🪨 Choledocholithiasis Stone Risk & Composition Simulator

Gallbladder Stones Present

Cholesterol or pigment stones crystallize inside the gallbladder lumen.

• 10–15%: Prevalence (of adults carry stones)
• 80%: Cholesterol stones (share of all gallstones)
• 20%: Pigment stones (bilirubin calcium salts)
• 80%: Asymptomatic (stay silent for years)

Stone formation

Supersaturated bile precipitates cholesterol crystals into stones.

Stones under 5mm carry the highest migration risk.

Composition matters

Cholesterol, pigment, or mixed stones affect passage and imaging.

Risk factors

Obesity, rapid weight loss, and female sex raise stone risk.

Cystic Duct Passage

Small stones squeeze through the narrow, valved cystic duct.

• 1–5mm: Duct diameter (typical cystic duct width)
• <5mm: Passable size (usually clears the duct)
• 2–4cm: Duct length (spiral valves of Heister)
• 70%: Biliary colic (of passing-stone cases)

Spiral valves

Valves of Heister slow but do not block small stones.

Size threshold

Stones near duct diameter risk impaction at the neck.

Duct width, not stone count, decides passage success.

Colic symptoms

Cystic duct spasm causes sudden right-upper-quadrant pain.

Common Bile Duct Migration

A stone that clears the cystic duct enters the CBD.

• 6–8mm: CBD diameter (wider than cystic duct)
• 10–15%: Choledocholithiasis (of gallstone patients)
• ~50%: Silent passage (reach duodenum unnoticed)
• 10%: Recurrence (after duct clearance)

Wider channel

The common bile duct is roomier than the cystic duct.

Transient stones

Many stones pass through into the duodenum without symptoms.

A wide CBD does not guarantee passage past the papilla.

Imaging clues

MRCP or endoscopic ultrasound best detects ductal stones.

Ductal Obstruction

An oversized stone lodges and blocks bile outflow completely.

• 100%: Complete block (bile flow at lodge site)
• 24–48h: Jaundice onset (after full obstruction)
• up to 30%: Cholangitis risk (if untreated)
• ~15%: Pancreatitis risk (stone impacted at papilla)

Impaction site

Stones most often lodge at the distal CBD or papilla.

Upstream pressure

Bile backs up, dilating ducts above the obstruction.

Obstruction risk rises once stone size exceeds duct diameter.

Infection danger

Stagnant bile invites bacterial ascending cholangitis.

Cholestasis Markers Elevated

Bilirubin, alkaline phosphatase, and GGT rise in blood tests.

• >2 mg/dL: Bilirubin threshold (visible jaundice appears)
• 3–10×: ALP elevation (above upper normal limit)
• up to 10×: GGT elevation (confirms hepatic origin)
• >90%: ERCP success (stone extraction rate)

Bilirubin rise

Conjugated bilirubin climbs first, causing jaundice and dark urine.

ALP and GGT

Both enzymes surge from bile duct epithelium under pressure.

GGT confirms ALP elevation is hepatic, not bone, in origin.

Treatment path

ERCP with sphincterotomy clears most obstructing bile duct stones.