The bladder has a rich parasympathetic nerve supply (Figure 50.2). The postganglionic cell bodies lie either in the bladder wall or pelvic plexuses, innervated by preganglionic fibres that originate from cell bodies in the grey columns of S2–4. There is little sympathetic innervation of the bladder, although greater quantities of noradrenergic terminals can be detected in the bladder neck or trigone. Noradrenergic effects can be either inhibitory or excitatory, depending on the receptor type present.

• α-Receptors, located predominantly in the bladder base, cause detrusor contraction. They can be manipulated with limited success with α-adrenergic agonists to treat mild stress incontinence.

• β-Receptors which cause detrusor relaxation are found in the dome of the bladder.

Figure 50.2 The major innervation pathways at the pelvic level that are basic to control of micturition and continence.

The cell bodies of the sympathetic nerves originate in the grey matter of T10–L2, and pass through the sympathetic chain via the lumbar splanchnic nerve and left and right hypogastric nerves to the pelvic plexus. It is thought that the sympathetic nervous system exerts its effects by inhibiting the parasympathetic nervous system rather than by direct action. The visceral nerve afferents pass along the sacral and thoracolumbar visceral efferents, relaying sensations of touch, pain and distension. However, transection has little or no effect on micturition. The urethra possesses similar autonomic innervation. Parasympathetic efferents cause contraction but the functional significance of this remains in doubt. There is no obvious sphincteric function, but contraction produces shortening and widening of the urethra along with detrusor contraction during micturition. Sympathetic efferents innervate the predominantly α-adrenoreceptors.

Innervation of striated muscle

The rhabdosphincter muscle is supplied via the pelvic splanchnic nerves travelling with the parasympathetic fibres to the intrinsic smooth muscle of the urethra. This is analogous to the puborectalis muscle.

The extrinsic periurethral muscle of the levator ani is innervated by motor fibres of the perineal branch of the pudendal nerve. This is in common with the external anal sphincter (EAS). The pudendal nerve also supplies the striated elements of the levator ani on both sides, and there are associated somatic afferent fibres which travel with the pudendal nerves. They ascend via the dorsal columns to convey proprioception from the pelvic floor.

Central nervous control of continence

The connections of the lower urinary tract within the central nervous system are complex (Figure 50.3). There are many discrete areas which influence micturition, and these have been identified within the cerebral cortex, in the superior frontal and anterior cingulate gyri of the frontal lobe and the paracentral lobule; within the cerebellum, in the anterior vermis and fastigial nucleus; and in subcortical areas, including the thalamus, the basal ganglia, the limbic system, the hypothalamus and discrete areas of the mesencephalic pontine medullary reticular formation. The full function and interactions of these various areas are incompletely understood, although the effects of ablation and tumour growth in humans and stimulation studies in animals have given some insights.

Figure 50.3 The interaction of the nervous system in micturition. Locations of possible nervous lesions are denoted by numbers. 1, lesions isolating superior frontal gyrus will prevent voluntary postponement of voiding; 2, lesions isolating paracentral lobule, often with hemiparesis, will cause spasticity of urethral sphincter and retention; 3, pathways of sensation are not known accurately; in theory, isolated lesion of sensation above brainstem would lead to unconscious incontinence, and defective conduction of sensory information would explain enuresis; 4, lesions above brainstem centres lead to involuntary voiding that is coordinated with sphincter relaxation; 5, lesions below brainstem centres but above the sacral spinal cord lead, after a period of bladder paralysis, to involuntary ‘reflex’ voiding that is not coordinated with sphincter relaxation.

The centres within the cerebral cortex are important in the perception of sensation in the lower urinary tract, and the inhibition and subsequent initiation of voiding. Lesions in the superior frontal gyrus and the adjacent anterior cingulate gyrus reduce or abolish both the conscious and unconscious inhibition of the micturition reflex. The bladder tends to empty at low functional capacity. Sometimes, the patient is aware of the sensation of urgency; sometimes, micturition may be entirely unconscious. These areas, which have been localized by functional magnetic resonance imaging (MRI), are supplied by the anterior cerebral and pericallosal arteries; spasm or occlusion of these arteries produces incontinence.

Localized lesions more posteriorly in the paracentral lobule may produce retention rather than incontinence because of the combination of impaired sensation and spasticity of the pelvic floor.

