Risk factors for developing a cystocele are:

- an occupation involving or history of heavy lifting

- pregnancy and childbirth

- chronic lung disease/smoking

- family history of cystocele

- exercising incorrectly

- ethnicity (risk is greater for Hispanic and whites)

- hypoestrogenism

- pelvic floor trauma

- connective tissue disorders

- spina bifida

- hysterectomy

- cancer treatment of pelvic organs* childbirth; correlates to the number of births

- forceps delivery

- age

- chronically high intra-abdominal pressures

- chronic obstructive pulmonary disease

- constipation

- obesity

Connective tissue disorders predispose women to developing cystocele and other pelvic organ prolapse. The tensile strength of the vaginal wall decreases when the structure of the collagen fibers change and become weaker.

In the US, greater than than 200,000 surgeries are performed each year for pelvic organ prolapse and 81% of these are to correct cystocele. Cystocele occurs most frequently compared to the prolapse of other pelvic organs and structure. Cystocele is found to be three times as common as vaginal vault prolapse and twice as often as posterior vaginal wall defects. The incidence of cystocele is around 9 per 100 women-years. The highest incidence of symptoms occurs between ages of 70-79 years old. Based on population growth statistics, the number of women with prolapse will increase by a minimum of 46% by the year 2050 in the US. Surgery to correct prolapse after hysterectomy is 3.6 per 1,000 women-years.

Rectoceles result from the weakening of the pelvic floor also called pelvic organ prolapse. Weakened pelvic structures occur as a result of an episiotomy during previous births, even decades later. Other causes of pelvic floor prolapse can be advanced age, multiple vaginal deliveries, and birthing trauma. Birthing trauma includes vacuum delivery, forceps delivery, and perineal tear. In addition, a history of chronic constipation and excessive straining with bowel movements are thought to play a role in rectocele. Multiple gynecological or rectal surgeries can also lead to weakening of the pelvic floor. Births that involve babies over nine pounds in weight, or rapid births can contribute to the development of rectocele.

A hysterectomy or other pelvic surgery can be a cause, as can chronic constipation and straining to pass bowel movements. It is more common in older women than in younger ones; estrogen which helps to keep the pelvic tissues elastic decreases after menopause.

Treatment depends on the severity of the problem, and may include non-surgical methods such as changes in diet (increase in fiber and water intake), pelvic floor exercises such as Kegel exercises, use of stool softeners, hormone replacement therapy for post-menopausal women and insertion of a pessary into the vagina. A high fiber diet, consisting of 25-30 grams of fiber daily, as well as increased water intake (typically 6-8 glasses daily), help to avoid constipation and straining with bowel movements, and can relieve symptoms of rectocele.

Genital prolapse occurs in about 316 million women worldwide as of 2010 (9.3% of all females).

Mechanistically, the causes of pelvic floor dysfunction are two-fold: widening of the pelvic floor hiatus and descent of pelvic floor below the pubococcygeal line, with specific organ prolapse graded relative to the hiatus. Associations include obesity, menopause, pregnancy and childbirth. Some women may be more likely to developing pelvic floor dysfunction because of an inherited deficiency in their collagen type. Some women may have congenitally weak connective tissue and fascia and are therefore at risk of stress urinary incontinence and pelvic organ prolapse.

By definition, "postpartum" pelvic floor dysfunction only affects women who have given birth, though pregnancy rather than birth or birth method is thought to be the cause. A study of 184 first-time mothers who delivered by Caesarean section and 100 who delivered vaginally found that there was no significant difference in the prevalence of symptoms 10 months following delivery, suggesting that pregnancy is the cause of incontinence for many women irrespective of their mode of delivery. The study also suggested that the changes which occur to the properties of collagen and other connective tissues during pregnancy may affect pelvic floor function.

Pelvic floor dysfunction can result after treatment for gynegological cancers.

Pelvic organ prolapse (POP) is characterized by descent of pelvic organs from their normal positions. In women, the condition usually occurs when the pelvic floor collapses after gynecological cancer treatment, childbirth or heavy lifting.

