Complaints of constipation account for 3% of primary care visits for infants and children and up to 25% of referrals to pediatrie gastroenterologists.1'2 Despite its frequency, a single definition for constipation has not been agreed on. Simplistically, constipation refers to an inability to defecate as frequently or as easily as one would like. Discussion of abnormal stool frequency obligates recognition of "normal" stool frequency; available data suggest that infants have a mean of 4 stools per day during the first week of life and this gradually declines to a mean of 1.7 stools per day at 2 years of age, and 1.2 stools per day at 4 years of age (resembling the adult pattern of stool frequency).3'5 Furthermore, in infants, the range of stool frequency considered normal by physicians is quite variable (and so often contrasts with what is believed to be normal by parents and grandparents). Normal, breast-fed infants may stool as often as 7 times per day or as infrequently as once per week. Older children may stool as infrequently as every 2 to 3 days. Therefore, it is simplest to define constipation as the difficult passage of large or hard stools, irrespective of frequency.
The epidemiology and clinical scenarios commonly associated with constipation vary with age. In young infants and toddlers, the male to female ratio is 1:1. In a study by lssenman et al,6 16% of parents reported constipation in their 22-month-old child. In older, prepubertal children, constipation is more common in boys than in girls (3:1 ratio). This ratio reverses in adolescence with constipation being three times more common in postpubertal females. Anatomic malformations and congenital intestinal disorders are more likely to present in infancy and must be carefully considered at any age. However, nonorganic or functional causes of constipation predominate at all ages.
Constipation is a symptom, not a disease; the etiology of the symptom may represent a definable organic disorder or a behavioral, functional one. All complaints of constipation need to be addressed by the clinician, be it by education of the parent and child or by medical intervention.
COLORECTAL PHYSIOLOGY AND THE PHYSIOLOGY OF DEFECATION
The colon serves as a site of fluid and electrolyte absorption as well as a conduit and storage reservoir for feces. The majority of the 1.5 L of fluid entering an adult colon daily are absorbed in the ascending and transverse colon, yielding a stool fluid volume of approximately 100 mL. Rapid emptying occurs from the cecum and ascending colon, but fecal matter generally is retained several hours in the transverse colon. Serving as a conduit, the descending colon propels feces into the sigmoid colon, where it is stored. Following the ingestion of a meal, and upon awakening, high-amplitude colonie contractions propagate from the proximal to distal sigmoid colon, pushing the stool mass into the rectum (gastrocolic reflex). Using ingested markers, normal colonie transit time from cecum to rectum occurs in 24 to 100 hours in adults7 and within 48 hours in healthy children.8
Normal defecation is controlled by the pelvic complex (Figure), an anatomic funnel consisting of two overlapping muscle sphincters surrounding the anus: an internal sphincter composed of involuntary smooth muscle and an external sphincter composed of voluntary skeletal muscle that maintains continence.9 The internal sphincter is contracted tonically, and the external sphincter is relaxed when the rectum is empty. When stool is propelled into the rectum, stretch receptors in the wall activate nerve cells in the intramural plexus, causing reflexive relaxation of the internal anal sphincter. When the internal sphincter relaxes, stool contacts the sensitive anoderm lining the external anal canal, and the need to defecate or pass flatus is recognized. Fortunately, this sensory system is so sensitive that it readily discriminates among solid, liquid, and gas phases to determine if the passage of the rectal contents is acceptable. Gas is passed when deemed appropriate. Liquids and solids are passed when toilet facilities are conveniently available. To defecate, a squatting position is assumed, which straightens the anal canal. A Valsalva maneuver increases intraabdominal pressure, the external anal sphincter relaxes, and defecation proceeds evacuating the rectum. If deemed inconvenient (or aversive), the external anal sphincter and gluteal muscles can be voluntarily contracted, ejecting the fecal mass out of the rectal ampulla back into the rectal vault. The urge to defecate subsides until the rectum again becomes distended.
ORGANIC CAUSES OF CONSTIPATION
Only a small minority of patients who present with the complaint of constipation have underlying organic disorders. However, anatomic, neurologic, endocrine, and metabolic entities should be considered in the differential diagnosis of constipation in infants and children to assure that appropriate therapy is selected.
