Constipation is a symptom rather than a disease and therefore represents a patient’s subjective interpretation of a real or imaginary somatic disturbance. Although no single definition is applicable to all patients with constipation, for clinical purposes one may use a frequency of defecation less than three times a week, either alone or in conjunction with difficulty during defecation, especially if this represents a distinct change in regular bowel habits (Fig. 6-1).
Constipation may be regarded conceptually as disordered movement through the colon or anorectum. From a pathophysiologic standpoint, this can occur because of a primary motor disorder, in association with various diseases or as a side effect of many drugs.
The classic example of neurogenic constipation is Hirschsprung disease, which results from a developmental arrest of caudal migration of neural crest cells from the notochord during embryonic development. This is
characterized by colonic dilation proximal to a contracted nonpropulsive segment of distal bowel, which can be seen at barium enema examination (Fig. 6-2). In these patients, the internal anal sphincter does not relax after rectal distention (Fig. 6-3). Because this finding is universal in all forms of Hirschsprung disease, demonstration at anorectal manometry of the rectosphincteric inhibitory reflex excludes the disease from consideration. On occasion, Hirschsprung disease presents itself as involvement of only a short segment of distal colon. In such cases, diagnosis may be delayed into adolescence or adulthood. Barium radiographs may be similar to those of children who have idiopathic constipation with megacolon (Fig. 6-4). Manometry should be performed, and the diagnosis can be confirmed by examination of rectal biopsy specimens to prove the absence of intramural ganglion cells in the distal rectum.
Most patients with constipation have no obvious cause to explain their symptoms but can be categorized into several broad groups on the basis of age at presentation, studies of colonic transit and anorectal sensorimotor function, and in some instances, psychologic profile. Studies of colonic transit are performed by having the patient ingest radiopaque markers and following transit of the markers through the colon with serial abdominal radiographs. Markers are counted in the right, left, and rectosigmoid regions of the colon, as defined by certain anatomic landmarks (Fig. 6-5). In such studies, approximately 30% of adults with infrequent defecation refractory to therapy have normal transit. The other patients have slow transit and may exhibit a pattern of delayed transit through the proximal colon (“colonic inertia”) or have a pattern in which stagnation of markers is confined to the rectosigmoid colon (“outlet obstruction”). The latter is not specific and occurs in a variety of conditions.
One possible cause of outlet obstruction is rectosphincteric dyssynergia, in which ineffective defecation is associated with failure to relax or with inappropriate contraction of the puborectalis and external anal sphincter muscles. This condition can be diagnosed with radiography, electromyography recordings, or anorectal manometry (Fig. 6-6).
The pathogenesis of this disorder is uncertain, but it may represent an acquired, learned dysfunction. Biofeedback techniques have been used to normalize defecation patterns of both children and adults with this abnormality (Fig. 6-7).

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Dr. Muhammad Umer Chawla and Dr. Humaira Mehwish Chawla
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