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Basic Information ⬇

Author: Fred F. Ferri, MD

Definition

Cholecystitis is acute or chronic inflammation of the gallbladder generally caused by gallstones (>95% of cases).

Synonyms

  • Gallbladder attack
  • Biliary colic
ICD-10CM CODES
K81.9Acute cholecystitis
K80.00Calculus of gallbladder with acute cholecystitis without obstruction
K81.9Cholecystitis, unspecified
Epidemiology & Demographics

  • •Acute cholecystitis occurs most commonly in women during the fifth and sixth decades. Approximately 120,000 cholecystectomies are performed for acute cholecystitis annually in the U.S.
  • •The incidence of gallstones is 0.6% in the general population and much higher in certain ethnic groups (>75% of Native Americans by age 60 yr). Most patients with gallstones are asymptomatic. Of such patients, biliary colic develops in 1% to 4% annually.
Physical Findings & Clinical Presentation

  • •Pain and tenderness in the right hypochondrium or epigastrium; pain possibly radiating to the infrascapular region
  • •Palpation of the right upper quadrant eliciting marked tenderness and stoppage of inspired breath (Murphy sign)
  • •Guarding
  • •Fever (33%)
  • •Jaundice (25% to 50% of patients)
  • •Palpable gallbladder (20% of cases)
  • •Nausea and vomiting (>70% of patients)
  • •Fever and chills (>25% of patients)
  • •Medical history often revealing ingestion of large, fatty meals before onset of pain in the epigastrium and right upper quadrant
Etiology

  • •Gallstones (>95% of cases). Factors contributing to gallstone formation are illustrated in Fig. E1
  • •Ischemic damage to the gallbladder, critically ill patient (acalculous cholecystitis)
  • •Infectious agents, especially in patients with AIDS (cytomegalovirus, Cryptosporidium)
  • •Strictures of the bile duct
  • •Neoplasms, primary or metastatic
  • •Risk factors for cholelithiasis include age, obesity, female sex, rapid weight loss, ethnicity/race (Native American), use of contraceptives, pregnancy, diabetes mellitus, use of glucagon-like peptide-1 (GLP-1) receptor agonists,1 hemolysis, total parenteral nutrition, biliary parasites

Figure E1 Five Primary Defects Work Together to Promote Formation of Cholesterol Gallstones

The five defects are genetic factors and LITH (gallstone) genes, hepatic hypersecretion of cholesterol, gallbladder hypomotility, rapid phase transitions, and intestinal factors. The hypothesis proposed is that hepatic hypersecretion of biliary cholesterol is the primary defect and is the outcome, in part, of a complex genetic predisposition. Downstream effects include gallbladder hypomotility and rapid phase transitions. A major result of gallbladder hypomotility is alteration in the kinetics of the enterohepatic circulation of bile salts (intestinal factors). Alterations in intestinal factors result in increased cholesterol absorption, as well as reduced bile salt absorption, that leads to abnormal enterohepatic circulation of bile salts and a diminished biliary bile salt pool size. Not only does gallbladder hypomotility facilitate cholesterol nucleation and crystallization, but it also allows the gallbladder to retain solid platelike cholesterol monohydrate crystals. Although a large number of candidate LITH genes have been identified in mouse models and many human LITH genes have been discovered, their contributions to gallstone pathogenesis require further investigation.

(From Feldman M et al: Sleisenger and Fordtran’s gastrointestinal and liver disease, ed 11, Philadelphia, 2021, Elsevier.)

Diagnosis ⬆ ⬇

Differential Diagnosis

  • •Hepatic: Hepatitis, abscess, hepatic congestion, neoplasm, trauma
  • •Biliary: Neoplasm, stricture, sphincter of Oddi dysfunction
  • •Gastric: Pelvic ulcer disease, neoplasm, alcoholic gastritis, hiatal hernia, nonulcer dyspepsia
  • •Pancreatic: Pancreatitis, neoplasm, stone in the pancreatic duct or ampulla
  • •Renal: Calculi, infection, inflammation, neoplasm, ruptured kidney
  • •Pulmonary: Pneumonia, pulmonary infarction, right-sided pleurisy
  • •Intestinal: Retrocecal appendicitis, intestinal obstruction, high fecal impaction, irritable bowel syndrome (IBS), inflammatory bowel disease (IBD)
  • •Cardiac: Myocardial ischemia (particularly involving the inferior wall), pericarditis
  • •Cutaneous: Herpes zoster
  • •Trauma
  • •Fitz-Hugh-Curtis syndrome (perihepatitis), ruptured ectopic pregnancy
  • •Subphrenic abscess
  • •Dissecting aneurysm
  • •Nerve root irritation caused by osteoarthritis of the spine
Workup

Workup consists of detailed history and physical examination coupled with laboratory evaluation and imaging studies. No single clinical finding or laboratory test is sufficient to establish or exclude cholecystitis without further testing. Acute acalculous cholecystitis is acute inflammation of the gallbladder in the absence of stones. The term acalculous cholecystitis has been questioned as incorrectly suggesting that the disease is simply cholecystitis without stones. Instead, the term necrotizing cholecystitis has been proposed to reflect the distinct etiology, pathology, and prognosis of the disease. The symptoms of acalculous biliary pain may be indistinguishable from those of cholelithiasis. For older adult patients at risk, a high index of suspicion for biliary tract sepsis is the best hope for early recognition and treatment. Table 1 delineates several diagnostic criteria for acute acalculous cholecystitis.