Constipation may occur in association with anterior location of the anus.10 Some infants and children with an anteriorly displaced anus have difficulty with defecation. Increased abdominal pressure with straining during attempted defecation thrusts stool into a cul-de-sac posterior to the displaced anus. Stool must be quite soft in order to "turn the corner" and exit through the anus. Most children with an anteriorly displaced anus respond well to laxative therapy affording the passage of soft stools. Surgical intervention usually can and should be avoided; however, occasionally a child may benefit from anoplasty.
Anal stenosis with constipation may be seen following surgical correction of anal atresia or may occur as an isolated finding in an otherwise healthy newborn. The young infant with constipation and a mild degree of anal stenosis will generally improve after simple dilatation by digital rectal examination (which may need to be repeated). If the child requires more than two dilatations, referral to a specialist to confirm the diagnosis and to initiate scheduled sequential dilatations should be considered. Anal stenosis also may occur after various anorectal surgical procedures, requiring intermittent dilatation postoperatively to allow the passage of stools.
Constipation frequently complicates the care of neurologically impaired children and may result from a variety of factors.11 Children with static encephalopathy may have abnormal skeletal muscle tone and poor coordination of pelvic floor musculature, resulting in poor defecatory effort. Others may have slow transit through the colon, resulting in excessively hard stool. Associated feeding disorder may obligate tube feedings; the use of nonfrber- containing formulas may further increase the risk for constipation.
Children with spinal cord injury OT dysraphism may have abnormal coordination or function of the external anal sphincter and levatoi ani muscle. In addition, depending in part on the level of the spinal cord lesion, these children may have abnormal motor and sensory function of the colon and rectum.
Figure. Schematic representation of the anorectum. (Reprinted with permission from Rudolph CD, Benaroch L. Hirschsprung disease. Pediatr Rev. 1995;16:5-11. Copyright ©1995.)
Between 10% and 30% of children with spina bifida maintain fecal continence, but may require an individualized bowel evacuation program to maintain social acceptability.12 This program often includes a high-fiber diet, digital stimulation, or even daily enema regimens. The preservation of some sensorimotor function in the perineal region in a cooperative child may allow for biofeedback training.13 Recent reports of the surgical creation of an appendiceal conduit for anterograde enema administration may benefit neurologically impaired children with severe fecal retention with or without incontinence, who are unresponsive to conventional medical management.14 This aggressive approach may be warranted in patients with myelomeningocele to allow for continence in school and other social settings.
Colonic Neuromuscular Disorders
Hirschsprung's disease (congenital aganglionic megacolon) is a rare disorder that must be considered in the differential diagnosis of any pediatrie patient with severe constipation. Failure to diagnose Hirschsprung's disease in a timely fashion places the patient at risk for toxic megacolon. Hirschsprung's disease is characterized by the absence of intramural ganglion cells of the submucosal and myenteric plexi from the distal rectum to a variable length proximalIy.9 This disorder occurs in 1 in 5000 live births, has a male to female predominance of almost 4 to 1, and has a higher incidence in infants and children with Down's syndrome.15,16
The usual presentation of neonatal Hirschsprung's disease consists of constipation, abdominal distension, vomiting, or diarrhea.17 Failure to pass meconium in the first 24 hours of life is a historical hallmark to suggest Hirschsprung's disease.18 Bloody diarrhea may herald potentially life-threatening enterocolitis. Older children may present with constipation and ribbon-like stools, abdominal distension and bloating, and perhaps with failure to thrive. The urge to defecate may be absent because stool is seldom in contact with the anoderm; retentive posturing is not demonstrated.