The thalamus is the principal relay centre for pathways projecting to the cerebral cortex, and ascending pathways activated by bladder and urethral receptors synapse on neurones in specific thalamic nuclei which have reciprocal connections with the cortex. Electrical stimulation of the basal ganglia in animals leads to suppression of the detrusor reflex, whereas ablation has resulted in detrusor hyper-reflexia; patients with Parkinsonism are commonly shown to have detrusor instability on cystometric examination.

Within the pontine reticular formation are two closely related areas with inhibitory and excitatory effects on the sacral micturition centre in the conus medullaris. Lesions of the cord below this level always lead to incoordinate voiding with a failure of urethral relaxation during detrusor contraction; lesions above this level may be associated with normal although involuntary micturition.

The mechanism of urinary continence

The mechanism of urinary continence is a complex dynamic process which relies on intact fascia, ligaments and muscles with their accompanying nerve and vascular supply. It relies on maximum urethral pressure being higher than maximum detrusor pressure. There are special features of physiology and anatomy that contribute to the maintenance of a low detrusor pressure, and adequate urethral closure and positioning. These features are discussed below.

Bladder

An intravesical pressure that exceeds urethral pressure will lead to incontinence. There are a number of factors which maintain a low intravesical pressure.

The hydrostatic pressure at the bladder neck

Any fluid within the bladder will itself have a pressure. This is due to a vertical gravitational pressure gradient. For clinical purposes, the intravesical pressure defines the pressure in the bladder with respect to atmospheric pressure measured at the level of the upper border of the symphysis pubis. This pressure works against the mechanisms that produce urethral closure, and very rarely amounts to more than 10 cmH₂O.

Transmission of intra-abdominal pressure

The bladder is normally an intra-abdominal organ and is subject to the pressures of adjacent organs and abdominal pressure. The pressures are normally equally transmitted to the bladder, the bladder neck and proximal areas of the urethra, and this helps to maintain continence.

Tension in the bladder wall

Due to higher control of the basic visceral reflexes, the bladder does not contract in response to stretch receptors within the bladder wall. This and the actual ability of the bladder to be compliant (i.e. to allow for a large rise in volume and little rise in pressure) make it an ideal storage organ.

Urethra

There are several components of urethral function that are necessary to maintain good urethral closure.

The hermetic seal

The vascularity in the submucosal urethral plexuses has been mentioned above, and there are also secretions that allow this seal to be maintained. This may fail after the menopause.

The intrinsic smooth and striated muscles and the extrinsic striated muscles

The intrinsic smooth and striated muscles exert a constant pressure from their constant tone, and the extrinsic striated muscle contracts during moments of stress to maintain urethral closure. It has been estimated from urethral pressure studies that resting urethral pressure is one-third due to external striated muscle effects, one-third due to smooth muscle effects and one-third due to its vascular supply. The highest pressure is found at the midurethral point.

Urethral support

From cadaveric studies, ultrasound and MRI, it is postulated that the urethra is supported by a hammock (Figure 50.4). This hammock is contributed to by its immediate intimate relationship with the vagina, and the pubocervical fascia that lies between them and attaches laterally to the arcus tendineus fascia pelvis, which attaches to muscle fascia and which are in connection with the levator ani muscles themselves. During any rise in abdominal pressure, these may cause compression of the urethra against the anterior vaginal wall. In this model, it is the stability of the supporting structures rather than the height of the urethra that determines stress continence. In an individual with a firm supportive layer, the urethral compression can be compared with the way that the flow of water through a garden hose can be stopped by stepping on it and compressing it against concrete. The pubourethral ligaments also contribute to midurethral support.

Figure 50.4 Fascial breaks.

Normal micturition cycle

Filling and storage phase

The bladder normally fills with urine by a series of peristaltic contractions at a rate of between 0.5 and 5 ml/min. Under these conditions, the bladder pressure only increases minimally. Urethral closure is maintained by the three mechanisms mentioned above. During the early stages of bladder filling, proprioceptive afferent impulses from the stretch receptors within the bladder wall pass via the pelvic nerves to sacral dorsal roots S2–4. These impulses ascend in the cord via the lateral spinothalamic tracts, and any detrusor motor response is inhibited by descending impulses from higher centres. As bladder filling continues, further afferent impulses ascend to the cerebral cortex, and eventually a first sensation to desire is appreciated. This is usually at approximately half of functional bladder capacity. The impulses increase as volume increases and reinforce conscious inhibition; micturition occurs when a suitable site and posture for micturition is found. At this time, in addition to the cortical suppression of detrusor activity, there may also be a voluntary pelvic floor contraction in an attempt to improve urethral closure.

