Orthotopic liver transplantation is the definitive treatment for end-stage liver disease and hepatocellular carcinomas. Biliary complications are the most common complications seen after transplantation, with an incidence of 10–25%. These complications are seen both in deceased donor liver transplant and living donor liver transplant. Endoscopic treatment of biliary complications with endoscopic retrograde cholangiopancreatography (commonly known as ERCP) has become a mainstay in the management post-transplantation. The success rate has reached 80% in an experienced endoscopist’s hands. If unsuccessful with ERCP, percutaneous transhepatic cholangiography can be an alternative therapy. Early recognition and treatment has been shown to improve morbidity and mortality in post-liver transplant patients. The focus of this review will be a learned discussion on the types, diagnosis, and treatment of biliary complications post-orthotopic liver transplantation.

Endoscopic stent placement is a common primary management therapy for benign and malignant biliary strictures. However, continuous use of stents is limited by occlusion and migration. Stent technology has evolved significantly over the past two decades to reduce these problems. The purpose of this article is to review current guidelines in managing malignant and benign biliary obstructions, current endoscopic techniques for stent placement, and emerging stent technology. What began as a simple plastic stent technology has evolved significantly to include uncovered, partially covered, and fully covered self-expanding metal stents (SEMS) as well as magnetic, bioabsorbable, drug-eluting, and antireflux stents.

Endoscopic stent placement is a common primary management therapy for benign and malignant biliary strictures. However, continuous use of stents is limited by occlusion and migration. Stent technology has evolved significantly over the past two decades to reduce these problems. The purpose of this article is to review current guidelines in managing malignant and benign biliary obstructions, current endoscopic techniques for stent placement, and emerging stent technology. What began as a simple plastic stent technology has evolved significantly to include uncovered, partially covered, and fully covered self-expanding metal stents (SEMS) as well as magnetic, bioabsorbable, drug-eluting, and antireflux stents.1

c Mycobacteria, the etiological agents of tuberculosis and leprosy, have coevolved with mammals for millions of years and have numerous ways of suppressing their host's immune response. It has been suggested that mycobacteria may contain genes that reduce the host's ability to elicit CD8 ؉ T cell responses. We screened 3,290 mutant Mycobacterium bovis bacillus Calmette Guerin (BCG) strains to identify genes that decrease major histocompatibility complex (MHC) class I presentation of mycobacterium-encoded epitope peptides. Through our analysis, we identified 16 mutant BCG strains that generated increased transgene product-specific CD8 ؉ T cell responses. The genes disrupted in these mutant strains had disparate predicted functions. Reconstruction of strains via targeted deletion of genes identified in the screen recapitulated the enhanced immunogenicity phenotype of the original mutant strains. When we introduced the simian immunodeficiency virus (SIV) gag gene into several of these novel BCG strains, we observed enhanced SIV Gag-specific CD8؉ T cell responses in vivo. This study demonstrates that mycobacteria carry numerous genes that act to dampen CD8 ؉ T cell responses and suggests that genetic modification of these genes may generate a novel group of recombinant BCG strains capable of serving as more effective and immunogenic vaccine vectors.

Fifty-four year-old man with recent history of myocardial infarction and a percutaneous coronary intervention who suffered a ventricular fibrillation arrest at home. He was resuscitated in the field. His heart rhythm was in atrial fibrillation. The cardiac catheterization showed a patent stent from his previous myocardial infarction and no new occlusions. He subsequently underwent hypothermia protocol using the Alsius CoolGard 3000 Temperature Control System and Icy Catheter. Heparin drip was started for atrial fibrillation 36 hours after catheter insertion and became therapeutic 2 hours before the end of cooling maintenance phase. Heparin drip was stopped 4 hours into the rewarming phase because of spontaneous conversion to sinus rhythm. Subcutaneous heparin was resumed for deep venous thrombosis prophylaxis. He was extubated to room air after hypothermia protocol. The cooling catheter was removed 88 hours after insertion. Within 1 minute of catheter removal, his oxygen saturation dropped to 80%. Transthoracic echocardiogram showed a mobile thrombus in the right atrium prolapsing into the right ventricle. Computer tomography angiography of the chest confirmed a large saddle embolus. Ninety minutes later, patient went into cardiac arrest with pulseless electrical activity while he was being considered for surgical embolectomy, but he could not be resuscitated. The temporal relationship of the catheter removal and his acute clinical decompensation led to believe that this was an intravascular cooling catheter (ICC)-related event. Providers should be cognizant of the complications of central venous catheters such as thrombosis formation, as it could lead to fatal pulmonary embolism. Physicians should promote frequent assessment of the access site(s) during routine physical examinations and potentially use point of care vascular ultrasound in high-risk cases to rule out a catheter-associated thrombus before catheter removal.