Usually, the diagnosis of Hirschsprung's disease can be excluded based on the history and physical examination (Table 1). Rectal examination reveals a paucity of stool in a small diameter vault (in contrast to a dilated rectal vault full of stool characteristic of functional fecal retention). An unprepped barium enema may demonstrate a transition zone at the junction of the dilated, normally innervated proximal colon and the narrowed, aganglionic distal colorectal segment; however, barium enema lacks adequate sensitivity to rule out Hirschsprung's disease, particularly in infants. Suction rectal biopsy reveals the absence of ganglion cells in the mysenteric and submucosal plexi; the proliferation of nerve trunks can be demonstrated by acetylcholinesterase staining, confirming the diagnosis of Hirschsprung's disease.19 Anorectal manometry reveals the failure of internal anal sphincter relaxation on rectal balloon dilatation in patients with Hirschsprung's disease.20 The appropriate confirmatory test, be it manometry or rectal biopsy, would depend on the availability of a skilled manometric laboratory or skilled pathologists in a given clinical setting.
Surgical management consists of resection of the aganglionic colonie segment. Difficulty with persistent constipation or fecal incontinence may be encountered following surgical resection for Hirschsprung's disease; a recent large series reported soiling in 1 2% of their 135 patients status postresection.21
Comparison of Functional Fecal Retention and Hirschsprung's Disease
Intractable constipation can be seen in other forms of intestinal nerve or muscle disease as well.11 Neuronal intestinal dysplasia is characterized by increased or altered ganglion cells on intestinal biopsy. Visceral myopathy, visceral neuropathy, and connective tissue disorders such as scleroderma and amyloidosis also may be associated with severe constipation. These intestinal nerve and muscle disorders may have more diffuse intestinal involvement and yield a clinical scenario more characteristic of pseudo-obstruction, with vomiting and diarrhea as the dominant symptoms.
In a child or adolescent with severe and debilitating constipation unresponsive to medical management, further studies of colorectal physiology may be warranted. Anorectal manometry can identify patients with Hirschsprung's disease or abnormal defecation dynamics (rectosphincteric dyssynergia discussed in a following section). Radiopaque markers may be used to measure intestinal transit time. In healthy children, swallowed markers are excreted within 48 hours.8'22 Given a patient with outlet obstruction, obstruction due to functional fecal retention, short-segment Hirschsprung's disease, or anatomic obstruction, markers remain in the rectum for a prolonged period.23 With colonie inertia, markers are scattered rather uniformly throughout the colon for many days. Colonie inertia has classically been a disorder of young adult females24; a recent report documents delayed colonie transit to greater than 100 hours in a subset of constipated children, half of whom had prolonged transit in all colonie segments suggestive of colonie inertia.25 The reproducibility of these data in other populations has not as yet been tested. Also, it is unclear whether these constipated children with impaired colonie transit represent a distinct clinical syndrome, as many of them improved with standard enema and laxative therapy; transit studies were not repeated following evacuation of rectal fecal masses. Colonie manometry also may be useful in a subset of children with severe constipation to elucidate the underlying alterations of colonie physiology; more experience with this methodology is needed prior to widespread application.26
Metabolic and Medication-Induced Constipation
Constipation may occur in hypothyroidism, Kypercalcemia, hypokalemia, renal acidosts, and diabetes insipidus, disorders in which water depletion or altered smooth muscle function is common. Also, constipation occurs in patients with cystic fibrosis; control may be achieved with oral laxative regimens. Lavage with polyethylene glycol-balanced salt solutions may be required for episodes of distal intestinal obstruction syndrome (meconium ileus equivalent).27
Drugs such as anticonvulsants, psychotherapeutic agents, and narcotic-containing analgesics and cough suppressants can cause constipation, and their contribution should be considered, particularly in children with multiple medical conditions.
NONORGANIC CAUSES OF CONSTIPATION
Three nonorganic clinical syndromes associated with the presenting complaint of constipation in infants and children have been classified.11 These include:
* the grunting, purple-faced baby,
* infant dyschesia, and
* functional fecal retention.
The Grunting Baby
The grunting baby syndrome is common among young infants aged 1 to 10 weeks. The parents of these young infants perceive that stooiing requires great effort for their child and is accompanied by significant discomfort. Distraught parents describe an infant with a red or purple face, straining and crying for 5 to 10 minutes before stool is produced. The stools are soft in consistency, normal in appearance, and occur on an almost daily basis. The infants are readily consoled after stooling has occurred. This classic history is most likely explained by the infant being unable to increase intraabdominal pressure coincident with the relaxation of pelvic floor musculature. The coordination of the two events is necessary to allow the easy passage of stools and is a learned phenomena. This learning process occurs faster in some infants than in others and generally occurs in the first few months of life. Explaining this process to parents and reassuring them that their infant is healthy is the charge of the pediatrie caretaker. Enemas and suppositories should be avoided in these grunting infants, as manipulation of the anus may increase aversion or may cause the infant to await external stimuli to encourage stooling behavior.
