The term ‘rectal prolapse’ implies a full thickness circumferential descent of the rectum through the anus. A prolapse of only the rectal mucosa is called incomplete or mucosal prolapse. A variant of complete rectal prolapse has been described in which the upper rectum prolapses into the middle or lower rectum without actually reaching the anal canal. This is called an internal prolapse, or intussusception of the rectum.

Rectal prolapse occurs at the extremes of life. Complete rectal prolapse is found chiefly in elderly female patients: 85 per cent of adults with full thickness rectal prolapse are women and the incidence is maximal in the fifth decade and upwards. Many patients are of very advanced age, being in their eighties or nineties. In men, though the incidence is much lower, rectal prolapse presents throughout the age range or may be more common in the second and third decades of life. Mucosal prolapse is most common in young children.

The increased incidence in female patients might imply an effect of childbirth on the pelvic floor, but in many series half of the patients are childless. Furthermore, uterine and rectal prolapse only rarely occur together.

In children there is usually some promoting factor such as diarrhoea, constipation, or bad defecatory habits. A chronic cough or severe coughing attacks can cause a rectal prolapse. In adults prolapsed mucosa is associated with third-degree haemorrhoids, and in older patients it may occur as a result of a weak anal sphincter. Parks et al. described the descending perineum syndrome in which the anterior wall of the rectum causes an evacuatory disorder.

Complete rectal prolapse is associated with a collection of distinct anatomical changes (Table 1) 347. The most striking of these is the abnormally deep rectovaginal, or in males rectovesical, pouch. This gave rise to the earliest theory of the cause of rectal prolapse, namely that it was a form of sliding hernia, the pouch of Douglas being the hernial sac pressing the anterior rectal wall into the rectal lumen.

Broden and Snellman described the radiographic changes seen when an intussusception was the lead point of a rectal prolapse found at 6 to 8 cm from the anal verge. In 60 per cent of patients this was anterior, in 32 per cent annular, and in 8 per cent posterior. An enterocele developed late, if at all (Fig. 1) 1119.

Most patients with complete prolapse have a weak atonic anal sphincter, and many also have a weak pelvic floor. It is not clear whether this is a cause or an effect of the prolapse: some patients have a large prolapse, but a normal anal sphincter once the prolapse has been reduced, while others with prolonged marked changes in the pelvic floor may have had a rectal prolapse for only weeks or months.

Although rectal prolapse may occur in patients with cauda equina lesions, most patients with rectal prolapse have no obvious neurological abnormality. Studies of anorectal physiology show a reduction of resting anal pressure and maximum voluntary contraction pressure, impaired rectal sensation, absence or abnormalities of the rectosphincteric reflex, an increase in pudendal nerve latency, and histological evidence of muscle denervation in the external anal sphincter. These changes are most apparent in those patients who have a combination of prolapse and incontinence. Denervation of the voluntary sphincter muscles may be due to stretching of the pudendal nerves during descent of the rectum in the course of prolapse.

Since the intussusception described by Broden and Snellman starts well above the pelvic floor, these changes are probably a result of the rectal prolapse rather than the cause of it. Of 250 patients with anterior mucosal prolapse 20 per cent developed a full thickness rectal prolapse within 10 years.

The aetiology of rectal prolapse is still not clear. Known initiating factors include diarrhoea, constipation, and disorders of the pelvic floor which, acting together with predisposing factors such as a deep pouch of Douglas, a redundant sigmoid colon, and a weak pelvic floor, together bring about intussusception as the first stage in the genesis of a rectal prolapse.

Rectal prolapse in a child usually becomes apparent during defecation. It may reduce itself spontaneously sometimes, while at other times it may need to be replaced digitally. There is sometimes discomfort and a slight discharge of mucus or blood, but the child is usually perfectly well and normally continent.

On examination the prolapse consists of a ring of mucosa projecting 2 to 4 cm beyond the perianal verge. Gentle palpation between finger and thumb usually reveals that the prolapse consists of only two layers of mucosa. Very little pressure is required to reduce the prolapse and the anal sphincter appears normal. If there is only a history of prolapse, it is important for the surgeon to see the prolapse occurring in the clinic. Rarely the prolapse may be a complete rectal prolapse. Differential diagnosis includes a prolapsed rectal polyp or the apex of an intussusception. In the latter case it is possible to pass the tip of an examining finger along the slit between the intussuscepted bowel and the wall of the anal canal.

Symptoms include those due to the prolapse itself and those due to the weakness of the anal sphincter. The prolapse first becomes apparent during evacuation or during episodes of raised intra-abdominal pressure. When the bowel wall is prolapsed mucus and blood may soil underclothes. There is also a degree of incontinence of faeces and flatus, giving rise to urgency and soiling episodes. Patients often have coincident constipation which aggravates the prolapsed condition.

