Originates in the bile duct epithelium and spreads by direct invasion. In total, 60% are perihilar (Klatskin tumours). Most present with hi...
Originates in the bile duct epithelium and spreads by direct invasion. In total, 60% are perihilar (Klatskin tumours). Most present with hilar obstruction and normal extrahepatic ducts. Risk factors include inflammatory bowel disease (10-fold), primary sclerosing cholangitis (15-year latency), choledochal cysts, chronic stones and viral hepatitis. It may appear as a frank mass, intraductal polyp or diffuse duct wall thickening. The tumour commonly invades nerves, infiltrates the liver and metastasises to coeliac lymph nodes and the peritoneum.
US
• Right hepatic lobe affected more commonly
• Nodules/focal bile duct wall thickening
• Hyperechoic bile duct walls
CT
• Can be subtle—tumour mass is often isodense.
• Peripheral enhancement.
• Delayed enhancement of the lesion (best seen at 10 minutes).
• Intrahepatic duct dilatation.
• May contain calcification.
• Liver infiltration is common.
• Check for peritoneal disease (10%).
• Most sensitive for diagnosis.
• Check for vascular encasement.
• Lesion is high signal on T2, low signal on T1.
• Enhancement characteristics as for CT.
• Does not take up superparamagnetic iron oxide (SPIO)
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