Pre-transplant Portal Vein Thrombosis Research Articles

Living donor liver transplantation for patients with portal vein thrombosis: high-volume single center experience.

End-stage liver disease is commonly associated with portal vein thrombosis (PVT). Lastly, PVT is no longer an absolute contraindication for liver transplantation, and many centers adopt portal vein thrombectomy. PVT imposes special technical difficulties during living donor liver transplantation (LDLT). In this research, the experience with PVT cases during LDLT in a high-volume center is introduced. Between January 2018 and July 2023, 312 patients underwent LDLT. After 88 cases were excluded, 224 cases were included, and their incidence of pre-transplant PVT was 16.5% (37/224). Demographic and clinical features, perioperative variables, and post-transplant outcomes of patients with PVT (PVT group, n=37) were compared to patients who had no PVT (non-PVT group, n=187). According to Yerdel classification, 16, 16, 2, and 3 patients had PVT grade I, II, III, and IV, respectively. Complete venous thrombectomy was accomplished in 34 patients, while for three patients, thrombectomy was not feasible, and graft inflow was established by interposition vascular graft. For portal flow modulation, splenectomy and splenic artery ligation were performed in 7 and 4 patients, respectively, while two patients underwent post-transplant splenic artery embolization. The PVT group had longer operation time (p<0.001), longer warm ischemia time (p=0.031), longer anhepatic phase (p<0.001), and intraoperatively required more than 3 packed RBCs units (p=0.029) and ≥1 platelet unit transfusion (p=0.021) than the non-PVT group. No statistically significant difference was found between groups in terms of re-exploration (p=0.954), post-transplant PVT (p=0.375), biliary (p=0.253) and arterial complications (p=0.593), ICU stay (p=0.633), hospital stay (p=896), and 30-day mortality (p=1.000). Survival analysis showed no statistically significant difference regarding 1-year survival (p=0.176) between both groups. This study showed that patients with different stages of PVT can successfully undergo LDLT in experienced centers and that they do not differ from patients without PVT in terms of post-transplant complications.

Liver transplantation for severe hepatic trauma: A multicenter analysis from the UNOS data set.

Orthotopic liver transplantation (OLT) is rarely indicated after hepatic trauma but it can be the only therapeutic option in some patients. There are scarce data analyzing the surgical outcomes of OLT after trauma. We used the UNOS data set to identify patients who underwent OLT for trauma from 1987 to 2022 and compared them to a cohort of patients transplanted for other indications. Cox proportional hazard and multivariable logistic regression analyses were performed to assess predictors of graft and patient survival. Seventy-two patients underwent OLT for trauma during the study period. Patients with trauma were more frequently on mechanical ventilation at the time of transplantation (26.4% vs. 7.6%, p < 0.001) and had a greater incidence of pretransplant portal vein thrombosis (12.5% vs. 4%, p = 0.002). Our 4:1 matched analysis showed that trauma patients had significantly shorter wait times, higher incidence of pretransplant portal vein thrombosis and prolonged length of stay. Trauma was associated with decreased overall graft survival (hazards ratio, 1.42; 95% confidence interval, 1.01-1.98), and increased length of stay ( p = 0.048). There were no significant differences in long-term patient survival. Unique physiological and vascular challenges after severe hepatic trauma might be associated with decreased graft survival in patients requiring liver transplantation. Prognostic and Epidemiological; Level III.

The Impact of Thrombophilic Factors on Disease Progression in Children with Biliary Atresia-A Single-Centre Cohort Study.

