Janimine

Constipation is usually defined in terms of alterations in the frequency, size, consistency and ease of passage of stool. Large differences in both the frequency and consistency of stools exist at varying ages. A number of studies reveal a decline in stool frequency from more than four stools per day during the first week of life to two stools per day by four months of age and one stool per day at four years of age, with a corresponding increase in stool size.[1-4] Bowel movements occur from three times per day to three times per week in 96 percent of children three to four years of age. By the age of four, an adult pattern of bowel movements is achieved.[5] Stool frequency is occasionally difficult to assess, because some children have several bowel movements each day but apparently evacuate incompletely, as evidenced by the periodic passage of large amounts of stool or the presence of a fecal mass on examination.

Constipation in infants and toddlers can be defined as a stool frequency of less than three per week. However, painful bowel movements and stool retention are symptoms of constipation even when stool frequency is three or more per week. The infrequent passage of stool in a contented breast-fed baby in the early weeks or months of life is normal.

Pathophysiology

Defecation, like the maintenance of continence, involves the coordination of many reflex mechanisms. In a healthy person, the entry of a fecal bolus into the rectum is followed by several automatic, coordinated reflexes. The right side of the colon, including the rectum, contracts as the internal sphincter relaxes. The external sphincter initially contracts but, with a sufficient fecal bolus, the initial contraction is followed by total inhibition of the external and internal anal sphincters, leading to defecation.

Fecal continence refers to the ability to control defecation voluntarily. It requires normal action of the anal sphincters, normal sensory receptors in the rectum and anus to identify the rectal contents as solid, liquid or gaseous matter, and a normal rectal reservoir.

Defecation can be delayed until it is convenient. At that time, intra-abdominal pressure is increased voluntarily by closure of the glottis, descent of the diaphragm and contraction of the abdominal wall muscles (Valsalva maneuver). As a result of this maneuver, the pelvic floor descends and stool is expelled.

Stool retention results when stool expulsion has not occurred. When stool retention remains untreated for a prolonged period, the rectal wall becomes stretched and a megarectum develops. The rectum can become so huge that the stored stool becomes a mass reaching up to the umbilicus. Occasionally, the whole colon is dilated and full of stool (megacolon).

Fecal impaction results when stool expulsion has not occurred for several days. By then the rectum is so distended with stool that the child is no longer able, with voluntary effort alone, to force the fecal mass through the anal canal. Hence, an impaction is probably irreversible without intervention.

Presentation

Difficulties with defecation are common in infants and toddlers. The problem is usually short-lived and of little consequence. In one study,[6] 16 percent of parents of 22-month-old children reported constipation in their toddlers. Chronic constipation, however, often follows an acute constipation problem that was inadequately managed.[7] Risk factors that may play a role in the development of chronic constipation are listed in Table 1.

In young children, attention must be given not only to stool frequency[1-4] and consistency, but also to the occurrence of pain during bowel movements, the degree of straining and the time it takes to complete the bowel movement.

When specifically asked, most parents can describe stool-holding maneuvers in their children, which they may have misinterpreted as extreme efforts to pass stool. They may describe their infant or toddler forcefully contracting the anal muscles, squeezing the buttocks together and assuming a straight posture. Toddlers often rise on their toes, hold their legs stiff, and rock back and forth, perhaps holding on to a piece of furniture. Some toddlers retire to a comer or go to another room to hide while standing stiffly or squatting.

Problems with the parent-child relationship, such as excessive parental anxiety and rigidity, tension, anger, coercion and punishment, may intensify a child's chronic constipation problems.[7-9]

Pain is another aggravating factor. If defecation is painful, the child learns to avoid the pain-producing activity. If the rectum is permissively large, the child will succeed in holding stools for a time interval proportional to the rectal capacity.[8] A vicious cycle is started when the stool is hard, large and passed with pain, leading to further avoidance of defecation. As the cycle is repeated, successively greater amounts of stool build up in the rectum, with longer exposure to its drying action. Passage of this harder and larger stool comes with even greater pain, reinforcing the desire to withhold stool.

Severe screaming can accompany the stool withholding maneuver. These screaming episodes stop when the stool is finally expelled, only to recur when the next "call to stool" is experienced. Screaming episodes in anticipation of or during defecation occur in approximately half of constipated children under two years of age.

