Hilar Inflammatory Pseudotumour with Hepatic Artery Atheroma- mimicker of Klatskin Tumour.

Inflammatory pseudotumour of hilar biliary structures is an extremely rare benign lesion that can mimic hilar cholangiocarcinoma. Clinical presentation and imaging findings often pose diagnostic difficulties. Main histopathological findings are the presence of myofibroblastic spindle cells, plasma cells, macrophages, and lymphocytes without cellular atypia or atypical mitotic figures. We describe a case of 62 year old male who presented with surgical obstructive jaundice. Imaging revealed a mass lesion involving the biliary confluence with upstream dilatation of biliary tree. Diagnosis of hilar cholangiocarcinoma with type III hilar block was made. Intraoperately hilar mass lesion was found which was encasing right hepatic artery with no evidence of metastasis. The patient underwent Right hepatectomy with caudate lobectomy with complete common bile duct (CBD) excision with Roux en Y hepaticojejunostomy. Unexpectedly histopathological examination showed no evidence of malignancy and revealed hilar inflammatory pseudotumour with hepatic artery atherosclerosis. Preoperative imaging, operative management, pathologic diagnosis and literature review are being presented in view of rarity of the case.

Analysis of biliary anatomy according to different classification systems.

PURPOSE: Variations in biliary anatomy are common, and different classifications have been described. These classification systems have not been compared to each other in a single cohort. We report such variations in biliary anatomy on magnetic resonance cholangiopancreatography (MRCP) using six different classification systems. METHODS: In 299 patients undergoing MRCP for various indications, biliary anatomy was classified as described by Couinaud (1957), Huang (1996), Karakas (2008), Choi (2003), Champetier (1994), and Ohkubo (2004). Correlation with direct cholangiography and vascular anatomy was done. Bile duct dimensions were measured. Cystic duct junction and pancreaticobiliary ductal junction (PBDJ) were classified. RESULTS: Normal biliary anatomy was noted in 57.8 %. The most common variants were Couinaud type D2, Choi type 3A, Huang type A1, Champetier type a, Ohkubo types D and J, and Karakas type 2a. The Ohkubo classification was the most appropriate; 3.1 % of right ducts and 6.3 % of left ducts with variant anatomy could not be classified using the Ohkubo classification. There was a good agreement between MRCP and direct cholangiography (ĸ = 0.9). Anomalous PBDJ was noted in 8.7 %. Variant biliary anatomy was not associated with gender (p = 0.194) or variant vascular anatomy (p = 0.24). CONCLUSION: Although each classification system has its merits and demerits, some anatomical variations cannot be classified using any of the previously described classifications. The Ohkubo classification system is the most applicable as it considers most clinically relevant variations pertinent to hepatobiliary surgery.

Treatment of portosystemic shunt myelopathy with a stent graft deployed through a transjugular intrahepatic route.

A case of surgically created splenorenal shunt complicated with shunt myelopathy was successfully managed by placement of a stent graft within the splenic vein to close the portosystemic shunt and alleviate myelopathy. To our knowledge, this is the first report of a case of shunt myelopathy in a patient with noncirrhotic portal fibrosis without cirrhosis treated by a novel technique wherein a transjugular intrahepatic route was adopted to deploy the stent graft.

Non-bleeding Spontaneous Rupture of Hepatocellular Carcinoma.

Rupture of hepatocellular carcinoma (HCC) is not uncommon and most ruptured HCC present with hemoperitoneum and hemorrhagic shock. Management of ruptured HCC is different than non-ruptured one. Short- and long-term mortality increases following rupture of HCC with increasing chances of tumor dissemination. We describe a case with non-bleeding spontaneous rupture of HCC. A 62-year-old male patient was admitted to our institute hospital with mild to moderate pain in the right upper part of the abdomen. He lost appetite and weight. Ultrasonography of the abdomen was performed and it suggested HCC and ascites. Triple phase computer tomography revealed HCC in segments 6 and 7 of liver with typical radiological characteristics. Portal vein was thrombosed. No extravasation of dye was seen. Ruptured of tumor through liver capsule was seen with necrosis and hemorrhage in the center of the tumor. Non-bleeding ruptured HCC has not been reported in the literature to the best of our knowledge. We herein describe this rare case.