Epidemiological evidence suggests that thrombophilic factors, including male sex, non-O blood type, MTHFRnt677TT mutation, factor V Leiden G1691A mutation, and prothrombin G20210A polymorphism, may contribute to the progression of fibrosis and occurrence of portal vein thrombosis in liver disease. We retrospectively investigated the effect of potentially thrombophilic factors on native liver survival as a patient-relevant endpoint of disease progression in a cohort of 142 children being followed up for biliary atresia at Hannover Medical School from April 2017 to October 2019. No significant association could be determined. There was no evidence for relevant differences in native liver survival for the Factor V Leiden G1691A mutation (hazard ratio [HR] = 0.86, 95% confidence interval [CI] 0.38-1.98, p = 0.73), prothrombin G20210A polymorphism (HR = 0.96, 95%CI 0.24-3.65, p = 0.96), non-O blood type (HR = 0.79, 95%CI 0.51-1.21, p = 0.28) or MTHFRnt677TT mutation (HR = 1.24, 95%CI 0.60-2.56, p = 0.56). A certain, albeit not strong, evidence of reduced native liver survival in male patients after Kasai hepatoportoenterostomy, particularly during the first 2000 days (42%; HR = 1.41, 95%CI 0.92-2.18, p = 0.11) was found. All children with pre-transplant portal vein thrombosis (n = 7) had non-O blood types. Larger multi-centre studies are necessary to show if the male sex or other thrombophilic factors could be potentially associated with reduced native liver survival.

Pre-transplant portal vein thrombosis in non-alcoholic fatty liver disease patients-pathogenesis, risk factors, and implications on management.

Along with the worldwide increase in obesity and metabolic syndrome, non-alcoholic fatty liver disease (NAFLD) and its more severe subset, non-alcoholic steatohepatitis (NASH), are on path to become the leading cause of liver transplantation in the United States. NAFLD, as well as obesity, create an inflammatory milieu via the release of adipocytokines. In turn, the inflammatory environment can trigger an increase in prothrombotic factors. Independent of inflammation, the severity of NASH is associated with a graded increase in hypercoagulability such as an increase in factor VIII, increase in plasminogen activator inhibitor-1, and decrease in protein C. Ultimately, this environment creates an increase in thrombotic risk, leading to higher rates of pre-transplant portal vein thrombosis (PVT) in patients with NASH cirrhosis vesus other causes of cirrhosis. Many studies have shown worse outcomes in liver transplant recipients with PVT as it complicates anastomotic reconstruction which can negatively affect portal blood supply needed for adequate liver functioning. Management and treatment of PVT is not standardized, but from a pharmacologic standpoint, multiple classes of anticoagulants have shown to be successful in recanalization of the portal vein and preventing recurrence of clot with minimal bleeding complications. The increasing prevalence of NASH cirrhosis and subsequent increase in PVT require further research for improved outcomes.

Meta-analysis and systematic review: Prevalence, graft failure, mortality, and post-operative thrombosis in liver transplant recipients with pre-operative portal vein thrombosis.

This study seeks to evaluate the association between pre-transplant portal vein thrombosis (PVT) and overall survival, graft failure, waitlist mortality, and post-operative PVT after liver transplantation. A conventional pairwise meta-analysis between patients with and without pre-transplant PVT was conducted using hazard ratios or odds ratios where appropriate. Prevalence of preoperative PVT was 11.6% (CI 9.70-13.7%). Pre-operative PVT was associated with increased overall mortality (HR 1.45, 95% CI 1.27-1.65) and graft loss (HR 1.58, 95% CI 1.34-1.85). In particular, grade 3 (HR 1.59, 95% CI 1.00-2.51) and 4 (HR 2.24, 95% CI 1.45-3.45) PVT significantly increased mortality, but not grade 1 or 2 PVT. Patients with PVT receiving living donor (HR 1.54, 95% CI 1.24-1.91) and deceased donor (HR 1.52, 95% CI 1.21-1.92) liver transplantation had increased mortality, with no significant difference between transplant types (P=.13). Furthermore, pre-transplant PVT was associated with higher occurrence of post-transplant PVT (OR 5.06, 95% CI 3.89-6.57). Waitlist mortality was not significantly increased in patients with pre-transplant PVT. Graft failure, mortality, and post-operative PVT are more common in pre-transplant PVT patients, especially in grade 3 or 4 PVT. Prophylactic anticoagulation can be considered to reduce re-thrombosis and improve survival.

