Living donor liver transplantation has become an essential surgical option to address the shortage of deceased donor organs. Unlike recipients, donors are healthy individuals who accept substantial surgical risks solely for the benefit of others. Thus, perioperative anesthetic management must emphasize donor safety, minimize morbidity, and optimize recovery. Key priorities include maintaining stable hemodynamics with minimal blood loss, implementing enhanced recovery after surgery protocols, and delivering effective multimodal pain control strategies. This review integrates current evidence and experience from recent publications to highlight the anesthetic principles guiding minimally invasive living liver donor surgery.

Living donor liver transplantation (LDLT) has become a critical strategy for addressing the global organ shortage, particularly in East Asia. While perioperative donor safety has been well established, the long-term hepatic and metabolic consequences of donor hepatectomy have only recently come under systematic investigation. A landmark Korean population-based study of 12,372 donors revealed elevated incidence rates of liver failure, diabetes, hypertension, cardiovascular events, and overall mortality compared with matched healthy controls. Post-donation steatotic liver disease develops progressively, reaching a cumulative incidence of approximately 28% at 15 years, with donation for a pediatric recipient, pre-donation body mass index, and male sex as independent predictors. Liver regeneration after right hepatectomy is generally robust, with most donors achieving 80%-90% of their original liver volume by 6-12 months, though factors such as donor age, portal hemodynamics, and body composition influence the regenerative response. This review synthesizes the current evidence on long-term hepatic regeneration, liver function, post-donation steatosis, and cardiometabolic morbidity in living liver donors. We discuss identifiable risk factors for adverse outcomes and propose a structured framework for lifelong donor surveillance. These data underscore the ethical obligation of transplant programs to ensure comprehensive, sustained follow-up for all living liver donors.

Background: A systematic evaluation of potential living liver donors is essential to ensure donor safety and optimize recipient outcomes in living donor liver transplantation (LDLT). This study aimed to assess donor acceptance rates and reasons for disqualification among individuals evaluated for LDLT at a high-volume transplant center over a one-year period. Methods: We retrospectively reviewed 1,087 potential living liver donors who presented for LDLT evaluation in 2023. Of these, 991 candidates advanced beyond the initial screening (Stage 1) and underwent comprehensive clinical, imaging, and pathological assessments (Stages 2 and 3). Candidates who discontinued after Stage 1 were excluded due to the absence of documented reasons for non-progression. Results: Among the 991 candidates who proceeded beyond initial screening, 473 (47.7%) completed the full donor evaluation, of whom 466 were judged to be suitable donors. Among suitable donors, 384 (82.4%) proceeded to donor hepatectomy, whereas 82 did not, primarily due to recipient-related factors such as clinical deterioration or withdrawal of consent. Donor ineligibility was determined in 422 candidates (42.6%), most commonly due to inadequate remnant liver volume (52.8%), hepatic steatosis (20.6%), and insufficient graft size (10.2%). Among candidates undergoing Stage 2 evaluation, 162 (16.3%) failed to meet steatosis criteria; 126 were excluded solely for steatosis and advised weight reduction, and 39 subsequently became eligible and successfully donated. Conclusion: In this high-volume LDLT center, donor disqualification was primarily driven by remnant liver volume and hepatic steatosis. Targeted interventions such as weight reduction enabled successful donation in a subset of initially ineligible candidates, underscoring the importance of individualized donor evaluation and pre-donation optimization.

Background: We developed a simplified variant of the ADV score, the AFP-PIVKA-II (AP) score for post-transplant hepatocellular carcinoma (HCC) prognosis, which considers only AFP and PIVKA-II levels excluding morphometric tumor size information from the ADV score. This study investigated the prognostic performance of the AP score in predicting HCC recurrence and overall survival (OS) after living donor liver transplantation (LDLT). Methods: We analyzed 843 patients with HCC who underwent LDLT between 2006 and 2015, assessing HCC recurrence and OS in relation to AP score. Results: The median pretransplant AFP and PIVKA-II levels were 12.8 ng/mL and 27 mAU/mL, respectively. The median and mean AP scores were 2.6 log (range: 0.6-9.2 log) and 2.9±1.1 log, respectively. The 5-year time-dependent area under the receiver operating characteristic curve for the AP score in predicting post-transplant HCC recurrence was 0.672 (p<0.001). HCC recurrence and OS curves along AP score intervals of 1.0 log showed statistical differences in accordance with the AP scores (both p<0.001). Using a Youden index J-derived AP score cutoff of 4.0 log, two-tiered groups (ADV <4.0 log vs. ADV ≥4.0 log) showed statistically significant differences in HCC recurrence and OS (both p<0.001). Harrell's c-indices for AP score with cutoff of 4.0 log and ADV scores with cutoff of 5.0 log regarding HCC recurrence and OS were similar. Conclusion: The AP score functions as an integrated surrogate marker for predicting post-transplant outcomes in patients with HCC undergoing LDLT. It may serve as a simplified alternative to the ADV score, particularly in patients with small HCCs.

