Cholelithiasis Choledocholithiasis
definitio gallstones in the gallbladder
n
Etiology:  Imbalance of bile salts, lecithin (stabilizer),
diluted substances (cholesterol, calcium
carbonate, bilirubin) and gallbladder stasis
 Risk factors
 Obesity
 Female sex, especially among those
receiving estrogen therapy
 Multiparity or pregnancy
 Age (> 40 years of age)
 European, Native American, or Hispanic
ancestry
 Family history
 Chronic hemolytic anemias (associated
with pigmented stones)
Rule of the 6 Fs: Fat, Female, Fertile, Forty, Fair-
skinned, Family history
Clinical  Only 25% of patients with gallstones have
features symptoms!
 Biliary colic (colicky RUQ pain)
 Especially postprandial
 May radiate to the epigastrium, right
shoulder, and back (referred pain)
 Nausea, vomiting, feelings of satiety
 Bloating, dyspepsia
Patof  Abnormal hepatic cholesterol
metabolism → ↑ cholesterol concentration
in bile + ↓ bile saltsand lecithin →
 Hypersaturated bile → biliary sludge
→ cholesterol stones or mixed
stones (most common, accounting for 80%
of all stones)
 Bile acids malabsorption (e.g., Crohn's
disease, cystic fibrosis)
→ cholesterol precipitation
 During pregnancy
 Increased estrogen levels → increased
secretion of lithogenic bile (rich
in cholesterol) → sludge and formation
Cholecystitis
Stones in the common bile duct
 Primary choledocholithiasis (less
common): conditions predisposing
to bile stasis (e.g., cystic fibrosis)
 Secondary choledocholithiasis: history
of cholelithiasis, though patients remain at
risk
of choledocholithiasis postcholecystectomy
 Colicky RUQ/epigastric pain
 Nausea, vomiting
 Extrahepatic cholestasis
 Obstructive jaundice, pale stool,
dark urine
 Pruritus with obstruction of gallbladder
drainage
 If complicated, may present
with pancreatitis and acute cholangitis
 Primary choledocholithiasis: conditions
causing cholestasis (e.g., prolonged total
parenteral nutrition, cystic fibrosis) →
intraductal stone formation
 Secondary choledocholithiasis (most
frequent): cholelithiasis → passage of
gallstones into the common bile
duct → common bile duct obstruction →
spasm of the biliary tracts
Inflammation of the gall bladder
Due to obstructing cholelithiasis: 90%
of cases, with secondary bacterial infection
(E. coli, Klebsiella, Enterobacter
A sterile inflammatory reaction ensues after
gallbladder outflow obstruction due to
gallstones (inflammatory mediators
released). Bowel pathogens infiltrate
the bileducts during the course of infection
and result in a local bacterial infection.
 RUQ pain
 More severe and prolonged (> 6
hours) than in cholelithiasis
 Worse after meals
 Radiation to the right scapula
 Guarding
 Positive Murphy's
sign describes sudden inspiratory
arrest during RUQ palpation.
 Fever, malaise
 Nausea and vomiting
 Cholelithiasis → passage of
gallstones into the cystic
duct → cystic duct obstruction →
distention and inflammation of the
gallbladder
 → superinfection
→ emphysematous cholecystitis
 of cholesterol gallstones
 Increased progesterone levels → smooth
muscle relaxation, decreased and impaired
gallblader contraction → bile stasis →
formation of gallstones
 Gallbladder hypomotility & bowel rest (e.g.,
prolonged total parenteral nutrition)
→ bile stasis
 Other stone types, caused by precipitation
of different substances:
 Black pigment stones (calcium
bilirubinate): 10% of all stones
 ↑ Hemolysis (e.g., chronic hemolytic
anemias, cirrhosis) → supersaturation
of bilirubin → bilirubin precipitation and
stone formation
 Brown pigment stones (mixed): 10% of all
stones
 Calcium carbonate stones (caused by
bacteria, biliary parasites such
as Clonorchis
sinensisand Opisthorcus species, and
stasis

Diagnose  Best initial test: ultrasonography  Approach: conduct laboratory tests and  Ultrasonography
 Shows gallstones with posterior transabdominal ultrasound to determine  Enlargement of the
acoustic shadow, possible risk of choledocholithiasis → further gallbladder
sludge confirmatory imaging if necessary (i.e.,  Wall thickening > 4
 Endoscopic ultrasound (EUS) of intermediate or low risk) mm (postprandial > 5 mm)
the bile ducts to exclude choledocholithiasis  Laboratory tests  Double wall sign
 Gastroscopy: exclude other etiologies of  Signs  Possible free fluid
abdominal pain of cholestasis: ↑ ALP, ↑ GGT, ↑ surrounding the gallbladder
total and ↑ direct bilirubin  Sonographic Murphy's sign
 Synthetic liver function  Presence
tests: ↑ AST, ALT of concrement or gallstone
 Possibly pancreatic inflammation: s in 90% of cases
↑ lipase, ↑ amylase  99mTc-hepatic iminodiacetic acid
 Imaging (HIDA) scan (cholescintigraphy)
 Transabdominal ultrasonograph  Perform if US is not
y diagnostic
 Dilated common bile  Procedure: radioactive tracer
duct with possible IV HIDA is injected →
intrahepatic biliary selective uptake
dilatation by hepatocytes →
 Depending on the location, subsequent excretion
the occluding stone may into bile → can be visualized
be visualized via a gamma camera
 Confirmatory diagnosis  Abnormal if gallbladder not
 If high risk
of choledocholithiasis → E
RCP (see “Treatment”
below)
 If intermediate risk
→ magnetic resonance
cholangiopancreatography
(MRCP) or EUS
 If low risk → treatment if
evidence
of cholelithiasis (no further
imaging)
visualized within 30–60
minutes: suggests cystic
duct obstructiondue
to edema or obstructing
stone
 CT scan: may be performed when
US is not diagnostic Finidings similar
to US would be seen. Gallstones
may be missed on CT scan.
 Laboratory tests
 Elevated inflammatory
markers (especially leukocyt
es and CRP)
 ↑ ALP, ↑ GGT,
possible ↑ AST & ↑ ALT