Etiology
Obstruction of the lumen of the appendix is the main cause of acute appendicitis. Fecalith (a hard mass of fecal matter), normal stool, or lymphoid hyperplasia are the main causes for obstruction. Retrospective appendectomy data suggest fecalith prevalence of 14% to 18% (among patients with a clinical indication/clinical syndrome of appendicitis or emergency appendectomy patients, respectively).[14][15] In emergency appendectomy patients, fecalith prevalence was 39.4% in perforated appendicitis, but only 14.6% in nonperforated appendicitis.[14]
Other postulated mechanisms of appendicitis, based on emerging research, include parasitic infection, schistosomal infection, and neuroimmune etiology.[16][17][18][19] These are ongoing areas of investigation.
Pathophysiology
The lumen distal to the appendiceal obstruction starts to fill with mucus and acts as a closed-loop obstruction. This leads to distension and an increase in intraluminal and intramural pressure. As the condition progresses, the resident bacteria in the appendix rapidly multiply. The most common bacteria in the appendix are Bacteroides fragilis and Escherichia coli.[20]
Distension of the lumen of the appendix causes reflex anorexia, nausea and vomiting, and visceral pain around the umbilicus, based on the embryonic origins of the appendix.
As the pressure of the lumen exceeds the venous pressure, the small venules and capillaries become thrombosed but arterioles remain open, which leads to engorgement and congestion of the appendix. The inflammatory process soon involves the serosa of the appendix, hence the parietal peritoneum in the region, which causes classical right lower quadrant pain at McBurney point.
Once the small arterioles are thrombosed, the area at the antimesenteric border becomes ischemic, and infarction and perforation ensue. Bacteria leak out through the walls and pus forms (suppuration) within and around the appendix. Perforations are usually seen just beyond the obstruction rather than at the tip of the appendix.[21]
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