Recipient-Specific Risk Factors Impairing Patient and Graft Outcome after Pediatric Liver Transplantation—Analysis of 858 Transplantations in 38 Years

(1) Background and Aim: Despite excellent long-term results in pediatric liver transplantation (pLTx), mortality and graft loss still are to be diminished. We aim to describe time-dependent changes and long-term outcome of a large single-center pLTx cohort and to identify independent recipient-related risk factors impairing patient and graft survival. (2) Methods: This is a retrospective single-center study analyzing all pediatric liver transplants from 1983–2020. Risk factors for mortality and graft loss were identified by univariable and multi-linear regression analysis. (3) Results: We analyzed 858 liver transplantations in 705 pediatric patients. Five-year patient/graft survival increased from 60.9%/48.0% (1983–1992) to 97.5%/86.5% (OR = 12.5; p < 0.0001/OR = 6.5; p < 0.0001) (2014–2020). Indications changed significantly over time, with a higher proportion of patients being transplanted for malignancies and metabolic disease and indications of PFIC and α1AT-deficiency declining. The era of transplantation (log7.378/9.657; p < 0.0001) and indication of acute liver failure (log = 1.944/2.667; HR = 2.015/1.772; p = 0.0114/0.002) impairs patient/graft survival significantly in the multivariate analysis. Furthermore, patient survival is worsened by re-transplantation (log = 1.755; HR = 1.744; p = 0.0176) and prolonged waiting times in high-urgency status (log = 2.588; HR = 1.073; p = 0.0026), whereas the indication of biliary atresia improved outcome (log = 1.502; HR = 0.575; p = 0.0315). Graft survival was additionally impaired by pre-existing portal vein thrombosis (log = 1.482; HR = 2.016; p = 0.0330). (4) Conclusions: Despite more complex indications, patient and graft survival after pLTx continue to improve.. Acute liver failure remains the indication with poorest outcome, and listing for high urgency liver transplantation should be considered carefully and early to keep waiting time on HU list short. Furthermore, pre-transplant portal vein thrombosis should be prevented whenever possible to improve graft survival.

Primary graft nonfunction in liver transplantation: can we predict? A single-center experience

Background Primary nonfunction (PNF) after liver transplantation is a lethal condition, requiring immediate retransplantation. The precise cause is not well known yet. The aim of this study is to determine the incidence of PNF in our liver recipients, potential risk factors, and outcome. Patients and methods A total of 248 adult liver transplant recipients from 2014 till 2017 at our Transplant Unit were included after excluding nine patients for missing data. Of 248 patients, five (2%) had PNF; two of these patients have been excluded for the purpose of data analysis, as they had machine perfusion (One Liver Assist, and the other Organox). Of the non-PNF 243 recipients, 36 patients receiving livers from donors undergoing in-situ normothermic regional perfusion or ex-situ normothermic perfusion were not included, leaving 207 patients, so the total number was 210 patients. Donor and graft variables studied including age, BMI, serum sodium, cold ischemia time, warm ischemia time, operative time, graft type, and severity of steatosis. Recipient variables included primary liver disease; United Kingdom Model for End-Stage Liver Disease (UKELD) score; posttransplant biochemistry; potential risk factors, including dialysis, inotropes, mechanical ventilation, and pretransplant portal vein thrombosis; hospital and ICU stay; and patient survival. Results UKELD score was the only significant recipient variable (P=0.044). Among donor and graft variables, notably all PNF patients received donation after circulatory death grafts. Posttransplant laboratory values were strikingly worse, clearly indicating more pronounced hepatic and renal impairment in PNF group. Creatinine levels on days 1, 3, and 5 were significantly worse. Hospital and ICU stays were longer for PNF group, with ICU stay significantly longer [median of 7 vs. 2 days (P=0.014)], with no death in PNF group. Conclusion The main risk factors for PNF in our practice were donation after circulatory death grafts and more sick (higher UKELD) recipients.

Analysis of portal vein thrombosis after liver transplantation.

