CHOLECYSTITIS (Robbins pp 895)

This is the inflammation of the gall bladder.

There are three subgroups:

1) acute calculous cholecystitis,

2) acute acalculous cholecystitis,

3) chronic cholecystitis.

Acute calculous cholecystitis:

This is cholecystitis as a result of impacted stones in the gall bladder. The types of stones, epidemiology/at risk individuals are the same as before.

Pathogenesis: A gall stone forms ≫ becomes impacted at neck/cystic duct ≫ chemical inflammation follows ≫ acute calculous cholecystitis. Following this, bacterial infection settles in and the organisms implicated are: E coli, enterococci, gram –ve bacilli, salmonella.

Clinical features / Sequaelae: Begins with epigastric pain ≫ sudden RUQ pain≫ sweating, nausea / vomiting. Sequelae is same as for gall stones.

Morphology: Macroscopically, you will see four things:

1) thickened gall bladder wall,

2) presence of multiple/single stones impacted onto wall of gall bladder,

3) oedematous changes in gall bladder wall,

4) focal areas of subserosal haemorrhage.

Acute acalculous cholecystitis:

This is cholecystitis without evidence of any stones.

Epidemiology/at risk individuals: Males and children are more susceptible. At risk patients are those that have had/have:

1) previous surgery,

2) diabetes,

3) intravenous hyperalimentation (nourishment),

4) severe trauma (burns, accidents),

5) post partum.

Pathogenesis: It is thought to arise from situations that compromise blood flow to the gall bladder (involves cystic artery). Addition factors include: 1) inflammation of wall ≫ leading to obstruction of artery, 2) too much biliary sludge obstructing the cystic duct (no stones though) etc.

Clinical features / Sequelae: clinical presentation is same as with acute calculous cholecystitis. The sequelae is fatal if not diagnosed quickly. Other sequelae are same as for gall stones.

Chronic cholecystitis:

This is a sequel to repeated bouts of acute cholecystitis. Calculi is present in 90% of cases, and certain bacteria are implicated: E coli, enterococci, Salmonella. Epidemiology/at risk individuals: Same as for cholilithiasis.

Clinical features / Sequalae: Same as for acute cholecystitis. Carcinoma occurs in about 0.5% of cases.

Morphology: Macroscopically:

1) subserosal fibrosis,

2) thickening of the wall / pale / rigid,

3) luminal stones.

Microscopically:

1) subepithelial / subserosal fibrosis,

2) chronic inflammatory cells,

3) fusion of mucosal folds – buried crypts within wall,

4) outpouchings of mucosal epithelium through wall (Rokitansky-Ashchoff sinuses).

Rarely: dystrophic calcification ≫ porcelain gallbladder.

Category: Pathology Notes