Anorectal manometry

Pressure in the anus and rectum is measured using a narrow diameter multichannel catheter. Each channel is perfused with water and connected to a pressure transducer and digital recording apparatus; sequential channels open at 0.75 cm intervals from the tip of the catheter (Fig 16.3). The pressure at rest reflects the strength of the internal sphincter, and pressure during voluntary contraction of the muscles is a measure of the external sphincter strength (Fig 16.4). Relaxation of the internal sphincter is tested by inflating a balloon positioned in the rectum at the tip of the manometry catheter, while recording anal pressure. Manometry is a very useful test because it defines which muscle is affected in a patient with sphincter weakness. It also demonstrates that sphincter function is normal in a patient whose incontinence is due to diarrhoea or excessive colonic propulsion, or due to a local anal condition such as haemorrhoids and, hence, confirms that sphincter weakness is not the cause of the incontinence.

Figure 16.3 Manometry catheter. Water perfusion catheter showing balloon at the tip inflated by water-filled syringe. Several pressure recording points are found at short intervals from the balloon to measure pressure along the anal canal.

Figure 16.4 Anorectal manometry. Manometry recording—pressures recorded simultaneously at three levels in the anal canal and one site in the rectum. Pressure at rest reflects the internal sphincter; an increase above the resting pressure is produced by a squeeze or cough, due to the external sphincter contraction. The rectoanal reflex (RAR) shows relaxation of the internal sphincter (seen as a fall in pressure in the anal recording) due to distension of the rectum with a balloon (seen as a rise in pressure in the rectum).

Electrophysiology

In patients with suspected neurogenic incontinence the function of the pudendal nerves is tested. Motor conduction is measured by transrectal stimulation of the nerves, using a fine disposable electrode mounted on the gloved index finger (Fig 16.5). The left and right pudendal nerves are stimulated at the point that each passes around the ischial spine and the conduction time to the external anal sphincter is recorded (Fig 16.6). Stretch-induced damage to the nerves caused by difficult vaginal delivery or chronic excessive straining at stool is reflected in the slowing of conduction in the nerves due to axonal degeneration. Sensory conduction is measured by delivering a small current to the anal mucosa. The current is increased in fractions of a milliamp until a slight, painless, tapping feeling is reported by the patient, and the threshold of stimulation is measured. With pudendal nerve damage there is loss of sensation, reflected as an increased threshold of stimulation.

Figure 16.5 Pudendal electrode strapped to index finger. Stimulating electrodes are at the tip and recording electrodes at the base of the finger.

Figure 16.6 Recording of pudendal motor latency. The arrow indicates the onset of the stimulus delivered to the pudendal nerve; there is then a delay (2 ms) due to the conduction time along the nerve (pudendal latency), followed by contraction of the external sphincter shown by a rise and fall in the trace. Damage to the pudendal nerve results in an increase in pudendal latency.

Electromyography is carried out using a fine needle electrode inserted into the external sphincter muscle. Muscle contraction is amplified and displayed as spikes of electrical activity. Normal muscle activity can be clearly distinguished from non-functional scar tissue, allowing the site and extent of a sphincter defect to be clearly defined (Fig 16.7). Electromyography is used less commonly, with the advent of endoanal ultrasound.

Figure 16.7 Electromyography of the external sphincter showing normal muscle activity at 3, 7, 8, 9 and 12 o’clock, and loss of activity at 6 and 11 o’clock due to sphincter damage.

Ultrasound

Endoanal ultrasound has become a valuable tool to study anal function. It is very accurate in identifying a defect in the internal or external sphincter, and is less invasive than electromyography. The ultrasound probe records through 360° to give a complete image of the sphincter (Figs 16.8 and 16.9).

Figure 16.8 Ultrasound machine, showing endoanal probe stored on the left side of the machine.

Figure 16.9 Endoanal ultrasound in a patient with incontinence. The internal sphincter is seen as a black ring, which is incomplete in this patient due to an anterior sphincter defect (shown between the arrows). The external sphincter is seen as the white band outside the internal sphincter.

Proctography

Barium studies of the anorectum are used to test the ability of the anal sphincter to maintain continence. Semisolid barium paste of similar consistency to soft stool is instilled into the rectum. Lateral x-ray examination is made of the rectum and anus while the patient coughs, moves and during a Valsalva manoeuvre, and the amount of leakage is assessed (Fig 16.10). This examination is used to confirm the diagnosis of neurogenic incontinence.

Figure 16.10 Proctography. Lateral X-ray film of the rectum (r) and anal canal (a) showing leakage of barium during coughing in a patient with neurogenic incontinence.