Portal vein thrombosis (PVT) is one of the most deadly complications after orthotopic liver transplantation (OLT). This study aimed to identify risk factors and summarize the experience of PVT management after OLT. The clinical data of 407 adult patients received OLT from July 2011 to December 2015 was retrospectively investigated. The incidence rate of PVT was 2.9% (12/407). Pre-transplant PVT (P = 0.001), post-operative transfusion of erythrocyte (P = 0.006) and platelet (P = 0.036) were significantly associated with PVT in the univariate analysis and the appearance of pre-transplant PVT (P = 0.002, odds ratio 6.05) was the independent risk factor according to binary logistic regression. Among patients with PVT, three cases (3/12) received balloon dilation through selective catheterization of portal vein, five (5/12) received balloon-expandable stent placement, three (3/12) received thrombectomy and surgical revascularization and one (1/12) received retransplantation. Six patients (6/12) died from various complications and the remaining six were followed up with normal liver function and patent portal vein. The risk factors were pre-transplant PVT and post-operative transfusion of erythrocyte and platelet. To recipients with high risk, early diagnosis and prompt management of PVT are essential to improve prognosis.

Re-transplantation for Hepatic Artery Thrombosis: A National Perspective.

Hepatic artery thrombosis (HAT) is a major complication after liver transplantation that commonly requires re-transplantation. We queried the UNOS dataset for all patients transplanted between 1995 and 2015 for HAT. We identified 623 patients who underwent re-transplantation for HAT with a mean age of 51.25 + 10.4years. The mean BMI was 26.72kg/m2, and mean MELD score was 19.62 + 9.09. There was a higher proportion of male patients, with higher prevalence of pre-transplant portal vein thrombosis (7.4 vs. 5.4%, p = 0.04), lower incidence of hepatitis C virus infection (29.5 vs. 35.8%, p = 0.002), and shorter waiting time (61 vs. 111days, p = 0.001) in the HAT group compared to those re-transplanted for other indications. The perioperative 90-day mortality was lower in patients re-transplanted for HAT (16 vs. 20%, p = 0.02). Patients undergoing re-transplantation for HAT had 13% decreased graft survival and 13% increased long-term survival. After case-control matched analysis, graft survival and patient survival were significantly better in the HAT group. Late re-transplantation (>30days) for HAT was linked to decreased graft and patient survival when compared to those undergoing early re-transplantation (within 30days). Improved outcomes were seen in patients undergoing re-transplantation for HAT compared to patients who underwent re-transplantation for other indications. Those re-transplanted late after HAT (>30days) were associated with worse outcomes when compared to early re-transplantation.

Advanced non-alcoholic steatohepatitis cirrhosis: A high-risk population for pre-liver transplant portal vein thrombosis

AIMTo examine if liver transplant recipients with high-risk non-alcoholic steatohepatitis (NASH) are at increased risk for pre-transplant portal venous thrombosis.METHODSData on all liver transplants in the United States from February 2002 through September 2014 were analyzed. Recipients were sorted into three distinct groups: High-risk (age > 60, body mass index > 30 kg/m2, hypertension and diabetes), low-risk and non-NASH cirrhosis. Multivariable logistic regression models were constructed.RESULTSThirty-five thousand and seventy-two candidates underwent liver transplantation and of those organ recipients, 465 were transplanted for high-risk and 2775 for low-risk NASH. Two thousand six hundred and twenty-six (7.5%) recipients had pre-transplant portal vein thrombosis; 66 (14.2%) of the high-risk NASH group had portal vein thrombosis vs 328 (11.8%) of the low-risk NASH group. In general, all NASH recipients were less likely to be male or African American and more likely to be obese. In adjusted multivariable regression analyses, high-risk recipients had the greatest risk of pre-transplant portal vein thrombosis with OR = 2.11 (95%CI: 1.60-2.76, P < 0.001) when referenced to the non-NASH group.CONCLUSIONLiver transplant candidates with high-risk NASH are at the greatest risk for portal vein thrombosis development prior to transplantation. These candidates may benefit from interventions to decrease their likelihood of clot formation and resultant downstream hepatic decompensating events. Prospective study is needed.

Liver transplant recipients with portal vein thrombosis receiving an organ from a high-risk donor are at an increased risk for graft loss due to hepatic artery thrombosis.

