PATHOPHYSIOLOGY OF APPENDICITIS

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

development of acute appendicitis from a normal appendix.

Understanding the pathophysiology of appendicitis helps to explain all the signs and
symptoms as well as complications seen in appendicitis.

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 by faecolith, enlarged lymph node, worms, tumour, or
indeed foreign objects, 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, 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 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 (faecolith, pus and mucus secretions) are then released into
the general abdominal cavity, bringing causing peritonitis.

So, in acute appendicitis, bacterial colonisation 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 distension 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.

The pathophysiology of appendicitis obviously correlates with the clinical picture.

Acute appendicitis pathophysiology follows the same pattern, even in children and
pregnant women.

In the elderly, the pathophysiology of appendicitis remains unaltered, but the

inflammatory response generated by the elderly is often less than that seen with young fit
individuals, accounting for the often benign presentation froth with a tendency to miss the
diagnosis, thus courting more complications.