GALL BLADDER STONES by greendramaqueen

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Bryan Bernard U. Ong Kian Koc MD
       Jocelyn M. Lledo MD
   Male: 8 %

   Female: 17%
Predisposing factors
   Obesity
   Multiparity
   DM
   Cirrhosis
   Pancreatitis
   Chronic hemolytic states
   Malabsorption
   Inflammatory bowel disease
   Racial/ genetic factors(Blacks/ Indians)
   Bile salts
    – primary- cholic,
    – secondary-
      deoxycholic and
      lithocholic acids
 Phospholipids (90%
 Cholesterol
1.       MIXED (80%)
         Most common, multiple
         Cholesterol, predominates(70%)
         15-20 % may calcify, becoming radio opaque

2.       PURE CHOLESTEROL (10%)
         Solitary , with large round configuration
         Usually not calcified
3. PIGMENT (10%)
 Unconjugated bilirubin, calcium and variable
    amounts of organic material
 50% radioopaque
 Black pigment stones are associated with
    cirrhosis and chronic hemolytic states
 Bile usually sterile and choledocholithiasis
 Ca bilirubinate stones- more frequently in CBD;
    associated with bile stasis
 80%- asymptomatic
 Yearly around 2 % with asymptomatic
  stones develop symptoms most commonly
  biliary colic
 Incidence of development of symptoms in
  patients with asymptomatic stones 15-30 %
  over 15 years
 Elective cholecystectomy
Biliary Colic
   Pain arising from the GB without
    established infection
   Etiology
    –   Due to transient gallstone obstruction of the
        cystic duct
   Clinical History: moderate intermittent
    RUQ pain
    – pain may radiate to the back or below the
    – pain begins abruptly and subsides gradually
      lasting from minutes to hours
    – pain of biliary colic usually steady
   Physical Exam
    – No associated fever
    – some mild epigastric pain or RUQ tenderness
      or palpable GB
Differential diagnosis
 Pancreatitis
 Hiatal hernia with reflux
 Gastritis
 Hepatic flexure carcinoma
 Hepatobiliary carcinoma
 Cardiopulmonary disease
   Prolonged cystic duct obstruction may
    allow bacterial growth and progress to acute

   Stones may pass into CBD with consequent
    obstruction or pancreatitis
   Lab findings
    – None are diagnostic
    – Liver function test, amylase and WBC count
    – Elevation of alkaline phosphatase common in
      biliary disease but non specific
    – 10-15 % of gallstones are radio opaque and
      may be detected on plain film of the abdomen
   Ultrasound
    – Diagnostic procedure of choice
    – Identifies stones, wall thickness, presence of
      masses, ductal dilatation, fluid collections
    – Technical difficulties
    – Sensitivity and specificity of 95%
   Cholecystectomy
    – Definitive treatment
    – Early (2-3 days of the illness) rather than
      delayed/interval cholecystectomy
    – Prophylactic cholecystectomy: diabetics, non
      functioning GB, calcified/ porcelain GB, biliary
Symptomatic Gallstones
   Chronic Cholecystitis
          Two-thirds of patients characterized by recurrent
           attacks of pain, often inaccurately labeled biliary
          Pain develops when a stone obstructs the cystic duct
           resulting in a progressive increase of tension in the
           gallbladder wall.
• Clinical Presentation:
   • Pain – constant and increases in severity
     over the first half hour or so and typically
     last 1 to 5 hours.
   • Pain is severe and comes on abruptly,
     typically during the night or after a fatty
   • Mild right upper quadrant tenderness
     during an episode of pain.
   • Stone in the cystic duct = pain last for more
     than 24 hours.
   • Hydrops of the gallbladder = impacted
     stone in the neck of the gallbladder 
     gallbladder becomes distended with
     mucinous material. (white bile)
   Hydrops of the
    – Elongated, tense
      gallbladder filled
      with clear, mucoid
      material protrudes
      through the wound.
 Diagnosis:
     Abdominal ultrasound: standard
     diagnostic test
     Cholesterolosis: caused by the
     accumulation of cholesterol in
     macrophages in the GB mucosa.
     Adenomyomatosis or cholecystitis
     glandularis proliferans = epithelial
     sinus formation.
   Acute cholecystitis:
        90 to 95% - gallstones
        Obstruction of the cystic duct by a gallstone.

