Updated: Oct 30, 2009
Concern about bowel function has been prevalent throughout history across many cultures. A normal bowel pattern is thought to be a sign of good health. Unfortunately, no uniform definition of childhood constipation is recognized. Moreover, health care providers have definitions of constipation that are very different than most parents' definitions.
The North American Society of Gastroenterology and Nutrition defines constipation as "a delay or difficulty in defecation, present for 2 weeks or more, and sufficient to cause significant distress to the patient."1 The Paris Consensus on Childhood Constipation Terminology defines constipation as "a period of 8 weeks with at least 2 of the following symptoms: defecation frequency less than 3 times per week, fecal incontinence frequency greater than once per week, passage of large stools that clog the toilet, palpable abdominal or rectal fecal mass, stool withholding behavior, or painful defecation."2 For practical clinical purposes, constipation is generally defined as infrequent defecation, painful defecation, or both. In most cases, parents are worried that their child's stools are too large, too hard, not frequent enough, and/or painful to pass.
Constipation in children is an extremely common problem with reported prevalence rates between 1-30%.3 Constipation is the principal complaint in 3-5% of all visits to pediatric outpatient clinics and as many as 35% of all visits to pediatric gastroenterologists.4
Most children with constipation have no underlying medical condition. They are often labeled as having functional constipation or acquired megacolon. In most cases, childhood constipation develops when the child begins to associate pain with defecation. Once pain is associated with the passage of bowel movements, the child begins to withhold stools in an attempt to avoid discomfort. As stool withholding continues, the rectum gradually accommodates, and the normal urge to defecate gradually disappears. The infrequent passage of very large and hard stools reinforces the child's association of pain with defecation, resulting in worsening stool retention and progressively more abnormal defecation dynamics with anal sphincter spasm. Chronic rectal distension ultimately results in both loss of rectal sensitivity, and loss of the urge to defecate, which can lead to fecal incontinence (ie, encopresis).
The differential diagnosis of childhood constipation can be extensive and may include Hirschsprung disease (ie, congenital megacolon), spinal or neuromuscular abnormalities, hypothyroidism, anal stenosis, imperforate anus with fistula, anterior displacement of the anus (this is a controversial diagnosis), allergy or sensitivity to cow's milk, and celiac disease. Fortunately, in most cases in which an underlying condition causes constipation, other stigmata of the disorder point to diagnosis. For example, constipation is rarely the only symptom of hypothyroidism.
For practical purposes, in an otherwise healthy child, the differential diagnosis of chronic constipation is Hirschsprung disease and functional constipation (not Hirschsprung disease). Although this differentiation sometimes may be difficult, a number of clues in the history and physical examination are helpful (see Media file 1).
Constipation is extremely common among infants and young children. Issenman et al found that 16% of parents reported that their 2-year-old children had constipation.5 Loening-Baucke reported that the prevalence of constipation was 22.6% among 482 children aged 4-17 years.6 In a longitudinal study of children aged 9-11 years, Saps et al reported an 18% overall prevalence of constipation.7
Yong and Beattie found that 34% of parents in the United Kingdom reported their children aged 4-7 years had at least intermittent difficulties with constipation.8 de Araujo Sant'Anna and Calcado found that 28% of Brazilian children aged 8-10 years were constipated.9
Before puberty, constipation appears to be equally common among girls and boys. After puberty and into young adulthood, females are more likely to develop constipation.
Constipation occurs in all pediatric age groups from infancy to young adulthood. Typically, childhood constipation develops during 3 stages of childhood: in infants during weaning, in toddlers during toilet training, and in school-aged children. In several published reports, approximately half of childhood constipation occurs during the first year of life.
Hirschsprung Disease
Hypercalcemia
Hypokalemia
Hypothyroidism
Imperforate Anus
Neurofibromatosis
Anal stenosis
Anterior displacement of the anus
Celiac disease
Cerebral palsy (static encephalopathy)
Currarino's triad (rectal stenosis, hemi sacrum, presacral mass)
Cow's milk intolerance
Mitochondrial disorders
Neuronal intestinal dysplasia
Prune-belly syndrome
Spinal muscular atrophy
Tethered cord
Although constipation is an extremely common problem among children, few studies have systematically evaluated different management strategies. Childhood constipation is treated in many ways, and virtually any therapeutic regime is likely to be effective as long as it is sufficiently aggressive and persistent.12 Because of the medical profession's understanding of the pathophysiology of the problem, the basic tenets of therapy include evacuation of the colon, elimination of pain with defecation, and establishing regular bowel habits.
