Intestinal Motility Disorders 

Updated: Jan 18, 2017
Author: Luigi Santacroce, MD; Chief Editor: Burt Cagir, MD, FACS 



The phrase intestinal motility disorders applies to abnormal intestinal contractions, such as spasms and intestinal paralysis. This phrase is used to describe a variety of disorders in which the gut has lost its ability to coordinate muscular activity because of endogenous or exogenous causes.[1, 2, 3] Such disorders may be primary or secondary and may manifest in a variety of ways, including the following:

  • Abdominal distention

  • Recurrent obstruction

  • Severe abdominal colicky pain

  • Severe constipation

  • Gastroesophageal reflux disease

  • Intractable, recurrent vomiting

In a broad sense, any alteration in the transit of foods and secretions into the digestive tract may be considered an intestinal motility disorder. The following are considered intestinal motility disorders[4, 5] :

  • Intestinal pseudo-obstruction(Ogilvie syndrome)

  • Irritable bowel syndrome(IBS)

  • Fecal incontinence

  • Constipation

Chronic intestinal pseudo-obstruction

Chronic intestinal pseudo-obstruction (CIP) is a clinical syndrome caused by ineffective intestinal propulsion and characterized by symptoms and signs of intestinal obstruction in the absence of an occluding lesion of the intestinal lumen.[6] CIP is caused by a group of heterogeneous nerve and muscle disorders and results in obstructive intestinal symptoms in the absence of any mechanical obstruction. Usually, CIP occurs in patients with severe comorbid clinical conditions or after traumas (even surgical) or in patients with other underlying medical diseases.

A consensus working group defined CIP as a “rare, severe disabling disorder characterized by repetitive episodes or continuous symptoms and signs of bowel obstruction, including radiographic documentation of dilated bowel with air-fluid levels, in the absence of a fixed, lumen-occluding lesion.”[7] However, this definition is really applicable only to the most severe forms of CIP; air-fluid levels may not always be present.

Thus, the criteria for diagnosis should include definite symptoms and signs of obstruction, with documentation of air-fluid levels on plain radiographs of the abdomen or a dilated duodenum, small intestine, or colon on barium radiographs. Even though severe dysmotility may otherwise be present, the term pseudo-obstruction should not be used when these radiographic findings are absent.


Coordinated movements of the stomach and intestines are required to digest and propel intestinal contents along the digestive tract. The complex patterns of contraction and relaxation necessary for proper motility of the gastrointestinal (GI) tract are generated in the nerves and muscles within the GI walls.

Every day, at any time, many factors can influence GI motility (eg, physical exercise, emotional distress). The pathogenesis of primary intestinal motility disorders probably is multifactorial, but neither biochemical abnormality nor structural abnormality has been demonstrated commonly, except in some forms of intestinal pseudo-obstruction. More recently, there is evidence that low-grade mucosal inflammation and immune activation (particularly with mast cell involvement) in association with impaired epithelial barrier function and aberrant neuronal sensitivity may play a role in functional gastrointestinal disorders.[8]

Although the overall structural organization is similar throughout the digestive tract, each part has distinct motor activities. The musculature of the digestive tract has either extrinsic innervation (both sympathetic and parasympathetic) or intrinsic innervation (Auerbach plexus or myenteric plexus).

Intrinsic innervation is fundamental to coordinating GI motor activity. A neural network branching between longitudinal and circular muscle layers of the GI tract constitutes intrinsic innervation. Another nervous intrinsic plexus in the GI tract (Meissner plexus or submucosal plexus) helps to modify mucosal absorption and secretion without influencing motility.

Random, unorganized motor activity with occasional peristaltic and antiperistaltic complexes occurs during feeding, and this allows gastric remixing of foods. After this, another motor activity occurs, which is more regular, and this begins the peristaltic waves (ie, contractions of the circular musculature of the small intestine) that allow progression of undigested food through the intestines.

These events happen because the gastric pacemaker area, which originates electric slow waves with a frequency of 3 cycles per minute, occurs at the junction between the body and the antrum of the stomach. These electric waves, called migrating myoelectric complexes, determine the frequency of muscular contractions in the antral and pyloric areas through electromechanical coupling.

Migrating myoelectric complexes regulate gastric emptying and move gastric contents distally. Every 90 minutes, a cluster of migrating myoelectric complexes arises in the stomach and migrates distally beyond the ileum. Vagal function and the release of nitric oxide, vasoactive intestinal polypeptide, motilin, and nutrients of the meal and other enterohormones also affect GI motility.