Encopresis, in most children, is a complication of longstanding constipation. Encopresis is usually defined as the involuntary seepage of formed, semiformed or liquid fecal material into the child's underwear (or other locations) on a regular basis, after the child has reached the age of four years.[10,11] Encopresis is not limited to children four years of age and older, however; infrequent or constant seepage of feces associated with fecal impaction also occurs in toddlers and even in young infants.

Diagnosis

Constipation is commonly functional. The etiology is believed to be abnormal functioning of normally innervated structures. However, rare organic conditions for constipation must be ruled out. This can usually be accomplished with a history and physical examination, including a rectal examination and, if necessary, anorectal manometry. Constipation is occasionally caused by anatomic, endocrinologic, metabolic or neurologic factors. Anatomic causes include anal fissure, anterior location of the anus, anal stenosis and anal atresia.

Endocrine and metabolic. causes include disorders such as hypothyroidism, renal acidosis, diabetes insipidus and hypercalcemia. Neurogenic causes include disorders of the spinal cord, such as myelomeningocele or tumor, cerebral palsy, hypotonia, neuronal intestinal dysplasia[12] and Hirschsprung's disease.[13-15]

Constipation may also result from use of such drugs as methylphenidate (Ritalin), phenytoin (Dilantin), imipramine (Janimine, Tofranil), phenothiazines, iron-containing preparations, aluminum-containing antacids and codeine-containing cough syrups.

A general physical examination should be performed, with the physician looking for an abnormal growth, dysmorphic features, the stigmata of hypothyroidism or spinal disease, and anorectal abnormalities.

The physical examination often provides further information regarding the presence of constipation. A large abdominal fecal mass can be palpated in 42 percent of constipated patients up to four years of age.[16] The fecal mass is commonly felt suprapubically and midline. Rarely does the mass extend throughout the entire colon. Inspection of the anal canal reveals protruding fecal material in only a few patients. The rectum is filled with stool in most patients. The stool may have a hard consistency or, more commonly, may be clay-like on the outside and hard at the core.

HIRSCHSPRUNG'S DISEASE

Most physicians are aware of the importance of early diagnosis of Hirschsprung's disease, which must always be considered in the differential diagnosis of severe constipation. The incidence of Hirschsprung's disease is approximately one in 5,000 births. The usual presentation of Hirschsprung's disease in the newborn period is constipation, abdominal distention, vomiting or diarrhea.[13] The severity ranges from transient retention of meconium to complete obstruction relieved only by surgery.[14]

Gastrointestinal bleeding and diarrhea are danger signs for enterocolitis of Hirschsprung's disease, an often fatal complication even today. Although Hirschsprung's disease is a congenital abnormality, only 40 percent of patients are diagnosed in the first three months of life, 61 percent by one year of age and 82 percent by four years of age.[15] An infant or toddler with Hirschsprung's disease may present with small-caliber stools, intermittent diarrhea or failure to thrive, in addition to severe constipation and abdominal distention.

On rectal examination of children with Hirschsprung's disease, the rectum is usually found to be empty and small. Barium enema, which should always be performed with a nonprepped bowel, may show a narrow segment of colon above the anus, which is the aganghonic bowel, and a dilated colon above the aganglionic segment, which is the normal ganglionic bowel.

Anorectal manometry can be diagnostic for Hirschsprung's disease, showing an absence of the relaxation reflex of the internal anal sphincter with rectal distention[17,18] (Figure 1). If, on rectal biopsy, ganglion cells are absent, the diagnosis of Hirschsprung's disease is confirmed.

One or several anorectal physiologic abnormalities are present in 97 percent of children with functional constipation who are tested with anorectal manometry.[19] A probe containing intraluminal transducers spaced 5 cm apart (P31-D3, Sandhill Scientific Inc., Littleton, Colo.) and a latex balloon are used for anorectal manometric evaluation of infants and toddlers.17,18,20-22 The responses of the anal canal and rectum to rectal distention are evaluated and recorded on paper, with the base of the distending balloon at 11 cm, one pressure transducer in the rectum at 6 cm, and one in the anal canal 1 cm above the anal verge.

