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Gastrointestinal · GI

Gallstones & Biliary Disease

A boards-focused walkthrough of biliary disease from lithogenic bile to next-best-step management, mapping each syndrome (colic, cholecystitis, choledocholithiasis, cholangitis, gallstone pancreatitis) to its buzzwords, labs, imaging, and definitive intervention. Emphasizes ultrasound-first workup, HIDA for equivocal cholecystitis, and ERCP for CBD stones and cholangitis.

13 min readHigh yield

Pathophysiology: lithogenic bile and where the stone lodges

Gallstones (cholelithiasis) form when bile turns lithogenic. Cholesterol stones (the majority — ~80–90% in the US) require three ingredients: cholesterol supersaturation of bile, gallbladder hypomotility/stasis, and accelerated nucleation. Pigment stones are calcium bilirubinate — black stones form in chronic hemolysis (sickle cell, hereditary spherocytosis, thalassemia) and cirrhosis; brown stones form within the ducts under stasis/infection (bacterial β-glucuronidase, Asian liver flukes such as Clonorchis).

The clinical syndrome reflects where a stone impacts:

  • Intermittent cystic-duct obstruction → biliary colic.
  • Sustained cystic-duct obstruction + inflammation → acute cholecystitis.
  • Passage into the common bile duct (CBD)choledocholithiasis, which can progress to ascending cholangitis (infection behind an obstruction) or, lodging at the ampulla, gallstone pancreatitis.

Key board point: most gallstones are asymptomatic and need no treatment.

Risk factors & stone types
  • Cholesterol-stone risk — the 5 F's: Female, Forty, Fat, Fertile, Fair. Add estrogen/OCPs, rapid weight loss or bariatric surgery, prolonged TPN, and fibrates.
  • Ileal disease/resection (Crohn's) → bile-salt malabsorption → cholesterol stones. Native American (Pima) ethnicity has the highest prevalence.
  • Black pigment stones: chronic hemolysis (sickle cell, spherocytosis, thalassemia) and cirrhosis.
  • Brown pigment stones: biliary infection/stasis, liver flukes (Clonorchis sinensis); typically intraductal.
  • X-ray visibility: only ~10–15% of stones are radiopaque (calcium); most cholesterol stones are radiolucentultrasound, not plain film, is the test.
  • Prophylactic cholecystectomy for asymptomatic stones is reserved for a porcelain gallbladder, stones >3 cm, or an anomalous pancreaticobiliary junction.
Opened gallbladder specimen containing numerous small gallstones
Opened gallbladder full of gallstones; cholesterol and mixed stones are the most common type in the US. · Wikimedia Commons — Emmanuelm at en.wikipedia (Original text : Emmanuelm (talk)) — CC BY 3.0, via Wikimedia Commons

Comparison of biliary syndromes

ConditionPain & systemic signsLabsImaging / dxNext step
Biliary colicRUQ pain <6 h after fatty meal, no feverNormalUS: stones, no wall changeElective lap chole
Acute cholecystitisRUQ pain >6 h, fever, +Murphy sign↑WBC, mild ↑LFTsUS: wall >3 mm, pericholecystic fluid; HIDA if equivocalIVF, antibiotics, early lap chole
CholedocholithiasisRUQ pain + jaundice↑ALP/GGT, ↑direct bili, CBD >6 mmUS → MRCP/EUS; ERCP if high-riskERCP extraction, then chole
Ascending cholangitisCharcot triad ± Reynolds pentad↑ALP/bili, ↑WBC, +culturesDilated CBD + stoneIVF, abx, urgent ERCP decompression
Gallstone pancreatitisEpigastric pain radiating to back↑lipase, ALT >3× ULNUS: stones ± dilated CBDSupportive; ERCP if cholangitis/obstruction; chole same admission
Vignette: equivocal ultrasound in suspected cholecystitis

Vignette: A 45-year-old obese woman has 8 hours of constant RUQ pain, fever 38.4°C, and nausea after a fatty meal. Palpation of the RUQ during inspiration causes her to catch her breath. WBC 14,000, mildly elevated ALT/AST, normal bilirubin. RUQ ultrasound shows gallstones but no wall thickening and an equivocal sonographic Murphy sign.

