Cholecystitis
Cholecystitis
Overview
Acute, chronic, or acute-on-chronic. Chronic=commoner. ACUTE=surgical emergency.
Acute cholecystitis
Resembles acute appendicitis — OBSTRUCTION first, infection later.
Etiopathogenesis (2 types):
- CALCULOUS (90%) — gallstone obstructs neck/cystic duct, MC location=HARTMANN’S POUCH. Distension→inflammation(chemical first)→secondary bacterial infection(E.coli, Strep faecalis)
- ACALCULOUS (10%) — no stones. Causes: non-biliary surgery, trauma, burns, childbirth, sepsis, dehydration, torsion, diabetes. Rare: salmonellosis/cholera, parasites
Morphology (both forms similar except calculi): Gross=distended tense, fibrinous exudate+congestion+haemorrhage on serosa, bright red mucosa, pus+green bile in lumen. Complete cystic duct obstruction+pus = EMPYEMA. Micro: oedema+congestion+neutrophilic exudate, ±abscesses, ±gangrenous necrosis+rupture (GANGRENOUS cholecystitis).
Clinical: severe pain+peritoneal irritation(guarding/hyperaesthesia), tender±palpable gallbladder, fever, neutrophilic leucocytosis, slight jaundice. EARLY cholecystectomy(<3 days)=<0.5% mortality, avoids complications(perforation/fistula/recurrence/adhesions). Medical treatment resolves many but recurrence risk persists.
Chronic cholecystitis
COMMONEST gallbladder disease clinically. Almost CONSTANT association with cholelithiasis.
Etiopathogenesis: virtually always with MIXED+COMBINED stones (NOT pure stones — key correlation). Trigger unclear — cholesterol supersaturation may predispose to both stones+inflammation; or repeated mild acute attacks→chronic.
Morphology: Gross=usually contracted(±normal/enlarged), wall thickened grey-white(fibrosis)±calcified, mucosal folds intact/thickened/flattened, lumen=multiple mixed or combined stones. Micro:
- Thickened congested mucosa (±destroyed)
- ROKITANSKY-ASCHOFF SINUSES (mucosal penetration to muscularis) — MOST SPECIFIC diagnostic finding
- Chronic infiltrate (lymphocytes/plasma/macrophages) in lamina propria+subserosa
- Variable subserosal/subepithelial fibrosis
Variants: CHOLECYSTITIS GLANDULARIS (fused mucosal folds→buried crypts), PORCELAIN GALLBLADDER (calcified, eggshell-cracking), ACUTE-ON-CHRONIC.
Clinical: vague symptoms. Classic patient = FAT, FERTILE, FEMALE of forty/fifty. Abdominal distension/epigastric discomfort post-fatty-meal, dull RUQ/epigastric ache+tenderness, nausea/flatulence, ±biliary colic. Cholecystography visualises stones.
Clinical relevance
Acute cholecystitis parallels acute appendicitis (obstruction-then-infection template) — cross-ref Appendicitis. Chronic cholecystitis’s near-universal MIXED/COMBINED stone association (NOT pure stones) = key morphologic correlation — a pure stone in an inflamed gallbladder should prompt reconsidering the pattern. Early(<3days) cholecystectomy’s <0.5% mortality vs delayed-management complication risk = practical argument for prompt surgery. Rokitansky-Aschoff sinuses = single most specific histologic anchor for chronic cholecystitis diagnosis.
Cholecystitis
Overview
Acute, chronic, or acute-on-chronic. Chronic=commoner. ACUTE=surgical emergency.
Acute cholecystitis
Resembles acute appendicitis — OBSTRUCTION first, infection later.
Etiopathogenesis (2 types):
- CALCULOUS (90%) — gallstone obstructs neck/cystic duct, MC location=HARTMANN’S POUCH. Distension→inflammation(chemical first)→secondary bacterial infection(E.coli, Strep faecalis)
- ACALCULOUS (10%) — no stones. Causes: non-biliary surgery, trauma, burns, childbirth, sepsis, dehydration, torsion, diabetes. Rare: salmonellosis/cholera, parasites
Morphology (both forms similar except calculi): Gross=distended tense, fibrinous exudate+congestion+haemorrhage on serosa, bright red mucosa, pus+green bile in lumen. Complete cystic duct obstruction+pus = EMPYEMA. Micro: oedema+congestion+neutrophilic exudate, ±abscesses, ±gangrenous necrosis+rupture (GANGRENOUS cholecystitis).
