Selective Trans-Catheter Coil Embolization of Cystic Duct Stump in Post-Cholecystectomy Bile Leak.

BACKGROUND: Percutaneous drainage is a first-line treatment for bilomas developed post-cholecystectomy in the setting of bile leak from the cystic duct stump. Percutaneous drainage is usually followed by surgical or endoscopic treatment to address the leak. AIMS: This study aimed to evaluate outcome of selective coil embolization of the cystic duct stump via the percutaneously placed drainage catheters in patients with post-cholecystectomy bile leak. METHODS: Seven patients with persistent bile leak after laparoscopic cholecystectomy who underwent percutaneous catheter placement for biloma/abscess formation in the region of the gallbladder fossa were followed. These patients underwent selective trans-catheter cystic duct stump coil embolization from Feb 2013 to Feb 2019. Procedural management, complications, and success rates were analyzed. RESULTS: All patients underwent placement of a percutaneous catheter for drainage of biloma formation in the gallbladder fossa post-cholecystectomy. Selective coil embolization of the cystic duct was performed through the existing percutaneous tract on average 3.5 weeks after percutaneous catheter placement, resulting in resolution of the biloma. All bile leaks were immediately closed. None of the patients showed recurrent bile leak or further clinical symptoms. Coil migration to the common bile duct was diagnosed in a single case, after 2.5 years, with no bile leak reported. CONCLUSIONS: Selective trans-catheter coil embolization of the cystic stump is a feasible and safe procedure, which successfully seals leaking cystic duct stumps and can circumvent the need for repeat surgical or endoscopic intervention in selected patient populations.

Regulation of cyclic nucleotides in the urinary tract.

Cyclic nucleotide levels are controlled through their synthesis from nucleotide triphosphates by cyclases and their degradation to 5'-monophosphates by phosphodiesterases (PDEs). Components controlling cyclic AMP-induced relaxation in the urinary tract include receptors, inhibitory and stimulatory G-proteins, isoforms of adenylyl cyclase and PDEs. The responsiveness of PDEs to a variety of physiological challenges is related to the presence of multiple families of isoenzymes with specific localization within tissues and within cells. At least 11 families of PDEs encode more than 50 PDE proteins produced in mammalian cells. In the urinary tract, characterization of PDE isoforms has lagged behind other systems and much of the literature was published prior to identification of PDE7, 8, 9, 10, 11. Specific PDE inhibitors regulate smooth muscle function in the bladder, urethra, prostate and ureter. The pharmacological potential of these inhibitors may include treatment of urge incontinence and the low compliance bladder, and treatment of prostate cancer. G-proteins also regulate cyclic AMP production. Changes in specific G- protein isoforms with aging, most prominently Gialpha2, cause decreased relaxation response in the aging bladder. As we have seen here with aging and certainly in other disease processes, levels of the components of adenylyl cyclase/phosphodiesterase/protein kinase can change and thus affect the relaxation response. By exploitation of differences in PDE expression in disease, such as the overexpression of PDEs in cancer, treatment options may present themselves.