Initiation phase

When a suitable time, site and posture for micturition have been selected, the process of voiding commences. Relaxation of the pelvic floor occurs early in the process of initiation and micturition. This can be observed radiologically and also by performing electromyography where an electrical silence is recorded. It is likely that a simultaneous relaxation of the intrinsic striated muscle also occurs, since a marked decrease in intraurethral pressure is seen before the intravesical pressure rises. A few seconds later, the descending inhibitory influences are suppressed, allowing rapid discharge of efferent parasympathetic impulses via the pelvic nerves to cause detrusor contraction at the bladder neck. In addition, there is probably efferent sympathetic discharge encouraging urethral relaxation.

Voiding phase

When the decreasing urethral pressure and increasing intravesical pressure equate, urine flow will commence. As bladder emptying occurs, the radius of the bladder decreases. However, the pressure remains constant during voiding, and therefore it is likely that the tension of the wall decreases as voiding continues. If micturition is voluntarily interrupted midstream by contraction of the periurethral striated muscle, the urethral pressure rises rapidly and urine flow stops. The detrusor is much slower to relax and therefore goes on contracting against the sphincter, and an isometric contraction occurs. At the end of micturition, the intravesical pressure gradually decreases as urine flow diminishes. The pelvic floor and intrinsic striated muscle are contracted, flow is interrupted in the mid urethra, and a process of milkback occurs where a few drops of urine are forced back into the bladder as urethral closure occurs in a cephalad direction.

Pathophysiology of urinary incontinence

The pathophysiology of major causes of incontinence is discussed in some detail in the following chapters. A few general principles are considered here.

If the lower urinary tract is intact, urine flow can only occur when the intravesical pressure exceeds the maximum urethral pressure or when the maximum urethral pressure becomes negative. Causes of this are discussed in later chapters but may be largely due to childbirth, with direct mechanical injury to the supports including muscle and connective tissue, and following denervation injury to those muscles. Ageing also plays a part, as does pelvic floor surgery and radiotherapy. Incontinence, therefore, may occur as a result of:

• a decrease in urethral pressure associated with an increase in intravesical pressure. This can occur during normal voiding or in cases of detrusor instability (Figure 50.5A);

• an increase in intravesical pressure associated with an increase in urethral pressure where the latter rise is insufficient to maintain a positive closure pressure. This may be the case in detrusor instability with associated detrusor sphincter dyssynergia (Figure 50.5B);

• an abnormally steep rise in detrusor pressure during bladder filling, suggesting impaired bladder compliance. This can occur after pelvic irradiation or with conditions that cause chronic inflammation such as tuberculosis or interstitial cystitis (Figure 50.5C);

• loss of urethral pressure alone. This can occur in urethral instability and also in women who have urethral insufficiency or, as it is otherwise termed, ‘intrinsic sphincter deficiency’. This can commonly occur in the menopause, or after radiotherapy or surgery (Figure 50.5D); or

• during periods of stress, the intravesical pressure rises to a greater extent than the intraurethral pressure. This is usually due to a lack of urethral support, or an abnormally positioned bladder neck and proximal urethra where equal pressure transmission does not occur (Figure 50.5E).

Figure 50.5 Mechanisms of urinary incontinence showing changes in urethral and intravesical pressure and pelvic floor electromyogram (EMG) at various stages of bladder filling in different types of incontinence. (A) Normal voiding or detrusor instability. (B) Detrusor instability with detrusor sphincter dyssynergia. (C) Impaired bladder compliance. (D) Urethral instability. (E) Genuine stress incontinence.

Effect of continence surgery on mechanisms of continence

There are many operations for stress incontinence and the mechanism of their actions is debated. Operations such as the Burch colposuspension and Marshall–Marchetti–Krantz elevate the bladder neck, and this is assumed to restore it to its zone of equal pressure transmission. This has been shown using pressure transmission ratios, where increased pressure is transmitted to the proximal quartile of the urethra, but there are obviously obstructive components that also contribute. Bladder neck injectables have been used to increase urethral length, allowing better transmission to the proximal urethra. Finally, tension-free vaginal tape and its evolutionary descendants obturator and single incision tapes are thought to work by increasing the support of the urethra in the midurethral zone, rather than influencing bladder neck position.

