PERCUTANEOUS CHOLANGIOSCOPY AND LASER BILIARY LITHOTRIPSY FOR BILIARY INTRAHEPATIC STONES MANAGEMENT: CASE REPORT.

Intrahepatic biliary stone disease is a difficult condition to treat, due to anatomical complexity of biliary tract, association with colestasis, and high recurrence rates, with potential short- and long-term complications, such as cholangitis and secondary biliary cirrhosis. Removal of biliary stones via intraductal access can be achieved endoscopically or percutaneously, with preference for cholangioscopy-guided laser lithotripsy in complex cases. The surgical approach, despite its prolonged results, is a more invasive and risky procedure. The authors present a case of cholangioscopy with percutaneous laser biliary lithotripsy as an option for the treatment of intrahepatic biliary stone disease associated with biliary stricture following biliodigestive anastomosis due to bile duct injury following cholecystectomy, a safe and effective alternative with low morbidity and satisfactory outcomes in follow-up.

Mechanical strength of biliary defect closure after topical sealing: Comparison of four sealants in a porcine model.

BACKGROUND/OBJECTIVE: Biliary leakage is a potential complication of liver resection and is still a concern. The aim of the present study was to evaluate the effectiveness of four routinely used sealants in preventing bile leakage under pressure from an induced perforation of the gallbladder in a porcine model. METHODS: Forty Landrace pigs were randomly assigned to one of five groups. These included a control group (n = 8) and one group each for the sealants TachoSil®, TissuCol Duo®, Coseal®, and FloSeal® (n = 8 per group). In the control group, the perforation was left unsealed. To evaluate the biliostatic potential of the sealants, we measured the pressure that was needed to induce leakage (mmHg) and the gallbladder volume (cc) at the time of leakage in each group. RESULTS: A significantly higher mean pressure was required to induce leakage in the sealant groups compared with the control group. However, the biliostatic effects were heterogeneous among the sealant groups. Sealants with the highest to lowest effectiveness were TachoSil, Coseal, TissuCol, and FloSeal. The mean gallbladder volume at the time of leakage also varied between sealant groups. CONCLUSION: Biliostatic properties are markedly improved by the use of modern sealants compared with using no sealant. However, the advantages and disadvantages of using sealants should be carefully considered in each clinical situation. The effectiveness of the sealants should be evaluated in chronic and clinical studies.

Intrahepatic subcapsular biloma after endoscopic retrograde cholangiopancreatography treated by endoscopic biliary drainage.

Several major complications from endoscopic retrograde cholangiopancreatography (ERCP), including pancreatitis, cholangitis, and hemorrhage have been discussed in detail; however, a few uncommon but severe complications have been reported. We encountered an unusual case of post-ERCP intrahepatic subcapsular biloma. An 89-year-old woman with a 25-mm mass located at the hepatic hilum, suggestive of cholangiocarcinoma, underwent ERCP which demonstrated complete stricture of the common hepatic duct. Subsequently, two plastic stents were placed from the common bile duct to the right and left intrahepatic branches. On day 3, serum inflammatory markers were elevated and computed tomography revealed a large subcapsular fusiform fluid collection in the right liver, consistent with biloma. On day 6, the biloma ruptured and 500 ml of biliary ascites were removed. On day 8, endoscopic nasobiliary drainage via the right intrahepatic branch was performed because of recurrence of biliary ascites. After the procedure, 150 ml of bile was collected through the drain every day and no ascites recurred. We believe that minor injury to the right intrahepatic bile duct due to guidewire manipulation caused the biloma. Biloma may become apparent several days after ERCP, and endoscopic biliary drainage placement adjacent to the bile duct rupture site can stop bile leakage.

Management of paediatric liver trauma.

