INTRODUCTION PVT is a common complication seen in about 25% of patients with cirrhosis due to alterations in the coagulation and portal hemodynamic systems. In cirrhosis, chronic PVT is much more common than acute PVT, contributes to portal hypertension, and is associated with the development of collateral circulation. The treatment of PVT is complicated in these patients, due to increased risk of bleeding and lack of universal benefit. This is especially true in patients being considered for liver transplantation, as there is a lack of clear guidance on the management of PVT in this patient population. This guide aims to shed light on the special attention that must be considered when managing cirrhosis in patients with PVT before, during, and after liver transplantation.1 EPIDEMIOLOGY AND NATURAL HISTORY OF PVT IN PERITRANSPLANT PATIENTS The prevalence of PVT is ~1% in compensated cirrhosis but increases up to 8%–25% in liver transplant candidates, with patients with NASH cirrhosis at greatest risk of PVT formation.1 In patients with cirrhosis with PVT who undergo liver transplantation, there is an increased risk of non–graft-related thrombosis, graft death, and post-LT mortality, without a significant increase in waitlist mortality.2,3 Post-LT complications arise more commonly in patients with cirrhosis with complete PVT as compared with partial PVT, especially if there is involvement of the superior mesenteric vein, which is an especially important surgical consideration as this can result in a lack of end-to-end portal vein (PV) anastomosis, subsequently increasing the risk of graft failure. Other key complications to monitor after liver transplant include biliary strictures, gastrointestinal bleeding, or infections.2Figure 1 summarizes the risk factors for PVT development, which are branch points of Virchow’s triad.FIGURE 1: “Shedding light on the key etiologies of PVT in cirrhosis.” Factors leading to PVT are often linked to Virchow’s triad and may present with unique risk factors in patients with cirrhosis.1 Abbreviations: HNT, hypertension.CLASSIFICATION OF PVT In addition to the Sarin classification system as described in Supplemental Figure S1, https://links.lww.com/XCL/A10, it is critical to take into consideration patient symptoms when diagnosing PVT.1,4 Clinical manifestations of acute PVT include nausea, abdominal pain, vomiting, lack of appetite, or diarrhea. Involvement of the superior mesenteric vein and its branches can lead to hematochezia, paralytic ileus, or peritonitis secondary to intestinal ischemia or infarction.1 On the contrary, many chronic PVTs are discovered incidentally on imaging without any particular symptom manifestation. Finally, PVTs can lead to hepatic decompensation and should be part of an evaluation in a newly decompensated patient with cirrhosis. DIAGNOSIS OF PVT AND TREATMENT The diagnosis of PVT is a radiologic diagnosis with the gold standard being Doppler ultrasound.5 Contrasted MRI can further determine flow within the portal venous system and assess for cavernoma presence.5 The prevalence of prothrombic mutations and conditions such as JAK2 mutation, factor V Leiden, and paroxysmal nocturnal hemoglobinuria are more common in patients with cirrhosis who develop PVT than patients with cirrhosis who do not develop PVT. Despite this finding, there is no specific guidance to pursue a hypercoagulability workup in this patient population given the provoked nature of PVT formation in the setting of cirrhosis-associated hypercoagulability derangements. Cases of PVT warrant a screening endoscopy within 2–3 months of diagnosis to assess variceal burden in need of eradication.5,6 Once screened, treatment should be offered in cases of acute PVT. In cases of chronic PVT, it is reasonable to discuss with the multidisciplinary transplant team regarding the benefits and risks of anticoagulation.5,6 Risk of PVT development after liver transplant is greatest in those with extensive PVT before liver transplant, history of severe portal hypertension, mismatch of recipient and donor PV, failure to achieve adequate anastomosis, or a high number of portosystemic collaterals. Thus, patients who fit this criterion should be considered for treatment with anticoagulation after liver transplant to reduce the risk of PVT post-transplant. Post-transplant anticoagulation practices have yet to be clearly defined resulting in various approaches.3 However, the Baveno VI guidelines recommend anticoagulation therapy in patients with chronic PVT to decrease post-transplant complications and mortality. Therefore, it is generally accepted that patients who are candidates for liver transplant qualify for pretransplant anticoagulation to prevent post-transplant complications. Therapy options include direct