Anal Incontinence

Definition

Faecal incontinence is defined as ‘the involuntary or inappropriate passage of faeces’ (Royal College of Physicians 1995). This definition, however, is incomplete as it may not include incontinence to flatus. Therefore, many adopt the term ‘anal incontinence’ to include flatus. Furthermore, this definition includes transient episodes of incontinence that may be experienced following a bout of gastrointestinal upset, and therefore a definition similar to that proposed by the International Continence Society for urinary incontinence may be more appropriate; namely, anal incontinence is the involuntary loss of flatus or faeces that is a social or hygienic problem.

Prevalence of anal incontinence

The estimated community prevalence of faecal incontinence is 4.2 per 1000 in men aged 15–64 years, 10.9 per 1000 in men aged 65 years or over, 1.7 per 1000 in women aged 15–64 years and 13.3 per 1000 in women aged 65 years or over. In residential homes for the elderly, the incidence was found to be 10.3% but may approach 60% in the elderly. Although the incidence of faecal incontinence in 45-year-old women is eight times higher than that in men of the same age, its prevalence has not been accurately assessed in the younger age groups. Even a minor degree of faecal incontinence can be very distressing and is a cause of great embarrassment; therefore, very few admit to it and seek medical assistance. In one study, half the patients referred to a gastrointestinal clinic complaining of diarrhoea were incontinent, but less than half of them volunteered this information. Moreover, clinicians may not enquire or document this symptom, and therefore the true prevalence of faecal incontinence can be grossly underestimated. A validated scoring system would therefore be more representative for epidemiological and research purposes. The Wexner scoring system is very popular and includes the need to wear a pad and alteration in lifestyle (Table 50.1). A modified version of the Wexner score has also been introduced to include faecal urgency, the ability to defer defaecation and the use of antidiarrhoeal medications.

Table 50.1 The Wexner score

The anal sphincter mechanism

The puborectalis and the external anal sphincter

Proximally, the EAS lies in contiguity with the posterior half of the puborectalis; distally, it merges with the perianal skin. Like the levator ani, it is primarily composed of striated muscle. There is lack of consistency in the literature with regard to the structural subdivisions of the EAS. Some authors describe it as one structure, while others have subdivided it into two or even three components: the subcutaneous and deep EAS as annular muscles not attached to the coccyx, and the superficial EAS (middle layer) as being elliptical with fibres running anteroposteriorly from the perineal body to the coccyx and the anococcygeal raphe (Figure 50.6). The deep EAS has anterior fibres which cross over to the opposite side and combine with the superficial transverse perinei attaching to the ascending ramus of the ischium. Electrophysiological techniques have shown that the motor supply of the puborectalis is via direct branches of the sacral nerves (S3 and S4), and that of the EAS is via the pudendal nerve (S2–4). This supports the contention that the puborectalis is part of the levator ani and separate from the anal sphincter. Nevertheless, close cohesion between these muscles would seem to be essential because without it, peristalsis would pull the rectum upwards and over its contents without expelling them through the anus. Frustration in attempts to identify these subdivisions of the EAS led some authors to propose that the EAS is, in fact, a single structure with no real subdivision. As these subdivisions are not identified during surgery, they do not appear to be clinically relevant. However, a clear understanding of normal anatomy and variants is important during imaging (ultrasound and MRI) of the anal sphincter in order to avoid misinterpretation.

Figure 50.6 The anal sphincter mechanism showing the puborectalis and external anal sphincter (EAS), the longitudinal muscle, and the internal anal sphincter (IAS).

The longitudinal muscle

The longitudinal muscle of the anal canal is a direct continuation of the smooth longitudinal muscle of the rectum. Between the lower border of the internal anal sphincter (IAS) and the upper border of the subcutaneous EAS, it attaches to the anal skin to form the anal intermuscular septum. Many of the fibres then pass outwards, traversing the subcutaneous EAS to insert into the perianal skin to form the corrugator cutis ani. The functional significance of this muscle is unknown.