Knowles and Martin attempted to define a novel classification for intestinal motility disorders,[9] in which these conditions are categorized as well-defined entities, entities with a variable dysfunction-symptom relation, questionable entities, and entities associated with behavioral disorders.

Well-defined entities in the Knowles-Martin classification include the following:

  • Delayed colonic transit - Slow transit constipation (eg, enteric neuropathy, enteric myopathy, Parkinson disease, endocrine disorders, spinal injury); the impairment of gastric motility in Parkinson disease patients, particularly in those with motor complications (42%), may be due in part to the effect of L-dopa on gastric dopaminergic receptors[10] ; in patients with spina bifida and spinal cord injuries, altered histology of the enteric nervous system as well as myenteric plexus neuronal loss and decreased nerve fiber density may play a major role in intestinal motility[11]

  • Dilated colon (diffuse or segmental) - Ogilvie syndrome, megacolon

  • Absent rectoanal inhibitory reflex - Hirschsprung disease

Entities with a variable dysfunction-symptom relation include the following:

  • Abnormally low anal canal pressure fecal incontinence (eg, diabetes mellitus, spinal injury)

Questionable entities include the following:

  • Accelerated transit bile salts

  • Short bowel

  • Rare endocrine and metabolic disorders

Entities associated with behavioral disorders include the following:

  • Impaired pelvic floor relaxation, prolonged storage in the rectosigmoid, outlet delay, anismus

  • Avoidance of defecation, functional fecal retention (eg, poor pelvic floor training, poor diet, fear of pain, learned suppression)


Causes of intestinal motility disorders seem to be multifactorial, and only a few have been detected.

Degenerative disorders cause pseudo-obstruction along with other problems; however, in patients with pseudo-obstruction, only changes in the nervous and muscular systems have been observed.

Many drugs that are commonly used (eg, tricyclic antidepressants, diuretics, laxatives) or have specific indications (eg, lithium salts, vinca alkaloids, and other chemotherapy agents) may interfere with intestinal motility. Stypsis may be related to drug abuse. Drugs such as benzodiazepines, lithium salts, laxatives, and codeine cause secondary stypsis. The latter can produce narcotic bowel syndrome, which is usually observed in patients who abuse opiates for chronic pain.

Endocrine disorders (eg, myxedema) can also cause pseudo-obstruction.

IBS, the more commonly diagnosed disorder of intestinal motility, has been considered a disease of the colon for decades, but research on GI motility has demonstrated that underlying motility disturbances can occur in the small bowel.

Irritable bowel syndrome

The causes of irritable bowel syndrome (IBS) remain unknown. According to some reports, the small intestine and colon of patients with IBS are more sensitive and reactive to mild stimuli than usual. IBS could be related to immature status of muscles and nerves in the intestinal wall of these persons.

Fecal incontinence

Aging, dementia, stroke, Parkinson disease, spinal cord injuries, rectal tears during birthing, diabetes, surgical complications, and neuromuscular disorders (eg, myasthenia gravis) may cause fecal incontinence.

Occasionally, fecal incontinence may occur after ingestion of certain foods. Sugars, insoluble fibers, and starches (except rice) are broken down in the intestines, forming a variable amount of gas that must be expelled. Most people who have lactase deficiency cannot digest lactose, a sugar common in several foods (eg, milk, cakes). People who have lactose deficiency may experience uncontrolled liquid diarrhea after lactose ingestion.


Constipation commonly has several causes, either primary or secondary. The most frequent of these are the following:

  • Diet that is very poor in fiber and high in animal fats and refined sugars

  • Pregnancy

  • Psychological constipation related to lifestyle changes (eg, travel, a new job, or divorce), in which the patient ignores the urge to defecate

  • Hypothyroidism

  • Electrolyte imbalance, especially if it involves Ca++ or K+

  • Tumors producing mechanical compression on an intestinal tract, either internally or externally

  • Nervous system injuries

  • Intoxication from lead, mercury, phosphorus, or arsenic

  • Constipation also may be secondary to rhagades (anal fissures) and piles.

Genetic factors

In a retrospective study investigating the association between mitochondrial disorders and CIP in 80 patients, Amiot et al determined that 15 patients (19% of the study cohort) had mitochondrial defects, including mutations in the thymidine phosphorylase gene (5 patients), the DNA polymerase-gamma gene (5 patients), and tRNA(leu(UUR)) (2 patients); 3 of the patients had no identifiable genetic defects.[12] Extradigestive symptoms occurred in all 15 patients.

