Choledocholithiasis

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Basics

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

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