The internal anal sphincter

The IAS is continuous with the inner circular smooth muscle of the rectum, and terminates in a sharply defined, thickened, rounded lower margin, separated from the subcutaneous EAS by the anal intermuscular septum. The IAS measures approximately 3 mm in length and 5 mm in thickness. It is tonically active and under autonomic control, namely excitatory (sympathetic L1–2) and inhibitory (parasympathetic S2–4).

The defaecation cycle

The main reservoir for faeces is the transverse colon, and the rectum is usually empty. Although the rectum has a poor supply of intraepithelial receptors, it is sensitive to distension. The first sensation of rectal filling occurs at a volume of 50 ml, with a maximum tolerated volume of 200 ml. Depending on various factors such as gut motility and stool consistency, colonic contents are delivered at a variable rate to the rectum.

Following rectal distension with either faeces or flatus, the internal sphincter relaxes to allow sampling of rectal contents to take place by the specialized sensory epithelium of the anal canal (Figure 50.7). This relaxation is mediated via myenteric connections modulated by the autonomic nervous system, and is known as the ‘rectoanal inhibitory reflex’ (RAIR). If it is socially convenient, the puborectalis and external sphincter relax and evacuation occurs. If the time for evacuation is inappropriate, EAS contraction extends the period of continence to allow the compliance mechanisms within the colon to make adjustments in order to accommodate the increased rectal volume. Thereafter, the stretch receptors are no longer activated and afferent stimuli are abolished, together with the sensation of faecal urgency.

Figure 50.7 The mechanism of defaecation. EAS, external anal sphincter; IAS, internal anal sphincter.

The factors contributing to the mechanism of incontinence will be discussed in detail below.

Anal continence mechanisms

The mechanism that maintains continence is complex and affected by various factors such as mental function, lack of a compliant rectal reservoir, changes in stool consistency and volume, diminished anorectal sensation and enhanced colonic transit (Figure 50.8). However, analogous to urinary continence, anal continence can be maintained provided that the anal pressure exceeds the rectal pressure. As shown in Figure 50.6, the ultimate barrier to rectal contents is provided by the puborectalis sling and anal sphincters. An increased volume of liquid stool coupled with rapid colonic transit may overwhelm the compliant rectal reservoir. Therefore, if the rectum is able to function effectively as a rectal reservoir and in the presence of normal stool consistency, faecal incontinence can usually be attributed to defective function of the anal sphincter complex.

Figure 50.8 The mechanism of anal continence.

The physiological role of various components of this complex in maintaining continence will be considered separately.

The puborectalis muscle and the anorectal angle

The anorectal angle is formed by the anteriorly directed pull of the puborectalis. The angle varies from 60° to 105° at rest; during defaecation, the angle straightens, allowing the rectum to empty. Two theories have been proposed to explain how the anatomical angulation at the anorectal junction may contribute to maintain continence. The first is the ‘flutter’ valve, which is created as the rectum passes through the slit-like aperture in the pelvic floor caused by the forward pull of the puborectalis; a rise in intra-abdominal pressure would create a high-pressure zone and result in apposition of the rectal walls at the anorectal junction. The second is the flap valve theory; contraction of the puborectalis creates an acute anorectal angle, and intra-abdominal forces compress the anterior rectal wall against the upper anal canal. However, both these theories have lost credibility; for a flutter valve to produce such a high-pressure zone, intra-abdominal forces would have to be applied below the pelvic floor. Moreover, both theories would account for rectal pressures in excess of anal canal pressures without evacuation of rectal contents. As rectal pressures have been shown to be consistently lower than anal pressures in healthy subjects, continence must be sphincteric and not valvular.

The puborectalis is considered by some to be the most important muscle in maintaining continence. In children with congenital anomalies and absence of the anal sphincter, a high degree of continence can be maintained with the puborectalis. However, posterior division of the puborectalis in the treatment of chronic constipation made no difference to the anorectal angle, and was not associated with incontinence of solid stool. Furthermore, following successful postanal repair for faecal incontinence, no significant change was observed in the anorectal angle. The role of the anorectal angle in maintaining continence therefore remains controversial.

The puborectalis muscle functions in concert with the EAS, and it is probable that if damage occurs to one muscle, the other may compensate functionally. Faecal incontinence may ensue if, in addition, other factors in the continence mechanism (see below) are compromised or if the remaining muscle cannot compensate adequately.