Clinical: severe pain+peritoneal irritation(guarding/hyperaesthesia), tender±palpable gallbladder, fever, neutrophilic leucocytosis, slight jaundice. EARLY cholecystectomy(<3 days)=<0.5% mortality, avoids complications(perforation/fistula/recurrence/adhesions). Medical treatment resolves many but recurrence risk persists.
Chronic cholecystitis
COMMONEST gallbladder disease clinically. Almost CONSTANT association with cholelithiasis.
Etiopathogenesis: virtually always with MIXED+COMBINED stones (NOT pure stones — key correlation). Trigger unclear — cholesterol supersaturation may predispose to both stones+inflammation; or repeated mild acute attacks→chronic.
Morphology: Gross=usually contracted(±normal/enlarged), wall thickened grey-white(fibrosis)±calcified, mucosal folds intact/thickened/flattened, lumen=multiple mixed or combined stones. Micro:
- Thickened congested mucosa (±destroyed)
- ROKITANSKY-ASCHOFF SINUSES (mucosal penetration to muscularis) — MOST SPECIFIC diagnostic finding
- Chronic infiltrate (lymphocytes/plasma/macrophages) in lamina propria+subserosa
- Variable subserosal/subepithelial fibrosis
Variants: CHOLECYSTITIS GLANDULARIS (fused mucosal folds→buried crypts), PORCELAIN GALLBLADDER (calcified, eggshell-cracking), ACUTE-ON-CHRONIC.
Clinical: vague symptoms. Classic patient = FAT, FERTILE, FEMALE of forty/fifty. Abdominal distension/epigastric discomfort post-fatty-meal, dull RUQ/epigastric ache+tenderness, nausea/flatulence, ±biliary colic. Cholecystography visualises stones.
Clinical relevance
Acute cholecystitis parallels acute appendicitis (obstruction-then-infection template) — cross-ref Appendicitis. Chronic cholecystitis’s near-universal MIXED/COMBINED stone association (NOT pure stones) = key morphologic correlation — a pure stone in an inflamed gallbladder should prompt reconsidering the pattern. Early(<3days) cholecystectomy’s <0.5% mortality vs delayed-management complication risk = practical argument for prompt surgery. Rokitansky-Aschoff sinuses = single most specific histologic anchor for chronic cholecystitis diagnosis.
Cholecystitis
Overview
Cholecystitis (gallbladder inflammation) may be acute, chronic, or acute-on-chronic. Chronic cholecystitis is commoner overall, but acute cholecystitis is a surgical emergency.
Acute Cholecystitis
Resembles acute appendicitis in many ways — usually begins with obstruction, followed later by infection.
Etiopathogenesis — two types:
Acute calculous cholecystitis (90%) — obstruction of the gallbladder neck or cystic duct by a gallstone, most commonly impacted in Hartmann’s pouch. Obstruction → gallbladder distension → acute inflammation, initially chemical irritation, later secondary bacterial infection (chiefly E. coli, Streptococcus faecalis).
Acute acalculous cholecystitis (10%) — no gallstones present. Causes: previous non-biliary surgery, multiple injuries, burns, recent childbirth, severe sepsis, dehydration, gallbladder torsion, diabetes mellitus. Rarer causes: primary bacterial infection (salmonellosis, cholera), parasitic infestations.
Morphology — the two forms are morphologically similar apart from calculi presence/absence. Gross: distended, tense gallbladder; serosa coated with fibrinous exudate, congestion, haemorrhages; bright red mucosa; lumen filled with pus mixed with green bile. In calculous disease, a stone may impact the neck/cystic duct; complete cystic duct obstruction with purulent lumen = empyema of the gallbladder. Micro: marked inflammatory oedema, congestion, neutrophilic exudate in the wall; frank abscesses may form; gangrenous necrosis with peritoneal rupture = gangrenous cholecystitis.
