MCQ Hepatobiliary Bile duct pathology

• During open cholecystectomy - 0.1–0.2%Q
• During laparoscopic cholecystectomy - 0.3–0.85%Q

• I - CBD mistaken for cystic duct but recognized; cholangiogram incision of cystic duct extended into CBD
• II - Lateral damage to common hepatic duct from cautery or clips placed on duct; associated bleeding, poor visibility
• III - CBD mistaken for cystic duct, not recognized; CBD, CHD, RHD, LHD transected or resected
• IV - RHD mistaken for cystic duct, RHA mistaken for cystic artery, RHD and RHA transected; lateral damage to the RHD from cautery or clips placed on ducts

• Type 1 - Low common hepatic duct stricture; hepatic duct stump >2cmQ
• Type 2 - Mid common hepatic duct stump < 2 cmQ
• Type 3 - High stricture (hilar), no hepatic duct stump; confluence intactQ
• Type 4 - Destruction of the hilar confluence; right and left hepatic ducts separatedQ
• Type 5 - Involvement of aberrant right sectoral hepatic duct alone with or without a concomitant hepatic duct strictureQ

• It did not stipulate the length of the stricture
• It did not take into account the presence of biliary leaks, which are more common after laparoscopic cholecystectomy.
• This, latter fact has been incorporated in Strasberg’s classification.

• Type A - • Bile leaks from minor ducts still in continuity with the CBDQ, Includes leakage from cystic duct stump and from a subvesical duct of LuschkaQ
• Type B • Occlusion of a part of the biliary tree, almost always an aberrant right sectoral ductQ
• Type C • Transection without ligation of an aberrant right sectoral ductQ
• Type D • A lateral injury to an extrahepatic ductQ
• Type E • Includes biliary strictures, divided into E1 to E5 as classified by Bismuth

Type A

1 or 2 daysQ

Dissection of the hilar plate to expose the left hepatic duct and allow for a side-to-side anastomosis of the left hepatic duct to the Roux-en-Y jejunal limb.

Biliary Sphincter of Oddi dysfunctionQ

• Dilated CBD (>12 mm diameter) or increase in CBD diameter in response to CCK is a typical ultrasound findingQ
• Endoscopic manometry is considered gold standard Q for diagnosis

Transduodenal sphincteroplasty with transampullary septectomyQ

Decreased number of bile ducts seen in liver biopsy specimensQ

• • Chronic rejectionQ after liver transplantation
• • Graft-versus-host diseaseQ after BM transplantation
• • SarcoidosisQ
• • Drugs: ChlorpromazineQ
• • IdiopathicQ

Biliary cirrhosis, portal hypertension, and death by 2 years of ageQ.

Polysplenia, malrotation, preduodenal portal vein, and intrahepatic vena cavaQ

• GB is shrunken and CBD is not visibleQ.
• Triangle cord signQ
• Gallbladder ghost triadQ - gallbladder is short (<1.9 cm) and irregular and lacks an echogenic inner lining

• Kasai hepatoportoenterostomyQ
• Liver transplantation - who develop progressive hepatic fibrosis with resultant portal hypertension and progressive cholestasisQ

Ursodeoxycholic acid (facilitate bile flow) + Methylprednisolone (anti-inflammatory agent) + TMP-SMX (antimicrobial prophylaxis)Q

Cholangitis

• • Age in days at diagnosis and initial surgery (30–60 days)Q
• • Length of time jaundice was present before surgeryQ
• • Successful and persistent bile flow postoperativelyQ
• • Size and nature of the microscopic ducts (>150 μm)Q
• • Degree and extent of fibrotic changes in the liverQ
• • Need for phototherapy as a neonateQ
• • Technical aspects of the portoenterostomy and anastomosisQ
• • Presence of bile in hepatic lobular zone

Cholestatic liver disease characterized by fibrotic strictures involving the intrahepatic and extrahepatic biliary treeQ in the absence of a known precipitating cause.

• • Chronic ulcerative colitisQ
• • Crohn's diseaseQ
• Riedel's thyroiditisQ
• SarcoidosisQ

UC and PSCQ

“Onion skin appearance”Q

• Involvement of large intrahepatic and extrahepatic ductQ distinguishes PSC from PBC.
• Absence of the smallest intrahepatic ducts leading to a reduction in the branching of the biliary tree (give rise to pruned-tree appearanceQ on direct cholangiography).

Asymptomatic elevation of GGTQ

ERCP

• • Multifocal stricturing and beadingQ throughout the biliary tree
• • Beaded or pruned tree appearanceQ
• • PseudodiverticulaQ (tiny diverticulum like outpouchings) of the extrahepatic bile ducts are nearly pathognomonic of PSC, seen in one fourth of the cases.
• • The hepatic duct bifurcation is the most severely stricturedQ segment of the biliary tree

• High dose UDCAQ (25–30 mg/kg/day).
• Recurrent biliary sepsis: antibiotics and surveillance
• Biliary strictures: Dilated or stented
• Liver transplantation - PSC and end-stage liver diseaseQ
• Cholestyramine, Phenobarbital, Ursodeoxycholic acid are approved for the treatment of pruritusQ

• PSC and Cholangiocarcinoma is more common in malesQ.
• PBC is more common in femalesQ.
• Colectomy has no effect on the course of PSCQ.

Autoimmune etiology, leading to progressive destruction of intrahepatic bile ductsQ

• Florid duct lesion is characterized by lymphocytic or granulomatous bile duct infiltrationQ.
• In the setting of positive AMA, the florid duct lesion is essentially diagnosticQ.

Pruritus

• Cholestyramine is mainstay of treatment of pruritusQ.
• Ursodeoxycholic acid - associated with significant delay to time of transplantationQ.
• Transplantation - intolerable lethargy or intractable pruritusQ

• • Infection is caused by bacterial contamination, usually biliary pathogens, and biliary parasites, such as Clonorchis sinensis, Opisthorchis viverrini, and Ascaris lumbricoidesQ.
• • Partial obstruction of biliary tree caused by biliary sludge and dead bacterial cell bodies, which form brown pigment stonesQ

Roux-en-Y hepaticojejunostomyQ with a subcutaneous afferent limb (Hudson loopQ) to provide access to the biliary tree for stone extractionsQ