Uncomplicated Gallstone Diseases

Be aware that gallstone disease can present as ANY of the following:

Condition	Pathophysiology	Clinical and biochemical manifestations	Key investigations	Management
Cholelithiasis	Presence of gallbladder stone/s	Asymptomatic, or Biliary colic	Ultrasound Normal WCC and CRP	Elective laparoscopic cholecystectomy if symptomatic
Choledocholithiasis	Presence of common bile duct stone	Obstructive jaundice Abdominal pain	Ultrasound Deranged LFT (cholestatic pattern) Normal WCC and CRP	Bile duct clearance + laparoscopic cholecystectomy
Acute cholecystitis	Persistent cystic duct obstruction → gallbladder inflammation	RUQ pain Murphy’s sign +ve Fever	Ultrasound ↑ WCC and CRP Normal / mildly deranged LFT (no cholestasis)	IV fluids + antibiotics → early laparoscopic cholecystectomy
Acute cholangitis	Common bile duct obstruction → ascending bacterial infection	Charcot’s triad: RUQ pain Fever Jaundice	MRCP ↑ WCC and CRP Deranged LFT (cholestatic pattern)	IV antibiotics + urgent ERCP
Gallstone pancreatitis	Stone impacts at ampulla of Vater → pancreatic duct obstruction → pancreatitis	Epigastric pain radiating to the back Nausea and vomiting	Ultrasound ↑ Amylase / lipase Deranged LFT (cholestatic pattern)	Supportive (IV fluids, analgesia, optimise nutrition) → cholecystectomy after recovery

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Gallstones are precipitated bile components. There are 3 main types, depending on their composition:

• Cholesterol stones (crystal precipitation) (~80%)
  • Mostly radiolucent
• Pigmented stones (contain calcium bilirubinate, due to excess unconjugated bilirubin) (~10%)
  • Radiopaque
• Mixed stones (~10%)

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Risk factors for gallstone formation can be divided according to the composition of the gallstone ^[Ref]

Cholesterol gallstone (most common)

5 Fs Female (oestrogen increases cholesterol secretion in bile) Fat (obesity / metabolic syndrome) Forty (middle-aged) Fertile (pregnancy / oestrogen therapy – due to state of increased oestrogen) Fair skin (caucasian ethnicity)   Other risk factors Ileal disease (e.g. Crohn’s disease) or ileal resection Normal physiology: 95% of bile acids are reabsorbed in the terminal ileum, and return to the liver via the enterohepatic circulation to maintain a stable bile acid pool In Crohn's disease / post-ileal resection, there is reduced bile acid reabsorption → ↓ bile acid concentration in bile → bile becomes more concentrated with cholesterol, precipitating cholesterol stone formation.  Cirrhosis (due to ↓ bile acid synthesis → ↑ relative cholesterol secretion) Drugs Oestrogen-containing drugs (e.g. COCPCombined oral contraceptive pill, HRTHormone replacement therapy) Fibrates GLP-1 agonists (e.g. liraglutide)

Pigmented gallstone

Causes of chronic haemolysis Sickle cell disease Hereditary spherocytosis Other causes of haemolytic anaemia Other causes Cirrhosis Chronic biliary tract infection or stasis

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Clinical presentation spectrum: ^[Ref]

• Asymptomatic – most common (~80% cases are discovered incidentally on imaging)
• If symptomatic → biliary colic

 

Biliary colic presents as episodic postprandial abdominal pain

Biliary colic is typically experienced after eating, because food intake (especially fatty foods) stimulates the release of cholecystokinin (CCK), which stimulates the gallbladder to contract

(NB biliary colic is NOT exclusively postprandial, it can also occur at night): ^[Ref]

• Constant dull RUQ / epigastric pain (contrary to its name, the pain is usually constant instead of colicky)
• May radiate to the right shoulder / scapula
• Typically worse after fatty meals
• The pain characteristically resolves spontaneously within 5 hours (if persisting >5 hours, complications such as acute cholecystitis OR choledocholithiasis are more likely)

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1st line and gold standard: ultrasound

• Direct visualisation of the stone: echogenic (bright) foci within the gallbladder lumen that produce posterior acoustic shadowing
• Normal gallbladder thickness confirms uncomplicated cholelithiasis

  Increased wall thickness (>3 mm) is associated with acute or chronic cholecystitis and raises suspicion for complicated disease or premalignant changes.

  Additional imaging findings pointing towards complicated disease include pericholecystic fluid, mural striation, and increased wall enhancement.

 

Laboratory test findings:

• Normal WCC, CRP and bilirubin level (as there is NO inflammation and NO cholestasis)
• LFTs are typically normal, or a transient mild elevation in AST and ALT

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Choledocholithiasis typically presents with: ^[Ref1][Ref2]

• Signs of obstructive cholestasis
  • Jaundice
  • Pale stools and dark urine
• RUQ / upper abdominal pain
  • Pain lasting >5 hours (unlike in biliary colic from cholelithiasis, which resolves after 1-5 hours)
  • May radiate to the back
• +/- Nausea, vomiting, anorexia

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1st line test:

• Ultrasound
  • Dilated common bile duct (>6mm) + direct visualisation of the stone (echogenic [bright] foci within the common bile duct lumen that produce posterior acoustic shadowing)
  • NB that a dilated common bile duct alone is NOT diagnostic, further testing is necessary, see below
• LFTs
  • Cholestatic pattern (↑↑ ALP and bilirubin) is classic
  • AST and ALT are typically normal or mildly elevated

 

Further tests:

• If ultrasound fails to detect stones but the bile duct is dilated and/or abnormal LFTs → consider MRCP
• If MRCP failed to establish a diagnosis → consider endoscopic ultrasound

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All patients (both symptomatic and asymptomatic) should be offered intervention:

• Bile duct clearance (surgically or ERCP), and
• Laparoscopic cholecystectomy

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