Unlike other CIP patients, patients in whom the condition was associated with a mitochondrial defect tend to require frequent and long-term parenteral nutrition.[12] Because of the frequent occurrence of digestive and neurologic complications, these patients also had a high incidence of premature death. The authors suggested that mitochondrial defects are an important cause of CIP and recommended that CIP patients be tested for such defects, particularly those with severe CIP who experience associated neurologic symptoms.


According to some epidemiologic reports, as many as 30 million Americans have intestinal motility disorders. Available data from the medical literature indicate that worldwide, 30-45% of all GI conditions are referable to intestinal motility disorders.

When intestinal motility disorders are idiopathic and not related to either malignancies or systemic diseases, morbidity is minimal and mortality from complications is low (1-1.5%); complications usually occur in patients with intestinal pseudo-obstruction.

Persons of any age group may be affected, depending on the specific intestinal motility disorder. For example, IBS occurs more frequently in people aged 20-40 years, whereas intestinal pseudo-obstruction may occur in either newborns or elderly patients. Most patients are female, with a female-to-male ratio of 2.8:1. Primary intestinal motility disorders are most common in white persons and are usually thought to be related to diet.


Primary intestinal motility disorders or disorders that are not secondary to malignancy or debilitating pathology have a good prognosis. According to many reports, the prognosis is excellent for patients with IBS and mild fecal incontinence.

The prognosis is worse for patients with intestinal pseudo-obstruction, which has a high mortality.




The clinical presentation of patients with intestinal motility disorders is protean and may range from simple nausea and indigestion to severe abdominal pain, vomiting, diarrhea, inability to eat, weight loss, and other symptoms. It should be kept in mind that during pregnancy, intestinal motility disorders may worsen as a consequence of uterine compression of intestinal loops.

Obtain a complete patient history, recording information about the following:

  • Feelings of abdominal discomfort, cramping, nausea or vomiting, pain, excessive gas, and rectal fullness

  • Frequency, amount, and timing of normal defecation and any recent change

  • Amount, consistency, and color of last passed feces

  • Type of diet, use of laxatives or enemas, and drug use

Chronic intestinal pseudo-obstruction

Patients with chronic intestinal pseudo-obstruction (CIP) generally experience abdominal distention, pain, dizziness, fatigue, nausea, and vomiting for several days or months before their condition is recognized.

One type of pain is directly related to intestinal distention and improves or temporarily disappears if intestinal distention decreases. A second type is probably secondary to smooth muscle spasm or visceral hyperalgesia and is independent of intestinal distention.

Abdominal distention ranges from almost none to the equivalent of a 9-month pregnancy, depending on the nature and extent of the underlying pathology. An audible succussion splash and loud borborygmi may be present. Pain and distention may be almost continuous or may be interrupted by periods of clinical improvement. The vomitus frequently consists of food ingested 12 or more hours previously and may be feculent.

In patients with predominant small intestinal involvement, bacterial overgrowth and stagnant loop syndrome often develop and may lead to steatorrhea and diarrhea. Predominant colonic involvement usually results in constipation, megacolon, or both. Patients with both types of involvement may cycle from diarrhea to constipation, depending on the severity of steatorrhea and the relative involvement of each organ.

Many patients have involvement of the esophagus, which may be asymptomatic or may produce dysphagia, chest pain, regurgitation, reflux, and heartburn. Visceral neuropathies may manifest as symptoms resembling achalasia or diffuse esophageal spasm.

Gastric involvement produces gastroparesis. The abdominal distention and pain produced by any combination of gastric, small intestine, and colonic involvement result in decreased food intake, weight loss, and malnutrition, especially when combined with malabsorption.

Patients with involvement limited to the colon and distal small bowel may have relatively normal weights because their unaffected proximal bowel allows for normal absorption. Patients may have a history of weight loss or previous abdominal operations with no obstructing lesion found, or they may have a family history positive for the condition.

Irritable bowel syndrome

Abdominal pain, nausea, and irregular bowel habits that intensify during stress are the most common symptoms in patients with irritable bowel syndrome (IBS).

Fecal incontinence

Fecal incontinence can be a life-threatening condition. In the mild form, patients may experience abdominal bloating and uproar, but in the severe form, they may experience serious abdominal pain. Patients may not experience symptoms if incontinence is related to a comorbid condition (eg, dementia, Parkinson disease, or a demyelinating disease of the spinal cord).

Constipation and fecal incontinence

Constipation can also be a life-threatening condition. Patients with constipation report abdominal discomfort, cramping, pain, rectal fullness, or, more rarely, nausea and vomiting.

Physical Examination

The clinical picture of patients with intestinal motility disorders is protean and may vary greatly, depending on the specific condition present.

