Acute cholecystitis is inflammation of the gallbladder that develops over hours, usually because a gallstone obstructs the cystic duct. Symptoms include right upper quadrant pain and tenderness, sometimes accompanied by fever, chills, nausea, and vomiting. Abdominal ultrasound detects the gallstone and sometimes the associated inflammation. Treatment is with early cholecystectomy when possible.
(See also Overview of Biliary Function.)
Acute cholecystitis is the most common complication of cholelithiasis. In fact, ≥ 90% of patients with acute cholecystitis have cholelithiasis (1). 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, can lead 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.
Acute acalculous cholecystitis
Acalculous cholecystitis is cholecystitis without stones. It accounts for 5 to 10% of cholecystectomies performed for acute cholecystitis (1). Risk factors include the following (2, 3):
Major surgery or critical illness (eg, burns, sepsis, shock, or trauma)
Prolonged fasting or parenteral nutrition, both of which predispose to bile stasis
Immune deficiency or HIV infection
Vasculitis (eg, systemic lupus erythematosus [SLE], polyarteritis nodosa)
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.
General references
1. Gallaher JR, Charles A. Acute Cholecystitis: A Review. JAMA. 2022;327(10):965-975. doi:10.1001/jama.2022.2350
2. Gu MG, Kim TN, Song J, et al. Risk factors and therapeutic outcomes of acute acalculous cholecystitis. Digestion. 2014;90(2):75-80. doi:10.1159/000362444
3. Barie PS, Eachempati SR. Acute acalculous cholecystitis. Curr Gastroenterol Rep. 2003;5(4):302-309. doi:10.1007/s11894-003-0067-x
Symptoms and Signs of Acute Cholecystitis
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 (peaking within 15 to 60 minutes and lasting > 6 hours) and is more severe. Vomiting is common, as is right subcostal tenderness. Pain may be referred to the right scapula or upper back. 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 will resolve without surgical treatment in approximately 85% of patients (1).
Complications
Without treatment, approximately 10% of patients may develop localized or free perforation and peritonitis (2). Perforated gallbladder has a mortality rate of up to 16%. 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, acholic stool, 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).
Acute acalculous cholecystitis
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.
Pearls & Pitfalls
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Symptoms and signs references
1. Loozen CS, Oor JE, van Ramshorst B, et al. Conservative treatment of acute cholecystitis: a systematic review and pooled analysis. Surg Endosc. 2017;31(2):504-515. doi:10.1007/s00464-016-5011-x
2. Sartelli M, Chichom-Mefire A, Labricciosa FM, et al. The management of intra-abdominal infections from a global perspective: 2017 WSES guidelines for management of intra-abdominal infections. World J Emerg Surg. 2017;12:29. doi:10.1186/s13017-017-0141-6
Diagnosis of Acute Cholecystitis
Ultrasound
Cholescintigraphy if ultrasound results are equivocal or if acalculous cholecystitis is suspected
Sometimes CT or MRI with magnetic resonance cholangiopancreatography (MRCP) if ultrasound/cholescintigraphy are inconclusive and high suspicion of perforation, abscess, or choledocholithiasis.
Laboratory testing
Acute cholecystitis is suspected based on symptoms and signs.
Transabdominal ultrasound 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). The use of cholescintigraphy is sometimes limited due to practical considerations, particularly in patients with hemodynamic instability (eg, in the intensive care unit) who cannot be transported and tolerate the scan duration. False-positive results may be due to the following:
A critical illness
Parenteral nutrition (because gallbladder stasis prevents filling)
Severe liver disease (because the liver does not secrete the radionuclide)
Previous sphincterotomy (which facilitates flow into the duodenum rather than the gallbladder)
Morphine provocation, which increases tone in the sphincter of Oddi and enhances filling, helps eliminate false-positive results.
Abdominal CT and MRI identify complications such as gallbladder perforation or pancreatitis, as well as choledocholithiasis and other extrabiliary involvement.
Laboratory tests are performed 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 [68.4 micromol/L] 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
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.
Cholescintigraphy is the most reliable diagnostic test for acute acalculous cholecystitis (1). As for other causes of cholecystitis, CT and MRI are generally considered adjunctive imaging modalities, particularly when ultrasound is equivocal, complications are suspected, or specific patient factors limit the use of other imaging.
Diagnosis reference
1. Gallaher JR, Charles A. Acute Cholecystitis: A Review. JAMA. 2022;327(10):965-975. doi:10.1001/jama.2022.2350
Treatment of Acute Cholecystitis
Supportive care (hydration, analgesics)
Usually antibiotics
Cholecystectomy, usually laparoscopic
Management includes hospital admission, IV fluids, and analgesics (eg, a nonsteroidal anti-inflammatory drug ([NSAID] such as ketorolac or an 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 in cases of mild acute cholecystitis (Management includes hospital admission, IV fluids, and analgesics (eg, a nonsteroidal anti-inflammatory drug ([NSAID] such as ketorolac or an 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 in cases of mild acute cholecystitis (1). Empiric coverage, directed at gram-negative enteric organisms, involves IV regimens such as ampicillin/sulbactam or piperacillin/tazobactam (). Empiric coverage, directed at gram-negative enteric organisms, involves IV regimens such as ampicillin/sulbactam or piperacillin/tazobactam (2).
While resolution without surgery can occur, early cholecystectomy is favored over conservative management given the relatively high rates of complication and recurrence. Cholecystectomy cures acute cholecystitis and relieves biliary pain. Cholecystectomy for both calculous and acalculous cholecystitis is recommended within 7 days of hospital admission and within 10 days of the onset of symptoms (1). Multiple studies demonstrate benefit if cholecystectomy is performed during the first 24 to 48 hours in the following situations (2):
The diagnosis is clear and patients are at low surgical risk.
Patients are older or have diabetes and are thus at higher risk of infectious complications.
Patients have empyema, gangrene, perforation, or acalculous cholecystitis.
Surgery may be delayed when patients have an underlying severe chronic disorder (eg, cardiopulmonary disease or severe liver disease) that increases surgical risks (1, 2). In such patients, cholecystectomy is deferred until medical therapy stabilizes the comorbid disorders or until cholecystitis resolves. If cholecystitis resolves, cholecystectomy may be performed ≥ 6 weeks later. Delayed surgery carries the risk of recurrent biliary complications. Early cholecystectomy is generally favored for patients > 80 years old, pregnant patients, and patients with cirrhosis.
Cholecystectomy is usually performed laparoscopically, although open cholecystectomy may be performed in cases of technical difficulty or severe inflammation (1).
Percutaneous cholecystostomy is an alternative to cholecystectomy for patients at very high surgical risk, such as those who are older, those with acalculous cholecystitis, those with severe liver disease, and those in an intensive care unit because of burns, trauma, or respiratory failure.
Treatment references
1. Pisano M, Allievi N, Gurusamy K, et al. 2020 World Society of Emergency Surgery updated guidelines for the diagnosis and treatment of acute calculus cholecystitis. World J Emerg Surg. 2020;15(1):61. doi:10.1186/s13017-020-00336-x
2. Gallaher JR, Charles A. Acute Cholecystitis: A Review. JAMA. 2022;327(10):965-975. doi:10.1001/jama.2022.2350
Key Points
Most (≥ 90%) 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 ultrasound and, if results are equivocal, cholescintigraphy.
Treat patients with IV fluids, antibiotics, and analgesics; favor early cholecystectomy when patients are stable.
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