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Gallbladder
Cholecystitis
Acute cholecystitis
Reviewer: Hanni Gulwani, M.D. (see Reviewers page)
Revised: 11 February 2013, last major update September 2012
Copyright: (c) 2003-2013, PathologyOutlines.com, Inc.
General
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● Present in 5-10% of cholecystectomy specimens
● Either gallstone associated (acute calculous cholecystitis) or not (acute acalculous cholecystitis)
● 10% perforate without treatment
● Note: diagnosis of dysplasia should be made cautiously if extensive ulceration or acute inflammation
Treatment
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● Cholecystectomy
Gross description
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● Enlarged, distended gallbladder
● Congested vessels (“angry red color”), serosal and mucosal exudate, thickened wall with edema and hemorrhage
● Ulcers with blood clot, pus and bile
Gross images
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Red mucosa
Acute (with empyema) and chronic cholecystitis with gallstone
Micro description
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● Initially edema, congestion, hemorrhage, fibrin deposition in and around muscular layer
● Later mucosal and mural necrosis with neutrophils
● Variable reactive epithelial changes resembling dysplasia
● Finally myofibroblastic proliferation with chronic inflammatory infiltrate
● Also fresh thrombi within small veins
Micro images
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Reactive changes in acute cholecystitis
Virtual slides
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Red mucosa
Differential diagnosis
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● Leptospirosis (Hum Pathol 2001;32:750)
Acute calculous cholecystitis
General
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● 90% of cases
● Mean age 60 years, 60% women
● Abdominal pain, right upper quadrant tenderness, nausea, vomiting, fever, leukocytosis, mild jaundice
● 50% of those with jaundice have coexisting choledocholithiasis
● Due to stone impaction, versus biliary colic, which is due to intermittent obstruction
● 50% have bacterial infection (E. coli, Enterobacter, Enterococcus, Klebsiella, Clostridium, Peptostreptococcus, Bacteroides)
● 1% mortality
● Perforation unlikely if early operation
Pathophysiology
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● Chronic obstruction causes increased intraluminal pressure, vascular compromise, stasis and concentration of bile within lumen, mucosal damage, release of cellular enzymes, release of inflammatory mediators such as lysolecithin and prostagladins
● Gall bladder volume increases as acute cholecystitis progresses to gangrene or empyema
● Gallstone formation is associated with poorer contractility and larger volume in gallbladders that contain stones
(World J Gastroenterol 2010;16:4341)
● As the weight, volume and size of the stone increases, gall bladder mucosa changes from cholecystitis, hyperplasia, metaplasia, dysplasia, to carcinoma (Trop Gastroenterol 2012;33:39)
● Eosinophils accumulate in gallbladder mucosa in young patients (Pol J Pathol 2011;62:41)
Acute acalculous cholecystitis
General
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● 10% of cases
● 2/3 male, mean age 50+ years
● Often only fever or hyperamylasemia
● Patients usually severely debilitated, due to severe trauma, sepsis, shock, burns, cancer, diabetes, multiple blood transfusions, surgery, torsion, cystic duct obstruction from various causes
● May be associated with infection by CMV, cryptosporidia or microsporidia in AIDS patients
● 10-50% mortality
Pathophysiology
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● Raised prostaglandin E levels (cause damage), tissue anoxia, bacterial contamination, stasis and changes in bile salt concentration
Micro description
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● Bile infiltration is more prominent and extends deep to muscle layer, WBC margination of blood vessels and lymphatic dilation
Additional references
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● Histopathology 2005;47:485,
Semin Gastrointest Dis 2003;14:178,
World J Gastroenterol 2003;9:2821,
Dig Dis Sci 2003;48:1960
Cocaine related acute cholecystitis
General
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● Young, otherwise healthy patients
● Vascular thrombi present
● Other parts of GI tract also affected
Additional references
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End of Gallbladder > Cholecystitis > Acute cholecystitis
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