Encopresis is the involuntary discharge of feces (ie, fecal incontinence). In most cases, it is the consequence of chronic constipation and resulting overflow incontinence (see the images below), but a minority of patients have no apparent history of constipation or painful defecation. No good prospective data suggest that encopresis is primarily a behavioral or psychological disorder. The behavioral difficulties associated with encopresis are most likely the result of the condition rather than its cause.
View Image | Overflow incontinence. |
View Image | Overflow incontinence. |
Encopresis, along with enuresis, is classified as an elimination disorder in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). It may be divided into 2 subtypes: encopresis with constipation (retentive encopresis) and encopresis without constipation.
Symptoms of encopresis may include the following:
Physical findings, other than those from abdominal and rectal examinations, are usually normal. Unless contraindicated, a digital rectal examination should be performed on every child with encopresis.
Examination may reveal the following:
Neurologic findings should be normal. Patients should have a normal anal wink and normal sensation, strength, and reflexes in the lower extremities.
See Presentation for more detail.
Other problems to be considered in the diagnosis include the following:
In most patients, the diagnosis of encopresis is established on the basis of the history and complete physical examination, including a rectal examination. Laboratory studies are rarely warranted. The following studies may be helpful:
See Workup for more detail.
Conventional medical therapy is commonly the first therapy attempted, generally consisting of the following:
Agents that can be used for disimpaction include the following:
Virtually any laxative can be used, provide that it is administered in sufficient quantity to produce 1-2 soft stools daily.
In addition to long-term laxative therapy, modalities that have been proposed for the treatment of chronic encopresis include the following:
Although the critical components of a successful intensive behavioral program have not been systematically elucidated, common elements of existing programs include the following:
See Treatment and Medication for more detail.
Encopresis is the involuntary discharge of feces (ie, fecal incontinence). In most cases, it is the consequence of chronic constipation and resulting overflow incontinence, but a minority of patients have no apparent history of constipation or painful defecation. No good prospective data suggest that encopresis is primarily a behavioral or psychological disorder. The behavioral difficulties associated with encopresis are likely the result of the condition rather than its cause.
In most patients, the diagnosis of encopresis is established with the history and complete physical examination, including a rectal examination. Laboratory studies are rarely warranted, though radiography, manometry, and biopsy may be helpful. Treatment remains largely experiential and generally consists of demystification and education, colonic disimpaction followed by routine laxative therapy, and “toilet training.”
For patient education resources, see the Esophagus, Stomach, and Intestine Center, as well as Encopresis and Constipation in Children.
The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), uses the term elimination disorder to classify both encopresis and enuresis.[1] Encopresis is further divided into 2 subtypes: encopresis with constipation (retentive encopresis) and encopresis without constipation. The latter subtype is much less common and most often occurs in association with oppositional defiant disorder or conduct disorder or as a consequence of anal masturbation.
DSM-5 criteria for encopresis are as follows[1] :
In the vast majority of cases, encopresis develops as a consequence of chronic constipation with resulting overflow incontinence (see the images below),[2] which is typically termed retentive encopresis; encopresis in the absence of a history of constipation or painful bowel movements is typically referred to as nonretentive. Many children with encopresis have a remote history of constipation or painful defecation[3] or demonstrate incomplete evacuation during defecation on physical examination or radiographic assessment.[4]
View Image | Overflow incontinence. |
View Image | Overflow incontinence. |
Chronic constipation due to irregular and incomplete evacuation results in progressive rectal distention and stretching of both the internal anal sphincter and the external anal sphincter (EAS). As the child habituates to chronic rectal distention, he or she no longer senses the normal urge to defecate. Soft or liquid stool eventually leaks around the retained fecal mass, resulting in fecal soiling.
In most cases, encopresis is thought to develop as a consequence of chronic constipation with resulting overflow incontinence. Approximately 80-95% of children with encopresis have a history of constipation or painful bowel movements. The remaining 5-20% appear to have nonretentive encopresis and no history of constipation or painful defecation; they generally have no evidence of incomplete evacuation on physical evaluation or radiographic evaluation.
No good prospective data suggest that encopresis, whether retentive or nonretentive, is primarily a behavioral or psychological disorder. Rather, most of the available evidence indicates that children with encopresis do not have an increased incidence of major behavioral or personality disorders when compared with age-matched peers.[5] Overall, the evidence suggests that behavioral difficulties associated with encopresis may be the result of the encopresis rather than the cause.[6, 7]
No good evidence suggests that encopresis is an indicator of sexual abuse.[8] The incidence of fecal soiling is comparable among children with a history of sexual abuse and among children with psychiatric and behavioral disorders.
