In live donor liver transplantation, rigorous standardized criteria for matching of liver volume between donor and recipient have prevented graft loss because of size mismatch. In deceased whole liver transplantation, the safe donor-recipient size mismatch range remains unknown. We developed a multivariate survival model (generalized additive model) to estimate hazard risk of body surface area index (BSAi) for 3-year graft survival using data derived from the national registry database between 2005 and 2010. BSAi was calculated by BSA of donor divided by BSA of recipient. 24 509 patients were included in the analysis. Small-for-size (SFS) grafts with BSAi less than 0.78 had a significant impact on graft dysfunction with progressive increase of hazard risk toward the lowest end and a higher incidence of primary graft nonfunction and vascular thrombosis. Large-for-size (LFS) grafts with BSAi greater than 1.24 had a significant impact on graft dysfunction with progressive increase of hazard risk toward the largest end. Our findings suggest that donor grafts with BSAi < 0.78 could be considered 'SFS' and donor grafts with BSAi > 1.24 could be considered 'LFS', with both extremes resulting in decreased graft survival. Therefore, BSAi > 0.78 and <1.24 appears to be a safe range to avoid adverse outcome associated with size mismatch.
AKI is a major clinical problem with extremely high mortality and morbidity. Kidney hypoxia or ischemia-reperfusion injury inevitably occurs during surgery involving renal or aortic vascular occlusion and is one of the leading causes of perioperative AKI. Despite the growing incidence and tremendous clinical and financial burden of AKI, there is currently no effective therapy for this condition. The pathophysiology of AKI is orchestrated by renal tubular and endothelial cell necrosis and apoptosis, leukocyte infiltration, and the production and release of proinflammatory cytokines and reactive oxygen species. Effective management strategies require multimodal inhibition of these injury processes. Despite the past theoretical concerns about the nephrotoxic effects of several clinically utilized volatile anesthetics, recent studies suggest that modern halogenated volatile anesthetics induce potent anti-inflammatory, antinecrotic, and antiapoptotic effects that protect against ischemic AKI. Therefore, the renal protective properties of volatile anesthetics may provide clinically useful therapeutic intervention to treat and/or prevent perioperative AKI. In this review, we outline the history of volatile anesthetics and their effect on kidney function, briefly review the studies on volatile anesthetic-induced renal protection, and summarize the basic cellular mechanisms of volatile anesthetic-mediated protection against ischemic AKI.
Aortohepatic conduits provide a vital alternative for graft arterialization during liver transplantation. Conflicting results exist with respect to the rates of comorbidities, and long-term survival data on primary grafts are lacking. To identify the complications associated with aortohepatic conduits in primary liver transplantation and their impact on survival, we conducted a single-center, retrospective cohort analysis of all consecutive adult (n 5 1379) and pediatric primary liver transplants (n 5 188) from 1998 to 2009. The outcomes of aortohepatic conduits were compared to those of standard arterial revascularization. Adults with a conduit (n 5 267) demonstrated, in comparison with adults with standard arterialization (n 5 1112), an increased incidence of late (>1 month after transplantation) hepatic artery thrombosis (HAT; 4.1% versus 0.7%, P < 0.001) and ischemic cholangiopathy (7.5% versus 2.7%, P < 0.001) and a lower 5-year graft survival rate (61% versus 70%, P 5 0.01). The adjusted hazard ratio (HR) for graft loss in the conduit group was 1.38 [95% confidence interval (CI) 5 1.03-1.85, P 5 0.03]. Notably, the use of conduits (HR 5 4.91, 95% CI 5 1.92-12.58) and a warm ischemia time > 60 minutes (HR 5 11.12, 95% CI 5 3.06-40.45) were independent risk factors for late HAT. Among children, the complication profiles were similar for the conduit group (n 5 81) and the standard group (n 5 107). In the pediatric cohort, although the 5-year graft survival rate for the conduit group (69%) was significantly impaired in comparison with the rate for the standard group (81%, P 5 0.03), the use of aortohepatic conduits did not emerge as an independent predictor of diminished graft survival via a multivariate analysis. In conclusion, in adult primary liver transplantation, the placement of an aortohepatic conduit should be strictly limited because of the greater complication rates (notably late HAT) and impaired graft survival; for children, its judicious use may be acceptable. Liver Transpl 19:916-925,
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