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PA23.5-7 | Intestinal TB, Appendicitis, IBD & Malabsorption — SDL Guide (Part 2)

Acute Appendicitis — Pathogenesis

A five-panel stepwise diagram shows acute appendicitis progressing from luminal obstruction to pressure build-up, venous congestion, bacterial invasion, transmural necrosis, and perforation. — **Panel A:** Luminal obstruction by faecolith; appendix lumen; mucosa; obstructed distal lumen; inset showing lymphoid hyperplasia in children/adolescents.. **Panel B:** Continued mucous secretion; distended appendiceal lumen; increased intraluminal pressure; outward pressure arrows.. **Panel C:** Compressed submucosal veins; venous congestion; mucosal ischaemia; arterial supply initially maintained.. **Panel D:** Bacterial proliferation and invasion by gut flora; E. coli; Bacteroides; Enterococcus; weakened mucosal barrier.. **Panel E:** Transmural neutrophilic inflammation; suppurative appendicitis; gangrenous necrosis; perforation; inflammatory exudate..

Acute appendicitis is the most common cause of an acute surgical abdomen worldwide. The pathogenetic sequence follows a logical cascade:

Luminal obstruction — by a faecolith (calcified stool, ~35%), lymphoid hyperplasia (commonest in children/adolescents), foreign body, tumour, or inspissated mucus.
Increased intraluminal pressure — continued mucous secretion behind the obstruction distends the lumen.
Venous obstruction and mucosal ischaemia — rising pressure compresses submucosal veins; arterial supply initially maintained.
Bacterial proliferation — mucosal ischaemia allows transmural invasion by gut flora (E. coli, Bacteroides, Enterococcus).
Transmural inflammation — the appendix becomes acutely inflamed → suppurative → gangrenous → perforation.

Note: In children, lymphoid hyperplasia (from viral infections — adenovirus, measles) is the most common precipitant, not a faecolith.

A six-panel timeline diagram shows appendicitis progressing from luminal obstruction by a faecolith to pressure build-up, venous congestion, bacterial invasion, suppurative inflammation, and transmural necrosis with perforation risk. — **Panel A:** Normal appendix, caecum, open appendiceal lumen, mucosa, submucosa, muscularis propria, serosa, normal arterial and venous flow. **Panel B:** Faecolith obstructing appendiceal lumen, trapped mucus, closed distal lumen, proximal obstruction point. **Panel C:** Distended appendix, increased intraluminal pressure, compressed wall, outward pressure arrows, compromised lymphatic drainage. **Panel D:** Venous congestion, dilated serosal veins, oedematous wall, impaired venous outflow, persistent arterial inflow, early ischaemia. **Panel E:** Bacterial invasion, mucosal ulceration, neutrophils in muscularis propria, transmural neutrophilic inflammation, microabscesses, fibrinous serosal exudate. **Panel F:** Gangrenous appendicitis, transmural necrosis, green-black friable wall, focal perforation, faecal flora spillage, peritonitis risk, periappendiceal abscess risk.

Acute Appendicitis — Morphology and Complications

A four-panel medical diagram shows anatomical, gross, microscopic, and complication features of acute appendicitis. — **Panel A:** Caecum, inflamed appendix, serosal inflammation, parietal peritoneum, right iliac fossa, McBurney's point, rebound tenderness correlate. **Panel B:** Acute early appendicitis, congested appendix, dilated serosal vessels, acute suppurative appendicitis, swollen tense red-purple appendix, fibrinous serosal exudate, gangrenous appendicitis, green-black necrosis, friable wall. **Panel C:** Mucosa, submucosa, muscularis propria, serosa, neutrophils in muscularis propria, transmural neutrophilic infiltration, mucosal ulceration, microabscesses, ischemic necrosis. **Panel D:** Perforated appendix, faecal flora spillage, generalized peritonitis, omental walling off, periappendiceal abscess, portal vein septic emboli, hepatic abscesses, pylephlebitis, subphrenic abscess.

Gross and microscopic stages:

Acute (early) appendicitis:
• Appendix mildly congested; serosal vessels dilated.
• Microscopy: neutrophil infiltration of the muscularis propria — this is the diagnostic criterion (neutrophils in the muscle layer, not just the mucosa).

Suppurative (acute suppurative) appendicitis:
• Appendix grossly swollen, tense, red-purple with fibrinous exudate on serosa.
• Microscopy: transmural neutrophil infiltration, mucosal ulceration, microabscesses.

Gangrenous appendicitis:
• Green-black discolouration, friable wall due to ischaemic necrosis.
• High risk of imminent perforation.

