Incontinence of urine

Normal urinary continence is dependent on several factors. These include normal mobility and normal brain function allowing a perception of when it is socially acceptable to void, normal bladder sensation, normal voluntary detrusor contraction producing good bladder emptying, a normally competent sphincter mechanism which relaxes appropriately during a voluntary detrusor contraction allowing good bladder emptying and good bladder capacity with normally low pressures during filling. This is clearly a fine balance and several factors can cause incontinence.

In the diagnosis of urinary incontinence, a careful history and physical examination may help, but it will be necessary to carry out urodynamic testing in most patients if surgical intervention is proposed. The urine should be cultured to exclude infection and the serum creatinine should be measured. It may be appropriate to have anatomical visualisation of the urinary tract by means of IVU if one suspects a ureteric fistula, although ultrasound examination will often provide adequate details.

Urodynamic testing

The key to the practical management of lower urinary tract dysfunction lies with urodynamic investigation. The principle is artificially to simulate bladder filling and emptying whilst obtaining pressure measurements (Fig. 65.14).

The patient attends with a full bladder and is allowed to void in private to measure maximum urinary flow rate. After voiding, the residual urine is measured by means of ultrasound to assess the completeness of bladder emptying. Urodynamic testing involves the aseptic passage of a small pair of catheters or a twin-lumen catheter into the bladder; this allows the bladder to be filled with saline or contrast medium at a rate of 50 mI/minute whilst a continuous recording of the intravesical pressure is made via a transducer. To obtain true detrusor pressure, a second pressure channel is required to assess intra­abdominal pressure which is usually measured by means of a small intrarectal or intravaginal balloon. The bladder is filled until the patient states that their bladder is full. Screening by means of radiographic imaging may be carried out to assess bladder neck closure, and urinary leakage during voiding or during bouts of phasic detrusor pressure (detrusor instability). The patient is then asked to void at the end of bladder filling after the filling catheter has been removed.

Usefulness of urodynamic testing

      Distinguishing genuine stress incontinence (due to sphincter weakness) from detrusor instability in women (Fig. 65.15)

      Classification of neurogenic bladder dysfunction

      Distinguishing bladder outflow obstruction from idiopathic detrusor instability in men

      Investigation of incontinence

The normal bladder will accept approximately 400—55 0 ml when filled with saline at room temperature at filling rates of 50 ml/minute. The pressure increase in the bladder should be less than 15 cmH2O. In addition, phasic pressure increases should not be seen. The normal voiding pressure should not exceed 60 cmH2O in men and about 40 cmH2O in women, with a flow rate of between 20 and 25 mI/second.

Common abnormalities identified during urodynamic testing in incontinence

  Phasic increases giving rise to sensations of urgency of micturition and urge incontinence (detrusor instability; Fig. 65.16). This abnormality is found in patients with several types of neurogenic bladder dysfunction such as multiple sclerosis (MS), Parkinson’s disease, or following a stroke or certain types of spinal injury when it is known as detrusor hyperreflexia. In addition, about 50 per cent of men with bladder outflow obstruction have detrusor instability, and in about half of these men the instability resolves after prostatectomy. Idiopathic detrusor instability is common and must be distinguished from genuine stress incontinence in women before performing bladder neck suspension procedures.

Genuine stress incontinence is defined as urinary leakage occurring during increased bladder pressure when this is solely due to increased abdominal pressure and not due to increased true detrusor pressure (Fig. 65.15). It is caused by sphincter weakness.

Chronic urinary retention with overflow incontinence. This is recognised by a large residual volume of urine (Fig. 65.17) and is usually associated with high pressures during bladder filling.

  Bladder outflow obstruction, which is associated with increased voiding pressures often being in excess of 90 cmH2O (Fig. 65.18), coupled with low urinary flow rates.

 Neurogenic bladder dysfunction.

Causes of incontinence

There are various ways of classifying causes of incontinence. A good functional method is as follows.

