Appendicitis — MRCS Part B Surgical pathology

A classic presentation of appendicitis, which the station uses to test the pathology of acute inflammation, the theatre preparation and the sterilisation questions that go with any operation.

Assessment and investigation

An ABC assessment, then the history of migrating pain, anorexia, nausea and vomiting, and examination for tenderness and guarding at McBurney's point, Rovsing's sign, the psoas sign of a retrocaecal appendix, and a pelvic appendix felt on rectal examination. Bloods: a raised white count and CRP, urea and electrolytes, a group and save, and a pregnancy test in any woman of childbearing age. Urinalysis to exclude a urinary cause, remembering that a pelvic appendix can inflame the bladder and put white cells in the urine. Imaging when the diagnosis is in doubt: ultrasound in the young and in women, CT in the older patient where a caecal tumour is the alternative. The Alvarado score puts the features together.

Why the pain moves

The appendix is midgut, and its early inflammation, confined to the wall and the visceral peritoneum, is carried by sympathetic afferents with the superior mesenteric artery to T10, so it is felt as a vague colicky ache around the umbilicus. When the inflammation reaches the parietal peritoneum of the right iliac fossa, which is supplied by the somatic nerves of the abdominal wall, the pain becomes sharp, localised and made worse by movement, and the muscles over it guard.

Causes

Obstruction of the lumen by a faecolith, by lymphoid hyperplasia after a viral infection in the young, by a foreign body or worms, by a caecal carcinoma at the base in the elderly, or by a carcinoid tumour of the appendix itself. The trapped mucus distends the lumen, the wall's venous drainage and then its arterial supply are compressed, bacteria invade the ischaemic wall, and gangrene and perforation follow, with peritonitis if the omentum fails to wall it off.

Skin preparation

Both are effective antiseptics for surgical skin preparation, and both are used in an alcoholic solution. Chlorhexidine binds to the skin and goes on working for hours, is not inactivated by blood or serum, and is the agent recommended for most incisions; it is toxic to the cornea and the middle ear, so iodine is used near the eye and the ear. Povidone-iodine works by releasing free iodine, is inactivated by blood and pus, acts for less time, stains, and can affect thyroid function in neonates and cause reactions, but it can be used on mucous membranes. Alcohol in either gives the fast kill.

Sterilisation and disinfection

Sterilisation removes all living organisms, including spores; disinfection reduces the number of pathogens to a safe level but does not kill spores. Sterilisation is by moist heat in an autoclave (steam under pressure at 134 degrees for 3 minutes, the method for surgical instruments), dry heat for glass and metal, ethylene oxide gas or low-temperature hydrogen peroxide plasma for heat-sensitive equipment, and gamma irradiation for single-use items in industry; the Creutzfeldt-Jakob prion survives all of them and instruments used on suspected cases are quarantined or destroyed. Disinfection is with chemicals such as chlorhexidine, alcohol, hypochlorite and glutaraldehyde, or by boiling or pasteurising.

Acute inflammation

Macroscopically the four signs of Celsus: redness, heat, swelling and pain, with loss of function added by Virchow. The vessels dilate, their walls leak protein-rich exudate, and neutrophils marginate, stick and migrate out into the tissue. Drawing a blunt instrument across the skin shows the vascular response in sequence, Lewis's triple response: a red line as the capillaries dilate, a flare around it as the arterioles dilate by an axon reflex, and a wheal as fluid leaks out of the vessels. Histamine from mast cells is the first mediator, causing the arteriolar dilatation and the increase in venular permeability of the first hour.

The acute response localises and dilutes the injury, brings in antibody, complement and neutrophils, and carries the antigen to the lymph nodes. Its outcomes are resolution, when the cause is removed and the tissue returns to normal; suppuration, when pus forms; organisation into fibrous tissue and scarring; and chronic inflammation, when the cause persists. Pus is a fluid of dead and dying neutrophils, bacteria, tissue debris and exudate; enclosed in an abscess it has no blood supply, so antibiotics cannot reach it and it will not resolve until it is drained.

Adhesions

Peritoneum damaged by surgery, ischaemia or infection loses its mesothelium and bleeds fibrin into the cavity; normally the fibrin is dissolved by plasmin within days, but where the fibrinolytic activity of the injured peritoneum is reduced, the fibrin persists and fibroblasts grow into it, producing bands of fibrous tissue between loops of bowel and the abdominal wall. They are the commonest cause of small bowel obstruction in the developed world.

Acute and chronic inflammation

Acute inflammation is short, exudative and neutrophil-led, with a vascular response as its centre; chronic inflammation lasts weeks to years, is led by lymphocytes, plasma cells and macrophages, proceeds with fibrosis and new vessels at the same time as tissue destruction, and may form granulomas, the organised collections of epithelioid macrophages seen in tuberculosis, Crohn's disease and around foreign bodies.