The anus is usually patulous and there is a degree of mucosal prolapse evident at the anal orifice. Distraction on the anal margin causes the anus to open widely and the patient will often be able to push down a prolapse if it is not immediately apparent (Fig. 2) 1120. On palpation the anal sphincter is usually very weak. Voluntary contraction is usually poor and there is blunting of anal and rectal sensation. The mucosa on the apex of the prolapse may show some granularity or even superficial ulceration from repeated trauma caused by contact with underclothing.

When the prolapse is produced with the patient straining, palpation between finger and thumb reveals the double thickness of tissue; this is especially evident anteriorly where the deep pouch of Douglas and any possible contained loops of small intestine may add to the bulk of the prolapsing rectum. Most prolapses over 5 cm in length are complete but it can sometimes be difficult to tell whether a shorter prolapse is simply mucosa or a complete procidentia. If the patient is unable to produce a prolapse on the examination couch the diagnosis can be made on allowing the patient to adopt the usual squatting position secluded in a toilet. Some patients may find it easier to produce the prolapse in these circumstances than in the clinic.

On reducing the prolapse it is important to carry out a sigmoidoscopic examination to exclude any other abnormality within reach of the instrument.

Large third-degree haemorrhoids, a large polypoid tumour of the rectum, sigmoid colon prolapsing and emerging at the anus, or a purely mucosal prolapse must all be differentiated from a complete procidentia.

Most patients can reduce the prolapse readily, although urgent admission may be required if the bowel becomes oedematous and cannot be reduced. It may be possible to reduce such a prolapse manually in the clinic with the patient lightly sedated. In the rare situation of a gangrenous rectal prolapse an emergency perineal rectosigmoidectomy may be necessary. Proctitis, ulceration, and rarely severe haemorrhage can occur but these are not usually clinically important.

Rectal prolapse in children is a self-limiting disease and usually responds to conservative measures. Correction of bowel habit and small doses of laxatives may be all that is necessary. Occasionally a submucosal injection of phenol or alcohol may be required to secure fixation of the prolapse.

Minor mucosal prolapse can be treated in the same way as third-degree haemorrhoids, either by conservative measures or surgical excision. In older patients, in whom a partial prolapse complicates a weak anal sphincter a postanal repair operation may be necessary.

Innumerable methods for fixing a rectal prolapse have been described in the surgical literature, and they can be divided into perineal, sacral, and abdominal procedures. A procedure should be chosen with consideration for the age and fitness of the patient. There is perhaps no single ideal operation, and the art of prolapse management is to match the procedure to the patient.

This operation is becoming increasingly popular. With the bowel fully prolapsed a circular incision is made through the mucosa of the prolapse 1 cm from the dentate line (Fig. 3) 1121. Infiltration with dilute adrenaline solution helps indicate the submucosal plane. The mucosa is then dissected from the underlying muscle coat as a sleeve until the apex of the prolapse is reached, and the dissection is carried on down into the prolapse as far as possible (Fig. 4) 1122. This leaves the outer aspect of the prolapse without any mucosal covering. The underlying muscle coat is imbricated with a series of longitudinal sutures to bunch up or reef it and bring the edges of the mucosa together (Fig. 5) 1123. The mucosa is then sutured with absorbable sutures and the prolapse gently reduced. Christiansen and Kirkegaard have advocated this operation for elderly frail patients. It has a particular place in this group and the procedure can also be used in patients with rectal prolapse complicating chronic ambulatory peritoneal dialysis.

Where there is coincident anal sphincter weakness it is possible to carry out a postanal repair at the same time. Only a small series of cases have been reported. Delorme's procedure is a compromise operation and if recurrence does occur then the procedure can simply be repeated. It may also have a further advantage in that it does not cause constipation or an evacuation disorder, and there is no danger of pelvic nerve damage.

With the patient in the lithotomy or jack-knife position the prolapse is pulled down, and the outer of the two tubes of rectal wall is divided circumferentially just above the dentate line. The inner tube of rectum can then be drawn down bringing the distal sigmoid to the anal canal, where it is divided and sutured to the anal remnant with absorbable sutures (Fig. 6) 1124. The specimen resected should be 15 to 20 cm in length, leaving no slack rectum or distal colon to allow further prolapse (Fig. 7) 1125. Popularity for this procedure has waned in the United Kingdom, but it is still very popular in the United States.

Experience in the United Kingdom in the 1960s was disappointing with a high recurrence rate. Altermeier has modified the procedure to include suturing of the levator muscles anterior to the rectum. This is a plication of the puborectalis sling which attempts to improve sphincter function postoperatively and to reduce the incidence of recurrence. Long-term recurrence rates are not known, and removal of the reservoir function of the rectum must have considerable physiological effects.