We hypothesize that recipients with pretransplant portal vein thrombosis (PVT) receiving organs from high-risk donors (HRD) are at an increased risk of HAT. Data on all liver transplants in the United States from February 2002 to March 2015 were analyzed. Recipients were sorted into two groups: those with PVT and those without. HRDs were defined by donor risk index (DRI) >1.7. Multivariable logistic regression models were constructed to assess the independent risk factors for HAT with the resultant graft loss ≤90 days from transplantation. A total of 60 404 candidates underwent liver transplantation; of those recipients, 623 (1.0%) had HAT, of which 66.0% (n = 411) received organs from HRDs compared with 49.3% (n = 29 473) in recipients without HAT (P < 0.001); 2250 (3.7%) recipients had pretransplantation PVT and received organs from HRDs. On adjusted multivariable analysis, PVT with a HRD organ was the most significant independent risk factor (OR 3.56, 95% CI 2.52-5.02, P < 0.001) for the development of HAT. Candidates with pretransplant PVT who receive an organ from a HRD are at the highest risk for postoperative HAT independent of other measurable factors. Recipients with pretransplant PVT would benefit from careful donor selection and possibly anticoagulation perioperatively.

429 Liver Transplant Recipients With Pre-Transplant Portal Vein Thrombosis Receiving an Organ From a High-Risk Donor Are at the Highest Risk for Graft Loss Due to Hepatic Artery Thrombosis

429 Liver Transplant Recipients With Pre-Transplant Portal Vein Thrombosis Receiving an Organ From a High-Risk Donor Are at the Highest Risk for Graft Loss Due to Hepatic Artery Thrombosis

Pre-transplant portal vein thrombosis is an independent risk factor for graft loss due to hepatic artery thrombosis in liver transplant recipients

BackgroundHepatic artery thrombosis is an uncommon but catastrophic complication following liver transplantation. We hypothesize that recipients with portal vein thrombosis are at increased risk. MethodsData on all liver transplants in the U.S. during the MELD era through September 2014 were obtained from UNOS. Status one, multivisceral, living donor, re-transplants, pediatric recipients and donation after cardiac death were excluded. Logistic regression models were constructed for hepatic artery thrombosis with resultant graft loss within 90 days of transplantation. Results63,182 recipients underwent transplantation; 662 (1.1%) recipients had early hepatic artery thrombosis; of those, 91 (13.8%) had pre-transplant portal vein thrombosis, versus 7.5% with portal vein thrombosis but no hepatic artery thrombosis (p < 0.0001). Portal vein thrombosis was associated with an increased independent risk of hepatic artery thrombosis (OR 2.17, 95% CI 1.71–2.76, p < 0.001) as was donor risk index (OR 2.02, 95% CI 1.65–2.48, p < 0.001). Heparin use at cross clamp, INR, and male donors were all significantly associated with lower risk. DiscussionPre-transplant portal vein thrombosis is associated with post-transplant hepatic artery thrombosis independent of other factors. Recipients with portal vein thrombosis might benefit from aggressive coagulation management and careful donor selection. More research is needed to determine causal mechanism.

Wow, that portal vein is small: Preventing portal vein thrombosis in liver transplantation for small children

