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PH-GI27

Peritonitis and foreign material in the peritoneum

How the peritoneum reacts to bacteria, acid, bile, enzymes, blood and foreign material; why infected ascites, a perforated gut and tuberculosis inflame it differently; and how peritonitis spreads to the whole body or is walled off into abscesses and adhesions.

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  • 6 steps · 10 questions
  • 3D anatomy, affected parts marked

By the end, you can

  • Describe the peritoneum’s absorbing surface, nerve supply and defences, including the omentum.
  • Distinguish primary, secondary, chemical and tuberculous peritonitis by route, organisms and fluid.
  • Explain how generalised peritonitis causes fluid loss, ileus, sepsis and organ failure.
  • Explain how inflammation is walled off into abscesses where fluid pools, and how fibrin organises into adhesions.
  • Relate blood, bile, chyle, mucin and foreign bodies in the cavity to the reaction each provokes.
  • Recognise the classic signs, fluid values and tests, and explain how source control, antibiotics, albumin and drainage act on the mechanism.

What it is

Peritonitis is inflammation of the peritoneum. Primary peritonitis is infection without a breach in the gut, mostly spontaneous bacterial peritonitis of ascites; secondary peritonitis, by far the commonest, follows perforation or leakage of a hollow organ or spread from an inflamed one; chemical (sterile) peritonitis is caused by gastric juice, bile, pancreatic enzymes or blood; tuberculous peritonitis is granulomatous. It may be generalised or walled off as an abscess, and heals by resolution or with adhesions. Foreign material in the cavity provokes its own reactions, from mild irritation to granulomas.

4 types to tell apart
Primary (spontaneous bacterial) peritonitis
Infected ascites with no gut perforation, mainly in cirrhosis; usually a single organism.
Secondary peritonitis
From a perforated or leaking hollow organ or an inflamed neighbour; polymicrobial gut flora; needs the source controlled.
Chemical peritonitis
Sterile inflammation from gastric acid, bile, pancreatic enzymes, blood or barium; often becomes infected later.
Tuberculous peritonitis
Granulomatous inflammation with tubercles over the peritoneum, lymphocyte-rich ascites or matted, adherent bowel.

US spelling: tumours → tumors, fibres → fibers.

Normal function

The peritoneum: a large absorbing surface with its own defences

The peritoneum lines the abdominal wall (parietal peritoneum) and covers most of the gut and its organs (visceral peritoneum). Between them is a closed space with only a little lubricating fluid, except in women, where the uterine tubes open into it. Its mesothelial surface is very large, roughly the area of the skin, and it is semipermeable: water and small molecules cross it readily, which is why peritoneal dialysis works, and fluid, bacteria and particles drain through lymphatic openings under the diaphragm (the circulation of peritoneal fluid is taught in the peritoneal tumours lesson). In peritonitis this surface lets fluid pour out and bacterial products pour in.

The parietal peritoneum is supplied by the somatic nerves of the body wall, and under the diaphragm by the phrenic nerves, so its inflammation causes sharp, well-localised pain that is worse on movement, and reflex contraction of the muscles over it. The visceral peritoneum has only autonomic fibres, sensitive to stretch, so pain from it is dull and felt in the midline, as the appendicitis lesson explains.

Macrophages patrol the fluid, and the mesothelium releases cytokines and normally dissolves fibrin. The , a mobile fatty apron rich in immune cells, moves towards an inflamed organ and sticks to it with the help of fibrin: the “abdominal policeman”. Fluid pools in predictable places: the pelvis, the spaces under the diaphragm and beside the , and the paracolic gutters beside the colon. These are the places where abscesses form.

Point to it on the model