At least 90% of patients have gallstones.[3][2][11]

Occasionally, acute cholecystitis occurs in the absence of gallstones.[3] Starvation, total parenteral nutrition, narcotic analgesics, and immobility are predisposing factors for acute acalculous cholecystitis. It has also been described as a rare occurrence during the course of acute Epstein-Barr virus (EBV) infection and can be an atypical clinical presentation of primary EBV infection.[12] Secondary infection with gram-negative flora occurs in most cases of acute acalculous cholecystitis.

Helminthic infection is one of the major causes of biliary disease in Asia, southern Africa, and Latin America, but not the US.[13] Infection with Salmonella organisms has been described as a primary event in cholecystitis secondary to typhoid fever. AIDS-related cholecystitis and cholangiopathy may be secondary to cytomegalovirus and Cryptosporidium organisms. Various micro-organisms can be identified early in the onset of disease. These include Escherichia coli, Klebsiella, enterococci, Pseudomonas, and Bacteroides fragilis.[14] It has been suggested that this bacterial invasion is not a primary perpetrator of injury, because in >40% of patients no bacterial growth is obtained from surgical specimens.[3][8][15][16] Generally, bacterial infection is a secondary feature and not an initiating event.


Fixed obstruction or passage of gallstones into the gallbladder neck or cystic duct causes acute inflammation of the gallbladder wall. The impacted gallstone causes bile to become trapped in the gallbladder, which causes irritation and increases pressure in the gallbladder. Trauma caused by the gallstone stimulates prostaglandin synthesis (PGI2, PGE2), which mediates the inflammatory response. This can result in secondary bacterial infection leading to necrosis and gallbladder perforation.[3]

The pathophysiology of acalculous cholecystitis is poorly understood, but it is probably multi-factorial. Functional cystic duct obstruction is often present and related to biliary sludge or bile inspissation caused by dehydration or bile stasis (due to trauma or systemic illness). Occasionally, extrinsic compression may play a role in the development of bile stasis. Some patients with sepsis may have direct gallbladder wall inflammation and localised or generalised tissue ischaemia without obstruction.

Jaundice occurs in up to 10% of patients and is caused by inflammation of contiguous biliary ducts (Mirizzi's syndrome).[1]

Acute cholecystitis may resolve spontaneously 5 to 7 days after symptom onset. The impacted stone becomes dislodged, with re-establishment of cystic duct patency. If cystic duct patency is not re-established inflammation and pressure necrosis may develop, leading to mural and mucosal haemorrhagic necrosis. Untreated acute cholecystitis can lead to suppurative, gangrenous, and emphysematous cholecystitis.


Types of acute cholecystitis[2]

1. Calculous - 90% to 95%.

2. Acalculous - 3.7% to 14%.

Pathological classification[2]

1. Oedematous

  • 2 to 4 days

  • Gallbladder tissue is intact histologically, with oedema in the subserosal layer.

2. Necrotising

  • 3 to 5 days

  • Oedema with areas of haemorrhage and necrosis

  • Necrosis does not involve the full thickness of the wall.

3. Suppurative

  • 7 to 10 days

  • WBCs present within the gallbladder wall, with areas of necrosis and suppuration

  • Intra-wall abscesses involving the entire thickness of the wall

  • Pericholecystic abscesses present.

4. Chronic

  • Occurs after repeated episodes of mild attacks

  • Mucosal atrophy and fibrosis of the gallbladder wall.

5. Emphysematous

  • Air appears in the gallbladder wall due to infection with gas-forming anaerobes

  • Often found in diabetic patients.

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