Internal anal sphincter

There are conflicting opinions on the role of the IAS in maintaining continence. As 70% of the resting tone is contributed by the IAS, it is a major factor in keeping the anal canal closed at rest. This is supported by the finding that symptoms of incontinence can develop in up to 40% of cases following lateral internal anal sphincterotomy. Faecal incontinence has also been reported following anal dilatation, with sonographic evidence of internal sphincter disruption and a reduced resting pressure.

Ultrastructural changes have been identified in the morphology of the internal sphincter of patients suffering from neurogenic faecal incontinence. Although these changes are probably not the primary cause of faecal incontinence, they may have some relevance to IAS function. In addition, abnormalities of adrenergic innervation with a diminished sensitivity of the IAS to α-adrenergic agents in vitro have been demonstrated in patients with idiopathic faecal incontinence. These changes could be attributed to an intrinsic degeneration of the muscle and its receptors, or to simultaneous direct injury to the striated muscle of the pelvic floor.

The rectoanal inhibitory reflex

The RAIR or rectosphincteric reflex is a transient relaxation of the IAS when the rectum is distended. This response has been shown to persist in patients with cauda equina lesions and after complete transection of the spinal cord, indicating that it occurs independently of central control. It appears that the RAIR is mediated by intramural myenteric neurones because topical anaesthesia of the rectal mucosa blocks the reflex, and it is absent in patients with Hirschsprung’s disease.

The RAIR causes equalization of rectal and upper canal resting pressures, and allows rectal contents to enter the anal canal. The contents are then analysed by the specialized sensory epithelium in the anal canal (sampling reflex). This is accompanied by a reflex contraction of the external sphincter and puborectalis (inflation reflex), which temporarily maintains the high-pressure zone in the anal canal until either evacuation occurs or the anal contents are pushed back into the rectum. The sampling reflex occurs as a normal physiological process about seven times per hour. The absence of the reflex in patients with faecal incontinence would indicate a weakness of the IAS, whereas in Hirschsprung’s disease (segmental aganglionosis), it would be associated with obstructive defaecation rather than faecal incontinence. However, the value of this test is limited as the RAIR may be difficult to elicit consistently, even in healthy subjects.

The external anal sphincter

The EAS is inseparable from the puborectalis posteriorly, and both muscles appear to function as a single unit electrophysiologically. It has been shown that while contraction of the puborectalis accentuates the anorectal angle, it does not increase the intraluminal pressure of the anal canal.

The EAS contributes up to 30% of the resting pressure, and the increment of the squeeze pressure above the resting pressure predominantly reflects EAS function. The maintenance of tone is, however, also dependent on a sensory input, as it is lost if the sensory roots are destroyed (e.g. tabes dorsalis).

The response to changes in intra-abdominal pressure suggests that the EAS is actively involved in the preservation of continence. Further support for this hypothesis is that division of the internal sphincter alone can be associated with minor degrees of incontinence to flatus and liquid stool, but not usually to solid stool. These properties of the EAS may be diminished either by denervation, mechanical trauma or a combination of factors.

The anal cushions

The anal cushions, consisting of epithelium, subepithelium and the underlying haemorrhoidal plexuses, can contribute up to 15% of resting pressure. The anal sphincters cannot obliterate the lumen completely without the sealing effect of the anal cushions. The thickened cushions may account for the increased resting pressures seen in patients with haemorrhoids. The decrease in resting pressure following haemorrhoidectomy may explain the development of minor anal incontinence, although inadvertent damage to the sphincter, particularly the internal sphincter, has been observed using anal endosonography.

Rectal compliance

A compliant rectal reservoir that can accommodate large volumes of stool without significant increases in pressure is an important prerequisite for the effective function of barrier mechanisms of continence. Patients who have a reduction in rectal capacity, as occurs in colitis and radiation proctitis, often suffer from faecal urgency and incontinence.

Anorectal sensation

The epithelium of the anal canal is richly supplied with sensory nerve endings, exquisitely sensitive to pain, heat and cold. The afferent nerve pathways for anal canal sensation is via the posterior inferior haemorrhoidal branches of the pudendal nerve and anterior haemorrhoidal branches of the perineal nerve to the sacral roots of S2, S3 and S4, but in addition, direct anal and urethral branches arise from S4 and S5. Sampling has been shown to occur less frequently in incontinent patients compared with controls.

