Several definitions have been offered:

- "Absence of normal relaxation of pelvic floor muscles during defecation, resulting in rectal outlet obstruction".

- "Malfunction (a focal dystonia) of the external anal sphincter and puborectalis muscle during defecation".

- "[...] failure of [the external anal sphincter and puborectalis] muscle[s] to relax, resulting in maintenance of the anorectal angle and the difficulty with initiating and completing bowel movements".

- "[...] failure of relaxation (or paradoxic contraction) of the puborectalis muscle sling during defaecation, attempted defaecation or straining."

Liquid stool is more difficult to control than formed, solid stool. Hence, FI can be exacerbated by diarrhea. Some consider diarrhea to be the most common aggravating factor. Orlistat is an anti-obesity (weight loss) drug that blocks the absorption of fats. This may give side effects of FI, diarrhea and steatorrhea.

This may occur when there is a large mass of feces in the rectum (fecal loading), which may become hardened (fecal impaction). Liquid stool elements are able to pass around the obstruction, leading to incontinence. Megarectum (enlarged rectal volume) and rectal hyposensitivity are associated with overflow incontinence. Hospitalized patients and care home residents may develop FI via this mechanism, possibly a result of lack of mobility, reduced alertness, constipating effect of medication and/or dehydration.

One review stated that the most common causes of disruption to the defecation cycle are associated with pregnancy and childbirth, gynaecological descent or neurogenic disturbances of the brain-bowel axis. Patients with obstructed defecation appear to have impaired pelvic floor function.

Specific causes include:

- Anismus and pelvic floor dysfunction

- Rectocele

- "Rectal invagination" (likely refers to rectal intussusception)

- Internal anal sphincter hypertonia

- Anal stenosis

- Fecal impaction

- Rectal or anal cancer

- Descending perineum syndrome

Anismus is classified as a functional defecation disorder. It is also a type of rectal outlet obstruction (a functional outlet obstruction). Where anismus causes constipation, it is an example of functional constipation. Some authors describe an "obstructed defecation syndrome", of which anismus is a cause.

The Rome classification subdivides functional defecation disorders into 3 types, however the symptoms the patient experiences are identical.

- Type I: paradoxical contraction of the pelvic floor muscles during attempted defecation

- Type II: inadequate propulsive forces during attempted defecation (inadequate defecatory propulsion)

- Type III: impaired relaxation with adequate propulsion

It can be seen from the above classification that many of the terms that have been used interchangeably with anismus are inappropriately specific and neglect the concept of impaired propulsion. Similarly, some of the definitions that have been offered are also too restrictive.

Obstructed defecation has many causes, so the management in any individual case is specific to the cause of the symptom. For rectal internal intususception treatment is surgical, either STARR or rectopexy. For rectocele STARR or mesh implantation. For anismus/ pelvic floor dessynergia: biofeedback exercise.

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.

Although SRUS is not a medically serious disease, it can be the cause of significantly reduced quality of life for patients. It is difficult to treat, and treatment is aimed at minimizing symptoms.

Stopping straining during bowel movements, by use of correct posture, dietary fiber intake (possibly included bulk forming laxatives such as psyllium), stool softeners (e.g. polyethylene glycol, and biofeedback retraining to coordinate pelvic floor during defecation.

Surgery may be considered, but only if non surgical treatment has failed and the symptoms are severe enough to warrant the intervention. Improvement with surgery is about 55-60%.

Ulceration may persist even when symptoms resolve.

The estimated prevalence of encopresis in four-year-olds is between one and three percent. The disorder is thought to be more common in males than females, by a factor of 6 to 1.

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.

A 2014 meta-analysis of three small trials evaluating probiotics showed a slight improvement in management of chronic idiopathic constipation, but well-designed studies are necessary to know the true efficacy of probiotics in treating this condition.

Children with functional constipation often claim to lack the sensation of the urge to defecate, and may be conditioned to avoid doing so due to a previous painful experience. One retrospective study showed that these children did indeed have the urge to defecate using colonic manometry, and suggested behavioral modification as a treatment for functional constipation.

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.

The prognosis for non-ischemic cases of SBO is good with mortality rates of 3–5%, while prognosis for SBO with ischemia is fair with mortality rates as high as 30%.

Cases of SBO related to cancer are more complicated and require additional intervention to address the malignancy, recurrence, and metastasis, and thus are associated with poorer prognosis.

All cases of abdominal surgical intervention are associated with increased risk of future small-bowel obstructions. Statistics from U.S. healthcare report 18.1% re-admittance rate within 30 days for patients who undergo SBO surgery. More than 90% of patients also form adhesions after major abdominal surgery.

Common consequences of these adhesions include small-bowel obstruction, chronic abdominal pain, pelvic pain, and infertility.

Encopresis is commonly caused by constipation, by reflexive withholding of stool, by various physiological, psychological, or neurological disorders, or from surgery (a somewhat rare occurrence).

The colon normally removes excess water from feces. If the feces or stool remains in the colon too long due to conditioned withholding or incidental constipation, so much water is removed that the stool becomes hard, and becomes painful for the child to expel in an ordinary bowel movement. A vicious cycle can develop, where the child may avoid moving his/her bowels in order to avoid the "expected" painful toilet episode. This cycle can result in so deeply conditioning the holding response that the rectal anal inhibitory response (RAIR) or anismus results. The RAIR has been shown to occur even under anesthesia and when voluntary control is lost. The hardened stool continues to build up and stretches the colon or rectum to the point where the normal sensations associated with impending bowel movements do not occur. Eventually, softer stool leaks around the blockage and cannot be withheld by the anus, resulting in soiling. The child typically has no control over these leakage accidents, and may not be able to feel that they have occurred or are about to occur due to the loss of sensation in the rectum and the RAIR. Strong emotional reactions typically result from failed and repeated attempts to control this highly aversive bodily product. These reactions then in turn may complicate conventional treatments using stool softeners, sitting demands, and behavioral strategies.

The onset of encopresis is most often benign. The usual onset is associated with toilet training, demands that the child sit for long periods of time, and intense negative parental reactions to feces. Beginning school or preschool is another major environmental trigger with shared bathrooms. Feuding parents, siblings, moving, and divorce can also inhibit toileting behaviors and promote constipation. An initiating cause may become less relevant as chronic stimuli predominate.

Chronic idiopathic constipation is similar to constipation-predominant irritable bowel syndrome (IBS-C); however, people with CIC do not have other symptoms of IBS, such as abdominal pain. Diagnosing CIC can be difficult as other syndromes must be ruled out as there is no physiological cause for CIC. Doctors will typically look for other symptoms, such as blood in stool, weight loss, low blood count, or other symptoms.

To be considered functional constipation, symptoms must be present at least a fourth of the time.

Possible causes are:

- Anismus

- Descending perineum syndrome

- Other inability or unwillingness to control the external anal sphincter, which normally is under voluntary control

- A poor diet

- An unwillingness to defecate

- Nervous reactions, including prolonged and/or chronic stress and anxiety, that close the internal anal sphincter, a muscle that is not under voluntary control

- Deeper psychosomatic disorders which sometimes affect digestion and the absorption of water in the colon

There is also possibility of presentation with other comorbid symptoms such as headache, especially in children.

Fetal and neonatal bowel obstructions are often caused by an intestinal atresia, where there is a narrowing or absence of a part of the intestine. These atresias are often discovered before birth via an ultrasound, and treated with using laparotomy after birth. If the area affected is small, then the surgeon may be able to remove the damaged portion and join the intestine back together. In instances where the narrowing is longer, or the area is damaged and cannot be used for a period of time, a temporary stoma may be placed.