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PA24.8 | Cholelithiasis & Cholecystitis — SDL Guide (Part 2)

Morphology of Gallstones and Clinical Presentation

A multi-panel hepatobiliary diagram comparing gallstone morphology with clinical effects including biliary colic, choledocholithiasis, and Murphy's sign. — **Panel A:** Liver, gallbladder, Hartmann's pouch, cystic duct, common hepatic duct, common bile duct, duodenum, impacted gallstone, bile flow obstruction. **Panel B:** Cholesterol stones: pale yellow, round or oval, faceted when multiple, radiating crystalline cut surface; black pigment stones: small, jet-black, irregular, crumbly; brown pigment stones: soft, tan-brown, laminated, variable size. **Panel C:** Transient cystic duct obstruction, right hypochondriac or epigastric pain, radiation to right shoulder, referred pain via phrenic nerve, fatty meal trigger. **Panel D:** Common bile duct stone, obstructive jaundice, pale stools, dark urine, blocked bile drainage into duodenum. **Panel E:** Right costal margin, gallbladder fundus, deep palpation during inspiration, inspiratory arrest, positive Murphy's sign in acute cholecystitis.

Gross morphology
• Cholesterol stones: pale yellow, round/oval, solitary or multiple, faceted when multiple; cut surface shows radiating crystalline pattern
• Black pigment stones: small, jet-black, multiple, irregular, crumble easily
• Brown pigment stones: soft, tan-brown, laminated, variable size

Clinicopathological correlations
• Asymptomatic: ~80% of gallstone carriers remain asymptomatic for years ('silent gallstones'); annual risk of symptoms is ~1–2%
• Biliary colic: stone transiently obstructs the cystic duct or Hartmann's pouch → right hypochondriac/epigastric pain, colicky, radiates to right shoulder (referred via phrenic nerve), lasts 30 min to several hours, triggered by fatty meals
• Choledocholithiasis: stone passes into the common bile duct → obstructive jaundice, pale stools, dark urine (cross-reference SDL 1: obstructive jaundice pathway)
• Murphy's sign: inspiratory arrest on deep palpation at the right costal margin (gallbladder fundus) — positive in acute cholecystitis

Acute Cholecystitis — Pathogenesis

Diagram showing gallstone obstruction causing bile stasis, chemical mucosal injury, ischaemia, secondary bacterial infection, and complications of acute cholecystitis, with an acalculous variant entering at the ischaemia step. — **Panel A:** Hepatobiliary anatomy showing liver, gallbladder, Hartmann's pouch, cystic duct, common hepatic duct, common bile duct, duodenum, impacted gallstone, bile accumulation, and gallbladder distension.. **Panel B:** Calculous cholecystitis cascade: stone impaction, bile stasis, chemical mucosal injury by bile salts and lysolecithin, wall distension with mucosal ischaemia, secondary bacterial infection by E. coli, Klebsiella, and Enterococcus, and complications including empyema, gangrene, and perforation.. **Panel C:** Acalculous cholecystitis pathway showing no stone obstruction, biliary stasis, splanchnic hypoperfusion, critically ill risk factors, entry at the ischaemia step, and higher perforation risk due to delayed diagnosis..

Acute calculous cholecystitis (~90% of cases) follows obstruction of the cystic duct or Hartmann's pouch by a gallstone. The sequence:

Stone impaction → bile accumulation behind the obstruction
Chemical irritation: concentrated bile salts and lysolecithin (from lecithin hydrolysis by phospholipase) damage the mucosa
Ischaemia: distension of the gallbladder wall compresses mural vasculature → mucosal ischaemia
Secondary bacterial infection: E. coli, Klebsiella, Enterococcus — superimposed in ~50% of cases via portal bacteraemia or ascending route

Note: The initial injury is chemical, not primarily bacterial; hence even culture-negative acute cholecystitis follows this identical morphological sequence.

Acute acalculous cholecystitis (~10%) occurs in critically ill patients — major surgery, severe trauma, burns, prolonged fasting/TPN, sepsis, AIDS. Pathogenesis: biliary stasis + ischaemia (hypoperfusion of splanchnic bed) without stone obstruction. Carries higher perforation risk because diagnosis is delayed.