Always perform a digital rectal examination in any patient with an intestinal motility disorder to detect the presence of a mass (eg, feces, tumor, or a foreign body) or blood in the rectum.

Chronic intestinal pseudo-obstruction

Decreased or absent bowel sounds and progressive loss of bowel movements are the most common signs in patients with CIP.[13] Patients’ symptoms increase in the 4-7 days before clinical onset and recognition of the disorder.

Physical examination findings may include weight loss, cachexia, and abdominal distention. Patients with small intestinal involvement usually have a succussion splash located in the midabdomen, whereas patients with gastric involvement may have a splash in the left upper quadrant.

Hypertympany to percussion is usually present, and contracting bowel loops are occasionally observed pushing up against the abdominal wall. Bowel sounds are of no value in making a diagnosis of pseudo-obstruction.

Evidence of central and peripheral nervous system disease should be sought, and autonomic nervous system testing should be performed when indicated.

Involvement of the genitourinary system may be indicated by the presence of a palpable urinary bladder. Patients may have positive neurologic findings with signs of systemic disease (eg, progressive sclerosis, amyloidosis, or myxedema).

Irritable bowel syndrome

Patients with IBS commonly have bloating, heartburn, burping, vomiting, and difficulty swallowing. Symptoms can fluctuate, disappearing during sleep and occurring again during stressing occasions. Heartburn, burping, and difficulty swallowing are usually due to concomitant gastroesophageal reflux disease, a very common condition in such patients.

Fecal incontinence

In the first stage of the disease, passing gas more than the normal 14-23 times a day characterizes fecal incontinence. In the second stage, liquid incontinence occurs, and patients are unaware that stools are being passed (stage of passive fecal incontinence). In the third stage, which is more severe, involuntary passage of feces through normal sphincter muscles occurs (stage of urge incontinence).


The pattern of at least 3 stools per week and no more than 3 per day is considered normal defecation. Any reduction in the frequency of defecation may be considered constipation. Abdominal colicky pains are frequent in these patients.


Complications of intestinal motility disorders vary greatly, depending on the specific type of disorder under consideration.

Intestinal pseudo-obstruction is often associated with a high mortality (15-30%), in most cases due to delayed diagnosis.

Constipation may have a severe complication, impaction. If this condition is not recognized early, the patient may die. Impaction is the collection of dry and hardened feces in the rectum or colon. Symptoms of impaction may be similar to those of constipation or may be unrelated to the gastrointestinal system.

If abdominal distention occurs, movements of the diaphragm are compromised and cause insufficient aeration with subsequent hypoxia and left ventricular dysfunction. In addition, hypoxia can precipitate angina or tachycardia. When a vasovagal response begins, the patient may have hypotension. Patients with impaction may experience vomiting, diarrhea, and resultant dehydration. They may present in an acutely confused and disoriented state, with tachycardia, fever, and altered blood pressure.

IBS is not usually associated with complications. Fecal incontinence may cause psychological problems in affected patients.



Diagnostic Considerations

Failure to make the correct diagnosis of an intestinal motility disorder is a medicolegal pitfall, especially in patients with irritable bowel syndrome (IBS), because several cancers of the digestive tract mimic this condition, even in late stages.

The criteria for diagnosis of intestinal pseudo-obstruction should include definite symptoms and signs of obstruction, with documentation of an ileus or air-fluid levels on plain radiographs of the abdomen or a dilated duodenum, small intestine, or colon on barium radiographs. Even though severe dysmotility may otherwise be present, the term pseudo-obstruction should not be used when these radiographic findings are absent.

In addition to the conditions listed in the differential diagnosis, other problems to be considered include the following:

  • Alcohol-related neuropathies

  • Electrolytic imbalance

  • Poisoning due to environmental agents

  • Maldigestion

Counseling with a neuropsychologist, evaluation by an endocrinologist, and research into toxins and drugs in the blood may be helpful for diagnosis.

Differential Diagnoses



Approach Considerations

A complete workup should be performed to exclude an organic cause for the patient’s symptoms (eg, myxedema, dynamic bowel obstruction, or malignancy, which are eminently treatable conditions). Only after the complete workup has been carried out can the patient be deemed to have a functional problem.

Workup may include laboratory studies, diagnostic imaging, manometry, electromyography (EMG), endoscopy, and diagnostic laparoscopy or laparotomy.[14]

Laboratory Studies

Routine laboratory examinations are not very useful for diagnosing primitive intestinal motility disorders, except pseudo-obstructive attacks. However, laboratory studies may be helpful for diagnosing motility disorders of the gut due to intestinal cancers or irritable bowel disease.

