GALL BLADDER STONES Bryan Bernard U. Ong Kian Koc MD Jocelyn M. Lledo MD Incidence Male: 8 % Female: 17% Predisposing factors Obesity Multiparity DM Cirrhosis Pancreatitis Chronic hemolytic states Malabsorption Inflammatory bowel disease Racial/ genetic factors(Blacks/ Indians) Etiology Bile salts – primary- cholic, chenodeoxycholic acids; – secondary- deoxycholic and lithocholic acids Phospholipids (90% lecithin) Cholesterol types 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 (>2.5cm) Usually not calcified types 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 unusual 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 scapula – 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 PUD Hiatal hernia with reflux Gastritis Hepatic flexure carcinoma Hepatobiliary carcinoma Cardiopulmonary disease Complications Prolonged cystic duct obstruction may allow bacterial growth and progress to acute cholecystitis Stones may pass into CBD with consequent obstruction or pancreatitis Diagnosis 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 Diagnosis Ultrasound – Diagnostic procedure of choice – Identifies stones, wall thickness, presence of masses, ductal dilatation, fluid collections – Technical difficulties – Sensitivity and specificity of 95% Treatment 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 pancreatitis Symptomatic Gallstones Chronic Cholecystitis Two-thirds of patients characterized by recurrent attacks of pain, often inaccurately labeled biliary colic. 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 meal. • 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 gallbladder. – 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 cholecystectomy. 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 organs. 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 cholecystitis. pain does not subside, persist for several days. 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 guarding Murphy’s sign Ancillary Procedures: CBC – mild to moderate leukocytosis (12,000 to 15,000) – High WBC ( > 20,000) = gangrenous cholecystitis, 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 cholecystectomy. 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 completely dissected free prior to the application of clips and transection. Choledocholithiasis 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 cholecystectomy – 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 ampulla – Retained of recurrent stones = endoscopic removal T H A N K Y O U !!!!
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