Aetiology

Diarrhoea, either acute or chronic, may overcome the ability of the normal sphincter to resist the forceful passage of liquid stool. High pressures generated in the colon may exceed the maximum pressure of the anal sphincter, and incontinence is then inevitable. Incontinence may even occur when stool consistency and frequency are normal, due to sudden excessive colonic propulsion.

Clinical features

In patients with diarrhoea, incontinence is sometimes preceded by lower abdominal pain or a sudden urgent call to stool. Other clinical features are discussed in Chapters 13 and 14.

Treatment

When there is a colonic cause for incontinence, simple antidiarrhoeal medication may produce a very dramatic improvement in some patients. Chronic diarrhoea should be investigated with fresh stool specimens sent for microscopy and culture, and with sigmoidoscopy or colonoscopy. Special tests for malabsorption or more rare causes of diarrhoea (see Ch 14) will be indicated in some cases.

Once secondary causes have been excluded, diarrhoea should be treated with a small regular prophylactic dose of loperamide, usually one 2 mg tablet taken daily in the morning. The aim of treatment is to suppress colonic activity sufficiently to produce slight firmness of the stool. There is no benefit gained from taking this medication after a loose stool is passed. Loperamide also has the added benefit of producing direct contraction of the internal sphincter muscle and, hence, raising resting anal pressure in some patients.

Treatment

With a normal sphincter, treatment, if successful, will result in the return of normal continence. Rectal cancer presenting with incontinence is treated by surgery according to conventional principles (Ch 22). Prolapsing haemorrhoids and anal mucosal prolapse causing incontinence usually require rubber-band ligation (Ch 12). Occasionally when the prolapse is large, surgical excision is required. Anal fissure causing incontinence is always a deep chronic fissure, which should be treated surgically by lateral sphincterotomy. Abnormalities in rectal sensation may respond to loperamide because of the constipating effect of the drug.

Supranuclear lesions

The cerebral control of sphincter function is located in the orbitofrontal cortex and conditions affecting this area, such as dementias, are particularly liable to present with incontinence. Upper motor neurone lesions also result from multiple sclerosis, multifocal atherosclerotic vascular disease or spinal trauma above the S2 level. Some disorders, especially motor neurone disease, are accompanied by widespread muscle wasting but relative preservation of the sphincter muscles because of sparing of the motor neurones in the Onuf nucleus.

Infranuclear lesions

Lower motor neurone lesions cause denervation of the sphincter muscles and hence incontinence. This results from damage to the sacral nerve roots in the pelvis or within the cauda equina. Cauda equina disease results from sacral spondylosis, disc prolapse, trauma, or intraspinal neoplasms. Pelvic lesions include tumours—either primary presacral tumours or recurrent carcinoma after excision of the rectum.

Treatment

There is no effective curative treatment for most supranuclear lesions, including multiple sclerosis, and for most dementias. Localised spinal conditions such as disc prolapse or tumours may be amenable to surgical treatment.

Aetiology

Rectal prolapse is a primary intussusception of the bowel. Constipation and impaired rectal evacuation leading to straining at stool are sometimes present and may contribute to the development of prolapse. Trauma during childbirth is probably not a significant contributing factor as many women with prolapse are nulliparous. Almost all cases of prolapse in children are due to constipation and straining.

Clinical features

The condition is most common over the age of 50 years, and a smaller number of patients are in the 20–50-year age group. It occasionally occurs in children.

Most elderly patients complain of a prolapse during defecation, which either reduces spontaneously or must be manually reduced. Sometimes the prolapse occurs spontaneously when the subject walks about. The prolapse is accompanied by mucus discharge.

There are two distinct forms of rectal prolapse:

Treatment

Rectal prolapse in children is usually due to constipation and straining and should be treated conservatively with dietary measures (Ch 11).

In adults, if the prolapse is small, it reduces spontaneously and is not accompanied by incontinence, it can be treated conservatively. With mild symptoms or a patient with poor functional status, conservative treatment including encouragement to avoid straining at stool and treatment of constipation with bulk-forming agents (e.g. psyllium or sterculia) might be all that are indicated.

If the prolapse is more severe surgery is needed. There are many operative procedures used in the treatment of rectal prolapse, indicating that no procedure produces an entirely satisfactory result. There are two approaches that can be used: an abdominal procedure or a perineal procedure. With an abdominal operation there is a low long-term incidence of recurrent prolapse and also a 75% chance of curing the incontinence, but this is achieved with the risks and morbidity that accompany a major abdominal operation. This is particularly relevant in very elderly patients with prolapse. Perineal procedures are associated with very little pain or other morbidity, but carry a higher incidence of recurrent prolapse. Incontinence is cured less frequently by these procedures than by an abdominal procedure. The choice of a particular procedure in a patient therefore needs to take into account such factors as the age and general medical status of the patient, the expected remaining lifespan, and the severity and nature of the symptoms. For example, a young patient with prolapse and severe incontinence would be well suited to abdominal rectopexy; an elderly, frail patient with a large prolapse and less severe incontinence would be treated with a perineal procedure.