Children with encopresis are significantly more likely to have attention-deficit disorder/hyperactivity (ADHD) than the general population.[9, 10]
Low self-esteem or parent-child conflict as a result of the disorder is not uncommon. Embarrassed youngsters also frequently deny having the problem.
Although few prospective studies have been conducted to examine the prevalence of encopresis in childhood, it is estimated that 1-2% of children younger than 10 years have encopresis. In a study of 482 children aged 4-17 years who were observed over a 6-month period in a primary care pediatric clinic in Iowa, 4.4% of the subjects experienced fecal incontinence at least once per week.[11]
Nearly all of the few published population-based studies examining the prevalence of encopresis have been conducted in North America and Europe. In one such study conducted in the Netherlands, 4.1% of children aged 5-6 years and 1.6% of children aged 11-12 years experienced fecal soiling at least once per month.[12] Studies conducted in Sweden and the United Kingdom[13] reported similar numbers.
In nearly all published series, boys are much more commonly affected than girls. In most series, approximately 80% of affected children are boys.
Even with aggressive medical and behavioral interventions, as many as 30% of children remain symptomatic.[14] Unfortunately, the available data are insufficient to enable clinicians to make reliable predictions as to which children will successfully respond to which specific treatment protocols.
Current evidence suggests that family disorganization correlates with a poor response to all forms of treatment. In contrast, no demographic, manometric, behavioral, social, academic, or self-esteem measures are clearly associated with response to therapy. No investigators have systematically examined the child’s motivation, the family’s motivation, or the state of change to determine whether any of these is predictive of the patient’s response to treatment.
Nonretentive encopresis may be associated with oppositional defiant disorder and conduct disorder. Urinary tract infection may be associated with encopresis, but is more frequently seen in females than in males.
Approximately 80-95% of children with encopresis have a history of constipation or painful defecation. In many patients, the history of constipation or painful defecation is remote, occurring years before the child presents with encopresis. On average, children who have encopresis are symptomatic 5 years before the problem is brought to medical attention.
Most children with encopresis deny the urge to defecate associated with their soiling episodes. Sometimes, affected children contend that they are unable to differentiate between passing gas and passing feces.
In most cases, soiling episodes occur during the daytime, when the child is awake and active. Soiling at night, when the child is asleep, is uncommon.
As evidence of functional megacolon, many children with retentive encopresis intermittently pass extremely large bowel movements.
Physical findings, other than those obtained from the abdominal and rectal examinations, are usually normal. Unless a physical or psychological contraindication is noted, a digital rectal examination should be performed on every child with encopresis to exclude any underlying anatomic or neurologic abnormality that might account for the encopresis (eg, imperforate anus with perineal fistula, low or unsuspected meningomyelocele, or ultrashort-segment Hirschsprung disease).
In many patients, stool can be palpated throughout the distribution of the colon, most notably in the left lower quadrant. On rectal examination, stool is often found smeared around the anus. The anal sphincter may appear somewhat lax and patulous because chronic rectal distention is associated with reflex relaxation of the internal sphincter. The rectum is typically enlarged and filled with soft stool that yields negative results on fecal occult blood testing.
Neurologic findings should be normal. Patients should have a normal anal wink and normal sensation, strength, and reflexes in the lower extremities.
In most patients, the diagnosis of encopresis is established in the basis of the history and complete physical examination, including a rectal examination.
Laboratory studies are rarely warranted, though radiography, manometry, and biopsy may be helpful.
Plain abdominal radiography may be helpful in determining whether a soft fecal impaction is present. This study can be very useful for documenting the nature of the problem and helping explain it to an older child and his or her parents, particularly when a history of constipation is not evident or is denied.
Anorectal manometry is sometimes helpful in delineating the child’s defecation dynamics.[15] Many children with encopresis have evidence of megarectum, as evidenced by diminished sensation to distention of the rectum during balloon insufflation. Many children who have encopresis also have paradoxical constriction of the external anal sphincter (EAS) during attempted defecation.
Anorectal manometry can also be helpful in excluding ultrashort-segment Hirschsprung disease, which is a rare cause of encopresis. With this disorder, intramural ganglion cells in the submucosa and myenteric plexuses of the distal colon are absent. In the absence of these ganglion cells, the internal anal sphincter does not relax in response to rectal distention by balloon inflation.
