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.

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

Reducing opiate-based medication (when possible, tolerable, and safe; prescription medication changes should be done under the supervision of a physician), and adequate intake of liquids (water) and dietary fiber and daily exercise.

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.

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.

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.

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."

Fecal incontinence to gas, liquid, solid stool, or mucus in the presence of obstructed defecation symptoms may indicate occult rectal prolapse (i.e. rectal intussusception), internal/external anal sphincter dysfunction, or descending perineum syndrome.

There are many possible causes; for example, physical inactivity, not eating enough (particularly of fiber), and not drinking enough water. Medications such as opioid pain relievers (suboxone, methadone, codeine, oxycodone, hydrocodone, etc.) and certain sedatives that reduce intestinal movement may cause fecal matter to become too large, hard and/or dry to expel. Specific diseases or conditions, such as irritable bowel syndrome, neurological disorders, diabetes, and autoimmune diseases such as amyloidosis, celiac disease, lupus, and scleroderma can cause constipation. Hypothyroidism can cause chronic constipation because of sluggish, slower, or weaker colon contractions. Iron supplements or increased blood calcium levels are also potential causes. Spinal cord injury is a common cause.

Manual removal of a fecal impaction is often required with obese patients in traction, after a barium enema, and in poorly hydrated older adults.

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.

Transient gastroparesis may arise in acute illness of any kind, as a consequence of certain cancer treatments or other drugs which affect digestive action, or due to abnormal eating patterns.

It is frequently caused by autonomic neuropathy. This may occur in people with type 1 or type 2 diabetes. In fact, diabetes mellitus has been named as the most common cause of gastroparesis, as high levels of blood glucose may effect chemical changes in the nerves. The vagus nerve becomes damaged by years of high blood glucose or insufficient transport of glucose into cells resulting in gastroparesis. Gastroparesis has also been associated with connective tissue diseases such as scleroderma and Ehlers–Danlos syndrome, and neurological conditions such as Parkinson's disease. It may also occur as part of a mitochondrial disease. Opioids and anticholinergic medications can cause medication-induced gastroparesis.

Chronic gastroparesis can be caused by other types of damage to the vagus nerve, such as abdominal surgery. Heavy cigarette smoking is also a plausible cause since smoking causes damage to the stomach lining.

Idiopathic gastroparesis (gastroparesis with no known cause) accounts for a third of all chronic cases; it is thought that many of these cases are due to an autoimmune response triggered by an acute viral infection. Gastroenteritis, mononucleosis, and other ailments have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.

Gastroparesis sufferers are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men. A hormonal link has been suggested, as gastroparesis symptoms tend to worsen the week before menstruation when progesterone levels are highest. Neither theory has been proven definitively.

Gastroparesis can also be connected to hypochlorhydria and be caused by chloride, sodium and/or zinc deficiency, as these minerals are needed for the stomach to produce adequate levels of gastric acid (HCl) in order to properly empty itself of a meal.

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.

Bethanechol (Management of overflow incontinence by activating muscarinic receptors in the bladder and stimulating contraction to void the urine, NOT a treatment modality; must rule out urinary obstruction prior to use.)

If an incontinence is due to overflow incontinence, in which the bladder never empties completely, or if the bladder cannot empty because of poor muscle tone, past surgery, or spinal cord injury, a catheter may be used to empty the bladder. A catheter is a tube that can be inserted through the urethra into the bladder to drain urine. Catheters may be used once in a while or on a constant basis, in which case the tube connects to a bag that is attached to the leg. If a long-term (or indwelling) catheter is used, urinary tract infections may occur.

Overflow incontinence occurs when the patient's bladder is always full so that it frequently leaks urine. Weak bladder muscles, resulting in incomplete emptying of the bladder, or a blocked urethra can cause this type of incontinence. Autonomic neuropathy from diabetes or other diseases (e.g. Multiple sclerosis) can decrease neural signals from the bladder (allowing for overfilling) and may also decrease the expulsion of urine by the detrusor muscle (allowing for urinary retention). Additionally, tumors and kidney stones can block the urethra. Spinal cord injuries or nervous system disorders are additional causes of overflow incontinence. In men, benign prostatic hyperplasia (BPH) may also restrict the flow of urine. Overflow incontinence is rare in women, although sometimes it is caused by fibroid or ovarian tumors. Also overflow incontinence can be from increased outlet resistance from advanced vaginal prolapse causing a "kink" in the urethra or after an anti-incontinence procedure which has overcorrected the problem. Early symptoms include a hesitant or slow stream of urine during voluntary urination. Anticholinergic medications may worsen overflow incontinence. NSAIDs medications may worsen overflow incontinence.