With sudden rectal distention, the internal sphincter relaxes. This reflex, called the rectosphincteric reflex or anorectal inhibitory reflex, is present in both healthy children and in children with chronic constipation due to a variety of causes, including idiopathic constipation, but not in children with Hirschsprung's disease (Figure 1).

Next, the physician determines the minimal amount of air required to produce a rectosphincteric reflex, a sustained complete relaxation of the anal canal (internal and external anal sphincters), an urge to defecate (often expressed by the beginning of withholding maneuvers, fussing or screaming) and rectal contractility, by adding air to the rectal balloon, 10 mL to 60 mL initially, and then 30 mL every 10 to 15 seconds until the urge to defecate is reached.

Mean distention volumes for all parameters are significantly increased in children with idiopathic constipation. These abnormalities are shown in Figure 2.

The anorectal function abnormalities in constipated children with or without encopresis include impaired rectal sensations to balloon distention, decreased spontaneous rectal motility, and decreased or absent rectal contractility induced by rectal distention.[19-22]

Treatment

Exact guidelines cannot be provided for the initiation of laxatives. However, any infant who has less than one stool a day and any young child who has less than one stool every two days--and who is passing firm, large-caliber stools, or cries or strains excessively during stooling--should be considered for laxative treatment. Treatment is especially required if the rectal or abdominal examination reveals a large stool mass. Stool withholding is much more difficult to treat and might be avoided by appropriate therapy in the initial period of constipation.

Treatment of chronic constipation includes education, fecal disimpaction, prevention of future impaction, promotion of regular bowel habits and, finally, toilet training in older children[7,8,10,11,23-30] (Table 2).

Parents should be informed that the child's stooling problem is caused by underlying chronic constipation. Parents must be reassured that constipation is not life-threatening and told that it cannot be treated in a short period of time. After they understand the situation and are given a detailed plan for treatment, parents usually lose their sense of frustration, compliance is improved, and they can adjust and modify their child's treatment in ways that result in regular elimination.[25]

DISIMPACTION

A first disimpaction should always be performed in the physician's office. A hypertonic phosphate enema (Fleet) is used, 2 oz per 5 kg body weight in very young infants and a 4.5 oz, adult-sized enema for children weighing more than 10 kg. In most children, one to two enemas result in a clean bowel.

LAXATIVES

Daily defecation is maintained by daily administration of laxatives, beginning the evening of the day of the office visit. Rectal stimulation by finger or suppository should be avoided as daily treatment. Laxatives are prescribed according to age, body weight and severity of the constipation.

Two problems need to be solved--the mechanical problem of too-large, too-firm stools, and the fear of painful bowel movements. An adequate dose of laxative improves the problem of large, firm stools immediately, but the fear of painful bowel movements resolves only with time.

Suggested dosages of commonly used laxatives are given in Table 3.[25] The actual choice of medication is not as important as a correct dosage and the child's and parents' compliance with the treatment regimen. Osmotic agents such as malt soup extract or corn syrup are beneficial. Recently the use of corn syrup has been discouraged by some infectious disease specialists, because of the risk of botulism.[31]

[TABULAR DATA 3 OMITTED]

The mechanism of action of milk of magnesia derives from the relative nonabsorption of magnesium and the resultant increase in luminal osmolality. In severe constipation with rock-hard stools, the starting dosage of milk of magnesia is approximately 2 mL per kg body weight per day, given with the evening meal. In children who have fecal retention of mostly soft stools, the starting dose is usually 1 mL per kg body weight daily. The laxative does not have a set dosage. A starting dosage is set for each child and adjusted to induce one to two bowel movements per day, loose enough to ensure complete daily emptying of the lower bowel and prevent stool withholding and pain.

Milk of magnesia can be given in liquid or tablet form. The liquid form is sometimes mixed with lemon juice, chocolate syrup or other ingredients to make it more palatable. The concentrated form of milk of magnesia can be given; it is approximately twice as potent as the regular form. Both the amount of milk of magnesia given daily and the consistency and size of each bowel movement should be recorded in a stool diary.

Mineral oil is converted into hydroxy fatty acids, which induce fluid and electrolyte accumulation. Mineral oil should never be force-fed or given to patients with dysphagia or vomiting, because of the risk of aspiration pneumonia. Other disadvantages to mineral oil are leakage and the possibility of developing fat-soluble vitamin deficiency with long-term use.