In men, it may occur after the prostrate gland is removed. The injury occurs to fascia membranes and other connective structures that can result in cystocele, rectocele or both. Treatment can involve dietary and lifestyle changes, physical therapy, or surgery.

The condition is widespread, affecting up to 50% of women at some point in their lifetime. Almost 10 percent of women will undergo surgery for urinary incontinence or pelvic organ prolapse. 30 percent of those undergoing surgery will have at least two surgeries in trying to correct the problem.

Some conditions are reversible, with pelvic floor exercises, or Kegel exercises recommended to strengthen the area muscles. Devices and probes are also available over the counter which purport to increase pelvic floor tone by stimulating muscle contractions with electrical impulses.

One of the main causes is suggested to be excessive and repetitive straining during defecation. Other causes include weakness of the pelvic floor muscles (secondary to age related neuropathic degeneration or traumatic injury during pregnancy and labor.

Surgical treatments may be used to treat the condition, and include retro-rectal levatorplasty, post-anal repair, retro-anal levator plate myorrhaphy.

A group of conditions known as Mucosal prolapse syndrome (MPS) has now been recognized. It includes SRUS, rectal prolapse, proctitis cystica profunda, and inflammatory polyps. It is classified as a chronic benign inflammatory disorder. The unifying feature is varying degrees of rectal prolapse, whether internal intussusception (occult prolapse) or external prolapse.

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 effected 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 rectum and anal canal's ability to contract and fully evacuate rectal contents. The intussusceptum itself may mechanically obstruct the rectoanal lumen, creating a blockage that straining, anismus and colonic dysmotility exacerbate.

Some believe that internal rectal intussusception represents the initial form of a progressive spectrum of disorders the extreme of which is external rectal prolapse. The intermediary stages would be gradually increasing sizes of intussusception. However, internal intussusception rarely progresses to external rectal prolapse. The factors that result in a patient progressing from internal intussusception to a full thickness rectal prolapse remain unknown. Defecography studies demonstrated that degrees of internal intussusception are present in 40% of asymptomatic subjects, raising the possibility that it represents a normal variant in some, and may predispose patients to develop symptoms, or exacerbate other problems.

The six-week period after pregnancy is called the postpartum stage. During this time, women are at increased risk of being constipated. Multiple studies estimate the prevalence of constipation to be around 25% during the first 3 months. Constipation can cause discomfort for women, as they are still recovering from the delivery process especially if they have had a perineal tear or underwent an episiotomy. Risk factors that increase the risk of constipation in this population include:

- Damage to the levator ani muscles (pelvic floor muscles) during childbirth

- Forceps-assisted delivery

- Lengthy second stage of labor

- Delivering a large child

- Hemorrhoids

Hemorrhoids are common in pregnancy and also may get exacerbated when constipated. Anything that can cause pain with stooling (hemorrhoids, perineal tear, episiotomy) can lead to constipation because patients may withhold from having a bowel movement so as to avoid pain.

The pelvic floor muscles play an important role in helping pass a bowel movement. Injury to those muscles by some of the above risk factors (examples- delivering a large child, lengthy second stage of labor, forceps delivery) can result in constipation. Women sometimes get enemas during labor that can also alter bowel movements in the days after having given birth. However, there is insufficient evidence to make conclusions about the effectiveness and safety of laxatives in this group of people.

Approximately 3% of children have constipation, with girls and boys being equally affected. With constipation accounting for approximately 5% of general pediatrician visits and 25% of pediatric gastroenterologist visits, the symptom carries a significant financial impact upon the healthcare system. While it is difficult to assess an exact age at which constipation most commonly arises, children frequently suffer from constipation in conjunction with life-changes. Examples include: toilet training, starting or transferring to a new school, and changes in diet. Especially in infants, changes in formula or transitioning from breast milk to formula can cause constipation. Fortunately, the majority of constipation cases are not tied to a medical disease, and treatment can be focused on simply relieving the symptoms.