Infants and toddlers without organic pathology may experience painful defecation as they pass hard, pelleted stools. The child tends to contract the anal sphincter while straining to stool, which further increases the likelihood of passing hard stool. A cycle of stool withholding may be initiated. The pattern often ensues at a time of dietary alteration such as weaning from breast milk to formula or from formula to cow's milk. Therapy is aimed at softening the stools to ensure painless defecation. This may be accomplished by dietary alteration with the addition of fruits, fruit juices, fiber-containing foods, or Karo syrup in an attempt to add bulk and nonabsorbed sugars. Alternatively, therapy may consist of a commercial fiber supplement such as Maltsupex (Wallace Laboratories, Cranbury, NJ) or the addition of laxative therapy with a nonabsorbed sugar (lactulose), fat (mineral oil), or an osmotic agent (milk of magnesia). The failure to establish the passage of frequent, soft stools may lead to stool aversion and chronic fecal retention. In one report, a history of painful defecation prior to age 36 months could be elicited in 63% of children presenting with constipation and fecal soiling.28
Functional Fecal Retention
Functional fecal retention with voluntary withholding of stool is by far the most common cause of constipation in childhood.29'31 Essentially synonymous with the term encopresis, functional fecal retention consists of a cycle of events initiated by the passage of painful stools or the development of fear of the toilet itself. The majority of children with functional fecal retention have a history of passing large stools associated with pain; occasionally, perianal streptococcal infection may incite painful stooling, or there may be a history of sexual abuse. Magical or imaginative thinking may occur on the part of a toddler, who becomes afraid of sitting on the toilet. Examples include fear of serpents in the toilet or fear of being swallowed by the toilet. For whatever reason, voluntary fecal retention ensues.
The incidence of functional fecal retention peaks at two times - during toilet training and at the beginning of school age. During toilet training, the previously involuntary act of stooling must become a voluntary act associated with social expectations. Attempts to toilet train before the child is cognitiveIy prepared or extremely coercive attitudes toward training can result in a child's decision to "hold back." In toddlers, retentive posturing is commonly displayed: contraction of the gluteal muscles perhaps rising on their toes and rocking back and forth while holding their legs and buttocks stiffly. Parents and grandparents frequently misinterpret this behavior as straining and pushing to have a stool and are perplexed when the child is "unable to stool" while displaying retentive posturing. In the older school-aged child, the innumerable distractions of school, play time, athletic activities, and television can successfully compete with the child's "call to stool," leading to fecal retention. School policies of restricting trips to the restroom to narrow time frames also may prove deleterious. Fecal withholding also may result from a lack of privacy if stalls with open doors are encountered in the school setting.
Fecal retention often leads to further symptoms of irritability, abdominal pain, abdominal distension, anorexia, and fecal soiling. Often, the passage of a large stool, perhaps of a caliber to obstruct the toilet, leads to marked improvement in symptoms until further retention occurs and the cycle repeats. Once a pattern of withholding is established, progressive rectal distension can lead to overflow incontinence, which is of particular concern to the parent and school-aged child. Many children cope with the soiling by denial that it occurs, often hiding underwear and maintaining an indifference to malodorous staining. Parents will become frustrated and perhaps frightened that their child cannot feel and cannot control the urge to defecate. Children may be punished inappropriately for soiling behavior or given antidiarrheal medication, which worsens the sentinel problem of fecal retention. The longer the problem persists, the greater the emotional burden on the child, with the negative impact of soiling on self-image.