Although Hirschsprung disease is rarely associated with encopresis, this diagnosis, if suspected, can be excluded by identifying ganglion cells in the submucosa and myenteric plexuses of the rectum.
A biopsy specimen can be obtained either by surgical means or through the use of a suction device.
Despite the frequency with which childhood encopresis occurs, no large, randomized, controlled therapeutic trials have been conducted.[16] As a result, treatment remains largely experiential rather than evidence based. Conventional medical therapy is commonly the first therapy attempted, generally consisting of the following:
The aim of this multimodal approach to therapy is to decrease the physical and emotional distress associated with defecation, to develop or restore normal bowel habits with positive reinforcement, and to encourage the child and parents to take an active role during the treatment.[19]
Conventional medical therapy proves successful in approximately one half of children with chronic constipation, encopresis, or both. If a child has not experienced significant clinical improvement after 2-4 months of therapy, a different therapy program may be indicated. Accordingly, it is appropriate to assess progress after 2-4 months of treatment. If the child remains symptomatic, consider enrolling him or her in an intensive behavior program that supplements conventional medical therapy.[20]
Although no surgical intervention has a proven role in the management of childhood encopresis, performing an appendicostomy or cecostomy to perform antegrade enemas in children who have proven refractory to medical therapy may improve their quality of life.[21] In most cases of encopresis, consultation with a subspecialist is not absolutely necessary. Affected children are often referred to a pediatric gastroenterologist, a behavioral psychologist, or both.
Although controversy remains and conflicting data have been reported, many authors advocate behavioral strategies, with or without long-term laxative therapy, to encourage bowel movements in patients with chronic encopresis. The addition of an intensive behavioral program to conventional medical therapy can be of substantial therapeutic benefit for most children with chronic encopresis (see Long-Term Monitoring).
Because more than 50% of children with chronic encopresis have paradoxical external anal sphincter (EAS) constriction (anismus) during attempted defecation, biofeedback training focusing on teaching the child how to relax the EAS during active straining and thus eliminate anismus has been used in this population since the mid-1980s. Although biofeedback may help selected children, there is no evidence that it adds any benefit to conventional treatment in the management of childhood encopresis.[20]
Because most children with encopresis have retentive encopresis as a consequence of chronic constipation with resulting overflow incontinence, medical therapy is initially focused on disimpaction of the distal colon,[22] which is followed by prolonged use of laxatives to ensure that the child passes soft stools frequently without any associated pain.
Disimpaction can be accomplished with aggressive use of oral cathartics (eg, polyethylene glycol [PEG], sodium phosphate, or magnesium citrate) or a series of enemas. In clinical trials, disimpaction is reported to be equally effective whether done via the oral route or via the rectal route.[23, 24]
Most enema preparations contain osmotically active agents that are not substantially absorbed in the colon (see Medication). To the author’s knowledge, no studies have yet been performed to compare the effectiveness of these preparations. In all likelihood, the effectiveness of any particular preparation depends more on the volume of the enema than on the composition of the enema solution.
After the colon is disimpacted, long-term laxative therapy is generally started. Virtually any laxative can be used, provide that it is administered in sufficient quantity to produce 1-2 soft stools daily.
No evidence suggests that dietary interventions are beneficial in the management of encopresis. Although many people advocate high-fiber diets, the authors know of no studies conducted to systematically evaluate the effectiveness of dietary therapy in childhood encopresis.
In addition to the long-term laxative therapy outlined above, various modalities have been proposed for the treatment of chronic encopresis.
As noted (see Behavioral Therapy and Biofeedback), EAS biofeedback focuses on teaching the child to reverse paradoxical constriction by learning how to relax the EAS during straining.[25] Most studies examining the use of biofeedback in childhood encopresis included biofeedback as a supplement to medical-behavioral treatment.[25]
Both manometric and electromyographic (EMG) biofeedback have been used to treat encopresis, but manometric biofeedback is more invasive than EMG biofeedback. Data from a meta-analysis suggested no significant differences in outcomes between intra-anal pressure biofeedback and surface EMG biofeedback of the perianal skin.[20]
Adding biofeedback therapy to conventional medical therapy appears not to offer substantial therapeutic benefit to most children with chronic constipation, encopresis, or both.[20, 26] Although biofeedback can be used to train children to tighten and relax their perineal muscles (thereby, in theory, increasing the efficiency of defecation), this achievement is not clearly correlated with successful resolution of chronic constipation or encopresis. In fact, outcomes tend to worsen when children are treated with biofeedback therapy.
