On the basis of experimental evidence, acute appendicitis seems to be the end result of a primary obstruction of the appendix lumen. Once this obstruction occurs the appendix subsequently becomes filled with mucus and swells, increasing pressures within the lumen and the walls of the appendix, resulting in thrombosis and occlusion of the small vessels, and stasis of lymphatic flow. Rarely, spontaneous recovery can occur at this point. As the former progresses, the appendix becomes ischemic and then necrotic. As bacteria begin to leak out through the dying walls, pus forms within and around the appendix (suppuration). The end result of this cascade is appendiceal rupture causing peritonitis, which may lead to septicemia and eventually death.
Among the causative agents, such as foreign bodies, trauma, intestinal worms and lymphadenitis, the occurrence of an obstructing fecalith has attracted attention. The prevalence of fecaliths in patients with appendicitis is significantly higher in developed than in developing countries, and an appendiceal fecalith is commonly associated with complicated appendicitis. Also, fecal stasis and arrest may play a role, as demonstrated by a significantly lower number of bowel movements per week in patients with acute appendicitis compared with healthy controls. The occurrence of a fecalith in the appendix seems to be attributed to a right sided fecal retention reservoir in the colon and a prolonged transit time. From epidemiological data it has been stated that diverticular disease and adenomatous polyps were unknown and colon cancer exceedingly rare in communities exempt for appendicitis. Also, acute appendicitis has been shown to occur antecedent to cancer in the colon and rectum. Several studies offer evidence that a low fiber intake is involved in the pathogenesis of appendicitis. This is in accordance with the occurrence of a right sided fecal reservoir and the fact that dietary fiber reduces transit time..