  Problems of social control — patients with Alzheimer ‘s disease, Parkinson’s disease or multi-infarct dementia often have urinary incontinence owing to a combination of uninhibited detrusor hyperreflexia and impaired social perception.

  Storage problems — patients with a small capacity owing to fibrosis from tuberculosis or interstitial cystitis can develop incontinence. Patients with a small functional capacity owing to severe idiopathic detrusor instability, neurogenic bladder dysfunction or urinary infection also can develop incontinence.

  Severe impairment of emptying — patients with chronic retention or some types of neurogenic bladder dysfunction often have small functional bladder capacities with detrusor overactivity causing incontinence, despite having large residual volumes of urine.

  Weak sphincter — patients with genuine stress incontinence owing to previous prolonged labour or with damage to the distal sphincter mechanism secondary to prostatectomy or with neurogenic bladder dysfunction often have impaired sphincter function which leads to stress incontinence. Congenital causes such as epispadias also result in sphinc­ter weakness.

  Fistulae leakage from fistulae or upper tract duplication with an ectopic ureter.

The common causes may be classified into male, female or mixed sex groups.

Male

Chronic urinary retention with overflow. This is a common cause of incontinence and may be due to benign prostatic hypertrophy, carcinoma of the prostate, urethral stricture and, in younger men, hypertrophy of the bladder neck. The key to the diagnosis lies with the history of prolonged hesi­tancy and a poor urinary stream with both daytime and nocturnal ‘dribbling incontinence’ coupled with the finding of a distended bladder. Examination may reveal that the bladder is visibly distended, the transverse suprapubic crease is lost and the painless distension of the bladder may be palpated or percussed. It may easily be diagnosed by means of ultrasound measurement of residual urine volume. The treatment is discussed in Chapter 66.

Postprostatectomy. Postprostatectomy incontinence may result from injury to the external sphincter mechanism which may be caused by clumsy surgery — urodynamic evaluation will demonstrate genuine sphincter weakness. The other cause of incontinence is idiopathic detrusor instability, although such patients often have significant irritative symptoms prior to prostatectomy and should be identified and investigated by means of urodynamic studies prior to prostatectomy.

Female

Stress incontinence. The commonest cause of leakage of urine in women is genuine stress incontinence (GSI), although in some parts of the world vesicourethral fistulae owing to neglected labour are very common. GSI occurs sec­ondary to weakness of the distal sphincter mechanism associated with laxity of the pelvic floor. It is usually found in multiparous women with a history of difficult labour often accompanied by the use of forceps. It can be found in normal young women who indulge in competitive trampolining and also in patients with epispadias. The classical symptoms are complaints of urine loss during coughing, laughing, sneezing or sudden change of posture. The symptoms may change with the menstrual cycle. The volume of urine loss can be measured during an exercise test which is performed by putting the patient through a standard set of tests with 300 ml of fluid in the bladder; in GSI the fluid losses usually range from 10 to 50 ml. Urinary frequency and urgency are, however, often found in such patients as they try to avoid incontinence by frequent voiding.

Idiopathic detrusor instability can closely mimic GSI and indeed can coexist with it. It is important to make a correct preoperative diagnosis by urodynamic measurements, as the outcome of surgery is significantly worse in women with idiopathic detrusor instability.

Minor degrees of stress urinary incontinence often can be controlled by means of teaching the patient a series of pelvic floor exercises. However, if this fails then surgery is indicated. The best standard operation is the Butch colposuspension.

This operation is carried out with the patient in the Lloyd-Davies position through a Pfannenstiel incision. The vaginal fascia is identified by sweeping the bladder off the vagina and three sutures are placed on each side between the vaginal fascia and the iliopubic ligament. A suprapubic catheter is placed. The operation corrects minor degrees of cystocoele. Voiding difficulties are frequent, but usually temporary. It is best to warn women with large bladder capacities and low voiding pressures that this complication may occur and that they may require to carry out CISC for a period. The operation is very successful in the treatment of GSI with 90 per cent 1-year good results, which are maintained in about 80 pet cent at 5 years. Endoscopic needle bladder neck suspension can now be carried out, but is less successful than open operation.