Abdominal rectopexy involves mobilising the rectum out of the pelvis, and then securing it to the sacrum with sutures to prevent prolapse. This procedure can now be done using laparoscopic techniques.

Anal encirclement procedures involve placing a stainless steel wire or nylon suture subcutaneously around the anal canal after reducing the prolapse. Although still used today in some centres for high-risk patients, it is rarely used since the wire (being too loose) inevitably fails to control the prolapse, or ulcerates through the skin, or is too tight, resulting in constipation.

The Delormes procedure involves excision of the mucosa over the prolapsing section of rectum and then plication of the underlying rectal wall. Reported recurrence rates range from 5% to 30%.

Perineal rectosigmoidectomy involves excision of the entire prolapsing section of rectum and sigmoid, with anastomosis of the colon to the anus. In principle this is a very sound procedure, but the reported recurrence rates are as high as with the Delorme procedure. The high rates found in some series are probably because of incomplete removal of the prolapsing bowel, and in those centres where a more complete excision is practised, recurrence rates as low as 5% are found. Since there is minimal blood loss with the procedure and virtually no morbidity, this is a very good option for elderly patients.

Aetiology

Direct trauma to the sphincter is most commonly due to an obstetric tear, or damage resulting from surgery for anal fistula. Other less common causes are impalement on a sharp object, pelvic fracture, stab wound or gunshot wound.

Obstetric injuries are the most common cause of sphincter trauma. In North America and some parts of Europe where midline episiotomy is practised routinely, division of the anal sphincter and imperfect repair may cause a sphincter defect; while in Australia, the UK and most of Europe, lateral episiotomy is made and third-degree perineal tears are the cause. Recent studies of the anal sphincter using the technique of intraanal ultrasound have identified injuries to the anterior sphincter in a much higher proportion of cases than is recognised clinically, and in some of these cases of occult sphincter injury incontinence will develop in later life.

Surgery for anal fistula is the most common iatrogenic cause of incontinence. Laying open of a fistula that has not been recognised as suprasphincteric or extrasphincteric will result in incontinence. However, these fistulae are rare, and more commonly incontinence results from treatment of a trans-sphincteric fistula that crosses more than 50% of the external sphincter muscle.

Impalement injuries generally result from falling astride a sharp object, such as a fence, and can result in severe damage. Secondary infection may occur if adequate surgical debridement is not performed, resulting in further tissue loss. There may be an associated injury to the rectum above the sphincter. Pelvic fractures may produce widespread disruption of the anal sphincter and can present a particularly difficult problem for surgical repair.

There are several iatrogenic injuries apart from those resulting from fistula surgery. These injuries are due to poor surgical technique and should be completely avoidable. Minor incontinence after haemorrhoidectomy is well recognised and occurs in up to 10% of cases in some series, usually due to damage to the internal sphincter or lower part of the external sphincter during the haemorrhoidectomy, but in some cases anal dilatation carried out at the time of haemorrhoidectomy may be the cause of the incontinence. Lateral sphincterotomy for anal fissure should include only the lower part of the internal sphincter—if the external sphincter is divided, incontinence will result. Anal dilatation has been advocated for haemorrhoids and anal fissure. Although this procedure is an effective treatment for these conditions by disrupting the internal sphincter spasm, it is a frequent cause of incontinence, particularly in multiparous women, and should be completely avoided.

Clinical features

A damaged sphincter may be recognised by a visible keyhole defect externally or a palpable defect on physical examination. The defect is best assessed prior to surgical intervention with endoanal ultrasound.

Treatment

Repair of the damaged sphincter ranges from a relatively simple procedure when the sphincter has been cleanly divided, to a very complex procedure when the sphincter has been widely disrupted with accompanying sepsis and tissue necrosis. Preoperative establishment of the precise extent of the scar tissue greatly facilitates planning of the procedure and accurate repair. In most cases, a covering stoma is not required, and the use of a stoma is restricted to three situations: underlying Crohn’s disease; repeat sphincter repair; or with a very extensive injury. The principles of surgery are to expose the injured area, excise the scar tissue, and create an overlapping repair using healthy muscle on either side of the scar.

The results of sphincter repair are very satisfactory. Almost 70% of patients will achieve continence and up to half of the remaining patients will be partially improved, although the results deteriorate over time. In those cases where there is no improvement and severe incontinence persists, the two available alternatives are a permanent colostomy or reconstruction of a new sphincter mechanism. Complete sphincter reconstruction involves the procedure called stimulated graciloplasty, in which the gracilis muscle in the thigh is detached from its insertion on the tibia and tunnelled around the anus to construct a neosphincter. Since the gracilis is a conventional fast-twitch skeletal muscle that fatigues quickly, it must be stimulated using an implanted subcutaneous pacemaker, which converts it to a fatigue-resistant slow-twitch muscle by continuous low-frequency stimulation, eventually allowing it to remain continuously contracted.

