Inflammation of the appendix probably results from obstruction of the lumen by a faecolith, but other causes of obstruction may be mural lymphoid hyperplasia, congenital bands, adhesions, and kinking of the whole appendix due to previous inflammation.
No particular organism has been consistently found to initiate inflammation. Histologically, a normal mixture of bowel flora is found invading the appendiceal wall.
Initially, there is inflammation of the mucosa which gradually extends through the submucosa to involve the muscular and serosal - peritoneal - layers. The accumulation of mucus causes ischaemia of deeper mural layers by a pressure effect, so allowing bacterial advancement until perforation. Fibrinopurulent exudate extends from the serosa into the adjacent peritoneal surface - the bowel or abdominal wall - causing a localised peritonitis. The appendix becomes distended with pus and there is blockage of its end-arteries. The distal appendix becomes infarcted and gangrenous. The necrotic appendix, if untreated, will perforate and discharge its purulent, faeculent contents into the peritoneal cavity.
If the discharged contents become walled-off, for example by omentum, then a localised abscess will form. If not, a generalised peritonitis will develop.
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