The complete blood count (CBC) is usually altered in patients with intestinal cancers (in whom it may show anemia) and in patients with irritable bowel disease (in whom leukocytosis is the more frequent result). In such patients, the protein electrophoresis pattern may show alterations of both albumin and globulins (especially alpha-1 and gamma globulins).

Electrolyte imbalance is common in patients with intestinal pseudo-obstruction. Serum levels of triiodothyronine, thyroxine, and glucose are also altered in these patients. Vitamin B-12 levels are reduced in persons with malabsorption. Transaminase levels can be altered in patients with liver metastases. A stool sample should be sent for analysis if the diagnosis of steatorrhea from small bowel bacterial overgrowth is suggested.

Tumor markers may be studied in patients who may have cancer of the digestive system. The most useful tumor markers for these patients are carbohydrate antigen 19-9, cancer antigen 125, and carcinoembryonic antigen (CEA). CEA is nonspecific but is useful in follow-up evaluations. Alpha-fetoprotein evaluation may help detect liver involvement by metastases from intestinal cancers.

Urinalysis is not useful in establishing a diagnosis of an intestinal motility disorder.

Radiography and Scintigraphy

Plain radiographic films of the abdomen may show bowel blockage (without any actual mechanical bowel obstruction) in patients with intestinal pseudo-obstruction, but findings are usually negative in patients with irritable bowel syndrome (IBS) or constipation (see the image below).

Dilated cecum (16 cm) and colon in patient with ps Dilated cecum (16 cm) and colon in patient with pseudocolonic obstruction.

A barium meal is a helpful study in the diagnosis of intestinal motility disorders, but it should never be administered to patients with symptoms of pseudo-obstruction, because it may cause irreversible blockage of intestinal transit. It may show a delay in transit time in persons with constipation, or the results may be normal in patients with IBS.

Computed tomography (CT) and nuclear magnetic resonance examinations are expensive and should be reserved for patients with possible intestinal malignancy.

Although defecography offers some information about the kinetics of rectal emptying, scintigraphic study of the small bowel or colonic transit time is currently preferred. Radionuclide gastric emptying tests are also performed when needed. Scintigraphic study of intestinal transit time, accomplished by oral administration of radiolabeled foods, allows study of gastric emptying and intestinal progression of the meal. It is not helpful in the diagnosis of patients with possible intestinal cancer.[15]

Guidelines for the scintigraphic measurement of solid-phase, liquid-phase, and combined liquid-phase/solid-phase gastric emptying are available from the American College of Radiology (ACR), the Society of Nuclear Medicine (SNM), and the Society for Pediatric Radiology (SPR).[16] The following are among the general indications for gastrointestinal scintigraphy[16] :

  • Demonstration of: Salivary gland function and tumors; presence and site of acute gastrointestinal bleeding; transit through the small/large intestine; presence/absence of peritoneal loculations before the administration of intraperitoneal chemotherapy or radiopharmaceutical therapy

  • Detection of: Ectopic functioning gastric mucosa; congenital/acquired perforation of the pleuroperitoneal diaphragm

  • Confirmation of suspected aspiration

  • Evaluation and quantification of transit through and reflux into the esophagus

  • Evaluation of patency of peritoneovenous shunts

  • Quantification of the rate of emptying of liquid and/or solid meals from the stomach

Manometry and Electromyography

Rectal manometry, a procedure for measuring the intestinal pressure exerted by the muscles of the pelvic floor, may provide some important information in patients with intestinal motility disorders, especially in those with fecal incontinence. Esophageal or gastroduodenal manometry or cystometrography may be performed as indicated. High-resolution manometry in conjunction with pressure-flow measurements appears to allow discrimination of the cause of dysphagia in children, such as differentiating weak peristalsis (poor bolus clearance) from abnormal bolus flow resistance (esophageal outflow obstruction), which may aid in treatment planning and decision making.[17]

EMG of the pelvic floor yields information about nervous conduction and muscle function, though it is not very accurate. Such information makes it possible to distinguish between functional and organic disorders of defecation.


Endoscopy usually provides information about morphologic and functional patterns of the digestive tract. Perform endoscopic studies of the upper and lower digestive tracts in any patient with an intestinal motility disorder because, in most of these patients, dysmotility has been described in the whole digestive tract.

A rectal mucosal or full-thickness biopsy may be useful in helping to diagnose amyloidosis or pathologic abnormalities of the muscularis propria or the nerve plexus (myopathies and neuropathies). Echoendoscopy may provide additional information about the muscular layer of the gastrointestinal (GI) tract.