Patients in whom there is an isolated internal anal sphincter injury may benefit from injection of a bulking agent into the sphincter. This bulking agent may be silicone-based (PTQ™) or carbon-based (Duosphere™). Continence has been shown to be improved in some patients.

Recent studies have suggested that sacral nerve stimulation (see below) probably improves continence even in the presence of a sphincter defect.

Aetiology

A global weakness of the anal sphincter and pelvic floor muscles is a common cause of severe incontinence requiring surgery. This condition was previously known as ‘idiopathic incontinence’, but new methods of investigation have shown that the sphincter weakness is due to an injury to the distal part of the nerve supply to the anal sphincter and pelvic floor muscles.

The nerve supply to the external anal sphincter is via the pudendal nerve (arising from S2–S4 sacral segments). The puborectalis and levator ani (pubococcygeus) muscles are supplied by direct branches from the sacral nerve plexus (S3, S4) (Fig 16.12). During vaginal delivery there is marked descent of the pelvic floor with stretching of the pudendal and sacral nerves, and a temporary reversible nerve injury occurs in some cases. Somatic nerves can normally withstand a stretch injury of up to 12% of their length and it has been calculated that stretching of 20% may occur during vaginal delivery. In the majority of cases, the neuropraxia resolves over a 6-week period, but a permanent injury remains in others. This may not result in muscle weakness immediately, but as the pelvic floor muscles age, particularly after menopause, a cumulative weakness develops, leading to incontinence.

Figure 16.12 Pudendal nerve supply to the external anal sphincter; sacral nerves to the puborectalis muscle.

From Henry MM, Swash M. Coloproctology and thepelvicfloor. London: Butterworths; 1985, with permission from the publisher.

Factors shown to be associated with nerve damage are prolonged second stage of labour, forceps delivery and high infant birth weight. In addition to vaginal delivery, chronic straining at stool due to constipation has a similar effect by causing a repeated stretch injury to the pelvic nerves. Women who have a combination of multiple vaginal deliveries and chronic constipation are, therefore, particularly likely to develop neurogenic incontinence.

It can be seen that since direct sphincter trauma and neurogenic muscle weakness are both associated with difficult vaginal delivery, these two conditions may co-exist in some women. Recognition of this dual pathology has important implications for surgical treatment in many cases.

Clinical features

On examination, the sphincter is found to be shortened and gaping, and voluntary squeeze is found to be reduced to absent. The puborectalis sling is lax and there is loss of posterior support of the anus. Anorectal manometry and electrophysiology will confirm the abnormalities.

Treatment

Initial treatment is with stool bulking agents such as psyllium, in combination with loperamide (Imodium™), which firms the stool and also directly stimulates the internal anal sphincter. Biofeedback may be used, where the patient is taught to contract the external sphincter muscle more effectively by showing the patient sphincter pressure measurements during physiotherapy exercises.

If this is not successful, sacral nerve stimulation may be effective. In this procedure an electrode is placed trancutaneously under x-ray control into the S3 or S4 sacral foramin. The electrode is connected to a stimulator that is implanted subcutaneously in the gluteal region. This has a success rate of over 70% in carefully selected patients.

Alternative surgical treatment is a procedure in which the left and right limbs of the puborectalis muscle are plicated posterior to the external sphincter (postanal repair). This has the effect of increasing the functional length of the anal sphincter and improving the efficacy of the puborectalis. This operation does not reverse the denervation process and merely realigns the weakened muscles to create a high-pressure sphincter zone. Over 50% of patients achieve satisfactory restoration of continence.

In selected patients in whom these procedures fail, or when there is a severe anatomical deficiency of the sphincter ring following sphincter trauma, and severe incontinence persists, the gracilis neosphincter can then be considered. In this procedure the gracilis muscle is mobilised from the thigh and wrapped around the weak anal sphincter to create a functioning neosphincter.

A further surgical option for the treatment of incontinence is antegrade colonic irrigation. This involves placing a caecostomy tube via the appendix (if present) or caecum. The patient is taught to irrigate the colon regularly (e.g. daily) while on the toilet until the colon is evacuated, thereby preventing soiling during the course of the day.

If all measures fail and incontinence is severe, formation of a stoma may be offered.

The treatment of faecal incontinence has multiple options, and treatment must be based on a sound clinical history and examination, assisted by tests of anorectal physiology. An algorithm for treatment is shown in Figure 16.13.

Figure 16.13 Incontinence algorithm.