Portal vein thrombosis after pediatric liver transplantation is a common and devastating complication. Occurring in up to 8% of pediatric liver transplant recipients who are less than 15 kg, it frequently leads to graft loss and the need for emergent retransplantation.1, 2 Children with biliary atresia are at particularly high risk and often develop an atretic portal vein; this makes the portal vein anastomosis particularly difficult. Adding further complexity is the frequent use of left lateral segment allografts, which frequently introduce portal vein size mismatching and orientation issues. Several options exist for managing the technical challenges related to portal vein anastomoses. Although the traditional approach has been end-to-end portal vein anastomoses, size differences often make this approach impossible. When this is the case, a proximal mesenteric vein anastomosis, branch vein patch, or donor venoplasty may be necessary to complete the anastomosis.3 When angulation issues result in low portal flow after transplantation, augmentation can be achieved through the ligation of the left renal vein or other mesocentral venous collaterals. Portocaval and porto-arterial anastomoses have also been proposed to increase flow. Although these approaches may effectively lower the risk of portal vein thrombosis after liver transplantation, they are less than optimal solutions for pediatric recipients with diminutive portal veins or preoperative portal vein thrombosis. A potential answer to this issue may be the use of a renoportal anastomosis. This approach has been described in adult liver transplantation with promising results.4 In pediatric patients, we believe that this technique provides a unique solution to issues relating to flow, size, and orientation mismatch. In general, there are no specific criteria for using a renoportal anastomosis; however, we find that size mismatch and portal flow issues are the most frequent indications. If the recipient portal vein measures 2 to 3 mm in size or is less than half the diameter of the donor portal vein, we often consider this technique. Additionally, if the portal vein flow is inadequate despite clamping of the left renal vein, we will also consider this approach. An appropriately sized venous conduit is prepared; this depends on the size relationship between the donor and recipient vessels. Suitable conduits include the external iliac vein, femoral vein, superior mesenteric vein, splenic vein, and saphenous vein (for living donors). The procurement of all these potential conduits is appropriate to facilitate as many technical options as possible during the transplant operation. The transplant hepatectomy proceeds as usual. As much length as possible of the recipient portal vein should be maintained. Before the completion of the hepatectomy and the clamping of the portal vein and inferior vena cava, the left renal vein of the recipient is exposed. On the back table, an end-to-end anastomosis is fashioned between the left portal vein of the donor and the vein conduit. The liver is brought to the field, and the hepatic vein anastomosis is completed. A clamp is placed on the recipient left renal vein toward the kidney, and the vein is ligated at the level of the inferior vena cava. The renoportal anastomosis is created between the conduit and the left renal vein. The clamps are removed, and the liver is reperfused. Once the bleeding is under control, a partial clamp is placed on the side of the vein conduit. An anastomosis is created between the end of the recipient portal vein and the side of the donor conduit (Fig. 1). The portal vein clamp is removed, and the arterial anastomosis is completed. In conclusion, using a renoportal anastomosis for hepatic portal inflow overcomes 2 issues that commonly challenge pediatric liver transplantation in small children. First, the renal vein, the donor left portal vein, and the conduit are well matched in size. Second, there frequently is little flow through the mesenteric venous system of these small children. Using the left renal vein as inflow provides a reliable amount of flow to the allograft. Although the sewing of the donor portal vein to the iliac vein conduit may not be necessary, it dilates with time and frequently becomes the dominant inflow to the liver. Even in the setting of pretransplant portal vein thrombosis, the left renal vein provides adequate inflow and likely also adequate mesenteric venous drainage. Michael J. Englesbe, M.D. Amit K. Mathur, M.D. Seth A. Waits, M.D. John C. Magee, M.D. Section of Transplant Surgery Department of Surgery University of Michigan Ann Arbor, MI

Readmission after living donor liver transplantation: predictors, causes, and outcomes.

Complications following liver transplantation requiring readmission may be serious and potentially life threatening. Most reports on readmission have been about after deceased donor liver transplantation (DDLT). We hypothesized that readmission after living donor liver transplantation (LDLT) is due to different reasons and analyzed our experience. We retrospectively analyzed the records of 172 consecutive patients who underwent liver transplantation at our institute between January 2010 and June 2012. The primary outcome measure was readmission. We classified readmission into early (<3months after discharge) and late (>3months). The study population was 140 after excluding pediatric patients (12), DDLT recipients (2), and those who died during the index admission (18). Their median age was 42years, and there were 117 males and 23 females. Thirty-eight patients were readmitted (56 episodes) after LDLT. There were 35 early and 21 late readmission episodes. The most common cause for early readmissions was infection (46%) and that for late readmissions was biliary stricture (62%). On univariate analysis, pretransplant portal vein thrombosis, more than one bile duct in the liver graft, revised arterial anastomosis or two arteries in the graft, and higher serum alkaline phosphatase levels at discharge were significantly associated with readmission. Readmission was also significantly associated with a higher overall mortality than non-readmission in which there was no mortality. Pretransplant portal vein thrombosis, more than one bile duct in the liver graft, revision of the arterial anastomosis or two arteries in the graft, and higher serum alkaline phosphatase levels at discharge were significantly associated with readmission. Infective and biliary complications were the commonest causes of early and late readmission after LDLT.

