Treatment Approach to Functional Constipation?

Yehuda Ringel, MD

Disclosures

September 11, 2003

Question

Can slow-transit constipation be caused by outlet obstruction? Is anal sphincterotomy indicated in patients with slow transit for improvement of symptoms?

Response from Yehuda Ringel, MD

The treatment approach to chronic constipation may differ with respect to the presumed etiology and the underlying pathophysiologic mechanisms. Chronic constipation may be secondary to systemic metabolic disorders (eg, hypothyroidism, diabetes mellitus, hypo-/hypercalcemia), neurogenic disorders (eg, autonomic neuropathy, chronic intestinal pseudo-obstruction, Parkinson's disease, spinal cord injury), various medications (eg, anticholinergics, antihypertensives, opiates), or structural abnormalities (eg, mechanical obstruction). However, in the majority of patients, no obvious morphologic or biochemical abnormalities can be identified. Thus, these patients are considered to have functional constipation.[1]

Three main pathophysiologic subgroups of functional constipation have been described: (1) Normal colonic transit refers to patients who complain of infrequent defecation, but have normal colonic transit on objective evaluation. These patients may misperceive their bowel frequency. They usually do not respond to medications (laxatives) and often have psychosocial contributing factors. (2) Slow-transit constipation refers to patients who have delayed transit of radio-opaque markers through their proximal colon (ie, colonic inertia). This disorder is thought to be related to abnormal functioning of the enteric nervous system (ENS). A recent study[2] suggested decreased volume of the interstitial cells of Cajal in these patients. (3) Functional outlet obstruction refers to abnormal defecation associated with delay or unsuccessful passage of stool through the rectum and anal canal. Functional outlet obstruction may occur in patients with normal colonic transit as well as in patients with slow colonic transit. Although a single study[3] in normal subjects has shown that voluntary suppression of defecation can delay colonic transit, there is no evidence that functional outlet obstruction is a cause for slow-transit constipation.

The treatment approach for each of these conditions is different. In patients with normal-transit constipation, reassurance and education may be sufficient. Further treatment may be determined by psychosocial assessment. The clinical approach for slow-transit constipation usually consists of dietary changes, including increased fluid and fiber intake, stool softeners, and various laxatives. Some prokinetic agents may also be considered, including prostaglandin analogs (misoprostol) and serotonin-receptor agonists such as cisapride (under restricted use only) and tegaserod (recently approved for irritable bowel syndrome with constipation).

The treatment for functional outlet obstruction depends on the underlying pathophysiologic mechanism. The differential diagnosis can include pelvic floor dyssynergia (dysfunction of the pelvic floor muscles during defecation), Hirschsprung's disease, fecal impaction, megarectum, and intermittent mechanical obstruction during defecation (eg, rectocele, enterocele, rectal intussusception, rectal/mucosal prolapse). The treatment for pelvic floor dyssynergia is behavioral and involves retraining of the pelvic floor and rectosphincteric muscles with the use of biofeedback. Surgical repair should be considered in cases of rectocele, enterocele, rectal intussusception, and rectal/mucosal prolapse only when they are believed to contribute to the patient's symptoms. Anal sphincterotomy (myomectomy) may be appropriate in some patients with a very short aganglionic segment of Hirschsprung's disease. However, surgical removal of the abnormal bowel is usually necessary in patients with longer aganglionic segments.

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