Clinical features: severe upper abdominal pain with peritoneal irritation signs (guarding, hyperaesthesia); tender, sometimes palpable gallbladder; fever, neutrophilic leucocytosis, slight jaundice. Early cholecystectomy (within 3 days) has <0.5% mortality and avoids complications (perforation, biliary fistula, recurrence, adhesions); medical treatment resolves a fair proportion but recurrence risk persists.
Chronic Cholecystitis
The commonest clinical gallbladder disease; almost constantly associated with cholelithiasis.
Etiopathogenesis: virtually always associated with mixed and combined gallstones. The initiating trigger for the inflammatory response is unclear — bile cholesterol supersaturation may predispose to both stone formation and inflammation; some cases arise from repeated mild acute cholecystitis attacks.
Morphology: Gross — usually contracted, but may be normal or enlarged; wall thickened, grey-white on cut section (dense fibrosis), sometimes calcified; mucosal folds intact, thickened, or flattened/atrophied; lumen commonly contains multiple mixed stones or a combined stone. Micro:
- Thickened, congested mucosa (occasionally totally destroyed).
- Mucosal penetration deep into the wall to the muscularis, forming Rokitansky-Aschoff sinuses.
- Variable chronic inflammatory infiltrate (lymphocytes, plasma cells, macrophages) in the lamina propria and subserosa.
- Variable subserosal/subepithelial fibrosis.
Morphologic variants:
- Cholecystitis glandularis — mucosal folds fuse from inflammation, forming buried epithelial crypts in the wall.
- Porcelain gallbladder — calcified wall cracking like eggshell.
- Acute-on-chronic cholecystitis — acute changes superimposed on chronic changes.
Clinical features: ill-defined, vague symptoms. Classic patient — fat, fertile, female of forty/fifty — presents with abdominal distension or epigastric discomfort, especially post-fatty-meal; constant dull right-hypochondrium/epigastric ache with tenderness; nausea, flatulence common; occasional biliary colic from stone passage. Cholecystography usually demonstrates the gallstones radiologically.
Clinical Relevance
- Acute cholecystitis’s parallel with acute appendicitis (obstruction-first, infection-second pathogenesis) is a useful cross-reference — both conditions follow the same mechanistic template applied to different organs, worth linking to the Appendicitis topic.
- The near-universal association of chronic cholecystitis specifically with mixed and combined stones (not pure stones) is the key morphologic correlation — finding a pure cholesterol or pigment stone in an inflamed gallbladder should prompt reconsidering the pattern.
- Early (within 3 days) cholecystectomy’s dramatically low mortality (<0.5%) versus the complication risks of delayed/medical management is the practical clinical argument for prompt surgical intervention in confirmed acute cholecystitis.
- Rokitansky-Aschoff sinuses are the single most specific histologic finding to anchor a chronic cholecystitis diagnosis — their presence (mucosal penetration to the muscularis) distinguishes true chronic cholecystitis from simple mucosal thickening.
Cholecystitis
Overview
Cholecystitis (gallbladder inflammation) may be acute, chronic, or acute-on-chronic. Chronic cholecystitis is commoner overall, but acute cholecystitis is a surgical emergency.
Acute Cholecystitis
Resembles acute appendicitis in many ways — usually begins with obstruction, followed later by infection.
Etiopathogenesis — two types:
Acute calculous cholecystitis (90%) — obstruction of the gallbladder neck or cystic duct by a gallstone, most commonly impacted in Hartmann’s pouch. Obstruction → gallbladder distension → acute inflammation, initially chemical irritation, later secondary bacterial infection (chiefly E. coli, Streptococcus faecalis).
Acute acalculous cholecystitis (10%) — no gallstones present. Causes: previous non-biliary surgery, multiple injuries, burns, recent childbirth, severe sepsis, dehydration, gallbladder torsion, diabetes mellitus. Rarer causes: primary bacterial infection (salmonellosis, cholera), parasitic infestations.