Incisions are made in front of and behind the anal margin to allow the passage of wire, stout nylon, or even silastic around the anal sphincter. It is usually overlapped and sewn together anteriorly to provide the right amount of tension (Fig. 8) 1126. The procedure can be carried out under regional or local anaesthesia in elderly frail patients. In principle, the technique works by supporting the reduced prolapse and causing a local reaction which induces fibrosis and stenosis of the anal canal.

In our experience this procedure can work quite well for small prolapses, but if the prolapse is large the wire or nylon tends to migrate and cut through the skin. Recurrences are common and the Thiersh operation cannot be regarded as anything more than a temporary solution.

Variations on the technique have been described, including placing a silastic band around the top of the external sphincter below the levator muscles, but there is no evidence that this produces better results.

In patients with a weak anal sphincter and marked symptoms of incontinence it is tempting to use a sphincter plication procedure to hold in the prolapse. Unfortunately this is rarely successful for long and the technique can only be used for small prolapses.

A number of operations have been described which exploit the Kraske approach alongside the coccyx and behind the sacrum. With the patient in the jack-knife position an incision is made over the coccyx and parasacral area, giving access to the presacral and postrectal space. The rectum is mobilized, shortened by imbricating sutures, and foreign material is placed in the presacral space. None of these procedures has stood the test of time and become particularly popular.

The general principle of these operations is to repair the prolapse by mobilizing the rectum and fixing it to the sacrum. Repair of the pelvic floor is sometimes performed simultaneously.

The mobilized rectum is fixed to the sacral hollow by means of a sling of Teflon mesh 5 cm wide. This is passed around the rectum and the ends are sutured behind it to the fascia on the front of the sacrum, just below the promontory. In addition, a few sutures are passed between the edges of the Teflon and the anterior and lateral rectal walls. Jurgeleit et al. reported 55 patients treated in this way at the Lahey clinic. There were no operative deaths, and there was a 7.5 per cent recurrence rate. In a postal survey of members of the American Society of Colon and Rectal Surgeons the recurrence rate was 2.3 per cent and significant problems with constipation and faecal impaction occurred in 6.7 per cent of patients. Stricturing at the site of the sling occurred in 2 per cent of patients. A modification of this operation, placing the mesh behind the rectum, has been reported by Keighley et al.

Following early experience with the use of polyvinyl alcohol sponge in the repair of herniae, Wells used a 3-mm thick sheet of Ivalon measuring 10 × 15 cm. After a full mobilization of the rectum the Ivalon is placed behind it, partially wrapping the full circumference of the rectum, and resutured, fixing it and the sponge to the sacral hollow. In 101 cases reported by Penfold and Hawley from St Mark's Hospital there were no operative deaths but four patients developed postoperative sepsis and the Ivalon had to be removed in one of these: sepsis in the implanted foreign body is a recognized hazard of this procedure. After 2 to 10 years, three patients had developed a recurrence and 31 suffered mucosal prolapse. Continence was improved in about 30 per cent of the patients postoperatively. Reasonable results have also been reported in a group of young patients with rectal prolapse treated by the same operation.

An alternative to the use of an implant of either Teflon or Ivalon is simply to mobilize the rectum and fix it to the sacral promontory. No major series has been reported, but six recurrences were noted in 79 patients treated in this way.

In this procedure the mobilized rectum is lifted out of the pelvis and the sigmoid colon is then fixed in an elevated position to the peritoneum of the anterior abdominal wall or the pelvic bone, and in female patients to the uterus. The procedure was popularized at the Mayo Clinic in the 1940s and gave a recurrence rate of 35 per cent.

Here the rectum is fully mobilized preserving the lateral ligaments which are pulled up and made taught. These tight bands are then sutured to the presacral fascia to keep the bowel up out of the pelvis. After mobilizing the descending colon the sigmoid loop is resected. Watts et al. reported 138 patients treated in this way, with a recurrence rate of 1.9 per cent.

Some surgeons favour a straight anterior resection. When the anal sphincter is very weak an abdominoperineal excision would be justified.

Variations on this procedure have been described by a number of surgeons. The rectum is fully mobilized but in addition the pelvic floor is plicated either in front of or behind the rectum. The aim of this part of the procedure is to maintain the rectum in an elevated position and to improve postoperative continence. Goligher felt that it provided no more than a temporary buttress which after several months could no longer be palpated.

