Peritoneum

What it normally does

• The inner layer wrapping the organs (visceral peritoneum) is supplied by autonomic afferents that travel back with the sympathetics to the spinal cord. It cannot sense cutting or burning — its adequate stimuli are stretch, distension, traction, ischaemia and chemical or inflammatory irritation — and the brain can only localise it to the midline at the level of the embryonic gut segment: foregut to the epigastrium, midgut to the umbilicus, hindgut to the suprapubic region.

  This is why early appendicitis hurts around the navel and why bowel obstruction is felt as central colic, nowhere near the actual diseased organ.

• The outer layer lining the abdominal wall (parietal peritoneum) is supplied by the same segmental somatic nerves as the overlying skin and muscle — T7 to L1 for the wall, and the phrenic nerve (C3, C4, C5) for the central diaphragm. Somatic means sharp, precisely localised, and wired to a reflex arc back to the muscle of that same segment.

  This is why pain becomes point-tender once inflammation reaches the wall, why the muscle contracts on its own (guarding and rigidity), and why blood or pus under the diaphragm is felt at the shoulder tip.

• The cavity between the two layers is only a potential space holding a small volume of lubricating fluid — usually well under 50 mL — but the membrane itself has a very large surface area, classically quoted as roughly that of the skin (about 1.7 square metres), though direct anatomical measurements give a smaller figure. It exchanges water and solutes in both directions across the capillaries of the tissues it covers, and drains via one-way lymphatic gaps (stomata) in the diaphragm.

  This large exchange surface explains how litres of ascites accumulate, how peritoneal dialysis works, and how infection and fluid loss spread so fast in peritonitis.

• Injured peritoneum repairs by regrowing mesothelium from islands across the whole surface, not from the edges inwards, and it normally dissolves the fibrin laid down during healing using its own plasminogen activator. Where tissue is ischaemic, dried out or handled roughly, that fibrinolysis fails and fibroblasts turn the fibrin into permanent fibrous bands.

  This is why abdominal surgery leaves adhesions, and why those adhesions later strangle or kink bowel.

What goes wrong

• Appendicitis and the migrating pain← from “The inner layer wrapping the organs (visceral …”

  The appendix lumen blocks (faecolith, lymphoid swelling). Mucus keeps being secreted behind the block, so the appendix distends. Stretch fires the visceral afferents, which run back with sympathetics to T10 — a midgut level — so the brain reports dull, poorly located pain around the umbilicus, often with nausea and anorexia. Over hours the wall becomes ischaemic and inflamed, and the inflammation reaches the parietal peritoneum lying against it. That layer is somatic, segmentally mapped, and now the pain is sharp, constant and precisely at McBurney point, with local guarding and rebound.

  Migration of pain from periumbilical to right iliac fossa is visceral peritoneum handing over to parietal peritoneum. A retrocaecal appendix — the commonest position, not a rare variant — may never touch the anterior parietal layer, so the abdomen stays soft and the diagnosis is missed. That is the classic trap.

  You would find: Pain that started around the navel and moved to the right iliac fossa. The patient reports it got worse on the drive in over speed bumps and hurts when they cough — both are the parietal layer being jarred. Percussion tenderness is a kinder test than rebound and means the same thing.

• Perforated viscus and generalised peritonitis← from “The outer layer lining the abdominal wall (par…”

  A hole in the stomach, duodenum or colon spills acid, enzymes and faecal organisms across the whole peritoneal surface. Every somatic nerve from T7 to L1 is irritated at once, and each fires a reflex contraction of the muscle in its own segment, so the whole abdominal wall contracts — board-like rigidity. The inflamed membrane pours protein-rich fluid into the cavity and the gut stops moving (ileus), so litres are lost from the circulation into a space that cannot be seen. Bacteria and endotoxin cross the same huge surface into the blood.

  Rigidity plus free gas is a surgical emergency, not a diagnostic puzzle. The shock is hypovolaemic before it is septic — the fluid has third-spaced into the peritoneal cavity. Resuscitate, give antibiotics, and get the source closed.

  You would find: A patient lying absolutely still (movement stretches the parietal layer), rigid silent abdomen, tachycardia and hypotension. Free gas under the diaphragm on an erect chest x-ray — but this is absent in roughly a quarter to a third of perforations, so a normal film does not exclude one and CT is the next step. If the irritant reaches the underside of the central diaphragm, the pain is felt at the shoulder tip, because the phrenic nerve is C3, C4, C5 and the brain maps that to the shoulder.

• Ascites and spontaneous bacterial peritonitis← from “The cavity between the two layers is only a po…”

  In cirrhosis, sinusoidal portal pressure rises. Hydrostatic pressure in the hepatic sinusoids and splanchnic capillaries now exceeds what the lymphatics can carry away, so hepatic lymph weeps from the liver capsule and splanchnic capillaries filter into the cavity faster than the diaphragmatic lymphatics can clear it; falling hepatic albumin production lowers plasma oncotic pressure and adds to this. Splanchnic vasodilation (largely nitric oxide driven) drops the effective arterial volume, so renin-angiotensin-aldosterone and ADH switch on and the kidney retains sodium and water — which feeds straight back into the ascites. That fluid is low in protein (a total protein below about 15 g/L is the risk marker) and poorly opsonised, so gut organisms that translocate across a leaky bowel wall are not cleared and multiply in it.

  Every new or worsening ascites gets a diagnostic tap, and so does any decompensation in a patient who already has ascites. In Australia the common causes are alcohol-related liver disease, chronic hepatitis B and C, and increasingly metabolic dysfunction-associated fatty liver disease; chronic liver disease and its complications fall disproportionately on Aboriginal and Torres Strait Islander communities, driven by higher chronic hepatitis B prevalence and poorer access to antiviral treatment.

  You would find: Distension with shifting dullness and a fluid thrill. Tap it: a serum-ascites albumin gradient of 11 g/L or more means portal hypertension. Ascitic neutrophils of 250 x 10^6/L or more is spontaneous bacterial peritonitis — and it often presents with nothing more than a low-grade fever or new confusion, with no rigidity at all, because the parietal peritoneum is barely involved.

• Adhesions and small bowel obstruction← from “Injured peritoneum repairs by regrowing mesoth…”

  Surgery, blood or infection damages the mesothelial surface. Fibrin is laid down. Normally the peritoneum lyses that fibrin and regrows mesothelium in about a week, but where the tissue is ischaemic or handled roughly, fibrinolysis fails and fibroblasts move in instead — the fibrin band becomes a permanent fibrous cord between loops of bowel or bowel and wall. Later, a loop kinks over or twists around that band. Gas and fluid build up proximally, the wall distends, and stretch fires visceral afferents in waves: colic. If the loop's blood supply is caught, the wall becomes ischaemic, then inflamed through to the parietal layer, and the pain turns constant and localised.

  Adhesions cause roughly two-thirds of small bowel obstruction in Australia, and previous surgery is the single most useful thing in the history. Colic that becomes constant, with fever, tachycardia and localised tenderness, means strangulation — that is the shift from visceral to parietal pain again, and it is the signal to operate.

  You would find: A laparotomy scar. Colicky central pain, vomiting, distension, no flatus. Bowel sounds are high-pitched and tinkling early, then absent. Abdominal x-ray shows dilated central loops with valvulae conniventes crossing the full width.

What we give, and how it works

Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.