Diagnostic Laparoscopy or Laparotomy

Diagnostic laparoscopy or laparotomy, with full-thickness biopsy or resection, and immunohistochemistry can be performed to assess for c-kit –positive cells. A full-thickness biopsy sample of the small intestine can be obtained via laparoscopy, with or without a feeding jejunostomy tube. Full-thickness biopsy specimens should be examined for muscle disease, inflammatory infiltrates of the myenteric plexus, neuronal intranuclear and intracytoplasmic inclusions, neuronal destruction, and absent or deficient c-kit immunoreactivity.

If laparotomy is performed, specimens should be taken from 2 sites, with tissue obtained from dilated and nondilated segments of intestine and processed for conventional light microscopy and immunohistochemistry.

Histologic Findings

Because of their functional origin, no specific histologic pattern has been associated with primary intestinal motility disorders. Some sort of molecular damage in muscle fibers of the digestive tract is thought to occur, or intrinsic innervation (enteric nervous system) may cause motor incoordination as a result of alterations of migrating myoelectric complexes.

Testing of c-kit immunoreactivity is used to assess the volume of the interstitial cells of Cajal. Literature suggests that a decrease in the volume of these cells is associated with slow transit of the bowel.[18, 19, 20, 21]



Approach Considerations

Because several different drugs can cause intestinal motility disorders, avoiding them, if possible, may resolve the condition. In selected patients, pharmacotherapy may be helpful. Gastric preprandial dysrhythmia may lead to impaired gastric emptying, thus contributing to irregular absorption of drugs from the small intestine and conducing to disabling response fluctuations of the therapy.

Cognitive interventions (eg, cognitive behavorial therapy, hypnotherapy) have been successful in managing abdominal pain in patients with irritable bowel syndrome; however, they have limited utility for routine use in daily practice owing to their labor intensiveness and tight availability.[22]

Surgery is not usually performed to treat patients with primary intestinal motility disorders, except in the treatment of idiopathic constipation that does not respond to medical therapies and in the treatment of intestinal pseudo-obstruction. Surgery for these patients is always palliative. Only patients who are incapacitated by their symptoms or those whose nutritional status is adversely affected undergo surgery.

Neural stem cell transplantation may be beneficial for patients with intestinal motility disorders associated with enteric neuropathy.[23] A murine study demonstrated that transplanted enteric neural progenitor cells could generate functional enteric neurons in the postnatal bowel.[23]

Patients with intestinal motility disorders must be educated in ways of coping with their condition and instructed to avoid any situation or substance that may cause the symptoms to worsen. Psychological counseling may be helpful.

Pharmacologic Therapy

Avoidance of drugs that can cause intestinal motility disorders is recommended if doing so is feasible. In patients with primitive (idiopathic) intestinal motility disorders, the administration of some drugs may be useful to control symptoms.

Drugs used in the management of intestinal motility disorders include parasympathomimetics, prokinetic agents, opioid antagonists, antidiarrheals, and antibiotics. The agents that are most useful in the treatment of these disorders are neostigmine, bethanechol, metoclopramide, cisapride, and loperamide.[24, 25, 26, 27] Prucalopride appears promising for the treatment of chronic constipation[28, 29] ; its low side-effect and drug-interaction profile appear to allow it to be a safe option in elderly patients with chronic constipation.[30]  

Tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs) provide symptomatic relief, but this has been demonstrated only for TCAs in meta-analyses.[22]

The use of injectable bulking treatment appears to be effective and safe in the long-term management of fecal incontinence.[31]  In one study, symptomatic reduction with non-animal stabilized hyaluronic acid/dextranomer (NASHA Dx) occurred in 52% of 136 patients at 6 months, with sustained results at 12 months (57%) and at 36 months (52%). Mean change from baseline Cleveland Clinic Florida Fecal Incontinence Score (CCFIS) and Fecal Incontinence Quality of Life Scale (FIQL) scores improved between baseline and at 36-month follow-up.[31]

Broad-spectrum antibiotics (not discussed in detail in this topic) may be needed to treat stagnant loop syndrome with bacterial colonization. A 7-day course of antibiotics (eg, tetracycline, doxycycline, ampicillin, quinolones, metronidazole) may lead to remission of the diarrhea.[32]

Endoscopy, Ostomy, and Bowel Resection

Before the decision is made to perform a particular operation, it is extremely important to determine which symptoms are being palliated and from which area of the intestine these symptoms emanate. Surgery is always indicated if the patient has complications such as perforation of the bowel or peritonitis.