Flow diagram showing acute calculous cholecystitis progressing from cystic duct obstruction by gallstone to bile stasis, chemical irritation, mucosal ischaemia, bacterial infection, and complications, with acalculous cholecystitis entering at the ischaemia step. — **Panel A:** Sequential cascade: cystic duct obstruction by stone, bile stasis, chemical irritation by bile salts and lysolecithin, mucosal ischaemia due to distension, secondary bacterial infection, empyema, gangrene, perforation.. **Panel B:** Gallbladder, cystic duct, impacted gallstone, distended lumen, bile stasis, thick oedematous wall, turbid bile.. **Panel C:** Acalculous cholecystitis variant, gallbladder hypomotility, ischaemia entry point, dashed arrow entering the mucosal ischaemia step..

Morphology of Acute and Chronic Cholecystitis

Medical diagram comparing acute and chronic cholecystitis, emphasizing gross acute inflammation and chronic Rokitansky-Aschoff sinuses with fibrosis, lymphocytic infiltrate, metaplasia, and porcelain gallbladder. — **Panel A:** Gross acute cholecystitis: enlarged tense gallbladder, dull serosa, fibrinopurulent exudate, oedematous haemorrhagic congested wall, turbid bile, gallstones, empyema with frank pus, gangrenous green-black necrotic area.. **Panel B:** Microscopic acute cholecystitis: mucosal ulceration, neutrophilic infiltration, oedema, vascular congestion, fibrinopurulent serosal exudate.. **Panel C:** Chronic cholecystitis histology: mucosa, lamina propria, muscularis propria, Rokitansky-Aschoff sinuses penetrating muscularis propria, sinus epithelium, perimuscular tissue, lymphocytic infiltrate, fibrotic wall thickening, intestinal or pyloric metaplasia.. **Panel D:** Porcelain gallbladder: dystrophic calcification of gallbladder wall on chronic cholecystitis background, radiologically detectable calcified wall, association with gallbladder carcinoma..

Acute cholecystitis — gross
• Gallbladder enlarged, tense, dull serosa with fibrinopurulent exudate
• Wall oedematous, haemorrhagic, congested
• Lumen contains turbid bile, pus, or stones
• Empyema: lumen distended with frank pus
• Gangrenous cholecystitis: transmural necrosis → green-black discolouration → perforation risk

Acute cholecystitis — microscopy
• Mucosal ulceration with neutrophilic infiltration
• Oedema and congestion of all layers
• Fibrinopurulent exudate on serosa

Chronic cholecystitis
Results from repeated bouts of acute inflammation or low-grade stone irritation. Key features:

Rokitansky-Aschoff sinuses: invaginations of the gallbladder epithelium through the muscularis propria into the perimuscular tissues — result of increased intraluminal pressure over time; characteristic on histology
Fibrosis and thickening of the wall
Mononuclear (lymphocytic) infiltrate
Metaplastic changes: intestinal or pyloric metaplasia
Porcelain gallbladder: dystrophic calcification of the gallbladder wall on a background of chronic cholecystitis — radiologically detectable; carries association with gallbladder carcinoma (though recent data suggest risk is lower than historically quoted)

Schematic histology diagram of chronic cholecystitis showing Rokitansky-Aschoff sinuses lined by epithelium penetrating through the muscularis propria with lymphocytic inflammation and fibrotic wall thickening. — **Panel A:** Gallbladder lumen, mucosal epithelium, lamina propria, lymphocytic infiltrate, Rokitansky-Aschoff sinuses, muscularis propria, perimuscular connective tissue, fibrotic wall thickening. **Panel B:** Rokitansky-Aschoff sinus close-up with sinus epithelium, smooth muscle bundles of muscularis propria, surrounding lymphocytes, fibrotic stroma. **Panel C:** Mechanism summary showing mucosal herniation through muscularis propria due to chronic inflammation and increased intraluminal pressure.

SELF-CHECK

On histology, invaginations of the gallbladder epithelium penetrating through the muscularis into the perimuscular connective tissue are termed:

A. Brunn's nests

B. Psammoma bodies

C. Rokitansky-Aschoff sinuses

D. Creola bodies

Reveal Answer

Answer: C. Rokitansky-Aschoff sinuses

Rokitansky-Aschoff sinuses are the hallmark histological feature of chronic cholecystitis. They form due to repeated elevation of intraluminal pressure (from stones, obstruction, or repeated bouts of acute inflammation), causing the mucosa to herniate through the muscularis propria. Brunn's nests are found in the urinary bladder; psammoma bodies are calcifications seen in papillary thyroid carcinoma, meningioma, and serous ovarian tumours.