In several randomized trials, laxatives have been shown to be beneficial in the treatment of chronic childhood constipation.18,19 Studies have shown that polyethylene glycol,20 mineral oil, magnesium hydroxide, and lactulose are effective and can be used for prolonged periods of time without risk. The key to therapy is to use a sufficient amount of laxative to produce the desired effect. The use of stimulant laxatives may be necessary intermittently in some children; however, routine usage of these agents in young children is not generally recommended. Continuous laxative therapy may be required for several months until the child extinguishes the association between pain and the passage of bowel movements.
These agents produce osmotic effect in colon that results in distention and promotes peristalsis.
Polyethylene glycol (PEG) is a long chain of ethylene glycol molecules. The resulting molecule is extremely large, is very poorly absorbed, and functions as an osmotic laxative. These powders are tasteless and odorless and dissolve completely in nearly all liquids including water. These agents often can also be used as purgatives in preparation for colonoscopy. At very large dosages, PEG is occasionally difficult to take and its usage may be associated with nausea, bloating, abdominal cramps, and vomiting.
Occasional constipation: 17 g mixed in 180 - 240 mL of fluid PO qd prn
Mix 1 packet (17 g) in 240 mL to yield approximately 1 g per 14 mL; may store refrigerated for 48 h
Disimpaction: 1-3 g (14-42 mL)/kg/d PO divided 2-4 doses
Maintenance therapy in children 6 months to 15 years: ~0.5 g (7 mL)/kg/d PO qd or divided bid
Do not administer PO medications within 1 h of initiation of therapy due to potential risk of reduced absorption
Documented hypersensitivity; colitis, ileus, megacolon, bowel perforation, gastric retention, GI obstruction
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Mixing the product in juice or other flavored fluids may make it more palatable; chilled product is more palatable; caution in ulcerative colitis and hot loop polypectomy
Magnesium is a divalent cation maximally absorbed in the distal small intestine. At low concentrations, magnesium appears to absorb by a saturable carrier-mediated process influenced by vitamin D. At higher concentrations, magnesium absorption appears to occur largely by diffusion and is quite inefficient. Increased serum magnesium levels may release cholecystokinin, which stimulates GI motility and secretion; this may explain why some children experience abdominal cramping. Mostly flavorless but has a thick, chalky texture. More palatable when mixed with a fluid (eg, milk, chocolate milk).
30-60 mL/d (as 400 mg/5 mL PO susp) PO qd or divided bid
1-3 mL/kg/d (as 400 mg/5 mL susp) PO qd or divided bid
Decreases absorption of tetracyclines, digoxin, indomethacin, and iron salts
Documented hypersensitivity; colostomy, ileostomy, fecal impaction, intestinal obstruction
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Infants may be more susceptible to magnesium poisoning than older children and adults; overdosage can lead to hypermagnesemia, hypophosphatemia, and secondary hypocalcemia; administer magnesium-containing laxatives cautiously among patients with renal insufficiency because most of a magnesium load is excreted in the urine
Synthetic, nonabsorbable disaccharide available as a 70% solution. Generally very well tolerated and tastes sweet. Contains 10 g lactulose/15 mL of PO solution.
10-30 mL PO qd
1-3 mL/kg/d PO qd or divided bid
Neomycin may eliminate certain colonic bacteria and interfere with the desired degradation of lactulose, thus preventing colonic content acidification
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Exercise caution in patients with diabetes mellitus; at commonly used doses, often produces flatulence and occasional abdominal cramping
This alcohol of glucose is largely nonabsorbable. Available as a 70% solution. As with lactulose, generally well tolerated and tastes quite sweet.
30-150 mL PO qd prn
1-3 mL/kg/d PO qd or divided bid
None reported
Documented hypersensitivity; anuria
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
At commonly used doses, often produces flatulence and occasional abdominal cramping
Magnesium is a divalent cation maximally absorbed in the distal small intestine. At low concentrations, magnesium appears to absorb by a saturable carrier-mediated process influenced by vitamin D. At higher concentrations, magnesium absorption appears to occur largely by diffusion and is quite inefficient. Increased serum magnesium levels may release cholecystokinin, which stimulates GI motility and secretion; this may explain why some children experience abdominal cramping.
