Choledocholithiasis

Description

• Stones in common bile duct (CBD)
• Several types: cholesterol (majority), calcium bilirubinate or pigment, and mixed stones
• System(s) affected: gastrointestinal; hepatobiliary
• Synonym(s): CBD stones; CBD calculi

Epidemiology

Incidence

• Gallstone disease affects >20 million Americans (14.2 million females, 6.3 million males).
  • Choledocholithiasis noted in 7–12% of patients undergoing cholecystectomy for symptomatic gallstones
  • Choledocholithiasis noted in 18–33% of patients with acute biliary pancreatitis
• Incidence increases with age (30–50% of patients >60 years with gallstones have concurrent CBD stones):
  • Patients with choledocholithiasis are, on average, 10 years older than those with cholelithiasis.
• Internationally, incidence is increased due to parasitic infections (e.g., Ascaris lumbricoides).
• Associated with chronic conditions such as dyslipidemia, obesity, cardiovascular disease, as well as increased risk of mortality

Prevalence

• Symptomatic gallstone disease affects 10% of the U.S. population, leading to ~700,000 cholecystectomies at an annual cost of ~$6.5 billion.
• Twice as common among women
• Increased prevalence among Hispanics, Asians, Native Americans

Etiology and Pathophysiology

• CBD stones may be primary or secondary:
  • Primary stones form within the biliary tract with bile stasis or chronic bactibilia.
  • Secondary stones (more common) form within the gallbladder and migrate to the biliary tree.
• Stones may migrate to the duodenum or remain in the CBD (due to small diameter of Vater papilla). Not all CBD stones are symptomatic.
• Obstruction leads to jaundice. Biliary stasis can trigger infection (e.g., ascending cholangitis).
• Dysfunction/obstruction of the CBD and/or main pancreatic duct can trigger acute pancreatitis.
• Chronic hemolytic states increase the risk for gallstone formation.
• Formation of de novo pigment stones can result from:
  • Dilated, sclerosed, or strictured ducts (e.g., recurrent cholangitis)
  • Hepatobiliary parasitism (A. lumbricoides or Clonorchis sinensis)

Genetics

• MDR3 defects may predispose to biliary sludge, cholelithiasis, cholestasis of pregnancy, and subsequent choledocholithiasis.
• Variants of UGT1A1 responsible for bilirubin conjugation may increase cholesterol and pigment gallstone formation.
• Hepatobiliary cholesterol hemitransporter ABCG8 variant p.D19H doubles the odds of gallstone recurrence after cholecystectomy.
• LITH genes are thought to increase susceptibility to development of gallstones. Studies in mice show this class of genes creates a lithogenic environment by altering various lipid transporters, nuclear hormone receptors, and enzymes.

Risk Factors

• Obesity; high caloric diet, low-fiber diet
• Rapid weight loss (>25% of original weight, especially after bariatric surgery) or prolonged fasting
• Gender (females > males)
• Family history
• Cirrhosis
• Crohn disease
• Gallbladder stasis: spinal cord injury, somatostatin
• Drugs (octreotide, thiazide diuretics)
• Pancreatitis
• Chronic estrogen exposure
• Prior cholecystectomy:
  • <2 years prior: Consider retained stone.
  • >2 years prior: Consider recurrent stone.

General Prevention

• Maintain healthy weight and lifestyle. Avoid rapid weight loss.
• Consider UDCA therapy in LPAC syndrome.

Commonly Associated Conditions

• Cholelithiasis, cholecystitis, cholangitis
• Gallstone pancreatitis