TABLE 1 Diagnostic Criteria for Acute Acalculous Cholecystitis

TechniqueFindings
Clinical evaluationRight upper quadrant tenderness, if present, supports the diagnosis but is lacking in 75% of cases
Unexplained fever, hypotension, leukocytosis, or hyperamylasemia is frequently the only finding
USThickened gallbladder wall (>4 mm) in the absence of ascites and hypoalbuminemia (serum albumin<3.2 g/dl)
Sonographic Murphy sign (maximum tenderness over the US-localized gallbladder)
Pericholecystic fluid collection
Bedside availability is a major advantage
CTThickened gallbladder wall (>4 mm) in the absence of ascites and hypoalbuminemia
Pericholecystic fluid, subserosal edema (in the absence of ascites), intramural gas, or sloughed mucosa
The best test for excluding other intraabdominal diseases but requires moving the patient to a scanner
Hepatobiliary scintigraphyNonvisualization of the gallbladder with normal excretion of radionuclide into the bile duct and duodenum indicates a positive result for acute cholecystitis
Results in critically ill, immobilized patients may be falsely positive because of viscous bile
Better at excluding than confirming acute cholecystitis

CT, Computed tomography; US, ultrasound.

From Feldman M et al: Sleisenger and Fordtran’s gastrointestinal and liver disease, ed 11, Philadelphia, 2021, Elsevier.

Laboratory Tests

  • •Leukocytosis (12,000 to 20,000) is present in >70% of patients.
  • •Elevated alkaline phosphatase, ALT, AST, bilirubin; bilirubin elevation >4 mg/dl is unusual and suggests presence of choledocholithiasis.
  • •Elevated amylase may be present (consider pancreatitis if serum amylase elevation exceeds 500 U).
Imaging Studies

  • •Ultrasound of the gallbladder (Figs. 2 and E3) is the preferred initial test; it will demonstrate the presence of stones and also dilated gallbladder with thickened wall and surrounding edema in patients with acute cholecystitis.
  • •Nuclear imaging (HIDA scan) (Fig. E4) is useful for diagnosis of cholecystitis when sonogram is inconclusive: Sensitivity and specificity exceed 90% for acute cholecystitis. This test is only reliable when bilirubin is <5 mg/dl. A positive test result (absence of gallbladder filling within 60 min after the administration of tracer) will demonstrate obstruction of the cystic or common hepatic duct; the test will not demonstrate the presence of stones.
  • •Computed tomography (CT) scan of abdomen (Fig. E5) is useful in cases of suspected abscess, neoplasm, or pancreatitis.
  • •Plain radiograph of the abdomen generally is not useful because <25% of stones are radiopaque.

Figure 2 Thickened gallbladder wall in acute cholecystitis.

The gallbladder contains echogenic calculi.

(From Grainger RG et al [eds]: Grainger and Allison’s diagnostic radiology, ed 4, Philadelphia, 2001, Churchill Livingstone.)

Figure E3 Ultrasound image of a gallbladder with acute acalculous cholecystitis.

The diffusely thickened gallbladder wall (arrows) is highly suggestive of cholecystitis.

(From Townsend CM et al: Sabiston textbook of surgery, ed 21, St Louis, 2022, Elsevier.)

Figure E4 Hepatic iminodiacetic acid (HIDA) scan showing nonfilling of the gallbladder.

With no filling of the gallbladder (arrows) even on delayed images, HIDA confirms occlusion of the cystic duct, the characteristic feature of acute cholecystitis.

(From Townsend CM et al: Sabiston textbook of surgery, ed 21, St Louis, 2022, Elsevier.)

Figure E5 Computed Tomography Scan Showing Dilated Biliary Tree (Arrow) at the Portal Confluence

This dilation continued down to the head of the pancreas and is suggestive of possible neoplastic process.

(Modified from Townsend CM et al: Sabiston textbook of surgery, ed 21, St Louis, 2022, Elsevier.)

Treatment ⬆ ⬇

Nonpharmacologic Therapy

Provide intravenous (IV) hydration; withhold oral feedings.

Acute General Rx

  • •Laparoscopic (percutaneous) cholecystectomy (PC) is considered the treatment of choice for most patients. The rate of conversion to open cholecystectomy is higher when laparoscopic cholecystectomy (CCY) is performed for acute cholecystitis rather than for uncomplicated cholelithiasis; conservative management with IV fluids and antibiotics (ampicillin-sulbactam 3 g IV q6h or piperacillin-tazobactam 4.5 g IV q8h) may be justified in some high-risk patients to convert an emergency procedure into an elective one with a lower mortality rate.
  • •Endoscopic retrograde cholangiopancreatography with sphincterotomy and stone extraction can be performed in conjunction with laparoscopic cholecystectomy for patients with choledochal lithiasis; approximately 7% to 15% of patients with cholelithiasis also have stones in the common bile duct.
Disposition

  • •Prognosis is good; elective laparoscopic cholecystectomy can be performed as outpatient procedure.
  • •Hospital stay (when necessary) varies from overnight with laparoscopic cholecystectomy to 4 to 7 days with open cholecystectomy.
  • •Complication rate is approximately 1% (hemorrhage and bile leak) for laparoscopic cholecystectomy and <0.5% (infection) with open cholecystectomy.
Referral

Surgical referral in all patients with acute cholecystitis

Pearls & Considerations ⬆ ⬇

Comments

  • •Patients should be instructed that stones may recur in bile ducts.
  • •Gallbladder aspiration, in which all fluid visualized by ultrasound is aspirated, represents a nonsurgical treatment when patients who are at high operative risk develop acute cholecystitis. Salvage cholecystectomy is reserved for nonresponders.
Related Content

Reference(s) ⬆

  1. Woronow D : Acute cholecystitis associated with the use of glucagon-like peptide-1 receptor agonists reported to the US Food and Drug AdministrationJAMA Intern Med. 182(10):1104-1106, 2022.