150-300 mL/d PO qd
<6 years: 1-3 mL/kg/d PO qd
6-12 years: 100-150 mL/d PO qd
>12 years: Administer as in adults
Decreases absorption and effects of tetracyclines, digoxin, indomethacin, and iron salts
Documented hypersensitivity; colostomy, ileostomy, fecal impaction, intestinal obstruction, diabetes mellitus, renal failure
A - Fetal risk not revealed in controlled studies in humans
Infants may be more susceptible to magnesium poisoning than older children and adults; overdosage can lead to hypermagnesemia, hypophosphatemia, and secondary hypocalcemia; administer magnesium-containing laxatives cautiously among patients with renal insufficiency, as most of a magnesium load is excreted in the urine; exercise caution in patients who are taking digoxin and lithium; product may be chilled to improve palatability
Phosphate is a divalent anion largely absorbed in the proximal small intestine. When administered as an enema, only small amounts are absorbed so the phosphate functions as an osmotic agent. Each 15 mL contains 7.2 g monobasic sodium phosphate monohydrate and 2.7 g dibasic sodium phosphate heptahydrate.
1 tablespoonful mixed with 8 oz water PO qd prn; may increase dose not to exceed 3 tablespoonfuls per day; drink at least 8 oz of extra fluid with each dose
<5 years: Not recommended
5-9 years: Up to 1/2 tablespoon PO qd taken with eight ounces of fluid
10-11 years: Up to 1 tablespoon PO qd taken with eight ounces of fluid
>12 years: Administer as in adults
Sucralfate or antacids that contain aluminum, calcium, or magnesium may bind phosphate in gut and decrease absorption (separate administration by at least 1 h); phosphate may also bind magnesium and reduce its absorption (separate administration by at least 1 h); anion exchange resins (eg, colestipol) may alter phosphate absorption; caution with other drugs that may lower seizure threshold (eg, antipsychotics); caution when coadministered with other drugs that prolong QT interval (eg, antipsychotics, macrolide antibiotics, class IA or class III antiarrhythmic agents); risk of acute phosphate nephropathy may increase with drugs that alter renal perfusion (eg, diuretics, ACE inhibitors, angiotensin II antagonists, NSAIDs)
Do not administer sodium phosphate to patients with renal insufficiency because severe and lethal episodes of hyperphosphatemia may develop with resultant hypocalcemia and tetany; fecal impaction
A - Fetal risk not revealed in controlled studies in humans
Caution in congestive heart failure, and cirrhosis; electrolyte disturbances (eg, hypernatremia, hypokalemia, hyperphosphatemia, hypocalcemia) dehydration, metabolic acidosis, renal failure, tetany, and death have been attributed to prescribing >45 mL as bowel preparation for colonoscopy, surgery, or barium enema and/or prescribing it for people at medical risk
These agents soften stools and decrease water absorption from the GI tract. They may also promote salt and water secretion by the colon.
Nonabsorbable fat that softens stool and decreases water absorption, partly by its metabolism in the colon to hydroxy fatty acids. Largely tasteless. Has an oily consistency. More palatable if cold or mixed into a fluid (eg, orange juice). When taken in high doses, many children experience seepage of orange oil into their underwear, which can produce perianal pruritus.
15-45 mL PO qd prn
<1 year: Not recommended
>1 year: 1-3 mL/kg/d PO qd or divided bid
Theoretically, mineral oil may interfere with absorption of fat-soluble vitamins; however, several long-term studies have not demonstrated any deleterious effects on vitamin levels; decreases effect of docusate sodium and may decrease absorption of warfarin, or PO contraceptives
Documented hypersensitivity; do not administer to people with increased aspiration risk because aspiration of mineral oil can result in lipoid pneumonia
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Do not administer with food or meals since may cause aspiration leading to lipid pneumonitis
These agents increase peristaltic activity in the GI tract. Most of these agents also stimulate salt and water secretion in the colon.
Sennosides are plant alkaloids that stimulate colonic salt and water secretion and promote colonic motility. At higher doses, these agents often produce abdominal cramping. Long-term use in animals has not been associated with any evidence of cathartic colon, tachyphylaxis, or secondary hyperaldosteronism.
10-15 mL PO qhs prn
<2 years: Not recommended
2-5 years: 2.5-5 mL/dose (8.8 mg of sennosides/5 mL) PO qd/bid
>5 years: 5-10 mL/dose (8.8 mg of sennosides/5 mL) PO qd/bid
Decreases effects of anticoagulants
Documented hypersensitivity; bowel obstruction, fecal impaction
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Chronic use of sennosides can be associated with melanosis coli (brown pigment accumulation in the colonic mucosa); this finding does not appear to have any pathological significance and resolves within several months of discontinuing the laxative
Colorless and odorless compound that is very poorly absorbed. Can be administered PO or rectally. Bisacodyl increases colonic peristalsis and stimulates salt and water secretion.
