No abstract

Background Acute kidney injury (AKI) occurs frequently after liver transplant surgery and is associated with significant morbidity and mortality. While the impact of intraoperative hypotension (IOH) on postoperative AKI has been well demonstrated in patients undergoing a wide variety of non-cardiac surgeries, it remains poorly studied in liver transplant surgery. We tested the hypothesis that IOH is associated with AKI following liver transplant surgery. Methods This historical cohort study included all patients who underwent liver transplant surgery between 2014 and 2019 except those with a preoperative creatinine > 1.5 mg/dl and/or who had combined transplantation surgery. IOH was defined as any mean arterial pressure (MAP) < 65 mmHg and was classified according to the percentage of case time during which the MAP was < 65 mmHg into three groups, based on the interquartile range of the study cohort: “short” (Quartile 1, < 8.6% of case time), “intermediate” (Quartiles 2–3, 8.6–39.5%) and “long” (Quartile 4, > 39.5%) duration. AKI stages were classified according to a “modified” “Kidney Disease: Improving Global Outcomes” (KDIGO) criteria. Logistic regression modelling was conducted to assess the association between IOH and postoperative AKI. The model was run both as a univariate and with multiple perioperative covariates to test for robustness to confounders. Results Of the 205 patients who met our inclusion criteria, 117 (57.1%) developed AKI. Fifty-two (25%), 102 (50%) and 51 (25%) patients had short, intermediate and long duration of IOH respectively. In multivariate analysis, IOH was independently associated with an increased risk of AKI (adjusted odds ratio [OR] 1.05; 95%CI 1.02–1.09; P < 0.001). Compared to “short duration” of IOH, “intermediate duration” was associated with a 10-fold increased risk of developing AKI (OR 9.7; 95%CI 4.1–22.7; P < 0.001). “Long duration” was associated with an even greater risk of AKI compared to “short duration” (OR 34.6; 95%CI 11.5-108.6; P < 0.001). Conclusions Intraoperative hypotension is independently associated with the development of AKI after liver transplant surgery. The longer the MAP is < 65 mmHg, the higher the risk the patient will develop AKI in the immediate postoperative period, and the greater the likely severity. Anesthesiologists and surgeons must therefore make every effort to avoid IOH during surgery.

Background and Aim The aim of this study is to describe the cholangiographic features and endoscopic management of biliary cast syndrome (BCS), a rare specific ischemic cholangiopathy following liver transplantation. Methods Patients with biliary complications were identified from prospectively collected database records of patients who underwent liver transplantation at the Erasme Hospital from January 2005 to December 2014. After excluding patients with hepatico‐jejunostomy or no suspicion of stricture, cholangiograms obtained during endoscopic retrograde cholangiopancreatography (ERCP) and magnetic resonance imaging were systematically reviewed. Biliary complications were categorized as anastomotic (AS) and non‐AS strictures, and patients with BCS were identified. Clinical, radiological, and endoscopic data were reviewed. Results Out of 311 liver transplantations, 14 cases were identified with BCS (4.5%) and treated with ERCP. Intraductal hyperintense signal on T1‐weighted magnetic resonance and a “duct‐in‐a‐duct” image were the most frequent features of BCS on magnetic resonance imaging. On initial ERCP, 57% of patients had no stricture. Complete cast extraction was achieved in 12/14, and one of these had cast recurrence. On follow‐up, 85% of the patients developed biliary strictures that were treated with multiple plastic stents reaching 60% complete stricture resolution, but 40% of them had recurrence. After a median follow‐up of 58 months, BCS patients had lower overall and graft survival (42.9% and 42.9%) compared with non‐AS (68.8% and 56.3%) and AS (83.3% and 80.6%), respectively. Conclusions Particular magnetic resonance‐cholangiographic and ERCP‐cholangiographic features of BCS have been identified. Outcomes for BCS are characterized by high complete cast extraction rates, high incidence of secondary strictures, and poorer prognosis.

LRYGBP post-TOGA apparently can be done without any trouble. The performance of TOGA does not seem to interfere with the short-term results of the LRYGBP.

The liver ischemia‐reperfusion (IR) injury that occurs consequently to hepatic resection performed in patients with metastases can lead to tumor relapse for not fully understood reasons. We assessed the effects of liver IR on tumor growth and the innate immune response in a mouse model of colorectal (CR) liver metastasis. Mice subjected to liver ischemia 2 days after intrasplenic injection of CR carcinoma cells displayed a higher metastatic load in the liver, correlating with Kupffer cells (KC) death through the activation of receptor‐interating protein 3 kinase (RIPK3) and caspase‐1 and a recruitment of monocytes. Interestingly, the immunoregulatory mediators, tumor necrosis factor‐α (TNF‐α) and heme oxygenase‐1 (HO‐1) were strongly upregulated in recruited monocytes and were also expressed in the surviving KC following IR. Using TNFflox/flox LysMcre/wt mice, we showed that TNF deficiency in macrophages and monocytes favors tumor progression after IR. The antitumor effect of myeloid cell‐derived TNF involved direct tumor cell apoptosis and a reduced expression of immunosuppressive molecules such as transforming growth factor‐β, interleukin (IL)‐10, inducible nitric oxyde synthase (iNOS), IL‐33 and HO‐1. Conversely, a monocyte/macrophage‐specific deficiency in HO‐1 (HO‐1flox/flox LysMcre/wt) or the blockade of HO‐1 function led to the control of tumor progression post‐liver IR. Importantly, host cell RIPK3 deficiency maintains the KC number upon IR, inhibits the IR‐induced innate cell recruitment, increases the TNF level, decreases the HO‐1 level and suppresses the tumor outgrowth. In conclusion, tumor recurrence in host undergoing liver IR is associated with the death of antitumoral KC and the recruitment of monocytes endowed with immunosuppressive properties. In both of which HO‐1 inhibition would reinforce their antitumoral activity.