oral anticoagulants (DOACs), vitamin K antagonists, or low–molecular-weight heparin, with each class providing advantages and disadvantages. Warfarin may be difficult to use in patients with cirrhosis as they may already have elevated international normalized ratio (INR). However, the reversibility with fresh frozen plasma provides an advantage over DOACs. Low–molecular-weight heparin is an injectable drug and needs to be dose adjusted in renal disease, but it does not require routine monitoring as would be needed in warfarin use. Finally, DOACs such as apixaban or rivaroxaban do not require routine monitoring, are not injectable, and are well tolerated in mild to moderate renal disease. However, DOACs are restricted to Child A patients and should be carefully considered in Child B or C patients as patients with cirrhosis have disruptions in their normal drug metabolism pathways, which may alter the pharmacokinetics of DOAC therapy.1 In patients undergoing liver transplant, the most common anticoagulation therapy is LWMH, but warfarin is often preferred due to its reversibility in the case of an organ offer.5 Given the increased risk of mortality in the postoperative period, it is recommended to anticoagulate after liver transplant to prevent the risk of thrombosis formation.5 Other PVT treatments as detailed in Figure 2 include thrombolytic therapy or PV recanalization. Thrombolytic therapy is often not pursued due to the increased complications after this procedure.5 However, TIPS creation usually leads to a decrease in portal hypertension symptoms by producing a shunt between the hepatic vein and PV.2 TIPS has been quite successful in patients with cirrhosis where some studies demonstrate >80% resolution of PVT.5 Patients who typically qualify for TIPS include those who fail to respond to anticoagulation or have severe portal venous system hypertension.5FIGURE 2: “Crafting accurate treatments for a patient with cirrhosis and PVT.” Treatment algorithm for a patient with cirrhosis and PVT based on PVT timing onset, extent of occlusion of the portal venous system, and response to therapy based on follow-up imaging.7 Abbreviations: PV, portal vein; SMV, superior mesenteric veins.OUTCOMES OF PVT IN LIVER TRANSPLANT PATIENTS Patients with PVT undergoing liver transplant are at an increased risk of complications, but these risks can be mitigated with appropriate therapy. A study examining the OPTN waitlist demonstrated an increased risk of post-transplant PVT in those with cryptogenic cirrhosis, diabetes mellitus, obesity, fatty liver disease, or ascites.8 Immediately after liver transplant, patients who previously had a PVT are at an increased risk of thrombosis recurrence with some studies denoting a 4%–39% risk of PVT redevelopment.7 A study by Zanetto and colleagues discovered that the rate of 1-year mortality was greater for patients with prior PVT at 13.5% as compared with 9.9% for patients without PVT after liver transplant.7,9 Yeo et al2 discovered that preoperative PVT grade 3 and 4 was associated with an increase in graft loss (HR: 1.58) and patient mortality (HR: 1.45), thought to be due to the requirement of extra-anatomic reconstruction in these patients during surgery. In addition, nonanatomical anastomoses, such as autologous veins, artificial grafts, cadaveric veins or arteries, or polytetrafluoroethylene increase the risk of post-transplant PVT due to the potential of graft kink formation, or anastomoses mismatch leading to portal venous stasis.7,9 A study by Yerdel et al determined that grade 2 and 3 PVT cases after medical or surgical thrombus elimination with subsequent creation of a successful end porto-portal anastomoses have similar outcomes to non-PVT comparator arms.10 In addition, patients with preoperative PVT grade 3 and 4 have an increased risk of developing post-transplant PVT; thus, initiation of prophylaxis anticoagulation should be carefully considered before liver transplant.2 Together these findings illustrate the critical nature of PVT treatment in liver transplant candidates to improve their long-term mortality and morbidity. CONCLUSION PVT used to be a significant barrier for patients who were seeking liver transplantation. As time has progressed, patients with PVT who have close follow-up can have similar mortality and graft survival outcomes to their non-PVT peers. This has been due to the evolution of anticoagulation management along with surgical techniques. However, it is imperative that PVT status be taken into consideration when caring for liver transplant patients in the postoperative period to decrease their risk of complications. Detailed care of this special patient population is essential for their long-term outcomes measured as mortality and morbidity to be optimized.