        An inflammatory process mediated by
         lysolecithin, as well as bile salts and platelet
         activating factor.
        Secondary bacterial contamination occurs
         50% of patients undergoing open
        GB wall grossly thickened and reddish with
         subserosal hemorrhage.
 When the gallbladder remains obstructed and
  secondary bacterial infection supervenes acute
  gangrenous cholecystitis
 Perforation of the GB contained in the
  subhepatic space by the omentum and adjacent
 Consequence of perforation: free perforation with
  peritonitis, intrahepatic perforation with
  intrahepatic abscesses and perforation into
  adjacent organs with cholecystoenteric fistula.
   When gas-forming organisms are part of the
    secondary bacterial infection , gas may be
    seen in the lumen of GB and the wall of the
    GB on abdominal radiograph and CT scan
     Emphysematous Gallbladder.
   Clinical Manifestations:
        80% - give a compatible history with chronic
        pain does not subside, persist for several
        Pain is typically in the right upper quadrant
         or epigastrium  radiate in the right upper
         part of the back or interscapular area.
        Febrile, anoreexia, nausea and vomiting

        On physical exam, RUQ tenderness with
        Murphy’s sign
   Ancillary Procedures:
          CBC – mild to moderate leukocytosis
           (12,000 to 15,000)
            – High WBC ( > 20,000) = gangrenous
                perforation or associated cholangitis.
        Serum liver chemistry = Normal
        Serum bilirubin, alkaline phosphatase,
         transaminases, and amylase= mildly elevated
   Mirizzi’s syndrome:
             • Common bile duct stones or
               obstruction of the bile ducts by
               severe pericholecystic
               inflammation secondary to
               impaction of a stone in the
               infundibulum of the gallbladder
               that mechanically obstructs the
               bile ducts.
 Management: Cholecystectomy
     Laparoscopic cholecystectomy

        – Chronic
       Open cholecystectomy
        – Acute
        – Early rather than delayed
        – symptomatic gallstone
   The standard sites of the four ports used in laparoscopic
   The gallbladder is retracted through the lateral port, and the
    laparoscope is inserted through the umbilical port.
   The entire
    cystic duct and
    the cystic
    artery are
    dissected free
    prior to the
    application of
    clips and
 In 6-12% of pts w/ stones in the GB
 Incidence increases w/ age (20-25% of >
  60 y/o)
 2 types:
    – Primary = assoc. w/ biliary stasis & infection;
      common in Asians; brown pigment stones
    – Secondary = formed in GB & migrate down the
      cystic duct to CBD; cholesterol stones
 S/sxs: biliary colic, nausea, vomiting,
  transient jaundice
 PE: mild epigastric or RUQ tenderness,
  mild icterus
 Stone completely impacted  severe
  progressive jaundice
 Labs: elevated serum bilirubin, alkaline
  phosphatase, transaminases
 UTZ: dilated CBD (> 8 mm in diameter)
 Endoscopic cholangiography: gold standard
   Tx:
    – Preoperative endoscopic cholangiography or
        intraoperative cholangiogram
    –   Endoscopic sphincterotomy & ductal clearance of
        stones followed by a laparoscopic
    –   Open common bile duct exploration if
        endoscopic method not available/feasible
    –   T-tube left in place if choledochotomy is done
    –   Choledochoduodenostomy or Roux-en-Y
        choledochojejunostomy if stone is impacted in
    –   Retained of recurrent stones = endoscopic
T H A N K Y O U !!!!

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