Evaluation. Evaluation of the child who presents with constipation and soiling often can be limited to a careful history and physical examination. A history of retentive posturing, infrequent stooling in the toilet, occasional passage of enormous stools, and soiling would strongly suggest functional fecal retention. One should inspect the skin overlying the lumbosacral spine for vascular, pigmented, or hairy patches to suggest spinal dysraphism. A normal neurologic examination, including intact cremasteric reflexes in male children, intact anocutaneous reflex (anal wink), and intact sensory innervation to sacral dermatomes, in a cooperative child is adequate to rule out underlying neurologic impairment.
The confirmation of a fecal mass in a distended rectal vault makes the diagnosis of functional fecal retention of high probability. Often, a rectal fecal mass may be appreciated by bimanual palpation of a mass on either side of the rectus sheath. Digital rectal examination can readily confirm a dilated rectal vault full of stool. The pediatrie caretaker must consider the degree of aversion to rectal inspection that each child may harbor; in the highly aversive child, further association of their perianal region with aversion and "trauma" may be counterproductive and hinder the ability to establish a therapeutic relationship with the child. Given an appropriate history, confirmation of a rectal mass by bimanual palpation of the abdomen (or in the obese or uncooperative child, by abdominal radiograph) is adequate to warrant a trial of therapy without rectal examination in the highly fearful child.
Therapy. The initial therapeutic goal is to educate the child and family to demystify the symptoms and to decompress a frequently tense, counterproductive relationship between parent and child regarding toileting habits. A simplistic description of the normal mechanics of stooling, a discussion of the likely initiating events for stool withholding (pain and fear of stooling), and admission that no "quick fix" is available for this long-standing disorder is generally adequate. The patient should be reassured that many children have been troubled by the same condition and that the success rate for resolution of the problem is high. Parents must recognize that the cycle of fecal withholding and soiling is not volitional, and that soiling generally occurs without the knowledge of the child; punishment is to be avoided. An explanation of the reduction in rectal sensation and the impaired function of the rectum due to chronic distension is warranted.
The family should be informed that it will require from 6 to 12 months for the rectum to regain normal tone, size, and sensitivity to distension. It is useful to warn parents that it is common for setbacks or recurrences to occur during the course of therapy. A therapeutic plan and "contract" with the child and family then should be outlined that allows the child to releam toileting behavior with the empathetic guidance of the pediatrician and parental caretakers.
The therapeutic regimen begins with disimpaction: enemas, mineral oil, polyethylene glycolbalanced electrolyte solutions, and citrate of magnesia can be used to mobilize the fecal mass. Consideration should be given to the degree of anal aversion for each child; although generally quite effective for disimpaction, enemas can be considered punitive in the mind of the child, and some authors suggest avoiding them entirely. Commercially available hypertonic phosphate enemas have been reported to cause hyperphosphatemia in infants and young children. Hyperosmolar milk and molasses enemas (3 oz milk:3 oz molasses) may offer a safe and efficacious means to cleanse the rectum in the child who is not allergic to cow's milk. For the aversive child or for the child who fails enema therapy, large oral doses of mineral oil ( 1 oz/year of age up to 8 oz/dose given twice daily for 3 days) have been used with great success.32 In severe cases, an inpatient admission for nasogastric lavage with large volumes of lavage solutions may be required.33
Following successful disimpaction, the maintenance phase begins with the major aim to alter maladaptive behavior and to prevent reaccumulation of stool. The child is started (or continued) on a laxative regimen; a clear benefit to laxative administration compared with behavior modification alone has been demonstrated in a controlled trial.34 Lactulose, mineral oil, and milk of magnesia are all used commonly and effectively (Table 2). It appears that the actual choice of medication is less important than achieving compliance with the treatment regimen on the part of the parent and child. Compliance is aided by finding a palatable means of administration; toward this goal, mineral oil may be given mixed with juice, root beer, or ice cream. A starting dose is recommended, and then the dose is titrated to achieve one to two soft to loose stools per day.
Of note, although efficacy is similar, mineral oil and milk of magnesia are significantly less expensive than lactulose. Despite theoretical concerns about alteration in fat-soluble vitamin absorption with long-term mineral oil therapy, clinical trials have supported its safety in this regard.35 A greater concern with mineral oil is the potential for aspiration and lipid pneumonitis in the young infant or neurologically impaired child.36 Patients and families should be warned about the potential for leaking mineral oil through the rectum, which produces an otherwise harmless orange stain; this is an indication for decreasing the dosage in a child whose stool frequency is appropriate. If leakage does occur, clothing stains can be removed with commercially available laundering soaps designed to remove grease.