Complications (in order of frequency):
1. Perforation and generalised peritonitis — most feared; spillage of faecal flora.
2. Pericaecal/periappendiceal abscess — if omentum walls off the perforation.
3. Portal pyaemia — septic emboli via portal vein → hepatic abscesses (rare but life-threatening).
4. Pylephlebitis — suppurative thrombophlebitis of the portal vein branches.
5. Subphrenic abscess — if peritonitis tracks superiorly.

CLINICAL PEARL

Rovsing's sign, McBurney's point, rebound tenderness — all well-known clinically. The pathological correlate is peritoneal irritation from serosal inflammation. Once the appendix perforates, pain may paradoxically diminish briefly (pressure release) before intensifying as peritonitis generalises. Never be reassured by sudden pain relief in a child with appendicitis — it may signal perforation, not recovery.

SELF-CHECK

On histology of a surgically removed appendix, which finding is the minimum diagnostic criterion for acute appendicitis?

A. Neutrophils in the submucosal layer only

B. Neutrophil infiltration of the muscularis propria

C. Mucosal ulceration with goblet cell depletion

D. Fibrinous exudate on the serosa alone

Reveal Answer

Answer: B. Neutrophil infiltration of the muscularis propria

The diagnostic criterion for acute appendicitis on histology is neutrophil infiltration of the muscularis propria. Mucosal neutrophils can be found in other conditions (enteritis). Serosal fibrin alone is non-specific. The muscle layer involvement confirms transmural acute inflammation specific to appendicitis.

Inflammatory Bowel Disease — Overview and Crohn Disease

A multi-panel medical diagram shows gross, comparative, cross-sectional, and microscopic features of Crohn disease including skip lesions, cobblestoning, creeping fat, strictures, transmural inflammation, fissures, and granulomas. — **Panel A:** Gross opened terminal ileum and right colon showing skip lesions, normal intervening mucosa, cobblestone appearance, longitudinal fissures, transverse fissures, creeping fat, terminal ileum, right colon. **Panel B:** Normal bowel versus Crohn disease comparison showing normal mucosa, thickened bowel wall, narrowed lumen, fibrotic stricture, linear knife-cut fissure, cobblestone mucosa, string sign on barium inset. **Panel C:** Transverse bowel wall section showing mucosa, submucosa, muscularis propria, serosa, transmural inflammation, fissuring ulcer extending into muscularis, lymphoid aggregates. **Panel D:** Microscopy schematic showing non-caseating granuloma, epithelioid macrophages, multinucleated giant cell, lymphocytes, transmural lymphoid aggregates, preserved goblet cells.

Inflammatory bowel disease (IBD) encompasses two chronic, relapsing immune-mediated disorders: Crohn disease (CD) and ulcerative colitis (UC). Both result from dysregulated mucosal immune responses to luminal antigens (gut microbiota) in genetically susceptible individuals.

Crohn disease — key pathological features:

Distribution: Any segment from mouth to anus; most commonly terminal ileum and right colon (ileocolitis, 40%). Characterised by skip lesions — diseased segments separated by normal 'skip' areas.

Gross morphology:
• Cobblestone appearance — transverse fissures intersecting with longitudinal fissures between oedematous mucosa islands.
• Creeping fat (fat wrapping) — mesenteric fat extending over the serosal surface.
• Strictures — fibrous thickening of the wall → 'string sign' on barium.
• Fistulae — enteroenteric, enterocutaneous, perianal (hallmark of Crohn, very rare in UC).
• Linear 'knife-cut' fissures penetrating deep into the wall.

Microscopy:
• Transmural inflammation — all layers involved.
• Non-caseating granulomas in 50-60% of cases — the histological hallmark (absent in UC).
• Transmural lymphoid aggregates ('Crohn rosary').
• Fissuring ulcers extending into muscularis.
• Relative preservation of goblet cells.

Medical illustration of Crohn disease gross bowel specimen showing cobblestone mucosa, longitudinal fissures, fat wrapping, skip lesions, and a normal bowel comparison inset. — **Panel A:** Opened bowel specimen showing cobblestone mucosa, longitudinal fissure, skip lesion, normal intervening mucosa, and transmural inflammation.. **Panel B:** External diseased bowel surface showing fat wrapping / creeping fat, thickened bowel wall, and narrowed lumen.. **Panel C:** Normal bowel comparison showing smooth mucosa, uniform wall thickness, and continuous mucosal pattern.. **Panel D:** Schematic intestinal map showing affected segments, normal segments, and discontinuous skip lesion pattern..