosa provides coaptation. The vascular submucosa creates the ‘washer effect’ for the continence mechanism. Functionally the surrounding smooth muscle coat contains this mechanism by directing submucosal expansile pressures inward towards the mucosa. Muscle tone is mediated by alpha adreno receptors in the sympathetic nervous system. All three layers are under oestrogen control.

For women in normal circumstances, the urethra is stabilised during stress by mainly three inter-related mechanisms.8 The first one is a reflex or voluntary closure of the pelvic floor. Contraction of the levator ani complex elevates the proximal urethra and bladder neck, tightens intact connective tissue supports and elevates the perineal body, which may serve as a urethral back stop. 

The second mechanism involves intact connective tissue support to the bladder neck and urethra. The pubo-cervico-vesical or anterior endopelvic connective tissue in the area of the bladder neck is attached to the back of the pubic bone, the arcus tendineus fascia pelvis and the perineal membrane. The pubo-urethral ligaments also suspend the mid urethra to the back of the pubic bone. These components form the passive supports to the urethra and bladder neck. During times of increased intra abdominal pressure, if these supports are intact they augment the supportive effect of muscular closure of the pelvic floor.
Finally the third mechanism involves two bundles of striated muscle, the urethro-vaginal sphincter and the compressor urethrae, found at the distal aspect of the striated urethral sphincter. These muscles may aid in compressing the urethra shut during stress manoeuvres. These muscles do not surround the urethra like the striated sphincter but lie along the lateral and ventral aspects.

The exact function and importance of these muscles are controversial. They may provide compression and increased pressure in the distal urethra during times of stress. UI occurs when there is dysfunction in either the storage function or occasionally in the emptying function of the lower urinary tracts. Urethral sphincter dysfunction and bladder dysfunction can co-exist and various components of the continence mechanism may compensate one another. For example, women may sustain anatomical or neuromuscular injury during childbirth but may remain asymptomatic until there is loss of urethral sphincter function due to ageing. 

The International Continence Society has defined the nomenclature for UI into different types and this classification of incontinence into diagnostic clinical types is useful in evaluation and planning treatment. The aetiology may be classified either on anatomical basis or functional basis. The anatomical classification will subdivide the causes in to bladder-related, urethra-related and ureter-related causes. It will take into account of the congenital and acquired causes of the anatomical abnormalities of the lower urinary tract. Functionally it may be divided into two—urge incontinence or stress incontinence.

Predisposing factors

Caucasian women are found more susceptible than African-American or Asian women.13

Family predisposition
Women whose mother and/or older sisters are incontinent have an increased risk (relative risk three) of developing stress and mixed urinary incontinence and more severe symptoms and if the woman has an incontinent mother and grandmother, the risk is even further increased.13

Anatomical abnormalities
Congenital defects of the ureters or urethra or urinary fistulae such as urethro-vaginal or vesico-vaginal or vesico-uterine fistulae can cause UI.

Neurological causes
Cerebral causes such as stroke, dementia, degenerative lesions such as Parkinson’s disease or spinal cord causes such as multiple sclerosis, spina bifida, trauma etc or peripheral nerve causes such as pelvic plexus injury, pelvic surgery etc are likely to induce neurogenic bladder and UI.

Pregnancy, childbirth and parity
UI is common among pregnant women and usually is a self-limiting condition for many women. Vaginal delivery, prolonged labour, episiotomy and instrumental delivery (mainly vacuum extraction) and increased birth weight (over 4kg) are thought to increase the risk of UI. Many studies support the link between the parity and UI. It is most common in women who had four or more children.13

Pelvic surgery and irradiation
Even though radical pelvic surgeries such as AP resection and radical hysterectomy have been implicated as contributing to pelvic floor dysfunction, routine pelvic surgeries such as hysterectomy still remains debatable.13 Other procedures such as pelvic irradiation is also known to cause damage of the nerves and muscles of lower urinary tract, but no data show convincing evidence that there is direct link to development of UI.

Pelvic organ prolapse
Women with anterior vaginal prolapse often have bladder neck hypermobility with stress incontinence. Some 30% of women with either small or large cystoceles have detrusor overactivity on urodynamic testing and a higher percentage have symptoms of urge incontinence.13

Promoting factors

Age and comorbidities
With ageing, changes in the bladder and pelvic floor structures occurs and will predispose to incontinence and furthermore several other factors associated with old age such as dementia, cognitive impairment, diabetes mellitus etc, may play a role in deterioration of UI.

It is an established risk factor for UI, particularly stress incontinence.14,15 The added weight in obese patients with increased intra-abdominal and intravesical pressure bear down on the pelvic tissues causing straining, stretching and weakening of the muscles, nerves and connective tissues of the pelvic floor. Obese women are 4.2 times more likely to develop stress incontinence and 2.2 times more likely to develop urge incontinence. Furthermore weight reduction in a group of morbidly obese women resulted in reduction of stress incontinence from 61% to 12%.13

Conditions that cause increased intra abdominal pressure
Chronic constipation with repeated and prolonged straining efforts can cause pudendal nerve damage and can eventually lead to neuropathy and dysfunction thus causing stress incontinence. Faecal impaction in the rectum also can cause physical outflow obstruction, even resulting in urinary retention and urinary leakage. There is no convincing evidence to support the link between smoking as a direct risk factor for urinary incontinence.16 Smoking is the primary risk factor for lung disease and it has an anti-oestrogen effect as well. Chronic lung diseases such as chronic bronchitis and emphysema cause increased intra-abdominal pressure.

