Faculty Bibliography

INTRODUCTION:The aim of this study is to investigate large volume therapeutic paracentesis using either a z-tract or axial (coxial) technique in a randomized controlled trial. MATERIALS AND METHODS:In this randomized, single blind study, patients with cirrhosis undergoing outpatient therapeutic paracentesis were randomized to the z-tract or the modified angular (coaxial) needle insertion technique. Subject and procedure characteristics were compared between the groups with ascites leakage as quantified by need for dressing changes with standardized sized gauze pads as a primary endpoint and subject procedural discomfort, operator preference, and procedure complications as secondary endpoints. RESULTS:72 paracenteses were performed during the study period: 34 to the z-tract and 38 to the coaxial insertion technique. Following exclusions, a total of 61 paracenteses were analyzed: 30 using the z-tract technique and 31 using the coaxial technique. There were equal rates of post-procedural leakage of ascites between groups (13% in both groups, p = 1.00). Using the visual analog scale (0 - 100), there was a statistically significant increase in the subject reported pain score with the z-tract compared with the coaxial method [26.4 (95% CI 18.7 - 34.1) vs. 17.2 (95% CI 10.6 - 23.8), p = 0.04]. Mean physician rated procedure difficulty (1 - 5) was significantly higher for the z-tract versus the coaxial technique [2.1 (95% CI 1.6 - 2.6) vs. 1.5 (95% CI 1.2 - 1.8), p = 0.04]. CONCLUSION:When compared to the z-tract technique, the coaxial insertion technique is superior during large volume paracentesis in cirrhosis patients.

AIM/OBJECTIVE:To investigate the incidence of spontaneous bacterial peritonitis (SBP) in pre-transplant patients and its effect on post transplant mortality and graft failure. METHODS:We conducted a retrospective cohort study of patient records from the organ procurement and transplant network data set. Patients were identified by the presence of SBP pre-transplant. Univariate post-transplant survival models were constructed using the Kaplan-Meier technique and multivariate models were constructed using the Cox proportional hazards model. Variables that affected post-transplant graft survival were identified in the SBP population. RESULTS:< 0.017) after liver transplantation. CONCLUSION/CONCLUSIONS:HCV patients prior to the advent of directing acting anti-viral agents had a higher incidence of pre-transplant SBP than other patients on the liver transplant wait list. SBP history pre-transplant resulted in a higher rate of graft loss due to recurrent HCV infection and chronic rejection.

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.

The coagulopathy of liver disease is distinctly different from therapeutic anticoagulation in a patient. Despite stable elevated standard clot-based coagulation assays, nearly all patients with stable chronic liver disease (CLD) have normal or increased clotting. Common unfamiliarity with the limitations of these assays in CLD may lead to inappropriate and sometimes harmful interventions, including blood product transfusions before a procedure. Knowledge of the distinct hemostatic alterations in CLD can allow identification of the small subset of patients with clinically significant coagulopathy who can benefit from hematologic optimization before invasive procedures.

INTRODUCTION/BACKGROUND:Autoimmune-like drug-induced liver injury (DI-AIH) is a rare but serious event with a growing body of scientific evidence and a fair degree of uncertainty. Areas covered: This review covers the definition, pathophysiology, treatment and patient-centered outcomes of DI-AIH and presents up-to-date information on the most commonly implicated drugs. Expert opinion: A high degree of clinical suspicion is required for the diagnosis of DI-AIH. This diagnosis should be considered in any patient with either acute or chronic elevations in liver-associated enzymes. Prevalence rates exceed 15% based on large international registry data. Autoantibodies, while common, are neither specific nor diagnostic of DI-AIH. Histology may be helpful in describing subtle differences between DI-AIH and de novo idiopathic autoimmune hepatitis (iAIH), but oftentimes the two are indistinguishable histologically. Alpha-methyldopa, fibrates, hydralazine, minocycline, nitrofurantoin, HMG-CoA reductase inhibitors (statins), iplimumab and tumor necrosis factor alpha antagonists are the most commonly associated drugs with DI-AIH. Complete recovery of liver injury is most often seen with DI-AIH, however, cases of prolonged injury may occur and may require treatment with immunosuppressive therapy. Relapse following cessation of corticosteroids for suspected DI-AIH should prompt reconsideration of the diagnosis and further exploration into possible iAIH.

BACKGROUND:Hepatic artery thrombosis is an uncommon but catastrophic complication following liver transplantation. We hypothesize that recipients with portal vein thrombosis are at increased risk. METHODS:Data 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. RESULTS:63,182 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. DISCUSSION/CONCLUSIONS:Pre-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.

AIM/OBJECTIVE:To determine the clinical impact of portal vein thrombosis in terms of both mortality and hepatic decompensations (variceal hemorrhage, ascites, portosystemic encephalopathy) in adult patients with cirrhosis. METHODS:We identified original articles reported through February 2015 in MEDLINE, Scopus, Science Citation Index, AMED, the Cochrane Library, and relevant examples available in the grey literature. Two independent reviewers screened all citations for inclusion criteria and extracted summary data. Random effects odds ratios were calculated to obtain aggregate estimates of effect size across included studies, with 95%CI. RESULTS:A total of 226 citations were identified and reviewed, and 3 studies with 2436 participants were included in the meta-analysis of summary effect. Patients with portal vein thrombosis had an increased risk of mortality (OR = 1.62, 95%CI: 1.11-2.36, P = 0.01). Portal vein thrombosis was associated with an increased risk of ascites (OR = 2.52, 95%CI: 1.63-3.89, P < 0.001). There was insufficient data available to determine the pooled effect on other markers of decompensation including gastroesophageal variceal bleeding or hepatic encephalopathy. CONCLUSION/CONCLUSIONS:Portal vein thrombosis appears to increase mortality and ascites, however, the relatively small number of included studies limits more generalizable conclusions. More trials with a direct comparison group are needed.

Portal vein thrombosis (PVT) is a common complication of cirrhosis sometimes implicated in hepatic decompensation. There are no consistent epidemiologic data to suggest an increased risk of thrombotic complications in nonalcoholic steatohepatitis (NASH); however, research suggests an increased risk of thrombosis. Our aim was to examine the independent association between NASH cirrhosis and PVT in patients who underwent liver transplantation (LT) in a cross-sectional study. Data on all LTs occurring in the United States between January 1, 2003 and December 31, 2012 were obtained from the United Network for Organ Sharing. Multivariable models were constructed to assess the statistical associations and risk factors for the development of PVT. A total of 33,368 patients underwent transplantation. Of these, 2096 (6.3%) had PVT. Of the patients with PVT, 12.0% had NASH. When we compared these patients to a composite of all other causes of cirrhosis, an increased prevalence of PVT was again found, with 10.1% having PVT at the time of transplantation versus 6.0% without NASH (P < 0.001). The strongest risk factor independently associated with a diagnosis of PVT in a multivariable analysis was NASH cirrhosis (odds ratio, 1.55; 95% confidence interval, 1.33-1.81; P < 0.001). NASH cirrhosis appears to predispose a patient to PVT independently of other risk factors. These epidemiological findings provide support for the idea that NASH is a prothrombotic state, and they should lead to more research in treatment and prevention in this population.