Central control of anal continence

The upper motor neurones for the voluntary sphincter muscles lie close to those of the lower limb musculature in the parasagittal motor cortex. They communicate by a fast conducting oligosymptomatic pathway, with the Onuf nucleus situated in the sacral ventral grey matter, mainly S2 and S3. The frontal cortex is important for the conscious awareness of the need to defaecate and appropriate social behaviour. Disease affecting the upper neurone motor pathway usually results in urgency and urge incontinence, and provided the lower motor pathway is still intact, reflex defaecation will still be possible. Neurological diseases such as multiple sclerosis, Parkinson’s disease and disorders of the spinal cord or cauda equina can be accompanied by incontinence because the central pathways which control sphincter function are located in the vicinity of the corticospinal tracts. Patients suffering with diabetes mellitus can have an autonomic neuropathy and this can also lead to faecal incontinence.

The lower motor neurones innervating the striated pelvic floor and urethral and anal sphincters arise from the Onuf nucleus. The most common cause of a lower motor neurone lesion in the adult is chronic stretching of the pudendal nerve, usually as a result of chronic straining at stool and/or childbirth. Damage to the pudendal nerve results in progressive denervation and reinnervation of the pelvic floor–anal sphincter complex, causing weakness and atrophy of these muscles.

Pathophysiology of anal incontinence

The development of anal incontinence may be due to either mechanical disruption or neuropathy, but sometimes both coexist. Obstetric trauma is a major cause of such injury, although the peak incidence appears to be in the perimenopausal years. The development of anal endosonography has revolutionized our understanding of anal incontinence, and it has now been demonstrated that approximately one-third of primiparous women develop anal sphincter injury that is not recognized during vaginal delivery. However, even when it is recognized and repaired, the outcome is suboptimal as one-third continue to suffer impaired continence. Attention is now being focused on improved training in anatomy and repair techniques. However, there are other factors such as the effect of ageing, collagen weakness, progression of pelvic neuropathy, oestrogen deficiency, concurrent irritable bowel syndrome, primary degeneration of the IAS, severe constipation and uterovaginal/rectal prolapse that may contribute to a deterioration in anorectal function.

Effects of continence surgery on mechanisms of continence

The most common operation for faecal incontinence is an overlap anterior sphincteroplasty which serves to re-establish the continuity of the anal sphincter muscle ring in patients with a sphincter defect. In addition, some surgeons perform a levatoroplasty while others imbricate the internal sphincter. This operation has a success rate of 70–80%, although this can deteriorate to nearer 50% by 5 years. Anal pressures, particularly the voluntary squeeze pressure, increase. Pelvic neuropathy can cause atrophy of the sphincter muscles and hence have an adverse outcome. Some studies have suggested that a prolonged pudendal nerve latency prognosticates a poor outcome, but other studies have failed to identify a correlation. An abnormally prolonged latency of >2.4 ms in isolation correlates poorly with anal squeeze pressures, and therefore some neurophysiologists believe that this is not a good test of neuropathy as it is only a measure of conduction in the fastest conducting motor fibres of the pudendal nerve.

The postanal repair is performed when faecal incontinence is due to a neurogenic cause leading to pelvic floor atrophy. The intention is to recreate the anorectal angle by placating the levators at the back of the rectum. However, current evidence indicates that this operation does not have a significant effect on the anorectal angle, but appears to increase the functional length of the anal canal and may improve anal canal sensation.

Other surgical options include stimulated gracilis muscle neoplasty and artificial anal sphincter.

Sacral nerve modulation is a relatively new technique that has added a new dimension to the management of faecal incontinence and defaecatory disorders. Short-term results are very encouraging with minimal morbidity. This technique provides new hope to women who otherwise would be left with no option but a stoma.

Comparison between Bladder and Bowel

Reflex adaptation of the rectum and bladder in response to filling are fairly analogous. There is an inverse relationship between distension and compliance. The ‘irritable bladder’ is more often found in patients with irritable bowel syndrome. The aetiology of faecal and urinary incontinence may also be comparable, and Table 50.2 compares bladder and bowel conditions.

Table 50.2 Comparison of bladder and bowel conditions

Bladder	Bowel
Detrusor overactivity	Irritable bowel syndrome
Urodynamic stress incontinence	Faecal incontinence
Detrusor sphincter dyssynergia	Anismus
Urgency	Urgency
Hypotonic bladder	Constipation