Common to both sexes

Idiopathic detrusor instability (DI). This condition is very common. Phasic increases in bladder pressure may occur during filling in otherwise normal patients (idiopathic) or it may be found in several conditions including neurogenic bladder dysfunction (then known as detrusor hyperreflexia) and blad­der outflow obstruction. Idiopathic detrusor instability may be symptomless, but usually results in symptoms of frequency, urgency, urge incontinence, nocturia or nocturnal incontinence (enuresis) depending on the severity of the instability. It must be distinguished from GSI and from bladder outflow obstruction as colposuspension or prostatectomy have poor results in patients with severe idiopathic DI. Most urologists will want to exclude infection, tuberculosis or carcinoma in situ by urine culture, cytological examination, cystoscopy and confirmation of the diagnosis by means of urodynamic investigation. The mainstay of treatment is the use of various anticholinergic medication (propantheline, oxybutinine, tolteroclise, and amytryptiline). Severe symptoms resistant to conventional conservative treatment resulting in major impairment of quality of life may need more aggressive treatment such as enterocystoplasty.

Ageing. In both sexes ageing can result in smooth muscle cell dysfunction that can cause combinations of small functional capacities, detrusor instability, impaired bladder emptying and symptoms of lower urinary tract dysfunction.

Congenital. Ectopic vesicae and severe epispadias. The abnormal entry of an ectopic ureter distal to the sphincter complex or into the vagina in a female should theoretically result in total urinary incontinence. This is discussed in Chapter 62.

Trauma. Trauma, whether from pelvic surgery or asso­ciated with pelvic fracture, may result in disruption of the nerve supply to the bladder or urethra or in fistula formation.

Infection. Simple lower urinary tract infection may be sufficient, particularly in a woman, to induce urinary incon­tinence. A history of frequency, burning and a fever should prompt the diagnosis. The bladder may be tender whether palpated suprapubically or  per vaginum. Symptoms will usually settle with a course of antibiotics, but in the case of recurrent infection further investigation of the urinary tract will clearly be indicated.

Neoplasia. Locally advanced cancers in the pelvis, partic­ularly carcinoma of the cervix in a woman and prostate in a man, may result in direct invasion of the sphincter mech­anism causing incontinence; occasionally, fistula formation may occur in women.

Other causes

Neurogenic incontinence

Neurogenic incontinence

This has been dealt with in the previous section. The common causes include:

  myelodysplasia;

  multiple sclerosis;

  spinal cord injuries;

  cerebral dysfunction [cerebrovascular accident (CVA), dementia);

  Parkinson’s disease (paralysis agitans).

These conditions lead to a combination of neurogenic vesical dysfunction often associated with loss of mobility. Careful investigation of the whole urinary tract is always required, and the treatment needs to strike a fine balance between preventing hydronephrosis from abnormally high bladder pressures yet at the same time maintaining con­tinence.

The mainstay of management is accurate urodynamic assessment to assess bladder emptying, incontinence and the risks to the upper tract. The upper tracts should be assessed with regular ultrasound scanning, and assessment of the patient’s mobility, intelligence and motivation is vital. The important factors to assess urodynamically are:

bladder emptying;

bladder capacity and bladder pressure during filling;

continence.

The standard way of dealing with impaired bladder emptying is the use of CISC. Occasionally, in an elderly immobile patient an indwelling urethral or suprapubic catheter or an ileal conduit external urinary diversion may be justified, or the performance of an endoscopic sphincterotomy followed by the use of a condom appliance should be considered.

