The pathophysiology of appendicitis is the constellation of processes that leads to the

development of acute appendicitis from a normal appendix. The main thrust of events leading to
the development of acute appendicitis lies in the appendix developing a compromised blood
supply due to obstruction of its lumen and becoming very vulnerable to invasion by bacteria
found in the gut normally

Obstruction of the appendix lumen or appendiceal lumen (inside the appendix) by fecalith,
enlarged lymph node, worms, tumor, or indeed foreign objects,

can cause inflammation of the appendix

that brings about a raised intra-luminal pressure, which causes the wall of the appendix to
become distended.

Normal mucus secretions continue within the lumen of the appendix, thus causing further build
up of intra-luminal pressures. This in turn leads to the occlusion of the lymphatic channels, then
the venous return or decreased venous drainage, and finally the arterial supply becomes
undermined.

Reduced blood supply to the wall of the appendix means that the appendix gets little or no
nutrition and oxygen. It also means a little or no supply of white blood cells and other natural
fighters of infection found in the blood being made available to the appendix.

The wall of the appendix will thus start to break up and rot. Normal bacteria found in the gut gets
all the inducement needed to multiply and attack the decaying appendix within 36 hours from the
point of luminal obstruction, worsening the process of appendicitis. This leads to necrosis (the
death of most or all of the cells in an organ or tissue due to disease) and perforation of the
appendix. Pus formation occurs when nearby white blood cells are recruited to fight the bacterial
invasion.

A combination of dead white blood cells, bacteria, and dead tissue makes up pus. The content of
the appendix (fecalith, pus and mucus secretions) are then released into the general abdominal
cavity, bringing causing peritonitis (inflammation of peritoneum).

So, in acute appendicitis, bacterial colonization follows only when the process have commenced.

These events occur so rapidly, that the complete pathophysiology of appendicitis takes about one
to three days. This is why delay can be deadly.

Pain in appendicitis is thus caused, initially by the distention of the wall of the appendix, and
later when the grossly inflamed appendix rubs on the overlying inner wall of the abdomen
(parietal peritoneum) and then with the spillage of the content of the appendix into the general
abdominal cavity (peritonitis).
Fever is brought about by the release of toxic materials (endogenous pyrogens) following the
necrosis of appendicael wall, and later by pus formation. Loss of appetite and nausea follows
slowing and irritation of the bowel by the inflammatory process.