  • Diagnosis: Acute cholecystitis (positive Murphy sign + fever + leukocytosis).
  • Best next step when US is equivocal: HIDA scan (cholescintigraphy)non-visualization of the gallbladder confirms cystic-duct obstruction (highest sensitivity/specificity).
  • Management: NPO, IV fluids, analgesia, IV antibiotics, and early laparoscopic cholecystectomy (within ~72 h). If the patient is too unstable or a poor surgical candidate → percutaneous cholecystostomy as a bridge.
Axial right upper quadrant ultrasound showing a thickened gallbladder wall and gallstones with posterior acoustic shadowing
RUQ ultrasound is first-line: gallstones with wall thickening (>3 mm) and pericholecystic fluid suggest acute cholecystitis. · Wikimedia Commons — Cerevisae — CC BY-SA 4.0, via Wikimedia Commons
Classic triads and pentad
  • 5 F's — cholesterol-stone risk: Female, Forty, Fat, Fertile, Fair.
  • Charcot triad — ascending cholangitis: fever, jaundice, RUQ pain.
  • Reynolds pentad — suppurative cholangitis: Charcot triad + hypotension + altered mental statusemergent biliary decompression.
  • Rigler triad — gallstone ileus: pneumobilia + small-bowel obstruction + ectopic (RLQ) gallstone on imaging.
Diagnostic algorithm & choledocholithiasis risk
  • First test for any RUQ biliary complaint: transabdominal ultrasound.
  • Acute cholecystitis on US: stones, wall thickening >3 mm, pericholecystic fluid, sonographic Murphy. Equivocal → HIDA (non-visualization = positive).
  • CBD-stone (choledocholithiasis) high-risk predictors (2019 ASGE): CBD stone seen on imaging, total bilirubin >4 mg/dL with a dilated CBD, or clinical cholangitisgo straight to ERCP.
  • Intermediate risk (abnormal LFTs, age >55, or dilated CBD alone): confirm first with MRCP or EUS before committing to ERCP.
  • ERCP is therapeutic (sphincterotomy + stone extraction) and carries a post-ERCP pancreatitis risk — avoid using it purely diagnostically when MRCP/EUS suffices.
  • Cholestatic pattern (↑ALP, ↑GGT, ↑direct bilirubin) = ductal obstruction; a hepatocellular bump with ALT >3× ULN points to gallstone pancreatitis.
Vignette: fever, jaundice, and hypotension

Vignette: A 70-year-old man has RUQ pain, fever with rigors, and jaundice. BP 88/54, and he is confused. WBC 18,000, total bilirubin 6 mg/dL, ↑ALP; ultrasound shows a dilated common bile duct with a stone.

  • Diagnosis: Ascending (acute) cholangitis — Charcot triad plus hypotension and altered mentation = Reynolds pentad (suppurative).
  • Immediate management: aggressive IV fluids and broad-spectrum IV antibiotics covering enteric gram-negatives/anaerobes; ICU-level resuscitation.
  • Definitive next step: urgent/emergent biliary decompression by ERCP (sphincterotomy + stone removal). If ERCP fails or is unavailable → percutaneous transhepatic cholangiography (PTC) drainage.
  • Cholecystectomy is done after the patient stabilizes, not acutely.
Complications & special situations
  • Acalculous cholecystitis: critically ill/ICU, TPN, major trauma, burns, sepsis; no stones, high mortality → often percutaneous cholecystostomy first.
  • Porcelain gallbladder: calcified wall on imaging; associated with gallbladder adenocarcinomacholecystectomy.
  • Gallstone ileus: cholecystoenteric fistula lets a large stone impact at the ileocecal valve → SBO; look for Rigler triad.
  • Mirizzi syndrome: a stone in the cystic duct/gallbladder neck externally compresses the common hepatic duct → obstructive jaundice.
  • Gallbladder cancer: risk factors — porcelain gallbladder, large stones (>3 cm), chronic cholecystitis; usually presents late.
  • Post-cholecystectomy recurrent RUQ pain/jaundice → suspect retained CBD stone or bile leakMRCP/ERCP.

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