<b><i>Background/Objectives:</i></b> Anastomotic leakage remains the most devastating postoperative complication in colorectal surgery. The mechanical integrity of the newly formed colorectal anastomosis can be evaluated by visual inspection intraoperatively; both air leak and liquid leak tests are also used to evaluate the integrity of stapled colorectal anastomoses. It is not clear whether double-stapled anastomoses are more prone to leaks than single-stapled anastomoses. The aim of our study was to compare the methylene blue and the air leak test in the experimental setting of single-stapled and double-stapled porcine bowels. <b><i>Methods:</i></b> Twenty-four distal colons were excised from slaughtered pigs without delay. The proximal bowel end was closed with a linear stapler using blue cartridges. The bowels were randomly divided into single-stapled or double-stapled groups. Air leak and methylene blue leak tests were performed. A digital pressure monitor with a gradual pressure increase function was used to both gradually increase pressure within the bowel and to determine the pressure at which the stapler line disintegrated. <b><i>Results:</i></b> Air leakage occurred at a mean pressure of 51.62 (±16.60) mm Hg and methylene blue leakage occurred at 46.54 (±16.78) mm Hg (<i>p</i> = 0.31). The air and methylene blue leaks occurred at comparable pressures in single-stapled bowels and in double-stapled bowels (47.21 [±14.02] mm Hg vs. 50.96 [±19.15] mm Hg, <i>p</i> = 0.6). <b><i>Conclusions:</i></b> The methylene blue solution leak test is not inferior to the air leak test. There is no significant difference in bursting pressure between single-stapled and double-stapled anastomoses.

No abstract

Ischemia-reperfusion injury (IRI) is encountered in various stages during solid organ transplantation (SOT). IRI is known to be a multifactorial inflammatory condition involving hypoxia, metabolic stress, leukocyte extravasation, cellular death (including apoptosis, necrosis and necroptosis) and an activation of immune response. Although the cycle of sterile inflammation during IRI is consistent among different organs, the underlying mechanisms are poorly understood. Receptor-interacting protein kinase 3 (RIPK3) and mixed-lineage kinase domain-like pseudokinase (MLKL) are thought to be crucial in the implementation of necroptosis. Moreover, apart from “silent” apoptotic death, necrosis also causes sterile inflammation—necroinflammation, which is triggered by various damage-associated molecular patterns (DAMPs). Those DAMPs activate the innate immune system, causing local and systemic inflammatory responses, which can result in graft failure. In this overview we summarize knowledge on mechanisms of sterile inflammation processes during SOT with special focus on necroptosis and IRI and discuss protective strategies.

No abstract