Morphology — the two forms are morphologically similar apart from calculi presence/absence. Gross: distended, tense gallbladder; serosa coated with fibrinous exudate, congestion, haemorrhages; bright red mucosa; lumen filled with pus mixed with green bile. In calculous disease, a stone may impact the neck/cystic duct; complete cystic duct obstruction with purulent lumen = empyema of the gallbladder. Micro: marked inflammatory oedema, congestion, neutrophilic exudate in the wall; frank abscesses may form; gangrenous necrosis with peritoneal rupture = gangrenous cholecystitis.
Clinical features: severe upper abdominal pain with peritoneal irritation signs (guarding, hyperaesthesia); tender, sometimes palpable gallbladder; fever, neutrophilic leucocytosis, slight jaundice. Early cholecystectomy (within 3 days) has <0.5% mortality and avoids complications (perforation, biliary fistula, recurrence, adhesions); medical treatment resolves a fair proportion but recurrence risk persists.
Chronic Cholecystitis
The commonest clinical gallbladder disease; almost constantly associated with cholelithiasis.
Etiopathogenesis: virtually always associated with mixed and combined gallstones. The initiating trigger for the inflammatory response is unclear — bile cholesterol supersaturation may predispose to both stone formation and inflammation; some cases arise from repeated mild acute cholecystitis attacks.
Morphology: Gross — usually contracted, but may be normal or enlarged; wall thickened, grey-white on cut section (dense fibrosis), sometimes calcified; mucosal folds intact, thickened, or flattened/atrophied; lumen commonly contains multiple mixed stones or a combined stone. Micro:
- Thickened, congested mucosa (occasionally totally destroyed).
- Mucosal penetration deep into the wall to the muscularis, forming Rokitansky-Aschoff sinuses.
- Variable chronic inflammatory infiltrate (lymphocytes, plasma cells, macrophages) in the lamina propria and subserosa.
- Variable subserosal/subepithelial fibrosis.
Morphologic variants:
- Cholecystitis glandularis — mucosal folds fuse from inflammation, forming buried epithelial crypts in the wall.
- Porcelain gallbladder — calcified wall cracking like eggshell.
- Acute-on-chronic cholecystitis — acute changes superimposed on chronic changes.
Clinical features: ill-defined, vague symptoms. Classic patient — fat, fertile, female of forty/fifty — presents with abdominal distension or epigastric discomfort, especially post-fatty-meal; constant dull right-hypochondrium/epigastric ache with tenderness; nausea, flatulence common; occasional biliary colic from stone passage. Cholecystography usually demonstrates the gallstones radiologically.
Clinical Relevance
- Acute cholecystitis’s parallel with acute appendicitis (obstruction-first, infection-second pathogenesis) is a useful cross-reference — both conditions follow the same mechanistic template applied to different organs, worth linking to the Appendicitis topic.
- The near-universal association of chronic cholecystitis specifically with mixed and combined stones (not pure stones) is the key morphologic correlation — finding a pure cholesterol or pigment stone in an inflamed gallbladder should prompt reconsidering the pattern.
- Early (within 3 days) cholecystectomy’s dramatically low mortality (<0.5%) versus the complication risks of delayed/medical management is the practical clinical argument for prompt surgical intervention in confirmed acute cholecystitis.
- Rokitansky-Aschoff sinuses are the single most specific histologic finding to anchor a chronic cholecystitis diagnosis — their presence (mucosal penetration to the muscularis) distinguishes true chronic cholecystitis from simple mucosal thickening.
Cholecystitis
- Acute cholecystitis obstruction-to-gangrene progression cascade with the empyema/gangrenous branch points marked
- Chronic cholecystitis’s four morphologic variants (classic, cholecystitis glandularis, porcelain gallbladder, acute-on-chronic) side by side
Cholecystitis
- Acute cholecystitis obstruction-to-gangrene progression cascade with the empyema/gangrenous branch points marked
- Chronic cholecystitis’s four morphologic variants (classic, cholecystitis glandularis, porcelain gallbladder, acute-on-chronic) side by side
My Sticky Notes
Personal revision notes, mnemonics and reminders.