Suggested Starting Doses of Commonly Prescribed Laxatives
Therapy of Functional Fecal Retention
In toilet-aversive toddlers, further attempts at toilet training are delayed until a normal stooling pattern is established. In the school-aged child, successful toileting is reinforced with a systematic behavior modification system. Twice-daily toilet sits, 5 to 15 minutes after each meal, are highly encouraged. Sitting after meals potentially takes advantage of the gastrocolic reflex. The parents and chud should cooperate in record keeping to document the frequency of stooling in the toilet, occasions of soiling, and the compliance with laxatives. A system of positive rewards should be established to reward appropriate toileting behaviors. Increased dietary fiber is recommended, and high-fiber suggestions (whole grain breads and cereals, fruits, vegetables, and legumes) are given to the parents. It has been documented that the fiber intake in constipated children is far below the recommended guidelines. In a study of children given simple instruction on the part of the primary caretaker "to increase their fiber intake," dietary fiber intake remained half that of control children and less than one fourth of the recommended fiber intake.37 Specific suggestions for "kid-friendly" fiber therapy and ongoing dietary counseling should be made a part of follow-up examinations.
After experiencing months of success with pain and accident-free defecation, the laxative dose should be weaned gradually. Parents should be alerted to pay careful attention to the child's stool frequency during holidays, travel, or significant changes in the family routine as this is a common time for relapse of fecal retention. The therapeutic regimen for treatment of functional fecal retention is summarized in Table 3.
Treatment failures for children with encopresis occur in approximately 20% of cases.11 Failure is more likely in children with long-standing functional fecal retention that has had negative impact on self-esteem or children who had secondary gain from encopretic behavior. In children who have experienced significant psychosocial trauma related to soiling, related to family interactions (divorce or other family discourse), or from sexual abuse, or in children with significant behavioral difficulties, psychological evaluation and therapy may prove to be a beneficial adjunct to medical therapy. One investigator administered the Child Behavior Checklist to 55 children presenting with encopresis; 49% of the sample children had behavior problem scores at or above the 90th percentile.38 The child with attention-deficit hyperactivity disorder may present a significant challenge; resistance to encopresis therapy due to an inability to focus and respond promptly to the urge to defecate is commonly encountered. Improvement in toileting behavior may or may not be recognized with initiation of medical therapy for attention-deficit hyperactivity disorder. Other novel therapeutic options from a behavioral model that have been reported to benefit children with refractory encopresis include group behavioral therapy and play therapy with the use of modeling clay.39,40
In a subgroup of patients, biofeedback can be beneficial in the therapy of functional fecal retention.41 Given a cooperative child, normal defecation dynamics can be taught using anorectal manometry and biofeedback. Occasionally, a child will not recognize that the sensation of rectal distension indicates the call to stool. A single teaching session demonstrating what rectal distension "feels like" can result in cognitive recognition of the need to defecate. This methodology also can be of particular benefit to those children with rectosphincteric dyssynergia; these children display paradoxical contraction of the external anal sphincter in response to rectal distension. The goal of biofeedback is to educate the child that the sensation of rectal distension should prompt the urge to defecate, and teach him or her under manometric guidance to relax the external sphincter and allow stooling to occur. In a controlled trial, biofeedback therapy for encopresis is superior to mineral oil only in those children with paradoxical contraction.41
An additional potential intervention for nonresponding children is the use of the prokinetic agent cisapride. Both open-labeled42 and placebocontrolled43 trials have demonstrated benefit for cisapride in children with chronic, intractable constipation. Stool frequency was increased, and gastrointestinal transit time and laxative use were decreased in the small controlled trial. The role for prokinetic therapy in the treatment of functional fecal retention remains to be elucidated; it seems rational that cisapride would be of use in a minority of children with an underlying motility disturbance who are refractory to standard medical therapy.
