Anorectal incontinence is a relatively common and profoundly disabling complaint, which can be defined as the inability to delay discharge from the anal canal until a suitable moment arises. In the community, the prevalence of anorectal incontinence increases with age such that 1.1 per cent of men and 1.3 per cent of women over 65 years of age are affected. Some groups, notably long-stay geriatric and psychogeriatric patients, are more commonly affected, with up to 60 per cent suffering leaks of faeces each day.

This is achieved by the interplay of functional sphincters, anorectal sensitivity, rectal compliance, and stool composition. Of these, the smooth muscle internal anal and striated muscle external anal sphincters are of prime importance. Both are tonically active at rest but the internal anal sphincter is responsible for 80 per cent of tone in this state. The internal sphincter relaxes in response to rectal distension (the rectosphincteric reflex) and its importance in normal and disordered continence is being increasingly recognized.

The external sphincter encircles the internal anal sphincter and is innervated by the pudendal nerve (sacral roots S3 and S4). Its activity is recruited when continence is threatened, either by raised intra-abdominal pressure (coughing or straining) or when the internal sphincter relaxes and defecation is not planned. Superiorly, the external and sphincter blends with puborectalis. The forward pull of this, the most medial part of the levator ani, produces angulation at the anorectal junction and luminal occlusion. The puborectalis therefore functions as a sphincter, enhancing continence to solids. It does not, however, act as a ‘flap valve’ as was previously thought.

The anal canal has a rich sensory innervation that is able to discriminate between gas, liquids, and solids. Sensory nerve endings may be brought into contact with the contents of the rectum in a process called anorectal sampling. Sampling occurs subconsciously several times each minute and is facilitated by internal sphincter relaxation which abolishes the pressure gradient between the rectum and upper anal canal (Fig. 1) 1182. Mechanoreceptors that lie in the muscles of the pelvic floor and side walls subserve the sensation of rectal fullness.

Even if the motor and sensory components of the anal canal function normally, continence can still be threatened by the arrival of copious amounts of fluid stool, especially if rectal compliance is diminished, as it is in patients with inflammatory bowel disease or following irradiation.

Anorectal incontinence can occur when any facet of the normal continence mechanism is defective. The causes of such abnormalities are outlined in Table 1 354, and some are discussed below.

This common cause of incontinence should always be considered in the elderly and patients in institutions. Those affected show diminished anorectal sensation combined with a failure of the external sphincter to respond to internal sphincter relaxations. In addition, the internal sphincter relaxes at lower levels of rectal distension when compared with normal age-related individuals.

The sphincters may be divided erroneously at the time of anorectal surgery or may be damaged by accidental injuries. Direct sphincter injury also occurs during childbirth, making this a significant and potentially preventable cause of incontinence. Patients who sustain anal sphincter injuries during childbirth should be offered elective caesarian section in subsequent pregnancies to prevent further damage.

This is the most common cause of primary anorectal incontinence seen in adult surgical practice, and it particularly affects middle-aged women. Histological and electrophysiological examination of the striated muscle components of the continence mechanism indicate the presence of a denervation/reinnervation injury which is probably caused by stretching of the pudendal and pelvic nerves. Such stretch injuries may occur first during childbirth and are then compounded by subsequent, chronic straining at stool. As well as striated muscle weakness, affected patients may have diminished anal sensation, abnormal anorectal sampling and weakness of the internal anal sphincter.

All patients attending coloproctology or gastroenterology clinics should be asked directly about anorectal incontinence as this may be a hidden symptom. Many patients complain of diarrhoea when they in fact have urgency and incontinence. The character and frequency of the leakage should be determined and careful attention paid to defecatory, previous medical, and obstetric histories. Neurological symptoms must be documented.

It is important to perform a complete examination since incontinence can be a manifestation of disease outside the anorectum. Particular attention should be paid to the abdomen and the innervation of the perineum and lower limbs. Inspection of the perineum, anus, and rectum should be performed with the patient in the left lateral position at rest and while performing the Valsalva manoeuvre. The presence of soiling, scarring, the external opening of a fistula, a patulous anus, perineal descent, and prolapse should be noted. The integrity of perineal innervation should be determined by testing pin-prick sensation and the anocutaneous reflex. Digital anorectal examination allows qualitative assessment of the resting anal pressure as well the changes which occur on voluntary contraction and coughing. Indeed, digital examination performed by an experienced physician may be as good as formal anal manometry in assessing anal sphincter function. The presence of impacted faeces, other masses, and tenderness should be noted. All patients should undergo proctoscopy and sigmoidoscopy to exclude neoplasia, inflammatory bowel disease, fistulae, fissures, mucosal prolapse, and haemorrhoids.

A thorough clinical assessment will usually disclose reveal a diagnosis without recourse to specialist investigations. These may, however, be required and are outlined here.

