Management of biliary complications following damage control surgery for liver trauma

Background: The liver is the most frequently injured solid intra-abdominal organ. The major cause of early death following severe liver trauma is exsanguination. Although perihepatic packing improves survival in severe liver trauma, this leaves parenchymal damage untreated, often resulting in post-traumatic biliary leakage and a subsequent rise in morbidity. The aim of this study was to analyze the incidence and treatment of biliary leakage following the operative management of liver trauma. Methods: Patients presenting between 2000 and 2009 to Erasmus University Medical Centre with traumatic liver injury were identified. Data from 125 patients were collected and analyzed. Sixty-eight (54 %) patients required operation. All consecutive patients with post-operative biliary complications were analyzed. Post-operative biliary complications were defined as biloma, biliary fistula, and bilhemia. Results: Ten (15 %) patients were diagnosed with post-operative biliary leakage following liver injury. Three patients with a biloma were treated with percutaneous drainage, without further intervention. Seven patients with significant biliary leakage were managed by endoscopic stenting of the common bile duct to decompress the internal biliary pressure. One patient had a relaparotomy and right hemihepatectomy to control biliary leakage and injury of the right hepatic duct. Conclusion: Biliary complications continue to occur frequently following damage control surgery for liver trauma. The majority of biliary complications can be managed without an operation. Endoscopic retrograde cholangiopancreatography (ERCP) and internal stenting represent a safe strategy to manage post-operative biliary leakage and bilhemia in patients following liver trauma. Minor biliary leakage should be managed by percutaneous drainage alone

Development and Validation of an Inflammatory Bowel Diseases Monitoring Index for Use With Mobile Health Technologies

Mobile health technologies are advancing rapidly as smartphone use increases. Patients with inflammatory bowel disease (IBD) might be managed remotely through smartphone applications, but no tools are yet available. We tested the ability of an IBD monitoring tool, which can be used with mobile technologies, to assess disease activity in patients with Crohn's disease (CD) or ulcerative colitis (UC). We performed a prospective observational study to develop and validate a mobile health index for CD and UC, which monitors IBD disease activity using patient-reported outcomes. We collected data from disease-specific questionnaires completed by 110 patients with CD and 109 with UC who visited the University of California, Los Angeles, Center for IBD from May 2013 through January 2014. Patient-reported outcomes were compared with clinical disease activity index scores to identify factors associated with disease activity. Index scores were validated in 301 patients with CD and 265 with UC who visited 3 tertiary IBD referral centers (in California or Europe) from April 2014 through March 2015. We assessed activity of CD based on liquid stool frequency, abdominal pain, patient well-being, and patient-assessed disease control, and activity of UC based on stool frequency, abdominal pain, rectal bleeding, and patient-assessed disease control. The indices identified clinical disease activity with area under the receiver operating characteristic curve values of 0.90 in patients with CD and 0.91 in patients with UC. They identified endoscopic activity with area under the receiver operating characteristic values of 0.63 in patients with CD and 0.82 in patients with UC. Both scoring systems responded to changes in disease activity (P < .003). The intraclass correlation coefficient for test-retest reliability was 0.94 for CD and for UC. We developed and validated a scoring system to monitor disease activity in patients with CD and UC that can be used with mobile technologies. The indices identified clinical disease activity with area under the receiver operating characteristic curve values of 0.9 or higher in patients with CD or UC, and endoscopic activity in patients with UC but not C

Mycophenolic acid is a potent inhibitor of the expression of tumour necrosis factor- and tumour necrosis factor-receptor superfamily costimulatory molecules

The tumour necrosis factor (TNF) ligands CD154, CD70 and TNF receptors CD134 and CD137 are all involved in allograft rejection. Because these molecules are not present on resting T cells, we investigated whether immunosuppressive drugs could inhibit their induction. Expression was induced in vitro on T cells by phorbol 12-myristate 13-acetate and ionomycin or by allogeneic dendritic cells in the presence or absence of cyclosporin A (CsA), tacrolimus (TAC), rapamycin derivative (SDZ RAD), or mycophenolic acid (MPA), and determined by flow cytometry. To study the effect of in vivo exposure to immunosuppressive drugs on these molecules, immunohistochemistry was performed on human lymph nodes from patients treated with TAC or TAC and MMF. The calcineurin inhibitors (CI) CsA and TAC strongly suppressed the induction of CD70, CD137 and CD154, but not of CD134, upon pharmacological stimulation of T cells in vitro. In allogeneic stimulations only CD137 and CD154 were inhibited by CI. SDZ RAD did not inhibit pharmacological induction, but in allogeneic stimulations all the investigated molecules were partially suppressed. Both in pharmacological and in allogeneic stimulations, MPA inhibited induction of all tested molecules on T cells nearly completely at 4 µg/ml. However, in lymph nodes obtained from patients chronically treated with MMF and TAC no reduction of the expression of these molecules was observed. This was possibly caused by trough levels which were in vivo lower (mean: 2·3 µg/ml) than the concentration giving complete inhibition in vitro. In conclusion, in contrast to CsA, TAC and SDZ RAD, MPA is a potent inhibitor of the induction of TNF- and TNF-receptor superfamily molecules on T cells. To obtain long-term suppression of these molecules in vivo, a plasma trough level of 4 µg/ml is indicated