Appendicitis

Overview

Commonest acute abdominal condition needing surgery. Older children/young adults; rare at extremes of age. More common West/affluent (low-fibre, high-protein diet).

Etiopathogenesis

Commonest mechanism: LUMINAL OBSTRUCTION → ↑intraluminal pressure → compresses vessels → ISCHAEMIA → bacterial proliferation → appendicitis.

A. Obstructive: faecolith, calculi, foreign body, tumour, worms (Enterobius vermicularis), diffuse lymphoid hyperplasia (esp. children) B. Non-obstructive: haematogenous spread of infection, vascular occlusion, low-roughage diet

Morphology

Gross (stage-dependent):

• Early: swollen, hyperaemic serosa
• Acute SUPPURATIVE: fibrinopurulent exudate coating serosa, engorged vessels
• Acute GANGRENOUS (advanced): mucosal necrosis+ulceration through wall, soft/friable, greenish-black gangrene

Micro: KEY diagnostic criterion = NEUTROPHILIC INFILTRATION OF MUSCULARIS (propria). Early: congestion+oedema. Late: mucosal sloughing, wall necrosis, vessel thrombosis, neutrophilic abscesses. ± impacted faecolith/foreign body/concretion in lumen. Gross-micro correlation is good.

Clinical course

Acute abdomen: colicky pain (periumbilical→RIF migration), N/V, mild pyrexia, tenderness, ↑pulse. Most significant lab finding: NEUTROPHILIC LEUCOCYTOSIS with toxic granules.

Predisposes to recurrent attacks → surgery. Interval appendicectomy (after acute attack) shows healing fibrosis + chronic inflammation.

Complications

1. Peritonitis — from perforation (gangrenous appendix), localised or generalised
2. Appendix abscess — from rupture, RIF localised; may spread to subphrenic space, pelvis (bladder-rectum), or in females uterus/tubes
3. Adhesions — late, to omentum/small intestine/other structures
4. Portal pylephlebitis — mesenteric vein spread → septic phlebitis → liver abscess
5. Mucocele — mucus distension of distal appendix post-recovery, usually proximal obstruction, sometimes benign/malignant neoplasm; infected mucocele→empyema

Tumours of appendix (rare)

• Carcinoid (COMMONEST) — argentaffin>argyrophil. Near tip, circumscribed nodule <1cm, rare mets. Resembles other midgut carcinoids
• Adenocarcinoma — uncommon, resembles GI adenocarcinoma elsewhere
• Pseudomyxoma peritonei — gelatinous mucinous ascites, 2° to appendiceal neoplasm (usually benign mucinous cystadenoma, occasionally invasive carcinoma), ±tumour cells (benign/signet-ring). KEY RULE: ovarian mucinous tumour + pseudomyxoma peritonei = presumed APPENDICEAL origin unless proven otherwise

Clinical relevance

Obstruction→pressure→ischaemia→bacteria = single mechanistic chain explaining progression swollen→suppurative→gangrenous if untreated. Neutrophilic muscularis infiltration = THE diagnostic histologic criterion (lead with this over more visually dramatic late-stage necrosis). Periumbilical→RIF pain migration = classic visceral-to-parietal peritoneal irritation transition, tested alongside leucocytosis. Pseudomyxoma peritonei appendix-origin rule = high-yield “check the other organ” fact.

Overview

Acute inflammation of the appendix — acute appendicitis — is the most common acute abdominal condition confronting the surgeon. Seen more commonly in older children and young adults, uncommon at the extremes of age. More frequent in the West and in affluent societies, possibly reflecting diet — a low-bulk/low-cellulose, high-protein diet more often causes appendicitis.

Etiopathogenesis

The most common mechanism is luminal obstruction from various etiologic factors, causing increased intraluminal pressure. This compresses the appendiceal blood vessels, producing ischaemic injury, which in turn favours bacterial proliferation and thus acute appendicitis.

A. Obstructive causes:

1. Faecolith
2. Calculi
3. Foreign body
4. Tumour
5. Worms (especially Enterobius vermicularis)
6. Diffuse lymphoid hyperplasia — especially in children

B. Non-obstructive causes:

1. Haematogenous spread of generalised infection
2. Vascular occlusion
3. Inappropriate diet lacking roughage

Morphology

Gross appearance depends on the stage examined:

• Early acute appendicitis: swollen organ, hyperaemic serosa.
• Acute suppurative appendicitis (well-developed): serosa coated with fibrinopurulent exudate, engorged surface vessels.
• Acute gangrenous appendicitis (advanced): mucosal necrosis and ulceration extending through the wall — the appendix becomes soft and friable, surface coated with greenish-black gangrenous necrosis.