Without diagnostic evaluation, the cause of UAB is unclear, as there are multiple possible causes. UAB symptoms can accurately reflect impaired bladder emptying due either to DU or obstruction (normal or large storage volumes, elevated post-void residual volume), or can result from a sense of incomplete emptying of a hypersensitive bladder (small storage volumes, normal or elevated postvoid residual volume). UAB potentially might also result from inaccurate perceptions of bladder function, such as in neurologic or psychiatric disease. DU itself is often linked to a weak detrusor muscle (impaired contractility), however this association is weak. Both UAB and DU have been associated with diminished sensitivity to bladder volumes rather than objective detrusor weakness, suggesting both symptoms (UAB) and function (DU) have a significant component of sensory dysfunction, leading to impaired bladder sensations and control (Smith et al., 2015).

The underlying contributors to UAB include neurologic disease, metabolic disease (e.g. diabetes), chronic bladder outlet obstruction (e.g. obstructive BPH or complications of anterior vaginal surgery), cognitive decline (such as with aging), psychiatric disorders, and adverse effects of medications. Additionally, structural abnormalities expanding the urinary reservoir beyond the bladder, such as massive vesicoureteral reflux or large bladder diverticulae, can result in UAB. While aging itself is often associated with UAB (and DU), there is scant evidence to support this claim.

Many pediatricians will recommend the following three-pronged approach to the treatment of encopresis associated with constipation:

1. cleaning out

2. using stool softening agents

3. scheduled sitting times, typically after meals.

The initial clean-out is achieved with enemas, laxatives, or both. The predominant approach today is the use of oral stool softeners like Movicol, Miralax, Lactulose, mineral oil, etc. Following that, enemas and laxatives are used daily to keep the stools soft and allow the stretched bowel to return to its normal size.

The child must be taught to use the toilet regularly to retrain his/her body. It is usually recommended that a child be required to sit on the toilet at a regular time each day and 'try' to go for 10–15 minutes, usually soon (or immediately) after eating. Children are more likely to be able to expel a bowel movement right after eating. It is thought that creating a regular schedule of bathroom time will allow the child to achieve a proper elimination pattern. Repeated voiding success on the toilet itself helps it become a releasor stimulus for successful bowel movements.

Alternatively, when this method fails for six months or longer, a more aggressive approach may be undertaken using suppositories and enemas in a carefully programmed way to overcome the reflexive holding response and to allow the proper voiding reflex to take over. Failure to establish a normal bowel habit can result in permanent stretching of the colon. Certainly, allowing this problem to continue for years with constant assurances that the child "will grow out of it" should be avoided.

Dietary changes are an important management element. Recommended changes to the diet in the case of constipation-caused encopresis include:

1. reduction in the intake of constipating foods such as dairy, peanuts, cooked carrots, and bananas

2. increase in high-fiber foods such as bran, whole wheat products, fruits, and vegetables

3. higher intake of water and liquids, such as juices, although an increased risk of tooth decay has been attributed to excess intake of sweetened juices

4. limit drinks with caffeine, including cola drinks and tea

5. provide well-balanced meals and snacks, and limit fast foods/junk foods that are high in fats and sugars

6. limit whole milk to 500 mL (16.9 ounces) a day for the child over 2 years of age, but do not completely eliminate milk because children need calcium for bone growth and strength.

The standard behavioral treatment for functional encopresis, which has been shown to be highly effective, is a motivational system such as a contingency management system. In addition to this basic component, seven or eight other behavioral treatment components can be added to increase effectiveness.

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.

Primary complications of gastroparesis include:

- Fluctuations in blood glucose due to unpredictable digestion times (in diabetic patients)

- General malnutrition due to the symptoms of the disease (which frequently include vomiting and reduced appetite) as well as the dietary changes necessary to manage it

- Severe fatigue and weight loss due to calorie deficit

- Intestinal obstruction due to the formation of bezoars (solid masses of undigested food)

- Bacterial infection due to overgrowth in undigested food

There is considerable research into the causes, diagnosis and treatments for FGIDs. Diet, microbiome, genetics, neuromuscular function and immunological response all interact. Heightened mast cell activation has been proposed to be a common factor among FGIDs, contributing to visceral hypersensitivity as well as epithelial, neuromuscular, and motility dysfunction.

Underactive Bladder Syndrome (UAB) describes symptoms of difficulty with bladder emptying, such as hesitancy to start the stream, a poor or intermittent stream, or sensations of incomplete bladder emptying. The physical finding of detrusor pressurization of insufficient strength or duration to ensure timely and efficient bladder emptying is properly termed "detrusor underactivity" (DU) (Abrams et al., 2002). Historically, UAB and DU (as well as others such as 'bladder underactivity') have been often used interchangeably (Rigby D, 2005), leading to both terminologic and pathophysiologic confusion.

Patients with UAB have a diminished sense of bladder filling and consequently are often found to have DU as an underlying finding, however bladder outlet obstruction and less frequently volume hypersensitivity ("OAB") can be associated with UAB symptoms (Chapple et al., 2015).

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.

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.

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.