Gallstones (cholelithiasis) are hardened deposits of bile components that form within the gallbladder. They affect approximately 10–15% of the adult population in Western countries and are one of the most common reasons for abdominal surgery. Most gallstones cause no symptoms, but when a stone obstructs the gallbladder's outflow, inflammation of the gallbladder (cholecystitis) develops — typically causing severe right upper abdominal pain and often requiring urgent surgical treatment.
Gallstone disease sits at the center of a cluster of closely related biliary conditions. When stones migrate from the gallbladder into the common bile duct (choledocholithiasis), they can cause biliary duct obstruction with jaundice and ascending cholangitis — a potentially life-threatening infection. A gallstone lodging at the ampulla of Vater blocks both the bile duct and the pancreatic duct, triggering gallstone pancreatitis — one of the most common causes of acute pancreatitis and an important cause of pancreatic injury. MRCP (MR cholangiopancreatography) maps the entire biliary and pancreatic ductal system on a single noninvasive examination, making MRI the definitive study for evaluating the full extent of gallstone-related complications.
Causes
Bile composition imbalance.
Gallstones form when bile — a digestive fluid produced by the liver and stored in the gallbladder — loses its normal chemical equilibrium. The majority (approximately 80%) are cholesterol gallstones, which form when bile is supersaturated with cholesterol relative to the bile salts and lecithin that normally keep it dissolved. When cholesterol crystallizes, it forms a nidus for stone growth — a process that occurs over months to years. Pigment stones (20%) form from excess bilirubin, most commonly in patients with chronic hemolytic conditions (sickle cell disease, hereditary spherocytosis), cirrhosis, or biliary infections, where unconjugated bilirubin precipitates as calcium bilirubinate. Impaired gallbladder motility — from prolonged fasting, total parenteral nutrition, pregnancy, or vagal nerve injury — allows bile to become more concentrated and stagnant, promoting stone nucleation even when bile composition is relatively normal.
Other risk factors.
The classic risk factor mnemonic is the "5 Fs" — Female, Forty, Fertile, Fat, and Family history. Women have twice the gallstone risk as men, driven by the effects of estrogen (which increases biliary cholesterol secretion) and progesterone (which reduces gallbladder motility). Pregnancy significantly accelerates stone formation through both mechanisms simultaneously. Obesity increases biliary cholesterol secretion. Rapid weight loss — including after bariatric surgery — causes massive mobilization of cholesterol from adipose tissue into bile. Diabetes mellitus impairs gallbladder contractility. Crohn disease of the terminal ileum impairs bile salt reabsorption, depleting the bile salt pool and leaving cholesterol relatively supersaturated. Certain medications including estrogen therapy, octreotide (which inhibits cholecystokinin release), and ceftriaxone (which precipitates in bile) increase stone risk.
Symptoms
Approximately 80% of gallstones are entirely asymptomatic throughout a person's lifetime and are found incidentally on imaging performed for an unrelated reason. The first symptomatic event — biliary colic — occurs when a stone transiently obstructs the cystic duct during gallbladder contraction after a fatty meal: the patient experiences a sudden, severe, crampy or steady pain in the right upper quadrant or epigastrium that typically builds to a plateau over 30–60 minutes, lasts 1–4 hours, and then resolves as the stone falls back from the cystic duct opening. Pain frequently radiates to the right shoulder or interscapular area via diaphragmatic irritation. Nausea and vomiting accompany most episodes. Importantly, biliary colic resolves completely between episodes — persistent right upper quadrant pain suggests progression to cholecystitis.
Acute cholecystitis develops when a stone becomes persistently impacted in the cystic duct — the gallbladder wall becomes inflamed, edematous, and ultimately infected. Pain is severe, constant, and associated with fever, leukocytosis, and a positive Murphy's sign (sharp inspiratory catch when the examiner's hand contacts the inflamed gallbladder during deep inspiration). Jaundice signals that a stone has migrated into the common bile duct, causing biliary duct obstruction — this requires urgent endoscopic intervention.
Diagnosis
Ultrasound is the standard first-line imaging test for suspected gallstone disease, with over 95% sensitivity for gallstones within the gallbladder. Gallstones appear as echogenic foci with acoustic shadowing. Signs of acute cholecystitis on ultrasound include gallbladder wall thickening (greater than 3–4 mm), pericholecystic fluid, and a sonographic Murphy's sign. Blood tests assess for leukocytosis (suggesting infection), elevated bilirubin (suggesting bile duct obstruction), elevated transaminases (hepatocellular injury from bile duct stone), and elevated lipase (gallstone pancreatitis).