Of all the intra-abdominal solid organs, the liver is the most vulnerable to blunt abdominal trauma. The majority of liver ruptures present in combination with other abdominal or extra-abdominal injuries. Over the last three decades, the management of blunt liver trauma has evolved from obligatory operative to non-operative management in over 90% of cases. Penetrating liver injuries more often require operative intervention and are managed according to adult protocols. The greatest clinical challenge remains the timely identification of the severely damaged liver with immediate and aggressive resuscitation and expedition to laparotomy. The operative management can be taxing and should ideally be performed in a dedicated paediatric surgical centre with experience in dealing with such trauma. Complications can occur early or late and include haemobilia, intrahepatic duct rupture with persistent biliary fistula, bilaemia, intrahepatic haematoma, post-traumatic cysts, vascular outflow obstruction, and gallstones. The prognosis is generally excellent.

A case of hepatocellular carcinoma treated by radiofrequency ablation confirming the adjacent major bile duct under hybrid contrast mode through a biliary drainage catheter.

Bile duct injury is a potential complication of radiofrequency ablation (RFA). Bipolar RFA devices have recently become available. Because visibility of the bipolar RFA electrodes is not good on ultrasonography, more careful usage of the electrodes to avoid bile ducts is needed. We present a case with hepatocellular carcinoma (HCC) located near the B5 intrahepatic bile duct. To view the bile duct, we used contrast medium for ultrasonography, administered through a biliary drainage catheter for endoscopic nasobiliary drainage (ENBD). Infusing the contrast medium allowed clear visualization of the HCC adjacent to the major bile duct during RFA. We also used a navigation system for bipolar RFA to confirm positions of the electrodes and HCC. We confirmed complete ablation of the HCC while avoiding bile duct injury and late bile duct stenosis. Administration of contrast medium for ultrasonography through an ENBD tube appears useful to avoid bile duct injury during RFA.

Epigallocatechin 3-gallate ameliorates bile duct ligation induced liver injury in mice by modulation of mitochondrial oxidative stress and inflammation.

Cholestatic liver fibrosis was achieved by bile duct ligation (BDL) in mice. Liver injury associated with BDL for 15 days included significant reactive oxygen/nitrogen species generation, liver inflammation, cell death and fibrosis. Administration of Epigallocatechin 3-Gallate (EGCG) in animals reduced liver fibrosis involving parenchymal cells in BDL model. EGCG attenuated BDL-induced gene expression of pro-fibrotic markers (Collagen, Fibronectin, alpha 2 smooth muscle actin or SMA and connective tissue growth factor or CTGF), mitochondrial oxidative stress, cell death marker (DNA fragmentation and PARP activity), NFκB activity and pro-inflammatory cytokines (TNFα, MIP1α, IL1ß, and MIP2). EGCG also improved BDL induced damages of mitochondrial electron transport chain complexes and antioxidant defense enzymes such as glutathione peroxidase and manganese superoxide dismutase. EGCG also attenuated hydrogen peroxide induced cell death in hepatocytes in vitro and alleviate stellate cells mediated fibrosis through TIMP1, SMA, Collagen 1 and Fibronectin in vitro. In conclusion, the reactive oxygen/nitrogen species generated from mitochondria plays critical pathogenetic role in the progression of liver inflammation and fibrosis and this study indicate that EGCG might be beneficial for reducing liver inflammation and fibrosis.

Management of biliary complications in 412 patients with liver injuries.

BACKGROUND: Bile leaks occur in 4% to 23% of patients after major liver injuries. The role of conservative management versus internal biliary drainage has not been clearly defined. The safety and efficacy of nonoperative management of bile leaks were studied. METHODS: Four hundred twelve patients with liver injuries were assessed in a prospective study between 2008 and 2013. All patients with clinically significant injuries to the intrahepatic biliary tract were evaluated. Bile leaks were classified as minor or major (>400 mL/d or persistent drainage >14 days). Minor leaks were managed conservatively, and major leaks underwent endoscopic retrograde cholangiogram and endoscopic biliary stenting. RESULTS: Fifty-one patients (12%) developed a bile leak after liver trauma. Eleven patients (22%) with an extrahepatic duct injury underwent open surgery. Forty patients (78%) had an intrahepatic bile leak. Twenty-six patients (65%) with minor bile leaks were treated conservatively, and 14 patients (35%) with major leaks underwent endoscopic retrograde cholangiogram and internal drainage. All bile leaks resolved. There was no significant difference in the two groups with respect to septic complications (p = 0.125), intensive care unit stay (p = 0.534), hospital stay (p = 0.164), or mortality (p = 1.000). CONCLUSION: Sixty-five percent of the intrahepatic bile leaks following trauma are minor and easily managed conservatively. Endoscopic retrograde cholangiogram and internal drainage should be reserved for major leaks. LEVEL OF EVIDENCE: Therapeutic study, level IV.