5-15 mg PO as single dose
10 mg PR as single dose
<2 years: Not recommended
>2 years: 0.5-1 of a 10-mg suppository/dose PR or one third of the 5-mg tab/dose PO
Decreases effects of warfarin and antacids
Documented hypersensitivity; intestinal obstruction
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
At higher doses, these agents often produce abdominal cramping
These agents allow incorporation of water and fat into stool, causing stool to soften.
Used to avoid straining during defecation. Allows incorporation of water and fat into stool causing stool to soften.
50-400 mg/d PO qd or divided qid
3-6 years: 20-60 mg/d PO qd or divided qid
6-12 years: 40-150 mg/d PO qd or divided qid
>12 years: Administer as in adults
Decreases effects of warfarin and increases effects of phenolphthalein
Documented hypersensitivity; nausea, vomiting, acute abdominal pain
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Prolonged use of medication may result in electrolyte imbalance
Emollient stool softeners cause stool to soften. Most of these agents also promote salt and water secretion by the colon. Stimulants increase peristaltic activity in the GI tract. Most of these agents also promote salt and water secretion by the colon.
Docusate sodium allows incorporation of water and fat into stool causing stool to soften. Casanthranol is an anthraquinone stimulant hydrolyzed by colonic bacteria into active compound. Usually produce action 8-12 h after administration.
1-4 cap or tab PO hs
Alternatively, 5-60 mL PO hs if syrup or emulsion administered
<6 years: Not recommended
>6 years: 1-2 cap or tab PO hs; alternatively, 5-15 mL PO hs if syrup or emulsion administered
Decreases effects of warfarin and increases effects of phenolphthalein
Documented hypersensitivity; nausea, vomiting, GI bleeding, appendicitis, GI bleeding, congestive heart failure, fecal impaction, appendicitis, nausea, vomiting, acute abdominal pain
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Excessive use may lead to electrolyte imbalance, osteomalacia, steatorrhea, cathartic colon
These agents produce osmotic effect in colon that results in distention and promotes peristalsis.
Phosphate is a divalent anion largely absorbed in the proximal small intestine. When administered as an enema, only small amounts are absorbed so the phosphate functions as an osmotic agent drawing water into intestinal lumen increasing intraluminal and hydrostatic pressure. May also decrease water and electrolyte absorption.
1 adult enema (4.5 fl oz) PR prn
<2 years: Do not use
2-5 years: 1 pediatric enema (2.25 fl.oz) PR once or twice daily prn
>5 years: 1 adult enema (4.5 fl. oz) PR once or twice daily prn
Do not administer aluminum, magnesium antacids, or sucralfate
Documented hypersensitivity; hypernatremia, hyperphosphatemia, renal failure, hypocalcemia, and fecal impaction
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in congestive heart failure, and cirrhosis; electrolyte disturbances (eg, hypernatremia, hypokalemia, hyperphosphatemia, hypocalcemia) dehydration, metabolic acidosis, renal failure, tetany, and death have been attributed to prescribing >45 mL as bowel preparation for colonoscopy, surgery, or barium enema and/or prescribing it for people at medical risk
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constipation, acquired megacolon, functional constipation, functional megacolon, megacolon, stool hoarding, stool retention, stool withholding, Hirschsprung disease, defecation, fecal incontinence, abdominal mass, rectal fecal mass, treatment, diagnosis
Stephen Borowitz, MD, Professor of Pediatrics and Public Health Sciences, Department of Pediatrics, Division of Gastroenterology and Nutrition, University of Virginia
Stephen Borowitz, MD is a member of the following medical societies: American Academy of Pediatrics, American Gastroenterological Association, American Pediatric Society, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research
Disclosure: Nothing to disclose.
Chris A Liacouras, MD, Director of Pediatric Endoscopy, Department of Pediatrics, Division of Gastroenterology and Nutrition, Associate Professor, Children's Hospital of Philadelphia and University of Pennsylvania
Chris A Liacouras, MD is a member of the following medical societies: American Gastroenterological Association
Disclosure: Nothing to disclose.
Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner
Carmen Cuffari, MD, Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine
Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.
Steven M Schwarz, MD, FAAP, FACN, AGAF, Professor of Pediatrics, Children's Hospital at Downstate, SUNY-Downstate Medical Center
Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, American Gastroenterological Association, American Pediatric Society, Gastroenterology Research Group, New York Academy of Medicine, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research
Disclosure: TAP Pharmaceuticals Honoraria Speaking and teaching; Curemark, LLC Consulting fee Board membership; Centocor, Inc. Grant/research funds Independent contractor
Carmen Cuffari, MD, Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine
Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.
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