page_title: Rectal prolapse
section_title: Cause
hierarchical_section_title: Rectal prolapse / Complete rectal prolapse / Cause
caption_attribution_description: English: Low magnification micrograph showing microscopic changes consistent with rectal prolapse. H&amp;E stain. The image shows a marked increase of fibrous tissue in the submucosa and fibrous tissue +/- smooth muscle hyperplasia in the lamina propria. Related images Very low mag. Low mag. Intermed. mag.
context_page_description: Rectal prolapse is when the rectal walls have prolapsed to a degree where they protrude out the anus and are visible outside the body. However, most researchers agree that there are 3 to 5 different types of rectal prolapse, depending on if the prolapsed section is visible externally, and if the full or only partial thickness of the rectal wall is involved.
  Rectal prolapse may occur without any symptoms, but depending upon the nature of the prolapse there may be mucous discharge, rectal bleeding, degrees of fecal incontinence and obstructed defecation symptoms.
  Rectal prolapse is generally more common in elderly women, although it may occur at any age and in either sex. It is very rarely life-threatening, but the symptoms can be debilitating if left untreated. Most external prolapse cases can be treated successfully, often with a surgical procedure. Internal prolapses are traditionally harder to treat and surgery may not be suitable for many patients.
context_section_description: The precise cause is unknown, and has been much debated. In 1912 Moschcowitzl proposed that rectal prolapse was a sliding hernia through a pelvic fascial defect.
  This theory was based on the observation that rectal prolapse patients have a mobile and unsupported pelvic floor, and a hernia sac of peritoneum from the Pouch of Douglas and rectal wall can be seen.  Other adjacent structures can sometimes be seen in addition to the rectal prolapse. Although a pouch of Douglas hernia, originating in the cul de sac of Douglas, may protrude from the anus (via the anterior rectal wall), this is a different situation from rectal prolapse.
  Shortly after the invention of defecography, In 1968 Broden and Snellman used cinedefecography to show that rectal prolapse begins as a circumferential intussusception of the rectum, which slowly increases over time. The leading edge of the intussusceptum may be located at 6–8 cm or at 15–18 cm from the anal verge. This proved an older theory from the 18th century by John Hunter and Albrecht von Haller that this condition is essentially a full-thickness rectal intussusception, beginning about 3 inches above the dentate line and protruding externally.
  Since most patients with rectal prolapse have a long history of constipation, it is thought that prolonged, excessive and repetitive straining during defecation may predispose to rectal prolapse. Since rectal prolapse itself causes functional obstruction, more straining may result from a small prolapse, with increasing damage to the anatomy. This excessive straining may be due to predisposing pelvic floor dysfunction (e.g. obstructed defecation) and anatomical factors:
  Abnormally low descent of the peritoneum covering the anterior rectal wall
  poor posterior rectal fixation, resulting in loss of posterior fixation of the rectum to the sacral curve
  loss of the normal horizontal position of the rectum with lengthening (redundant rectosigmoid) and downward displacement of the sigmoid and rectum
  long rectal mesentery
  a deep cul-de-sac
  levator diastasis
  a patulous, weak anal sphincter
  Some authors question whether these abnormalities are the cause, or secondary to the prolapse. Other predisposing factors/associated conditions include: 
  pregnancy (although 35% of women who develop rectal prolapse are nulliparous) (have never given birth)
  previous surgery (30-50% of females with the condition underwent previous gynecological surgery)
  pelvic neuropathies and neurological disease
  high gastrointestinal helminth loads (e.g. Whipworm)
  COPD
  cystic fibrosis
  The association with uterine prolapse (10-25%) and cystocele (35%) may suggest that there is some underlying abnormality of the pelvic floor that affects multiple pelvic organs. Proximal bilateral pudendal neuropathy has been demonstrated in patients with rectal prolapse who have fecal incontinence. This finding was shown to be absent in healthy subjects, and may be the cause of denervation-related atrophy of the external anal sphincter. Some authors suggest that pudendal nerve damage is the cause for pelvic floor and anal sphincter weakening, and may be the underlying cause of a spectrum of pelvic floor disorders.
  Sphincter function in rectal prolapse is almost always reduced. This may be the result of direct sphincter injury by chronic stretching of the prolapsing rectum. Alternatively, the intussuscepting rectum may lead to chronic stimulation of the rectoanal inhibitory reflex (RAIR - contraction of the external anal sphincter in response to stool in the rectum). The RAIR was shown to be absent or blunted. Squeeze (maximum voluntary contraction) pressures may be affected as well as the resting tone. This is most likely a denervation injury to the external anal sphincter.
  The assumed mechanism of fecal incontinence in rectal prolapse is by the chronic stretch and trauma to the anal sphincters and the presence of a direct conduit (the intussusceptum) connecting rectum to the external environment which is not guarded by the sphincters.
  The assumed mechanism of obstructed defecation is by disruption to the rectu
caption: Micrograph showing a rectal wall with changes seen in rectal prolapse. There is a marked increase of fibrous tissue in the submucosa and fibrous tissue +/- smooth muscle hyperplasia in the lamina propria. H&E stain
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