In patients with acute intestinal pseudo-obstruction, endoscopic decompression is suitable and may resolve the problem. When indicated, endoscopic decompression should always be attempted before any open surgical intervention. Some patients may benefit from laparoscopy and lysis of adhesions. Surgical procedures such as feeding jejunostomies, decompressive gastrostomy, or ileostomy also may be necessary.

Transplantation of the small intestine is still in the experimental stages, but steady progress has been made, and improved survival is being reported.[33, 34]

Patients with chronic intestinal motility disorders may experience symptom relief after total colectomy in conjunction with near-total proctectomy. This surgical procedure is successful in nearly 90% of patients. Some surgeons prefer to perform a total proctocolectomy with ileoanal anastomosis on a J-pouch.

This procedure may be necessary in patients who have a megacolon and severe abdominal distention. However, even with such treatment, some patients continue to have severe symptoms from coexisting disease of the small intestine. In addition, colectomy may exacerbate diarrhea. Accordingly, palliative surgery should be undertaken only after careful consideration; unnecessary surgery must be avoided at all costs.

After any abdominal procedure, exclusion of mechanical obstruction caused by adhesions may be difficult if the patient returns with symptoms of intestinal obstruction. On the other hand, surgery may be necessary for acute problems, such as intestinal volvulus, perforation, or herniation, all of which can occur in patients with pseudo-obstruction.

Extensive, sometimes radical, small-bowel resection may be necessary in rare cases of unrelenting intestinal obstruction and massive intestinal fluid secretion that make it impossible to keep up with fluid losses or control severe obstructive symptoms. Some patients continue to have abdominal pain or such copious intestinal secretion that vomiting and fluid and electrolyte losses remain substantial. They may require a decompressive enterostomy or an extended small-bowel resection; in such cases, they are invariably on home parenteral nutrition.

If the patient is unable to maintain adequate nutritional intake or continues to have severe symptoms despite palliative treatment, long-term home parenteral nutrition may be necessary. Many patients who are on home parenteral nutrition seem to do well, though some develop sepsis and thrombotic complications of the central intravenous catheter, depression, prolonged suffering, and analgesic dependence.

Support groups, such as the American Association of Gastrointestinal Motility Disorders and the American Pseudo-Obstruction and Hirschsprung Society, provide advice, information, educational meetings, and psychological support to patients and their families.

Diet and Activity

Changes in dietary habits alone can help cure motility disorders. Correct fiber intake is useful in patients with either constipation or stool leakage. Fiber and water must be abundant in the diet of patients with constipation; fermentable foods should be avoided. Patients should take small frequent meals (6-8 times a day), avoid foods high in fat or lactose, and avoid residue- and gas-producing foods.[22] Pureed foods (via a blender or other means) may be tolerated by some individuals.

Patients can receive supplementation with liquid formulations, vitamins, and minerals (eg, vitamin B-12, iron, calcium, folic acid, water-soluble vitamins, vitamin A, vitamin D, vitamin E, vitamin K, trace elements) as needed to meet the requirements. Consultation with a dietitian helps provide the patient with a number of options.

Mild physical exercise is not contraindicated and may be very useful for symptom relief in patients with irritable bowel syndrome or constipation.


A healthy lifestyle is the best prevention for intestinal motility disorders. A diet rich in fiber, especially insoluble fibers, cannot prevent colon cancer, but it may prevent constipation and impaction, its more severe complication. In addition, because insoluble fibers create a mass effect in the stomach, they may be helpful in weight control, preventing diseases related to obesity (eg, cardiovascular accidents and endocrine disturbances).

Prescriptions of laxatives, diuretics, benzodiazepines, and anticholinergic drugs should be limited. Such agents may interfere with gastrointestinal motility; they should be administered only if they are clearly useful for patients, and only for a limited time.

Any patients older than 50 years should be scheduled for colonoscopy, even if they are not symptomatic.

Patients with a history of abdominal surgery who have recurrent bowel habit disorders should be carefully evaluated with an eye to detecting eventual adhesions. The same consideration is valid for patients with a history of radiotherapy of the abdomen or pelvis.



Medication Summary

Drugs used in the management of intestinal motility disorders include cholinergic agonists, prokinetic agents, opioid antagonists, antidiarrheals, and antibiotics. The agents that are most useful in the treatment of these disorders are neostigmine,[35] bethanechol, metoclopramide, cisapride, and loperamide. Neostigmine appears to increase antral and intestinal motor activity in patients with hypomotility, including intestinal dysmotility.[35]

Cholinergic Agonists

Class Summary

Excessive parasympathetic suppression appears to be involved in the genesis of intestinal pseudo-obstruction. Cholinergic agents may allow early resolution of pseudo-obstruction and obviate surgery.