Patients with a small functional bladder capacity (< 150 ml), a high-pressure increase during filling (> 25 cmH2O) and a large residual volume of urine are at high risk of developing upper tract dilatation, and in the past would have undergone endoscopic sphincterotomy. However, there have been major changes in the management of mobile, well-motivated patients with impaired bladder emptying or with high-risk bladders. Such treatment will often involve major bladder reconstruction with replacement of the high-pressure bladder with a low-pressure substitute made of a detubularised bowel segment, often accompanied by surgery to the bladder out­flow using artificial urinary sphincters or a colposuspension. Such treatment will usually need to be accompanied by the patient carrying out CISC afterwards.

Small bladder capacity

The capacity of the bladder may be considerably diminished in several conditions. This can cause crippling urinary frequency and incontinence. It may follow tuberculosis, radio­therapy or interstitial cystitis. Radiotherapy for pelvic cancer can also cause this problem.

Drug-induced incontinence

The detrusor muscle is basically under postganglionic parasympathetic control and the main neurotransmitter system is cholinergic. Recent studies have established the presence of a number of neurotransmitters including  alpha adrenergic fibres in the region of the bladder neck and other neuropeptides, whose function is uncertain as yet, are present throughout the bladder. A number of drugs can induce urinary retention (anticholinergic agents, tricyclic antidepressants, lithium and some antihypertensives). Overflow incontinence may ensue. Drugs giving extrapyramidal side-effects may induce urinary frequency and incontinence, for example phenothiazine.

Constant dribbling of urine coupled with normal micturition

This occurs when there is a ureteric fistula or an ectopic ureter associated with a duplex system opening into the urethra beyond the urethral sphincter in females, or into the vagina. The history is diagnostic, and intravenous pyelography or ultrasound scanning may reveal the upper pole segment which is often poorly functioning. These segments are very liable to infection. Treatment is by excision of the aberrant ureter and portion of kidney which needs it. A ureteric fistula can be difficult to diagnose and may require retrograde ureterography and a high degree of suspicion to demonstrate.

Nocturnal enuresis

This is a condition of young children and young adults. The time at which children become dry at night varies, of course, and in some of them it is merely a delayed onset of continence. In others it persists until late adolescence and is classified into primary and secondary nocturnal enuresis.

Primary nocturnal enuresis occurs in patients with nocturnal enuresis alone and with no daytime symptoms. Often, they have been dry for a period and the vast majority of patients will eventually become dry. In the meantime a sympathetic approach to these children is essential. They often respond to a system of rewards using a ‘star’ chart. In addition, the use of DDAVP (vasopressin analogues) can produce increased urinary concentration at night with a decrease in nocturnal incontinence. Other treatments include the use of amytryptiline and alarms which wake the child (or at least the child’s parents) when incontinence occurs.

Patients with secondary nocturnal enuresis have daytime symptoms of urinary frequency, urgency and urge incontinence. Essentially, these patients have idiopathic detrusor instability and should be treated in a similar way (see subsection on ‘Treatments for incontinence’).

Treatments for incontinence

Treatments are listed below. Management is dependent on making a correct working diagnosis. The treatment depends on the cause. The aim is to keep the patient dry, free of odour, to lessen the incidence of skin excoriation, and to protect the kidneys from the effects of infection and back pressure.

Management and treatment

Problems of social functioning. Patients with Alzheimer’s disease, Parkinson’s disease and multi-infarct dementia are difficult to treat. Often these patients will respond to regular toileting. Anticholinergic agents can cause confusion in these patients and often, in severe cases, an indwelling catheter is needed.

Storage problems. Patients with a small capacity owing to fibrosis may require augmentation cystoplasty. Patients with a small functional bladder capacity owing to detrusor over­activity from neurogenic bladder dysfunction or idiopathic detrusor instability should be tried on anticholinergic medi­cation, but in severe cases, particularly in neuropathic patients at high risk of upper tract dilatation, bladder sub­stitution (near-total supratrigonal cystectomy followed by the need for detubularised ileocaecal segment bladder substitution) or augmentation (enterocystoplasty) may be needed. These procedures should only be carried out after careful assessment in units used to dealing with these problems. Patients with very impaired mobility and MS may require ileal conduit diversion.