JAK2 exon 12 mutations were not found in liver transplant recipients with or without pretransplant portal vein thrombosis

JAK2 exon 12 mutations were not found in liver transplant recipients with or without pretransplant portal vein thrombosis

Obesity is an independent risk factor for pre-transplant portal vein thrombosis in liver recipients

BackgroundPortal vein thrombosis is a frequent complication in end-stage cirrhosis with a considerable peri-operative risk for liver transplant candidates. We aimed to characterize the pre-transplant portal vein thrombosis in a cohort of liver transplant recipients, and to identify independent risk factors for this complication.Methods380 consecutive primary orthotopic liver transplants were performed in the Digestive Surgery Department of “12 de Octubre” Hospital (Madrid, Spain), between January 2001 and December 2006. The main risk factors considered were smoking, obesity, metabolic disorders, previous immobility, surgery or trauma, nephrotic syndrome, associated tumor, inflammatory disease, neoplasm myeloprolipherative. Furthermore we have reported genetic thrombophilia results for 271 recipients.ResultsSixty-two (16.3%) patients developed pre-transplant portal vein thrombosis and its presence had no impact in the overall survival of liver recipients. Obesity was the only independent risk factor for pre-transplant portal vein thrombosis.ConclusionWe recommend close control of cardiovascular factors in patients with liver cirrhosis in order to avoid associated thrombosis.

Portal vein thrombosis, cirrhosis, and liver transplantation

Portal vein thrombosis is not uncommon in candidates for transplantation. Partial thrombosis is more common than complete thrombosis. Despite careful screening at evaluation, a number of patients are still found with previously unrecognized thrombosis per-operatively. The objective is to recanalize the portal vein or, if recanalization is not achievable, to prevent the extension of the thrombus so that a splanchnic vein can be used as the inflow vessel to restore physiological blood flow to the allograft. Anticoagulation during waiting time and transjugular intrahepatic portosystemic shunt (TIPS) are two options to achieve these goals. TIPS may achieve recanalization in patients with complete portal vein thrombosis. However, a marked impairment in liver function, which is a characteristic feature of most candidates for transplantation, may be a contraindication for TIPS. Importantly, the MELD score is artificially increased by the administration of vitamin K antagonists due to prolonged INR. When patency of the portal vein and/or superior mesenteric vein is not achieved, only non-anatomical techniques (renoportal anastomosis or cavoportal hemitransposition) can be performed. These techniques, which do not fully reverse portal hypertension, are associated with higher morbidity and mortality risks. Multivisceral transplantation including the liver and small bowel needs to be evaluated. In the absence of prothrombotic states that may persist after transplantation, there is no evidence that pre-transplant portal vein thrombosis justifies long term anticoagulation post-transplantation, provided portal flow has been restored through conventional end-to-end portal anastomosis.

The Effect of Recipient-Specific Surgical Issues on Outcome of Liver Transplantation in Biliary Atresia

Biliary atresia (BA), the most common reason for orthotopic liver transplantation (OLT) in children, is often accompanied by unique and challenging anatomical variations. This study examines the effect of surgical-specific issues related to the presence of complex vascular anatomic variants on the outcome of OLT for BA. The study group comprised 944 patients who were enrolled in the Studies of Pediatric Liver Transplantation (SPLIT) registry and underwent OLT for BA over an 11-year period. 63 (6.7%) patients met the study definition of complex vascular anomalies (CVA). Patient survival, but not graft survival, was significantly lower in the CVA group, (83 vs. 93 % at 1-year post-OLT). The CVA group had a significantly higher incidence of all reoperations, total biliary tract complications, biliary leaks and bowel perforation. The most frequent cause of death was infection, and death from bacterial infection was more common in the CVA group. Pretransplant portal vein thrombosis and a preduodenal portal vein were significant predictors of patient survival but not graft survival. This study demonstrates that surgical and technical factors have an effect on the outcome of BA patients undergoing OLT. However, OLT in these complex patients is technically achievable with an acceptable patient and graft survival.