Finally, not all children with fecal soiling have functional fecal retention. A minority of children present with a history of sporadically passing entire stools in their underpants. A history of prior constipation is absent, and fecal retention is not evident on examination. Generally, other maladaptive behaviors are displayed. Nonretentive functional soiling, or antisocial soiling as it has been termed, is usually a behavioral manifestation of emotional disturbance and requires psychological intervention. Laxative therapy in this setting will likely only worsen soiling behavior.
1. Levine MD. Ckitthen with encopresis: a descriptive analysis. Pediatrics. 1975;56:412-416.
2. Tain LS, Water JKH1 Uiwin OM, Motnar D. Factors associated with outcome in management of defecation disorders. Arch Du Chad. 1986:61:472-477.
3. Lemon AN, Brooke OG. Frequency and weights of normal stools in infancy. Andi Dis OiU. 1979;54:719-722.
4. Colon AK. Jacob LJ. Defecation pattern in American infants and children. CIm Pediatr (Phila). 1977; 16599- 1003.
5. Weaver LT. Steiner H. The bowel habits of young children. Arch Dis Chad. 1984:59:049-652.
6. Issenman RM, Hewson S, Piihonen D, Taylor W. Are chronic digestive complaints the result of abnormal dietary patterns? Am J IXtCMd. 1987 i141 ?79-682.
7. Metealf AM, Hullips SF. Zinsmeister AR. MacCarcy RL, Bean FW, WoW BG. Simplified assessment of segmentai colonie transit time. Gastroenterology. 1987;92:40-47.
8. Bautista Casanovas A, Várela Cives R, VUIanueva J, Castro-Gago M, Cadrant! S, Tojo Siena R. Measurement of colonie Damit time in children. J Pedían Gastroenterol Nwr. 1991;I3:42-45.
9. Rudolph C, Bearoc L. Hinchaprung disease. PBUOB Kw. 1995;16:5-11.
10. Leape LL, Raemnofsky, NL. Anterior ectopicanus: a common cause of constipation In children. J PwtatrSurg. 1978; 13-627-629.
11. DiLorenio C. Constipation. In: Hyman P1 DtLorento C, eds. Pediatrie Gastrointestinal Motility Disorders. New York, NY: Academy Professional Information Services; 1994:129-143.
12. Younoezai MK. Scooling problem in patients wtthmyelomeningoeele. SotuhMal J. 1992;85:718-723.
13. Wald Use of biofeedback of fécal incontinence in patients with meningomyelocele. Paterna. 1981 i68:45 -49.
14. Koyle MA, Kaji DM, duque M Wild J. Galanky SJ. The Malone antergrade continence enema dor neurogenic ans structural fecal incontinece and constipation. J. Urology. 1995;154:759-761.
15. Kleinhauee S, Boley S]. Sheran M, et al Hírachjpnmg*i disease: a Njrvey of the members of the Surgical Sección of the American Academy of Pediatrics. jPedtar Surg- 1979114:588-597.
16. Martin LW. Torre« AM. Htochsprung'i disease. Surg CLin North Am. 1985;5:1171-1180.
17. Klein MD. Corara AG, Wesley JR, Drongowiki RA- Hirachsprungs disease in the newborn. J Pefcw Sarg. 1984; 19 3 70-374.
18. Landman GB. A five-year chart review of children btopsied to rule out Hirtcheprungï disease. Cbi Pefcar (PMa). 1987;2&288-291.
19. Campbell PE, Noblen HR. Experience with rectal Mction biopty in the diagnosis of Hitichflirimg's disease. J PafcarSwrg. 1969:4:410-415.
20. Lanfrancbi GA, Baaocchi O, Federici S. et at Anorectal menometry in the diagnotii of Hinchtpruru's disease - comparison with clinical and radiological criteria. Am J Gostroentserol. 1984:79:270-275.
21. Marty TL. Seo T. Mtlak ME, Sullivan JJ, Black RE, Johnson DG. Gatroentestinal function after surgical correction of Hirchsprug's disease: long-term follow-up in 135 patients. J Pediatr SUTJ. 1995 i30:65 5 -65 S.
22, Arhan P, Devroede O, Hehannin G, et al. Segmentai colonie transit time. Dis quency on Rectum. 1981:42:625-629.
