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Cholelithiasis

1. CHOLECYSTOLITHIASIS

  • MC in fat, fertile, forty, flatulent, female
  • If symptomatic first line treatment is surgery.

Etiology

Pathophysiology

  • Classified into cholesterol and pigment stones (although majority are mixed composition)
  • Cholesterol stones – MC in developed countries
  • Pigment stones – MC in developing countries
  • Gallstones contain a varying amount of calcium salts – bilirubinate, carbonate, phosphate, palmitate

Cholesterol gallstones

  • Cholesterol held in solution in bile by its association with bile acids and phospholipids in the form of micelles
  • Admirand’s triangle  shows the relationship between lecithin, bile, cholesterol in stone formation.
  • Biliary lipoproteins may also have a role in solubilising cholesterol
  • In gallstone disease, the liver produces bile that contains ↑ cholesterol
    • Because there is either a relative deficiency of bile salts or a relative excess of cholesterol
      • ‘lithogenic bile’ – see box
  • Nucleation factors (which initiate crystallisation of cholesterol in lithogenic bile) determine rate at which crystals form
    • Factors favouring nucleation – mucus, calcium, fatty acids
    • Antinucleating factors – apolipoproteins

Pigment stones

  • Brown + crumbly – MC as a result of bacterial/parasitic biliary infection
  • Infection allows bacterial β-glucoronidase to hydrolyse CBR to its free form
    • Which then present as calcium bilirubinate
  • Black pigment stones – assoc with chronic haemolytic disease

Biliary sludge

  • Gelatinous bile that contains numerous microspheroliths of calcium bilirubinate and cholesterol crystals
  • Precursor to the formation of gallstones
  • Frequently formed under normal conditions, but then is dissolved/cleared by the Gallbladder (GB)
  • Fasting, parenteral nutrition, pregnancy are associated with biliary sludge

Clinical features

  • Only 10% develop sx of gallstones – biliary pain (colic) or cholecystitis
  • Biliary colic – pain occurs suddenly, persists for 2 hours. Non continuous pain.
    • MC in epigastrium of RUQ – radiates to R.scapula
    • Can mimic oesophagitis, AMI or aneurysm
  • Fatty food intolerance, dyspepsia and flatulence
    • Mucocele (hydropic GB) – if there is slow distension of the GB from continuous sec of mucus
    • Can become empyema if gets infected
    • Calcium secreted into the lumen of hydropic GB – limey GB
    • If calcium salts are precipitated in the GB wall – porcelain GB
  • Stone can migrate to the common bile duct (CBD) and cause pain
  • Fistula can develop b/w GB and duodenum/colon/stomach (rare – Mirizzi syndrome)
    • XR – air in biliary tree
    • If stone >2.5cm migrates into gut, it can impact at the terminal ileum
      • Causes intestinal obstruction – gallstone ileus (Rigler’s triad for diagnosis)
  • Stone impacts in the GB wall and compresses it – pressure necrosis which further gets adherent to CBD wall
    • Causes compression and may lead to cholecystocholedochal fistula (rare – Mirizzi syndrome)

Investigations

USS, MRCP  

LFT

Management

  • Asymptomatic gallstones found incidentally don’t need to be treated
  • Symptomatic gallstones – laparoscopic cholecystectomy
  • If surgery contra-indicated may use endoscopic retrograde cholangiopancreatography (ERCP) but higher risk of complications such as pancreatitis

2. CHOLECYSTITIS

Acute cholecystitis

Pathophysiology

  • MC in association with obstruction of the GB neck or cystic duct by gallstone
    • Obstruction can also be due to mucus, parasitic worms or bile tumour
  • Chemically induced inflammation → GB mucosal damage → release of phospholipase → converts biliary lecithin to lysolecithin (a mucosal toxin)
  • Eventually infection occurs

Clinical features

  • Pain in RUQ + epigastrium, R.shoulder, non-biliary colic (constant and progressive)
  • Difficult to differentiate between biliary colic and acute cholecystitis
    • Cholecystitic pain – more severe and prolonged pain, fever, leucocytosis
  • Murphy’s sign – pain on inspiration during deep palpation of R.hypochondrium
  • Occasional gallbladder mass
  • Jaundice (uncommon) – only when stone passes into CBD or Mirizzi syndrome

Investigations

  • Peripheral blood leucocytosis
  • Minor ^transaminases and amylase (amylase >1000U/L means pain is due to acute pancreatitis)
  • XR – radio-opaque gallstones, intrabiliary gas (due to fistula formation into intestine)
  • USS – thickened and distended gallbladder

Management

  • Medical – bed rest, analgesia (NSAIDs/opiates), ABs (cefuroxime [1.5g/8hrs]/piperacillin), IV fluids
    • Some doctors say opioids are contra-indicated
  • Surgical – urgent if empyema/perforation develop

DDx

Acute pancreatitis, AMI, cholangitis, renal failure, diabetic ketoacidosis, ectopic pregnancy

Chronic cholecystitis

  • Chronic inflam of GB nearly always associated with gallstones
  • CF – recurrent attacks of upper abdominal pain, often at night, after a heavy meal
  • Patient may recover spontaneously after analgesia and ABs
  • Patients usually advised to undergo elective laparoscopic cholecystectomy
  • Gallbladder is usually smaller and thicker
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