Etiology
At least 90% of patients with acute cholecystitis have gallstones.[2][7][13] Helmintic infection is one of the major causes of biliary disease in Asia, southern Africa, and Latin America, but not the US.[14] 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 microorganisms can be identified early in the onset of disease. These include Escherichia coli, Klebsiella, enterococci, Pseudomonas, and Bacteroides fragilis.[15] 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.[7][10][16][17] Generally, bacterial infection is a secondary feature and not an initiating event.
Starvation, total parenteral nutrition, opioid analgesics, and immobility are predisposing factors for acute acalculous cholecystitis.[2][7][18] 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.[19] Secondary infection with gram-negative flora occurs in most cases of acute acalculous cholecystitis.
Pathophysiology
The presence of an impacted gallstone in the neck of the gallbladder or in the cystic duct causes bile to become trapped in the gallbladder, which increases pressure in the gallbladder. Trauma caused by the gallstone stimulates prostaglandin synthesis (PGI2, PGE2), which mediates an acute inflammatory response in the gallbladder wall. This can be compounded by secondary bacterial infection of the stagnant bile, leading to necrosis and gallbladder perforation.[7]
The pathophysiology of acalculous cholecystitis is poorly understood, but it is most likely multifactorial. 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 localized or generalized tissue ischemia without obstruction.
Jaundice occurs in up to 10% of patients and is caused by inflammation of contiguous biliary ducts (Mirizzi syndrome).[1]
Acute cholecystitis may resolve spontaneously 5-7 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 hemorrhagic necrosis. Untreated acute cholecystitis can lead to suppurative, gangrenous, and emphysematous cholecystitis.
Classification
Types of acute cholecystitis[2][3][4][5][6]
1. Calculous - 90% to 95%.
2. Acalculous - 5% to 10%.
Pathologic classification[2]
1. Edematous
2-4 days
Gallbladder tissue is intact histologically, with edema in the subserosal layer.
2. Necrotizing
3-5 days
Edema with areas of hemorrhage and necrosis
Necrosis does not involve the full thickness of the wall.
3. Suppurative
7-10 days
WBCs present within the gallbladder wall, with areas of necrosis and suppuration
Intrawall 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 anerobes
Often found in diabetic patients.
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