Bethanechol (Urecholine)

Bethanechol is a synthetic muscarinic stimulant. It should never be administered intravenously (IV) or intramuscularly (IM).

Prokinetic Agents

Class Summary

Prokinetics are promotility agents, proposed for use with severe constipation-predominant symptoms.

Tegaserod (Zelnorm)

Tegaserod was temporarily withdrawn from the US market in March 2007; however, as of July 27, 2007, restricted use of tegaserod is now permitted via a treatment investigational new drug (IND) protocol. This protocol allows tegaserod treatment of irritable bowel syndrome with constipation (IBS-C) or chronic idiopathic constipation (CIC) in women younger than 55 years who meet specific guidelines. Its use is further restricted to those in critical need who have no known or preexisting heart disease. (See the FDA MedWatch Product Safety Alert.)

Tegaserod is used for short-term treatment of women with IBS in which constipation is the predominant symptom. It is also indicated to treat CIC. Tegaserod is a serotonin type 4 receptor partial agonist with no affinity for 5-HT3 receptors. It may trigger peristaltic reflex via 5-HT4 activation, which enhances basal motor activity and normalizes impaired gastrointestinal (GI) motility. Research studies have shown inhibitory activity of the drug on visceral activity in the GI tract.

Metoclopramide (Reglan, Metozolv)

Metoclopramide is characterized by remarkable coordination of gastric and duodenal motility.

Cisapride (Propulsid)

Cisapride indirectly improves GI motility by promoting acetylcholine release from postganglionic nerve endings in the myenteric plexus. It was withdrawn from the US market on July 14, 2000, but the manufacturer will make it available to certain patients meeting clinical eligibility criteria for a limited-access protocol only.

Opioid Reversal Agents

Class Summary

Consider using a peripherally selective opioid antagonist to treat constipation in patients who have advanced illness requiring chronic opioid analgesia and are unresponsive to laxatives.

Methylnaltrexone (Relistor)

Methylnaltrexone is a peripherally acting mu-opioid receptor antagonist. It selectively displaces opioids from mu-opioid receptors outside the central nervous system (CNS), including those located in the GI tract, thereby decreasing constipating effects. Methylnaltrexone is indicated for opioid-induced constipation in patients with advanced illness who are receiving palliative care and whose response to laxatives has not been sufficient. It is available as a 12-mg/0.6-mL injectable solution for subcutaneous use.

Naloxegol (Movantik)

Naloxegol selectively antagonizes peripheral mu-opioid receptors, inhibiting opioid-induced GI hypomotility. In chronic constipation, dosing is 25 mg PO once daily 1 hour prior to eating or 2 hours post-prandial. If creatinine clearance is < 60, then start at 12.5 mg PO once daily.


Class Summary

Antidiarrheal agents inhibit peristalsis and slow intestinal motility.

Loperamide (Imodium)

Loperamide inhibits peristalsis by acting directly on the muscles of the intestinal wall, thereby slowing intestinal motility. It prolongs movement of electrolytes and fluid through the bowel and increases viscosity and loss of fluids and electrolytes.

Diphenoxylate and atropine (Lomotil)

Diphenoxylate and atropine is an antidiarrheal drug combination wherein diphenoxylate is chemically related to the narcotic analgesic meperidine. It acts on intestinal muscles to inhibit peristalsis and slow intestinal motility. It prolongs the movement of electrolytes and fluid through the bowel and increases viscosity and loss of fluids and electrolytes. A subtherapeutic dose of anticholinergic atropine sulfate is added to discourage overdosage, in which case diphenoxylate may clinically mimic the effects of codeine.

Difenoxin and atropine (Motofen)

Difenoxin and atropine is an antidiarrheal drug combination wherein diphenoxylate is chemically related to the narcotic analgesic meperidine. Difenoxin is the active metabolite of diphenoxylate, and it is active at one fifth the dose of diphenoxylate.


Class Summary

Erythromycin is a prokinetic agent for the stomach. It is indicated in patients with gastroparesis.

Erythromycin (E.E.S., Erythrocin, Ery-Tab)

Erythromycin is a macrolide antibiotic that duplicates the action of motilin and is responsible for migrating motor complex activity by binding to and activating motilin receptors. IV administration enhances the emptying rate of liquids and solids. The effect can be seen with oral erythromycin. The enteric-coated form may be better tolerated.