23. Coraaiari Em Cucchìara S, Statano A1 et al. Gastrointestinal transit time, frequency of defecation, and anorectal manometrey in healthy and constipated chil· dren .} Pedina. 1 985; 106:3 79-3 82.
24. Preston DM, Lennard-Jones JE. Severe chronic constipation of young women: 'idiopathic slow transit constipation.' GUI. 1986;27:41-48.
25. Benninga MA. Buller HA, Tytgat NJ, Akkeimans LMA, Bossuyt PM, Taminiau JA]M. Colinic transit time in constipated children: does pédiatrie slow- transit constipation exist!.! Pediotr Gaaroenterol Nun. 1996;23:241-251.
26. Di Loremo C, Reddy SN, Hyman PK. The clinical value of colonie manomeny in children. Gastrontorolog}. 1996-1 10:A798.
27. Cleghom GJ. Forstner GG, Stringer DA, Dutie PR. Treatment of distal intestinal obstruction syndrome in cystic fibrosis with a balanced intestinal electrolyte solution. Lancet I986;i:8-Il.
28. Pattin JC, Haml! SK, Fischel JE. Partin JS. Painful defecation and fecal soiling in childten. Poultries. 1992:89:6.
29. Sondheimer JM. Helping the child with chronic constipation. Contemporary Pediatria. 1985; 12-28.
30. Seth R, Heyman MB. Management of constipacion and encopiesis in infants and children. Gastmenterol COn North Am. 1994:4:621-636.
31. Loening-Baucke V Chronic constipacion in children. Gasrroentenaogy. 1993; 105:1557-1564.
32. Gleghem EE, Rudolph C, Heyman MB. No-enema therapy fot idiopathic constipation and encopresis. CIm Peaatr (Phila). 1991;3ft669-672.
33. Ingebo KB, Heyman MB. Polyethelene glycoelectrolyte solution fat intestinal clearance in childten with refractory encopresis. Am J Dis Child. 1988; 142:340-342.
34. Nolan T, Debelle G. Oberklaid F, Coffey C, Randomised trial of laxatives in treatment of childhood encoptesis. Lancet. 1991:338:523-527.
35. Clark J, Russell O, Fitzgerald J. Serum beta-caiotene, relhol, and alphatocopherol level during mineral oil therapy fot constipation. AmJ Dis Child. 1987:141:12101212.
36. Fan LL, Graham LM. Lipotd pneumonia from mineral oil aspiration. Arch Pcdiarr Adolesc Md. 1994; 148:205-206.
37. McCtung HJ, Boyne L, Heitlinger L Constipation and dietary flux intake in children. Pediatrici. 1995;96(suppl):999-1001.
38. Gabel S. Hegedus AM, WaId A, Chandra R, Chiponis D. Prevalence of behaviot problems and mental health utilization among encopretic children: implications for behavioral pediatrics. ) Dev Behav Pediarr. 1986; 15:639-671.
39. Stark LJ, Owens-Stively J, Spirito A, Lewis A, Guevremonl D. Group behavioral treatment of retentive encopresis. J PetSaa PijchoL 1995i1 5:639-671.
40. Feldman PC, Villanueva S, Lanne V, Devroede G. Use of play with clay to Beat children with intracrable encopresis. J Pedimr. 1993:122:483-488.
41. WaId A. Chandra R, Gabel S, Chiponii D. Evaluation of biofeedbac!; in childhood encopresis. J Pediatr Gostroenterol Nuttr. 1987:6:554-558.
42. Murray RD, Ulysses B, Li K, McClugn J. Heitlinger L, Rehm D. Cisapride for intractable constipation in children: observations from an open trial. J Pediarr Gasrrointerd NUIT. 1990:11:503-508.
43. Saiano A, Cucchiaia S. Andreotti MR, Minella R, Mami G. Effect of cUaprioe on chronic idiopathic constipation in children. Dig Dis Sci. 199 1 ;36: 733-736.
Comparison of Functional Fecal Retention and Hirschsprung's Disease
Suggested Starting Doses of Commonly Prescribed Laxatives
Therapy of Functional Fecal Retention