Diagnosis and treatment modalities of hilar biliary duct stricture in hepatic cystic echinococcosis after endocystectomy

Aim: Hilar biliary duct stricture may occur in hepatic cystic echinococcosis (CE) patients after endocystectomy. This study aimed to explore diagnosis and treatment modalities. Methods: Clinical data of 26 hepatic CE patients undergoing endocystectomy who developed postoperative hilar biliary duct stricture were retrospectively analyzed and were classified into three types: type A, type B, and type C. Postoperative complications and survival time were successfully followed up. Results: Imaging showed biliary duct stenosis, atrophy of ipsilateral hepatic lobe, reactive hyperplasia, hepatic hilum calcification, and dilation or discontinuity of intrahepatic biliary duct. All patients received partial hepatectomy to resect residual cyst cavity and atrophic liver tissue, and anastomosis of hepatic duct with jejunum or common bile duct exploration was applied to handle hilar biliary duct stricture. Twenty-five patients were successfully followed up. Among type A patients, one patient died of organ failure, and upper gastrointestinal bleeding and liver abscess occurred in one patient. Moreover, calculus of intrahepatic duct was found in one type B and type C patient. Conclusion: Long-term biliary fistula, infection of residual cavity or obstructive jaundice in hepatic CE patients after endocystectomy are possible indicators of hilar bile duct stricture. Individualized and comprehensive treatment measures, especially effective treatment of residual cavity and biliary fistula, are optimal to avoid serious hilar bile duct stricture

Collateral circulation caused by end-stage hepatic alveolar echinococcosis

Abstract Background Hepatic alveolar echinococcosis (HAE), as a benign parasitic disease with malignant infiltrative activity, grows slowly in the liver, allowing sufficient time for collateral vessels to emerge in the process of vascular occlusion. Methods The portal vein (PV), hepatic vein and hepatic artery were observed by enhanced CT and the inferior vena cava (IVC) by angiography, respectively. Analysis of the anatomical characteristics of the collateral vessels helped to look into the pattern and characteristics of vascular collateralization caused by this specific etiology. Results 33, 5, 12 and 1 patients were included in the formation of collateral vessels in PV, hepatic vein, IVC and hepatic artery, respectively. PV collateral vessels were divided into two categories according to different pathways: type I: portal -portal venous pathway (13 cases) and type II: type I incorporates a portal-systemic circulation pathway (20 cases). Hepatic vein (HV) collateral vessels fell into short hepatic veins. The patients with IVC collateral presented with both vertebral and lumbar venous varices. Hepatic artery collateral vessels emanating from the celiac trunk maintains blood supply to the healthy side of the liver. Conclusions Due to its special biological nature, HAE exhibited unique collateral vessels that were rarely seen in other diseases. An in-depth study would be of great help to improve our understanding related to the process of collateral vessel formation due to intrahepatic lesions and its comorbidity, in addition to providing new ideas for the surgical treatment of end-stage HAE

Diagnosis and treatment modalities of hilar biliary duct stricture in hepatic cystic echinococcosis after endocystectomy

Aim: Hilar biliary duct stricture may occur in hepatic cystic echinococcosis (CE) patients after endocystectomy. This study aimed to explore diagnosis and treatment modalities. Methods: Clinical data of 26 hepatic CE patients undergoing endocystectomy who developed postoperative hilar biliary duct stricture were retrospectively analyzed and were classified into three types: type A, type B, and type C. Postoperative complications and survival time were successfully followed up. Results: Imaging showed biliary duct stenosis, atrophy of ipsilateral hepatic lobe, reactive hyperplasia, hepatic hilum calcification, and dilation or discontinuity of intrahepatic biliary duct. All patients received partial hepatectomy to resect residual cyst cavity and atrophic liver tissue, and anastomosis of hepatic duct with jejunum or common bile duct exploration was applied to handle hilar biliary duct stricture. Twenty-five patients were successfully followed up. Among type A patients, one patient died of organ failure, and upper gastrointestinal bleeding and liver abscess occurred in one patient. Moreover, calculus of intrahepatic duct was found in one type B and type C patient. Conclusion: Long-term biliary fistula, infection of residual cavity or obstructive jaundice in hepatic CE patients after endocystectomy are possible indicators of hilar bile duct stricture. Individualized and comprehensive treatment measures, especially effective treatment of residual cavity and biliary fistula, are optimal to avoid serious hilar bile duct stricture