German Clinical Trials Register

Acronym/abbreviation of the study

No Entry

URL of the study

No Entry

Brief summary in lay language

This study is based on the hypothesis that obstructed defecation is an obligatory precondition for the pathogenesis of colonic diverticular disease. Morphological, functional, or behavioural causes for obstructed defecation impede sigmoid peristalsis. This causes stasis of faecal contents within the bowel above the obstruction which in turn causes increase of intraluminal pressure by itself and by additional reflectory overmodulation of persitaltic efforts. This causes the herniation of mucosa through the "weak points" of the muscular wall, defined by the locations where the colonic wall is pierced by its vasculature.

Brief summary in scientific language

Since the seminal publication by Graser (1899) (11) it has been known and accepted that colonic diverticula are in fact "false" (Graser) or "pseudo-"diverticula. Colonic diverticula consist mainly of colonic mucosa which is pushed through points of least resistance in the bowel wall. In contrast, "true" diverticula are sacculations which consist of all layers of the wall and may be congenital (such as "Meckel diverticulum") or acquired (e.g. "Zenker diverticulum"). It is also established that colonic "pseudo"-diverticula are "pulsion"-diverticula which implies that they are caused by excess intraluminal pressure pushing them out. They are distinguished from so-called "traction"-diverticula, which are basically caused by extraluminal "traction" caused by fibrosis and scarring in general as sequel to an inflammatory process. The cause for the development of the excess intraluminal pressure to cause colonic "pulsion"-diverticula is still considered unclear. Many theories have been advanced which have either been entirely or in part refuted afterwards or which do not suffice to satisfactorily explain all aspects of this disorder (20,26,27). Unrelated to these considerations various degenerative structural disorders of the rectum are over the last years increasingly recognised and treated. In this context the occult rectal prolapse is in the main focus of medical attention and is increasingly acknowledged as a major morphological cause for obstructed defecation. This has gained increasing acceptance particularly among colorectal and proctological surgeons and is summarized as a pathophysiological concept under the descriptive label "obstructed-defecation-syndrome" or by the acronym "ODS" (1-3,6,8,17,18,21,22,25) The occult ("inner") rectal prolapse is an intussusception of the rectum into itself. The intussusception acts like an obstructing plug which has to be overcome to permit the passage of faecal content. Variants to this disorder include the mucosal prolapse which is the precursor-stage to the "full-thickness" rectal prolapse, but also haemorrhoidal prolapse, as the notorious and often highly symptomatic accompanying phenomenon. In females, prolapse is commonly associated with rectoceles which are typically located anteriorly and are easily detected digitally as structural weakness primarily of the rectovaginal septum. The defecatory disturbances caused by direct obstruction are probably further enhanced by increasing functional deficits. During defaecation the rectum plays an important role as propulsive and sensory organ (12,15,16,19). All of the acquired degenerative changes are detrimental to the structural integrity of the rectal wall. This will most likely entail secondary motoric and sensory functional deficits (4,5,7,10,13,23,28). In addition to rectal prolapse, further morphological changes have meanwhile been identified which potentially contribute to defecation disturbances. These changes include the "descending perineum", the caudally sagging pelvic floor which is in essence an acquired weakness of the pelvic floor muscles and ligaments. The descending perineum evolves from an initially dynamic stage (the pelvic floor descends on straining only) to the advanced stage with the pelvic floor being descended already at rest. The main anatomical landmark to assess descending perineum clinically is the level of the ischiatic tuberosities. The degree of descending perineum is classified by the approximation or transgression of the external anal ring with respect to an imagined line connecting both tuberosities. Descending perineum impedes stool evacuation because the pelvic floor evades all straining efforts. Therefore the evacuatory effect of straining is lost as much as the pelvic floor evades the straining (9). A so-called ""cul-de-sac" proximal to the rectosigmoid junction is another common and morphologically definded cause for obstructed defecation. "Cul-de-sac" describes a frequently noted syphon-like kinking of the sigmoid colon into the pelvis and onto the rectum. The kinking strangulates the rectosigmoid and compresses the rectum externally. Persons with a wide pelvis (and particularly following hysterectomy) are predisposed to acquire this disturbance. Obstructed defecation may be oligo- or asymptomatic for many years. It is well known to clinicians that even advanced cases of post-inflammatory intestinal stenosis such as in cases of stnosing diverticulitis or Crohn's disease may be compensated for long periods of time and cause little or no symptoms. This may not least be due to the fact that visceral sensation reacts only little to gradual and compensated changes (23). However, not infrequently obstructed defecation causes symptoms such as stool irregularities, frequent bowel motions, changes in stool consistency, abdominal bloating etc. which may invite other diagnostic conclusions. Therefore, several acquired morphological conditions contributing to obstructed defecation have been identified. These changes are common, their incidence increases and their severity progresses with advancing age. These changes are, as described above, conceptionally grasped, diagnosed, and treated as a "syndrome". It is further known and accepted that diverticular disease of the colon is an acquired condition which progresses in severity and extent with age. It is also well established for over a century that colonic diverticuli are "false" pulsion diverticuli. They develop due to intraluminal pressure pushing mucosa through the colonic wall. A causal linkage between distal obstruction and proximal rise in intraluminal pressure appears obvious. However, this causality has so far not been investigated.