Occupational and recreational activities
The occupational and recreational activities that cause an increase in the intra-abdominal pressure would worsen existing UI, but it does not primarily induce incontinence.13,16

Urinary tract infections
It has been considered as a transient cause for UI.

The atrophic changes occurring during menopause increase the susceptibility to UTIs and can cause storage symptoms. Lower urinary tract tissue is oestrogen sensitive but the exact role of oestrogen in the continence mechanism is not yet clear.13 No good evidence can be found that menopause is an independent risk factor for UI may be because it is difficult to separate it from the effect of age.13

Medications and alcohol
Antihypertensives that are alpha antagonists can cause stress incontinence, anticholinergics can cause urinary retention and overflow, diuretics can induce increased urinary volume and frequency and urgency, ACE inhibitors can cause chronic cough, which can result in stress incontinence and NSAIDs, iron, calcium, antacids can cause constipation. Alcohol is a known cause for transient incontinence by its effects on sedation, mobility impairment and diuresis. 

Definitions and classifications
According to the International Continence Society, incontinence is defined as involuntary loss of urine,14 which is objectively demonstrable and is a social or hygienic problem. It can be thought of as a symptom as reported by the patient, as a sign that is demonstrable on clinical examination and as a disorder observed on urodynamic study.

Common types of UI in females are:16 urge incontinence, stress incontinence and mixed incontinence. In addition there are other types which are not typical of stress or urge incontinence. They are, transient incontinence, overflow incontinence, unconscious (unaware) incontinence, continuous incontinence, extra-urethral incontinence, nocturnal enuresis and post micturition dribble.

UI is common in women but it is under reported and undertreated. Generally UI is caused by ageing, childbirth, pelvic surgery and neurological disorders. Most UI can be evaluated and treated in the primary care setting after careful history and simple clinical assessment. This can include lifestyle modifications, pelvic floor muscle training, bladder training and pharmacotherapy. If there is complex symptomatology or if the primary management fails, then referral to a specialist is suggested. 

UI can be very distressing both physically and psychologically and impacts on quality of life and health. GPs, as primary care providers, should evaluate, treat and refer high risk patients. The treating clinicians should make use of the guidelines such as EAU guidelines and NICE guidelines in the management of these patients in a cost effective and safer way.

Part two of this article will review the common types of UI and management options.

Conflict of interest: none declared.

1. Nygaard IE, Heit M. Stress urinary incontinence. Obstet Gynecol 2004; 104: 607–20
2. Hunskaar S, Burgio K, Diokno AC, et al. Epidemiology and natural history of urinary incontinence. In: Abams P, Cardozo L, Khoury S,Wein A [eds]: Incontinence(2nd edition) 2nd International Consultation on Incontinence. UK, Health Publications 2002: 165–201
3. Perry S, Shaw C, et al. An epidemiological study to establish the prevalence of urinary symptoms and felt need in the community: The Leicestershire MRC incontinence study. Journal of Public Health Medicine 2000; 22: 427–34
4. Odeyemi AO, Dakin HA, et al. Epidemiology, prescribing patterns and resource use associated with overactive bladder in UK primary care. The International Journal of Clinical Practice 2006; 60: 949–58
5. Hu TW, Wagner TH, et al. Costs of urinary incontinence and overactive bladder in the United States: a comparative study. Urology 2004; 63: 461–65
6. Urinary Incontinence in women. Costing report. Implemending NICE guidance in England.UK: National Institute for Health and Clinical Excellence; 2006
7. Turner DA, Shaw C, et al. The cost of clinically significant urinary storage symptoms for community dwelling adults in the UK. BJU International 93: 1246–52
8. O’Shaughnessy M. Urinary incontinence, medical and surgical aspects. emedicine 2007; 257260: 1-91 [ www.emedicine.medscape.com/article/257260]
9. Urinary Incontinence: The management of urinary incontinence in women. NICE clinical guideline 40 .UK: National Institute for Health and Clinical Excellence; 2006. http://www.nice.org.uk/guidance/cg40 (accessed 2/2/15)
10. Kelly HA, Dumm WM. Urinary incontinence in women, without manifest injury to the bladder. Journal of the American College of Surgeons 1914: 18; 444–50
11. Cundiff GW. The pathophysiology of stress urinary incontinence: A historical perspective. Rev Urol 2004; 6(suppl 3): S10–S18
12. Wein AJ. Pathophysiology and classification of voiding dysfunction. In: Campbell-Walsh Urology International Edition. Philadelphia: Saunders Elsevier; 2007: 3; 1973–85
13. Abrams P. Artibani W, et al. Clinical Manual of Incontinence in Women Based on the Reports of the 3rd International Consultation on Incontinence. Paris; Health Publications Ltd; 2005
14. Nitti VW, Blaivas JG. Urinary Incontinence: Epidemiology, Pathophysiology, Evaluation and Management Overview. In: Campbell-Walsh Urology International Edition. Philadelphia: Saunders Elsevier 2007: 3; 2046–78
15. Hunskaar S.,Burgio K, et al. Epidemiology of Urinary and Faecal incontinence and pelvic organ prolapse .In: Abrams P,Cardozo L. Khoury S,Wein A[eds]: Incontinence (edition 2005) 3rd International Consultation on incontinence.UK, Health Publications, 2005; 255–312
16. Schroder A, Abrams P, et al Guidelines on Urinary Incontinence. In: European Association of Urology Guidelines 2009. Arnhem: EAU 2009. 15: 1–52