Choleperitoneum due to intrahepatic bile duct rupture - case report.

Non-traumatic perforations of the bile ducts are unfrequently encountered entities, all the more when they affect the intrahepatic bile ducts, exteriorizing their biliary content in the great peritoneal cavity. Reporting such a case has determined the authors to perform a careful overview of the cases present in the literature. An observation that can be made based on these is that the obstruction of the main bile duct due to lithiasis determines, by pressure increase, the dilation of the bile system branches, all on the background of an unknown malformation of the intrahepatic bile ducts.

Notch signaling regulates tubular morphogenesis during repair from biliary damage in mice.

BACKGROUND & AIMS: Repair from biliary damages requires the biliary specification of hepatic progenitor cells and the remodeling of ductular reactive structures into branching biliary tubules. We hypothesized that the morphogenetic role of Notch signaling is maintained during the repair process and have addressed this hypothesis using pharmacologic and genetic models of defective Notch signaling. METHODS: Treatment with DDC (3,5-diethoxycarbonyl-1,4-dihydrocollidine) or ANIT (alpha-naphthyl-isothiocyanate) was used to induce biliary damage in wild type mice and in mice with a liver specific defect in the Notch-2 receptor (Notch-2-cKO) or in RPB-Jk. Hepatic progenitor cells, ductular reaction, and mature ductules were quantified using K19 and SOX-9. RESULTS: In DDC treated wild type mice, pharmacologic Notch inhibition with dibenzazepine decreased the number of both ductular reaction and hepatic progenitor cells. Notch-2-cKO mice treated with DDC or ANIT accumulated hepatic progenitor cells that failed to progress into mature ducts. In RBP-Jk-cKO mice, mature ducts and hepatic progenitor cells were both significantly reduced with respect to similarly treated wild type mice. The mouse progenitor cell line BMOL cultured on matrigel, formed a tubular network allowing the study of tubule formation in vitro; γ-secretase inhibitor treatment and siRNAs silencing of Notch-1, Notch-2 or Jagged-1 significantly reduced both the length and number of tubular branches. CONCLUSIONS: These data demonstrate that Notch signaling plays an essential role in biliary repair. Lack of Notch-2 prevents biliary tubule formation, both in vivo and in vitro. Lack of RBP-Jk inhibits the generation of biliary-committed precursors and tubule formation.

Intrahepatic biliary ablation with pure ethanol: an experimental model of biliary atresia.

PURPOSE: We describe a new rat model of biliary atresia, induced by biliary ablation with pure ethanol. METHODS: A catheter was inserted and fixed in the common bile duct of male rats. Saline or pure ethanol was injected through the catheter and the animals were monitored for 8 weeks thereafter. We measured total bilirubin (T-Bil), aspartate aminotransferase (AST), alanine transaminase (ALT), and hyaluronic acid (HA) and examined liver biopsy specimens immunohistochemically for α-smooth muscle actin staining (α-SMA) and transforming growth factor-ß1 (TGF-ß1). RESULTS: The ethanol injection group animals were further divided into a temporary and a persistent liver dysfunction group. In the persistent group, T-Bil, AST, ALT and HA levels were significantly higher after 8 weeks in the persistent group than in the control group and the temporary group. In the ethanol injection group, α-SMA expression was prominent in the surrounding proliferative bile ducts and portal areas. The distribution of TGF-ß1 was found prominently in hepatocytes in the center of nodules and in ductular epithelial cells. CONCLUSIONS: This study characterizes the effects of ethanol-induced bile duct injury in rats, resulting in sclerosing cholangitis and its secondary effects. We believe that this experimental model will prove useful in the study of biliary atresia.