Lactulose (1,4 beta-galacto-fructose; Cephulac, Chronulac) is an unabsorbable carbohydrate that is hydrolyzed to acids by the colonic flora, resulting in increased water content in the stool through the osmotic effects of lactulose and its metabolites.[28] Drawbacks to this medication are gaseousness, increased flatulence, cramps and a relatively high cost.

Senna (Perdiem, Senokot) affects intestinal motility as well as fluid and electrolyte transport and stimulates defecation. Stool softeners and other laxatives are often ineffective in the initial treatment of megacolon in patients who have disease states that limit the act of defecation, such as hypotonia, cerebral palsy, severe mental retardation and spina bifida, and patients who still suffer from constipation after surgery for anal atresia or Hirschsprung's disease. In these patients, senna, 1 to 2 tsp of syrup or 1/2 to 1 tsp of granules given daily, stimulates defecation.

To be successful, treatment must change stool frequency and/or stool consistency. Treatment failures are the result of laxatives being given either in minimal dosage or for too short a time. The laxative dosage required to treat constipation in the young child is much higher than the suggested dosages on the over-the-counter laxative label. In addition, the warning on the label may lead parents to doubt the safety of its use in young children. Therefore, the first step of the treatment protocol is to educate parents about constipation, the chronicity of the problem, the requirement for long-term treatment and the safety of nonstimulant laxatives.

Dietary corrective measures should be tried initially in patients with simple constipation of short duration. Dietary measures include increasing fluid intake and dietary residue. No evidence suggests that dietary factors alleviate chronic constipation once stool withholding and stool retention have become a problem.

TOILET TRAINING

Toilet training of toddlers during the initial stages of treatment for constipation should be discouraged. In fact, these children should initially be put back in diapers. The first goal is to use laxatives to restore regular bowel patterns. Toilet training can usually be restarted about one month after laxative treatment is begun.

The child should be asked to sit on the toilet with proper foot support for 5 minutes after every meal to take advantage of the gastrocolic reflex. Rewards are given for toilet sitting and, later, for bowel movements into the toilet. Intense psychologic intervention in children under four years of age is rarely necessary, even in the most extreme cases.

FOLLOW-UP

The management of constipation in young children requires considerable patience and effort on the part of both the child and the parents. It is important to provide support and encouragement during the treatment period through frequent office visits and/or telephone consultations, especially until an appropriate laxative dosage has been established.

Parents should be encouraged to call the physician's office. The stool records should be reviewed, progress should be assessed and the abdominal and rectal examinations should be repeated to assure that the constipation is being adequately treated.

If necessary, a dosage adjustment is made, and the child and parents are again encouraged to continue with the treatment regimen. After two to three months, the laxative dosage can be decreased gradually to a level that maintains one daily bowel movement and prevents pain and stool withholding. In about 50 percent of infants and toddlers, discontinuation of the laxative should be possible in three to six months. Some patients, however, continue to need laxatives for years to prevent constipation.

A patient information handout on managing constipation in children is provided on page 411.