Background: Warm ischemia is a major contributor to ischemic cholangiopathy and non-anastomotic biliary strictures (NAS) after liver transplantation, particularly in donation-after-circulatory-death grafts. However, the isolated impact of warm ischemia on peribiliary fibrosis is difficult to delineate because clinical settings involve overlapping effects of cold ischemia, reperfusion injury, and alloimmunity. This study aimed to establish a non-transplant rat model that isolates warm ischemic biliary injury and to compare the antifibrotic effects of rapamycin and tacrolimus. Methods: Warm ischemia was induced in Sprague-Dawley rats by ligating both ends of the peribiliary vascular plexus and the hepatic artery, followed by 30 minutes of portal vein clamping. Rats were randomly assigned to control, tacrolimus (1 mg/kg/day), or rapamycin (1 mg/kg/day) groups (n=15 per group). Serum alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transferase, and total bilirubin were measured serially. Hematoxylin and eosin (H&E) and Sirius red staining were performed at 1, 3, and 6 weeks. Peribiliary fibrosis was quantified using digital image analysis of collagen area fraction. Results: Warm ischemia induced acute hepatobiliary injury with transient enzyme elevations, but no significant intergroup differences were observed. Histologically, biliary epithelial proliferation and collagen deposition increased progressively and became prominent at 6 weeks. At this time point, fibrosis ratios differed significantly (overall p=0.002): controls showed the highest fibrosis (4.8%), followed by tacrolimus (2.4%) and rapamycin (1.7%). Both immunosuppressants significantly reduced fibrosis compared with controls (p<0.05), whereas the difference between tacrolimus and rapamycin was not significant. Conclusion: This warm ischemia model demonstrates that isolated ischemic injury alone can induce progressive peribiliary fibrosis. Rapamycin and tacrolimus attenuated fibrosis, with rapamycin producing the lowest collagen deposition. These findings provide mechanistic insight into ischemic cholangiopathy after liver transplantation-particularly in donation after circulatory death grafts-and underscore the need for further studies using models that incorporate cold ischemia, reperfusion, and alloimmune factors.

Background: In the era of nucleoside analogs (NA), we investigated the safety of using hepatitis B surface antigen (HBsAg)-positive grafts in liver transplantation (LT) using nationwide KOTRY data. Methods: Among 4,265 adult LTs in the KOTRY registry (April 2014-January 2020), 20 (0.5%) used HBsAg(+) grafts. The S(+) group was compared with HBsAg-negative groups, both HBcAb(+) (C[+]) and HBcAb(-) (SC[-]), using 1:1 propensity score matching. Patient and graft survival were evaluated using Kaplan-Meier analysis. Cox regression was used to identify prognostic factors. Results: No significant differences were observed in patient or graft survival between S(+) and C(+) or SC(-) groups. Key prognostic factors for patient survival included age, HCC, MELD score, ascites, and encephalopathy. For graft survival, HCC, preoperative HCC treatment, MELD score, ascites, and encephalopathy were significant. HBV recurrence occurred in the S(+) group, but did not compromise outcomes. Conclusion: In HBV-endemic regions, HBsAg(+) liver grafts can be safely used to expand the donor pool without compromising LT outcomes when combined with appropriate prophylaxis.

Replacing the retrohepatic inferior vena cava (IVC) following concurrent resection of the IVC and tumor-involved liver is an emerging surgical technique in living donor liver transplantation (LDLT), particularly for managing hepatocellular carcinomas near the IVC. This approach makes the extent of hepatectomy in LDLT comparable to that of deceased donor liver transplantation. We report a pediatric LDLT case involving IVC and portal vein (PV) replacement with an iliac vein homograft to treat advanced hepatoblastomas. The patient was a 24-month-old girl weighing 9.1 kg, presenting with large, multiple hepatoblastomas infiltrating the retrohepatic IVC and PV. After a 2-week waiting period, a cold-stored iliac vein graft was obtained, and the transplantation was performed using a left lateral section graft from her father. A 4-cm iliac vein homograft was anastomosed between the suprahepatic and suprarenal IVC stumps. The liver graft was implanted following standard procedures, with the PV reconstructed via a telescope-shaped anastomosis using the vein graft interposition. The patient experienced an uncomplicated recovery and is currently receiving scheduled adjuvant chemotherapy. In conclusion, IVC and PV replacement with vein homografts represents a feasible and effective surgical strategy for pediatric LDLT patients with advanced liver malignancies involving vascular invasion.