ANATOMY Three places the common bile duct may join the pancreatic duct in the wall of the

e duodenum within the pancreas prior to insertion into the duodenal wall may enter the duodenum separately from the pancreatic duct Parts of the gallbladder: neck, infundibulum with Hartmanns pouch, body, fundus Gallbladder capacity 30 - 60 mL of bile Where the gallbladder attaches the liver, Glisson's capsule does not form Cystic duct length 1 5 cm Common bile duct >8mm is dilated Spiral valves of Heister: folds of mucosa oriented in a spiral pattern to keep gallstones from entering the common bile duct Hepatic parenchyma segments based on hepatic venous drainage and portal inflow Three major hepatic veins drain into the inferior vena cava The entire biliary tree is supplied solely by the arterial anatomy In most cases the right hepatic artery passes posterior to the common hepatic duct to supply the right lobe of the liver The cystic artery normally arises from the right hepatic artery Although variable, the cystic artery generally lies superior to the cystic duct and is usually associated with the lymph node (Calot's node) Bile ducts generally my superior to the corresponding portal veins The left duct drains segments II, III and, IV, IVa The right duct drains segments V, VI, VII, and VIII Right duct is short, left duct is long PHYSIOLOGY bile excretes toxins plays critical role in the absorption of most lipids vagal activity, gastrointestinal hormone secretin and cholecystokinin all induce mobile secretion Cholecystokinin is secreted by intestinal mucosa Bilirubin is the breakdown products of hemoglobin and myoglobin The gallbladder is efficient at absorbing water and concentrating bile components With absorption of sodium chloride and water across the gallbladder epithelium bile is concentrated Fasting state causes increase in tonic activity of sphinceter of Oddi

IMAGING Hepatic Iminodiacetic Acid scan (H I DA) Biliary scintigraphy used to evaluate the physiologic secretion of Bile Failure to fill the gallbladder two hours after injection demonstrates obstruction of the cystic duct Call bladder function can be determined by a HIDA scan because the injection cholecystic kinin during scan will document physiological injection the gallbladder Triple phase CT: arterial phase, portal venous face, delayed phase Indications for intraoperative cholangiography: pain at the time of operation abnormal hepatic function panel Anomalous or confusing biliary anatomy inability to perform ERCP following cholecystectomy dilated biliary tree preoperative suspicion ofColey Delco lithiasis

ERCP or PTC (percutaneous transhepatic cholangiography) prophylactic antibiotics equals first or second generation cephalosporin or flouroquinolone GALLSTONES In US 70% of gallstones are calcium and cholesterol Increased gallbladder stone formation impaired gallbladder emptying prolonged fasting TPN use post Vagotomy Somatostatin analogues

Black stones: hemolytic conditions and cirrhosis Brownstones: occur within the biliary tree 20 to 30% of patients with asymptomatic gallstones will develop symptoms within 20 years Rapid weight-loss favors stone formation Nonoperative treatments of Cholelithiasis oral salt therapy contact dissolution extracorporeal shockwave Lithotripsy

Acute Vs. Chronic Cholecystitis Acute: Pain lasting longer than 2 hours or when associated with fever suggests acute cholecystits Acute = inflammation with edema and subserosal hemorrhage Tenderness and positive Murphys sign Biliary colic (no inflammatory process, and thus no tenderness or Murphys sign) Acute Calculous Cholecystitis: Most common organisms: Gram negative aerobes Anaerobes

Gram positive aerobes Tx: NPO IVF Parenteral antibiotics (broad-spectrum) Cholecystectomy: Within one week Too much intraoperative inflammation: partial cholecystectomy (transecting gallbladder at infundibulum with cauterization of remaining mucosa) Cholecystostomy tube: allows for 3-6 months of medical optimization before operation Choledocholithiasis: Primary (arising in the duct) Most commonly brown stones More common in Asian populations Associated with bacterial infection of bile duct Secondary (passing from the gallbladder) Most common in US Retained common duct stones when found within 2 years of cholecystectomy Symptoms Biliary colic obstructive jaundice (dark urine, scleral icterus, lightening of stools), fever, RUQ pain (Charcots triad) Charcot + hypotension and metnal status changes (Reynolds pentad) Findings >8mm CBD Tests ERCP 75% clearance of stones on first try, 90% on repeat tries MRI >90% sensitive, 100% specific 1488 Treatment ERCP as above Common bile duct exploration (lap or open) Impacted stone at ampulla Nondilated biliary tree Transduodenal sphincterotomy Dilated biliary tree Cholodochoenterostomy Choledochoduodenostomy Preserves endoscopic access Can create sump syndrome Roux-en-Y choledochojenjunostomy Difficult to access endoscopically Gallstone pancreatitis Stone passing into CBD and temporarily blocking pancreas outflow Stone usually passes spontaneously Lap chole to prevent repeat episode of gallstone pancreatitis is warranted Can do it during the same hospitalization just prior to discharge Biliary dyskinesia

Presents are calculous biliary disease without evidence of stones or sludge CCK-stimulated HIDA scan Ejection fraction <1/3 at 20 min after CCK is diagnostic of dyskinesia Cholecystectomy

Sphincter of Oddi dysfunction Suspect in patients with biliary pain and CBD diameter >12mm Manometry Sphincter pressure >40mmHg

Laparoscopic Cholecystectomy Contraindications Intolerance of general anesthesia End-stage liver disese with portal hypertension Coagulopathy Severe COPD (relative) with poor gas exchange CHF(relative) Orogastric tube 12mm umbilical port + 5-mm ports critical view of safety view of the lver bed through the space between cystic duct and cystic artery and above the cystic artery glucagon relaxes spincter of Oddi Postcholecystectomy syndromes: inferolateral traction on gallbladder infundibulum helps dissociate structures cholangiography does not eliminate but reduces incidence and extent of bile duct injury bile duct injury presentation complaints that persist or increase over time should raise suspicion after lap chole of bile duct injury elevated alk phos bile leak (subsequent bile peritonitis) presents early bile duct stricture presents later and with jaundice repair simple ligation ducts smaller than 3mm and by cholangiography drain only a single segment or subsegment of liver reimplantation into biliary tree t-tube placement reanastomosis to the gastrointestinal tract choledochoduodenostomy roux-en-y should be stented if anastomosis will be within 2 cm of hepatic duct bifurcation or involves intrahepatic ducts Lost stones Do not necessitate conversion to open operation Treat with Extensive irrigation Significant attempt to retrieve lost stones Course of antibiotics Documentation in operative report Gallstone ileus

Mechanical small bowel obstruction from a gallstone passed through a spontaneous cholecystoenteric fistula Distal ileum most common site of stone impaction Pneumobilia is ubiquitous Exploration and enterotomy, possible resection of impacted area

Acute cholangitis Pathogenesis Bacteria in biliary tree Klebsiella, E. coi, Enterobacter, Pseudomonas, Citrobacter Obstruction of flow Charcots triad Jaundice, RUQ pain, fever 50% of patients (jaundice the most variable) pain can be severe but usually not associated with abdominal tenderness Diagnosis Liver enzymes Ultrasound (dilation of biliary ducts) CT ERCP/PTC Treatment Hydration IV antibiotics Emergency decompression of biliary tree if go into shock Endoscopic, percutaneous, or surgical Recurrent Pyogenic Cholangitis Cholangiohepatitis or intrahepatic stones East Asians Clonorchis sinensis or Ascaris lumbricoides in biliary tree Cholangitis with fever, RUQ pain, jaundice