Internal rectal intussusception is an early stage of rectal prolapse, where the proximal rectum has prolapsed into the ampulla but has not progressed through the anal canal. Symptoms include constipation and an incomplete sense of evacuation. Less commonly reported are incontinence, pain, and soiling. Endoscopy may reveal a solitary rectal ulcer on the anterior rectal wall 8 to 10 cm above the anal verge. Defecography is the diagnostic test of choice and shows the rectum intussuscepting several centimeters above the level of the levators. Classically, a funnel-shaped pattern is seen reflecting circular prolapse of the rectal wall. Rectal intussusception previously had been thought to be a common cause of obstructed defecation. However, because operative repair of rectal intussusception has met with little success, current thought suggests that intussusception may be the result of, and not the cause of, obstructed defecation.
Full-thickness rectal prolapse is the protrusion of the full thickness of the wall of the rectum through the anal canal (Fig. 3.4). Symptoms correlate with the degree of prolapse through the anal canal. With complete prolapse through the anal canal, the extruded rectum becomes excoriated, resulting in ulceration, bleeding, and mucous discharge. In this latter stage, fecal incontinence is the rule. A history of constipation is a common finding. Physical examination discloses a protruding mass of reddened friable tissue. Digital rectal examination may easily reduce the prolapse, and a widely patent, poorly contractile, anal canal is noted. Concentric folds of colonic mucosa are observed in contrast to the radial folds seen in patients with prolapsed internal hemorrhoids. Uterine prolapse or cystocele may be identified concomitantly.
Patients with slow-transit constipation are almost always women, usually presenting in their second or third decade. They have two or fewer bowel movements per week. Malaise, bloating, nausea, and abdominal cramping are frequent complaints. Symptoms are typically unresponsive to bulk laxatives and stool softeners. There is often a strong association with gynecologic complaints such as irregular menstrual cycles, ovarian cysts, and galactorrhea. Many patients have delayed gastric emptying, biliary dyskinesia, and delays in small bowel transit, suggesting the presence of a panenteric motility disorder.18-20 A diagnosis of colonic inertia is made only after excluding systemic neurologic processes such as diabetes mellitus or multiple sclerosis, or a pelvic floor abnormality as a cause.
Investigation typically reveals a normal-caliber but often very redundant colon on barium enema (Fig. 3.5). Defecography and manometry are essential to exclude pelvic floor dysfunction as an etiology of constipation. Colonic transit studies show markedly delayed transit of ingested radiopaque markers. Interestingly, there are two categories of transit studies. The first displays pancolonic inertia, as markers have delayed transit beginning in the cecum and
continuing throughout the remainder of the colon. The second shows passage of markers without delay through the ascending and transverse colon and a slowing of transit through the left colon and rectosigmoid.
Studies in animal models suggest that colonic transit can be accelerated by serotonin, serotonin analogues, or both. Zhao et al21 evaluated the distribution, density, and staining intensity of ente-rochromaffin and serotonin cells in the colonic mucosa of patients with colonic inertia compared to controls. The number of enterochro-maffin cells and serotonin-producing cells was increased in the group with colonic inertia, with a greater number found in the left colon. Compared with controls, these cells contained fewer hormones as measured by the intensity of staining but were present in greater numbers. It is unknown whether an increased level of serotonin is the cause of motility impairment or a consequence.
The mechanism by which serotonin exerts an effect on colonic motility is not completely understood. Work by Haga et al22 indicates that serotonin, both endogenously produced and exogenously applied, stimulated acetylcholine release via 5-hydroxytryptamine (5-HT3) receptors, resulting in increased colonic transit.
Alterations of hormones at the enteric level also may play a role in the etiology of idiopathic slow-transit constipation. Substance P levels have been found to be decreased in the mucosa and submucosa of patients with slow-transit constipation.23 Altomare et al18 and others have suggested that slow-transit constipation is a manifestation of autonomic nervous system dysfunction, pointing out that such disorders are characterized by abnormalities in diverse systems such as cardiovascular, urinary, sexual, and digestive. A recent review found that more than 70% of patients suffering from slow-transit constipation also showed some degree of auto-nomic dysfunction, such as biliary dyskinesia and delayed small bowel transit. This group has also shown that women with slow-transit constipation exhibit impaired sweat production after acetylcholine application. Impaired extrinsic autonomic control of mechanisms controlling colonic motility via acetylcholine and serotonin-regulated pathways may result in multisystem dysregulation and subsequent clinical symptoms. Pharmacologic treatment of such patients will be a rapidly expanding field in the future.
Slow-Transit Constipation with Megarectum/Megacolon
In contrast to the condition previously described, some patients with constipation present with a markedly dilated colon and rectum. Males and females are affected equally. This condition usually presents in childhood or adolescence. Patients often require chronic laxative use to maintain bowel function. The symptoms of chronic constipation with abdominal pain, bloating, and often fecal incontinence can have a significant adverse affect on lifestyle.24
Radiographic evaluation shows dilatation of the colon and rectum to the pelvic floor. Although any part of the colon may be affected, the process usually begins in the rectum or involves the rectum. A rectal diameter of 6.5 cm at the pelvic rim on lateral view defines megarectum.25 Colonic transit studies are abnormal, with marked delay in the dilated segment of affected bowel.26 Small bowel transit studies are generally
normal. The diagnosis of idiopathic megacolon and megarectum is a diagnosis of exclusion, made only after other causes of constipation such as Hirschsprung's disease have been ruled out (Fig. 3.6). This syndrome can be distinguished from Hirschsprung's disease by the presence of anorectal inhibitory reflex, the absence of a normal caliber or stenotic length of distal bowel, and the presence of ganglion cells on rectal biopsy. Subtle histologic abnormalities have been identified in both smooth muscle and intrinsic innervation. There is thickening of the bowel wall due to smooth muscle hypertrophy and fibrosis of the muscularis mucosa, circular muscle, and longitudinal muscle layers. These findings, however, are not specific to this syndrome.
Several investigators have found decreased vasoactive intestinal peptide levels in the muscu-laris externa in patients with idiopathic mega-colon,27,28 suggesting a loss of inhibitory nerves that normally innervate colonic smooth muscle. Other researchers have noted reduced numbers of argyrophilic neurons and structural abnormalities in these neurons, such as decreased neuronal processes and variable-size nuclei in the ganglia.
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Did you ever think feeling angry and irritable could be a symptom of constipation? A horrible fullness and pressing sharp pains against the bladders can’t help but affect your mood. Sometimes you just want everyone to leave you alone and sleep to escape the pain. It is virtually impossible to be constipated and keep a sunny disposition. Follow the steps in this guide to alleviate constipation and lead a happier healthy life.