Micro: the most important diagnostic histological criterion is neutrophilic infiltration of the muscularis (propria). Early stage: congestion and oedema of the appendiceal wall alongside acute inflammatory change. Later stages: mucosa sloughs off, the wall becomes necrotic, blood vessels may thrombose, and neutrophilic abscesses may form in the wall. Either stage may show an impacted foreign body, faecolith, or concretion in the lumen. Macroscopic and microscopic findings correlate well.

Clinical Course

Presents as an acute abdomen:

1. Colicky pain — initially periumbilical, later localising to the right iliac fossa
2. Nausea and vomiting
3. Mild-grade pyrexia
4. Abdominal tenderness
5. Increased pulse rate
6. Neutrophilic leucocytosis with toxic granules — the most significant laboratory finding

An attack predisposes to repeated attacks (recurrent acute appendicitis), usually prompting surgery. If appendicectomy is done later, following the acute attack (interval appendicectomy), the specimen shows healing by fibrosis and chronic inflammation of the wall.

Complications

1. Peritonitis — a perforated appendix, as in gangrenous appendicitis, may cause localised or generalised peritonitis.
2. Appendix abscess — from rupture of the appendix, giving a localised right-iliac-fossa abscess; may spread to other sites — between liver and diaphragm (subphrenic abscess), into the pelvis between bladder and rectum, and in females may involve the uterus and fallopian tubes.
3. Adhesions — a late complication: fibrous adhesions to the greater omentum, small intestine, and other abdominal structures.
4. Portal pylephlebitis — spread of infection into mesenteric veins, producing septic phlebitis and liver abscess.
5. Mucocele — distension of the distal appendix by mucus following recovery from an attack, generally from proximal obstruction, but sometimes from a benign or malignant appendiceal neoplasm. An infected mucocele may progress to empyema of the appendix.

Tumours of the Appendix

Rare. Include carcinoid tumour (the most common), pseudomyxoma peritonei, and adenocarcinoma.

Carcinoid tumour — both argentaffin and argyrophil types occur, argentaffin being more common. Gross: mostly near the tip, a circumscribed nodule usually <1 cm, involving the wall; metastases are rare. Histologically resembles other midgut carcinoids.

Adenocarcinoma — uncommon; morphologically similar to adenocarcinoma elsewhere in the alimentary tract.

Pseudomyxoma peritonei — accumulation of gelatinous mucinous ascites, generally secondary to an appendiceal neoplasm; the mucinous collection may be acellular or contain tumour cells (benign or signet-ring). The associated appendiceal tumour is frequently a benign mucinous cystadenoma of the appendix, though occasionally invasive appendiceal carcinoma is found. When assessing an ovarian mucinous tumour associated with pseudomyxoma peritonei, the appendix’s state matters: such an ovarian mucinous tumour with mucinous ascites is presumed to be of appendiceal origin unless proved otherwise.

Clinical Relevance

• The obstruction→raised intraluminal pressure→ischaemia→bacterial proliferation chain is the single mechanistic thread that explains why the disease can progress from swollen-and-hyperaemic to suppurative to frankly gangrenous if untreated — each morphologic stage is just a further step along that one pathway.
• Neutrophilic infiltration of the muscularis is the histologic feature to lead with when asked for “the” diagnostic criterion — it is specifically emphasised as the most important one, ahead of the more visually obvious necrosis/abscess changes seen in later stages.
• The migratory pain pattern (periumbilical → right iliac fossa) is a classic, testable clinical sequence directly explained by the visceral-to-parietal peritoneal irritation transition, though the source material’s emphasis is on recognising it as part of the acute-abdomen presentation alongside leucocytosis.
• The pseudomyxoma peritonei / appendix-vs-ovary origin rule is a genuinely high-yield “always check the other organ” fact: an ovarian mucinous tumour with pseudomyxoma peritonei should be presumed appendiceal in origin unless proven otherwise, reflecting how often the appendix is the true primary site.

• Obstruction → raised intraluminal pressure → ischaemia → bacterial proliferation cascade, with the three gross stages (early/suppurative/gangrenous) branching off
• Complication map radiating from a perforated appendix (peritonitis, abscess with its spread sites, adhesions, pylephlebitis, mucocele)