(See also Overview of Biliary Function.)
Acute cholecystitis is the most common complication of cholelithiasis. In fact, ≥ 95% of patients with acute cholecystitis have cholelithiasis. When a stone becomes impacted in the cystic duct and persistently obstructs it, acute inflammation results. Bile stasis triggers release of inflammatory enzymes (eg, phospholipase A, which converts lecithin to lysolecithin, which then may mediate inflammation).
The damaged mucosa secretes more fluid into the gallbladder lumen than it absorbs. The resulting distention further releases inflammatory mediators (eg, prostaglandins), worsening mucosal damage and causing ischemia, all of which perpetuate inflammation. Bacterial infection can supervene. The vicious circle of fluid secretion and inflammation, when unchecked, leads to necrosis and perforation.
If acute inflammation resolves then continues to recur, the gallbladder becomes fibrotic and contracted and does not concentrate bile or empty normally—features of chronic cholecystitis.
Acalculous cholecystitis is cholecystitis without stones. It accounts for 5 to 10% of cholecystectomies done for acute cholecystitis. Risk factors include the following:
The mechanism probably involves inflammatory mediators released because of ischemia, infection, or bile stasis. Sometimes an infecting organism can be identified (eg, Salmonella species or cytomegalovirus in immunodeficient patients). In young children, acute acalculous cholecystitis tends to follow a febrile illness without an identifiable infecting organism.
Most patients have had prior attacks of biliary colic or acute cholecystitis. The pain of cholecystitis is similar in quality and location to biliary colic but lasts longer (ie, > 6 hours) and is more severe. Vomiting is common, as is right subcostal tenderness. Within a few hours, the Murphy sign (deep inspiration exacerbates the pain during palpation of the right upper quadrant and halts inspiration) develops along with involuntary guarding of upper abdominal muscles on the right side. Fever, usually low grade, is common.
In older patients, the first or only symptoms may be systemic and nonspecific (eg, anorexia, vomiting, malaise, weakness, fever). Sometimes fever does not develop.
Acute cholecystitis begins to subside in 2 to 3 days and resolves within 1 week in 85% of patients even without treatment.
Without treatment, 10% of patients develop localized perforation, and 1% develop free perforation and peritonitis. Increasing abdominal pain, high fever, and rigors with rebound tenderness or ileus suggest empyema (pus) in the gallbladder, gangrene, or perforation. When acute cholecystitis is accompanied by jaundice or cholestasis, partial common duct obstruction is likely, usually due to stones or inflammation.
Other complications include the following:
Mirizzi syndrome: Rarely, a gallstone becomes impacted in the cystic duct and compresses and obstructs the common bile duct, causing cholestasis.
Gallstone pancreatitis: Gallstones pass from the gallbladder into the biliary tract and block the pancreatic duct.
Cholecystoenteric fistula: Infrequently, a large stone erodes the gallbladder wall, creating a fistula into the small bowel (or elsewhere in the abdominal cavity); the stone may pass freely or obstruct the small bowel (gallstone ileus).
The symptoms are similar to those of acute cholecystitis with gallstones but may be difficult to identify because patients tend to be severely ill (eg, in an intensive care unit) and may be unable to communicate clearly. Abdominal distention or unexplained fever may be the only clue. Untreated, the disease can rapidly progress to gallbladder gangrene and perforation, leading to sepsis, shock, and peritonitis; mortality approaches 65%.
Acute cholecystitis is suspected based on symptoms and signs.
Transabdominal ultrasonography is the best test to detect gallstones. The test may also elicit local abdominal tenderness over the gallbladder (ultrasonographic Murphy sign). Pericholecystic fluid or thickening of the gallbladder wall indicates acute inflammation.
Cholescintigraphy is useful when results are equivocal; failure of the radionuclide to fill the gallbladder suggests an obstructed cystic duct (ie, an impacted stone). False-positive results may be due to the following:
Morphine provocation, which increases tone in the sphincter of Oddi and enhances filling, helps eliminate false-positive results.
Abdominal CT identifies complications such as gallbladder perforation or pancreatitis.
Laboratory tests are done but are not diagnostic. Leukocytosis with a left shift is common. In uncomplicated acute cholecystitis, liver tests are normal or only slightly elevated. Mild cholestatic abnormalities (bilirubin up to 4 mg/dL and mildly elevated alkaline phosphatase) are common, probably indicating inflammatory mediators affecting the liver rather than mechanical obstruction. More marked increases, especially if lipase (amylase is less specific) is elevated > 3-fold, suggest bile duct obstruction. Passage of a stone through the biliary tract increases aminotransferases (alanine, aspartate).
Acute acalculous cholecystitis is suggested if a patient has no gallstones but has ultrasonographic Murphy sign or a thickened gallbladder wall and pericholecystic fluid. A distended gallbladder, biliary sludge, and a thickened gallbladder wall without pericholecystic fluid (due to low albumin or ascites) may result simply from a critical illness.
CT identifies extrabiliary abnormalities. Cholescintigraphy is more helpful; failure of a radionuclide to fill may indicate edematous cystic duct obstruction. Giving morphine helps eliminate a false-positive result due to gallbladder stasis.
Management includes hospital admission, IV fluids, and analgesics, such as a nonsteroidal anti-inflammatory drug (NSAID; ketorolac) or opioid. Nothing is given orally, and nasogastric suction is instituted if vomiting or an ileus is present. Parenteral antibiotics are usually initiated to treat possible infection, but evidence of benefit is lacking. Empiric coverage, directed at gram-negative enteric organisms, involves IV regimens such as ceftriaxone 2 g every 24 hours plus metronidazole 500 mg every 8 hours, piperacillin/tazobactam 4 g every 6 hours, or ticarcillin/clavulanate 4 g every 6 hours.
Cholecystectomy cures acute cholecystitis and relieves biliary pain. Early cholecystectomy is generally preferred, best done during the first 24 to 48 hours in the following situations:
Surgery may be delayed when patients have an underlying severe chronic disorder (eg, cardiopulmonary disease) that increases the surgical risks. In such patients, cholecystectomy is deferred until medical therapy stabilizes the comorbid disorders or until cholecystitis resolves. If cholecystitis resolves, cholecystectomy may be done ≥ 6 weeks later. Delayed surgery carries the risk of recurrent biliary complications.
Percutaneous cholecystostomy is an alternative to cholecystectomy for patients at very high surgical risk, such as those who are older, those with acalculous cholecystitis, and those in an intensive care unit because of burns, trauma, or respiratory failure.
Most (≥ 95%) patients with acute cholecystitis have cholelithiasis.
In older patients, symptoms of cholecystitis may be nonspecific (eg, anorexia, vomiting, malaise, weakness), and fever may be absent.
Although acute cholecystitis resolves spontaneously in 85% of patients, localized perforation or another complication develops in 10%.
Diagnose via ultrasonography and, if results are equivocal, cholescintigraphy.
Treat patients with IV fluids, antibiotics, and analgesics; do cholecystectomy when patients are stable.