Benign biliary disease Dr. Gili Halfteck Department of General Surgury Shaare Zedek Medical Center January 2014

Embed Size (px)

Citation preview

  • Slide 1
  • Benign biliary disease Dr. Gili Halfteck Department of General Surgury Shaare Zedek Medical Center January 2014
  • Slide 2
  • Anatomy
  • Slide 3
  • Slide 4
  • Slide 5
  • Calots triangle
  • Slide 6
  • Physiology Roles of bile secretion: 1.Excretion of toxins and cellular metabolites (bilirubin) 2.Lipids absorption Components of bile: 1.Bile salts 2.Lipids (phospholipids and cholesterol) 3.proteins 4.pigments
  • Slide 7
  • Bile flow
  • Slide 8
  • Stimuli of bile secretion 1.Vagal activity 2.Secretin 3.CCK (bile secretion and gallbladder wall contraction)
  • Slide 9
  • Slide 10
  • Fasting state: -entero-hepatic circulation -Accumulation of bile in the gallbladder -Retrograde filling of the gallbladder - tonic activity of the sphincter of Oddi Fed state: -CCK (acid, fat and protein in duodenum) -Vagal activity
  • Slide 11
  • Symptoms of biliary tree disease Pain Fever Juandice
  • Slide 12
  • Pain Biliary colic Usually constant pain Location: RUQ/epigatrium Can be associated with meals (1 hour or more after a meal) Caused by contraction of the gallbladder against an obstructed neck Stasis + pressure + bacterial inoculum infection and inflammation (RUQ tenderness on palpation) Murphys sign
  • Slide 13
  • Fever Accompanies infection and inflammation of the gallbladder or biliary tree Not present in biliary colic
  • Slide 14
  • Juandice Elevation of serum bilirubin Surgical (obstruction) / medical (hepatocellular) >2.5 mg/dl scleral icterus >5 mg/dl cutaneous juandice Pathogenesis: failure to excrete bile from the liver to the intestine Charcots triade: fever, RUQ pain, juandice Reynolds pentad: + hypotension and altered mental status
  • Slide 15
  • Laboratory tests Bilirubin (conjugated/unconjugated) Alkaline phosphatase, GGT Serum transaminases (AST, ALT)
  • Slide 16
  • Imaging 1. US study of choice for initial evaluation of jaundice and gallbladder or biliary disease Surgical/medical jaundice High sensitivity and specificity for gallstones
  • Slide 17
  • 2. HIDA (hepatic iminodiacetic acid) scan Nuclear medicine test demonstrated physiologic bile flow but does not provide anatomic delineation Failure to fill the gallbladder 2 hours after injection cystic duct obstruction (cholecystitis) Obstruction of the biliary tree, bile leaks
  • Slide 18
  • 3. CT scan Superior anatomic information Most gallstones are isodense to bile Identifies cause and site of biliary obstruction Preoperative planning in pancreatic/hepatic neoplastic processes 4. MRI/MRCP Superior anatomic definition of intra- and extrahepatic biliary tree and pancreas Non-invasive No radiation exposure
  • Slide 19
  • Slide 20
  • 5. ERCP (endoscopic retrograde cholangiopancreatography) Invasive test using endoscopy and fluoroscopy Contrast injection through the ampulla and imaging of the biliary tree Able to diagnose and treat many biliary tree diseases (choledocholithiasis, tissue sampleing, CBD stenting) Complication rate - 10%
  • Slide 21
  • Bacteriology Without previous biliary intervention bile is considered sterile The presence of gallstones or obstruction and stasis increases the likelihood of bacterial contamination Mostly gram-negative aerobes passage of bacteria upward from the duodenum into the biliary tree E. Coli, Klebsiella, Enterobacter, Enterococcus spp.
  • Slide 22
  • Gallstones Types: 1.Mixed stones (70%) cholesterol and calcium 2.Pure cholesterol stones (10%) 3.Pigment stones brown/black (10%) Gallstones formation: -Supersaturation of bile -Concentration of bile in the gallbladder -Crystal nucleation -Gallbladder dysmotility
  • Slide 23
  • Natural history of gallstones Vast majority are asymptomatic incidentale finding Biliary colic temporary obstruction of the cystic duct or gallbladder neck 1% of patients with asymptomatic stones develop complications before onset of symptoms - prophylactic cholecystectomy is not warranted High risk patients: -Hemolytic anemias -Porcelain gallbladder -Large (>2.5 cm) stones -Long common channels of bile and pancreatic duct -Bariatric surgery (sleeve, bypass) -Immunocompromised patients