An MRI of the abdomen with MRCP (magnetic resonance cholangiopancreatography) is the most comprehensive noninvasive evaluation of the biliary system and provides the definitive anatomic roadmap for complex gallstone disease. MRCP acquires heavily T2-weighted images in which bile appears bright — creating a "cast" of the entire biliary and pancreatic ductal tree without contrast or radiation. Gallstones within the common bile duct appear as dark (T2-hypointense) filling defects within the bright bile — MRCP is more accurate than CT (which often misses isodense soft stones) and avoids the procedural risks of diagnostic ERCP. MRI also characterizes gallbladder wall involvement, identifies gallbladder perforation or pericholecystic abscess in complicated cholecystitis, detects Mirizzi syndrome (a large cystic duct stone compressing the common hepatic duct), evaluates for gallbladder carcinoma when the gallbladder wall is irregularly thickened, and assesses for associated pancreatic injury in gallstone pancreatitis.
Classification
Gallstone-related disease is classified by the location of the stones and the severity of associated complications.
- Asymptomatic cholelithiasis: Gallstones without symptoms. Annual risk of developing symptoms is approximately 1–2%. Observation without prophylactic surgery is standard; exceptions include patients with porcelain gallbladder or a very large single stone.
- Symptomatic cholelithiasis (biliary colic): Recurrent pain episodes from transient cystic duct obstruction. Cholecystectomy is recommended to prevent progression to acute cholecystitis or stone migration.
- Acute cholecystitis: Persistent cystic duct obstruction with gallbladder wall inflammation and infection. Tokyo Guidelines grade I (mild), II (moderate with organ dysfunction), III (severe with single organ failure) guide timing of surgery and need for ICU support.
- Chronic cholecystitis: Repeated episodes producing a scarred, fibrotic, contracted gallbladder. Often asymptomatic between episodes but cholecystectomy is indicated.
- Choledocholithiasis: Stones within the common bile duct, causing jaundice, cholangitis, or pancreatitis. Requires ERCP for stone removal, followed by cholecystectomy.
- Gallstone pancreatitis: Gallstone obstruction at the ampulla of Vater triggering acute pancreatitis. Severity ranges from mild (self-limiting) to severe (necrotizing pancreatitis). ERCP within 24–48 hours for concurrent cholangitis; cholecystectomy before discharge in mild cases.
- Acalculous cholecystitis: Gallbladder inflammation without stones, most common in critically ill, fasting, or post-surgical patients. Treated with percutaneous cholecystostomy drainage in patients too unstable for surgery.
Treatments
Treatment depends on symptom severity, stone location, and the presence of complications.
Observation for asymptomatic gallstones: Asymptomatic gallstones do not require prophylactic surgery — the annual complication risk (1–2%) does not justify the operative risk for most patients. Exceptions include patients scheduled for bariatric surgery (where post-operative stone migration risk is elevated), immunocompromised patients (where cholecystitis may present atypically), and those with a porcelain gallbladder (associated with gallbladder carcinoma in some series) or a single stone larger than 3 cm.
Laparoscopic cholecystectomy.
Surgical removal of the gallbladder is the definitive treatment for symptomatic gallstones and acute cholecystitis. Laparoscopic cholecystectomy — performed through four small incisions with excellent visualization — is the gold standard, with a complication rate under 1% and typical hospital stay of less than 24 hours. Early laparoscopic cholecystectomy within 24–72 hours of presentation for acute cholecystitis produces better outcomes than delayed surgery and is now the standard recommendation at most centers. The bile duct is routinely imaged intraoperatively (intraoperative cholangiography) to identify unsuspected bile duct stones.
ERCP for bile duct stones.
Endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy is the standard treatment for choledocholithiasis — the endoscopist passes a scope through the mouth into the duodenum, cannulates the common bile duct, cuts the sphincter of Oddi, and extracts the stones with a balloon or basket catheter. ERCP is followed by laparoscopic cholecystectomy (to remove the stone source) once the patient has recovered. For patients with concurrent cholangitis, ERCP within 24–48 hours is urgent.
Management of acute cholecystitis.
Hospitalization, IV hydration, bowel rest, and intravenous antibiotics covering gram-negative enteric organisms (ceftriaxone, piperacillin-tazobactam, or carbapenems for severe cases) stabilize the patient. Early laparoscopic cholecystectomy within 24–72 hours is preferred for grade I and II cholecystitis. For grade III (severe) cholecystitis or patients too medically unstable for surgery, percutaneous cholecystostomy — ultrasound or CT-guided drainage tube placement into the gallbladder — decompresses the infected organ until definitive surgery can be safely performed.
Prevention.
Gradual rather than rapid weight loss, a diet rich in fiber, unsaturated fats, and coffee (which reduces biliary cholesterol saturation), regular physical activity, and ursodeoxycholic acid (UDCA) prophylaxis during rapid weight loss programs reduce gallstone formation risk. UDCA is routinely prescribed for 6 months following bariatric surgery.
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