Patients should undergo a full bowel preparation in case the rectum is damaged during mobilization. Prophylactic intravenous antibiotics should be given. The patient is placed in Lloyd-Davis stirrups, a urinary catheter is passed and a lower abdominal incision is made. A head down tilt makes access to the pelvis easier. The small bowel is packed off, and the uterus is hitched up with stay sutures. Peritoneal cuts are then made to mobilize the rectum, starting on the right side of the base of the mesosigmoid but a little way up the mesentery so that the peritoneum can be preserved and closed over the repair. The incision is carried down to the bottom of the often deep pouch of Douglas, crossing anteriorly and joining a similar cut on the left side. The presacral space is opened, identifying and preserving the presacral nerves posterolaterally and the left ureter. The posterior dissection can now be carried right down to the pelvic floor (Fig. 9) 1127. Anteriorly, the plane between the posterior vaginal wall and the rectum is opened and dissected with a combination of blunt and sharp dissection. There is debate over whether the lateral ligaments should be divided: some evidence suggests that bilateral division results in abnormal rectal function.

A 15 × 10 cm sheet of implantable material (Ivalon sponge, Marlex, Mersiline, or Teflon) is fixed to the presacral fascia, care being taken not to puncture middle sacral vessels or pelvic veins (Fig. 10) 1128. The use of several sutures increases the risk of damage to sacral veins: two or three probably suffice. Once the implanted material has been attached to the sacral promontory and presacral fascia either the same sutures or a new set of sutures can be used to attach this in turn to the fully mobilized and stretched up mesorectum, taking in a section of the serosa of the rectal wall at the same time. The implant is then partially wrapped around the lateral sides of the mobilized rectum (Fig. 11) 1129, leaving one-third of the anterior circumference of the rectal wall uncovered to minimize the risk of stenosis or functional constipation. Sutures are then placed to fix this in position. The pelvic peritoneum can then be covered over all of this, leaving two suction drains in the cavity to prevent a haematoma.

Variations on this procedure include the use of a transverse abdominal incision and limited peritoneal incisions gaining access to the presacral space and the mesorectal plane.

The procedure is usually well tolerated, even by elderly patients. Intravenous fluids should be given for 48 h since some patients suffer marked postoperative paralytic ileus. A mild laxative is prescribed from the second or third postoperative day to prevent constipation and straining at stool. There is often an irregularity of bowel habit and continence in the immediate 2 or 3 weeks postoperatively.

During straining the anal canal should not descend more than 2 cm below a line joining the ischial tuberosities. In patients with descending perineum syndrome the anal canal at rest lies at a lower level; straining causes the perineum itself to balloon well below the lower margin of the bony pelvis. It is more common in women and may occur at any age, although it is rare before the third decade.

It is probable that excessive straining weakens the pelvic floor muscles and stretches the pudendal nerves supplying the pelvic floor, which then bulges and allows the anterior wall of the rectum to prolapse into the upper anal canal (Fig. 12) 1130. This anterior mucosal prolapse results in a feeling of incomplete evacuation, to which the patient will respond by further straining efforts.

Gross perineal descent on its own does not always cause symptoms and some patients remain continent.

The patient's main symptoms are of intractable tenesmus but there may also be the passage of mucus and blood. There is often a past history of haemorrhoidectomy, inappropriately performed for what was thought to be haemorrhoidal symptoms. There may be anorectal incontinence, and others have a dragging perineal pain. Physical examination usually reveals reduced resting anal tone and descent of the perineum at rest and on straining. Proctoscopy may reveal an anterior rectal mucosal prolapse, and in intractable cases a solitary ulcer of the rectum may develop (see below).

Treatment consists of avoiding further straining by alterations in diet and the administration of bulking agents, suppositories, and enemata.

Anterior mucosal prolapse or prolapsing haemorrhoids can be treated by injection therapy or band ligation. Great care must be taken with surgical excision, since the haemorrhoidal tissue may be an important component of the patient's remaining continence.

The solitary ulcer syndrome is often, but not always, associated with the descending perineum syndrome. It rarely takes the form of a single large depressed ulcer, and is more commonly an area of mucosal change on the anterior wall of the lower rectum. This may be ulcerated in places, but the mucosa is oedematous, heaped up, and bleeds easily on contact. Sometimes these appearances can extend around the whole rectal circumference. Histologically, there is replacement of the lamina propria by fibroblasts and smooth muscle cells, typically arranged at right angles to the muscularis mucosa.

It is now thought that these changes are the result of mucosal trauma. The lower, anterior ulcers are usually associated with the mucosal prolapse, while higher ulcers are associated with intussusception of the rectum. The mucosal changes probably result from a straining effort in the presence of a contracting sphincter muscle which then pinches and damages the prolapsing mucosa. This gives rise to the common symptoms of the passage of mucus and blood, and the thick, ridged, oedematous mucosa gives a sense of anal obstruction and pain, resulting in prolonged and excessive straining. There may be multiple fruitless attempts at defecation.

These symptoms and the appearance of a rectal ulcer can be easily mistaken for a carcinoma and it is important to obtain a biopsy sample.

This is usually conservative. Straining efforts are discouraged. If symptoms become intractable they may be improved by an abdominal rectopexy, fixing both the anterior and posterior walls of the rectum.

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