  • Slide 24
  • Non-operative treatment of cholelitiasis Generally unsuccessfull and rarely used!!! -Oral dissolution -Contact dissolution -Shock-wave lithotripsy Up to 50% recurrence rate
  • Slide 25
  • Acute calculus cholecystitis Pathogenesis: unresolved cystic duct obstruction Inflammation, edema, subserosal hemmorhage Infection of stagnant bile pool Can progress to ischemia and necrosis (gangrenous cholecystitis) Presentation: -Fever -RUQ pain -Tenderness to palpation Laboratory finding: leukocytosis, mild elevation of bilirubin, transaminases, alk-phos.
  • Slide 26
  • diagnosis 1. Transabdominal US -sensitive, inexpensive and reliable -Sensitivity 85%, specificity 95% -Gallstones, gallbladder wall thickening, pericholic fluid, sonographic murphys sign 2. Hida scan -Atypical cases -Cystic duct obstruction 3. CT scan - Less sensitive then US
  • Slide 27
  • Treatment NPO IV fluids IV antibiotics (broad-spectrum) Pain control Cholecystectomy (open/lap.) Percutaneous cholecystostomy
  • Slide 28
  • Chronic cholecystitis Inflammation and scarring of the gallbladder neck and cystic duct Pathogenesis: recurrent biliary colic which cause temporary cystic obstruction and do not cause acute cholecystitis Presentation: recurrent biliary colic (usually after fatty meals), nausea, vomiting RUQ/epigatric pain radiating to the scapula, usually resolves within few hours Symptomatic cholelithiasis indication for chlecystectomy
  • Slide 29
  • Diagnosis History Transabdominal US stones, sludge Treatment Elective cholecystectomy Curative in > 90% of patients
  • Slide 30
  • choledocholithiasis 1.Primary common duct stones -De novo in the bile duct -Usually brown pigment stones -More common in Asian population -Associated with bacterial bile duct infection 2. Secondary common duct stones -Arising from the gallbladder -Most common bile duct stones in the USA Retained common duct stones found within 2 years of cholecystectomy
  • Slide 31
  • Presentation 80-90% of common duct stones remain clinically silent Routine cholangiography 10% choledocholithiasis Selective cholangiography (pain, abnormal liver function test) 1-2% of patients will present with retained stones Symptoms: -Biliary colic -Obstructive juandice -Ascending cholangitis (fever, pain, juandice)
  • Slide 32
  • Diagnosis Hepatic function panel abnormalities Leukocytosis US choledocholithiasis, biliary ductal dilatation, gallstones Bile duct dilatation (>8 mm) in the presence of biliary colic, juandice or gall stones is suggestve of choledocholithiasis ERCP -highly sensitive and specific -Usually therapeutic -Sphincterotomy, balloon stone extraction -Complication rate 5-8% MRCP - highly sensitive and specific - Does not provide therapeutic solution
  • Slide 33
  • treatment 1.ERCP -Sphincterotomy and stone extraction -Reasons for endoscopic failure: large stones, multiple stones, intrahepatic stones, altered anatomy, duodenal diverticula, impacted stones -Does not eliminate the risk of recurrent biliary stone disease (up to 50% recurrence) 2.Common bile duct exploration (lap./open) -Intraoperative cholangiogram -Trans-cystic/common duct incision
  • Slide 34
  • Ascending cholangitis Acute ascending bacterial infection of the biliary tree cause by obstruction Obstruction: stones, malignancy Presentation: Charcots triad (fever, RUQ pain, jaundice), Reynolds pentad (+hypotension, altered mental status)
  • Slide 35
  • Diagnosis Tachycardia, shock symptoms Laboratory test: leukocytosis, abnormal liver panel US dilatation of the biliary tree CT site of obstruction ERCP/PTC diagnostic as well as therapeutic
  • Slide 36
  • Treatment NPO IV fluids IV antibiotics Most patients respond to medical therapy Emergent decompression of the biliary tree (ERCP/PTC)
  • Slide 37
  • Questions?