REFERENCES

[1.] Nyhan WL. Stool frequency of normal infants in the first week of life. Pediatrics 1952;10:414-25. [2.] Lemoh JN, Brooke OG. Frequency and weight of normal stools in infancy. Arch Dis Child 1979;54: 719-20. [3.] Wolman IJ. Laboratory applications in clinical pediatrics. New York: Blakiston Division, 1957:696-7 [4.] Weaver LT, Steiner H. The bowel habit of young children. Arch Dis Child 1984;59:649-52. [5.] Weaver LT. Bowel habit from birth to old age. J Pediatr Gastroenterol Nutr 1988;7:637-40. [6.] Issenman RM, Hewson S, Pirhonen D, Taylor W, Tirosh A. Are chronic digestive complaints the result of abnormal dietary patterns? Diet and digestive complaints in children at 22 and 40 months of age. Am J Dis Child 1987;141:679-82. [7.] Fitzgerald JF. Constipation in children. Pediatr Rev 1987;8:299-302. [8.] Clayden G. Chronic constipation in childhood. Postgrad Update 1989; June:1243-55. [9.] Pinkerton P. Psychogenic megacolon in children: the implications of bowel negativism. Arch Dis Child 1958;33:371-80. [10.] Levine MD. Encopresis: its potentiation, evaluation, and alleviation. Pediatr Clin North Am 1982;29:315-30. [11.] Fitzgerald JF. Difficulties with defaecation and elimination in children. Clin Gastroenterol 1977;6: 283-97 [12.] Scharli AF, Meier-Ruge W. Localized and disseminated forms of neuronal intestinal dysplasia mimicking Hirschsprung's disease. J Pediatr Surg 1981; 16:164-70. [13.] Ehrenpreis T. Hirschsprung's disease. Am J Dig Dis 1971;16:1032-52. [14.] Klein MD, Coran AG, Wesley JR, Drongowski RA. Hirschsprung's disease in the newborn. J Pediatr Surg 1984;19:370-4. [15.] Kleinhaus S, Boley SJ, Sheran M, Sieber WK. Hirschsprung's disease--a survey of the members of the Surgical Section of the American Academy of Pediatrics. J Pediatr Surg 1979;14:588-97. [16.] Loening-Baucke VA. Constipation in early childhood: patient characteristics, treatment, and longterm follow up. Gut 1993;34:1400-4. [17.] Loening-Baucke VA. Anorectal manometry: experience with strain gauge pressure transducers for the diagnosis of Hirschsprung's disease. J Pediatr Surg 1983;18:595-600. [18.] Loening-Baucke V, Pringle KC, Ekwo EE. Anorectal manometry for the exclusion of Hirschsprung's disease in neonates. J Pediatr Gastroenterol Nutr 1985;4:596-603. [19.] Meunier P, Louis D, Jaubert de Beaujeu M. Physiologic investigation of primary chronic constipation in children: comparison with the barium enema study. Gastroenterology 1984;87:1351-7 [20.] Loening-Baucke V. Factors determining outcome in children with chronic constipation and faecal soiling. Gut 1989;30:999-1006. [21.] Loening-Baucke V. Assessment of the pediatric patient. In: Kumar D, Waldron DJ, Williams NS, eds. Clinical measurement in coloproctology. New York: Springer-Verlag, 1991:201-12. [22.] Loening-Baucke V. Persistence of chronic constipation in children after biofeedback treatment. Dig Dis Sci 1991;36:153-60. [23.] Davidson M, Kugler MM, Bauer CH. Diagnosis and management in children with severe and protracted constipation and obstipation. J Pediatr 1963;62:261-75. [24.] Levine MD, Bakow H. Children with encopresis: a study of treatment outcome. Pediatrics 1976;58:845-52. [25.] Loening-Baucke V. Elimination disorders. In: Greydanus DE, Wolraich ML, eds. Behavioral pediatrics. New York: Springer-Verlag, 1992:280-97 [26.] Lewis AV, Hillemeier AC. Pediatric constipation: diagnosis and treatment. Practical Gastroenterol 1989; September:31-9,67 [27.] Partin JC, Hamill SK, Fischel JE, Partin JS. Painful defecation and fecal soiling in children. Pediatrics 1992;89(6 Pt 1):1007-9. [28.] Younoszai MK, Tolaymat N. Chronic functional constipation in infants and children. In: Lebenthal E, ed. Textbook of gastroenterology and nutrition in infancy. 2d ed. New York: Raven, 1989:1311-26. [29.] Polanco I, Prieto G. Chronic functional constipation. Semin Pediatr Gastroenterol Nutr 1992;3:1-14. [30.] Sondheimer JM. Helping the child with chronic constipation. Contemporary Pediatr 1985; March:12-28. [31.] Spika JS, Shaffer N, Hargrett-Bean N, Collin S, MacDonald KL, Blake PA. Risk factors for infant botulism in the United States. Am J Dis Child 1989;143:828-32 [Published erratum appears in Am J Dis Child 1990;144:60].

The Author

VERA LOENING-BAUCKE, M.D. is professor of pediatrics in the Division of General Pediatrics at the University of Iowa, Iowa City, where she is also director of the Encopresis Clinic. Dr. Loening-Baucke earned her medical degree at the University of Erlangen-Nurnberg, Erlangen, Germany. She completed a residency in pediatrics at Mary Hitchcock Memorial Hospital, Dartmouth Medical School, Hanover, N.H.

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