This study identified patient and operative risk factors for anastomotic leak on a national scale. It also demonstrates that these patients have increased morbidity and 30-day mortality rates, experience multiple readmissions to the hospital, and have a higher likelihood of requiring further operative intervention.

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A complete evaluation of living donor liver transplantation (LDLT) in the United States has been difficult because of the persistent low volume and the lack of adequate comparisons with deceased donor liver transplantation (DDLT). Recent reports have suggested outcomes equivalent to those for DDLT, but these studies did not adjust for differences in recipient selection. From a linkage between the University HealthSystem Consortium and Scientific Registry of Transplant Recipients databases, we identified 14,282 patients at 62 centers who underwent DDLT from 2007 to 2012 and 715 patients at 35 centers who underwent LDLT during the same period. Then, we performed 1:1 propensity score matching for 708 LDLT recipients based on age, Model for End-Stage Liver Disease (MELD) score, and pretransplant patient status. The median follow-up was 2 years. Compared with DDLT recipients, LDLT recipients were more likely to be white (84.5% versus 72.2%) and female (41.1% versus 31.7%), to have lower MELD scores (15 versus 19), and to be classified preoperatively as independent (65.3% versus 46.7%) and not hospitalized (91.3% versus 78.4%). The posttransplant length of stay (LOS), in-hospital mortality, costs, and survival were similar between the groups, but LDLT recipients were more likely to be readmitted within 30 days (44.9% versus 37.1%, P 5 0.001). After matching, the difference in 30-day readmission rates persisted (45.1% versus 33.8%, P 5 0.001), but there were no differences in the LOS, costs, patient survival, or graft survival. This national report shows that LDLT is associated with higher readmission rates in comparison with DDLT, but the results are comparable for other key patient metrics.

Background The pathophysiology that drives the subacute hypercoagulable state commonly seen after traumatic brain injury (TBI) is not well understood. Alterations caused by TBI in platelet and microparticle (MP) numbers and function have been suggested as possible causes; however, the contributions of platelets and MPs are currently unknown. Materials and methods A weight-drop technique of TBI using a murine model of moderate head injury was used. Blood was collected at intervals after injury. MP enumeration and characterization were performed using Nanoparticle Tracking Analysis, and platelet counts and coagulation parameters were determined using thromboelastometry. A MP procoagulant assay was used to compare activity between injured and sham mice. Results At 24 h after injury, there were no changes in circulating platelet numbers. However, there was a decrease in platelet contribution to clot formation. In contrast, there was a decline in circulating total MP numbers. When MPs from sham mice were added to the blood from head-injured animals, there was a normalization of platelet contribution to clot formation. Conversely, when MPs from TBI mice were added to sham blood, there was a significant decrease in platelet contribution to clot formation. Notably, there was an increase in MP procoagulant activity in head-injured mice. Conclusions MPs generated after TBI likely contribute to altered coagulation after head injury and may play a key role in the development of a posttraumatic hypercoagulable state in TBI patients.

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