Cholecystitis

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Cholecystitis

Cholecystitis is inflammation of the gallbladder. It is one of the most common indications for abdominal surgery in the United States, and its epidemiologic distribution closely parallels that of gallstone disease.

Classification

Type	Key feature
Acute calculous	Obstruction by gallstone (~90% of acute cases)
Acute acalculous	No stone; stasis/ischemia in critically ill (5-12%)
Chronic	Repeated bouts; fibrosis; almost always with stones
Emphysematous	Gas-forming organisms; diabetics/elderly men
Gangrenous	Necrosis of gallbladder wall; most severe

Acute Calculous Cholecystitis

Pathogenesis

Acute cholecystitis begins when a stone becomes persistently embedded in the cystic duct (rather than causing transient obstruction as in biliary colic). Three parallel mechanisms drive the inflammatory response:

Mechanical - increased intraluminal pressure and distension cause mucosal ischemia
Chemical - phospholipase A released from the mucosa converts lecithin to lysolecithin, which is toxic to the epithelium; the glycoprotein mucous layer is disrupted, exposing mucosa to bile salt detergent action; prostaglandins E and F2α amplify mucosal inflammation
Bacterial - enteric organisms (E. coli, Klebsiella, Streptococcus, Clostridium) are cultured from gallbladder bile in 50-85% of patients, but are considered a secondary event, not the initiator

The role of prostaglandins is supported by evidence that diclofenac (a prostaglandin synthetase inhibitor) given early resolves biliary pain and prevents acute cholecystitis from developing - Sleisenger and Fordtran's, p. 1242.

Clinical Features

Pain: RUQ or epigastric pain that is steady and severe, lasting >6 hours (contrast with biliary colic, which resolves within 5 hours). Radiates to the right scapula or interscapular area.
Fever: low-grade fever typical; temperature >102°F (>39°C) suggests gangrene or perforation
Nausea/vomiting: common; may cause volume depletion
Murphy's sign: during deep palpation of the RUQ, the patient arrests inspiration when the inflamed gallbladder descends to meet the examiner's hand. Positive predictive value >90% for acute cholecystitis when gallstones are also present.
Palpable gallbladder: in ~25-50% of patients, especially on first attack. Repeat attacks cause scarring that prevents distension.
Jaundice: mild (bilirubin <4 mg/dL) in ~20% overall, up to 40% in elderly. Bilirubin >4 mg/dL raises concern for choledocholithiasis or Mirizzi syndrome.
Approximately 75% of patients report prior attacks of biliary pain before their first episode of acute cholecystitis. - Sleisenger and Fordtran's, p. 1242

Laboratory Findings

Test	Finding
WBC	10,000-15,000/mm³ with left shift
WBC >15,000	Suggests empyema or perforation
Serum bilirubin	Mildly elevated (<4 mg/dL) in <50%
Bilirubin >4 mg/dL	Suggests bile duct stones or Mirizzi syndrome
ALT/AST, ALP	Mildly elevated; up to 5-fold
Amylase/lipase	Mildly elevated nonspecifically; >1000 U/L suggests pancreatitis

Harrison's Principles of Internal Medicine, 22E (2025), p. 2775

Imaging

Ultrasound (US) is the first-line and most useful study:

Identifies gallstones in 90-95% of cases
Gallbladder wall thickening >4 mm (loses specificity in ascites/hypoalbuminemia)
Pericholecystic fluid
Sonographic Murphy sign: focal gallbladder tenderness under the US probe

HIDA scan (hepatobiliary scintigraphy): highly sensitive and specific (~95%). Non-visualization of the gallbladder (isotope appears in bile duct and small bowel but not the gallbladder within 60 minutes) confirms cystic duct obstruction. A normal scan effectively excludes acute cholecystitis.

CT: shows gallbladder wall thickening, pericholecystic inflammation; useful when US is inconclusive and for detecting complications (gangrene, perforation, emphysematous cholecystitis).

Morphology (Pathology)

Acute cholecystitis:

Enlarged, tense gallbladder; bright red or violaceous (from subserosal hemorrhage)
Serosal fibrinous or fibrinopurulent exudate
In 90% of cases, stones obstruct the neck or cystic duct
Lumen contains cloudy/turbid bile, fibrin, blood, pus
Empyema: lumen filled predominantly with pus
Gangrenous cholecystitis: green-black necrotic wall
Histology: edema, leukocytic infiltration, vascular congestion, abscess formation, gangrenous necrosis

Chronic cholecystitis:

Marked subepithelial and subserosal fibrosis
Lymphocytic infiltrate in the wall (when not superimposed acute)
Rokitansky-Aschoff sinuses: outpouchings of mucosal epithelium through the gallbladder wall - a hallmark finding

FIG. 14.43 Chronic cholecystitis. (A) Gallbladder mucosa infiltrated by chronic inflammatory cells. (B) Rokitansky-Aschoff sinus containing a fragmented bile pigment stone. - Robbins & Kumar Basic Pathology, p. 633

Acute Acalculous Cholecystitis

Accounts for 5-12% of acute cholecystitis cases. Thought to result from gallbladder stasis and ischemia rather than stone obstruction.