Impaired bladder emptying. Patients with overflow incontinence owing to bladder outflow obstruction will respond well to prostatectomy, after an initial period of catheterisa­tion to allow bladder and renal function to recover to some extent. Patients with impaired bladder emptying owing to neurogenic bladder dysfunction should be treated in the first place by means of CISC.

  Weak sphincter. Patients with genuine stress incontinence owing to previous prolonged labour should be treated by means of pelvic floor exercises or colposuspension. Those with post-prostatectomy incontinence or with neurogenic bladder dysfunction may require fitment of an artificial urinary sphincter (Fig. 65.19) if they are well motivated and mobile.

Leakage from fistulae or upper tract duplication with an ectopic ureter. This will require the appropriate surgical treatment.

Appliances in women are usually unsatisfactory. In elderly, immobile or mentally impaired patients, an indwelling cathe­ter drained constantly into a leg urinal is usually a satisfactory solution, although in some instances diversion via an ileal conduit is necessary. In men, a condom urinary appliance may be satisfactory, and can avoid an indwelling catheter.

More major surgical treatments

Various types of urinary diversion. This may be required for the treatment of end-stage incontinence that is not otherwise treatable (see later in this chapter).

Bladder substitution procedures. The principle behind these operations is the creation of a low-pressure, large capacity reservoir. These can be made using any segment of bowel isolated on its vascular pedicle (Figs 65.20,65.21,and 65.22). This is then detubularised by dividing its antimesenteric border and suturing this into a plate. This can then be re­configured into a spherical structure. This reservoir can then be anastomosed to the bladder remnant after excision of the fundus above the trigone. If necessary, the ureters can be re­implanted into the bowel segment. This new bladder (Fig. 65.23) will almost certainly need to be emptied by means of intermittent self-catheterisation (CISC).

‘Clam’ enterocystoplasty. This procedure was originally described by Bramble for the treatment of nocturnal enuresis. It is now being used more frequently in the treatment of idiopathic detrusor instability. It involves the isolation of a 16-cm segment of ileum on its vascular pedicle. This is divided on its antimesenteric border and sutured into the opened out bladder. The bladder is divided along a circumference from bladder neck at 3 o’clock to 9 o’clock in the coronal plane (Fig. 65.24). This procedure can also be used as an augmentation procedure in patients with neurogenic bladder dysfunction and a reasonable preoperative bladder capacity (approximately 300 ml).

Fitment of artificial urinary sphincter. See Fig. 65.19.

Treatments for incontinence

1.  Devices for collection            External penile condom, indwelling
     or control                               catheter, penile clamps
2.  Drugs                                     To increase the strength of the
                                                   bladder neck (e.g. a-adrenergic
                                                   agonists), to decrease the
                                                   strength of the bladder neck (e.g.
                                                   a-adrenergic blockers), mixed
                                                   action on the bladder neck and
                                                   central nervous system (e.g.
                                                   tricyclic drugs), inhibit bladder
                                                   activity (e.g. anticholinergic drugs)

3. Intermittent self­-
  catheterisation

     to improve emptying

4.  Surgery to decrease outlet         Prostatectomy, urethrotomy in
     resistance                                 females with obstruction

5. Increasing outlet                         Pelvic floor physiotherapy,
     resistance                                 colposuspension or slings,
                                                     periurethral collagen or silicone
                                                     particles, artificial urinary sphincter

6. Denervation of bladder             Neurectomy procedures,
     (to inhibit bladder activity          transection of bladder
     and improve functional
     capacity)
7. Augmentation of bladder ‘         Clam’ enterocystoplasty, bladder
     capacity                                   substitution with detubularised
                                                     bowel segment

8.  Urinary diversion                     Ileal conduit, continent urinary
                                                     diversion