Measurement of anal canal pressures allows assessment of the function of both sphincters. A variety of pressure measuring devices which use perfused, balloon-tipped (air- or water-filled) or microtransducer-tipped catheters is now available. These are inserted into the rectum and then gradually withdrawn. Once the high-pressure zone of the sphincters is reached, the distance from the anal verge is noted and the pressure recorded at 1-cm intervals (stations) as the catheter is removed. The pressure produced by the internal sphincter (maximum resting pressure) and the resting sphincter length can thus be measured (Fig. 1) 1182. The procedure is then repeated with the patient attempting to close the anal canal as tightly as possible so that a measure of external sphincter performance is derived (maximum voluntary contraction pressure).

The integrity of the rectosphincteric reflex can be assessed by measuring anal pressures during incremental inflation of a rectal balloon (Fig. 1) 1182. Inflation of a balloon in the rectum allows measurement of rectal sensation (recording when distension is first perceived as well as the maximum tolerated volume) and rectal compliance. These features can also be assessed by the saline continence test in which up to 1500 ml of warmed saline is infused into the rectum while anal and rectal pressures are recorded. The volume at which leakage occurs provides another measure of external sphincter function.

Sensation within the anal canal is routinely quantified by measuring anal mucosa electrosensitivity. A constant current of increasing strength is applied between two platinum electrodes mounted on a catheter placed within the anal canal, and the level (mA) at which it is first perceived (a tingling or pulsing sensation) is recorded for the upper, middle, and lower zones of the canal. Sensation is reduced in some patients with anorectal incontinence.

Nerve-mediated muscle contraction is initiated by membrane depolarization, which generates electrical activity. The analysis of this activity forms the basis of electromyography. A single efferent motor nerve, arising from an anterior horn cell, may innervate a number of muscle fibres. Together these constitute a ‘motor unit’, the characteristics of which are altered in various disease states. For example, in idiopathic anorectal incontinence some muscle fibres are denervated by a traction injury. As reinnervation occurs, both from ingrowth of adjacent nerves and from regrowth of the damaged neurone, the number of muscle fibres innervated by a single motor nerve will increase, and they will tend to be clumped together rather than being dispersed normally. These changes can be detected using either concentric or single fibre needle electrodes. The former has a relatively large uptake area and records the activity of several motor units. It is particularly helpful when direct sphincter injury is suspected, since the damaged area is electrically silent. Single fibre electromyography allows analysis of changes in single muscle fibres.

Surface electrodes are used in nerve conduction studies and in the measurement of nerve latency. The pudendal nerve is most commonly studied, using a specially designed glove, with electrodes attached to the tip of the finger. These stimulate the pudendal nerve at the ischial spine and additional electrodes positioned more proximally on the finger detect the resulting contraction of the external sphincter. The speed with which the nerve conducts impulses can thus be measured: this is slowed in idiopathic anorectal incontinence (Fig. 2) 1183. Similar studies, using transcutaneous nerve stimulation, can be performed to assess the integrity of the cauda equina.

In most patients with anorectal incontinence it is wise to assess the entire large bowel to ensure that there is no proximal contributory lesion such as an unsuspected carcinoma. A colorectal survey can be achieved either by barium enema or by colonoscopy; it can be difficult to achieve adequate bowel preparation since incontinent patients have difficulty retaining preparatory enemas. The anorectum can also be assessed at proctography, by endoluminal ultrasound and by magnetic resonance imaging (MRI).

Anal ultrasonography yields high resolution images of both sphincters. Defects in the external sphincter caused by direct sphincter injury correspond with areas of electrical silence on electromyography. Damage to the internal sphincter can also be assessed.

Magnetic resonance imaging has several advantages. It does not rely on ionizing radiation, it allows images to be generated in multiple planes, and it provides good soft tissue characterization. MRI is of great value in assessing patients with congenital anorectal anomalies, either when they first present or later when they suffer from poor anal function and when further surgery is contemplated.

Investigations are useful when they aid diagnosis, direct management, or if they can predict the outcome of a particular treatment. To a large extent anorectal investigations are useful because they aid diagnosis and objectively measure abnormalities but, as yet, they do not have a more extended role in management. Although they have been used to assess the effects of treatment in clinical research, they do not generally predict outcome in individual patients. Electromyography and MRI are, however, useful in the management of congenital anorectal anomalies, while anal endosonography and concentric needle electromyography is of use in the diagnosis of sphincter tears. Nerve conduction studies are useful if they define a treatable cauda equina lesions such as a disc prolapse.

Conservative treatment should be tried in all patients, except when the clinical features and results of investigations suggest an underlying pathology such as inflammatory bowel disease, carcinoma or prolapse when appropriate treatment is required. Counselling of patients should aim at production of a solid stool once each day. Codeine phosphate or loperamide may be helpful and a low fibre diet is recommended. Such measures will be most beneficial in patients with mild symptoms. If their problem is transient or intermittent, or if they are satisfied with conservative treatment, nothing further need be done. A successful outcome can be expected in up to 40 per cent of patients treated by diet and drugs alone.