Predisposing conditions:

Major surgery or severe trauma (motor vehicle crashes)
Severe burns
Sepsis
Prolonged fasting / parenteral nutrition
Postpartum after prolonged labor
Vasculitis, cholesterol emboli
DM, adenocarcinoma, gallbladder torsion

Important organisms in unusual cases: Leptospira, Salmonella, Vibrio cholerae, parasitic infestations.

The complication rate exceeds that of calculous cholecystitis. Management depends on early diagnosis and prompt surgical or percutaneous drainage. - Harrison's 22E, p. 2775

Emphysematous Cholecystitis

Acute cholecystitis complicated by ischemia/gangrene + gas-producing organisms
Common organisms: Clostridium perfringens/welchii (anaerobes), E. coli (aerobes)
Most common in elderly men and diabetics
Diagnosis: plain film or CT showing gas in the gallbladder lumen, gas dissecting the wall (ring sign), or pericholecystic gas
Carries high morbidity and mortality; urgent surgery + antibiotics mandatory

Natural History

Untreated acute cholecystitis pain resolves in 7-10 days; often remits within 48 hours of hospitalization
~83% resolve without complication medically
Complications occur in ~17%: gangrenous cholecystitis (7%), empyema (6%), perforation (3%), emphysematous (<1%)
Of those who remit medically: ~25% recur within 1 year, ~60% within 6 years
Therefore acute cholecystitis is best treated by early surgery when possible

Complications

Empyema of the gallbladder (pus-filled lumen)
Gangrenous cholecystitis with risk of perforation
Perforation - local abscess or diffuse peritonitis
Cholangitis/sepsis from bacterial superinfection
Biliary-enteric (cholecystoenteric) fistula - drainage into adjacent bowel, entry of air/bacteria into biliary tree, risk of gallstone ileus
Mirizzi syndrome - impacted stone in cystic duct compresses the common hepatic duct, causing jaundice

Treatment

Acute Cholecystitis

IV fluids, NPO, analgesia (NSAIDs - ketorolac, diclofenac are preferred; also reduce prostaglandin-driven inflammation)
Antibiotics covering enteric gram-negatives and anaerobes
Early laparoscopic cholecystectomy is the treatment of choice - ideally within 72 hours to 1 week of symptom onset
Conversion to open surgery in ~5%; death rate <0.1%; bile duct injury rate 0.2-0.6%

High-risk/non-surgical candidates: Percutaneous cholecystostomy (gallbladder drainage) followed by interval cholecystectomy once the patient is stabilized.

A recent 2025 systematic review and meta-analysis (PMID 40483437) comparing percutaneous treatment vs. cholecystectomy found that both approaches are viable, with percutaneous drainage being preferred for high-risk surgical patients.

A 2024 meta-analysis (PMID 39607476) challenged the traditional "7-day barrier," showing that early laparoscopic cholecystectomy remains safe even beyond 7 days of symptom onset.

Chronic Cholecystitis

Elective laparoscopic cholecystectomy is definitive
Medical dissolution with UDCA (10-15 mg/kg/d) is an option only for radiolucent stones <5 mm in a functioning gallbladder; complete dissolution in ~50% within 6-24 months; high recurrence rate (30-50% over 3-5 years)

Chronic Cholecystitis

Develops with or without a prior history of acute attacks. Almost always associated with gallstones, though the stones appear to create a milieu of bile supersaturation rather than directly causing inflammation. Microorganisms (E. coli, enterococci) cultured in ~one-third of cases.

Chronic symptoms: recurrent RUQ pain, fatty food intolerance, bloating. Gallbladder may be contracted (fibrotic) and non-functioning on imaging.

Sources:

Sleisenger and Fordtran's Gastrointestinal and Liver Disease, pp. 1241-1244
Harrison's Principles of Internal Medicine, 22E (2025), pp. 2774-2776
Robbins & Kumar Basic Pathology (Robbins Pathology), pp. 632-633
Tintinalli's Emergency Medicine: A Comprehensive Study
Robbins, Cotran & Kumar Pathologic Basis of Disease

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