Some authors advocate the use of behavioral strategies, with or without long-term laxative therapy, to encourage frequent bowel movements.[27, 25, 28, 20] A Cochrane review concluded that the addition of an intensive behavioral program to conventional medical therapy can be of substantial therapeutic benefit in most children with chronic encopresis.[20] Although the critical components of a successful intensive behavioral program have not been systematically elucidated, common elements of existing programs include the following:
Preliminary evidence suggests that this type of intensive behavioral intervention can be successfully performed by using the Internet.[30, 31]
Because most children with encopresis have retentive encopresis as a consequence of chronic constipation with resulting overflow incontinence, therapy is initially focused on evacuating the distal colon. Disimpaction can be accomplished with aggressive use of oral cathartics or a series of enemas. After the colon is evacuated, long-term laxative therapy is generally started. Virtually any laxative can be used as long as it is used in sufficient quantity to produce 1-2 soft stools daily.
Clinical Context: Polyethylene glycol (PEG) 3350 consists of a long chain of ethylene glycol molecules. The resulting molecule is extremely large, is very poorly absorbed, and functions as an osmotic laxative. The powder is tasteless and odorless to most people and completely dissolves in nearly all liquids, including water. This agent can also be used as a purgative in preparation for colonoscopy. At very large dosages, PEG is occasionally difficult to take, and its use may be associated with nausea, bloating, abdominal cramps, and vomiting.
Clinical Context: Magnesium is a divalent cation that is maximally absorbed in the distal small intestine. At low concentrations, it appears to be absorbed in a saturable carrier-mediated process influenced by vitamin D. At high concentrations, absorption appears to occur largely and inefficiently through diffusion. Increased serum magnesium levels may cause cholecystokinin release, which stimulates gastrointestinal (GI) motility and secretion; this may explain why some children have abdominal cramping.
Magnesium hydroxide formulations are mostly flavorless, with a thick and chalky texture. They are most palatable when mixed with a fluid (eg, milk or chocolate milk).
Clinical Context: Lactulose is a synthetic nonabsorbable disaccharide that is available as a 70% solution. It is generally well tolerated and tastes sweet. Bloating, borborygmi, and flatulence are common side effects as a result of colonic flora fermenting the lactulose.
Clinical Context: Sorbitol is a hyperosmotic laxative that is available as a 70% solution. It has cathartic actions in the GI tract and is largely nonabsorbable. Sorbitol is generally well tolerated and tastes sweet. Bloating, borborygmi, and flatulence are common side effects as a result of colonic flora fermenting the sorbitol.
Clinical Context: Magnesium is a divalent cation that is maximally absorbed in the distal small intestine. At low concentrations, it appears to be absorbed in a saturable carrier-mediated process influenced by vitamin D. At high concentrations, absorption appears to occur largely and inefficiently through diffusion. Increased serum magnesium levels may cause cholecystokinin release, which stimulates gastrointestinal (GI) motility and secretion; this may explain why some children have abdominal cramping.
Magnesium citrate may be chilled to improve palatability.
Osmotic laxatives cause fluid retention in the colon, lowering the pH, resulting in distention, and increasing colonic peristalsis.
Clinical Context: Mineral oil is a nonabsorbable fat that softens stool and decreases water absorption, partly through its metabolism to hydroxy fatty acids in the colon. It is largely tasteless and has an oily consistency. It is most palatable if taken cold or mixed into a fluid (eg, orange juice). In many children given high doses, mineral oil causes seepage of orange oil into underwear, which can produce perianal pruritus.
Lubricants and emollients retard colonic absorption of fecal water and thus soften stool.
Clinical Context: Sennosides are plant alkaloids that stimulate colonic salt and water secretion and promote colonic motility. They often produce abdominal cramping at high doses. Long-term use in animals has not been associated with any evidence of cathartic colon, tachyphylaxis, or secondary hyperaldosteronism.
Clinical Context: Bisacodyl is a colorless and odorless compound that is poorly absorbed. It may be administered either orally or rectally. It increases colonic peristalsis and stimulates salt and water secretion.
Stimulant laxatives act directly on the intestinal mucosa or nerve plexus. They alter water and electrolyte secretion.
Clinical Context: Phosphate is divalent anion absorbed largely in proximal small intestine. Functions as osmotic agent and only small amounts are absorbed when administered as enema.
Most enema preparations contain osmotically active agents that are not substantially absorbed in the colon. In all likelihood, the effectiveness of any particular preparation in the setting of encopresis depends more on the volume of the enema than on the composition of the enema solution.