Other non-operative therapies include pelvic floor physiotherapy, biofeedback conditioning, and electrical stimulation. Promising early results have recently been reported in patients given repeated stimulation of the pudendoanal reflex arc, and biofeedback conditioning has been used successfully in some centres. These techniques are, however, time-consuming and have not yet proven to be of long-term benefit. In addition to these, we are currently investigating the use of an anal plug which is made of specially coated synthetic sponge. Plugs are inserted into the anal canal like a conventional suppository and expand once inside. Initial trials have shown that a ‘tulip’ shaped plug is tolerated best and is, on average, retained for 11 to 12 h. They are comfortable, easy to insert and remove, and only 20 per cent of plugs allow leakage whilst in use. Once available, it is hoped that plugs will be used alone or as an adjuvant to other measures.

If conservative measures fail to ameliorate the problem then surgical intervention should be considered. The options available are outlined in Fig. 3 1184. Patients undoubtedly fear the prospect of a permanent stoma and this should only be considered as a last resort when other measures have proved unsuccessful.

All patients should receive thorough preoperative bowel preparation with Picolax (Nordic, Feltham, UK) and appropriate antibiotic chemoprophylaxis, such as broad-spectrum antibiotics administered intravenously every 8 h on the day of operation, followed by oral administration for 6 days. Operations are performed in the lithotomy position, with the buttocks strapped apart. Adrenaline can be injected locally to reduce bleeding.

These should be explored through a curved perianal incision in the area of the previously defined defect (Fig. 4) 1185. The ends of the external sphincter are isolated by dissection and with the aid of peroperative nerve stimulation. Enough muscle is mobilized to allow an overlapping repair over a reasonable distance cranially (3–4 cm) so that an anal canal of adequate length can be reconstructed. The fibrous scar at the abrupted ends of the injured muscle can be used to secure the overlap. The repair is performed using non-absorbable sutures and, where possible, the internal anal sphincter is also tightened by imbrication.

This is the most commonly performed operation when pelvic floor and external sphincter weakness is due to neuropathy (Fig. 5) 1186. The sphincters are exposed through a curvilinear or ‘V’-shaped postanal incision and the intersphincteric plane is sought. This is the bloodless anatomical key to the operation which, when entered and followed superiorly, leads up to the pelvic floor, where Waldeyer's fascia is incised to gain access to the presacral space above. The levators—pubococcygeus and puborectalis—are approximated in turn, using interrupted non-absorbable sutures. The external sphincter is then imbricated with a similar suture. The muscles must not be opposed under tension as this may result in necrosis.

It is usually possible to close the skin after both procedures but, if this is not the case, the wound should be left to heal by secondary intention. A defunctioning stoma is not required routinely. In the postoperative period, patients remain on fluids only for 2 days before commencing a low residue diet. All receive a stool softening agent and are instructed to defecate only when they have the urge and to refrain from straining.

Anorectal incontinence is a complicating factor in 75 per cent of patients who present with complete rectal prolapse. Surgical correction of the prolapse by rectopexy fails to relieve incontinence in 30 per cent of these, particularly when there is marked weakness of the pelvic floor and sphincteric striated muscle. In such instances a combined approach is advised, rectopexy and postanal repair being performed at the first operation.

Repair of a direct sphincter injury restores full continence in 78 to 90 per cent of patients, with less than 10 per cent achieving no benefit at all. The results of postanal repair are outlined in Table 2 355. Although most patients gain some benefit, perfect continence is often not achieved. Technical failures may arise in the presence of concomitant proximal disease such as the irritable bowel syndrome or due to continuing neuropathy. It was formerly thought that the success of postanal repair is determined by restoration of anorectal angulation; however, it has now been shown that success is related to increasing sphincter pressures and enhancing anal canal sensation. Similar results are achieved with anterior sphincter plication and levatorplasty.

Patients who fail to benefit from these procedures are difficult to manage. A repair can be repeated or, if there has already been a posterior repair, an anterior repair can be performed. Anterior and posterior repairs can be undertaken simultaneously in patients with very weak sphincters. These procedures can be technically difficult and may again be unsuccessful. Alternative approaches which have been suggested, include the construction of a neosphincter by transposition of the gracilis muscle and the implantation of an artificial sphincter based on a device used in urinary incontinence. Gracilis transposition has been combined with prolonged neurostimulation, with the effect of converting it from a fast twitch to a slow twitch muscle. Problems arising from muscle necrosis and electrode instability seem to have been overcome. These techniques are still in their developmental phases, but hold promise for the future.

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